Trauma.mattox.7th.ed..pdf

TRAUMA

NOTICE Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required. The authors and the publisher of this work have checked with sources believed to be reliable in their efforts to provide information that is complete and generally in accord with the standards accepted at the time of publication. However, in view of the possibility of human error or changes in medical sciences, neither the authors nor the publisher nor any other party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of the information contained in this work. Readers are encouraged to confirm the information contained herein with other sources. For example and in particular, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this work is accurate and that changes have not been made in the recommended dose or in the contraindications for administration. This recommendation is of particular importance in connection with new or infrequently used drugs.

TRAUMA Seventh Edition

Editors Kenneth L. Mattox, MD Distinguished Service Professor Baylor College of Medicine Michael E. DeBakey Department of Surgery Chief of Staff Chief of Surgery Ben Taub General Hospital Houston, Texas

Ernest E. Moore, MD Professor and Vice Chairman Department of Surgery University of Colorado at Denver and Health Sciences Center Bruce M. Rockwell Distinguished Chair of Trauma Surgery Rocky Mountain Regional Trauma Center Chief of Surgery Denver Health Medical Center Denver, Colorado

David V. Feliciano, MD Attending Surgeon, Atlanta Medical Center Atlanta, Georgia Attending Surgeon, Medical Center of Central Georgia Macon, Georgia Professor of Surgery Mercer University School of Medicine Macon, Georgia Adjunct Professor of Surgery Uniformed Services University of the Health Sciences Bethesda, Maryland

ERRNVPHGLFRVRUJ New York Chicago San Francisco Lisbon London Madrid Mexico City Milan New Delhi San Juan Seoul Singapore Sydney Toronto

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DEDICATION The editors of Trauma, Seventh Edition, gratefully dedicate this edition to our five unique “families”: our spouses, children, grandchildren, and extended families; our trainees, who now dot the globe—our lasting legacy; our medical schools and academic anchors; our organizations and associations; and our patients, who continue to teach us so very much.

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CONTENTS Contributors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .xi Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .xix

SECTION 1 TRAUMA OVERVIEW 1. Kinematics . . . . . . . . . . . . . . . . . . . . . . . . . 2 John P. Hunt, Alan B. Marr, and Lance E. Stuke

4. Trauma Systems, Triage, and Transport . . 54 Raul Coimbra, David B. Hoyt, and Vishal Bansal

2. Epidemiology . . . . . . . . . . . . . . . . . . . . . 18 Thomas J. Esposito and Karen J. Brasel

3. Injury Prevention. . . . . . . . . . . . . . . . . . . 36 Ronald V. Maier and Charles Mock

5. Injury Severity Scoring and Outcomes Research . . . . . . . . . . . . . . . . . 77 Robert D. Becher, J. Wayne Meredith, and Patrick D. Kilgo

6. Acute Care Surgery . . . . . . . . . . . . . . . . . 91 Gregory J. Jurkovich

SECTION 2 GENERALIZED APPROACHES TO THE TRAUMATIZED PATIENT 7. Prehospital Care . . . . . . . . . . . . . . . . . . 100 Jeffrey P. Salomone and Joseph A. Salomone III

8. Disaster and Mass Casualty . . . . . . . . . . 123 Eric R. Frykberg and William P. Schecter

9. Rural Trauma . . . . . . . . . . . . . . . . . . . . . 140 Charles F. Rinker II and Nels D. Sanddal

10. Initial Assessment and Management . . 154 Panna A. Codner and Karen J. Brasel

11. Airway Management . . . . . . . . . . . . . . 167 Eric A. Toschlog, Scott G. Sagraves, and Michael F. Rotondo

12. Management of Shock . . . . . . . . . . . . . 189 Louis H. Alarcon, Juan Carlos Puyana, and Andrew B. Peitzman

13. Postinjury Hemotherapy and Hemostasis . . . . . . . . . . . . . . . . . . . 216 Fredric M. Pieracci, Jeffry L. Kashuk, and Ernest E. Moore

14. Emergency Department Thoracotomy . . . 236 Clay Cothren Burlew and Ernest E. Moore

15. Diagnostic and Interventional Radiology . . 251 Salvatore J.A. Sclafani

16. Surgeon-Performed Ultrasound in Acute Care Surgery . . . . . . . . . . . . . . 301 Christopher J. Dente and Grace S. Rozycki

17. Principles of Anesthesia and Pain Management . . . . . . . . . . . . . . . . . 322 Dirk Younker

18. Infections . . . . . . . . . . . . . . . . . . . . . . . 330 Michael A. West and Daniel Dante Yeh vii

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Contents

SECTION 3 MANAGEMENT OF SPECIFIC INJURIES 19. Injury to the Brain . . . . . . . . . . . . . . . . . 356 Alexander F. Post, Thomas Boro, and James M. Ecklund

20. Eye . . . . . . . . . . . . . . . . . . . . . . . . . . . . 377 Petros E. Carvounis and Yvonne I. Chu

21. Face . . . . . . . . . . . . . . . . . . . . . . . . . . . . 395 Robert M. Kellman

22. Neck . . . . . . . . . . . . . . . . . . . . . . . . . . . 414 David V. Feliciano and Gary A. Vercruysse

23. Vertebrae and Spinal Cord . . . . . . . . . . 430 Maneesh Bawa and Reginald Fayssoux

24. Trauma Thoracotomy: Principles and Techniques . . . . . . . . . . . 461 Kenneth L. Mattox, Matthew J. Wall, Jr., and Peter Tsai

25. Lung, Trachea, and Esophagus . . . . . . . 468 Joseph A. DuBose, James V. O’Connor, and Thomas M. Scalea

26. Heart and Thoracic Vascular Injuries . . . . 485 Matthew J. Wall, Jr., Peter Tsai, and Kenneth L. Mattox

27. Trauma Laparotomy: Principles and Techniques . . . . . . . . . . . 512 Asher Hirshberg

28. Diaphragm . . . . . . . . . . . . . . . . . . . . . . 529 Kevin M. Schuster and Kimberly A. Davis

29. Liver and Biliary Tract . . . . . . . . . . . . . . 539 Timothy C. Fabian and Tiffany K. Bee

30. Injury to the Spleen . . . . . . . . . . . . . . . 561 David H. Wisner

31. Stomach and Small Bowel . . . . . . . . . . 581 Lawrence N. Diebel

32. Duodenum and Pancreas . . . . . . . . . . . 603 Walter L. Biffl

33. Colon and Rectal Trauma . . . . . . . . . . . 620 Demetrios Demetriades and Kenji Inaba

34. Abdominal Vascular Injury . . . . . . . . . . 632 Christopher J. Dente and David V. Feliciano

35. Pelvis . . . . . . . . . . . . . . . . . . . . . . . . . . . 655 George C. Velmahos

36. Genitourinary Trauma . . . . . . . . . . . . . . 669 Michael Coburn

37. Trauma in Pregnancy . . . . . . . . . . . . . . 709 M. Margaret Knudson and Daniel Dante Yeh

38. Trauma Damage Control . . . . . . . . . . . . 725 Amy D. Wyrzykowski and David V. Feliciano

39. Upper Extremity . . . . . . . . . . . . . . . . . . 747 Nata Parnes, Peleg Ben-Galim, and David Netscher

40. Lower Extremity . . . . . . . . . . . . . . . . . . 783 Philip F. Stahel, Wade R. Smith, and David J. Hak

41. Peripheral Vascular Injury . . . . . . . . . . . 816 Michael J. Sise and Steven R. Shackford

Contents

SECTION 4 SPECIFIC CHALLENGES IN TRAUMA 42. Alcohol and Drugs . . . . . . . . . . . . . . . . . 850 Larry M. Gentilello

43. The Pediatric Patient . . . . . . . . . . . . . . . 859 David W. Tuggle and Nathaniel S. Kreykes

44. The Geriatric Patient . . . . . . . . . . . . . . . 874 Jay A. Yelon

45. Ethics of Acute Care Surgery . . . . . . . . . 886 Laurence B. McCullough

46. Social Violence . . . . . . . . . . . . . . . . . . . 890 James W. Davis

47. Wounds, Bites, and Stings. . . . . . . . . . . 896 Charles A. Adams, Jr., Daithi S. Heffernan, and William G. Cioffi

49. Temperature-Related Syndromes: Hyperthermia, Hypothermia, and Frostbite . . . . . . . . . . . . . . . . . . . . . 938 David H. Ahrenholz

50. Organ Procurement for Transplantation . . . 944 Aditya K. Kaza and Max B. Mitchell

51. Rehabilitation . . . . . . . . . . . . . . . . . . . . 950 Paul F. Pasquina, Caitlin L. McAuliffe, and Kevin F. Fitzpatrick

52. Modern Combat Casualty Care . . . . . . . 964 Jay Johannigman, Peter Rhee, Donald Jenkins, and John B. Holcomb

53. Genomics and Acute Care Surgery . . . . 991 Grant E. O’Keefe and J. Perren Cobb

48. Burns and Radiation . . . . . . . . . . . . . . . 922 Jong O. Lee and David N. Herndon

54. Trauma, Medicine, and the Law . . . . . . 997 Kenneth L. Mattox and Stacey A. Mitchell

SECTION 5 MANAGEMENT OF COMPLICATIONS AFTER TRAUMA 55. Principles of Critical Care . . . . . . . . . . . 1006 Raul Coimbra, Jay Doucet, and Vishal Bansal

56. Cardiovascular Failure . . . . . . . . . . . . . 1041 Mary Margaret Wolfe and Fred Luchette

57. Respiratory Insufficiency . . . . . . . . . . . 1055 Jeffrey L. Johnson and James B. Haenel

58. Gastrointestinal Failure . . . . . . . . . . . . 1073 Rosemary A. Kozar and Frederick A. Moore

59. Renal Failure . . . . . . . . . . . . . . . . . . . . 1084 Charles E. Lucas, Michael T. White, and Anna M. Ledgerwood

60. Nutritional Support and Electrolyte Management . . . . . . . . . . . . . . . . . . . . 1100 Kenneth A. Kudsk and Caitlin Curtis

61. Multiple Organ Failure. . . . . . . . . . . . . 1128 Angela Sauaia, Frederick A. Moore, and Ernest E. Moore

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Contents

SECTION 6 ATLAS OF TRAUMA Introduction to the Atlas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1148 Head and Neck . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1149 Thoracic Outlet and Chest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1155 Abdomen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1175 Vascular . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1192

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1201

CONTRIBUTORS Charles A. Adams, Jr., MD, FACS

Peleg Ben-Galim, MD

Assistant Professor of Surgery Alpert Medical School of Brown University Chief Division of Trauma and Surgical Critical Care Department of Surgery Rhode Island Hospital Providence, Rhode Island Chapter 47: Wounds, Bites, and Stings

Assistant Professor Department of Orthopedic Surgery Baylor College of Medicine Houston, Texas Chapter 39: Upper Extremity

David H. Ahrenholz, MD, FACS Associate Professor of Surgery University of Minnesota Medical School St. Paul, Minnesota Chapter 49: Temperature-Related Syndromes: Hyperthermia, Hypothermia, and Frostbite

Louis H. Alarcon, MD Associate Professor of Surgery and Critical Care Medicine Medical Director of Trauma Surgery University of Pittsburgh Pittsburgh, Pennsylvania Chapter 12: Management of Shock

Vishal Bansal, MD, FACS Assistant Professor of Surgery Assistant Director Trauma Services University of California, San Diego San Diego, California Chapter 4: Trauma Systems, Triage, and Transport Chapter 55: Principles of Critical Care

Maneesh Bawa, MD San Diego Orthopaedic Associates/Mercy Hospital San Diego, California Assistant Professor Chief of Trauma Spine Surgery Emory University Department of Orthopaedic Surgery Atlanta, Georgia Chapter 23: Vertebrae and Spinal Cord

Robert D. Becher, MD Howard H. Bradshaw Surgical Research Fellow Department of General Surgery Wake Forest University School of Medicine Winston-Salem, North Carolina Chapter 5: Injury Severity Scoring and Outcomes Research

Tiffany K. Bee, MD Associate Professor of Surgery University of Tennessee Health Science Center Memphis, Tennessee Chapter 29: Liver and Biliary Tract

Walter L. Biffl, MD Professor of Surgery Denver Health Medical Center University of Colorado School of Medicine Denver, Colorado Chapter 32: Duodenum and Pancreas

Thomas Boro, MD Chief Trauma Resident Department of Surgery Inova Fairfax Hospital Falls Church, Virginia Chapter 19: Injury to the Brain

Karen J. Brasel, MD, MPH Professor of Surgery, Bioethics and Humanities Medical College of Wisconsin Milwaukee, Wisconsin Chapter 2: Epidemiology Chapter 10: Initial Assessment and Management

Clay Cothren Burlew, MD Director Surgical Intensive Care Unit Associate Professor of Surgery Denver, Colorado Chapter 14: Emergency Department Thoracotomy

Petros E. Carvounis, MD Assistant Professor Baylor College of Medicine Houston, Texas Chapter 20: Eye

Yvonne I. Chu, MD Assistant Professor Baylor College of Medicine Houston, Texas Chapter 20: Eye

William G. Cioffi, MD J. Murray Beardsley Professor and Chairman Department of Surgery Alpert Medical School of Brown University Surgeon-in-Chief Rhode Island Hospital Providence, Rhode Island Chapter 47: Wounds, Bites, and Stings

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Contributors J. Perren Cobb, MD, PhD

Demetrios Demetriades, MD, PhD, FACS

Director Critical Care Center Massachusetts General Hospital Associate Professor of Anaesthesia and Surgery Harvard Medical School Boston, Massachusetts Chapter 53: Genomics and Acute Care Surgery

Professor and Vice-Chairman of Surgery University of Southern California Director of Trauma Division of Emergency Surgery and Surgical Intensive Care Unit Los Angeles County and University of Southern California Medical Center Sierra Madre, California Chapter 33: Colon and Rectal Trauma

Michael Coburn, MD Professor and Chair Scott Department of Urology Baylor College of Medicine Chief of Urology Ben Taub General Hospital Houston, Texas Chapter 36: Genitourinary Trauma

Panna A. Codner, MD, FACS Assistant Professor Department of Surgery Medical College of Wisconsin Milwaukee, Wisconsin Chapter 10: Initial Assessment and Management

Raul Coimbra, MD, PhD, FACS The Monroe E. Trout Professor of Surgery Executive Vice-Chairman Department of Surgery Chief Division of Trauma, Surgical Critical Care, and Burns Director Surgical Critical Care Fellowship Program University of California San Diego School of Medicine San Diego, California Chapter 4: Trauma Systems, Triage, and Transport Chapter 55: Principles of Critical Care

Caitlin Curtis, MD Nutrition Support Pharmacist University of Wisconsin Hospital and Clinics Madison, Wisconsin Chapter 60: Nutritional Support and Electrolyte Management

James W. Davis, MD, FACS Professor of Clinical Surgery University of California, San Francisco, Fresno Chief of Trauma Community Regional Medical Center Fresno, California Chapter 46: Social Violence

Kimberly A. Davis, MD, FACS, FCCM Associate Professor of Surgery Vice Chair for Clinical Affairs Chief of the Section of Trauma, Surgical Critical Care and Surgical Emergencies Department of Surgery Yale University School of Medicine New Haven, Connecticut Chapter 28: Diaphragm

Christopher J. Dente, MD, FACS Assistant Professor of Surgery Emory University School of Medicine Associate Director of Trauma Grady Memorial Hospital Atlanta, Georgia Chapter 16: Surgeon-Performed Ultrasound in Acute Care Surgery Chapter 34: Abdominal Vascular Injury

Lawrence N. Diebel, MD Professor of Surgery Department of Surgery Wayne State University School of Medicine Detroit, Michigan Chapter 31: Stomach and Small Bowel

Jay Doucet, MD, MSc, FRCSC, FACS Associate Professor of Clinical Surgery Director Surgical Intensive Care Unit University of California, San Diego San Diego, California Chapter 55: Principles of Critical Care

Joseph A. DuBose, MD Major USAF MC University of Maryland Medical System R Adams Cowley Shock Trauma Center Air Force/C-STARS Baltimore, Maryland Chapter 25: Lung, Trachea, and Esophagus

James M. Ecklund, MD, FACS Chairman Department of Neurosciences Inova Fairfax Hospital Medical Director Neurosciences Inova Health System Professor of Surgery Uniformed Services University Professor of Neurosurgery George Washington University Professor of Neurosurgery Virginia Commonwealth University, School of Medicine – Inova Campus Falls Church, Virginia Chapter 19: Injury to the Brain

Contributors Thomas J. Esposito, MD, MPH

James B. Haenel, RRT

Professor and Chief Division of Trauma, Surgical Critical Care & Burns Department of Surgery Director Injury Analysis & Prevention Programs Loyola University Burn & Shock Trauma Institute Loyola University Stritch School of Medicine Maywood, Illinois Chapter 2: Epidemiology

Surgical Critical Care Specialist Department of Surgery Denver Health Medical Center Denver, Colorado Chapter 57: Respiratory Insufficiency

Timothy C. Fabian, MD, FACS Harwell Wilson Professor and Chairman Department of Surgery University of Tennessee Health Sciences Center Memphis, Tennessee Chapter 29: Liver and Biliary Tract

Reginald Fayssoux, MD Eisenhower Medical Center Rancho Mirage, California Chapter 23: Vertebrae and Spinal Cord

David V. Feliciano, MD Attending Surgeon, Atlanta Medical Center Atlanta, Georgia Attending Surgeon, Medical Center of Central Georgia Macon, Georgia Professor of Surgery Mercer University School of Medicine Macon, Georgia Adjunct Professor of Surgery Uniformed Services University of the Health Sciences Bethesda, Maryland Chapter 22: Neck Chapter 34: Abdominal Vascular Injury Chapter 38: Trauma Damage Control

Kevin F. Fitzpatrick, MD Physiatrist Inova Fairfax Hospital Falls Church, Virginia Major U.S. Army Medical Corps Walter Reed Army Medical Center Washington, District of Columbia Chapter 51: Rehabilitation

Eric R. Frykberg, MD, FACS Professor of Surgery University of Florida College of Medicine Chief Division of General Surgery Shands Jacksonville Medical Center Jacksonville, Florida Chapter 8: Disaster and Mass Casualty

Larry M. Gentilello, MD Professor of Surgery University of Texas Texas Chapter 42: Alcohol and Drugs

David J. Hak, MD Professor Department of Orthopaedic Surgery Denver Health Medical Center University of Colorado School of Medicine Denver, Colorado Chapter 40: Lower Extremity

Daithi S. Heffernan, MD, AFRCSI Department of Surgery Division of Trauma and Surgical Critical Care Rhode Island Hospital Assistant Professor of Surgery Brown University Providence, Rhode Island Chapter 47: Wounds, Bites, and Stings

David N. Herndon, MD Jesse H. Jones Distinguished Chair in Burn Surgery Professor of Surgery Chief of Staff Shriners Hospitals for Children University of Texas Medical Branch Galveston, Texas Chapter 48: Burns and Radiation

Asher Hirshberg, MD, FACS Professor of Surgery SUNY Downstate College of Medicine Director Emergency Vascular Surgery Kings County Hospital Center Brooklyn, New York Chapter 27: Trauma Laparotomy: Principles and Techniques

John B. Holcomb, MD, FACS Vice Chair and Professor of Surgery Chief Division of Acute Care Surgery Director Center for Translational Injury Research Jack H. Mayfield, M.D. Chair in Surgery University of Texas Health Science Center Houston, Texas Chapter 52: Modern Combat Casualty Care

David B. Hoyt, MD Executive Director American College of Surgeons Chicago, Illinois Chapter 4: Trauma Systems, Triage, and Transport

John P. Hunt, MD, MPH Professor of Surgery Louisiana State University Health Science Center New Orleans, Louisiana Chapter 1: Kinematics

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Contributors Kenji Inaba, BS, MS, MD, FRCSC, FACS

Patrick D. Kilgo, MS

Assistant Professor of Surgery University of Southern California Medical Director Surgical Critical Care Fellowship Program Division of Trauma, Emergency Surgery and Surgical Intensive Care Unit Los Angeles and University of Southern California Medical Center Los Angeles, California Chapter 33: Colon and Rectal Trauma

Senior Associate Faculty Department of Biostatistics Emory University School of Public Health Atlanta, Georgia Chapter 5: Injury Severity Scoring and Outcomes Research

Donald Jenkins, MD Consultant Division of Trauma, Critical Care and General Surgery Associate Professor of Surgery College of Medicine Medical Director Trauma Center Mayo Clinic Rochester, Minnesota Chapter 52: Modern Combat Casualty Care

Jay Johannigman, MD Professor of Surgery University of Cincinnati College of Medicine Cincinnati, Ohio Chapter 52: Modern Combat Casualty Care

Jeffrey L. Johnson, MD Associate Professor of Surgery University of Colorado Denver Denver, Colorado Chapter 57: Respiratory Insufficiency

Gregory J. Jurkovich, MD Professor of Surgery University of Washington Chief of Trauma Harborview Medical Center Seattle, Washington Chapter 6: Acute Care Surgery

Jeffry L. Kashuk, MD, FACS Associate Professor of Surgery University of Colorado Denver Health Medical Center Trauma, Acute Care Surgery and Surgical Critical Care Denver, Colorado Chapter 13: Postinjury Hemotherapy and Hemostasis

Aditya K. Kaza, MD Assistant Professor of Surgery University of Utah and Primary Children’s Medical Center Salt Lake City, Utah Chapter 50: Organ Procurement for Transplantation

Robert M. Kellman, MD, FACS Professor and Chair SUNY Upstate Medical University Syracuse, New York Chapter 21: Face

M. Margaret Knudson, MD Professor of Surgery University of California, San Francisco San Francisco, California Chapter 37: Trauma in Pregnancy

Rosemary A. Kozar, MD Professor of Surgery The University of Texas Medical School at Houston Houston, Texas Chapter 58: Gastrointestinal Failure

Nathaniel S. Kreykes, MD Surgeon Pediatric Surgical Associates, LTD Minneapolis, Minnesota Chapter 43: The Pediatric Patient

Kenneth A. Kudsk, MD Professor of Surgery University of Wisconsin-Madison Madison, Wisconsin Chapter 60: Nutritional Support and Electrolyte Management

Anna M. Ledgerwood, MD Professor of Surgery Wayne State University School of Medicine-Trauma Medical Director Detroit Receiving Hospital Detroit, Michigan Chapter 59: Renal Failure

Jong O. Lee, MD Associate Professor of Surgery Annie Laurie Howard Chair in Burn Surgery University of Texas Medical Branch Attending Surgeon Shriners Hospitals for Children Galveston, Texas Chapter 48: Burns and Radiation

Charles E. Lucas, MD Professor Department of Surgery Wayne State University Detroit, Michigan Chapter 59: Renal Failure

Fred Luchette, MD The Ambrose and Gladys Bowyer Professor of Surgery Loyola University Chicago Stritch School of Medicine Maywood, Illinois Chapter 56: Cardiovascular Failure

Contributors Ronald V. Maier, MD, FACS

Charles Mock, MD, PhD

Jane and Donald D. Trunkey Professor and Vice Chair Department of Surgery University of Washington Surgeon-in-Chief Harborview Medical Center Seattle, Washington Chapter 3: Injury Prevention

Professor Department of Surgery and Department of Epidemiology Harborview Injury Prevention and Research Center University of Washington Seattle, Washington Chapter 3: Injury Prevention

Alan B. Marr, MD, FACS

Professor and Vice Chairman Department of Surgery University of Colorado at Denver and Health Sciences Center Bruce M. Rockwell Distinguished Chair of Trauma Surgery Rocky Mountain Regional Trauma Center Chief of Surgery Denver Health Medical Center Denver, Colorado Chapter 13: Postinjury Hemotherapy and Hemostasis Chapter 14: Emergency Department Thoracotomy Chapter 61: Multiple Organ Failure

Professor of Clinical Surgery Vice Chairman of Education and Informatics Louisiana State Univeristy Health Sciences Center at New Orleans Attending in Trauma and Critical Care Medical Center of Louisiana in New Orleans New Orleans, Louisiana Chapter 1: Kinematics

Kenneth L. Mattox, MD Distinguished Service Professor Baylor College of Medicine Michael E. DeBakey Department of Surgery Chief of Staff Chief of Surgery Ben Taub General Hospital Houston, Texas Chapters 24: Trauma Thoracotomy: Principles and Techniques Chapters 26: Heart and Thoracic Vascular Injuries Chapters 54: Trauma, Medicine, and the Law

Ernest E. Moore, MD

Frederick A. Moore, MD Professor of Surgery The Methodist Hospital Research Institute Chief, Division of Acute Care Surgery and Critical Care The Methodist Hospital Houston, Texas Chapters 58: Gastrointestinal Failure Chapters 61: Multiple Organ Failure

Caitlin L. McAuliffe, BS

David Netscher, MD

Research Assistant Center for Neuroscience and Regenerative Medicine Uniformed Services University of the Health Sciences Bethesda, Maryland Chapter 51: Rehabilitation

Clinic Professor Division of Plastic Surgery Professor Department of Orthopedic Surgery Chief of Hand Surgery Baylor College of Medicine Houston, Texas Chapter 39: Upper Extremity

Laurence B. McCullough, PhD Dalton Tomlin Chair in Medical Ethics and Health Policy Center for Medical Ethics and Health Policy Baylor College of Medicine Houston, Texas Chapter 45: Ethics of Acute Care Surgery

J. Wayne Meredith, MD Richard T. Myers Professor and Chair Department of General Surgery Director Division of Surgical Sciences Wake Forest University School of Medicine Winston-Salem, North Carolina Chapter 5: Injury Severity Scoring and Outcomes Research

Max B. Mitchell, MD Professor of Surgery University of Colorado at Denver and Children’s Hospital Colorado Heart Institute Aurora, Colorado Chapter 50: Organ Procurement for Transplantation

Stacey A. Mitchell, DNP, MBA, RN, SANE-A, SANE-P Director Forensic Nursing Services Harris County Hospital District Houston, Texas Chapter 54: Trauma, Medicine, and the Law

James V. O’Connor, MD, FACS Trauma Medical Director CaroMont Health Gastonia, North Carolina Chapter 25: Lung, Trachea, and Esophagus

Grant E. O’Keefe, MD Professor Department of Surgery University of Washington Harborview Medical Center Seattle, Washington Chapter 53: Genomics and Acute Care Surgery

Nata Parnes, MD Director Tri-County Orthopaedics Carthage Area Hospital Carthage, New York Chapter 39: Upper Extremity

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Contributors Paul F. Pasquina, MD

Scott G. Sagraves, MD, FACS

Colonel U.S. Army Medical Corps Chief Department of Orthopaedics and Rehabilitation Walter Reed National Military Medical Center Washington, District of Columbia Chapter 51: Rehabilitation

Chief Division of Trauma and Surgical Critical Care Associate Professor of Surgery Brody School of Medicine at East Carolina University Greenville, North Carolina Chapter 11: Airway Management

Andrew B. Peitzman, MD

Associate Professor of Surgery Emory University School of Medicine Deputy Chief of Surgery Grady Memorial Hospital Atlanta, Georgia Chapter 7: Prehospital Care

Mark M. Ravitch Professor Executive Vice-Chair Department of Surgery University of Pittsburgh Pittsburgh, Pennsylvania Chapter 12: Management of Shock

Fredric M. Pieracci, MD, MPH Assistant Professor of Surgery Denver Health Medical Center University of Colorado School of Medicine Denver, Colorado Chapter 13: Postinjury Hemotherapy and Hemostasis

Alexander F. Post, MD Assistant Professor George Washington University and Virginia Commonwealth University Pediatric Neurosurgery Department of Neuroscience Inova Fairfax Hospital Falls Church, Virginia Chapter 19: Injury to the Brain

Juan Carlos Puyana, MD, FACS, FACCP, FRCSC Director Global Health – Surgery Associate Professor Surgery and Clinical Translational Science University of Pittsburgh President Pan-American Trauma Society Pittsburgh, Pennsylvania Chapter 12: Management of Shock

Peter Rhee, MD, MPH, FACS, FCCM, DMCC Professor of Surgery Chief of Trauma, Critical Care, Emergency Surgery University of Arizona Tucson, Arizona Chapter 52: Modern Combat Casualty Care

Charles F. Rinker II, MD, FACS Adjunct Clinical Professor of Medicine Montana State University Bozeman, Montana Chapter 9: Rural Trauma

Michael F. Rotondo, MD, FACS Professor and Chair Department of Surgery Brody School of Medicine at East Carolina University Greenville, North Carolina Chapter 11: Airway Management

Grace S. Rozycki, MD, RDMS, FACS Professor of Surgery Emory University School of Medicine and Grady Memorial Hospital Atlanta, Georgia Chapter 16: Surgeon-Performed Ultrasound in Acute Care Surgery

Jeffrey P. Salomone, MD, FACS, NREMT-P

Joseph A. Salomone III, MD, FAAEM Associate Professor of Emergency Medicine University of Missouri Kansas City School of Medicine EMS Medical Director Kansas City Fire Department Kansas City, Missouri Chapter 7: Prehospital Care

Nels D. Sanddal, MS, REMT-B President and CEO Critical Illness and Trauma Foundation Bozeman, Montana Chapter 9: Rural Trauma

Angela Sauaia, MD, PhD Associate Professor of Medicine Public Health and Surgery Department of Surgery University of Colorado Denver, School of Medicine Aurora, Colorado Chapter 61: Multiple Organ Failure

Thomas M. Scalea, MD Physician-in-Chief R Adams Cowley Shock Trauma Center Baltimore, Maryland Chapter 25: Lung, Trachea, and Esophagus

William P. Schecter, MD, FACS Professor of Clinical Surgery University of California, San Francisco San Francisco General Hospital San Francisco, California Chapter 8: Disaster and Mass Casualty

Kevin M. Schuster, MD, FACS Assistant Professor of Surgery Section of Trauma, Surgical Critical Care and Surgical Emergencies Department of Surgery Yale University School of Medicine New Haven, Connecticut Chapter 28: Diaphragm

Salvatore J.A. Sclafani, MD Professor and Chairman of Radiology Professor of Clinical Surgery and Clinical Emergency Medicine State University of New York Health Science Center at Brooklyn Brooklyn, New York Chapter 15: Diagnostic and Interventional Radiology

Contributors Steven R. Shackford, MD

George C. Velmahos, MD, PhD, MSEd

Professor of Surgery Emeritus University of Vermont School of Medicine Director Trauma Graduate Medical Education Scripps Mercy Hospital San Diego, California Chapter 41: Peripheral Vascular Injury

John F. Burke Professor of Surgery Chief Division of Trauma, Emergency Surgery, and Surgical Critical Care Harvard Medical School Massachusetts General Hospital Boston, Massachusetts Chapter 35: Pelvis

Michael J. Sise, MD, FACS Clinical Professor of Surgery UCSD School of Medicine Trauma Medical Director Scripps Mercy Hospital San Diego, California Chapter 41: Peripheral Vascular Injury

Wade R. Smith, MD, FACS Professor Department of Orthopaedics University of Colorado School of Medicine Englewood, Colorado Chapter 40: Lower Extremity

Gary A. Vercruysse, MD Assistant Professor of Surgeon Emory University School of Medicine Co-Director Burn Center Attending Surgeon Grady Memorial Hospital Atlanta, Georgia Chapter 22: Neck

Matthew J. Wall, Jr., MD

Professor of Orthopaedics and Neurosurgery University of Colorado (CU) School of Medicine Denver Health Medical Center Denver, Colorado Chapter 40: Lower Extremity

Professor of Surgery Michael E. DeBakey Department of Surgery Baylor College of Medicine Deputy Chief of Surgery/Chief of Thoracic Surgery Ben Taub General Hospital Chairman of the Executive Medical Board Ben Taub General Hospital Houston, Texas Chapters 24: Trauma Thoracotomy: Principles and Techniques Chapters 26: Heart and Thoracic Vascular Injuries

Lance E. Stuke, MD, MPH

Michael A. West, MD, PhD, FACS, FCCM

Philip F. Stahel, MD, FACS

Assistant Professor of Surgery Department of Surgery Louisiana State University Health Science Center New Orleans, Louisiana Chapter 1: Kinematics

Eric A. Toschlog, MD, FACS, FCCM Associate Professor of Surgery Director Surgical Critical Care Brody School of Medicine at East Carolina University Greenville, North Carolina Chapter 11: Airway Management

Peter Tsai, MD Assistant Professor of Cardiothoracic Surgery Michael E. DeBakey Department of Surgery Baylor College of Medicine Staff Surgeon Ben Taub General Hospital Houston, Texas Chapters 24: Trauma Thoracotomy: Principles and Techniques Chapters 26: Heart and Thoracic Vascular Injuries

David W. Tuggle, MD Chief Pediatric Surgery The University of Oklahoma College of Medicine Oklahoma City, Oklahoma Chapter 43: The Pediatric Patient

Professor and Vice Chair Department of Surgery University of California, San Francisco Chief of Surgery San Francisco General Hospital San Francisco, California Chapter 18: Infections

Michael T. White, MD Assistant Professor of Surgery & Director Burn Center Detroit Receiving Hospital Department of Surgery Detroit Medical Center/Wayne State University Detroit, Michigan Chapter 59: Renal Failure

David H. Wisner, MD Professor and Chairman Department of Surgery University of California, Davis Sacramento, California Chapter 30: Injury to the Spleen

Mary Margaret Wolfe, MD Assisstant Clinical Professor of Surgery University of California, San Francisco - Fresno Fresno, California Chapter 56: Cardiovascular Failure

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Contributors Amy D. Wyrzykowski, MD

Jay A. Yelon, DO, FACS, FCCM

Assistant Professor of Surgery Emory University School of Medicine Grady Memorial Hospital Atlanta, Georgia Chapter 38: Trauma Damage Control

Chairman Department of Surgery Lincoln Medical Center Bronx, New York Chapter 44: The Geriatric Patient

Daniel Dante Yeh, MD

Dirk Younker, MD

Clinical Instructor Harvard Medical School Massachusetts General Hospital Boston, Massachusetts Chapter 18: Infections Chapter 37: Trauma in Pregnancy

Shelden Professor and Vice-Chairman Department of Anesthesiology and Perioperative Medicine University of Missouri at Columbia Chapter 17: Principles of Anesthesia and Pain Management

PREFACE Almost 30 years ago, two ambitions and competitive surgeons, both of whom had received some specialized advanced training in cardiovascular surgery and surgical research, were acquiring reputations in the exploding field of “trauma.” Physicians and physiologists have been interested in the field of trauma for thousands of years, as manifest by the earliest of surgical writings, the Edwin Smith Surgical Papyrus, in which almost all case studies focused on the injured patient. The explosion of interest in trauma during the 1970s and 1980s was brought about by the simultaneous juxtaposition of many factors: • • • • • • • • •

EMS development Emergency medicine as a specialty Critical care as a discipline Increased sophistication in human physiological monitoring Advances in blood banking and hemotherapy Advances in vascular surgery Surgeons returning from the Vietnam conflict Broadening the scope of military medicine via the Uniformed Services University of the Health Sciences Last, but far from least, a large group of young, aggressive, eager surgeons who enjoyed the challenge of taking care of acutely injured patients with severe anatomic and physiological derangements

During the 1970s and early 1980s, trauma textbooks available to an aspiring academic surgeon or a practicing community surgeon seeking to master new techniques were few and rather limited in scope. Most recommendations contained therein were based on “expert opinion” and trial and error, rather than any evidence-based approach. Injury classification was in its infancy, and quality management matrix analyses had yet to be described. Almost simultaneously, Doctor Kenneth Mattox, in Houston, and Doctor Ernest Eugene (Gene) Moore, in Denver, recognized “there has to be a better way and a better textbook.” Doctors Moore and Mattox, independently and unbeknownst to each other, began to construct outlines for a practical trauma book employing the leading “trauma surgeons” of the day to contribute. While both were in the challenging “convincing stages” with their respective publishers, they were assembling a group of authors to participate in their respective endeavors. At this point, they discovered, they were pursuing similar projects and recruiting similar authors. A major merger followed, and at our initial meeting, the current format for the book Trauma was born. David Feliciano was invited to be the third editor, and the legacy began. We agreed to rotate the first editor spot with each subsequent edition, and the subsequent six editions are

history. During the past 30 years, Trauma has been the dominant textbook in its field throughout the world. It led in the fields of surgical critical care and acute care surgery, long before these were disciplines. This Seventh Edition marks a milestone in a textbook that continues to be the best seller in its field and have the same three medical editors. Since the mid-1980s, we have seen many changes in our society, medicine, and surgery, in general. HIV and AIDS introduced new immunological and treatment dilemmas. Inflammatory mediators, cytokines, and immunomodulation have grown into scientific fields, all their own. The wars in the Middle East have underscored the contemporary changes in trauma management. We have witnessed the emergence of damage control surgery and staged treatment. The most pronounced aspect of this concept is the ability to transport combat causalities across continents after initial damage control treatment, administer intermediate treatment in a European military hospital, and then transport, again, in a literal flying ICU. During the growth and development of Trauma, trauma center verification, designation, and recognition have become widespread. The terms Level I, Level II, and Level III Trauma Centers are now commonplace, and society expects every major city to have appropriate trauma treatment capability. Tenets of aggressive crystalloid resuscitation, precontrol elevation of the blood pressure, and other traditional aggressive resuscitation cultures have changed dramatically. Each edition of Trauma is different from the previous one. In preparing for the Seventh Edition and this preface, I reviewed each edition, chapter by chapter. For this edition, as in previous ones, we have invited new authors for many chapters, and we requested that the number of references be reduced to less than 50, when feasible for the subject, with both historic and recent citations. We have again attempted to avoid duplication of a subject or conflicting opinion, recognizing that this is not always possible when we also ask that each author make original contributions. For this edition, we are very excited about the inclusion of a Trauma Atlas of anatomic drawings and recognized surgical approaches. The three editors selected the drawings we believe best illustrate our current best practice for exposure and reconstruction. The descriptors with each drawing are short and succinct. Finally, and most importantly, the authors acknowledge the assistance of many people who make it possible to successfully accomplish this major endeavor, edition after edition. We are grateful to the authors who have contributed their knowledge, experience, writing talent, and valuable time. The expertise of the support personnel at all levels at McGraw-Hill Publishers is essential and appreciated at each step for each edition. Each xix

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Preface editor has office assistants who have performed many tasks, from interacting with authors to pushing the editors to meet deadlines. Mary Allen, in Kenneth Mattox’s office, Jo Fields in E. Eugene (Gene) Moore’s office, and Samantha Buckner in David Feliciano’s office all worked diligently to support this project. As assistant to the senior editor of the Seventh Edition, Mary Allen was tireless in coordinating the work of editors and authors to bring this project to fruition. Mary was present at

the very first concept formulation meeting, when Trauma was just a dream, and has been present at all editorial meetings since. Thank you, Mary, for your significant efforts in this and all previous editions of Trauma. Kenneth L. Mattox, MD Ernest E. Moore, MD David V. Feliciano, MD

SECTION 1

TRAUMA OVERVIEW

2

CHAPTER 1

Kinematics John P. Hunt, Alan B. Marr, and Lance E. Stuke

Kin·e·mat·ics (kn-mtks) n: The branch of mechanics that deals with pure motion without reference to the masses or forces involved in it. From Greek knma, knmat-, movement.1 As can be presumed from the derivation of the word kinematics, its essence revolves around motion. All injury is related to the interaction of the host and a moving object. That object may be commonplace and tangible, such as a moving vehicle or speeding bullet or more subtle as in the case of the moving particles and molecules involved in injury from heat, blasts, and ionizing radiation. Newtonian mechanics, the basic laws of physics, and the anatomic and material properties of the human body explain many of the injuries and injury patterns seen in blunt and penetrating trauma. Injury is related to the energy of the injuring element and the interaction between that element and the victim. Although most patients suffer a unique constellation of injuries with each incident, there are quite definable and understandable energy transfer patterns that result in certain predictable and specific injuries. Knowing the details of a traumatic event may aid the treating physician to further investigative efforts to uncover occult but predictable injuries. This chapter has been organized in a stepwise fashion. First, the basic laws of physics and materials that dictate the interaction between the victim and the injuring element are reviewed. This is followed by a more detailed examination of penetrating and blunt trauma and a synopsis of mechanisms specific to organs and body regions. It is hoped that this will offer the reader a better understanding of specific injury patterns, how they occur, and which injuries may result.

BASIC PRINCIPLES ■ Newton’s Laws, Impulse, Momentum, Energy and Work, Elastic and Inelastic Collisions Newton’s first law states that every object will remain at rest or in uniform motion in a straight line unless compelled to change its state by the action of an external force. This is the definition of inertia. Newton’s second law builds on the first and further defines a force (F ) to be equal to the product of the mass (m) and acceleration (a). F  ma. The application of a force does not occur instantaneously, but over time. If we multiply both sides of the above equation by time ∫Fdt  ma(t). The product of force and time is known as impulse and multiplying acceleration by time yields velocity. Momentum (p) is defined to be the mass (m) of an object times its velocity (v). p  mv, hence impulse  change in momentum. The important fact is that a force or impulse will cause a change in momentum and, likewise, a change in momentum will generate a force.2 This folds into Newton’s third law, which

Kinematics

W  ∫Fdx, with F  ma and a  vdv/dx

passenger compartment. If the momentum of car A was greater than that of car B by having a greater mass or velocity, the resultant mass C will have momentum in the previous direction in which car A was traveling. In T-bone type crashes the directions of the momentum of cars A and B are perpendicular. Therefore, in the momentum axis of car A, car B has 0 momentum and, in the momentum axis of car B, car A has no momentum. The conglomerate C conserves momentum in both the A and B axes with the resultant direction as shown in Fig. 1-1(B). As a consequence, the changes in momentum and force generated are far less than that of a head-on collision. Also, C continues to have a velocity and, as such, kinetic energy. This means that some of the initial kinetic energy was not converted to work, and less damage to the automobiles will occur. In general, the closer to a head-on collision the greater the change in momentum and, thus, the greater the force generated. In rear-end collisions the momentum of both cars is typically in the same direction, Fig. 1-1(C). Therefore, the changes

W  ∫mvdv/dx (dx), which after integration yields the familiar formula for kinetic energy: 1/2mv2

A

C

B

W  1/2mv  1/2mv . 2 2

2 1

Therefore, the work being done by a moving object, which interacts with a second object, equals the kinetic energy of the first object prior to doing work minus the kinetic energy after the interaction. In other words, the work done is equal to the change in kinetic energy of the first object.5 When this interaction sets the other body in motion, the second body now has kinetic energy of its own, equal to the work done. James Joule described the first law of thermodynamics in 1840, which simply states that energy can be neither created nor destroyed.6 Interactions in which both momentum and energy are conserved are termed elastic. In trauma most collisions are inelastic. Inelastic collisions conserve momentum, but not kinetic energy. In these instances the kinetic energy “does work” in the deformation of materials even to the point where objects can conglomerate and form a single object. This is the hallmark of the inelastic collision. This energy transfer or work done is what is typically responsible for the injury sustained by the host. Energy transfer and momentum conservation can be illustrated in the collision of two cars. Fig. 1-1(A) represents a head-on collision of two cars with equal mass and velocity and, thus, equal kinetic energy and momentum. The momentums are equal, but in opposite directions. Thus, the total momentum for the system is 0 prior to the crash and, by the law of conservation of momentum, must be 0 after the crash. Upon impact, both cars will come to rest. It is as if one of the cars struck an immovable wall. Recalling Newton’s second and third laws, this sudden change in momentum represents a force, which is equally applied to both cars. Because the final velocity is 0, the final kinetic energy is 0, meaning that all the kinetic energy has been converted to work that stops the other car and causes deformation such as breaking glass, bending metal, and causing physical intrusion into the

A. Frontal collisions

A

B C

B. T-bone collision C

A

B

C

C. Rear-end collision

FIGURE 1-1 Energy and momentum available in various motor vehicle crash scenarios. (A) Frontal collisions have the greatest change in momentum over the shortest amount of time and hence the highest forces generated. (B) T-bone collision. When cars A and B collide their resultant momentum directs them toward their final position C; the individual momentums in the x and y axis are dissipated over a greater time resulting in smaller forces then head-on collision. (C) Rear-end collision. Since these vehicles move in the same direction the change in momentum and forces generated are smaller.

CHAPTER 1 X

states that for every action or force there is an equal and opposite reaction.3 For instance, when two objects of equal velocity and mass strike each other, there velocities are reduced to zero (at the moment of impact). This change in velocity and, hence, momentum was caused by each object applying a force to the other. During impact the forces are equal and opposite. Recalling Newton’s second law, a force is associated with a change in momentum. In this system, the net force is zero and, therefore, the change in momentum is zero. This illustrates the law of conservation of momentum. The total momentum of a system will remain constant unless acted upon by an external force. The momentum of this two object system is the same after a collision as it was prior to impact.4 The next important basic principles are those of work and energy. Work (W) is defined as a force exerted over a distance and is frequently written as

3

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Trauma Overview

SECTION 1 X

in momentum and resultant forces generated are typically small as is the conversion of kinetic energy to work. These principles apply to all collisions whether they are a bullet penetrating a victim, a car hitting a pedestrian, or a driver impacting the windshield.

■ Penetrating Trauma and Ballistics Although the above principles were elaborated in the setting of blunt trauma, they are equally applicable to penetrating trauma. The study of ballistics details the energy of projectiles as they leave the firearm and the energy transfer once the bullet strikes the victim. Theodore Kocher first proposed that the kinetic energy possessed by the bullet was dissipated in the four following ways: namely, heat, energy used to move tissue radially outward, energy used to form a primary path by direct crush of the tissue, and energy expended in deforming the projectile.7 Despite limited techniques for studying ballistics, Kocher was for the most part correct. Our more extensive knowledge of the behavior of projectiles in a host comes from the observed performance of bullets in gelatin, which has properties similar to that of muscle and is thought to reflect the way in which energy is transferred through tissue. From such experiments several characteristics of a projectile piercing tissue have been described. These include the following: (a) penetration (the distance the projectile passes through tissue is reflected in the distance from the cut edge of the gelatin block to where the projectile comes to rest); (b) fragmentation (the pattern is assessed by biplaner x-rays and the degree reflected in the difference of the weight of the prefired projectile minus the weight of the collected fragments); (c) permanent cavity (the tissue disintegrated by direct contact with the missile and preserved in the gelatin); and (d) temporary cavity (the amount of “stretch” caused by the passing projectile). This is reflected by the distance from the edge of the permanent cavity to the outer perimeter of the cracks within the gelatin.8 The performance of the bullet and the injury sustained is reliant upon velocity, construction of the bullet, and composition of the target.9 The energy and construction characteristics of the projectile will be discussed here while target properties will be reviewed in the section on biomaterials. The prominent 18th-century surgeon John Hunter stated, “If the velocity of the ball is small, then the mischief is less in all, there is not so great a chance of being compounded with fractures of bones etc.”10 This astute observation reflects the exponential importance of velocity in determining the amount of kinetic energy that a particular projectile is capable of transmitting to a given target (kinetic energy  1/2mv 2). As such, high-velocity missiles will generally cause more tissue destruction than their lower velocity counterparts. The velocities and kinetic energies11,12 of common handguns and rifles are listed in Table 1-1. The amount of energy imparted (or work) to the tissue by a projectile is equal to the kinetic energy of the missile as it enters the tissue minus the kinetic energy as it leaves the tissue. Bullets are extremely aerodynamic, causing little disturbance while passing through the air. To some extent, this is similar in tissue (i.e., if the projectile moves with the point forward and passes in and out of the tissue, only a small portion of its kinetic energy will

TABLE 1-1 Velocity and Kinetic Energy Characteristics of Various Guns Velocity (ft/s)

Muzzle Energy (ft-lb)

810 745 1,410 855 985 1,470 850 935 1,340

73 140 540 255 390 1,150 370 345 425

Long guns/military weapons 0.243 Winchester 3,500 M-16 3,650 2,830 7.62 NATO 1,500 Uzi 3,770 AK47

1,725 1,185 1,535 440 1,735

Caliber Handguns 0.25 in. 0.32 in. 0.357 in. 0.38 in. 0.40 in. 0.44 in. 0.45 in. 9 mm 10 mm

be transferred to the target). The characteristics of damage created along the track of a bullet are divided into two components, the temporary and the permanent cavities. The temporary cavity is the momentary stretch or movement of tissue away from the path of the bullet. This could be construed as an area of blunt trauma surrounding the tract of the projectile. The temporary cavity increases in size with increasing velocity. The largest portion of the temporary cavity is on the surface where the velocity of the striking missile is the greatest.12 The concept of the temporary cavity has been used to advocate excessive tissue debridement in high-velocity wounds. In truth, postinjury observation of wound healing and animal experiments involving microscopic examination of tissue in the temporary cavity demonstrate that the momentary stretch produced does not usually cause cell death or tissue destruction.13 As such, debridement of highvelocity injuries should be confined to obviously devitalized tissue. Bullets can be constructed to alter their performance and increase the permanent cavity after they strike their target. This can be enhanced in four ways that all work by increasing the surface area of the projectile–tissue interface that facilitates the transfer of kinetic energy to the target. These include the following: (a) yaw, the deviation of the projectile in its longitudinal axis from the straight line of flight; (b) tumbling, the forward rotation around the center of mass; (c) deformation, a mushrooming of the projectile that increases the diameter of the projectile, usually by a factor of 2, increases the surface area, and, hence, the tissue contact area by four times; hollow point, soft nose, and dum–dum bullets all promote deformation; and (d) fragmentation, in which multiple projectiles can weaken the tissue in multiple places and enhance the damage rendered by cavitation. This usually occurs in high-velocity missiles. Nonfragmenting bullets will have a deeper penetration, whereas a fragmented

Kinematics

A

(W/W1)1/3  D/D1 B

C

D

FIGURE 1-2 Yaw, tumble, deformation, and fragmentation. (A) Yaw describes deviation from flight path along the longitudinal axis. (B) Tumble is deviation in a “head over heels” manner. (C) Deformation occurs on impact and increases the actual surface area of the projectile. (D) Fragmentation involves the bullet scattering. All of these increase surface area of the projectile/ tissue interface.

where W/W1 is a ratio of weights of a given explosive and D/D1 a ratio of distances from the epicenter. A compilation of experimental results showed that if a peak overpressure for one weight of explosive occurred at one distance, the same overpressure could be produced with a smaller weight of explosive at a shorter distance and for a larger weight of explosives at a longer distance (Fig. 1-3A). This relationship is known as the cube root rule or Hopkinson’s rule, and has been demonstrated to hold true for numerous modern-day explosive materials.18 At any given distance from the explosion there will be a distinct pressure–time curve with an abrupt increase in overpressure. Peak overpressure is dictated by the cube root rule and a decay in pressure that varies with the particular explosive compound and the time past the initial blast wavefront. As the wave moves past a given point, this positive pressure phase will be followed by a negative pressure phase19 (Fig. 1-3B). Pressure is a force applied per unit area. When a force is applied over a

A. The Scaling Laws Epicenter Do D

projectile will not penetrate as deeply, but will affect a larger cross-sectional area.14–16 If the bullet deforms, yaws, tumbles, or fragments, it will cause more tissue destruction. This occurs in deeper structures, not at the surface (Fig. 1-2). Wounds caused by knives are of very low energy and cause only a permanent cavity. With little energy transferred to the tissue, serious injury is caused by directly striking vital structures such as the heart, major vessels, lung, or abdominal organs.

Blast waves

B. The Pressure-Time relationship at any given distance from the epicenter Peak overpressure

Positive phase

The transfer of energy that results from explosions follows the previously stated rules of physics, but also has additional dimensions that deserve mention. The transmission of energy from an explosive blast is best understood in the context of wave mechanics. All conventional explosions have in common several characteristics in that they all involve a solid or liquid mixture that undergoes a rapid chemical reaction producing a gaseous by-product and a large amount of released energy. This release of energy pushes gaseous molecules from the explosion and within the atmosphere radially away from the explosion center producing a spherical wave of compressed gas, known as the blast wave, with increased density, pressure, and temperature when compared with the ambient air. The movement of these molecules creates what is known as a blast wind, and the compression of these molecules into a given space increases the density and pressure. This blast overpressure is defined

Pressure

■ Blast Injury and Ionizing Radiation

Decay Negative phase Time

FIGURE 1-3 Physical characteristics of an explosive blast. (A) The Scaling Laws relate the overpressure at specific distances to the ratio of distances from the epicenter of a blast and the cube root of the ratios of corresponding weights of the charges. (B) The Pressure–time relationship at any given distance from the epicenter—the peak overpressure represents the passing wave front with a subsequent decrease in pressure until ambient pressure is reached. This is known as the positive phase. The passing wave will then cause a decrease in pressure below baseline resulting in a relative vacuum, or negative pressure phase.

CHAPTER 1 X

as the wavefront pressure generated above ambient pressure. This peak overpressure is a function of the energy released from the blast and the distance from the point of detonation, and its decay is expressed as a scaling function17

5

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given time, an impulse is present and has the ability to change momentum. This force when applied across a distance has the ability to transfer energy and do work. Nuclear blast waves have a similar pressure–time relationship, but their positive phase may last several seconds as compared to the milliseconds of conventional munitions.20 The energy released from a nuclear explosion is on the order of thousands of times greater than conventional explosives with a corresponding increase in overpressure. The energy available is dictated by Einstein’s mass–energy equivalency formula:21

A

B

E  mc2. A large portion of this energy is released in the form of kinetic energy that dictates the wave characteristics of the blast. Also, there is the production of high-energy subatomic particles, such as gamma radiation, which has the ability to cause destruction at the cellular level. Where h  Planck’s constant, the energy of these particles is directly related to their frequency (v).22

C

D

E  hv They can be released at the time of the blast, but also for a period of time after the explosion as unstable products of a nuclear reaction undergo radioactive decay. Therefore, a nuclear explosion has the ability to transfer energy to a victim and do damage long after the initial blast.

PROPERTIES OF BIOMATERIALS ■ Stress, Strain, Elasticity, and Young’s modulus When a force is applied to a particular material, it is typically referred to as a stress, which is a load or force per unit area. This stress will cause deformation of a given material. Strain is the distance of the deformation caused by the stress, divided by the length of the material to which the stress was applied.23 Strain can be tensile, shear, compressive, or overpressure (a relative of compressive strain) (Fig. 1-4). Tensile strain of a particular structure or organ occurs as opposing forces are applied to the same region. The forces are opposite and concentrated upon a particular point. This essentially interrupts the integrity of the structure by pulling it apart. Shear strain occurs as opposing forces are applied to a particular structure, but at different points within that structure. This can be caused by an application of opposing external forces or can arise from a relative differential in the change of momentum within a single structure or between structures that are attached to one another.24 Compressive strain is the direct deformation that occurs as a result of impact. The energy involved with a particular force does work on the structure causing a crushing-type injury resulting in deformation and interruption of the structural integrity of the injured organ. Overpressure is a type of compressive strain that is applied to a gas- or fluid-filled cavity. The energy applied to a gas- or fluid-filled viscus can deform that

FIGURE 1-4 Biomechanical mechanisms of injury. (A) Tensile strain—Opposite forces stretching along the same axis. (B) Shear strain—Opposite forces compress or stretch in opposite direction but not along the same axis. (C) Compressive strain—Stress applied to a structure usually causing simple deformation. (D) Overpressure—A compressive force increases the pressure within the viscus passing the “breaking point” of the wall.

structure and cause a decrease in the volume of the structure. Following Boyle’s law: P1V1  P2V2 The product of the pressure and the volume prior to an applied force must be equal to the product afterward.4 Therefore, a decrease in its original volume will increase the pressure inside that viscus. If the rise in pressure, which is a force, overcomes the tensile strength of the viscus, it will rupture.25 When stress is plotted on the same graph as strain, there are several clear and distinct aspects to the curve. The elastic modulus is that part of the curve in which the force does not cause permanent deformation, and a material is said to be more elastic if it restores itself more precisely to its original configuration.26 The portion of the curve beyond this is called the plastic modulus and denotes when an applied stress will cause permanent deformation.27 The tensile, compressive, or shear strength is the level of stress at which a fracture or tearing occurs.28 This is also known as the “failure point.” The area under the curve is the amount of energy that was applied to achieve the given stress and strain (Fig. 1-5).29 How well tissue tolerates a specific insult varies with the type of force applied and the tissue in question. In blunt and penetrating trauma, the higher the density of a particular tissue, the less elastic it is and the more energy is transferred to it in a collision. Lung is air-filled and extremely elastic. In lower velocity

Kinematics L

■ Motor Vehicle Crashes

Tensile strain = ΔL/L

Tensile Strength Plastic Modulus

Stress

Elastic Modulus

Energy

Strain

FIGURE 1-5 The concept of stress, strain, elastic modulus, plastic modulus, tensile strength and energy as demonstrated by a tensile stress applied to a given structure. The tensile strain is the change in length under a stress divided by the original length. This concept is applicable to compressive and shear strain. In the stress/strain relationship the elastic modulus is the portion of the curve where permanent deformation does not occur as opposed to the plastic modulus where it does fracture or tearing occurs at the tensile strength. The energy applied is the area under the curve.

blunt trauma, energy tends to be dissipated across the lung easily, while in penetrating trauma the actual destruction of the permanent cavity and stretch caused by the temporary cavity are better tolerated because of the elasticity of the lung. In contrast, solid organs such as spleen, liver, or bone tend to absorb energy and will have greater tissue destruction as a consequence.30 In blast injury it is the air-filled structures of the lung and bowel that tend to be injured because of their ability to transmit the blast wave and cause localized pressure increases that overcome the structural failure point of the organ.20

BLUNT TRAUMA MECHANISMS AND PATTERNS OF INJURY The transfer of energy and application of forces in blunt trauma is often much more complex than that of penetrating trauma. The most frequent mechanisms of blunt trauma include motor vehicle crashes, auto–pedestrian crashes, and falls from a significant height. In these instances there are typically varying energies and forces in both the victim and the

Although there are frequently confusing vectors for energy transfer and force in a victim of a motor vehicle crash, mortality is directly related to the total amount of energy and force available. Mortality from motor vehicle crashes is accounted for in large part by head-on collisions with mortality rates up to 60%. Side impact collisions (20–35%) and rollovers (8–15%) have progressively lower mortality rates with rear-end collisions (3–5%) having the lowest.31–32 Rollover crashes have a lower than expected mortality because the momentum is dissipated, and forces generated and projected to the passenger compartment are in a random pattern that frequently involves many different parts of the car. Although there are certain forces and patterns of energy exchange that occur in a motor vehicle crash, the vehicle itself does offer some degree of protection from the direct force generated by a collision. Patients who are ejected from their vehicle have the velocity of the vehicle as they are ejected and a significant momentum. They typically strike a relatively immobile object or the ground and undergo serious loads. Trauma victims who were ejected from the vehicle were four times more likely to require admission to an intensive care unit, had a 5-fold increase in the average Injury Severity Score, were three times more likely to sustain a significant injury to the brain, and were five times more likely to expire secondary to their injuries in one study.33 Understanding the changes in momentum, forces generated, and patterns of energy transfer between colliding vehicles is important. For example, the principal direction of force in a head-on collision is affected by the degree of overlap of the vehicles.34 Yet, the behavior of the occupants of the passenger compartment in response to this is what helps identify specific patterns of injury. In frontal collisions the front of the vehicle decelerates as unrestrained front-seat passengers continue to move forward in keeping with Newton’s first law. Lower extremity loads, particularly those to the feet and knees, occur early in the crash sequence and are caused by the floorboard and dashboard that are still moving forward. Therefore, relative contact velocity and change in momentum are still low. Contact of the chest and head with the steering column and windshield occurs later in the crash sequence; therefore, contact velocities and deceleration, change in momentum, and contact force are higher.31,35 Types of injuries are dependent on the path the patient takes. The patient may slide down and under the steering wheel and dashboard. This may result in the knee first impacting the dashboard causing a posterior dislocation and subsequent injury to the popliteal artery. The next point of impact is the upper abdomen or chest. Compression and continued movement of solid organs results in lacerations to the liver or spleen.

CHAPTER 1 X

ΔL

L

striking object. Other variables that complicate care include the larger surface area over which the energy is dispersed as compared to penetrating trauma and the multiple areas of contact that can disperse energy to different regions of the victim’s body. The interactions and directions of these lines of force and energy dispersion are often instrumental in causing specific kinds of injury.

7

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Trauma Overview

SECTION 1 X

Compression of the chest can result in rib fractures, cardiac contusion, or a pneumothorax from the lung being popped like a paper bag. Finally, the sudden stop can cause shear forces on the proximal descending thoracic aorta resulting in a partial- or full-thickness tear. The other common path is for the occupant to launch up and over the steering wheel. The head then becomes the lead point and strikes the windshield resulting in a starburst pattern on the windshield. The brain can sustain direct contusion or can bounce within the skull causing brain shearing and a contrecoup injury. Once the head stops, forces are transferred to the neck that may sustain hyperflexion, hyperextension, or compression injuries, depending on the angle of impact. Once the head and neck stop, the chest and abdomen strike the steering wheel with similar injuries to the down and under path. Lateral collisions, specifically those that occur on the side of a seated passenger, can be devastating because of the small space between the striking car and the passenger. Therefore, resistance to slow momentum of the striking car prior to contact with the passenger is limited. If the side of the car provides minimal resistance the passenger can be exposed to the entire momentum change of the striking car. These loads are usually applied to the lateral chest, abdomen, and pelvis and, as such, injuries to the abdomen and thorax are more frequent in lateral collisions than in frontal collisions.35 Injuries to the chest include rib fractures, flail chest, and pulmonary contusion. Lateral compression often causes injuries to the liver, spleen, and kidneys, as well. Finally, the femoral head can be driven through the acetabulum. Rear-end collisions are classically associated with cervical whiplash-type injury and are a good example of Newton’s first law at work. When the victim’s car is struck from behind, the body, buttressed by the seat, undergoes a forward acceleration and change in momentum that the head does not. The inertia of the head tends to hold it in a resting position. The forward pull of the victim’s trunk causes a backward movement on the head leading to hyperextension of the neck. Similarly, this injury pattern can also be seen in head-on collisions where a sudden deceleration of the victim’s trunk with a continued forward movement of the head is followed by a backward rotation resulting from recoil.36,37

■ Pedestrian Injuries Pedestrian injuries frequently follow a well-described pattern of injury depending on the size of the vehicle and the victim. Nearly 80% of adults struck by a car will have injuries to the lower extremities. This is intuitively obvious as the level of a car’s bumper is at the height of the patient’s knee and this is the first contact point in this collision sequence. A victim struck by a truck or other vehicle with a higher center of mass will more frequently have serious injuries to the chest and abdomen because the initial force is applied to those regions. In the car–pedestrian interaction, the force applied to the knee region causes an acceleration of the lower portion of the body that is not shared by the victim’s trunk and head, which tend to stay at rest, by Newton’s first law. As the lower extremities

are pushed forward they will act as a fulcrum bringing the trunk and head forcefully down on the hood of the car applying a secondary force to those regions, respectively. The typical injury pattern in this scenario is a tibia and fibula fracture or dislocation of the knee joint, injury to the trunk such as rib fractures or rupture of the spleen, and injury to the brain.38,39

■ Falls Falls from height can result in a large amount of force transmitted to the victim. The energy absorbed by the victim at impact will be the kinetic energy at landing. This is related to the height from which the victim fell. The basic physics formula describing the conservation of energy in a falling body states that the product of mass, gravitational acceleration, and height, the potential energy prior to the fall, equals the kinetic energy as the object strikes the ground. With mass and gravitational acceleration being a constant for the falling body, velocity, and, therefore, momentum and kinetic energy are directly related to height.4 The greater the change in momentum upon impact the larger the load or force applied to the victim. Injury patterns will vary depending upon which portion of the victim strikes the ground first and, hence, how the load is distributed. The typical patient with injuries sustained in a free fall has a mean fall height of just under 20 ft. One prospective study of injury patterns summarized the effects of falls from heights ranging between 5 and 70 ft. Fractures accounted for 76.2% of all injuries, with 19–22% of victims sustaining spinal fractures and 3.7% developing a neurological deficit.40 Nearly 6% of patients had intra-abdominal injuries, with the majority requiring operative management for injury to a solid organ. Bowel and bladder perforation were observed in less than 1% of injuries.41

ANATOMIC CONSIDERATIONS ■ Injury to the Head (Brain and Maxillofacial Injury) The majority of closed-head injuries are caused by motor vehicle collisions (MVCs), with an incidence of approximately 1.14 million cases each year in the United States.42,43 The severity of traumatic brain injury represents the single most important factor contributing to death and disability after trauma and may contribute independently to mortality when coexistent with extracranial injury.37,44,45 Our knowledge of the biomechanics of injury to the brain comes from a combination of experiments conducted with porcine head models, biplaner high-speed x-ray systems, and computer-driven finite element models.46 There are a multitude of mechanisms that occur under the broad heading of traumatic brain injury. All are a consequence of loads applied to the head resulting in differing deceleration forces between components of the brain. Brain contusion can result from impact and the associated direct compressive strain. The indirect component of injury to the brain on the side opposite to that of impact is known as the contrecoup

Kinematics

■ Thoracic Injury The primary mechanism of blunt trauma to the chest wall involves inward displacement of the body wall with impact.

Musculoskeletal injury in the chest is dependent upon both the magnitude and rate of the deformation of the chest wall and is usually secondary to compressive strain from the applied load. Patterns of injury for the internal organs of the thorax frequently reflect the interactions between organs that are fixed and those that are relatively mobile and compressible. This arrangement allows for differentials in momentum between adjacent structures that lead to compressive, tensile, and shear stresses. The sternum is deformed and rib cage compressed with a blunt force to the chest. Depending on the force and rate of impact in a collision, ribs may fracture from compressive strain applied to their outer surface and consequent tensile strain on the inner aspects of the rib. Indirect fractures may occur due to stress concentration at the lateral and posterolateral angles of the rib. Furthermore, stress waves may propagate deeper into the chest resulting in small, rapid distortions or shear forces in an organ with significant pressure differential across its parenchymal surface (i.e., the air and tissue interface of the lung). This is thought to be the mechanism causing a pulmonary contusion. Blunt intrusion into the hemithorax and a pliable lung could also result in overpressure and cause a pneumothorax. A direct load applied to the chest compresses the lung and increases the pressure within this air-filled structure beyond the failure point of the alveoli and visceral pleura. This overpressure mechanism may also be seen with fluid (blood) instead of air in a blunt cardiac rupture. High-speed cine-radiography in an anterior blunt chest trauma model in the pig has demonstrated that the heart can be compressed to half of its pre-crash diameter with a doubling of the pressure within the cardiac chambers.52 If the failure point is reached, rupture occurs with disastrous results. There are several examples of indirect injury secondary to asynchronous motion of adjacent, connected structures and development of shear stress at sites of attachment.53 Mediastinal vascular injury and bronchial injury are examples of this mechanism. Rupture or transection of the descending thoracic aorta is a classic deceleration injury mediated by shear forces. This injury can occur in frontal or lateral impacts and occurs because of the continued motion of the mobile and compressible heart in relation to an aorta that is tethered to more fixed structures.54 In frontal and lateral impacts the heart moves in a horizontal motion relative to an aorta that is fixed to the spinal column by ligamentous attachments. This causes a shear force applied at the level of the ligamentum arteriosum. When the stress is applied in a vertical direction, such as a fall from a height in which the victim lands on the lower extremities, the relative discrepancy in momentum is in that plane and a tensile strain is generated at the root of the ascending thoracic aorta (Fig. 1-6). Injury to a major bronchus is another example of this mechanism. The relatively pliable and mobile lung generates a differential in momentum in a horizontal or vertical plane depending on the applied load as compared to the tethered trachea and carina. This creates a shear force at the level of the mainstem bronchus and explains why the majority of blunt bronchial injuries occur within 2 cm of the carina (Fig. 1-7).

CHAPTER 1 X

injury. This occurs because the brain is only loosely connected to the surrounding cranium. As a result, after a load is applied to the head causing a compressive strain at the point of impact and setting the skull in motion along the line of force, the motion of the brain lags behind the skull. As the skull comes to rest, or even recoils, the brain, still moving along the line of the initial load, strikes the calvarium on the opposite side and another compressive strain is generated. The existence of the coup–contrecoup injury mechanism is supported by clinical observation and has been confirmed by a three-dimensional finite element head model and pressure-testing data in cadavers.47 It is even suspected that this forward acceleration of the brain relative to the skull may set up a tensile strain in the bridging veins causing their laceration and formation of a subdural hematoma.48 Injury to the superficial regions of the brain is explained by these linear principles; however, injury to the deep structures of the brain, such as diffuse axonal injury (DAI), is more complicated. Several authors have tried to explain DAI as a result of shear strain between different parts of the brain, but there is also another model known as the stereotactic phenomenon. This model relies more on wave propagation and utilizes the concavity of the skull as a “collector,” which focuses multiple wave fronts to a focal point deep within the brain, causing disruption of tissue even in the face of minimal injury at the surface of the brain.49 This “wave propagation” through deeper structures within the brain, such as the reticular-activating system, with subsequent disruption of their structural integrity is thought to account for a loss of consciousness, the most frequent serious sign after blunt trauma to the brain.50 Current research characterizes DAI as a progressive process induced by the forces of injury, gradually evolving from focal axonal alteration to eventual disconnection. Traumatically induced focal axolemmal permeability leads to local influx of Ca2 causing the release of proteases that digest the “membrane skeleton.” This ultimately leads to local axonal failure and disconnection.51 An injury caused by shear strain is a laceration or contusion of the brainstem. This is explained by opposing forces applied to the brain and the spinal cord perpendicular to their line of orientation, with the spinal cord and brainstem being relatively fixed in relation to the mobile brain. Maxillofacial injuries are associated with injuries to the head and brain in terms of mechanism and are a common presentation after motor vehicle crashes. The classic force vector that results in mid-face fractures is similar to that of traumatic brain injury and occurs when a motor vehicle occupant impacts the steering wheel, dashboard, or windshield. Nearly all of these subtypes of injury are secondary to compressive strain. This mechanism is associated with the greatest morbidity for the driver and front-seat passenger, while the forces are attenuated for the back-seat passenger impacting the more compliant front seat.

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Trauma Overview

■ Abdominal Injury

Shear Force

SECTION 1 X

Reactive Force

Reactive Force

Initial Force

Initial Force Horizontal Deceleration

Vertical Deceleration

FIGURE 1-6 Various mechanisms of injury for thoracic aorta injury. In a horizontal deceleration the heart and arch move horizontally away from the descending aorta causing shear strain and tearing at the ligamentum arteriosum. A vertical deceleration causes caudad movement of the heart, causing a strain at the root of the ascending aorta.

Abdominal organs are more vulnerable than those of the thorax because of the lack of protection by the sternum and ribs. A number of different mechanisms account for the spectrum of injury observed in blunt trauma to the abdomen. With regard to the solid abdominal organs, a direct compressive force with parenchymal destruction probably accounts for most observed injuries to the liver, spleen, and kidney. Shear strain can also contribute to laceration of these organs. As with the previous description of strain forces, a point of attachment is required to exacerbate a differential in movement. This can occur at the splenic hilum resulting in vascular disruption at the pedicle or at the ligamentous attachments to the kidney and diaphragm. Shear forces in the liver revolve upon the attachments of the falciform ligament anteriorly and the hepatic veins posteriorly, explaining injuries to the parenchyma in these areas. Another significant injury related to this mechanism is injury to the renal artery. The renal artery is attached proximally to the abdominal aorta, which is fairly immobile secondary to its attachments to the spinal column, and distally to the kidney, which has more mobility. A discrepancy in momentum between the two will exact a shear stain on the renal artery resulting in disruption.55 This same relation to the spinal column occurs with the pancreas (Fig. 1-8). The relatively immobile spine and freely mobile pancreatic tail

Splenic Hilum

Falciform Ligament

Pancreas L-Spine

Shear Strain

Hepatic Veins

Ligament of Treitz

Initial Load

FIGURE 1-7 Mechanisms of injury for bronchial injury. The carina is tethered to the mediastinum and spinal complex while the lungs are extremely mobile, setting up shear strain in the mainstem bronchus upon horizontal or vertical deceleration.

Terminal Ileum

FIGURE 1-8 Points of shear strain in blunt abdominal trauma. All of these points occur where a relatively fixed structure is adjacent to a mobile structure.

Kinematics The type and extent of injury is determined by the momentum and kinetic energy associated with impact, underlying tissue characteristics, and angle of stress of the extremity. High-energy injuries can involve extensive loss of soft tissue, associated neurovascular compromise, and highly comminuted fracture patterns. Low-energy injuries are often associated with crush or avulsion of soft tissue in association with simple fractures. Injuries to soft tissue are usually secondary to compressive strain with crush injury as an example. Tensile and shear strain mechanisms, however, are present with degloving and avulsion injuries, respectively. Most of that written about musculoskeletal injury involves fractures of long bones. Although each fracture is probably a consequence of multiple stresses and strains, there are four basic biomechanisms (Fig 1-9). In a lateral load applied to the mid shaft of a long bone, bowing will occur and compressive strain occurs in the cortex of the bone where the load is applied. The cortex on the opposite side of the bone will undergo tensile strain as the bone bows away from the load. Initially, small fractures will occur in the cortex undergoing tensile strain because bone is weaker under tension than it is under

Lateral Load

Compressive Strain

Longitudinal Load W/Bowing

Tensile Strain

Tensile Strain

Load Compressive Strain Load

Torsional Load

Longitudinal Load

■ Musculoskeletal Injury By far, the most common type of blunt injury in industrialized nations is to the musculoskeletal system. The ratio of orthopedic operations to general surgical, thoracic, and neurosurgical operations is nearly 5:1. As stated earlier, seatbelts and air bags have significantly decreased the incidence of major intracranial and abdominal injuries; however, they have not decreased the incidence of musculoskeletal trauma. Although these are not usually fatal injuries, they often require operative repair and rehabilitation and can leave a significant proportion of patients with permanent disability.60 With the advent of seatbelt laws, improved restraint systems, and air bags in motor vehicles, the incidence of lower extremity trauma, in particular, has increased. It is thought that these patients in the past may have suffered fatal injuries to the brain or torso and, therefore, their associated fractures of the femur, tibia, and fibula were not included in the overall list of injuries.

Load

Compressive Strain Load

FIGURE 1-9 Fracture mechanics. A lateral load causing “bowing” will create tensile strain in the cortex opposite the force and compressive strain in the adjacent cortex. If a longitudinal stress caused “bowing” a similar strain pattern occurs. If no bowing occurs the strain is all compressive. A torsion load will cause a spiral fracture.

CHAPTER 1 X

predispose to a differential in momentum between the two in a deceleration situation leading to fracture in the neck or body of the pancreas. The biomechanics of such injuries suggest that the body’s tolerance to such forces decreases with a higher speed of impact, resulting in an injury of greater magnitude from a higher velocity collision.29 Perforation of a hollow viscus in blunt abdominal trauma occurs in approximately 3% of victims.56 The exact cause is a matter of debate. Some believe that it is related to compressive forces, which cause an effective “blowout” through generation of significant overpressure, whereas others believe that it is secondary to shear strains. Both explanations are plausible, and clinical observations have supported the respective conclusions. Most injuries to the small bowel occur within 30 cm of the ligament of Treitz or the ileocecal valve, supporting the shear force theory57 (Fig. 1-8). Yet, injuries do occur away from these points of fixation. Also, experiments have documented that a “pseudo-obstruction” or temporarily closed loop under a load can develop bursting pressures as described by the overpressure theory.58 Clinically, this is confirmed by the largest percentage of small intestinal injuries being of the “blowout” variety.59 Most likely, both proposed mechanisms are applicable in individual instances. The most common example of the pseudo-obstruction type is blunt rupture of the duodenum, where the pylorus and its retroperitoneal location can prevent adequate escape of gas and resultant high pressures that overcome wall strength. Another important example of overpressure is rupture of the diaphragm. The peritoneal cavity is also subject to Boyle’s law, which states that volume of a gas is inversely proportional to pressure. A large blunt force, such as that related to impact with the steering wheel, applied to the anterior abdominal wall will cause a temporary deformation and decrease in the volume of the peritoneal cavity. This will subsequently raise intraabdominal pressure. The weakest point of the cavity is the diaphragm with the left side being the preferred route of pressure release as the liver absorbs pressure and protects the right hemidiaphragm. The relative deformability of the lung on the other side of the diaphragm facilitates this.

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SECTION 1 X

compression.61 Once the failure point is reached on the far side from the load, the compressive strain increases markedly and the failure point for the side near the applied load is reached, also, resulting in a complete fracture. This mechanism can be seen in passengers in lateral collisions, pedestrians struck by a passenger car in the tibia and fibula region, or in the upper extremities from direct applied force in victims of assault with a blunt instrument. When a longitudinal load is placed on a long bone, bowing can also occur, and the compressive and tensile strain patterns will be similar to that previously described. If bowing does not occur, then only a compressive strain is seen and a compression fracture can occur. In the case of the femur this usually occurs distally with the shaft being driven into the condyles. These mechanisms can be seen in falls from a height, but are more frequently seen in head-on collisions resulting in fractures of the femur or tibia. In these cases deceleration occurs and the driver’s or passenger’s feet receive a load from the floorboard or the knee receives a load from the dashboard upon deceleration. This causes a longitudinal force to be applied to the tibia or femur, respectively. A torsional load will cause the bone to fracture in a spiral pattern.

■ Injury to the Spine and Whiplash Injury to the vertebral column and spinal cord can be devastating and is frequently the result of a complex combination of specific anatomic features and transmitted forces. These can cause a wide variety of injury patterns distributed through the different portions of the vertebral column. Deceleration forces in motor vehicle crashes, such as impact with the windshield, steering assembly, and instrument panel, inertial differences in the head and torso, or ejection are responsible for both flexion and hyperextension injuries. Although the biomechanics of transmission of force can be readily demonstrated for the vertebral column’s individual components (disks, vertebrae, etc.), a model demonstrating injury patterns in the intact spinal unit is lacking.36 The cervical spine is most frequently injured in motor vehicle crashes, due to its relatively unprotected position compared to the thoracic and lumbar regions. Injuries are related to flexion, extension, or lateral rotation, along with tension or compression forces generated during impact of the head. The direction and degree of loading with impact account for the different injury patterns in trauma to the cervical spine.29 Approximately 65% of injury is related to flexion–compression, about 30% to extension–compression, and 10% to extension–tension injuries.62 Fracture dislocations of the vertebrae are related to flexion and extension mechanisms, whereas fractures of the facets are related to lateral-bending mechanisms. In contrast to trauma to the cervical spine, injury to the thoracic or lumbar spine is more likely related to compressive mechanisms. The rib cage and sternum likely provide stabilizing forces in motor vehicle crashes and lessen the risk of injury in these regions. Whiplash refers to a pattern of injury seen often in MVCs with a rear-end impact. The injury is usually a musculoligamentous sprain, but may be combined with injury to cervical

nerve roots or the spinal cord. Patients typically experience neck pain and muscle spasm, although an additional spectrum of symptoms has been described.63 The etiology of whiplash probably relates to acceleration and extension injury, with some rotational component in non–rear-impact crashes. Factors related to poor recovery following whiplash injury are a combination of sociodemographic, physical, and psychological, and include female gender, low level of education, high initial neck pain, more severe disability, increased levels of somatization, and sleep difficulties.64

■ Kinematics in Prevention The ideas of William Haddon have become the cornerstone of injury prevention, and approximately a third of his strategies involve altering the interaction of the host and the environment.65 Understanding forces and patterns of energy transfer have allowed the development of devices to reduce injury. Most of this understanding has been applied to the field of automotive safety. The first set of design features revolve around the concept of decreasing the force transmitted to the passenger compartment. This includes the “crumple zone,” which allows the front and rear ends of a car to collapse upon impact. The change in momentum the passenger compartment undergoes in a collision will, therefore, occur over a longer period. Going back to the impulse and momentum relation, this means less force will be transmitted to the passenger compartment. In terms of energy, work is done in the crumple zone and energy is expended before reaching the passenger compartment.66 The second design feature directs the engine and transmission downward and not into the passenger compartment decreasing intrusion into the passenger compartment. Passenger restraint systems, which include safety harnesses and child car seats, keep the passengers’ velocity equal to that of the car and prevent the passengers from generating a differential in momentum and striking the interior of the car. Also, they more evenly distribute loads applied to the victim across a greater surface area thus decreasing stress. Even with restraint systems the occupants of a car can develop relative momentum and kinetic energy during a crash. This energy and momentum can be dissipated by air bags, which convert it into the work of compressing the gas within the device. The helmets used by cyclists and bicyclists work on a similar principle in that a compliant helmet absorbs some of the energy of impact, which is therefore not transmitted to the brain. Many studies have demonstrated the benefits of using seatbelts and air bags with mortality reductions ranging from 41 to 72% for seatbelts, 63% for air bags, 80% for both, and 69% for child safety seats.61 Seatbelts and air bags have also significantly reduced the incidence of injuries to the cervical spine, brain, and maxillofacial region by keeping the forward momentum of the passenger to a minimum and preventing the head from striking the windshield.46 Also worth mentioning is the headrest that has decreased whiplash-type injury by 70% by preventing a difference in momentum between the head and body and hyperextension of the neck in rear-end collisions.67

Kinematics

SPECIAL CONSIDERATIONS ■ Pediatrics Differences have been noted between adults and children in both patterns of injury and physiological responses to injury. In one analysis of adults and children sustaining comparable degrees of injury from blunt trauma, significant differences were noted in the incidence of thoracic, spinal, and pelvic injuries in children. Although the overall incidence of injury to the brain is higher in blunt pediatric trauma, thoracic and pelvic injuries occur less frequently.71 Overall mortality is generally higher for adults than it is for children sustaining comparable degrees of injury. When assessed by mechanism, however, mortality is slightly higher for children in motor vehicle crashes.72 The most significant difference between adults and children is in the compliance of the bony structures. This difference is seen commonly in the resilience of the chest wall. The incidence of rib fractures, flail chest, hemo-pneumothorax, and injury to the thoracic aorta in children is significantly less than that in adults, though the incidence of pulmonary contusion is higher. Because of this resilience, the chest wall can absorb a greater impact in children while demonstrating less external sign of injury. In children the index of suspicion for a pulmonary contusion, in the absence of rib fractures, must be higher than in an adult. Injury to the spinal cord is rare in children, representing only 1–2% of all pediatric trauma. The cervical spine is injured in the majority of cases (60–80%), compared to 30–40% in adult injury. The immature spinal column has incomplete ossification, a unique vertebral configuration, and ligamentous laxity, which accounts for this difference in pattern of injury. The proportionally larger head and less developed neck musculature of younger children (10 years old) account for more

torque and acceleration stress in the higher cervical spine during injury, as well. Young children have high rates of dislocations and spinal cord injury without radiographic abnormality (SCIWORA), and these are more likely to be seen at the upper cervical levels. As older children have a low fulcrum of cervical motion (C5–C6) and more ossification and maturity of the vertebral bodies and interspinous ligaments, they have a high incidence of fractures in the lower cervical spine.73 SCIWORA is associated with 15–25% of all injuries to the cervical spine in pediatrics and represents a transient vertebral displacement and realignment during injury, resulting in damage to the spinal cord without injury to the vertebral column. Childhood obesity is recognized as a leading public health issue in the United States. Childhood obesity is defined as an age and sex-specific body mass index at the 95th percentile or higher. Based on this definition, 14–17% of all children were obese from 1999 to 2004.69 When compared to their nonobese counterparts, obese children between the ages of 2 and 5 who are injured in a MVC are at an increased risk for major injuries to the brain and chest. Obese children above the age of 5 involved in an MVC are at an increased risk for major thoracic and lower extremity injuries in comparison to nonobese children of the same age and sex.74 Nothing has reduced the incidence of injury to children and infants more than the mandatory use of safety belts and restraints. The problem still to be faced is the different contours and shapes with infant restraints. Also, there has been increased interest in the issue of pediatric restraint systems because of a number of injuries related to air bags. It is recommended that restrained infants and children not be placed in a front seat and that all children under age 12 ride in the rear seat. Injuries related to air bags have ranged from minor orthopaedic trauma to fatal injury to the brain.75 Unfortunately, child abuse is a reality in the pediatric population and must be considered when evaluating a child who has been injured in less than clear circumstances or has multiple injuries of varying ages. Although injury to soft tissue is the most common presentation, fractures follow as a close second. There is a high rate of spiral fractures of the humerus and femur secondary to a torsional force, applied by an adult grabbing the child’s extremity in a twisting motion. Injury to the brain is the third most common injury, with skull fractures thought to be secondary to direct blows to the child’s head or the dropping and throwing of the child. Intracranial hemorrhage has been noted in the “shaken impact syndrome” and is thought to result from significant acceleration and deceleration forces followed by direct force transfer with impact. Subdural and subarachnoid hemorrhages can often result, as blood vessels between the brain and skull are ruptured. Retinal hemorrhage may also be identified in this pattern of injury and occurs in approximately 3% of cases. Impact injury to the abdomen is common in child abuse and can result in injury to solid organs (liver, spleen, or kidney), duodenal hematoma (sometimes with delayed symptoms of intestinal obstruction), pancreatitis, injury to the colon or rectum, or mesenteric bleeding. In addition, falls from even very small heights may cause severe intracranial hemorrhage in the infant or child.76

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Despite their effectiveness, air bags can be responsible for injury in motor vehicle crashes. Approximately 100 air bag– related deaths were confirmed by National Highway Traffic Safety Administration (NHTSA) over a 5-year period, many associated with improper restraint of small adults or children in front-seat locations. Additionally, a spectrum of minor injuries such as corneal abrasions and facial lacerations have been seen in low-speed impacts. Injuries can occur from the use of safety belts, as well. Lap seatbelts can cause compressive injuries such as rupture of the bowel, pelvic fractures, and mesenteric tears and avulsions. They can also act as a fulcrum for the upper portion of the trunk and be associated with hyperflexion injuries such as compression fractures of the lumbar spine. As a consequence, newer automobiles are required to have the more extensive and protective lap and shoulder harness style belts. Even still, shoulder harnesses can cause intimal tears or thrombosis of the great vessels of the neck and thorax and fracture and dislocation of the cervical spine in instances of submarining, where the victim slides down under the restraint system.68 Even when a shoulder harness system works as intended, clavicular and rib fractures or perforations of hollow viscera in the abdomen secondary to a compressive-type mechanism can occur.69, 70

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Trauma Overview

■ Pregnancy SECTION 1 X

Injury to pregnant women in motor vehicle crashes is estimated to account for 1500 to 5000 fetal deaths each year. There has been little investigation into specific forces and the kinematics of injury in pregnancy. Several studies have demonstrated that the most common cause of fetal demise in motor vehicle crashes with a viable mother is placental abruption. The biomechanics of this injury involves generation of tensile and shear forces, with the circumferential forces in the uterine wall inducing a shear strain across the placental surface, resulting in placental strain and subsequent abruption. Shorter women have a higher incidence of fetal demise with automotive crashes because of their close proximity to the steering wheel. As in other populations, restraints have been demonstrated to increase survival in both mother and fetus.77

■ Geriatrics Trauma remains a disease of the young, though there is a significant incidence of morbidity and mortality in the elderly population. Death from trauma represents the fifth leading cause of mortality in persons over 65 years of age. The most common mechanisms of injury in the elderly are falls, fires, and vehicular trauma. When patients with similar injury levels are compared with respect to age and mortality, the incidence of fatality in older persons is 5- to 10-fold higher than it is in the younger population. It is not the severity of injury that is crucial, but rather the incidence of comorbid factors in this population, especially cardiac and vascular disease. Most likely it is the patient’s inability to demonstrate a cardiovascular reserve that is a contributing factor to their subsequent increased morbidity and mortality. The Injury Severity Score and other predictors of outcome do not hold up in the geriatric or pediatric populations. Another significant finding in this population is that most (as many as 88%) of these patients never return to their previous level of independence.78 The incidence of falls in the geriatric population is high, with an annual incidence of approximately 30% in those over 65, and approximately 50% in those over 80 years of age. Falls account for approximately half the cases of geriatric trauma. Most falls in the elderly occur from standing with mortality secondary to the comorbid factors mentioned earlier.79 The propensity for fracture is also increased secondary to a loss of bone density with aging, with hip fractures being one of the most common injuries.

BLAST INJURIES Blast injuries are among the most dramatic and devastating wounds encountered by the trauma community. The National Counterterrorism Center documented approximately 11,800 terrorist attacks in 2008, resulting in over 54,000 deaths and injuries.80 Although the number of terrorist incidents decreased from the previous year, overall fatalities had increased.80, 81 The vast majority of these attacks occurred in the Middle and Far East, but the United States was not immune from blast incidents. The Bureau of Alcohol, Tobacco, and Firearms

noted an average of 182 annual injuries and 23 annual deaths from explosive incidents in the United States from the period of 2004 to 2006.82 Blast injuries are broadly categorized as primary, secondary, tertiary, quaternary, and quinary, based on a taxonomy of explosive injuries published by the Department of Defense in 2006.83 The trauma practitioner should be familiar with each of these patterns of injury and be able to predict associated injuries from each category (Table 1-2). Primary blast injuries occur when the blast overpressure transmits forces directly onto a person, causing tissue damage. The air-filled organs are the most likely affected by a primary blast injury and include the tympanic membrane, lungs, and gastrointestinal tract.84 Primary blast injuries are less common in open-space explosions but are increased in situations where the explosion occurs within a confined space, which allows the blast wave to reflect off of fixed structures.85 Rupture of the tympanic membrane is the most common manifestation of primary blast injury, occurring in up to one half of patients injured in an explosion.84 Some have considered an intact tympanic membrane to be a strong negative predictor of severe blast injury, although this has proven not to be the case.86, 87 The orientation of the patient to the blast wave (perpendicular vs. parallel), the presence or absence of cerumen in the ear canal, and whether the patient was wearing hearing protection at the time of the blast will all work to alter the true impact of the blast on the tympanic membrane.84 Therefore, an intact tympanic membrane does not rule out blast injury. The most common fatal injury among blast victims is to the lung, often referred to as “blast lung injury.” The blast wave causes tissue disruption at the capillary–alveolar interface, resulting in pulmonary edema, pneumothorax, parenchymal hemorrhage, and, occasionally, air embolus from alveolovenous fistulas.84 Clinical diagnosis of blast lung injury is dependent on the presence of the triad of hypoxia, respiratory distress, and bilateral or central infiltrates on a chest radiograph.88 The infiltrates are usually present on admission and can worsen with aggressive fluid resuscitation. These central infiltrates are also referred to as “butterfly” or “batwing” infiltrates and are pathognomonic for blast lung injury, in contrast to the peripheral infiltrates commonly seen with pulmonary contusions from blunt injury. Management of the ventilated patient with blast lung injury includes avoidance of positive pressure ventilation, minimization of positive-end expiratory pressure (PEEP), and judicious fluid resuscitation.84 Fluid management in these patients will often be challenging due to associated injuries from secondary and tertiary blast effects, which often require greater amounts of intravenous fluid for adequate resuscitation. Secondary blast injuries are created by debris from the explosive device itself or from surrounding environmental particles. Many devices contain additional munitions consisting of nails, pellets, ball bearings, and scrap metal designed to increase the lethality of the explosion. Fragments from the surrounding environment, including glass and small rocks, can become secondary missiles, as well. Secondary blast injuries are more common than primary blast injuries as the debris and added fragments travel over a much greater distance than does the shock wave from the primary blast.89 Lacerations, penetrating

Kinematics

15

TABLE 1-2 Department of Defense Classification of Blast Injuries from Explosive Devices Definition Blast overpressure injury (blast wave) Direct tissue damage from the shock wave Air-filled organs at highest risk (ears, lungs, gastrointestinal tract)

Common Injuries Tympanic membrane rupture Blast lung Gastrointestinal tract perforation/hemorrhage Ocular Concussion

Secondary

Primary fragments—from the exploding device (either from pieces of the device itself or from projectiles placed intentionally into the device to increase the lethality of the device) Secondary fragments—from the environment (glass, small rocks, etc.)

Lacerations Penetrating injury Significant soft tissue injury (including traumatic amputations) Ocular

Tertiary

Acceleration/deceleration of the body onto nearby objects or displacement of large nearby objects onto an individual

Blunt trauma Traumatic amputation Crush injury

Quaternary

Injuries due to other “explosive products” effects—heat, toxidromes from fuel and metals, and so on

Burns Inhalation injury

Quinary

Clinical consequences from postdetonation environmental contaminants including bacteria, radiation, and tissue reaction to fuels and metals

Radiation Sepsis

injury, and significant soft tissue defects are the most common injuries seen from secondary blast injuries. Tertiary blast injuries are caused by the body being physically thrown a distance or from a solid object falling onto a person as a result of the explosion. Most tertiary injuries are from a blunt mechanism, and crush injuries or traumatic amputations are not uncommon. Quarternary and quinary blast injuries have only recently been defined. They are miscellaneous blast injuries caused directly by the explosion but often due to other mechanisms, such as burns, inhalation injuries, and radiation effects. Children injured by explosions suffer a different injury pattern as compared to adults.90 Children are more likely to sustain life-threatening injuries and traumatic brain injury. They are less likely to have an extremity injury or significant open wounds. The adolescent injury pattern resembles that of the adult, although they are more likely to have fewer internal injuries, more contusions, and have a higher risk of requiring surgical intervention for mild or moderate wounds when compared to adults.

REFERENCES 1. The American Heritage Dictionary of the English Language. 4th ed. Houghton Mifflin; 2000. 2. Dennis JT. The Complete Idiot’s Guide To Physics. New York, NY: Alpha Books; 2006.

3. Newton I. Philosophiae Naturalis Principia Mathematica. New York: Prometheus Books; 1995. 4. Cutnell J, Johnson K. Physics. 4th ed. New York: John Wiley and Sons; 1997. 5. Sears FW, Zemansky MW. University Physics. Reading, MA: AddsionWesley; 1949. 6. Reif F. Statistical Physics. New York: McGraw-Hill; 1967. 7. Fackler ML, Dougherty PJ. Theodor Kocher and the Scientific Foundation of Wound Ballistics. Surg Gynecol Obstet. 1991;172(2):153–160. 8. Fackler ML, Malinowski JA. The wound profile: a visual method for quantifying gunshot wound components. J Trauma. 1985;25(6): 522–529. 9. Williams M. Practical Handgun Ballistics. Springfield, IL: Charles C. Thomas; 1980. 10. Hunter J. A Treatise on the Blood, Inflammation and Gunshot Wounds. London: John Richardson; 1794. 11. McSwain NE. Ballistics. In: Ivatury RR, Cayten CG, eds. The Textbook of Penetrating Trauma. Media, PA: Williams & Wilkens; 1996:105. 12. Fackler ML, Bellamy RF, Malinowski JA. Wounding mechanism of projectiles striking at more than 1.5 km/sec. J Trauma. 1986;26(3): 250–254. 13. Fackler ML. Wound ballistics. A review of common misconceptions. JAMA. 1988;259(18):2730–2736. 14. Fackler ML, Surinchak JS, Malinowski JA, Bowen RE. Bullet fragmentation: a major cause of tissue disruption. J Trauma. 1984;24(1): 35–39. 15. Swan KG, Swan RC. Gunshot Wounds: Pathophysiology and Management. Littleton, MA: PSG Publishing; 1980. 16. Fackler ML, Bellamy RF, Malinowski JA. A reconsideration of the wounding mechanism of very high velocity projectiles—importance of projectile shape. J Trauma. 1988;28(1 suppl):S63–S67. 17. Baker WE. Explosions in Air. Austin, TX: University of Texas Press; 1973. 18. Koper KD, Wallace TC, Reinke RE, et al. Emperical scaling laws for truck bomb explosions based on seismic and acoustic data. Bull Seismol Soc Am. 2002;92(2):527–542.

CHAPTER 1 X

Classification Primary

16

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SECTION 1 X

19. Ramamurthi K. Prediction of overpressure from finite-volume explosions. Defence Sci J. 1995;45(1):35–41. 20. Stuhmiller JH, Phillips YY, Richmond DR. The physics and mechanisms of primary blast injury. Conventional warfare: ballistic, blast, and burn injuries. In: General OotS, ed. Textbook of Military Medicine: Warfare, Weaponry, and the Casualty. Vol 5. Washington, DC: Office of the Surgeon General; 1991:241–270. 21. Einstein A. Ist die Trägheit eines Körpers von seinem Energieinhalt abhängig? . Annalen der Physik. 1905;18:639–643. 22. Planck M. Ueber das Gesetz der Energieverteilung im Normalspectrum. Ann Phys. 1901;309(3):553–563. 23. Weast RC. CRC Handbook of Chemistry and Physics. Boca Raton, FL: CRC Press; 1986. 24. Viano DC, King AI, Melvin JW, Weber K. Injury biomechanics research: an essential element in the prevention of trauma. J Biomech. 1989;22(5): 403–417. 25. McSwain N. Kinematics of trauma. In: Mattox KL, Moore EE, Feliciano DV, eds. Trauma. 4th ed. New York: McGraw-Hill; 1996. 26. Halliday D, Resnick RE. Fundamentals of Physics. 3rd ed. New York: Wiley; 1988. 27. Hoadley BR. Understanding Wood. A Craftsman’s Guide To Wood Technology. Newton, CT: The Taunton Press; 1980. 28. Pugh J, Dee R. Properties of musculoskeletal tissues and biomaterials. In: Dee R, Mango E, Hurst LC, eds. Principles of Orthopaedic Practice. New York: McGraw-Hill; 1988:134. 29. Frankel VH, Burnstein AH. Orthopaedic Biomechanics. Philadelphia: Lea & Febinger; 1970. 30. Ryan JM, Rich NM, Dale RF, et al. Ballistic Trauma: Clinical Relevance in Peace and War. New York, NY: Oxford University Press; 1997. 31. Mackay M. Mechanisms of injury and biomechanics: vehicle design and crash performance. World J Surg. 1992;16(3):420–427. 32. Gikas PW. Mechanisms of injury in automobile crashes. Clin Neurosurg. 1972;19:175–190. 33. Gongora E, Acosta JA, Wang DS, Brandenburg K, Jablonski K, Jordan MH. Analysis of motor vehicle ejection victims admitted to a level I trauma center. J Trauma. 2001;51(5):854–859. 34. Lindquist MO, Hall AR, Bjornstig UL. Kinematics of belted fatalities in frontal collisions: a new approach in deep studies of injury mechanisms. J Trauma. 2006;61(6):1506–1516. 35. Daffner RH, Deeb ZL, Lupetin AR, Rothfus WE. Patterns of high-speed impact injuries in motor vehicle occupants. J Trauma. 1988;28(4): 498–501. 36. Panjabi MM, White AA, 3rd. Basic biomechanics of the spine. Neurosurgery. 1980;7(1):76–93. 37. Swierzewski MJ, Feliciano DV, Lillis RP, Illig KA, States JD. Deaths from motor vehicle crashes: patterns of injury in restrained and unrestrained victims. J Trauma. 1994;37(3):404–407. 38. Vestrup JA, Reid JD. A profile of urban adult pedestrian trauma. J Trauma. 1989;29(6):741–745. 39. Lane PL, McClafferty KJ, Nowak ES. Pedestrians in real world collisions. J Trauma. 1994;36(2):231–236. 40. Helling TS, Watkins M, Evans LL, Nelson PW, Shook JW, Van Way CW. Low falls: an underappreciated mechanism of injury. J Trauma. 1999;46(3):453–456. 41. Velmahos GC, Demetriades D, Theodorou D, et al. Patterns of injury in victims of urban free-falls. World J Surg. 1997;21(8):816–820; discussion 820–811. 42. Peek-Asa C, McArthur D, Hovda D, Kraus J. Early predictors of mortality in penetrating compared with closed brain injury. Brain Inj. 2001;15(9):801–810. 43. Guerrero JL, Thurman DJ, Sniezek JE. Emergency department visits associated with traumatic brain injury: United States, 1995–1996. Brain Inj. 2000;14(2):181–186. 44. Gennarelli TA, Champion HR, Copes WS, Sacco WJ. Comparison of mortality, morbidity, and severity of 59,713 head injured patients with 114,447 patients with extracranial injuries. J Trauma. 1994;37(6):962–968. 45. McMahon CG, Yates DW, Campbell FM, Hollis S, Woodford M. Unexpected contribution of moderate traumatic brain injury to death after major trauma. J Trauma. 1999;47(5):891–895. 46. Park HK, Fernandez II, Dujovny M, Diaz FG. Experimental animal models of traumatic brain injury: medical and biomechanical mechanism. Crit Rev Neurosurg. 26 1999;9(1):44–52. 47. King AI, Ruan JS, Zhou C, Hardy WN, Khalil TB. Recent advances in biomechanics of brain injury research: a review. J Neurotrauma. 1995;12(4):651–658. 48. Gennarelli TA, Thibault LE. Biomechanics of acute subdural hematoma. J Trauma. 1982;22(8):680–686.

49. Holbourn AHS. Mechanics of head injuries. Lancet. 1943;242(6267): 438–441. 50. Blumbergs PC, Scott G, Manavis J, Wainwright H, Simpson DA, McLean AJ. Staining of amyloid precursor protein to study axonal damage in mild head injury. Lancet. 15 1994;344(8929):1055–1056. 51. Buki A, Povlishock JT. All roads lead to disconnection?—Traumatic axonal injury revisited. Acta Neurochir (Wien). 2006;148(2):181–193; discussion 193–184. 52. Cooper GJ, Maynard RL, Pearce BP, Stainer MC, Taylor DE. Cardiovascular distortion in experimental nonpenetrating chest impacts. J Trauma. 1984;24(3):188–200. 53. Cooper GJ, Taylor DE. Biophysics of impact injury to the chest and abdomen. J R Army Med Corps. 1989;135(2):58–67. 54. Shkrum MJ, McClafferty KJ, Green RN, Nowak ES, Young JG. Mechanisms of aortic injury in fatalities occurring in motor vehicle collisions. J Forensic Sci. 1999;44(1):44–56. 55. Rabinovici R, Ovadia P, Mathiak G, Abdullah F. Abdominal injuries associated with lumbar spine fractures in blunt trauma. Injury. 1999;30(7):471–474. 56. Neugebauer H, Wallenboeck E, Hungerford M. Seventy cases of injuries of the small intestine caused by blunt abdominal trauma: a retrospective study from 1970 to 1994. J Trauma. 1999;46(1):116–121. 57. Dauterive AH, Flancbaum L, Cox EF. Blunt intestinal trauma. A modernday review. Ann Surg. 1985;201(2):198–203. 58. Geoghegan T, Brush BE. The Mechanism of intestinal perforation from nonpenetrating abdominal trauma. AMA Arch Surg. 1956 1956;73(3): 455–464. 59. Munns J, Richardson M, Hewett P. A review of intestinal injury from blunt abdominal trauma. Aust N Z J Surg. 1995;65(12):857–860. 60. Morris S, Lenihan B, Duddy L, O’Sullivan M. Outcome after musculoskeletal trauma treated in a regional hospital. J Trauma. 2000;49(3):461–469. 61. Harkess JW, Ramsey CW, Harkess JW. Biomechanics of fractures. In: Rockwood CA, Green DP, Bucholz RW, eds. Fractures in Adults. New York: Lippincott; 1991:1. 62. Viano DC. Causes and control of spinal cord injury in automotive crashes. World J Surg. 1992;16(3):410–419. 63. Pennie B, Agambar L. Patterns of injury and recovery in whiplash. Injury. 1991;22(1):57–59. 64. Hendriks EJ, Scholten-Peeters GG, van der Windt DA, Neeleman-van der Steen CW, Oostendorp RA, Verhagen AP. Prognostic factors for poor recovery in acute whiplash patients. Pain. 2005;114(3):408–416. 65. Haddon W, Jr. Energy damage and the ten countermeasure strategies. J Trauma. 1973;13(4):321–331. 66. Mashaw J. The Struggle for Auto Safety. Cambridge, MA: Harvard Press; 1990. 67. Viano DC, Olsen S. The effectiveness of active head restraint in preventing whiplash. J Trauma. 2001;51(5):959–969. 68. Miller PR, Fabian TC, Bee TK, et al. Blunt cerebrovascular injuries: diagnosis and treatment. J Trauma. 2001;51(2):279–285; discussion 285–276. 69. Feliciano DV, Wall MJ. Patterns of injury In: Moore EE, Mattox KL, Feliciano DV, eds. Trauma. 2nd ed. Norwalk, CT: Appleton & Lange; 1991:81. 70. Hendey GW, Votey SR. Injuries in restrained motor vehicle accident victims. Ann Emerg Med. 1994;24(1):77–84. 71. Arbogast KB, Moll EK, Morris SD, Anderko RL, Durbin DR, Winston FK. Factors influencing pediatric injury in side impact collisions. J Trauma. 2001;51(3):469–477. 72. Snyder CL, Jain VN, Saltzman DA, Strate RG, Perry JF, Jr., Leonard AS. Blunt trauma in adults and children: a comparative analysis. J Trauma. 1990;30(10):1239–1245. 73. Kokoska ER, Keller MS, Rallo MC, Weber TR. Characteristics of pediatric cervical spine injuries. J Pediatr Surg. 2001;36(1):100–105. 74. Haricharan RN, Griffin RL, Barnhart DC, Harmon CM, McGwin G. Injury patterns among obese children involved in motor vehicle collisions. J Pediatr Surg. 2009;44(6):1218–1222; discussion 1222. 75. Mehlman CT, Scott KA, Koch BL, Garcia VF. Orthopaedic injuries in children secondary to airbag deployment. J Bone Joint Surg Am. 2000; 82(6):895–898. 76. Berkowitz CD. Pediatric abuse. New patterns of injury. Emerg Med Clin North Am. 1995;13(2):321–341. 77. Pearlman MD, Klinich KD, Schneider LW, Rupp J, Moss S, AshtonMiller J. A comprehensive program to improve safety for pregnant women and fetuses in motor vehicle crashes: a preliminary report. Am J Obstet Gynecol. 2000;182(6):1554–1564. 78. Tornetta P, 3rd, Mostafavi H, Riina J, et al. Morbidity and mortality in elderly trauma patients. J Trauma. 1999;46(4):702–706.

Kinematics 85. Leibovici D, Gofrit ON, Stein M, et al. Blast injuries: bus versus open-air bombings—a comparative study of injuries in survivors of open-air versus confined-space explosions. J Trauma. Dec 1996;41(6):1030–1035. 86. DePalma RG, Burris DG, Champion HR, Hodgson MJ. Blast injuries. N Engl J Med. Mar 31 2005;352(13):1335–1342. 87. Ashkenazi I, Olsha O, Alfici R. Blast injuries. N Engl J Med. Jun 23 2005;352(25):2651–2653; author reply 2651–2653. 88. Avidan V, Hersch M, Armon Y, et al. Blast lung injury: clinical manifestations, treatment, and outcome. Am J Surg. Dec 2005;190(6): 927–931. 89. Wolf SJ, Bebarta VS, Bonnett CJ, Pons PT, Cantrill SV. Blast injuries. Lancet. Aug 1 2009;374(9687):405–415. 90. Jaffe DH, Peleg K. Terror explosive injuries: a comparison of children, adolescents, and adults. Ann Surg. Jan 2010;251(1):138–143.

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79. Sterling DA, O’Connor JA, Bonadies J. Geriatric falls: injury severity is high and disproportionate to mechanism. J Trauma. 2001;50(1):116–119. 80. NCTC Report on Incidents of Terrorism 2008 National Counterterrorism Center; 2010. http://wits-classic.nctc.gov/ReportPDF.do?f=crt2008 nctcannexfinal.pdf. Accessed April 22, 2010 81. Champion HR, Holcomb JB, Young LA. Injuries from explosions: physics, biophysics, pathology, and required research focus. J Trauma. 2009;66(5):1468–1477; discussion 1477. 82. U.S. Bomb Data Center. Available 2008; http://www.atf.gov/publications/ factsheets/factsheet-us-bomb-data-center.html. Accessed April 22, 2010. 83. Medical Research for Prevention, Mitigation, and Treatment of Blast Injuries. Number. Department of Defense Directive 2006; July 2006:http:// www.dtic.mil/whs/directives/corres/html/602521.htm. Accessed April 22, 2010. 84. Ritenour AE, Baskin TW. Primary blast injury: update on diagnosis and treatment. Crit Care Med. Jul 2008;36(7 Suppl):S311–317.

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18

CHAPTER 2

Epidemiology Thomas J. Esposito and Karen J. Brasel

From the public health perspective, injury is not considered an “accident” but rather a disease, much like malaria, tuberculosis and other public health scourges, or cancer and heart disease. Injury, like other diseases, has variants such as blunt or penetrating. It has degrees of severity, rates of incidence, prevalence, and mortality that can differ by race and other sociodemographic factors. Injuries have a pattern of occurrence related to age, gender, alcohol and other drugs, and again, sociodemographic factors, among others. When public health concepts are applied to this disease of injury, it, like the aforementioned public health diseases, can be controlled to a socially acceptable level. The first step, however, is to characterize the disease such that control strategies can be applied. Epidemiology is the study of patterns of disease occurrence in human populations and the factors that influence these patterns.1 Descriptive epidemiology refers to the distribution of disease over time, place, and within or across specific subgroups of the population. It is important for understanding the impact of injury in a population and identifying opportunities for intervention. Analytic epidemiology, in contrast, refers to the more detailed study of the determinants of observed distributions of disease in terms of causal factors. The epidemiological framework traditionally identifies these factors as related to the host (i.e., characteristics intrinsic to the person), the agent (physical, chemical, nutritive, or infectious), and the environment (i.e., characteristics extrinsic to the individual that influence exposure or susceptibility to the agent). The environment can be physical or sociocultural. It is the understanding of how these multiple factors interact to increase the risk of injury and their influence on injury outcome that exemplifies the epidemiological approach to the study of disease and injury. By studying patterns of occurrence across and within populations of individuals, one can learn how best to potentially mitigate them. The concepts of the public

health approach applied to injury control seek to modulate factors related to the host and agent and/or their interactions within the environment utilizing a number of strategies. These strategies encompass engineering, education, the enactment and enforcement of laws, and economic incentives and disincentives. Injuries can result from acute exposure to physical agents such as mechanical energy, heat, electricity, chemicals, and ionizing radiation in amounts or rates above or below the threshold of human tolerance.2 The transfer of mechanical energy accounts for more than three quarters of all injuries.3 The extent and severity of injury is largely determined by the amount of energy outside the threshold of human tolerance. Both the exposure to energy and the consequences of that exposure are greatly influenced by a variety of factors both within and beyond individual or societal control.4 The public health approach as it applies to injury was first conceptualized by William Haddon in the late 1960s.2 He developed and promulgated a phase-factor matrix that incorporated the classic epidemiological framework of host, agent, and environment in a time sequence that encompasses three phases: pre-event, event, and post-event. Factors related to the host, agent, or environment in the pre-event phase determine whether the event will occur (e.g., motor vehicle crash). Factors in the event phase determine whether an injury will occur as a result of the event and the degree of injury severity. Factors in the post-event phase influence the outcome from, or consequences of, any injuries of any severity that do occur. An example of the Haddon Matrix applied to an actual injury event is depicted in Table 2-1. The addition of potential control strategies to the matrix in a three-dimensional fashion results in an “injury control cube,” suggesting that injury prevention and control are not unidimensional or unifactorial and that the greater the number of sections of the “cube” that are addressed, the greater the control of the injury event (Fig. 2-1A). For example, gun control laws focus on only the

Epidemiology

19

TABLE 2-1 Haddon Matrix Conceptually Applied to a Motor Vehicle Crash Incident Event Use of safety belts Deployment of air bag

Environment

Speed limits

Impact-absorbing barriers

Post-event Care delivered by bystander Assessment of vehicle characteristics that may have contributed to event Access to trauma system

Source: Reproduced with permission from ATLS Course, 8th ed. Chicago, IL: American College of Surgeons.

agent, in the pre-event phase, using a legislative strategy (Fig. 2-1B). However, there are many other counter measures that can be applied in other phases and to the host or environment (Table 2-2). The public health approach to injury control will be detailed further in Chapter 3.

OVERVIEW OF EPIDEMIOLOGY IN THE UNITED STATES Injuries rank fourth as a cause of death for all age groups in this country. It is the leading cause of death among children, adolescents, and young adults ages 1–34 (Table 2-3).5 In 2009 nearly 150,000 persons died in the United States as a result of an injury. This yields an overall death rate of 54.4 injury deaths per 100,000 population translating into over 400 injury deaths per day with nearly 50 of these being children. Approximately 8 of every 10 deaths in young people

ages 15–24 are injury related and more deaths among the young ages 1–34 are attributable to injury than all other causes of death in that age group combined. Trends in annual rates of death due to the nine leading causes among persons ages 25–44 over time are shown in Fig. 2-2. Specific trends for injuries over the past several decades show an overall decline in the death rate from unintentional causes primarily due to advances in traffic and work place safety. Intentional injuries, particularly those related to firearms, have fluctuated over the last decade. Homicide deaths are predominantly responsible for the fluctuations, as suicide deaths have remained relatively stable. The societal impact of injury is further emphasized when comparing the total years of potential life lost before age 65 across the leading causes of death (Fig. 2-3). Intentional and unintentional deaths account for over 30% of the total years of potential life lost for all deaths occurring in that age range.

Social environment

Physical environment

Agent Economic – Incentives/Disincentives Education Engineering

Host

Legislation – Enactment/Enforcement A

Pre-event

Event

Post-event

FIGURE 2-1 (A) Injury control “cube” graphic depiction—general concept.

CHAPTER 2

Host Vehicle

Pre-event Avoidance of alcohol use Antilock brakes

20

Trauma Overview

SECTION 1

Social environment

Physical environment

Agent Economic – Incentives/Disincentives Education Engineering

Host

Legislation – Enactment/Enforcement B

Pre-event

Event

Post-event

FIGURE 2-1 (continued) (B) Positioning of gun control laws in the injury control “cube” model.

Therefore, injuries account for more premature deaths than cancer, heart disease, or HIV infection.5 Previously, trauma deaths were characterized as having a trimodal distribution.6 However, more recent studies suggest a bimodal pattern with a reduction in late deaths7,8 The majority of all deaths still occur within minutes of the injury, either at the scene prior to arrival of emergency medical services (EMS), en route to the hospital, or in the first hours of care. These immediate deaths are typically the result of massive hemorrhage or severe neurological injury. Many fatalities succumb primarily due to central nervous system (CNS) injury within several hours to several days of the event. Far fewer than in original studies now die of infection or multiple organ failure many days to weeks after the injury (Fig. 2-4 A and B). Currently, even the best EMS and trauma systems are largely ineffective in preventing those deaths that occur at the scene of the incident. Efforts at preventing the occurrence of the injury event or reducing the severity of the injuries incurred by the incident will be the most effective means of reducing this large number of immediate deaths. Continued efforts at developing trauma systems that foster rapid and efficient means of triage and transfer to higher levels of care, and efforts at clinical and translational research in the area of trauma, hemorrhage, and infection will eventually serve to reduce the delayed and late deaths. Deaths represent only one small aspect of the injury disease burden. Each year, over 1.5 million people are hospitalized as the result of an acute injury and survive to discharge. Another 28 million are treated and released from emergency departments (EDs) or urgent care centers.8 Fig. 2-5 depicts these

statistics for 2004. Injuries account for an estimated 6% of all hospital discharges and 30% of all ED visits annually. Many of these nonfatal injuries have far-reaching consequences with potential for reduced quality of life and high costs accrued to the health care system, employers, and society. The estimated total lifetime costs associated with both fatal and nonfatal injuries occurring in any 1 year amount to over 406 billion dollars9,10 (Table 2-4). The costs associated with injury deaths account for a disproportionate share of total injury costs. Estimates show that deaths account for less than 1% of all injuries but account for 31% of total injury costs. The majority, or the remaining 69% of costs due to injury, is associated with nonfatal injuries. These costs include direct expenditures for health care and other goods and services purchased as a result of the injury. Direct expenditures account for approximately 30% of the total cost of injury. The value of lost productivity due to temporary and permanent disabilities is also taken into account and represents 41% of the total costs. It is often mentioned that these are merely the financial costs and do not take account the pain and suffering to the patients, their families and associates that are the sequelae of nonfatal injuries.

OVERALL INJURY PATTERNS BY AGE AND GENDER Injury is a disease predominantly affecting young males. Seventy percent of injury deaths and over half of nonfatal injuries occur among males.3,5,8 In every age group except ages 0–9, the rate of injury death for males is more than twice as

TABLE 2-2 The Ten Leading Causes of Death by Age Group and Rank 1–4

5–9

10–14

15–24

Age Groups 25–34

35–44

45–54

55–64

65

All Ages

1

Congenital Anomalies 5,785

Unintentional Injury 1,588

Unintentional Injury 965

Unintentional Injury 1,229

Unintentional Injury 15,897

Unintentional Injury 14,977

Unintentional Injury 16,931

Malignant Neoplasms 50,167

Malignant Neoplasms 103,171

Heart Disease 496,095

Heart Disease 616,067

2

Short Gestation 4,857

Congenital Anomalies 546

Malignant Neoplasms 480

Malignant Neoplasms 479

Homicide 5,551

Suicide 5,278

Malignant Neoplasms 13,288

Heart Disease 37,434

Heart Disease 65,527

Malignant Neoplasms 389,730

Malignant Neoplasms 562,875

3

SIDS 2,453

Homicide 398

Congenital Anomalies 196

Homicide 213

Suicide 4,140

Homicide 4,758

Heart Disease 11,839

Unintentional Injury 20,315

Chronic Low. Respiratory Disease 12,777

Cerebrovascular 115,961

Cerebrovascular 135,952

4

Maternal Pregnancy Comp. 1,769

Malignant Neoplasms 364

Homicide 133

Suicide 180

Malignant Neoplasms 1,653

Malignant Neoplasms 3,463

Suicide 6,722

Liver Disease 8,212

Unintentional Injury 12,193

Chronic Low. Respiratory Disease 109,562

Chronic Low. Respiratory Disease 127,924

5

Unintentional Injury 1,285

Heart Disease 173

Heart Disease 110

Congenital Anomalies 178

Heart Disease 1,084

Heart Disease 3,223

HIV 3,572

Suicide 7,778

Diabetes Mellitus 11,304

Alzheimer’s Disease 73,797

Unintentional Injury 123,706

6

Placenta Cord Membranes 1,135

Influenza & Pneumonia 109

Chronic Low. Respiratory Disease 54

Heart Disease 131

Congenital Anomalies 402

HIV 1,091

Homicide 3,052

Cerebrovascular 6,385

Cerebrovascular 10,500

Diabetes Mellitus 51,528

Alzheimer’s Disease 74,632

7

Bacterial Sepsis 820

Septicemia 78

Influenza & Pneumonia 48

Chronic Low. Respiratory Disease 64

Cerebrovascular 195

Diabetes Mellitus 610

Liver Disease 2,570

Diabetes Mellitus 5,753

Liver Disease 8,004

Influenza & Pneumonia 45,941

Diabetes Mellitus 71,382

8

Respiratory Distress 789

Perinatal Period 70

Benign Neoplasms 41

Influenza & Pneumonia 55

Diabetes Mellitus 168

Cerebrovascular 505

Cerebrovascular 2,133

HIV 4,156

Suicide 5,069

Nephritis 38,484

Influenza & Pneumonia 52,717

9

Circulatory System Disease 624

Benign Neoplasms 59

Cerebrovascular 38

Cerebrovascular 45

Influenza & Pneumonia 163

Congenital Anomalies 417

Diabetes Mellitus 1,984

Chronic Low. Respiratory Disease 4,153

Nephritis 4,440

Unintentional Injury 38,292

Nephritis 46,448

10

Neonatal Hemorrhage 597

Chronic Low. Respiratory Disease 57

Septicemia 36

Benign Neoplasms 43

Three Tied 160

Liver Disease 384

Septicemia 910

Viral Hepatitis 2,815

Septicemia 4,231

Septicemia 26,362

Septicemia 34,828

Source: From WISQARS. Produced By: Office of Statistics and Programming, National Center for Injury Prevention and Control, Centers for Disease Control and Prevention. Atlanta, GA: Data Source: National Center for Health Statistics (NCHS), National Vital Statistics System.

Epidemiology

1

Rank

21

CHAPTER 2

22

Trauma Overview

TABLE 2-3 Counter Measures Available for Controlling Firearm-related Injury

high as the rate for females. For nonfatal injuries, males are only 1.3 times as likely as females to be affected. This gender-related risk reverses after the age of 65 with females being 1.3 times as likely as males to suffer nonfatal injury in that age category. The disease of injury has a bimodal distribution of mortality that peaks for both genders in the 16- to 40-year-old age group and then again in those older than 65 years of age. Persons under the age of 45 account for 53% of all injury fatalities (Fig. 2-6), just over 50% of hospitalizations, and nearly 80% of

Part II-FLCOT-Injury Prevention Countermeasures in Injury Control Interpose material barriers between hazard and host Bulletproof vest Bulletproof glass Modify basic qualities of the hazard Small gauge ammunition Nonfragmenting bullets Nonlethal chemical ammunition Lessen effects of hazard after occurrence EMS access and care Hospital care Rehabilitation

ED visits.3,5,8 Hospitalizations and ED visits also follow this pattern of a bimodal peak related to age and a predominance among the male gender. The elderly, while being less likely to be injured, are more likely to be hospitalized or die from those injuries with a lesser degree of severity than their younger counterparts. The rate of injury death among persons age 65 and older is 113/100,000 population and for persons age 75 and older it is 169/100,000. The elderly are overrepresented in the pool of injury fatalities

Trends in annual rates of death due to the 9 leading causes among persons 25–44 years old, United States, 1987–2006 40 35 Deaths per 100,000 population

SECTION 1

Part I-FLCOT-Injury Prevention Countermeasures in Injury Control Prevent creation of the hazard Ban manufacture of guns/ammunition Reduce amount of hazard Limit manufacture and sale Guns buy-back programs Prevent release of existing hazard Trigger locks Storage Alternative conflict resolution Modify rate or spatial distribution of hazard release from source Lower caliber/velocity No automatic weapons Separate host and agent in time or space Curfews Safe-havens

Unintentional injury Cancer Heart disease Suicide Homicide HIV disease Chronic liver disease Diabetes Stroke

30 25 20 15 10 5 0 1987 1988 1989 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006

Note: For comparison with data for 1999 and later years, data for 1987–1998 were modified to account for ICD-10 rules instead of ICD-9 rules.

FIGURE 2-2 Trends in annual rates of death due to the nine leading causes of death in the United States for those age 25–44 (1987–2006). (From Centers for Disease Control and Prevention, Atlanta, Georgia.)

Epidemiology

23

Years of Potential Life Lost (YPLL) Before Age 65 2007 United States All Races, Both Sexes All Deaths

All Causes

YPLL

11,795,817

Unintentional Injury

2,371,575

Malignant Neoplasms

1,858,935

Heart Disease

1,395,829

Percent

100.0% 20.1% 15.8% 11.8%

Perinatal Period

947,061

Suicide

703,199

Homicide

605,158

Congenital Anomalies

491,957

Liver Disease

247,188

2.1%

Cerebrovascular

243,667

2.1%

Diabetes Mellitus

222,303

1.9%

All Others

8.0% 6.0% 5.1% 4.2%

2,708,945

23.0%

FIGURE 2-3 Comparison of years of potential life lost before age 65 stratified by disease/condition. (From Centers for Disease Control and Prevention, Atlanta, Georgia.)

and hospitalized patients. Although representing only 3% of the U.S. population, those over the age of 65 accounted for approximately 26% of all injury deaths and 30% of all injuryrelated hospitalizations. The proportion of citizens over the age of 65 is projected to increase to nearly 20% by the year 2030.11 This has significant implications for the future of health care as over the next several decades it is expected that the elderly will account for approximately 40% of all injury deaths and hospitalizations.

PATTERNS OF INJURY BY MECHANISM AND INTENT Injuries are typically categorized by their mechanism, intent, and place of occurrence. Mechanism refers to the external agent or particular activities that were associated with the injury (e.g., motor vehicle related, falls, firearm related, etc.). Intent of the injury is classified as either unintentional (often referred to as “an accident”) or intentional. Injuries that are intentionally inflicted can be further subcategorized into interpersonal (e.g., homicide) or intrapersonal (e.g., suicide). Intent may not be always determinable. Injuries resulting from legal interventions and operations of war are typically classified separately as an “other intent” category.

The classification system most often used in describing the specific mechanism and intent of injury is the international classification of disease (ICD). This classification system was developed and promulgated by the World Health Organization and is now in its tenth edition.12,13 The E-Code, which is the acronym for external cause of injury code, provides detailed information about the circumstances associated with injuryrelated ED visits and hospitalizations. These codes are considered essential to the epidemiology of injury and its accurate study. They provide critical public health information for monitoring health status, setting injury prevention priorities, and developing and evaluating injury prevention programs at the local, state, and national levels. E-Codes are also useful for injury-related quality-of-care assessments (e.g., risk of falls among older persons) in the emergency care, hospital, assisted living/nursing care, and home health care settings. As an example, fall prevention (e.g., reducing fall-related hip fractures) is one of the priority areas for quality and patient safety initiatives relevant to the present-on-admission (POA) Codes required for billing by the federal government (Center for Medicare and Medicaid Services [CMS]). E-Codes can also be useful for other quality initiatives associated with injury-related claims (e.g., motor vehicle crashrelated injuries) that may assist CMS in making payment

CHAPTER 2

Cause of Death

24

Trauma Overview 120 84% 100 # of patients

SECTION 1

120 100 80 60 40 20 0

80 60

5%

<1hr 2hrs

11%

3hrs 4hrs

40

20 0 1-4 hrs

< 1 hr

5-12 hrs 13-24 hrs 25-48 hrs 3-7 days 2nd week 3rd week 4th week 5th week > 5 weeks

Time from injury to death

CNS

A

Exsanguination

Other causes

60

# of patients

50

40 Blunt Penetrating 30

20

10

0 < 1 hr

B

1-4 hrs

5-12 hrs

13-24 hrs 25-48 hrs 3-7 days 2nd week 3rd week 4th week 5th week > 5 weeks

Time from injury to death

FIGURE 2-4 (A) Temporal distribution of trauma deaths, excluding individuals who were found dead by police. (B) Temporal distribution of trauma deaths caused by blunt and penetrating injuries, excluding individuals who were found dead by police. (Reproduced with permission from Sauaia A, Moore FA, Moore EE, et al. Epidemiology of trauma deaths: A reassessment. J Trauma. 1995;38:185.)

decisions. Hence, numerous professional organizations, including the American College of Surgeons Committee on Trauma, the American College of Emergency Physicians, the Emergency Nurses Association, and the National Safety Counsel, have published position statements to endorse the need for improving E-Coding in state mortality and morbidity data systems. They have also urged that the capture of at least three codes as part of the electronic health record that is being proposed by CMS be essential. Two of the E-Code fields can be used for coding the precipitating and immediate causes (e.g., the mechanism/intent of injury such as falls, motor vehicle traffic, fire/ burn, cut/pierce, assault, self-harm, etc.) and one other field to

delineate place of occurrence (e.g., home, street/highway, residential, institution, etc.). The distribution of injuries by mechanism varies for deaths, hospitalizations, and ED visits. The two leading mechanisms of injury death are related to motor vehicles and firearms. Using 2007 statistics from the Centers for Disease Control and Prevention (CDC), it appears there were over 182,000 deaths caused by injuries.5 Approximately 46,000 of these (25%) were traffic related with just over 31,000 (17%) related to firearms. Another 23,000 (13%) were related to falls. In contrast, using 2008 statistics, of the nearly 30 million nonfatal injuries reported to the CDC, approximately 8.5 million (29%) were

Epidemiology

25

Injuries in the United States, 2004 167,184 injury deaths (7%)

31 million initial emergency department visits for injury (32%)

Deaths

Hospital discharges

35 million initial visits for injury to physician offices and outpatient departments (12%)

Initial emergency department visits

33 million episodes of medically-attended injuries were reported in a national household survey.

Initial physician office and outpatient department visits

FIGURE 2-5 Injuries in the United States, 2004. (From Centers for Disease Control and Prevention, National Center for Health Statistics, Atlanta, Georgia. Injuries in the United States; 2007 Chartbook, Figure 1.)

related to falls whereas approximately 4 million (14%) were traffic-related injuries. Less than 1% of reported nonfatal injuries were related to firearms. When all intents are considered, burns account for approximately 2% of all injury deaths and 1.4% of nonfatal injuries reported by the CDC.5 These differences in distribution by cause and class of injury underscore the lethality of injuries involving firearms and motor vehicles. Perhaps also emphasizing this point are statistics on intentionality of injury, which reveal that 93% of nonfatal injuries are unintentional whereas 68% of fatal injuries are unintentional. Nearly 30% of all injury deaths are violence related. In 2007 over 18,000 deaths were a result of homicide (34% of all violence related deaths) and over 34,000 deaths were caused by successful suicide attempts (66% of all violent deaths).

Injury in the workplace also constitutes a not uncommon occurrence. A total of 5,071 fatal work injuries were recorded in the United States in 2008. This represents 3.6 fatal work injuries per 1,000,000 full-time equivalent workers.14 Overall, transportation-related incidents accounted for the majority (40%) of occupational injury deaths. Assaults and violent acts accounted for 16% of fatalities, contacts with objects and equipment 18%, and falls 13%. Ten percent of occupational-related deaths in 2008 were a result of homicide, with firearm-related fatalities compromising 80% of these homicides. Five percent of deaths were a result of self-inflicted injuries. In addition to the fatalities associated with work-related activities, there were a total of 4.6 million nonfatal injuries recorded by the Bureau of Labor Statistics (3.9 cases per 100 workers).15

TABLE 2-4 Incidence and Cost of Injury in the United States, 2000 Fatal Hospitalized Nonhospitalized Total

Incidence 149,075 1,869,857 48,108,166 50,127,098

Medical Costs $1 billion $34 billion $45 billion $80 billion

Productivity Losses $142 billion $59 billion $125 billion $326 billion

Total Costs $143 billion $92 billion $171 billion $406 billion

Cost estimates based on 2000 data. Finkelstein et al. (2006) Source: From the Incidence and Economic Burden of Injuries in the United States. Atlanta, GA: Centers for Disease Control and Prevention.

CHAPTER 2

1.9 million hospital discharges for injury (6%)

26

Trauma Overview Injury deaths and injury death rates by age, 2003–2004 90

350 Injury deaths as percent of total deaths

300

70 250 Percent

60 200

50 40

150 Injury death rate

30

100 20

Deaths per 100,000 population

SECTION 1

80

50

10

0

0 Under 5 1

10 15 20 25 30 35 40 45 50 55 60 65 70 75 80 85 and Age in years over

FIGURE 2-6 Injury death and injury death rates by age, 2003–2004. (From Centers for Disease Control and Prevention, National Center for Health Statistics, Atlanta, Georgia. Injuries in the United States; 2007 Chartbook, Figure 3.)

Seventy-one percent of these occurred in service providing industries and nearly half produced disability.

DISTRIBUTION OF INJURIES BY NATURE AND SEVERITY Cataloging and analyzing the distribution of injuries by their nature and severity is important to efforts at establishing priorities for prevention as well as treatment and trauma system development. Several systems for classifying the nature and severity of injury exist and a number of these are described elsewhere in this textbook. The international collaborative effort on injury statistics has published an injury diagnosis matrix that provides a uniform framework for using the ICD codes in categorizing injury diagnosis by the body region involved and the specific nature of the injury.16 The most prevalent source of national data on the nature of injury death is death certificate data. However, these data have significant limitations due to variations and inaccuracy in the diagnosis listed as cause of death, terminology, and reporting practices for injury by geographic region and over different time periods.17,18 The National Trauma Data Bank (NTDB)19 also provides some insight as to the nature, severity, and types of injuries encountered utilizing a nonscientific sample of trauma centers that voluntarily contribute data to the data bank. Some of what is known about the overall nature of trauma deaths is based on a limited number of studies conducted in selected geographic regions using coroners’ reports and autopsy records.20,21 These types of records, much like the death certificates that are often based upon them, are variable in completeness, accuracy, and utility. Although the results of autopsy studies vary, they do suggest a trend that implicates CNS injuries as the most common cause of injury death,

accounting for 40–50% of the total number of deaths. The second ranking cause tends to be hemorrhage, accounting for an additional 30–35%. More recent and reliable data from the CDC confirms that traumatic brain injury (TBI) is a serious public health issue in America.22 TBI resulting from many mechanisms poses a serious public health problem contributing to a substantial number of deaths and cases of permanent disability each year. Like other injuries, TBI can range from mild to severe with many of the mild cases going undiagnosed. An estimated 1.7 million TBIrelated deaths, hospitalizations, and ED visits occur in the United States each year. As suggested by autopsy studies, TBI is a contributory factor in nearly one third of all injury-related deaths in the United States or about 52,000 deaths annually (Fig. 2-7). The distribution of all nonfatal injuries by nature and severity is somewhat different from that described for fatal injuries. Many injuries occurring each year affect isolated body systems and are associated with a low severity. Even among injuries that result in hospitalization, only one quarter have an Abbreviated Injury Scale (AIS)23 score of 3 or greater on a scale of 0–6. Injuries to the lower and upper extremities constitute the leading cause of hospitalizations and ED visits related to nonfatal injury. They account for over half (56%) of all nonfatal occurrences and 47% of all injury hospitalizations.8,9 Slightly over one third of hospitalizations for extremity injuries are for moderately severe to severe injuries as measured by an AIS score of 3 or more.9 For many of these injuries, recovery can be protracted and costly. Even optimal treatment can result in permanent impairment and disability.24–26 The second ranking cause of nonfatal injury hospitalization is head injury, accounting for 10–15% of total hospitalizations for injury.27 Mild head injuries are predominantly treated on an outpatient basis, comprising 2–5% of all injury-related ED

Epidemiology

27

Injury and Traumatic Brain Injury (TBI) Death rates, by age group — United States, 2006 Estimated average percentage of annual TBI by external cause in the United States, 2002–2006

Injury death rate

Per 100,000 population

TBI death rate 150 10% Assault 100 35.2% Falls

50

16.5% Struck by/ Against

75+

65–74

55–64

45–54

35–44

25–34

20–24

15–19

10–14

5–9

0–4

0

17.3% Motor Vehicle-traffic

Age group (years) Nearly one third of all injury deaths involve TBI.

FIGURE 2-7 Traumatic brain injury death rates in comparison to overall injury death rates stratified by age—United States, 2006. (From Centers for Disease Control and Prevention, Atlanta, Georgia.)

visits.28 Nearly 80% are treated and released. However, these ED statistics may actually be an underestimate, as many mild head injuries may be treated at urgent care centers and private physician offices and therefore not counted in the statistics. Estimates of the total incidence of head injury vary widely and range between 152 and 367 per 100,000 population.29 Although the majority of head injuries are classified as mild, conservative estimates suggest that between 70,000 and 90,000 people survive a significant head injury that often results in long-term disability.30 Head injuries incurred as a result of recreational activities are also not uncommon.31–33 Approximately 300,000 such injuries occur annually. The estimated average proportion of annual TBI stratified by external cause is noted in Fig. 2-8. Spinal cord injuries account for a relatively small proportion of all nonfatal injuries accounting for an estimated 10,000–15,000 hospitalizations per year.34 Once again, motor vehicles are the major cause of these types of injuries with 30–60% being a result of traffic incidents. Falls follow closely accounting for an additional 20–30%. Approximately 5–10% of all spinal cord injuries are due to diving. The total burden of injury stratified by body region is depicted in Fig. 2-9.

DISTRIBUTION OF INJURIES BY GEOGRAPHIC LOCATION The overall incidence and patterns of injury vary between urban and rural populations and across different regions of the country.3,8 Unintentional injury death rates are highest in rural

21% Unknown/ Other

FIGURE 2-8 Estimated average percentage of annual traumatic brain injury by external cause—United States, 2002–2006. (From Centers for Disease Control and Prevention, Atlanta, Georgia.)

areas, whereas homicide rates are several times higher in central cities compared to rural and suburban communities (Fig. 2-10). Injury death rates also vary by region of the country. Death rates for unintentional injury tend to be highest in the west and south, whereas suicide rates are highest in the west and homicide rates highest in the south. However, there is a substantial state-by-state and even county-by-county variation. To date, local data relating to nonfatal injuries are not uniformly

Total of all burden, by body region

35% 30% 25% 20% 15% 10% 5% 0%

Incidence Medical costs Productivity losses Total costs

I I e c o k n m m TB nec SC lum Tors xtre xtre spe -wid / n o r e r/u tem re ad lc s pe owe the he ra p b r Sy e e L U O rt th e O V

FIGURE 2-9 Total of all injury burden stratified by body region. (From Centers for Disease Control and Prevention, National Center for Health Statistics, Atlanta, Georgia.)

CHAPTER 2

200

28

Trauma Overview Injury death rates by level of urbanization, 2003 – 2004

SECTION 1 FIGURE 2-10 Injury death rates stratified by degree of urbanization. (From Centers for Disease Control and Prevention, National Center for Health Statistics, Atlanta, Georgia. Injuries in the United States: 2007 Chartbook, Figure 11.)

Deaths per 100,000 population

60

Large central metro

50 40

Micropolitan (nonmetro)

Small metro

Noncore (nonmetro)

30 20 10 0

Unintentional

Suicide

Homicide

Intent

available to examine trends by rurality or geographic region. The observed differences related to geographic location and population density may be a function of a number of confounding factors such as access to care, economic, or educational climate, to name a few. When these factors are controlled for, these geographic disparities can be less prominent, or nonexistent.

CONFOUNDERS OF INJURY ANALYSIS AND INTERPRETATION

Deaths per 100,000 population

There are a number of confounding factors that may influence results and, more critically, the interpretation and conclusions drawn from epidemiological analyses of injury. These include race, ethnicity, culture, socioeconomic status, access to health

care, mental health, alcohol and other drugs, as well as others. Due to their number and multiplicity, adequate control for any or all is difficult at best. Hence, forethought and caution should be exercised in making generalizations regarding some epidemiological findings. Although on the surface there may appear to be certain associations between race and injuries, particularly violent injuries, controlling for socioeconomic status, there is little disparity between races as perpetrators or victims of violence. For example, homicide rates have been shown to vary significantly by economic status (Fig. 2-11). Homicide rates for black males of age 15–24 show urban rates to be 96/100,000 population and in nonurban areas only 41/100,000. Therefore, data that are stratified by race and Hispanic origin must be interpreted carefully. First, the number of people in the population that is used as the denominator in the

3 2.5 Black

White

2 1.5 1 0.5 0 < $3,000

FIGURE 2-11 Violence-related deaths stratified by per capital income and race.

Medium metro

Large fringe metro

$3,000-

$4,000-

$5,000-

Per capita income of area

$6,000-

Epidemiology

LEADING MECHANISMS OF MAJOR TRAUMA ■ Traffic-related Injuries Traffic-related incidents involving motor vehicles are the leading cause of injury death and rank second as a cause of nonfatal injury in the United States. It is the leader of all causes of death in the 1–34 age group. There were 44,128 trafficrelated deaths in 2007 and over 298,000 hospitalizations in 2008 for these types of injuries. They also accounted for nearly 5 million ED visits. Adolescents and young adults are at the highest risk for both fatal and nonfatal injuries due to motor vehicles. Their rates of death, hospitalization, and ED visits are approximately twice

the rate for all ages combined. White males age 15–24 are at particular risk. For black males in that same age group, trafficrelated injury death rank second as a cause of death behind firearm-related injuries. The elderly, age 75 and older, are also at relatively high risk for dying from motor vehicle incidentrelated injury. Males are more than twice as likely as females to die from motor vehicle crashes. Males under the age of 45 are also more likely to be hospitalized as a result of motor vehicle-related injuries, although the gender differential is not as great as for fatalities. Males and females age 45 and older, in contrast, are equally likely to be hospitalized. Determinants of injury occurrence and severity in a motor vehicle-related incident relate to speed of impact, vehicle crash worthiness and the use of safety devices and restraints including safety belts, air bags, and helmets. When used, safety belts have been shown to reduce fatalities to front-seat occupants by 45% and the risk of moderate-to-critical injury by 50%. Currently, safety belt usage rates in the United States range from 68 to 98% with a national average of 84% in 2009.41 The additional presence of an air bag in belted drivers provides increased protection resulting in an estimated 51% reduction in fatality rate. Despite some success in reducing the role of alcohol in motor vehicle injuries, it remains a major factor in fatal crashes among adolescents and young adults. Approximately 50% of all traffic fatalities including the driver, occupant, bicyclist, or pedestrian have been found to have a blood alcohol concentration (BAC) of 0.08 g/dL or greater. The proportion of fatally injured drivers with elevated BAC varies with age. For all age groups, it has slowly declined over time but has remained unchanged in recent years (Fig. 2-12). Also of note is distracted driving. Distracted driving is an increasingly recognized risk factor for traffic-related injuries and deaths, which may supersede impaired driving as a contributor to these injury incidents. The practice of distracted driving has become a dangerous epidemic on America’s roadways. In 2009 alone, nearly 5,500 people were killed and over 450,000 more were injured in distracted driving crashes. In that year, 16% of fetal crashes and 20% of crashes resulting in non-fatal injuries involved reports of distracted driving.41 This does not include injuries and deaths incurred by distracted pedestrians and bicyclists. Distracted driving is not limited to the high profile activity of texting while driving but also includes other behaviors such as eating, grooming, reading (including maps and directions), or watching videos while driving. However, because text messaging requires visual, manual, and cognitive attention from the driver, it is by far the most concerning and risky distraction. It has been reported that one is 23 times more likely to be involved in a crash while texting and driving. Legislation to ban texting while driving is currently in place or in process in many states and municipalities. At present, nine states, the District of Columbia, and the US Virgin Islands prohibit all drivers from using handheld cell phones while driving. Thirty-five states and D.C. ban text messaging for all drivers, with 12 of these laws being enacted in 2010 alone.

CHAPTER 2

calculation of the death rate generally comes from U.S. Census Bureau estimates and the characteristics of those who died used in the numerator generally stems from either the funeral director or the medical examiner. As a result, to the extent that race and Hispanic origin are reported inconsistently by the different data sources generating the numerator and denominator, rates may be biased. Second, bias in estimates by race and ethnicity also can result from undercounting of specific populations in the census, thereby potentially producing an overestimation of death rates. Differences in health status by race and Hispanic origin also are known to exist and may be explained by factors including socioeconomic status, health practices, psychosocial stress and resources, environmental exposures, discrimination, and access to health care.35 As these factors are not routinely collected or controlled for, analysis of injury mortality and morbidity by race and ethnicity may lead to incorrect inferences. With specific regard to data on violence, estimates may be misinterpreted because attention may have been directed to the victim rather than to the perpetrator, for whom sufficient data are not routinely collected. The National Violent Death Reporting System (NVDRS)36,37 may improve this particular problem by attempting to acquire data, when possible, on the perpetrator as well as the victim. Although this chapter emphasizes the concept of injury being a disease entity in and of itself, data suggest that for a significant number of trauma patients, injuries may be an unrecognized symptom of an underlying alcohol or other drug use problem. Therefore, it may be that injury is actually a comorbidity of the disease that is alcohol and substance use disorder. Nearly 50% of injury deaths are alcohol related. Traumatic injury accounts for roughly the same number of alcohol-related deaths as cirrhosis, hepatitis, pancreatitis, and all other medical conditions associated with excessive alcohol use combined. A multicenter study that included data on more than 4,000 patients admitted to six trauma centers demonstrated that 40% had some level of alcohol in their blood upon admission,38 when other drug use is included up to 60% of patients test positive for one or more intoxicants.38–40 Therefore, it is clear that alcohol and substance use must be considered in the epidemiology of injury as well as in the equation leading to effective injury control.

29

30

Trauma Overview Fatally injured drivers with BAC of 0.08 percent or greater, 1982–2004 70

SECTION 1

60 21–30 years

Percent

50 40

31 years and over

30

16–20 years

20 10 0

1982 1984 1986 1988 1990 1992 1994 1996 1998 2000 2002 2004 Year

FIGURE 2-12 Fatally Injured Drivers with Blood Alcohol Level 0.08%—United States, 1982–2004. (From Centers for Disease Control and Prevention, National Center for Health Statistics, Atlanta, Georgia. Injuries in the United States: 2007 Chartbook, Figure 13.)

■ Firearm-related Injuries In 2007 there were 31,224 intentional and unintentional gun related deaths in the United States, which equates to approximately 86 deaths per day. The overwhelming majority of these deaths are intentional (98%) and related to violence, with only 2% being unintentional.5 Firearm-related deaths rank second as a cause of injury death over all ages in the United States being responsible for 17% of all injury deaths. More than half (57%) of all firearm deaths were suicide and an additional 40% were homicides. Firearm-related injuries disproportionately affect males and younger people. Approximately 87% involve males. In the 15–34 age group, firearm-related death rates for males are nearly seven times that for females. Firearm-related injuries are the leading cause of death in black males ages 15–34. From a global and cultural standpoint, firearm-related mortality is eight times higher in the United States than other high-income countries in the world. The majority of firearm-related deaths among males ages 15–34 in the United States (67%) are homicides. Suicide accounts for an additional 33%. Suicide in the elderly is also a significant problem with 3,895 firearm-related suicides among the elderly between ages 65 and 84 or greater. This represents 22% of all firearm-related injuries for both genders and all ages. Over 90% of the suicides in the elderly population were among males. Data on nonfatal firearm-related injuries are not as complete; however in 2008, there were 78,622 reported nonfatal injuries caused by firearms. The majority were again intentional; however, 17,215 were determined to be unintentional (22%).5 Both fatal and nonfatal firearm injuries are estimated to account for approximately 9% of the 406 billion dollar overall cost of injury in 2006, or nearly 37 billion dollars.10 Close to 8 billion (22%) were related to direct medical costs and over

29 billion (78%) were related to productivity losses. In analyzing firearm homicides, the firearm used in well over 80% of cases, where firearm type was known, involved handguns. It is estimated that firearms of some type are present in about 38% of all U.S. households and carried by one in 12 students.42,43 Some studies suggest that those who live in homes that harbor guns are more likely to die from homicide and suicide in the home than are residents of homes without firearms.44,45 There is evidence to suggest that few firearm deaths in the home stem from acts of self-protection. It is reported that half of those murdered in the home knew their assailant. Less than 2% of homicides committed with a firearm are judged to be justifiable, that is, in self-defense. In one survey, results revealed an average of just under 110,000 defensive uses of guns each year compared to approximately 1.3 million crimes committed with a firearm.46 With regard to suicide and guns, firearms are the primary method of suicide in both males and females. Firearms are utilized in well over 50% of successful suicide attempts. Suicides are five times more likely to be committed in homes that harbor firearms. Ninety-two percent of suicide attempts utilizing firearms are successful in comparison to only 27% that employ poisons and 4% involving cutting or stabbing.

■ Falls There were 23,443 fatal falls in 2007 and over 8.5 million nonfatal injuries that were a result of falls. The overwhelming majority of these were unintentional. Falls represent approximately 13% of all injury deaths. Falls account for over one third of all injury hospitalizations and one quarter of all injuryrelated visits to the ED.5 The greatest occurrence rate is witnessed in the younger and older age groups; however, the severity profile in the two groups is quite different. In children, falls are common but generally

Epidemiology

DATA SOURCES There are a plethora of data available nationally52 and locally to define and research injury epidemiology. A number of these data sources have been used in the production of this chapter and are referenced. Although data on nonfatal injuries are not

as comprehensive or robust as those on fatal injuries, significant improvement has occurred in recent years relating to the scope and quality of data collection. This has enhanced the understanding of the magnitude and significance of injury as a major public health problem. Several of these databases provide information on several types of work-related injuries with a number of others focusing on injuries and injury deaths related to other unintentional and intentional injuries. Many are ongoing surveillance systems. This collective group of databases varies in scope and the extent to which they provide information on mechanism and intent, nature and severity, risk factors, health services use, costs, and health outcomes. Some are population based and some are not. Comprehensive data on fatalities are available from vital statistics data, although these data do not provide detailed information about the extent and nature of injury sustained. Standardized data on nonfatal injuries treated in the ED, including those treated and released, transferred, or hospitalized are available from the National Electronic Injury Surveillance System—All Injury Program (NEISS-AIP).53 The NEISS-AIP is a collaborative effort between the National Center for Injury Prevention and Control (NCIPC) and the U.S. Consumer Products Safety Commission (CPSC). This database acquires information on over half a million injury-related ED visits to a nationally representative sample of 66 hospitals on an annual basis. The NEISS-AIR is the most comprehensive database on all nonfatal injuries presenting to hospitals with EDs that is currently available. These data, together with injury mortality data, can be accessed through WISQARS (Web-based Injury Statistics Query and Reporting System), which is an interactive database system supported by the NCIPC.5 Injuries that result in hospitalization can also be obtained from both the National Hospital Discharge Survey (NHDS) and the Healthcare Costs and Utilization Project (HCUP-3)54,55 Although both these sources can provide detailed information regarding the nature and severity of injuries, treatment, and discharge disposition, they are limited in that codes for classifying the mechanism and intent of the injury are not routinely recorded. Although strategies exist for estimating distribution by mechanism and intent given incomplete data, the lack of uniform E-coding of hospital discharges as well as the exclusion of ED cases that are treated and released remains a significant impediment to the optimal use of these databases for studying the entire spectrum of injury epidemiology. Initiatives to rectify this situation, as mentioned earlier in this chapter, are currently being undertaken. An additional confounder in the reliability and accuracy of these essentially administrative databases is the extent, prioritization, and accuracy of ICD coding. Also, it should be pointed out that these are only population based from the standpoint of the population of hospitalized patients. They do not capture all deaths and will not ever include patients with minor injuries not seeking treatment at hospitals. Softer and perhaps more subjective data on nonfatal injuries not resulting in hospital admission or death are available from the National Health Interview Survey (NHIS),56 The National Ambulatory Care Survey (NAMCS), and the National Hospital Ambulatory Medical Care Survey (NHAMCS).57 The NHIS

CHAPTER 2

not severe or fatal. Falls are the leading cause of nonfatal injuries for all children ages 0–19. Approximately 8,000 children are treated daily in U.S. EDs for fall-related injury.47 This totals almost 2.8 million children each year. Less than 3% of these visits result in hospitalization. Approximately one half of all pediatric falls occur in the home and one quarter occur at school. Falls in children ages 0–4 years are most commonly from furniture or stairs. In older children, falls are commonly from standing and/or associated with recreational activities related to playground equipment, bicycling, or sports. In adults of working age, most fatal falls are from buildings, ladders, and scaffolds. Falls on stairs increase in significance starting at age 45.3 Gender ratios for injury deaths in adults differ by mechanism. ED visit rates for falls are consistently higher for men up to the age of 44. From age 45 and older, this trend reverses and by age 65, ED visit rates and hospitalizations for falls in women are nearly three times those in men. This finding is consistent with the increased fracture risk in women after menopause and, specifically, those with osteoporosis. In the elderly, falls are a significant cause of mortality and morbidity being the cause of death in 23% of injury deaths for those 65 and over and 32% of injury deaths in those 85 years of age and older. The death rate from falls after age 85 is over three times that for people age 75–84 years old. Falls are also the most common cause of nonfatal injury in the elderly, accounting for nearly 60% of injury-related ED visits and approximately 80% of injury-related hospitalizations for persons age 65 years and older. In the United States, one in five people over the age of 65 will sustain a fall annually. Of these, about one quarter will be injured and another quarter will restrict their daily activities for fear of another fall. Fractures occur in approximately 5% of falls. Risk for hip fractures from falls increases dramatically with age. The elderly over age 85 are 10–15 times as likely to sustain hip fractures as people age 60–65.48,49 The economic impact of falls in the elderly is sizable and estimated to reach nearly 55 billion dollars in 2020.50 Major risk factors for falls among the elderly include those related to the host (advanced age, anticoagulant medications history of previous falls, hypotension, psychoactive medications, dementia, difficulties with postural stability and gait, visual disturbances, cognitive and neurological deficits, or other physical impairment) and environmental factors (loose rugs and loose objects on the floor, ice and slippery surfaces, uneven flooring, poor lighting, unstable furniture, absent handrails on staircases) to name a few. The risk of falling increases linearly with the number of risk factors present, and it has been suggested that falls and some other geriatric syndromes may share a set of predisposing factors. All of these factors are potentially modifiable with combinations of environmental, rehabilitative, psychological, medical, and/or surgical interventions.51

31

32

Trauma Overview

SECTION 1

relies on self-reports of injury events, whereas both the NAMCS and the NHIS rely on data abstracted from injury-related visits to hospital EDs, hospital outpatient departments, and/or physician offices. These databases do generally include E-codes. In addition to these sources of comprehensive data across all types and severities of injury, several sources of national data exist that are specific to a particular mechanism or intent. Examples include the Fatal Analysis Reporting System (FARS),58 the National Automotive Sampling System—General Estimates System,59 and the Crash Injury Research and Engineering Network (CIREN).60 Also worthy of note are the National Occupant Protection Use Survey (NOPUS), National Fire Incident Reporting System (NFIRS), the National Traumatic Occupational Fatality Surveillance System and the Survey of Occupational Injuries and Illness for Occupational Injuries, the National Crime Victimization Survey (NCVS) and the Uniform Crime Reporting System for Intentional Injuries (which excludes suicides and self-inflicted injuries),61 as well as the American Burn Association Burn Repository.62 These databases are particularly useful for monitoring injury rates specific to certain mechanisms and for identifying risk factors associated with their occurrence. Less developed are the data systems that deal with violencerelated injuries overall and firearm-related injuries in particular. NVDRS37 catalogues violent incidents and deaths, death rates, and causes of injury mortality. However, data are only provided from 16 states and are not nationally representative. There has also been some movement toward developing a data collection system similar to that developed for motor vehicle crashes, which would be an essential component to a nationwide effort at reducing the epidemic of violence currently being experienced in this country.63 The development of a national violent injury statistics system64 has initially focused on evolving a national reporting system for firearm-related injuries; however, it has since expanded to include deaths from all homicides and suicides, regardless of weapon type. The ongoing efforts to develop this reporting system have focused on collection of current data for use in planning and evaluating policies aimed at reducing violent deaths. Of particular interest to trauma clinicians and clinical researchers are clinical databases. The most noteworthy of these is NTDB.19 This database is the largest aggregation of U.S. trauma registry clinical data ever assembled. Since its inception, nearly 4 million records have been amassed emanating from over 900 trauma centers of various levels. Despite the robust nature of this database, it only contains data from trauma centers that have voluntarily contributed data. This introduces a notable element of sample bias. Additionally, data completeness, accuracy, and validity, have been continuous concerns, which have been increasingly ameliorated over time. As a partial solution to these issues, the American College of Surgeons Committee on Trauma, which administrates the NTDB, has instituted the National Sample Program that specifically seeks more highly controlled data from a nationally representative sample of 100 Level I and Level II trauma centers in the United States. A number of research data sets containing highly scrutinized and reliable data have also been created for use by researchers.

Two additional phases of trauma care where data have been lacking are the prehospital phase and the post–acute care phase or rehabilitation. The National Emergency Medical Services Information System (NEMSIS)65 is the national repository that is being developed to store prehospital EMS data from every state in the nation. Since the 1970s, the need for EMS information systems and databases has been well established, and many statewide data systems have been created. However, these databases vary significantly in their ability to acquire patient and systems data and allow analysis at a local, state, and national level. Currently 26 states contribute to the NEMSIS database, which is being characterized as the National EMS Registry and utilizing the NEMSIS data dictionary. The registry now includes over 10 million records for 2008–2010. An additional 12 states are close to implementing a statewide EMS data collection system that will allow for contribution this registry. There is an increasing impetus due to initiatives from professional organizations and regulatory agencies to have prehospital run sheets and data systems be NEMSIS compliant, which will facilitate submission of consistent and valid data to the national database. Information from the post–acute phase of care is essential to long-term clinical and financial outcome studies. The Uniform Data System for Medical Rehabilitation (UDSMR)66 catalogs data from rehabilitation hospitals nationwide for use in evaluating the effectiveness and efficiency of their rehabilitation programs. It provides the most comprehensive data available on rehabilitation patients across many diagnostic categories, including injuries. The database includes information on demographics, type of injury, length of stay, primary payor, and postinjury rehabilitation circumstances such as employment status, living situation and Functional Independence Measure (FIM), which is the most widely accepted functional assessment measure in use by the rehabilitation community. The FIM is an 18-item ordinal scale used with all diagnoses within a rehabilitation population.67 The USDMR has been used in at least one long-term study of motor vehicle crash outcomes and costs.68 National data can be used for drawing attention to the magnitude of the injury problem, for monitoring the impact of federal legislation, and for examining variations in injury rates by region of the country and by rural versus urban/suburban environments. They can also be useful in aggregating sufficient numbers of cases of a particular type of injury to analyze causal patterns and clinical or other outcomes on an individual or systems basis.69 Often, however, these national data are not appropriate for the same or other purposes or for developing and sustaining injury prevention programs at the state and local level. State and local data are more likely to reflect injury problems specific to the local area and therefore more useful in setting priorities and evaluating the impact of policies and programs in these more limited catchment areas. Additionally, local data are typically more persuasive than are national data in advocating to establish a policy or to achieve funding of injury control programs at the local level. Some of the previously described national databases do provide subsets of data at the state or even county level; however, many do not.

Epidemiology present an enticing opportunity for facilitating both short- and long-term trauma research and evaluation, it should be noted that linkage for the sake of linkage and analysis for the sake of analysis serves no useful purpose. Appropriate data must be turned into relevant information, which is then used to answer pertinent questions about injury, epidemiology, treatment, cost efficiency, and prevention. Many of these questions can be answered adequately, and perhaps more appropriately and accurately, by analyzing a single database rather than employing sophisticated schemes of data linkage that are often complicated and costly.

SUMMARY In summary, injury imposes a heavy burden on society in terms of both mortality and morbidity along with its sizable economic burden on the health care system and society. Largely unrecognized is the fact that many fatal and nonfatal injuries are preventable and controllable using specific strategies guided by the analysis of injury epidemiology. Hence there is no societal level of tolerance, or perhaps intolerance, and fear of incidence as there is for HIV or West Nile virus and H1N1 influenza. Yet, these diseases contribute much less to the burden of public health disease than do injuries. Risks of injury death vary by age and gender. The majority of injury deaths are unintentional, with elderly people at a particularly high risk of death from unintentional injuries. Considering intentional injuries, overall, suicide greatly exceeds homicides, but rates again vary by age, gender, and urban or rural residence. Mechanisms of injury death also vary be age. The risk of injury death on the job varies by occupation. From a global perspective, the United States compares less than favorably with other countries in terms of fatal injury, particularly those related to firearms (Fig 2-13). The risks of hospitalization for injury vary by age and gender with elderly women at particularly high risk. Teens and young adults have the highest rates of initial ED visits for injury with many of these injuries occurring around the home. In total, injury deaths declined slightly during the 1985– 2004 period with some variation by intent of injury. Injury mortality trends vary considerably by mechanism of injury. Some causes are on the rise with others declining or remaining essentially unchanged. Injury morbidity rates have demonstrated declining trends among all age groups except the elderly. Although certain assumptions or “profiling” may arise from the association of injury and certain mechanisms thereof, a number of confounding factors unrelated to racial origin have been outlined, which should dissuade broad generalizations that are unfounded. Alcohol and other drugs continue to be intimately associated with all types and mechanisms of injury. In conclusion, although significant strides have been made in reducing the rate at which injury occurs, trauma remains a major public health issue. More efficient ways of treating injuries as they occur, or tertiary prevention, should and will continue to be the major thrust of clinical care providers and researchers. However, it is equally important that efforts to develop appropriate programs and policies that will prevent

CHAPTER 2

Availability, accuracy and completeness of local injury data varies substantially by state and county. Vital statistics and death certificate data are generally available for 100% of injuryrelated deaths. As previously discussed, however, these data are limited in the information they provide about the nature and circumstances of the injury, cause of death, and risk factors associated with the death. Medical examiner and coroner reports can be a useful adjunct to death certificate data, but once again, the completeness and quality of these data vary substantially from state to state. Autopsy rates are equally variable and are generally biased toward being performed in cases of suspected homicide. State and local data on trauma hospitalizations are generally available from two principal sources, those being uniform hospital discharge data including the UB-04 along with its predecessor UB-9270 and hospital or system trauma registries. Hospital discharge data are predominantly administrative in nature, whereas trauma registry data are primarily clinical. Both types of databases have limitations, which have been alluded to previously. Trauma registries suffer from selection bias and generally inconsistent inclusion criteria as well as highly variable data integrity. In both types of databases, ICD coding is not uniform. Administrative databases in general are not useful in attempting to analyze clinical issues despite available methods to estimate injury severity using ICD codes.71 Both hospital discharge databases and trauma registries do not include information on trauma deaths that occur at the scene, in transport, or in the ED nor do they routinely include patients treated and released. Specifically, in comparison to hospital discharge data, trauma registries typically include more detailed information regarding the cause, nature, and severity of the injury. Some trauma registries will also include data on deaths occurring in the ED. Trauma registries, for the most part, collect information only on “major trauma” patients, generally excluding those patients who survive but remain in the hospital less than 3 days. Again, this leads to sample bias of a small subset of all injured patients in a population. It is important to reemphasize that caution should be exercised in using these databases for describing the epidemiology of trauma as neither is population based. Uniform data on trauma patients treated and released from EDs, hospital clinics, and physicians offices are generally less accessible on a county or state level. Other data sources, often available at the state and local levels that can be useful in studying the epidemiology of injury, include routinely collected information from EMS, police, fire departments, poison control centers and child protective surgery, among others. The utility of existing data at the state and local level can be significantly enhanced by linking data across multiple data sources. Single data sources are often limited in their content or scope of coverage, or both. Techniques have been developed and are continually being improved to facilitate linkage of these databases to avoid the high costs of gathering new data.72 Several states have now linked hospital discharge data, vital statistics, police crash reports, and prehospital run sheet data to examine patterns and outcomes of motor vehicle-related crashes.73 Although these linkage strategies and methods

33

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Trauma Overview Motor Vehicle Traffic

Firearm United States New Zealand

SECTION 1

France Canada Australia Denmark Israel The Netherlands Norway England/Wales Scotland 65 60

55

50 45 40

35

30

25 20 15 10

5

0

Deaths per 100,000 population

0

5

10 15

20 25 30

35 40 45

50 55 60 65

Deaths per 100,000 population

FIGURE 2-13 Firearm and motor vehicle traffic injury death rates, males 15–34, 1992–1995 for selected countries. (Reproduced with permission from Annest JL, Conn JM, James SP. Inventory of Federal Data Systems in the United States. Atlanta, GA: National Center for Injury Prevention and Control; 1996.)

them from occurring, that is, primary and secondary prevention also be prioritized. Education of policy makers and the public that this public health epidemic can and must be controlled is also an essential component of this effort. Taken as a whole, integrated efforts at primary, secondary, and tertiary prevention, along with public information and education programs, are the only effective means to effect injury control and reduce the burden of injury on individuals, the health care system and society at large.74 Accurate and comprehensive data are essential to these collective efforts. Studying the epidemiology of injuries provides the opportunity for understanding how, when, and with whom to intervene.

REFERENCES 1. Lilienfeld AM, Lilienfeld DE. Foundations of Epidemiology. New York: Oxford University Press; 1980:3–22. 2. Haddon W Jr. The changing approach to epidemiology, prevention, and amelioration of trauma: the transition to approaches etiologically rather than descriptively based. Am J Public Health. 1968;58:1431. 3. Centers for Disease Control and Prevention. The Injury Fact Book. http:// www.cdc.gov/Injury/Publications/FactBook. Accessed June 2010. 4. Robertson LS. Injury Epidemiology. New York: Oxford University Press; 1998. 5. http://www.cdc.gov/ncipc/wisqars/default.htm. Accessed June 2010. 6. Trunkey DD. Trauma. Sci Am. 1983;249:28. 7. Sauaia A, Moore FA, Moore EE, et al. Epidemiology of trauma deaths: a reassessment. J Trauma. 1995;38:185. 8. Demetriades D, Kimbrell B, Salim A, et al. Trauma deaths in a mature urban trauma system: is “trimodal” distribution a valid concept? JACS. 2005;201:343–348. 9. Center for Disease Control and Prevention. Injury in the United States: 2007 Chartbook. http://www.cdc.gov/nchs/data/misc/injury 2007. pdf. Accessed June 2010. 10. Rice DP, MacKenzie EJ, Jones AS, et al. Cost of Injury in the United States. San Francisco: Institute for Health and Aging, University of California and the Injury Prevention Center, The Johns Hopkins University; 1989. 11. Finklestein EA, Corso PS, Miller TR. Incidence and Economic Burden of Injuries in the United States. New York: Oxford University Press; 2006. 12. Administration on Aging. Department of Health and Human Services, 2010. http://www.aoa.gov/aoaroot/aging_statistics/index.aspx. Accessed June 2010.

13. World Health Organization. Manual for the International Statistical Classification of Diseases, Injuries, and Causes of Death, Based on the Recommendations of the Tenth Revision Conference, 1975. Geneva: World Health Organization; 1977. 14. U.S. Department of Labor, Bureau of Labor Statistics. National Census of Fatal Occupational Injuries in 2000. http://www.bls.gov/iif/oshcfoi1.htm. Accessed June 2010. 15. U.S. Department of Labor, Bureau of Labor Statistics. Workplace Injuries and Illnesses in 2000. http://www.bls.gov/news.release/osh.nr0.htm. Accessed June 2010. 16. http://www.cdc.gov/nchs/injury/ice/barellmatrix.htm. Accessed June 2010. 17. Isreal RA, Rosenberg HA, Curtin LR. Analytic potential for multiple cause of death data. Am J Epidemiol. 1986;124:161. 18. Sosin DM, Sacks JJ, Smith SM. Head injury-associated deaths in the United States from 1979–1986. JAMA. 1989;362:2251. 19. http://www.facs.org/trauma/ntdb/index.html. Accessed June 2010. 20. Baker CC, Oppenheimer L, Stephens B, et al. Epidemiology of trauma deaths. Am J Surg. 1980;140:144. 21. Shackford SR, Mackersie RC, Holbrook TL, et al. The epidemiology of traumatic death: a population-based analysis. Arch Surg. 1993;128:571. 22. Centers for Disease Control and Prevention. Traumatic Brain Injury in the U.S. http://www.cdc.gov/features/dstbi_braininjury. Accessed June 2010. 23. Committee on Injury Scaling. The Abbreviated Injury Scale. Des Plaines, IL, Association for the Advancement of Automotive Medicine; 1990. 24. Jurkovich GJ, Mock C, MacKenzie EJ, et al. The sickness impact profile as a tool to evaluate functional outcome in trauma patients. J Trauma. 1995;39:625. 25. MacKenzie EJ, Morris JA, Jurkovich GJ, et al. Return to work following injury. The role of economic, social and job-related factors. Am J Pub Health. 1998;88:1630. 26. Wesson DE, Williams JI, Sapence LJ, et al. Functional outcomes in pediatric trauma. J Trauma. 1989;29:589. 27. Thurman DJ, Guerrero J. Trends in hospitalization associated with traumatic brain injury. JAMA. 1999;282(10):954–957. 28. Guerrero J, Thurman DJ, Sniezek JE. Emergency department visits associated with traumatic brain injury: United States, 1995–1996. Brain Injury. 2000;14(2):181–186. 29. Kraus JF. Epidemiologic features of injuries to the central nervous system. In: Anderson DW, ed. Neuroepidemiology: A Tribute to Bruce Schoenberg. Boca Raton, FL: CRC Press; 1991:333. 30. U.S. Department of Health and Human Services. Interagency Head Injury Task Force Report. Washington, DC: U.S. Department of Health and Human Services; 1989. 31. Frankowski RF, Annegers JF, Whitman S. The descriptive epidemiology of head trauma in the United States. In: Becker DP, Povlishock JT, eds. Central System Trauma Status Report: 1985 Bethesda, MD: National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health; 1985.

Epidemiology 53. Centers for Disease Control and Prevention. MMWR. 2001;50(17): 340–346. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5017a4. htm. Accessed June 2010. 54. Centers for Disease Control and Prevention. National Hospital Discharge Survey. http://www.cdc.gov/nchs/nhds.htm. Accessed June 2010. 55. Agency for Health Care Policy and Research. http://www.ahcpr.gov/data/ hcup. Accessed June 2010. 56. Centers for Disease Control and Prevention. National Health Interview Survey http://www.cdc.gov/nchs/nhis.htm. Accessed June 2010. 57. Centers for Disease Control and Prevention. Ambulatory Health Care Data. http://www.cdc.gov/nchs/ahcd.htm. Accessed June 2010. 58. National Highway Traffic Safety Administration Fatal Analysis Reporting System. http://www.nhtsa.gov/dot/nhtsa/ncsa/content/pdf/farsbrochure. pdf. Accessed June 2010. 59. National Highway Traffic Safety Administration NASS-General Estimates System. http://www.nhtsa.gov/data/automotive+sampling+system+(Nass) /NASS+general+estimates+system. Accessed June 2010. 60. National Highway Traffic Safety Administration Crash Injury Research and Engineering Network. http://www.nhtsa.gov/ciren. Accessed June 2010. 61. McKenzie EJ, Fowler CJ. Epidemiology. In: Moore EE, Feliciano DV, Mattox K, eds. Trauma. 6th ed., Chapter 2. New York: McGraw Hill; 2007. 62. American Burn Association. http://www.ameriburn.org/nbr2005.pdf. 63. Barker C, Hemmenway D, Hargarten S, et al. A “call to arms” for a national surveillance system on firearm injuries (editorial). Am J Public Health. 2000;90:1191–1193. 64. http://www.hsph.harvard.edu/hicrc/nviss/about_main.htm. Accessed June 2010. 65. http://www.nemsis.org. Accessed June 2010. 66. Granger CV. Quality and Outcome Measures for Rehabilitation Programs. http://www.emedicine.medscape.com/article/317865-overview. Accessed June 2010. 67. http://www.usdmt.org/webmodule/fim/fim_about.aspx. Accessed June 2010. 68. http://www.nhtsa.gov/people/injury/research/rehabcosts/execsum.htm. Accessed June 2010. 69. Fingerhut L, Gallagher S, Warner M, Heinen M. Injury Data Basics. http://www.cdc.gov/nchs/injury/injury_presentations.htm. Accessed June 2010. 70. http://www.ingenix.com/content/attachment/insight316.pdf. Accessed June 2010. 71. MacKenzie EJ, Steinwachs DM, Shankar B. Classifying trauma severity based on hospital discharge diagnoses. Med Care. 1989;27:412. 72. Johnson SW. So You Want to Link Your Data? DOT HS 808426. Washington DC. Department of Transportation, National Highway Traffic Safety Administration; 1996. 73. http://www.nhtsa.gov/data/state+data+program+&+codes. Accessed June 2010. 74. Bonnie RJ, Fulco CE, Liverman CT, eds. Reducing the Burden of Injury: Advancing Prevention and Treatment. Washington, DC: Committee on Injury Prevention and Control, Division of Health Promotion and Disease Prevention, Institute of Medicine. National Academy Press; 1999.

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32. Sosin DM, Sniezek JE, Thurman DJ. Incidence of mild and moderate brain injury in the United States, 1991. Brain Injury. 1996;10:47. 33. Kelly J. Sports-related recurrent brain injuries-United States. MMWR Morb Mortal Wkly Rep. 1997;46:224. 34. Kraus JF. Epidemiological aspects of acute spinal cord injury: a review of incidence, prevalence, causes and outcome. In: Becker DP, Povlishock JT, eds. Central System Trauma Status Report: 1985. Bethesda, MD: National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health; 1985. 35. Williams DR, Rucker TD. Understanding and addressing racial disparities in health care. Health Care Finan Rev. 2000;21:75–90. 36. Stankamp M, Frazier L, Lipskey N, et al. The National Violent Death Reporting System: an exciting new tool for public health surveillance. Inj Prev. 2006;12(suppl 2):ii3–ii5. 37. http://www.cdc.gov/injury/wisqars/nvdrs.html. 38. Soderstrom CA, Dischinger PC, Smith GS, et al. Psychoactive substance dependence among trauma center patients. JAMA. 1992;267: 2756–2759. 39. Madan AK, Yu K, Beech DJ. Alcohol and drug use in victims of lifethreatening trauma. J Trauma. 1999;47:568–571. 40. Soderstrom CA, Dischinger PC, Kerns TJ, et al. Epidemic increases in cocaine and opiate use by trauma center patients: documentation with a large clinical toxicology database. J Trauma. 1992;33:709–713. 41. National Highway Traffic Safety Administration. http://www.nhtsa.dot. gov. 42. Johns Hopkins Center for Gun Policy and Research. 1998 National Gun Policy Survey: Questionnaire With Weighted Frequencies. Baltimore, MD: The Johns Hopkins Center for Gun Policy and Research; 1999. 43. Kann L, Warren CW, Harris WA, et al. Youth Risk Behavior Surveillance, 1995. Atlanta: Centers for Disease Control and Prevention; 1996. 44. Kellermann AL, Rivara FP, Rushforth NB, et al. Gun ownership as a risk factor for homicide in the home. N Engl J Med. 1993;329:1084. 45. Kellermann AL, Rivara FP, Somes G, et al. Suicide in the home in relation to gun ownership. N Engl J Med. 1992;327:467. 46. Cook PJ, Ludwig J, Hemenway D. The gun debate’s new mythical number: how many defensive uses per year? J Policy Anal Manage. 1997;16:463. 47. Centers for Disease Control and Prevention. http://www.cdc.gov/ safechild/fact_sheets/falls-fact-sheet-a.pdf. Accessed June 2010. 48. Melton LJ III, Riggs BL. Epidemiology of age-related fractures. In: Avioli LV, ed. The Osteoporotic Syndrome. New York: Grune and Stratton; 1983. 49. Centers for Disease Control and Prevention. Falls Among Older Adults: An Overview. http://www.cdc.gov/homeandrecreationsafey/falls/adultfalls. html. Accessed June 2010. 50. Centers for Disease Control and Prevention. Costs of Falls Among Older Adults. http://www.cdc.gov/homeandrecreationsafety/falls/fallcost.html. 51. Tinetti ME, Inouye SK, Gill TM, et al. Shared risk factors for falls, incontinence, and functional dependence. JAMA. 1995;273:1348. 52. Centers for Disease Control and Prevention. Inventory of National Injury Data Systems. http://www.cdc.gov/injury/wisqars/inventoryinjurydatasys. html. Accessed June 2010.

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CHAPTER 3

Injury Prevention Ronald V. Maier and Charles Mock

INTRODUCTION Trauma has been termed the “neglected disease of modern society.” It is also now the costliest medical problem, with trauma costs nearly doubling since the mid-1990s.1 Until recently, injuries were considered to be due to “accidents,” or randomly occurring, unpredictable events. Injuries were thus regarded in a fundamentally different manner from other diseases, which are viewed as having defined and preventable causes. This viewpoint, on the part of the public, professionals, and policy makers, induced a nihilistic attitude and severely limited the development of injury prevention efforts. Trauma, as with any other disease, should be approached from a scientific vantage point, with delineation of causative factors and with development of preventive strategies targeting such factors. This scientific approach has been successful in decreasing the toll of mortality and morbidity from most diseases. However, this same organized scientific approach has only recently been applied to the prevention of injury.2–7 The importance of injury prevention efforts is pointed out by trauma mortality patterns. One-third to one-half of trauma deaths still occur in the field,8,9 before any possibility of treatment even by the most advanced trauma treatment system. Such deaths can only be decreased by prevention efforts. In terms of severely injured persons who survive long enough to be treated by prehospital personnel, very few “preventable deaths” occur in a modern trauma system with a well-run emergency medical system and designated trauma centers. Even among those who survive to reach the hospital, a significant portion of in-hospital deaths are directly related to head injuries and occur despite optimal use of currently available therapy. Hence, injury prevention is critical to further significantly reduce the toll of death caused by trauma. Moreover, prevention efforts can also decrease the severity of injuries and thus the likelihood of disability that arises after trauma.

In the following chapter, the historical development of the scientific approach to prevention is discussed and practical considerations for implementation of prevention efforts and for assessment of their effectiveness are reviewed. The chapter will discuss how these basic principles have been successfully applied to the prevention of both unintentional and intentional injuries. Finally, the chapter will conclude with a discussion of surgeons’ roles in injury prevention programs.

SCIENTIFIC APPROACH TO PREVENTION OF INJURIES ■ Historical Development of the Science of Injury Prevention Early attempts at injury prevention were largely based on the premise that injured individuals had been careless or were “accident prone.” Although this may be true in some circumstances, the resulting injury prevention strategies, limited to generic admonitions to be careful, were greatly limited in their scope and success.7,10 The current foundation for the scientific approach to understanding the causation of injuries and to developing rational prevention programs was laid by several pioneers. One of the earliest developments of the science of injury prevention was the work of Hugh DeHaven in the 1930s–1940s. DeHaven demonstrated that during an injury-producing event such as a crash or a fall, the body could withstand varying amounts of kinetic energy depending on how that energy was dissipated. He pointed out the possibility of disconnecting the linkage of “accident” and the resultant “injury.”11,12 He provided a biomechanical foundation for subsequent injury prevention work and introduced the concept of injury thresholds. His groundwork is credited with eventually leading to the introduction of automotive seatbelts.11,12

Injury Prevention A. Pre-Event Phase 1. Prevent the creation of the hazard; prevent the development of the energy that would lead to a harmful transfer. For example, prevent manufacture of certain poisons, fireworks, or handguns. 2. Reduce the amount of the hazard. For example, reduce speeds of vehicles. 3. Prevent the release of the hazard that already exists. For example, placing a trigger lock on a handgun. B. Event Phase 4. Modify the rate or spatial distribution of the release of the hazard from its source. For example, seatbelts, airbags. 5. Separate in time or space the hazard being released from the people to be protected. For example, separation of vehicular traffic and pedestrian walkways. 6. Separate the hazard from the people to be protected by a mechanical barrier. For example, protective helmets. 7. Modify the basic structure or quality of the hazard to reduce the energy load per unit area. For example, breakaway roadside poles, rounding sharp edges of a household table. 8. Make what is to be protected (both living and nonliving) more resistant to damage from the hazard. For example, fire and earthquake resistant buildings, prevention of osteoporosis. C. Post-Event Phase 9. Detect and counter the damage already done by the environmental hazard. For example, emergency medical care. 10. Stabilize, repair, and rehabilitate the damaged object. For example, acute care, reconstructive surgery, physical therapy.7,10,14

TABLE 3-1 Examples of the Interactions of Phases and Factors Within Haddon’s Matrix of Injury Etiology FACTOR Vector/Vehicle Condition of brakes, tires Accessibility of moving parts in machinery in factories Window bars at high elevations

PHASE PRE-EVENT

Human/Host Driver intoxication Experience

EVENT

Use of safety belts

Airbags Collapsible steering column Side impact protection

POST-EVENT

Age Physical conditioning

Integrity of fuel system/ fire proof gasoline tanks

Environment: Social and Physical Speed limits Traffic regulations Societal attitudes and laws on intoxicated driving Highway design (road curvature, intersections, road conditions) Highway design (guard rails, breakaway poles) Societal attitudes and laws regarding seatbelt use Trauma care systems

CHAPTER 3 X

In the 1940s, John E. Gordon introduced the use of epidemiology to the evaluation of injury. He pointed out how, similar to any other disease, injuries occurred with recognizable patterns across time and populations. He also pointed out how, as with other diseases, injuries were the result of the interaction of the host, the agent of injury production, and the environment within which they interacted.13 The most notable of the early pioneers of injury prevention was William Haddon, the first director of the National Highway Traffic Safety Administration (NHTSA). Haddon advanced these early works and developed a systematic approach to the evaluation and prevention of injuries. He based his approach upon the recognition that virtually all injuries resulted from rapid and uncontrolled transfer of energy to the human body. Furthermore, such energy transfers were understandable and predictable, and hence preventable. Haddon expanded Gordon’s ideas on the interaction of the three factors of host, agent, and environment into what ultimately became known as Haddon’s Matrix (Table 3-1). In this model, each of the three factors influences the likelihood of injury during each of the three phases: pre-event, event, and post-event. In the pre-event phase, each of the three factors influences the likelihood of an injury-producing event, such as a crash, to occur. During the event phase, they influence the probability that such an event will result in an injury and determine the severity of that injury. During the post-event phase, these same components determine what ultimate consequences the injury will have. Table 3-1 gives examples of such interactions.14 Haddon provided a firm basis for the modern approach to injury control. The principles summarized in his matrix have also served as guidelines for the development of prevention efforts. He went on to develop 10 strategies to dissociate potentially injury-producing “energy” from the host. Most current strategies for prevention and control of injuries are conceptually derived from these 10 strategies. They are listed below with examples.

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■ Practical Considerations in Injury Prevention Work SECTION 1 X

Almost all prevention efforts can be conceptually derived from Haddon’s 10 strategies. However, implementing such strategies in the real world involves a variety of practical considerations. In general, interventions can be thought of as either being active or passive on the part of the person being protected. Active interventions involve a behavior change and require people to perform an act such as putting on a helmet, fastening a seatbelt, or using a trigger lock for a handgun. Passive interventions require no action on the part of those being protected and are built into the design of the agent or the environment, such as airbags or separation of vehicle routes and pedestrian walkways. In general, passive interventions are considered more reliable than active ones.14,15 However, even passive interventions require an action on the part of some segment of society, such as passage of legislation to require certain safety features in automobiles. The accomplishment of injury prevention strategies in society can be undertaken through three primary modalities: (i) legislation and enforcement, (ii) education and behavior change, and (iii) engineering and technology. These are often referred to as the three “E’s.” Enforcement and legislation can work at different governmental levels. For example, national or federal level legislation regulates safety features built into the design of motor vehicles. States define what constitutes drunk driving and establish the strictness with which such laws are enforced. Local governments establish safety-related building codes. Education and behavior change were once the mainstay of injury prevention work. However, if used uncritically and without evaluation, they usually have limited effect.16 Educational efforts need to be delivered in a well-thought-out manner, utilizing the techniques of social marketing, to succeed in actually effecting behavior change. Moreover, educational work is often most effective when coupled with other methods of injury prevention, such as informing the public of the risk of being apprehended and prosecuted under new and more stringent anti-drunk driving laws. Also, to be most effective, a committed and ongoing program is required. Engineering and technology address a variety of issues, such as development of safer roadways, more effective safety features for automobiles, and automatic protection for manufacturing equipment. These three main modalities are frequently complementary. For example, seatbelts are a technological development. Convincing people to adopt the behavior of using them requires education and is reinforced through legislation. Convincing legislators to pass seatbelt laws requires lobbying and education.7 In the later sections of this chapter, specific examples of use of these modalities are discussed. Certain common principles run through many successful injury prevention programs. These include a multidisciplinary approach, community involvement, and should involve ongoing evaluation of both the process and outcome of the program. Depending on the targeted injury type, a program might involve contributions from health care professionals, public

health practitioners, epidemiologists, psychologists, manufacturers, traffic safety and law enforcement officials, experts in biomechanics, educators, and individuals associated with the media, advertising, and public relations. Health care professionals might include those in primary care, such as pediatricians, and those involved in acute trauma care. Finally, individual members of the public might be involved.15,17 There is frequently the need to organize several groups with diverse interests into a coalition focusing on one particular injury prevention goal. Such groups might include governmental agencies, such as the health department, schools, and transportation department. They might also include academic institutions, the media, community groups, private foundations, corporations, and medical associations.14–16 Coordination of these diverse groups and interests is an important component of the overall prevention program and is often best performed by having one organization act as a “lead agency.”7 Programs are more likely to be successful when they have specific objectives and focus on a few or even just one key intervention. In general, interventions that can be integrated into existing programs will be more sustainable than will be shortterm, temporary programs. When a prevention program achieves ongoing support and commitment from the agency, organization, or community in which it is based, it can be considered to be “institutionalized”.7 Such sustainability is especially necessary for interventions based on education and behavior change. Funding for injury prevention is frequently a limiting factor, as these programs are almost always nonprofit endeavors. However, much can be accomplished by utilizing available community resources. These can include volunteer labor, publicity from the media in the form of free advertising space or special interest stories, and gifts in kind, such as donations of safety devices from manufacturers. The greater the level of involvement of the community, the greater the availability of such resources. Hence, a key component of many injury prevention programs is to elicit and sustain the interest of the community. A critical element of injury prevention programs, which is frequently given inadequate attention, is evaluation of effectiveness. This requires two main activities: evaluation of both the process and the outcome. Process evaluation can be regarded, in part, as quality assurance of the program. For example, are the various items in a public information campaign progressing at the scheduled rate? The main purpose of such evaluation is to provide feedback for modification of the intervention. Most importantly, outcome assessment evaluates possible changes or impact in the incidence of injury. Ideally, outcomes would monitor the most severe consequences of injury, namely, fatalities and injuries producing disability. This may not always be possible, given the limitations of size of the target population and the influence of other factors influencing injury rates. In these circumstances, measurement of “proxy outcomes” can be suitable, if carefully chosen. These are outcomes that are more frequent and hence more easily measurable, but that are less important and represent less tangible benefit than the more important outcomes. However, they should reflect or initiate a change ultimately in the more serious outcomes. For example, a program to promote bicycle helmet use would reasonably

Injury Prevention

1. 2. 3. 4. 5. 6. 7.

Injury fatalities Injury admissions Injury cases treated as outpatients All injury cases Direct observation of behavior or the physical environment Measures of self-reported behavior Measures of knowledge, attitudes, beliefs, or intentions

Factors that influence the choice of outcome to measure include size of project, size of population to be studied, specific intervention planned, and funding available. Larger programs should focus on more important and tangible outcomes such as injury fatalities and injury admissions. However, these are not usually possible for smaller programs. Moreover, if smaller programs are implementing an intervention that has had proven success in other areas or in similar circumstances, then changes in behavior or attitudes regarding this intervention may suffice to prove success. Whichever outcome is chosen, it is important to build outcome assessment into the design of the prevention program. In this way baseline measurements can be obtained, which will subsequently enable comparisons before and after an intervention and comparisons of groups with and without an intervention. Such outcome assessment is useful for identifying strategies that have been successful and hence are worth promulgating on a wider scale. Outcome assessment is also useful for identifying those strategies that are not working and hence should be changed or discontinued.

■ Ethical Issues In circumstances where educational efforts seek to increase voluntary compliance with safety measures, ethical issues in injury prevention are minimal. Ethical issues usually arise with laws mandating compliance with safety practices. These issues typically involve the balancing of an individual’s personal rights with the overall good of society. In circumstances where an individual’s actions adversely affect others, the ethical questions

are usually straightforward. For example, an individual’s “right” to drink and then drive is easily deprived in favor of protecting other members of society from the potential harm of such an action. Similarly, laws mandating use of restraint seats for children in automobiles may be viewed as an infringement on the rights of their parents to choose how they wish to treat their children. However, the vulnerable state of children and the precedent of protecting them from potentially harmful acts of their parents is well established and such laws, once passed, have easily stood. The difficult issues in injury prevention arise with laws to protect against injuries in which the potential victims are primarily harming themselves. One of the best examples of this is mandatory motorcycle helmet laws. Such laws have been opposed by motorcycle groups, who feel that they are only risking their own safety by riding without a helmet. Proponents of helmet laws have generally pointed to the societal costs of treatment of severely head-injured motorcyclists as the rationale as to why the issue affects society as a whole.18 Courts have consistently backed the latter view, as best summed up in the case of Simon v Sargent in Massachusetts: “From the moment of the injury, society picks the person up off the highway; delivers him to a municipal hospital and municipal doctors; provides him with unemployment compensation, if after recovery, he cannot replace his lost job and, if the injury causes permanent disability, may assume the responsibility for his and his family’s continued subsistence. We do not understand the state of mind that permits the plaintiff to think that only he himself is concerned.”19 Ethical issues related to injury prevention will continue to evolve. Most activities in life require some degree of risk taking. Societal norms and legal standards as to what represents acceptable risk taking are continually shifting. As these values change and as injury prevention strategies evolve, which might call upon legislation for mandatory compliance, new ethical issues will continue to arise.

■ Political Issues Even when scientifically proven and cost-effective, the acceptance by society and government of safety measures to prevent important causes of injury are often blocked by a variety of political issues.3,20 In some cases, there is resistance to behavior change on the part of a specific segment of society. For example, motorcycle helmet laws are frequently challenged by motorcycle groups. Besides ethical issues, the actual alternating legislative enactment and repeal of state motorcycle helmet laws have been due to political pressures from motorcycle groups on one hand and safety advocates on the other.3 In other cases, however, safety measures have been specifically blocked by the active efforts of special interests that would stand to loose financially. For example, one of the major advances in automotive safety in recent decades has been the enactment of the Federal Motor Vehicle Safety Standards (FMVSS). These have been estimated to have saved 10,000– 20,000 lives per year since their initial enactment in the

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start by measuring changes in the percentage of bicycle riders wearing a helmet rather than changes in head injuries or deaths. Such a program would be more likely to demonstrate changes in the proxy measure, helmet use, in a shorter period or in a smaller population, whereas serious head injuries and deaths are more likely to change only over longer periods. Using such measurable outcomes are critical to “document” the success of a program and hence to increase or sustain community “buy-in” and support. Injury outcomes can be thought of as a hierarchy, with the highest level being fatalities. These are the most desirable to prevent, but the hardest in which to reliably evaluate changes, due to their relatively infrequent occurrence. The lower levels of the outcome hierarchy are the easiest in which to assess change, especially in small-scale projects. However, the lower levels have the disadvantage of being less directly and less definitely associated with ultimate decreases in the more serious outcomes. The list below indicates this hierarchy from most desirable, but more difficult to assess, to less important, but more easily measured:

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1960s.3,21–23 Despite their effectiveness, efforts to promote such safety advances are often hindered by lobbying from the automobile industry or opposition from anti-regulatory– minded members of the government.3,24 Another example of political opposition involves efforts to legislate mandatory setting of hot water heater temperatures at 120–125°F. As will be described later, this is a tremendously effective strategy to prevent scald burns in young children. Initial work on such regulation was carried out at the state level. Despite the obvious low-cost and significant benefits of such laws, they were frequently opposed. As one particular example, the legislative fight to pass a 120°F water heater temperature bill in Wisconsin has been well documented.20 This bill was opposed by legislators who considered it to be anti-business. Although a state level bill, it was lobbied against by national interests, such as the Gas Appliance Manufacturers Association, as representing too much government interference in their business. Such opposition was eventually overcome by lobbying from several groups, including the State Medical Association and the state chapter of the American Academy of Pediatrics (AAP), and by a public letter writing campaign. Unfortunately, many other examples are also common. Among these is the opposition to efforts to promote responsible alcohol advertising on the part of alcohol manufacturers and retailers.20 One of the more extreme examples is the vehement opposition to efforts to any limit on availability of firearms by the National Rifle Association and its allies in the gun manufacturing industry. Such groups have opposed even efforts such as closing the gun-show loophole, which has allowed convicted criminals to continue to purchase guns. In addition to specific injury prevention issues, addressing deeper issues in our society is pertinent in protecting the health of the public from injury-related death and disability. Virtually every form of injury is more common in the lower socioeconomic strata of society. The inequities that produce this situation need to be confronted as well. This has been well stated by Christoffel and Gallagher in their book, Injury Prevention and Public Health: “Truly effective injury prevention interventions challenge the structural underpinnings of the status quo. Effective injury prevention means things like worker participation in production decisions, community involvement in land use policy, equitable distribution of risk… These are dangerous ideas; they challenge unbridled free-market competition. Yet they are necessary for long-term, meaningful advances in injury prevention.”3 These deep-seated political challenges indicate the need for those who wish to promote injury prevention to develop skills in advocacy and lobbying. This includes becoming proficient at efforts such as testifying before legislatures, pushing behind the scenes as individuals or through organizations such as professional societies, publicly countering unproven or non–evidence-based arguments used by safety opponents (such as motor cycle helmets increase the risk of crashes), and by working to mobilize public support for safety-related measures. Simultaneously, this challenge places the burden on the injury prevention community to develop scientific, evidence-based proposals that can withstand the appropriate public scrutiny before imposing legislative constraints on selected components of society.

STRATEGIES TO PREVENT UNINTENTIONAL INJURIES The remaining portions of this chapter will demonstrate how Haddon’s principles of injury causation and his strategies for prevention, as well as three main modalities for implementation (legislation, education, and technology), can be utilized in programs directed at specific types of both unintentional and intentional injury.

■ Motor Vehicle and Transportation Several well-established groups have been working in motor vehicle–related safety, including NHTSA, the Centers for Disease Control and Prevention (CDC), state and local highway departments, as well as various injury prevention coalitions. Progress in road safety has been made along multiple avenues, as indicated by the examples given in Table 3-1. Some of those warranting special discussion are detailed below.

■ Safety-related Vehicle Design and Occupant Protection Much has been accomplished to make motor vehicles safer. This includes engineering features that make it less likely for a vehicle to crash. This is referred to as crash avoidance and takes into account such features as brakes, headlights, triple brakelights, and signals. Automotive safety also includes engineering features that make occupant injury less likely in the event of a crash. This is referred to as crashworthiness and takes into account such features as collapsible steering columns, shatter proof glass, and improved side impact protection. These improvements have resulted from both improved car design on the part of the automobile manufacturers and regulations from NHTSA, in the form of FMVSS. One of the greatest advances in automotive safety was the realization that a significant component of the injuries sustained in crashes were due to ejections and to secondary collision of the occupant with the vehicle interior after the vehicle had collided with another object. This understanding led to the development of seatbelts to allow occupants to “ride down” the crash, dissipating their kinetic energy more slowly and in a controlled fashion. However, this accomplishment of engineering is an active intervention, requiring the occupant to decide to put on the belt each time they begin a new journey. Hence, convincing people to use seatbelts remains a major injury prevention challenge. Even though the addition of airbags has enhanced safety and is a completely passive intervention, concomitant use of seatbelts is required to optimize their benefit and avoid airbag-related injuries. Efforts to increase belt usage include both education and legislation. Legislation includes mandatory seatbelt laws. Although some form of such a law has been passed in most states, only 27 states have laws allowing primary enforcement. Belt usage in the United States remains incomplete, at 84% overall, including 88% in those states with primary enforcement and 77% in states with secondary enforcement of seatbelt laws.25

Injury Prevention

■ Helmets Occupant protection is obviously difficult to engineer for motorcycles and bicycles due to the exposed position of the riders. However, head injuries are the primary cause of death and prolonged disability for crashes involving both types of vehicles.5,6 Helmets have been shown to decrease the probability of a head injury during crashes, to decrease the severity of head injuries when they occur, and to decrease the probability of death in both bicycle and motorcycle crashes.30–34 As with seatbelts, helmets are an active intervention and the challenge has been to get riders to wear them. Programs to accomplish this have involved both education and legislation. The two case studies at the end of this section of the chapter detail examples of each approach.

■ Speed Limits In the precrash, environmental segment of Haddon’s Matrix, two factors that stand out are roadway design and traffic regulations, including speed limits. Safety aspects of roadway design have been greatly advanced by such features as greater use of limited access highways, which have eliminated the risk of head-on collisions and decreased intersection-related conflicts. One of the most important safety-related traffic regulations has been the speed limit. The nationwide 55 MPH speed limit contributed significantly to lowering the motor vehicle crash fatality rate. The move toward higher speed limits can be considered a societal sacrifice to directly appease personal freedom demands.

As a consequence, the nation sustained a rise in motor vehicle–related deaths in the early and mid-1990s.25

■ Alcohol Another of the major risk factors for motor vehicle crashes is alcohol-impaired driving. Risk of a crash increases dramatically with increasing blood alcohol concentration (BAC). The risk of a crash increases 5-fold at a BAC of 80 mg/dL; 7-fold at a BAC of 100 mg/dL; and 25-fold at 150 mg/dL.7,35 On weekend nights, when a large percentage of severe crashes occur, 2% of all drivers are legally intoxicated. Drunk driving is associated currently with 32% of all fatal crashes in the United States.36,37 In light of these dramatic facts, anti-drunk driving efforts have been a cornerstone of road safety efforts in the United States and most other developed nations. These have employed both educational and legislative approaches.38 A great many anti-drunk driving educational campaigns have been undertaken by diverse groups such as NHTSA, state agencies, and citizen groups such as Mothers Against Drunk Driving. Many of these have targeted younger drivers, who are at especially high risk for drunk driving.7 In terms of legislation, all states have adopted per se laws, in which any driver with an alcohol level above a specified level is considered impaired, regardless of any witnessed driving infractions. This legal limit has now been decreased to 80 mg/dL in all states. Likewise, many states have moved toward zero tolerance laws for underage drivers.25 However, legislation must be linked to enforcement because any law is only as good as its enforcement. Drunk-driving laws are enforced to extremely varying degrees in different jurisdictions. Random sobriety checkpoints and administrative license suspension are just two methods to increase enforcement effectiveness and should strongly be considered.7 Another avenue to pursue in the fight against drunk driving is identification of injured, alcohol-impaired drivers following hospital admission. There is a documented high rate of recidivism among intoxicated trauma patients in general, and not only among drunk drivers. Hence, identification and appropriate treatment of injured persons with alcohol abuse problems is a means toward decreasing the level of alcohol-related injury from all causes.5,6,39,40 Blood alcohol screening on admission, accompanied by brief questioning, such as the Short Michigan Alcohol Screening Test, Michigan Alcohol Screening Test, or CAGE, can detect patients at a high risk for alcohol-related injury recidivism. The CAGE questionnaire consists of four basic questions: Have you every tried to Cut down on your drinking? Are you Annoyed when people complain about your drinking? Do you ever feel Guilty about your drinking? Do you ever drink Eye-Openers?5,6,39,40 Referring these patients for counseling or even engaging in very brief interventions by trained professionals in the hospital is a potentially effective way of getting these patients to decrease their alcohol intake. In a prospective, randomized, controlled trial of screening and brief intervention (SBI) among admitted trauma patients, it was found that patients who had undergone this brief counseling demonstrated a longterm (1 year) decrease in their alcohol intake. This group

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A particular subset of restraint use that warrants special attention is that of infant and child car seats and booster seats. These are necessitated by the fact that infants and children do not fit into adult-size seatbelts and hence such seatbelts do not provide adequate protection for these age groups. The need for infant car seats was recognized many years ago. These are required by legislation in all states. These laws require infant/child harness seats that are appropriate for children ages 0–4 years. These have played a major part in decreasing occupant deaths for children ages 0–4 years from 682 deaths nationwide in 1994 to 261 deaths in 2006.26,27 The need for booster seats for children ages 4–9 years (under 4 ft 9 in.) has been more recently recognized. The need for these arises from the fact that adult seatbelts rarely fit children of this age group. The shoulder belt portion typically lies over the face, leading children to place it behind their backs. Likewise, the lap belt portion rides high, over the abdomen. These factors have been associated with intra-abdominal and spinal injuries, known as seatbelt syndrome.28 Such factors have contributed to the minimal declines in occupant death rates for children of this age group. Booster seats raise the child into a position where the shoulder belt fits more properly over the chest and shoulder and where the lap belt is properly positioned low, across the pelvis. Booster seats reduce severe injuries to child occupants.29 The recognition of the importance of booster seats has led an increasing number of states to pass booster seat laws.

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reduced their alcohol intake by more than 20 drinks per week compared to only 7 per week in patients not undergoing such brief counseling. In addition, there was a 43% reduction in new injuries in treated individual compared to controls.41 Brief interventions generally entail one or more counseling sessions, adding up to less than 1 hour. These have been shown to be effective in the context of acute injury hospitalization for all except the most severely impaired patients. The reader is directed to the cited references for more details on brief intervention counseling methods.39–41 The effectiveness and importance of alcohol SBI has recently led the American College of Surgeons Committee on Trauma (ACSCOT) to add a requirement that SBI programs must be present to its list of requirements for trauma center verification for Level I and II trauma centers. CMS has recognized the merit of intervention programs and created a specific billing code to enable reimbursement.

■ Graduated Drivers Licensing Systems A particularly high-risk group for crashes is new adolescent (16–17-year-old) drivers. Rates of crashes and crash-related death are higher than for older drivers due to having less experience and skill coupled with more risk-taking behavior. Drivers ages 16–20 have an annual rate of involvement in fatal crashes of 44/100,000 licensed drivers, compared with 24/100,000 for the general public.25 One particularly effective method to decrease the crash rate in this age group has been graduated driver licensing (GDL). Details vary from state to state and between countries; however, several common features include (1) new adolescent drivers first obtain a learner’s permit that allows them to drive only while supervised by a licensed adult; (2) a provisional license is next obtained that allows new adolescent drivers to drive unsupervised only under restricted conditions, such as only during certain times of day (usually not late at night), and with restrictions on the numbers and ages of passengers (e.g., with only limited numbers of other adolescents). Progression from one stage to the next and to a full license can only occur after specified minimum time periods and is contingent upon the absence of traffic violations or at-fault crashes.42 GDL programs have been shown to be effective in decreasing rates of crashes and crash-related death among new adolescent drivers. For example, after institution of a GDL system for 16-year-old drivers in North Carolina, rates of fatal crashes involving 16-year-old drivers declined by 57%, from 5 to 2/10,000 population per year.43 As of 2010, all states and several other countries have adopted GDL. However, only 35 such states have achieved a rating of “good” according to the scale developed by the Insurance Institute for Highway Safety, which takes into account the toughness of the restrictions and the length of the period after the 16th birthday for which these restrictions apply. Factors in this rating include the hour at which nighttime restrictions apply, the number of adolescent passengers that are allowed, and the age at which a full license may be obtained, among other criteria. The other states have been

rated as fair, marginal, or poor, indicating that much work still needs to be done.42

■ Distracted Driving The rapidly growing use of cellphones has brought the subject of distracted driving to the forefront of road safety. Distracted driving is one of several forms of driver inattention and can be defined as occurring when “a driver’s attention is diverted away from driving by a secondary task that requires focusing on an object, event, or person not related to the driving task.”44 Various forms of distraction include conversations with passengers, eating, smoking, reaching for objects inside the vehicle, manipulating controls, and cellphone use.44 Such distracted driving, in general, is a significant contributor to crash causation. NHTSA estimates that 10.5% of crashinvolved drivers were distracted at the time of their crash involvement44 and that, in 2008, there were 5,870 deaths in crashes in which at least one form of driver distraction was reported on the police crash report.45 Given the difficulties in knowing whether distraction was occurring or contributing to a crash, these figures are likely underestimates. Use of cellphones while driving has been shown in driving simulator studies to result in driving performance degradation, slowed response times (including braking), and reduced awareness of other traffic.44,46 Studies have consistently shown an increase of approximately 4-fold (i.e., 400% increase) in risk of a crash compared to baseline.44,46,47 This increased risk becomes especially problematic, given the widespread and growing use of cellphones, both in the USA and globally. Observational studies show 1–6% of drivers using cellphones at any given time while driving.46 Furthermore, use of hands-free units does not appear to eliminate the risk. Some studies indicating no change in risk and others decreased risk, but not to baseline. This is likely because drivers are still at risk due to the diversion of attention away from driving caused by the conversation itself.44,46,47 In an attempt to confront this problem, several states have adopted laws prohibiting use of cellphones while driving. As of 2010, 7 states had bans on handheld cellphones, 21 states had bans on text messaging while driving, and 24 had bans on teen drivers use of cellphones.48 In general, these laws lead to 50% reductions in cellphone use after they become effective. However, long-term effectiveness appears weaker.46 For example, a law in New York state in 2001 (the first such law in the USA) resulted in a decrease in the percentage of drivers using handheld mobile phones from 2.3% before the law to 1.1% one month after the law became effective, at which time there had been considerable publicity and enforcement. However, after 1 year the percentage of drivers using handheld mobile phones had risen back to 2.1%.46,49 Thus, as with many other road safety and injury prevention laws, there is a need for ongoing social marketing and law enforcement for the safety effect of the law to be realized. Furthermore, there are no data at this time confirming that such laws have an effect in lowering rates of crashes or injuries.46 There is considerable need for research on this topic. Priorities include better definition of the extent of the problem,

Injury Prevention

■ Residential Safety: Burns Improved residential safety encompasses poisoning, suffocation, drowning, falls, and burns. In the United States, burns are the fourth leading cause of injury-related mortality. There are three major causes of death and injury due to burns. House fires account for 75% of burn deaths, but only 4% of burn admissions, due to their high case fatality rate. Many of these deaths from fires are actually due to smoke inhalation.5,6,50 Scalds from hot liquids and burns from clothing ignition each account for only about 3% of burn deaths, but these mechanisms account for a large percentage of burn admissions (scalds—29%; clothing—10%).51 Hence, burn prevention efforts have been oriented toward these three most common causes.

■ House Fires Most house fire deaths occur because of entrapment in burning buildings. In many cases, people do not know their building is on fire until it is too late to escape or to call the fire department. Many injuries and deaths could be prevented if people knew earlier that a fire had started and had time to escape. Therefore, a key component to injury prevention for house fires is the early warning system provided by smoke detectors. Smoke detectors are an extremely effective injury prevention tool. They have been found to lower the potential for death in 86% of fires.7 This is an example of the use of engineering in injury prevention. However, the tool is of no value if people do not use it. Use of smoke detectors has been promulgated by both education and legislation. Educational campaigns have been run on a regular basis by local fire departments and nonprofit groups, such as the Northwest Burn Foundation in Seattle. These activities educate people about the importance of having a smoke detector in their home and the need to change the batteries every 6–12 months. In addition, most states have laws that require placement of smoke detectors in all new buildings. These measures have been extremely effective. The percentage of homes having smoke detectors rose from 5% in 1970 to 67% in 1982. Primarily based on increased use of smoke detectors, fire-related deaths in the United States decreased by 20% between the 1970s and the 1980s.7,51 Other efforts to prevent deaths due to house fires have attempted to attack root causes.52 Most house fires arise from (1) faulty heating equipment, especially in lower-income housing, and (2) ignition of mattresses or upholstered furniture from cigarettes. The first has been addressed primarily through legislation regarding housing codes. The second,

cigarette-related fires, has been worked on by (a) educating people about the dangers of smoking in bed and (b) laws that require mattresses to be made with less flammable materials.7 Unfortunately, the most effective measure, manufacture of self-extinguishing cigarettes, has been effectively blocked by the industry, even though the technology exists.20

■ Scalds Young children, ages 0–4 years, account for half of scald injuries.51 The leading cause is hot water, especially hot tap water used for bathing. A typical scenario is a child being bathed and the faucet being turned on too hot, either unintentionally by a child playing with the knobs or by an adult not realizing how hot the water is. Thus, a major prevention focus is lowering the temperature in hot water heaters. Hot water heaters can heat water as high as 160°F (71°C), which can produce a first-degree burn in 1 second of exposure, and more severe burns with longer periods of exposure. However, temperatures of 125°F (52°C) require three or more minutes of exposure to produce burns. Hence, essentially all scald burns due to tap water can be prevented by keeping the temperature in hot water heaters to 125°F or less.7,51 Reduction in thermostat settings is the engineering aspect. To achieve this, injury prevention groups have been educating parents of the dangers of high temperatures for hot water heaters and the importance of lowering the thermostat on the heater. Liquid crystal thermometers have been made specifically for the purpose of checking the temperature at the faucet. As regards legislation, many states have introduced laws that require manufacturers to preset their hot water heaters at 120–125°F (49–52°C). These scald prevention efforts have been very effective. Between the 1960s and the 1980s, scald-related deaths have decreased by over half for all age groups and by 75% for children.7,51

■ Clothing Ignition The second leading cause of burn-related admissions is ignition of clothing. This may happen from contact with stoves, electrical heating units (space heaters), cigarettes, matches, or other sources. The two major groups in whom these occur are young children, who do not realize the dangers, and the elderly, in whom reaction time is slowed. One of the most notable examples of burn prevention efforts is in this field. Most of the clothing ignition burns to children occurred from sleepwear, which was formerly made of easily flammable fabrics. In the 1970s, the Children’s Sleepwear Standard law required children’s sleepwear to be made of less flammable materials and required that any new sleepwear products pass a flame test before being allowed in the market. These measures have resulted in a dramatic decrease in childhood clothing related burns to the point where burns related strictly to clothing ignition are very rare. However, a major problem remains in clothing ignition burns among the elderly, which currently account for over 75% of clothing ignition burns. Likewise, clothing industry lobbyists have had some recent success in loosening some of the sleepwear standards for children, thus indicating that vigilance and continued advocacy are required even after safety-related laws are passed.7,51

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especially the contribution of cellphone use and other types of distracted driving to the number of crashes and crash deaths. There is especially a need to understand the effect of interventions, such as laws and methods for their enforcement, as well as new, potential, technological solutions such as methods to block mobile use while driving similar to the use of interlocks to prevent alcohol-impaired driving or speed governors to automatically limit vehicle speed. There is also a need to approach the use of cellphones within the broader context of other sources of driver distraction.46

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■ Two Contrasting Case Studies: Helmet Promotion SECTION 1 X

These two case studies address a similar issue, the use of protective helmets: in one case for bicycle riders and in the other for motorcycle riders. Both affect the crash phase and human factor of Haddon’s Matrix (i.e., decreasing the likelihood of injury once an injury-producing event has occurred). In addition, both involve the same concepts of Haddon’s 10 principles of prevention, namely, separation of the hazard from the people to be protected by a mechanical barrier. This particular strategy has been shown to decrease the severity of head injuries in victims of both bicycle and motorcycle crashes.30–34 From an implementation viewpoint, use of helmets for bicyclists and motorcyclists is an active intervention, requiring the rider to put on a helmet, voluntarily and repetitively, each time he or she performs the act of riding. The challenge in both circumstances has been to increase compliance with this behavior. However, due to selective social circumstances and pressures in the populations to be protected, very different modalities of implementation have been required.

■ The Seattle Bicycle Helmet Campaign The Seattle bicycle helmet campaign has been considered a model program in health promotion and injury prevention. It utilized a multidimensional approach, emphasizing a broadbased community coalition building and focusing on young elementary school-aged children. The initial step consisted of a background survey of schoolchildren and their parents, undertaken to assess the current knowledge, attitudes, and practices regarding bicycle helmets. Over 1,000 elementary school-aged children and their parents were surveyed. Only 12% of children who had bicycles reported that they used helmets when they rode. Among the large majority of children who did not use helmets, three main barriers to helmet use were identified. (1) Parents were largely unaware of the danger of head injuries to bicycle riders and were also unaware of the effectiveness of helmets in preventing such injuries. (2) The price of helmets at the time was $40–60 and was considered too high. (3) Children were reluctant to wear helmets as most other children did not do so and hence wearing a helmet would result in them being viewed as “nerds.”53,54 These barriers subsequently became the main targets of the bicycle helmet campaign. After this background survey, the Harborview Injury Prevention and Research Center (HIPRC) elicited the support and involvement of a number of organizations in forming a coalition to promote helmet use. This coalition relied on use of volunteer labor and gifts in kind. Members of this coalition included the Cascade Bicycle Club, local and state health departments, the Washington State Medical Association, the Parent Teachers Association (PTA), local television and radio stations, local sports figures, manufacturers of bicycle helmets, and Group Health Cooperative, the state’s largest health maintenance organization. The HIPRC acted as the lead agency in the program and coordinated the activities of the other coalition members.54–56

The program focused on elementary school-aged children as these were felt to be most amenable to changes in behavior. Increasing parental awareness was primarily undertaken via the mass media. Air time was donated as a gift in kind from local radio and television stations for public service announcements about bicycle helmets. The media provided reports by the Level I trauma center at Harborview Medical Center to publicize, as human interest stories, head injuries to unhelmeted children bicyclists. Families of bicycle crash victims were asked if their child’s case could be publicized on behalf of the helmet campaign. Compliance was usually high with these requests. The pediatricians and surgeons caring for these children played a key role in identifying their cases for publicity and also acted as spokespersons for helmets in the subsequent news stories. The trauma registry at Harborview Medical Center provided up to date statistics on bicycle trauma, which were popular with reporters and news broadcasters. In addition to the direct mass media approach, articles on bicycle helmets appeared in the newsletters of the Washington State PTA and the Boy Scouts. Similar articles, directed at health care providers, also appeared in the newsletters of the Washington State Medical Association and the state chapter of the AAP. Such items stressed the importance of injury prevention counseling in general and, in particular, about bicycle helmets, in primary care practices involving children. Through the state medical association, informational pamphlets were provided to physicians to distribute to their patients. At the start of the campaign, helmets were primarily sold at specialty bicycle shops catering to adults and retailed for $40–60. Few stores that sold children’s bicycles also sold helmets. A “partnership” was developed between the helmet coalition and Mountain Safety Research, a Seattle-based helmet manufacturer. This company mass produced and marketed helmets for children under a different label for $20–25. In exchange, retailers of bicycles who were involved with the coalition, agreed to attach “hang tags” on children’s bicycles they sold to promote helmets. Large chain stores that sold children’s bicycles were convinced to also provide helmets at reduced costs. The retail outlets likewise received public commendation and hence publicity from the state chapter of the AAP. In addition, helmets were made available through the PTA. Other cost-lowering activities included distribution of discount coupons through physicians’ offices, schools, and youth and community groups. Other helmet manufacturers eventually became involved in the campaign. To promote helmet use among school-aged children, bicycle safety programs were conducted in Seattle public elementary schools. These included posters, assemblies, and endorsements by local sports figures. Outside of school, bicycle rodeos and rallies were put on in city parks and other public sites, hosted by radio stations, and the Cascade Bicycle Club. At these bicycling events, rewards were given to children wearing helmets, including coupons for free French fries and free tickets to Seattle Mariner baseball games.54–56 This campaign has been held annually since 1986 with most intensive activities from April to September each year.54–56 The direct monetary costs of the program were primarily for printing and mailing. The only full-time personnel was a health

Injury Prevention mortality rate for admitted bicyclists also decreased from 7% in 1986–1990 to 3% in 1991–1993.57

■ Washington State Motorcycle Helmet Law In contrast to the bicycle helmet campaign, efforts to improve use of helmets by motorcyclists in Washington State have emphasized legislation. Mandatory motorcycle helmet laws have been the subject of nationwide debate. During the 1960s and 1970s many states enacted such legislation, primarily due to the threat of the withholding of federal highway funds. In 1976, Congress withdrew the U.S. Department of Transportation’s authority to withhold highway funds based on individual states’ helmet laws. Many states, including Washington, repealed their mandatory motorcycle helmet laws, primarily due to lobbying by motorcyclists groups. Increases in motorcycle related deaths and severe head injuries were noted nationwide.7,18 In Washington State, attempts were made to reinstitute a motorcycle helmet law during the 1980s. Such efforts were defeated twice in the legislature. A third and final lobbying effort by proponents of the helmet law utilized not only information on the terrible human consequences of preventable motorcycle-related head trauma but also data on the financial cost of these injuries. These data showed that not only does helmet use decrease the incidence of severe head injury by more than 50% but also that the average cost ($15,592) of an admission for motorcycle-related trauma was increased dramatically by the presence of a severe head injury ($46,936), with even more costs accruing for subsequent rehabilitative and custodial care of those with these severe head injuries.58 Of special interest to the state legislature was the fact that 63% of the costs of treatment for motorcycle-related injuries were borne by general public funds, primarily state Medicaid.59 In part, because of these data showing the stake of taxpayers and the state budget in the motorcycle helmet debate, the Washington State Legislature passed a law the following year requiring helmets for all motorcycle drivers and passengers, effective June 7, 1990. Follow-up of the results of the reinstitution of the motorcycle helmet law has re-established the efficacy of this law. Among victims of motorcycle crashes admitted to the state’s Level I trauma center, the proportion of those sustaining severe (AIS 4 or 5) head injuries declined from 20% before enactment of the helmet law to 9% afterward. The mortality rate declined from 10% to 6%.57 These case studies point out several important principles about injury prevention efforts. First, they show the need for multidisciplinary collaboration and point out the important role that surgeons and other clinicians caring for injured patients can play in both education and advocacy work. Second, they show the importance of considering the political and cultural environment in which the prevention effort is occurring. Parents were more than ready to listen to messages about the safety of their children, when those messages were properly delivered. Although many motorcyclists were utilizing helmets without a mandatory law, those who were not using helmets have been unlikely to appreciably respond to educational efforts, hence the need for legislation.23 Advocacy for passage of

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educator for years two and three of the campaign. A public relations specialist was employed on a part-time basis for the most intensive periods of the campaign, during the riding season. Otherwise, the bulk of activities of the campaign were provided for by “in-kind” donations of services.55 A key element in the program was assessment, both of the process of the campaign and of its outcome. Process factors that were followed included (i) number of discount coupons distributed and percentage redeemed; and (ii) number of helmets sold. During the first 2 years of the campaign, 109,450 discount coupons were distributed, of which 4.7% were redeemed, a figure that is deemed very high by standards of product promotion. Discount coupons distributed at the bicycle rodeos and fairs were especially productive, with an 8.7% redemption rate. Seattle area bicycle helmet sales also rose dramatically during the early years of the campaign, from 1500 in 1986 to 20,000 in 1988.55 In terms of assessment of outcome, death or major neurological disability related to bicycle crashes would be the most important to decrease. Given the proven efficacy of helmets at preventing severe head injuries and death in bicycle crashes it was felt that a change in helmet use behavior would be a reasonable surrogate measure of the program’s effectiveness.54–56 Observations on randomly chosen bicyclists were carried out throughout the Seattle area, utilizing a formal epidemiological sampling strategy. To fully assess the effectiveness of the helmet campaign, such observations were carried out before the initiation of the public information campaign. Moreover, as a control for general societal trends in helmet use, similar observations were carried out simultaneously in Portland, Oregon, a city without a helmet promotion campaign at the time.54,56 These observations were carried out on 8,860 Seattle area bicycle riders from 1987 to 1993. During the first 2 years of the program, the percentage of helmeted riders rose from 5% in 1987 to 16% in 1988, during which time the helmet use rates in Portland remained below 3%54 Helmet use rates in Seattle continued to rise to 62% in 1993.57 This helmet promotion campaign has continued for the past 15 years, becoming partially “institutionalized” in that pamphlets and other educational materials are available on a regular basis from the state medical association; helmets are now a routine item for sale at stores that sell children’s bicycles; free helmets are available for all children on public assistance through the state welfare office; and many pediatricians and family practitioners routinely work injury prevention and bicycle helmet promotion into their counseling of families. In turn, over the years of the program, the program’s success at decreasing the more serious sequelae of bicycle crashes has materialized. In a study of the population enrolled in the state’s largest health maintenance organization, Group Health Cooperative, it was found that from 1987 to 1992, medically treated (admitted or emergency room) bicycle-related head injuries decreased by 72% among 5- to 9-year-olds and by 78% among 10- to 14-year-olds.56 Likewise, at the state’s only Level I trauma center, at Harborview Medical Center, among patients admitted for bicycle crashes, the proportion of patients with severe head injuries (Abbreviated Injury Scale [AIS] for head of 4 or 5) declined from 29% in 1986 to 11% in 1993. The

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this legislation was aided by publicizing information on the public costs of motorcycle trauma at a time when fiscal conservatism was a priority. Third, these efforts each focused on one key injury prevention strategy, rather than a wide array of activities, such as promotion of safe riding habits by riders of both types of vehicles. Although such efforts might be useful and should be promoted, intensive efforts, as in the helmet campaigns, are more likely to succeed when focused on a simple message.55 Fourth, outcome assessment was a key component, especially of the bicycle campaign. Outcomes that were feasible to measure and that would reliably indicate the success of the campaign were chosen (e.g., change in behavior of wearing helmets). Assessment of this outcome was built into the design of the campaign, both in before-and-after comparisons and in comparisons with a control community. Finally, both efforts were accomplished largely with a minimum of funding and in the case of the bicycle campaign with a generous input of volunteer labor.

■ Nationwide Effectiveness of Prevention Efforts Aimed at Unintentional Injury Other examples of successful prevention programs aimed at unintentional injuries abound, so do examples of the complementary use of the three primary injury prevention modalities. These have been applied particularly well to traffic-related trauma. On a nationwide scale, this is especially well seen with promotion of restraints. The technological advancements, first of seatbelts and then the development of child safety seats and airbags have been complemented by promotion and education and by advocacy for legislation. Increased awareness of the importance of seatbelts has enabled passage of mandatory safety seats for children under 4 years old in all states and of mandatory seatbelt laws for all occupants in many states.7,25 The field of traffic-related injury prevention has also been advanced by other means, including vehicle design, highway design, lower speed limits, increased minimum legal drinking age, and increased public awareness about and increased enforcement of laws against driving while intoxicated. Similar advancements have been recorded in other types of unintentional injuries such as occupational injuries, residential injuries, and burn prevention. These advances in prevention, coupled with advances in trauma treatment, have reduced the death rate for unintentional injuries to some of the lowest rates recorded since statistics were first collected in the early part of the past century.51 The accomplishments have been especially notable in the last two decades. During the 1980s and 1990s, the rate of death due to unintentional injury declined by 19%, from 42.8 deaths/100,000/year (1981) to 34.9/100,000/year (2000). Obviously, there is still much to do. In fact, there has been some erosion of gains in the past few years, with rates increasing from the nadir of 34.9 deaths/100,000/year in 2000 to 39.8/100,000/year in 2006.26,60 Priorities for future work in the prevention of unintentional injuries include decreasing public acceptance of driving while intoxicated, especially among younger drivers; increasing use of seatbelts both through educational efforts and through

advocacy for passage of mandatory seatbelt laws with provisions for primary enforcement in all states; further promotion of helmets for motorcyclists and bicyclists; and increased occupational safety especially in the highest risk professions of mining, construction, logging, and transportation.

STRATEGIES FOR PREVENTION OF INTENTIONAL INJURIES Organized injury prevention efforts do not have as long a history for intentional injuries as it does for unintentional injuries. Prevention of intentional injuries has traditionally been the realm of the criminal justice system, with health care professionals and injury prevention personnel being relative newcomers. However, the same basic principles of injury etiology apply. Likewise, prevention work can be based on the development of strategies to identify and decrease risk factors. These strategies can use the same modalities of engineering, education, and enforcement to accomplish change in society. Some of the prevention efforts that have been utilized against some of the more common forms of intentional injury will be reviewed briefly. Fatal intentional injury is commonly categorized as either homicide or suicide. However, it is important to remember that homicide is a final common pathway for several types of violent behavior, each of which produces many more nonfatal injuries. These include domestic violence, child abuse, elder abuse, and assaultive behavior in general. Prevention strategies for each of these are fairly different and examples will be considered separately.

■ Assaultive Behavior A minority of interpersonal violence occurs between strangers. The majority occurs between people who know each other and occurs in the course of interpersonal relationships, which have evolved into conflicts. Hence, a focus for violence prevention has been to promote nonviolent “conflict resolution.” The teaching and promotion of conflict resolution skills has been undertaken within two broad categories of programs: school based and community based.7,61–64

School-based Programs These usually involve an educational curricula aimed at changing students’ attitudes toward violence and teaching adaptive interpersonal skills for nonviolent conflict resolution. Several standardized curricula are available, oriented for a variety of grades, from primary through high school. These curricula have been shown to change students’ attitudes toward violence and to decrease interpersonal aggression in the short term. However, their long-term effectiveness at decreasing assaultive behavior is not known.7 An example of one such curriculum is Second Step: A Violence Prevention Curriculum, Grades 1–3. The curriculum consists of 30, half-hour lessons. Each lesson involves the presentation of a social scenario, with an accompanying photograph. This scenario forms the basis for discussion and role playing by the students. Teachers who participate are usually given a 2-day training session. The lessons are arranged in three

Injury Prevention

Community-based Programs These programs focus on decreasing youth violence outside of the school environment. This has the advantage of reaching older adolescents and dropouts. Some community-based programs utilize conflict resolution education, similar to school-based programs. Such education is delivered by public education campaigns and via neighborhood health centers. In some cases, high-risk youths, such as those seen in emergency rooms for assaultive injuries, are identified and referred for violence prevention counseling.65 Some community-based programs are parts of more general youth development programs, featuring mentoring, as well as recreational and cultural activities. These include some traditional approaches that have been active for years, such as the Boys Club. Such programs seek to decrease violent behavior as part of decreasing overall delinquency and drug dependency. An example of a successful community-based program is the Harlem Hospital Injury Prevention Program (HHIPP). This program, founded in 1988, sought to decrease childhood injuries from all causes, including violence. The program used a broad multidimensional approach, including educational programs on health and safety; increased environmental safety in parks and playgrounds; and increased availability of supervised recreational activities for children and adolescents. The program was community based, with the HHIPP acting as the lead agency in building a coalition, which included neighborhood organizations and agencies of the local and state government.61,62 The results of these activities were evaluated using the Northern Manhattan Injury Surveillance System. The incidence of all injuries targeted by the HHIPP decreased by 44% after the institution of the program. Violent injuries decreased by 50%, in comparison to control communities, where such violent injuries increased by 93% during the study period.61,62

■ Domestic Violence Although a large proportion of all violent acts involve persons living in the same household, a specific subset of such violence warrants special attention. This is violence involving spouses or other intimate partners and hence is often know as intimate

partner violence. The vast majority of such abuse involves a man injuring his female partner. This is often regarded as a separate entity because of the interpersonal dynamics involved and the associated prevention implications. Domestic violence usually is a chronic, repetitive phenomenon. It is usually associated with psychological abuse and verbal intimidation. It is usually characterized by a man who seeks to dominate his partner both physically and emotionally and by a woman who is afraid to leave the relationship because of psychological and/or financial dependency. The more extreme forms of domestic violence, including homicide, are usually the endpoints of long abusive relationships.7,66,67 It is the identification of domestic violence at its earlier stages upon which most preventive strategies are built. For years, the mainstay of domestic violence prevention has been the criminal justice system. This has included both active interventions, such as restraining orders against abusive men, and deterrence by threat of punishment. None of the other newer interventions are likely to work unless such a system is functional. However, as traditionally used, the criminal justice system is underutilized primarily because many women are afraid to step forward and file complaints. Hence, other modalities have been deemed necessary. These have included the use of hot lines, counseling services, and shelters for battered women. Another component of prevention has included early identification of battered women through the health care system. This has included identification in the setting of both emergency departments and primary care practices. Although many battered women may not volunteer information as to a history of battering, many are willing to divulge the information when asked. Hence, questioning about domestic violence is critical for screening and identification. Both the American Medical Association and the American College of Emergency Physicians strongly recommend routine screening for domestic violence.66–69 Specific programs aimed at domestic violence have included programs to improve training of health care workers (including doctors, nurses, and receptionists) in such screening for domestic violence. This includes techniques for eliciting confidential information from victims, for establishing severity and risk, and for presenting options for safety and counseling. Such programs have been documented to improve screening and case identification of abused women.7,66,67,70 In addition, further work is needed to identify the most effective interventions, once a woman at risk for repeated domestic violence has been identified. The same rigor that has been applied to outcome assessments for unintentional injury needs to be applied for intentional injury. This implies a furthering of scientific inquiry into domestic violence and other forms of intentional injury. As one example of such evaluation, Holt et al. demonstrated that year-long restraining orders were more likely to lead to a decrease in subsequent acts of violence against women than short-term orders.71

■ Suicide High-risk groups for suicide include adolescents and young adults in all races, but especially Native Americans. Unlike

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groups: (1) empathy training, (2) impulse control, and (3) anger management. In a study to evaluate the effectiveness of this curriculum, 12 elementary schools in King County, Washington State, were randomized to have the curriculum taught or to be a control. Observers rated specific children’s interactions with other children and with teachers using a standardized social science behavior coding system. These observers were blinded as to whether or not a given school or specific children had received the curriculum. There was a decrease in physical aggression and an increase in neutral/prosocial behavior in the group receiving the curriculum compared with the control group. This was true at both 2 weeks and at 6 months after the course was taught. These changes were significant at both time periods, but less pronounced at 6 months. The ultimate effect on violent behavior in adolescence and adulthood remains unknown.63

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other forms of intentional injury however, one of the highest risk groups is older white men.51 A common problem with suicide prevention efforts is the relative lack of evaluation of their effectiveness. In part, this has been due to a difficulty in monitoring suicides due to underreporting. Also, the sporadic nature of actual suicides mandates very large sample sizes in order to assess effectiveness. Thus, a variety of different prevention strategies have been utilized.

■ Identification and Treatment of Individuals at High Risk of Suicide Such identification has most often been done within the health care system, especially in emergency departments and primary care practices. Patients who present to an emergency department having just made an unsuccessful suicide attempt are obviously one high-risk group to identify. Identifying patients with depression or other “warning signs” of impending suicide within the context of a primary care practice, however, is much more difficult.72 In addition to a history of prior suicide attempt, studies have shown several risk factors for future attempts, including alcohol or substance abuse and mental illness, especially affective disorders.73 However, none of these factors is sufficiently sensitive or specific to be a good screening test in and of itself. Special efforts to upgrade the training of primary care providers to improve recognition of these risk factors and to increase their familiarity with treatment for these disorders has shown some promise in improving the detection and treatment of high-risk individuals.74–77

■ Education Programs Aimed at General Public These have most notably been utilized in school-based settings. The goals of such programs are to educate teachers, students, and parents about warning signs of impending suicide attempts and to provide them with information about available resources for help.7,78

■ Crisis Intervention Services Accessible self-referral resources for suicidal persons have included hot lines and personal counseling. In addition to the services they directly provide, these also function as an entry point into the mental health system. Such crisis intervention services have been the most frequently utilized suicide prevention strategies. However, their impact on lowering the suicide incidence rate has not been well demonstrated.7,78

■ Reducing the Availability of the Means of Suicide Reducing access to the means of suicide can be considered on both an individual and a societal level. It might seem that someone who wishes to commit suicide would find alternative means. However, most cases of suicide involve complex psychological processes in which both ambivalence and spontaneity play major roles. Elimination of a convenient and acceptable

way to commit suicide may not lead to choosing another alternative, but rather to a decision not to complete the act.7,78 One of the best examples of the effects of decreasing the availability of the means of suicide was in England. Prior to the 1960s, half of the persons committing suicide in England used cooking gas to asphyxiate themselves. At the time, cooking gas was coal-based and consisted of 10–20% carbon monoxide. During the 1960s and 1970s, this was replaced by natural gas, both for safety and for economic reasons. The overall suicide rate in Britain decreased by 35% in the years after the gas supply had changed.79,80 This example has obvious implications for the United States, where the majority of suicides are committed with firearms.

■ The Roles of Alcohol and Firearms As can be seen, there are a variety of interventions to decrease specific types of intentional injury, based on the human, psychological, and interpersonal factors at play. However, there are several common risk factors for all forms of intentional injury. These are the high frequency of involvement of alcohol and firearms. Between 30–60% of all homicides involve alcohol on the part of at least either the assailant or victim.7 Alcohol involvement in suicides also appears frequent, although the exact percentages are more difficult to identify. Similarly, firearms are used in 60% of suicides and 70% of homicides.5–7,51 Strategies to decrease the availability or impact of alcohol in society are also ways to decrease alcohol’s involvement in intentional injuries. Such strategies include institution of a 21-yearold drinking age, higher alcohol excise taxes, and increased availability of alcohol rehabilitation services. Hospital- and trauma center-based counseling interventions aimed at patients who present with any type of alcohol-related injury are another strategy to consider, as discussed in the section on unintentional injury.39–41 Likewise, strategies to decrease the availability or impact of firearms are ways to decrease intentional injuries in general. However, probably no other aspect of injury prevention engenders a greater debate than this issue. Firearms are more common in American society than in almost any other developed country. The United States has higher rates of firearmrelated injury than any other developed country that is not at war. Attempts to decrease the availability of firearms have met with sustained, emotional resistance from Americans who consider unrestricted ownership of firearms a constitutionally guaranteed right. However, it is important to recognize that communities with differing gun laws causing resultant differences in the prevalence of gun ownership also demonstrate decreases in homicide rates in those communities with more restrictive gun control laws.81 Data on the effects of the institution of more restrictive gun ownership laws in a given area over time are less clear cut. However, the weight of the evidence does indicate a net reduction in firearm-related deaths from such laws.5,6,82,83 The CDC recommends a greater use of restrictive licensing for firearms, especially for handguns. Such gun control laws restrict possession of handguns to those with a clearly demonstrated need. The CDC also recommends greater enforcement

Injury Prevention

RECENT GLOBAL INITIATIVES This chapter primarily addresses the circumstances of North America and other high-income countries. However, the vast majority of injury-related deaths occur in low- and middle-income countries (LMICs). This is because this is where the majority of people live; injury rates are higher; there have been limited application of organized injury prevention efforts; and trauma care systems are less than optimally developed. Moreover, injury rates are declining in most highincome countries, but rising, sometimes rapidly, in most LMICs.87,88 Many of the general injury prevention principles discussed in the current chapter are applicable under any circumstances. However, some of the specific applications need to vary to fit the circumstances of most of the world. This is due to varying injury mechanisms, resource restrictions, and cultural differences. There is a need to develop local injury prevention expertise and locally applicable strategies. After years of neglect by international agencies, injury control has been gradually receiving justifiable increases in attention worldwide. One of the groups spearheading these efforts has been the World Health Organization (WHO). Two recent landmark publications by the WHO have addressed two of the biggest injury problems, road traffic injury and violence. The World Report on Road Traffic Injury Prevention has helped raise awareness about the problem and to promote practical policy solutions for countries at varying economic levels worldwide.89 The World Report on Violence and Health has emphasized the role that the health sector can have in violence prevention, in addition to sectors, such as criminal justice, that have traditionally been the foundation of violence prevention.90 This report points out the complementary role

that the health sector brings by its focus on changing the behavioral, social, and environmental factors that give rise to violence. Health also brings its focus on prevention, its scientific outlook, and its potential to coordinate multidisciplinary approaches. In similar fashion, the Global Burden of Surgical Disease working group has been formed, consisting of surgeons, anesthesiologists, public health specialists, and others from the United States and from many other countries. This group has worked closely with the American College of Surgeons and WHO. It is working to get increased global attention to a spectrum of issues that involve surgical care, including trauma, obstetrics, and emergency surgical conditions. Among other activities, the group is attempting to get better estimates of the toll of surgical conditions especially within the Global Burden of Disease study, and to promote increased attention to planning for surgical care within the world’s ministries of health.91 This increased attention to global injury control has gradually resulted in increasing political commitment. In 2009, the First Global Ministerial Conference on Road Safety was held. This was attended by ministers of health and/or transportation and other senior officials from 150 countries, who committed their countries to greater attention to road safety. This was followed shortly thereafter, in March 2010, by the United Nations General Assembly declaring 2011–2020 as the Decade of Action for Road Safety. Through this Decade of Action, country governments worldwide committed to action in such areas as developing and enforcing legislation on key risk factors, including speed reduction, reducing drunk-driving, and increasing the use of seatbelts, child restraints, and motorcycle helmets. Efforts will also be undertaken to improve trauma care, upgrade road and vehicle safety standards, promote road safety education and enhance road safety management generally.92 Of course, it is still up to injury control advocates to actively lobby their governments to see that these commitments become reality. There has also been increasing commitment to injury control by funders. For example, the U.S. National Institutes of Health established the Fogarty International Collaborative Trauma and Injury Research Training Program. This funds collaborative training programs linking U.S. universities with partners in developing countries for the purpose of increasing the capacity of developing country institutions to conduct research on injury prevention and trauma care. Similarly, several private foundations have begun funding injury control issues. For example, the Bloomberg Philanthropies has recently funded a consortium of partners, headed by WHO, to improve road safety in 10 developing countries that currently account for half of all road traffic deaths globally.93 Nonetheless, overall funding for injury prevention remains inadequate compared to the extent of the problem and major bilateral donors, such as USAID, have not yet established programs that encompass injury prevention. Readers interested in learning more about the application of injury prevention programs in LMICs are encouraged to read these and other related2,88,93,94 publications, as well as the WHO website (www.who.int/violence_injury_ prevention/en/).

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of existing firearms laws, such as requiring waiting periods and background checks for those wishing to purchase guns.7 In addition, another matter requiring attention is closing the current gun-show sales loophole. Other preventive measures directed at firearms include educational programs to teach safe gun handling, as a way primarily to decrease unintentional firearm injuries. However, similar to other generic nonfocused educational programs, the efficacy of such programs is not well demonstrated. Moreover, unintentional injuries account for only a small proportion of all firearm-related injuries.7 Finally, there has been increased emphasis lately on safer storage of firearms. This includes keeping guns stored unloaded with ammunition stored separately. Other alternatives include the use of trigger locks and locked gun boxes. These devices allow a loaded gun to be kept more immediately available for those who feel the need to have such weapons rapidly available for self-protection. All these techniques are felt to be ways to decrease not only unintentional firearms injuries, but also both assaultive and suicidal use of firearms.84–86 In addition to social marketing efforts to promote use of these devices, mandated trigger locks on all guns sales is a currently proposed approach.

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BOX 3-1 COMPONENTS OF A SUCCESSFUL INJURY PREVENTION PROGRAM

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1. Identify a significant, eminently preventable, injury problem and a potential, eminently feasible, intervention. Problem should be a significant health problem, in terms of mortality or morbidity. Focus on injuries that are severe or common, or both. An effective intervention should exist, especially one which is being suboptimally utilized in a given environment. Gather information on the extent of the problem and the effectiveness of possible interventions. Be able to communicate this information in terms understandable to the public, politicians, and other constituencies. 2. Identify and elicit the support of potential partners. Create a coalition of those with similar interests and goals. This coalition could include clinicians, public health practitioners, government, members of the lay public, insurance companies and other industry representatives, and others. Having one of these partners function as a “lead agency” is helpful to coordinate and stimulate the actions of the other partners. 3. Identify barriers to the use of the intervention. Such barriers could include: The knowledge and attitudes of the public. Available interventions may need to be modified or presented differently to certain high-risk groups. Lack of political will. Opposition by special interest groups. 4. Develop and implement a plan to address these barriers. Such a plan could involve a wide variety of actions and goals, such as, among other items: A public information campaign to change a dangerous behavior. A change in a law or the enforcement/application of a law. Change in the availability or characteristics of a product. Change in a hazardous environment. Surgeons and other clinicians can play key roles in all of the above, through actions, such as, among others: Bearing witness to the human toll of injury, so as to increase public and political will for changes. Advocacy for changes with local, state, and national government. Institute changes in injury prevention practice in their own institutions, such as with instituting alcohol interventions in hospitals. Injury prevention related counseling and advice for patients and their families. Successful programs usually involve: Multidisciplinary approach. Community involvement. Ongoing evaluation. Need to mobilize resources: Funding. Volunteer labor. Publicity/free advertising/human interest stories. Gifts-in-kind. More resources usually available with increased community interest and involvement. Other aspects of successful programs. Specific tasks assigned to specific partners. Set reasonable, meaningful, yet achievable goals. Regular meetings and updates by coalition members. 5. Evaluate the outcome of this program. Potential items to assess. Change in a law or its enforcement. Change in behavior, such as use of safety devices (e.g., smoke detectors, helmets). Decreases in rates of death or severe injury. Be prepared to change plans, if needed, based on feedback from outcome assessment. 6. Prevent the erosion of success. Most successful injury prevention campaigns are those that eventually become “institutionalized” and thus a regular part of the function of government or other groups. Guard against successful programs being rolled back by opposing interest groups or apathy by the public.

Injury Prevention

CONCLUSION: THE SURGEON’S ROLE IN INJURY PREVENTION

REFERENCES 1. American Trauma Society. Trauma Watch; February 13, 2006. 2. Barss P, Smith G, Baker S, Mohan D. Injury Prevention: An International Perspective. New York: Oxford University Press; 1998. 3. Christoffel T, Gallagher S. Injury Prevention and Public Health. Gaithersburg, MD: Aspen Publishers, Inc; 1999. 4. Doll L, Bonzo S, Sleet D, Mercy J. Handbook of Injury and Violence Prevention. New York: Springer; 2007. 5. Rivara FP, Grossman DC, Cummings P. Injury prevention: First of two parts. N Engl J Med. 1997;337:543–548. 6. Rivara FP, Grossman DC, Cummings P. Injury prevention: Second of two parts. N Engl J Med. 1997;337:613–618. 7. The National Committee for Injury Prevention and Control. Injury Prevention: Meeting the Challenge. New York: Oxford University Press; 1989. 8. Mock CN, Jurkovich GJ, nii-Amon-Kotei D, Arreola-Risa C, Maier RV. Trauma mortality patterns in three nations at different economic levels: implications for global trauma system development. J Trauma. 1998; 44:804–814. 9. Sauaia A, Moore FA, Moore EE, Moser KS, Read RA, Pons P. Epidemiology of trauma deaths: a reassessment. J Trauma. 1995;38:185–193. 10. Waller J. Injury: conceptual shifts and preventive implications. Annu Rev Public Health. 1987;8:21–49. 11. DeHaven H. Mechanical analysis of survival in falls from heights of fifty to one hundred and fifty feet. War Med. 1942;2:586–596. 12. DeHaven H. Research on crash injuries (editorial). JAMA. 1946; 131:524. 13. Gordon JE. The epidemiology of accidents. Am J Pub Health. 1949;39: 504–515. 14. Haddon W. Advances in the epidemiology of injuries as a basis for public policy. Public Health Rep. 1980;95:411–421. 15. Hazinski MF, Francescutti LH, Lapidus GD, Micik S, Rivara FP. Pediatric injury prevention. Ann Emerg Med. 1993;22(pt 2):456–467. 16. Insurance Institute for Highway Safety. Education alone won’t make drivers safer. It won’t reduce crashes. Insurance Institute for Highway Safety: Status Report. 2001;36(5):1–7. 17. Brown ST, Foege WH, Bender TR, Axnick N. Injury prevention and control: prospects for the 1990s. Annu Rev Public Health. 1990;11: 251–266. 18. McSwain NE, Belles A. Motorcycle helmets: medical costs and the law. J Trauma. 1990;30:1189–1197. 19. Simon v Sargent FSM. Affirmed in 409 U.S. 1020 (1972). 20. Bergman AB. Political Approaches to Injury Control at the State Level. Seattle: University of Washington Press; 1992. 21. Robertson LS. Automobile safety regulation in the United States. Am J Pub Health. 1981;71:818–822. 22. Robertson LS. Automobile safety regulation: rebuttal and new data. Am J Pub Health. 1984;74(12):1390–1394.

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Injury prevention efforts do work. Such efforts have had considerable success in lowering the toll of injury-related death and disability. These successes have been most notable in unintentional injury, especially due to road safety. Organized injury prevention work is also being increasingly applied to intentional injury. Obviously, much more remains to be done. This is especially true in light of recent setbacks in highway safety, motorcycle helmet use, and flame retardant clothing for children’s sleepwear. In addition, the raising of speed limits in most states resulted in an increase in the motor vehicle crash death rate in the early 1990s with stagnation in the death rate thereafter, until the most recent few years.25 The accomplishments and successes of injury prevention programs rely on multidisciplinary input. Although many surgeons may not consider themselves as a usual part of injury prevention work, there is much they can contribute. In some injury prevention programs, they have played a pivotal role. Their contributions can be on both individual and societal levels. Surgeons, along with emergency physicians and prehospital providers, have more direct contact with acutely injured patients than do any other health care professionals. Hence, they are in a position to provide individual patient counseling regarding safety at a time when many injured persons are in a receptive state. Examples include emphasizing the importance of bicycle helmets to the parents of a child who has been injured bicycling without one and stressing the necessity of wearing a seatbelt to a motorist injured without one. Perhaps one of the biggest roles for surgeons is to screen patients for alcohol abuse. Surgeons in hospitals that receive large numbers of injured persons should make sure that their hospitals institute mandatory screening, counseling, and referral programs, as now required by the American College of Surgeons for Level I and II trauma centers. The voice of authority with which health care professionals speak allows them to be effective advocates for injury prevention educational campaigns and for legislation. Surgeons and other clinicians were instrumental in the public information campaigns that formed a component of the Seattle bicycle helmet campaign. Likewise, surgeons and other clinicians provided testimony in the motorcycle helmet debate, which eventually led to the passage of numerous state motorcycle helmet laws. Research is another avenue through which surgeons have and can contribute to injury prevention. This includes research that demonstrates the extent of a problem. For example, research on the costs of nonhelmeted motorcyclists in Washington State has provided useful data in the motorcycle helmet debate.31,58,59 Such research also includes evaluation of the effectiveness of injury prevention programs.57 In addition to such analytic research, surgeons have contributed to the development of systems to collect basic information on the extent of the toll from injury. For example, surgeons have been actively involved in the ongoing development of the National Violent Death Reporting System, created by the CDC. This system is seeking to provide information on the toll of violence in our

society and to provide answers to questions about violence prevention strategies (http://www.cdc.gov/ViolencePrevention/ NVDRS/index.html). For surgeons and other clinicians wishing to get involved in injury prevention, many of the references cited in this chapter offer useful practical information. We especially recommend Injury Prevention: Meeting the Challenge, published by the CDC,7 Injury Prevention and Public Health by Christoffel and Gallagher,3 and the Handbook of Injury and Violence Prevention by Doll et al.4 Finally, the American Association for the Surgery of Trauma and the American College of Surgeons both have prevention sections on their websites (http://www.aast.org and http://www.facs.org/trauma/injmenu.html). These sites provide useful, practical information on injury prevention and on important injury-related legislation, which is pending. They also have multiple links to other injury prevention resources, including a large number of local programs. A summary of the components of a successful injury prevention program, with emphasis on a surgeon’s involvement, is included in Box 3-1.

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23. Robertson LS. Injury Epidemiology: Research and Control Strategies. New York: Oxford University Press; 1998. 24. Nader R. Unsafe at Any Speed: The Designed-in Dangers of the American Automobile. New York: Grossman Publishers; 1965. 25. National Highway Traffic Safety Administration. Traffic Safety Facts 2008. DOT HS 811 170. Washington, DC: National Center for Statistics and Analysis, US DOT; 2009. 26. Centers for Disease Control and Prevention. Web-based Injury Statistics Query and Reporting System. 2010. http://www.cdc.gov/injury/wisqars/ index.html. Accessed April 20, 2010. 27. Ebel B, Grossman D. Crash proof kids? An overview of current motor vehicle child occupant safety strategies. Curr Probl Pediatr Adolesc Health Care. 2003;33:35–55. 28. Anderson P, Rivara F, Maier R, Drake C. The epidemiology of seatbeltassociated injuries. J Trauma. 1991;31:60–67. 29. Durbin D, Elliott M, Winston F. Belt-positioning booster seats and reduction in risk of injury among children in vehicle crashes. JAMA. 2003;289:2835–2840. 30. Evans L, Frick M. Helmet effectiveness in preventing motorcycle driver and passenger fatalities. Accid Anal Prev. 1988;6:447–458. 31. Rowland J, Rivara FP, Salzberg P, Soderberg R, Maier R, Koepsell T. Motorcycle helmet use and injury outcome and hospitalization costs in Washington State. Am J Publ Health. 1996;86:41–45. 32. Sosin DM, Sacks JJ. Motorcycle helmet use laws and head injury prevention. JAMA. 1992;267:1649–1651. 33. Thomas S, Acton C, Nixon J, Battistutta D, Pitt WR. Effectiveness of bicycle helmets in preventing head injury in children: case-control study. BMJ. 1994;308:173–176. 34. Thompson RS, Rivara FP, Thompson DC. Case-control study of the effectiveness of bicycle safety helmets. N Engl J Med. 1989;320: 1361–1367. 35. Borkenstein RF, Crowther RF, Shumate RP, Ziel WB, Zylman R. The role of the drinking driver in traffic accidents. Alcohol Drugs Behav. 1974;2 (suppl 1):8–32. 36. National Highway Traffic Safety Administration. 2007 Traffic Safety Annual Assessment: Alcohol-Impaired Driving Fatalities. DOT HS 811 016. NHTSA’s National Center for Statistics and Analysis. Washington, DC: NHTSA; 2008. 37. National Highway Traffic Safety Administration. Results of the 2007 National Roadside Survey of Alcohol and Drug Use by Drivers. DOT HS 811 175. NHTSA’s National Center for Statistics and Analysis. Washington, DC: NHTSA; 2009. 38. DeJong W, Hingson R. Strategies to reduce driving under the influence of alcohol. Annu Rev Public Health. 1998;19:359–378. 39. Dunn CW, Donovan DM, Gentilello LM. Practical guidelines for performing alcohol interventions in trauma centers. J Trauma. 1997; 42:299–304. 40. Gentilello LM, Donovan DM, Dunn CW, Rivara FP. Alcohol interventions in trauma centers. JAMA. 1995;274:1043–1048. 41. Gentilello L, Rivara F, Donovan D, et al. Alcohol interventions in a trauma center as a means of reducing the risk of injury recurrence. Ann Surg. 1999;230:473–480. 42. Insurance Institute for Highway Safety. Licensing Ages and Graduated Licensing Systems. 2010. http://www.iihs.org/laws/graduatedLicenseIntro. aspx. Accessed April 20, 2010. 43. Foss R, Feaganes J, Rodgman E. Initial effects of graduated driver licensing on 16-year-old driver crashes in North Carolina. JAMA. 2001; 286:1588–1592. 44. Ranney TA. Driver Distraction: A Review of the Current State-of-Knowledge. DOT HS 810 787. Washington, DC: NHTSA; 2008. 45. National Highway Traffic Safety Administration. An Examination of Driver Distraction as Recorded in NHTSA Databases. DOT HS 811 216. Washington, DC: NHTSA’s National Center for Statistics and Analysis; 2009. 46. Breen J. Car telephone use and road safety. Final report. An overview prepared for the European Commission. June 2009. http://ec.europa.eu/transport/ road_safety/specialist/knowledge/mobile/car_telephone_use_and_road_ safety.pdf. Accessed April 20, 2010. 47. Redelmeier DA, Tibshirani RJ. Association between cellular-telephone calls and motor vehicle collisions. N Engl J Med. 1997;336: 453–458. 48. American Automobile Association. State Distracted Driving Laws. 2010. http://www.aaaexchange.com/main/Default.asp?CategoryID=3&SubCat egoryID=35. Accessed April 20, 2010. 49. McCartt AT, Braver ER, Geary LL. Drivers’ use of handheld cell phones before and after New York State’s cell phone law. Prev Med. 2003;36: 629–635.

50. Rivara F, Koepsell T, Grossman D, Mock C. Effectiveness of automatic shoulder belt systems in motor vehicle crashes. JAMA. 2000;283: 2826–2828. 51. Baker SP, O’Neill B, Ginsburg MJ, Li G. The Injury Fact Book. New York: Oxford University Press; 1992. 52. Wanda L, Tenenbein M, Moffatt ME. House fire injury prevention update. Inj Prev. 1999;5:217–225. 53. DiGuiseppi CG, Rivara FP, Koepsell TD. Attitudes toward bicycle helmet ownership and use by school-age children. AJDC. 1990;144: 83–86. 54. DiGuiseppi CG, Rivara FP, Koepsell TD, Polissar L. Bicycle helmet use by children: evaluation of a community-wide helmet campaign. JAMA. 1989;262:2256–2261. 55. Bergman AB, Rivara FP, Richards DD, Rogers LW. The Seattle children’s bicycle helmet campaign. AJDC. 1990;144:727–731. 56. Rivara FP, Rogers LW, Thompson DC, et al. The Seattle children’s bicycle helmet campaign: effects on helmet use and head injury admissions. Pediatrics. 1994;93:567–569. 57. Mock CN, Maier RV, Boyle E, Pilcher S, Rivara FP. Injury prevention strategies to promote helmet use decrease severe head injury at a level I trauma center. J Trauma. 1995;39:29–35. 58. Offner PJ, Rivara FP, Maier R. The impact of motorcycle helmet use. J Trauma. 1992;32:636–642. 59. Rivara FP, Dicker BG, Bergman AB, Dacey R, Herman C. The public cost of motorcycle trauma. JAMA. 1988;260:221–223. 60. National Safety Council. Accident Facts. Chicago: National Safety Council; 1990. 61. Davidson LL, Durkin MS, Kuhn L, O’Connor P, Barlow B, Heagarty MC. The impact of the Safe Kids/Healthy Neighborhoods Injury Prevention Program in Harlem, 1988 through 1991. Am J Public Health. 1994;84:580–586. 62. Durkin MS, Kuhn L, Davidson LL, Laraque D, Barlow B. Epidemiology and prevention of severe assault and gun injuries to children in an urban community. J Trauma. 1996;41:667–673. 63. Grossman DC, Neckerman HJ, Koepsell TD, et al. Effectiveness of a violence prevention curriculum among children in elementary school. JAMA. 1997;277:1605–1611. 64. Wright JL, Cheng TL. Successful approaches to community violence intervention and prevention. Pediatr Clin North Am. 1998;45:459–467. 65. Prothrow-Stith D. The violence prevention project: a public health approach. Sci Tech Human Values. 1987;12:67–69. 66. El-Bayoumi G, Borum ML, Haywood Y. Domestic violence in women. Med Clin North Am. 1998;82:391–401. 67. Melvin SV, Rhyne MC. Domestic violence. Adv Intern Med. 1998; 43:1–25. 68. American College of Emergency Physicians Policy Statement. Emergency Medicine and Domestic Violence. Dallas: American College of Emergency Physicians; 1994. 69. American Medical Association. Diagnostic and Treatment Guidelines on Domestic Violence. Chicago: American Medical Association; 1992. 70. Thompson RS, Rivara FP, Thompson DC, et al. Identification and management of domestic violence: a randomized trial. Am J Prev Med. 2000;19:253–263. 71. Holt VL, Kernic MA, Lumley T, Wolf ME, Rivara FP. Civil protection orders and risk of subsequent police-reported violence. JAMA. 2002;288:589–594. 72. Mock CN, Grossman D, Mulder D, Stewart C, Koepsell T. Detection of suicide risk during health care visits on a Native American reservation. J Gen Intern Med. 1996;11:519–524. 73. Fowler RC, Rich CL, Young D. San Diego Suicide Study, II: substance abuse in young cases. Arch Gen Psychiatry. 1986;43:962–965. 74. Katon W, VonKorff M, Lin E, et al. Collaborative management to achieve treatment guidelines: impact on depression in primary care. JAMA. 1995;273:1026–1031. 75. Rutz W, LvonKnorring, Walinder J. Frequency of suicide in Gotland after systematic postgraduate education of general practitioners. Acta Psychiatr Scand. 1989;80:151–154. 76. Rutz W, LvonKnorring, Walinder J. Long-term effects of an educational program for general practitioners given by the Swdish Committee for the Prevention and Treatment of Depression. Acta Psychiatr Scand. 1992; 85:83–88. 77. Simon GE, VonKorff M. Recognition, managment, and outcomes of depression in primary care. Arch Fam Med. 1995;4:99–105. 78. O’Carroll PW, Rosenberg ML, Mercy JA. Suicide. In: Rosenberg ML, Fenley MA, eds. Violence in America. New York: Oxford University Press; 1991. 79. Brown JH. Suicide in Britain. Arch Gen Psychiatry. 1979;36:1119–1124.

Injury Prevention 88. Mock C, Quansah R, Krishnan R, Arreola-Risa C, Rivara F. Strengthening the prevention and care of injuries worldwide. Lancet. 2004;363: 2172–2179. 89. Peden M, Scurfield R, Sleet D, et al. World Report on Road Traffic Injury Prevention. Geneva: World Health Organization; 2004. 90. Krug E, Dahlberg L, Mercy J, Zwi A, Lozano R. World Report on Violence and Health. Geneva: World Health Organization; 2002. 91. Global Burden of Surgical Disease Working Group. 2010. http:// globalhealthdelivery.org/2008/05/global-burden-of-surgical-diseaseworking-group-need-and-impact-of-surgical-services-in-low-resourcecountries-unaccounted-for/. Accessed April 20, 2010. 92. World Health Organization. Decade of Action for Road Safety. 2010. http://www.who.int/violence_injury_prevention/road_traffic/rs_decade_ of_action/en/. Accessed April 20, 2010. 93. World Health Organization. Country Work. 2010. http://www.who.int/ violence_injury_prevention/road_traffic/countrywork/en/index.html. Accessed April 20, 2010. 94. Berger LR, Mohan D. Injury Control: A Global View. Delhi: Oxford University Press; 1996.

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80. Kreitman N. The coal gas story: United Kingdom suicide rates, 19601971. Br J Prev Soc Med. 1976;30:89–93. 81. Sloan JH, Kellermann AL, Reay DT, et al. Handgun regulations, crime, assaults, and homicide: a tale of two cities. N Engl J Med. 1988;319: 1256–1262. 82. Loftin C, McDowall D, Wiersema B, Cottey TJ. Effects of restrictive licensing of handguns on homicide and suicide in the District of Columbia. N Engl J Med. 1991;325:1615–1620. 83. Rosengart M, Cummings P, Nathens A, Heagerty P, Maier R, Rivara F. An evaluation of state firearm regulations and homicide and suicide death rates. Inj Prev. 2005;11:77–83. 84. Cummings P, Grossman DC, Rivara FP, Koepsell TD. State gun safe storage laws and child mortality due to firearms. JAMA. 1997;278: 1084–1086. 85. Denno DM, Grossman DC, Britt J, Bergman AB. Safe storage of handguns: what do the police recommend. Arch Pediatr Adolesc Med. 1996;150:927–931. 86. Grossman DC, Cummings P, Koepsell TD, et al. Firearm safety counseling in primary care pediatrics: a randomized, controlled trial. Pediatrics. 2000;106:22–26. 87. Krug EG, Sharma GK, Lozano R. The global burden of injuries. Am J Pub Health. 2000;90:523–526.

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CHAPTER 4

Trauma Systems, Triage, and Transport Raul Coimbra, David B. Hoyt, and Vishal Bansal

DEFINITION OF TRAUMA SYSTEMS A trauma system is an organized approach to acutely injured patients in a defined geographic area that provides full and optimal care and that is integrated with the local or regional emergency medical service (EMS) system. A system has to achieve cost efficiency through the integration of resources with local health and EMS system to provide the full range of care (from prehospital to rehabilitation).1–3 Regionalization is an important aspect of trauma as a system because it facilitates the efficient use of health care facilities within a defined geographic area and the rational use of equipment and resources. Trauma care within a trauma system is multidisciplinary and is provided along a continuum that includes all phases of care.2–6 The major goal of a trauma system is to enhance the community health. This can be achieved by identifying risk factors in the community and creating solutions to decrease the incidence of injury, and by providing optimal care during the acute as well as the late phase of injury including rehabilitation, with the objective to decrease overall injury-related morbidity and mortality and years of life lost. Disaster preparedness is also an important function of trauma systems, and using an established trauma system network will facilitate the care of victims of natural disasters or terrorist attacks. The Model Trauma System Planning and Evaluation Standard has recently been completed by the U.S. Department of Health and Human Services.7

THE NEED FOR TRAUMA SYSTEMS—HISTORY The need for a trauma system seems obvious and intuitive. However, trauma is not yet recognized as a disease process. Many people still think of trauma as an accident. Trauma is an epidemic that affects all age groups with devastating personal, psychological, and economic consequences. Recent calculations

have estimated the total cost of injury in the United States to be about $260 billion per year.8 Because of the association of injury and personal behavior, trauma is often predictable and preventable. The modern approach to trauma care is based on lessons learned during war conflicts. Advances in rapid transport, volume resuscitation, wound care management of complex injuries, surgical critical care, early nutritional management, and deep venous thrombosis prophylaxis were all derived from the military experience. The American College of Surgeons Committee on Trauma (ACSCOT) was created in 1949 and evolved from the Committee on the Treatment of Fractures that was established in 1922. A specific trauma unit was opened in 1961 at the University of Maryland. In 1966, the National Academy of Sciences and the National Research Council published the important “white” paper entitled Accidental Death and Disability: The Neglected Disease of Modern Society.9 The outgrowth of this document was the development and propagation of systems of trauma care. This publication increased public awareness and led to a federal agenda for trauma system development. Two trauma centers were simultaneously formed in Chicago and San Francisco. The Maryland Institute of Emergency Medicine became the first completely organized, statewide, regionalized system in 1973. Similar initiatives were taken in 1971 in Illinois,10 where the designation of trauma centers was established by state law, and in Virginia in 1981, where a statewide trauma system based on volunteer participation and compliance with national standards as defined by the ACSCOT was established. In 1973, the Emergency Medical Services Systems Act became law, providing guidelines and financial assistance for the development of regional EMS systems. In addition, state and local efforts were initiated by using prehospital care systems to deliver patients to major hospitals where appropriate care could be provided. Prehospital provider programs were

Trauma Systems, Triage, and Transport

TABLE 4-1 Criteria for Statewide Trauma Care System Legal authority for designation Formal process for designation Use American College of Surgeon’s standards Use out-of-area survey teams Number of trauma centers population or volume based Triage criteria allow direct transport to trauma center Monitoring systems in place Full geographic coverage Source: West JG, Williams MJ, Trunkey DD, Wolferth CC. Trauma systems: current status—future challenges. JAMA . 1988;259:3597.

initiatives from this legislation were noteworthy: (1) planning grants for statewide trauma system development were provided to states on a competitive basis and (2) the Model Trauma Care System Plan was published as a consensus document.15 The Model Trauma Care System Plan established an apolitical framework for measuring progress in trauma system development and set the standard for the promulgation of systems of trauma care. The program was again funded in fiscal year 2001 but lost funding in 2006. New legislation is being written to further this effort. The newest document for trauma system planning uses the public health care model of assessment, policy development, and evaluation of the outcome. With appropriate federal funding, this approach will be very successful.7

TRAUMA SYSTEM DEVELOPMENT The criteria for a statewide EMS and trauma systems have been determined and are identified in Tables 4-1 and 4-2. The first step is to establish legal authority for the development of a system. This usually requires legislation at a state or local level that provides public agency authority. The next step in the development of a trauma system is to determine the need of

TABLE 4-2 Emergency Medical Service System Components Regulation and policy Resource management Human resources and training Transportation Facilities Communications Trauma systems Public information and education Medical direction Evaluation Source: Development of Trauma Systems (DOT). Washington, DC: National Highway Traffic Safety Administration; 1988.

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formalized, and training programs were established for paramedics and emergency medical technicians (EMTs). At that time, major teaching hospitals in large cities were, by default, recognized as regional trauma centers. With strong academic leadership, these centers were able to develop regionalization of systems of trauma care by setting examples. ACSCOT developed a task force to publish Optimal Hospital Resources for the Care of the Seriously Injured in 1976, establishing a standard for evaluation of care. This document was the first to set out specific criteria for the categorization of hospitals as trauma centers. This document is periodically revised and is recognized nationally and internationally as the standard for hospitals aspiring to be trauma centers. The current version entitled Resources for Optimal Care of the Injured Patient was published in 2006.4 It establishes criteria for prehospital and trauma care personnel and the importance of ongoing quality assessment. In addition, ACSCOT developed the Advanced Trauma Life Support (ATLS) course in 1980, which has contributed to the uniformity of initial care and the development of a common language for all care providers. In 1985, the National Research Council and the Institute of Medicine published Injury in America: A Continuing Health Care Problem. This document concluded that despite considerable funding used to develop trauma systems, little progress had been made toward reducing the burden of injury.11 This document also reinforced the necessity of investments in epidemiological research and injury prevention. Following the publication of this document, the Centers for Disease Control and Prevention (CDC) was chosen as the site for an injury research center, to coordinate efforts at the national level in injury control, injury prevention, and all other aspects of trauma care. In 1987, the ACSCOT instituted the Verification/ Consultation Program, which provided further resources and incentive for trauma system development and trauma centers’ designation. More recently, the ACSCOT published a document entitled Consultation for Trauma Systems with the objective of providing guidelines for trauma system evaluation and enhancement.12 In 1987, the American College of Emergency Physicians (ACEP) published Guidelines for Trauma Care Systems.13 This document focused on the continuum of trauma care, and identified essential criteria for trauma care systems. In 1988, the National Highway Safety Administration (NTHSA) established the Statewide EMS Technical Assessment Program and the Development of Trauma Systems Course, both important tools to assess the effectiveness of trauma system components as well as for system development. NHTSA also developed standards for quality EMS, including trauma care. The standard required that the trauma care system be fully integrated into the state’s EMS system and have specific legislation (Table 4-1). The trauma care component must include designated trauma centers, transfer and triage guidelines, trauma registries, and initiatives in public education and injury prevention. In 1990, the Trauma Systems Planning and Development Act created the Division of Trauma and EMS (DTEMS) within the Health Resources and Services Administration (HRSA) to improve EMS and trauma care. Unfortunately, the program was not funded between 1995 and 2000 in many states that were in the process of developing trauma systems. Two

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Legal Authority

SECTION 1 X

Inclusive Trauma System

Needs Assessment

Trauma Center Designation

FIGURE 4-1 Regional trauma system development must progress in a sequential fashion; a comprehensive needs assessment is a pivotal early step. (Reproduced with permission from Moore EE. Trauma systems, trauma centers, and trauma surgeons: opportunity in managed competition. J Trauma. 1995;39:1.)

such a system. In general, this has been done in communities by reviewing the outcome of trauma cases in the region. Traditionally, such reviews have focused on preventable deaths. The surgeon’s role is critical in both leadership and commitment to establish a better standard of care. The designated agency in combination with local trauma surgeons and other medical personnel develops criteria for the trauma system, determines which facilities will be designated trauma centers, and establishes a trauma registry, a fundamental component of a quality assurance program4,14–17 (Fig. 4-1).

TRAUMA SYSTEM COMPONENTS The most significant improvement in the care of injured patients in the United States has occurred through the development of trauma systems. However, recent data show that only 60% of states in the United States have statewide trauma

systems, and about 20% have no trauma system at all. The necessary elements of a trauma system are: access to care, prehospital care, hospital care, and rehabilitation, in addition to prevention, disaster medical planning, patient education, research, and rational financial planning. Prehospital communications, transport system, trained personnel, and qualified trauma care personnel for all phases of care are of utmost importance for a system’s success (Fig. 4-1). External peer review generally is used to verify specific hospital’s capabilities and its ability to deliver the appropriate level of care. The verification process can be accomplished through the ACSCOT or by inviting experts in the field of trauma as outside reviewers. Finally, quality assessment and quality improvement is a vital component of the system, as it provides directions for improvement as well as constant evaluation of the system’s performance and needs. The Model Trauma Care System Plan introduced the concept of the “inclusive system”15 (Fig. 4-2). Based on this model, trauma centers were identified by their ability to provide definitive care to the most critically injured. Approximately 15% of all trauma patients will benefit from the resources of a Level I or II trauma center. Therefore, it is appropriately expected in an inclusive system to encourage participation and to enhance capabilities of the smaller hospitals. Surgical leadership is of fundamental importance in the development of trauma systems. Trauma systems cannot develop without the commitment of the surgeons of a hospital or community.

PUBLIC INFORMATION, EDUCATION, AND INJURY PREVENTION Death following trauma occurs in a trimodel distribution. Effective trauma programs must also focus on injury prevention, since more than half of the deaths occur within minutes of injury, and will never be addressed by acute care.

FIGURE 4-2 Diagram showing the growth of the trauma care system to become inclusive. Note that the number of injured patients is inversely proportional to the severity of their injuries.

Trauma Systems, Triage, and Transport

HUMAN RESOURCES Because the system cannot function optimally without qualified personnel, a quality system provides quality education to its providers. This includes all personnel along the trauma care continuum: physicians, nurses, EMTs, and others who impact the patient and/or the patient’s family.

PREHOSPITAL Trauma care prior to hospital arrival has a direct effect on survival. The system must ensure prompt access and dispatch of qualified personnel, appropriate care at the scene, and safe and rapid transport of the patient to the closest, most appropriate facility. The primary focus is on education of paramedical personnel to provide initial resuscitation, triage, and treatment of trauma patients. Effective prehospital care requires coordination between various public safety agencies and hospitals to maximize efficiency, minimize duplication of services, and provide care at a reasonable cost.

COMMUNICATIONS SYSTEM A reliable communications system is essential for providing optimal trauma care. Although many urban centers have used modern electronic technology to establish emergency systems, most rural communities have not. A communications system must include universal access to emergency telephone numbers (e.g., 911), trained dispatch personnel who can efficiently match EMS expertise with the patient’s needs, and the capability of EMS personnel at the trauma incident to communicate with prehospital dispatch, the trauma hospital, and other units. Access also requires that all users know how to enter the system. This can be achieved through public safety and information and school educational programs designed to educate health care providers and the public about emergency medical access.

MEDICAL DIRECTION Medical direction provides the operational matrix for care provided in the field. It grants freedom of action and limitations to EMTs who must rescue injured patients. The medical director

is responsible for the design and implementation of field treatment guidelines, their timely revision, and their quality control. Medical direction can be “off-line” in the form of protocols for training, triage, treatment, transport, and technical skill operations or “online,” given directly to the field provider.

TRIAGE AND TRANSPORT The word triage derives from the French word meaning “to sort.” When applied in a medical context, triage involves the initial evaluation of a casualty and the determination of the priority and level of medical care necessary for the victim. The purpose of triage is to be selective, so that limited medical resources are allocated to patients who will receive the most benefit. Proper triage should ensure that the seriously injured patient be taken to a facility capable of treating these types of injuries—a trauma center. Patients with lesser severity of injuries may be transported to other appropriate medical facilities for care. Each medical facility has its own unique set of medical resources. As such, triage principles may vary from one locale to another depending on the resource availability. Likewise, established triage principles may be modified to handle multiple casualty incident or mass casualties. Then, a different set of triage criteria may be employed that will attempt to provide medical care to the greatest number of patients. In this scenario, some critically injured patients may not receive definitive care as this may consume an “unfair share” of resources. The goal of triage and acute medical care is to provide the greatest good to the greatest numbers. From a historical perspective, war has been the catalyst for developing and refining the concept of medical triage. Dominique Jean Larrey, Napoleon’s chief surgeon, was one of the first to prioritize the needs of the wounded on a mass scale. He believed “… it is necessary to always begin with the most dangerously injured, without regard to rank or distinction.” He evacuated both friend and foe on the battlefield and rendered medical care to both. He refined his techniques for evacuation and determining medical priorities for injured patients over the 18 years and 60 battles while being a member of the French army. During World War I, the English developed the “casualty clearing station,” where the injured were separated based on the extent of their injuries. Those with relatively minor injuries received first aid, while those with more serious injuries underwent initial resuscitative measures prior to definitive care. As medical and surgical care of battlefield injuries expanded, a system of triage and tiered levels (echelons) of medical care was designed. Echelons of medical care and triage of single, multiple, and mass casualties remain the paradigm for military combat medical care. There are five echelons (or levels) of care in the present military medicine. The first line of medical care is that which is provided by fellow soldiers. Principles of airway management, cessation of bleeding, and basic support are offered by fellow soldiers. Organized medical care begins with a medic or corpsman who participates in echelon 1 care. They are assigned to functional military units and serve as the initial medical

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Because trauma is not considered an important public health problem by the general population, efforts to increase awareness of the public as well as to instruct the public about how the system operates and how to access the system are important and mandatory. A recent Harris Poll conducted by the Anemia Trauma Society showed that most citizens value the importance of a trauma system with the same importance as fire and police services. Trauma system must also focus on injury prevention based on data relevant to injuries and what interventions will likely reduce their occurrence. Identification of risk factors and high-risk groups, development of strategies to alter personal behavior through education or legislation, and other preventive measures have the greatest impact on trauma in the community, and, over time, will have the greatest effect on nonfatalities.18–20

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SECTION 1 X

evaluation and care of the injured patient. Echelon 2 is a battalion aid station or a surgical company. Resuscitation and basic lifesaving surgical procedures may be performed at these stations. Echelon 3 is a Mobile Army Surgical Hospital (MASH) or Fleet Surgical Hospital. Advanced surgical and medical diagnostic and therapeutic capabilities are available at these facilities. An Echelon 4 facility is larger and has enhanced medical capacity. Examples include a hospital ship (USNS Mercy or Comfort) or an out-of-country medical facility (Landstuhl Region Medical Center [Army], Germany). An Echelon 5 facility is a large tertiary and rehabilitative medical facility and is located within the home country (Naval Medical Center San Diego). Each increasing echelon has a more comprehensive medical and surgical capacity. As patients are identified on the battlefield, they are triaged and transferred to the next higher echelon for care. During the Vietnam War, air medical transport enabled the triage of a seriously injured soldier from the battlefield directly to an MASH unit. The time to definitive surgical care was less than 2 hours compared to 6 hours during World War II. The lessons learned from the triage and treatment of combat casualties were slow to translate into civilian use. Injured patients, regardless of the severity of injury, were simply taken to the nearest hospital for treatment. Neither a triage system nor an organized approach to injury existed. The ATLS course was created in the late 1970s and with it the concept of requisite skills and facilities to treat injured patients emerged.

PURPOSE AND CHALLENGES OF TRIAGE The purpose of triage is to match the patient with the optimal resources necessary to adequately and efficiently manage his or her injuries. It is a dynamic process of patient evaluation and reevaluation until the patient receives definitive care. The challenge of a triage system lies in correctly identifying which patient has injuries in need of a designated trauma center. Studies have demonstrated better outcomes in major trauma victims who have been treated at hospitals that have a commitment for this specialized care.16 Of all trauma patients, only 7–15% have injuries that require the facilities of a dedicated trauma center. The ideal triage system would direct patients with serious injuries to the most appropriately staffed hospital while transporting those with less serious injuries to all other hospitals within the geographic area. Due to the complexities of patient evaluation and injury determination, “the perfect triage system” is yet to be developed. The primary goal of an effective triage system is to identify which casualties are seriously injured and in need of immediate surgical or medical care. This requires a rapid evaluation of the patient and a decision about the level of emergency care that will be needed for the patient. Once this is determined, they are matched and transported to the appropriate medical facility. The triage physician often has limited resources, information, and time to make this important decision. While many triage methods can be used, they often rely on physiologic, anatomic, and mechanism of injury information to assist in the triage decision. Once the patient has been routed to a treatment

facility, information concerning the patient’s injuries and physiologic state should be transmitted to the receiving facility if possible. This will give the receiving physician an opportunity to gather the appropriate personnel and equipment to treat the incoming casualty. A concise prehospital radio report will enable the receiving medical personnel to anticipate emergent equipment and personnel needs. In some instances, a direct operative resuscitation may be indicated to stabilize the patient.21 In other cases, emergent airway control may be the primary concern. The few minutes of preparation, prior to the patient’s arrival, may be the difference in patient survival. The other goal is to define the “major trauma victim.” While this term may be easy to conceptualize, it is very difficult to quantify. A precise definition is important so that triage, treatment, and outcomes can be compared. Prompt recognition of those patients who are in immediate risk of life (e.g., loss of airway or hemorrhagic shock) or loss of a limb (ischemia) or will need immediate operative or lifesaving interventions is paramount. These patients are in need of definitive care in an expedient fashion where delays in care may result in excess morbidity or mortality. The Injury Severity Score (ISS) provides the means for a trauma system to retrospectively identify major trauma victims with an ISS of greater than 15 being a commonly accepted level.22 Another definition of major trauma is provided by the Major Trauma Outcome Study (MTOS), which defines the trauma patient as all patients who died due to their injuries or were admitted to the hospital.23 The threshold that defines the major trauma victim within a trauma system is based not only on the resources of a particular trauma center but also on the inability of the nondesignated hospitals to consistently provide appropriate care for an injury exceeding the threshold. This may vary from system to system. After a traumatic event, the effectiveness of a triage system should be analyzed based on expected performance standards. Data monitoring and quality assessment tools should be applied after a disaster or after any one patient who has been treated so that system or operator errors can be identified and corrected. Each multiple casualty event presents unique problems to a triage system. Constant reevaluation and refinement are cornerstones for improved performance. One of the accepted performance markers to an effective triage system is found in the determination of the undertriage and overtriage rates. Undertriage is defined as a triage decision that classifies a patient as not needing a higher level of care (e.g., trauma center), when in fact they do. This is false-negative triage classification.44 Undertriage is a medical problem that may result in an adverse patient outcome. The receiving medical facility may not be adequate to diagnose and treat the trauma victim. Defining an acceptable level of undertriage is dependent on how one defines the patient requiring trauma center care. One method is to identify all the potentially preventable causes. Using this method, a target undertriage rate would be 1% or less. Using a broader definition, undertriage would also result in patients being sent to institutions without the capability to render appropriate care. In this instance, an undertriage rate of 5–10% is accepted.

Trauma Systems, Triage, and Transport

COMPONENTS OF TRIAGE TOOLS AND DECISION MAKING Trauma triage decisions are usually made within a limited time frame and are based on information that can be difficult to obtain. These decisions are based on evidence gathered in the field that estimates the potential for severe injury. Physiologic and anatomic criteria, mechanism of injury, and comorbid factors are used in the triage decision-making process. Unfortunately, all these criteria have limitations that affect their validity in certain situations. The judgment of experienced EMS personnel is also a key factor in triage.

PHYSIOLOGIC CRITERIA Physiologic data are felt to represent a snapshot into the wellbeing of an injured patient. Physiologic criteria include measurements of basic life-sustaining functions such as heart rate, blood pressure, respiratory rate and effort, level of consciousness, and temperature. The advantage of physiologic data is that they are readily assessable in the field with a simple physical examination. These data can be ranked into a numerical format, which allows them to be quantified, and used in various trauma scoring systems such as the Revised Trauma Score (RTS). The larger the deviation from normal, the more likely there is a severe injury. In this way, physiologic data may correlate to severity of injury and may predict serious injury or death. Patients who have sustained a mortal injury tend to have the greatest deviation in their vital signs.25 The problem is that their ability to detect physiologic derangement is time dependent. A single set of physiologic signs is only a snapshot to the patient’s state. Patients who have sustained significant injury may not manifest physiologic changes immediately after the event and, as a result, are at risk for undertriage. A significant injury may take some time to manifest life-threatening hemorrhage or tension pneumothorax. This is especially true of young, otherwise healthy adults who have significant physiologic compensation mechanisms that may mask the true extent of the injury.

ANATOMIC CRITERIA The anatomic location and external appearance of the injury aid in the immediate field triage decisions. This visual picture of the injured patient may be sufficient for an experienced triage officer

to make a disposition decision without further evaluation. In a mass casualty event, rapid triage may be performed with a quick visual exam of the patient. Anatomic criteria that suggest triage to a trauma center may include, but are not limited to: penetrating injury to the head, neck, torso, or proximal extremity; two or more proximal long-bone fractures; pelvic fracture; flail chest; amputation proximal to the wrist or ankle; limb paralysis; or greater than 10% total body surface area burn or inhalation injury. Each regionalized trauma system must decide what constitutes significant anatomic injury as a triage criterion. Anatomic injury may be challenging to predict reliably based on physical examination in the field. Fracture of long bones, amputations, and skin and soft tissue injuries may appear devastating in the field but are rarely life threatening and may distract the field examiner as well as the patient from more subtle and serious injuries. Significant blunt chest and abdominal injuries can have little external evidence of internal injury and initial physical examination lacks diagnostic accuracy.26,27 Other significant injuries missed on initial examination include spine28 and certain types of pelvic injuries. A pelvic bony injury can be diagnosed on physical examination in the awake, cooperative patient; however, a significant number of trauma victims have altered mental status due to head injury or ingestion of drugs or alcohol. The distinction between blunt and penetrating injury is an important triage distinction. Oftentimes there may be little external trauma to the patient. However, recognition of the penetrating wounds correlated with the likelihood of internal injury is needed to effectively triage these patients. Penetrating injuries to trunk and proximal extremities are of concern because of their proximity to vital structures; however, it is nearly impossible to know the direction or depth of penetration while in the field. Finally, the triage officer must expeditiously evaluate patients and not perform time-consuming physical examinations in the field that only slow down the triage process. Complex patients may be better served by urgent transport to a trauma center.

MECHANISM OF INJURY Evaluation is more than the simple determination of how a trauma injury occurred. To the trained eye, it can give information on the type, amount, and direction of force or energy applied to the body. Prehospital personnel, who view the effects of the forces that were applied during the injurious event, can estimate the amount of energy involved. This, in turn, helps predict the likelihood of injury. Mechanisms of injury felt to have a high potential for major trauma include falls of more than 15 ft; motor vehicle accidents with a fatality at the scene, passenger ejection, prolonged extrication (20 minutes), or major intrusion of the passenger compartment; pedestrians struck by a motor vehicle; motorcycle accidents of more than 20 mph; or any penetrating injuries to the head, neck, torso, or proximal extremities. When used as a triage criterion by itself, mechanism of injury results in the high overtriage rate. However, when combined with other triage components, such as physiologic indices and anatomic injury, mechanism of injury improves the sensitivity and specificity of the triage process.29,30

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Another method is to determine how many major trauma patients were incorrectly transported to a nontrauma center. If an ISS of greater than 16 or more is used to define the major trauma patient, undertriaged patients would be those patients (ISS 16) who were taken to a nontrauma center hospital. Using this method, an acceptable undertriage rate can be as high as 5%. Overtriage is a decision that incorrectly classifies a patient as needing a trauma center, although retrospective analysis suggests that such care was not justified. It has been said to result in overutilization of finite material, that is, financial and human resources.24

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AGE, COMORBID DISEASE, AND ENVIRONMENTAL CONCERNS SECTION 1 X

Age has been shown to impact the outcome of trauma victims and should be taken into consideration when triaging a patient. Elderly trauma victims, using a variety of definitions (i.e., 55 years old, 65 years old, etc.), have been shown to have increased morbidity and mortality compared to younger trauma victims. When compared to young patients, the elderly are at risk for undertriage, because a similar amount of force may cause a greater magnitude of injury.31 The effect of age on morbidity and mortality is not as clear in the pediatric population.32 There are significant differences in physiology and anatomy in the pediatric population that require specialized equipment, facilities, and personnel. Certainly, the optimal treatment involves identifying the unique resources needed to care for the injured child and having those available when needed. These differences are significant enough that specialized triage criteria have been developed for the pediatric population.33 Chronic diseases have also been shown to have a significant impact on morbidity and mortality in the trauma victim independent of age and injury severity.34 Acute conditions such as ethanol or cocaine intoxication or systemic anticoagulation may also impact morbidity and mortality. Comorbidities such as cardiopulmonary, hepatic, renal disease, diabetes mellitus, malignancy, or neurologic disorders have been found to have increased mortality rates compared to their disease-free counterparts. The problem is that many times the associated medical condition of the patient cannot be ascertained in the prehospital arena unless the patient has identification such as a medical alert bracelet or a relative who can provide the necessary history to the field personnel. Environmental extremes can have serious consequences for the trauma patient. Hypothermia is known to have adverse physiologic effects, prolongs blood coagulation time, and contributes to mortality.35 Prolonged heat exposure may lead to dehydration. Burn injuries require accurate assessment for resuscitation and wound care, as well as evaluation for potential inhalation injury. When combined with associated trauma, patient management can be complex36 (Table 4-3).

PARAMEDIC JUDGMENT A working familiarity of clear, concise, and reliable triage guidelines is essential for effective triage. Experience and judgment of EMS personnel are crucial to this mission. EMS personnel are in a unique position to directly assess the trauma scene, ascertain the mechanism of injury, determine the extent of the patient’s injuries, and estimate the patient’s physiologic response. For example, a patient with a fractured femur due to a frontal, high-speed motor vehicle collision will be evaluated and triaged differently than will a patient with a femur fracture due to a low-speed collision. Paramedic triage is outlined in the prehospital trauma life support manual. Several studies have shown that prehospital field personnel judgment can be as good or better than the available triage scoring methods commonly in use37 and, when combined with

TABLE 4-3 Commonly Used Trauma Triage Criteria Physiologic and anatomic criteria Glasgow Coma Scale of 13 or less Systolic blood pressure of 90 or less Respiratory rate of 10/min or less, or greater than 29/min Sustained pulse rate of 120/min or more Head trauma with altered state of consciousness, hemiplegia, or uneven pupils Penetrating injuries of the head, neck, torso, and extremities proximal to the elbow or knee Chest trauma with respiratory distress or signs of shock Pelvic fractures Amputations above the wrist or ankle Limb paralysis Two or more proximal long-bone fractures Combination of trauma with burns Mechanism of injury and high-energy impact Fall of 20 ft or more Patient struck by a vehicle moving 20 mph or more Patient ejected from a vehicle Vehicle rollover with the patient unrestrained High-speed crash (initial speed of 40 mph) with 20 in of major front-end deformity, 12 in or more deformity into the passenger compartment Patient was a survivor of a MVA where a death occurred in the same vehicle Other criteria Age of less than 5 years old, or over 55 years old History of cardiac disease, respiratory disease, insulindependent diabetes, cirrhosis, or morbid obesity Pregnancy Immunosuppressed patients Patients with bleeding disorders, or patients on anticoagulants Burns of greater than 30% of body surface area in adults, or 15% body surface area in children Burns of the head, hands, feet, or genital area Inhalation injuries Electrical burns Burns associated with multiple trauma or severe medical problems

other triage criteria, improves on the identification of major trauma victims. In a systematic review of Mulholland et al. there was no conclusive evidence for or against paramedic judgment in the field.38 The one constant theme in triage at all levels of medical personnel was the level of clinical experience. Pointer et al.39 studied the compliance of paramedics to established triage rules. Paramedic triage was best when evaluating triaging based on a patient’s injury patterns. Compliance was intermediate when based on mechanism of injury and the lowest for patients evaluated for physiologic triage criteria. They demonstrated a paramedic undertriage rate of 9.6%, which is relatively close to the acceptable 5% or less undertriage rate.

Trauma Systems, Triage, and Transport

CURRENT FIELD METHODS FOR FIELD TRIAGE SCORING

SPECIFIC TRIAGE METHODS—DEFINITIONS ■ Trauma Index The Trauma Index was one of the earliest triage scoring methods, first reported in 1971 by Kirkpatrick and Youmans.41 It included measures of five variables: blood pressure, respiratory status, central nervous system (CNS) status, anatomic region, and type of injury. One study showed some correlation with injury severity42; however, the Trauma Index never saw widespread use. A revision of the Trauma Index in 1990 reported undertriage and overtriage rates comparable to those of the Trauma Score (TS); circulation, respiration, abdominal/thoracic, motor, and speech (CRAMS); Prehospital Index (PHI); and mechanism of injury scales and correlated to the final ISS.43

■ Glasgow Coma Scale When Teasdale and Jennett first introduced the Glasgow Coma Scale (GCS),44 it was intended as a description of the functional status of the CNS, regardless of the type of insult to the brain, and was never intended to be used as a prehospital assessment tool. The three components of the score reflect different levels of brain function with eye opening corresponding to the brainstem, motor response corresponding to CNS function, and verbal response corresponding to CNS integration. Because the degree of injury to the CNS is considered to be a major determinant of outcome in trauma victims, many of the field triage tools measure CNS function, including the TS,45 the RTS,46 the CRAMS scale,47 and the Trauma Triage Rule (TTR).48 Interpretation of GCS in the presence of an intubated patient diminishes the ability to use the GCS as a

■ Triage Index, Trauma Score, Revised Trauma Score The Triage Index (TI) was described in 1981, and analyzed physiologic parameters of an injured patient. These variables were examined alone and in combination in an effort to make the TI more precise. One year later, Champion et al. modified the TI by adding systolic blood pressure and respiratory effort in an effort to be more discriminatory in patient severity identification. The resulting TS was designed to look at those physiologic parameters known to be associated with higher severity of injury if found to be abnormal.45 Central to this idea was the fact that the known leading causes of traumatic death were related to dysfunction of the cardiovascular, respiratory, and CNS. The authors recommended trauma center care for trauma victims with a TS of 12 or less. The TS was revised in 1989 because of concerns about accurate assessment of capillary refill and respiratory effort at night as well as potential underestimation of CNS injury.46 These components were deleted and the RTS consists of three parameters: GCS, systolic blood pressure, and respiratory rate.

■ CRAMS Scale CRAMS was first proposed as a simplified method of field triage.47 These parameters are individually assessed and assigned a value corresponding to normal, mildly abnormal, or markedly abnormal. With a range of 0–10, a score of 8 or less signifies major trauma, indicating that the patient should be taken to a designated trauma center. Both retrospective and prospective studies have shown that the CRAMS method of triage is accurate in identifying major trauma victims with relatively high specificity and sensitivity and is easy to use.49

■ Prehospital Index The PHI consists of field measurements of blood pressure, pulse, respiratory status, and level of consciousness, which were determined to have the best correlation with mortality or the need for surgery. A subsequent prospective multicenter validation study by the same authors showed that the PHI is accurate in predicting the need for lifesaving surgery within 4 hours and death within 72 hours following injury.50 Furthermore, the attachment of non-time-dependent variables such as age, body region injured, and mechanism of injury to the PHI improved the predictive power to select those patients who were likely to need intensive care or a surgical procedure.

■ Trauma Triage Rule The TTR proposed by Baxt et al. consists of measurements of blood pressure, the GCS motor response, and the anatomic region and type of injury.48 Rather than comparing the scoring method to traditional outcome measures to determine the

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In order for a triage scoring method to be acceptable for use in the field, it must meet certain criteria. The components of the scoring scheme must be credible, meaning that they have some correlating relationship with the injuries being described. Because there is no “gold standard” to test the accuracy of the scoring scheme, the results of the scoring scheme must be in general agreement with other, currently accepted scoring methods.40 The triage scoring method must correlate with outcome. The scores that indicate more severe injury should identify the patients with worse outcomes. The better the correlation with outcome, the lower the undertriage and overtriage rates within a trauma care system. Outcomes for major trauma victims are usually classified as death, need for urgent/emergent surgical intervention, length of intensive care unit (ICU) and/or hospital stay, and major single-system or multisystem organ injuries. The scoring scheme must also have interobserver and intraobserver reliability, that is, it should be able to be consistently applied between observers and by the same observer at another point in time with the same results. Finally, the scoring scheme must be practical and easily applied to trauma victims for a variety of mechanisms, by a variety of personnel without the need of specialized training or equipment.

prehospital evaluation tool. A more recent study found that the motor component of the GCS is almost as good as the TS and better than the ISS in predicting mortality. This suggests that the motor component score could be used to identify patients who are likely to require urgent trauma center care.

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factors that constitute a major trauma victim, major trauma was defined a priori as a systolic blood pressure of less than 85 mm Hg; a GCS motor component score of 5 or less; or penetrating trauma to the head, neck, or trunk. Retrospective review revealed major trauma victim identification with a sensitivity and specificity of 92%. The TTR was concluded to potentially reduce overtriage while maintaining an acceptable undertriage rate. However, it has not been adapted widely.

potential injury to a trauma victim. As shown earlier in the chapter, mechanism of injury, anatomic region and type of injury, preexisting illnesses, and paramedic judgment are important considerations in providing additional information in the field to help determine whether a patient requires transport to a designated trauma center. Combination field triage methods make use of this additional information by including it in the initial evaluation of the trauma victim.

■ Disaster Triage: Simple Triage and Rapid Treatment (START)

■ American College of Surgeons Field Triage System

In the event of a mass casualty or disaster, EMS personnel may utilize the START triage system initially developed to be used in earthquakes in California. The object of this system is to triage large numbers of patients rapidly. It is relatively simple and can be used with limited training.51 The focus of START is to evaluate four physiologic variables: the patient’s ability to ambulate, respiratory function, systemic perfusion, and level of consciousness. It can be performed by lay and emergency personnel. Victims are usually divided into one of the four groups with color codes according to the timing of care delivery based on the clinical evaluation as follows: (a) green—minor injuries (walking wounded); (b) red—immediate; (c) yellow—delayed; and (d) black—unsalvageable or deceased. If the patient is able to walk, he or she is classified as a delayed transport, but if not, ventilation is assessed. If the respiratory rate is 30, the patient is an immediate transport. If the respiratory rate is 30, perfusion is assessed. A capillary refill of 2 seconds will mandate an immediate transport. If the capillary refill is 2 seconds, the patient’s level of consciousness is assessed. If the patient cannot follow commands, he or she is immediately transported; otherwise he or she is a delayed transport. The Fire Department of New York used this system during the World Trade Center disaster. Unfortunately, due to the collapse of the buildings and concern for the safety of the rescue workers, the START system came to a complete halt.52 It resumed only when it was declared safe to approach ground zero. In some systems the START system is coupled with severity scores: in the immediate category the TS varies from 3 to 10, in the urgent category the TS varies from 10 to 11, and in the delayed (nonurgent) group the TS is 12. The triage principles are the same for children and adults. However, due to differences in physiology, response to insults, ability to talk and walk, and anatomic differences, disaster triage in the pediatric age group is not straightforward. Assessment tools have been proposed to increase the accuracy of the process but were found to have major limitations. The START system is important in the triage of severely injured trauma patients because those requiring surgical care are transported by air or ground ambulances to trauma centers distant enough from the incident where the number of victims is lower and the resources are still available to provide optimal care.

The ACS Field Triage System is a more complete, advanced triage scoring scheme that is described in the Resources for Optimal Care of the Injured Patient. This decision scheme describes indications for transport of the trauma victim to a trauma center based on specific physiologic and anatomy of injury variables. In addition, mechanism of injury and comorbid factors are evaluated and, if specific criteria are met, may also indicate transport to a trauma center. Finally, if there is concern on the part of the prehospital medical personnel that the victim may have significant injuries, consideration is given to taking the patient to the designated trauma center. Fig. 4-3 shows the triage decision scheme that is widely used throughout the country.

■ Combination Methods While most of the field triage criteria are based on physiologic criteria, there are other methods for assessing the severity of the

APPLICATION OF TRIAGE PRINCIPLES FOR MULTIPLE PATIENT SCENARIOS Triage principles may need to be modified to include triage of multiple patient and mass casualty situations.

■ Single Patient Triaging a single trauma victim is relatively straightforward. The prehospital care provider assesses the patient according to the defined triage criteria for that particular regionalized trauma system. If the patient meets the criteria of a major trauma victim, he or she is transported to the nearest designated trauma center.

■ Multiple Casualties In the situation of multiple patients, such as seen with multiple cars involved in the same accident, the same essential principles apply; however, decisions must be made in the field as to which patients have priority. A state of multiple casualties occurs when the numbers of patients and injury severity do not exceed the hospital resources. Those patients who are identified as major trauma victims by field triage criteria have priority over those who appear less injured. All major trauma patients should be transported to a trauma center as long as the trauma center has adequate resources to manage all the patients effectively. This type of situation can stress local resources, and possible diversion of the less critically injured to another trauma center should be considered. Monitoring transports with online computer assistance allows for contemporaneous determination if one trauma center is overwhelmed.

Trauma Systems, Triage, and Transport

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FIELD TRIAGE DECISION SCHEME

Measure vital signs and level of consciousness Glasgow Coma Scale Systolic blood pressure Respiratory rate

< 14 or < 90 or < 10 or > 29 (< 20 in infant less than one year)

Yes

No

Take to a trauma center. Steps 1 and 2 triage attempts to identify the most seriously injured patients in the field. These patients would preferentially be transported to the highest level of care within the trauma system.

Step Two

• • • • • • • •

Assess anatomy of injury

All penetrating injuries to head, neck, torso, and extremities proximal to elbow and knee Flail chest Two or more proximal long-bone fractures Crush, degloved or mangled extremity Amputation proximal to wrist and ankle Pelvic fractures Open or depressed skull fracture Paralysis

Yes

No

Take to a trauma center. Steps 1 and 2 triage attempts to identify the most seriously injured patients in the field. These patients would preferentially be transported to the highest level of care within the trauma system. •

• Step Three

• •

Assess mechanism of injury and evidence of high-energy impact

Falls Adults: > 20 feet (one story is equal to 10 feet) Children: > 10 feet or two to three times the height of the child High-risk auto crash Intrusion: > 12 inches occupant site > 18 inches any site Ejection (partial or complete) from automobile Death in same passenger compartment Vehicle telemetry data consistent with high risk of injury Auto v pedestrian/bicyclist thrown, run over, or with significant (> 20 mph) impact Motorcycle crash > 20 mph

No

Yes Transport to closest appropriate trauma center which, depending on the trauma system, need not be the highest level trauma center •

Step Four

• •

• • • •

Assess special patient or system considerations

Age Older Adults: Risk of injury death increases after age 55 Children: Should preferentially be triaged to pediatric-capable trauma centers Anti-coagulation and bleeding disorders Burns Without other trauma mechanism: Triage to burn facility With trauma mechanism: Triage to trauma center Time sensitive extremity injury End stage renal disease requiring dialysis Pregnancy > 20 weeks EMS provider judgment

Yes

No

Contact medical control and consider transport to trauma center or a specific resource hospital.

Transport according to protocol

When in doubt, transport to a trauma center

FIGURE 4-3 Prehospital triage decision scheme recommended by the American College of Surgeons Committee on Trauma. (Reproduced with permission from The American College of Surgeons Committee on Trauma. Resources for Optimal Care of the Injured Patient: 2006. Chicago, IL: American College of Surgeons; 2006.)

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Step One

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■ Mass Casualties SECTION 1 X

Triage in this situation is unique in that priorities are different from those in the single- or multiple-victim scenarios. In the instance of mass casualties, the resources of the designated trauma center, as well as the regional trauma system, are overwhelmed. When resources are inadequate to meet the needs of all the victims, priority shifts from providing care to those with the most urgent need to providing care to those with the highest probability of survival. A severely injured patient, who would consume a large amount of medical resources, is now a lower triage priority. Despite the potential salvageability of this patient, the medical resources are focused on other patients who would benefit from advanced medical and surgical care. This method provides the greatest good for the greatest number of people. Field triage in this situation is probably the most difficult to perform as one has to make choices of quantity over quality with very limited amounts of information. These issues are further complicated when dealing with children.53 The most experienced and best-trained personnel available should make these field triage decisions. Physicians may be the best qualified to make these triage decisions; however, if they are the only receiving physicians available, direct patient care should take precedence and triage decisions would fall to other personnel. Patients are identified according to a triage code, based on the severity of injuries and likelihood of survival, and are treated accordingly. Occasionally, there may be an indication for a specialized surgical triage team with the capability to render acute lifesaving care of an injured trapped patient.54 In some disaster scenarios moving the intensive care into a disaster zone may be beneficial when evacuation of patients may be unrealistic due to logistical reasons. In order to optimize patient care in these situations, it is important for regionalized systems to periodically have mock disaster drills. These drills allow for the proper training of all individuals who might be involved as well as the identification and correction of potential problems. With increasing terrorist activity, specific triage algorithms have been developed for specific scenarios such as biologic, chemical, radiologic, or blast attacks.55

■ Disaster Management Events surrounding the recent terrorist attacks of the Oklahoma Federal Building, World Trade Center, and the Pentagon, and natural disasters such as Katrina, should crystallize the resolve of all medical personnel to become educated and proficient in disaster management. The approach to disasters, whether natural or man-made, requires a coordinated relief effort of EMS, hospital, fire, police, and public works personnel. This multiorganizational operation can function in a crisis environment only if it is well directed and controlled. The ability to assess a disaster scene, call in appropriate personnel to provide damage control, fire and rescue operations, and crowd control is dependent on an organization structure that permits dynamic information processing and decision making of vital scene information. The military uses the concept of command and control for its combat operations. Key personnel continually monitor and

manage the battlefield situation. The Fire Service of the US Department of Forestry, in 1970, adapted command and control into an incident command structure. Within this framework, a centralized group of disaster personnel works to command and control all of resources at the disaster site. Dynamic disaster scene information is processed at the incident command and decisions as to how best to engage the rescue resources are implemented. The incident command center structure is composed of seven key groups. If the disaster is small in scope, a single person may fill all seven areas. As the disaster increases in scope, more personnel are required to fulfill these functions. The incident commander is responsible for the entire rescue or recovery operation. Under the direction of the incident commander are the seven group commanders: operations, logistics, planning, finance, safety, information, and liaison. Each of these section commanders has well-defined areas of authority and responsibility. Continuous on-scene information will be communicated to the command center. This will enable the incident command center to plan and direct the rescue or recovery operation. Thus, limited resources and key personnel will be directed to produce the greatest benefit. The disaster scene is typically divided into zones of operation. Ground zero is the inner hazard zone where the fire and rescue operations occur. EMS and other nonessential personnel are kept out of this area. Rescued victims are brought out of this area to the EMS staging area. This is the second zone, a primary casualty receiving area, and it is here that EMS personnel perform triage and initial care for the patient. Disposition directly to the hospital may occur or the patient may be sent to a distant receiving area for care and ultimate triage and transport. The distant casualty receiving areas provide for additional safety in the environment. This downstream movement of injured patients prevents the primary triage sites from being overrun. Transportation of the wounded from the primary receiving site is reserved for the most seriously injured patients. Thus, a tiered triage approach is developed. A temporary morgue is also set up at a distant site. Typically, groups of patients, the walking wounded, will migrate toward the nearest medical treatment facility. This process is called convergence. Medical facilities will often set up a triage area in front of the emergency department to handle these patients. Present-day medical teaching supports the treatment of any patient who arrives at an institution’s doorstep. Perhaps thought should be given to transporting groups of these patients to secondary medical facilities so that the closer hospitals do not become overburdened with an influx of patients. The use of outpatient operating facilities is being considered for this purpose. The final operational zone of the disaster site is the outer perimeter. Police permit only essential personnel access into the disaster site. Crowd and traffic control ensure the safety and security of the disaster scene as well as to provide emergency vehicles rapid transit to and from the site. Disasters may be of a small scale such as an intrafacility fire or explosion and may remain only a local or regional problem. As was seen at the World Trade Center, the magnitude of a local disaster was of such proportions that a national response was

Trauma Systems, Triage, and Transport

CURRENT EVIDENCE FOR TRIAGE GUIDELINES There is little argument that a regionalized trauma system reduces the number of potentially preventable deaths due to trauma.16,61 To do so, one must accurately select which trauma victim will benefit from the resources of a trauma center. The dilemma is 2-fold: (1) Which criteria should be used to define the “major trauma” victims? (2) How are these patients identified in the field? Other relevant questions include: Does selective triage of patients in terms of hospital resources at the time of hospital admission benefit the major trauma patient, and, if

so, what selection criteria are the most appropriate? Do transport times modify the definition of a major trauma victim, and does this influence outcome? Finally, do present field triage criteria provide adequate rates of undertriage and overtriage? Each of these questions will be addressed individually.

■ Major Trauma Patient The definition of a major trauma patient is a person who has sustained potentially life- or limb-threatening injuries and is based on retrospective analysis of the patient’s injuries. The major trauma definition is used primarily to monitor field triage criteria as well as calculate undertriage and overtriage rates within a regional trauma system. Unfortunately, there is no absolute standard for the criteria that have been used when defining major trauma. The best that can be accomplished is to retrospectively compare quantified injury severity data to mortality and then use a predefined threshold as defining major trauma. The ISS is a measure of physical injury, based on adding up the square of the three highest individual anatomic injury scores (Abbreviated Injury Scale [AIS], range 1–6) calculated from all of the patient’s known injuries.22 When used to define major trauma, an ISS of 15 or more has been the most frequently utilized threshold. Using this definition, a trauma victim must have a single anatomic injury score of 4 or two AIS 3 injuries in order to be categorized as sustaining “major trauma.” Because ISS has been shown to have a good correlation with mortality over a wide range of ages and different types of injuries, it has been the most frequently utilized method for stratifying the injuries of patients for comparison with prehospital triage scores. However, it has several shortcomings when used as a determinant of major trauma with regard to analysis of field triage criteria. Several studies have shown that preventable deaths can occur with a single AIS 3 injury.14,62 For example, a patient with a closed head injury and an AIS of 3 is at a higher risk of death than if the patient had a similar grade extremity injury. In a retrospective autopsy analysis of all patients dying within 24 hours, Bansal et al. demonstrated that closed head injury was the most common cause of death; however, there was a significant variation in ISS and therefore ISS alone could not be used as a predictor of early death.63 As a result, there is no consensus on the numeric value of ISS that defines major trauma. Stewart et al. used an ISS of greater than 12 to define their study population when they reported on the improvement in outcomes of motor vehicle accident victims after trauma center designation.64 Similarly, Petrie et al. also used an ISS of greater than 12 when they reported on the improvement of outcomes of patients who had trauma team activation when compared to those who did not.65 However, Morris et al. defined major trauma as a patient with an ISS of 20 or more when they reported on the ability of the TS to prospectively identify patients with life-threatening injuries.66 Additionally, Norwood and Myers stratified their patient sample into two groups based on ISSs of 19 or less and 20 or more—when they reported on outcomes from a rural-based trauma center.67 Thus, comparing studies that define major trauma becomes very difficult due to the differences in the ISS threshold.

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needed to address the rescue and recovery efforts. The standard appeal for this today is to activate the National Disaster Medical System. Interestingly, in some of the more recent natural disasters, there have been approximately 10–15% of the survivors who were seriously injured. The remaining people either were dead or had mild to moderate trauma. It becomes a pivotal task to rapidly sort through the survivors and identify the level of care needed by each patient. In the World Trade Center, the New York Fire Department and EMS utilized the START system. The initial scene casualties were from the planes striking the building. Fire and rescue personnel could not reach these patients. With the collapse of the first tower, rescue operations were aborted and attempts to evacuate rescue personnel became paramount.52 Following the collapse, victims injured in the street or from the surrounding buildings required medical treatment. As rescue operations resumed, injured rescue workers began to arrive at medical treatment facilities. Unfortunately, there were only five survivors of the Twin Tower collapse with over 3,000 fatalities, which included civilians and rescue personnel. The experience in Israel with terrorist attacks has demonstrated that rapid and accurate triage is critical to decrease or minimize mortality. Therefore, it has been suggested that the best triage officer, at least in bombings and shooting massacres, which are the most common form of terrorist violence, is the trauma surgeon. This is important to guarantee that those in real need of immediate surgical attention are seen and treated in a timely fashion without inundating the hospitals with patients who can be treated at a later time. Critical concepts have been learned from the Israeli experience. These include rapid and abbreviated care, unidirectional flow of casualties, minimization of the use of diagnostic tests, and relief of medical teams ever so often to maintain quality and effectiveness in care delivery. The concepts of damage control should be liberally applied in the operating room (OR) to free up resources for the next “wave” of injured individuals.56–59 In mass casualties, hospitals become overwhelmed very easily. Therefore, communication between hospitals is critical to distribute the casualties in an evenly fashion. Surgeons should be familiar with the basic principles of mass casualty management. Trauma surgeons should be the leaders in this field, as trauma systems serve as a template for the triage, evacuation, and treatment of mass casualty victims. The American College of Surgeons has emphasized on this critical role for surgeons.60

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A second problem with ISS is that it is based on injuries identified within specific anatomic regions and takes into account only one injury per body region. Therefore, ISS may not be a sensitive indicator of certain types of injuries. Several studies have found that ISS is not as accurate in identifying the severity of the injury in penetrating or blunt trauma, in which several organ systems may be injured within the same anatomic location. This has led to the development of specialized anatomic injury scoring systems such as the Penetrating Abdominal Trauma Index (PATI)68 and, ultimately, the Organ Injury Scale (OIS)69 that may more accurately reflect the severity of the injury. A modification to the calculation of ISS scoring has been introduced as the New Injury Severity Score (NISS), which is defined as the sum of the squares of the AIS scores of each of a patient’s three most severe AIS injuries regardless of the body region in which they occur. This method has been found to be more predictive of survival, but may overestimate the severity of injury for lesser injury grades.70 In addition, injury severity scoring may also be inaccurate, as the ISS fails to differentiate between severity of injury and mismanagement of injury and, as a result, assigns an increased injury severity to lesser injuries of inappropriately managed patients. Transport times may need to be included in the definition of the major trauma patient when used for triage or interfacility transport purposes, particularly when they exceed 30 minutes. When time is added to lesser injuries before definitive care, ongoing bleeding, the magnitude of the resuscitation, and the relative stability of the patient may increase the injury severity of otherwise equivalent injuries. A number of studies have shown that hemodynamic and respiratory dysfunction, as well as mortality, is increased with increasing transport times.71 As such, when long transport times are a problem and complications due to long transport and inadequate resuscitation can be anticipated, these patients should be considered for a higher level of care where critical care resources are more likely to be available. Patient transport modalities and point to trauma center time of transport are unique to each region. Goldstein et al. validated a transport decision process that utilized a modification of the PHI (the pretransport index) and documented the time and distance from a trauma center for these trauma transfer patients in British Columbia. The pretransport index adds onto the two PHI variables: intubation and pneumothorax. Accurate recognition of the more seriously injured patients and the knowledge of the quickest modality to transport the patient to a trauma center resulted in a quicker time to definitive time to care.72 Recently, an analysis by the Resuscitation Outcomes Consortium (ROC) of the association between EMS intervals and in-hospital mortality following serious injury was conducted. A total of 3,656 patients were prospectively collected and a secondary retrospective analysis was performed studying mortality as a function of EMS transport time. All patients were seriously injured with a mean systolic blood pressure less than 90 mm Hg and a GCS less than or equal to 12. Of those studied, 22.0% died after EMS transport to the hospital and most within the same day. The overall mean EMS time was 36.3 minutes; however, when EMS time was delineated into 10-minute increments, there was no evidence of increased mortality. Similarly, total EMS times, grouped by

lowest to highest quartile, did not reveal any increase in mortality. The authors concluded that even though decreased EMS transport times may improve mortality for select patients, overall this relationship across a wide field of injured victims does not seem to affect mortality. Therefore, utilization of the most appropriate transport mode for specific patients should maximally utilize health care resources and dollars.73

■ Field Triage Scores Triage scores that are based on physiologic data are accurate in doing so. The original “first step” field trauma triage criteria were published by consensus from the ACSCOT that stratified them by GCS 12, SBP 90 mm Hg, and RR 10 or 29.74 The TS, CRAMS scale, RTS, and the PHI have good correlation with the ISS and are able to predict mortality with a sensitivity of at least 85%. However, no single field triage scoring scheme has been universally accepted as the gold standard. This is due, in part, to the fact that there is no agreed-upon standard that defines “major trauma” that allows for comparison of the individual triage scoring systems. An evidence-based analysis is limited by this problem. As a result, each of the individual scoring systems has its advocates as well as critics. When Gormican originally described the CRAMS scale, rather than using an ISS threshold to define major trauma, he defined it as the patient who died in the emergency department or went directly to the OR.47 Minor trauma was defined as a patient who was discharged home from the emergency department. Using a CRAMS score of 8 or less to signify major trauma, he found a sensitivity of 92% and a specificity of 98% in identifying major trauma victims. Others examined the ability of the CRAMS scale to accurately identify patients who required admission to the hospital or any operation for their injuries. Using this definition for major trauma, they found that a CRAMS score of 8 or less failed to identify two out of three patients. Champion et al., who constructed the TS by analyzing CNS, cardiovascular, and respiratory data, a priori defined major trauma as a TS of 12 or less because it correlated with a decreased probability of survival.45 It has been shown that a TS of 12 or less also failed to identify two out of three patients who required admission or an operation. Similar criticisms in the literature can be found for the PHI for its failure to accurately identify patients requiring emergency surgery, and the RTS for its low sensitivity in identifying patients requiring emergency treatment.75 The addition of the variables of age, body region injured, mechanism of injury, comorbidity, and the PHI improved prediction of the PHI alone by 10% (sensitivity of 76% vs. 66%). Unfortunately, the addition of the mechanism of injury to the PHI was almost as accurate as all of the major descriptors. It has been shown that the physiologic-based triage scores were unable to accurately identify survivors of major injuries, each score having a sensitivity and specificity of less than 70%. Holcomb et al. recently evaluated the utility of manual vital signs plus the GCS (motor and verbal scores) to predict the need for lifesaving interventions in nonclosed head injured patients. In this group, patients with a weak radial arterial pulse had an 11-fold increase in the need for a lifesaving intervention. A GCS verbal score of 2–3 in a nonclosed head injured patient

Trauma Systems, Triage, and Transport (GCS score 3, 4–12, and 13–15) and the same analysis was performed, they found that each group had a different factor that best predicted mortality. Systolic blood pressure was the strongest predictor of mortality in the GCS 3 group, ISS in the GCS 4–12 group, and age in the GCS 13–15 group.80 Finally, the use of non-time-dependent data requires that the prehospital personnel have enough training and experience to recognize, interpret, and report them to the physician. Burstein et al. reviewed the prehospital EMS reports for specific ACS mechanism of injury triage criteria and found that it was underreported in standard EMS reporting documentation. Reporting improved with the use of a structured data instrument that requested the presence or absence of the criteria.81 A paramedic’s ability to recognize and report this type of criteria may explain the discrepancy in studies reporting on the ability of paramedic judgment to correctly or incorrectly triage patients to a trauma center. The mechanism of injury does seem to have a correlation with the need for a higher intensity of medical care or operation. In a study by Santaniello et al., nearly 50% of patients who met a mechanism of injury criteria needed an operative intervention.82

■ In-Hospital Triage Secondary, or in-hospital, triage complements field triage by stratifying the immediate needs of the trauma patient at the time of admission. The emphasis of this retriage is to direct the patient into the proper hospital area: urgent care, emergent care, trauma bay, or the OR. During a multiple casualty event, this in-hospital triage is essential to maximize hospital resource allocation and patient flow. Tinkoff et al. reported on a two-tiered trauma response protocol.83 They used field triage criteria to identify patients requiring either a surgery-supervised “trauma code” or an emergency medicine-supervised “trauma alert.” Using this protocol, they found that accurate identification of the most seriously injured patients was achieved as demonstrated by the improved ability to predict those patients who would require direct disposition to the OR or ICU. Prehospital prediction models as well as admission systemic inflammatory response syndrome (SIRS) scores may be useful to predict the need for ICU services, and estimate length of stay and potential mortality of seriously injured patients. Hoyt et al. originally described predefined field criteria that indicated OR resuscitation.21 Indications included cardiac arrest with one vital sign present, persistent hypotension despite field intravenous fluid, and uncontrolled external hemorrhage. They found that penetrating and blunt trauma patients who underwent operation in less than 20 minutes had a significantly greater probability of survival versus that predicted by MTOS data. A more recent analysis of their 10-year experience with OR resuscitation shows the survival advantage predominates in the penetrating trauma victims.84 Rhodes et al. used a variety of triage criteria to indicate need for OR resuscitation: systolic blood pressure of 80 mm Hg or less, penetrating torso trauma, multiple long-bone fractures, major limb amputation, extensive soft tissue wounds, severe maxillofacial hemorrhage, and witnessed arrest.85 The mean ISS and survival rate of all patients

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had a 6-fold increase while a GCS motor score of 2–3 had a 20-fold increase in the need for a lifesaving intervention. An additional conclusion was that the addition of automated vital sign reporting, oxygen saturation monitors, or end-tidal CO2 monitors did not improve the predictive model of which patients might need a lifesaving intervention.76 The ROC group studied mortality and hospital length of stay in 6,259 adult trauma patients meeting ACSCOT “first step” physiologic triage criteria. Patients who died or had an LOS 2 days were considered high risk, whereas survivors and LOS 2 days were low risk. Total patient mortality in the high-risk category was 58.0%. Those patients were found to have a statistically significant increase in abnormal respiratory rate as well as depressed GCS as sole criteria for triage. The authors further evaluated the need for advanced airway management, outside of the ACSCOT criteria, and found that 31% of high-risk patients compared to 5% of low-risk patients required advanced airway interventions. The authors conclude that no specific physiologic parameter using present ACSCOT physiologic criteria can be omitted, but perhaps airway intervention should be added to further risk stratify high-risk trauma patients.74 The incorporation of non-time-dependent data, such as mechanism of injury, anatomic injury, and comorbid factors, has been shown to make physiologic-based triage scores more sensitive in identifying the major trauma victim. However, questions have also been raised as to whether this type of data identifies the major trauma patient. Its ability to do so appears to be dependent on the context in which it is used. For example, Cooper et al. found that mechanism of injury had a positive predictive value of only 6.9% when used to identify patients with an ISS of 16 or greater. They concluded that it did not justify bypass of local hospitals when used as a sole criterion for triage to a trauma center.77 There are conflicting reports when analyzing non-timedependent criteria as a determinant of outcome in trauma patients. Smith and colleagues stratified patients into age over 65 and age under 65, and they found that preexisting conditions did not significantly affect outcome. Age, however, was a significant determinant of mortality. DeKeyser et al. compared the mortality and functional outcomes of patients who were stratified into three groups based on age: age 35–45, age 55–64, and age 65 and over. They found that there were no differences between the three groups in terms of ISS, mortality rates, or functional outcome.78 Van der Sluis et al. also evaluated differences in mortality and long-term outcome between young and elderly patients. They analyzed two groups of patients with an ISS of 16 or greater: age 20–29 and age 60 and over. They reported that while there was a significant difference in terms of early mortality, survivors of both groups were discharged in equal percentages and their functional outcome 2 years after injury was essentially the same.79 A possible explanation for these contradictory findings may be that there are interactions between all the possible factors that have not been previously appreciated. Hill et al. analyzed multiple factors as possible determinants of outcome in major trauma patients (ISS 15). They found that preresuscitation GCS was the overall strongest predictor of mortality. However, when the patients were stratified into different GCS categories

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meeting these criteria were 29.3% and 70.4%, respectively, which were better than those predicted by TRISS methodology. Finally, Barlow et al. have advocated triage of pediatric patients (age 16 and younger) directly to the OR based on mechanism of injury and have reported survival rates of 100% for patients admitted with stab wounds and 94% for patients admitted with gunshot wounds.86,87 Secondary triage has also been shown to benefit the hospital in terms of human and financial resources. DeKeyser et al. reported that the institution of a two-tiered, in-hospital trauma response system, based on patient status at the time of admission, reduced the cost of trauma care by more than $600,000 over a 1-year period by reducing the utilization of personnel, OR, laboratory work, and protective wear.88 Secondary triage characteristics such as patient response to resuscitation measures, newly diagnosed major injuries, or the presence of markedly abnormal blood values (e.g., elevated lactate levels) portend the need for enhanced medical resources and ICU care.

■ Undertriage/Overtriage The determination of the rates of undertriage and overtriage based on the use of each of the current field triage scoring methods would provide an answer to the main question of which method best identifies the major trauma patient in the field. The best method would have the lowest rates of both undertriage and overtriage. However, the variability over an equivalent definition of a major trauma patient makes this type of analysis subject to criticism. It is impossible to achieve perfect overtriage and undertriage rates using current field triage methods. West and colleagues found that the addition of non-time-dependent criteria to traditional physiologic triage criteria reduced the undertriage rate from 21% to 4.4%, when undertriage is defined as non-CNSrelated motor vehicle accident deaths occurring in non-traumadesignated hospitals. However, depending on the definition of major trauma, overtriage ranged from 36% to 80%. Other factors also appear to confound analysis of undertriage and overtriage. Studies have found that major trauma patients (defined by ISS) were more likely to be undertriaged if they were elderly or had single-system injuries. Patients with minor injuries were more likely to be overtriaged if they were intoxicated, obese, or had an injury to the head or face. In reality, acceptable rates of undertriage and overtriage are dependent on how a trauma system defines major trauma and the type of field triage criteria employed. The San Diego Trauma System has reported overtriage rates by comparing patients transported to those entered into the trauma registry using MTOS criteria. Data regarding preventable deaths are also available because all nontrauma centers have trauma deaths reviewed. Using this approach the data suggest that combining physiologic and non-time-dependent criteria leads to an overtriage rate of approximately 35% and an undertriage rate of less than 1%. These rates have been found to be stable over time and would seem to be reasonable targets. Looked at another way, this translates to about 30% unnecessary transports, which calculates to 2,000 patients per year or about 6 patients per day. This amounts to no more than one to

two extra patient evaluations per trauma center per day, hardly a significant overburden to a trauma system. At present, a combination of methods may provide the most accurate field assessment of the seriously injured trauma victim and represents the current state of the art in identification of major trauma victims. A number of studies have shown that the sensitivity and specificity of physiologic-based triage scoring methods are improved by the addition of anatomic and/or mechanistic injury data. The addition of the mechanism of injury with the PHI did not improve the ability to identify seriously injured trauma patients. The structure of triage decisions must be based on the individual trauma system’s unique resources and capabilities in both the prehospital and hospital phases of care and then employed such that patient morbidity and mortality are minimized.

■ Interhospital Transfer Many trauma victims who live in rural communities do not have immediate access to a designated trauma center or regional trauma system. These patients are generally taken to the local community hospital for their initial care. While most are adequately cared for by these facilities, there are a significant number of patients who will require the services found only at a hospital dedicated to the overall care of the trauma patient. Previous studies have shown that these patients are at an increased risk of death. Some of the factors that have been implicated in contributing to potentially avoidable mortality in this situation include failure to recognize the severity of the injury, lack of adequate resuscitative measures, and delay in or lack of necessary treatment procedures for stabilization. It is imperative that the initial treating physician should be able to recognize that the trauma victim may have injuries that require diagnostic and/ or therapeutic modalities beyond the scope of the initial receiving hospital. If this situation is identified, then transfer of the patient to a “higher level of care” is appropriate. Interhospital transfers should occur from one facility to another that will provide the additional resources needed. This generally occurs from a Level III or IV hospital as part of a regionalized trauma system. Patients may also need care from specialized centers such as a burn center or a pediatric trauma center. However, one must recognize that the period of transport is one of potential instability for the patient, and the risks of transport must be balanced against the benefits of a higher level of care. Risk to the patient can be minimized with the use of proper equipment, personnel, and planning. The patient may need to undergo a period of resuscitation and stabilization prior to transfer.89 Some patients may not stabilize and require more definitive intervention prior to transfer. Communication with the trauma center will assist in this determination as well as interventional planning. A patient with an unstable intra-abdominal hemorrhage may need a damage control surgery with abdominal packing in order to be stable enough for transfer. The trauma surgeon could be in constant communication with the outlying surgeon to assist in the decision making for the operative procedure. This concept is particularly important with distant interhospital transfers. In addition to the medical aspects of interhospital transfer,

Trauma Systems, Triage, and Transport physicians must also comply with certain federal and local legal regulations. Failure to do so has serious ramifications for the transferring hospital as well as the individual physician.90

Identification of a trauma victim who may benefit from transfer to a designated trauma center is based on specific criteria. A number of factors must be examined when making this decision, including patient status and recognition of possible injuries and/or comorbid factors as well as the personnel and equipment resources necessary for optimal patient care. Criteria for transfer are often not followed because of financial conflicts or failure to appreciate the long-term complexities of certain injuries.91 This may be best addressed in a trauma system through a legislative process that defines which patients should be transferred to which level of care. The Colorado State Board of Health has published Rules and Regulations pertaining to the Statewide Trauma System in which criteria for interhospital transfer have been defined.92 Patient criteria are based primarily on physiologic and anatomic injury data (aortic tears, liver injuries requiring intraoperative packing, bilateral pulmonary contusions requiring nonconventional ventilation, etc.), and on the level of care (Level II, III, IV) that the patient’s facility is able to provide. If the patient meets the criteria for that specific health care facility, then consultation with a Level I trauma surgeon and discussion of possibility for interhospital transfer is mandatory. Interhospital transfer may be essential in multiple casualty events whereby a single hospital is overburdened by casualties. In this case the criteria for the transfer of patients change in order to offload the primary hospital patient load. Good triage principles need to apply so that those patients who would benefit the most would be transferred. These transfers may even occur between two equivalent level institutions in order to facilitate the distribution of trauma victims. As was demonstrated in the World Trade Center disaster, the walking wounded inundated the closest medical facilities to ground zero. This condition has the potential to make it more difficult to identify and treat the most seriously injured patients from the mass of patients who arrive at the hospital.

■ Methods of Transfer Transfer of the trauma victim must be organized in a way that minimizes the risk to the patient during the transfer process. This includes establishing transfer protocols at the EMS and institutional levels prior to transport. It also includes the planning that is necessary after the decision for transfer is made in individual cases with respect to the type of equipment, mode of transport, and personnel necessary to maximize patient safety.

■ Transfer Agreement Minor delays can have adverse consequences for the major trauma victim; it is therefore necessary to expedite the transfer process once its need is recognized. Transfer agreements are established protocols between hospitals that ensure rapid and efficient passage of pertinent patient information prior to the

■ Transport Modality The objective is to get the trauma victim to the receiving hospital as quickly and safely as possible. However, the mode of transportation is dependent on the availability of a particular mode, distance, geography, weather, patient status, and the skills of the transport personnel and equipment that will likely be needed during transport. This should be discussed between the referring and receiving physicians with each transfer. Knowledge of transporting agencies in the area and their availability should be ascertained as soon as the need for transport is recognized. The patient should have appropriate monitoring of physiologic indices, including invasive monitoring, during the transport period. This may include monitoring of respiratory rate, cardiac rhythm and blood pressure, intracranial pressure, and central venous or pulmonary artery pressure. If the patient is intubated, end-tidal CO2 should be monitored and the transport ventilator should have alarms to indicate disconnects and high airway pressures. The other additional equipment necessary for safe transport is that needed for effective ACLS/ ATLS interventions and has been outlined in a number of publications.

■ Transport Team The patient should be accompanied by at least two people in addition to the vehicle operator, one of whom should have requisite training in advanced airway management, intravenous therapy, cardiac dysrhythmia recognition and treatment, and ATLS. If the transporting personnel do not have the necessary training or skills, a nurse or physician should accompany the patient during transport to ensure optimal care.

IMPROVED OUTCOME FROM TRANSFER Reduction in the morbidity and mortality of trauma patients who require the resources of a trauma center depends on early identification of the severely injured, proper initial stabilization,

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■ Criteria for Interhospital Transfer

actual transfer. This should include patient identification, history and physical examination findings, diagnostic and therapeutic procedures performed and their results, and the initial impression and a clear identification of the referring and receiving physicians. This information then allows the trauma surgeon at the receiving hospital to suggest possible diagnostic or therapeutic maneuvers that may be required prior to transfer, such as intubation, insertion of a nasogastric tube, Foley catheter, or thoracostomy tube. It also allows for mobilization of resources, such as an ICU bed or OR, at the receiving hospital in anticipation of possible injuries. The physicians involved should also discuss the mode of transportation, accompanying personnel, and equipment that may be needed for optimal transfer. Discussion should also include who will assume medical control of the patient during transport. Full documentation, including a summary of care from the referring hospital and copies of all studies, should accompany the patient to the receiving hospital.

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and safe interhospital transfer.93 There is evidence that patients who sustain major trauma in a rural or small community setting are at an increased risk for adverse outcomes. A high incidence of departure from well-defined standards in the initial evaluation and management of major trauma victims in rural community hospitals has been demonstrated. A report on the care of fatally injured patients in a rural state found that 22% of fatally injured patients with non-CNS injuries reaching the emergency department alive had potentially survivable injuries. Errors in initial volume replacement, airway control, and recognition of the need for surgical intervention were factors complicating the care of these patients. The adequacy of initial care of patients subsequently transferred to a trauma center with regard to neurologic, chest, abdominal, and orthopedic injuries has also been studied. Major departures from accepted standards of care, promoted by the ASCOT and the ACEP, in more than 70% of these cases were found. The care of patients initially treated at local community hospitals during initial management and subsequent transport to a referral trauma center was reviewed. Quality of care was assessed based on ATLS guidelines. Lifethreatening deficiencies occur in 5% and serious deficiencies in 80% of cases reviewed, including inadequate cervical spine immobilization, inadequate intravenous access, and inadequate oxygen delivery. Veenema and Rodewald demonstrated that, while initial triage and management of rural trauma victims at a Level III trauma center prior to Level I transfer provide outcomes similar to MTOS data, there were still unexpected deaths.93 Timely transfer of major trauma victims to trauma centers improves patient care and subsequent outcome. Trauma centers not only provide the resources for the early management of severely injured patients, but can also provide more extensive support for the patient beyond the initial 24 hours. There are few studies that have looked at specific criteria as markers for patients who would benefit from interhospital transfer. Lee et al. attempted to clarify specific anatomic criteria that would indicate the need for interhospital transfer from Level III centers.94 They found that the presence of three or more rib fractures was a marker for potential serious injury, as evidenced by significant differences in outcome when compared to patients with one or two rib fractures. A subsequent population-based study confirmed that these patients have a significantly higher mortality rate, higher ISS, and longer ICU and overall hospital stay.95 Clark et al. reviewed their experience with major hepatic trauma (Grade III or more) in patients transferred from rural facilities. However, they did not delineate specific transfer criteria.96 Similar studies have looked at mechanistic and physiologic criteria as reasons for bypassing rural/ local community hospitals or determining the need for a specific transport modality.

MODE OF TRANSPORT—INTERFACILITY TRANSFER The question of whether air or ground transport is more appropriate for the transfer of the trauma victim is dependent on a number of factors. This includes the distance to be traveled,

geography, weather, and overall patient status. Because outcome is directly related to time to definitive care, the quickest mode of transport that ensures patient safety should be chosen. Several options are available at many major trauma centers, including traditional ground transport and helicopter and fixed-wing air transport. The data on transport modality may not directly correlate to interhospital transfer because much of them come from analyzing transports from the scene of the accident rather than from one hospital to another. Baxt and Moody found that patients transported from the scene of the accident by helicopter had a 52% reduction in mortality compared to those transported by ground.97 Similar results were found by Moylan et al. when they looked at factors improving survival in multisystem trauma patients who were transported by air versus ground.98 There were no differences in the prehospital times between these two sets of patients, and the air-transported patients were more frequently intubated and transfused blood, and had larger volumes of fluid given than the ground-transported patients. The main benefit of air transport appears to be its use for long-distance transport. Several studies have shown that there is an improved survival in patients who need higher level of care when transported by air, and this benefit can be realized up to an 800-mile radius from the trauma center. This mode of transport may not be appropriate for short-distance transfer due to prolonged response time for interhospital transport. For local urban transport, helicopters offer no advantage over an organized ground transportation system, and the increased cost for air transport, especially that of helicopters, is probably not justified. Trauma triage and the interhospital transfer process have many similarities. Both have the same goal: to minimize potentially avoidable deaths. In order to accomplish this, both attempt to accurately identify the trauma patient who will require the specialized skills and resources provided by a Level I or II trauma center. Both utilize the same type of limited information early in the course of events in order to make that decision. While certain types of obvious injuries warrant expeditious transport of the trauma victim, it is best to look at all of the available information in terms of physiologic indices, mechanism of injury, comorbid factors, and known or suspected injuries. This approach allows one to assess potential problems that may be more appropriately handled at a major trauma center. If there is any doubt, it is in the patients’ best interest to be taken to a facility providing the highest level of care available.

TRAUMA CENTER FACILITIES AND LEADERSHIP Hospital care of the injured patient requires commitments from specific facilities to provide administrative support, medical staff, nursing staff, and other support personnel. The trauma center integrates the trauma care system by providing local or regional leadership. Trauma centers are categorized by level, as described below.

■ Level I Trauma Center The Level I trauma center is a tertiary care hospital usually serving large inner-city communities that demonstrates a leadership

Trauma Systems, Triage, and Transport

■ Level II Trauma Center The Level II trauma center also provides definitive care to the injured and may be the principal hospital in the community or may work together with a Level I trauma center, in an attempt to optimize resources and clinical expertise necessary to provide optimal care for the injured victim. Its approach to trauma is generally not as comprehensive as the Level I facility. The attending trauma surgeon’s availability is equivalent and he or she must participate early in the care of the patient. Graduate education and research are not required.

■ Level III Trauma Center A Level III trauma center generally serves a community that lacks Level I or II facilities. Maximum commitment is required to assess, resuscitate, and, when necessary, provide definitive operative therapy. For the major trauma patient, the principal role of the Level III center is to stabilize the injured patient and effect safe transfer to a higher level of care when capabilities for definitive care are exceeded. Transfer agreements and protocols are essential in a Level III trauma center. Education program for health care personnel may be part of a Level III center’s role, as the hospital may be the only designated trauma center in the community.

■ Level IV Trauma Center A Level IV trauma center is usually a hospital located in a rural area. Level IV trauma centers are expected to provide the initial evaluation and care to acutely injured patients. Transfer agreements and protocols must be in place, since most of these hospitals have no definitive surgical capabilities on a regular basis.

■ Acute Care Facilities within the System Many general hospitals exist within a trauma care system but are not officially designated as trauma centers. Circumstances often exist in which less severely injured patients reach these hospitals and appropriate care is provided. The system should provide for interfacility transfer of patients if a major trauma patient is mistriaged and registry entry for injured patients managed at nondesignated facilities.

■ Specialty Trauma Centers Regional specialty facilities concentrate expertise in a specific discipline and serve as a valuable resource for patients with critical specialty-oriented injuries. Examples include pediatric trauma,

bums, spinal cord injuries, and hand (replantation) trauma. Where present, these facilities provide a valuable resource to the community and should be included in the design of the system.

REHABILITATION Rehabilitation is as important as prehospital and hospital care. It is often the longest and most difficult phase of the trauma care continuum for both patient and family. Only 1 of 10 trauma patients in the United States has access to adequate rehabilitation programs, although it is critically important to reintegrating the patient into society. Rehabilitation can be provided in a designated area within the trauma center or by agreement with a freestanding rehabilitation center.

SYSTEM EVALUATION A trauma system has to monitor its own performance over time and determine areas where improvement is needed. To achieve this goal, reliable data collection and analysis through a statewide or systemwide trauma registry is necessary. Information from each phase of care is important and must be linked with every other phase. Compatibility between data collection during different phases of care is important to accurately determine the effects of certain interventions on long-term outcome. The practical use of a system evaluation instrument is to identify where the system falls short operationally and allow for improvements in system design. This feedback mechanism must be part of the system plan for evaluation. The implementation of trauma care systems coupled with trauma registry databases, injury severity indices, and measurable outcome indicators has led to improved validity for investigations across the entire spectrum of injury control research. The system also has to be evaluated by the American College of Surgeons Committee on Trauma Verification Review Committee or by inviting experts as outside reviewers in addition to internal review.

TRAUMA SYSTEM QUALITY IMPROVEMENT (QI) The systemwide QI program’s most important role is to monitor the quality of trauma care from incident to rehabilitation and create solutions to correct identified problems. The purpose of quality improvement is to provide care in a planned sequence, measure compliance with defined standards of care, and reduce variability and cost while maintaining quality. A comprehensive downloadable guide to this process is detailed on the American College of Surgeons Web site. It allows health care providers to monitor several aspects of medical care using explicit guidelines to identify problems that have a negative impact on patient outcome. This is accomplished by establishing standards of trauma care and a mechanism to monitor the trauma care provided (surveillance), usually with audit filters designed to identify outliers. Errors occur due to the complexity of trauma care and because of the involvement of multiple providers. It is of fundamental importance to make a distinction between process

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role in system development, optimal trauma care, quality improvement, education, and research. It serves as a regional resource for the provision of the most sophisticated trauma care, from resuscitation to rehabilitation and managing large numbers of severely injured patients to immediate 24-hour availability of an attending trauma surgeon. Level I trauma centers address public education and prevention issues on a regional basis and provide continuing education for all levels of trauma care providers. They lead research efforts to advance care.

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complexity and human errors when developing a quality improvement program in trauma.99–102 A peer process must be established to review QA/QI problems.103 The process must be accurately documented, corrective action instituted and applied uniformly across the system, and the results reassessed. These principles apply to systemwide QA/QI as well as to the process within the hospital. Corrective action is taken through changes in existing policies or protocols, through education targeted at the problem, or by restriction of privileges. A successful trauma system monitors the performance of the EMS agency and prehospital operations, individual trauma hospitals, and care in nondesignated hospitals. The prehospital audit process should include timeliness of arrival, timeliness of transport, application of prehospital procedures and treatments, and outcomes. To develop this part of the quality improvement process, extensive involvement by the regional authority, the regional medical director, the provider agencies, and the trauma hospitals is required. Standards of care are defined in relation to the availability of resources and personnel, timeliness of physician response, diagnosis, and therapy. These standards have been defined by the ACS and published in the Resources for Optimal Care of the Injured Patient.4 Guidelines or protocols are then developed and audit filters are established to monitor the guidelines. Audit filters are useful tools to provide continuous monitoring of established practices. Standard audit filters and complications that need to be monitored have been established by the ACSCOT and include timeliness of care, appropriateness of care, and death review. Tracking of complications and illnesses allows trends to be monitored over time. Death reviews should be conducted in an attempt to determine preventability. Guidelines reduce variability, and, consequently, fewer errors are made. The process of quality improvement requires accurate documentation and this is achieved by using the trauma registry. The trauma registry provides objective data to support continuous quality improvement. The registry should be designed to collect and calculate response times, admission diagnoses, diagnostic and therapeutic procedures, discharge diagnoses, complications, costs, and functional recovery. The trauma coordinator is of utmost importance in making the quality improvement process effective. This person assures timely recognition of problems, use of the registry to document problems, and that problems are resolved. Cases identified as noncompliant with established standards of care are reviewed at the hospital level and by a trauma medical audit committee overseeing the trauma system.103 Peer review identifies the problem, the results are documented and determination of problem recurrence is made, trends are identified, and a decision is made if more specific action for problem resolution is required. Actions may include simple education of the staff or revision of the guidelines, or eventually development of new guidelines, hiring additional staff, or even removing a staff member. The monitoring process should continue after action was taken to determine its effectiveness. Quality improvement processes in trauma are a multidisciplinary task.

STANDARDIZED DEFINITION OF ERRORS AND PREVENTABLE DEATH The development of trauma systems led to a significant reduction in the number of preventable deaths after injury. A preventable death rate of less than 1–2% is now widely accepted as ideal in a trauma system. However, a small number of patients continue to die, or eventually, to develop complications that could otherwise be avoided or prevented. These errors occur in different phases of trauma care (resuscitative, operative, and critical care phases), and are named provider related, as a group. These include events that lead to delays or errors in technique, judgment, treatment, or communication. A delay in diagnosis is defined as an injury-related diagnosis made greater than 24 hours after admission resulting in minimum morbidity. An error in diagnosis is an injury missed because of misinterpretation or inadequacy of physical examination or diagnostic procedures. An error in judgment is defined as a therapeutic decision or diagnostic modality employed contrary to available data. An error in technique occurs during the performance of a diagnostic or therapeutic procedure.102 According to the ACSCOT Resources for Optimal Care of the Injured Patient: 2006 document, an event is defined as nonpreventable when it is a sequela of a procedure, disease, or injury for which reasonable and appropriate preventable steps had been observed and taken. Potentially preventable is an event or complication that is a sequela of a procedure, disease, or injury that has the potential to be prevented or substantially ameliorated. A preventable event or complication is an expected or unexpected sequela of a procedure, disease, or injury that could have been prevented or substantially ameliorated.4 With regard to mortality, the same definitions apply. Nonpreventable deaths are defined as fatal injuries despite optimal care, evaluated and managed appropriately accordingly to standard guidelines (ATLS), and with a probability of survival, estimated by using the TRISS methodology, of less than 25%. A potentially preventable death is defined as an injury or combination of injuries considered very severe but survivable under optimal conditions. Generally these are unstable patients at the scene who respond minimally to treatment. Evaluation and management are generally appropriate and suspected care, however, directly or indirectly is implicated in patient demise. The calculated probability of survival varies from 25% to 50%. A preventable death usually includes an injury or combination of injuries considered survivable. Patients in this category are generally stable, or if unstable, respond adequately to treatment. The evaluation or treatment is suspected in any way, and the calculated probability of survival is greater than 50%. The causes of preventable deaths in trauma centers are different than those occurring at nontrauma hospitals. In nontrauma hospitals, preventable deaths occur because the severity or multiplicity of injuries is not fully appreciated, leading to delays in diagnosis, lack of adequate monitoring, and delays to definitive therapy. In trauma hospitals, the causes of preventable death include errors in judgment or errors in technique. In trauma centers the diagnostic modalities used are normally adequate, and delays in diagnosis or treatment are uncommon and have minimal impact on outcome.

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ANALYSIS OF TRAUMA SYSTEM PERFORMANCE Different study designs have been used to evaluate trauma system effectiveness. The most common scientific approaches include panel review preventable death studies, trauma registry performance comparisons, and population-based studies. Panel review studies are conducted by a panel of experts in the field of trauma who review trauma-related deaths in an attempt to determine preventability. Well-defined criteria and standardized definitions regarding preventability have been used, but significant methodological problems (Table 4-4) can lead to inconsistencies in the results and interpretation of the data.16,103 Registry studies are frequently used to compare data from a trauma center or a trauma system with a national reference norm available, between trauma centers within the same system, TABLE 4-4 Limitations of Current Trauma System Evaluation Studies Panel studies Inconsistent definition of preventability Case mix of the population Size, composition, and expertise of the panel Process and criteria to determine preventability Inconsistent report of prehospital and autopsy data Registry-based studies Missing or incomplete data sets Coding inconsistencies and errors Inconsistent report of autopsy data MTOS limitations Outdated data set Data are not population based Mostly blunt trauma Differences in trauma centers’ level of care Inconsistencies in trauma registry inclusion criteria Lack of data on comorbid factors Lack of data on long-term follow-up Population-based studies Mechanism of injury, physiologic, and anatomic data usually not available Autopsies not performed consistently in all trauma deaths Limited number of secondary diagnoses in claims data Autopsy findings not always included in claims data Hospital discharge data are inaccurate in transfers and deaths in the emergency department Inconsistencies in obtaining AIS scores Outcome measure is in-hospital mortality. No long-term or functional outcomes data available

or in the same trauma center at different periods. The MTOS23 has been used as the national reference, although several of its limitations have been recognized, compromising the reliability of the comparison with data from other systems or centers (Table 4-4). The advantages of registry-based studies include a detailed description of injury severity and physiologic data. Population-based studies use information obtained from death certificates, hospital discharge claim data, or fatal accident reporting system (FARS) on all injured patients in a region. These methodologies of data collection and analysis are important to evaluate changes in outcome before and after, or at different time periods following the implementation of trauma systems in a defined region. Limited information on physiologic data, injury severity, and treatment is available.104 The limitations of the most commonly used databases in population-based studies are described in Table 4-4. The data on trauma system effectiveness published in the literature are difficult to interpret due to great variability in study design, type of analysis, and definition of outcome variables. In an attempt to review the existing evidence on the effectiveness of trauma systems, the Oregon Health Sciences University with support from the NTHSA and the National Center for Injury Prevention and Control of the CDC organized the Academic Symposium to evaluate Evidence regarding the Efficacy of Trauma Systems, also known as the Skamania Symposium.105 Trauma care providers, policy makers, administrators, and researchers reviewed and discussed the available literature in an attempt to determine the impact of trauma systems on quality of patient care. The available literature on trauma system effectiveness does not contain class I (prospective randomized controlled trials) or class II studies (well-designed, prospective or retrospective controlled cohort studies, or case-controlled studies). There are several class III (panel studies, case series, or registry based) studies that were reviewed and discussed during the symposium. According to Mann et al. reviewing the published literature in preparation for the Skamania Symposium, it is appropriate to conclude that the implementation of trauma systems decreases hospital mortality of severely injured patients.106 Independently of the used methodology (panel review, registry based, or population based), and despite the above-mentioned limitations of each study design, a decrease in mortality of 15–20% has been shown with the implementation of trauma systems. The participants of the symposium also concluded that not only mortality but also functional outcomes, financial outcomes, patient satisfaction, and cost-effectiveness should be evaluated in future prospective, well-controlled studies. Outcomes data are difficult to interpret due to differences in study design. One recent area of interest has been in comparing outcomes in inclusive and exclusive systems. As mentioned previously, in an inclusive system, care is provided to all injured patients and involves all acute care facilities, whereas in exclusive systems specialized trauma care is provided only in highlevel trauma centers that deliver definitive care. In inclusive systems, patients may be transferred to a higher level of care (trauma center) after initial stabilization based on the availability of resources and expertise in the initial treating facility. Two problems arise: (a) delay in transfer and (b) dilution of trauma centers’ experience. Utter et al. have recently investigated

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These definitions are useful to monitor trauma system’s performance and to compare different trauma systems. Once preventable death rate reaches a plateau after trauma system implementation, system performance should focus on tracking provider-related complications. This approach has been proved adequate to identify problems and to implement solutions.

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whether mortality is lower in inclusive systems compared to exclusive systems. They concluded that severely injured patients are more likely to survive in states with the most inclusive trauma system, independent of the triage system in place. A possible explanation to these findings includes better initial care in referring hospitals.107 A more recent study confirms a mortality reduction of 25% in patients under the age of 55.61

SPECIAL PROBLEMS Despite the experience acquired on trauma system development in the United States during the last three decades, trauma systems still face multiple problems and challenges. The financial aspect, linked to the problem of uncompensated care, has led to the closure of several trauma centers and the collapse of some trauma systems. Alternative and stable sources for funding indigent care have to be part of an agenda for legislative action in support of trauma systems. This is particularly important given recent published reports showing that the risk of death is significantly lower in trauma centers than nontrauma centers. In an important study, MacKenzie et al. compared rates of both in-hospital and 1-year mortality in trauma victims treated in trauma centers versus nontrauma centers. After risk and case mix adjustment, trauma centers had an in-house mortality of 7.6%, significantly less than nontrauma centers where mortality was 9.5%. After 1 year, trauma center mortality was 10.4% compared to 13.8% in nontrauma centers.61 Funds for prevention strategies should also be provided, targeting particularly the pediatric and the elderly population. Table 4-5 lists the actual problems faced by regionalized trauma systems as documented through an SWOT analysis conducted by the Health Resources and Service Administration in 2003. One effort that has been developed recently is the Consultations for Trauma Systems document and accompanying process developed by the ACSCOT.12 It follows previous efforts to develop trauma systems and the original Model Trauma System Care Plan.108 The consultation provides two unique services: (1) an exceptional and experienced team enables examination and a knowledgeable perspective to optimize hospital and community trauma resources and (2) the consultant team brings the credibility of the ACSCOT to hospitals developing a trauma center. A more recent effort has led to the Model Trauma System Planning and Evaluation Program developed in collaboration with the HRSA of the U.S. Department of Health and Human Services.7 This is the most comprehensive tool available to help develop regional trauma systems. As important is the issue related to the ideal number of trauma centers needed in an organized system. Many states with organized trauma systems, as well as many counties with developed trauma systems, have not performed a needs assessment prior to the implementation of the system. Similar to other fields of surgery and medicine, data suggest that the patient volume correlates with outcomes. Severely injured patients should be treated at high-volume trauma centers within a community, and the number of Level I trauma centers should be based on a needs assessment. Limiting the number of trauma centers and “concentrating” the experience of managing severely injured patients in Level I trauma centers improves

TABLE 4-5 Current Problems of Trauma Systems Urban Financial Uncompensated care Closure of trauma centers Source of funding for indigent care Overdesignations of trauma center Rural Sparse population Long distances Difficult patient access Weather conditions Delays in notification Treatment delays due to interfacility transfer needs Lack of medical oversight Pediatric Integral part of the system Education Elderly Increased costs Increased morbidity and mortality Prevention Lack of federal/state funding needs to be addressed in order to increase the number of states engaged in developing statewide or regional trauma systems in the United States Funding required: National level: national trauma system development State/local level: to finance the EMS system Research/prevention/avoidance of duplication

outcomes, reduces costs, improves efficiency, facilitates transfers, and enhances education and research.3,5,109 Despite the realization that trauma systems reduce morbidity and mortality, there remain several barriers to full implementation. A trauma system agenda for the future has been recently written and endorsed as a template for going forward. Critical elements are defined in Table 4-6. It is imagined that trauma systems when fully implemented will enhance community health through an organized system of injury prevention, acute care, and rehabilitation that is fully integrated into the public health system of a community. In addition to addressing the daily demands of trauma, it will form the basis for disaster preparedness and possess the distinct ability to identify risk factors and early interventions to prevent injuries in a community while integrating a delivery of optimal resources for patients who ultimately need acute trauma care. The availability of federal dollars to assist in the development of trauma systems will be essential. At the same time, a developing consensus to build trauma systems that do not cover designated trauma centers yet meet the needs of all components of the trauma patient will be equally critical. The biggest challenge in the future will be the implementation of what we already know how to do. Developing the political and public will to do so remains the challenge before us.

Trauma Systems, Triage, and Transport

TABLE 4-6 Critical Targets for Future Trauma System Development

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Regionalization of trauma care Development of disaster preparedness Identification of trauma as a disease process Recognition of the continuum of care required Recognition that trauma requires a multidisciplinary approach Improving cost-effectiveness Coordination of resources, services, and special populations Reimbursement, funding, and legislation

21. Hoyt DB, Shackford SR, McGill T, et al. The impact of in-house surgeons and operating room resuscitation on outcome of traumatic injuries. Arch Surg. 1989;124:906. 22. Baker SP, O’Neill B. The injury severity score: an update. J Trauma. 1976;16:882. 23. Champion HR, Copes WS, Sacco WJ, et al. The major trauma outcome study: establishing national norms for trauma care. J Trauma. 1990; 30:1356. 24. Hoff WS, Tinkoff GH, Lucke JF, Lehr S. Impact of minimal injuries on a level I trauma center. J Trauma. 1992;33:408. 25. Guzzo JL, Bochicchio GV, Napolitano LM, et al. Predictions of outcomes in trauma: anatomic or physiologic parameters? J Am Coll Surg. 2005;201:891. 26. Mackersie RC, Tiwary AD, Shackford SR, et al. Intra-abdominal injury following blunt trauma. Identifying the high-risk patient using objective risk factors. Arch Surg. 1989;124:809. 27. Rizoli SB, Boulanger BR, McLellan BA, et al. Injuries missed during initial assessment of blunt trauma patients. Accid Anal Prev. 1994;26:681. 28. Frankel HL, Rozycki GS, Ochsner MG, et al. Indications for obtaining surveillance thoracic and lumbar spine radiographs. J Trauma. 1994; 37:673. 29. Lowe DK, Oh GR, Neely KW, et al. Evaluation of injury mechanism as a criterion in trauma triage. Am J Surg. 1986;152:6. 30. Knopp R, Yanagi A, Kallsen G, et al. Mechanism of injury and anatomic injury as criteria for prehospital trauma triage. Ann Emerg Med. 1988; 17:895. 31. McCoy GF, Johnstone RA, Duthie RB. Injury to the elderly in road traffic accidents. J Trauma. 1989;29:494. 32. Nakayama DK, Copes WS, Sacco WJ. The effect of patient age upon survival in pediatric trauma. J Trauma. 1991;31:1521. 33. Phillips S, Rond PC III, Kelly SM, et al. The need for pediatric-specific triage criteria: results from the Florida Trauma Triage Study. Pediatr Emerg Care. 1996;12:394. 34. Sacco WJ, Copes WS, Bain LW Jr, et al. Effect of preinjury illness on trauma patient survival outcome. J Trauma. 1993;35:538. 35. Gentilello LM. Advances in the management of hypothermia. Surg Clin North Am. 1995;75:243. 36. Dougherty W, Waxman K. The complexities of managing severe burns with associated trauma. Surg Clin North Am. 1996;76:923. 37. Emerman CL, Shade B, Kubincanek J. A comparison of EMT judgement and prehospital trauma triage instruments. J Trauma. 1991;31:1369. 38. Mulholland SA, Gabbe BJ, Cameron P. Is paramedic judgment useful in prehospital trauma triage? Injury. 2005;36:1298. 39. Pointer JE, Levitt MA, Young JC, et al. Can paramedics using guidelines accurately triage patients? Ann Emerg Med. 2001;38:268. 40. Senkowski CK, McKenney MG. Trauma scoring system: a review. J Am Coll Surg. 1999;189:491. 41. Kirkpatrick JR, Youmans RL. Trauma index: an aide in evaluation of injury victims. J Trauma. 1971;14:934. 42. Hedges JR, Sacco WJ, Champion HR. An analysis of prehospital care of blunt trauma. J Trauma. 1982;22:989. 43. Smith JS Jr, Bartholomew MJ. Trauma index revisited: a better triage tool. Crit Care Med. 1990;18:174. 44. Teasdale G, Jennett B. Assessment of coma and impaired consciousness: a practical scale. Lancet. 1974;2:81. 45. Champion HR, Sacco WJ, Carnazzo AJ, et al. Trauma score. Crit Care Med. 1981;9:672. 46. Champion HR, Sacco WJ, Copes WS, et al. A revision of the trauma score. J Trauma. 1989;20:188. 47. Gormican SP. CRAMS scale: field triage of trauma victims. Ann Emerg Med. 1982;11:132. 48. Baxt WG, Jones G, Fortlage D. The trauma triage rule: a new, resourcebased approach to the prehospital identification of major trauma victims. Ann Emerg Med. 1990;19:1401. 49. Clemmer TP, Orme JF Jr, Thomas F, et al. Prospective evaluation of the CRAMS scale for triaging major trauma. J Trauma. 1985;25:188. 50. Keohler JJ, Malafa SA, Hillesland J, et al. A multicenter validation of the prehospital index. Ann Emerg Med. 1987;16:380. 51. Risavi BL, Salen PN, Heller MB, et al. A two-hour intervention using START improves prehospital triage of mass casualty. Prehosp Emerg Care. 2001;5:197. 52. Asaeda G. The day that the START triage system came to a STOP: observations from the World Trade Center. Acad Emerg Med. 2002;9:255. 53. Maconochie I, Hodgetts T, Hall J. Planning for major incidents involving children by implementing a Delphi study. Letter to the editor. Arch Dis Child. 2000;82:266.

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54. Blank-Reid C, Santora TA. Developing and implementing a surgical response and physician triage team. Disaster Manag Response. 2003;1:41. 55. Subbarao I, Johnson C, Bond WF, et al. Symptom-based, algorithmic approach for handling the initial encounter with victims of a potential terrorist attack. Prehosp Disaster Med. 2005;20:301. 56. Frykberg ER. Principles of mass casualty management following terrorist disasters. Ann Surg. 2004;239:319. 57. Einav S, Feigenberg Z, Weissman C, et al. Evacuation priorities in masscasualty terror-related events. Implications for contingency planning. Ann Surg. 2004;239:304. 58. Almogy G, Belzberg H, Mintz Y, et al. Suicide bombing attacks: update and modifications of the protocol. Ann Surg. 2004;239:295. 59. Feliciano DV, Anderson GV, Rozycki GS, et al. Management of casualties from the bombing at the Centennial Olympics. Am J Surg. 1995;176:538. 60. American College of Surgeons. Statement on disaster and mass casualty management by the American College of Surgeons. Bull Am Coll Surg. 2003;88:14. 61. MacKenzie EJ, Rivara FP, Jurkovich GJ, et al. A national evaluation of the effect of trauma-center care on mortality. N Engl J Med. 2006;354:366. 62. Trunkey DD, Lim RC. Analysis of 425 consecutive trauma fatalities: an autopsy study. J Am Coll Emerg Phys. 1974;3:368. 63. Bansal V, Fortlage D, Lee JG, Costantini T, Potenza B, Coimbra R. Hemorrhage is more prevalent than brain injury in early trauma deaths: the golden six hours. Eur J Trauma Emerg Surg. 2009;35:26–30. 64. Stewart TC, Lane PL, Stefanits T. An evaluation of patient outcomes before and after trauma center designation using Trauma and Injury Severity Score analysis. J Trauma. 1995;39:1036. 65. Petrie D, Lane P, Stewart TC. An evaluation of patient outcomes comparing trauma team activated versus trauma team not activated using TRISS analysis. Trauma and Injury Severity Score. J Trauma. 1996;37:870. 66. Morris JA Jr, Auerbach PS, Marshall GA, et al. The Trauma Score as a triage tool in the prehospital setting. JAMA. 1986;256:1319. 67. Norwood S, Myers MB. Outcomes following injury in a predominantly rural-population-based trauma center. Arch Surg. 1994;129:800. 68. Moore EE, Dunn EL, Moore JB, et al. Penetrating abdominal trauma index. J Trauma, 1981;21:439. 69. Moore EE, Shackford SR, Pachter HL, et al. Organ injury scaling: spleen, liver, and kidney. J Trauma. 1989;29:1664. 70. Osler T, Baker SP, Long W. A modification of the injury severity score that both improves accuracy and simplifies scoring. J Trauma. 1997;43:922. 71. Feero S, Hedges JR, Simmons E, et al. Does out-of-hospital EMS time affect trauma survival? Am J Emerg Med. 1995;13:133. 72. Goldstein L, Doig CJ, Bates S, et al. Adopting the pre-hospital index for interfacility helicopter transport: a proposal. Int J Care Injured. 2005;34:3. 73. Newgard CD, Schmicker RH, Hedges JR, et al.; Resuscitation Outcomes Consortium Investigators. Emergency medical services intervals and survival in trauma: assessment of the “golden hour” in a North American prospective cohort. Ann Emerg Med. 2010;55(3):235–246. 74. Newgard CD, Rudser K, Hedges JR, et al.; ROC Investigators. A critical assessment of the out-of-hospital trauma triage guidelines for physiologic abnormality. J Trauma. 2010;68:452–462. 75. Roorda J, Van Beeck EF, Stapert JW, et al. Evaluation performance of the Revised Trauma Score as a triage instrument in the prehospital setting. Injury. 1996;27:163. 76. Holcomb JB, Salinas J, McManus JM, et al. Manual vital signs reliably predict need for life-saving interventions in trauma patients. J Trauma. 2005;59:821. 77. Cooper ME, Yarbrough DR, Zone-Smith L, et al. Application of field triage guidelines by pre-hospital personnel: is mechanism of injury a valid guideline for patient triage? Am Surg. 1995;61:363. 78. DeKeyser F, Carolan D, Trask A. Suburban geriatric trauma: the experiences of a level I trauma center. Am J Crit Care. 1995;4:379. 79. Van der Sluis CK, Klasen HJ, Eisma WH, et al. Major trauma in young and old: what is the difference? J Trauma. 1996;40:78. 80. Hill DA, Delaney LM, Roncal S. A chi-square automatic interaction detection (CHAID) analysis of factors determining trauma outcomes. J Trauma. 1997;42:62. 81. Burstein JL, Henry MC, Alicandro JM, et al. Evidence for and impact of selective reporting of trauma triage mechanism criteria. Acad Emerg Med. 1996;3:1011. 82. Santaniello JM, Esposito TJ, Luchette FA, et al. Mechanism of injury does not predict acuity or level of service need: field triage criteria revisited. Surgery. 2003;134:698.

83. Tinkoff GH, O’Connor RE, Fulda GJ. Impact of a two-tiered trauma response in the emergency department: promoting efficient resource utilization. J Trauma. 1996;41:735. 84. Steele JT, Hoyt DB, Simons RK, et al. Is operating room resuscitation a way to save time? Am J Surg. 197;174:683. 85. Rhodes M, Brader A, Lucke J, et al. Direct transport to the operating room for resuscitation of trauma patients. J Trauma. 1989;29:907. 86. Barlow B, Niemirska M, Gandhi RP. Stab wounds in children. J Pediatr Surg. 1983;18:926. 87. Barlow B, Neimirska M, Gandhi RP. Ten years’ experience with pediatric gunshot wounds. J Pediatr Surg. 1982;17:927. 88. DeKeyser FG, Paratore A, Seneca RP, et al. Decreasing the cost of trauma care: a system of secondary inhospital triage. Ann Emerg Med. 1994; 23:841. 89. Rogers FB, Osler TM, Shackford SR, et al. Study of the outcome of patients transferred to a level I hospital after stabilization at an outlying hospital in a rural setting. J Trauma. 1999;46:328. 90. Strobos J. Tightening the screw: statutory and legal supervision of interhospital patient transfers. Ann Emerg Med. 1991;20:302. 91. Nathens AB, Maier RV, Copass MK, et al. Payer status: the unspoken triage criterion. J Trauma. 2001;50:776. 92. State of Colorado, Board of Health. Rules and Regulations pertaining to the Statewide Trauma System-Chapter 2. Area Trauma Advisory Councils; 1999. 93. Veenema KR, Rodewald LE. Stabilization of rural multiple trauma patients at Level III emergency departments before transfer to a Level I regional trauma center. Ann Emerg Med. 1995;25:175. 94. Lee RB, Morris JA Jr, Parker RS. Presence of three or more rib fractures as an indicator of need for interhospital transfer. J Trauma. 1989; 29:795. 95. Lee RB, Bass SM, Morris JA Jr, et al. Three or more rib fractures as an indicator for transfer to a Level I trauma center: a population-based study. J Trauma. 1990;30:689. 96. Clark DE, Cobean RA, Radke FR, et al. Management of major hepatic trauma involving interhospital transfer. Am Surg. 1994;60:881. 97. Baxt WG, Moody P. The impact of a rotocraft aeromedical emergency care service on trauma mortality. JAMA. 1983;249:3047. 98. Moylan JA, Fitzpatrick KT, Beyer AF III, et al. Factors improving survival in multisystem trauma patients. Ann Surg. 1988;27:679. 99. Hoyt DB, Hollingsworth-Fridlund P, Winchell RJ, et al. An analysis of recurrent process errors leading to provider-related complications on an organized trauma service: directions for care improvement. J Trauma. 1994;36:377. 100. Davis JW, Hoyt DB, McArdle MS, et al. The significance of critical care errors in causing preventable death in trauma patients in a trauma system. J Trauma. 1991;31:813. 101. Davis JW, Hoyt DB, McArdle MS, et al. An analysis of errors causing morbidity and mortality in a trauma system: a guide for quality improvement. J Trauma. 1992;32:660. 102. Hoyt DB, Hollingsworth-Fridlund P, Fortlage D, et al. An evaluation of provider-related and disease-related morbidity in a Level 1 university trauma service: directions for quality improvement. J Trauma. 1992; 33:586. 103. Shackford SR, Hollingsworth-Fridlund P, McArdle MS, et al. Assuring quality in a trauma system—the medical audit committee: composition, cost, and results. J Trauma. 1987;27:866. 104. Nathens AB, Jurkovich GJ, Cummings P, et al. The effect of organized systems of trauma on motor vehicle crash mortality. JAMA. 2000; 283:1990. 105. Mullins RJ, Mann NC. Introduction to the academic symposium to evaluate evidence regarding the efficacy of trauma systems. J Trauma. 1999;47:S3. 106. Mann NC, Mullins RJ, Mackenzie EJ, et al. Systematic review of published evidence regarding trauma system effectiveness. J Trauma. 1999;47:S25. 107. Utter GH, Maier RV, Rivara FP, et al. Inclusive trauma systems: do they improve triage or outcomes of the severely injured? J Trauma. 2006; 60:529. 108. U.S. Department of Health and Human Services, Health Resources and Services Administration. Model Trauma Care System Plan. Rockville, MD: U.S. Department of Health and Human Services, Health Resources and Services Administration; 1992. 109. Moore EE. Trauma systems, trauma centers, and trauma surgeons: opportunity in managed competition. J Trauma. 1995;39:1–11.

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CHAPTER 5

Injury Severity Scoring and Outcomes Research Robert D. Becher, J. Wayne Meredith, and Patrick D. Kilgo

INTRODUCTION Traumatic accidents have long been classified in terms of their severity. The world’s oldest known surgical document, the Edwin Smith Surgical Papyrus (ca. 17th century BC), classified 48 traumatic injuries from ancient Egyptian battlefields and construction sites as successfully treatable, possibly curable, or untreatable.1 Such predictions about patient outcomes, and attempts to quantify the severity of traumatic accidents, are today the realm of injury severity scores (ISSs). Trauma injury severity scoring quantifies the risk of an outcome following trauma. Injury scoring provides a single metric based on elements of clinical acumen and statistical theory to describe aspects of the patient condition after a traumatic incident. The primary outcome of interest is usually survival, though the outcome can be whatever one wants to measure: hospital or ICU length of stay (LOS), a vital sign such as blood pressure, performance of a procedure, or any other endpoint of interest. Clinically, these “scores” assist in the prehospital triage of trauma patients and can help to more accurately predict patient outcomes to assist with clinical decision making, especially at the end of life. In the outcomes research setting, ISSs allow valid comparisons between disparate groups, which in turn can be translated into myriad applications: quality improvements in patient care, advancements in trauma systems and health care delivery, enhancements in injury prevention, valid benchmarking and quality control “report cards,” and epidemiological studies of trauma, among others. Outcomes research is defined as a method of creating “empirically verified information” to better understand how variables in the real-world setting (from injury to treatment) affect a wide range of outcome variables (from mortality to satisfaction with care).2 Because outcomes are the product of many influences, the outcomes researcher must isolate the effects he or she wants to study from the effects of other “noisy”

factors that can influence the outcome. This is called risk adjustment, or “case mix” adjustment, and is essential for proper outcomes analysis. In trauma outcomes research, trauma ISSs are the essential tools for stratified risk adjustment, thereby allowing accurate comparisons among disparate patient populations with varied degrees of risk. The goal is to compare populations with similar degrees of traumatic injury so that other risk factors (time to treatment, mechanism, injury prevention equipment, etc.) may be properly isolated to examine their relationship to particular outcomes. Risk adjustment might be as simple as defining classes of a variable to stratify risk groups or as complicated as using a risk adjustor in a multivariable regression model.3 This chapter provides a background into injury severity scoring and outcomes research, reviewed in three sections. The first section, Injury Coding, discusses the two major schemes used to classify traumatic injury in the United States, the Abbreviated Injury Scale (AIS) and the International Classification of Diseases (ICD). The second section, Injury Severity Scoring, highlights the major trauma scoring systems used for outcome prediction and risk adjustment. The final section, Outcomes Research, discusses the increasingly important role of outcomes research in the field of trauma, the databases used for such research, and the basic approaches to risk adjustment and statistical analysis.

INJURY CODING Accurate classification of a patient’s injuries, also known as “injury coding,” is fundamental to the validity and success of severity scoring. This is because ISSs are uniformly based on two classification schemes: the AIS and the ICD (Table 5-1). The most advanced trauma-specific, anatomically based coding lexicon is the AIS, which was first conceived as a system to define the type and severity of injuries arising from motor vehicle

78

Trauma Overview

TABLE 5-1 Injury Coding/Classification Schemes: A Comparison

SECTION 1 X

Name (Year First Introduced; Year Last Revised) Brief Description AIS (1971; Trauma-specific, 2008) anatomically based coding system with two numerical components: (1) an injury descriptor (“pre-dot”) that is unique to each injury and (2) a severity score (“post-dot”) graded from 1 (minor) to 5 (critical injury); all unsurvivable injuries scored a 6; severity scores are consensus assessments assigned by a group of experts. ICD-9-CM General, all-purpose (1893;2004) diagnosis classification system/taxonomy for all health conditions/ diseases; codes exist for over 10,000 medical conditions; each medical condition is assigned a specific code.

Primary Use Classification of type and severity of injury based on tissue damage.

Interpretation For post-dot scores, any score 3 is “serious”; any score of 6 is unsurvivable; pre-dot codes include nine anatomic regions: 1, head; 2, face; 3, neck; 4, thorax; 5, abdomen and pelvic contents; 6, spine; 7, upper extremity; 8, lower extremity; 9, unspecified.

Benefits Continually updated, with last update in 2008; also found to be a valid tool to predict survival based on “postdot” severity score; can be treated as nominal data if only use “pre-dot” injury descriptors.

Limitations Proprietary system that requires specialized training for coding and is time consuming; severity scores are based on consensus assessments and are not totally objective.

Administrative purposes, specifically billing and event reporting.

Codes 800.0 to 959.9 are traumaspecific; this includes roughly 2000 codes.

Codes often used to define health conditions in large national databases and therefore contribute to research and epidemiology.

ICD taxonomy has no specific severity dimension included with the diagnoses of a traumatic injury.

AIS  Abbreviated Injury Score; ICD-9-CM  International Classification of Diseases, 9th Revision, Clinical Modification.

accidents.4 The last major revision to the AIS occurred in 2005,5 with a subsequent update in 2008.6 To calculate AIS scores, medical records of traumatic incidents are transcribed into specific codes that capture individual injuries. AIS is a proprietary classification system, meaning it requires specialized training for coding personnel. Therefore, AIS is not captured at every hospital. The actual AIS code consists of two numerical components. The first component is a six-digit injury descriptor code (“pre-dot”), which is unique to each traumatic injury; pre-dots classify the injury by region, type of anatomic structure, specific structure, and level. The second component is a severity score (“post-dot”), graded from 1 (minor) to 5 (critical injury), with the caveat that all unsurvivable injuries are scored a 6 (Table 5-2); these severity scores, or “AIS severity,” are consensus-derived assessments assigned by a group of experts. Of note, AIS is used as both a classification scheme for injury coding (the pre-dots) and a severity score (the post-dots; see next section). The second method to classify traumatic injury is the ICD coding system. ICD is not trauma-specific, but rather is a

general, all-purpose diagnosis taxonomy for all health conditions; it is over 110 years old and is currently in its 10th revision (ICD-10),7 though in the United States the 9th revision (ICD-9)8 is most commonly used (though a conversion to using ICD-10 will be complete by the year 2013). Codes exist for over 10,000 medical conditions, about 2,000 of which are physical injuries (the block of ICD-9 codes from 800.0 to 959.9 encompasses all traumatic injuries). ICD-9 codes are used by all hospitals in the United States, primarily to classify diagnoses for administrative purposes, such as billing and event reporting. For the trauma outcomes researcher, AIS codes are generally preferred over ICD-9 because of their greater specificity of injury description (the pre-dot classification). However, as discussed in the next section, valid severity scores can be formulated from either system. Additionally, while the AIS classification scheme attaches an ordinal 1–6 severity level to each injury, ICD-9 codes are only nominal classifications and therefore do not measure the severity of injury.

Injury Severity Scoring and Outcomes Research

TABLE 5-2 AIS Components, Definition of 1–6 Ordinal Description Minor injury Moderate injury Serious injury Severe injury Critical injury Virtually unsurvivable injury

AIS  Abbreviated Injury Score.

INJURY SEVERITY SCORES ISSs quantify the risk of an outcome after trauma, for both clinical and research purposes. The selection of which trauma severity score to use should be based on a clear sense of what one wants to measure and why. The scores vary considerably, from complexity of calculation to ease of use. The majority of scores are based on either the trauma-specific AIS coding classification or the more general ICD-9 taxonomy. However, trauma scoring systems are continuously being revised, tested, and compared to each other, and still today there is no consensus on a “best” injury scoring system. The trauma outcomes researcher needs to be familiar with the various scoring schemes (Table 5-3) in order to most accurately risk adjust their patient population to best isolate the effects of an independent predictor variable on a dependent outcome variable. In general, four types of risk adjustments (equally called “scores”) are calculated to account for trauma severity: (1) Anatomic Injury Scores; (2) Physiological Derangement Scores; (3) Comorbidity Scores; and (4) A combination of the three. Unlike other circumstantial factors (time to treatment, quality of care, etc.), each of these scores is intrinsic to the patient and are therefore important to understand and quantify.

■ Anatomic Scoring Systems Anatomic injury scores are the most developed types of risk adjustment following trauma. Many scores have been proposed in the literature, but this review will be limited to scores that have gained practical acceptance. The majority of scoring algorithms are designed to predict mortality (Table 5-3) and are not specifically validated on other outcomes, such as LOS or functional status, though moderate correlations may exist. The AIS is not only a method to classify injuries, as described earlier, it is also a validated method to score injury severity. The AIS severity designation (ordinal scale from 1 to 6; Table 5-2) that accompanies each coded injury is the simplest form of a score. The maximum AIS (maxAIS), which is the largest AIS severity among all of a patient’s injuries, is highly associated with mortality but ignores information provided from other injuries. In 1974, Baker et al. first posited a multiinjury score by introducing the ISS.9 ISS divides the body into six regions: head or neck, face, abdominal, chest, extremities, and external.

CHAPTER 5 X

AIS Severity 1 2 3 4 5 6

Injuries in each region are given an AIS score and the highest AIS scores in the 3 most severely injured regions are squared and summed to form the ISS. ISSs have a range from 1 (least severe) to 75 (unsurvivable); higher scores reflect higher likelihood of mortality. Any patient with an AIS severity of 6 is automatically given an aggregate score of 75. ISS correlates well with mortality and remains the most widely used anatomical scoring system. However, ISS has many limitations.10 ISS is often incorrectly treated as a continuous, monotonic function of mortality, though it is none of these (Fig. 5-1).11,12 There are only 44 distinct values of ISS, some of which are possible in two different combinations of sums of squares. Optimally, each combination would be treated nominally (as its own class) in terms of risk adjustment, but in practice this seldom occurs. Furthermore, ISS only considers one injury in each of the body regions and thus ignores important injury information. Because of these shortcomings we continue to believe ISS should be retired and replaced by one of the more modern injury scores that are now available (see below). The New Injury Severity Score (NISS) was formulated by Osler et al. to address some of the ISS shortcomings, specifically its omission of multiple occurrences of serious injuries within the same body region.13 NISS is the sum of the squares of the three most severe AIS severities, regardless of body region (and keeping the convention that an AIS of 6 automatically results in a NISS of 75). This permutation offers a slight prediction advantage but has several of the same shortcomings as ISS (Fig. 5-2). The Anatomic Profile Score (APS), developed by Copes et al., adjusted for body region differences and AIS severity.11 Three “modified components” are weighted to form a single scalar based on anatomic location of all serious injuries (AIS severity of 3). Although APS represents a logical approach to anatomic scoring, it has failed to supplant ISS. The International Classification of Diseases Injury Severity Score (ICISS), created by Osler et al., took an empirical estimation approach to injury severity scoring with the formulation of ICD-9 survival risk ratios (SRRs).14 An SRR is an ICD-9 codespecific estimate of the survival probability associated with that particular injury. For a set of patients, the SRR for a particular injury code is the number of patients that survive that injury divided by the number of patients who display the injury. The ICISS score is the product of the SRRs corresponding to a patient’s set of injuries, and ranges from 0 (unsurvivable) to 1 (high likelihood of survival). ICISS offers several advantages over other anatomic scores. First, because of its ICD-9 base coding lexicon, it can be used in any clinical setting, including smaller centers that typically do not perform AIS coding. Second, unlike the consensusderived AIS severity scores, ICISS’ empirical approach means that powerful statistical estimates of injury-specific survival can be computed if enough representative patients are available for study. Consequently, unlike ISS and NISS, ICISS is a smooth, if nonlinear, function of mortality (Fig. 5-3). However, ICISS does have limitations. First, although it resembles an overall probability, ICISS can only be considered a scalar since most SRRs are “contaminated” by patients with multiple injuries. Independent SRRs can be calculated from

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SECTION 1 X 80

Name (Year Predicts First Introduced) What? Anatomic scoring systems

How Calculated?

Score Range/ Interpretation

AIS (1971)

Patient survival

See Table 1

See Table 1

ISS (1974)

Patient survival

44 distinct possible scores ranging from 1 (least severe) to 75 (unsurvivable); higher scores reflect higher likelihood of mortality.

NISS (1997)

Patient survival

Body divided into six anatomical regions: head/neck, face, chest, abdomen/pelvis, extremities, skin/general; injuries in each region given an AIS score; the highest AIS scores in the three most severely injured regions are squared and summed for ISS; any patient with an AIS severity of 6 is automatically given an aggregate score of 75. Sum of the squares of the three most severe AIS severities, regardless of body region; as with ISS, any patient with an AIS severity of 6 is automatically given an aggregate score of 75.

APS (1990)

Patient survival

ICDMAP-90 (1997)

Injury severity

Three “modified components” (head/brain and spinal cord injury; thorax and neck injury; all other serious injuries) are scored based on AIS and weighted to form a single APS; only “serious” injuries included. Translates ICD-9 discharge diagnosis codes into AIS “pre-dot” codes, injury descriptors, and severity scores, which in turn are translated into an ISS, NISS, and APS for the patient.

Benefits

Limitations

Initially developed to classify severity of injury, but has been validated to measure probability of death; used for trauma center evaluation and quality improvement. Most widely used trauma severity score; relates AIS to patient outcomes.

Cannot predict functional impairment; proprietary scoring system.

44 distinct possible scores ranging from 1 (least severe) to 75 (unsurvivable); higher scores reflect higher likelihood of mortality. Range varies; higher numbers have worse prognosis.

Addresses the ISS omission of multiple occurrences of serious injuries within one body region; slight prediction advantage over ISS and ICISS in predicting mortality. Logical, analytical approach; based on location and severity of illness.

Scored on three injuries only; requires specialized training; not widely used, but should be.

ICD/AIS scores vary.

Conservative estimates of injury severity.

Based on a computer software program; loss of certain injury information in the translation between diagnosis systems; out of date as not mapped to ICD-9-CM, ICD-10-CM, or most recent AIS.

No physiologic predictors; does not account for 1 injury in the same region, only the highest score; scored on three regions only, not all six; requires specialized training.

Failed to supplant ISS as predominant severity scoring modality.

Trauma Overview

TABLE 5-3 Injury Severity Scores: A Comparison by Type of Score

ICISS (1996)

Patient survival

Computed directly from ICD-9 codes; conversion of a specific ICD-9 code into a SRR for that code, with higher SRRs reflecting higher likelihood of survival; the final ICISS score in the product of each SSR for each injury the patient has.

Scores range from 0 (unsurvivable) to 1 (high likelihood of survival).

One of the few severity scores not based on AIS/ ISS; accounts for all injuries; no specialized training required; multiple studies show it outperforms ISS; some evidence that most severe SRR outperforms multiplicative SRR.

TRAIS (2003)

Patient survival

Scores range from 0 (unsurvivable) to 1 (high likelihood of survival).

OIS (1987)

Not for patient outcomes

Exact same calculation as ICISS except TRAIS uses AIS injury descriptor codes to create SRRs; the TRAIS score is the product of AIS-derived SRRs for each injury the patient has. Anatomic injury within an organ system graded on an ordinal scale, with Grade 1 being a minor injury and Grade 5 being tissue-destructive and likely fatal.

Behaves very similarly to ICISS; out-predicts its AIS counterparts ISS, NISS, and APS; used in models to predict mortality. Enhances communication between trauma surgeons.

Designed to standardize the descriptive language of injury for 32 organ and body system regions.

Multiple databases can be used to calculate SRRs (ICD-9-CM, NTDB, etc.), and thus SRRs are databasespecific; SRRs from different sources are not comparable; SRRs are not independent of each other; no consensus yet on best practice; some argue ICISS measures hospital survival not injury survival. Not widely adopted.

No predictive abilities; not widely adopted; not used for risk adjustment.

Physiological scoring systems Aggregate score of motor activity (scale of 1–6 points), verbal activity (1–5 points), and eye-opening (1–4 points); higher scores indicate more function.

Range from 3 (no or minimal neurological function) to 15 (normal or near-normal neurological function).

Simple to use; quickly calculated; well validated; used by many other scoring systems; can use motor score alone.

RTS (1989)

Patient survival

APACHE-II (1985)

Patient survival; disease severity

Computed by logistic regression equation based on indexed values of GCS, systolic blood pressure, and respiratory rate on presentation to ED. Based on the worst 12 routine physiological measurements (heart rate, blood pressure, etc.) in the first 24 hours of ICU admission, as well as age and chronic health conditions.

Range from 0 (severe physiological derangement) to 7.84 (no physiological derangement). Range from 0 (very low risk of mortality) to 71 (very high risk of in-hospital mortality); scores 15 considered moderate moderate-to to-severe risk.

Provides physiological assessment of patient; high association with mortality; contributes to TRISS. ICU specific; superior to TRISS and ISS at predicting mortality in TICU.

Hard to measure all components in some patients (if sedated, intubated, etc.); score changes with time (not fixed on admission). Intubation and sedation prior to ED arrival alter accuracy; use limited by missing data. Very time consuming and complex to calculate.

(continued)

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CHAPTER 5 X

Patient survival; brain function

Injury Severity Scoring and Outcomes Research

GCS (1976)

SECTION 1 X 82

Name (Year Predicts First Introduced) What? How Calculated? Comorbidity scoring systems

Score Range/ Interpretation

Charlson (1987)

Patient survival

Score consists of 19 possible comorbid conditions, each allocated a weight of 1–6 based on the relative risk of 1-year mortality; values are summed to provide a total score.

Range from 0 (low chance of death) to 37 (high cumulative mortality attributable to comorbid disease).

TRISSCOM (2004)

Patient survival

Similar to TRISS with adjustments to age (dichotomized at 65 years old as opposed to 55 years old) and the addition of eight comorbidity variables (recorded as a binary yes/no variable).

Scores range from 0 (unsurvivable) to 1 (high likelihood of survival).

Benefits

Limitations

Simple to calculate; validated in medicine patients; good indicator of disease burden; adapted for use with administrative databases with ICD-9 codes. Reflects the aging population.

Charlson score is not trauma-specific.

Scores range from 0 (unsurvivable) to 1 (high likelihood of survival).

Useful for quality improvement initiatives; separate probability equations for blunt and penetrating patients.

Requires multiple variables; if one not captured you are unable to calculate TRISS.

Range varies.

Out-predicts TRISS for penetrating trauma.

Complex calculation.

Comorbidities are not weighted based on severity.

Combination scoring systems TRISS (1987)

Patient survival

ASCOT (1990)

Patient survival

Combines ISS, RTS (respiratory rate, systolic blood pressure, GCS), and age; regression coefficients derived from MTOS database; equations vary between blunt versus penetrating trauma. Uses APS to define injury severity, with different regression coefficients for blunt versus penetrating trauma.

AIS  Abbreviated Injury Score; APACHE-II  Acute Physiologic and Chronic Health Evaluation II; APS  Anatomic Profile Score; ASCOT  A Severity Characterization of Trauma; Charlson  Charlson Comorbidity Index (CCI); ED  emergency department; ICDMAP-90  International Classification of Disease “map”; ICISS  International Classification of Disease Injury Severity Score; ICU  Intensive Care Unit; ISS  Injury Severity Score; GCS  Glasgow Coma Score; MCOT  Major Trauma Outcomes Study; NISS  New Injury Severity Score; NTDB  National Trauma Data Bank; OIS  AAST Organ Injury Scale; RTS  Revised Trauma Score; SRR  Survival Risk Ratios; TRAIS  Trauma Registry Abbreviated Injury Score; TRISS  Trauma and Injury Severity Score; TRISSCOM  Trauma and Injury Severity Score Comorbidity.

Trauma Overview

TABLE 5-3 Injury Severity Scores: A Comparison by Type of Score (Continued )

1

0

15

30

45

60

75

ISS

FIGURE 5-1 ISS versus actual mortality. This graph plots the mortality associated with each ISS value. Of note is the erratic choppiness of the curve, indicating that ISS is not a monotonically increasing function of mortality. It is characterized in places by steep decreases in mortality as ISS gets larger. Ideally, ISS would be considered nominal and not ordinal.

Mortality

patients who only have an isolated injury, but these are not available for all codes because many injuries rarely occur in isolation.15 Second, SRRs are database-specific and the degree to which they are applicable within disparate populations remains uncertain.16 ICD-9 codes are nominal, meaning they are unordered, qualitative categories not ranked by severity. If one ignores the AIS severity score, AIS codes can also be treated nominally, taking advantage of their specificity in injury classification. As such, AIS injury descriptor codes can be used to create SRRs, similar to the SRR calculated from ICD-9 codes for ICISS. AIS-based SRRs are used for the TRAIS score (Trauma Registry Abbreviated Injury Score), which is the product of AIS-derived SRRs. Kilgo et al. showed that ICISS and TRAIS behave very similarly in a large group of patients coded both ways (Fig. 5-4) and that TRAIS out-predicts its AIS counterparts ISS, NISS, and APS.17 Trauma clinicians, outcomes researchers, and hospital administrators may ask: which of these approaches is the best? There is no consensus, and many publications each year continue to debate this question. Several large studies, including Sacco et al. and Meredith et al., compared these anatomic scores in terms of their ability to predict mortality.18,19 Both studies found that APS and ICISS better discriminate survivors from nonsurvivors than ISS,

90% 80% 70% 60% 50% 40% 30% 20% 10% 0%

Mortality

90% 80% 70% 60% 50% 40% 30% 20% 10% 0%

90% 80% 70% 60% 50% 40% 30% 20% 10% 0%

0.9 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.1 0 ICISS

FIGURE 5-3 ICISS versus actual mortality. ICISS, unlike ISS and NISS, has a very smooth association with mortality, though it too is nonlinear. In the places where ICISS mortality decreases from one value to the next, the decrease is very slight, never more than about 7% and corrects itself quickly. Contrast these small decreases with the decreases seen in ISS and NISS, which can be as large as 20% from one value to the next and 30% in the span of two values.

NISS, and the ICDMAP versions of ISS, NISS, and APS. A surprising finding was that maxAIS performed better than its multiinjury counterparts ISS and NISS. Based on this result, Kilgo et al. showed that the patient’s worst injury, regardless of the coding lexicon (ICD-9 or AIS) or the estimation approach (AIS severity-consensus or empirical SRRs), was a better predictor of mortality than multiinjury scores, though there remains no consensus on this.17 More recently, however, Harwood et al. found that NISS was better than the ISS and equivalent to the maxAIS in the prediction of mortality in blunt trauma patients.20 Finally, in 1987, the American Association for the Surgery of Trauma (AAST) introduced the AAST Organ Injury Scale (OIS).21 The goal of the scale was not to predict outcomes, but to standardize the descriptive language of injuries to improve communication between trauma surgeons and physicians. Like AIS, the OIS provides an ordinal scale to each level of organ disfigurement, with Grade 1 injuries being relatively minor and Grade 5 injuries being destructive injuries that are thought to be fatal. These scales, originally developed by Moore et al. via a series of journal articles, exist for 32 organ and body region systems.22–27 Although descriptions using this lexicon are common, the scale has not been widely adopted into formal risk adjustment methods. The potential exists for these scales to make an enduring impact on outcomes research. The validation of OIS should be carried out with a large representative database.

■ Physiological Scoring Systems

0

15

30

45

60

75

NISS

FIGURE 5-2 NISS versus actual mortality. This graph plots the mortality associated with each NISS value. The NISS curve is also very nonmonotonic, even more so than ISS.

Physiological status is a powerful predictor of mortality. Clinical markers, including respiratory rate (RR), systolic blood pressure (SBP), base deficit, and others, are important prognosticators of outcome and are routinely used in clinical management. However, unlike anatomic injuries and preexisting comorbidities, which are fixed at the time of hospital admission, physiological parameters are ever-changing, both spontaneously and in response to therapy. This makes them difficult to utilize in risk adjustment. The solution, even though imperfect and with

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Mortality

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ICISS

FIGURE 5-4 TRAIS and ICISS by mortality rate. ICISS and TRAIS behave very similarly in terms of their association with mortality (the vertical axis) despite being derived from two very different types of codes. This suggests that empirical approaches might obviate the inherent structure of the coding systems.

some exceptions, is to use a “snapshot” of physiological status at one point in time, usually immediately upon emergency department (ED) arrival. Perhaps the most widely employed physiological adjuster is the Glasgow Coma Scale (GCS), first proposed first by Teasdale and co-workers as a means to monitor postoperative craniotomy patients.28,29 The GCS was subsequently adopted by trauma surgeons as a measure of overall physiological derangement. The scale has three components—motor (GCS-M), verbal (GCS-V), and eye (GCS-E)—each with ordinal characterizations of severity (Table 5-4). The scales can be

TABLE 5-4 Descriptors of GCS Components Function Eye

Verbal responses

Motor response

Description Spontaneous To voice To pain None Oriented Confused Inappropriate Incomprehensible None Obeys commands Localizes pain Withdraw (pain) Flexion Extension (pain) None

GCS  Glasgow Coma Score.

GCS Scaled Value 4 3 2 1 5 4 3 2 1 6 5 4 3 2 1

summed to produce the Glasgow Coma Score, or equally the GCS. The GCS is labeled a measure of brain injury but in actuality it measures brain function. It ranges from 3 (completely unresponsive) to 15 (completely responsive) and has been shown to be highly associated with survival. Osler and co-workers used the National Trauma Data Bank (NTDB) to show that the Glasgow Motor Component was almost as powerful as the full GCS score and had better statistical properties in general.30 As such, the motor score alone could replace the full GCS score. The Trauma Score, later updated to the Revised Trauma Score (RTS), was designed by Champion et al. as an approach to combining clinical and observational physiological data into one score.31,32 Two forms of the RTS exist, one for triage (Triage-RTS) and one for outcomes evaluation and risk adjustment. Both are based on variable physiological breakpoints for GCS, SBP, and RR (Table 5-5). The Triage-RTS score is calculated by summing the coded values for each of the three variables; it has a minimum score of 0 and maximum of 12.

TABLE 5-5 Revised Trauma Score (RTS) Variable Breakpoints Coded Value 0 1 2 3 4

GCS 3 4 to 5 6 to 8 9 to 12 13 to 15

SBP (mm Hg) 0 1 to 49 50 to 75 76 to 89 89

RR (breaths/min) 0 1 to 5 6 to 9 29 10 to 29

GCS  Glasgow Coma Score; RR  respiratory rate; SBP  systolic blood pressure.

Injury Severity Scoring and Outcomes Research

RTS  0.9368(GCS)  0.7326(SBP)  0.2908(RR) The RTS score ranges from 0 to 7.84; lower scores translate into more physiological derangement. RTS is highly associated with mortality and remains important in injury scoring through its contribution to the TRISS model (see below). Studies have also shown that the combined use of SBP and GCS-M are just as effective at predicting patient survival as the RTS.33 The Acute Physiologic and Chronic Health Evaluation II (APACHE-II) was first introduced in 1985.34 It is calculated from 12 physiological parameters (the worst values within 24 hours of ICU admission), age, and chronic health conditions. It has long been validated for the use in both medical and surgical ICU patients, though its use in the trauma intensive care unit (TICU) has been limited and debated. This is because of APACHE-II’s poor correlation with ISS and its inability to predict hospital LOS.35 However, APACHE-II very accurately predicts mortality in the TICU population.36,37 APACHE-II has also been shown to be superior to TRISS and ISS at predicting TICU mortality,38 and we advocate for its use in risk adjustments in critically injured patients.

■ Comorbidity Scoring Systems Trauma outcomes research has long recognized the importance of comorbidities on patient outcomes. Morris et al., among others, identified several preexisting conditions that worsen prognosis following trauma, most notably liver cirrhosis, chronic obstructive pulmonary disease (COPD), congenital coagulopathy, diabetes, and congenital heart disease.39 Morbid obesity has now been added to this list.40 Accordingly, specific comorbidity adjustments, such as the Charlson Comorbidity Index (CCI), which are widely used in other disciplines,41 have been incorporated into current injury severity models in attempts to enhance their predictive abilities. Results, however, have been poor.42 The incorporation of preexisting conditions into injury severity models is difficult because so many potential comorbidities exist, each of which may itself occur with variable severity. Further, many are relatively rare, confounded by age, and may be inconsistently recorded. One accepted convention is to simply use patient age as a surrogate for comorbidities because age is moderately associated with serious preexisting disease. Another approach is to use the presence of individual comorbidities or classes of conditions (ICD-9 ranges) in risk adjustment methods. Either of these is acceptable but eventually a generalized score that incorporates all of this information might improve the accuracy of trauma scoring. One trauma-specific score that adjusts for comorbidities is available, based on adjustments to TRISS.43 The Trauma and Injury Severity Score Comorbidity (TRISSCOM) adjusts the initial TRISS model (see below) to dichotomize age at 65 years old (as opposed to 55 years old) and to include eight

comorbidities recorded as a binary yes/no variable if any one of the eight was present in the patient (based on ICD-9 diagnosis ranges: pulmonary disease, cardiac disease, diabetes, coagulopathy/anticoagulation, neurological disease or dementia, hepatic insufficiency, chronic renal insufficiency on dialysis, active neoplasia of the hematological or lymphatic system, or metastatic cancer). The end result was that the TRISSCOM model improved the predictive performance of TRISS but not its ability to discriminate.

■ Combined Scoring Systems The three types of risk adjustments—anatomic, physiological, and comorbid—can be easily combined so that information from all three sources is used to predict outcomes. The first such attempt from resulted in the Trauma and Injury Severity Score (TRISS).44 TRISS has become the standard tool to estimate survival probabilities. TRISS incorporates ISS (anatomic component), RTS (physiological component), and an age indicator (55, 55; comorbidity component) to estimate survival. Two separate equations, one each for blunt and penetrating patients, represent weighted sums of each of the three components; the equations were calculated from data gathered in the Major Trauma Outcomes Study (MTOS).45 From these equations, a probability of survival can be calculated for an individual patient (Table 5-6). This probability (usually called the TRISS Score) can be used as a risk adjustor. However, the TRISS approach has shortcomings.46 It requires 8–10 variables (depending on the number of injuries used by ISS); failing to capture even a single predictor renders TRISS incalculable. This is the case in as many as 28% of all trauma cases. TRISS could be improved by replacing ISS with ISS squared or replacing it with a better anatomic predictor, accounting for comorbidities more accurately, and updating the MTOS equations with more modern NTDB coefficients that reflect the advancements made since TRISS first appeared.47,48 Other TRISS-like models aim to account for all three risk adjustments.48 The ASCOT score (A Severity Characterization

TABLE 5-6 Equation for TRISS: Probability of Survival  1/(1  e(LOGIT)) where LOGIT is Given by: LOGIT  Intercept  βISS∗ (ISS)  βRTS∗ (RTS)  βAGE (AGE) MTOS Mechanism Intercept βISS βRTS βAGE

Blunt 1.2470 0.0768 0.9544 1.9052

Penetrating 0.6029 0.1516 1.1430 2.6676

Age is dichotomized as follows: 0–55 years  0;  55 years  1. ISS  Injury Severity Score; MCOT  Major Trauma Outcomes Study; RTS  Revised Trauma Score; TRISS  Trauma and Injury Severity Score.

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The RTS equation for outcomes evaluation computes indexed values of GCS, SBP, and RR (Table 5-5) by weighting them with logistic regression coefficients and summing them.

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of Trauma) was introduced to address some weaknesses in TRISS, in particular its poor prediction for certain types of trauma (e.g., penetrating torso trauma) and the reliance upon ISS.49 Like TRISS, ASCOT relies upon anatomic descriptors, emergency department physiological status, age, and mechanism. However, instead of ISS, the Anatomic Profile (AP), which is the basis for the APS score, is used to adjust for anatomic severity.11 Further, age is parsed into five ordinal categories rather than two. Similar to TRISS, all the values are statistically weighted in such a manner as to produce a probability of survival. Although ASCOT provides better predictions than TRISS, it has failed to replace TRISS as the standard survival predictor.

OUTCOMES RESEARCH Trauma outcomes research was at one point focused solely on predicting patient survival. Today, it has become much more complex, as contemporary trauma outcomes research keeps pace with the changes in the medical and scientific research communities on the whole. This has translated into a move away from a predominate focus on quantitative outcome measures, such as mortality and hospital LOS, and toward much more qualitative and subjective measures, such as health-related quality of life, chronic functional impairment, and qualityadjusted life years (QALYs). These changes reflect a trauma community that has begun to embrace the World Health Organization’s definition of health, which is a “state of complete physical, mental, and social well-being and not merely the absence of disease or infirmity.”50 Current severity scoring systems are inadequate for predicting nonfatal, subjective outcome measures. There is considerable room for growth and advancement in the scores’ ability to predict myriad potential outcomes in trauma patients, such as appropriateness of care, cost-utility, satisfaction with care, and functionality.51–53 This will be essential given the renewed national focus on comparative-effectiveness research (CER).54 To create such tools requires a basic understanding of the process of outcomes research, which is the focus of this section.

■ Outcomes Research Basics There are five essential steps in outcomes research as outlined by Kane,2 and each step is to be performed sequentially (Kane RL. Understanding Health Care Outcomes Research. 2nd ed. Sudbury, MA: Jones & Bartlett Learning; 2005. www.jblearning.com. Reprinted with permission): 1. 2. 3. 4. 5.

Define a research question Develop a conceptual model Identify the critical dependent and independent variables Identify appropriate measures for each Develop an analysis plan

Each step is critical, though none more so than refining your research question (step 1) by use of a conceptual model (step 2). Such a model (often a drawn diagram) outlines all the determinants

thought to influence/cause an outcome, either directly or indirectly. The practice of creating a conceptual model should fully elucidate the multifactorial and multidimensional nature of the outcome under study. As such, the conceptual model is the foundation for outcomes research, and can be simplistically written as follows (and can be amended based on specific outcomes): Outcomes  f (baseline, patient clinical characteristics, patient demographics, psychosocial characteristics, treatment, setting).2 Quality outcomes research attempts to define the determinants of an outcome in a quantifiable relationship. This therefore depends on quality, comprehensive data collection. Kane maintains that the ultimate goal of outcomes research analysis is to isolate the true relationship between an outcome of interest and its determinants. In order to do this, the researcher must risk adjust the data, meaning he must control for the effects of the other relevant variables in the outcomes model (see below). Accordingly, the more accurate the data, the better the risk adjustment, and in turn the more valid the statistical conclusions.

■ Identifying the Critical Variables The goal of trauma outcomes research is to discover true relationships between input variables and outcome variables, collectively known as the “critical variables.” To do this requires statistical hypothesis testing, which enables inferences about populations based on samples from those populations. From these samples powerful inferences can be made if studies are properly designed and adequately powered. The statistical “model” is usually the modus operandi for exploring relationships among the critical variables. In general, three types of variables are used in the statistical modeling of data.

Outcome/Dependent Variables The dependent, or outcome, variable is the one that is described in terms of the other variables (the independent variables) in the model under study. The outcome variables in trauma research include mortality, ICU and hospital LOS, the presence of some complication, functional status, and others. The data type of the outcome (continuous, dichotomous, ordinal, etc.) drives the type of statistical model chosen.

Predictor/Independent Variables The independent, or predictor, variables are those variables that are hypothesized to influence the outcome of interest (the dependent variable). Independent variables are measured or observed. Examples would be ICD-9 code of an injury or a patient’s preexisting condition.

Covariates Covariates are variables that are known to influence the study outcome, but whose relationship to the outcome is not of primary interest. These variables are called covariates and their purpose is to account for as much of the variance in the

Injury Severity Scoring and Outcomes Research

■ Analysis and Risk Adjustment Approaches Unlike in randomized controlled trials, which are controlled experiments under controlled conditions in populations comparable on every level except the intervention being studied (termed “efficacy” studies), outcomes research evaluates the results of interventions and health care processes in real-world conditions (termed “effectiveness” studies). In such studies, patient populations can be vastly different, with varied degrees of injury severity, physiological derangement, and comorbidities. To address these differences, risk adjustments are made that allow accurate comparisons among such disparate patient populations.

Risk adjustment in trauma outcomes research uses the injury severity scoring systems mentioned above. Risk adjustment is increasingly simpler because of the advent of large relational databases and powerful, easily implemented statistical software. Researchers interested in risk adjustment should choose carefully which methods best accommodate their data constraints. Here are some factors to consider when planning a risk-adjusted study.

Database Choices The type of patient database one uses for their research will determine what type of risk adjustments can be made (Table 5-7). Trauma registries, such as the NTDB,55 exist at most verified trauma centers for clinical documentation, research, and quality control purposes. These data include the pertinent medical records outcomes for each patient over a range of variables, including anatomic injury measures, physiological parameters, and comorbidities. In most cases, any of the aforementioned risk adjustments can be made to NTDB data. Absent large amounts of missing data, comprehensive TRISS-like risk models are fit and probabilities of survival are computed, if desired. This situation is optimal because the best available risk adjustments are derived from scoring

TABLE 5-7 Databases Used in Trauma Outcomes Research and to Populate Injury Severity Scores Name (Year First Introduced) NTDB (1997, though trauma registries began in 1973)

Administrative Databases (database dependent)

TQIP (2007)

Brief Description Dataset compiled by participating hospitals and validated trauma centers; contains injury, demographic, and hospitalization-related information on admitted trauma patients. Databases of discharge data complied by medical records specialists. Often have ICD-9 diagnosis and procedure codes, but no physiological parameters. Uses NTDB-collected data to provide risk-adjusted mortality and morbidity analysis of participating trauma centers to track outcomes and improve patient care.

Primary Use Quality improvement and research on all aspects of trauma, which can lead to improvements in outcomes and trauma care.

Benefits Widely used; over 10 years of data; efforts to standardize data collection with the NTDB National Trauma Data Standard.

Limitations Currently not standardized; not a population-based dataset.

Primarily for billing purposes, though increasingly used for outcomes research.

Many options for available datasets (on national versus state levels).

No physiological data; can often only risk adjust based on anatomic severity scores.

Evaluation of trauma outcomes and improvements in trauma care, both on a local and national level.

Similar to the NSQIP, huge potential for overall improvements in trauma care; riskadjusted morbidity and mortality measures; O/E ratios for benchmarking and improvements.

Remains in pilot stages; low incidence of penetrating trauma makes benchmarking based on O/E ratios difficult; resource intense.

NTDB  National Trauma Data Bank; NSQIP  National Surgical Quality Improvement Program; O/E  Observed to Expected Ratio; TQIP  Trauma Quality Improvement Project.

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outcome as possible. Sometimes called “confounders” or “nuisance variables,” covariates are included in the model so that the association between predictors and outcomes is properly ascribed. The significance of the covariates are of no interest; all that matters is the association of the predictors to the outcome in the presence of covariates. In observational and interventional studies, trauma severity scores are usually used as covariates, hence removing (or adjusting) the confounding effect coincident with some other predictor of interest.

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approaches that use all three types of trauma severity adjustments. Administrative databases, on the other hand, exist primarily for billing purposes and aren’t meant specifically to be used for clinical research. In many cases administrative databases will have at least some injury ICD-9 codes and some comorbidity information, but seldom do they have physiological data. Therefore, risk adjustments on administrative data are usually limited to anatomic severity adjustments.56 If only a principal ICD-9 diagnosis code exists, then the worst injury approach is indicated and the SRR for this code is used for adjustments. If a complete set of injury codes is present, the evidence suggests that ICISS should be used. Finally, the Trauma Quality Improvement Program (TQIP) uses NTDB-collected data to provide risk-adjusted mortality and morbidity analysis of participating trauma centers to track outcomes and improve patient care.57 Although still in its pilot stages, TQIP will eventually lead to the creation of an entire risk-adjusted database. The risk adjustment will be based on observed outcome to expected outcome ratios (O/E ratio; see below) for both survival and complications.

Risk Adjustment Choices The use of AIS severities for risk adjustment have the advantage of familiarity, but studies show that SRR approaches account for more variance in the outcome, discriminate dichotomies better, and contain more information. The problem is that conglomerate scores such as TRISS and ASCOT use AIS severities, and no established, empirically based alternative exists. Hence, it is advisable to take empirical approaches such as TRAIS or ICISS when adjusting only with anatomic scores. Otherwise, TRISS-like combined scores that are AIS-based offer a substantial improvement over single anatomic adjustments. Finally, O/E ratios in databases such as TQIP provide population-based expected outcome probabilities, which can be used for risk stratification. Overall, a low O/E ratio indicates better than expected outcome and a high O/E ratio indicates poorer than expected outcome.

Injury Coding/Classification Choices Injury classification is based on either AIS or ICD taxonomy. When the variables necessary for TRISS or ASCOT are available then AIS codes should be used. TRAIS may be calculated for any case where AIS codes are present, though it only represents the effect due to anatomic injury. Alternatively, when only ICD-9 codes are available (as with most administrative databases), the literature suggests that the ICISS score be used rather than mapping software. When both types of codes are available, the decision is more difficult and no consensus exists. AIS codes possess more specificity in describing the trauma landscape and have in the past been used for these types of adjustments. However, ICD-9 scores repeatedly have been shown to possess similar statistical properties. Although most trauma surgeons will prefer AIS scoring, these decisions are usually guided by other facets of the study design.

■ Evaluation of Trauma Severity Codes Several statistical criteria are employed when evaluating the efficacy of the trauma severity scores. The choice of the modelbased evaluation depends on the data type of the outcome. When the outcome is continuous, multiple linear regression analysis or analysis of variance methods including model R-square values, information criterion, and tests of significance of risk factors suffice to evaluate the association of these scores to the outcome.58 If the outcome is dichotomous (i.e., it takes on one of the two possible values), then logistic regression is warranted.59,60 Logistic regression has two important functions. First, it establishes the relationships between the outcome and the predictors. Within logistic models, the strength of the association between predictors and outcomes is directly measured and inferences about statistical significance are made. Second, logistic regression returns an estimated probability of exposure to the outcome of interest. This estimated (expected) probability can be compared with the observed outcomes in the following ways: Tests of Discrimination—a score that discriminates well is able to efficiently separate dichotomies. For example, survivors get accurately classified as survivors with minimal probability for misclassification as nonsurvivors. Popular tests of discrimination include the area under the Receiver Operating Characteristic (ROC) curve and Harrell’s c-index.60,61 Tests of Goodness-of-Fit—These tests measure the degree of agreement between empirically observed and statistically predicted probabilities. The Hosmer–Lemeshow (HL) statistic is probably used the most, but it has severe limitations.60 Many researchers prefer to graph predicted and observed classes in deciles and compare them visually. Information Criterion Scores—Because models can be compared using different criteria (ROC, HL, etc.) that may disagree among themselves as to which model is preferred it is desirable to have a mathematically consistent approach to comparing models. Based upon the work of Kullback and Leibler, it is possible to measure the distance between any two models in terms of the amount of information contained in each model.62 In order to compare two models of a system (say, two models predicting death from trauma), it is enough to measure the Kullback–Leibler distance from each putative model to the “true model.” The “true model” is never known (of course, otherwise we would have no interest in modeling it), but by means of a mathematically rigorous sleight of hand it is possible to substitute another measure of information content, the Akaike Information Criterion (AIC), for the Kullback–Leibler distance and avoid the need to explicitly specify the true model.60 Fortuitously, the AIC is a simple function of the likelihood function (available from all standard statistical software) and the number of parameters estimated for the model of interest, and is thus straightforward to calculate. Once the AICs for each model are available, it is a simple matter to order them and to further assign probabilities to each model as to the likelihood that it is, in fact, the true model.63

Injury Severity Scoring and Outcomes Research

REFERENCES 27. 28. 29. 30. 31. 32. 33. 34. 35. 36.

37. 38. 39. 40. 41.

42. 43. 44. 45. 46. 47. 48. 49. 50. 51. 52. 53.

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1. Breasted JH. The Edwin Smith Surgical Papyrus: Published in Facsimile and Hieroglyphic Transliteration with Translation and Commentary in Two Volumes. Chicago, IL: The University of Chicago Press, Oriental Institute Publications; 1930. 2. Kane RL. Understanding Health Care Outcomes Research. 2nd ed. Jones & Bartlett; 2005. 3. Iezzoni LI. Risk Adjustment for Measuring Healthcare Outcomes. 3rd ed. Health Administration Press; 2003. 4. Rating the severity of tissue damage. I. The abbreviated scale. JAMA. 1971;215(2):277–280. 5. Association for the Advancement of Automotive Medicine, Committee on Injury Scaling. The Abbreviated Injury Scale 2005. Des Plains, IL: Committee on Injury Scaling; 2005. 6. AAAM. Abbreviated Injury Scale (AIS) 2005-Update 2008. 1st ed. AAAM; 2008. 7. Organization WH. International Statistical Classification of Diseases and Health Related Problems (The) ICD-10. 2nd ed. World Health Organization; 2004. 8. Association AM. International Classification of Diseases 9th Revision Clinical Modification ICD-9-Cm 2001. Volumes 1 and 2. AMA Press; 2000. 9. Baker SP, O’Neill B, Haddon W, Long WB. The injury severity score: a method for describing patients with multiple injuries and evaluating emergency care. J Trauma. 1974;14(3):187–196. 10. Linn S. The injury severity score—importance and uses. Ann Epidemiol. 1995;5(6):440–446. 11. Copes WS, Champion HR, Sacco WJ, et al. Progress in characterizing anatomic injury. J Trauma. 1990;30(10):1200–1207. 12. Kilgo PD, Meredith JW, Hensberry R, Osler TM. A note on the disjointed nature of the injury severity score. J Trauma. 2004;57(3): 479–485; discussion 486–487. 13. Osler T, Baker SP, Long W. A modification of the injury severity score that both improves accuracy and simplifies scoring. J Trauma. 1997;43(6): 922–925; discussion 925–926. 14. Osler T, Rutledge R, Deis J, Bedrick E. ICISS: an international classification of disease-9 based injury severity score. J Trauma. 1996; 41(3):380–386; discussion 386–388. 15. Meredith JW, Kilgo PD, Osler TM. Independently derived survival risk ratios yield better estimates of survival than traditional survival risk ratios when using the ICISS. J Trauma. 2003;55(5):933–938. 16. Meredith JW, Kilgo PD, Osler T. A fresh set of survival risk ratios derived from incidents in the National Trauma Data Bank from which the ICISS may be calculated. J Trauma. 2003;55(5):924–932. 17. Kilgo PD, Osler TM, Meredith W. The worst injury predicts mortality outcome the best: rethinking the role of multiple injuries in trauma outcome scoring. J Trauma. 2003;55(4):599–606; discussion 606–607. 18. Sacco WJ, MacKenzie EJ, Champion HR, Davis EG, Buckman RF. Comparison of alternative methods for assessing injury severity based on anatomic descriptors. J Trauma. 1999;47(3):441–446; discussion 446–447. 19. Meredith JW, Evans G, Kilgo PD, et al. A comparison of the abilities of nine scoring algorithms in predicting mortality. J Trauma. 2002;53(4): 621–628; discussion 628–629. 20. Harwood PJ, Giannoudis PV, Probst C, et al. Which AIS based scoring system is the best predictor of outcome in orthopaedic blunt trauma patients? J Trauma. 2006;60(2):334–340. 21. The American Association for the Surgery of Trauma. AAST Injury Scoring Scale Resource for Trauma Care Professionals. Available at: http://www.aast. org/Library/TraumaTools/InjuryScoringScales.aspx. Accessed March 19, 2010. 22. Moore EE, Shackford SR, Pachter HL, et al. Organ injury scaling: spleen, liver, and kidney. J Trauma. 1989;29(12):1664–1666. 23. Moore EE, Cogbill TH, Malangoni MA, et al. Organ injury scaling, II: pancreas, duodenum, small bowel, colon, and rectum. J Trauma. 1990;30(11):1427–1429. 24. Moore EE, Cogbill TH, Jurkovich GJ, et al. Organ injury scaling. III: chest wall, abdominal vascular, ureter, bladder, and urethra. J Trauma. 1992;33(3):337–339. 25. Moore EE, Malangoni MA, Cogbill TH, et al. Organ injury scaling. IV: thoracic vascular, lung, cardiac, and diaphragm. J Trauma. 1994;36(3): 299–300. 26. Moore EE, Jurkovich GJ, Knudson MM, et al. Organ injury scaling. VI: extrahepatic biliary, esophagus, stomach, vulva, vagina, uterus

(nonpregnant), uterus (pregnant), fallopian tube, and ovary. J Trauma. 1995;39(6):1069–1070. Moore EE, Malangoni MA, Cogbill TH, et al. Organ injury scaling VII: cervical vascular, peripheral vascular, adrenal, penis, testis, and scrotum. J Trauma. 1996;41(3):523–524. Teasdale G, Murray G, Parker L, Jennett B. Adding up the Glasgow Coma Score. Acta Neurochir Suppl (Wien). 1979;28(1):13–16. Segatore M, Way C. The Glasgow Coma Scale: time for change. Heart Lung. 1992;21(6):548–557. Healey C, Osler TM, Rogers FB, et al. Improving the Glasgow Coma Scale score: motor score alone is a better predictor. J Trauma. 2003; 54(4):671–678; discussion 678–680. Champion HR, Sacco WJ, Carnazzo AJ, Copes W, Fouty WJ. Trauma score. Crit Care Med. 1981;9(9):672–676. Champion HR, Sacco WJ, Copes WS, et al. A revision of the Trauma Score. J Trauma. 1989;29(5):623–629. Oyetunji T, Crompton JG, Efron DT, et al. Simplifying Physiologic Injury Severity Measurement for Predicting Trauma Outcomes1. J Surg Res. 2010;159(2):627–632. Knaus WA, Draper EA, Wagner DP, Zimmerman JE. APACHE II: a severity of disease classification system. Crit Care Med. 1985;13(10):818–829. McAnena OJ, Moore FA, Moore EE, et al. Invalidation of the APACHE II scoring system for patients with acute trauma. J Trauma. 1992;33(4): 504–506; discussion 506–507. Rutledge R, Fakhry S, Rutherford E, Muakkassa F, Meyer A. Comparison of APACHE II, Trauma Score, and Injury Severity Score as predictors of outcome in critically injured trauma patients. Am J Surg. 1993;166(3): 244–247. Aslar AK, Kuzu MA, Elhan AH, Tanik A, Hengirmen S. Admission lactate level and the APACHE II score are the most useful predictors of prognosis following torso trauma. Injury. 2004;35(8):746–752. Dossett LA, Redhage LA, Sawyer RG, May AK. Revisiting the validity of APACHE II in the trauma ICU: improved risk stratification in critically injured adults. Injury. 2009;40(9):993–998. Morris JA, MacKenzie EJ, Edelstein SL. The effect of preexisting conditions on mortality in trauma patients. JAMA. 1990;263(14):1942–1946. Byrnes MC, McDaniel MD, Moore MB, Helmer SD, Smith RS. The effect of obesity on outcomes among injured patients. J Trauma. 2005;58(2):232–237. Needham DM, Scales DC, Laupacis A, Pronovost PJ. A systematic review of the Charlson Comorbidity Index using Canadian administrative databases: a perspective on risk adjustment in critical care research. J Crit Care. 2005;20(1):12–19. Gabbe BJ, Magtengaard K, Hannaford AP, Cameron PA. Is the Charlson Comorbidity Index useful for predicting trauma outcomes? Acad Emerg Med. 2005;12(4):318–321. Bergeron E, Rossignol M, Osler T, Clas D, Lavoie A. Improving the TRISS methodology by restructuring age categories and adding comorbidities. J Trauma. 2004;56(4):760–767. Boyd CR, Tolson MA, Copes WS. Evaluating trauma care: the TRISS method. Trauma Score and the Injury Severity Score. J Trauma. 1987; 27(4):370–378. Champion HR, Copes WS, Sacco WJ, et al. The Major Trauma Outcome Study: establishing national norms for trauma care. J Trauma. 1990; 30(11):1356–1365. Gabbe BJ, Cameron PA, Wolfe R. TRISS: does it get better than this? Acad Emerg Med. 2004;11(2):181–186. Osler TM, Rogers FB, Badger GJ, et al. A simple mathematical modification of TRISS markedly improves calibration. J Trauma. 2002; 53(4):630–634. Kilgo PD, Meredith JW, Osler TM. Incorporating recent advances to make the TRISS approach universally available. J Trauma. 2006;60(5): 1002–1009. Champion HR, Copes WS, Sacco WJ, et al. A new characterization of injury severity. J Trauma. 1990;30(5):539–545; discussion 545–546. WHO|WHO Constitution. Available at: http://www.who.int/governance/ eb/constitution/en/index.html. Accessed March 23, 2010. Lee CN, Ko CY. Beyond outcomes—the appropriateness of surgical care. JAMA. 2009;302(14):1580–1581. Holtslag HR, van Beeck EF, Lindeman E, Leenen LPH. Determinants of long-term functional consequences after major trauma. J Trauma. 2007; 62(4):919–927. Schluter PJ, Neale R, Scott D, Luchter S, McClure RJ. Validating the functional capacity index: a comparison of predicted versus observed total body scores. J Trauma. 2005;58(2):259–263.

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54. Iglehart JK. Prioritizing comparative-effectiveness research—IOM recommendations. N Engl J Med. 2009;361(4):325–328. 55. American College of Surgeons: Trauma Programs: National Trauma Data Bank (NTDB). Available at: http://www.facs.org/trauma/ntdb/index. html. Accessed March 22, 2010. 56. Clark DE, Winchell RJ. Risk adjustment for injured patients using administrative data. J Trauma. 2004;57(1):130–140; discussion 140. 57. American College of Surgeons: Trauma Programs: National Trauma Data Bank (NTDB) Trauma Quality Improvement Program (TQIP). Available at: http://www.facs.org/trauma/ntdb/tqip.html. Accessed March 22, 2010.

58. Kutner M, Nachtsheim C, Neter J, Li W. Applied Linear Statistical Models. 5th ed. McGraw-Hill/Irwin; 2004. 59. Hosmer DW, Lemeshow S. Applied Logistic Regression. 2nd ed. WileyInterscience; 2000. 60. Harrell FE. Regression Modeling Strategies. Corrected. Springer; 2001. 61. Hanley JA, McNeil BJ. The meaning and use of the area under a receiver operating characteristic (ROC) curve. Radiology. 1982;143(1):29–36. 62. Kullback S, Leibler R. On information and sufficiency. Ann Math Statist. 1951;22:79. 63. Burnham KP. Model Selection and Multi-Model Inference: A Practical Information-Theoretic Approach. New York: Springer; 2010.

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Acute Care Surgery Gregory J. Jurkovich

The training and scope of practice of today’s trauma surgeon has evolved into a burgeoning field known as acute care surgery. Acute care surgery both defines an advanced surgical training paradigm and describes a type of surgical practice. The history of this evolution is short, and somewhat cyclic. In 1922 Charles L. Scudder, a general surgeon from Boston who had a strong academic interest in fracture management, established the Committee on Fractures within the American College of Surgeons. This early forerunner of today’s Committee on Trauma was composed of 22 fellows of the College, and the work of this committee encouraged the specialization of trauma surgeons and laid the foundation for the modern concept of quality improvement. As the results of physical force injury from wars, motor vehicle crashes, and interpersonal violence fostered the training of “trauma care” during the mid-20th century, the scope of the trauma surgeon encompassed more than fracture management. In 1950 the Regents of the College authorized the current title—the Committee on Trauma—to emphasize this expanding scope of practice.1 Further advancement of a surgical discipline uniquely dedicated to the care of the injured patient in the United States occurred in the 1960s with the establishment of civilian trauma centers. These early trauma centers were almost exclusively within the domain of city–county hospitals in urban areas such as Chicago, Dallas, and San Francisco, but their impact and influence was rapidly spread by devotees of the charismatic leaders of these centers.2 During the ensuing two decades, trauma surgery became an attractive career based largely on the mentorship of trauma surgeons in urban city–county hospitals who epitomized the master technician, and who developed an academically productive career based on the physiology of the injured patient and lessons learned from the Vietnam War. These trauma surgeons operated confidently and effectively in all body cavities, and perhaps were the last of the “master surgeons” that once were the hallmark of general surgery. Operating primarily in large-volume public, “safety net” hospi-

tals, these surgeons were also typically referred the most challenging surgical problems from the surrounding city or region, particularly if there was a financial disincentive to providing care in a private for-profit hospital. As a result, the city–county or “safety net” hospital trauma surgeons developed an active elective and emergency surgical practice while providing trauma coverage and care to the most critically ill and injured surgical patients.3 The academic success of these leading trauma surgeons (Blaisdell, Carrico, Davis, Freeark, Lucas, Ledgerwood, Mattox, Moore, Shires, Feliciano) fostered their incorporation into university hospitals, and the economic viability of civilian blunt trauma care, particularly in no-fault auto insurance states, led to an expansion of trauma programs out of the safety net hospitals and into private hospitals. The American College of Surgeons contributed to the widespread adoption of trauma programs by the remarkably successful and innovated activities of the Committee on Trauma, including hospital verification, the ATLS course, and the National Trauma Data Bank (NTDB). The federal government fostered the “inclusive trauma system” concept and encouraged the widespread development of trauma centers, in large part by reports of high preventable death rates in nontrauma hospitals, and by publications from the prestigious and influential National Research Council that characterized trauma as “the neglected disease” of modern society.4 The result is that today there are over 1,600 trauma centers in the United States, including 203 Level I centers, 271 Level II centers, 392 Level III centers, and 43 pediatric-specific trauma centers,5,6 with 84% of the population within 1 hour of a Level I or II trauma center.7 This remarkable adaptation of regionalized medical care is nearly unique to trauma, and has been fostered by the recognition of the specialty of its care model and the evidence of its survival benefit.8 Yet the attractiveness of this career, and indeed this type of practice, has been challenged and changed by a number of forces. As trauma surgery became more specialized and expanded

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out of the domain of the urban safety net hospital, the trauma surgeon no longer remained the “renaissance surgeon” of the urban/county hospitals of the 1970s. This success may in and of itself have paradoxically led to a declining interest and commitment to the practice of trauma surgery. The requirement of a surgical presence for the resuscitation and early decision making was interpreted by many hospitals (and surgeons) as a preclusion to developing a competitive elective practice, thereby discouraging technically proficient and talented clinicians from accepting such positions. Yet perhaps most importantly, as pointed out in an essay by Gene Moore and his “senior active trauma surgeon colleagues,” a declining interest in trauma surgery as a career was influenced by the loss of operative practice due to a number of factors: the nonoperative management of solid organ injuries, effective injury prevention strategies, the emergence of surgical specialties diverting thoracic and vascular injuries away from trauma surgeons, the explosion of technical capabilities of interventional radiology, and the emergence of surgical critical care as a part and parcel of trauma care.9 These forces challenged the viability of a career in trauma surgery, noted by a lack of interest in a trauma by residents and students toward the end of the 20th century. A number of articles have focused on the perceived lack of interest in any on-call practice, the aging of the trauma surgeon workforce, the focus on “lifestyle” residencies that result in highly remunerative and restricted practices, and concern that trauma surgery was primarily a nonoperative field.10–13 Equally pressing has been the continued and unabated emphasis on specialty training beyond core general surgery training. This is a universal trend in medicine as evidenced by the 145 subspecialty certificates awarded by the 24 member boards of the American Board of Medical Specialties (ABMS).14 The exodus of general surgery trainees into surgical subspecialties has created a void of general surgeons with broad-based training who are capable of providing the expertise needed to continue the type of practice once common in city–county hospitals as well as in many rural communities. Many general surgeons, particularly those in group practices, will “subspecialize” within their group by virtue of additional training. Increasingly, surgical subspecialists exhibit less interest in providing emergency and trauma on-call coverage, often concluding that they “aren’t comfortable” or “don’t feel qualified” to do so. Lifestyle interests and an elective practice volume that does not require taking emergency room call to enhance billing often fuel this attitude. This is a reflection of both a demand in surgical manpower that has not yet been addressed and a tendency of hospitals and surgical departments to acquiesce to this demand in order to attract and retain these lucrative and desirable elective clinical practices. Stitzenberg and Sheldon report that 70% of trainees who complete general surgery residencies pursue further training.15 The greatest interest has been in newer subspecialties, particularly surgical oncology (including breast surgery), endocrine surgery, and “minimally invasive surgery,” which usually includes gastrointestinal and bariatric diseases. In contrast, cardiothoracic surgery and vascular surgery have experienced a decline in interest as evidenced by the marked reduction of applicants to fellowships in these areas and a number of vacant positions in the match. Each of these specialties has had a decline in traditional open

operative caseload primarily because of technological advances. Vascular surgeons have responded to this challenge by adding required training in endovascular techniques to their fellowship programs, and have been rewarded by a renewed interest in resident applicant. Cardiothoracic surgery has chosen to increase its focus on thoracic surgical procedures. There is a common thread here. Specialties that have declining operative caseloads are not as attractive to those interested in a career in surgery.16 In response to these changing social, economic, and demographic forces, a joint meeting of the leadership of the American College of Surgeons, the Association for the Surgery of Trauma (AAST), Eastern Association for the Surgery of Trauma (EAST), and Western Trauma Association (WTA) was held in August 2003, with the AAST taking the lead in considering how to restructure the training and practice of trauma surgery to make it a viable, attractive, and sustainable career, in the best interest of patient care, and, importantly, to keep trauma a surgical care disease. The result was the formation of a working group within the AAST to develop a surgical training curriculum that would be attractive to new trainees, and provide the training for a practice that would be viable, sustainable, and, importantly, in the best interest of the patients.17 Surveys of membership of the major trauma societies of the United States were undertaken to document the factors influencing the thinking of current trauma surgeons in both academic and nonacademic settings.18 The average workweek was 80 hours, with one half reporting mandatory in-house night call. Two thirds (67%) of the respondents care for trauma, surgical critical care, and emergency general surgery while on call. Widely valued and enjoyed by these surgeons were the intellectual challenges and the diverse aspect of a trauma career, but the major disincentives to participating in trauma care were the disproportionately poor income, irregular-hour time demands, and an inadequate trauma operative practice spurred by a preponderance of blunt trauma and interference or prohibition from developing an elective general surgical practice. These practicing trauma surgeons largely felt the best current model of trauma care was a training and practice paradigm that included trauma, surgical critical care, and emergency general surgery, and also allowed the option of an elective surgical practice if desired. They generally endorsed an option to include limited orthopedic and neurosurgical skills such as external fixation of uncomplicated long-bone fractures and ICP monitoring, but only if such specialty coverage was unavailable. They envision the ideal practice model as one involving a group practice at a designated trauma center, supported financially by the hospital and regionalized care. They would not mind mandatory in-house night call if such call was necessary for good care, limited in its frequency, predictable, compensated, and earns the next day off. These results, along with a careful consideration of the needs of society and access to emergency surgical care, result in the development of a recommendation for a new advanced training fellowship to provide the expert surgical workforce to manage trauma and surgical emergencies. The AAST Committee on Acute Care Surgery developed and has promulgated a training curriculum for a specialist that has broad training in elective and emergency general surgery, trauma surgery, and surgical critical care.17 As reflected by the name of this committee, this new

Acute Care Surgery reduced. Finally, in academic centers, the ready availability of an in-house surgical specialist will increase the exposure of medical students and residents to surgical attendings. The acute care surgeon specialist will be filling a niche, which now might be termed a void in our provision of acute surgical care to the American public. This void needs to be filled as many of our surgical specialty brethren are increasingly refusing to participate in the surgical call schedule. Although the field of trauma surgery would benefit from these changes, those who will benefit most are our patients. With this in mind, these changes should be welcome in the future of trauma surgery.9 The Acute Care Surgery Fellowship is also designed to have the flexibility to adapt to the possible shortening of core general surgery training to 4 years, or the concept of early specialization. Early specialization is an attractive option to many surgical specialties (but not all) if the core general surgery training can be adequately defined, and completion or advancement dependent on the accomplishment of measures of competency. This is a distinct change from the paradigm of “immersion” training that has been evident in surgical training for the past 50 years. No longer are the work hours unlimited, no longer is independent experience of residents acceptable, and the operative experience of surgery residents continues to fall. Extensive discussions and the development of the Surgical Council on Resident Education (SCORE) curriculum are a direct response to these changes, and hold the possibility of a competency-based core curriculum for all surgeons, with careful integration into early specialization by limiting core general surgery to 3 or 4 years, followed by self-selected area of concentration.20 This pathway for vascular surgery was approved by the American Board of Surgery (ABS) in 2003.21 The training paradigm of the acute care surgeon would fit well within this construct, with core general surgery followed by 2–3 years of trauma, surgical critical care, and advanced general surgical procedures. The genesis of this concept can be traced to recommendations of some members of American Surgical Association committee on the future of surgical training in 2004 and modified in Fig. 6-1.22 This concept of abbreviated

Core surgery 2-3 years

Verification of competency Specialists in General Surgery lead to board certification

Optional research track

Urban track 3 years

Cardiothoracic

Plastics

Vascular

Rural track 3 years

Transplant

FIGURE 6-1 Proposal for restructured surgical residency training.

Subspecialty in surgery 3 years

Acute care surgery

Pediatrics

Colo-rectal

Surgical oncology

CHAPTER 6

surgical specialist has been called the acute care surgeon. A graduate of these fellowship-training programs is trained for a career in managing acute general surgical problems, providing surgical critical care and managing acute trauma. A group practice of these surgical specialists would allow for rotating coverage, with dedicated time off or protected time for elective practice, administration, or research. The training of this surgical specialist requires core general surgery training, as well as advanced thoracic, vascular, and GI surgery, so as to not just allow but also encourage the development of a diverse elective surgical practice, as local practice patterns permit. It has also been proposed that the acute care surgeon specialist could also perform selected and limited neurosurgical, orthopedic, or interventional radiology procedures, with national and local support from these fellow surgical and interventional specialists, and when such subspecialty coverage is not immediately available. While there has been considerable resistance to this part of the proposal, the fact that many hospitals are having difficulty with surgical emergency coverage argues for its addition.19 Current practicing trauma surgeons find that this new specialty makes sense. The broadened training in thoracic, vascular, and GI operative skills and techniques makes this a more desirable surgical specialty. Further training in these areas is required given the shrinking training time brought on by the limited workweek and the siphoning of advanced operative cases by other fellowship trainees. The option of working on a preset schedule allows for a more controllable lifestyle, and potentially makes this specialty more attractive to surgeon who wishes to take a more active part in childrearing or other family activities. This is more than a “surgical hospitalist” who would only cover the on-call window or take care of the patients of other physicians during undesirable hours; rather, the acute care surgeon could well be seen as the most experienced surgeon for most circumstances in most hospitals, a resource for all the medical staff. Also, since this surgical specialist will most commonly be “in-house” 24 hours a day, the likelihood of significant complications due to lack of an experienced surgeon at night and on weekends will be reduced; thus, the cost of care is likely to be

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core training followed by specialty training ultimately leading to board certification in both general surgery and the specialty of choice is being considered and trialed or considered at this time by thoracic, vascular, and plastic surgery. The ABS has also recently added four new Advisory Councils, including one in Trauma, Burns, and Critical Care, along with Advisory Councils in Surgical Oncology (including breast and endocrine), Transplantation, and Gastrointestinal Surgery (includes endoscopy, hepatobiliary, and bariatric surgery) to provide advise and guidance from these specialty areas,23 and in 2006 the ABS hired Dr Richard H. Bell, Jr, MD, for a newly created administrative leadership role of assistant executive director to specifically facilitate the development of a standardized surgery residency curriculum defined by the SCORE (http://www. surgicalcore.org/). The SCORE is a nonprofit consortium formed in 2006 by the principal organizations involved in US surgical education. SCORE’s mission is to improve the education of general surgery residents (trainees) in the United States through the development of a standard national curriculum

for general surgery residency training. This competency-based curriculum is meant to define the specialty of general surgery and provide greater assurance that residents are receiving sufficient training in all areas. The curriculum design is to focus on the 5 years of progressive education and training, which constitute general surgery residency, but prior to independent practice.24

ACUTE CARE SURGERY CURRICULUM Acute care surgery is an advanced surgical training paradigm (fellowship) that is 2 years in length and follows general surgery training (residency). The outline of this curriculum is presented in Table 6-1. The curriculum includes a dedicated minimum of 9 months of surgical critical care, as mandated for Residency Review Committee (RRC)–approved surgical critical care residencies. Only programs with an RRC-approved surgical critical care training residency can be acute care surgery training programs. The remaining 15 months are focused

TABLE 6-1 Acute Care Surgery Curriculum Length Required clinical rotation Surgical critical care including ● Trauma/surgical critical care, including other relevant critical care rotations ❍ This portion of the fellowship must comply with ACGME requirements for a surgical critical care residency

12 months

Emergency and elective surgery including ● Trauma/emergency surgery

12 months 2–3 months

Total

24 months

Suggested clinical rotations ● Thoracic ● Transplant/hepatobiliary/pancreatic ● Vascular/interventional radiology ● Orthopedic surgery ● Neurological surgery ● Electives ❍ Recommended: burn surgery and pediatric surgery ❍ Also include: endoscopy, imaging, plastic surgery, etc.

2–3 months 2–3 months 2–3 months 1 month 1 month 1–3 months

Total

12 months

Notes to curriculum outline: It is a requirement that over the 2-year fellowship, trainees participate in acute care surgery call for no less than 12 months. Fellows are required to take 52 night calls in trauma and emergency surgery during the 2-year fellowship. 1. Flexibility in the timing of these rotations and the structure of the 24-month training should be utilized to optimize the training of the fellow. 2. Rational for out-of-system rotations for key portions of the training must be based on educational value to the fellow. 3. Acute Care Surgery Fellowship sites must have RRC approval for surgical critical care residency. 4. Experience in elective surgery is an essential component of fellowship training. 5. An academic environment is mandatory and fellows should be trained to teach others and conduct research in acute care surgery.

Acute Care Surgery the clinical challenges of emergency surgery. Limited time is suggested on orthopedics and neurosurgical services, with additional elective time to be allocated to meet the needs of the trainee. The expectation is that trainees will be competent in the management of a wide spectrum of acute care surgical needs, and have specific operative competency in the procedures listed in Table 6-2. Essential elements of the training program will be the operative experience, the presence of an RRC-approved surgical critical care fellowship, and the commitment of the hospital and surgical colleagues to support this new paradigm. The

TABLE 6-2 Operative Management Principles and Technical Procedure Requirements of Acute Care Surgery Fellowship Area/Procedure Airway Cricothyroidotomy Nasal and oral endotracheal intubation including rapid sequence induction Tracheostomy, open and percutaneous Head/face Nasal packing (for complex facial fracture bleeding) ICP monitor Lateral canthotomy Ventriculostomy Neck Exposure and definitive management of vascular and aerodigestive injuries Elective neck dissection Parathyroidectomy Chest Advanced thoracoscopic techniques as they pertain to the described conditions Bronchoscopy: diagnostic and therapeutic for injury, infection, and foreign body removal Damage control techniques Definitive management of empyema: decortication (open and VATS) Diaphragm injury, repair Exposure and definitive management of cardiac injury, pericardial tamponade Exposure and definitive management of esophageal injuries and perforations Exposure and definitive management of thoracic vascular injury Exposure and definitive management of tracheobronchial and lung injuries Pulmonary resections Spine exposure: thoracic and thoracoabdominal Video-assisted thoracic surgery (VATS) for management of injury and infection Partial left heart bypass Repair blunt thoracic aortic injury: open or endovascular Abdomen and pelvis Abdominal wall reconstruction following resectional debridement for infection, ischemia Advanced laparoscopic techniques as they pertain to the described procedures Damage control techniques

Essential

Desirable

X X X X X X X X X X X X X X X X X X X X X X X X X X X (continued)

CHAPTER 6

on operative rotations in emergency and elective surgery, with the expectation that there will be at least 12 months of acute care surgical on-call experience, or a minimum of 52 nights of trauma and emergency general surgery call. The 15 months of operative rotations are as a foundation time spent on an intact, functioning, active Acute Care Surgical service. This is supplemented by three core rotations in thoracic, vascular, and hepatobiliary–pancreatic surgery, with the expectation that these rotations will provide adequate exposure to advanced surgical skills and patient care challenges that often are inadequate in core general surgery training to prepare a surgeon for

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TABLE 6-2 Operative Management Principles and Technical Procedure Requirements of Acute Care Surgery Fellowship (continued)

SECTION 1

Area/Procedure Abdomen and pelvis Exposure and definitive management of duodenal injury Exposure and definitive management of gastric, small intestine and colon inflammation, bleeding, perforation, and obstructions Exposure and definitive management of gastric, small intestine and colon injuries Exposure and definitive management of major abdominal and pelvic vascular injury Gastrostomy (open and percutaneous) and jejunostomy Hepatic resections Management of abdominal compartment syndrome Management of all grades of liver injury Management of pancreatic injury, infection, and inflammation Management of rectal injury Abdomen and pelvis Management of renal, ureteral, and bladder injury Management of splenic injury, infection, inflammation, or disease Pancreatic resection and debridement Exposure and definitive management of major abdominal and pelvic vascular rupture or acute occlusion Management of acute operative conditions in the pregnant patient Management of injuries to the female reproductive tract Place IVC filter Extremities Amputations, lower extremity (hip disarticulation, AKA, BKA, trans-met.) Damage control techniques in the management of extremity vascular injuries, including temporary shunts Exposure and management of lower extremity vascular injuries Exposure and management of upper extremity vascular injuries Fasciotomy, lower extremity Radical soft tissue debridement for necrotizing infection Acute thromboembolectomy Applying femoral/tibial traction Fasciotomy, upper extremity Hemodialysis access, permanent On-table arteriography Reducing dislocations Splinting fractures Other procedures Skin grafting Treatment of hypothermia Lower GI endoscopy Operative management of burn injuries Thoracic and abdominal organ harvesting for transplantation Upper GI endoscopy Pediatric surgical procedures Inguinal hernia repair Trauma management Treatment of bowel obstruction Ventral hernia repair

Essential

Desirable

X X X X X X X X X X X X X X X X X X X X X X X X X X X X X X X X X X X X X X X X

Acute Care Surgery

1. The program should supply the necessary volume and variety of trauma, critical care, and emergency general surgery to assure adequate training of fellows. 2. Each fellow must have ample opportunity and responsibility for the care of patients with acute surgical problems, and the operative experience consistent with developing competency in technical skills and procedures required to provide acute surgical care. 3. Elective general surgery is an essential component of the training of acute care surgeons. 4. Emergency surgical call and trauma call are mandatory components of the training curriculum. Fellows will take a minimum of 52 trauma and emergency surgery night calls during the 2-year fellowship. 5. Elective operative experience in thoracic, vascular, and complex hepatobiliary and pancreatic procedures is encouraged as a means of developing competency in the management of acute surgical emergencies in these anatomic regions. 6. Experience in the diagnosis, management, and operative treatment of neurosurgical and orthopedic injuries is encouraged. 7. Experience with the use of interventional radiology techniques is encouraged. 8. Experience and competency with diagnostic upper and lower GI endoscopy and bronchoscopy are encouraged. Further details on the program requirements and the currently approved acute care surgery training sites can be found on the AAST Web site (http://www.aast.org/Library/AcuteCareSurgery/ Default.aspx). As of mid-2010 there were 7 formally approved training sites, with another estimated 10–20 programs in various stages of considering submitting applications for approved training sites. The AAST Committee on Acute Care Surgery had considered two other options for the future of trauma surgery: (1) de-emphasize the field from surgery, that is, encourage nonsurgeons to assume responsibility for initial care and SICU management (“United Kingdom model”), and (2) expand the discipline of trauma surgery to include more orthopedics (“European model”). The vast majority of current trauma surgeons are unwilling to abandon trauma care to nonsurgical disciplines.18,25 Others, exampled by the writing of Richardson and Malangoni, have argued that the acute care surgeon is a general surgeon, and that trauma training and practice is part of the broader practice of general surgery.16,26–28 Yet the Louisville

group practice of trauma care has closely exemplified the acute care surgeon model, in that their trauma service is designed to include all emergency operations and inpatient consults, and indeed is referred to as “the crucible, where high-volume, highintensity, results matter, life or death decisions are made, and treatment is provided.”29 Additionally, all (trauma) surgeons are encouraged (and supported) to pursue an elective surgical practice. The acute care surgery paradigm is exactly that, where trauma and general surgery together create a specialist that has broad training in elective and emergency surgery, trauma surgery, and surgical critical care.17 A large number of academic urban trauma centers, mostly safety net hospitals, have always employed this model to ensure optimal care of the injured patient—convinced that emergent torso trauma surgery and elective general surgery are inseparable.30 Moreover, this has always been the scope of practice for rural trauma surgeons, and the possibility of Acute Care Surgery Fellowship training that is tailored to the rural trauma surgeon has great appeal.31–33 Likewise, the training of modern military surgeons seems ideally suited to the acute care surgeon model, as exemplified by the incorporation of military surgeons into urban trauma center hospital staffs to expand their clinical operative experience. The options of including surgical skills and patients with some orthopedic and neurological injuries with the domain of the acute care surgeons (option 2 above) has been challenged by the leadership of neurosurgical societies and the Orthopedic Trauma Association. The initial proposals ranged from including decompressive craniotomies for mass lesions from bleeding and ORIF of all long bone fractures to as little as splinting simple fractures, reducing dislocations, and placing ICP monitors. All have been met with significant resistance, which seems incongruous given the data on lack of specialty coverage from many hospitals for exactly this type of care.25,34 While this represents the model of much of European trauma care,35,36 without the support of these leading organizations, the lack of neurosurgical and orthopedic emergency surgical coverage affecting many hospitals will not be solved by acute care surgery. These societies and professional organizations recognized this, and are taking step to encourage regionalization of trauma/ emergency care, and the training and practice interests in trauma/emergency care. The name acute care surgery was chosen carefully. The term surgical hospitalist, no doubt appealing to hospital administrators, was rejected because the connotation of primarily providing surgical care deemed burdensome and undesirable to other surgical disciplines. Emergency surgery is a recent discipline championed in Europe, including a new World Journal of Emergency Surgery. This name, however, was viewed as suboptimal because of the implication that acute surgical care can be relegated to shift work and is limited to patients seen in the ED. Acute care surgery, as with existing trauma surgery, must provide comprehensive patient management from ED arrival to hospital discharge and seamless 24/7 services. In some ways current trauma surgeons are responding to the stresses of health care that are external to the discipline of surgery, and are effecting a change in all fields of medicine. The public, payers, and legislators are expecting improvements in

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curriculum will meet the ACGME requirements for competency-based training, and the evaluation of the fellows’ performance will reflect that expectation. The ABS, along with the RRC and the American Council on Graduate Medical Education, will be considering how all of surgical training might be evolving over this time as well, and specifically how Acute Care Surgery Fellowship training meets the needs of patients, the populations, and trainees. The clinical component of these fellowships includes the following key areas:

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both the process and outcome of care. The expectation of a continuous in-house physician is no longer confined to the emergency room, but extends to the ICU, the trauma team, and the inpatient floors. Yet this expectation of continuous presence is challenged by equally strong expectations of a limited workweek, and a nonsustainable health care budget. The demographics of medicine are changing as well, with more women entering higher education, medical school, and surgery. This changing demographic will inevitably impact the future of surgery. Acute care surgery is part of this evolution.

REFERENCES 1. A.C.o.S.C.o. Trauma, ed. Blue Book: A Guide to Organization, Objectives and Activities of the Committee on Trauma. Chicago: American College of Surgeons; 2005. Available at: http://www.facs.org/trauma/publications/ bluebook2005.pdf. 2. Blaisdell FW. Development of the city–county (public) hospital. Arch Surg. 1994;129(7):760–764. 3. Moore EE. Acute care surgery: the safety net hospital model. Surgery. 2007;141(3):297–298. 4. Division of Medical Sciences, Committee on Trauma and Shock. Accidental Death and Disability: The Neglected Disease of Modern Society. Washington, DC: National Academy of Sciences–National Research Council; 1966. 5. American Trauma Society. Trauma Centers by State or Regional Designation; 2010. Available at: http://www.amtrauma.org/tiep/reports/Designation Status.jsp. Cited July 20, 2010. 6. MacKenzie EJ, Hoyt DB, Sacra JC, et al. National inventory of hospital trauma centers. JAMA. 2003;289(12):1566–1567. 7. Branas CC, MacKenzie EJ, Williams JC, et al. Access to trauma centers in the United States. JAMA. 2005;293(21):2626–2633. 8. MacKenzie EJ, Rivara FP, Jurkovich GJ, et al. A national evaluation of the effect of trauma-center care on mortality. N Engl J Med. 2006:354(4): 366–378. 9. Moore EE, Maier RV, Hoyt DB, Jurkovich GJ, Trunkey DD. Acute care surgery: eraritjaritjaka. J Am Coll Surg. 2006;202(4):698–701. 10. Meredith J, Miller P, Chang M. Operative Experience at ACS Verified Level I Trauma Centers. Cashiers, NC: Halstead Society; 2002. 11. Fakhry SM, Watts DD, Michetti C, Hunt JP; EAST Multi-Institutional Blunt Hollow Viscous Injury Research Grup. The resident experience on trauma: declining surgical opportunities and career incentives? Analysis of data from a large multi-institutional study. J Trauma. 2003;54(1):1–8. 12. Aucar J, Hicks L. Economic modeling comparing trauma and general surgery reimbursement. Am J Surg. 2005;190:932–940. 13. Esposito TJ, Kuby AM, Unfred C, Young HL, Gamelli RL. Perception of differences between trauma care and other surgical emergencies: results from a national survey of surgeons. J Trauma. 1994;37(6):996–1002. 14. American Board of Medical Specialties. 2010. Available at: http://www .abms.org/. Cited July 20, 2010.

15. Stitzenberg KB, Sheldon GF. Progressive specialization within general surgery: adding to the complexity of workforce planning. J Am Coll Surg. 2005;201(6):925–932. 16. Malangoni M. Acute care surgery: the general surgeon’s perspective. Surgery. 2007;141(3):324–326. 17. Committee to Develop the Reorganized Specialty of Trauma Surgical Critical Care and Emergency Surgery. Acute care surgery: trauma, critical care, and emergency surgery. J Trauma. 2005;58(3):614–616. 18. Esposito T, Leon L, Jurkovich G. The shape of things to come: results from a national survey of trauma surgeons on issues concerning their future. J Trauma. 2006;60(1):8–16. 19. Gore L, Huges C. Two-Thirds of Emergency Department Directors Report On-Call Specialty Coverage Problems; 2004. Available at: http://www.acep. org/webportal/Newsroom/NR/general/2004/TwoThirdsofEmergency DepartmentDirectorsReportOnCallSpecialtyCoverageProblems.htm]. Cited February 16, 2006. 20. Lewis FJ. The American Board of Surgery. Bull ACS. 2004;69(4):52–55. 21. American Board of Surgery. Early Specialization Program in Vascular Surgery; 2010. Available at: http://home.absurgery.org/default.jsp? policyesp. Cited July 20, 2010. 22. Pellegrini CA, Warshaw AL, Debas HT. Residency training in surgery in the 21st century: a new paradigm. Surgery. 2004;136(5):953–965. 23. ABS Newsletter. Winter 2005. Available at: http://home.absurgery.org/ default.jsp?newsletter&ref=news. Cited 16 February, 2006. 24. American Board of Surgery News. Philadelphia: American Board of Surgery; 2006. Available at: http://home.absurgery.org/default.jsp? newsdrbell. 25. Esposito TJ, Rotondo M, Barie PS, Reilly P, Pasquale MD. Making the case for a paradigm shift in trauma surgery. J Am Coll Surg. 2006;202(4):655–667. 26. Cheadle WG, Franklin GA, Richardson JD, Polk HC Jr. Broad-based general surgery training is a model of continued utility for the future. Ann Surg. 2004;239(5):627–632 [discussion 632–636]. 27. Richardson JD. Training surgeons to care for the injured: the general surgery model. Bull Am Coll Surg. 1994;79(8):31–37. 28. Richardson JD, Miller FB. Is there an ideal model for training the trauma surgeons of the future? J Trauma. 2003;54(4):795–797. 29. Richardson JD. Trauma centers and trauma surgeons: have we become too specialized? J Trauma. 2000;48(1):1–7. 30. Ciesla DJ, Moore EE, Moore JB, Johnson JL, Cothren CC, Burch JM. The academic trauma center is a model for the future trauma and acute care surgeon. J Trauma. 2005;58(4):657–661 [discussion 661–662]. 31. Finlayson SR. Surgery in rural America. Surg Innov. 2005;12(4): 299–305. 32. Hunter J, Deveny K. Training the rural surgeon. Bull Am Coll Surg. 2003;88(5):13–17. 33. Cogbill T. What is a career in trauma. J Trauma. 1996;41(2):203–207. 34. Esposito TJ, Reed RL 2nd, Gamelli RL, Luchette FA. Neurosurgical coverage: essential, desired, or irrelevant for good patient care and trauma center status. Ann Surg. 2005;242(3):364–370 [discussion 370–374]. 35. Goslings JC, Ponsen KJ, Luitse JS, Jurkovich GJ. Trauma surgery in the era of non-operative management: the Dutch model. J Trauma. 2006;61:111–115. 36. Allgower M. Trauma systems in Europe. Am J Surg. 1991;161:226–229.

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GENERALIZED APPROACHES TO THE TRAUMATIZED PATIENT

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Prehospital Care Jeffrey P. Salomone and Joseph A. Salomone III

Critically injured patients must receive high-quality care from the earliest postinjury moment to have the best chance of survival. Most trauma victims first receive health care from the emergency medical services (EMS) system, which is responsible for rendering aid and transporting the trauma patient to an appropriate facility. The practice of medicine in the prehospital setting presents numerous challenges not encountered in the hospital. Hazardous materials along with environmental and climatic conditions may pose dangers to rescuers as well as to patients. If the patient is entrapped in a mangled vehicle or a collapsed building, there must be meticulous coordination of medical and rescue teams. Providers of prehospital care are expected to deliver high-quality medical care in situations that are austere and unforgiving and, often, for prolonged periods. The role of the EMS system is far more complex than simply transporting the trauma victim to a medical facility. In most EMS systems in the United States, specially trained health care professionals are responsible for the initial assessment and management of the injured patient. Experience from the last several decades has shown that these paraprofessionals can safely perform many of the interventions that were previously performed only by physicians or nurses in the emergency department. While many of these procedures have proven beneficial for victims of cardiac emergencies, critically injured patients may need two items not available on an ambulance—blood and a surgeon. As EMS systems mature and additional prehospital care research is conducted, the question is no longer, “What can the Emergency Medical Technician (EMT) do for the trauma patient in the prehospital setting?” but rather, “What should the EMT do?”

HISTORICAL PERSPECTIVE While the roots of prehospital trauma care can be traced back to military physicians, modern civilian prehospital trauma

care began about four decades ago. J.D. “Deke” Farrington and Sam Banks instituted the first trauma course for ambulance personnel in 1962.1 This course, initiated with the Chicago Committee on Trauma and the Chicago Fire Academy, marked the beginning of formal training in prehospital care of injured patients. Farrington is generally acknowledged as the father of modern EMS.2 In September, 1966, the National Academy of Sciences and National Research Council published the landmark monograph, Accidental Death and Disability: The Neglected Disease of Modern Society.3 This document argued that there were no standards for ambulances with respect to design, equipment, or training of personnel. As a direct result of this monograph, the Department of Transportation funded the development of the Emergency Medical Technician–Ambulance (EMT-A) curriculum, which was published in 1969. Continued public pressure resulted in the passage of the Emergency Medical Services (EMS) Systems Act of 1973 (PL 93-154). This act revolutionized EMS in this country and resulted in federal funding for the establishment of EMS systems. In the late 1960s, Pantridge, an Irish physician practicing in Belfast, developed a mobile coronary care unit that was staffed by physicians.4 He conceived of a system in which the victim of an acute myocardial infarction was stabilized at the scene by bringing advanced life support (ALS) to the patient. The physicians worked to restore normal cardiac rhythm through medications and defibrillation at the location where the victim was stricken. In the United States, the concept of advanced prehospital care involved training emergency medical technicians (EMTs) to perform these lifesaving skills. The original “paramedic” programs began in Los Angeles, California; Houston, Texas; Jacksonville, Florida; and Columbus, Ohio; and were often associated with fire departments. Paramedics were trained to serve as the “eyes and ears” of the physicians in their base hospitals and provide care under their direction.

Prehospital Care

EMERGENCY MEDICAL SERVICES SYSTEM The modern EMS system involves the integration of a number of complex components. Essential elements include the following: personnel, equipment, communications, transport modalities, medical control, and an ongoing quality improvement process. Different configurations of EMS systems result when these components are integrated in varying combinations. The EMS system represents a significant component of the trauma system, described elsewhere (see Chapter 4). The Department of Transportation, through the EMS Office of the National Highway Traffic Safety Administration, provides federal leadership for the EMS system. With input from national stakeholder organizations, NHTSA developed the EMS Agenda for the Future, published in 1996.14 This document detailed a vision for improving 14 aspects of EMS including the following: integration of health services, EMS research, legislation and regulation, system finance, human resources, medical direction, education systems, public education, prevention, public access, communication systems, clinical care, information systems, and evaluation. Two related documents that expand on concepts addressed in the original Agenda are the EMS Education Agenda for the Future: A Systems Approach (2000) and the National EMS Research Agenda (2001).15,16

retained the original 1985 curriculum. The Blueprint divided the major areas of prehospital instruction into 16 “core elements.” For each core element, there are progressively increasing knowledge and skill objectives, representing a continuum of education and practice. A National Standard Curriculum (NSC) provided lesson plans for each level. With the publication of the EMS Education Agenda for the Future, the foundation was laid to replace the NSC with a system that would hopefully standardize EMS training and certification across the country. This system is based on a medical model that includes a defined scope of practice, accredited education programs, certifying exams that assure baseline competency, and licensure to permit one to practice. Three of the five components of this system focus on the levels and education of EMS providers, and each had input from national stakeholder organizations and the public during its development: National EMS Core Content. Published in 2005, this document describes the domain of prehospital care, identifying the universal body of knowledge and skills that could potentially be utilized by EMS providers who do not function as independent practitioners.18 National EMS Scope of Practice Model. Published in 2007, this document identifies four new levels of prehospital care practitioners19 (Table 7-1). The knowledge and skills described in the Core Content are divided among the four levels. During the development of the Scope of Practice Model, there was insufficient support in the EMS and medical communities to support the development of a fifth level of EMS provider with a scope of practice greater than that of the paramedic. National EMS Education Standards. Published in 2009, these standards describe the minimal, entry-level competencies that EMS personnel must achieve for each of the levels described in the Scope of Practice.20 Compared to the NSC, the Education Standards allow for more diverse methods of implementation, more frequent updates of content, and some variation at the state or local level. Each level builds upon the knowledge and skills of the previous level.

■ EMS Personnel EMTs comprise the vast majority of prehospital care providers employed in the United States, and only a small number of nurses and physicians deliver care in the out-of-hospital setting.

Emergency Medical Technicians For more than a decade, the National Emergency Medical Services Education and Practice Blueprint, published by NHTSA in 1993, provided the basis for the levels and training of EMTs utilized in the United States.17 The four levels of EMTs described in the document are the First Responder, EMT-Basic, EMT-Intermediate (EMT-I), and EMT-Paramedic. An enhanced EMT-I level was introduced in 1999, but many states

TABLE 7-1 EMS Provider Levels National EMS Standard Curricula First Responder (FR) Emergency Medical Technician-Basic (EMT-B) Emergency Medical Technician-Intermediate (EMT-I) Emergency Medical Technician-Paramedic (EMT-Paramedic)

National EMS Scope of Practice (2007) Emergency Medical Responder (EMR) Emergency Medical Technician (EMT) Advanced Emergency Medical Technician (AEMT) Paramedic

CHAPTER 7

While prehospital ALS proved beneficial for victims of cardiac emergencies, it was not until the 1980s that it became obvious that definitive care for trauma patients was fundamentally different than that for the cardiac patient. Efforts to restore circulating blood volume proved to be unsuccessful in the face of ongoing internal hemorrhage. The exsanguinating trauma patient requires operative intervention, and any action that delays the trauma patient’s arrival in the operating room is ultimately detrimental to survival. During this period, significant controversy surrounded prehospital ALS for trauma patients as expert panels and editorialists debated its pros and cons.5,6 Several studies documented the detrimental effect of prolonged attempts at field stabilization on seriously injured trauma patients,7–9 while others showed that paramedics could employ ALS measures in an expeditious manner.10–13

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Generalized Approaches to the Traumatized Patient The four levels of prehospital care providers described in this new system are described below.

SECTION 2

Emergency Medical Responder. This level was previously named “First Responder.” Following the terrorist attacks of September 11, 2001, this term now refers to those who are the initial responders to emergencies and could include law enforcement personnel or firefighters who may lack medical training. The EMR uses a limited amount of equipment to perform initial assessment and rudimentary intervention until EMS providers with a higher level of training arrive at the scene. Skills utilized by the EMR include oral airways, suctioning, automated external defibrillators, cardiopulmonary resuscitation (CPR), oxygen therapy, hemorrhage control, and manual stabilization of the spine and injured extremity. New skills included at the EMR level that were not taught in the FR include measurement of blood pressure, eye irrigation, and use of a bag-valve mask (BVM) device and auto-injectors for self or peers. Emergency Medical Technician. Previously termed the EMT-Basic, the EMT has greater knowledge and skills than the first responder and holds the minimum qualifications to staff an ambulance. The EMT possesses expanded assessment skills and is trained to perform spinal immobilization and splinting, assist with uncomplicated childbirth, and use limited medications (oral glucose, sublingual nitroglycerine, and subcutaneous epinephrine). Compared to the EMT-Basic, the new EMT is trained to use more types of oxygen masks, automated transport ventilators, auto-injectors, and oral administration of aspirin. Advanced EMT. In the current system, the EMT-I is the least well defined of all the levels of EMS providers, as training requirements and skills vary widely from state to state. The AEMT replaces both the versions of the EMT-I, although the AEMT is closer to the scope of practice of the 1999 EMT-I than to the 1985 version. Additional time is devoted to acquiring a more in-depth knowledge of pathophysiology, advanced techniques of patient assessment, and advanced skills for airway management, but not endotracheal intubation. The AEMT is trained in intravenous access and can perform fluid resuscitation with crystalloid solutions. Medications an AEMT may administer include epinephrine, glucagon, 50% dextrose, naloxone, and inhaled beta-agonists and nitrous oxide. Paramedic. In addition to the knowledge and skills of the previous levels, the paramedic is trained in the use of a wider range of medications and the performance of a greater number of advanced skills. The scope of practice of the EMTParamedic includes endotracheal intubation, needle decompression of the pleural cavity, cardiac monitoring and interpretation of arrhythmias, and administration of numerous medications. The paramedic has had a major impact on the resuscitation of patients with cardiac or major medical problems and is very effective in urban areas in which response times are short. Compared to the EMT-Paramedic, the new paramedic is trained to administer continuous positive airway pressure (CPAP), monitor and manage chest

tubes, access indwelling venous devices, perform eye irrigation using a Morgan lens, initiate and monitor thrombolytic agents, and perform analysis of limited blood chemistry utilizing portable devices. Education and Certification of EMS Personnel. In addition to the three components of the EMS Education Agenda for the Future described above, the two additional elements that complete this system of EMS education are national certification and national accreditation of paramedic training programs. National EMS Certification. In medical practice, certification exams serve to protect the public by ensuring that practitioners have minimal, entry-level competency on entering the workforce. Traditionally, individual states have offered certification exams for their EMS personnel, but this results in issues related to cost for test development, legal challenges, and reciprocity as EMS providers move from one state to another. The National Registry of EMTs (NREMT), a nonprofit organization founded in 1970, has emerged as the only national entity that offers certification exams for all recognized EMS levels. Through its careful test development, NREMT offers psychometrically sound, legally defensible examinations that states may use for licensure of their EMS personnel. Currently, 45 states utilize the NREMT examination process. While current exams are based on the National Standard Curricula, NREMT will phase in new exams based on the National EMS Scope of Practice Model between 2011 and 2013. National EMS Education Program Accreditation. The Committee on Accreditation of EMS Programs (CoAEMSP), also a nonprofit corporation, is the only organization that offers accreditation of paramedic training programs on a national basis. CoAEMSP itself is accredited by the Commission on Accreditation of Allied Health Education Programs (CAAHEP). Established in 1994, this group had its origins as the Council on Medical Education of the American Medical Association. CoAEMSP utilizes a combination of self and peer assessment to a set of defined standards that ensure a quality educational experience for the student. While some states require that all paramedic training programs be approved by CoAEMSP, many states have no such requirements. In fact, EMS (i.e., paramedic) is the only allied health profession that does not require graduation from an accredited program in order to work in the field. One recent study demonstrated that graduates of accredited paramedic programs are more likely to successfully achieve certification by the NREMTs.21 For these reasons, the NREMT will require applicants for the paramedic certification exam to have graduated from an accredited education program after January 1, 2013.

Nurses Nurses occupy a unique position in the EMS system. They serve as prehospital providers, instructors, and proctors of quality improvement. While nursing education imparts an excellent

Prehospital Care patients in the prehospital setting. In such situations, the physician should realize that the vast majority of EMTs are well trained and capable of performing their job and that they work under the medical direction of a licensed physician. Additionally, should the physician begin to direct care for a patient, he or she must remain with the patient until care is formally transferred over to an accepting physician, either by radio communication or by face-to-face turnover in the emergency department. Failure to do so may constitute abandonment of the patient and leave the physician exposed to serious legal repercussions.

Ground Nurses. When dual trained as a nurse and an EMT, the individual can function in the field as a prehospital provider under the auspices of EMT certification. Nurses are utilized by many critical care transport services to assist in the care of special patients (e.g., neonatal and cardiac). In this context, nurses can function to the extent of their training, abilities, and license restrictions. Most states have not developed standards for the prehospital role of nurses. Because of the paucity of trained EMTs, nurses often serve as ambulance attendants in foreign countries.

■ SYSTEM DESIGN

Flight Nurses. Almost all air medical services in the United States utilize nurses in the delivery of prehospital care and transport. The composition of the flight crews varies widely, and common configurations are two nurses, a nurse and a paramedic or EMT, or a physician with either a nurse or paramedic. In this context, nurses are limited in their roles just as in ground transport. They provide important knowledge and skills in critical care, but need to be paired with a partner who is licensed to perform in the prehospital arena in most states. Nurses who are dual trained as both an EMT and a nurse can provide care in the prehospital phase as dictated by their EMS certification and license.

Physicians In the United States, it is unusual for physicians to directly participate in the provision of care to the injured patient in the field, although some air medical services utilize physicians as members of their flight crew. The physicians assigned to such crews are usually emergency medicine residents who rotate onto the aircraft as a formal part of their residency. Another use of physicians in the prehospital setting involves neonatologists or pediatric residents or fellows who staff units used for interfacility transport of critically ill infants. In Europe and Central and South America it is common for physicians to function as primary members of the EMS team. Because of a surplus of physicians or a lack of attractive employment opportunities, physicians may work for an EMS service, either staffing an ambulance or responding in a separate vehicle. The standards of EMT training in the United States suggest that little is gained by employing physicians on EMS units, and this use of a valuable resource in the field is a challenging one to defend. Physicians who happen upon the scene of a motor vehicle crash may be tempted to assume control of the patient despite the fact that they possess little experience caring for

Prior to the early 1970s, EMS in the United States were very rudimentary and focused primarily on transportation of patients. Actual medical care began only after the patient’s arrival at the hospital. Today, numerous models of EMS systems exist, as the various elements of the system are combined in different ways. No definitive evidence exists that one model is superior in performance to any other, and community leaders design their system around the available resources in the community. An EMS service may be operated by a private company, a hospital, a fire department, a police department, or an agency funded by the government that is solely responsible for emergency medical care (a public “third service”). Regardless of which agency provides EMS, prehospital care generally fits into one of two distinct categories, that is, basic life support (BLS) and ALS.22

Basic Life Support BLS is a term used to describe a level of care that provides noninvasive emergency care and includes care rendered by personnel trained at the EMR and EMT levels. While EMRs may drive an ambulance, the minimum level for providing patient care during transportation should be the EMT. BLS involves providing basic airway management, supplemental oxygen, and rescue breathing; CPR; control of external hemorrhage; splinting; spinal immobilization; and uncomplicated childbirth. The goal of BLS care is to maintain breathing and circulation and transport the patient without causing further harm. Many BLS services utilize automatic or semi-automatic external defibrillators (AEDs) that identify ventricular fibrillation and deliver electrical countershocks. Because of the limited equipment and training, BLS systems are less costly to establish and maintain than are more advanced levels of care.

Advanced Life Support ALS describes care that involves the use of more advanced, invasive procedures such as those performed by personnel in an emergency department. EMS providers at the ALS level are capable of advanced airway management, cardiac monitoring and defibrillation, insertion of intravenous lines, and administration of numerous medications. ALS systems utilize individuals trained at the AEMT or paramedic level. In contrast to BLS systems, ALS systems provide advanced therapy to the patient at the scene, rather than waiting until arrival at a hospital to institute care. ALS systems have had

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understanding of patient assessment, the pathophysiology of disease processes, and administration of medications, most nursing programs do not teach many of the skills necessary for prehospital care. This includes splinting, spinal immobilization, and advanced airway management, so dual training is often required to function in the EMS setting. Nurses may also be employed by EMS services as on-site instructors for continuing education and may be utilized as field observers for quality improvement. They can provide insight to the EMTs on the smooth integration of patient care from the field to the emergency department.

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impressive results in the care of cardiac patients, especially when CPR is started within 4 minutes of a cardiopulmonary arrest and ALS can be initiated within 8 minutes of the arrest. These types of systems, however, are very expensive to establish and maintain, primarily because of the equipment and amount of training required. ALS systems also must invest more in continuing education for their personnel in order to maintain their skills.

Tiered Response Systems An EMS system that is not purely BLS or ALS but a combination of both is called a tiered response system.23 The goal of a tiered EMS system is to match the training level of the provider with the needs of the patient. The first level of care is typically BLS with the providers being from a public safety agency (e.g., fire or police) or EMS units staffed by EMTs. In this model, BLS personnel would initiate transport if the patient did not require ALS procedures. If ALS interventions are needed, the BLS crews initiate basic care and attempt to stabilize the patient until the ALS unit arrives. This allows ALS units to respond only when needed. Proponents of this system argue that it functions in a more cost-effective manner, providing ALS-level care only to those patients who require it. In many communities, especially those in rural settings, a third tier comprised of air medical transport may be utilized. This tier usually provides a slightly higher level of training and expertise, combined with the more rapid transport capabilities of the aircraft.

■ Equipment for EMS Units The American College of Surgeons Committee on Trauma (ACSCOT) joined with the American College of Emergency Physicians (ACEP), the National Association of EMS Physicians, and other organizations to publish a document delineating the necessary equipment that should be stocked on an EMS unit.24 This document includes separate recommendations for both BLS and ALS ambulances. The most recent revision requires EMS units to include sufficient sizes of equipment to adequately care for infants and children in addition to adults. In most jurisdictions, state law mandates the equipment carried by EMS units, and administrative agencies periodically inspect ambulances to ensure that necessary equipment is present. Medical directors may also require that certain equipment or medications be added to units under their direction.

■ Communications Communications comprise an essential component of the EMS system. The EMS dispatch center must be able to readily locate the unit closest to the incident and provide them with an exact location and description of the call. EMS units must also be able to communicate with other agencies that provide first responder care (i.e., law enforcement and fire department) and those that serve an adjunctive role such as extrication and control of hazardous materials. EMS units must also have two-way communication with receiving facilities and with the physicians who provide medical oversight. EMS personnel may request

specific orders from a physician when a patient’s condition falls outside established treatment protocols.

■ Transport Modalities Ground Units EMS units operating on the ground may possess transport capabilities (i.e., an ambulance) or they may be a “quick response” unit that contains only equipment and personnel, and a separate ambulance is required for transport. Such quick response vehicles are common in rural areas or in tiered EMS systems. Ambulances should conform to size and performance specifications as outlined by governmental agencies and authoritative organizations and possess required equipment as described earlier. In areas primarily covered by BLS units, a tiered response arrangement should be in place so that ALS backup is available when needed.22 To qualify as an ALS unit, at least one member of the team must possess training beyond the EMT level. Most commonly, ALS units now are staffed by at least one paramedic, although many ALS services utilize units staffed by two paramedics. Additional equipment and supplies must be available on the ALS unit to support the defined scope of practice.

Rotor-Wing Aircraft Helicopter evacuation of military casualties began during the Korean War and matured during the Vietnam War.25 The improvement noted in survival was largely attributed to the speed of evacuation to facilities capable of providing initial trauma care. Civilian air medical services were established in the United States as a result of the success during wartime and have proliferated throughout the industrialized world. In the United States, helicopter EMS (HEMS) programs are most commonly operated by a private EMS service or are hospital based; however, the Coast Guard, military, law enforcement agencies, or park services may also provide helicopter transport. Crew configurations vary from service to service. The two most common combinations are two flight nurses or a flight nurse and a paramedic. Helicopters are equipped as ALS units and often function as compact intensive care units. HEMS personnel generally have an expanded scope of practice compared to ground EMS providers, including a greater variety of medications and additional skills (e.g., management of an intra-aortic balloon pump, etc.), but only a small portion may be applicable to the care of trauma patients. The typical maximum transport radius for a helicopter is 150 miles. Helicopter transport appears to be beneficial for wilderness rescue and for the transport of critically injured patients from a rural facility with limited resources to a major trauma center.26–30 When outcome for trauma patients transported by HEMS has been studied, conflicting results have been found. While some studies have correlated an improvement in the outcome of victims of blunt trauma transported by helicopter,31–34 other studies have found little or no benefit.26,35,36 Unfortunately, many trauma patients transported by HEMS are not critical and, in many trauma centers, it is not unusual for up to one third of the patients transported by HEMS to be discharged from the emergency department.

Prehospital Care

Fixed-Wing Aircraft Fixed-wing aircraft are constrained by the need for a runway and, therefore, lack the versatility of rotor-wing units that can land at an accident scene or at a trauma center. With the additional time required to transport a patient to and from a local airport, fixed-wing aircraft only become more time-efficient when a patient requires transfer over a distance greater than about 150 miles. Aircraft equipped for air medical transport often serve to transfer patients to regional specialized facilities such as those for burns or spinal cord injuries or to transplant centers. The equipment and supply requirements for fixed-wing aircraft are not as well defined as for ground or rotor-wing units.

■ Performance Improvement Quality medical care is a vital issue in all areas of the health care system. This is attained by developing a small performance improvement (PI) process. PI is an ongoing cycle of evaluation, data collection, interpretation, and modification of the system to improve patient care.41 An EMS service should have its own internal PI program, with oversight by the service medical director. Key aspects of this program include evaluation of the care rendered and monitoring the efficiency of the EMS system. A variety of methods are utilized in order to determine if care is rendered in a timely, efficient, and medically sound fashion. Equipment must be reliable and durable in order to withstand the sometimes harsh conditions associated with the delivery of prehospital care and not contribute to injury. Trauma centers should also evaluate the care of the patients transported to their facilities and provide appropriate feedback to EMS system administrators, medical directors, and field personnel.

System Efficiency The evaluation process for any EMS system must determine the efficiency of all components involved in providing care to the patient. One method of evaluating efficiency of the system is to

review notification time, response time, on-scene time, and transport time. Notification time. This represents the time interval between the injury and notification of the EMS dispatch center. In the United States, most requests for EMS arrive via the 911 phone system. By 2006, 75% of the US population lived in an area covered by enhanced 911 (E911), although that only represents about 50% of the counties in the country.42 Many rural and frontier areas still lack this coverage. E911 is capable of delivering a wireless caller’s number and location to the appropriate Public Safety Answering Point (PSAP). The PSAP may still have to pass information along to the EMS dispatch center. Response time. This is defined as the period that starts when an emergency call is received by the EMS dispatch center and ends with the arrival of the ambulance at the scene. This time frame encompasses several actions as follows: (a) the call must be physically received; (b) the dispatcher must analyze the call and decide on the appropriate response; (c) the ambulance must be contacted and dispatched; and (d) the ambulance must leave its current location and travel to the scene. The final factor, ambulance travel time, is a function of location and availability of the ambulance, weather, and traffic conditions. The desired response time for any system directly impacts the number of ambulances that the system requires. In order to meet the target response times, sufficient EMS units must be available to meet the expected number of emergency calls in the coverage area. While many urban systems have set a response time standard of 8 minutes that must be met 90% of the time, the ideal response time for trauma is unknown. A retrospective study failed to identify an association between shorter EMS response times and improved outcome in trauma patients.43 On-scene time (scene time). This is the interval from the arrival of EMS at the scene until their departure en route to the receiving facility. This time will vary according to environmental conditions, geography of the scene and location, accessibility of the patient, entrapment, injuries present, and requirements for packaging of the patient. When caring for a critically injured patient, the EMS personnel should strive to limit their on-scene time to 10 minutes or less.44 Approximately 85–90% of trauma patients encountered by EMS are not critically injured and, thus, do not require rapid packaging and immediate transport. Continuous monitoring of on-scene times should be performed to ensure that time is not being lost in the performance of unnecessary procedures on patients with severe injuries. Transport time. This is the length of time required to transport the patient from the scene to an appropriate facility. The factors that affect this time are distance from the facility, weather, transport modality (air vs. ground), and traffic conditions, if transported by ground. The choice of a destination facility is an important decision in the care of the critical patient. A patient who requires emergent operative intervention to control hemorrhage

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The benefits of on-scene HEMS response are also debatable in an urban or suburban setting when a well-trained ground EMS service is present and transport times are brief.37,38 A recent study by Diaz et al.39 found that ground transport is always faster than air medical transport when the distance from the scene to the trauma center is 10 miles or less, while helicopter transport is always faster when the scene is more than 45 miles from the trauma center. These findings are not surprising considering the time it takes to power up and power down a helicopter. There is a noteworthy element of risk associated with air medical transport, and a study by Bledsoe and Smith40 documented a steady and marked increase in the number of crashes of medical helicopters over the decade of 1993–2002. This trend has continued at an alarming rate since that study was published, resulting in significant loss of life of both patients and the air medical crews. For all these reasons, increasing controversy surrounds the utility of HEMS for transportation of injured patients in the civilian setting.

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should be taken to a hospital staffed and equipped to move the patient to the operating room immediately, if such a facility is available. PI reviews should address these issues in an ongoing manner.

Care Rendered The medical director and leadership of an EMS service must be able to objectively review the care rendered by the personnel they supervise. Evaluation of medical care can be separated into prospective, concurrent, and retrospective phases. Prospective evaluation. This form of evaluation attempts to improve the level of care rendered prior to the actual delivery of the care. Evaluating continuing education programs and periodic assessment of skills are examples of prospective evaluation tools. Concurrent evaluation. Concurrent evaluation involves direct observation of the EMS personnel during the delivery of care. The medical director or a designated member of the staff of the EMS system (e.g., field training officer) accompanies the crew in order to observe the delivery of care in the field. Trauma surgeons may also evaluate the EMS personnel’s assessment and care as they deliver patients to their facility. Steps can be taken immediately to correct deficiencies and improve patient care. Retrospective evaluation. Retrospective evaluation occurs after care has been delivered. This form of review is the easiest and least costly of the methods and comprises chart audits, case reviews, and debriefings to review the events of any particular EMS call. Trauma surgeons should participate in the retrospective evaluation of EMS services that transport patients to their facility. Such involvement helps EMS providers gain perspective into the entire spectrum of trauma care. Examples of audit filters that may be utilized to evaluate prehospital care are shown in Table 7-2.

■ Medical Control One of the most important relationships in EMS is that between the prehospital providers and the physician. In the United States, EMS personnel practicing at the ALS level can

TABLE 7-2 Audit Filters for Prehospital Trauma Care Lack of adequate airway Misplaced endotracheal tube Hypoxia (SpO2  90%) Inability to control external hemorrhage (i.e., no tourniquet for extremity) Spinal immobilization for penetrating torso trauma Scene time 10 min for critical patient Appropriateness of needle decompression of pleural cavity Failure to transport critical patient to closest appropriate facility

be thought of as physician extenders.45 While State EMS offices issue licenses to prehospital care providers, they are not allowed to function independently and function under the auspices of their medical director. Thus, EMS personnel perform under delegated practice, which is typically described in the Medical Practice Act in state law. Numerous terms have been applied to the association between EMS providers and the supervising or responsible physicians, including medical control, medical direction, and medical oversight. Medical direction of an EMS system is provided in a variety of fashions that differ from region to region. In some systems a single physician provides medical direction, and, in other circumstances, medical direction is carried out by a group of physicians acting collectively through a consensus process. In 1986, Holroyd et al.46 recommended that the EMS medical director be a physician with the following qualifications: (a) knowledge and demonstrated ability in planning and operation of prehospital EMS systems; (b) experience in the prehospital provision of emergency care for acutely ill or injured patients; (c) experience in the training and ongoing evaluation of all levels of participants in the prehospital care system; (d) knowledge and experience in the application of medical control to an EMS system; and (e) a knowledge of the administrative and legislative processes affecting regional and/ or state prehospital EMS systems. The medical director must be interested in and committed to the day-to-day activities of the EMS service. The role of medical director for an EMS service is not limited to emergency physicians, and trauma/critical care surgeons are well suited to function in this role once they have gained the prerequisite knowledge of how EMS systems function. The National Association of EMS Physicians has developed a workshop for EMS medical directors. Medical control is divided into two categories including indirect (off-line/protocols) and direct (on-line).47

Indirect (Off-Line/Protocols) This form of medical direction involves the development of written protocols and the review of EMT performance. The amount of time required to accomplish these administrative duties varies with the size and complexity of the particular EMS system. The medical director’s review of care is a PI function and has been discussed previously. Protocols are the overall steps in patient management that are to be followed by the prehospital provider at every patient contact. As an accurate diagnosis is often not possible in the field, protocols are usually developed based on the patient’s complaints or condition. For ease of memorization and integration with those of other conditions, many protocols are designed in an algorithmic fashion. Trauma surgeons should participate in the development of EMS protocols regarding care for injured patients in their region.

Direct (On-Line) Direct or on-line medical control by the medical director is clinical in nature.48 This form of direction involves providing

Prehospital Care

TRAUMA EDUCATION FOR EMS PERSONNEL Two continuing education courses have been developed to provide EMS personnel with the essential knowledge and skills to manage critically injured patients. Both courses have been promulgated nationally and internationally.

■ Prehospital Trauma Life Support The Prehospital Trauma Life Support (PHTLS) program was developed by the National Association of EMTs in cooperation with the ACSCOT.44 The PHTLS course is based on the tenets of the Advanced Trauma Life Support course developed by ACSCOT, but has been modified to meet the needs of the patient in the prehospital setting.50 The central philosophy of the PHTLS course is that EMS providers, when given an appropriate fund of knowledge, can make appropriate decisions regarding patient care. Thus, the course emphasizes “principles” of management, rather than focusing on individual preferences or protocols. A new edition of the course is produced every 4 years, 1 year after the revised ATLS course has been released. This strategy guarantees that PHTLS continues to disseminate any changes in treatment or philosophy that have been introduced in ATLS and ensures a seamless interface between the prehospital providers and personnel in the emergency department in the initial management of the trauma patient. PHTLS is currently taught throughout the United States and in almost 50 foreign countries.

■ International Trauma Life Support About the same time that PHTLS was developed by NAEMT, the Alabama Chapter of the ACEP developed the Basic Trauma Life Support course.51 The course was subsequently transitioned to BTLS International, a not-for-profit organization, and, in 2005, the name was changed to International Trauma Life Support (ITLS). Like PHTLS, ITLS is also based on the philosophies of ATLS and taught both in the United States and internationally.

ASSESSMENT AND MANAGEMENT Assessment and management of the injured patient in the prehospital setting should proceed in an orderly manner, despite the fact that the EMT must frequently make rapid decisions

about patient care under adverse conditions. While the general approach is based on that taught in the ATLS course, one important modification is that the EMT first performs a “scene assessment” prior to evaluating an individual patient. Next, a “primary survey” is conducted to identify life-threatening conditions and initiate immediate therapy. At the end of the primary survey the EMT considers whether life-threatening or potentially life-threatening injuries have been identified. If so, the patient is expeditiously packaged and transported to the closest appropriate facility. Definitive care for severe, uncontrolled internal hemorrhage cannot be provided in the field, and surgery is usually required. Interventions such as direct pressure on a bleeding wound and infusion of intravenous fluids are not substitutes for rapid transportation to an appropriate facility with immediate surgical capabilities.

■ Assessment of the Scene In the prehospital setting, assessment of the patient actually begins before reaching the patient’s side. As an EMS crew is dispatched to a scene, they begin to consider numerous factors that may play a role in caring for the patient, as well as ensuring their safety and that of the patient. These factors include such things as mechanism of injury, environmental conditions, and hazards present at the scene. The important aspects of this assessment can be divided into the following two key categories: safety/standard precaution and situation.

Safety/Standard Precaution Prehospital personnel must first evaluate the safety of the scene. EMS must not enter into a situation that puts their health and well-being at risk as this puts them in jeopardy of becoming patients as well. EMS workers are dependent on law enforcement personnel to ensure that the scene has been cleared of violent assailants and their weapons. In addition to their personal safety, the EMS providers need to consider concerns that threaten the safety of the patient. The scene of a traumatic incident may include dangers such as traffic, downed power lines, hazardous materials, and harsh environmental conditions. In light of incidents of terrorism there is heightened concern of chemical, biological, or nuclear contamination of a scene, or secondary devices planted with the intent of killing rescuers. Standard Precautions. One hazard ubiquitous to virtually all trauma scenes is blood. Blood and other body fluids may contain communicable diseases including hepatitis and human immunodeficiency viruses. In any patient encounter, health care workers are encouraged to employ measures to decrease the risk of contracting these pathogens. Standard precautions involve the use of impermeable gloves, gowns, masks, and goggles. In addition to wearing this protective gear, EMS providers must also exercise caution when handling sharp devices, such as needles that are contaminated with a patient’s blood or body fluid.

Situation The second component of the scene assessment is evaluation of the situation. The EMS providers should consider the

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radio or telephone instructions to prehospital providers for conditions that are not covered in their protocols and direct observation of individual performance. Early in the development of EMS systems, a great deal of emphasis was given to direct medical control. Many authorities believed that direct communication between the physician and the prehospital providers would be the mainstay of good prehospital care. Despite this, several studies have demonstrated that there is no difference in survival with and without on-line medical control and less time is spent in the field when there is no requirement to call the hospital.49

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following issues: the number of patients and their ages; the need for specialized personnel or equipment (power company, heavy rescue); the need for additional EMS units, including summoning an air medical helicopter; the need for a physician at the scene to assist with triage; and the possibility that the traumatic event was triggered by a medical emergency (acute myocardial infarction or a cerebrovascular accident). Because the EMS personnel are essentially the “eyes and ears” of the emergency physician and trauma surgeon at the scene, they are in the position to observe key data about the mechanism of injury. Kinematics. An understanding of the mechanism of injury assists in evaluating the patient for potential injuries (see Chapter 1). Certain mechanisms frequently result in specific injury patterns. Recognition of the mechanism may guide providers in the assessment of the patient. If the incident involves a motor vehicle crash, the EMS crew should evaluate the type of collision (frontal, rear, or lateral impact, etc.) and note the degree of damage to the vehicles. The location of the patient at the time of the crash and the use of restraints or protective gear is also valuable information. For penetrating trauma, the caliber of the weapon and distance from the assailant should be documented.

■ Primary Survey After assessing the scene, EMS personnel perform a primary survey of the patient (see Chapter 10). As taught in ATLS, this survey serves to identify life-threatening or potentially lifethreatening conditions. While it is taught in a stepwise A–B– C–D–E approach, one must remember that many aspects of this evaluation can be done simultaneously. EMS personnel employ a “treat as you go” philosophy, wherein care is initiated for life-threatening conditions as they are identified. Thus, the primary survey establishes a framework for setting priorities for management.

Airway Management Management of the airway is given highest priority, but care must be taken not to aggravate a potential injury to the cervical spine (see Chapter 11). One EMS provider applies manual inline stabilization to the head and neck while a coworker begins assessment and management of the airway. This stabilization of the cervical spine is continued either until the patient is completely immobilized on a long backboard or until it is determined that the patient does not require spinal immobilization. All EMS providers, regardless of their level of training, must master the “essential skills” of airway management.44 These skills include the following: manually clearing the patient’s airway of foreign material, manually opening the airway using the trauma jaw thrust or trauma chin lift, suctioning the oropharynx, and inserting basic oral or nasal airways. An algorithm for prehospital management of the airway is provided (Fig. 7-1).44 Endotracheal Intubation. While this has long been the “gold standard” for securing an airway in the hospital, its role

in prehospital care has become increasingly controversial. This skill is typically limited to advanced providers, though all levels of EMTs have now been taught to safely insert endotracheal tubes. The use of this technique is almost universally accepted at the EMT-Paramedic level throughout the United States. A limited number of communities have allowed EMT-Bs to be trained in endotracheal intubation. In most EMS systems, the success rate for endotracheal intubation exceeds 90%. With good, indirect medical control and field preceptors, training in endotracheal intubation can be successfully accomplished.52 Because of the concern of potential fractures of the cervical spine, endotracheal intubation should be performed concurrently with in-line stabilization of the cervical spine.53,54 While intubation is most commonly accomplished via the orotracheal route using a laryngoscope, other techniques include blind nasotracheal intubation, digital intubation, and retrograde intubation, although these are rarely utilized in the field.55–57 Indications for endotracheal intubation in the field include the following: • Inability of patient to maintain an airway due to altered level of consciousness (Glasgow Coma Scale [GCS] score 8) • Need for assisted ventilations • Threatened airway (e.g., respiratory burns, expanding hematoma of the neck) Concern has arisen that endotracheal tubes placed in the prehospital setting may be misplaced or may become dislodged more commonly than previously believed.58 Once endotracheal intubation has been performed, care should be taken to confirm proper placement using a combination of clinical assessments and adjunctive devices. The clinical assessments include presence of bilateral breath sounds and the absence of ventilatory sounds over the epigastrium, chest rise with ventilation, fogging of the endotracheal tube, and the provider watching the tube pass through the vocal cords. Adjuncts that help confirm a successful intubation include colorimetric CO2 detectors, capnography, and the esophageal detector device.59 Following intubation, the tube is carefully secured and its position checked each time the patient is moved. A recent publication suggests that continuous capnography in the prehospital setting may significantly reduce the incidence of misplaced or dislodged ET tubes.60 A number of EMS services, especially air medical programs, permit their providers to perform rapid sequence intubation (RSI). This involves the administration of both a sedating agent and a neuromuscular blocking agent prior to endotracheal intubation. In skilled hands, this technique can facilitate effective airway control in patients when other methods fail or are otherwise unacceptable (e.g., the patient with trismus). The role of RSI in the prehospital setting is controversial, primarily because of both concerns related to the risks of losing a partially patent airway by administration of a paralytic agent and data suggesting that patient outcomes may be compromised when RSI is performed by EMS personnel.

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ESSENTIAL SKILLS Manual clearing of airway Manual maneuvers • Trauma jaw thrust • Trauma chin lift Suctioning Basic adjuncts • Oropharyngeal airway • Nasopharyngeal airway

No

DIFFICULT AIRWAY

Able to ventilate?4

No

Yes

Options • Essential skills • Supraglottic airway • Laryngeal mask airway • Retrograde intubation5 • Digital intubation6

Options • Laryngeal mask airway • Supraglottic airway Able to ventilate?

Assist ventilations FiO2 >0.85 Complete primary survey

Yes

No PTV7

Rapid transport Assist ventilations FiO2 >0.85 Complete primary survey Rapid transport

FIGURE 7-1 Airway management. (Reproduced with permission from Salomone JP, Pons PT, McSwain NE, eds. PHTLS: Prehospital Trauma Life Support. 7th ed. St. Louis: Mosby; 2011:140. Copyright © Elsevier.)

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With adequate medical control, several studies have documented that EMS personnel can safely perform this procedure.61–63 Data from one case–control study, however, demonstrated an interesting paradox. While paramedics using RSI had a higher success rate at performing endotracheal intubation, the patients with suspected severe traumatic brain injury (TBI) intubated with RSI had a higher mortality than did those in the control group.64 Davis et al.65 recently published the findings of an expert panel on the role of prehospital RSI. Wang and Yealy66 reviewed the data on prehospital intubation and concluded that there is little literature to support maintaining endotracheal intubation as the standard airway of choice. More studies have documented worsened outcomes than improved outcomes. If intubation is utilized, the EMS systems must carefully review each intubation attempt and ensure that it is being performed safely. Supraglottic Airways Percutaneous Transtracheal Ventilation (PTV). These are devices that are inserted without a laryngoscope (i.e., blindly) into the hypopharynx. Although various models differ in design, properly positioned devices have openings that allow for passage of air from the device into the adjacent glottic opening to ventilate the lungs. Some devices have two ports and ventilations are then administered through the port that results in chest excursion and breath sounds (pharyngotracheal lumen (PtL) airway, Gettig Pharmaceutical Instrument Company, Spring Hills, PA; Combitube, Nell-cor, Typo Healthcare, Pleasanton, CA). A newer but similar alternative has a single ventilation port making it even easier to use (King LT airway, King Systems, Noblesville, IN). Another supraglottic device is the laryngeal mask airway (LMA) (LMA North America, San Diego, CA), consisting of an inflatable silicone ring attached to a silicone tube. This device is blindly inserted into the hypopharynx so that the ring seals around the glottic opening. Ventilation is then provided through the tube. This device has replaced endotracheal intubation for general anesthesia in a significant percentage of shorter operations, especially in Great Britain. LMAs have been popular in the prehospital setting in Europe and with some air medical services in the United States.67 The primary advantage of supraglottic airways is that minimal training is necessary to achieve competency because of their design and the blind insertion. A potential disadvantage of these devices is that the risk of aspiration is believed to be greater than with endotracheal intubation. Supraglottic devices are valuable backup (“rescue”) airways when endotracheal intubation cannot be accomplished. Because of the controversies with endotracheal intubation, these airways are increasingly utilized as the initial airway of choice. This is especially true in the urban setting where transport times are generally brief. This involves the insertion of a large-bore needle through the cricothyroid membrane and connecting it to high-pressure oxygen. The lungs are then insufflated periodically. This technique possesses the following advantages: it does not require paralysis, is less invasive than surgical cricothyroidotomy, affords easy access and insertion, and requires minimal education and very basic equipment. The technique has been

demonstrated experimentally to be safe and effective even in the presence of complete obstruction of the airway. While oxygenation is adequate, studies have shown that the patient may become hypercarbic.68 PTV is indicated when an injured patient is unable to be intubated and cannot be ventilated using a BVM device and an alternative airway. Surgical Cricothyroidotomy. This involves incising the skin and the cricothyroid membrane, followed by the insertion of a small endotracheal or tracheostomy tube. Because it is highly invasive, complications have included significant hemorrhage and injury to adjacent nerves, blood vessels, and the larynx. Air medical crews have utilized surgical cricothyroidotomy in the prehospital setting for several decades.69 Groups from Indianapolis and Tucson have reported on their experiences with this procedure when performed by ground ambulance crews.70,71 Although these authors concluded that surgical cricothyroidotomy could be safely performed by paramedics assigned to ground units, many experts have argued that the procedure was excessively utilized. In the studies, between 10% and 20% of the total field airways were surgical, and, of these, 20–25% were performed as the initial technique of airway management. Well-trained air medical crews who have been allowed to perform this skill have demonstrated a much smaller need. In systems with tight medical control, EMS providers could consider this procedure when faced with the “can’t intubate, can’t ventilate” situation.

Ventilatory Support The patient’s ventilatory status (“breathing”) is next examined. If the patient’s ventilatory rate is 10 or less, ventilations should be assisted with a BVM device connected to 100% oxygen. The tidal volume should be estimated if the patient is tachypneic. Rapid, shallow breaths indicate inadequate minute ventilation and require assistance with a BVM. Auscultation of breath sounds should be performed during the primary survey if the patient has an abnormal ventilatory rate or evidence of respiratory distress. Most patients who have suffered an injury benefit from supplemental oxygen. Pulse oximetry should be monitored, and oxygen administered to maintain an SpO2 95%. Prehospital care providers must exercise caution while providing ventilatory support, as deleterious effects may ensue. Hyperventilation by EMS personnel in one study was associated with increased mortality in patients with suspected TBI.72 Additionally, data from animal models suggest that hyperventilation resulted in auto-positive end-expiratory pressure (PEEP) that further compromised the hemodynamic status of a hypovolemic swine.73 For an adult patient, a reasonable tidal volume of 350–500 mL delivered at a rate of 10 breaths/min is probably sufficient to maintain a satisfactory oxygen saturation while minimizing the risk of hyperventilation. Continuous pulse oximetry and capnography can help guide the ventilatory support.

Circulation Assessment of a patient’s circulatory status involves examining for external hemorrhage and evaluating the adequacy of

Prehospital Care

FIGURE 7-2 Protocol for tourniquet application. (Reproduced with permission from Salomone JP, Pons PT, McSwain NE, eds. PHTLS: Prehospital Trauma Life Support. 7th ed. St. Louis: Mosby; 2011:201. Copyright © Elsevier.)

perfusion. Most life-threatening external hemorrhage can be controlled with direct pressure. If man power is limited, a pressure dressing with gauze pads and an elastic bandage can be placed around an extremity. Should direct pressure alone not control bleeding in an extremity, a tourniquet should be applied just proximal to the site of hemorrhage and tightened until bleeding ceases. No published data document any significant decrease in hemorrhage when a bleeding extremity is elevated, and such manipulation may result in the conversion of a closed fracture to an open one. The efficacy of applying pressure over “pressure points” in the axilla and groin has also not been studied in the prehospital setting and is labor intensive. In the operating room, arterial tourniquets have been used safely for periods of 120–150 minutes. Options for a tourniquet include a blood pressure cuff, a cravat tied into a “Spanish windlass,” and the use of a manufactured tourniquet.74 If a manufactured tourniquet is used, it should be one that has been tested and recommended by the Committee on Tactical Combat Casualty Care (CoTCCC).75 A sample protocol for application of a tourniquet is described as follows and is shown in Fig. 7-2. Kragh et al.76,77 studied the outcomes of casualties who had tourniquets applied for their extremity wounds. Their data demonstrated that prehospital use of tourniquets was lifesaving and that complications were low. Less than 2% of the patients suffered transient nerve palsy at the level where the tourniquet was applied, and no limbs were sacrificed because of tourniquet use. In patients who had a tourniquet on for 2 hours or less, 28% required fasciotomy, while a slightly higher percentage (36%) required fasciotomy if the tourniquet was in place longer than 2 hours. A topical hemostatic agent should be considered for significant external hemorrhage from body areas not amenable

Traumatic Cardiopulmonary Arrest. Trauma patients who are found in cardiopulmonary arrest require special consideration. Unlike cardiopulmonary arrest associated with an acute myocardial infarction, most patients who suffer cessation of their vital signs prior to the arrival of EMS have exsanguinated. CPR, defibrillation, antidysrhythmic medications, and crystalloid resuscitation will not reverse this. Attempts at resuscitation are typically futile and place the EMS personnel at unnecessary risk from automobile crashes during emergency transport and exposure to blood. The National Association of EMS Physicians and the ACSCOT have collaborated on a position paper that endorses the following guidelines81: • For victims of blunt trauma, resuscitation efforts may be withheld if the patient is pulseless and apneic on the arrival of EMS. • For victims of penetrating trauma, resuscitation efforts may be withheld if there are no signs of life (papillary reflexes, spontaneous movement, or organized cardiac rhythm on the electrocardiogram greater than 40/min). • Resuscitation efforts are not indicated when the patient has sustained an obviously fatal injury (such as decapitation) or when evidence exists of dependent lividity, rigor mortis, and decomposition. • Termination of resuscitation should be considered in trauma patients with an EMS-witnessed cardiopulmonary arrest and 15 minutes of unsuccessful resuscitation including CPR. • Termination of resuscitation should be considered for a patient with traumatic cardiopulmonary arrest who would require transport of greater than 15 minutes to reach an emergency department or trauma center. • Victims of drowning, lightning strike, or hypothermia, or those in whom the mechanism of injury does not correlate with the clinical situation (suggesting a nontraumatic cause) deserve special consideration before a decision is made to withhold or terminate resuscitation.

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1. Attempt to control hemorrhage with direct pressure or pressure dressing must fail. 2. A commercially manufactured tourniquet, blood pressure cuff, or “Spanish windlass” is applied to the extremity just proximal to the bleeding wound. 3. The tourniquet is tightened until hemorrhage ceases, and then it is secured in place. 4. The time of tourniquet application is written on a piece of tape and secured to the tourniquet (“TK 21:45” indicates that the tourniquet was applied at 9:45 pm). 5. The tourniquet should be left uncovered so that the site can be seen and monitored for recurrent hemorrhage. If bleeding continues after application and tightening of the initial tourniquet, a second tourniquet can be applied just above the first. 6. Pain management should be considered unless the patient is in Class III or IV shock. 7. The patient should ideally be transported to a facility that has surgical capability.

to placement of a tourniquet (neck, torso, axilla, and groin). In laboratory and clinical studies the military has found several of these agents to be effective, including those incorporating chitosan, zeolite (a derivative of volcanic rock), or kaolin clay.78,79 Zeolite been associated with thermal injury as a result of an exothermic reaction that takes place when the material comes in contact with water.80 The CoTCCC currently recommends Combat Gauze that is impregnated with kaolin clay as the topical hemostatic agent of choice.75 Perfusion is assessed primarily by evaluating pulse rate and quality, skin color, temperature, and moisture; however, prolonged capillary refill time may add further evidence that the patient is in shock. Time should not be taken in the primary survey to measure blood pressure. Even mild tachycardia (heart rate 100/min) should always make one consider that the injured patient is hypovolemic. Significant tachycardia (120/ min), weak peripheral pulses, and anxiety are associated with loss of 30–40% of the blood volume of an adult.50

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During the primary survey, the EMS provider assesses neurologic function by evaluating the patient’s GCS score and pupillary response. The GCS score comprises three components including eyes, verbal, and motor.82 If a painful stimulus is required to complete the assessment, the EMT can either apply pressure to the nail bed or squeeze the axillary tissue. If the patient has an altered level of consciousness (GCS 15), pupillary response to light is assessed. Any belligerent, combative, or uncooperative patient should be considered to be hypoxic or have a TBI until proven otherwise. In a trauma patient, a GCS score of 13, seizure activity, or a motor or sensory deficit are all reasons for concern.

Scene assessment

Primary survey • Airway/spinal stabilization • Breathing • Circulation • Disability • Expose/environment • Treat as needed

Life-threatening or multisystem injuries

Exposure and Environmental Control The final part of the primary survey involves a quick scan of the patient’s body to note any other potentially life-threatening injuries. In general, this requires removal of the patient’s clothes, but environmental conditions and the presence of bystanders may make this impractical. Hypothermia from failure to preserve body heat can contribute to a serious coagulopathy in the trauma patient. Heavy, dark colored woolen clothing may absorb significant amounts of blood. On occasion, patients may have more than one mechanism of injury, that is, blunt trauma from a motor vehicle crash that occurred while trying to flee the assailant who had shot them. Injuries cannot be treated unless they are identified.

■ Resuscitation On completion of the primary survey, the EMS provider determines whether or not the patient is critical (Fig. 7-3). Because the primary survey involves a “treat as you go” philosophy, airway management, ventilatory support, and control of external hemorrhage are initiated as the problems are identified. When a critically injured patient is identified (Table 7-3), scene time should ideally be less than 10 minutes, unless extenuating circumstances, such as extrapment or an unsafe scene, preclude this. A retrospective study of the outcome of seriously injured trauma patients (Injury Severity Score 15) in an urban setting demonstrated improved survival when the patient was transported by private vehicle compared to an ALS unit, primarily because the EMS crews were spending, on average, more than 20 minutes on scene.83 If indicated, spinal immobilization should be performed expeditiously and the patient moved to the ambulance. Time is not taken to splint each individual fracture. For the critically injured patient, immobilization to the long backboard provides satisfactory immobilization of potential musculoskeletal injuries. Because definitive care cannot be provided to the critically injured patient in the field, EMS personnel must realize that initiation of transport to the closest appropriate facility demonstrates good judgment. Originally developed by the ACSCOT, the Field Triage Decision Scheme was recently revised by a national expert panel convened by the Centers for Disease Control and Prevention (CDC) (Fig. 7-4).84 The revi-

YES

NO

Spinal immobilization if indicated

Secondary survey AMPLE history

Initiate rapid transport (closest appropriate facility)

Manage injuries as appropriate

Reevaluate primary survey

Reevaluate primary survey

Secondary survey if appropriate

Initiate transport

En route interventions and continued assessment

FIGURE 7-3 Prehospital care overview. (Reproduced with permission from Salomone JP, Pons PT, McSwain NE, eds. PHTLS: Prehospital Trauma Life Support. 7th ed. St. Louis: Mosby; 2011:429. Copyright © Elsevier.)

sion has been endorsed by more than 35 national organizations with EMS or trauma care. According to this algorithm, patients who meet specific anatomic or physiologic criteria should be transported to the highest level of care in the system, typically a Level I or II trauma center. Patients who meet mechanism of injury criteria should be transported to the closest trauma center, which need not be a Level I or II. Protocols should be written so that EMS personnel may bypass a closer hospital in order to take a patient with lifethreatening injuries to a trauma center.

Fluid Therapy Infusions of crystalloid solutions and blood transfusion are the mainstays of therapy for the in-hospital treatment of severe hypovolemic shock (see Chapter 12). Because it requires refrigeration and typing, blood is not available in the prehospital environment. Isotonic crystalloid solutions, such as lactated

Prehospital Care

TABLE 7-3 Critical Trauma Patient

Reproduced with permission from Salomone JP, Pons PT, McSwain NE, eds. PHTLS: Prehospital Trauma Life Support. 7th ed. St. Louis: Mosby; 2011:424. Copyright © Elsevier.

Ringer’s or normal saline (0.9% sodium chloride), can be used for volume resuscitation. Although hypertonic saline (7.5% sodium chloride) initially showed promise, a meta-analysis of several studies failed to demonstrate an improvement in survival rates compared to those patients treated with isotonic solutions.85 En route to the receiving facility, the EMS providers should insert two large-bore (14- or 16-gauge) intravenous catheters in veins of the forearm or antecubital area. If possible, lactated Ringer’s solution (or normal saline) should be warmed (102°F/38.8°C) prior to administration. Fluid resuscitation in the prehospital setting must be based on the clinical scenario.44 If the patient has suspected uncontrolled hemorrhage in the thorax, abdomen, or retroperitoneum, fluid infusions should be titrated to maintain a systolic blood pressure (SBP) in the range of 80–90 mm Hg (mean arterial pressure of 60–65 mm Hg) in the hope of perfusing vital organs while limiting the risk of increased, uncontrollable internal hemorrhage. If the patient has a suspected

■ Secondary Survey Secondary survey refers to a more thorough history and physical examination. For the patient with life-threatening conditions identified in the primary survey, the EMS provider performs the secondary survey when those conditions have been addressed and are stable or improving and the patient is being transported. If the primary survey fails to indicate that the injured patient is critical, then the provider proceeds on to the secondary survey.

AMPLE History This brief history from the patient or family includes the following: • • • • •

Allergies to medications Prescription or over-the-counter Medications Pertinent Past medical history Last eaten Recall of Events leading up to the injury

CHAPTER 7

Limit scene time to 10 min or less when any of the following life-threatening conditions are present: Inadequate or threatened airway Impaired ventilation as demonstrated by the following: Abnormally fast or slow ventilatory rate Hypoxia (SpO2  95% even with supplemental oxygen) Dyspnea Open pneumothorax or flail chest Suspected pneumothorax Significant external hemorrhage or suspected internal hemorrhage Shock, even if compensated Abnormal neurologic status GCS score 13 Seizure activity Sensory or motor deficit Penetrating trauma to the head, neck, or torso, or proximal to the elbow and knee in the extremities Amputation or near amputation proximal to the fingers or toes Any trauma in the presence of the following: History of serious medical conditions (e.g., coronary artery disease, chronic obstructive pulmonary disease, bleeding disorder) Age 55 Hypothermia Burns Pregnancy

injury to the central nervous system injury (TBI or injury to spinal cord), intravenous fluids should be administered at a rate sufficient to maintain the SBP at 90 mm Hg. If the patient has identifiable shock that resulted from external hemorrhage that has been controlled, fluids are titrated to maintain a normal pulse rate and blood pressure. If the patient again becomes hypotensive, further intravenous fluids should be titrated to maintain an SBP in the range of 80–90 mm Hg. Controversy exists regarding the role of therapy with intravenous fluids in the prehospital setting. No published study has ever demonstrated an improvement in survival resulting from the prehospital administration of fluids. One computer model of prehospital fluid therapy suggested that intravenous therapy is potentially beneficial when all of the following occur: (a) the bleeding rate is initially 25–100 mL/min; (b) the prehospital time exceeds 30 minutes; and (c) the intravenous infusion rate is approximately equal to the bleeding rate.86 Opponents of prehospital fluid therapy cite data from animal models of uncontrolled internal hemorrhage. In these studies, attempts to improve blood pressure with crystalloid infusions have resulted in increased blood loss and mortality.87–90 Data from a prospective, randomized prehospital trial of intravenous fluid therapy in patients with penetrating torso trauma found an improved outcome when intravenous fluids were withheld until operative control of hemorrhage was obtained.91 Unfortunately, there were long delays until operation was performed in this study. Several blood substitutes that have shown promise in the laboratory have encountered difficulty in clinical trials, and none has been approved for routine use by the FDA. Although further studies will be needed to clarify this issue, EMS providers should never delay transport simply to initiate intravenous therapy. In one sense, the most important fluid in the prehospital care of critically injured patients is fuel—to transport patients rapidly to the closest appropriate facility.

113

114

Generalized Approaches to the Traumatized Patient Measure vital signs and level of consciousness

SECTION 2

Step One

Glasgow coma scale ≤13 Systolic blood pressure (mm Hg) <90 mm Hg Respiratory rate <10 or > 29 breaths per minute* (<20 in infant aged <1 year), or need for ventilatory support

Yes

Transport to a trauma center.† Steps One and Two attempt to identify the most seriously injured patients. These patients should be transported preferentially to the highest level of care within the defined trauma system.

Yes

Transport to a trauma center, which, depending upon the defined trauma system, need not be the highest level trauma center.§§

Yes

Transport to a trauma center or hospital capable of timely and thorough evaluation and initial management of potentially serious injuries. Consider consultation with medical control.

No Assess anatomy of injury

Step Two§

• All penetrating injuries to head, neck, torso and extremities proximal to elbow or knee • Chest wall instability or deformity (e.g., flail chest) • Two or more proximal long-bone fractures • Crushed, degloved, mangled, or pulseless extremity • Amputation proximal to wrist or ankle • Pelvic fractures • Open or depressed skull fracture • Paralysis No Assess mechanism of injury and evidence of high-energy impact

Step Three§

• Falls – Adults: > 20 feet (one story is equal to 10 feet) – Children¶ >10 feet or two or three times the height of the child • High-risk auto crash – Intrusion,** including roof: >12 inches occupant site; >18 inches any site – Ejection (partial or complete) from automobile – Death in same passenger compartment – Vehicle telemetry data consistent with high risk of injury • Auto vs. pedestrian/bicyclist thrown, run over, or with significant (>20 mph) impact†† • Motorcycle crash >20 mph No Assess special patient or system considerations

Step Four

• Older adults¶¶ – Risk of injury/death increases after age 55 years – SBP <110 might represent shock after age 65 years – Low impact mechanisms (e.g. ground level falls) might result in severe injury • Children – Should be triaged preferentially to pediatric capable trauma centers • Anticoagulants and bleeding disorders – Patients with head injury are at high risk for rapid deterioration • Burns – Without other trauma mechanism: triage to burn facility*** – With trauma mechanism: triage to trauma center*** • Pregnancy >20 weeks • EMS provider judgment No Transport according to protocol††† When in doubt, transport to a trauma center

FIGURE 7-4 Field Triage Decision Scheme. Abbreviation: EMS, emergency medical services. (Reproduced from Sasser SM, Hunt RC, Sullivent EE, et al. Guidelines for field triage of injured patients: recommendations of the national expert panel on field triage. MMWR. 2009;58:1.)

Prehospital Care

Head-to-Toe Survey This complete physical examination begins with obtaining a complete set of vital signs. Injuries to the head, neck, chest, abdomen, pelvis, and extremities are noted. The patient is then turned using the log roll maneuver if spinal injury is suspected, and the patient’s back is examined. Finally, a neurologic examination that involves reassessing the GCS score, pupillary reaction, and motor and sensory functions in the extremities is completed.

■ Specific Conditions Scalp Wounds Because of the high concentration of blood vessels in the skin and soft tissues of the scalp, face, and neck, even a small wound can result in serious external hemorrhage. EMS providers and other health care workers often fail to appreciate that patients with a complex scalp wound may bleed sufficiently to develop shock. A compression dressing created with gauze pads and an elastic bandage often provides satisfactory control of hemorrhage.

Traumatic Brain Injury TBI remains one of the leading causes of mortality in injured patients. Secondary brain injury refers to the extension of the original injury and may result from numerous causes. These include hypoxia, hypocapnia and hypercapnia, anemia, hypotension, hypoglycemia and hyperglycemia, seizures, and intracranial hypertension as the result of edema or mass effect. Optimal prehospital care of the patient with TBI involves preventing secondary brain injury, maintaining cerebral perfusion pressure (mean arterial pressure minus intracranial pressure), and expeditious transfer to a facility capable of caring for the injury.

A patient with a severe TBI may be unable to control his or her airway, and endotracheal intubation should be considered for patients with a GCS score of 8 or less, although an alternative airway device may provide a satisfactory airway. Ventilatory support should be administered and the patient maintained eucapneic as prophylactic hyperventilation is no longer indicated.92,93 Data from patients with TBI indicate that those who arrive in the emergency department with either hypocapnia (arterial pCO2  30 mm Hg) or hypercapnia (pCO2  45 mm Hg) have poorer outcomes compared to those who arrive in a eucapneic condition.94 Unfortunately, capnography has not proven to be a useful noninvasive method for keeping a patient in the target pCO2 range. Warner et al.95 found a poor correlation between ETCO2 and arterial pCO2, especially in patients with impaired perfusion. Blood loss should be minimized by controlling external sources and splinting fractures as appropriate. Because of the risk of an associated injury to the spine, patients with suspected TBI should undergo spinal immobilization. Intravenous fluids should be initiated en route to the receiving facility with a goal of maintaining the SBP at 90 mm Hg. During prolonged transport, blood glucose can be monitored and dextrose administered if the patient is hypoglycemic. Benzodiazepines are appropriate for control of seizures, but they should be carefully titrated intravenously because of the risk of hypotension and respiratory depression. Intracranial hypertension may cause cerebral herniation and brain death, but it cannot be measured in the prehospital setting. Signs of possible intracranial hypertension include the following: a decline in the GCS score of 2 points or more, development of a sluggish or nonreactive pupil, development of hemiplegia or hemiparesis, or Cushing’s phenomena (bradycardia associated with arterial hypertension). An algorithm for the prehospital management of TBI has been developed (Fig. 7-5).44

CHAPTER 7

FIGURE 7-4 (Continued) *The upper limit of respiratory rate in infants is 29 breaths per minute to maintain a higher level of overtriage for infants. † Trauma centers are designated Level I-IV. A Level I center has the greatest amount of resources and personnel for care of the injured patient and provides regional leadership in education, research, and prevention programs. A Level II facility offers similar resources to a Level I facility, possibly differing only in continuous availability of certain subspecialties or sufficient prevention, education, and research activities for Level I designation; Level II facilities are not required to be resident or fellow education centers. A Level III center is capable of assessment, resuscitation, and emergency surgery, with severely injured patients being transferred to a Level I or II facility. A Level IV trauma center is capable of providing 24-hour physician coverage, resuscitation, and stabilization to injured patients before transfer to a facility that provides a higher level of trauma care. § Any injury noted in Step Two or mechanism identified in Step Three triggers a “yes” response. ¶ Age 15 years. **Intrusion refers to interior compartment intrusion, as opposed to deformation which refers to exterior damage. †† Includes pedestrians or bicyclists thrown or run over by a motor vehicle or those with estimated impact 20 mph with a motor vehicle. §§ Local or regional protocols should be used to determine the most appropriate level of trauma center within the defined trauma system; need not be the highest-level trauma center. ¶¶ Age 55 years. ***Patients with both burns and concomitant trauma for whom the burn injury poses the greatest risk for morbidity and mortality should be transferred to a burn center. If the nonburn trauma presents a greater immediate risk, the patient may be stabilized in a trauma center and then transferred to a burn center.

115

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Generalized Approaches to the Traumatized Patient

Suspected TBI

SECTION 2

Yes

GCS ≤ 8

Consider need for airway management1

No

Notes: 1See Airway Management algorithm (p. 125). 2

Ventilate at these rates: adult 10/min; children 20/min; infants 25/min. ETCO2 only provides a rough estimate of hypoventilation or hyperventilation; consider maintaining ETCO2 at 30–35 mm Hg, if available. 3Ideal

facility should have neurosurgical coverage and functioning CT scan.

Apply oxygen Maintain SpO2 ≥ 95%

Maintain SBP ≥ 90 mm Hg if possible.

4

5Use

Assist

ventilations2

6

Signs of possible increased ICP: decline in GCS score of two points or more, development of a sluggish or nonreactive pupil, development of hemiplegia or hemiparesis, or Cushing’s phenomenon.

Control external hemorrhage Initiate transport3

benzodiazepine titrated intravenously.

7Titrate

small doses of benzodiazepine intravenously.

8Consider

IV fluid

long-acting neuromuscular blocking agent (vecuronium).

resuscitation4

9Consider

mannitol (0.25 to 1 g/kg).

Treat seizures5 10Ventilate

Check blood glucose level

at these rates: adult 20/min; children 30/min; infants 35/min. Consider maintaining ETCO2 at 25–30 mm Hg, if available.

Signs of increased ICP?6

No

Yes

Options: • Remove cervical collar • Sedation7 • Paralysis8 • Osmotherapy9 • Controlled mild hyperventilation10

Continue transport

FIGURE 7-5 Algorithm for the prehospital management of TBI. (Reproduced with permission from Salomone JP, Pons PT, McSwain NE, eds. PHTLS: Prehospital Trauma Life Support. 7th ed. St. Louis: Mosby; 2011:240. Copyright © Elsevier.)

Thoracic Trauma Flail Chest and Pulmonary Contusion. In the prehospital setting, the administration of oxygen and ventilatory support are the primary therapies for a flail chest and suspected pulmonary contusion (see Chapters 24–26). Oxygen saturation should be kept at 95% or higher by applying supplemental oxygen. CPAP, a therapy which is becoming increasingly common among EMS services, may be of benefit. If these measures fail to provide adequate oxygenation, ventilations should be assisted and endotracheal intubation considered if the patient’s tidal volume appears inadequate. Tension Pneumothorax . Tension pneumothorax should be suspected whenever the following three criteria are identified: increasing respiratory distress or difficulty ventilating

with a BVM device, decreased or absent breath sounds, and hemodynamic compromise. Needle decompression of the pleural space can be lifesaving.44,96,97 The intravenous catheter inserted should be left in place, but there is no need to create a one-way (“flutter”) valve as any air exchange through the catheter is clinically insignificant. Recent data suggest that a catheter length of at least 8 cm is necessary to reach and decompress the pleural space.98–100 Open Pneumothorax . An open pneumothorax should be sealed with an occlusive dressing. One of the four sides of the dressing may be left untaped so that air can decompress from the pleural space as needed. After an occlusive dressing has been applied to an open pneumothorax, any signs of a developing tension pneumothorax should prompt the EMS

Prehospital Care worker to remove the dressing. If this does not result in improvement of the patient’s status, needle decompression should be considered.

Abdominal Trauma

Musculoskeletal Trauma

Intra-Abdominal Hemorrhage. In the absence of an obvious sign such as a bullet wound, intra-abdominal hemorrhage is difficult to identify in the prehospital setting, especially in the unconscious trauma patient (see Chapters 27–34). Unexplained hypovolemic shock should lead the EMS provider to suspect this condition. Management involves rapid transport to a facility that offers immediate operative intervention.

Hemorrhage. This is the only immediately life-threatening condition associated with trauma to an extremity (see Chapters 39–41). External hemorrhage should be controlled with direct pressure or a pressure dressing, followed by a tourniquet if these measures fail. Internal hemorrhage is best managed in the field by immobilization of the extremity. In the critically injured patient, immobilization to a long backboard is sufficient stabilization. If the patient does not have life-threatening injuries, time can be taken to splint each suspected fracture individually. A traction splint provides reasonable pain control and will stabilize a suspected fracture of the femur.

Pelvic Fractures. The presence of a severe pelvic fracture may be suspected if the EMS provider finds instability on examination of the pelvis, especially if the patient has evidence of hypovolemic shock (see Chapter 35). Pelvic binders, which are often placed on hypotensive trauma patients with proven pelvic fractures in the hospital, have limited utility in the field. EMS providers may not be able to identify a fractured pelvis on physical examination alone and the pelvic binders are costly. These binders may be useful in the setting of a hypotensive trauma patient with a known pelvic fracture who requires interfacility transport. Pregnancy. Prehospital management of the injured pregnant patient focuses on adequately resuscitating the mother, especially if shock is present (see Chapter 37). In the third trimester, pregnant individuals may exhibit hypotension while lying supine due to compression of the inferior vena cava by the uterus. Supine hypotension is treated by gently rolling the mother into the left lateral decubitus position or, if immobilized on a long backboard, placing sufficient padding under the right side of the board to elevate it 30° or so. If hypotension does not correct with this measure, hemorrhagic shock should be suspected. Oxygen should be administered, and the patient transported to a facility that has both trauma and obstetrical capabilities.

Spinal Trauma An algorithm has been developed that details the indications for spinal immobilization in the prehospital setting (see Chapter 23) (Fig. 7-6).44,101 Patients with penetrating trauma to the torso almost never have an unstable vertebral column.102 A recent analysis of data from the National Trauma Data Bank showed that victims of penetrating trauma who received

Amputation. The ACSCOT has published guidelines for the management of amputated parts.104 These include the following: • Cleansing the amputated part by gentle rinsing with lactated Ringer’s solution • Wrapping the part in sterile gauze moistened with lactated Ringer’s solution and placing it in a plastic bag • Labeling the bag or container and placing it in an outer container filled with crushed ice • The part should not be allowed to freeze, and it should be transported along with the patient to the closest appropriate facility. Pain Control. In the prehospital setting, analgesics are indicated for an isolated injury to an extremity, but not in a patient with multisystem trauma.44,105,106 After appropriately splinting the extremity, small doses of narcotics, titrated intravenously, may help relieve pain. The patient should be observed for side effects including hypotension and respiratory depression. Narcotics should not be administered in the trauma patient who exhibits signs of shock or when the patient appears to be under the influence of drugs and alcohol.

TRIAGE Disasters may be the result of natural phenomena, such as tornadoes, hurricanes, and earthquakes, or man-made in the case of a building collapse or terrorist event. When situations such

CHAPTER 7

Pericardial Tamponade. Pericardial tamponade is generally encountered following penetrating trauma to the heart; however, it may be a complication of a blunt cardiac rupture. In the prehospital setting, the classic symptoms of Beck’s triad (elevated venous pressure, muffled heart tones, and hemodynamic compromise) may be difficult to identify. While some EMS systems permit ALS personnel to perform pericardiocentesis if pericardial tamponade is suspected, the emphasis should be placed on transporting that patient with a suspected tamponade to a facility that has immediate surgical capabilities.

prehospital spinal immobilization had a higher risk of death compared to those who did not.103 Therefore, spinal immobilization is indicated in the setting of penetrating trauma only when the patient has a neurologic complaint or finding. In patients with blunt trauma, spinal immobilization should be performed if the patient has an altered level of consciousness (GCS score  15) or if spinal pain or tenderness, a neurologic deficit or complaint, or an anatomic deformity of the spine is present. In the absence of these findings, the mechanism of injury should be evaluated. If the mechanism is considered to be concerning, the patient should be evaluated for evidence of alcohol or drug intoxication, presence of a distracting injury, or the inability to communicate. If any of these are present, spinal immobilization should be performed. In their absence, spinal immobilization is not indicated.

117

118

Generalized Approaches to the Traumatized Patient INDICATIONS FOR SPINAL IMMOBILIZATION

SECTION 2

Blunt trauma

Penetrating trauma to head, neck, or torso

Altered level of consciousness (GCS <15)

Neurologic deficit/complaint?

Yes

No

Yes

No

IMMOBILIZE

Spinal pain or tenderness? or Neurologic deficit or complaint? or Anatomic deformity of spine?

IMMOBILIZE

IMMOBILIZATION NOT INDICATED

Rapid transport

Yes

Rapid transport Rapid transport ** USE CLINICAL JUDGEMENT. IF IN DOUBT, IMMOBILIZE**

No

IMMOBILIZE Transport

Concerning Mechanism of injury1

Yes

No

Presence of: Evidence of alcohol/drugs or Distracting injury2 or Inability to communicate3

Immobilization not indicated

Yes

No

IMMOBILIZE

Immobilization not indicated

Transport

Transport

Transport

Notes: 1 Concerning mechanisms of injury • Any mechanism that produced a violent impact to the head, neck, torso, or pelvis (e.g., assault, entrapment in structural collapse, etc.) • Incidents producing sudden acceleration, deceleration, or lateral bending forces to the neck or torso (e.g., moderate- to high-speed MVC, pedestrian struck, involvement in an explosion, etc.) • Any fall, especially in elderly persons • Ejection or fall from any motorized or otherwise-powered transportation device (e.g., scooters, skateboards, bicycles, motor vehicles, motorcycles, or recreational vehicles) • Victim of shallow-water diving incident 2

Distracting injury Any injury that may have the potential to impair the patient’s ability to appreciate other injuries. Examples of distracting injuries include a) long bone fracture; b) a visceral injury requiring surgical consultation; c) a large laceration, degloving injury, or crush injury; d) large burns, or e) any other injury producing acute functional impairment. (Adapted from Hoffman JR, Wolfson AB, Todd K, Mower WR: Selective cervical spine radiography in blunt trauma:methodology of the National Emergency X-Radiography Utilization Study [NEXUS], Ann Emerg Med 461, 1998.)

3

Inability to communicate. Any patient who, for reasons not specified above, cannot clearly communicate so as to actively participate in their assessment. Examples: speech or hearing impaired, those who only speak a foreign language, and small children.

FIGURE 7-6 Indications for spinal immobilization. (Reproduced with permission from Salomone JP, Pons PT, McSwain NE, eds. PHTLS: Prehospital Trauma Life Support. 7th ed. St. Louis: Mosby; 2011:257. Copyright © Elsevier.)

Prehospital Care

PREHOSPITAL RESEARCH Over the last decade the entire health care field has seen a growing trend toward evidence-based medicine. EMS, in general, and prehospital trauma care, specifically, need quality research to separate sound medical practice from conjecture. Management of the airway and fluid therapy are two areas that deserve intensive investigation in the prehospital setting. Far too few treatment protocols in EMS are based on highquality data. More commonly, protocols are written that include the biases of the authors and extrapolations from inhospital care. Several major obstacles to the development of quality EMS research exist.14 Funding is woefully inadequate and integrated information systems are needed to link data on patient care with information on outcome. Few academic institutions possess a long-term commitment to EMS research. Governmental regulations regarding informed consent inhibit the conduct of research in the emergency situation, as well. Finally, EMS personnel lack an appreciation of the importance of research in their own field. As these challenges are overcome, new research will lead us to better care for our patients. NHTSA has published a document detailing numerous issues in prehospital care that are awaiting investigation.16

SUMMARY AND GOLDEN PRINCIPLES Prehospital management of the injured patient remains a topic of some debate. Few experts recommend a return to a mere “scoop and run” approach in which EMS personnel would leave the patient without support of vital functions during the transport to the hospital. Conversely, delays on the scene to perform unnecessary interventions are associated with increased mortality.83,103 A recent publication compared trauma mortality before and after the implementation of a

TABLE 7-4 Golden Principles of Prehospital Trauma Care 1. Ensure the safety of the prehospital care providers and the patient 2. Assess the scene situation to determine the need for additional resources 3. Recognize the kinematics that produced the injuries 4. Use the primary survey approach to identify life-threatening conditions 5. Provide appropriate airway management while maintaining cervical spine stabilization 6. Support ventilation and deliver oxygen to maintain an SpO2  95% 7. Control any significant external hemorrhage 8. Provide basic shock therapy, including appropriately splinting musculoskeletal injuries and restoring and maintaining normal body temperature 9. Maintain manual spine stabilization until the patient is immobilized on a long backboard 10. For critically injured trauma patients, initiate transport to the closest appropriate facility within 10 min of arrival on scene 11. Initiate warmed, intravenous fluid replacement en route to the receiving facility 12. Ascertain the patient’s medical history and perform a secondary survey when life-threatening conditions have been satisfactorily managed or have been ruled out 13. Provide thorough and accurate communication regarding the patient and the circumstances of the injury to the receiving facility 14. Above all, do no further harm Reproduced with permission from Salomone JP, Pons PT, McSwain NE, eds. PHTLS: Prehospital Trauma Life Support. 7th ed. St. Louis: Mosby; 2011:421. Copyright © Elsevier.

province-wide ALS program and found no significant change in survival between the two periods.110 While these findings could be the result of inexperienced ALS providers or inappropriate ALS protocols, it remains unclear which, if any, ALS procedures improve survival. A more moderate approach focuses on limited, key field interventions, as taught in the PHTLS program: • Rapid assessment to identify life-threatening injuries • Key field interventions including management of the airway, ventilatory support with administration of oxygen, control of external hemorrhage, etc. • Rapid transport to the closest appropriate facility PHTLS summarizes optimal prehospital trauma care into 14 golden principles (Table 7-4).44 One study from Trinidad

CHAPTER 7

as these occur, the EMS and health care systems must try to match their resources with the needs of the community. A multiple-patient incident refers to a situation where numerous individuals may be injured, but the EMS system possesses the ability to provide adequate care. In a mass casualty incident, the number of injured patients overwhelms the resources of the community, and additional aid from other locations is required. The number of patients involved in each of these circumstances may vary, depending on the size of the EMS system and the resources of the community. In either situation, EMS personnel and health care workers must employ the principles of triage in order that the most seriously injured patients receive care before those with minor injuries. Simple Triage and Rapid Treatment (START) is an easily taught, simple triage system that is widely used by EMS providers when faced with numerous injured patients.44,107,108 A national expert panel, assembled by the CDC, reviewed all available triage schemes (“SALT”) and proposed a new method, comprised of the best components of the others.109 A more comprehensive discussion of disaster care is presented in Chapter 8.

119

120

Generalized Approaches to the Traumatized Patient

SECTION 2

and Tobago compared the overall mortality of trauma patients following the introduction of PHTLS training with the period preceding PHTLS. The authors documented a decrease in mortality of about 33% following the PHTLS training of EMS personnel.111

REFERENCES 1. McSwain NE Jr. Pre-hospital care. In: Feliciano DV, Moore EE, Mattox KL, eds. Trauma. 3rd ed. Stamford, CT: Appleton & Lange; 1996:107. 2. Rockwood CA, Mann CM, Farrington JD, et al. History of emergency medical services in the United States. J Trauma. 1976;16:299. 3. National Academy of Sciences/National Research Council. Accidental Death and Disability: The Neglected Disease of Modern Society. Rockville, MD: U.S. Department of Health, Education, and Welfare; 1966. 4. Pantridge JF, Adgey AA. Prehospital coronary care: the mobile coronary care unit. Am J Cardiol. 1969;24:666. 5. Border JR, Lewis FR, Aprahamian C, et al. Panel: prehospital trauma care—stabilize or scoop and run. J Trauma. 1983;23:708. 6. Trunkey DD. Is ALS necessary for pre-hospital trauma care? J Trauma. 1984;24:86. 7. Gervin AS, Fischer RP. The importance of prompt transport in salvage of patients with penetrating heart wounds. J Trauma. 1982;22:443. 8. Smith JP, Bodai BI, Hill AS, et al. Prehospital stabilization of critically injured patients: a failed concept. J Trauma. 1985;25:65. 9. Ivatury RR, Nallathambi MN, Roberge RJ, et al. Penetrating thoracic injuries: in-field stabilization vs. prompt transport. J Trauma. 1987;27: 1066. 10. Jacobs LM, Sinclair A, Beiser A, et al. Prehospital advanced life support: benefits in trauma. J Trauma. 1984;24:8. 11. Pons PT, Honigman B, Moore EE, et al. Prehospital advanced trauma life support for critical penetrating wounds to the thorax and abdomen. J Trauma. 1985;25:828. 12. Cwinn AA, Pons PT, Moore EE, et al. Prehospital advanced trauma life support for critical blunt trauma victims. Ann Emerg Med. 1987;16: 399. 13. Honigman B, Rohweder K, Moore EE, et al. Prehospital advanced trauma life support for penetrating cardiac wounds. Ann Emerg Med. 1990;19:145. 14. U.S. Department of Transportation, NHTSA. EMS Agenda for the Future. Washington, DC: U.S. Department of Transportation. Available at: http://ems.gov/pdf/2010/EMSAgendaWeb_7-06-10.pdf. Accessed September 19, 2010. 15. U.S. Department of Transportation, NHTSA. EMS Education Agenda for the Future: A Systems Approach. Washington, DC: U.S. Department of Transportation. Available at: http://www.nhtsa.gov/people/injury/ ems/FinalEducationAgenda.pdf. Accessed September 19, 2010. 16. U.S. Department of Transportation, NHTSA. National EMS Research Agenda. Washington, DC: U.S. Department of Transportation. Available at: http://www.nhtsa.gov/people/injury/ems/ems-agenda/EMSResearch Agenda.pdf. Accessed September 19, 2010. 17. National Emergency Medical Services Education and Practice Blueprint. Columbus, OH: National Registry of Emergency Medical Technicians; 1993. 18. U.S. Department of Transportation, NHTSA. National EMS Core Content. Washington, DC: U.S. Department of Transportation. Available at: http://www.nhtsa.gov/people/injury/ems/EMSCoreContent/index. htm. Accessed September 19, 2010. 19. U.S. Department of Transportation, NHTSA. National EMS Scope of Practice Model. Washington, DC: U.S. Department of Transportation. Available at: http://www.nhtsa.gov/people/injury/ems/EMSScope.pdf. Accessed September 19, 2010. 20. U.S. Department of Transportation, NHTSA. National EMS Education Standards. Washington, DC: U.S. Department of Transportation. Available at: http://ems.gov/pdf/811077a.pdf. Accessed September 19, 2010. 21. Dickison P, Hostler D, Platt TE, et al. Program accreditation effect on paramedic credentialing examination success rate. Prehosp Emerg Care. 2006;10:224. 22. Mustalish AC, Post C. Appendix I: scope and specificity of each component in EMS systems. In: Kuehl AE, ed. National Association of EMS Physicians: Prehospital Systems & Medical Oversight. 2nd ed. St. Louis: Mosby Year Book; 1994:24.

23. Giordana LM, Davidson SJ. Urban systems. In: Kuehl AE, ed. National Association of EMS Physicians: Prehospital Systems & Medical Oversight. 2nd ed. St. Louis: Mosby Year Book; 1994:35. 24. American College of Surgeons Committee on Trauma, American College of Emergency Physicians, National Association of EMS Physicians, et al. Equipment for Ambulances. Chicago, IL; 2009. Available at: http://www. facs.org/fellows_info/bulletin/2009/ambulance0709.pdf. Accessed September 21, 2010. 25. Neel S. Army aeromedical evacuation procedures in Vietnam: implications for rural America. JAMA. 1968;204:99. 26. Fischer RP, Flynn TC, Miller PW, et al. Urban helicopter response to the scene of injury. J Trauma. 1984;24:946. 27. Baxt WG, Moody P. The impact of a rotorcraft aeromedical emergency care service on trauma mortality. JAMA. 1983;249:3047. 28. Law DK, Law JK, Brennan R, et al. Trauma operating room in conjunction with an air ambulance system: indications, interventions, and outcomes. J Trauma. 1982;22:759. 29. Urdaneta LF, Miller BK, Ringenberg BJ, et al. Role of an emergency helicopter transport service in rural trauma. Arch Surg. 1987; 122:992. 30. Boyd CR, Corse KM, Campbell RC. Emergency interhospital transport of the major trauma patient: air versus ground. J Trauma. 1989;29: 789. 31. Baxt WG, Moody P, Cleveland HC, et al. Hospital-based rotorcraft aeromedical emergency care services and trauma mortality: a multicenter study. Ann Emerg Med. 1985;14:859. 32. Moront ML, Gotschall CS, Eichelberger MR. Helicopter transport of injured children: system effectiveness and triage criteria. J Pediatr Surg. 1996;31:1183. 33. Bartolacci RA, Munford BJ, Lee A, et al. Air medical scene response to blunt trauma: effect on early survival. Med J Aust. 1998;169:612. 34. Thomas SH, Harrison TH, Buras WR, et al. Helicopter transport and blunt trauma mortality: a multicenter trial. J Trauma. 2002;52: 136. 35. Cunningham P, Rutledge R, Baker CC, et al. A comparison of the association of helicopter and ground transport with the outcome of injury in trauma patients transported from the scene. J Trauma. 1997;43:940. 36. Brathwaite CEM, Rosko M, McDowell R, et al. A critical analysis of on-scene helicopter transport on survival in a statewide trauma system. J Trauma. 1998;45:140. 37. Schiller WR, Knox R, Zinnecker H, et al. Effect of helicopter transport of trauma victims on survival in an urban trauma center. J Trauma. 1988;28:1127. 38. Schwartz RJ, Jacobs LM, Yaezel D. Impact of pre-trauma center care on length of stay and hospital charges. J Trauma. 1989;29:1611. 39. Diaz MA, Hendey GW, Bivins HG. When is the helicopter faster? A comparison of helicopter and ground ambulance transport times. J Trauma. 2005;58:148. 40. Bledsoe BE, Smith MG. Medical helicopter accidents in the United States: a 10-year review. J Trauma. 2004;56:1325. 41. Swor RA, ed. National Association of EMS Physicians: Quality Management in Prehospital Care. St. Louis: Mosby Year Book; 1993. 42. Longdistanceus.com. 75% of the US Covered by E911 Service. Available at: http://www.longdistanceus.com/news/75_percent_of_us_covered_ by_e-911_service.html. Accessed September 21, 2010. 43. Pons PT, Markovchick VJ. Eight minutes or less: does the ambulance response time guideline impact trauma patient outcome? J Emerg Med. 2002;23:43. 44. Salomone JP, Pons PT, McSwain NE, eds. PHTLS: Prehospital Trauma Life Support. 7th ed. St. Louis: Mosby; 2011. 45. McSwain NE Jr. EMS medical director. In: McSwain NE Jr, Paturas JL, eds. The Basic EMT: Comprehensive Prehospital Patient Care. 2nd ed. St. Louis: Mosby Year Book; 2001:42. 46. Holroyd BR, Knopp R, Kallsen G. Medical control: quality assurance in pre-hospital care. JAMA. 1986;256:1027. 47. McSwain NE Jr. Medical control in prehospital care. J Trauma. 1984;24:172. 48. Braun O. Direct medical control. In: Kuehl AE, ed. National Association of EMS Physicians: Prehospital Systems & Medical Oversight. 2nd ed. St. Louis: Mosby Year Book; 1994:196. 49. McSwain NE Jr. Indirect medical control. In: Kuehl AE, ed. National Association of EMS Physicians: Prehospital Systems & Medical Oversight. 2nd ed. St. Louis: Mosby Year Book; 1994:186. 50. American College of Surgeons Committee on Trauma. Advanced Trauma Life Support for Doctors. 8th ed. Chicago: American College of Surgeons; 2008.

Prehospital Care 79. Alam HB, Uy GB, Miller D, et al. Comparative analysis of hemostatic agents in a swine model of lethal groin injury. J Trauma. 2003; 54:1077. 80. McManus J, Hurtado T, Pusateri A, et al. A case series describing thermal injury resulting from zeolite use for hemorrhage control in combat operations. Prehosp Emerg Care. 2007;11:67. 81. Hopson LR, Hirsch E, Delgado J, et al. Guidelines for withholding or termination of resuscitation in prehospital traumatic cardiopulmonary arrest: Joint Position Statement of the National Association of EMS Physicians and the American College of Surgeons Committee on Trauma. J Am Coll Surg. 2003;196:106. 82. Teasdale G, Jennett B. Assessment of coma and impaired consciousness: a practical scale. Lancet. 1974;2:81. 83. Demetriades D, Chan L, Cornwell E, et al. Paramedic vs. private transportation of trauma patients: effect on outcome. Arch Surg. 1996;131:133. 84. Sasser SM, Hunt RC, Sullivent EE, et al. Guidelines for field triage of injured patients: recommendations of the national expert panel on field triage. MMWR. 2009;58:1. 85. Wade CE, Kramer GC, Grady JJ. Efficacy of hypertonic 7.5% saline and 6% dextran in treating trauma: a metaanalysis of controlled clinical trials. Surgery. 1997;122:609. 86. Lewis FR. Prehospital intravenous fluid therapy: physiologic computer modeling. J Trauma. 1986;26:804. 87. Gross D, Landau EH, Assalia A, et al. Is hypertonic saline resuscitation safe in “uncontrolled” hemorrhagic shock? J Trauma. 1988;28: 751. 88. Gross D, Landau EH, Klin B, et al. Quantitative measurement of bleeding following hypertonic saline therapy in “uncontrolled” hemorrhagic shock. J Trauma. 1989;29:79. 89. Krausz MM, Bar-Ziv M, Rabinovici R, et al. “Scoop and run” or stabilize hemorrhagic shock with normal saline or small-volume hypertonic saline? J Trauma. 1992;33:6. 90. Craig RL, Poole GV. Resuscitation in uncontrolled hemorrhage. Am Surg. 1994;60:59. 91. Bickell WH, Wall MJ, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994;331:1105. 92. Muizelaar JP, Marmarou A, Ward JD, et al. Adverse effects of prolonged hyperventilation in patients with severe brain injury: a randomized clinical trial. J Neurosurg. 1991;75:731. 93. Brain Trauma Foundation. Guidelines for Prehospital Management of Traumatic Brain Injury. 2nd ed. New York, NY: Brain Trauma Foundation; 2007. Available at: http://braintrauma.org/pdf/Prehospital_Guidelines_ 2nd_Edition.pdf. Accessed September 25, 2010. 94. Warner KJ, Cuschieri J, Copass MK, et al. The impact of prehospital ventilation on outcome after severe traumatic brain injury. J Trauma. 2007;62:1330. 95. Warner KJ, Cuschieri J, Garland B. The utility of early end-tidal capnography in monitoring ventilation status after severe injury. J Trauma. 209;66:26. 96. Eckstein M, Suyehara D. Needle thoracostomy in the prehospital setting. Prehosp Emerg Care. 1998;2:132. 97. Davis DP, Petit K, Rum CD, et al. The safety and efficacy of prehospital needle and tube thoracostomy by aeromedical personnel. Prehosp Emerg Care. 2005;9:191. 98. Cullinane DC, Morris JA, Bass JG. Needle thoracostomy may not be indicated in the trauma patient. Injury. 2001;32:749. 99. Givens ML, Ayotte K, Manifeld C. Needle thoracostomy: implications of computer tomography chest wall thickness. J Acad Emerg Med. 2004;11:211. 100. Marinaro JL, Kenny CV, Smith SR, et al. Needle thoracostomy in trauma patients: what catheter length is adequate? Acad Emerg Med. 2003;10:495. 101. Domeier RM, National Association of EMS Physicians Standards and Clinical Practices Committee. Indications for prehospital spinal immobilization. Prehosp Emerg Care. 1997;3:251. 102. Cornwell EE, Chang DC, Bonar JP, et al. Thoracolumbar immobilization for trauma patients with torso gunshot wounds: is it necessary? Arch Surg. 2001;136:324. 103. Haut ER, Kalish BT, Efron DT, et al. Spinal immobilization in penetrating trauma: more harm than good? J Trauma. 2010;68: 15. 104. Seyfer AE, American College of Surgeons Committee on Trauma. Guidelines for Management of Amputated Parts. Chicago, IL; 1996. Available at: http://www.facs.org/trauma/publications/amputatedparts. pdf. Accessed September 25, 2010.

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51. Campbell JE, ed. International Trauma Life Support for Prehospital Care Providers. 6th ed. Upper Saddle River, NJ: Brady/Prentice Hall Health; 2007. 52. Stewart RP, Paris PM, Pelton GH, et al. Effect of various training techniques on field endotracheal intubation success rates. Ann Emerg Med. 1984;13:1032. 53. Scannell G, Waxman K, Tominaga G, et al. Orotracheal intubation in trauma patients with cervical fractures. Arch Surg. 1993;128:903. 54. Shatney CH, Brunner RD, Nguyen TQ. The safety of orotracheal intubation in patients with unstable cervical spine fracture or high spinal cord injury. Am J Surg. 1995;170:676. 55. Iserson KV. Blind nasotracheal intubation. Ann Emerg Med. 1981;10:468. 56. Hardwick WC, Bluhm D. Digital intubation. J Emerg Med. 1983;1:317. 57. McNamara RM. Retrograde intubation of the trachea. Ann Emerg Med. 1987;16:680. 58. Katz SH, Falk JL. Misplaced endotracheal tubes by paramedics in an urban emergency medical services system. Ann Emerg Med. 2001; 31:32. 59. O’Connor RE, Swor RA. Verification of endotracheal tube placement following intubation. Prehosp Emerg Care. 1999;3:248. 60. Silvestri S, Ralis GA, Krauss B, et al. The effectiveness of out-of-hospital use of continuous end-tidal carbon dioxide monitoring on the rate of unrecognized or misplaced intubations within a regional emergency medical services system. Ann Emerg Med. 2005;45:497. 61. Hedges JR, Dronen SC, Feero S, et al. Succinylcholine-assisted intubations in prehospital care. Ann Emerg Med. 1988;17:469. 62. Wayne MA, Friedland E. Prehospital use of succinylcholine: a 20-year review. Prehosp Emerg Care. 1999;3:107. 63. Ochs M, David D, Hoyt D, et al. Paramedic-performed rapid sequence intubation of patients with severe head injuries. Ann Emerg Med. 2002;40:159. 64. Davis DP, Hoyt DB, Ochs M, et al. The effect of paramedic rapid sequence intubation on outcome in patients with severe traumatic brain injury. J Trauma. 2003;54:444. 65. Davis DP, Fakhry SM, Wang HE, et al. Paramedic rapid sequence intubation for severe traumatic brain injury: perspectives from an expert panel. Prehosp Emerg Care. 2007;11:1. 66. Wang HE, Yealy DM. Out-of-hospital endotracheal intubation: where are we? Ann Emerg Med. 2006;46:532. 67. Martin SE, Ochsner MG, Jarman RH, et al. Use of the laryngeal mask airway in air transport when intubation fails. J Trauma. 1999; 47:352. 68. Frame SB, Simon JM, Kerstein MD, et al. Percutaneous transtracheal catheter ventilation (PTCV) in complete airway obstruction—a canine model. J Trauma. 1989;29:774. 69. Boyle MF, Hatton D, Sheets C. Surgical cricothyroidotomy performed by air ambulance flight nurses: a 5-year experience. J Emerg Med. 1993;11:41. 70. Jacobson LE, Gomez GA, Sobieray RJ, et al. Surgical cricothyroidotomy in trauma patients: analysis of its use by paramedics in the field. J Trauma. 1996;41:15. 71. Fortune JB, Judkins DG, Scanzaroli D, et al. Efficacy of prehospital surgical cricothyroidotomy in trauma patients. J Trauma. 1997; 42:832. 72. Davis DP, Dunford JV, Poste JC, et al. The impact of hypoxia and hyperventilation on outcome after paramedic rapid sequence intubation of severely head injured patients. J Trauma. 2004;57:1. 73. Pepe PE, Raedler C, Lurie KG. Emergency ventilatory management in hemorrhagic states: elemental or detrimental? J Trauma. 2003;54:1048. 74. Walters TJ, Mabry RL. Use of tourniquets on the battlefield: a consensus panel report. Mil Med. 2005;170:770. 75. Committee on Tactical Combat Casualty Care. Tactical Combat Casualty Care Guidelines. Washington, DC; November 2009. Available at: http:// www.health.mil/Libraries/Presentations_Course_Materials/TCCC_ Guidelines_091104.pdf. Accessed September 26, 2010. 76. Kragh JP, Walters TJ, Baer DG, et al. Practical use of emergency tourniquets to stop bleeding in major limb trauma. J Trauma. 2008;64:S38. 77. Kragh JP, Walters TJ, Baer DG, et al. Survival with emergency tourniquet use to stop bleeding in major limb trauma. Ann Surg. 2009; 249:1. 78. Pusateri AE, McCarthy S, Gregory KW, et al. Effects of a chitosan-based hemostatic dressing on blood loss and survival in a model of severe venous hemorrhage and hepatic injury in swine. J Trauma. 2003;54:177.

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105. White LJ, Cooper JD, Chambers RM, et al. Prehospital use of analgesia for suspected extremity fractures. Prehosp Emerg Care. 2000;4:205. 106. Alonso-Serra HM, Wesley K. Prehospital pain management. Prehosp Emerg Care. 2003;7:482. 107. Arnold T, Cleary V, Groth S, et al. START. Newport Beach, CA: Newport Beach Fire and Marine Department; 1994. 108. Risavi BL, Salen PN, Heller MB, et al. A two-hour intervention using START improves prehospital triage of mass casualty incidents. Prehosp Emerg Care. 2001;5:197.

109. Lerner EB, Schwartz RB, Coule PL. Mass casualty triage: an evaluation of the data and development of a proposed national guideline. Disaster Med Public Health Preparedness. 2008;2:S25. 110. Stiell IG, Nesbitt LP, Pickett W, et al. The OPALS Major Trauma Study: impact of advanced life-support on survival and morbidity. Can Med Assoc J. 2008;178:1141. 111. Ali J, Adam RU, Gana TJ, et al. Trauma patient outcome after the prehospital trauma life support program. J Trauma. 1997;42:1018.

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CHAPTER 8

Disaster and Mass Casualty Eric R. Frykberg and William P. Schecter

INTRODUCTION The term disaster is subject to a variety of interpretations and misperceptions that typically relate to one’s background and experience, but there are specific characteristics on which most would agree. An essential feature of a disaster involves a major disruption of the infrastructure of a community or geographic region and its inhabitants. Another is that the magnitude of destruction exceeds that of routine emergency situations to such an extent that the response to it must be entirely different in order to restore some semblance of order and normalcy. Approaching a disaster with the mindset of simply doing more of the same, using the same methods as routine emergencies, is generally doomed to failure and tends to extend rather than curtail the adverse consequences.1 True disasters are rare. Very few events in a century result in more than 1,000 casualties, and only about 10–15 events each year throughout the world result in more than 40 casualties.2 Because they are rare, as well as unpredictable, random, sudden, and unexpected, their successful management requires established and well-rehearsed plans that anticipate necessary consequences, procedures, and needs.2–4 The feature that best distinguishes the medical response to a disaster from the routine medical care of patients is that resources are overwhelmed by the casualty load. The receiving hospital is therefore unable to provide each casualty with the optimal level of care that is standard in routine medical management.5,6 External assistance is necessary to manage the event. This has significant impact on the approach to medical care and the associated ethical considerations, as, by definition, the limited resources must be rationed according to who most merits care so as to avoid squandering these resources and leaving many other casualties without care that may be more effectively applied in terms of overall casualty salvage. This means that some casualties who would ordinarily be treated may have to be denied full care for the sake of saving many more. These altered standards of care

that must prevail in true disasters tend to be unfamiliar and morally repugnant to health care providers, and they are not taught in medical or nursing schools or residency training. This emphasizes the necessity of education and training in these principles if a medical response is to succeed.7 This response cannot just be more of the same, but an entirely different approach to care. The longer it takes to learn this as a medical response unfolds, the more property and lives will be lost unnecessarily.1 A multiple casualty event is one in which hospital resources are strained, but not overwhelmed, by the patient load, as we experience on busy nights in urban trauma centers and emergency rooms. All patients are ultimately fully treated according to our standard principle of the greatest good for each individual, although the costs include extra personnel, financial losses, delays in care, and difficulty in finding beds, operating rooms (ORs), and equipment. A mass casualty event is distinctly different, referring to casualty loads that overwhelm available resources, preventing optimal individual care. This requires a paradigm shift in focus on a new principle of the greatest good for the greatest number. A disaster response must revolve around the population rather than the individual, with all the difficult ethical implications of rationed care.7,8 The average medical provider may never see a true mass casualty disaster in an entire career, which all the more emphasizes the importance of education and training to prepare for them.

CLASSIFICATION OF DISASTERS Several classification schemes (Table 8-1) have been applied to disasters.3 The number of casualties is often used to define a mass casualty event and its severity, although it is a relative measure that does not necessarily reflect the magnitude of an event. Five victims of a motor vehicle crash could be handled easily at a major urban trauma center, while this could overwhelm a small rural hospital and be seen there as a true mass casualty disaster. Classification according to mechanism, such

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Generalized Approaches to the Traumatized Patient Closely related to this are finite disasters, which occur within a defined and usually short period of time with a clear beginning and end, such as tornados or terrorist bombings. The response challenges in terms of resources and personnel would be quite different in open disasters occurring over a wide geographic area, such as hurricanes, and in ongoing disasters, in which destruction occurs over a prolonged and uncertain time period, such as aftershocks following an earthquake, disease pandemics, or armed conflicts and wars. The most useful classification scheme groups events according to the level and extent of response and resources necessary to manage the destruction of people and property. A common system involves three levels of response, from local to regional to statewide, national or international. This tends to work best and is widely used because it corresponds to the most basic disaster characteristic of overwhelmed resources, and magnitude is reflected by the extent of external assistance that is needed.

TABLE 8-1 Disaster Classification Schemes

PLANNING Plans are nothing. Planning is everything. Dwight David Eisenhower

as tornados, hurricanes, earthquakes, fires, floods, shootings, or bombings, natural or man-made, allows identification of distinct patterns of damage, injury, and logistical demands. Classification according to injury type similarly allows distinction of these patterns to facilitate response planning, such as burns, blast injuries, and chemical or radiation poisoning. Extent and timing of a disaster may be a useful means of classification in view of the very different types of response required for specific geographic and time course considerations. A closed disaster refers to a single event occurring in a specific location, with a clearly defined scene, such as a building collapse.

The word disaster is derived from the Latin words for “evil star,” suggesting that these events are random and unpredictable acts of God for which anticipation and preparation is futile. In fact, the very rarity and unpredictability of disasters make advance preparations essential for a successful response to occur, as the complexity and very different approaches of such a response tend to be counterintuitive and cannot be cobbled together at the time of the event. Furthermore, there are patterns of property damage, bodily injury, behavior, response elements, and pitfalls that are common to all disasters. Once such patterns can be identified (Fig. 8-1), preparation and

ISS distribution, Beirut and Bologna bombings 50 40 No. casualties

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Number of casualties Mechanism: shootings, explosions, natural Natural Weather related: hurricanes, tornados Geophysical: earthquakes, tsunamis Man-made Intentional: industrial accidents Unintentional: terrorism Nature of injuries: burns, blast, crush Extent and timing Closed Open Finite Ongoing Level of response Local (I) Regional (II) State/national/international (III)

BER BOL

30 20 10 0 0-5 6-10 11-15 16-20 21-25 26-30 31-4041-50 51-65 66-75 Mean ISS: Beirut 11.7, Bologna 11.0

FIGURE 8-1 Graphic comparison of the range of Injury Severity Scores (ISS) of survivors of the terrorist bombings of the train station in Bologna, Italy, in 1980 and the U.S. Marines barracks in Beirut, Lebanon, in 1983,6,19,63 showing the common pattern seen in most disasters of only a minority with critical injuries. (From Frykberg ER. Disaster and mass casualty management. In: Britt LD, ed. Acute Care Surgery. 2007:235, Fig. 16-2, with kind permission of Springer ScienceBusiness Media.)

Disaster and Mass Casualty

TABLE 8-3 Key Stakeholders in Disaster Planning

Communications Authority and responsibility Security Organization of medical care Desire to help Media Original disaster plan

Hospital Assets Medical and nursing staffs Administration Security Food services Hospital Incident Command (HICS) Volunteer services Blood bank/laboratory Poison control center Pharmacy Radiation biologist Imaging services Operating room staff Intensive care unit staff Public Information Office Chaplains/social workers Rehabilitation assets

planning are entirely possible, and moreover are the most essential factors that lead to a successful outcome in terms of minimizing the loss of infrastructure and lives.4,9–12 Disaster planning begins with education. Knowledge of the abundant published reports of past disasters and of basic principles of disaster response is necessary for the formulation of a realistic and workable disaster plan. The plan must be based on valid assumptions derived from actual experience so as to accurately anticipate the most likely injury patterns, resource requirements, human behavior, and threats.13 Without this knowledge, plans tend to be based on imagination rather than reality. It is common for plans to assume model behavior, rather than incorporate how people actually behave in this setting.2,13 The problems and lessons learned in past disasters serve as an important planning tool that allows the plan to avoid their repetition (Table 8-2), and to thus be more useful in future events. Failure of communications has been the most common and consistent pitfall of disaster responses, due to damage to telephone, cellular phone, and radio infrastructure, and to overloading of that infrastructure by overuse. Communication is the thread that weaves the complex fabric of a disaster response together. Its breakdown impairs the coordination and interoperability of this response. Without redundant systems in place to maintain this interoperability, the response will falter. Another major pitfall of most disaster responses is the uncertainty of who is in charge, which must be designated and understood by all responders in advance to avoid a loss of command and control. Failure of security at the disaster scene and in the hospital increases the dangers to casualties, responders, and medical providers. The system of medical care for mass casualties must be workable to optimize their outcomes. The control of volunteers, the worried well, families, and the media is necessary to prevent confusion of roles, misinterpretation of instructions and messages, and mass confusion by these well-meaning but uninformed and untrained entities. Finally, the original disaster plan has consistently been found to be unworkable very early into the response of virtually every reported disaster, demonstrating a widespread failure of valid and effective planning.14 Disaster plans and the process of planning must integrate the many multidisciplinary entities that will contribute to the disaster response and work toward the common goal of recovery (Table 8-3). Plans should be developed by the people who will be executing them. The formulation of a plan should begin with an assessment of the most likely threats that may give rise to a disaster event in any given community or region, which is known as a hazards vulnerability analysis (HVA). The plan should

Community Assets Emergency operations center Public Health Department Prehospital EMS services Law enforcement/forensics Fire department Search and rescue Media Local/state government Medical examiner Business leaders Transportation/evacuation services Area blood banks/Red Cross Area hospital representatives Mental health services Local medical society Civil/structural engineers

then be built around such threats. Examples include radiation leaks from a nearby nuclear reactor, airplane crashes near airports, floods near major bodies of water, frequent clusters of large numbers of people such as in a sports stadium or theme park, and common weather events such as tornados or hurricanes. Disaster plans should follow an all-hazards approach, which refers to the creation of only one generic plan encompassing those factors common to all disasters. This is far more effective than multiple plans for each specific type of disaster, as these are unlikely to all be read and remembered by responders and providers. A robust all-hazards plan will have the necessary flexibility to adapt to the unique challenges of each specific event. An example of how to provide such flexibility is to attach appendices to the generic plan for such categories as burns, radiation or chemical poisoning, and blast injuries. The basic premise of all-hazards planning is that all disasters should have the same broad principles of response.4 The planning process is more important than the written plan, which often sits on a shelf unread. The collective interaction of the many different response elements in this process allows all participants to understand the capabilities and needs of each other, and thus how everyone fits into the overall disaster response (see Table 8-3). This provides flexibility and adaptability to the unique exigencies of any specific event, which is independent of the written plan and allows a response to proceed despite an unrealistic written plan. This process helps to prevent the paper plan syndrome, or the false sense of complacency that a written plan may confer even though it is not read or tested. Once formulated, disaster plans must be tested regularly through both hospital drills of a single facility and communitywide exercises that integrate multiple response elements. These simulations are meant to test the plan for its ability to guide the response to actual events, and should be as realistic as

CHAPTER 8

TABLE 8-2 Common Pitfalls in Disaster Response

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possible in order to confirm its effectiveness and uncover weaknesses that should be improved.4,15 A postevent analysis of all drills and actual disasters is another essential element of disaster planning. This should involve all key participants in the response and should occur within 24–48 hours of the event while memories are fresh. Documentation of all parts of the disaster response should be objectively and comprehensively reviewed to identify those things that worked and those that did not. The plan should then be revised and strengthened accordingly to make it more workable and successful the next time. Disaster planning must be a dynamic process. It is also important to disseminate the lessons learned so as to extend the existing knowledge base.14 Such a postevent critique of the New Orleans response to Hurricane Katrina in 2005 showed a number of weaknesses in the disaster plan despite its thoughtful formulation and testing.16

COMMAND AND CONTROL In order to coordinate the complex structure of a disaster response, there must be a recognized prevailing authority to exert command and control. The absence of clear authority is one of the most common barriers to a successful disaster response (see Table 8-2), as each of the many participating agencies and personnel tends to believe that it is in charge, and is reluctant to yield its individual missions, agendas, and independence to an overriding command element. This, of course, prevents the smooth coordination and interoperability of all these entities that is necessary to achieve a common goal, as none of these entities have the perspective to appreciate the “big picture.” It is clear that the longer it takes to exert effective command and control of a disaster scene, the longer will chaos, and destruction of property and lives, persist.9,14,17,18 An effective disaster response command structure incorporates three widely recognized command principles. Unity of command refers to a designated hierarchy in which all personnel have specific roles and responsibilities with regard to the common goal. Chain of command refers to the reporting process in this hierarchy, in which each person reports to one

supervisor, and no more than five to seven people report to one person (span of control). Unified command refers to the consolidation of all response elements under a single authority who determines the overall mission and objectives toward which all efforts are directed in a coordinated fashion. Deviation from these principles, such as bypassing the chain of command, weakens the structure as a whole by impairing the commander’s situational awareness, and thus the ability to properly execute the mission. This weakness has manifested in a number of major disasters. In New York City on September 11, 2001, no clear authority existed to coordinate the independent actions of multiple response elements following the collapse of the World Trade Center. This same problem was evident following Hurricane Katrina in New Orleans in 2005, and following the earthquake in Haiti on January 12, 2010. The result in these and many similar events was large-scale confusion over the roles of responders, loss and waste of equipment and supplies, lack of enforcement of safety precautions with exposure of responders and medical providers to safety risks, and delays in provision of food, water, shelter, and medical care. Following a series of wildfires in California in the 1970s, the problem of poor coordination of multiple response units from multiple jurisdictions was identified. The Incident Command System (ICS) was developed as a management tool to address these command and control issues in the setting of major disasters, by incorporating all response elements under a single Incident Commander (IC). ICS is based on functional requirements that are allocated among five major management activities carried out by a general staff—command, planning, logistics, operations, and finance/administration. The operations section is directly responsible for the nuts and bolts of the response, including casualty care, and all other sections support this element. A command staff directly supports the IC with interaction with the media and the public, assurance of safety, and facilitating coordination of all elements, through a Public Information Officer, a Safety Officer, and a Liaison Officer, respectively. The ICS incorporates the three command principles described above to be highly flexible and adaptable to any form of disaster or emergency (Fig. 8-2). Its success and effectiveness

Incident commander

Public information officer

Liaison officer

Safety officer

Technical specialist

Planning

Logistics

Operations

Finance/Admin.

Organization Intelligence Pt tracking assess needs Advise/predict

Supplies Equipment Transport Food Sanitation

Medical care Search and rescue Security Site clearing Forensics/law Fire services

Records Contracts Procurement Costs/charges Payments

FIGURE 8-2 The structure and major functional elements of the Incident Command System.

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127

9 8

No. casualties/hour

7

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CC/HR (surge capacity) Non-CC/HR (overtriage load)

6 5 4 3 2 1 0 0

50

25

75

Overtriage rate (%)

FIGURE 8-3 Effect of increasing overtriage (arrival rate of noncritical casualties, non-cm3/h) on hospital capability to optimally care for arriving critical casualties, or surge capacity (cm3/h). (From data in Hirshberg A, Scott BG, Granchi T, et al. How does casualty load affect trauma care in urban bombing incidents? A quantitative analysis. J Trauma. 2005;58:686–695, with permission of Lippincott Williams & Wilkins.)

is demonstrated by its adoption as the official model for disaster response in the United States and many other countries. All participants in a disaster response must learn this system and their specific role within it.18

TRIAGE The sorting and prioritization of casualties according to their needs is known as triage. This is generally a minor consideration in routine medical care, where there are essentially unlimited resources and all may be provided optimal treatment. However, in austere environments and in mass casualty events, the process of triage assumes major importance because, by definition, resources are limited, and must therefore be allocated, or rationed, according to the principle of the greatest good for the greatest number. This is a major departure from routine standards of medical care, as necessary considerations of salvageability and resource availability must enter into these decisions.7 The most severely injured casualties with the lowest chance of survival, yet with the greatest resource requirements, may have to be put aside and treated last, if at all, rather than first, in order to conserve the limited resources for the greater number who will most benefit. Rapid identification of this expectant category of casualties provides the best opportunity for maximizing casualty salvage.3,6,9,19–22

■ Triage Accuracy The challenge of triage lies in the very consistent pattern of injury severity found in most mass casualty disasters (see Fig. 8-1), in which a large majority of survivors are not critically injured and therefore do not require immediate care or even hospitalization.6,19,21,23 The rapid identification of that small minority (10–20%) who are critically injured is vitally important

in order to direct the limited resources where they are most needed, and not squander them on those not in need. This is the key challenge of health care providers. The two errors of triage include undertriage, or the inappropriate assignment of critically injured casualties to a delayed, nonurgent category, and overtriage, or the assignment of noncritical casualties to immediate, urgent care. Undertriage is always considered a medical problem that results in preventable mortality, because necessary care is delayed. In routine medical care, overtriage is more of a logistical, economic, and administrative problem, resulting in strained financial, personnel, supply, and equipment resources, but does not impact patient outcomes. However, in a mass casualty setting, when large numbers inundate a hospital all at once, overtriage impairs the ability to detect the critically injured minority who require early lifesaving interventions, and could therefore be as much a threat to casualty survival as undertriage. Hirshberg et al. have provided data to support this contention with a computer modeling study of mass casualty events24 that demonstrates a diminishing capability to optimally care for critical casualties as the rate of overtriage, or influx of noncritical casualties, increases (Fig. 8-3). They have extended this finding with another recent computer model25 showing an improvement in the ability of hospital trauma teams to manage an increasing influx of critically injured mass casualties as triage accuracy increases (Fig. 8-4). That this degradation in care may lead to increased mortality among critically injured mass casualties, as most appropriately measured by the critical mortality rate (CMR), is suggested by a meta-analysis of published data from 14 major terrorist bombing disasters comprising 3,105 casualties (Table 8-4).6,19,23,26 Graphic depiction of these data confirms a highly consistent linear relationship (r  0.92) between overtriage and CMR (Fig. 8-5).

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Generalized Approaches to the Traumatized Patient Triage accuracy 50% Triage accuracy 80% Triage accuracy 100%

180

Time to saturation (min)

SECTION 2

160 140

A

B

120 100 80 60 40 20 0 0

2

4 6 8 10 12 14 Severe casualties per hour

16

FIGURE 8-4 Computer model of mass casualty hospital management showing improving surge capacity (arrival rate of critical casualties) at which trauma teams can provide optimal care (time to saturation of teams) with improving triage accuracy (% correct decisions), with reference surge capacity at 6 critical casualties/h. (From Hirshberg A, et al. Triage and trauma workload in mass casualty: a computer model. J Trauma. 2010;69:1074–1081. Wolters Kluwer Health, Lippincott Williams & Wilkins, with permission.)

TABLE 8-4 Relation of Overtriage to Critical Mortality in Survivors of 14 Terrorist Bombings and 3 Nonbombing Mass Casualty Events Event (Reference) Cu Chi Craigavon Old Bailey Guildford Birmingham Tower of London Bologna Beirut Keystoned AMIA Oklahoma City 9/11 NYC Helsinki Mall Rhode Islandd Madrid London Virginia Techd Total

Year 1969 1970s 1973 1974 1974 1974 1980 1983 1987 1994 1995 2001 2002 2003 2004 2005 2007

No. of Survivors 34 339 160 64 119 37 218 112 60 200 597 30 161 215 312 722 26 3,406

No. of Critically Injured (%)a 3 (9) 113 (33) 4 (2.5) 22 (34) 9 (8) 10 (27) 48 (22) 19 (17) 12 (20) 14 (7) 52 (9) 7 (23) 13 (8) 79 (37) 29 (9.3) 20 (2.7) 5 (19) 459 (13.5)

No. of Overtriageb (%) 9 (75) 29 (20) 15 (79) 2 (8.3) 12 (57) 9 (47) 133 (73.5) 77 (80) 7 (21)e 47 (56) 31 (37) 23 (77) 11 (52) 23 (10.6) 62 (68) 35 (64) 18 (69) 543 (54)

No. of Critical Mortality (%)c 1 (33) 5 (4) 1 (25) 0 2 (22) 1 (10) 11 (23) 7 (37) 1 (8.5) 4 (29) 5 (10) 2 (29) 2 (15) 4 (5) 5 (17) 3 (15) 1 (20) 55 (12)

a

Percentage of total survivors.

b

Number of noncritical survivors triaged to immediate care or hospital, as a percentage of all casualties triaged to immediate care or hospital. c

Number and percentage of all critically injured survivors who died.

d

Nonbombing events described in text.

e

Based on 33 patients presenting to hospitals. Adapted from Frykberg ER. Medical management of disasters and mass casualties from terrorist bombings: how can we cope? J Trauma. 2002;53:201–212. Wolters Kluwer Health, Lippincott Williams & Wilkins, with permission.

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129

40 Beirut

CHAPTER 8

35 Cu Chi

Critical mortality rate (%)

30

AMIA

9/11 Old Bailey

25 Birmingham

Bologna

20

Va Tech* Madrid

15

London

Helsinki Keystone*

10

Oklahoma City

Tower of London

Rhode Island* 5

Craigavon

R = 0.92

Guildford 0 0

10

20

30

40

50

60

70

80

90

Overtriage rate (%)

FIGURE 8-5 Relationship of overtriage and critical mortality rate in mass casualties from 14 terrorist bombing events (in black) and 3 nonbombing events (in red), from data in Table 8-4. (Adapted from Frykberg ER. Medical management of disasters and mass casualties from terrorist bombings: how can we cope? J Trauma. 2002;53:201–212, Wolters Kluwer Health, Lippincott Williams & Wilkins, with permission.)

This same relationship holds true with the application of data from 3 additional nonbombing mass casualty disasters with a total of 301 surviving casualties—the 1987 Keystone, Colorado, chairlift accident,27 the 2003 Station nightclub fire in Rhode Island,12 and the 2007 mass shooting at Virginia Tech.28,29 This overall analysis of 3,406 casualties from 17 disasters (see Table 8-4 and Fig. 8-5) demonstrates that the adverse effect of overtriage is not confined to any one disaster mechanism, but relates to the common pattern of all disasters, regardless of mechanism, in which the inundation of hospitals with a sudden large casualty load interferes with the delivery of urgent medical care. It is clear that triage accuracy, which involves minimizing both undertriage and overtriage, is essential to the success of a disaster medical response. In fact, it is the one element of a disaster response in which medical providers can directly impact casualty outcomes in the initial aftermath of a disaster. The triage officer who makes these decisions therefore has an important role in this setting. This person must be experienced in the types of injuries that each disaster is likely to cause, and should also be trained in the unique standards that must be applied to mass casualty care in order to optimize triage accuracy, and thus casualty survival. Who should be designated as the triage officer is dependent more on training and experience than on

professional background, and it need not even be a physician. It is important to recognize that this position involves only decision making and not treatment, and therefore any physician or surgeon in this role is being removed from casualty care. Available resources must thus impact the decision as to who should be in this position. In some events, nurses or prehospital personnel may best perform this duty. In unconventional disasters, such specialists as infectious disease or public health personnel, radiation biologists, or toxicologists may be the most appropriate triage officer. However, most disasters result in bodily injury, in which setting surgeons and emergency medicine physicians are best in this role because of their experience with the acute care of trauma victims.5,6,9,12,17,21,30 Whoever assumes this role must have the leadership qualities to exert authority and make prompt and firm decisions that will be followed, and must have situational awareness of evolving conditions and resource constraints to make accurate decisions.

■ Triage Decisions Triage decisions must be rapid as well as accurate in order to move casualties along to accommodate the continuing influx of more casualties. The greater the casualty load, the more rapid must this process be. Therefore, these decisions must be as

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simple and abbreviated as possible. It should not be surprising that the many complex triage methodology schemes currently in vogue, which require assessment of multiple physiologic and anatomic parameters on each casualty, prove unworkable in true disasters.31 Those who are most experienced in mass casualty triage consistently assert that decisions must derive from no more than a clinical judgment, or gestalt, after a quick look at the victim for a few seconds.5,17,32–36 Casualty dispositions must also be simple. In the prehospital sector, all that is necessary is to determine if a casualty is alive or dead, and, if alive, whether hospitalization is warranted or not. Those judged to require hospitalization are then moved on, and at the hospital the decision is made as to entrance or not. Once in the hospital, the basic decision is whether the casualty requires one of the critical resources of OR, intensive care unit (ICU), or not. Further segregation into delayed and minimal categories may be made at this point, but it should be noted that if minimally injured casualties are in the hospital, there was a failure in the triage process to keep them out, as they should not be burdening this critical resource. Those casualties judged as expectant should also be kept out of the hospital to avoid wasting resources. The dead should be recognized and segregated from the living to avoid unnecessary application of resources on their resuscitation.17 What constitutes an expectant casualty cannot be specifically defined in advance, as it will differ for each specific disaster according to such variables as casualty numbers, type and severity of injuries, and available resources. The leaders of the medical care operations should agree on this determination in the earliest phases of the disaster response, when the magnitude and needed resources can best be assessed. Examples of determining factors include the number of mechanical ventilators, availability of electrical power, the presence of toxic contamination, and the number of available ORs and surgeons.9,20–22 Triage must be a dynamic process that involves continued reassessment at each successive echelon of care, precisely because injury is dynamic and the status of casualties could change over time. Casualties put aside into delayed or expectant categories should be closely monitored for changes that may warrant reassignment to other levels of urgency. This monitoring is an essential backup mechanism for any triage errors made by the triage officer at any point along the casualty care continuum. Errors must be expected in major mass casualty events, but anticipating them, and instilling flexibility in the system to mitigate their adverse consequences, creates error tolerance. Once the casualty influx subsides, resources can be reevaluated, and expectant and delayed casualties may be reconsidered for immediate treatment or other change in status.5,17

MEDICAL CARE OF CASUALTIES ■ Prehospital Considerations Disaster responses typically evolve through four phases—chaos, initial reorganization, site clearing, and recovery.17 The initial chaos that characterizes all disaster scenes is brought to order with the arrival of the first responders and their establishment of command and control. Protection of first responders must be the priority at this point, to prevent them from becoming

secondary casualties and thus depriving the response of their necessary skills. Responders must adhere to the use of personal protective gear and avoid potentially unstable settings that may result in a “second hit” phenomenon that then kills or disables them, such as leaking gas mains that may later explode, damaged buildings that may later collapse, or second bombs that explode later in terrorist events.6,10,15,17,19 As the command structure becomes organized in the initial reorganization phase, a needs assessment is performed, which guides the mobilization and transport of necessary resources. The initial triage and evacuation of surviving casualties from the scene occurs simultaneously with search and rescue and scene stabilization. Casualties should not be transported directly to hospitals from the scene, but should go to one or more casualty collection areas (CCAs), where medical providers may further assess and decide on the need for hospitalization. Without the early establishment of a command authority and CCAs, all casualties tend to go, or be sent, to the nearest hospital, which then becomes overwhelmed and unable to render proper care. This is called the geographic effect. It is best avoided by a systematic distribution of casualties among all available hospitals, called leapfrogging, thereby converting the mass casualty event into many more manageable multiple casualty events at each hospital.9,18,34,36,37 This process must be rapid as well as organized, as the time from injury to definitive treatment is a major prognostic factor for casualty survival.6,19 These prehospital phases of response typically play out over a longer period of time following major natural disasters, such as earthquakes, floods, and destructive weather events. In this setting, early medical care is often nonexistent, due to destruction of medical infrastructure, and the opportunity to save critically injured casualties in the initial aftermath is lost. The needs assessment of these scenes is approached from a longterm relief perspective, targeting food, shelter, sanitation, and long-term care of medical problems. In the early phases, surgical interventions most commonly involve the management of complex limb trauma, including crush syndrome, amputations, and wound care. Longer-term issues include definitive limb rehabilitation, wound healing, and rebuilding medical and surgical infrastructure.38

■ Hospital Considerations The hospital care of the most seriously injured casualties is among the most important elements of a disaster response. Most other response elements revolve around the support of this key function, with the goal of saving lives. In order to best achieve this goal, hospitals must rapidly organize a command structure and implement the disaster plan for casualty care and resource mobilization. In the United States, the most commonly utilized command structure is the hospital version of ICS, termed HICS, in view of its modular structure around the same five key elements as ICS (see Fig. 8-2) that provides the flexibility to adapt to all forms of emergency events.18

Surge In most disasters, there is no standard method for notification of a hospital to which casualties are being transported. It is not

Disaster and Mass Casualty casualty evaluation moves it to the right to increase the casualty load that can be optimally treated. The downslope portion of this curve therefore represents a true mass casualty event in which resources are overwhelmed, while the upper flat portion represents a multiple casualty event in which standard medical care is still effective. It should not be surprising that the relationship of triage accuracy to trauma team workload is also described by a sigmoid curve (see Fig. 8-4), as this workload is an appropriate surrogate for quality of care. The relationship of overtriage to critical mortality discussed in the section “Triage” (see Fig. 8-5) indicates that the result of this degradation of care with increasing casualty loads is death. Together these studies emphasize the essential dependence of casualty outcomes on triage accuracy and efficient casualty throughput.

Resource Utilization Disaster plans must be formulated around realistic expectations of casualty flow patterns and hospital resource utilization following disasters, which are derived from published experiences. Only a minority of 10–15% of casualties will be critically injured (see Fig. 8-1 and Table 8-4), and the less seriously injured tend to be the first to arrive. Triage accuracy is essential to avoid overtriaging these casualties into the hospital and wasting the limited resources where they are not needed, leaving the second critical casualty wave with nothing.5 Within the first hour, 50–65% of all casualties to be admitted will arrive at the hospital, during which time a strong command authority and organized system of care is most important. In urban bombing disasters, which could be considered a universal model for all disasters, OR utilization peaks within 1.5 hours but may continue for 48 hours or longer. Anesthesiologists and general,

Mean global level of care (%)

100

Surge capacity

80

Mean global level of care Nonlinear regression line

60

40

20

0 0

5

10

15

20

Critical casualty load (patients/hour)

FIGURE 8-6 Computer model of mass casualty hospital influx using data from 22 urban terrorist bombings to demonstrate diminishing quality of care with increasing critical casualty load, defining surge capacity as the highest arrival rate (critical casualties/h) at which at least 90% of the optimal level of care can still be delivered to each casualty. (From Hirshberg A, Scott BG, Granchi T, et al. How does casualty load affect trauma care in urban bombing incidents? A quantitative analysis. J Trauma. 2005;58:686–695, Wolters Kluwer Health, Lippincott Williams & Wilkins, with permission.)

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uncommon for hospital personnel to first become aware of a disaster and imminent casualty arrival from the news media, or even from the arrival of the first casualties without warning. Hospitals should expect no more than 10 minutes of warning before casualties arrive following most urban disasters.17 In this time the most urgent preparation that must be made in order to avoid an uncontrolled inundation is a rapid development of space for the casualties (surge capacity), and a rapid mobilization of resources such as stretchers, medical supplies and equipment, and medical and nursing personnel to care for the casualties (surge capability). The priority for this surge must be in the three most needed and utilized hospital units in mass casualty events, the emergency department (ED), where all casualties are initially evaluated, the OR, and the ICU.39 Other spaces should also be cleared for less urgent casualties. Surge capacity requires the discharge or movement of existing patients in these areas to the greatest extent possible, using the process of reverse triage to determine priorities.40,41 Without established and rehearsed hospital disaster plans in place, this immediate mobilization of resources would not be possible, and chaos would soon overwhelm the facility with the incoming casualties. Perhaps the most appropriate functional definition of surge capacity has been provided in the previously discussed computer modeling study by Hirshberg et al.,24 as the arrival rate of critically injured casualties per hour permitting optimal care to still be provided to individual casualties. Once this is exceeded, degradation in individual quality of care must occur, at which point the welfare of the population must prevail over that of the individual as altered standards of care must be applied. As discussed in the section “Triage,” the sigmoid curve that describes this relationship (Fig. 8-6) is moved to the left with increasing overtriage (see Fig. 8-3), while effective planning and efficient

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thoracic, and vascular surgeons are in immediate demand, while orthopedic and plastic surgeons are required later. Of all casualties requiring surgery, 36% went directly to the OR from the ED. Approximately one third of all hospitalized casualties were admitted to the ICU, 31% directly from the ED, and as many as 73% required mechanical ventilation.34,39

Principles of Casualty Care Mass casualty needs are best accommodated by an efficient and organized system of care. ED personnel should be organized into small teams around each stretcher to provide rapid assessment, triage decisions, necessary urgent interventions, and adequate documentation, followed by rapid movement of the casualty onward to successive echelons of care to make way for the next wave of incoming victims.6,12,14,19 Imaging and laboratory tests must be minimized if used at all during this phase of acute casualty influx, to facilitate rapid forward flow of casualties with no backward movements that would create traffic gridlock and chaos.5,6,17 Records must be brief and should be kept with the casualties as they move onward, where they are progressively added so as to provide each new echelon of care sufficient information to allow the appropriate interventions and treatment to proceed. ED, OR, and ICU supervisors, or controllers, should be designated, who are not directly involved in care, to oversee the proper and expeditious movement of casualties to assure an organized response and prevent bottlenecks and confusion.5,6,17,34,42,43 Designated case managers who are assigned to individual casualties as their advocate, to assure continuity of care and proper treatment, have been shown to improve mass casualty care and throughput in this potentially chaotic process.44 Blood utilization tends to be greatly overestimated in disaster casualties, resulting in large amounts of waste of this critical resource as misguided calls go out for donations.14 In fact, it has been shown that only about 1 U of blood is necessary on average for each casualty of smaller disasters, and about 2 U for larger events, which fall well within the normal surge capability of blood banks.45 In both combat and civilian mass casualty events, most blood products that are used tend to be given to a small number of victims.45,46 External and internal security of the hospital facility is an essential component of the disaster medical response and optimal casualty care.14 The priority of a hospital disaster response must be the safety of its staff and physical structure before all else. The hospital should undergo a lockdown as soon as possible to restrict entry to all except staff and those casualties allowed by the triage officer, to prevent its inundation by the media, worried well, families of victims, minimally injured casualties, and volunteers, all of whom consistently flock to the hospital due to its perception as a safe haven for all. A lockdown contributes to reducing overtriage into the facility. Another component of lockdown is to establish a perimeter around the facility to keep people and vehicles away from the actual entrance as an added measure of safety.15 Internal security is also necessary to prevent the critical patient care areas from being overwhelmed and rendered ineffective by the inevitable influx of well-meaning but misguided medical providers who have no role in these areas. Hospital personnel must also be prevented from leaving

to run to the scene to “help,” where they have no role and no training, and will become an added burden and possibly secondary victims.17 There should be provision for ongoing care of those routine emergencies that will continue to arrive at any hospital even during a mass casualty event, such as acute chest or abdominal pain, urgent labor in pregnant women, and motor vehicle crashes. The best system for managing these patients is to consider them as casualties and have them get in line and undergo triage and treatment according to the same priorities as the disaster casualties. Without this provision, routine emergency patients will tend to be ignored. Once the acute casualty influx subsides, all triage and care dispositions can be reassessed in the light of what resources remain. The quality of care can return to normal medical standards. Expectant casualties may now be rendered care if still alive, and all injuries can undergo definitive treatment. Secondary casualty distribution to other hospitals with greater capacity may now occur to expedite definitive and long-term treatment measures.5,6

PATHOPHYSIOLOGY AND PATTERNS OF INJURY FOLLOWING DISASTERS There are distinct patterns of injury that result from mass casualty disasters, in terms of mechanism and severity. Approximately 80% of all disasters have resulted in bodily injury, emphasizing the importance of surgical leadership in disaster planning and management.5,6,36,43 Furthermore, trauma centers and trauma systems should be the foundation of all local, regional, state, and national disaster response systems, as they have the personnel, equipment, liaisons, and daily experience with managing large numbers of injured patients and rapid decision making that are so necessary in disasters.6,27,37 However, the trauma community has only rarely been confronted with those mechanisms and agents that commonly result in mass casualty disasters, and have little education and training in their detection and management.47 The following section reviews the mass casualty mechanisms most likely to confront health care providers.

■ Explosive Mass Casualty Events Explosions, whether accidental or deliberate, have a demonstrated capacity for severe injury of large populations. In addition to the devastation of accidental blasts, they are currently the most common weapons of war and terrorism in view of how easily and inexpensively they can inflict immense destruction (Table 8-5).48,49 Of the 93 major terrorist attacks that occurred globally between 1991 and 2000, 88% involved explosions.50

Blast Physics A high-energy explosion results from the virtually instantaneous conversion of solids or liquids into gas in the process of detonation. This releases a large amount of energy in a condensed volume, which creates a high pressure in the surrounding medium that propagates radially at hypersonic speeds of 3,000–8,000 m/s as a blast wave. An intense fireball typically

Disaster and Mass Casualty

TABLE 8-5 Major Global Terrorist and Accidental Explosive Events

Year 1917 1946 1980 1983 1993 1994 1995 1996 1996 1998 2000 2001 2002 2003 2004

166 (7) 100 (17) 1,300 (160)

2004 2005

2,092 (191) 722 (55) 25,780 (6,696)

a

Accidental explosion.

b

Confined space explosion.

c

Involved some element of building collapse.

surrounds the immediate blast source, representing the strongest energy field, before degrading into the blast wave, and finally into the lower amplitude of sound waves that provides the sound of the explosion. The energy of the blast wave dissipates rapidly in air according to the cube of the distance from the source. In the greater density of water, blast waves propagate three times more powerfully and farther. However, in confined spaces the blast wave magnifies, rather than dissipates, due to its reflection off floors, walls, and ceilings, resulting in a greater magnitude of destruction and injury.51 Terrorist bombings in crowded buses have resulted in mortality rates of 48%, while in open air they have a mortality of only 3–8%.52 An explosion inside a building may collapse the structure, further magnifying injury and death beyond the confined-space effects of the blast alone (see Table 8-5). The Murrah Federal Building in Oklahoma City was partially collapsed by its bombing in 1995. All 163 immediate deaths among 759 total casualties (21.5%) were occupants of this building. Furthermore, among the 361 building occupants, 94% of immediate deaths were in the collapsed portion of the building.53

Blast Pathophysiology These characteristics of high-energy blast waves cause significant destructive forces on exposed living organisms. Aircontaining organs are most susceptible to injury due to the

Primary blast injury (PBI) results from the effects of the blast wave traversing the body, and is characterized by the absence of external signs of injury. The air-containing organs— lungs, GI tract, and ears—are most commonly injured, and may take hours to days to manifest this injury.57 Tympanic membrane rupture is a sensitive marker of exposure to the blast wave, but does not correlate well with the severity of injury.58,59 Over 99% of PBI victims are immediately killed, and the small minority of survivors have a relatively high risk (10–20%) of mortality. Immediate deaths are usually due to fatal air emboli from disruption of the alveolar:vascular barrier characteristic of blast lung injury (BLI). Late deaths among survivors are due to intractable respiratory failure. Another marker of severity among victims of PBI is traumatic amputation, which is also characterized by most victims being immediately killed and a high mortality among survivors.6,19,48 Secondary blast injury refers to the impact of objects and debris secondarily stirred up by the blast wave on the body. Tertiary blast injury results from the body itself being thrown into objects by the force of the blast wave, and is more commonly seen in children due to their lighter weight. Glass shards from shattered windows are a common form of secondary blast injury.60 These are the most common injuries in survivors of blasts, and they are typically noncritical skeletal and soft tissue trauma, though more complex and severe than gunshot wounds and routine trauma as a result of the large magnitude of energy involved.61 A more destructive pattern of terror-related secondary blast injury has been seen in recent years with the inclusion of metal fragments in bombs.54,62 Quaternary blast injury includes miscellaneous forms of tissue damage only indirectly related to the blast. This includes severe burns from exposure to the fireball in the immediate vicinity of the blast source, which also serves as a marker of proximity to the blast and the potential for PBI and multisystem critical injuries that kill most victims immediately, and is associated with a high mortality among the minority of afflicted survivors. Among the survivors of the 1983 suicide bombing of the U.S. Marine barracks in Beirut, 57% of late deaths were from burns.63 Following the Madrid train bombings in 2005, 17.4% of hospitalized survivors suffered thermal burns, of which 64% were second and third degree.59 Other forms of quaternary blast injury are complex extremity and crush injuries from structural collapse, and inhalation injuries from toxic dust and chemicals. Among survivors of the 1993 terrorist bombing of the World Trade Center in New York City, 93% were afflicted with such

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Event Halifax harbor ship explosiona,b Texas City ship explosionsa,b Train terminal, Bolognab U.S. Marine barracks, Beirutb,c World Trade Center, New Yorkb AMIA, Buenos Airesb,c Murrah Building, Oklahoma Cityc Centennial Olympics, Atlanta Khobar Towers, Saudi Arabia US Embassies, Tanzania/Kenyac USS Cole, Yemen World Trade Center, New York Cityc Shopping mall, Helsinki, Finlandb U.N. Headquarters, Baghdadb,c Ryongchon, North Korea, train blasta Train terminals, Madridb Subways and bus, Londonb Total

No. of Total Casualties (Deaths) 9,000 (2,000) 2,000 (600) 291 (85) 346 (241) 1,042 (6) 286 (85) 759 (168) 111 (2) 574 (20) 4,100 (223) 52 (17) 2,839 (2,819)

pressure differentials and inertial mismatches at air:liquid interfaces, where turbulence known as spalling shears tissues. A number of studies have shown blast injury to be more severe than routine trauma, with higher ISS, more complex and extensive injuries that require more surgical procedures, longer ICU and hospital stays, and higher mortality. Children tend to be more susceptible to these injuries than adults.22,54–56 There are 4 categories of blast injury:

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inhalation injures. The dissemination of biological, chemical, or radiological agents through dirty bombs is included in this category. Both casualties and responders are susceptible to psychological sequelae of major blast events. Early and aggressive mental health interventions for acute stress reactions may prevent the development of long-term problems with post-traumatic stress disorder (PTSD).64 The organic effects of blast injury on the brain may mimic the manifestations of PTSD.59,65

Implications for Mass Casualty Management An understanding of the pathophysiology of blast injury allows effective planning for its distinct injury patterns. Recognition of the markers of severity, including BLI, thermal burns, penetrating torso injuries, and traumatic amputation, should facilitate accurate triage decisions, and promote effective utilization of hospital resources in the mass casualty setting typically created by major explosions. The prognostic factors that affect the severity and outcome of casualties afflicted by blast injury are essential for meaningful disaster planning and casualty triage and care (Table 8-6).

■ Biological Mass Casualty Events Bioterrorism is defined as the intentional infliction of disease and death on large populations through the use of microorganisms or their toxins. In the fall of 2001, separate anthrax attacks on the news media, political figures, and government institutions using letters contaminated with anthrax spores resulted in 5 deaths, 30 documented exposures, and 13,000 people placed on prophylactic antibiotics. A mass casualty event due to a biological pathogen or toxin is therefore a significant risk. This could occur as a result of a viral pandemic or weaponization of bacteria, viruses, or certain toxins produced by microorganisms. Although the skin, mucous membranes, and gastrointestinal tract are potential portals of entry, the respiratory tract is the most efficient avenue for disease transmission. Exposure of the respiratory tract to certain aerosolized biological products (e.g., anthrax, plague, Q fever, and staphylococcal enterotoxin B) causes primarily a pulmonary syndrome. Aerosolization of botulinum toxin and most viruses, on the other hand, produces systemic disease. The number of possible victims is dependent on the type of agent, its virulence, the susceptibility of the population to infectious or toxic effects, and the degree of exposure of the population.66 The US Centers for Disease Control and Prevention (CDC) has defined three categories of biological weapons, classified according to their likelihood and success of use in a terrorist attack.67 Category A weapons have a high potential for largescale dissemination, adverse effects on public health, and a high mortality rate. In decreasing order of concern, these include anthrax, smallpox, plague, botulinum toxin, tularemia, and viral hemorrhagic fevers. Category B weapons are moderately easy to disseminate, cause significant morbidity and mortality, and require special diagnostic tests. Category C weapons are emerging pathogens that could be weaponized in the future, and include Nipah virus, hantavirus, tick-borne encephalitis (TBE) viruses, yellow fever virus, and multidrug-resistant

TABLE 8-6 Prognostic Factors for Explosive Disasters Blast-related factors Magnitude of explosive energy Proximity to blast Extent of bomb fragmentation Orientation to blast Environmental factors Surrounding medium—underwater versus air Confined space versus open air Rural or isolated locale—resource availability Toxic fumes, dust, and debris Occurrence of building collapse Anatomic and physiologic injuries Multiple body systems injured Injury Severity Score 15 Age, comorbidities Primary blast injury Tympanic membrane rupture Blast lung injury with respiratory failure Bowel/GI injury Brain injury Bowel injury Spine and spinal cord injury Traumatic amputation Secondary and tertiary blast injury Blunt and penetrating torso injuries Impalement Skull fractures Glasgow Coma Score 10 Foreign body implantation (metallic, glass, human remains) Quaternary blast injury Extensive and deep burns Crush injuries Toxic inhalation injuries Biological, chemical, radiological exposure/ contamination/ingestion Casualty management factors Hospital overload Treatment delay Triage accuracy Efficiency of casualty flow Efficiency of resource management Availability of surgical capability

Mycobacterium tuberculosis. Frontline medical providers who will most likely be confronted with these casualties must know the clinical manifestations of these agents and maintain a high index of suspicion for their occurrence in order to contain any outbreak most rapidly.68 Delayed recognition of a biological event causing mass casualties is a major problem that most distinguishes it from other forms of disaster. In contrast to other conventional and nonconventional weapons, there is usually no obvious scene of

Disaster and Mass Casualty contaminate the entire building, but was destroyed by the blast.71 Sarin nerve agent attacks by the Aum Shinrikyo Japanese cult in Matsumoto, Japan, in 1994 (7 deaths and 240 hospital visits) and the Tokyo subway in 1995 (12 deaths and 5,000 hospital visits) resulted in a relatively small number of deaths and a large number of unexposed but worried citizens flooding the health care system. There was also an attempted cyanide release in the latter attack that was unsuccessful.72 There are five types of chemical weapons that could be used in a terrorist attack or otherwise give rise to a mass casualty disaster: nerve agents, blood agents (cyanide), vesicants (blistering), incapacitating agents, and pulmonary agents. Nerve agents and cyanide are the most likely chemicals to be used. Medical providers must have a working knowledge of the clinical manifestations and treatment of these agents if mass casualties are to be most effectively managed (Table 8-7). Nerve agents are organophosphate compounds that inhibit the action of cholinesterase at the postsynaptic and neuromuscular junctions resulting in excess acetylcholine causing a cholinergic crisis.73 Most insecticides are in this category. The symptoms and signs of a cholinergic crisis are due to the muscarinic (postsynaptic nerve cell membrane, smooth muscle cell, and secretory glands) and nicotinic (skeletal muscle and postsynaptic ganglia) effects of acetylcholine. The muscarinic effects involve hypersecretion and an overall wet patient, and may be classified according to the DUMBBELS mnemonic (diarrhea, urination, miosis, bronchorrhea, bronchospasm, emesis, lacrimation, salivation). The pulmonary effects result in a low pulmonary compliance. The nicotinic effects include fasciculations,

Blood agents

Cyanide

■ Chemical Mass Casualty Events

Incapacitating agents (anticholinergics) Nerve agents

BZ

Toxic chemicals have a well-demonstrated potential to cause severe morbidity and mortality among large populations from either unintentional or intentional release. The worst chemical disaster in history was caused by the accidental release of 40 tonnes of gaseous methyl isocyanate from the Union Carbide plant in Bhopal, India, in 1984, resulting in 6,000 deaths and 400,000 injuries.70 Poison gases caused over 1 million casualties in World War I. The bomb that exploded in the World Trade Center in New York City in 1993 contained enough cyanide to

TABLE 8-7 Potential Chemical Terrorism Agents Category Vesicants (blistering)

Pulmonary irritants

Agents Mustard Lewisite Phosgene oxime Phosgene Chlorine Ammonia Mace

GA—tabun GB—sarin GD—soman VX

Treatment Decontamination, hypochlorite (bleach), dimercaprol Decontamination, water cleansing, bronchodilators, mechanical ventilation Decontamination, 100% oxygen, amyl nitrite IV hydration Physostigmine Decontamination Atropine 2-PAM Diazepam Airway management Mechanical ventilation

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attack, and the slower time course of the evolution of the outbreak leads to a slower disaster response that may play out over days to weeks rather than minutes to hours. Victims are often unaware of their exposure and symptoms may take hours or days to develop because of the incubation period required for disease to manifest after the initial exposure. In the interim, the disease may unknowingly be spread to multiple contacts. The patient may first seek help at a doctor’s office, a freestanding medical clinic, or an emergency room risking further spread of the disease to the medical and nursing staff. The principles of management of a naturally occurring epidemic and an attack with a biological weapon are similar and include: (1) rapid detection and strict isolation of patients, (2) identification and treatment of contacts, (3) strict hospital infection control possibly including hospital lockdown, (4) avoidance of funeral practices allowing close contact with bodies, and (5) vaccination of the at-risk population. An effective system of syndromic surveillance is necessary to rapidly detect patterns of illness over a wide area in order to identify and contain the disease outbreak most expeditiously. These essential community-based public health measures take time and are difficult to achieve. In the meantime, hospitals have to deal with large numbers of patients requiring care. Most or all of these patients will become infected via the inhalation route.69 Routine reverse isolation is sufficient for most diseases except the highly contagious viral hemorrhagic fevers that require strict isolation. Staff must use a Level A protective ensemble in this situation including a self-contained breathing apparatus. ICU beds, critical care medical and nursing staff, and ventilators will be the critical resources limiting hospital response to seriously ill patients with respiratory failure following mass casualty events of all kinds.34,39 The CDC maintains a supply of 6,000 ventilators in the Strategic National Stockpile, which has recently been augmented by an additional 3,900 LTV 1200 ventilators in October 2009 as recommended by the American Association of Respiratory Care. However, effective use of these unfamiliar ventilators, and the time required to disseminate them for clinical use by ICU staff in afflicted hospitals, represents major challenges. Lack of experience with a biological mass casualty event in the modern era, lack of functional personal protective equipment permitting effective intensive care, and lack of experience with rapid deployment of stockpiled ventilators are limiting factors to an effective medical response to a biological mass casualty event.68

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flaccid paralysis, tachycardia, and hypertension. The heart rate may vary during a cholinergic crisis due to the opposing actions of the nicotinic and muscarinic effects. These patients tend to die of respiratory failure. The overwhelming majority of casualties who arrive at the hospital will have either mild or no exposure to the nerve agent. Patients who are comatose, seizing, or apneic are classified as severely injured. Supine patients who are wheezing, fasciculating, or incontinent are classified as moderately injured. Ambulatory patients are classified as mildly injured. Five nerve agents have been produced as weapons in increasing order of toxicity (see Table 8-7). The G and V designations are from NATO nomenclature. G agents are water soluble and tend to wash off more easily, and are therefore less toxic than the more oily and persistent V agents. VX is so toxic that a fraction of one droplet on the skin could kill an adult human. There are two separate antidotes for a cholinergic crisis caused by these chemicals. Atropine blocks the muscarinic effects of acetylcholine by competitive inhibition of acetylcholine at the postsynaptic cholinergic receptors. Atropine, however, does not block the nicotinic effects because it has no effect on the neuromuscular (striated muscle) end plate. The antidote for the nicotinic effects is pralidoxime chloride (2-PAM), a drug that functions like a “molecular crowbar” separating the organophosphate nerve agent from cholinesterase thereby enabling metabolism of the acetylcholine. Unfortunately irreversible binding between the organophosphate and cholinesterase occurs with time, a phenomenon known as aging. The aging time varies from 2 minutes for soman to several hours for sarin. 2-PAM must be given prior to the onset of aging in order to be effective. Its efficacy will obviously depend on how quickly after initial exposure it is administered.72 The recommended initial antidote is atropine 2 mg IM and 2-PAM 600 mg IM for mild to moderate nerve injury and atropine 6 mg IM and 2-PAM 1,200 mg IM for severe injury. Subsequent doses of atropine in hospital should be titrated to control the muscarinic symptoms.72 Blood agents are basically forms of cyanide, which is a highly effective chemical weapon when used in a closed space such as the “gas chambers” of the Nazi concentration camps. It is a highly volatile gas and disperses rapidly, making it unsuitable as a military or terrorist weapon in an open area. The cyanide ion has a high affinity for the ferrous ion in the mitochondrial cytochrome system. Oxidative phosphorylation is interrupted when cyanide binds to cytochrome A3 rapidly leading to anaerobic metabolism and lactic acidosis. The cyanide ion is generated by two chemicals: hydrogen cyanide and cyanogen chloride. The portals of entry for both are the respiratory tract, the GI tract, and the skin.74 The signs of moderate or severe exposure are a bright red appearance of the skin and venous blood, metabolic acidosis, and the odor of “bitter almonds,” although these tend to be very late and premorbid signs not likely to respond to treatment. Severe exposure causes coma, apnea, and cardiac arrest. Patients exposed to cyanide should be brought into open air and well-ventilated spaces as soon as possible. They are treated by inhalation of a 0.3-mL ampule of amyl nitrite or 10 mL of 3% sodium nitrite (300 mg) IV over 3 minutes. The goal is to

produce methemoglobin that binds to the cyanide ion creating cyanomethemoglobin. Following nitrite administration, 50 cm3 of a 25% solution of sodium thiosulfate (12.5 g) should be administered IV to convert cyanomethemoglobin to the inactive thiocyanate ion that is excreted in the urine. Protective clothing and masks should be used by the treatment teams, and treatment should be carried out in open and well-ventilated spaces. Vesicants are liquid chemical weapons that cause burns to the skin and mucous membranes after initial exposure and longterm bone marrow suppression. The principles of management include decontamination to remove the agent and minimize time of exposure, and treatment of the burn wound and hematologic abnormalities. Large-scale use of vesicants during World War I and the Iran–Iraq War in the 1980s resulted in tens of thousands of casualties. However, it is unlikely that vesicants will be used in a terrorist attack because of the difficulty in deploying the weapon on a large scale. Chlorine and phosgene are pulmonary agents that cause pulmonary edema and respiratory insufficiency. Exposure to these chemicals causes chest tightness progressing to cough, hoarseness, stridor, and hypoxia over a period of 2–4 hours. The pulmonary injury is similar to the effects of inhalation of smoke from burning plastic. Chlorine binds with the water of the respiratory tract’s mucous membranes to form hydrochloric acid, creating severe injury. It tends to only involve the upper respiratory tract as it is so noxious that it will be expelled before reaching the lower tract. Phosgene tends to injure the pulmonary parenchyma of the lower tract. Terrorist deployment of pulmonary agents would be difficult because a large volume of gas is required to cause a mass casualty event unless the gas is released in a closed space. A chemical mass casualty event requires specific alterations to the hospital response. If a nerve agent or pulmonary agent is used in the attack (the most likely scenarios), the result will most likely be a “mass hysteria” rather than “mass casualties.” Most of the severe cases will die in the field in view of how rapidly the symptoms progress to respiratory failure, making more of a mass mortality rather than mass casualty event. Therefore, the preparation for treatment of mass casualties from these agents is largely futile, as the treatment regimens described above for single patients will not be amenable to dozens, hundreds, or thousands of casualties within the short time period required to treat those most at risk of death. Treatment facilities would also be unlikely to have enough ventilators or ICU capacity and capability immediately available to manage mass casualties. A large number of worried well and mildly exposed patients will flood the hospital as happened after the Aum Shinrikyo sarin attacks in Japan. Hospital security and hospital lockdown are critical elements in response to a chemical event to prevent contamination of the facility and the hospital staff, as happened in Tokyo where many casualties were hospital personnel.72 Decontamination showers complete the process. Decontamination outside of the hospital is important. Early decontamination protects the patient from further exposure. Late decontamination protects the medical staff. Simple removal of clothing, or gross decontamination, eliminates 80% or more

Disaster and Mass Casualty

■ Radiological Mass Casualty Events The dispersal of radioactive agents to inflict injury and death on large populations is theoretically possible, and has occurred in a limited number of documented instances. However, the fears of mass casualty events from radiological agents are far out of proportion to actual risks, making this more of a weapon of mass hysteria than mass destruction. There are three types of radiological mass casualty events: a “dirty” bomb, an attack or accident at a nuclear facility (including nuclear-powered ships and submarines), and the detonation of a nuclear bomb in an urban area. The clinical and social consequences of these three scenarios differ significantly.75 A “dirty” bomb is a conventional explosive device mixed with radioactive powder or pellets. The explosion results in dispersion of a radioactive plume to the surrounding area. The blast effect depends on the size of the bomb. The radioactive contamination is usually clinically insignificant and limited to the immediate area surrounding the blast. Although a “dirty” bomb is not a “nuclear” device, the “radioactivity” associated with the explosion is likely to create panic sending a large number of uncontaminated worried well patients to the hospital. Most of the injuries will be due to the blast effects of the explosion. A small fraction of the patients will require radioactive decontamination.75,76 The accident at the Chernobyl nuclear reactor in the Ukraine on April 26, 1986, was caused by a chain of human errors and technical malfunctions causing a series of explosions ultimately expelling 25% of the reactor core. Two people died from blast injury, 1 from a myocardial infarction, and 28 from massive radiation exposure. Two hundred and thirty-eight survivors had acute radiation syndrome (ARS). Many of these patients had cutaneous burns. Thousands of people in Northern Europe were exposed to the radioactive fallout with long-term adverse health consequences.76 The casualty profile of a nuclear reactor incident includes some patients with blast injury, a group of patients with lethal radiation exposure, and a larger group of survivors with burns

and ARS. The magnitude of such an incident depends on whether or not the integrity of the reactor is breached. The explosion of a nuclear bomb results in massive release of energy in the form of heat, light, air pressure, and radiation after either fission (splitting of uranium-235 or plutonium) or fusion of the hydrogen isotopes deuterium and tritium. A large fireball occurs at the center of the explosion vaporizing everything including soil and water. The radioactive material is thrust high into the atmosphere creating the “mushroom” cloud. This material, carried by the prevailing winds, solidifies and eventually falls to the ground creating radioactive fallout. Two types of nuclear devices are of concern: a tactical nuclear weapon in the form of an artillery shell (“suitcase bomb”) and a strategic nuclear bomb. A tactical nuclear device can be delivered and detonated by a single person causing an explosion ranging in power from 72 tonnes to 15 kilotonnes of TNT. The power of strategic nuclear weapons ranges from hundreds of kilotonnes to megatonnes of TNT. Following explosion of a nuclear device, there will be a zone of destruction extending several kilometers from ground zero depending on the size of the device. There will be very few, if any, survivors in the zone of destruction. The electromagnetic pulse accompanying the explosion will likely destroy all electronic equipment inactivating cars, cell phones, computers, and other devices. The treatment of blast and burn injuries following a nuclear explosion is based on the accepted principles of trauma care. Radiation injury is uniquely associated with a nuclear incident, and is caused by any form of ionizing radiation. This damages living tissue through its immediate direct energy, as well as indirectly from the long-term creation of toxic hyperoxide molecules. The rapidly dividing tissues of the gastrointestinal tract and bone marrow are most susceptible to injury. The factors that determine the severity of the biological effects are time of exposure, distance from the source, and degree of shielding.75,76 It is important to distinguish radiation exposure from radiation contamination, as only the latter poses any level of risk to health care workers, and usually that risk is minimal. Radiation exposure does not make a person “radioactive.” ARS is a series of incremental symptoms after exposure to at least 0.7 Gy (1 Gy  100 rad of absorbed radiation). It is characterized by an initial prodromal phase of rapid onset of nausea, vomiting, and malaise. This is followed by a latent phase. After approximately 1 week GI symptoms develop. Bone marrow depression can develop within 6 weeks after radiation exposure.75–78 Exposure to 6–8 Gy results in bloody diarrhea after a latency period of several days. All of these patients develop bone marrow depression. Initial treatment includes fluid and electrolyte replacement. Although there are a number of isotope-specific treatments that have been used, including potassium iodide, chelating agents, binders, and purgatives, none of these have any substantial benefit. Even bone marrow transplant has shown disappointing results in casualty outcomes. A dose of 10 Gy is the maximum survivable absorbed dose of radiation. Exposure to 20–40 Gy of radiation results in hypotension, coma, and seizures. Death typically occurs within 3 days of exposure even with maximal medical therapy. This dose of radiation is so great that victims would be unlikely to survive

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of most contaminants and can be done quickly to allow treatment and hospital admission of the most seriously injured. More thorough technical decontamination involves a thorough washing with soap and water and shaving of hair. All clothing and effluent from this process must be carefully collected for proper disposal to prevent further spread. Patients in a cholinergic crisis require resuscitation by health care personnel wearing personal protective equipment in the decontamination zone. Well-ventilated spaces are important for this process to prevent off-gassing of fumes from the casualties that may afflict providers. Efficient resuscitation of large numbers of casualties in cholinergic crisis or with cyanide or pulmonary agent poisoning by unpracticed staff wearing bulky protective clothing is unrealistic. The decontamination process cannot involve treatment to any clinically relevant extent. Surgeons and anesthesiologists should be aware of the potentiating effects of nerve agents on neuromuscular blockade in the event that surgery is required to treat a trauma patient exposed to nerve agents.

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the blast effect. However, any victims with the neurovascular syndrome who do survive should receive comfort care only.77,78 Time to first emesis and time to first lymphocyte depression are very reliable triage tools as they directly correlate with the absorbed radiation dose. Emesis or diarrhea within 1 hour indicates an expectant patient who will die even with maximal medical treatment and should be given comfort care only. Onset of these symptoms within 2–4 hours indicates potential salvageability and should have immediate treatment, while longer onset should indicate minimal treatment. Clinically apparent bone marrow depression begins 10 days to 6–8 weeks following exposure. A 50% drop in the lymphocyte within 24 hours indicates significant radiation exposure and an expectant triage assignment. Treatment options include hematopoietic growth factors, prophylactic antibiotics, and bone marrow transplantation. Early severe bone marrow depression is a bad prognostic sign and has important implications for triage in a mass casualty situation.75,76 Casualties must undergo initial decontamination outside of the ER. Gross decontamination with removal of clothing and a soap and water shower eliminates more than 90% of the radioactive contamination. The clothing should be placed in plastic bags. This allows initial triage and evaluation to proceed with minimal risk to the health care team. Technical decontamination should then be done for stable patients. This procedure involves a thorough scrubbing of the body with bleach products, shaving or washing all hair, and covering all open wounds after cleansing to prevent them from becoming portals of entry for radioactive material. The results of technical decontamination should be monitored with dose-meter devices. All water, clothing, and other products of decontamination should be collected and stored in plastic bags to prevent contamination of the environment. The US Department of Energy maintains a 24-hour hotline for questions about radiation exposure at the Radiation Emergency Assistance Center/Training Site (REAC/TS) in Oak Ridge, Tennessee (865-576-1005).77 Unstable patients should not have necessary hospital admission or immediate lifesaving treatment delayed for radiological decontamination as there is no danger to the hospital or health care providers as long as standard universal precautions are practiced. Medical care trumps decontamination in this setting.77

SUMMARY Disasters and mass casualty events pose unique challenges in surgical management. Surgeons will be among the most prominent first receivers of casualties from most disasters. They should be leaders in the disaster planning process, and must understand the altered approaches to medical care, and the importance of being a part of a larger team framework, which are necessary to optimize casualty outcomes in these settings.43 Trauma centers and trauma systems have the necessary infrastructure, in terms of supplies, equipment, personnel, liaisons, and experience for disaster management, and should serve as the foundation for local, regional, and national disaster systems.27,36,37

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Disaster and Mass Casualty 55. Peleg K, Savitsky B, Israeli Trauma Group. Terrorism-related injuries versus road traffic accident-related trauma: 5 years of experience in Israel. Disaster Med Public Health Preparedness. 2009;3:196–200. 56. Jaffe DH, Peleg K, Israeli Trauma Group. Terror explosive injuries: a comparison of children, adolescents, and adults. Ann Surg. 2010;251: 138–143. 57. Bochicchio GV, Lumpkins K, O’Connor J, et al. Blast injury in a civilian trauma setting is associated with a delay in diagnosis of traumatic brain injury. Am Surg. 2008;74:267–270. 58. Leibovici D, Gofrit ON, Shapira SC. Eardrum perforation in explosion survivors: is it a marker of pulmonary blast injury? Ann Emerg Med. 1999;34:168–172. 59. Turegano-Fuentes F, Caba-Doussoux P, Jover-Navalon JM, et al. Injury patterns from major urban terrorist bombings in trains: the Madrid experience. World J Surg. 2008;32:1168–1175. 60. Thompson D, Brown S, Mallonee S, Sunshine D. Fatal and non-fatal injuries among U.S. Air Force personnel resulting from the terrorist bombing of the Khobar Towers. J Trauma. 2004;57:208–215. 61. Sheffy N, Rivkind AI, Shapira SC. Terror-related injuries: a comparison of gunshot wounds versus secondary-fragments-induced injuries from explosives. JACS. 2006;203:297–303. 62. Bala M, Rivkind AI, Zamir G, et al. Abdominal trauma after terrorist bombing attacks exhibits a unique pattern of injury. Ann Surg. 2008;248:303–309. 63. Frykberg ER, Tepas JJ, Alexander RH. The 1983 Beirut airport terrorist bombing: injury patterns and implications for disaster management. Am Surg. 1989;55:134–141. 64. Galea S, Ahern J, Resnick H, et al. Psychological sequelae of the September 11 terrorist attacks in New York City. N Engl J Med. 2002; 346:982–987. 65. Walilko T, North C, Young LA, et al. Head injury as a PTSD predictor among Oklahoma City bombing survivors. J Trauma. 2009;67: 1311–1319. 66. Henderson DA. The looming threat of bioterrorism. Science. 1999; 283:1279–1282. 67. Eachampati SR, Flomenbaum N, Barie PS. Biological warfare: current concerns for the health care provider. J Trauma. 2002;52:179–186. 68. Fry DE, Schecter WP, Parker JS, Quebbeman EJ. The surgeon and acts of civilian terrorism: biologic agents. JACS. 2005;200:291–302. 69. Green MS, Kaufman Z. Syndromic surveillance for early detection and monitoring of infectious disease outbreaks associated with bioterrorism. In: Shemer J, Shoenfield Y, eds. Terror and Medicine: Medical Aspects of Biological, Chemical and Radiological Terrorism. Lengerich, Germany: Pabst Science Publishers; 2003:81–95. 70. Wikipedia. Bhopal Disaster. Available at: http://en.wikipedia.org/wiki/ Bhopal_Disaster. Accessed March 3, 2010. 71. Jenkins BM. Understanding the link between motives and methods. In: Roberts B, ed. Terrorism with Chemical and Biological Weapons: Calibrating Risks and Responses. Alexandria, VA: Chemical and Biological Arms Control Institute; 1997:43–52. 72. Schecter WP, Fry DE, Governors’ Committee on Blood Borne Infection and Environmental Risk of the American College of Surgeons. The surgeon and acts of civilian terrorism: chemical agents. JACS. 2005;200: 128–135. 73. Ben Abraham R, Rudick V, Weinbroum AA. Practical guidelines for acute care of victims of bioterrorism: conventional injuries and concomitant nerve agent intoxication. Anesthesiology. 2002;97:989–1004. 74. Ballantyne B. Toxicology of cyanides. In: Ballantyne B, Marrs TC, eds. Clinical and Experimental Toxicology of Cyanides. Bristol, UK: Wright; 1987:41–126. 75. Fry DE, Schecter WP, Hartshorne MF. The surgeon and acts of civilian terrorism: radiation exposure and injury. JACS. 2006;202:146–154. 76. National Council on Radiation Protection and Measurements. NCRP Report No. 138: Management of Terrorist Events Involving Radioactive Material. Bethesda, MD: NCRP; 2001. 77. Mettler FA, Voelz GL. Major radiation exposure—what to expect and how to respond. N Engl J Med. 2002;346:1554–1560. 78. Chambers JA, Perdue GF. Radiation injury and the surgeon. JACS. 2007;204:128–137.

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30. Frykberg ER. Disaster and mass casualty management: a commentary on the American College of Surgeons position statement. JACS. 2003;197:857–859. 31. Asaeda G. The day that the START triage system came to a STOP: observations from the World Trade Center disaster. Acad Emerg Med. 2002;9:255–256. 32. Coupland RM, Parker PJ, Gray RC. Triage of war wounded: the experience of the International Committee of the Red Cross. Injury. 1992;23:507–510. 33. Kluger Y. Bomb explosions in acts of terrorism—detonation, wound ballistics, triage and medical concerns. Isr Med Assoc J. 2003;5: 235–240. 34. Avidan V, Hersch M, Spira RM, et al. Civilian hospital response to a mass casualty event: the role of the intensive unit. J Trauma. 2007;62: 1234–1239. 35. Kashuk JI, Halperin P, Caspi G, et al. Bomb explosions in acts of terrorism: evil creativity challenges our trauma systems. JACS. 2009; 209:134–140. 36. Lennquist S. Management of major accidents and disasters: an important responsibility for the trauma surgeons. J Trauma. 2007;62:1321–1329. 37. Jacobs LM, Goody MM, Sinclair A. The role of a trauma center in disaster management. J Trauma. 1983;23:697–701. 38. Ryan JM. Natural disasters: the surgeon’s role. Scand J Surg. 2005;94: 311–318. 39. Einav S, Aharonson-Daniel L, Weissman C, et al. In-hospital resource utilization during multiple casualty incidents. Ann Surg. 2006;243: 533–540. 40. Einav S, Feigenberg Z, Weissman C, et al. Evacuation priorities in mass casualty terror-related events—implications for contingency planning. Ann Surg. 2004;239:304–310. 41. Kelen GD, McCarthy ML, Kraus CK, et al. Creation of surge capacity by early discharge of hospitalized patients at low risk for untoward events. Disaster Med Public Health Preparedness. 2009;1(suppl):S1–S7. 42. Almogy G, Rivkind AI. Surgical lessons learned from suicide bombing attacks. JACS. 2006;202:313–319. 43. Einav S, Spira RM, Hersch M, et al. Surgeon and hospital leadership during terrorist-related multiple-casualty events: a coup d’etat. Arch Surg. 2006;141:815–822. 44. Einav S, Schecter WP, Matot I, et al. Case managers in mass casualty incidents. Ann Surg. 2009;249:496–501. 45. Soffer D, Klausner J, Bar-Zohar D, et al. Usage of blood products in multiple-casualty incidents: the experience of a level I trauma center in Israel. Arch Surg. 2008;143:983–989. 46. Propper BW, Rasmussen TE, Davidson SB, et al. Surgical response to multiple casualty incidents following single explosive events. Ann Surg. 2009;250:311–315. 47. Ciraulo DL, Frykberg ER, Feliciano DV, et al. A survey assessment of preparedness for domestic terrorism and mass casualty incidents among Eastern Association for the Surgery of Trauma members. J Trauma. 2004;56:1033–1041. 48. Born CT. Blast trauma: the fourth weapon of mass destruction. Scand J Surg. 2005;94:279–285. 49. Champion HR, Holcomb JB, Young LA. Injuries from explosions: physics, biophysics, pathology, and required research focus. J Trauma. 2009;66:1468–1477. 50. Arnold JL, Tsai M-C, Halpern P, Smithline H, Stok E, Ersoy G. Masscasualty, terrorist bombings: epidemiological outcomes, resource utilization, and time course of emergency needs (part I). Prehosp Disaster Med. 2003;18:220–234. 51. Wightman JM, Gladish SL. Explosions and blast injuries. Ann Emerg Med. 2001;37:664–678. 52. Leibovici D, Gofrit ON, Stein M, et al. Blast injuries: bus versus open-air bombings—a comparative study of injuries in survivors of open-air versus confined-space explosions. J Trauma. 1996;41:1030–1035. 53. Mallonee S, Shariat S, Stennies G, et al. Physical injuries and fatalities resulting from the Oklahoma City bombing. JAMA. 1996;276: 382–387. 54. Kluger Y, Peleg K, Daniel-Aharonson L, et al. The special injury pattern in terrorist bombings. JACS. 2004;199:875–879.

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Rural Trauma Charles F. Rinker II and Nels D. Sanddal

THE RURAL ENVIRONMENT While the majority of the population of the United States lives in an urban environment, 70% of the trauma deaths occur in a rural locale. “It is surprising that a disease that kills rural citizens at nearly twice the rate of urban citizens has not received more attention.”1,2 The chance of dying in a rural area from a severe injury sustained in a motor vehicle–pedestrian collision is three to four times greater than in urban areas.3 The relative risk of a rural victim dying in a motor vehicle crash is 15:1 compared with a victim of an urban crash,4 and death from motor vehicle crashes is inversely related to population density.5 In fact, death rates from all unintentional injuries combined are generally 50% greater in rural, sparsely populated counties of the western United States than they are in the densely populated northeastern counties.6,7 And pediatric deaths from injury in a rural setting are more frequent than they are in an urban setting, despite the recent increase in gunshot wounds in the urban population.8,9 Finally, autopsy studies have suggested preventable trauma death rates of 20–30% in rural populations.10–13 Not only are mortality rates higher, but outcomes in survivors based on Functional Independence Measure (FIM) scores are also worse. When fatalities are excluded, the rural to urban odds ratio of poor outcome is 1.52.14 Poor functional outcomes have also been documented in patients with traumatic brain injury sustained in rural versus urban locales. What are the reasons for these differences?15 In this chapter we will attempt to identify circumstances that make rural trauma care difficult and consider some solutions. An illustrative case will help to explain some of the unique features of trauma care outside an urban setting. A 48-year-old real estate developer was mountain biking with friends in a national forest in the Rocky Mountains. While unhelmeted, he rode ahead of the group and down a steep slope. Several minutes later his companions found him

unconscious at the bottom of a ravine after he had apparently lost control of his mountain bike. One of the friends rode out for help, which arrived 45 minutes following the crash in the form of a basic life support (BLS) ambulance unit from the local ski area. The patient had to be extricated from a ravine and carried several hundred yards to the ambulance, which then had a 1-hour trip to the nearest hospital, a Level III trauma center. Communication (handheld radio) with the hospital was not possible until the ambulance exited a narrow mountain canyon about 15 minutes before arrival. His Glasgow Coma Scale (GCS) score on the scene and in the emergency department was 8. He was hemodynamically normal, but a computed tomography (CT) scan of the head showed a large epidural hematoma with 5-mm shift. No other injuries were identified. Following consultation with a neurosurgeon at the nearest Level II center (150 air miles away), a general surgeon trained in emergency limited craniotomy (and following established local protocols) drilled a burr hole and enlarged it sufficiently to permit evacuation of the clot and to control the hemorrhage. The patient was transferred directly from the operating room to a helicopter, which flew him to the neurosurgeon for a formal craniotomy. He survived with a Glasgow Outcome Score of 4 and is now independent, although no longer able to function in his former capacity. This true scenario could have any of the following plausible variables: unaccompanied victim hours or days to discovery, less accessible to rescuers, greater distance to hospital, lack of trauma team and trained surgeon, or adverse weather preventing air transport to Level II trauma center. He might have been a hunter injured by firearm or animal, a backcountry skier caught in an avalanche, a rancher thrown from a horse, or the driver of a car on a remote rural road. Remoteness, rugged beauty, and “nature” are powerful magnets for tourists, recreationists, and those seeking a quieter, less stressful lifestyle. Such visitors are often shocked to

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DEFINING RURAL Rural spaces are sparsely populated and support only one third as many physicians as do urban areas.1 Specialists and, sometimes, even primary care physicians cannot make a living in communities under a certain population threshold. Lack of physicians skilled in rapid assessment and treatment of the critically injured has a significant effect on outcomes. Conversely, the number of physicians in a given county, and particularly emergency physicians who have taken the Advanced Trauma Life Support (ATLS) course, is associated with lower death rates from trauma.17 An urban area consists of a central city and its environs with a combined population of greater than 50,000 and a population density of 1,000 or more per square mile. As far as the US Bureau of the Census is concerned, everything else is rural. Not all rural environments, however, support farming, and many are surprisingly close to cities, but separated by geographic barriers such as mountains or large bodies of water. Residents of coastal Marin County, only a few miles north of San Francisco, may have difficulty accessing a trauma center because of intervening steep mountains, narrow roads, and local regulations prohibiting noisy and disruptive helicopters. San Diego County, home of a model trauma system, reports morbidity and mortality from delayed discovery of victims of motor vehicle crashes on remote county roads.18 North Carolina is the 10th most populous state, but 29 counties in the eastern part of the state are served by a single trauma center, 12 counties have no general surgeon, 17 no orthopedic surgeon, and 23 no neurosurgeon. In only 14 of these counties can a victim of trauma reach an emergency department staffed with emergency physicians in less than 30 minutes.17 Hypothermia is an independent predictor of mortality in injured patients, with mortality rising as core temperature falls. Urban trauma centers, with more rapid discovery and transport times than rural prehospital systems, have reported a 5% incidence of trauma patients with low core temperatures.19 A Level I trauma center in North Carolina serving 29 mostly rural counties and a combined population of 1.4 million reported transport times averaging 1 hour and time from injury to definitive care of 4 hours. Their trauma registry identified 1,490 of 9,482 (16%) patients suffering from hypothermia (36°C) on arrival. These hypothermic patients had a 14.6% mortality rate, compared with 4.5% among normothermic patients.20 Virtually all regions of our country have many areas that are sparsely populated and relatively poor in resources. In the central and northern plains, one sees the combination of few people and great distances from urban centers as nowhere else in the lower 48 states. Alaska, of

course, along with some portions of the northern Rocky Mountains, is more accurately described as a frontier area (six or fewer people per square mile). The state of Western Australia forms the western third of the country, with an area of 2.5 million km2, and a population density of 0.8 people/km2. Because of a lack of doctors and hospitals, some trauma patients may be transported in excess of 2,000 km over more than 24 hours to receive initial care. Investigators there developed an Accessibility/Remoteness Index of Australia (ARIA+) to reflect the ease or difficulty people face accessing services in nonmetropolitan areas of the country. The index is a continuous variable with values ranging from 0 (high accessibility) to 15 (high remoteness). Employing ARIA+, with Perth (the most isolated capital city in the world) as the reference point, they demonstrated that the remote rural trauma death rate is over four times the rate in major cities.21 Rural, then, may be defined in accordance with census data based on metropolitan statistical areas, in terms of geography and distance, or by virtue of limited resources. In a recent analysis of the general surgery workforce, Thompson et al.22 identified significant differences between communities with a population between 10,000 and 50,000 (large rural) and those with 2,500–10,000 residents (small, or isolated rural). Large rural towns are far more likely to have the necessary resources such as general surgery, medical and surgical subspecialties, advanced life support (ALS) ambulance services, and essential equipment to provide prompt and sophisticated trauma care. Environmental factors are also important as “rural trauma occurs in areas where geography, population density, weather, distance, or availability of professional and institutional resources combine to isolate the patient in an environment where access to definitive care is limited.”23 An alternate, somewhat more precise definition has been proposed as follows: “… A rural trauma region would be an area in which the population served is fewer than 2500, has a population density of fewer than 50 persons per square mile, has only basic life support prehospital care, has prehospital transport times that exceed 30 minutes on average, and is lacking in subspecialty coverage for specific injuries (such as a neurosurgeon to manage the patient with head injuries).”1 In any event, though we may think we know it when we see it, it is apparent that “rural” is difficult to define.

EPIDEMIOLOGY There are reasons why few people live in rural locations. The climate may be harsh, the terrain rugged and remote from services, the roads badly engineered and maintained, communications rudimentary, and the economy marginal. Career opportunities for the young are limited, so the young leave. As a result, significant segments of the population are elderly, poor, poorly educated, and in ill health. Population density (low) and personal income (also low) are the strongest predictors of per capita trauma death rates.17 Nearly one fourth of adults in this environment sustain some form of unintentional injury per year. The injuries are usually relatively minor, but they can be major and/or fatal. Binge drinking and depression are strongly

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discover that medical services they take for granted at home are simply unavailable in a rural setting. In contrast, local residents tend to be independent, fatalistic and accepting of limitations, suspicious of outsiders, resistant to both change and regulations (helmet and seatbelt laws; gun control), and unaware of trauma as a public health problem because, in their limited experience, it is a rare event.1,16

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associated comorbid factors, and suicide accounts for 10% of all rural trauma deaths.1,24 Elderly rural patients tend to start out with a lower Injury Severity Score (ISS) and are less likely to die at the scene, but have a higher complication rate and worse overall survival for comparable severity of injury. Based on data from the Major Trauma Outcome Study (MTOS), rural geriatric trauma patients fare less well than do those in an urban cohort.25 In addition, older age and lower population density independently increase vehicle-related mortality.26 A study by Wigglesworth27 compared two groups of five states each with the highest (Group 1) and lowest (Group 2) traffic death rates, respectively. Epidemiologic data from the Centers for Disease Control and Prevention (CDC) indicated that the fatality rates for falls, poisoning, drowning, fire, suffocation, homicide, and suicide conformed closely to the traffic death rates in the two groups of states. Group 1 states were rural, western, and below national averages for per capita income; Group 2 states were urban, eastern, and financially well-off.27 Overall, 60–70% of all trauma deaths occur in rural areas despite the fact that only 20–30% of the nation’s population lives in these areas.28 Unintentional blunt injury comprises about 90% of cases, largely because of the prevalence of motor vehicle crashes and the paucity of injuries from firearms. The most common causes of fatal injury are motor vehicle crashes, suicide, homicide, and falls. For these and the next 10 most frequent causes, rural death rates exceed urban rates for all but poisonings. Some of the most hazardous occupations such as mining, logging, and farming are almost exclusively rural by their very nature.29 Large animal injuries may occur on a farm or ranch in the course of daily work or in conjunction with such recreational pursuits as hunting, pleasure riding, or rodeo. Typical injuries are falls (horses), tramplings and gorings (bulls, wild game), and kicks (cows).30 Travel on rural highways entails the additional hazard of motor vehicle crashes with wild animals (elk, deer, bear, or moose). As a mature moose weighs half a tonne or more, a driver unfortunate enough to strike one risks significant injury to the brain or death.31 Fatal accidents are significantly higher for loggers (140/100,000) than they are for workers in other industries (94/100,000), and are typically the result of being struck by falling trees, limbs, or snags. Crush injury between moving logs and encounters with heavy equipment are other common mechanisms, and access to care is often a problem.32 Recreation also provides endless opportunities for serious injury and death. Particularly dangerous are four-wheeled all-terrain vehicles (ATVs). In 2004, ATV crashes were shown to result in more than 136,000 injuries and 500 deaths and one third of the deaths were in children. In Oregon, the rate of such injuries and deaths doubled between 2002 and 2005.33 Small community hospitals bear the brunt of these misadventures, particularly when situated in proximity to ski hills, wilderness areas, national parks, and seashores or lakefronts. Most people feel safe in rural setting as the risk of violent assault and penetrating trauma is very low as noted above. The low homicide rates, however, are negated by high suicide rates, particularly among adolescents and young adults.34–36 Blunt trauma comprises 95% or more of the trauma case load at most

rural community hospitals, 85% of which is minor or moderate (ISS  10) and can be treated without the need for transfer to a trauma center. Blunt trauma is less time dependent, which is fortunate since it is far more difficult to mount a rapid response in a small community hospital. It can be subtle, however, requiring experience and a high index of suspicion to avoid missed injuries.37 Although motor vehicle crashes cause the greatest number of trauma deaths in this country and in the rest of the world, they are sporadic events in small towns and the countryside. In essence, the greatest problems confronting rural trauma care are access to the system and lack of resources. The challenge is to devise a system, ensure access, and make the most of limited resources.

RURAL RESOURCES AND LIMITATIONS ■ Discovery and Access to the System Discovery of the victim and access to appropriate care are the most important explanations for the high mortality rates of trauma victims in rural areas. When people are scarce and distances between population centers are great, the injured may be lost or misplaced, whether in the backcountry or on a remote highway.1,16,38–40 Delays of hours are common, and, occasionally, days may pass before a victim can be found. In rural systems of care, time of crash until time of arrival at the hospital is more than an hour in 30% of cases, as opposed to 7% in urban systems.41 Prolonged mean prehospital times have been reported in rural Vermont (105 minutes), upstate New York (96 minutes), northern California (55 minutes), rural Washington (48 minutes), and Georgia (40 minutes). Thus, the “golden hour” is often spent on the road and not in the hospital.1 In extreme cases, crash victims in a snow-filled roadside ditch or ravine, a hunter, or a backcountry Nordic skier may not be found until spring breakup. Retrieval is equally challenging and often relies on the special skills of search-andrescue volunteers equipped to go into swamps and tidal flats, high mountains, or dense forests and other wilderness areas. Even when a helicopter is at hand, victims must often be moved over rough terrain by litter, watercraft, snowmobile, ATV, horse, or other conveyance to a suitable and safe landing area. Fortunately, most guides and outfitters now carry global positioning satellite (GPS) units, cellular phones, and/or handheld radios to facilitate rescues in emergency situations. If a hospital lacks a trauma program and leader, the response to a major trauma event tends to be disorganized as the patient will often arrive unannounced. Obvious extremity injuries may overshadow more critical internal injuries and prompt a call for an orthopedic surgeon when a trauma team led by a general surgeon is more appropriate. Even when notification occurs, the physician in the emergency department may wait to see just how badly a patient is injured, instead of mobilizing the trauma team and alerting the helicopter for interhospital transfer. The opportunity to eliminate a critical rate-limiting step is then lost. The patient proceeds from scene to litter to ambulance to local hospital and then, perhaps, on to the next higher level of care sequentially, and precious time is wasted (see Fig. 9-1).

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FIGURE 9-1 Roadside crosses on rural Montana highways mark fatal crash sites. (Reproduced with permission of the Critical Illness and Trauma Foundation, Bozeman, MT.)

One of the most important steps a small hospital can take toward improving trauma care is the establishment of a trauma team. When possible, the team should be led by a general surgeon.42–44 Criteria for team activation should be established, and team members should commit to come to the patient’s bedside immediately when called. In very small hospitals lacking general surgery support, it is still possible to provide appropriate emergency care.45 The Rural Trauma Subcommittee of the American College of Surgeons Committee on Trauma conducted an informal survey of small rural hospitals and found that most could mobilize three health care providers most of the time including physician extenders, nurses, and technicians (lab, x-ray, respiratory therapy). Drawing on these resources (as well as primary care physicians, or surgeons, in slightly larger facilities) the committee’s Rural Trauma Team Development Course trains these individuals in the team approach to the initial assessment, resuscitation, and transfer to definitive care for the injured patient. This 1-day interactive course is patterned on ATLS, but is inexpensive to present and may be given in modular form. The program is coordinated through the state chair of the Committee on Trauma.46 Obstacles to this logical solution include the following: (1) medical staff reluctance to participate in trauma care; (2) fears that overtriage will place greater demands on surgeons; (3) turf wars between ambulance services, hospitals, and communities; and (4) financial incentives to treat patients locally rather than transport them. In addition, the Emergency Medical Treatment and Active Labor Act (EMTALA) may have the unintended consequence of discouraging efficient transfers within a trauma system.

MANPOWER Physicians who practice in rural areas likely grew up in a small town, were influenced by a mentor, or have an independent streak.47 They usually have no fears of being overworked,

underpaid, and unable to obtain backup or guidance. If the social and cultural deprivations bear heavily on a spouse, the sojourn will be brief. Patient volumes are insufficient to support specialty services, and generalists with little or no formal trauma training predominate. Such individuals are expected to treat a significant number of minor trauma cases as well as the occasional complex major trauma case for which they have not been trained. A study of five small hospitals in rural Washington and Idaho revealed that they averaged three patients per year with an ISS greater than 19, and each physician saw, on average, 0.6% of these patients.48 Because trauma events are sporadic and infrequent, rural physicians may develop a fear of or aversion to care of the injured. Furthermore, despite evidence to the contrary, general surgeons believe they are more likely to be sued by trauma patients.49 Rural surgeons, more so than their urban counterparts, have traditionally viewed trauma care as an integral part of their service to their communities.50 Perhaps the greatest threat to our future ability to treat the injured in rural America is the unwelcome fact that this sense of commitment is changing. Rural surgeons are, for the most part, general surgeons. And this specialty has lost its appeal among young trainees who increasingly (70–80%) choose a subspecialty and avoid embarking on rural practice. Currently, the vast majority of rural surgeons are men, while more than half of medical school graduates are women. Women now account for 25% of surgical residents, and surveys confirm that they are much more inclined to practice in an urban or suburban setting.51,52 Furthermore, declining reimbursements compounded by a heavy burden of debt accrued during medical school have led many general surgeons to insist on compensation for call. Small rural hospitals may not be able to afford underwriting emergency call. Finally, the current cadre of rural general surgeons is retiring because of advancing age or because of burnout. As they are not being replaced, the net effect is that access to

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definitive trauma care at the local level is rapidly disappearing. This places a greater burden on regional Level I and II trauma centers, while at the same time denying essential revenue to the small community hospital. Perhaps most distressing, loss of surgical services may lead to the closing of the only hospital in a large geographic area.53 In many communities, a nurse practitioner or autonomous physician’s assistant is the town “doctor.” Their educational background and experience, as well as that of their supervising physician, rarely includes exposure to sufficient cases of major injury. Ambulance workers are predominantly volunteers trained in advanced first aid, emergency medical technician (EMT)-Basic, or, at most, EMT-I level, usually at their own expense. Their experience with trauma is also very limited, though trauma may be one third to one half of the case load in some rural ambulance services.54 Outside the academic medical center it is uncommon for resident staff or independent practitioners to stay in-house after hours. In hospitals with less than 30 inpatient beds it is unusual to have emergency physicians. In many small communities, a nurse or physician’s assistant is the only professional at the hospital on nights and weekends. The doctor may be at home or out of town and may or may not be willing to come in if called for a trauma emergency. If the doctor does come in, he or she will conduct the resuscitation with minimal assistance and limited equipment. Despite these shortcomings, there usually is no other choice since the next hospital may be many miles distant and may be no better equipped. It is for reasons such as these that it is so important for rural physicians, physician assistants, and nurses to take or audit the ATLS course and to become involved in the regional trauma system. An effective emergency medical service (EMS) program is vital for proper trauma care. In rural areas, the configuration of such systems varies and may include fire department– based, hospital-based, or freestanding entities. Personnel may be volunteers, salaried, or partially subsidized. Most are trained to the EMT-Basic level, which permits noninvasive interventions to reduce the morbidity and mortality associated with acute, out-of-hospital medical and trauma emergencies.55 Skills and capabilities may be enhanced with the addition of certain modules, under the guidance of their medical director. Some rural communities have personnel trained at higher levels of care.56 Specific trauma training (i.e., Prehospital Trauma Life Support [PHTLS]) may be challenging to conduct in rural areas for lack of instructors, but should be supported and encouraged. The nomenclature for the various levels of training is in transition, which may be clarified by the publication of a new scope of practice document in 2007.57 Currently, the primary challenges to rural EMS are maintenance of skills in a low-volume environment and dealing with collapse of infrastructure as a result of an aging volunteer workforce that is not being replaced. One proposed solution is to upgrade volunteer EMT-Bs to paramedics, employ their new skills as an adjunct to a broader community health program, and pay them.58,59 Aeromedical and ground transport systems that furnish critical care are becoming more common; however, their availability lags behind in many rural areas. In some locations

direct scene responses may be available while in others rendezvous with such units is more practical. Thoughtful incorporation of all resources into a regionalized response system for time-sensitive, life-threatening conditions (high-risk obstetrics, stroke, and STEMI as well as trauma) is beginning to evolve. Surgical leadership into the evolution of such systems is essential to ensuring the needs of the injured patient are not overshadowed by other acute conditions.

COMMUNICATIONS The original EMS legislation and subsequent funding bills recognized the need for effective and reliable communication between field and hospital. Availability of funds to improve communications infrastructure following the 9/11 bombings has improved radio coverage in many metropolitan areas. Paradoxically, those same systems have in some instances resulted in poorer rather than better coverage in rural areas due to terrain and distance issues. Skilled dispatchers are hard to find in small towns. Physicians and nurses at the hospital may be unfamiliar with and wary of communications equipment, and, accordingly, reluctant to talk with field personnel to provide medical guidance. Cellular telephones have improved prehospital provider-to-physician dialogue in many areas. In some areas with appropriate infrastructure and networks, telemedicine technology permits audio, video, and data transmission from field to hospital. Many 9-1-1 systems have upgraded to E9-1-1 (associates caller’s telephone number with a physical address). Even as rural areas are beginning to catch up in E9-1-1 availability, next generation NG9-1-1 is beginning to be deployed. NG9-1-1 is a network of systems that enables the transmission of voice, data, video, and text from various types of communication devices to a public service answering point. It makes that information actionable so that it can be moved into interconnected emergency responder networks. With the explosion of cell phone use that is not attached to a specific address, the FCC is mandating that cell phone services develop the ability to provide the latitude and longitude coordinates of the calling handset, accurate to within 50–300 m, to any Public Safety Answering Point (PSAP). Ultimately, cell phones will be able to transmit images and data. Communication between the local hospital and regional trauma center may also be difficult and unrewarding. Local practitioners often complain of unpleasant encounters with flight crews, emergency room personnel at the receiving hospital, and surgical staff on the trauma service. Attending surgeons are infrequently available for telephone consultation, despite the fact that they are, in essence, being referred a patient by a colleague. Feedback and constructive criticism regarding transferred patients are frequently sought by referring physicians, but not often attainable. In addition, they may receive mixed messages including criticism for overtriage on the one hand to holding onto a patient too long on the other. The net effect of problems in communication is that the rural practitioner ends up functioning in a relative vacuum, receiving little advance warning from the field, limited help at the hospital, and negative or no feedback from the regional center.

Rural Trauma

TRANSPORT

FACILITIES Urban trauma systems attempt to identify those hospitals with the resources and staff commitment to care for the critically injured patient and direct patients to those facilities. The system bypasses hospitals unable or unwilling to provide appropriate response and treatment. In less populated areas, where resources are not so abundant, bypass may not be an option. In the two decades following introduction of state EMS programs, most authors have asserted that rural community hospitals are the logical destination for critically injured patients.10,13,25,44,64,68–71 Following stabilization, they can then be transferred to the nearest trauma center. While this time-honored principle still applies in remote areas, studies indicate that bypass may be possible in some rural areas. With improved triage criteria, astute prehospital personnel, and good communications, a system can allow for transport of some stable rural patients with severe injuries directly to the trauma center without stopping at the local hospital.72–76 In rural Georgia, where one third of all ambulance trips were trauma related, 50% of patients were taken to the local hospital, but the remainder could be taken

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Evacuation of rural trauma victims is generally accomplished by surface conveyances. If the victim is inaccessible to an ambulance, various methods, all of them slow, may be employed to convey the patient to a road. The ambulance may then need to negotiate a sequence of roads from unsurfaced or gravel to county or state highway. Even the latter may be narrow, winding, and poorly maintained. Most often the destination is the nearest hospital, which will vary in its capabilities, and may be many miles distant. Response times, which include travel from the dispatch site to scene, extrication or retrieval, packaging, and travel to the hospital, are sometimes measured in hours, not minutes, as previously noted. Ambulance services may be freestanding or, in some instances, an integral part of the local fire department. Funding may be through a special ambulance district or as part of the county budget, jealously guarded by county commissioners.37 Frequently, because of limited funding, the ambulance service may employ aging although lovingly maintained vehicles, which are limited in number. In Vermont, it is estimated that the average local ambulance is unavailable 15% of the time.1 Surveys of state EMS directors in 2000 and 2004 indicated that the greatest need for rural services is the adequate recruitment and retention of staff. In the same surveys, 24/7 coverage rose from the 22nd to the 2nd most important rural EMS issue. Response time rose from 20th to 5th. If an ambulance is in service on a call or out of service for maintenance, the next call might have to be answered by a crew in a neighboring district through a mutual aid agreement.60 Multiple incidents or victims can easily overwhelm the transport system. Helicopters can be used both for scene rescue and for interhospital transport. Ideally, evacuation from the scene of injury directly to the trauma center should afford the patient the best opportunity for recovery. Due to reimbursement changes, there has been a proliferation and associated overutilization of helicopter services in some areas. In the urban environment, ground ALS has actually been shown to be preferable for relatively short distances, since it takes time to prepare the aircraft for flight. With flight times above 15 minutes, helicopters gain the advantage.61 In Fresno County, California, a study of ground versus helicopter transport in a relatively flat, nonmountainous area served by one Level I trauma center concluded that, within 10 miles of the hospital, ground transport yielded the shortest 9-1-1–hospital interval. Beyond that distance, the simultaneous dispatch of ground and air transport was the most efficient as ground personnel could extricate and resuscitate in advance of the arrival of the helicopter. For surface transports of more than 45 miles, helicopter was faster even if dispatched after the ground unit.62 In the rural environment, provided the scene is within the range of aircraft without the need to refuel, direct transport may be worthwhile if the time to the local hospital by ground ambulance is greater than that of the helicopter flight.63 If not, surface transport is preferable.64 A helicopter may also be invaluable in wilderness rescue if a suitable landing site can be assured. The downside is that such aircraft are expensive ($900,000–2,200,000 start-up; $500,000–2,000,000 annual

maintenance), hazardous (fatal accident rate 4.7/100,000 hours),65 and have a limited range. They are also sensitive to weather and altitude and are not always available. Although newer models are roomier, it is still difficult to examine, monitor, and resuscitate unstable patients while airborne. Finally, their effectiveness is open to question. In one study of scene (18.8%) and interhospital (79.5%) transports, the most severely injured patients (17%) died en route or shortly after arrival at the medical center, while 55% had relatively trivial injuries that did not require the use of the rotorcraft.66 The group with intermediate severity of injury (27%) benefited from use of the helicopter, but was difficult to identify in advance. ISS was not used in this study, but, in another study of scene transports alone, the group that benefited appeared to be those with an ISS of 22–30.65 In the remote rural setting, helicopters are used primarily for interhospital transfers, following stabilization at the local facility. Even in this circumstance, the solution is not ideal. Once the initial outlay for equipment and personnel has been made, an incentive exists to use it, even when surface conveyance may be an acceptable alternative. Helicopters become an important part of the sponsoring hospital’s marketing program. Overtriage reflected in an average ISS of 19 is a major problem that remains to be solved.61,65 In some mature programs, as many as 55% of patients transported were determined retrospectively to have minor trauma. It would appear that continued refinement of triage criteria is necessary to ensure that helicopters are used judiciously and effectively. Fixed-wing transfers are another option, but are restricted to interhospital transfer. These aircraft are fast and, when properly equipped, can function as an airborne intensive care unit.67 Their use is common in the noncoastal western states in helping to bridge vast distances. Drawbacks include the 30 minutes or more needed to get the plane airborne and the need to transport the victim by ground ambulance between airport and hospital on both ends of the transfer.

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directly to a regional trauma center or urban hospital. The more remote the county, the more likely the patient was taken first to the local hospital.54 It is still true that in many rural systems, it is simply not feasible to transfer unstable patients, whether by ground or helicopter, directly and over long distance to a trauma center. Bypass of the local hospital is, most often, not appropriate in these circumstances. A corollary of this observation is that rural health care facilities should be prepared, within their capabilities, to treat the sporadic seriously injured patient. Unfortunately, as a result of trauma legislation, malpractice concerns, uncertainty regarding the appropriate role of the local hospital, and lack of surgeon commitment, many patients are now transferred to trauma centers when they could have been treated locally.72 In a few select locations, a Level I academic trauma center may be strategically situated close to a large rural referral base. (For purposes of this discussion, Levels I–IV are those defined by the American College of Surgeons Committee on Trauma.23) More commonly, particularly in the plains and mountainous western states, huge distances intervene between regional trauma centers. Also, there may be no Level I, or, in some cases, even a Level II center. These trauma centers serve the population with equipment and technical expertise unavailable in smaller hospitals and furnish system development, performance improvement, professional and lay education, prevention programs, and rehabilitation services. Some rural Level II centers are located close enough to a Level I that their job is primarily to share some of the burden of the trauma case load as well as responsibility for education and outreach.42 Many serve a vast geographic area, however, and must assume a larger role. They will differ from a Level I center in terms of lower volumes, mostly blunt trauma, surgeons who take calls from home, and lack of certain sophisticated services such as limb replantation or management of complex pelvic and acetabular fractures.71 Most will provide helicopter and/or fixed-wing transport to their region. They may have resident house staff and medical students, but most do not. Leadership in education, outreach, performance improvement, and system development, normally the purview of Level I academic centers, becomes their mission. A rural Level III trauma center, even though it may lack many of the capabilities of the regional Level II, is a critical resource that will receive patients from many smaller hospitals in its region.2,44,77 It is expected to provide full-time emergency medicine, general surgeons, orthopedic surgeons, and operating room availability. Size will vary from about 40 to 150 beds. Case volumes are low with approximately 50–125 trauma registry patients per annum, and most have an ISS less than 15. In addition, the medical staff will usually have specialists in internal medicine, a variety of medical subspecialists, and family practitioners. Anesthesia is provided by anesthesiologists or nurse anesthetists. Services that are important to the care of trauma patients, but are usually unavailable, include neurosurgery, cardiovascular surgery, plastic and reconstructive surgery, interventional radiology, dialysis, comprehensive blood banking, in-house operating room team, and backup. Imaging services will include ultrasound and a CT scanner, while angiography, nuclear medicine, and magnetic

resonance imaging may be available. The trauma team takes call from home and is committed to early evaluation and treatment of critically injured individuals. This is based on prehospital triage and timely notification from the field so that the team may be present when the patient arrives. Physicians in the emergency department and, sometimes, surgeons should provide both online and off-line medical direction for local ambulance services. The hospital has sufficient equipment and personnel to provide definitive care for the majority of patients, but must recognize those patients who exceed local capabilities and need rapid, efficient stabilization followed by transport to the next appropriate level of care.78 The trauma program, aided by a trauma registry, is expected to conduct ongoing performance improvement for itself and prehospital personnel and to provide outreach services to smaller hospitals within its catchment area. The rural Level III is more likely to encounter and provide definitive care for moderately injured patients (ISS 9–25) and to serve as a regional resource than its urban or suburban conterpart.73,74 Level IV hospitals may or may not have surgical capability. If they do, there is often only one surgeon, who accordingly will not be available at all times.40,42,44 With the aid of improved triage criteria and prompt assembly of the trauma team, a group of nondesignated, isolated rural hospitals (size 18–77 beds) in northern California demonstrated the ability to provide care to 266 patients (mean ISS 26) that exceeded MTOS norms. They lacked the financial resources to be designated by the state as Level III, but were able to provide operative and inpatient care under the proper circumstances. Above all, they demonstrated commitment to care of the injured, without which no hospital, regardless of other resources, will succeed as a trauma center.79 In many small hospitals, however, those requiring surgical or inpatient care will usually need to be transferred early. Observation of patients with blunt injury to a solid organ is not advisable in this setting unless the surgeon and operating room staff commit to being available at a moment’s notice if nonoperative management fails. The trauma team and trauma program will be led by a surgeon when possible, but will include family physicians, physician assistants, and nurse practitioners. Damage control surgery or operative stabilization before transport should be undertaken when indicated, provided the surgeon and operating room staff are available. Several trauma systems (WA, CO, MT, UT, and WY, among others) include Level V trauma centers in their designation process. These are health care facilities lacking inpatient capability, but which commit to early availability for resuscitation, stabilization, and transport within the system. Some regions of California have developed Emergency Department Approved for Trauma (EDAT) in rural areas of the state to serve the same stabilization and transport function. Most hospitals in most states are undesignated, but also have an important role to play in an inclusive system.

EDUCATION AND MAINTENANCE OF SKILLS Severe trauma represents 5% or less of the workload of most rural general surgeons.2,44,48 Rural health care workers at all levels have difficulty maintaining their skills because they will

Rural Trauma

TREATMENT OPTIONS ■ Stabilization and Transfer to Definitive Care When a trauma patient is en route or has already arrived at a small hospital with limited resources, one of the most critical decisions to be made is whether the patient can be treated locally or whether transfer is necessary. Trauma outcome is directly related to time to definitive care. If it is clear from the field report that the victim’s injuries will exceed local resources,

that is the time to begin making transfer arrangements in order to eliminate the principal rate-limiting step (i.e., dispatch and arrival of the transport team and conveyance).84 Hospitals that need to transfer patients frequently know in advance which trauma centers will receive them and should have transfer agreements in effect. Once the patient is in the emergency department, it is the responsibility of the surgeon or physician leading the team to recognize the need for transfer and initiate arrangements as soon as possible. From that point onward, all efforts should be directed at optimizing the patient’s physiology. ATLS should be the guide to the resuscitation, and testing and interventions should be limited to essentials and should not delay the departure.85 Unfortunately, inappropriate imaging particularly with CT has been shown to delay some transfers. Compounding the problem is the fact that, because of unavailability of images or reports from the referring hospital, many of these studies are repeated at the receiving Level I or II center, creating further delay, expense, and risk to the patient. One institution reported that 53% of 410 patients required repeat imaging at an average cost of $2,985 per patient.86 Referring physicians appear to obtain such studies out of liability concerns or because the trauma center may not accept the patient without confirmation of the severity of injury. A potential solution, beyond education and outreach, could be the establishment of regional Picture Achieving and Communication System (PACS) networks that are connected by broadband technology between referring and receiving hospitals. The team leader should speak directly with the receiving trauma surgeon and should avoid transferring care directly to a subspecialist (orthopedic surgeon, neurosurgeon, plastic surgeon). If the receiving hospital is on diversion, its representatives should help the referring hospital find an alternate destination. Federal law now governs transfer of patients from an emergency department to another hospital, to another area within the same hospital, or to home. Violation of the Emergency Medical Treatment and Active Labor Act (EMTALA) regulations can lead to draconian penalties for hospitals and individuals. Punishments include denial of the ability to care for Medicare and Medicaid patients, as well as civil liability. This set of rules, originally enacted in 1985 to prevent patient “dumping” (inappropriate transfer of unstable indigent patients from private to public emergency rooms), has been expanded to what is essentially a federal right to emergency care and a federal malpractice act. The receiving hospital is obligated to report whenever a patient was “unstable” or inappropriately transferred. A complaint by any concerned party must be investigated by the Office of the Inspector General (OIG).87 Most traumatic events will be viewed by the patient, although not necessarily by health care workers, as an emergency. Any patient has a right to request a medical screening exam (MSE) for a perceived emergency medical condition (EMC). The hospital or clinic is required to determine by this exam whether or not an EMC in fact exists. If the patient has an EMC, “the hospital must stabilize the emergency condition, or, if it is unable to stabilize the patient, the hospital must transfer the patient to a hospital that is capable of stabilizing the

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have few opportunities to exercise them. ATLS was designed specifically to teach physicians how to manage patients in the early minutes and hours after a critical injury. The target audience was the rural physician or surgeon who sees such patients infrequently and must cope with very limited resources to resuscitate and transfer such patients. It has now become the international standard for early care of the injured and has had a positive impact on rural trauma care. PHTLS has been developed in conjunction with ATLS to educate EMTs about trauma. In the early 1980s and early 1990s, before the general dissemination of ATLS, most articles on rural trauma care were in agreement that a significant proportion of preventable trauma morbidity and mortality resulted from inappropriate care at the local hospital.10,13,16,18,40 More recent studies indicate that, at least in some areas, patients are now being stabilized much more effectively before transport to the regional Level I or II trauma center, and delays in discovery, retrieval, and transport are the principal causes of death.1,17,38,39,76,80–82 On the other hand, a recent report from Rhode Island where ATLS is not mandated for emergency room staff demonstrated frequent departures from ATLS guidelines, with resultant delays in transport to the centrally located Level I trauma center.78,83 New technology and techniques take time to arrive in rural areas. Expense and lack of need contribute to the delay. For instance, most rural surgeons and physicians in the emergency department will not encounter enough patients with serious abdominal injuries to become adept in the use of ultrasound to identify intra-abdominal hemorrhage. For them, time and expenditures for capital equipment may be better directed at more basic and utilitarian items. Ignorance of new methods, however, is not acceptable. Members of the trauma team should assume responsibility for remaining sufficiently current in the trauma literature and in ATLS. They should know how to evaluate and resuscitate severely injured patients, recognize the need for operative intervention before transfer, know when nonoperative management is appropriate and safe, and realize when a patient’s needs exceed local resources. Feedback on specific cases and trauma educational outreach programs are primary responsibilities of the leading trauma center in the area. Intramural offerings, particularly if based on local registry information, will help all members of the team to remain up to date. Prevention programs will help raise public awareness of the impact trauma has on individual lives and may assist in increasing support for the purchase of equipment and development of a regional trauma system.

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emergency condition. Hospitals with specialized capabilities or facilities are required to accept transfers of patients who require such specialized services ….”87 What constitutes an EMC, and the details of the MSE, is open to interpretation. How are hospitals and physicians to respond (Table 8-2)? One strategy already being employed is for surgeons to refuse to take trauma calls and for hospitals to close their doors to injured patients. The ethical and legal ramifications of this approach are debatable and will undoubtedly be subjected to close scrutiny. The proactive response is for health care workers and facilities to familiarize themselves with the provisions of the law and to establish, in cooperation with each other, a trauma program that will be in compliance. Properly executed transfer agreements should, in most cases, streamline the process. It is likely that the strongest defense in any given instance will be the ability to demonstrate that actions were directed toward the patient’s best interest. For the trauma patient, the following would be appropriate: 1. Prehospital triage protocols for identification of critically injured patients 2. A mechanism for ensuring early evaluation at the bedside by the appropriate surgeon or emergency medicine physician 3. Prompt initiation of resuscitation and stabilization measures 4. Early decision regarding the medical need for transfer 5. Consultation with the receiving hospital (ideally with the trauma surgeon) 6. Documentation of indications for, and acceptance of, transfer 7. Arrangement of the appropriate transfer team, conveyance, and equipment 8. Before transfer, stabilization of the patient’s condition to the degree possible given the resource imitations of the transferring hospital Managed care may also interfere with the orderly transfer of patients as established by a regional trauma system. Several types of problems have arisen. Payments for emergency and after-hours transfers have been denied for lack of prior authorization, even though such authorization was impossible to obtain at the time. Triage to a hospital within the managed care system may be mandated, even though that facility may not be an authorized trauma center. The American College of Surgeons has issued a statement condemning such practices and encouraging cooperation of managed care and trauma systems.88

■ Operative Stabilization and Transfer Most patients respond to standard resuscitative measures and, once stabilized, can be admitted locally, discharged home, or transferred to a higher level of care. A small proportion, probably less than 10%, will be either transient or nonresponders and will remain hemodynamically abnormal despite continued skilled resuscitation. If the patient has multiple injuries, suffers from significant medical comorbidity, is at the extremes of age, or has injuries requiring subspecialty (i.e., neurosurgical) or

complex intensive care, transfer will likely be necessary. The more remote the primary facility is, the greater the risk that the patient will deteriorate during transfer unless something is done to address the underlying problem, generally hemorrhage. In this circumstance, the local general or subspecialty surgeon should be prepared to operate and stabilize the patient before transfer.89 With a properly equipped transport vehicle, usually a fixed-wing aircraft or helicopter, the patient may often be transferred immediately thereafter into the hands of the flight team without any compromise of care.67,90 Operative stabilization of this sort falls into the following two categories: definitive surgery and damage control surgery.

Definitive Surgery Under most circumstances a stabilizing procedure can be conducted and completed in conventional fashion, such that no further treatment will be required for that particular problem. Examples would include, but are not limited to, the following: 1. Establishment of a surgical airway 2. Splenorrhaphy or splenectomy, hepatorrhaphy, resection and debridement, or insertion of perihepatic packs 3. Closure of evisceration 4. Closure of injuries to the gastrointestinal tract 5. Repair or shunting of truncal and extremity vascular injuries 6. Reduction of dislocations 7. Debridement and control of hemorrhage from open fractures in an extremity or mangled extremities

Damage Control Surgery Damage control operations followed by temporary closure of the abdomen have been described for a variety of truncal injuries with an emphasis on limiting time in the operating room and avoiding the triad of acidosis, hypothermia, and coagulopathy.91–93 Candidates for these desperate measures typically have an overwhelming constellation of injuries. Most reports on damage control surgery and temporary closure techniques have come from urban trauma centers. Following a period of rewarming and correction of hypothermia, acidosis, and a coagulopathy in the intensive care unit, the patient is then returned to surgery for definitive repair of the remaining injuries. Rural surgeons can apply the same principles. Occasional patients will have such complex injuries that definitive management exceeds the technical abilities or resources of the local surgeon and hospital, but may be amenable to temporizing maneuvers, followed by rapid transfer in an aircraft equipped as an airborne intensive care unit.94 Examples include packing of the liver for complex hepatic injuries; peritoneal cleansing, hemorrhage control, and stapling or rapid suture of multiple bowel perforations; temporary abdominal closure; and abbreviated thoracotomy, hemorrhage control, and temporary chest closure for patients with extensive pulmonary and thoracic vascular injuries.95 If interventional radiology is not available locally, patients with unstable pelvic fractures may benefit from application of external fixators prior to transfer.

Rural Trauma

1. A general surgeon trained in indications for and technique of burr holes with limited craniotomy 2. Traumatic brain injury with lateralizing signs and threatened herniation 3. Surgical lesion present on CT scan 4. Consultation with, and approval of, neurosurgeon at receiving trauma center 5. Limited craniotomy for decompression and hemorrhage control 6. Immediate transfer to definitive care97

■ Local Definitive Care Most trauma patients can be cared for at a local community hospital capable of offering continuous surgical care. “The mindset that a well-trained general surgeon is not able to care for many trauma patients must be corrected.”72 Although triage and transfer guidelines address anatomic, physiologic, and mechanism of injury parameters, there are few publications that describe specifically which patients might reasonably be cared for in small hospitals. Currently accepted examples are patients with isolated extremity fractures, minor burns, lacerations, a hemothorax and/or pneumothorax, multiple rib fractures, traumatic brain injury with GCS of 14–15, and a variety of organ and vessel injuries within the ability and comfort range of the attending surgeon. It is important for surgeons to remember that colleagues, nursing staff, and ancillary services must also be able to provide the necessary

adjunctive care. Patients at the extremes of age, with multiple organ system involvement, the need for prolonged ventilator support and/or intensive care, and serious underlying illnesses, will probably benefit from care in a trauma center under most circumstances. Patients should always be advised of the option to be transferred. It is important to be aware of pertinent state statutes or transfer guidelines used by the regional trauma system and to realize that in the event of misadventures, the burden of proof will rest with the doctor who chooses not to transfer a patient. The management of patients with blunt injury to solid abdominal viscera (particularly spleen and liver) presents some difficult logistical problems for the rural surgeon. Most patients with injuries to the spleen or liver and normal hemodynamics can be managed without an operation. When an operation is necessary, the well-trained general surgeon is certainly fully capable of performing a splenectomy or splenorrhaphy. Major hepatic injuries have the potential for overwhelming the technical ability of the surgeon or the resources of a small blood bank, but may be amenable to simple suture repair, resectional debridement, or packing and immediate transfer. It is to the patient’s advantage to be managed in the local hospital rather than be transferred to a distant Level I or II center, if it can be done safely. The problem lies with the patient who deteriorates unexpectedly, becomes hypotensive, and requires urgent surgery. In a hospital lacking house staff, immediate availability of the surgeon, and a plan for rapid preparation of the operating room, there is a small but real potential for death from exsanguinating hemorrhage. In these circumstances, a lower threshold for early operation or transfer is appropriate.102 When patients are selected properly for local treatment, a number of advantages accrue. It is generally more convenient for patient and family as friends, clergy, and support groups in the area provide moral support and can hasten recovery and reintegration into the community. Risks inherent in emergency transfers are eliminated. Use of local services keeps money in the community. Because most rural trauma is motor vehicle related, insurance coverage is better than average and supports the financial stability of the hospital. Finally, appropriate local care reduces the burden on busy regional trauma centers.72,103 A downside for many surgeons is that trauma of this sort, particularly in the era of observation of injuries to solid organs, is not very exciting and produces relatively few operations. Overseeing care for patients while subspecialists perform a variety of operative procedures does not appeal to many general surgeons. Hours are inconvenient, and trauma emergencies can wreak havoc with elective schedules. The high incidence of substance abuse in association with traumatic events is well documented and may make evaluation and management of injured patients difficult or unpleasant. Surveys of surgeons’ attitudes toward trauma reflect many of these concerns and yet, interestingly, demonstrate that rural surgeons are significantly more willing to accept these burdens than are their urban colleagues.50,104 In fact, the opportunity to provide potentially lifesaving treatment to friends, neighbors, or acquaintances and to see its long-term effects is one of the benefits of a general surgery practice in a small town.72

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Surgeons in Alberta compared outcomes in patients referred to a Level I center from Level III and IV hospitals in the region, focusing on those patients arriving in unstable condition and requiring emergency laparotomy. Most had multisystem injuries and required operations by surgical subspecialists, as well. Despite the presence of serious concurrent injuries, however, they concluded that while the community surgeons in the Level III hospitals were triaging patients appropriately, some patients might have benefited from a damage control operation prior to transfer.96 Injury to the brain remains the single greatest source of morbidity and mortality for trauma victims.18 Many patients sustain their closed head injuries far from the nearest neurosurgeon, and time becomes the enemy. Under most circumstances, the only option is to minimize secondary brain injury with appropriate ventilatory and pharmacologic maneuvers and expedite transfer.97,98 A small proportion of these patients, however, will have lesions amenable to surgical drainage. While rural hospitals generally lack neurosurgical services, most hospitals in the United States now have CT scanners. General surgeons can be trained to perform burr holes and/or limited craniotomy for decompression and hemorrhage control in patients with epidural or subdural hematomas noted on a CT scan.99,100 When a patient with an injury to the brain shows signs of rapid deterioration and a delay of more than 90 minutes to definitive neurosurgical care is anticipated, consideration should be given to emergency decompression of the hematoma.98,101 The necessary components are as follows:

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■ Population Shifts SECTION 2

Population shifts in the coming years will have an impact on the problems of rural trauma. Although many parts of the Great Plains are becoming progressively depopulated, rural areas of the coastal regions, Rocky Mountains, Southwest, and Sunbelt states are experiencing an influx of young, active people who are tired of city life and eager for what small town America has to offer. Equipped with cell phones, modems, GPS-based equipment, and sport utility vehicles, these members of generations X and Y (and their baby boom parents) are very much into hiking, camping, climbing, skiing, and other activities that are best pursued in rural and frontier settings. They are affluent and well educated and accustomed to getting what they want. It is likely that, in order to support their desired lifestyles, they will expect or demand a trauma infrastructure that is sophisticated, efficient, effective, and comparable to what is available in a resource-rich environment. Whether they will be willing to pay for it through taxes or user fees is another matter. An important mission for rural systems will be convincing constituents of the importance of financial support for trauma activities.

WIRELESS TECHNOLOGY Many of the problems of rural communities could be mitigated with the use of technology for prevention and for discovery. In the 1990s, rural EMS notification times (from time of motor vehicle crash) dropped significantly with the advent of wireless phones. In mountainous terrain, wireless communication is hampered by line of sight, but this problem is already being addressed through the installation of low-power, short-distance relay boxes. Vehicles produced by the leading automobile manufacturers can now include advanced automatic crash notification (AACN) equipment. For those vehicles lacking such systems, however, all is not lost. Provided ambulances are equipped with GPS units, law enforcement at a crash scene can radio either an actual address or latitude/ longitude coordinates to EMS personnel to guide them. Using such a system, mean rural response times have been reduced from 13.7 to 9.9 minutes, a differential which can prove lifesaving in some circumstances.105 A combination of crash sensors, GPS devices, and a wireless phone allows for automatic phone activation on impact to notify EMS of the location and severity of a crash.41 Crash avoidance is possible with sensors installed in the roadway to measure road edge, lane tracking, intersections, and merging traffic. Vehicle sensors can assist with avoidance of rear-end crashes, vision enhancement, navigation and routing information, and driver condition. The development of smart highways will be expensive, however, and, predictably, rural areas will be the last to benefit. Improvements in crash protection will result from refinements of existing passive restraints (seatbelts, airbags) and structural characteristics of vehicles. While the advances just described are specific for automobile occupants, wireless communication and location systems will also benefit hikers, hunters, workers, and others in the backcountry, provided they equip themselves with cell phones

and GPS monitors. Another device under investigation is the personal status monitor (PSM), which is worn like a wristwatch and combines pulse, blood pressure, and arterial hemoglobin saturation with GPS.106 The resulting improvement in notification and location will guide rescuers to victims more efficiently and eliminate much of the delay to definitive care that currently plagues rural EMS.

TRANSPORT Transport systems are another area where technology combined with a secure funding source could improve outcomes for trauma victims. Helicopters are very expensive, but may have the greatest potential for eliminating delay and downtime in the process of getting the right patient to the right hospital at the right time. Extended range, expanded capacity for onboard equipment and access to the patient, safer landing areas, and creative methods of funding are all possible areas for investigation. If national health policy moves toward regionalization of medical and surgical care, improved transport from scene or local hospital will be essential.

TELEMEDICINE If we are unable to improve on methods of transporting the patient to the trauma center, investigators are now actively studying strategies for bringing the trauma center to the patient. Telemedicine, particularly digital radiology, is already in use in many parts of the country. Outpatient follow-up of patients discharged from a trauma center to a remote rural area has been successfully accomplished using videoconferencing over T1 lines at 768 kbps. Internet broadband technology is increasingly available in rural areas and is also being successfully used for video and data transmission. Cable-based broadband technology is increasingly available in rural areas and is an even faster mode of data transmission. Adjuncts include an analog electronic stethoscope, document cameras and close-up cameras with macro lenses, and a fax line, scanner, or document camera for document transmission.107 Satellite uplinks on emergency vehicles and appropriate audiovisual equipment can allow trauma experts at the medical center to observe a rescue in real time and offer suggestions regarding appropriate evaluations, interventions, and disposition at a distance.108,109 Laptops and landlines have been used to transmit real-time images of trauma resuscitations at remote rural hospitals. In one case the trauma surgeon talked a local doctor through a lifesaving cricothyroidotomy in a patient with an injury to the brain, and, in another, recommended a diagnostic peritoneal lavage that was positive and led to local laparotomy for control of abdominal hemorrhage prior to transfer.110 The Internet has been used to transfer images to aid in assessing candidates for replantation of an extremity.111 Improvements in compression/ decompression software have overcome some of the previous bandwidth limitations in rural areas. Limiting factors include money and infrastructure including T1 lines at 2 Mbps, broadband fiber-optic lines at 155 Mbps, and advanced communication satellite access at 622 Mbps. Surgeons in Taiwan have

Rural Trauma

TELEPRESENCE SURGERY These strictures will also apply in another area under investigation, telepresence surgery, in which a surgeon uses a robotic system designed to make him or her feel as if he or she is actually at the remote site with the patient. Much of the research in this area has been sponsored by the Defense Advanced Research Projects Agency (DARPA) for the US military to develop methods for safely operating on troops at or near a battlefield. If it can be done under those circumstances, it surely can be applied to less hostile rural environments. One limitation is the latent

period required to transmit signals (currently 200–300 km by terrestrial cable, and 35–50 km by wireless transmission) at an acceptable delay of 200 minutes. Communications satellites, by comparison, have a latent period of 1.5 seconds.116 Laparoscopic surgery lends itself ideally to this technology and has, in fact, been accomplished by specially trained surgeons performing cholecystectomies from a “remote” console within the same operating suite.117,118 Efforts are underway to accomplish similar surgery at a much greater distance. The equipment utilized was originally designed for endoscopic coronary bypass surgery and has been used with success for that purpose, as well.119 At the moment, the acquisition cost of one of these robotic systems is approximately $1 million.

TRAUMA SYSTEMS Trauma systems are covered in depth elsewhere in this book. Most trauma experts are convinced that an inclusive and integrated approach to trauma will be necessary in the future. Computer models are now available that can help policymakers decide where to place trauma hospitals and helicopters in order to best meet the trauma needs of a given region and population.120 It is important to emphasize that a system will offer rural hospitals and health care workers the best opportunity to expand their limited resources. By pooling efforts with others in the region in common purpose, small hospitals benefit from educational and prevention services, improved patient transport, increased political influence, better financial support, and access to new technology. Failure to take advantage of these opportunities may consign a rural hospital and its patients to isolation and inadequate trauma care. “One of the most important functions of a trauma system is to ensure that patients do not die of simple injuries. Death caused by easily correctable and relatively minor injuries still occurs with an alarming frequency in the rural setting.”121

REFERENCES 1. Rogers F, Shackford S, Osler T, Vane D, Davis J. Rural trauma: the challenge for the next decade. J Trauma. 1999;47:802–821. 2. Wayne R. Rural trauma management. Am J Surg. 1989;157:463–466. 3. Muelleman R, Walker R, Edney J. Motor vehicle deaths: a rural epidemic. J Trauma. 1993;35:717–719. 4. Maio R, Green P, Becker M, Burney R, Compton C. Rural motor vehicle crash mortality: the role of crash severity and medical resources. Accid Anal Prev. 1992;24:631–642. 5. Baker S, Whitfield R, O’Neill B. Geographic variations in mortality from motor vehicle crashes. N Engl J Med. 1987;316:1384–1387. 6. Baker S, Whitfield R, O’Neill B. County mapping of injury mortality. J Trauma. 1988;28:741–745. 7. Kearney P, Stallones L, Swartz C, Barker D, Johnson S. Unintentional injury death rates in rural Appalachia. J Trauma. 1990;30:1524–1532. 8. Vane D, Shackford S. Epidemiology or rural traumatic death in children: a population-based study. J Trauma. 1995;38:867–870. 9. Rausch TK, Sanddal ND, Sanddal TL, Esposito TJ. Changing epidemiology of injury-related pediatric mortality in a rural state: implications for injury control. Pediatr Emerg Care. 1998;14(6): 388–392. 10. Certo T, Rogers F, Pilcher D. Review of care of fatally injured patients in a rural state: 5-year follow up. J Trauma. 1983;23:559–565. 11. Esposito T, Sanddal N, Hansen J, Reynolds S. Analysis of preventable trauma deaths and inappropriate care in a rural state. J Trauma. 1995;39:955–962.

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reported on 35 patients with a total of 60 traumatic digital amputations who were evaluated at a distance with the aid of a camera phone to determine whether transfer for replantation was appropriate.112 The trauma service at the University of Vermont has developed a remote teleconsultation service to provide immediate access to the trauma surgeon for physicians and physician extenders in rural northern New York. Each of the on-call surgeons has a telemedicine workstation at home that can communicate by interactive video with a similar workstation at one of the nine participating community hospitals using three ISDN lines. (ISDN is a digital network capable of transmitting voice, video, and data over telephone lines at speeds up to 1.4 Mbps.) The surgeon can observe the physical exam, monitor vital signs, and view x-rays. In one case, the surgeon walked a physician’s assistant through reduction of an elbow dislocation prior to transfer (3.5 hours by ground) to definitive care at the Level I trauma center. Telemedicine has also been used to evaluate burns, enhancing early management, while in some cases avoiding the need to transfer to a burn center.113 Adaptation of similar technology to moving ambulances is under development by the same group.114 Medicolegal considerations, including licensure if the supervising doctor is in another state, and the essence of the doctor–patient relationship if he or she never physically encounters the patient, have yet to be resolved. The Arizona Telemedicine Program, based at the University of Arizona in Tucson, was developed in the mid-1990s and funded by the state legislature. It is now a well-established service providing real-time consultations to hospitals around the state over a broad range of specialties. Trauma surgeons participating in the program have obtained credentials at the referring hospitals, dictate their consultations, and charge a nominal fee. They report experience with 35 trauma patients evaluated by telemedicine (audio, video via single camera with 12x zoom capability in the ED, data transfer by T1 line at 1.0 Mbps) at six separate rural hospitals since 2004. As a result of the consultation process, 27 patients were transferred to Tucson, 9 of whom underwent surgical intervention. Four of those transferred were felt to have life-threatening conditions that were significantly impacted by the consultation process. Equally important is the finding that 17 patients who might otherwise have been transferred were treated locally, saving an estimated $105,000 in transfer costs alone. Furthermore, physicians at the local sites appear to appreciate the backup provided by this service.115

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12. West J, Trunkey D, Lim R. Systems of trauma care: study of two counties. Arch Surg. 1979;114:455–460. 13. Houtchens B. Major trauma in the rural mountain West. J Am Coll Emerg Phys. 1977;6:343–350. 14. Sihler KC, Hemmila MR. Injuries in nonurban areas are associated with increased disability at hospital discharge. J Trauma. 2009;67: 903–909. 15. Schootman M, Fuortes L. Functional status following traumatic brain injuries: population-based rural–urban differences. Brain Inj. 1993;13:995–1004. 16. Waller J. Urban-oriented methods: failure to solve rural emergency care problems. JAMA. 1973;226:1441–1446. 17. Rutledge R, Fakhry S, Baker C, et al. A population-based study of the association of medical manpower with country trauma death rates in the United States. Ann Surg. 1994;219(5):547–563. 18. Shackford S, Mackersie R, Holbrook T, et al. The epidemiology of traumatic death: a population-based analysis. Arch Surg. 1993;128: 571–575. 19. Wang HE, Callaway CW, Peitzman AB, Tisherman S. Admission hypothermia and outcome after major trauma. Crit Care Med. 2005;33:1296–1301. 20. Waibel BH, Schlitzkus LL, Newell MA, Durham C, Sagraves S, Rotondo M. Impact of hypothermia (below 36°) in the rural trauma patient. J Am Coll Surg. 2009;209:580–588. 21. Fatovich DM, Jacobs IG. The relationship between remoteness and trauma deaths in Western Australia. J Trauma. 2009;67:910–914. 22. Thompson M, Lynge D, Larson E, Tachawachira P, Hart L. Characterizing the general surgery workforce in rural America. Arch Surg. 2005;140: 74–79. 23. Anderson JA. Rural Trauma Care: Resources for Optimal Care of the Injured Patient. Chicago: American College of Surgeons; 2006. 24. Nordstrom D, Zwerling C, Stromquist A, Burmeister L, Merchant J. Epidemiology of unintentional adult injury in a rural population. J Trauma. 2001;51:758–766. 25. Rogers F, Osler T, Shackford S, et al. A population-based study of geriatric trauma in a rural state. J Trauma. 2001;50(4):604–609. 26. Clark D. Motor vehicle crash fatalities in the elderly: rural versus urban. J Trauma. 2001;51:896–900. 27. Wigglesworth E. Do some US states have higher/lower injury mortality rates than others? J Trauma. 2005;58:1144–1149. 28. Deaths and Injuries in the Workplace, Home and Community, and on Roads and Highways. Available at: http://www.nsc.org/library/report_injury_ usa.htm. 29. Pratt D. Occupational health and the rural worker: agriculture, mining and logging. J Rural Health. 1990;6:399–417. 30. Norwood S, Myers M. Outcomes following injury in a predominantly rural-population-based trauma center. Arch Surg. 1994;129:800–805. 31. Farrell T, Sutton JJ, Clark D, et al. Moose-motor vehicle collisions: an increasing hazard in northern New England. Arch Surg. 1996;131: 377–381. 32. Helmkamp J, Derk S. Nonfatal logging-related injuries in West Virginia. J Occup Environ Med. 1999;41:967–972. 33. Mullins R, Brand D, Lenfesty B, Newgard C, Hedges J, Ham B. Statewide assessment of injury and death rates among riders of off-road vehicles treated at trauma centers. J Am Coll Surg. 2007;204: 216–224. 34. Coben JH, Tiesman HM, Bossarte RM, Furbee PM. Rural–urban differences in injury hospitalizations in the U.S., 2004. Am J Prev Med. 2009;36(1):49–55. 35. Perkins R, Sanddal TL, Howell M, Sanddal ND, Berman A. Epidemiological and follow-back study of suicides in Alaska. Int J Circumpolar Health. 2009;68(3):212–223. 36. Centers for Disease Control and Prevention. Web-Based Injury Statistics Query and Reporting System. Atlanta, GA: Centers for Disease Control and Prevention; 2010. 37. Robertson R, Mattox R, Collins T, Parks-Miller C, Eidt J, Cone J. Missed injuries in a rural area trauma center. Am J Surg. 1996;172: 564–567. 38. Rogers F, Osler T, Shackford S, Martin F, Healey M, Pilcher D. Population-based study of hospital trauma care in a rural state without a formal trauma system. J Trauma. 2001;50(3):409–414. 39. Rogers F, Osler T, Shackford S, Cohen M, Camp L, Lesage M. Study of the outcome of patients transferred to a level I hospital after stabilization at an outlying hospital in a rural setting. J Trauma. 1999;46:328–333. 40. Martin G, Cogbill T, Landercasper J, Strutt P. Prospective analysis of rural interhospital transfer of injured patients to a referral trauma center. J Trauma. 1990;30:1014–1019.

41. Champion H, Cushing B. Emerging technology for vehicular safety and emergency response to roadway crashes. Surg Clin North Am. 1999;79:1229–1240. 42. Zulick L, Dietz P, Brooks K. Trauma experience of a rural hospital. Arch Surg. 1991;126:1427–1430. 43. Bintz M, Cogbill T, Bacon J. Rural trauma care: role of the general surgeon. J Trauma. 1996;41:462–464. 44. Rinker C, Sabo R. Operative management of rural trauma over a 10-year period. Am J Surg. 1989;158:548–551. 45. Sariego J. Impact of a formal trauma program on a small rural hospital in Mississippi. South Med J. 2000;93:182–185. 46. Foley T, Kessel J, Schmitz G, RTTDC©. New course to improve rural trauma care. Bull Am Coll Surg. 2005;90. 47. Rabinowitz H, Diamond J, Markham F, Paynter N. Critical factors for designing programs to increase the supply and retention of rural primary care physicians. JAMA. 2001;286:1041–1048. 48. Smith N. The incidence of severe trauma in small rural hospitals. J Fam Pract. 1987;25:595–600. 49. Stewart R, Johnson J, Geoghegan K, et al. Trauma surgery malpractice risk: perception versus reality. Ann Surg. 2005;241:969–975. 50. Esposito T, Maier R, Rivara F, Carrico C. Why surgeons prefer not to care for trauma patients. Arch Surg. 1991;126:129–133. 51. Doty B, Zuckerman R. Rural surgery: framing the issues in surgical practice in rural areas. Surg Clin North Am. 2009;89:1279–1284. 52. Lynge D, Larson E. Workforce issues in rural surgery. Surg Clin North Am. 2009;89(6):1285–1291. 53. Doty B, Zuckerman R, Gold M, et al. General Surgery in Small Rural New York Hospitals. A Pilot Survey of Hospital Administrators; 2009. Available at: http://www.aamc.org/workforce/pwrc06/doty.pdf. 54. Morrisey M, Ohsfeldt R, Johnson V, Treat R. Trauma patients: an analysis of rural ambulance trip reports. J Trauma. 1996;41: 741–746. 55. Institute of Medicine. Emergency Medical Services: At the Crossroads. Washington, DC: Institute of Medicine; 2008. 56. Messick W, Rutledge R, Meyer A. The association of advanced life support training and decreased per capita trauma death rates: an analysis of 12,417 trauma deaths. J Trauma. 1992;33:850–855. 57. National Highway Traffic Safety Administration. National EMS Scope of Practice Model. Washington, DC: National Highway Traffic Safety Administration; 2007. 58. McGinnis K. Rural and Frontier EMS Agenda for the Future. Kansas City, MO: National Rural Health Association; 2003. 59. Mason S, Wardrope J, Perrin J. Developing a community paramedic practitioner intermediate care support scheme for older people with minor conditions. Emerg Med J. 2006;23:479–481. 60. McGinnis K. State EMS Rural Needs Survey 2004. Falls Church, VA: National Association of State EMS Directors; 2004. 61. Brathwaite C, Rosko M, McDowell R, Gallagher J, Proenca J, Spott M. A critical analysis of on-scene helicopter transport on survival in a statewide trauma system. J Trauma. 1998;45140–144. 62. Diaz M, Hendey G, Bivins H. When is helicopter faster? A comparison of helicopter and ground ambulance transport times. J Trauma. 2005;58:148–153. 63. Gabram S, Jacobs L. The impact of flight systems on access to and quality of care. Probl Gen Surg. 1990;7:203–222. 64. Grossman D, Hart L, Rivara F, Maier RV, Rosenblatt R. From roadside to bedside: the regionalization of trauma care in a remote rural county. J Trauma. 1995;38:14–21. 65. Cunningham P, Rutledge R, Baker C, Clancy TV. A comparison of the association of helicopter and ground ambulance transport with the outcome of injury in trauma patients transported from the scene. J Trauma. 1997;43:940–946. 66. Urdaneta L, Miller B, Ringenberg B, Cram A, Scott D. Role of an emergency helicopter transport service in rural trauma. Arch Surg. 1987;122:992–996. 67. Sharar S, Luna G, Rice C, Valenzuela T, Copass M. Air transport following surgical stabilization: an extension of regionalized trauma care. J Trauma. 1988;28:794–798. 68. Wald S, Shackford S, Fenwick J. The effect of secondary insults on mortality and long-term disability in a rural region without a trauma system. J Trauma. 1993;34:377–381. 69. Veenema K, Rodewald L. Stabilization of rural multiple trauma patients at Level III emergency departments before transfer to a Level I regional trauma center. Ann Emerg Med. 1995;25:175–181. 70. Rutledge R, Shaffer V, Ridky J. Trauma care reimbursement in rural hospitals: implications for triage and trauma system design. J Trauma. 1996;40:1002–1008.

Rural Trauma 97. Mann N, Mullins R, Hedges J, Rowland D, Arthur M, Zechnich A. Mortality among seriously injured patients treated in remote rural trauma centers before and after implementation of a statewide trauma system. Med Care. 2001;39:643–653. 98. Committee on Trauma, American College of Surgeons. Head injury. In: Advanced Trauma Life Support Program for Physicians. 8th ed. Chicago: American College of Surgeons; 2002. 99. Rinker CF, McMurry FG, Groeneweg VR, Bahnson FF, Banks KL, Gannon DM. Emergency craniotomy in a rural Level III trauma center. J Trauma. 1998;44:984–989. 100. Schecter W, Peper E, Tuatoo V. Can general surgery improve the outcome of the head-injury victim in rural America? A review of the experience in American Samoa. Arch Surg. 1985;120:1163–1166. 101. Cohen J, Montero A, Israel Z. Prognosis and clinical relevance of anisocoria-craniotomy latency for epidural hematoma in comatose patients. J Trauma. 1996;41:120–122. 102. Mangus R, Mann N, Worrall W, Mullins R. Statewide variation in the treatment of patients hospitalized with spleen injury. Arch Surg. 1999;134:1378–1384. 103. Engelhardt S, Hoyt D, Coimbra R, Fortlage D, Holbrook T. The 15-year evolution of an urban trauma center: what does the future hold for the trauma surgeon? J Trauma. 2001;51:633–637. 104. Richardson J, Miller F. Will future surgeons be interested in trauma care? Results of a resident survey. J Trauma. 1992;32:229–233. 105. Gonzalez RP, Cummings GR, Mulekar MS, Harlan SM, Rodning CB. Improving rural emergency medical service response time with global positioning system navigation. J Trauma. 2009;67:899–902. 106. Maniscalco-Theberge M, Elliott D. Virtual reality, robotics, and other wizardry in 21st century trauma care. Surg Clin North Am. 1999;79: 1241–1248. 107. Boulanger B, Kearney P, Ochoa J, Tsuei B, Sands F. Telemedicine: a solution to the follow up of rural trauma patients? J Am Coll Surg. 2001;192:447–452. 108. Kirkpatrick A, Brenneman F, McCallum A, Breeck K, Boulanger B. Prospective evaluation of the potential role of teleradiology in acute interhospital trauma referrals. J Trauma. 1999;46:1017–1023. 109. Aucar J, Granchi T, Liscum K, Wall M, Mattox K. Is regionalization of trauma care using telemedicine feasible and desirable? Am J Surg. 2000;180:535–539. 110. Rogers F, Ricci M, Shackford S, et al. The use of telemedicine for real time video consultation between trauma center and community hospital in a rural setting improves early trauma care. J Trauma. 2001;51: 1037–1041. 111. Buntic R, Siko P, Buncke G, Ruebeck D, Kind G, Buncke H. Using the internet for rapid exchange of photographs and x-ray images to evaluate potential extremity replantation candidates. J Trauma. 1997;43: 342–344. 112. Hsieh C, Jeng S, Chen C, et al. Teleconsultation with the mobile camera-phone in remote evaluation of replantation potential. J Trauma. 2005;58:1208–1212. 113. Saffle J. Telemedicine for acute burn treatment: the time has come. J Telemed Telecare. 2006;12:1–3. 114. Mahoney D. Telemedicine program serves rural Vermont. Surg News. 2005;1(10):1, 20–21. 115. Latifi R, Hadeed G, Rhee P, et al. Initial experiences and outcomes of telepresence in the management of trauma and emergency surgical patients. Am J Surg. 2009;198:905–910. 116. Satava R, Bowersox J, Mack M, Krummel T. Robotic surgery. State of the art and future trends. Contemp Surg. 2001;57. 117. Satava R. Emerging technologies for surgery in the 21st century. Arch Surg. 1999;134:1197–1202. 118. Marescaux J, Smith M, Folscher D, Jamali F, Malassagne B, Leroy J. Telerobotic laparoscopic cholecystectomy: initial clinical experience with 25 patients. Ann Surg. 2001;234:1–7. 119. Reichenspurner H, Damiano R, Mack M, et al. Use of the voicecontrolled and computer-assisted system ZEUS for endoscopic coronary artery bypass graft. J Thorac Cardiovasc Surg. 1999;118:11–16. 120. Branas C, ReVelle C, MacKenzie E. To the rescue: optimally locating trauma hospitals and helicopters. LDI Issue Brief. 2000;6:1–4. 121. Norwood S, McAuley C, Vallma V, Fernandez L, McLarty J, Goodfried G. Mechanisms and patterns of injuries related to large animals. J Trauma. 2000;48:740–744.

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71. Wenneker W, Murray D, Ledwich T. Improved trauma care in a rural hospital after establishing a Level II trauma center. Am J Surg. 1990;160: 655–657. 72. Richardson J. Trauma centers and trauma surgeons: have we become too specialized? J Trauma. 2000;48:1–7. 73. Richardson J, Cross T, Lee D, et al. Impact of Level III verification on trauma admissions and transfer: comparisons of two rural hospitals. J Trauma. 1997;42:498–502. 74. Sampalis J, Denis R, Frechette P, Brown R, Fleiszer D, Mulder D. Direct transport to tertiary trauma centers versus transfer from lower level facilities: impact on mortality and morbidity among patients with major trauma. J Trauma. 1997;43:288–295. 75. Barquist E, Pizzutiello M, Tian L, Cox C, Bessey P. Effect of trauma system maturation on mortality rates in patients with blunt injuries in the Finger Lakes region of New York State. J Trauma. 2000;49: 63–69. 76. Esposito TJ, Sanddal TL, Reynolds SA, Sanddal ND. Effect of a voluntary trauma system on preventable death and inappropriate care in a rural state. J Trauma. 2003;54(4):663–670. 77. Tinkoff GH, O’Connor RE, Alexander EL, Jones MS. The Delaware trauma system: impact of Level III trauma centers. J Trauma. 2007;63(1):121–127. 78. Svenson J. Trauma systems and timing of patient transfer: are we improving? Am J Emerg Med. 2008;26:465–468. 79. Karsteadt L, Larsen C, Farmer P. Analysis of a rural trauma program using the TRISS methodology: a three-year retrospective study. J Trauma. 1994;36:395–400. 80. Ali J, Adam R, Butler A, et al. Trauma outcome improves following the Advanced Trauma Life Support program in an developing country. J Trauma. 1993;34:890–889. 81. Ali J, Adam R, Stedman M, Howard M, Williams J. Advanced Trauma Life Support program increases emergency application of trauma resuscitative procedures in a developing country. J Trauma. 1994;36: 391–394. 82. Rogers F, Shackford S, Hoyt D, et al. Trauma deaths in a mature urban vs. rural trauma system. A comparison. Arch Surg. 1997;132: 376–381. 83. Harrington D, Connolly M, Biffl W, Majercik SD, Cioffi WG. Transfer times to definitive care facilities are too long. A consequence of an immature trauma system. Ann Surg. 2005;241:961–966. 84. Cone J. Tertiary trauma care in a rural state. Am J Surg. 1990;160: 652–654. 85. Committee on Trauma, American College of Surgeons. Stabilization and Transport. In: Advanced Trauma Life Support Program for Physicians. 8th ed. Chicago: American College of Surgeons; 2002. 86. Haley T, Ghaemmaghami V, Loftus T, Gerkin RD, Sterrett R, Ferrara JJ. Trauma: the impact of repeat imaging. Am J Surg. 2009;198: 858–862. 87. Bitterman R. Overview of hospital and physician responsibilities mandated by EMTALA. In: Providing Emergency Care under Federal Law EMTALA. Dallas: American College of Emergency Physicians; 2000. 88. ACS statement on managed care and the trauma system. Bull Am Coll Surg. 1995;80:86–87. 89. Wemyss-Holden S, Bruening M, Launois B, Maddern G. Management of liver trauma with implications for the rural surgeon. ANZ J Surg. 2002;72:400–404. 90. Gilligan J, Griggs W, Jelly M, et al. Mobile intensive care services in rural South Australia. Med J Aust. 1999;171:617–620. 91. Hirshberg A, Walden R. Damage control for abdominal trauma. Surg Clin North Am. 1997;77:813–820. 92. Granchi T, Liscum K. The logistics of damage control. Surg Clin North Am. 1997;77:909–920. 93. Mattox K. Introduction, background, and future projections of damage control surgery. Surg Clin North Am. 1997;77:753–759. 94. Kudsk K, Ivatury R, Morris J, Rotondo M. Symposium: damage control in the trauma patient. Contemp Surg. 2001;57:325–343. 95. Vargo D, Battistella F. Abbreviated thoracotomy and temporary chest closure: an application of damage control after thoracic trauma. Arch Surg. 2001;136:21–24. 96. Ball C, Sutherland F, Dixon E, et al. Surgical trauma referrals from rural level III hospitals: should our community colleagues be doing more, or less? J Trauma. 2009;67:180–184.

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Initial Assessment and Management Panna A. Codner and Karen J. Brasel

INTRODUCTION Time is of the essence in caring for patients with multiple injuries. To emphasize the time-sensitive nature of this care, the critical period immediately following injury was historically termed the “golden hour.”1 Mortality from trauma during this crucial time was estimated to be approximately 60%. This high mortality rate has been attributed in part to inadequate assessment and resuscitation. In order to minimize morbidity and mortality for these patients, appropriate and aggressive initial care must be delivered. The “golden hour” is no longer sacred, as we know that patient outcome is directly related to the time from injury to definitive care. Rapid assessment of injuries and institution of life-preserving measures have helped to reduce the preventable death rate of 35% to 10%.2–4 In order to save time, the initial assessment and management should follow a systematic approach that can be easily learned and practiced. This approach is the foundation for the Advanced Trauma Life Support (ATLS) course.5 Lack of a systematic approach to the initial assessment can result in errors from which the resuscitation team, and ultimately the patient, do not recover.6 Initial assessment and management includes the following: • • • • • • •

Preparation Triage Primary survey (ABCDEs) Resuscitation Adjuncts to the primary survey and resuscitation Consideration of need for transfer Secondary survey (more detailed evaluation, diagnosis, and treatment) • Adjuncts to the secondary survey • Continued postresuscitation monitoring and reevaluation • Definitive care Initial assessment and management is a linear progression of steps that includes both the primary and secondary surveys.

The name of this phase—initial assessment and management— highlights the need for evaluation and simultaneous intervention for life-threatening injury when identified. During the primary survey, remembered by the mnemonic ABCDE (airway, breathing, circulation, disability, exposure/environment), the patient is rapidly assessed for life-threatening injury. It is not always possible to dissociate diagnostic procedures from simultaneous resuscitation and treatment measures during this phase, and the treatment of life-threatening injury should not be delayed for definitive evaluation. Following the primary survey and its adjuncts, the secondary survey is performed. During the secondary survey, the patient is evaluated for potentially life-threatening and/or occult injuries. It is important to emphasize that both the primary and secondary surveys may be repeated as often as necessary. Once adjuncts to the secondary survey are completed, definitive care requirements such as type of facility and location are considered while postresuscitation monitoring is continued.

PREPARATION The preparatory phase is an integral component of trauma care and occurs in two different clinical settings: the prehospital and hospital settings.

■ Prehospital Phase The first aspect of the prehospital phase occurs before patient involvement and concerns the establishment of protocols aimed at directing the safe transport of the right patient to the appropriate trauma center at the earliest possible time using the ideal transport method. Physicians involved in trauma care should be familiar with these protocols, and should optimally be involved in their establishment, review, and revision. When an actual patient is injured, care is provided according to protocol by the personnel who receive initial notification of the trauma and are

Initial Assessment and Management

■ Hospital Phase The hospital phase of preparation is initiated with advance notice of the arrival of the injured patient. There is a tiered response in place at every trauma center. Depending on the severity of injury, a level of activation is initiated. For example, patients who are hypotensive (systolic blood pressure 90 mm Hg), bradycardic or tachycardic (heart rate [HR] 50 beats/min or 130 beat/min), or intubated in the field or with respiratory compromise, meet criteria for the highest level of activation which requires the presence of the full trauma team consisting of trauma surgery faculty, surgical residents, emergency medicine faculty and residents, and ED nurses. The activation criteria are developed by each hospital and guided by published resources and take into account the needed level of expertise and resources that should be available for the patient’s circumstances. Ideally, there should be a designated arrival area with adequate space to accommodate the personnel and equipment needed to carry out a trauma resuscitation. An often overlooked part of this phase is preparation of the resuscitation team, ensuring that all personnel understand their roles and have received any information communicated by the prehospital personnel. Airway supplies such as laryngoscopes and tubes should be tested and readily available. When the patient arrives, intravenous access and fluid resuscitation should be started in conjunction with a determination of airway and breathing status. In the trauma bay, pulse oximetry and ECG monitors should be available and applied to the patient. All trauma evaluations require proper personnel.8 In addition to physicians and nurses, respiratory therapists, radiology technicians, and social workers (for family issues) should be available. Resources such as the laboratory, x-ray, and bedside diagnostic equipment such as an ultrasound machine for FAST (Focused Assessment Sonography in Trauma) examination should be present. Last but definitely not least is the safety of the hospital team caring for the patient. All personnel who will be in close contact with the patient should wear universal precautions including hair covers, facemasks, eye protection, appropriate length gowns, shoe and/or leg coverings, and gloves to minimize exposure to communicable diseases.9 As many trauma patients either do not know or are unable to communicate their personal health

history due to altered mental status, it is important that strict universal precautions are observed and in place at the time of patient arrival.10

TRIAGE Triage is the process in which the severity of patient injuries, the number of injuries per patient, and the resources of the accepting facility determine priority of treatment. Communication between the accepting facility, other area facilities, and prehospital personnel is important prior to such an event as well as during such an event. One helpful triage scheme is based on the aforementioned ABCDE mnemonic, which is further outlined below. There are two typical triage situations encountered: multiple casualty incidents and mass casualty events. The former involves multiple patients whose injuries do not exceed the capabilities of the receiving facility. In this situation, patients with lifethreatening or multiple injuries are transported and treated first. In-hospital care is affected little, other than accessing normal surge capacity. In the latter situation, the number of patients and the severity of their injuries exceed the equipment, supplies, and personnel limitations of the receiving facility. Patients with the greatest chance of survival and requiring the least use of resources are transported and treated first. Triage continues in the hospital phase, as changing patient conditions and a variable number of patients transported may change initial estimations of survival and resource consumption.

PRIMARY SURVEY The primary survey is a sequence of steps to identify immediately life-threatening but treatable injuries. Assessment and management proceed simultaneously, and life-threatening situations are managed as they are encountered during the course of resuscitation. This is made possible through close coordination of the trauma team, with each team member performing his or her designated role under the direction of the captain. The primary survey involves airway maintenance with cervical spine protection, breathing and ventilation, circulation with hemorrhage control, disability with respect to neurologic status, and exposure/environmental control, where the patient is completely undressed but kept warm to prevent hypothermia. The priorities of the primary survey can be applied to all patients with certain caveats that do not alter the underlying alphabet or priorities, including pediatric patients, the elderly, pregnant women, and obese patients. Pediatric patients: When caring for the pediatric patient, the size of the child and specific injury patterns must be kept in mind. Serious pediatric trauma is usually blunt trauma, often involving the brain. Brain injuries can lead to apnea, hypoventilation, and hypoxia, and protocols for pediatric trauma patients stress aggressive management of the airway and breathing to prevent these consequences. These physiologic derangements occur more often than hypovolemia with hypotension in seriously injured children. Geriatric patients: The geriatric patient has overall less physiologic reserve to withstand injury. Their response may

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first to respond at the scene. During this phase, all events are ideally coordinated with the physicians at the receiving hospital to ensure adequate time to prepare personnel and resources in the emergency department (ED). The treatment goals for the prehospital phase include maintenance of airway, control of external bleeding and shock, patient immobilization, and transport to the closest appropriate facility, preferably a trauma center. In addition, obtaining important information concerning the mechanism of injury, related events, and past medical history of the patient may alert the receiving team to the possibility of particular injuries and their severity to enable faster diagnosis and treatment. The National Association of Emergency Medical Technicians Prehospital Trauma Life Support course is a resource for those interested in further information about this phase of care.7

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also be altered or blunted by comorbidities and chronic medication use. Resuscitation of these patients must take into account possible preexisting cardiac, pulmonary, and metabolic diseases.11 For example, minor injuries can cause serious complications due to multiple medications, especially anticoagulant use. Pregnant women: The anatomic and physiologic changes of pregnancy can be a challenge, and the response of the pregnant patient may be modified.12 Knowledge of pregnancy and early monitoring of the fetus are important in maternal and fetal survival. Unnecessary x-ray exposure should be avoided, but treatment of the mother takes precedence. Obese patients: The problem of obesity is on the rise.13 These patients pose a particular challenge in the trauma setting, as their anatomy can make procedures such as intubation difficult and hazardous.14 In addition, obese patients typically have cardiopulmonary disease limiting their ability to compensate for injury and stress. Treatment of these patients may exacerbate their underlying comorbidities. Although these special populations each have their unique characteristics, the assessment and management priorities are the same. Treatment of these patients is elaborated elsewhere in this text.

■ Airway Maintenance with Cervical Spine Protection Maintenance of the airway is the most important priority in caring for the trauma patient. Inadequate ventilation leads to hypoxia and inadequate oxygen delivery to tissues. Although important in all patients, this is particularly important in patients with head injury, as hypoxia contributes to secondary brain injury and hypoventilation may increase intracerebral pressure.15 Application of a pulse oximeter as an early adjunct to the primary survey in all patients helps in recognition and monitoring of hypoxemia. In acute trauma, upper airway obstruction is the most common cause of inadequate ventilation. Structures of the upper airway such as the tongue, edematous soft tissues, blood, foreign bodies, teeth, and vomitus are common causes of obstruction. Quick assessment of the airway begins by asking the patient his or her name. A normal response implies the airway is not in immediate jeopardy, but frequent reassessment is required. Breathlessness, weak or absent voice, or hoarseness suggests airway compromise. Objective signs of potential airway problems include noisy breathing, cyanosis, and the use of accessory muscles. Unconscious and obtunded patients with a Glasgow Coma Score (GCS) of less than 8 should have their airway protected with an endotracheal tube to provide oxygenation and ventilation, and reduce the chance of aspiration. Indications for a definitive airway are listed in Table 10-1. A definitive airway is defined as a cuffed endotracheal tube in the trachea.5 In children under 9 years of age, an uncuffed tube should be used to prevent tracheal injury from the cuff. The most important aspect of securing the airway involves preparation. A skilled physician must be present with the necessary medication and equipment close at hand for intubation.16

TABLE 10-1 Indications for Definitive Airway Need for Airway Protection Unconscious

Severe maxillofacial fractures

Risk for aspiration Bleeding Vomiting

Risk for obstruction Neck hematoma Laryngeal or tracheal injury Stridor

Need for Ventilation or Oxygenation Apnea Neuromuscular paralysis Unconscious Inadequate respiratory efforts Tachypnea Hypoxia Hypercarbia Cyanosis Severe closed head injury with need for brief hyperventilation if acute neurologic deterioration occurs Massive blood loss and need for volume resuscitation

Adapted with permission from American College of Surgeons Committee on Trauma. Advanced Trauma Life Support for Doctors. 8th ed. Chicago, IL: American College of Surgeons Committee; 2008: p. 33.

When airway compromise occurs, initial maneuvers to maintain the airway are performed. The first involves opening the mouth and inspecting for foreign bodies or other obstructive causes. Either a chin lift or jaw thrust in conjunction with an oral or nasal airway can relieve obstruction caused by the tongue (Fig. 10-1). Care must be taken to protect the cervical spine during these maneuvers. The chin lift or jaw thrust can temporarily maintain oxygenation in preparation for a definitive airway. Rapid sequence intubation is employed for obtaining the definitive airway in the potentially combative trauma patient.17 An induction agent (often etomidate) is used in combination with a short-acting depolarizing agent such as succinylcholine to minimize duration of paralysis. In case of failed orotracheal intubation, the team should be ready to perform a surgical airway. Confirmation of tube placement occurs by auscultation over the epigastrium and the bilateral chest wall. There should be no breath sounds over the epigastrium and equal breath sounds heard over the chest. A CO2 monitor is attached to the endotracheal tube and confirms the presence of CO2 by color change.18 A chest x-ray is also obtained to confirm position. Once a definitive airway is established, securing by means of tape or a commercial device is imperative. In addition, frequent evaluation of tube position should be performed to prevent dislodgement of the tube and subsequent airway loss.

Initial Assessment and Management

■ Breathing and Ventilation After securing the airway, attention may be turned to breathing and ventilation. This includes both oxygenation and adequate exchange of carbon dioxide. Pulse oximetry is an effective noninvasive means of measuring arterial blood saturation by colorimetric measurement.19 Pulse oximetry may be inaccurate in the presence of peripheral vasoconstriction, carbon monoxide poisoning, or jaundice. Pulse oximetry may also be unreliable in hypothermic or severely anemic patients.20 Depending on the patient’s partial pressure of oxygen and its location on the oxyhemoglobin dissociation curve, oxygen levels may change more quickly than indicated by the pulse oximeter measurement due to limitations in instrument response time. In these situations, the partial pressure of oxygen is more accurately determined using an arterial blood gas measurement. A patent airway does not ensure adequate ventilation.5 Evaluation of breathing begins by looking at, listening to, and feeling the chest wall. Inspection of the chest wall can reveal asymmetry in chest expansion, accessory muscle use, contusions, penetrating chest wounds, open or sucking chest wounds, and distended neck veins. Auscultation of breath sounds can help diagnose pneumo- or hemothorax by detecting differences

■ Circulation with Hemorrhage Control Hemorrhage is the leading cause of preventable death after injury. Shock is the result of inadequate oxygen delivery to tissues. Although hypovolemic shock from bleeding is the most

CHAPTER 10

FIGURE 10-1 Chin lift and jaw thrust maneuvers to establish an airway. (Reproduced with permission from American College of Surgeons Committee on Trauma. Advanced Trauma Life Support For Doctors. 8th ed. Chicago, IL: American College of Surgeons Committee; 2008: p. 30.)

in breath sounds between the left and right chest. Palpation of the chest wall can be used to diagnose an unstable chest wall, tenderness, crepitance, deformity, or subcutaneous air. Finally, percussion has been suggested to identify hyperesonance, dullness, or tympany. Due to an often noisy resuscitation area, it is rarely helpful in diagnosing or differentiating chest trauma. Breathing problems can be life-threatening. A tension pneumothorax develops from either blunt or penetrating injury where air continuously enters the pleural space from the trachea, bronchi, or chest wall causing the lung to collapse. Clinical signs include shifting of the mediastinum with deviation of the trachea away from the affected side, distended neck veins, respiratory distress, decreased venous return due to elevated intrathoracic pressure with low cardiac output, hypotension, and shock. Tension pneumothorax is a clinical diagnosis and a chest x-ray should be obtained after treatment by chest tube insertion. Differentiation between a tension pneumothorax and cardiac tamponade may be difficult. Neck veins may not be distended secondary to hypovolemic shock. Heart sounds are usually muffled with the latter but this may be difficult to appreciate in a noisy trauma bay. Absent breath sounds may be the only differentiating sign. A massive hemothorax can also cause mediastinal shift due to blood instead of air and circulatory compromise. Fortunately, the treatment is similar and involves tube thoracostomy. Ultrasound may be extremely useful in the rapid detection of pneumothorax, hemothorax, and cardiac tamponade. Accuracy for diagnosis of pneumo- and hemothoraces compares favorably with portable chest radiograph, and it can be performed much more quickly. The diagnosis of cardiac tamponade is also done efficiently by ultrasound, although the presence of a left hemothorax decreases accuracy.21–23 A flail chest can also cause breathing problems. The definition of a flail segment is three or more consecutive ribs broken in at least two places each, or one or more rib fractures along with a costochrondral separation or fracture of the sternum. A flail chest is most often associated with underlying hemo- or pneumothorax and/or pulmonary contusion, which is the usual cause of associated respiratory compromise.24 An open pneumothorax is defined as a chest wall defect greater than two thirds the diameter of the trachea. This is also known as a “sucking chest wound”. In an open pneumothorax air is drawn through the defect (the path of least resistance) into the chest. Larger defects cause greater respiratory distress. Treatment involves immediate temporary coverage of the defect on three sides, ipsilateral chest tube placement, and operative closure of the defect.25 Finally, a massive hemothorax (1,200 mL of blood evacuated initially) can cause mediastinal shift, respiratory distress, and hypovolemic shock, which must be managed immediately. This is managed with tube thoracostomy, transfusion, and immediate operation.

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TABLE 10-2 Estimated Blood Lossa Based on Patient’s Initial Presentationb

SECTION 2

Blood loss (mL) Blood loss (% blood volume) Pulse rate Blood pressure Pulse pressure (mm Hg) Respiratory rate Urine output (mL/h) CNS/mental status Fluid replacement

Class I Up to 750 Up to 15%

Class II 750–1500 15–30%

Class III 1,500–2,000 30–40%

Class IV 2,000 40%

100 Normal Normal or increased 14–20 More than 30 Slightly anxious Crystalloid

100–120 Normal Decreased 20–30 20–30 Mildly anxious Crystalloid

120–140 Decreased Decreased 30–40 5–15 Anxious/confused Crystalloid and blood

140 Decreased Decreased 35 Negligible Confused/lethargic Crystalloid and blood

CNS  central nervous system. a

For 70-kg male.

b

The guidelines in this table are based on the 3-for-1 rule. Adapted with permission from American College of Surgeons Committee on Trauma: Advanced Trauma Life Support for Doctors. 8th ed. Chicago, IL: American College of Surgeons Committee; 2008: p. 61.

common form of shock in trauma victims, other types of shock can occur in these patients, and occasionally a combination of several types of shock are simultaneously present. Treatment for shock begins with placement of two large-bore peripheral IVs (16-gauge or larger) and appropriate isotonic fluid replacement. There are four classes of shock based on initial blood loss and presentation (Table 10-2). STOP THE BLEEDING!!! The most important treatment for hemorrhage is control of bleeding.26,27 Hemorrhage in the adult trauma patient comes from one of five places—the thoracic cavity, abdominal cavity, pelvic fracture, long bones, or obvious external bleeding. The rapidity with which each source is investigated depends on the degree of shock. Some sources may be excluded by physical examination (external bleeding, thigh deformity), whereas others require the radiologic adjuncts to the primary survey. Bleeding into the chest and pelvis can be difficult to determine by physical examination alone, making early radiologic examinations essential in the patient in shock. The scalp is quite vascular and profuse bleeding from scalp wounds may require suture ligation or Raney clips to stop bleeding.28 For obvious external bleeding, direct pressure on the bleeding vessel is the most effective method of hemorrhage control. For less well-defined areas of bleeding, proximal pressure over the femoral artery in the groin or the brachial artery in the upper extremity can be used. Tourniquets are effective in massive exsanguination from an extremity, but run a high risk of ischemic injury to that extremity and should only be used when direct pressure is not effective.15 However, the use of tourniquets is increasing, especially in the prehospital phase. Kragh et al. investigated tourniquet use at a combat hospital in Baghdad. They found that tourniquet use when shock was absent was strongly associated with survival (90% vs. 10%; P 0.0001), that prehospital use was associated with survival, and no limbs were lost due to

tourniquet use.29 Hemothorax is treated with tube thoracostomy and operative control, intra-abdominal hemorrhage in the setting of shock requires laparotomy, and bleeding from a significant pelvic fracture requires pelvic stabilization with a sheet or binder followed by angiography or pelvic packing if necessary. The diagnosis of shock begins with a check of the patient’s pulse rate and character, skin color and temperature, and mental status. A slow, regular pulse suggests normovolemia, whereas a weak or thready pulse suggests hypovolemia. Patients with pink and warm skin and extremities are less likely to have a circulation problem. Mental status changes may be due to inadequate end organ perfusion caused by hypovolemia, brain injuries, or drug use. Blood pressure is an important indicator of response to resuscitation, but should not be relied upon during the initial evaluation for the presence of shock. Urine output and central venous monitoring may also be used later to assess volume status and response to resuscitation. Tachycardia results from a compensatory response to intravascular volume depletion via stimulation of the sympathetic nervous system and should always raise the suspicion of hemorrhagic shock. This efferent response to low intravascular volume also results in vasoconstriction of peripheral arteries, making the skin cool and clammy to the touch. Certain medications common in the elderly may blunt the tachycardic response, including beta-blockers, calcium-channel blockers, and diuretics. Although tachycardia is the most common compensatory response to hemorrhagic shock, paradoxical bradycardia has also been observed. Paradoxical bradycardia is associated with rapid large-volume hemorrhage. Bradycardia in hemorrhagic shock predicts a poor prognosis, and traditional teaching associates a decrease in heart rate with irreversible shock (terminal

Initial Assessment and Management chest trauma.36 Few patients with this injury have life-threatening cardiogenic shock. Blunt cardiac injury has a variable incidence depending on the method of diagnosis. It also has variable importance, ranging from clinically insignificant to life-threatening cardiac failure. In patients that sustain blunt chest trauma, a normal electrocardiogram is the only test necessary to exclude clinically significant blunt cardiac injury. Cardiac enzymes are not helpful, as troponin I and T have poor sensitivity and predictive value despite relatively high specificity.37 With no evidence of blunt cardiac injury and no respiratory distress, ICU admission for either telemetry or aggressive pulmonary therapy is also unnecessary.38 If blunt myocardial injury is present, treatment usually involves monitoring in the ICU and appropriate management of hypotension if present.39 Neurogenic shock results from spinal cord injury. It is not seen with traumatic brain injury alone unless there is imminent death from the brain injury and a state of preterminal shock. Hemorrhagic shock should be ruled out in these patients. The pathophysiology of neurogenic shock is loss of sympathetic tone due to spinal cord injury. Loss of sympathetic innervation to peripheral blood vessels and unopposed vagal stimulation of the heart lead to warm extremities and normocardia or even bradycardia with shock. This may be seen in patients with injuries at T6 or above.40 Injuries below T6 should prompt an aggressive search for alternative causes of the hemodynamic derangements. Treatment initially begins with fluid resuscitation, and vasoactive medications are usually necessary. Neurogenic shock differs from spinal shock, which refers to the temporary loss of muscle tone and reflexes occurring after total or near-total spinal cord injuries. Septic shock is usually not seen in the acutely injured trauma patient, but may appear in hospitalized patients many hours to days after their injury due to causes such as missed hollow viscus injuries. Septic patients may be normovolemic with normal blood pressure or minimal hypotension, warm skin, and wide pulse pressure, or hypovolemic and displaying signs of shock. All patients with suspected serious injuries require the placement of two large-bore peripheral IVs. Higher flow rates are best achieved with short, large-diameter catheters. Peripheral IVs are usually placed in the upper extremities unless there is significant injury to the upper extremities or upper chest with vascular or soft tissue compromise. When peripheral IVs cannot be placed, the next preferred choice for access is a femoral central venous catheter. Use of the subclavian or jugular veins is not initially recommended because of the higher likelihood of complications such as a pneumothorax.41 Central venous catheter insertion should be performed by a physician trained in these procedures. A cutdown of the saphenous vein in the lower extremity or basilic or cephalic vein in the upper extremity can also be performed in difficult situations. In children under 6 years of age, intraosseous cannulation of the proximal tibia may be used until adequate volume resuscitation and circumstances allow venous access.42 In the out of hospital setting, intraosseous cannulation is now being used more frequently in adult patients as well (Fig. 10-2). As in the pediatric population, this access may be used in-hospital until intravenous access is obtainable.43,44 At the time of placement, blood should be

CHAPTER 10

response). However, research has revealed that bradycardia as an acute response to hemorrhage is potentially reversible. The key to treatment is quick recognition that bradycardia is a sign of major bleeding requiring massive and rapid fluid loading. Administration of atropine can precipitate cardiac arrhythmias and is contraindicated.30 Traditional predictors of physiologic reserve such as age, injury severity, and lactic acidosis on admission have been criticized for lack of sensitivity and/or specificity in predicting trauma mortality. Heart rate variability (HRV) is a recently applied biomarker reflecting physiologic reserve and cardiac control and describes changes in the beat-to-beat interval rather than variations in the instantaneous heart rate. HRV may be measured using either time-domain or frequency-domain approaches. A Holter monitor or EKG may be used to measure the R-R interval in milliseconds, which can be used to derive the standard deviation of the normal RR interval (SDNN), an important and clinically useful time-domain measurement. The gold standard for time-domain measurements is to examine HRV over a 24-hour period, but a brief 5-minute assessment of HRV can also be clinically valid and meaningful. Reduced HRV reflects loss of physiologic reserve and control of the heart. This cardiac uncoupling has been used to predict severely injured patients in the prehospital setting and as a measure of a patient’s clinical course over the first 24 hours of intensive care unit (ICU) stay.31,32 Traumatic brain injury, metabolic causes such as intoxication, and shock can all cause mental status changes.33 Decreased cerebral blood flow from any cause leads to decreased cerebral perfusion and alteration of mental status. It is important to recognize and treat shock in brain-injured patients because mortality and morbidity in these patients doubles with concurrent hypotension, and there is a 3-fold increase in mortality and morbidity if both hypotension and hypoxia are present.34 Blood pressure can be a misleading sign in the shock patient. Hypotension may not be evident until 30% of blood volume is lost. The numeric difference between systolic and diastolic pressures (known as the pulse pressure) is a more sensitive indicator of blood loss. A narrowed pulse pressure is detectable after loss of as little as 15% of blood volume. In the adult trauma patient, a systolic blood pressure less than 90 mm Hg is considered shock until proven otherwise.35 Cardiogenic shock can occur as a result of cardiac tamponade or blunt myocardial injury. Cardiac tamponade may be caused by penetrating injuries to the “box,” a three-dimensional region bounded by the clavicles superiorly, the nipples inferiorly, and the mid-clavicular lines laterally. This life-threatening condition must be diagnosed and treated emergently. On clinical examination, jugular venous distension (JVD), muffled heart sounds, and hypotension are the classic signs known as Beck’s triad. Cardiac tamponade can be confused with tension pneumothorax but the latter causes diminished or absent breath sounds on the side of the pneumothorax as well as tracheal deviation. Temporary treatment of tamponade involves needle pericardiocentesis to relieve the tamponade, but definitive treatment with emergent sternotomy or thoracotomy may be necessary. Blunt myocardial injury may result from blunt

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SECTION 2 FIGURE 10-2 Demonstration of intraosseous puncture via the proximal tibial route. (Reproduced with permission from American College of Surgeons Committee on Trauma. Advanced Trauma Life Support for Doctors. 8th ed. Chicago, IL: American College of Surgeons Committee; 2008: p. 77.)

drawn for basic hematologic and chemistry analysis and typeand cross-matching. The treatment for hypovolemic shock is fluid resuscitation and hemorrhage control. Remember, STOP THE BLEEDING!!! Severely injured patients should receive a 2-L bolus of warm, isotonic fluid such as Ringer’s lactate. Patients whose blood pressure responds to this initial fluid bolus can undergo further work-up for potential injuries and continued crystalloid resuscitation. If blood pressure remains low, blood should be given. Historically, red blood cells were used alone, but recent studies have indicated that administering a combination of fresh frozen plasma and packed red blood cells during massive resuscitation is associated with improved mortality. The optimum ratio of fresh frozen plasma to packed red blood

cells is still under investigation.45–47 O-negative blood should be used until type-specific blood becomes available. In hypotensive children a 20-mL/kg fluid bolus should be administered. Patient response to fluid can be categorized into three groups. Rapid responders have a return of normal vital signs after the 2-L bolus. Transient responders undergo transient normalization of blood pressure and heart rate followed by recurrence of hypotension and tachycardia. Patients who fall into the final category are referred to as minimal to no responders and their vital signs remain abnormal after the initial fluid resuscitation. These three categories correspond to minimal (10–20%), moderate and ongoing (20–40%), and severe (40%) blood loss, respectively (Table 10-3). For patients who present in extremis or after cardiac arrest from penetrating chest trauma, an ED thoracotomy performed by a trained surgeon may be life-saving. Resuscitation efforts may be withheld in any blunt trauma patient who is apneic, pulseless, and without organized ECG activity upon the arrival of Emergency Medical System (EMS) personnel at the scene. Termination of resuscitation efforts should be considered in blunt trauma patients with EMS-witnessed cardiopulmonary arrest and 15 minutes of unsuccessful resuscitation and cardiopulmonary resuscitation.48 Anticipating which patients will require blood can be challenging. In the case of patients who are hypotensive and tachycardic, the preparation is simplified by ensuring the availability of O-negative blood. However, the need for blood may be less obvious in patients with significant injury mechanisms such as high-speed crashes with prolonged extrication. These patients may initially be reported as awake and alert with minimal alterations in vital signs, but may have occult injuries. If the need for blood is not anticipated and blood is not readily available, the delay in appropriate resuscitation may affect morbidity and mortality.

■ Disability: Neurologic Status Once life-threatening injuries are found and treated during the ABCs, a brief neurologic examination can be performed.

TABLE 10-3 Responses to Initial Fluid Resuscitationa Vital signs Estimated blood loss Need for more crystalloid Need for blood Blood preparation Need for operative intervention Early presence of surgeon a

Rapid Response Return to normal Minimal (10–20%)

Minimal or No Response Remain abnormal Severe (40%)

Low Low Type and crossmatch Possibly

Transient Response Transient improvement Moderate and ongoing (20–40%) High Moderate to high Type specific Likely

Yes

Yes

Yes

High Immediate Emergency blood release Highly likely

Two liters of isotonic solution in adults; 20 mL/kg bolus of Ringer’s lactate in children. Adapted with permission from American College of Surgeons Committee on Trauma: Advanced trauma life support for doctors. 8th ed. Chicago, IL: American College of Surgeons Committee; 2008: p. 65.

Initial Assessment and Management

■ Exposure and Environmental Control The patient’s clothing must be completely removed for complete and adequate evaluation, while ensuring the patient does not become hypothermic. Clothing is cut when there is severe injury or risk of injury to the spine. During exposure of the patient, prevention of hypothermia with warmed air, fluids, oxygen, and blankets is necessary. The temperature of the patient should be obtained as soon as possible and reassessed frequently.51 In colder climates where the threat of hypothermia is more serious, the inaccuracy of standard thermometers below 30°C becomes an important consideration. In this situation, a temperature-sensing urinary catheter placed in the bladder is ideal. The best way to avoid hypothermia in the trauma patient is to stop bleeding. Prevention of hypothermia and rewarming of the patient are equally important parts of the primary survey and resuscitation. Reevaluation throughout the primary survey is important to detect changes in the patient’s condition. If the patient is not responding to the treatment provided then revisiting the steps in the primary survey is crucial. In some cases, an operation is required to control circulation and the secondary survey is completed at a later time.

■ Adjuncts to the Primary Survey Monitoring Monitors should be placed on the trauma patient upon arrival. Heart rate, respiratory rate, temperature, and blood pressure should be checked as soon as possible. Continuous ECG monitoring of cardiac rhythm is essential. Arterial blood gas with base deficit and/or lactate measurements should be added in severely injured patients to identify presence and severity of shock.52,53 Continuous pulse oximetry provides a means to monitor the status of oxygenation and ventilation. When the patient arrives intubated, end-tidal CO2 can confirm tube position. An arterial or central venous line or pulmonary artery catheter may be

useful in the seriously injured patient in the ICU, but their initial use is not indicated.

Catheters and Tubes The main catheters and tubes are the Foley catheter and the nasogastric or orogastric tube. The Foley catheter is placed to monitor urine output. Certain injuries or signs may be a contraindication to placement of a Foley catheter.54 In the male patient, blood at the urethral meatus, a scrotal or penile hematoma, or a high-riding prostate on digital rectal examination are contraindications to placement of a Foley catheter. Placement should be deferred until a retrograde urethrogram (RUG) can be performed to rule out disruption of the urethra. If the urethrogram is normal, gentle placement of the Foley can be undertaken. If the RUG is abnormal, subspecialty consultation and placement of a suprapubic tube or definitive repair is necessary. The measurement of hourly urine output can be helpful in assessing volume status. Decompression of the stomach is important, especially in patients where gastric distention can occur as a result of intubation. Children are especially sensitive to gastric distention, and decompression of the stomach may improve hemodynamics in this population. In the presence of severe maxillofacial trauma or the suspicion of a cribiform plate or basilar skull fracture with blood or cerebrospinal fluid (CSF) drainage from the nose or ears, placement of an orogastric tube is safer to avoid inadvertent insertion of the nasogastric tube into the brain, which is a potentially fatal injury.55 Blood return from the oro- or nasogastric tube is usually from swallowed blood but can be an indicator of traumatic injury to the upper gastrointestinal tract.

X-rays and Other Diagnostic Studies A chest radiograph is mandatory during the primary survey/ resuscitation for both blunt and penetrating trauma. The chest x-ray can be used to identify rib fractures, pneumo- or hemothorax, and a widened mediastinum possibly indicative of blunt aortic injury. In the hemodynamically abnormal blunt trauma patient, a portable pelvic x-ray is also obtained as the physical examination of the pelvis may be misleading, particularly in the obtunded patient. Significant pelvic fractures or separation of the pelvic bones can explain blood loss in the patient in shock. The results of these tests frequently alter treatment plans. In the hemodynamically normal patient with significant mechanism for injury, CT scans of the head, cervical spine, chest, abdomen, and pelvis are obtained after completion of the primary and secondary survey. The decision of which CT scans to obtain is based on mechanism of injury as well as the findings of the primary and secondary surveys. For example, a head CT should be obtained in patients with suspected head injuries, altered GCS, or anticoagulation use. A more recently recognized injury involves the use of seat belts with a shoulder strap. Significant deceleration with the harness belt in place can cause seatbelt marks on the neck and chest. In these situations, the physician should be concerned about blunt carotid, vertebral, or aortic injuries, and a CT angiogram of

CHAPTER 10

The neurologic examination includes the GCS and pupil examination including size, symmetry, and reaction to light. A complete and detailed neurologic examination is not accurate or warranted until the patient is hemodynamically normal. The GCS is the sum of scores for three areas of neurologic evaluation: eye opening, verbal response, and best motor response. Abnormal pupillary size, asymmetry, or reaction to light can indicate a lateralizing brain lesion. The eye examination can be misleading if drugs, ocular prostheses, or direct injury to the globe are present. The pupils and GCS should be frequently reevaluated to detect changes signaling deterioration of mental status. Accurate record keeping is important, particularly in those patients requiring transfer, as a change is GCS may be the earliest sign of increased intracranial pressure and worsening head injury. Computed tomography (CT) scanning should be used liberally in patients with suspected head injuries or signs or symptoms of trauma to the brain.49,50

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SECTION 2

the neck and chest should be performed.56 Judicious selection of CT scans is important because CT contrast agents can interfere with the sequence of tests and lead to contrast nephropathy.57 In addition, the increased use of CT scans, especially of the chest and abdomen, has been linked to a higher incidence of cancer later in life.58 If the patient’s hemodynamics do not allow safe transport to the CT scanner, the abdomen must be evaluated for blood loss not explained by chest or pelvic radiographs. A FAST59,60 examination and/or diagnostic peritoneal lavage (DPL)61,62 may be performed to identify occult abdominal blood loss.63 During the FAST examination, an experienced physician uses an ultrasound machine to look for fluid, presumed blood, in the recesses of the peritoneal cavity. The four windows examined include the spaces between the liver and the kidney (Morison’s pouch), between the spleen and the kidney (splenorenal recess), over the bladder, and at the heart to identify fluid in the pericardial sac.64 In the case of a negative FAST, other sources for hemorrhage should be sought. An indeterminate result and persistent hypotension warrants a DPL as the next step. With a positive FAST, the patient is taken directly to the operating room for definitive control of hemorrhage.

Decision for Early Transfer Early recognition of the patient that requires transfer is essential, as patient outcome is directly related to the time between injury and definitive care. The decision to transfer is based on patient injury and local resources. Once the decision is made to transfer the patient, the efforts of the team should be directed to resuscitation of the patient and restoration of normal perfusion. Any unnecessary diagnostic tests take up valuable time and should be avoided. Physician-to-physician contact should occur to relay vital information about the mechanism of injury, the injuries identified and their treatment so far, and to make arrangements for transportation, accompanying health professionals, and tasks that must be completed before and during transport. The selected mode of transport may carry its own set of risks. In recent years, the number of helicopter crashes during medical transport has risen. These crashes are often related to bad weather conditions or flight at night. Although seriously injured patients may need immediate flight transport, and “critical care” ground transport continues to evolve, older guidelines published by the National Association of EMS Physicians (consensus with American College of Surgeons) speak to the issues regarding air medical utilization. New guidelines through NAEMSP are still being drafted.65 The patient should be continuously monitored during transport. The evaluation and resuscitation of the patient continues throughout transport until safe arrival at the receiving facility. While waiting for transport, the secondary survey may be completed including a complete history, “head-to-toe” examination, laboratory tests, and only those x-ray studies that assist in treatment without adding delay. Once the patient arrives at the receiving hospital, the definitive care phase begins and treatment continues in the ED, operating room, or ICU. During direct physician-to-physician contact, arrangements are

made at the receiving facility for surgical subspeciality care such as trauma surgeons, orthopedic surgeons, or neurosurgeons.

SECONDARY SURVEY The secondary survey is a thorough history and physical examination, which begins only after the primary survey is completed and resuscitative efforts have produced some normalization of the patient’s vital signs. Reevaluation of the patient’s vital signs and response to resuscitation during the secondary survey are key. If the patient becomes hemodynamically abnormal, then the ABCDEs of the primary survey are revisited. If definitive care (e.g., in the operating room) is necessary to complete the primary survey then the secondary survey is completed after surgery.

■ History A complete history of the mechanism of injury and the patient’s medical history are important in understanding injury patterns, in searching for occult injuries, and in identifying comorbidities and medications that may affect the physiologic response to injury. Severely injured trauma patients are usually unable to provide the history, and prehospital personnel and the patient’s family if available are consulted to obtain this history. Allowing 15–90 seconds for the prehospital personnel to provide a report before they leave may yield invaluable information. Members of the team should be silent, but not inactive, during this time to ensure adequate transfer of this information. A quick mnemonic to obtain the history is shown below: A—Allergies M—Medications currently used P—Past illness/Pregnancy L—Last meal E—Events/Environment related to the injury The patient’s tetanus status should also be determined.66 Allergies are important to avoid administering medications that could cause an allergic reaction. A current list of the patient’s medications can not only provide insight into the patient’s medical condition, but also help explain the patient’s physiologic response to shock. Use of anticoagulant or antiplatelet drugs suggests the need for early administration of either plasma or platelets. In patients with head injury, rapid identification of patients on chronic anticoagulation with resultant rapid reversal of coagulopathy improves outcome.67 When the patient ate his or her last meal is important for diabetic patients and also for estimating the risk of vomiting and aspiration. The mechanism of injury is crucial to understanding injury patterns and predicting occult injuries based on the direction and amount of energy producing the injury. Injuries may be broadly characterized as blunt or penetrating. Vehicular and pedestrian impacts, falls, occupational injuries, and recreational injuries fall into the former category. Important details about

Initial Assessment and Management

■ Physical Examination Head and Face Significant bleeding can occur from the scalp and lacerations in the posterior occiput may be difficult to locate. When the patient is turned to examine the back, the back of the head should be inspected and the examiner’s gloved finger should palpate for any depressions. Scalp bleeding can result in a large volume of blood loss and hypotension, particularly with long transport times and inadequate prehospital control of hemorrhage. Quick application of direct pressure, sutures, staples, or Raney clip closure of the laceration may be necessary to control bleeding. Once active hemorrhage is controlled, the wound can be definitively managed during the secondary survey. Facial injuries are detected by inspecting and then palpating for facial instability. Orbital fractures are the most commonly missed facial injury. In conscious patients, asking the patient if their bite feels normal can help detect any jaw fractures influencing alignment. Bleeding from the nose can usually be controlled by direct pressure. More troublesome bleeding usually occurs from the posterior nasopharynx, and nasal packing or angiography and embolization may be required. A more thorough pupillary examination should be performed, evaluating visual acuity, pupil size and reactivity, direct globe injury, hyphema, foreign body contamination including contact lenses, and extraocular movement. Bruising around the eyes (raccoon’s eyes) or behind the ears (Battle’s sign) may indicate a basilar skull fracture. Hemotympanum or clear drainage from the nose or ears (CSF) confirms this diagnosis. If there is suspicion of a basilar skull fracture or cribriform plate fracture, an orogastric and not a nasogastric tube should be inserted and the patient should

undergo a CT scan of the head. Treatment of facial fractures can be deferred unless bleeding compromises the airway.

Neurologic Assessment A quick examination of the pupils and determination of GCS is performed during the primary survey. A more detailed neurologic examination is performed during the secondary survey, involving a complete motor and sensory examination. Asymmetry in the motor examination could reflect a localized intracranial injury. A CT of the head should be obtained in all patients with an abnormal neurologic examination or altered level of consciousness at any time since the trauma occurred.

Neck and Spine All patients with a mechanism conducive to neck injuries must have a thorough examination. This includes inspection for seatbelt signs, hematomas, or a penetrating wound. A seatbelt mark across the neck or chest is associated with a 3% incidence of blunt carotid injury. A CT angiogram of the neck should be performed upon identification of a seatbelt mark or other related injuries such as cervical spine fractures, skull and facial fractures, Horner’s syndrome, or neurologic deficit.73 Penetrating neck wounds require careful investigation or surgery depending on local practices if the platysma is violated in order to rule out injury to blood vessels or other neck structures. Patients with blunt injury and/or abnormal neurologic examination require initial cervical spine protection with a cervical collar. If the patient is thought to be alert and cooperative without distracting injuries the cervical spine may be cleared clinically. Otherwise, a CT of the spine is necessary to rule out fracture or dislocation. Plain films of the cervical spine may also be performed but obtaining adequate views can sometimes be difficult. If any spinal fracture is identified, the entire spine must be evaluated due to a 10% incidence of noncontiguous injury.

Chest Inspection and palpation of the chest may detect pain, chest wall tenderness, or crepitance. A flail segment appears as asymmetry in the chest wall compared to the contralateral side or to another segment on the same side. Auscultation may be hard in a noisy trauma bay but is mandatory. Decreased or absent breath sounds can indicate a pneumothorax. By listening for hyperresonance or muffled heart tones and looking for JVD and symmetric chest rise in the hypotensive trauma patient, a tension pneumothorax or cardiac tamponade may be differentiated. Listening for hyperesonance is difficult because of the noisy environment, and is therefore unlikely to be helpful. Excluding the life-threatening condition of a tension pneumothorax, a chest x-ray is obtained. If the chest x-ray shows rib fractures, pneumo- or hemothorax, pulmonary contusion, or widened mediastinum, further evaluation should be performed using chest CT. Significant deceleration forces can also cause blunt aortic injury which can be evaluated with the use of chest CT.

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car crashes include the speed of the crash, seatbelt use, air bag deployment, location of the victim in the vehicle, structural deformation, and extrication time. For example, seatbelt marks on the abdomen may be associated with “blowout” injuries of the small bowel on the antimesenteric side.68–70 Car versus pedestrian, bicycle, or motorcycle collisions have a high incidence of extremity fractures as well as brain and torso injuries. Penetrating injuries are less predictable, particularly those due to gunshot wounds. Several factors affect the injury patterns seen with gunshot wounds, including the distance of the weapon, the mass and velocity of the missile (kinetic energy), and the location of the impact. High-velocity bullets from weapons such as rifles have the most kinetic energy and therefore the greatest potential to cause extensive injuries. The distance of shotgun blasts determines the extent of injuries. Close-range shotgun wounds are more likely to result in injury, especially to vascular structures.71 In the case of thermal or chemical burn injuries, information about the injury environment is important. There is significant potential for inhalation injury and carbon monoxide poisoning with burns.72 Chemical burns can pose serious hazards to the patient and health care providers. It is important for emergency personnel to determine the possibility of chemical burns and the appropriate precautionary measures.

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The abdomen may be a source of occult bleeding in hemodynamically abnormal patients with normal chest and pelvic x-rays. Inspection of the abdomen may reveal a seatbelt sign, which is associated with an increased risk of small bowel injuries near the ligament of Treitz or ileocecal valve. At these locations, the bowel is fixed between two points: the ligament or ileocecal valve and the seatbelt. When there is a significant deceleration force, the bowel blows out on the antimesenteric side. Deceleration injury may also result in pancreatic trauma. Inspection may also reveal penetrating injuries. Some centers surgically explore all anterior abdominal gunshot wounds. Stab wounds to the anterior abdomen are usually managed differently. Palpation of the abdomen may elicit tenderness or masses. Obviously, if peritonitis is present, the patient should be taken to the operating room emergently. The pelvis is included in the abdominal examination. Stability of the pelvis should be checked preferably only once by a skilled examiner. The perineum should also be examined for injuries. A mandatory rectal and/or vaginal examination is performed when a pelvic fracture is identified to rule out an open fracture. A pelvic x-ray should be obtained in the unstable patient to look for fractures that open the pelvis and increase the pelvic volume. As discussed previously, a FAST should be performed to look for hemoperitoneum. A DPL may be performed if the FAST is equivocal or is not available. With an unstable pelvic injury, a pelvic binder or sheet should be placed to help control bleeding.

Musculoskeletal and Peripheral Vascular System The upper and lower extremities should be examined and palpated for tenderness and deformities. Each extremity is gently moved to determine range of motion. A neurovascular examination is performed. Decreased or absent pulses in one extremity must be quickly evaluated and acted upon. Arterial hemorrhage or expanding hematomas require an urgent operation. Local practice determines the course of action for a discrepancy in pulses, loss of pulses, or proximity of penetrating injuries to large vessels of the arms or legs. An injured extremity is at risk for ischemia and compartment syndrome. The greatest risk for compartment syndrome occurs in patients with tibial fractures. The development of compartment syndrome may be insidious. A high index of suspicion is necessary, especially in unconscious patients. If the diagnosis of compartment syndrome is made, compartment pressures can be checked with a needle attached to a pressure transducer. Tissue pressures greater than 30 mm Hg require fasciotomy. Due to the catastrophic consequences of delayed response to compartment syndrome, immediate treatment with four-compartment fasciotomies is sometimes performed without measurement of pressures.

Adjuncts to the Secondary Survey Additional tests such as x-rays of the spine or extremities, angiography, or other diagnostic procedures may be necessary.

In the patient in shock, or the patient in whom transfer has already been deemed necessary, these should not be performed until the patient is at the institution that will provide definitive care due to treatment delays as well as the possible need for repeat examinations. During the secondary survey, laboratory test results may be available depending on turnaround time. Base deficit and lactate values are important for determining the status of volume resuscitation.52,53 In critically ill patients, the severity of lactic acidosis correlates with overall oxygen debt and survival.53,74 The base deficit is part of the standard arterial blood gas panel and usually returns much sooner than the lactate level. The base deficit can be important for determining the duration and magnitude of hypoperfusion, for example, in patients who underwent prolonged extrication following a vehicular crash. If the patient has received bicarbonate for metabolic acidosis, then lactate levels (which are not influenced by bicarbonate administration) are a more useful measure of the adequacy of resuscitation.

REEVALUATION After the secondary survey, reassessment of the patient and his or her response to treatment thus far is important. If problems are detected, the steps to the primary survey are repeated.

DEFINITIVE CARE An injured patient’s physiologic status, anatomic injuries, mechanism of injury, and comorbidities, as well as available local resources, determine the need for transfer to a higher level of care. When the decision is made to transfer a patient, the referring physician is responsible for continued resuscitation and attempted stabilization of that patient. Physicianto-physician communication can determine urgency of transport, mode of transport, and level of care during transport. Transfer agreements and patterns of communication within regions are best established prior to patient arrival, so that individual patient transfers happen efficiently and smoothly. The pertinent history, treatment, and potential unsolved problems must be communicated to the accepting physician and transport personnel. The level of care during transport should be commensurate with the severity of injuries, and transport personnel should be capable of continuing resuscitative efforts, including management of the ABCDEs. Finally, the patient must be “packaged” appropriately for transport. Endotracheal tubes must be secured. At times, it is difficult to secure an airway during transport, so if there is potential for airway compromise or severe head injury requiring a definitive airway with maintenance of adequate ventilation and oxygenation, intubation should be performed prior to transport. The patient should also have two large-bore intravenous lines, crystalloid and/or blood infusing, gastric and urinary catheters in place, and continuous cardiac monitoring prior to transport.

Initial Assessment and Management

MEDICAL RECORD DOCUMENTATION

REFERENCES 1. Trunkey DD. Trauma. Sci Am. 1983;249(2):20–27. 2. Cales RH, Trunkey DD. Preventable trauma deaths. A review of trauma care systems development. JAMA. 1985;254:1059–1063. 3. Acosta JA, Yang JC, Winchell RJ, et al. Lethal injuries and time to death in a Level I Trauma Center. J Am Coll Surg. 1998;186:528–533. 4. Esposito TJ, Sanddal TL. Reynolds SA, Sanddal ND. Effect of a voluntary trauma system on preventable death and inappropriate care in a rural state. J Trauma. 2003;54(4):663–669. 5. American College of Surgeons Committee on Trauma. Advanced Trauma Life Support for Doctors. 8th ed. Chicago, IL: American College of Surgeons Committee; 2008:1–18. 6. Lubbert PH, Kaasschieter EG, Hoorntje LE, et al. Video registration of trauma team performance in the emergency department: the results of a 2-year analysis in a level 1 trauma center. J Trauma. 2009;67: 1412–1420. 7. National Association of Emergency Medical Technicians: PTHLS. 6th ed. Philadelphia, PA: National Association of Emergency Medical Technicians; 2007. 8. Hadfield L. Preparation for the nurse as part of the trauma team. Accident and Emergency Nursing. 1993;1(3):154–160. 9. Brooks AJ, Phipson M, Potgieter A, et al. Education of the trauma team: video evaluation of the compliance with universal barrier precautions in resuscitation. Eur J Surg. 1999;165:1125–1128. 10. Hammond JS, Eckes JM, Gomez GA, et al. HIV, trauma, and infection control: universal precautions are universally ignored. J Trauma. 1990;30(5): 555–561. 11. Schwab CW, Kauder DR. Trauma in the geriatric patient. Arch Surg. 1992;127(6):701–706. 12. Mattox KL, Goetzl L. Trauma in Pregnancy. Crit Care Med. 2005;33(10): S385–S389. 13. Centers for Disease Control: National Health and Nutrition Examination Survey. Available at: www.cdc.gov/nchs/data/nhanes/databriefs/ adultweight.pdf. Bethesda, MD. Accessed December 25, 2009.

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Detailed record keeping and review of patient records and outcomes is essential in providing good patient care. Although in-person or phone communication is emphasized during the transfer process, communication also occurs via the medical record, and is facilitated with comprehensive and accurate documentation. The medical record of the trauma patient should include records of prehospital care, care in the ED, and inpatient care at all facilities in which care was provided. Minimum documentation for care provided in the emergency setting must include patient identification, how the patient arrived, care that was rendered before arrival, pertinent history, chronologic notation of the physical examination including vital signs, and the results of diagnostic and therapeutic procedures and tests. For the trauma patient, mechanism of injury, GCS, vital signs, respiratory rate, spinal immobilization, and the status of airway, breathing, and circulatory systems also must be recorded. Chronology and response to treatment are particularly important for subsequent care providers. The medical record is the legal documentation of care provided, and protects the legal interests of both patient and healthcare providers.75 When patient information is shared between facilities to provide continuity of care, the rules of the Health Insurance Portability and Accountability Act (HIPAA) do not apply.76 There are many ways that trauma resuscitations are recorded depending on the facility. The choice of which documentation form to use is up to each hospital caring for the injured patient. Review of medical records is an essential aspect of performance improvement.

14. Mort TC. Does the body mass index influence emergency airway management: morbid obesity versus normal. J Clin Anesth. 2006;18(4): 322–323. 15. Zuidema GD, Rutherford RB, Ballinger WF. The management of trauma. Chicago, IL: Saunders; 1968:1–27. 16. Rosenthal ME, Adachi M, Ribaudo V, et al. Achieving housestaff competence in emergency airway management using scenario based simulation training: comparison of attending versus housestaff training. Chest. 2006;129(6):1453–1458. 17. Bergen JM, Smith DC. A review of etomidate for rapid sequence intubation in the emergency department. J Emerg Med. 1997;15(2): 221–230. 18. Goldberg JS, Rawle PR, Zehnder JL, et al. Colorimetric end-tidal carbon dioxide monitoring for tracheal intubation. Anesth Analg. 1990;70: 191–194. 19. Yelderman M, New W Jr. Evaluation of pulse oximetry. Anesthesiology. 1983;59(4):349–351. 20. Jubran A. Pulse oximetry. Crit Care. 1999;3:R11–R17. 21. Knudtson JL, Dort JM, Helmer SD, et al. Surgeon-performed ultrasound for penumothorax in the trauma suite. J Trauma. 2004;56:527–530. 22. Sisley AC, Rozycki GS, Ballard RB, et al. Rapid detection of traumatic effusion using surgeon-performed ultrasound. J Trauma. 1998;44: 291–296. 23. Ball CG, Williams BH, Wyrzykowski AD, Nicholas JM, Rozycki GS, Feliciano DV. A caveat to the performance of pericardial ultrasound in patients with penetrating cardiac wounds. J Trauma. 2009;67: 1123–1124. 24. Pettiford BL, Luketich JD, Landreneau RJ. The management of flail chest. Thorac Surg Clin. 2007;17(1):25–33. 25. Mattox KL, Allen MK. Systematic approach to pneumothorax, hemothorax, pneumomediastinum and subcutaneous emphysema. Injury. 1986;17:309–312. 26. Bickell WH, Wall MJ, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso trauma. N Engl J Med. 1194;331:1105–1109. 27. Capone AC, Safar PK, Sterzoski SW, et al. Uncontrolled hemorrhagic shock outcome model in rats. Resuscitation. 1995;29:143–152. 28. Turnage B, Maull KI. Scalp laceration: an obvious ‚occult’ cause of shock. South Med J. 2000;93:265–266. 29. Kragh JF, Walters TJ, Baer DG, et al. Survival with emergency tourniquet use to stop bleeding in major limb trauma. Ann Surg. 2009;249(1):1–7. 30. Barriot P, Riou B. Hemorrhagic shock with paradoxical bradycardia. Intens Care Med. 1987;13(3):203–207. 31. Morris JA, Norris PR, Ozdaz A, et al. Reduced heart rate variability: an indicator of cardiac uncoupling and diminished physiologic reserve in 1,425 trauma patients. J Trauma. 2006;60(6):1165–1174. 32. Cancio LC, Batchinsky AI, Salinas J, et al. Heart-rate complexity for prediction of prehospital lifesaving interventions in traumatic patients. J Trauma. 2008;65(4):813–819. 33. Ries RK, Miller S, Fiellin DA, et al. Principles of Addiction Medicine. 4th ed. Philadelphia, PA: Lippincott, William and Wilkins; 2009:1049. 34. Chestnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma. 1993;34:216–222. 35. Stern SA. Low-volume fluid resuscitation for presumed hemorrhagic shock: helpful or harmful? Curr Opin Crit Care. 2001;7(6):422–430. 36. Illig FA, Swierzewski MJ, Feliciano DV, et al. A rational screening and treatment strategy based on the electrocardiogram alone for suspected cardiac contusion. Am J Surg. 1991;162:537–544. 37. Bertinchant JP, Polge A, Mohty D, et al. Evaluation of incidence, clinical significance, and prognostic value of circulating cardiac troponin I and T elevation in hemodynamically stable patients with suspected myocardial contusion after blunt chest trauma. J Trauma. 2000;48(5):924–931. 38. Nagy KK, Krosner SM, Roberts RR, et al. Determining which patients require evaluation for blunt cardiac injury following blunt chest trauma. World J Surg. 2001;25:108–111. 39. Beresky R, Klingler R, Peake J. Myocardial contusion: when does it have clinical significance? J Trauma. 1988;28:64–68. 40. Krassioukov AV, Karlsson AK, Wecht JM, et al. Assessment of autonomic dysfunction following spinal cord injury: rationale for additions to International Standards for Neurological Assessment. J Rehabil Res Dev. 2007;44:103–112. 41. McGee DC, Gould, MK. Preventing complications of central venous catherization. N Engl J Med. 2003;348(12):1123–1133. 42. Banerjee S, Singhi SC, Singh S, Singh M. The intraosseous route is a suitable alternative to intravenous route for fluid resuscitation in severely dehydrated children. Indian Pediatr. 1994;31(12):1511–1520.

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43. http://www.naemsp.org/position.html. Accessed March 20, 2010. 44. Fowler R, Gallagher JV, Isaacs M, et al. The role of intraosseous vascular access in the out-of-hospital environment. Prehospital Emerg Care. 2007;11:63–66. 45. Holcomb JB, Wade CE, Michalek JE, et al. Increased plasma and platelet to red blood cell ratios improves outcome in 466 massively transfused civilian trauma patients. Ann Surg. 2008;248:447–458. 46. Zink KA, Sambasivan CN, Holcomb JB, Chisholm G, Schreiber MA. A high ratio of plasma and platelets to packed red blood cells in the first 6 hours of massive transfusion improves outcomes in a large multicenter study. Am J Surg. 2009;197:565–570. 47. Stansbury LG, Dutton RP, Stein DM, Bochicchio GV, Scalea TM, Hess JR. Controversy in trauma resuscitation: do ratios of plasma to red blood cells matter? Transfus Med Rev. 2009;23:255–265. 48. Hopson LR, Hirsh E, Delgado MD, Domeier RM, McSwain NE, Krohmer J. Guidelines for withholding or termination of resuscitation in prehospital traumatic cardiopulmonary arrest: joint position statement of the national association of EMS physicians and the American college of surgeons committee on trauma. J Am Coll Surg. 2003;196:1106–1112. 49. Jennett B, Teasdale G. Aspects of coma after severe head injury. Lancet. 1977;1:878–881. 50. Smits M, Dippel DW, deHaan GG, et al. Minor head injury: guidelines for the use of CT—a multicenter validation study. Radiology. 2007;245(3):831–838. 51. Gentilello LM. Practical approaches to hypothermia. In: Maull KI, et al. Advances in Trauma and Critical Care. St. Louis: Mosby; 1994. 52. Davis JW, Parks SN, Kaups KL, Gladen HE, O’Donnell-Nicol S. Admission base deficit predicts transfusion requirements and risk of complications. J Trauma. 1996;41:769–774. 53. Rixen D, Siegel JH. Bench-to-bedside review: oxygen debt and its metabolic correlates as quantifiers of the severity of hemorrhagic and posttraumatic shock. Crit Care. 2005;9:441–453. 54. Morey AF, Rozanski TA. In: Wein AJ, Kavoussi LR, Novick AC, et al. Campbell-Walsh Urology. 7th ed. Philadelphia, PA: Elsevier; 2007: 2649–2655. 55. Fremstad JD, Martin SH. Lethal complications from insertion of nasogastric tube after severe basilar skull fracture. J Trauma. 1978;18:818–820. 56. Berne JD, Norwood SH. Blunt vertebral artery injuries in the era of computed tomographic angiographic screening: incidence and outcomes from 8292 patients. J Trauma. 2009;67(6):1333–1338. 57. Rudnick MR, Kesselheim A, Goldfarb S. Contrast-induced nephropathy: how it develops, how to prevent it. Cleve Clin J Med. 2006;73(1):75–80. 58. Berrington de Gonzales A, Mahesh M, Kim KP, et al. Projected cancer risks from computed tomographic scans performed in the United States in 2007. Arch Intern Med. 2009;169(22):2071–2077.

59. Rozycki GS, Oschner MG, Jaffin JH, et al. Prospective evaluation of surgeons’ use of ultrasound in the evaluation of trauma patients. J Trauma. 1993;34(4):516–527. 60. Dolich MO, McKenney MG, Varela JE, et al. 2, 576 ultrasounds for blunt abdominal trauma. J Trauma. 2001;50:108–112. 61. McAnena OJ, Marks JA, Moore EE. Peritoneal lavage enzyme determinations following blunt and penetrating abdominal trauma. J Trauma. 1991;31(8):1161–1164. 62. Feliciano DV. Diagnostic modalities in abdominal trauma. Peritoneal lavage, ultrasonography, computerized tomography scanning, and arteriography. Surg Clin North Am. 1991;71(2):241–256. 63. Liu M, Lee C, Veng F. Prospective comparison of diagnostic peritoneal lavage, computed tomographic scanning, and ultrasonography for the diagnosis of blunt abdominal trauma. J Trauma. 1993;35(2):267–270. 64. Rozycki GS, Feliciano DV, Ochsner MG, et al. The role of ultrasound in patients with possible penetrating cardiac wounds: a prospective multicenter study. J Trauma. 1999;46(4):542–552. 65. Thomson DP, Thomas SH. Guidelines for air medical dispatch. Prehospital Emerg Care. 2003;7(2):265–271. 66. Rhee P, Nunley M, Demetriades D, et al. Tetanus and trauma: a review and recommendations. J Truama. 2005;58(5):1082–1088. 67. Ivascu FA, Janczyk RJ, Junn FS, et al. Treatment of trauma patients with intracranial hemorrhage on preinjury warfarin. J Trauma. 2006;61(2): 318–321. 68. Dehner JR. Seatbelt injuries of the spine and abdomen. Am J Roentgenol. 1971;111(4):833–843. 69. Frick EJ Jr, Pasquale MD, Cipolle MD. Small-bowel and mesentery injuries in blunt trauma. J Trauma. 1999;46:920–926. 70. Chandler CF, Lane JS, Waxman KS. Seatbelt sign following blunt trauma is associated with increased incidence of abdominal injury. Am Surg. 1997;63:885–888. 71. Sherman RT, Parrish RA. Management of shotgun injuries: a review of 152 cases. J Trauma. 1963;3(1):76–86. 72. Head JM. Inhalation injury in burns. J Trauma. 1981;21(1):86. 73. Rozycki GS, Tremblay L, Feliciano DV, et al. A prospective study for the detection of vascular injury in adult and pediatric patients with cervicothoracic seat belt signs. J Trauma. 2002;52:618–623. 74. Mizock BA, Falk JL. Lactic acidosis in critical illness. Crit Care Med. 1992;20(1):80–93. 75. Southard P, Frankel P. Trauma care documentation: a comprehensive guide. J Emerg Nurs. 1989;15:393–398. 76. U.S. Department of Health and Human Services Health Information Privacy. Available at: http://www.hhs.gov. Washington, DC. Accessed February 2, 2010.

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CHAPTER 11

Airway Management Eric A. Toschlog, Scott G. Sagraves, and Michael F. Rotondo

INTRODUCTION ■ The Priority of the Airway In the crucial initial management of the injured patient, securing the airway is quite literally the single most important priority; failure to oxygenate and ventilate represents the difference between life and death as well as functionality and disability. Airway loss initiates a terminal and irreversible cascade of events. Not only are hypoxia and hypoventilation common injury-related causes of mortality, but also they additionally represent one of the most common causes of preventable mortality following injury. The trauma patient represents a unique and exquisite airway challenge, from both anatomic and physiologic perspectives. The multisystem trauma patient represents the culmination of interrelated insults to oxygenation and ventilation, where under extreme duress, clinicians must rapidly recognize compounding injury and prioritize the airway in what may be multiple conflicting priorities.

BASIC AIRWAY EQUIPMENT AND PREPARATION ■ Preparation for Airway Management Successful airway management starts with planning and preparation. Planning begins by assembling an airway kit or cart containing the necessary equipment for intubation. The practitioner should take the time to inventory the equipment prior to the intubation, ensuring function and availability.

Equipment The airway cart should consist of drugs, endotracheal tubes, airways, laryngoscopes, airway adjuncts, a variety of syringes and needles, and equipment to establish a surgical airway. The primary components of the airway kit are the endotracheal tube and laryngoscope. The airway cart should have a variety of tubes in both cuffed and uncuffed types, including

tubes down to a 2.0 internal diameter size for pediatrics, and a variety of stylet sizes. Both Miller and Macintosh laryngoscope blades should be included. In addition, the airway cart should be stocked with both the oropharyngeal airway (OPA) and nasopharyngeal airway (NPA) in all sizes. In the event of failed intubation, several airway adjuncts should be included in the standard airway cart. An array of adjuncts is now available to assist with difficult intubation and failed airway, including supralaryngeal airways, lighted wand stylets, retrograde intubation kits, a variety of video laryngoscopic devices, and the gum elastic bougie (GEB). The goal of airway management in the trauma admitting area is to closely simulate the control of the operating room. Key personnel should work as a team to assure a successful intubation (Fig. 11-1). The optimal intubating team should consist of at least three members including the intubator, a respiratory therapist, and an assistant to maintain cervical spine alignment or to provide the Sellick maneuver to prevent aspiration.

Monitoring and Troubleshooting Pulse Oximetry. The pulse oximeter is a portable, noninvasive, and reliable device that measures SpO2. Although very accurate in analysis of peripheral oxygen delivery, the pulse oximeter may display inaccurate readings in the case of carbon monoxide poisoning, high-intensity lighting, hemoglobin abnormalities, and a pulseless extremity or in severe anemia. Capnography. End-tidal carbon dioxide (ETCO2) detectors measure the partial pressure of carbon dioxide in a sample gas. The patient’s PaCO2 is typically 2–5 mm Hg higher than the ETCO2 and a normal reading in a trauma patient is approximately 30–40 mm Hg. ETCO2 reading may be used to confirm placement of an endotracheal tube. The presence of carbon dioxide in the exhaled air strongly suggests correct placement of the endotracheal tube in the trachea in a perfusing patient. The

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position. Due diligence with respect to preparation of both personnel and equipment makes for a less stressful intubation and improves the practitioner’s chances of successfully intubating the patient.1

Manual Airway Maneuvers

FIGURE 11-1 The optimal rapid sequence intubation team is comprised of (1) the intubating provider at the head of the bed, (2) an assistant to the patient’s right to facilitate passage of necessary equipment from the airway cart (to the intubating provider’s right) and to provide cricoid cartilage pressure, (3) a provider to administer drugs to the patient’s left, and (4) a respiratory therapist to assist with airway maneuvers. Note the presence of full barrier precautions, pulse oximetry, telemetry, colorimetry, and two functioning large-bore intravenous catheters.

disposable capnometer indicates the presence of carbon dioxide with a color change. The electronic capnometer provides the health care provider with a numerical ETCO2 and plots the CO2 concentration against time. Although the use of capnometry as an adjunct to monitor the patient’s exhaled carbon dioxide has met some success, conditions such as hypotension, increased intrathoracic pressure, and pulmonary embolus resulting in an increased dead space ventilation may decrease the accuracy of the capnometer. Troubleshooting. The intubating team should have the patient attached to a cardiac monitor, blood pressure cuff, and pulse oximeter (Fig. 11-1). Intravenous access should be established. The patient should receive supplemental oxygen via a nonrebreather mask or a bag valve mask (BVM) depending on the patient’s inherent respiratory drive. The correct size of endotracheal tube should be brought to the bedside and a correctly sized stylet should be inserted. The endotracheal balloon should be checked for leaks. Once the balloon has been checked, a 10-cm3 syringe is left attached to the pilot balloon. A suction device with a large catheter tip should be readily available and be placed near the right side of the patient’s head. The laryngoscope handle/blade connection should be checked for a functional light source. A means to secure the endotracheal tube should be available. Dentures should be removed just before intubation, particularly if the patient is being bagged and his or her dentures allow for a tight mask seal. If cervical spine injury has been excluded, the patient should be positioned with the neck slightly flexed and the head slightly extended on an imaginary axis through the patient’s ears. Placing a pillow or towel under the patient’s occipital region and elevating the head approximately 10 cm may facilitate this

Before any airway maneuver is undertaken, a quick visual inspection of the oropharyngeal cavity should be done. Any foreign or loose material should be swept clear with a gloved finger or removed with suction. Blood may be present in the mouth of a trauma patient and adequate suctioning is essential to maintaining an open airway. Administration of oxygen prior to suctioning may prevent hypoxemia due to prolonged suctioning. The tongue can cause airway obstruction in the unresponsive patient as it often lacks tone and falls into the oropharynx. Manual airway maneuvers serve to elevate the tongue out of the hypopharynx. Jaw Thrust. The cervical spine should be kept in normal alignment. The provider should grasp the sides of the patient’s face with fingers 3-5 along the ramus portion of the mandible. The provider’s thumb is on the patient’s cheek and the index finger on the chin and lower lip. These two fingers can open the patient’s lips or serve to seal the mask on a BVM. The provider’s fingers should form an “E” with the three lower fingers and a “C” with the thumb and index finger. Force is applied to the angle of the mandible forcing the mandible forward and anteriorly, while simultaneously opening the mouth with the index finger on the chin. Chin Lift. With either a free, gloved hand or another provider’s gloved hand, the provider’s thumb is placed into the patient’s mouth, the patient’s lower incisors and chin are grasped, and the patient’s mandible is lifted anteriorly. This maneuver supplements the jaw thrust and works to lift the mandible anteriorly, elevating the tongue out of the oropharynx. Sellick Maneuver. The injured patient may have swallowed large amounts of air, or air has been forced into the stomach during BVM ventilation. The use of the Sellick maneuver, particularly during BVM ventilation, aids in preventing aspiration. The maneuver is accomplished by applying gentle posterior pressure with the thumb and index finger to the patient’s cricoid cartilage. This pressure causes the cricoid cartilage to be displaced posteriorly, effectively closing off the esophagus.

■ Basic Mechanical Airway Devices Oropharyngeal Airway Oropharyngeal and nasopharyngeal devices can be inserted into either the mouth or nose of the patient, serving to elevate the tongue out of the oropharynx. The OPA is a curved, plastic or hard rubber device, which comes in various sizes and has channeling for suction catheters. The device is sized by placing the OPA in the space between the patient’s ear and corner of the mouth. A correctly sized OPA will extend from the patient’s mouth to the angle of the jaw.

Airway Management

1. Prevention of obstruction by the patient’s teeth and lips 2. Maintenance of the airway in a spontaneously breathing unconscious patient 3. Ease of suctioning 4. Use as a bite block in a patient who is having a seizure The OPA is contraindicated in a conscious patient as it may stimulate a gag reflex. In addition, it does not isolate the trachea, nor can it be inserted through clenched teeth. It may obstruct the airway if it is improperly placed and can be dislodged easily. To place the OPA, the mouth is opened and the OPA is inserted with the curve reversed and the tip pointing toward the roof of the patient’s mouth. Using a twisting motion the OPA is rotated into position behind the base of the patient’s tongue. Alternatively, a tongue blade can be used to depress the tongue with the OPA placed directly into the oropharynx.

Nasopharyngeal Airway The NPA is a soft rubber or latex uncuffed tube that is designed to conform to the patient’s natural nasopharyngeal curvature. It is designed to lift the posterior tongue out of the oropharynx. Like the OPA, it is indicated for patients who cannot maintain their airway. The advantages of the NPA include ease and speed of insertion, patient tolerance and comfort, and effectiveness when the patient’s teeth are clenched. Disadvantages of the NPA include its smaller size, the risk of nasal bleeding during insertion, and lack of utility when a basilar skull fracture is suspected.2 The provider should first size the NPA by selecting an NPA that is slightly smaller than the patient’s nostril. The distance from the patient’s nose to earlobe determines the length. The NPA should be liberally lubricated with lidocaine gel prior to insertion. The right nare is preferentially chosen, as it is typically larger. Gentle pressure should be applied until the flange rests against the patient’s nostril. After a basic mechanical airway has been inserted, the patient should be oxygenated with supplemental oxygen or a BVM.

Bag Valve Mask The BVM assists the provider with oxygenation and ventilation in the apneic or hypoventilating patient. With an effective mask seal and an open airway, the BVM can deliver tidal volumes approaching 1.5 L and nearly 100% inspired oxygen with an attached oxygen reservoir. The BVM consists of a bag with a volume of 1.6 L and a standard face mask attached via a oneway, nonrebreathing valve. A reservoir bag and oxygen source is attached to the opposite end of the bag. Multiple sizes are available to treat neonatal, infant, children, and adult patients. To effectively use the BVM, a second provider may be required to establish a properly fitted mask seal while the second provider squeezes the bag. Maintenance of oxygenation and ventilation

can be improved by utilizing a basic mechanical airway and proper jaw thrust and chin lift techniques while “bagging” the patient.

ASSESSMENT OF THE AIRWAY A single indicator has not been identified that accurately predicts the inability to intubate. However, an attempt at airway assessment is mandatory to assist with the prediction of difficulty to intubate or ventilate.3

■ History Time permitted, a history should be quickly obtained. The patient should be interrogated as to prosthetic dental devices, any previous difficulty with anesthesia or intubation, sleep apnea, trismus, and the timing of his or her last meal.

■ Physical Examination A general assessment of the oropharynx, nose, maxilla, mandible, and neck should be rapidly undertaken. An assessment of the patient’s overall level of consciousness (e.g., Glasgow Coma Score) and the ability of the patient to open his or her mouth should also be performed. If possible, have the patient stick out his or her tongue to evaluate the size of the tongue. The vocal quality of the patient should be noted during the physical exam, as well. The presence of stridor usually indicates some degree of injury to the upper airway. Assess for dentures or other prosthetic devices that may need to be removed prior to intubation.

INTUBATION OF THE TRACHEA The majority of injured patients are able to undergo successful orotracheal intubation (OTI). In compliance with the ATLS course, the preferred definitive airway is tracheal intubation through the mouth using direct laryngosocopy.1

■ Guidelines for Emergency Tracheal Intubation Indications for intubation relate to the following three simple questions: • First, is the patient able to oxygenate and ventilate? • Second, is the patient able to maintain an airway? • Third, will the underlying injury and physiology of the patient lead to a failure to maintain the airway, oxygenate or ventilate? The practice management guidelines of the Eastern Association for the Surgery of Trauma (EAST) for tracheal intubation secondary to trauma reveal no Level I data (evidence from randomized, controlled trials) that predict the need for urgent intubation.4 The guideline calls for emergency tracheal intubation in trauma patients exhibiting the following characteristics: • Acute airway obstruction • Hypoventilation

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Indications for the use of the OPA include a patient who is unable to maintain his or her airway or to prevent an intubated patient from biting the endotracheal tube. Advantages for use of the OPA include the following:

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• Severe hypoxemia despite supplemental oxygen • Severe cognitive impairment (Glasgow Coma Scale score 8) • Cardiac arrest • Severe hemorrhagic shock In concordance with ATLS, the EAST guidelines promulgate the concept that OTI utilizing direct laryngoscopy is the procedure of choice for airway control following trauma.4

■ Anatomy and Technique of Direct Laryngoscopy and Intubation Success in intubating the injured patient is dependent on thorough knowledge of the anatomy of the upper airway and a meticulous adherence to proper technique. The vocal cords lie posterior and inferior to the pliable epiglottis, which should be visualized as a constant reference point during laryngoscopy. The posterior-most esophagus may be lifted into view with sufficient elevation of the epiglottis. Since the majority of intubations occur prior to cervical spine clearance, head and neck immobilization is of highest priority. In the rare instance that the cervical spine is cleared, the patient should be placed in the sniffing position initially (extension of the head, slight flexion of the lower cervical spine), which optimizes the alignment of the oral, pharyngeal, and laryngeal axes. Following preparation of equipment and personnel, the laryngoscope is grasped firmly with the left hand. It should be emphasized that the right hand should be kept free, for suctioning, manipulation of oral structures, and placement of the endotracheal tube. Selection of a straight versus curved blade has less to do with proven efficacy in a particular scenario than the comfort and proficiency of the laryngoscopist with a particular blade. In general, the straight blade is utilized to pass beneath, and directly elevate, the epiglottis. The straight blade is inserted into the esophagus, with the blade withdrawn slowly under direct visualization to expose the glottic opening. The same technique can be applied with a curved blade of sufficient size, although the curved blade technique typically utilizes insertion of the tip of the blade into the vallecula, with anterior traction of the epiglottis, exposing the glottic opening. The tongue should be displaced by the blade to the patient’s left for best visualization of the epiglottis. The motion and direction of the laryngoscope in the left hand during laryngoscopy is of critical importance to safe and successful intubation of the trachea. The proper technique of laryngoscopy employs upward motion of the laryngoscope in the parallel plane of the handle. A “rocking” motion, during which the handle is rotated counterclockwise and posterior, should never be used. This posterior circular motion can impart dangerous extension on the cervical spine or fracture or dislodge teeth. In addition, the left elbow should not be placed on the bed or spine board for stabilization. As the blade is positioned to visualize the glottic opening, the right hand can be utilized to employ the BURP maneuver if the glottic opening is not readily visible. This technique includes Backward, Upward, Rightward, Pressure on the thyroid cartilage and is distinct from the Sellick maneuver.

RAPID SEQUENCE INTUBATION ■ Overview Intubation by rapid sequence induction (RSI) has become the gold standard for management of the airway in trauma and critical illness. The technique of RSI has been demonstrated to increase intubation success rates and reduce complications compared to pre-RSI techniques in a variety of emergent settings.5–9 RSI benefits include provision of optimal intubating conditions for injured patients, rapid airway control, high success rates, and reduction of pulmonary aspiration. The adaptability of RSI to individual patient conditions renders the technique optimal for airway control in the injured. First developed to facilitate operating room intubations in patients with full stomachs, thereby minimizing risk of aspiration,10 the technique is now widely utilized by prehospital paramedics,11,12 emergency medicine physicians,13 and trauma surgeons, with a high reported intubation success rate by nonanesthesiologists.5,14 Approximately 80% of intubations performed in North American emergency departments utilize RSI, with a 90% success rate by the first intubator.14 In the technique of RSI, laryngoscopy and intubation are facilitated by use of sedating induction agents and short-acting neuromuscular blockade (NMB). Rapid sequence intubation (RSI) can be divided into five phases: (1) patient and equipment preparation, (2) preoxygenation, (3) premedication, (4) paralysis, and (5) placement of the tube. A time line for RSI is demonstrated in Table 11-1.

■ Preparation Although significant injury with physiologic instability may preclude prolonged preparation for RSI, all efforts should be made to allow for individualized assessment of comorbid conditions, airway status, predictors of difficult intubation, and anticipated pharmacologic regimen. The selection and sequence of pharmacologic agents should be determined, with all agents ready and available in clearly labeled syringes. A horizontal approach to the preparatory phase of RSI is optimal, during which multiple personnel with predetermined responsibilities and positions work simultaneously (Fig. 11-1). In this manner, the preoxygenation phase is initiated during preparation

■ Preoxygenation Although not originally considered an essential component of RSI, preoxygenation is now considered optimal if the oxygenation, ventilation, and hemodynamic status of the patient permit. The purpose of preoxygenation is to replace the nitrogen-dominant room air occupying the pulmonary functional residual capacity with a 100% oxygen reservoir, such that saturation of arterial hemoglobin (SaO2) is prolonged. Preoxygenation can be accomplished by gently assisting spontaneous respirations with 100% oxygen or simply allowing the patient to breathe 100% oxygen. Forceful BVM ventilation should be assiduously avoided during the intubation sequence, as it may produce unnecessary gastric distention, increasing

Airway Management

Step Preparation

Timing Zero–10 min

Preoxygenation

Zero–5 min

Premedication

Paralysis

Placement

Action ✓ Prepare equipment ✓ Assess patient ✓ Position personnel ✓ Select drugs ✓ Passive administration of high-flow oxygen via bag valve mask

PHARMACOLOGY OF RAPID SEQUENCE INTUBATION

✓ Lidocaine 100 mg IVP ✓ Vecuronium 10 mg IVP ✓ Etomidate 20 mg IVP

Zero–2 min

Zero  20 s

✓ Succinylcholine 100 mg IVPF ✓ Sellick maneuver

Zero  45 s Zero  1 min

✓ Intubation ✓ Tube confirmation

Zero

the risk for pulmonary aspiration of gastric contents. Recommendations for the duration of preoxygenation necessary for optimal hemoglobin saturation range from 3 to 5 minutes; however, the effectiveness of preoxygenation is

It is imperative that providers caring for the injured be facile with all pharmacologic agents utilized for RSI, including both barbiturate and nonbarbiturate hypnotics, neuromuscular blocking agents, benzodiazepines, dissociative agents, and opiates (Table 11-2). A “one method fits all” approach is not always applicable,16 and each patient should be individualized based on type and mechanism of injury, comorbidities, and potential for adverse events. However, the majority of trauma patients can be effectively intubated using a generalized pharmacologic regimen. Clinical predictors of need for sedation and paralysis have been identified. In data from a prospective study of endotracheal intubation, factors associated with drug-facilitated intubation, defined as intubation facilitated by the use of sedatives or paralytics, included clenched jaw or trismus, declining verbal Glasgow Coma Scale score, and use of cervical spine precautions.17 The vast majority of patients currently undergoing RSI received both sedative and paralytic agents. Evidence-based principles identified by the EAST

TABLE 11-2 Pharmacology of Rapid Sequence Intubation Agent Premedication agents Fentanyl Midazolam Lidocaine Esmolol Vecuronium

Dose

Onset

Duration

Precautions

1.0–5.0 mcg/kg 0.1–0.3 mg/kg 1.0–1.5 mg/kg 2.0 mg/kg 0.01 mg/kg

30–45 s 2–3 min 30–90 s 2–5 min 90–120 s

0.5–1.0 h 2–3 h 10–20 min 9–30 min 60–75 min

Chest wall rigidity Slow onset Hypotension Hypotension Extended duration

Induction agents Etomidate Propofol Thiopental Methohexital Ketamine

0.05–0.15 mg/kg 0.5–2.0 mg/kg 1.0–3.0 mg/kg 1.0–3.0 mg/kg 0.5–2.0 mg/kg

10–60 s 10–50 s 10–60 s 30 s 30–120 s

2–5 min 2–10 min 5–30 min 5–10 min 5–15 min

Adrenal suppression Hypotension Hypotension Hypotension Intracranial hypertension

Neuromuscular blockade Succinylcholine Rocuronium

0.6–1.0 mg/kg 1.0 mg/kg

30–60 s 45–60 s

5–15 min 30–60 min

Hyperkalemia Long duration

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dependent on the physiologic status of the patient as well as age, size, and comorbid conditions. For example, an optimally preoxygenated healthy 70-kg adult will maintain SaO2 over 90% for approximately 8 minutes, an obese adult less than 3 minutes, and a 10-kg child less than 4 minutes.15 More importantly, the desaturation from 90% SaO2 to 0% occurs much more rapidly than the fall from 100% to 90%. The approximate Pao2 at 90% SaO2 is 60 mm Hg, falling to 27 mm Hg at an SaO2 of 50%. An injured patient with little compensatory reserve can decline from 90% to 0% literally in seconds.

TABLE 11-1 How We Do It: Steps and Timing of Rapid Sequence Intubation in a 70-kg Adult

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SECTION 2

• • • • • •

Neuromuscular paralysis Sedation Regimen that maintains hemodynamic stability Regimen that minimizes intracranial hypertension Regimen that prevents vomiting Regimen that prevents intraocular content extrusion

Premedication Agents Airway stimulation, including laryngoscopy and endotracheal tube placement, results in the pressor response, an intense autonomic sympathetic discharge producing tachycardia, hypertension, and increased intracranial pressure.10,18 The degree of airway stimulation is proportional to the magnitude of the pressor response. Correspondingly, increased intragastric, intrathoracic, and intracranial pressures may result from Valsalva, bronchospasm, or coughing. As the foundation of RSI relates to abrogating the untoward effects of airway stimulation, preinduction agents are routinely utilized to blunt the physiologic response to laryngoscopy and endotracheal tube placement. A common mnemonic for the preinduction regimen is LOAD, which includes Lidocaine, Opiates, Atropine, and a Defasciculating agent, although atropine is typically utilized in pediatric populations only. Opioids. Depth of sedation may correlate with speed of intubation in RSI.19 The sedative and analgesic effects of opioids may provide benefit to the injured patient prior to induction. A commonly used opioid for RSI in the prehospital and emergency department setting is fentanyl, which at 5.0 mcg/kg has been shown to be hemodynamically neutral compared to midazolam and thiopental during RSI.19 Fentanyl effectively blunts airway reactivity,20 and confers the significant added benefit of analgesia in the injured patient. Benzodiazepines. Benzodiazepines, a family of gamma aminobutyric acid (GABA) agonists, have been utilized in RSI for sedation. Midazolam is the most widely studied agent, having favorable pharmacokinetics for RSI, including rapid onset and short half-life. Advantages include hemodynamic neutrality and retrograde amnesia, although onset is slower than comparable agents and the intubation reflex is not attenuated,19 rendering it less commonly used in RSI protocols than opioids. Antiarrhythmics. Despite a great deal of controversy regarding the potential benefits of lidocaine during RSI, it is a preinduction agent common to RSI protocols,21 and is advocated in many emergency airway courses. Lidocaine has a number of theoretical beneficial preintubation effects, including abrogation of airway reactivity following placement of the endotracheal tube, the tachycardic response to intubation, and succinylcholine-induced myalgia and fasciculations.22 The two primary potential benefits of lidocaine use in RSI are to

mitigate against reflex bronchospasm and increased intracranial pressure. Although definitive data are lacking regarding effects on intracranial pressure, the potential benefits outweigh the negligible side effects of the RSI dose. Beta-Adrenergic Blockers. Esmolol has been utilized as a preinduction agent for mitigation of the tachycardic component of the pressor response. In comparison to lidocaine and fentanyl, esmolol has demonstrated superiority in attenuating the pressor response.23 Beneficial pharmacokinetics include rapid onset and short action; however, the bradycardic and negative inotropic effects of esmolol may blunt the compensatory response to hemorrhage. The cardiac effects may produce corresponding reductions in cerebral blood flow. Therefore, esmolol should be considered only in controlled circumstances in which hemorrhage of brain injury have been definitively excluded. The availability of other safer agents that effectively minimize the pressor response relegates beta-blockers to clear second-line status. Defasciculation Paralytic Agents. Succinylcholine, the standard neuromuscular blocking agent utilized for RSI, produces significant myoclonal fasciculations, prompting a rise in intracranial pressure in patients at risk for intracranial hypertension. Therefore, a defasciculating dose of a competitive neuromuscular blocking is administered during RSI. Common defasciculating agents include vecuronium and rocuronium, and, less commonly, pancuronium. Defasciculating doses are administered as 10% of the paralyzing dose, given 3–5 minutes prior to administration of succinylcholine. It is unusual for defasciculating doses of neuromuscular blockers to cause apnea. However, patient weight is commonly an estimate during RSI following injury, and preparations to assist with ventilation should be made.

Induction Agents The perfect induction agent would possess rapid onset and elimination, render the patient unconscious but also amnestic, possess analgesic properties, and have negligible side effects. In injured and critically ill patients, the ideal agent would produce little cardiovascular effects and maintain cerebral perfusion pressure. Regrettably, such an agent does not yet exist. Because many agents produce side effects, including myocardial depression with the potential for hypoperfusion, careful attention should be dedicated to the selection of individual agents. Etomidate. Etomidate is a short-acting carboxylated imidazole hypnotic agent frequently utilized for rapid sequence induction. It possesses ideal characteristics for urgent and emergent RSI in trauma patients, including rapid onset and clearance, reduction in cerebral metabolic rate,24 and negligible effects on hemodynamics. This favorable pharmacokinetic profile has led to the widespread use of etomidate for RSI in head injury and hemodynamically labile patients. Accordingly, the American College of Surgeons Committee on Trauma added etomidate to the Advanced Trauma Life Support course as an

Airway Management

Propofol. Propofol is a nonbarbiturate hypnotic agent that rapidly induces deep sedation and significant relaxation of laryngeal musculature.10 When used for induction, propofol produces intubation conditions equal to thiopental and equal to or superior to etomidate.28 Propofol should be used with caution in head-injured or hemodynamically labile patients due to a consistent hypotensive effect and potential reduction of cerebral blood flow. Barbiturates. Thiopental is the most commonly used barbiturate for RSI. Like other induction agents, thiopental has rapid onset and clearance. In the aeromedical setting, thiopental has been shown equally efficacious to etomidate as an adjunct to RSI.29 Similarly, in an evaluation of 2,380 RSI procedures, patients were more likely to be successfully intubated using thiopental or propofol as compared to etomidate or a benzodiazepine.28 Thiopental reduces cerebral oxygen consumption and exhibits anticonvulsant effects, rendering it useful in closed head injury (CHI). However, the significant limitation of thiopental use in trauma relates to inhibition of central nervous system sympathetic response. Consequently, thiopental produces reduced myocardial contractility and systemic vascular resistance, inducing hypotension. Therefore, it is best reserved for patients who are euvolemic and normotensive, limiting its application in critically ill patients. Methohexital is an additional barbiturate that has been used for RSI. It exhibits similar effects to thiopental, although it is significantly more potent and has shorter onset and duration than thiopental. Dissociative Agents. Ketamine, a rapid-onset dissociative sedative and anesthetic agent, is frequently used for RSI in the pediatric population and in adults with chronic obstructive pulmonary disease. In addition to its sedative effects, ketamine exhibits the beneficial properties of potent analgesia and a partial amnesia. As a sympathomimetic agent, ketamine may induce tachycardia and increased blood pressure. In addition, ketamine induces cerebral vasodilatation, potentially exacerbating intracranial hypertension. Trauma patients with documented or potential CHI should therefore not undergo induction for RSI with ketamine.

■ Paralysis Neuromuscular Blocking Agents Pharmacologic paralysis represents an integral component of RSI, facilitating emergent intubation for more than three decades.30 Paralysis of facial musculature facilitates visualization during laryngoscopy, confers total control of the patient, and reduces complications during intubation. Prehospital NMB has been demonstrated to be safe,8,9 and to improve intubation success in injured patients undergoing RSI.31,32 Potential adverse effects should be diligently assessed, particularly with use of succinylcholine. In addition, preparations for rescue techniques must be made prior to administration of a paralytic agent, in the event of intubation failure. Because paralytic agents provide no sedative, analgesic, or amnestic effect, it is imperative to combine paralytic use with an appropriate induction agent. Succinylcholine. Succinylcholine, a depolarizing acetylcholine dimer, acts noncompetitively at the acetylcholine receptor in a biphasic manner to produce muscular paralysis at the motor end plate. Succinylcholine stimulates all muscarinic and nicotinic cholinergic receptors of both parasympathetic and sympathetic systems. Initial brief depolarization results in clinically notable muscular fasciculations, followed by sustained myocyte depolarization. Succinylcholine degradation is dependent on hydrolysis by pseudocholinesterase, and resistant to acetylcholinesterase. Due to rapid onset of action and short half-life, succinylcholine remains the gold standard for RSI in patients not at risk for adverse events. The standard dose of succinylcholine for RSI is 1.0 mg/kg, although recent data suggest a smaller dose of 0.5–0.6 mg/kg is sufficient for RSI,33 facilitating more rapid resumption of spontaneous respiration. Intramuscular injection of succinylcholine has been described, although the required dose, 4 mg/kg, is higher, and onset is slower, than intravenous injection. A clear understanding of the potential adverse effects of succinylcholine is critical to its appropriate use in RSI. Contraindications are primarily related to conditions that accentuate the hyperkalemic effects of succinylcholine, as it normally produces a 0.5- to 1.0-mEq/L elevation of serum potassium. Contraindications related to hyperkalemia include thermal injury of age exceeding 24 hours, although receptor upregulation likely does not become clinically relevant until postburn day 5. Therefore, it is safe to use succinylcholine for RSI in most acute burns. Contraindications include crush injury or rhabdomyolysis with hyperkalemia, congenital or acquired myopathies, and conditions of subacute and chronic upper and motor neuron denervation including paralysis and polyneuropathy of critical illness.10 Contraindications related to known comorbid conditions include history of malignant hyperthermia and pseudocholinesterase deficiency. In addition, succinylcholine is reported to raise intragastric and intracranial pressure due to muscle fasciculations, and may contribute to increased intraocular pressure. It should be used with caution in head injury and penetrating globe injury, although the evidence that succinylcholine raises intraocular pressure is anecdotal at best.34

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induction agent for hypotensive trauma patients.1 The most significant side effect of etomidate relates to adrenal insufficiency, as it produces a reversible blockade of adrenal 11-betahydroxylase. In patients at risk for adrenal insufficiency, including head-injured, mechanically ventilated, and septic populations, etomidate has been independently correlated with reductions in serum cortisol.25,26 The controversial question relates to whether transient adrenal suppression produces lasting effects on outcome. In a recent large single-center study, a single induction dose of etomidate was independently associated with ARDS and multiple organ dysfunction syndrome.27 Further studies are warranted to determine the long-term safety of etomidate for RSI; however, given the multiple favorable characteristics of the drug, etomidate remains the standard induction agent in most RSI protocols.

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Nondepolarizing Agents. Nondepolarizing NMBAs, through competitive blockade of acetylcholine transmission at postjunctional, cholinergic nicotinic receptors, provide an alternative for patients not appropriate for succinylcholine. The aminosteroid compounds, including rocuronium, pancuronium, and vecuronium, represent the commonly used NMBAs for RSI. Nondepolarizing agents for RSI are selected based on the ability to best approximate the rapid onset and elimination of succinylcholine. The most intensively studied nondepolarizing agent utilized for RSI is rocuronium, which exhibits short onset and intermediate duration of action. When contraindications to succinylcholine exist, rocuronium produces acceptable intubating conditions and should remain in the RSI armamentarium as an alternative to succinylcholine.

RSI involves airway failure, particularly esophageal intubation. The National Emergency Airway Registry (NEAR) classifies adverse events related to intubation as immediate, technical, and physiologic.37 Immediate events include witnessed aspiration, airway trauma, and undetected esophageal intubation. Technical events include recognized esophageal intubation and mainstem intubation. Physiologic events, often difficult to separate from underlying patient conditions related to injury, include pneumothorax, dysrrhythmia, and cardiac arrest.

■ Cricoid Cartilage Pressure (Sellick Maneuver)

Nasotracheal intubation (NTI) is identified within the ATLS course as an alternative to OTI under select circumstances.1 Any discussion of NTI should begin by noting two absolute contraindications: apnea and severe midface trauma or suspicion of basilar skull fracture during which NTI could breech the cranial vault. Relative contraindications include coagulopathy, combativeness, intracranial hypertension, and suspected upper airway obstruction. NTI should also be avoided in patients with little oxygenation or ventilatory reserve due to significant delay incurred with the technique. Because of contraindications, failure rate, and complications, NTI has been nearly supplanted by RSI. The primary indication for NTI relates to the difficult airway. In a spontaneously breathing patient with an anticipated difficult airway in whom RSI is predicted to fail, NTI can be considered for tracheal intubation. Following preparation of all necessary equipment, as well as planning an algorithm for procedure failure, the patient is preoxygenated as in RSI. The nares, nasopharynx, and trachea should be anesthetized. Lidocaine jelly or topical cocaine solution can be instilled into the selected nare, topical anesthetic sprayed into the oropharynx and nasopharynx, and lidocaine solution injected through the cricothyroid membrane. An appropriate size tube should be selected, typically having an internal diameter of 6.0–7.5 mm. The tube should be well lubricated and gently inserted into the nare, with the tip directed toward the occiput. When the tube passes into the posterior nasopharynx, it should be directed caudad, and resistance is commonly encountered. The tube should be rotated approximately one quarter turn toward the opposite nare, and advanced. When the tube advances into the distal nasopharynx, it should be restored to neutral and advanced. When breath sounds are heard through the tube (condensation may be visible), the tube should be advanced carefully but rapidly approximately 3–5 cm. If the tube has entered the trachea, the patient will cough repeatedly, and condensation may be seen. Placement should be confirmed with auscultation of breath sounds and use of an ETCO2 detector.

The Sellick maneuver is reported to reduce aspiration and improve vocal cord visualization during RSI. The efficacy of Sellick maneuver requires a force of greater than 40 N. When attempting the Sellick maneuver, proper technique is imperative. In a review of videotaped RSI evaluating deviations from RSI protocol in emergency medicine residents, 45% employed improper use of the technique.35

■ Placement Confirmation Accurate confirmation of tube placement is critical. The first method to confirm placement is visualization of the endotracheal tube passing through the vocal cords, although this relies on the subjective impression of the operator and is not infallible. Other useful but nonspecific methods include auscultation of breath sounds in both lung fields, and visualization of both rise and fall of the chest and endotracheal tube condensation with exhalation. The standard confirmatory method for RSI is detection of exhaled carbon dioxide, through use of capnography or colorimetric end-tidal devices, which change from purple to yellow in the presence of exhaled carbon dioxide.36 The two primary clinical circumstances that may render the colorimetric device inaccurate include false-positive detection after esophageal intubation when sufficient carbon dioxide is present in the esophagus and false-negative detection during cardiac arrest with undetectable levels of tracheal carbon dioxide. If color change is not noted within two to three breaths, improper placement is likely and the endotracheal tube should be replaced.

■ Complications and Outcomes after Rapid Sequence Intubation Success rates for RSI are well established, and a recent international study including a database with over 10,000 intubations noted a success rate exceeding 97% for trauma patients.37 However, complications do occur. Sedative and paralytic agents utilized in RSI place injured patients at risk for cardiovascular collapse, diminution of respiratory effort, pulmonary aspiration, and abrupt loss of airway. The primary complication of

ALTERNATIVES AND ADJUNCTS TO ENDOTRACHEAL INTUBATION ■ Nasotracheal Intubation

■ Retrograde Intubation First described by Butler and Cirillo in 1960 as an alternative to conducting unplanned preoperative tracheostomies,38

Airway Management

175

■ Gum Elastic Bougie

retrograde endotracheal intubation (REI) represents another potential adjunctive airway rescue procedure. Conceptually REI involves needle cannulation of the trachea through the cricothyroid membrane, with passage of a flexible guide wire or epidural catheter into the oropharynx (Fig. 11-2). If a catheter is utilized, it can be affixed to the Murphy’s eye of an endotracheal tube, which is pulled in an anterograde fashion into the trachea. When the ET tube is at the cricothyroid membrane, the catheter is cut flush with the skin and removed. More commonly, an ET tube is passed over a flexible guide wire or obturator into the trachea, with the wire removed by transection at the skin and withdrawal through the oropharynx. Current commercial kits include a large-bore needle, a flexible guide wire, and a thicker flexible obturator to guide passage of the ET tube. The cited mean time to intubation utilizing REI has been reported to be from approximately 1 minute in simulators39 and cadavers40 to approximately 3–5 minutes in actual patient scenarios.41,42 A recent retrospective review of REI over an 8-year period at a Level I trauma center documented use of the technique in only eight patients (0.5% of intubations), with success and complication rates of 50% and 38%, respectively.42

■ Esophageal Tracheal Combitube (ETC) The ETC is a relatively new device that is primarily used as a rescue airway in the prehospital arena. Although inserted as a single tube, it is essentially a two-tube system with a divider in the distal tube. The device has two balloons: one proximal to occlude the oropharynx and a second balloon distally to occlude either the esophagus or trachea depending on into which structure the device is placed (Fig. 11-3). The ETC is inserted blindly and commonly is inserted into the esophagus. Both balloons are inflated. The longer, blue tube is ventilated first. If sounds are auscultated in the chest and there are no sounds auscultated over the epigastrium, the ETC is in the esophagus and ventilation should continue through the blue tube. If sounds are heard in the epigastrium, this suggests that the ETC is in the trachea. Ventilation should then be changed to the clear, shorter tube, while not changing the position of the ETC. Indications for its use include the following: 1. Immediate intubation cannot be performed 2. Unsuccessful endotracheal intubation in a patient requiring an airway 3. The patient may be entrapped and access to the patient’s head is poor 4. Direct visualization of the larynx cannot be obtained due to secretions Contraindications for ETC use include age less than 16 years and height less than 5 ft. Potential advantages include its ease in insertion, the ability to ventilate through either tube, no requirement of visualization during insertion, and prevention of aspiration with inflation of the proximal balloon. Disadvantages to ETC use include: endotracheal intubation becomes more difficult as the ETC obscures the trachea, the trachea cannot be directly

CHAPTER 11

FIGURE 11-2 Retrograde intubation. An epidural size 17 Tuohy needle is inserted through the cricothyroid membrane as close to the upper border of the cricoid cartilage as possible and angled cephalad (A). An epidural catheter (B) is advanced through the vocal cords into the oropharynx and pulled out of the mouth. The epidural needle is withdrawn, and the catheter is tied to the Murphy’s eye of a size ID 7- to 8-mm endotracheal tube (C), which is then pulled thorough the vocal cords. Once through or at the vocal cords, the endotracheal tube is pushed into the trachea, and once in position, the epidural catheter can be cut at the skin. Modifications include threading the endotracheal tube or a tube changer over the catheter or a J wire, and railroading the endotracheal tube into the trachea; or feeding the distal end of a J wire through the suction port of a bronchoscope over which an endotracheal tube has been loaded.

The GEB or Eschmann stylet is a semirigid, malleable endotracheal tube introducer that has been used for airway emergencies in a variety of settings. The 60-cm bougie, which has a diameter of 5 mm, is angled at 40°, 3.5 cm from the distal end. During difficult laryngoscopy, when the vocal cords are not well visualized, the GEB is advanced to the level of the epiglottis, with the angled portion directed anteriorly. With further advancement, the tube may enter the trachea, and if successful, a “washboard” effect is palpated, as the bougie tip passes over tracheal rings. An ETT can then be passed over the GEB into the trachea. If a smooth unobstructed course is encountered, and the GEB passes greater than 40–45 cm, a presumed esophageal intubation has occurred. In a prospective blinded trial in 20 human cadavers, the accuracy of tracheal ring “clicks” for tracheal intubation was assessed.43 Overall, 93% of tracheal placements were correctly identified, with ring clicks being 95% sensitive for tracheal intubation. In a recent review of 1,442 prehospital intubations, the GEB was utilized in 41 patients.44 Of the 3% requiring GEB use, intubation was successful in 33 cases (78%).

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SECTION 2 A

B FIGURE 11-3 (A) Lateral photograph of the combitube double-lumen tube. (B) The combitube in place for emergency airway control. The tube is inserted blindly by lifting the jaw and tongue upward until the two printed rings (R) are at the teeth. The tip of the tube usually enters the esophagus. The pharyngeal cuff (P) is inflated with 100 mL of air and, when correctly placed, seals off the nasopharynx and oral cavity. The distal cuff (E) is inflated with 15 mL of air. Ventilation through the longer (blue) connecting tube (L) will inflate the lungs via the eight side holes in the pharyngeal portion of the combitube (as illustrated). If no breath sounds are heard, ventilation is attempted through the other lumen (the shorter tube) as the distal tube and cuff (E) has probably entered the larynx.

Airway Management suctioned with the ETC in place, and it cannot be used in the conscious patient with a gag reflex.

Laryngeal Mask Airway The laryngeal mask airway (LMA North America, Inc, San Diego) was introduced over 20 years ago by Dr Archie Brain,45 and has evolved into a viable temporizing rescue maneuver for the difficult airway. The LMA Classic™ consists of a flexible tube attached to an inflatable cuff that is passed into the hypopharynx and advanced over the larynx (Fig. 11-4). When the cuff is inflated, a seal is created around the glottic aperture, permitting selective ventilation of the trachea. Since introduction of the LMA, a number of incarnations have ensued, each with theorized situation-specific advantages. The LMA may be utilized in the difficult airway during resuscitation in an unconscious patient, when intubation skills are lacking or intubation has been unsuccessful. Accordingly, the primary clinical indications for use of the LMA include: airway rescue and maintenance in an “unable to intubate, able to ventilate” situation, and as a firstline adjunct in an “unable to intubate, unable to ventilate” situation. Under the latter condition, LMA placement should proceed while preparations for cricothyroidotomy are underway. Under such conditions, the LMA may offer temporizing delivery of supplemental oxygen and assist ventilation. The Classic™ LMA has been successfully placed as an airway adjunct by prehospital personnel,46 Navy SEAL corpsmen under fire,47 emergency medicine physicians, and trauma surgeons. Placement of an LMA does not constitute a definitive airway. Contraindications to the use of an LMA exist, and complications have been reported. Use of the LMA should never delay cricothyroidotomy when need and expertise exist. The LMA is contraindicated in patients who are not obtunded or deeply sedated, as irritation of the airway may exacerbate cervical spine injury and intracranial hypertension. Under conditions of severe craniofacial or pharyngeal trauma, care should be taken not to worsen injury. Leakage from around the cuff may occur in patients with fixed reductions in pulmonary compliance secondary to thoracic injury. Reported complications include aspiration; although the LMA may prevent aspiration of secretions or blood secondary to nasopharyngeal trauma, it does not effectively separate the respiratory and alimentary tracts.48

Laryngeal Tube Airway The laryngeal tube airway (LTA), a relatively new supralaryngeal device, is a variation on the form and function of the combitube, although it is reported to exhibit substantially less resistance on insertion. The LTA is primarily intended as an emergency airway device.49 It is a single-lumen silicon tube with low-pressure oropharyngeal and esophageal cuffs, with the esophageal cuff terminating in a rounded tip. Between the two cuffs lies a ventilation outlet for selective ventilation of the

Video Laryngoscopy The morbidity and mortality associated with the difficult airway, compounded by potential litigation and the burgeoning epidemic of obesity, have fostered rapid growth in video laryngoscopy. A myriad of devices are now available, including the Truphatek Truview EVO2®, Pentax Airway Scope®, GlideScope®, Airway Scope®, and AirTraq Laryngoscope®. All devices have a rigid blade for laryngoscopy combined with videoscopic visualization of the anatomy in proximity to the end of the blade. The visual field is located through an eyepiece in proximity to the blade handle or on a separate portable monitor. The technology provides direct visualization of the glottic opening, facilitating intubation. Video laryngoscopes are being utilized in essentially any scenario in which a difficult airway may be encountered, including the emergency department, operating room, and intensive care unit. Application in the prehospital environment has been limited by financial constraints, lack of comparative data, and need for provider training. In comparisons of the effectiveness of video and conventional laryngoscopy, visualization of the glottis appears to be superior using video devices, but data regarding speed and efficacy of intubation are conflicting.

Cricothyroidotomy In this era of constantly evolving gadgetry, the surgical airway remains the mainstay for rapid control of the difficult airway. Cricothyroidotomy is an ancient procedure that, despite having undergone a myriad of incarnations in the past two decades, remains an effective method to secure a compromised airway. Multiple reviews of surgical cricothyroidotomy in recent years have redemonstrated a success rate of greater than 90% at obtaining an airway,51–53 including performance by prehospital providers.53 Cricothyroidotomy may be performed as the first airway control maneuver in cases of craniofacial trauma precluding oral or NTI; however, it is more commonly utilized after translaryngeal intubation attempts have failed. The greatest impediment to cricothyroidotomy is the recognition that it is necessary and subsequent performance of the procedure. Acute complications include procedure failure, pneumothorax, hemorrhage, and misplaced tube, while late complications

CHAPTER 11

■ Supralaryngeal Airways

trachea. Four variations of the LTA now exist, with addition of distal suction capabilities representing the primary design development. Literature assessing the role of the LTA in trauma patients and the emergent airway is limited. Due to the positive attributes demonstrated in the scant literature to date, the LTA warrants study in the emergent, difficult airway, particularly in comparison to the combitube. A variation of the LTA is the King LT®, approved for use in 2003, which is being utilized with increasing frequency by prehospital providers. In comparisons between the King LT® and the combitube, prehospital providers tested under conditions of simulated emergent airway placed the King LT equally effectively and significantly faster than the combitube.50

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SECTION 2 A

B FIGURE 11-4 (A) Anterior and lateral photograph of the Brain laryngeal mask airway (LMA). (B) The LMA in position. The LMA is inserted blindly with the cuff deflated or partly inflated over the tongue and pushed as far as it will go. The cuff is inflated with 20–30 mL of air. When correctly placed, the cuff lies in the pharynx, its tip obstructing the upper esophageal lumen, and the mask interposed between the base of the tongue and the posterior pharyngeal wall to open the airway. Patients can breathe spontaneously through it (when it is used to reduce upper airway obstruction) or can be ventilated via the LMA if apneic.

Airway Management cricothyroid membrane is punctured with a needle, a flexible guide wire is passed, and a tracheostomy tube is passed over a dilator. Alternatively, other kits utilize a tracheostomy tube placed over a puncture device without the intervening placement of a guide wire.

Technique of Cricothyroidotomy

Percutaneous needle cricothyroidotomy with transtracheal jet ventilation is an alternative to surgical cricothyroidotomy. The neck should be rapidly sterilized and the skin anesthetized. The cricothyroid cartilage and membrane are identified. A 14- to 16-gauge catheter is attached to a syringe half-filled with saline. The cricothyroid membrane is cannulated in an inferior and caudal direction, at an angle of 30–60° from the trachea. The trachea is aspirated, with position confirmed by bubbles in the saline. The needle is removed, and the catheter is attached to a jet ventilation system using a Luer lock. Alternatively, a 5-mL syringe can be cut and attached directly to oxygen tubing or the tubing can be wedged into the open end of the syringe, and connected to high-flow 100% oxygen. An alternative method is to attach a 3-cm3 syringe to a 14-gauge catheter with an endotracheal tube adapter inserted into the open end of the syringe (Fig. 11-5). This technique allows direct attachment of the BVM to the syringe. Whatever system is utilized, an aperture should be created such that when occluded, jet insufflation occurs, and when open, flow may escape. Jet insufflation should proceed at approximately 1 second of flow (inspiration) for every 3 seconds of release (expiration). Because ventilation is not actually occurring, alveolar carbon dioxide rises. A point of emphasis is the temporizing nature of the procedure; life may be sustained for approximately 30 minutes until a definitive airway can be achieved.

Preparation for a difficult airway should include securing necessary equipment for cricothyroidotomy, and all difficult airway carts should include the necessary instruments. An evaluation of surface anatomy and sterile preparation of the neck may facilitate the procedure in the event of airway failure. The most important instrument for surgical cricothyroidotomy is a scalpel, with many procedures having been performed with little else. Additional instruments may include tissue forceps and a hemostat. Cuffed endotracheal tubes with internal diameters of 5.0–7.0 mm should be at the ready. The procedure is initiated under universal precautions with a rapid antiseptic preparation of the skin, followed by identification of the position of the cricothyroid membrane just superior to the cricoid cartilage. The trachea and larynx are then stabilized with the nondominant hand, with the thumb, index, and long fingers immobilizing the superior cornua of the larynx. A generous vertical incision is made over the membrane. The pretracheal tissue and fascia anterior to the membrane are rapidly divided with the scalpel, followed by a horizontal incision in the membrane. The index finger of the stabilizing hand may be utilized to palpate the membrane, guiding correct orientation of the incision. Many descriptions of the technique include insertion of the scalpel handle through the incised membrane to dilate the opening; however, given the conditions under which the procedure is typically performed, this technique may lead to inadvertent injury. The cricoid incision can be dilated with artery forceps, a hemostat, and a Trousseau dilator, or digitally. The index finger of the stabilizing hand should be used to maintain control of the cricoidotomy and guide tube insertion. Care should be taken to insert the endotracheal tube in a controlled fashion to a depth of approximately 5 cm. Insertion is facilitated by use of a rigid stylet; otherwise the tube may selectively pass retrograde toward the vocal cords. It should be emphasized that cricothyroidotomy is a poorly visualized or blind procedure in many instances. The obese neck may render superficial landmarks less than obvious, and transaction of anterior jugular vein branches or thyroid tissue can lead to significant and unnerving hemorrhage. The stabilizing hand on the larynx may prove invaluable under such circumstances, and should not be removed until the airway is secure. A number of commercial alternatives to traditional surgical cricothyroidotomy have been developed, in an attempt to expedite the procedure and reduce the degree of expertise required. The devices, cricothyrotomes, typically utilize one of two techniques to cannulate the trachea, depending on whether a Seldinger technique is utilized. For Seldinger-type kits, the

Needle Cricothyroidotomy

FIGURE 11-5 A photograph of a useful setup for needle cricothyroidotomy, consisting of a standard 8-mm diameter endotracheal tube adapter, a 3-cm3 syringe, and a 14-gauge angiocatheter. The endotracheal tube adapter is removed and inserted into the open end of the 3-cm3 syringe (plunger removed). The angiocatheter is affixed to the syringe. A bag valve mask is then able to be attached to the adapter, allowing easy ventilation of the patient.

CHAPTER 11

include tracheal stenosis. In a series of 122 patients undergoing emergency department cricothyroidotomy identified by the EAST workgroup, the complication rate was 28.7%.4 A single contraindication to cricothyroidotomy exists, young age. Traditional recommendations suggest needle cricothyroidotomy for children less than 12 years of age, although body size should be taken into account.

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AIRWAY CHALLENGES IN THE INJURED PATIENT ■ Maxillofacial Trauma SECTION 2

Craniofacial, maxillofacial, and tracheolaryngeal injuries commonly present with threatened airways. Direct injury to the facial soft tissues and bony skeleton, tongue, and larynx may cause intrinsic and extrinsic airway obstruction from edema, hemorrhage, secretions, or loss of bony architecture. In a recent large review of craniomaxillofacial trauma at a Level I trauma center, 16,465 patients sustained head, neck, or facial injuries over a 12-year period, many of which required advanced airway techniques or cricothyroidotomy.54 In a review of 92 maxillofacial civilian gunshot wounds, 22% presented with a threatened airway, 60% of which required an emergent surgical airway.55 Similarly, in a separate 4-year review of 84 maxillofacial gunshots, 21% required urgent tracheostomy.56 Although emergent surgical intervention is often required, many patients with severe bony and soft tissue injury are able to clear blood and secretions. If the cervical spine is cleared, slight forward positioning, suctioning, and calming of the patient frequently allow for forward displacement of a bilateral mandibular fracture or macerated soft tissue and maintenance of a patent airway. Close observation and transport to the operating room may optimize conditions for definitive airway procedures such as an awake tracheostomy or submental intubation. In the context of massive bony and soft tissue injury (Fig. 11-6), such as the catastrophic self-inflicted submental gunshot wound, an urgent need for definitive airway does not necessarily require a surgical airway. Despite the intimidating appearance of such injuries, many can be easily orotracheally intubated due to loss of restrictive anatomy.

■ Laryngotracheal Trauma The management of laryngotracheal injuries is based foremost on airway status. In the previously mentioned study of craniomaxillofacial trauma, 0.2% of patients with head, neck, or facial injuries over a 12-year period sustained laryngeal fractures, of which 97% sustained concomitant maxillofacial trauma.54 Seventy-four percent of laryngeal fractures required advanced airway maneuvers. In another report, 71 patients with laryngotracheal trauma were identified over an 8-year period.57 Of note, 73% of injuries were penetrating, but blunt mechanism was more likely to require an emergent airway (79% vs. 46%). Clues to the diagnosis of laryngotracheal injury include marked pain, tenderness and ecchymosis across the anterior neck or larynx, hoarseness or stridor, or the presence of subcutaneous emphysema. Subcutaneous emphysema or crepitance is the chief clinical sign. In a review of 19 patients presenting to a Level I trauma center with upper aerodigestive tract injury, 100% had radiographic evidence of subcutaneous emphysema or palpable crepitance, 21% had dysphagia, and 63% had stridor or hoarseness.58 Treatment options for this constellation of injuries include fiber-optic techniques, OTI, and surgical airway. In patients who are oxygenating, ventilating, and protecting their airway, in which clinical suspicion of tracheolaryngeal injury is present, the procedures of choice are fiber-optic laryngoscopy or bronchoscopy to assess airway integrity under controlled conditions, with performance of a surgical airway if necessary. If tracheolaryngeal injury is visualized, an attempt at endotracheal tube passage over the scope may ensue. Under urgent conditions, unless obvious tracheal or laryngeal disruption is evident, OTI remains the procedure of choice. However, if resistance is met, intubation should be aborted, and a surgical airway performed, corresponding to the suspected level of injury. Temporizing supralaryngeal devices should be avoided in this circumstance, as the potential for worsening subcutaneous emphysema and distortion of anatomy exists. For open wounds in which a tracheal injury is visualized, the trachea may be cannulated directly, with conversion to OTI under controlled conditions.

■ Cervical Spine Trauma

FIGURE 11-6 Despite the extreme destructive nature of the maxillofacial injury, orotracheal intubation is the first method to secure a definitive airway. If orotracheal intubation fails and hypoxia ensues, cricothyroidotomy should be performed inferior to the tissue destruction. If the patient is able to oxygenate, an urgent yet controlled tracheostomy in the operating room is an alternative.

The critical need to immobilize the cervical spine in virtually all blunt trauma patients is a significant additive element in the difficulty of airway management following injury. Fear of spinal cord injury by cervical manipulation during laryngoscopy led to the purely theoretical practice of blind NTI for all multisystem blunt trauma patients. Accumulating evidence suggests that OTI, with strict cervical spine stabilization, is safe as a standard of care. A number of studies in the past decade have assessed the effects of various intubation techniques on cervical spine motion. The majority has utilized fluoroscopic images, in cadavers or in the controlled setting of the operating room.59,60 Nearly all studies compare cervical motion incurred during direct laryngoscopy with a Macintosh blade and techniques that utilize either fiber-optic laryngoscopy or devices to

Airway Management

■ Thermal Trauma Multiple scenarios in thermal injury may precipitate airway compromise. Airway edema with obstruction can be multifactorial following thermal injury, and, alone or in combination, may include: major nonfacial burns with shock with requisite large-volume crystalloid resuscitation, circumferential thoracic burns, direct thermal or caustic injury to the lips, tongue, or pharynx, and inhalational injury. The Advanced Burn Life Support course, similar to ATLS, emphasizes the primacy of airway in thermal and inhalational injury.1 The incidence of smoke inhalation, the most common inhalational injury, is approximately 20% in all patients admitted to Level I burn centers and in isolation carries a 5–8% mortality rate.61 Inhalational injury can affect any of three distinct areas of the respiratory tract, including supraglottic, tracheobronchial, and pulmonary parenchymal regions. Inhalation injury is defined as aspiration of superheated gases, steam, hot liquids, or noxious products of incomplete combustion. Inhalational injury causes a number of pulmonary physiologic derangements that ultimately lead to acute respiratory failure. The injuries evolve over time and parenchymal lung dysfunction is often minimal for 24–72 hours. Normal oxygenation and chest radiographs do not exclude the diagnosis.62 Because the etiology of early death from smoke inhalation is most commonly airway compromise, a high clinical index of suspicion is integral to survivability. Recent consensus recommendations from the American Burn Association (ABA) state: “Inhalation injury is suspected in the presence of one or more specific points of history (closed space exposure to hot gasses, steam or products of combustion), physical examination (singed vibrissae and carbonaceous sputum), or laboratory findings (elevated carboxyhemoglobin or cyanide level).”62 Inhalation injury alone is an ABA criterion for transfer to a burn center. Because the onset of symptoms from inhalational injury is variable and frequently insidious, significant clinical suspicion should prompt establishment of a definitive airway prior to transfer. Currently, bronchoscopic examination is the standard definitive diagnostic measure,62 assessing for the presence of carbonaceous debris and mucosal erythema or

ulceration. Although intubation alone is fraught with both early and late sequelae, a window of opportunity may exist for controlled intubation. Subsequent airway edema and rapid pulmonary deterioration can convert a controlled situation into an emergent, difficult airway at an inopportune time during transport. If clinical suspicion is significant or bronchoscopy suggests an inhalational component, clinicians should err on the side of intubation. The EAST Management Guidelines Workgroup completed an extensive review of the literature evaluating the need for intubation following inhalational injury. The committee identified airway obstruction, severe cognitive impairment (Glasgow Coma Scale score 8), cutaneous burn exceeding 40% total body surface area, prolonged transport time, and impending airway obstruction (due to moderate to severe facial burn, oropharyngeal burn, and airway injury visualized on endoscopy) as indications for intubation.4 Due to efficient cooling capabilities of the upper respiratory tract, thermal injury is usually confined to the upper airways, unless smoke with high water content or steam is inhaled.63 Significant oropharyngeal or facial burns with mucosal edema do not preclude oral intubation. Attempts at laryngoscopy are warranted, although failure of OTI should prompt rapid transition to surgical airway. Circumferential third-degree burns of the chest may impair oxygenation and ventilation secondary to reductions in chest wall compliance, pulmonary static compliance, and increased intra-abdominal pressure.64 Under these circumstances, it is imperative for clinicians to address the airway definitively with endotracheal intubation or rescue maneuvers, and to concurrently address the need for chest wall escharotomy as expeditiously as possible.

■ Closed Head Injury Perhaps no injury imparts more importance on precise airway management than CHI. Injury to the brain is the most common, single indication for a definitive airway in blunt trauma. Initial goals focus on airway protection and maintenance, while sustained goals focus on secondary brain injury prevention through optimization of oxygenation and regulation of carbon dioxide. Airway management is particularly challenging in head-injured patients with potential for intracranial hypertension. It is well recognized that hypoxia, even a single episode, has deleterious effects on outcome, and uncontrolled hyperventilation, with resultant cerebral vasoconstriction, may worsen outcome as well.65 The Brain Trauma Foundation guidelines state that hypoxia, defined as apnea, cyanosis, oxygen saturations 90%, or partial pressure of arterial oxygen 60 mm Hg, must be scrupulously avoided.66 In addition to prevention of hypoxia, the avoidance of hypercarbia is of critical importance. Hypercarbia results in cerebral vasodilatation, increasing intracranial blood volume, with resultant elevated intracranial pressure. Early definitive airway control is theoretically appealing, and the recommendation that Glasgow Coma Score 8 prompt intubation remains in the Advanced Trauma Life Support course.1 RSI may help to eliminate prolonged awake intubation attempts and therefore the risk of hypercarbia.

CHAPTER 11

facilitate blind intubation. To summarize findings to date, direct laryngoscopy produces more extension at all levels of the cervical spine than fluoroscopic and videoscopic techniques and the intubating LMA.59,60 However, nearly all techniques are significantly more time consuming than direct laryngoscopy, and the degree of extension, depending on the cervical level, ranges from 3.5° to 22.5°.60 If sufficient time, equipment, and expertise exist, alternative techniques to direct laryngoscopy may be considered, particularly with the intubating LMA, which has been reasonably well studied in the prehospital environment. However, given the emergent nature of most field and emergency department intubations and constraints of equipment and expertise, combined with the small degree of extension with proper cervical stabilization during direct laryngoscopy, the tried and true method of airway control in the injured patient remains RSI using direct laryngoscopy.

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SECTION 2

Despite the intuitive belief that early intubation may prevent hypoxia or extremes of ventilation, data assessing prehospital intubation in CHI are conflicting. In two recent studies, prehospital use of RSI by paramedics was shown to correlate with poor functional outcome and death in head-injured patients.67,68 Conversely, other recent studies have demonstrated outcome benefit in traumatic brain injury patients undergoing RSI, particularly when neuromuscular blocking agents are utilized.69 In a recent swine model evaluating the effects of various RSI regimens on intracranial pressure, those utilizing paralytic agents produced 3-fold increases in peak intracranial pressure compared to regimens using sedation only.70 The association between RSI and mortality may have little to do with the procedure itself; rather, preintubation hypoxia, and postintubation hyperventilation, may represent the mortality causation. In a study of 291 CHI patients, 144 patients underwent continuous ETCO2 measurement.71 Patients with ETCO2 monitoring had a lower incidence of inadvertent severe hyperventilation (defined as partial pressure carbon dioxide 25 mm Hg), and patients with severe hyperventilation had significantly higher mortality than those without hyperventilation.71 In further work from the San Diego Paramedic RSI trial, 79% of patients were documented to have ETCO2 values less than 30 mm Hg during RSI or transport, and 59% of patients had levels less than 25 mm Hg.72 In a study assessing the frequency of hypoxia (defined as oxygen saturation measured by oximetry 90%) during paramedic RSI, 57% of patients demonstrated hypoxia lasting a median duration of 160 seconds.73 The median decrease in oxygen saturation was 22%. In summary, RSI should be undertaken with strict attention to preoxygenation and rate of postintubation ventilation in CHI.

THE PEDIATRIC AIRWAY Airway management in the critically ill and injured child presents a number of unique challenges rendering emergent management less successful by clinicians primarily trained in the adult airway.74 In general, airway management principles for the pediatric population are similar to the adult population, although anatomy, physiology, and pharmacology may differ.

■ Anatomy The pediatric cranium comprises a larger relative percentage of body surface and mass, flexing the cervical spine in the supine position, and emphasizing the requirement for cervical stabilization. Internal airway differences at laryngoscopy that have the potential to render the pediatric airway challenging include a larger amount of distensible soft tissue. Children may have significant tonsilar and adenoid tissue as well as a large tongue that collapses into the posterior pharynx, each having the potential to obstruct laryngoscopy and hemorrhage with instrumentation. Compounded by the fact that the glottic opening of the trachea is at the level of C-1 in infancy, and the larynx is more anterior with decreasing age, the angle between the laryngeal orifice and the glottic opening is more acute. Other anatomic variations from adults include a narrower

cricoid ring, narrower and shorter trachea, and smaller cricothyroid membrane. As a rule, children less than 2 years of age have high anterior airways while children greater than 8 years of age approximate adult alignment. Children aged 2–8 have transitional airways with less consistency among individuals.

■ Physiology More rapid onset of hypoxemia in children is related to higher basal oxygen consumption, 6–8 mL/(kg min) in infants versus 3–4 mL/(kg min) in adults. Increased susceptibility to hypoxemia leads to a higher percentage of cardiac arrest due to airway compromise than in the adult population. The higher metabolic rate, compounded by reduced cardiovascular tolerance to hypoxia, accentuates the urgency of airway maintenance necessary in hemorrhagic, obstructive, or neurogenic shock. In addition, rapid desaturation in children is coupled to a relative reduction in functional residual capacity.

■ Equipment Anatomic and physiologic attributes of children mandate alterations in airway equipment and drug preparation, as well as anticipated algorithms for management of the difficult airway. The Broselow™ Pediatric Emergency Tape, although intended as a guide only, is an excellent airway resource for clinicians unfamiliar with standard sizes and doses. The tape includes length-based estimates of kilogram body weight, with corresponding recommendations for drug dosing and equipment sizing. The tape includes recommendations for size of endotracheal tube, insertion length, stylet, suction catheter, laryngoscope, BVM, ETCO2 detector, as well as oral airways, NPAs, and LMAs. The BVM apparatus should be selected with attention to size of face mask, proper seal, and delivered tidal volume. Although pop-off valves set at 35–45 cm H2O are often recommended, a higher generated airway pressure may be required to ventilate the injured child, and air may escape from the valve unrecognized. Circular masks often provide a better seal in infants and children. Endotracheal tube internal diameter may based on the Broselow™ tape or formulas, including age/4  4, or (16  age)/4. Uncuffed endotracheal tubes are recommended in younger children, with cuffed tubes employed for children requiring a 5.5-mm internal diameter or greater. Given the short tracheal length in children, right mainstem intubation is a potential complication following endotracheal intubation. In addition to Broselow™ tape recommendations, depth of insertion may be calculated as the internal diameter of the tube multiplied by 3. An NPA is selected based on the approximate distance from the tip of the nose to the angle of the tragus. The size of ETCO2 measurement also differs with use in children. The pediatric model should be used for children weighing less than 15 kg.

■ Technique Although all clinicians caring for the injured should be facile with the pediatric airway, it is frequently difficult to recall

Airway Management

EMERGENCY AIRWAY ALGORITHMS Airway algorithms provide a reproducible structural framework for recognition and response, guiding management under complex and stressful situations. Once the need for definitive airway protection has been identified, a concise and logical approach to airway control, based on situational and patient characteristics, is imperative.

■ Definitions The failed airway and the difficult airway are distinct. The two entities are not unrelated; the difficult airway frequently leads to the failed airway. To negotiate the sequence of both the failed and difficult airways, an understanding of current definitions is necessary. A failed airway is defined as any clinical scenario in which a patient is unable to oxygenate or ventilate. A failed airway may exist on presentation secondary to a disease process, or after a clinician has initiated any one of a number of airway interventions that have failed to maintain oxygenation or ventilation The difficult airway refers to any preintubation characteristics, related to injury type or pattern, physiology, anatomy, comorbidities, or skills of the practitioner that predict difficulty with the standard OTI algorithm. In the emergent situation, scant time may be available to plan or enact alternatives to OTI, such as an awake technique or NTI. Alternatively, an identified difficult airway may be followed by an uneventful progression through standard RSI technique. In summary, the difficult airway does not always portend a failed airway, nor does the failed airway universally arise from a predicted difficult

airway. In the words of one author, “The difficult airway is something one anticipates, the failed airway is something one experiences.”15

■ Decision Making in the Failed Airway When airway control is required, the first assessment relates to the urgency of the airway: determination of airway failure. Patients who are apneic, in extremis, or manifest inability to protect the airway with resultant oxygenation and ventilation failure represent airway failure. The first step in airway failure is BVM ventilation while rapid preparations for tracheal intubation are made (Fig. 11-7). Further management steps are based on success of BVM.

Airway Failure: Bag-Valve-Mask Ventilation, SpO2 .90% The effectiveness of BVM ventilation determines the progression to either OTI or urgent surgical intervention. If BVM results in successful oxygenation and ventilation, OTI should be attempted. If OTI is unsuccessful, further treatment always depends on the ability to oxygenate and ventilate the patient with BVM. If at any point the patient cannot be ventilated or desaturates, an emergent surgical airway should be undertaken. Following an initial failure of OTI, an assessment of reasons for failure should quickly follow. If paralysis is deemed beneficial based on the status of facial musculature on the first attempt at OTI, succinylcholine should be administered followed by a repeat attempt at OTI. If a second failure occurs, a third attempt should only occur if BVM remains effective and a more experienced clinician is available. If a third failure at OTI occurs, two options exist. First, a surgical airway is always acceptable after three OTI failures, and should be the mainstay for a definitive airway at this juncture. If surgical expertise is unavailable, alternative methods of tracheal intubation such as retrograde intubation or the intubating LMA may be considered provided BVM ventilation remains effective. If alternatives fail, temporizing measures to maintain oxygenation and ventilation, including ETC and supralaryngeal airways, should be utilized until surgical expertise is available.

Airway Failure: Bag-Valve-Mask Ventilation, SpO2 ,90% The foundation of this scenario is rapid transition to definitive surgical airway (Fig. 11-7). If SpO2 cannot be maintained 90% using BVM, emergent transition to a rapid single attempt at OTI or a surgical airway should be undertaken. The decision at this point should be based on available equipment and expertise. If a surgical airway is possible, delay for even a single attempt at tracheal intubation may be lethal. The decision to attempt tracheal intubation should be predicated on anticipated ease of placement and lack of surgical expertise. If OTI fails and a surgical airway is not possible, alternative methods of tracheal intubation should be avoided, with progression to attempts at temporizing measures to oxygenate and ventilate.

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specific differences in airway drug doses. Again, the Broselow™ tape may be invaluable when determining appropriate dosing. During RSI, defasciculating doses of nondepolarizing neuromuscular blocking agents are not recommended for children less than 20 kg body weight. In addition, it is imperative to remember that children have a higher percentage of extracellular volume than adults, requiring higher dose of succinylcholine (2 mg/kg). Finally, due to the potential for reflex bradycardia during RSI, all children when receiving succinylcholine and children less than 5 years of age undergoing any form of airway manipulation should receive atropine, although atropine does not always abrogate bradycardia.75 Given the unique impact of hypoxia on pediatric physiology, failure to gain definitive control of the airway can be catastrophic. Conversely, the decision to intubate has unique ramifications in children. BVM offers an excellent means to oxygenate and ventilate children. When definitive airway control is necessary, RSI is the technique of choice for definitive control of the pediatric airway, and is now recommended by pediatric life support courses. Surgical cricothyroidotomy is considered a contraindication in infants76 and small children, due to the size of the cricothyroid membrane, although data are limited. For children less than 8–10 years, needle cricothyroidotomy should be utilized, although limited data exist regarding the efficacy of this technique.

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Airway Control Necessary

SECTION 2

Emergent Failed Airway?

SpO2 < 90%?

Bag-Valve-Mask Ventilation

SpO2 > 90%?

Orotracheal Intubation

Surgical Airway

Failure

Three Failures?

Repeat Orotracheal Intubation with Succinycholine

Adjuncts Supralaryngeal Devices Combitube Retrograde Intubation

FIGURE 11-7 Algorithm for the failed airway.

Spontaneous Respirations A number of trauma patients may be alert, breathing spontaneously, yet not adequately oxygenating or ventilating, therefore representing a failed airway. Under these circumstances, vigorous BVM should be avoided, with supplemental oxygen applied to spontaneous breaths. The patient should be assessed for injuries potentially not requiring intubation, such as pneumothorax, with oxygen administered in the highest concentration possible. Emergent RSI should follow. If unable

to intubate, a surgical airway should be undertaken. In the event that surgical airway is not possible, temporizing alternatives, including supralaryngeal airway or ETC, should be considered.

■ The Difficult Airway For patients who have need for definitive airway but do not present with airway failure, time permits for assessment of, and preparation for, a potentially difficult airway (Fig. 11-8).

Airway Management

185

Airway Control Necessary

CHAPTER 11

Emergent Airway Failure Absent

Preparation

Difficult Airway?

Rapid Sequence Intubation

Laryngoscopy with Sedation Only

Orotracheal Intubation

Desaturation < 90% with Bag-Valve-Mask Ventilation at Any Time During Sequence?

Failure?

Rapid Sequence Intubation

Failure?

Bag-Valve-Mask SpO2 > 90%?

Bag-Valve-Mask SpO2 < 90%?

Fiberoptic or Other Adjunctive Techniques

Failed Airway

FIGURE 11-8 Algorithm for the difficult airway.

The most commonly used predictive scheme used in anesthesiology is the Mallampati airway classification system. The degree of airway difficulty is based on the ability to visualize the structures of the oropharynx, and the tongue’s ability to obscure the oropharynx is a predictor of the difficulty to establish an airway. The “Rule of Threes” was developed to combine the physical characteristics of mouth

opening, jaw size, and mandible size (thyromental distance) as a predictor of a difficult airway at the bedside. If three provider finger breaths can be placed between the following distances: the patient’s upper and lower teeth, the hyoid bone and the chin, and the thyroid cartilage and the sternal notch, the provider has a higher success rate in direct laryngoscopy.

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Equipment and Technique for the Difficult Airway

SECTION 2

In a survey of emergency medicine program directors regarding airway adjunct availability, the frequency of various adjuncts was reported and included: cricothyroidotomy kits (95%), fiber-optic scopes (76%), bougies (70%), LMAs (66%), intubating LMAs (61%), lighted stylets (54%), retrograde intubation kits (49%), combitube (46%), and esophageal obturator airways (15%). Despite the preparedness, 94% of airways consisted of OTI.77 Although difficult airway criteria are common, the majority of difficult airways are managed with RSI, with a low incidence of complications. Therefore, anticipation of a difficult airway, with preparation for alternatives to OTI, is critical. The step in RSI that may prompt airway failure is paralysis. Therefore, the single deviation from a standard RSI approach is laryngoscopy without paralysis (Fig. 11-8). In patients not meeting airway failure criteria, the pharynx and trachea can be topically anesthetized followed by administration of a short-acting sedative. Sedation alone may be sufficient to allow endotracheal intubation. In addition, the process may identify the airway as amenable to RSI with paralysis. If RSI fails to secure the difficult airway, management proceeds according to a failed airway (Fig. 11-7).

COMPLICATIONS ASSOCIATED WITH THE EMERGENCY AIRWAY Complications associated with emergency airway management are multiple and common, conferring significant morbidity and mortality both during and subsequent to airway procedures. For RSI, morbidity increases concordant to number of attempts at laryngoscopy.78 The most common and ominous immediate complications are failure to intubate, failure to recognize esophageal intubation, and failure to ventilate. Pulmonary aspiration of gastric contents, an immediate complication, imparts both early and late morbidity, secondary to the potential for acute lung injury and pneumonia.

■ Failure to Intubate Failure to intubate is the most feared complication of emergent airway intervention, initiating the critical pathway of alternative means of oxygenation and ventilation. Published rates of intubation failure are as varied as the patient populations and environments from which they originate. The majority of recent series, evaluating a range of providers including paramedics, residents, and attending physicians, report emergent intubation failure rates of 2–13%.17,36 In a recent multicenter prospective trial, the endotracheal intubation success rate across providers for out-of-hospital intubation was 86.8%.17 Unrecognized misplaced intubation represents a potentially lethal subset of failed intubation. Rates of prehospital misplaced intubation, primarily esophageal, reported in the multiple studies evaluating this complication range from 0.4% to 25%, with most documenting rates of less than 10%.79

■ Esophageal Intubation Esophageal intubation, comprising a subset of intubation failure, can represent a minor or catastrophic complication, depending on time of recognition. Early recognition is facilitated by lack of appropriate color change on colorimetry, desaturation, lack of breath sounds over bilateral lung fields, and auscultation of inspired air over the epigastrium. Unrecognized esophageal intubation incidence ranges from 0% in small series to 10% in larger studies.80 When esophageal intubation is proven or suspected, it is imperative to rapidly remove the tube and reintubate.

■ Aspiration The untoward effects of aspiration range from obscuration of vocal cords during intubation to death secondary to failed intubation, chemical pneumonitis with acute respiratory distress syndrome, and pneumonia. Studies of emergent airway management have reported the incidence of aspiration to range from 1% to 20%, depending on the patient population and environment.81 The few early studies focusing on the prehospital setting have reported an aspiration incidence of 34–39%.82 A recent study, using pepsin assay of tracheal aspirates, identified an aspiration incidence of 22% for urgent intubations in the emergency department compared to 50% in the prehospital environment.81

■ Pneumonia Emergency intubation has been identified as a risk factor for pneumonia after trauma, likely related to pulmonary aspiration during the procedure. In a review of 99 cases of early onset ventilator-associated pneumonia (VAP), multivariate regression identified emergency intubation and aspiration as factors independently associated with multidrug-resistant infections.83 The incidence of pneumonia is significantly higher after a field versus emergency department airway,84 and has been independently associated with paramedic RSI.85

REFERENCES 1. Krantz BE. Advanced Trauma Life Support for Doctors. American College of Surgeons, Committee on Trauma, Advanced Trauma Life Support (ATLS) Course. 7th ed. Chicago, IL: American College of Surgeons; 2004. 2. Schade K, Borzotta A, Michaels A. Intracranial malposition of nasopharyngeal airway. J Trauma. 2000;49:967–968. 3. Levitan RM, Everett WW, Ochroch EA. Limitations of difficult airway prediction in patients intubated in the emergency department. Ann Emerg Med. 2004;44(4):307–313. 4. Dunham CM, Barraco RD, Clark DE, et al. Guidelines for emergency tracheal intubation immediately after traumatic injury. J Trauma. 2003; 55(1):162–179. 5. Kovacs G, Law JA, Ross J, et al. Acute airway management in the emergency department by non-anesthesiologists. Can J Anaesth. 2004; 51(2):174–180. 6. Bair AE, Filbin MR, Kulkarni RG, et al. The failed intubation attempt in the emergency department: analysis of prevalence, rescue techniques, and personnel. J Emerg Med. 2002;23:131–140. 7. Bernard S, Smith K, Foster S, et al. The use of rapid sequence intubation by ambulance paramedics for patients with severe head injury. Emerg Med. 2002;14:406–411.

Airway Management 34. Vachon CA, Warner DO, Bacon DR. Succinylcholine and the open globe. Tracing the teaching. Anesthesiology. 2003;99(1):220–223. 35. Olsen JC, Gurr DE, Hughes M. Video analysis of emergency residents performing rapid-sequence intubations. J Emerg Med. 2000;18(4): 469–472. 36. Bair AE, Smith D, Lichty L. Intubation confirmation techniques associated with unrecognized non-tracheal intubations by pre-hospital providers. J Emerg Med. 2005;28(4):403–407. 37. Sagarin MJ, Chiang V, Sakles JC, et al. Rapid sequence intubation for pediatric emergency airway management. Pediatr Emerg Care. 2002; 18(6):417–423. 38. Butler FS, Cirillo AA. Retrograde endotracheal intubation. Anesth Analg. 1960;39:333–338. 39. Van Stralen DW, Rogers M, Perkin RM, et al. Retrograde intubation training using a mannequin. Am J Emerg Med. 1995;13:50–52. 40. Stern Y, Spitzer T. Retrograde intubation of the trachea. J Laryngol Otol. 1991;105:746–747. 41. Barriot P, Riou B. Retrograde technique for tracheal intubation in trauma patients. Crit Care Med. 1988;16:712–713. 42. Gill M, Madden MJ, Green SM. Retrograde endotracheal intubation: an investigation of indications, complications, and patient outcomes. Am J Emerg Med. 2005;23(2):123–126. 43. Bair AE, Laurin EG, Schmitt BJ. An assessment of a tracheal tube introducer as an endotracheal tube placement confirmation device. Am J Emerg Med. 2005;23(6):754–758. 44. Jabre P, Combes X, Leroux B, et al. Use of gum elastic bougie for prehospital difficult intubation. Am J Emerg Med. 2005;23(4): 552–555. 45. Matioc AA, Wells JA. The LMA-Unique in a prehospital trauma patient: interaction with a semirigid cervical collar: a case report. J Trauma. 2002;52(1):162–164. 46. Martin SE, Ochsner MG, Jarman RH, et al. Use of the laryngeal mask airway in air transport when intubation fails. J Trauma. 1999;47: 352–357. 47. Calkins MD, Robinson TD. Combat trauma airway management: endotracheal intubation versus laryngeal mask airway versus combitube use by Navy SEAL and Reconnaissance combat corpsmen. J Trauma. 1999;46(5):927–932. 48. Butler KH, Clyne B. Management of the difficult airway: alternative airway techniques and adjuncts. Emerg Med Clin North Am. 2003;21(2):259–289. 49. Bein B, Scholz J. Supraglottic airway devices. Best Pract Res Clin Anaesthesiol. 2005;19(4):581–593. 50. Tumpach EA, Lutes M, Ford D, Lerner EB. The King LT versus the combitube: flight crew performance and preference. Prehosp Emerg Care. 2009;13(3):324–328. 51. Wright MJ, Greenberg DE, Hunt JP, et al. Surgical cricothyroidotomy in trauma patients. South Med J. 2003;96(5):465–467. 52. Salvino CK, Dries D, Gamelli R, et al. Emergency cricothyroidotomy in trauma victims. J Trauma. 1993;34(4):503–505. 53. Jacobson LE, Gomez GA, Sobieray RJ, et al. Surgical cricothyroidotomy in trauma patients: an analysis of its use by paramedics in the field. J Trauma. 1996;41(1):15–20. 54. Verschueren DS, Bell RB, Bagheri SC, et al. Management of laryngotracheal injuries associated with craniomaxillofacial trauma. J Oral Maxillofac Surg. 2006;64(2):203–214. 55. Tsakiris P, Cleaton-Jones PE, Lownie MA. Airway status in civilian maxillofacial gunshot injuries in Johannesburg, South Africa. S Afr Med J. 2002;92(10):803–806. 56. Hollier L, Grantcharova EP, Kattash M. Facial gunshot wounds: a 4-year experience. J Oral Maxillofac Surg. 2001;59(3):277–282. 57. Bhojani RA, Rosenbaum DH, Dikmen E, et al. Contemporary assessment of laryngotracheal trauma. J Thorac Cardiovasc Surg. 2005;130(2): 426–432. 58. Goudy SL, Miller FB, Bumpous JM. Neck crepitance: evaluation and management of suspected upper aerodigestive tract injury. Laryngoscope. 2002;112(5):791–795. 59. Turkstra TP, Craen RA, Pelz DM, et al. Cervical spine motion: a fluoroscopic comparison during intubation with lighted stylet, GlideScope, and Macintosh laryngoscope. Anesth Analg. 2005;101(3):910–915. 60. Sahin A, Salman MA, Erden IA, et al. Upper cervical vertebrae movement during intubating laryngeal mask, fibreoptic, and direct laryngoscopy: a video-fluoroscopic study. Eur J Anaesthesiol. 2004;21(10):819–823. 61. Rocker GM. Acute respiratory distress syndrome: different syndromes, different therapies? Crit Care Med. 2001;29:202–219. 62. American Burn Association. Inhalational injury: diagnosis. J Am Coll Surg. 2003;196(2):307–312.

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8. Zonies DH, Rotondo MF, Sing RF, et al. The safety of urgent paralysis and intubation (UPI) in the trauma admitting area (TAA): a review of 570 consecutive patients. J Trauma. 1998;44(2):431. 9. Rotondo MF, McGonigal MD, Schwab CW, et al. Urgent paralysis and intubation of trauma patients: is it safe? J Trauma. 1993;34(2): 242–246. 10. Reynolds SF, Heffner J. Airway management of the critically ill patient rapid-sequence intubation. Chest. 2005;127(4):1397–1412. 11. Smith CE, Kovach B, Polk JD, et al. Prehospital tracheal intubating conditions during rapid sequence intubation: rocuronium versus vecuronium. Air Med J. 2002;21(1):26–32. 12. Sing RF, Rotondo MF, Zonies DH, et al. Rapid sequence induction for intubation by an aeromedical transport team: a critical analysis. Am J Emerg Med. 1998;16(6):598–602. 13. Sagarin MJ, Barton ED, Chng YM. Airway management by US and Canadian emergency medicine residents: a multicenter analysis of more than 6,000 endotracheal intubation attempts. Ann Emerg Med. 2005; 46(4):328–336. 14. Dibble C, Maloba M. Best evidence topic report. Rapid sequence induction in the emergency department by emergency medicine personnel. Emerg Med J. 2006;23(1):62–64. 15. Walls RM. Rapid sequence intubation. In: Walls RM, Murphy MF, Luten RC, Schneider RE, eds. Manual of Emergency Airway Management. 2nd ed. Philadelphia: Lippincott, Williams and Wilkins; 2004:24–25. 16. Blanda M, Gallo U. Emergency airway management. Emerg Med Clin North Am. 2003;21:1–26. 17. Wang HE, Kupas DF, Paris PM, et al. Preliminary experience with a prospective, multi-centered evaluation of out-of-hospital endotracheal intubation. Resuscitation. 2003;58(1):49–58. 18. Tong JL, Ashworth DR, Smith JE. Cardiovascular responses following laryngoscopic assisted, fiberoptic orotracheal intubation. Anaesthesia. 2005;60(8):754–758. 19. Sivilotti ML, Ducharme J. Randomized, double-blind study on sedatives and hemodynamics during rapid-sequence intubation in the emergency department: the SHRED study. Ann Emerg Med. 1998;31:313–324. 20. Tagaito Y, Isono S, Nishino T. Upper airway reflexes during a combination of propofol and fentanyl anesthesia. Anesthesiology. 1998;88: 1433–1434. 21. Robinson N, Clancy M. In patients with head injury undergoing rapid sequence intubation, does pretreatment with intravenous lignocaine/ lidocaine lead to an improved neurologic outcome? A review of the literature. Emerg Med J. 2001;18:453–457. 22. Schreiber JW, Lysakowski C, Fuchs-Buder T, et al. Prevention of succinylcholine-induced fasciculation and myalgia: a meta-analysis of randomized trials. Anesthesiology. 2005;103(4):877–884. 23. Kindler CH, Schumacher PG, Schneider MC, et al. Effects of intravenous lidocaine and/or esmolol on hemodynamic responses to laryngoscopy and intubation: a double-blind, controlled trial. J Clin Anesth. 1996;8: 491–496. 24. Rodricks MB, Deutschman CS. Emergent airway management: indications and methods in the face of confounding conditions. Crit Care Clin. 2000;16(3):389–409. 25. Cohan P, Wang C, McArthur DL, et al. Acute secondary adrenal insufficiency after traumatic brain injury: a prospective study. Crit Care Med. 2005;33(10):2358–2366. 26. Jackson WL Jr. Should we use etomidate as an induction agent for endotracheal intubation in patients with septic shock? A critical appraisal. Chest. 2005;127(3):1031–1038. 27. Warner KJ, Cuschieri J, Jurkovich GJ, Bulger EM. Single-dose etomidate for rapid sequence intubation may impact outcome after severe injury. J Trauma. 2009;67(1):45–50. 28. Sivilotti ML, Filbin MR, Murray HE, et al. Does the sedative agent facilitate emergency rapid sequence intubation? Acad Emerg Med. 2003; 10:612–620. 29. Sonday CJ, Axelband J, Jacoby J, et al. Thiopental vs. etomidate for rapid sequence intubation in aeromedicine. Prehosp Disaster Med. 2005;20(5): 324–326. 30. Thompson JD, Fish S, Ruiz E. Succinylcholine for endotracheal intubation. Ann Emerg Med. 1982;11:526–529. 31. Bozeman WP, Kleiner DM, Huggett V. A comparison of rapid-sequence intubation and etomidate-only intubation in the prehospital air medical setting. Prehosp Emerg Care. 2006;10(1):8–13. 32. Davis DP, Ochs M, Hoyt DB, et al. Paramedic administered neuromuscular blockade improves prehospital intubation success in severely head-injured patients. J Trauma. 2003;54:444–453. 33. Naguib M, Samarkandi A, Riad W, et al. Optimal dose of succinylcholine revisited. Anesthesiology. 2003;99(5):1045–1049.

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63. Rabinowitz PM, Siegel MD. Acute inhalation injury. Clin Chest Med. 2003;23(4):707–715. 64. Tsoutsos D, Rodopoulou S, Keramidas E. Early escharotomy as a measure to reduce intraabdominal hypertension in full-thickness burns of the thoracic and abdominal area. World J Surg. 2003;27(12):1323–1328. 65. Davis DP, Dunford JV, Poste JC, et al. The impact of hypoxia and hyperventilation on outcome after paramedic rapid sequence intubation of severely head-injured patients. J Trauma. 2004;57(1):1–8. 66. Brain Trauma Foundation. Guidelines for Prehospital Management of Traumatic Brain Injury. Available at: http://www.braintrauma.org. Accessed January 2006. 67. Wang HE, Peitzman AB, Cassidy LD, et al. Out-of-hospital endotracheal intubation and outcome after traumatic brain injury. Ann Emerg Med. 2004;44(5):439–450. 68. Davis DP, Hoyt DB, Ochs M. The effect of paramedic rapid sequence intubation on outcome in patients with severe traumatic brain injury. J Trauma. 2003;54:444–453. 69. Bulger EM, Copass MK, Sabath DR, et al. The use of neuromuscular blocking agents to facilitate prehospital intubation does not impair outcome after traumatic brain injury. J Trauma. 2005;58(4): 718–723. 70. Bozeman WP, Idris AH. Intracranial pressure changes during rapid sequence intubation: a swine model. J Trauma. 2005;58(2):278–283. 71. Davis DP, Dunford JV, Ochs M, et al. The use of quantitative end-tidal capnometry to avoid inadvertent severe hyperventilation in patients with head injury after paramedic rapid sequence intubation. J Trauma. 2004;56(4):808–814. 72. Davis DP, Heister R, Poste JC, et al. Ventilation patterns in patients with severe traumatic brain injury following paramedic rapid sequence intubation. Neurocrit Care. 2005;2(2):165–171. 73. Dunford JV, Davis DP, Ochs M, et al. Incidence of transient hypoxia and pulse rate reactivity during paramedic rapid sequence intubation. Ann Emerg Med. 2003;42(6):721–728.

74. Orenstein JB. Prehospital pediatric airway management. CPEM. 2006;7(1):31–37. 75. Fastle RK, Roback MG. Pediatric rapid sequence intubation: incidence of reflex bradycardia and effects of pretreatment with atropine. Pediatr Emerg Care. 2004;20(10):651–655. 76. Navsa N, Tossel G, Boon JM. Dimensions of the neonatal cricothyroid membrane—how feasible is a surgical cricothyroidotomy? Paediatr Anaesth. 205;15(5):402–406. 77. Reeder TJ, Brown CK, Norris DL. Managing the difficult airway: a survey of residency directors and a call for change. J Emerg Med. 2005;28(4): 473–478. 78. Mort TC. Emergency tracheal intubation: complications associated with repeated laryngoscopic attempts. Anesth Analg. 2004;99(2):607–613. 79. Silvestri S, Ralls GA, Krauss B, et al. The effectiveness of out-of-hospital use of continuous end-tidal carbon dioxide monitoring on the rate of unrecognized misplaced intubation within a regional emergency medical services system. Ann Emerg Med. 2005;45(50):497–503. 80. Davis DP, Fisher R, Buono C, et al. Predictors of intubation success and therapeutic value of paramedic airway management in a large, urban EMS system. Prehosp Emerg Care. 2006;10(3):356–362. 81. Ufberg JW, Bushra JS, Karras DJ, et al. Aspiration of gastric contents: association with prehospital intubation. Am J Emerg Med. 2005;23(3): 379–382. 82. Lockey DJ, Coats T, Parr MJ. Aspiration in severe trauma: a prospective study. Anaesthesia. 1999;54(11):1097–1098. 83. Akca O, Koltka K, Uzel S, et al. Risk factors for early-onset, ventilatorassociated pneumonia in critical care patients: selected multiresistant versus nonresistant bacteria. Anesthesiology. 2000;93(3):638–645. 84. Eckert MJ, Davis KA, Reed RL 2nd, et al. Urgent airways after trauma: who get pneumonia? J Trauma. 2004;57(4):750–755. 85. Davis DP, Stern J, Sise MJ. A follow-up analysis of factors associated with head-injury mortality after paramedic rapid sequence intubation. J Trauma. 2005;59(2):486–490.

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CHAPTER 12

Management of Shock Louis H. Alarcon, Juan Carlos Puyana, and Andrew B. Peitzman

Shock is defined as the inadequate delivery of oxygen to tissues leading to cellular dysfunction and injury. In 1872 Gross described shock as a “rude unhinging of the machinery of life.”1 Although this definition is less than precise, to this day it illustrates the physiologic derangements of decompensated shock. Significant hypoperfusion and cellular injury may occur despite normal systemic blood pressure, so equating shock with hypotension and cardiovascular collapse is a vast oversimplification and results in delayed recognition of early shock, when intervention may be most effective at preventing end-organ dysfunction. Shock is most precisely defined as inadequate delivery of oxygen and nutrients necessary for normal tissue and cellular function. The initial cellular injury that occurs is reversible. However, this injury will become irreversible if tissue hypoperfusion is prolonged or severe enough such that, at the cellular level, compensation is no longer possible. Rapid recognition of the patient in shock and the prompt institution of steps to correct shock is a critical skill for the trauma surgeon. Surgeons caring for injured patients must initiate active treatment empirically, prior to a definitive diagnosis of the cause of shock. The management of the patient in shock has been an integral component of the surgeon’s realm of expertise for centuries. Bernard suggested that an organism attempts to maintain constancy in the internal environment despite external forces that attempt to disrupt the milieu intérieur.2 In the intact animal, the failure of physiologic systems to buffer the organism against these external forces results in the shock state. Cannon described the “fight or flight response” generated by elevated levels of catecholamines in the bloodstream and introduced the term homeostasis in 1926. He spent 2 years on the battlefields of Europe and published his classic monograph, Traumatic Shock, in 1923. Cannon’s observations led him to propose that shock was due to a disturbance of the nervous system that resulted in vasodilatation and hypotension. He

proposed that secondary shock with its attendant capillary permeability leak was caused by a “toxic factor” released from the tissue.3,4 Interestingly, Cannon is also credited with first proposing deliberate hypotension in patients with penetrating wounds of the torso to minimize internal bleeding since “if the pressure is raised before the surgeon is ready to check the bleeding that may take place, blood that is sorely needed may be lost.”5 Blalock documented that shock after hemorrhage was associated with reduced cardiac output and that hemorrhagic shock was due to volume loss, not a “toxic factor.”6 He also noted, however, that toxins could be important initiators of shock. In 1934, Blalock proposed the following four categories of shock that are still utilized today: hypovolemic, vasogenic, cardiogenic, and neurogenic (Table 12-1). Hypovolemic shock, the most common type, results from loss of circulating blood or its components. Thus, loss of circulating volume may be due to decreased whole blood (hemorrhagic shock), plasma, interstitial fluid, or a combination thereof. Vasogenic shock as seen in sepsis results from decreased resistance to blood flow within capacitance vessels of the circulatory system causing an effective decrease in circulating volume. Neurogenic shock is a form of vasogenic shock in which spinal cord injury (or spinal anesthesia) causes vasodilatation. Cardiogenic shock results from failure of the pump function as may occur with arrhythmias or acute heart failure. Two additional categories of shock have been added to those originally proposed by Blalock. Obstructive shock occurs when circulatory flow is mechanically impeded as with pulmonary embolism or a tension pneumothorax. Laboratory experiments and clinical experience have also confirmed the appropriateness of Cannon’s proposal of traumatic shock as a unique entity. Injuries to soft tissue and fractures of long bones that occur in association with multisystem trauma can produce an upregulation of proinflammatory mediators that can create a state of shock that is more complex than simple hemorrhagic shock.

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TABLE 12-1 Forms of Shock

SECTION 2

Hypovolemic Cardiogenic Neurogenic Inflammatory (septic) Obstructive Traumatic

In addition to seminal observations on the clinical syndrome of shock on the battlefield, the early and mid-20th century witnessed important laboratory contributions to our understanding of shock. In 1947, Wiggers developed a model of graded hemorrhagic shock based on the uptake of shed blood into a reservoir to maintain a prescribed level of hypotension.7 Shires and coworkers performed a series of classical laboratory studies in the 1960s and 1970s that demonstrated that a large extracellular fluid (ECF) deficit occurred in severe hemorrhagic shock that was greater than could be attributed to vascular refilling alone.8 A triple isotope technique in dogs revealed that this ECF deficit persisted when shed blood or shed blood plus plasma was used in resuscitation. Only the infusion of both shed blood and lactated Ringer’s solution (an ECF mimic) repleted the red blood cell mass, plasma volume, and ECF.9 Mortality after hemorrhage dramatically illustrated the importance of this observation: resuscitation with blood alone (80%), blood plus plasma (70%), and blood plus lactated Ringer’s solution (30%). The existence of this ECF deficit was subsequently confirmed in patients. Additional studies by this group demonstrated significant dysfunction of the cellular membrane in prolonged hemorrhagic shock.10 Depolarization of the cell membrane resulted in an uptake of water and sodium by the cell and loss of potassium in association with the loss of membrane integrity.10 The depolarization of the cell membrane was proportional to the degree and duration of hypotension. Studies in red blood cells, hepatocytes, and skeletal muscle suggested that an abnormality in membrane active transport (Na-K-ATPase pump) was the basis of the cellular membrane dysfunction.10 In addition, the uptake of fluid by the intracellular compartment was a major site of fluid sequestration following prolonged hemorrhagic shock. These changes were reversible with appropriate resuscitation. Thus, the importance of fluid resuscitation of severe hemorrhagic shock with isotonic saline or lactated Ringer’s solution in addition to red blood cells was confirmed. These studies also emphasized the important cellular effects from what had previously appeared to be a global circulatory phenomenon. With advances in our understanding of the pathophysiology and treatment of shock, new clinical problems soon became apparent. The Vietnam War provided a clinical laboratory for the rapidly expanding field of shock research. Aggressive fluid resuscitation with red blood cells, plasma, and crystalloid solutions allowed patients who previously would have succumbed to hemorrhagic shock to survive. Renal failure became a less frequent clinical problem, but fulminant pulmonary failure appeared as an early cause of death after severe hemorrhage.

Initially labeled “shock lung” or “DaNang lung,” the clinical problem soon became recognized as the acute respiratory distress syndrome (ARDS). Flooding of the lung with large volumes of crystalloid solution was initially proposed as the primary mechanism of ARDS. Currently, ARDS is seen as a component of the multiple organ dysfunction syndrome (MODS), a result of the complex upregulation of proinflammatory mediators and mechanisms of the homeostatic response. The concept of MODS will be discussed in a subsequent chapter (see Chapter 61). Several decades of research utilizing modified Wiggers’ models of hemorrhagic shock emphasized the importance of early control of hemorrhage in conjunction with restoration of intravascular volume with red blood cells and crystalloid solutions. Studies over the past decade have extended the observations initially made by Cannon in 1918 on the futility of vigorously resuscitating patients with ongoing bleeding and have challenged traditional thinking on the appropriate end points of resuscitation from uncontrolled hemorrhage.11 The concepts of delayed fluid resuscitation and hypotensive resuscitation are still being debated, fueled by the clinical study by Bickell et al. of patients with penetrating torso trauma.12 Several essential concepts in the management of shock in the trauma patient, however, have withstood the test of time: (a) early definitive control of the airway must be achieved; (b) delays in control of active hemorrhage increase mortality; (c) poorly corrected hypoperfusion increases morbidity and mortality, that is, inadequate resuscitation results in avoidable early deaths; and (d) excessive fluid resuscitation exacerbates problems, that is, uncontrolled resuscitation is harmful.

PATHOPHYSIOLOGY ■ Pathophysiology of Shock Shock exists when the delivery of oxygen and metabolic substrates to tissues and cells is insufficient to maintain normal aerobic metabolism. This concept implies an imbalance between substrate delivery (supply) and substrate requirements (demand) at the cellular level. Tissue hypoperfusion is associated with cardiovascular and neuroendocrine responses designed to compensate for and reverse inadequate tissue perfusion. The pathophysiologic sequelae of shock may be due to either the direct effects of inadequate tissue perfusion on cellular and tissue function or the body’s adaptive responses producing undesirable consequences. The magnitude of the shock insult and, therefore, the magnitude of the response varies depending on the depth and duration of shock.13,14 The consequences of shock may also vary from minimal physiologic disturbance with complete recovery at one end of the spectrum to profound circulatory disturbance, end-organ dysfunction, and death at the other (Fig. 12-1). The accumulating evidence suggests that, while the quantitative nature of the host response to shock may differ between the various etiologies of shock, the qualitative nature of the body’s response to shock is similar regardless of the cause of the insult. This response consists, in part, of profound changes in cardiovascular, neuroendocrine, and immunologic function. Furthermore, the pathophysiologic responses

80

Compensation end point 100%

90%

50% 30% 10%

40 % Shed blood return

0% 10% 20% 30% 40% 50% B

Compensated

A

Decompensated

0% Death

Irreversible

A

Transition to acute irreversible shock

B

Transition to subacute lethal shock

FIGURE 12-1 A rodent model of hemorrhagic shock depicting the relation between volume loss, duration of shock, and transition from reversible to fatal, irreversible shock. (Reproduced with permission from Peitzman AB, Harbrecht BG, Udekwu AO, et al. Hemorrhagic shock. Curr Probl Surg. 1995;32:974, © Elsevier.)

vary with time and in response to resuscitation. For example, in hemorrhagic shock, the initial compensation for blood loss occurs primarily through the neuroendocrine responses to maintain hemodynamics. This represents the compensated phase of shock. With ongoing hypoperfusion, cellular death and injury are ongoing and the decompensated phase of shock ensues. Microcirculatory dysfunction, cellular injury, and activation of inflammatory cells can perpetuate the hypoperfusion and exacerbate tissue injury. The ischemia/reperfusion injury will often further exacerbate the initial insult. Persistent hypoperfusion results in further hemodynamic derangements and cardiovascular collapse, which has been termed the irreversible phase of shock. At this point, extensive parenchymal and microvascular injury has occurred, such that further volume resuscitation fails to reverse the process, leading to death of the patient.

AFFERENT SIGNALS Afferent impulses transmitted from the periphery are processed within the central nervous system (CNS) and activate the reflexive effector responses or efferent impulses designed to expand plasma volume, maintain peripheral perfusion and tissue oxygen delivery, and reestablish homeostasis. The afferent impulses that initiate the body’s intrinsic adaptive responses converge in the CNS and originate from a variety of sources. The initial inciting event is often loss of circulating blood volume; other stimuli that can produce the neuroendocrine response include tissue trauma, pain, hypoxemia, hypercarbia, acidosis, infection, change in temperature, emotional arousal, or hypoglycemia. The sensation of pain from injured tissue is transmitted via the spinothalamic tracts and activates the hypothalamic–pituitary–adrenal axis.15 The sensation of pain can also activate the autonomic nervous system (ANS) and increase direct sympathetic stimulation of the adrenal medulla to release catecholamines. Baroreceptors represent an important afferent pathway in initiating adaptive or corrective responses to shock. Volume receptors are present within the atria of the heart and are

sensitive to changes in both chamber pressure and wall stretch.15 They become activated with low-volume hemorrhage or mild reductions in right atrial pressure. Receptors in the aortic arch and carotid bodies respond to alterations in pressure or stretch of the arterial wall and respond to greater reductions in intravascular volume or changes in pressure. These receptors normally inhibit activation of the ANS. When these baroreceptors are activated, their output is diminished. Thus, there is increased ANS output principally via sympathetic activation at the vasomotor centers of the brainstem, and this produces centrally mediated constriction of peripheral vessels. Chemoreceptors in the aorta and carotid bodies are sensitive to changes in oxygen tension, H ion concentration, and CO2 level.16 These receptors also provide afferent stimulation when the circulatory system is disturbed and activate effector response mechanisms. In addition, a variety of protein and nonprotein mediators produced at the site of injury and inflammation act as afferent impulses and induce a host response to shock and trauma. Some of these compounds are components of the host immunologic response to shock and include histamine, cytokines, eicosanoids, endothelins, and others that will be discussed in greater detail both in this chapter and in subsequent chapters.

EFFERENT SIGNALS ■ Cardiovascular Response The neuroendocrine and ANS responses to shock result in changes in cardiovascular physiology, which constitute a prominent feature in the body’s adaptive response and the clinical presentation of the patient in shock. Stimulation of sympathetic fibers innervating the heart leads to activation of β1-adrenergic receptors that increase heart rate and contractility in an attempt to increase cardiac output.16 Increased myocardial oxygen consumption occurs as a result of the increased workload. Myocardial oxygen supply must be maintained or myocardial ischemia and dysfunction will develop. Direct sympathetic stimulation of the peripheral circulation via the activation of α1-adrenergic receptors on arterioles increases vasoconstriction and causes a compensatory increase in systemic vascular resistance and blood pressure. Selective perfusion of tissues due to regional variations in arteriolar resistance from these compensatory mechanisms occurs in shock. Blood is shunted away from organs such as the intestine, kidney, and skin that are less essential to the body’s immediate need to correct and respond to shock.17 Organs such as the brain and heart have autoregulatory mechanisms that attempt to preserve their blood flow despite a global decrease in cardiac output. Direct sympathetic stimulation also induces constriction of venous vessels, decreasing the capacitance of the circulatory system, and accelerating blood return to the central circulation. Increased sympathetic output increases catecholamine release from the adrenal medulla. Catecholamine levels increase and peak within 24–48 hours of injury before returning to baseline.16 Most of the epinephrine that circulates systemically

191

CHAPTER 12

Mean arterial pressure

Management of Shock

192

Generalized Approaches to the Traumatized Patient

SECTION 2

is produced by the adrenal medulla, while norepinephrine is derived from synapses of the sympathetic nervous system.17 Catecholamines also have profound effects on peripheral tissues in ways that support the organism’s ability to respond to shock and hypovolemia. They stimulate hepatic glycogenolysis and gluconeogenesis to increase the availability of circulating glucose to peripheral tissues, increase glycogenolysis in skeletal muscle, suppress the release of insulin, and increase the release of glucagon.15 These responses increase the availability of glucose to the tissues that require it for maintenance of essential metabolic activity.

angiotensin II by angiotensin-converting enzyme (ACE) produced in the lung. While angiotensin I has no significant functional activity, angiotensin II is a potent vasoconstrictor of both splanchnic and peripheral vascular beds and also stimulates the secretion of aldosterone, ACTH, and ADH. Aldosterone, a mineralocorticoid, acts on the nephron to promote reabsorption of sodium and, as a consequence, water in exchange for potassium and hydrogen ions that are lost in the urine.

■ Neuroendocrine Response

The inflammatory and immune responses are a complex set of interactions between circulating soluble factors and cells that can arise in response to trauma, infection, ischemia, toxic, or autoimmune stimuli.22 The function of the host’s immune system after shock is intimately related to alterations in the production of mediators generally considered part of the body’s response to localized inflammation and infection. When these mediators gain access to the systemic circulation, they induce changes in a number of tissues and organs. Therefore, activation of proinflammatory pathways is an integral component of the host response to shock. While proinflammatory activation is a central feature of septic shock, proinflammatory cytokine production and mediator release also occurs in other forms of shock such as hypovolemic shock.23–25 As initially proposed by Cannon in the early part of the 20th century, inflammatory mediators can be a cause of shock as well as a by-product of the body’s response to shock. Most mediators have a variety of effects due to the redundant and overlapping nature of the host response to injury. Therefore, in addition to regulating immune function in the host, many of these mediators have effects on the cardiovascular system, cellular metabolism, and cellular gene expression. It deserves to be mentioned, however, that many compounds already discussed that have substantial effects on the cardiovascular or neuroendocrine response to shock, such as catecholamines, can also have effects on immune function and the activation of proinflammatory cytokines.26 Cytokines are small polypeptides and glycoproteins that exert most of their actions in a paracrine fashion and are responsible for fever, leukocytosis, tachycardia, tachypnea, and the upregulation of other cytokines. Their levels are elevated in hemorrhagic, septic, and traumatic shock.22 The overexpression of certain cytokines is associated with the metabolic and hemodynamic derangements often seen in septic shock or decompensated hypovolemic shock, and cytokine production after shock correlates with the development of the MODS.23–25,27 The immune response to injury and infection is discussed in greater detail in Chapter 61. A brief review of several of the key components of the immune response is provided below. Tumor necrosis factor-α (TNF-α) is one of the earliest proinflammatory cytokines released by monocytes, macrophages, and T cells in response to injurious stimuli.28 The classic model of TNF-α production is the injection of bacterial endotoxin in an animal or human subject. Under these controlled conditions, TNF-α levels peak within 90 minutes of the insult and return to baseline within 4 hours. Endotoxin stimulates TNF-α release and may be a primary inducer of

As discussed earlier, a variety of afferent stimuli lead to activation of the hypothalamic–pituitary–adrenal axis that functions as an integral component of the adaptive response of the host following shock. Shock stimulates the hypothalamus to release corticotrophin-releasing hormone, which results in the release of adrenocorticotropin hormone (ACTH) by the pituitary. ACTH subsequently stimulates the adrenal cortex to release cortisol. Cortisol acts synergistically with epinephrine and glucagon to induce a catabolic state.16 It stimulates gluconeogenesis and insulin resistance, resulting in hyperglycemia. It also induces protein breakdown in muscle cells and lipolysis, which provide substrates for hepatic gluconeogenesis. Cortisol causes retention of sodium and water by the kidney that aids in restoration of circulating volume. In the setting of severe hypovolemia, ACTH secretion occurs independently of negative feedback inhibition by cortisol. Absence of appropriate cortisol secretion during critical illness or after injury has been postulated as a contributor to ongoing circulatory instability in critically ill patients.18–20 The pituitary also releases vasopressin or antidiuretic hormone (ADH) in response to hypovolemia, changes in circulating blood volume sensed by baroreceptors and stretch receptors in the left atrium, and increased plasma osmolality detected by hypothalamic osmoreceptors.15 Epinephrine, angiotensin II, pain, and hyperglycemia enhance the production of ADH. ADH levels remain elevated for about 1 week after the initial insult, depending on the severity and persistence of the hemodynamic abnormalities. ADH acts on the distal tubule and collecting duct of the nephron to increase water permeability, decrease losses of water and sodium, and preserve intravascular volume. Also known as arginine vasopressin, ADH acts as a potent mesenteric vasoconstrictor, shunting circulating blood away from the splanchnic organs during hypovolemia.21 The intense mesenteric vasoconstriction produced by vasopressin may contribute to intestinal ischemia and predispose to dysfunction of the intestinal mucosal barrier in shock states. Vasopressin also regulates hepatocellular function by increasing hepatic gluconeogenesis and hepatic glycolysis. The renin–angiotensin system is activated in shock, as well. Decreased perfusion of the renal artery, β-adrenergic stimulation, and increased sodium concentration in the renal tubules cause the release of renin from the juxtaglomerular cells.16 Renin catalyzes the conversion of angiotensinogen (produced by the liver) to angiotensin I, which is then converted to

■ Immunologic and Inflammatory Response

Management of Shock contribute to the development of organ dysfunction.43,44 The development of ARDS and MODS in trauma patients correlates with the intensity of complement activation.23,25 Activation of neutrophil is one of the early changes induced by the inflammatory response, and neutrophils are the first cells to be recruited to sites of injury and inflammation. These cells are important in the clearance of infectious agents, foreign substances that have penetrated host barrier defenses, and nonviable tissue. On the other hand, activated neutrophils and their products may also produce cell injury and organ dysfunction. Activated neutrophils generate and release a number of substances such as reactive oxygen species, lipid peroxidation compounds, proteolytic enzymes (elastase, cathepsin G), and vasoactive mediators (leukotrienes, eicosanoids, and platelet-activating factor [PAF]). Oxygen radicals such as superoxide anion, hydrogen peroxide, and the hydroxyl radical are potent inflammatory molecules that activate peroxidation of lipids, inactivate cellular enzymes, and consume cellular antioxidants (such as glutathione and tocopherol). Intestinal ischemia and reperfusion cause activation of neutrophils and induce neutrophil-mediated organ injury in experimental animal models.45 In animal models of hemorrhagic shock, activation of neutrophils correlates with irreversibility of shock and mortality,46 and neutrophil depletion prevents the pathophysiologic sequelae of hemorrhagic and septic shock.47,48 Human data corroborate the activation of neutrophils in trauma and shock and suggest that neutrophil activation may play a role in the development of MODS after injury.49 Plasma markers of neutrophil activation such as elastase may correspond to phagocytic activity or correlate with severity of injury.24 In this context, elastase and other markers of neutrophil activation may predict the development of ARDS and MODS after shock. Interactions between endothelial cells and leukocytes are important in host defense and the initiation and perpetuation of the inflammatory response in the host. The vascular endothelium regulates blood flow, adherence of leukocytes, and activation of the coagulation cascade. Adhesion molecules such as intercellular adhesion molecules (ICAMs), vascular cell adhesion molecules (VCAMs), and the selectins (E-selectin, P-selectin) are expressed on the surface of endothelial cells and are responsible for the adhesion of leukocytes to the endothelium. The interaction of surface proteins on leukocytes and vascular endothelial cells allows activated neutrophils to marginate into the tissues in order to engulf invading organisms. Unfortunately, the migration of activated neutrophils into tissues can also lead to neutrophil-mediated cytotoxicity, microvascular damage, and tissue injury.50 This tissue damage may contribute to organ dysfunction after shock.

■ Cellular Effects Depending on the magnitude of the insult and the intrinsic compensatory mechanisms present in different cells, the response at the cellular level may be one of adaptation, dysfunction and injury, or death. The aerobic respiration of the cell, that is, oxidative phosphorylation by mitochondria, is the pathway most susceptible to inadequate oxygen delivery. As oxygen

CHAPTER 12

cytokines, as in the case of septic shock. TNF-α release may also be a secondary event following the release of bacteria from the intestinal lumen that may occur after hemorrhage and ischemia.29,30 Also, TNF-α levels are increased after hemorrhagic shock,31 and TNF-α levels correlate with mortality in animal models of hemorrhage.32 In humans, TNF-α, interleukin-6 (IL-6), and IL-8 levels increase during hemorrhagic shock, although the magnitude of the increase is less than that seen in septic patients.33 Once released, TNF-α can cause peripheral vasodilation, activate the release of other cytokines such as IL-1β and IL-6, induce procoagulant activity, and stimulate a wide array of cellular metabolic changes.28 TNF-α has also been associated with mechanisms of host defense against infection by promoting activation of macrophages and intracellular killing of pathogens.34 During the stress response, TNF-α contributes to breakdown of muscle protein and cachexia, as well.28 Despite being linked to tissue injury and dysfunction, TNF-α may be essential in combating bacterial infection since neutralizing TNF-α in infection models using live bacteria (peritonitis, pneumonia) increases mortality.35–37 IL-1β has actions that are similar to TNF-α and can cause hemodynamic instability and vasodilation.28 It has a very short half-life (6 minutes) and primarily acts locally in a paracrine fashion. IL-1β produces a febrile response by activating prostaglandins in the posterior hypothalamus and causes anorexia by activating the satiety center. This cytokine also augments the secretion of ACTH, glucocorticoids, and β-endorphins.28 In conjunction with TNF-α, IL-1β can induce the release of other cytokines such as IL-2, IL-4, IL-6, IL-8, granulocyte/macrophage colony-stimulating factor (GM-CSF), and interferon-γ (IFN-γ). IL-2 expression is important for the cell-mediated immune response, and its attenuated expression has been associated with transient immunosuppression of injured patients. IL-6 has consistently been shown to be elevated in animals subjected to hemorrhagic shock or trauma and in patients with major surgery or trauma. And elevated IL-6 levels correlate with mortality in some forms of shock.38 IL-6 contributes to neutrophil-mediated injury to the lung after hemorrhagic shock39 and may play a role in the development of diffuse alveolar damage and ARDS. IL-6 and IL-1β are mediators of the hepatic acute phase response to injury and enhance the expression and/or activity of complement, C-reactive protein, fibrinogen, haptoglobin, amyloid A, and α1-antitrypsin. Activation of neutrophils is promoted by IL-6, IL-8, and GM-CSF, and IL-8 also serves as a potent chemoattractant to neutrophils. The complement cascade is activated by injury and shock and contributes to proinflammatory activation in both animal models and human patients. Complement consumption can occur after hemorrhagic shock and may contribute to the hypotension and metabolic acidosis observed following resuscitation.40 The degree of complement activation is proportional to the magnitude of the traumatic injury and may serve as a marker for severity of injury in trauma patients.41 Patients in septic shock also demonstrate activation of the complement pathway with elevation of the activated complement proteins C3a and C5a.42 Activation of the complement cascade can

193

194

Generalized Approaches to the Traumatized Patient

SECTION 2

tension within cells decreases, oxidative phosphorylation decrease and the generation of adenosine triphosphate (ATP) slows or stops. The loss of ATP, the cellular “energy currency,” has widespread effects on cellular function, physiology, and morphology.51 As oxidative phosphorylation slows, the cells shift to anaerobic glycolysis that generates ATP from the rapid breakdown of cellular glycogen.52 However, anaerobic glycolysis is much less efficient than oxygen-dependent mitochondrial pathways. Under aerobic conditions, pyruvate, the end product of glycolysis, is fed into the Krebs cycle for further oxidative metabolism. Under hypoxic conditions, the mitochondrial pathways of oxidative catabolism are impaired and pyruvate is instead converted to lactate. The accumulation of lactic acid and inorganic phosphates is accompanied by a reduction in pH resulting in intracellular metabolic acidosis. As cells become hypoxic and ATP depleted, other ATP-dependent cell processes are affected: synthesis of enzymes and structural proteins, repair of deoxyribonucleic acid (DNA) damage, and intracellular signal transduction. Tissue hypoperfusion also results in decreased availability of metabolic substrates and the accumulation of metabolic by-products such as oxygen radicals and organic ions that may be toxic to cells. The consequences of intracellular acidosis on cell function can be quite profound. Decreased intracellular pH can alter the activity of cellular enzymes, lead to changes in cellular gene expression, impair cellular metabolic pathways, and interfere with ion exchange in the cell membrane.53–55 Acidosis can also lead to changes in cellular calcium (Ca2) metabolism and Ca2-mediated cellular signaling that can, by itself, interfere with the activity of specific enzymes and alter cell function.53,56 These changes in normal cell function can produce cellular injury or cell death.57 Changes in both cardiovascular function and immune function in the host can be induced by acidosis,58,59 although translating these in vitro effects to the physiologic sequelae of shock produced in the intact organism may be difficult. As cellular ATP is depleted under hypoxic conditions, the activity of the membrane Na, K-ATPase slows and thus the regulation of cellular membrane potential and volume is impaired.10 Na accumulates intracellularly while K leaks into the extracellular space. The net gain of intracellular sodium is accompanied by an increase in intracellular water and the development of cellular swelling. This cellular influx of water is associated with a corresponding reduction in ECF volume.60 Swelling of the endoplasmic reticulum is the first ultrastructural change seen in hypoxic cell injury. Eventually, swelling of the mitochondria and cells is observed. The changes in cellular membrane potential impair a number of cellular physiologic processes such as myocyte contractility, cell signaling, and the regulation of intracellular Ca2 concentrations. Once intracellular organelles such as lysosomes or cell membranes rupture, the cell will undergo death by necrosis.61 Hypoperfusion and hypoxia can induce cell death by apoptosis, as well. Animal models of shock and ischemia/ reperfusion have demonstrated apoptotic cell death in lymphocytes, intestinal epithelial cells, and hepatocytes.62 Apoptosis has also been detected in trauma patients with ischemia and reperfusion injury. Apoptosis of lymphocytes and

intestinal epithelial cells occurs within the first 3 hours of injury.63 Apoptosis in intestinal mucosal cells may compromise barrier function of the intestine and lead to translocation of bacteria and endotoxin into the portal circulation during shock. Also, lymphocyte apoptosis has been hypothesized to contribute to the immune suppression that is observed in trauma patients. Tissue hypoperfusion and cellular hypoxia result not only in intracellular acidosis but also in systemic metabolic acidosis as metabolic by-products of anaerobic glycolysis exit the cells and gain access to the circulation. In the setting of acidosis, oxygen delivery to the tissues is altered as the oxyhemoglobin dissociation curve is shifted toward the right.15 The decreased affinity of hemoglobin for oxygen in erythrocytes results in increased tissue O2 release and increased tissue extraction of oxygen. In addition, hypoxia stimulates the production of erythrocyte 2,3-diphosphoglycerate (2,3-DPG), which also contributes to the shift to the right of the oxyhemoglobin dissociation curve and increases O2 availability to the tissues during shock. Epinephrine and norepinephrine released after shock have a profound impact on cellular metabolism in addition to their effects on vascular tone. Hepatic glycogenolysis, gluconeogenesis, ketogenesis, breakdown of skeletal muscle protein, and lipolysis of adipose tissue are all increased by these catecholamines.21 Cortisol, glucagon, and ADH also participate in the regulation of catabolism during shock. Epinephrine induces the release of glucagon while inhibiting the release of insulin by pancreatic β-cells. The result is a catabolic state with glucose mobilization, hyperglycemia, protein breakdown, negative nitrogen balance, lipolysis, and insulin resistance during shock and injury.21,60 The relative underutilization of glucose by peripheral tissues preserves it for the glucosedependent organs such as the heart and brain. In addition to inducing changes in cellular metabolic pathways, shock also induces changes in cellular gene expression. The DNAbinding activity of a number of nuclear transcription factors is altered by the production of oxygen radicals, nitrogen radicals, or hypoxia that occurs at the cellular level in shock.64 The expression of other gene products including heat shock proteins,65 vascular endothelial growth factor (VEGF), inducible nitric oxide synthase (iNOS), and cytokines is also increased in shock.66–68 Many of these shock-induced gene products, such as cytokines, have the ability to subsequently alter gene expression in specific target cells and tissues.28 These pathways will be discussed in greater detail elsewhere but they emphasize the complex, integrated, and overlapping nature of the response to shock. Shock induces profound changes in tissue microcirculation that may contribute to organ dysfunction, and the systemic sequelae of severe hypoperfusion. These changes have been studied most extensively in the microcirculation of skeletal muscle in models of sepsis and hemorrhage. Whether microcirculatory changes are primarily a result of the development of shock or a pathophysiologic response that promotes tissue injury and organ dysfunction has been difficult to determine. Intuitively, it would seem that both are likely to be true. After hemorrhage, larger arterioles vasoconstrict, most likely due to sympathetic stimulation, while smaller distal arterioles dilate,

Management of Shock

Hypoperfused tissues and cells experience what has been called oxygen debt, a concept first proposed by Crowell.80 The oxygen debt is the deficit in tissue oxygenation over time that occurs during shock. When oxygen delivery (DO2) is limited, oxygen consumption (VO2) may be inadequate to match the metabolic needs of cellular respiration creating a deficit in oxygen at the cellular level. The measurement of oxygen deficit is calculated by taking the difference between the estimated oxygen demand and the actual value obtained for oxygen consumption (VO2). Under normal circumstances, cells can “repay” the oxygen debt during reperfusion. The magnitude of the oxygen debt correlates with the severity and duration of hypoperfusion. In a canine model of hemorrhagic shock, Crowell and Smith demonstrated a direct relation between survival and degree of shock.81 They determined that a marker of mortality was the inability to repay the oxygen debt. The median lethal dose (LD50) occurred at 120 mL/kg of oxygen debt. Dunham et al. showed via regression analysis that the probability of death could be directly correlated to the calculated oxygen debt in a canine model of hemorrhagic shock.82 Their study demonstrated that the LD50 for oxygen debt was similar (113.5 mL/kg) to that found by Crowell in their earlier studies. Dunham et al. were also able to confirm a relation between the rate of accumulation of the oxygen debt and survival. In human patients a relation between oxygen debt and survival has also been shown. In over 250 high-risk surgical patients, the calculated oxygen debt correlated directly with

1.000

pDEATH = .0715 LACT - .4219 N = 51 R2 = .854 F1.49 = 286.1 p' .0001

0.900 0.800

LDLD75 = 16.39 mMol • 1

0.700 Probability of Death

■ Quantifying Cellular Hypoperfusion

organ failure and mortality.83 The maximum oxygen debt in nonsurvivors (33.2 L/m2) was greater than that of survivors with organ failure (21.6 L/m2) and survivors without organ failure (9.2 L/m2). In addition, the total duration of oxygen debt and the time required to repay it correlated with outcome in this study. Survivors were able to repay the oxygen debt while the hallmark of nonsurvivors was the inability to repay the oxygen debt. Thus, the magnitude of the oxygen debt, its rate of accumulation, and the time required to correct it may all correlate with survival. It is difficult to directly measure the oxygen debt in the resuscitation of trauma patients. The easily obtainable parameters of arterial blood pressure, heart rate, urine output, central venous pressure, and pulmonary artery occlusion pressure are poor indicators of the adequacy of tissue perfusion. Therefore, surrogate parameters have been sought to estimate the oxygen debt. Experimental animal studies show that serum lactate and base deficit (BD) correlate with oxygen debt.82 Cardiac output, blood pressure, and shed blood volume were all inferior to the BD and lactate in estimating the oxygen debt and in predicting mortality in hemorrhaged animals.82 Dunham et al. showed a direct correlation between arterial lactate and probability of survival in a model of canine hemorrhage (Fig. 12-2).82 The LD50 for lactate was 12.9 mmol/L in hemorrhaged dogs. BD is the amount of base in millimoles that is required to titrate 1 L of whole blood to a pH of 7.40 with the blood fully saturated with O2 at 37°C (98.6°F) and a PaCO2 of 40 mm Hg. It is usually measured by arterial blood gas analysis using automated devices and has a rapid turnaround time. Good correlation between the BD and survival has been shown in patients with shock.84 At a BD of 0 mmol/L there was an 8%

0.600

S DS

LD50 = 12.9 mMol • 1

0.500 D S

0.400 0.300 0.200 0.100 0 −0.100 0.0

LD25 = 9.4 mMol • 1

S SS

DSS DSS DS S DSS S SS DSS S 4.0

8.0

12.0

16.0

20.0

Lactate (mMol • L)

FIGURE 12-2 The relation between mortality and serum lactate levels is described by data generated in a canine hemorrhagic shock model. (Reproduced with permission from Dunham CM, Siegel JH, Weireter L, et al. Oxygen debt and metabolic acidemia or quantitative predictors of mortality and the severity of the ischemic insult in hemorrhagic shock. Crit Care Med. 1991;19:231.)

CHAPTER 12

presumably due to local mechanisms.69 Flow at the capillary level, however, is heterogeneous with swelling of endothelial cells and the aggregation of leukocytes producing diminished capillary perfusion in some vessels both during shock and following resuscitation.70,71 Hemorrhage-induced microcirculatory dysfunction also occurs in vascular beds besides skeletal muscle and may contribute to tissue injury and organ dysfunction.72,73 In sepsis, similar changes in microcirculatory function occur. Regional differences in blood flow can be demonstrated after proinflammatory stimuli, and the microcirculation in many organs is heterogeneous.74–78 Aggregation and sludging of neutrophils in the microcirculation can aggravate shock-induced hypoperfusion, induce direct cellular injury via toxic neutrophil-dependent processes such as production of oxygen radicals or release of proteolytic enzymes, and impair cellular metabolism.79 The decreases in microcirculatory blood flow and capillary perfusion result in decreased capillary hydrostatic pressure. The changes in hydrostatic pressure promote an influx of fluid from the extravascular or extracellular space into the capillaries in an attempt to increase circulating volume. These changes are associated, however, with additional decrements in the volume of ECF due to increased cellular swelling. These basic cellular and microcirculatory changes have significant physiologic importance in the ability of the organism to recover from circulatory shock. Resuscitation with volumes of fluid sufficient to restore the ECF deficit is associated with improved outcome after shock as described earlier.9

195

Generalized Approaches to the Traumatized Patient 100 95 90 85 80 75 70 65 60 55 50 45 40 35 30 25 20 15 10 5 0

% Mortality =

–19.2 – 23.5

100

eλ × 100 1 + eλ

90

–16.4

80 % Observed death

SECTION 2

% Mortality

196

LD50

Base excess = –11.8

70

2

–6 –14 –22 Extracellular BEA, mmol/L

–38

–11.8

50

– 9.7

40 30 20

10

–14

60

–7.5 – 4.5 –.17

10 –.19 0 0 10 20 30 40 50 60 70 80 90 100 % Predicted death on the basis of linear logistic model from BEAECF

FIGURE 12-3 The relation between base deficit (negative base excess) and mortality is depicted for patients who suffered blunt hepatic injury. (Reproduced with permission from Siegel JH, Rivkind AI, Dalal S, et al. Early physiologic predictors of injury severity and death in blunt multiple trauma. Arch Surg. 1990;125:498, Copyright © 1990 American Medical Association. All rights reserved.)

mortality, while there was a 95% mortality at a BD of 26 mmol/L. The LD50 occurred at a BD of 11.8 mmol/L (Fig. 12-3).84 Other clinical parameters such as blood pressure, heart rate, hemoglobin, plasma lactate, and oxygen transport variables were not nearly as accurate as the BD in determining the probability of death in these trauma patients. Neither BD nor serum lactate, however, is as precise at measuring physiologic stress as the oxygen debt. When compared in a model of hemorrhage and resuscitation, the lactate level decreased more slowly and tended to estimate higher residual oxygen debt while the BD decreased more rapidly and tended to estimate lower values of oxygen debt.81 However, the BD appeared to reflect the measured oxygen debt more accurately. As will be discussed more fully later in the chapter (see Section “End Points in Resuscitation of the Trauma Patient”), both lactate and BD are useful in the assessment of trauma patients and in the evaluation of the patient’s response to resuscitation.

EVALUATION OF THE TRAUMA PATIENT IN SHOCK ■ General Overview Shock represents a condition of abnormal tissue perfusion. The manifestations of shock may be dramatic, as in the patient with profound hypotension or obvious external sources of blood loss, or findings may be subtle. As with other traumainduced injuries, the evaluation, diagnosis, and treatment of the trauma patient in shock begin with the ABCs of the primary survey.85 Advanced shock may produce coma with loss of the ability to maintain and protect the airway, so that endotracheal intubation is necessary. Marked tachypnea may be present as the respiratory system attempts to compensate for metabolic acidosis or in response to generalized anxiety from hypoperfusion of the CNS. In the primary survey, the circula-

tion can be rapidly assessed by evaluation of the presence and location of the pulse (central vs. peripheral), its rate, and its character. Absent peripheral pulses (radial, pedal) associated with weak, rapid central pulses (femoral, carotid) denote a profound circulatory disturbance that requires prompt intervention. Associated findings that may be manifestations of abnormal tissue perfusion include cool clammy skin, altered sensorium (confusion, lethargy, coma), and tachycardia. Low urine output, often used as an indicator of hypovolemia, is unlikely to be a useful tool in the initial assessment of the patient in shock in the trauma resuscitation area. Measurement of blood pressure may be misleading. Compensatory mechanisms to maintain cerebral and coronary perfusion may maintain relatively normal systemic arterial pressure despite hypovolemia and significant underperfusion of splanchnic and peripheral tissues. Up to 30% of the blood volume may be lost before significant changes in blood pressure occur.85 When present, however, hypotension represents a profound circulatory derangement and the failure of compensatory mechanisms and requires immediate attention. The correction of shock should begin immediately once it is recognized. Treatment generally begins before an etiology for shock is identified. The forms of shock are listed in Table 12-1, but the most common etiology for shock in the trauma patient is hypovolemia from loss of circulating volume (see algorithm, Fig. 12-4). Two large-bore intravenous lines (at least 14- or 16-gauge peripheral or number 7.5–8.5 French resuscitation lines) should be inserted and volume resuscitation instituted. The availability of rapid infusion systems in many trauma centers facilitates rapid volume expansion with the delivery rate limited predominantly by the size and length of the intravenous cannula. Warmers to heat the infusate are essential to prevent hypothermia. For patients in profound shock, immediate blood replacement may be necessary. As soon as possible, fresh frozen plasma (FFP) and platelets should be infused as well, to prevent

Management of Shock

Yes

No

Volume Infusion

Diagnostic Studies as Indicated

Nonresponder

Responder

Transient Responder

Operating Room Rapid Diagnostic Evaluation

Diagnostic laparotomy and/or thoracotomy

Operating Room Obstructive Chest tube Decompress pericardium Treat cardiac injury

Hemorrhagic Consider Operative Tx

Neurogenic

Septic

Supportive Care Tx spinal injury

Supportive Care Tx Primary infection

Cardiogenic, Traumatic Supportive Care

FIGURE 12-4 Tissue hypoperfusion algorithm. The most common etiology for shock in the trauma patient is hypovolemia from loss of circulating volume.

worsening of the patient’s coagulopathy. As correction of the shock state is underway, the etiology for shock is rapidly sought. Physical examination may indicate potential etiologies (i.e., obvious external hemorrhage, flaccid extremities from spinal cord injury, or penetrating precordial wounds). Rapidly performed radiologic examinations (x-rays of chest and pelvis, diagnostic ultrasound) can provide additional information while the initial resuscitation is being conducted and the response to resuscitation is evaluated. Diagnostic maneuvers that do not directly contribute to the identification and treatment of shock should be deferred until shock has been corrected. Trauma patients can be categorized into three general groups with respect to their response to resuscitative maneuvers (see treatment algorithm, Fig. 12-5). Responders are those patients who rapidly correct their shock state with minimal replacement of intravascular volume. These patients often have an intravascular volume loss that is not ongoing, bleeding that has stopped or been tamponaded (multiple extremity fractures), or an etiology for hypoperfusion other than hypovolemia such as neurogenic shock or obstructive shock. Transient responders

represent patients who initially improve with resuscitative efforts, but subsequently deteriorate. This group of patients frequently has intracavitary bleeding that requires surgical control. Nonresponders represent those patients who have persistent manifestations of shock despite vigorous resuscitative efforts. These patients are gravely ill and often present in extremis. These patients typically have high-volume bleeding from injuries to major vessels or severe injuries to solid organs that require immediate operative control. They will rapidly expire from circulatory collapse or develop the progressive spiral of hypothermia, coagulopathy, and irreversible shock unless bleeding is rapidly controlled. Patients who have active, ongoing hemorrhage cannot be successfully resuscitated until hemorrhage has been controlled, and rapid identification of patients who require operative intervention is essential.

Vascular Access for Patients with Severe Hemorrhage In the trauma patient presenting with multiple serious injuries and hemorrhagic shock, vascular access is necessary to restore

CHAPTER 12

Tissue Hypoperfusion

197

198

Generalized Approaches to the Traumatized Patient

SECTION 2

Tissue Hypoperfusion Yes

No

Presentation Delayed

Diagnostic Studies as Indicated

Acute

Consider Septic Shock

Volume Status Hypervolemic Normal

Hypovolemic

Hemorrhagic Shock

Assess Cardiac Function Hyperdynamic Normal

Hypodynamic

Spinal Cord Injury at appropriate level Yes

No

Neurogenic Shock

Tension PTX or Cardiac Tamponade No

Traumatic Shock

Cardiogenic Shock

Yes

Obstructive Shock

FIGURE 12-5 Tissue hypoperfusion algorithm. Trauma patients can be categorized into three general groups with respect to their response to resuscitative maneuvers.

circulatory volume rapidly. The most important factor in considering the procedure and route for vascular access is the anatomical location and magnitude of hemorrhagic injuries and the individual physician’s level of skill and expertise. Venous access must never be initiated in an injured limb. In patients with injuries below the diaphragm, at least one IV line should be placed in a tributary of the superior vena cava, as there may be vascular disruption of the inferior vena cava. In patients with severe multiple trauma in whom occult thoracoabdominal damage is suspected, it is recommended to have one IV access site above the diaphragm and one below the diaphragm, thus accessing both the superior vena cava and inferior

vena cava, respectively. For rapid administration of large amounts of intravenous fluids, short large-bore catheters should be used. Doubling the internal diameter of the venous cannula increases the flow through the catheter 16-fold. When using 8.5 French pulmonary catheter introducers, the side port should be removed, as this increases the resistance roughly 4-fold. ATLS™ guidelines recommend rapid placement of two large-bore (16-gauge or larger) IV catheters in the patient with serious injuries and hemorrhagic shock.85 The first choice for IV insertion should be a peripheral extremity vein. The most suitable veins are at the wrist, the dorsum of the hand, the

Management of Shock it is possible to achieve IV access through standard percutaneous IV catheters or a central venous catheter.

Resuscitation Fluids The type of fluid used for resuscitation is as important as the volume infused. Despite the fact that lactated Ringers continue to be used in most civilian trauma centers, there is an increasing experience being accrued with the use of 6% hetastarch in a balanced salt solution (Hextend) as a fluid of choice for combat casualties. This conduct resulted from the tactical need to provide effective intravascular volume repletion with smaller volumes of fluids. Unfortunately there are little data available at this time to ascertain whether or not clinical outcomes with Hextend are superior when compared to what has been recommended traditionally by the ATLS. There are recent studies indicating that other fluids may have a greater positive impact as first line for resuscitation therapy. These include the use of FFP and lyophilized frozen plasma. A large animal model comparing Hextend to FFP and treatment with an equal ratio of FFP to PRBC showed that Hextend-treated animals displayed a greater coagulopathy, yet it could be rapidly reversed with the administration of blood components. In this study, infusion of FFP, even without any red blood cells, corrected the coagulopathy and resulted in high early survival.86 It is likely that we will see newer and more sophisticated choices available for fluid therapy in shock. A promising alternative is the introduction of lyophilized plasma (LP). In a recent large animal model, the use of LP was found to be safe and effective as FFP for resuscitation after severe trauma.87 LP was analyzed for factor levels and clotting activity before lyophilization and after reconstitution. Animals were subjected to a clinically comparable injury complex including multiple trauma characterized by extremity fracture, hemorrhage, severe liver injury, acidosis, and hypothermia. The authors reported that submitting FFP to lyophilization decreased clotting factor activity by an average of 14%. However, animals treated with LP had similar coagulation profiles, plasma lactate levels, and postinjury blood loss compared with those treated with FFP. Finally, it is now clear that the role of hypertonic saline as a first-line resuscitative fluid can no longer be recommended. The Resuscitation Outcomes Consortium (ROC) trials for both shock and traumatic brain injury were halted after preliminary data showed no beneficial effect of hypertonic saline for either one of the groups studied in the clinical trials. In both the shock and traumatic brain injury ROC hypertonic saline trials, patients were randomly selected to receive approximately 250 mL of intravenous normal saline, 250 mL of hypertonic saline, or 250 mL of hypertonic saline with dextran thought to prolong the effect of the hypertonic saline. The trauma shock study tested whether hypertonic solutions improve survival by 28 days after injury. Both the hypotensive shock study and the traumatic brain injury study were halted.

Hypotensive Resuscitation Traditionally, the management of patients in shock has been focused on providing aggressive fluid resuscitation with crystalloid or colloid solutions to rapidly restore circulating blood

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antecubital fossa in the arm, and the saphenous in the leg. These sites can be followed by the external jugular and femoral vein. The complication rate of properly placed intravenous catheters is low. Intravascular placement of a large-bore IV should be verified by checking for backflow. An IV site should infuse easily without added pressure. Intravenous fluids can leak into soft tissues when pumped under pressure through an infiltrated IV line, and may create a compartment syndrome. Patient in extremis who lose pulses in the trauma bay need a cut down in the femoral vein. Subclavian and internal jugular (IJ) catheterization should not be used routinely in hypovolemic trauma patients. The incidence of complications is higher and the rate of success is low due to vascular venous collapse. Rapid peripheral percutaneous IV access may be difficult to achieve in patients with hypovolemia and venous collapse, edema, obesity, scar tissue, history of IV drug abuse, or burns. Under such circumstances, central access with wide-bore catheters may be attempted by percutaneous femoral puncture or cutdown. Subclavian catheterization provides rapid and safe venous access in experienced hands. The most frequent complication of subclavian venipuncture is pneumothorax. Pneumothorax is more likely to occur on the left side because the left pleural dome is anatomically higher. Subclavian and IJ catheters should be inserted on the side of injury in patients with chest wounds, reducing the chances of collapse of the uninjured lung. A simple pneumothorax may result in respiratory compromise in individuals with pulmonary contusions or a pneumothorax in the contralateral hemithorax. It is extremely rare that a subclavian catheterization may be used as a first line of resuscitation in the trauma bay. Regardless of the site of insertion, it is extremely important not to force the wire or the introducer if resistance is encountered. Forcing the introducer could result in perforation of large veins or arteries and bleeding. Venous air embolism is another complication of central line insertion. Any lines placed during resuscitation of a trauma patient without strict aseptic technique should be removed as soon as the patient’s condition allows for it. Although percutaneous placement of IJ catheters is an excellent means of attaining rapid large-bore catheter access, this is a rather unusual site for intravenous insertion in trauma patients because of the possibility of cervical trauma and the need for cervical collar immobilization. Femoral vein cannulation is another alternative for line placement and is associated with fewer acute complications. Penetration of the hip could result in septic arthritis. Thrombophlebitis occurs more often with femoral than with IJ or subclavian catheters; however, this is most likely with prolonged use. Venous cutdowns can be performed when rapid, secure, large-bore venous cannulation is desirable, such as in hemodynamic shock and in situations where percutaneous peripheral or central access is either contraindicated or impossible to achieve. Strict aseptic technique should be used. Surgical masks and caps should be worn. Venous cutdown has a low potential for anatomical damage. Cutaneous nerve injury is the most common problem. The infection rate is relatively low when used acutely but increases over time. Therefore, it is recommended that venous cutdown catheters be removed as soon as

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volume and thus maintaining vital organ perfusion. This approach can potentially increase bleeding by elevating the blood pressure and dislodging established blood clots.88 Other unwanted effects of aggressive fluid resuscitation include worsening coagulopathy and increased tissue edema, which may play a role in the occurrence of abdominal compartment syndrome and multiple organ failure (MOF). Hypotensive resuscitation is not a new concept; in 1918, Cannon et al. described the deleterious effects of injecting fluids before the surgeon could achieve vascular control of the injury.5 Cannon suggested an end point of resuscitation prior to definitive hemorrhage control of a systolic pressure of 70–80 mm Hg, using a crystalloid/colloid mixture as his fluid of choice. In World War II, Cannon’s recommendations were followed by Beecher89 who developed Cannon’s hypotensive resuscitation principals specifically for the care of combat casualties with truncal injuries. This approach was primarily an attempt to minimize transfusion volume and blood loss in the operating room. Bickell et al. in 1994 published a classic prospective analysis comparing immediate and delayed fluid resuscitation in hypotensive adult trauma patients with penetrating torso injuries in the city of Houston.12 In the delayed group, fluid administration was withheld until the time of operative intervention. Improved survival was seen in this study population, with a trend toward fewer complications. These data corroborated the concept that delaying fluid resuscitation until hemorrhage is controlled improves outcome in a selected group of penetrating trauma patients. In subsequent publications following Bickell’s original paper, other investigators have shown that increased prehospital time associated with attempts to place an intravascular access as well as the prehospital use of rapid infusion was correlated with increased mortality.90–92 More importantly, the findings reported by Dutton in 2002 were not significantly different when patients were randomized to either a blood pressure of 70 mm Hg or systolic blood pressures of 100 mm Hg.90 This study showed once more that blood pressure is a poor end point of resuscitation in injured patients. Management protocols currently instituted by the military recommend the use of radial pulse and the presence of a normal mental status as the most appropriate indicators of adequate perfusion. Combat casualties found at the scene with a palpable radial pulse and normal mentation are given intravenous access but no intravenous fluids are infused until arriving to a far-forward facility where initial surgical management can be instituted. Preservation of native hemostatic mechanisms is best achieved by allowing for a lower than normal blood pressure and therefore reducing the rate of bleeding. The characteristics of the local environment, the type of injury, and whether fast and adequate hemostasis can be promptly achieved are the current determinants for the use of hypotensive resuscitation during prehospital care.

FORMS OF SHOCK ■ Hypovolemic Shock Hypovolemic shock occurs when rapid loss of fluids results in inadequate circulating volume and subsequent inadequate

perfusion. As previously noted, the most common cause of shock in the trauma patient is loss of circulating volume from hemorrhage. Acute blood loss causes decreased stimulation of baroreceptors (stretch receptors) in the large arteries resulting in decreased inhibition of vasoconstrictor centers in the brainstem, increased stimulation of chemoreceptors in vasomotor centers, and diminished output from atrial stretch receptors. These changes increase vasoconstriction and peripheral arterial resistance. Hypovolemia also induces sympathetic stimulation leading to the release of epinephrine and norepinephrine, activation of the renin–angiotensin cascade, and increased release of vasopressin. Peripheral vasoconstriction is prominent while lack of sympathetic effects on cerebral and coronary vessels and local autoregulation promote maintenance of blood flow to the heart and brain.15

Diagnosis Shock in a trauma patient should be presumed to be due to hemorrhage until proven otherwise. Treatment is instituted as soon as shock is identified, typically before a source of hemorrhage is located. The clinical and physiologic response to hemorrhage has been classified according to the magnitude of volume loss.85 Loss of up to 15% of the circulating volume (700–750 mL for a 70-kg patient) may produce little in terms of obvious symptoms, while loss of up to 30% of the circulating volume (1.5 L) may result in mild tachycardia, tachypnea, and anxiety. Hypotension, marked tachycardia (pulse 110–120 beats/min), and confusion may not be evident until more than 30% of the blood volume has been lost, while loss of 40% of circulating volume (2 L) is immediately life-threatening. Thus, there is a fine line between the development of mild symptoms of shock and the presence of life-threatening blood loss. Young, healthy patients with vigorous compensatory mechanisms may tolerate larger volumes of blood loss while manifesting fewer clinical signs. These patients may maintain a near-normal blood pressure until a precipitous cardiovascular collapse occurs. Elderly patients may be taking medications that either promote bleeding (warfarin, aspirin) or mask the compensatory response to hypovolemia (β-blockers). In addition, atherosclerotic vascular disease, diminished cardiac compliance with age, inability to elevate heart rate or cardiac contractility in response to hemorrhage, and overall decline in physiologic reserve decrease the ability of the elderly patient to tolerate hemorrhage.93,94 Understanding the mechanism of injury of the patient in shock will help direct the evaluation and management. Identifying the source of blood loss in patients with penetrating wounds is relatively simple since potential bleeding sources will be located along the known or suspected path of the wounding agent. Patients with penetrating injuries who are in shock usually require operative intervention. Occasionally, patients in shock from penetrating injuries may have problems that are readily treated by simple maneuvers outside the operating room. Treatment of a tension pneumothorax with insertion of a thoracostomy tube in the emergency department (ED) is one example. Generally speaking, though, shock from penetrating wounds is typically due to ongoing hemorrhage that mandates operative control.

Management of Shock

Treatment Control of ongoing hemorrhage is a central component of resuscitation of the patient in shock, and is part of the primary survey. Treatment of hemorrhagic shock is instituted concurrently with diagnostic evaluation to identify a source. As mentioned earlier, all trauma patients in shock should be presumed to have hemorrhage until proven otherwise. The method of treatment will depend on the patient’s response to resuscitation, the specific injury or injuries responsible for the blood loss, and consideration of factors such as mechanism of injury, age of the patient, associated injuries, and institutional resources. Patients who fail to respond to initial resuscitative efforts should be assumed to have ongoing active hemorrhage from major vessels (external bleeding, pleural cavity, peritoneal cavity, retroperitoneum, or both thighs) and require prompt operative intervention. Identification of the body cavity harboring active hemorrhage will help focus operative efforts, but since time is of the essence, rapid treatment is essential and diagnostic laparotomy or thoracotomy may be indicated. The

actively bleeding patient cannot be resuscitated until control of ongoing hemorrhage is achieved. Patients who respond to initial resuscitative efforts but then deteriorate hemodynamically frequently have injuries that require operative intervention. The duration of their response will dictate whether diagnostic maneuvers can be performed to identify the site of bleeding. Usually, however, hemodynamic deterioration denotes ongoing bleeding for which some form of intervention (operation, interventional radiology) is required. As noted above, patients who have lost significant intravascular volume with cessation of hemorrhage will often respond to resuscitative efforts if the depth and duration of shock have been limited. A subset of patients fails to respond to resuscitative efforts despite adequate control of ongoing hemorrhage. These patients present in the following manner: have ongoing fluid requirements despite adequate control of hemorrhage; have persistent hypotension despite restoration of intravascular volume; often require vasopressor support to maintain their systemic blood pressure; and may exhibit a futile cycle of uncorrectable hypothermia, hypoperfusion, acidosis, and coagulopathy that cannot be interrupted despite maximum therapy. These patients have classically been described to be in decompensated or irreversible shock,60 and mortality is inevitable once the patient manifests shock in its terminal stages; however, this is always a diagnosis made in retrospect. Hemodynamic decompensation or the paradoxical peripheral vasodilation that occurs with prolonged hemorrhage has been studied in animal models of shock,13,96 but the mechanisms responsible for its development and the clinical factors that predict its onset in humans with shock have not been elucidated. In patients with hemorrhagic shock, survival is improved if the time between injury and control of bleeding is reduced. Clarke et al. demonstrated that trauma patients with major abdominal injuries requiring emergency laparotomy had an increased probability of death with increasing length of time in the ED.97 This probability increased approximately 1% for every 3 minutes in the ED up to 90 minutes. The priorities in patients with hemorrhagic shock are (a) secure the airway, (b) support breathing and ventilation, and (c) control the source of hemorrhage and volume resuscitation. In trauma, identifying the body cavity harboring active hemorrhage will help focus the operative effort. Because time is of the essence, simultaneous and rapid evaluation and treatment is essential. Diagnostic laparotomy or thoracotomy may be indicated. The actively bleeding patient cannot be resuscitated until control of ongoing hemorrhage has been achieved. There has been evolution in the management of these patients known as damage control resuscitation.98 This strategy begins in the ED, continues into the operating room, and into the intensive care unit. Initial resuscitation is limited to keep systolic blood pressure around 90 mm Hg. Overly aggressive resuscitation during this phase has been shown to increase bleeding from recently clotted injured vessels. Intravascular volume resuscitation is accomplished with blood products and limited crystalloids. Too little volume infusion with resultant persistent hypotension and hypoperfusion is dangerous, yet overly vigorous resuscitation may be just as deleterious, and results in dilutional coagulopathy,

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Patients who suffer multisystem injuries from blunt trauma have multiple sources of potential hemorrhage. There are a limited number of sites, however, that can harbor sufficient extravascular blood volume to induce hypoperfusion or hypotension. Prehospital medical reports may confirm a significant blood loss at the scene of an accident, history of massive blood loss from wounds, visible brisk bleeding, or presence of an open wound in proximity to a major vessel. Injuries to major arteries or veins should be suspected when there is ongoing hemorrhage from an open pelvic fracture. Persistent bleeding from uncontrolled small vessels can, over time, precipitate shock if left untreated. However, attributing profound blood loss to these wounds (i.e., scalp lacerations) should be done only after major intracavitary bleeding has been excluded. When major blood loss is not immediately visible, internal (intracavitary) blood loss should be suspected. Intraperitoneal hemorrhage is probably the most common source of blood loss inducing shock. Its presence may be suspected based on physical examination (distended abdomen, abdominal tenderness, visible abdominal wounds), although the sensitivity of the physical exam for detecting substantial abdominal injuries after blunt trauma is unreliable. A large volume of intraperitoneal blood from abdominal injuries may be present before the physical examination is abnormal. Therefore, ultrasound Focused Assessment Sonography in Trauma (FAST) or diagnostic peritoneal lavage is used frequently in the resuscitation area to rapidly identify intraperitoneal blood. In selected patients, diagnostic laparotomy may be indicated. Each pleural cavity can hold 2–3 L of blood and can, therefore, also be a site of significant blood loss. Diagnostic and therapeutic tube thoracostomy may be indicated in patients based on clinical findings, clinical suspicion, or evidence of a hemopneumothorax on a chest x-ray or pleural FAST. Major retroperitoneal hemorrhage occurring in association with a pelvic fracture can be diagnosed by pelvic radiography in the resuscitation bay. The pattern of the pelvic fracture may provide clues as to the risk of massive blood loss.95

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compartment syndromes, acute lung injury, cerebral edema, acid–base and electrolyte disorders, and immune dysfunction. Control of hemorrhage is achieved in the operating room or angiography suite, and efforts to prevent hypothermia and coagulopathy are employed in emergency department (ED), operating room, and intensive care unit. Cannon made the observation that attempts to increase systolic blood pressure in soldiers with uncontrolled sources of hemorrhage are counterproductive, with increased bleeding and higher mortality.3 Several animal studies have confirmed the observation that attempts to restore normal blood pressure with fluids or vasopressors in the setting of active bleeding were rarely achievable and resulted in increased bleeding and higher mortality. A prospective, randomized clinical study compared delayed fluid resuscitation (on arrival in the operating room) with standard fluid resuscitation (with arrival of the paramedics) in hypotensive patients with penetrating torso trauma.12 The authors report that delayed fluid resuscitation resulted in a lower patient mortality. From these and other studies it is reasonable to conclude that in the setting of uncontrolled hemorrhage, any delay in surgical control of bleeding may increase mortality; with uncontrolled hemorrhage, attempting to achieve normal blood pressure may increase mortality, particularly with penetrating injuries and short transport times; a goal of systolic blood pressure of 80–90 mm Hg may be adequate in the patient with penetrating injury; and profound hemodilution should be avoided by early transfusion of red blood cells. For the patient with blunt injury, where the major cause of death is traumatic brain injury, the increase of mortality with hypotension in the setting of brain injury must be avoided. In this setting, a systolic blood pressure of 110 mm Hg would seem to be more appropriate. Transfusion of packed red blood cells and other blood products is essential in the treatment of the patient in hemorrhagic shock. FFP should also be transfused in patients with massive bleeding or patients with bleeding and associated coagulopathy. Civilian and military trauma data show that the severity of coagulopathy after injury is predictive of mortality.99,100 A number of retrospective studies in military and civilian studies support the early use of FFP in bleeding trauma patients who require massive transfusion. Data collected from a US Army combat support hospital in patients who required massive transfusion of packed red blood cells (defined as the requirement for 10 U of packed red blood cells in a 24-hour period) suggest that a high plasma to RBC ratio (1:1.4 U) was independently associated with improved survival.100 A number of retrospective studies in the civilian population support the concept of transfusing FFP, platelets, and packed red blood cells in a 1:1:1 ratio.101,102 While these data are retrospective, a number of civilian trauma centers have adopted this paradigm. A multicenter prospective study of massive transfusion is currently ongoing to address this question.

capacitance, decreased venous return, and decreased cardiac output. Neurogenic shock is usually due to injuries to the spinal cord from fractures of the cervical or high thoracic vertebrae that disrupt sympathetic regulation of peripheral vascular tone. Occasionally, an injury such as an epidural hematoma impinging on the spinal cord can produce neurogenic shock without an associated vertebral fracture. Penetrating wounds to the spinal cord can produce neurogenic shock, as well. Sympathetic input to the heart that normally increases heart rate and cardiac contractility and input to the adrenal medulla that increases the release of catecholamines can be disrupted by a high injury to the spinal cord, preventing the typical reflex tachycardia that occurs with the relative hypovolemia from increased venous capacitance and loss of vasomotor tone. Acute spinal cord injury results in activation of multiple secondary injury mechanisms: (a) vascular compromise to the spinal cord with loss of autoregulation, vasospasm, and thrombosis, (b) loss of cellular membrane integrity and impaired energy metabolism, and (c) neurotransmitter accumulation and release of free radicals. Importantly, hypotension contributes to the worsening of acute spinal cord injury as a result of further reduction in blood flow to the injured spinal cord.

■ Neurogenic Shock

Treatment

Neurogenic shock refers to diminished tissue perfusion as a result of loss of vasomotor tone to peripheral arterial beds. Loss of vasoconstrictor impulses results in increased vascular

After the airway is secured and ventilation is adequate, fluid resuscitation and restoration of intravascular volume will often improve systemic blood pressure and perfusion in neurogenic

Diagnosis The classic description of neurogenic shock consists of decreased blood pressure associated with bradycardia (absence of reflexive tachycardia due to disrupted sympathetic discharge), warm extremities (loss of peripheral vasoconstriction), motor and sensory deficits indicative of an injury to the spinal cord, and radiographic evidence of a fracture in the vertebral column. Determining the presence of neurogenic shock may be difficult, however, since patients with multisystem trauma that includes an injury to the spinal cord often have a traumatic brain injury that may make identification of motor and sensory deficits difficult. Furthermore, associated injuries may cause hypovolemia and complicate the clinical presentation. In a subset of patients with injuries to the spinal cord from penetrating wounds, most patients with hypotension had blood loss as the etiology (74%) and not a neurogenic cause, and few (7%) had all the classic findings of neurogenic shock.103 Hypovolemia should be sought and excluded before the diagnosis of neurogenic shock is made. To assume that the cause of hypotension in a multiply injured patient is due to neurogenic shock without first evaluating and treating potential hemorrhage is often a costly mistake. In patients who have neurogenic shock, the severity of the spinal cord injury seems to correlate with the magnitude of the cardiovascular dysfunction. Patients with complete motor deficits from spinal cord injury are over five times more likely to require vasopressors for neurogenic shock compared to those with incomplete lesions.104

Management of Shock

■ Cardiogenic Shock Cardiogenic shock refers to a failure of the circulatory pump leading to diminished forward flow and subsequent tissue hypoxia, in the setting of adequate intravascular volume. Hemodynamic criteria for cardiogenic shock include sustained hypotension (i.e., systolic blood pressure 90 mm Hg for at least 30 minutes), reduced cardiac index (2.2 L/(min m2)), and elevated pulmonary artery occlusion pressure (15 mm Hg).106 Acute myocardial infarction is the most common cause of cardiogenic shock. In this population, mortality for cardiogenic shock ranges between 50% and 80%. In the trauma patient, inadequate cardiac function after blunt thoracic trauma can be due to blunt myocardial injury, cardiac arrhythmia, myocardial infarction, or direct injury to a cardiac valve. As the average age of the population increases, the prevalence of comorbid medical conditions in trauma patients will also increase. Elderly patients with preexisting intrinsic cardiac disease will be more susceptible to suffering an acute myocardial infarction or significant arrhythmia associated with the stress of injury that can also induce cardiac failure and cardiogenic shock. Diminished cardiac output or contractility in the face of adequate intravascular volume (preload) may lead to underperfused vascular beds and reflexive sympathetic discharge. Increased sympathetic stimulation of the heart, either through direct neural input or from circulating catecholamines, increases heart rate, myocardial contraction, and myocardial oxygen consumption. Patients with fixed, flowlimiting stenoses of the coronary arteries may not be able to increase coronary perfusion to meet the increased myocardial oxygen demands and these lesions, therefore, further increase the risk for myocardial damage.15 Diminished cardiac output decreases coronary artery blood flow, resulting in a scenario of increased myocardial oxygen demand at a time when

myocardial oxygen supply may be limited. Acute heart failure can also result in fluid accumulation in the pulmonary microcirculatory bed, impairing the diffusion of oxygen from the alveolar space and decreasing myocardial oxygen delivery even further.

Diagnosis Rapid identification of the patient with pump failure and institution of corrective actions are essential in preventing further decreases in cardiac output after such an injury. If increased myocardial oxygen needs cannot be met, there will be progressive and unremitting cardiac dysfunction. Blunt injury to the heart is rarely severe enough to induce pump failure,107 but manifestations of shock in the setting of a patient at risk should raise one’s index of suspicion. Evidence of blunt thoracic injury such as sternal fracture, multiple rib fractures, tenderness or hematomas in the chest wall or precordial area, or a history of a direct precordial impact identifies a patient at increased risk for a blunt cardiac injury. Elderly patients with known preexisting cardiac disease are at increased risk of suffering injury-related cardiac complications including cardiac failure. Furthermore, elderly patients with intrinsic cardiac disease are at risk to suffer a primary cardiac event that induces syncope, a fall, or loss of control of one’s vehicle that then leads to presentation to a trauma center. Making the diagnosis of cardiogenic shock involves the identification of cardiac dysfunction or acute heart failure in a susceptible patient. Since patients with blunt cardiac injury typically have multisystem trauma,108,109 hemorrhagic shock from intra-abdominal bleeding, intrathoracic bleeding, and bleeding from fractures must be excluded. Most instances of blunt cardiac injury are self-limited with no long-term cardiac sequelae. Relatively few patients with blunt cardiac injury will develop dysfunction of the cardiac pump and those who do generally exhibit cardiogenic shock early in their evaluation.107 Therefore, establishing the diagnosis of blunt cardiac injury is secondary to excluding other etiologies for shock and establishing that significant cardiac dysfunction is present. Invasive cardiac hemodynamic monitoring, which generally is not necessary, may be useful in the complex patient with the combination of hemorrhagic shock and cardiogenic shock, or when it is necessary to exclude right ventricular infarction and mechanical cardiac complications, or in the patient with known preexisting myocardial disease. This typically involves continuous monitoring of cardiac output and other hemodynamic variables using the pulmonary artery catheter.110–113 Invasive hemodynamic monitoring with a pulmonary artery catheter can reveal diminished cardiac output and elevated pulmonary artery pressures and also may be used to guide the response to therapy. Transesophageal echocardiography (TEE) provides excellent views of the pericardium that are not interfered with by subcutaneous air, bandages covering chest wounds, chest tubes, or unfavorable body habitus that may limit evaluation of cardiac function by transthoracic echocardiography. The rapid evaluation of cardiac function by TEE may be problematic, however, in the presence of severe cervical trauma, maxillofacial trauma, or unstable injuries to the cervical spine that can interfere with placement of the probe. TEE also requires

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shock. Most patients with neurogenic shock will respond to volume resuscitation alone, with adequate improvement in perfusion and resolution of hypotension. Administration of vasoconstrictors can improve peripheral vascular tone, decrease vascular capacitance, and increase venous return, but should only be considered once hypovolemia is excluded and the diagnosis of neurogenic shock established. If the patient’s blood pressure has not responded to appropriate volume resuscitation, continuous infusion of dopamine or a pure α-agonist such as phenylephrine may be used. Specific treatment for the shock state per se is often brief and the need to administer vasoconstrictors typically lasts only 24–48 hours. The duration of the need for vasopressor support for neurogenic shock may correlate with the overall prognosis for improvement in neurologic function.104 Appropriate rapid restoration of blood pressure and circulatory perfusion may also improve perfusion to the spinal cord, prevent progressive ischemia of the spinal cord, and minimize secondary injury to the spinal cord.105 Restoration of normal hemodynamics should precede any operative attempts to stabilize the vertebral fracture. Patients who are hypotensive from spinal cord injury are best monitored in intensive care unit, and carefully followed for evidence of cardiac or respiratory dysfunction.

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experienced ultrasonographers who may not be rapidly available at all hours. Trauma surgeons are becoming increasingly more experienced in the use of ultrasound as part of the initial resuscitation. While the sensitivity of surgeon-performed ultrasound to diagnose penetrating cardiac wounds may be high,114,115 the ability of surgeons to effectively evaluate cardiac performance as part of the ultrasound examination for trauma has not been established.

Treatment Patients with blunt cardiac injury will often have associated injuries that produce hypovolemia, and expansion of intravascular volume as an initial maneuver can improve perfusion significantly. However, hypervolemia can magnify the physiologic derangements produced by cardiac dysfunction and should be avoided. When profound cardiac dysfunction exists, ionotropic support may be indicated to improve cardiac contractility and cardiac performance.116 Dobutamine stimulates primarily cardiac β1 receptors to increase cardiac output, but may also vasodilate peripheral vascular beds, lower total peripheral resistance, and lower systemic blood pressure through effects on β2 receptors. Ensuring adequate preload and intravascular volume is, therefore, essential prior to instituting therapy with dobutamine. Dopamine stimulates α receptors (vasoconstriction), β1 receptors (cardiac stimulation), and β2 receptors (vasodilation) with its effects on receptors predominating at low doses. Epinephrine stimulates β receptors and may increase cardiac contractility and heart rate, but can also cause intense peripheral vasoconstriction that can further impair cardiac performance. It is important to balance the beneficial effects of improved cardiac performance versus the potential side effects of excessive reflex tachycardia and peripheral vasoconstriction. This will require serial assessment of tissue perfusion including capillary refill, character of peripheral pulses, adequacy of urine output, or improvement in laboratory parameters of resuscitation such as arterial blood pH, BD, and lactate. Patients whose cardiac dysfunction is refractory to cardiotonics may require mechanical circulatory support with an intra-aortic balloon pump.116 This can be inserted at the bedside in the intensive care unit via the femoral artery through either a cutdown or percutaneous approach. Aggressive circulatory support of patients with cardiac dysfunction from intrinsic cardiac disease has led to more widespread application of these devices and more familiarity with their operation by both physicians and critical care nurses. Patients who have suffered an acute myocardial infarction following injury should have preservation of existing myocardium and cardiac function as priorities of therapy. This is accomplished by the following: ensuring adequate systemic oxygen delivery and peripheral tissue oxygenation, maintaining adequate preload with judicious volume restoration, minimizing sympathetic discharge through adequate relief of pain, and correcting electrolyte imbalances. The use of anticoagulation or thrombolytic therapy for the management of acute coronary syndromes will depend on associated injuries and the risk of secondary intracavitary or intracranial bleeding. Patients in cardiac failure from an acute myocardial infarction may benefit from pharmacologic or mechanical circulatory support in a

manner similar to that of patients with cardiac failure related to blunt cardiac injury. There are additional pharmacologic tools that are useful in patients with cardiac ischemia from intrinsic coronary artery disease. These include the use of β-blockers to control heart rate and myocardial oxygen consumption, nitrates to promote coronary blood flow through vasodilation, and ACE inhibitors to reduce ACE-mediated vasoconstriction that increases myocardial workload and oxygen consumption.117 Selected patients who do not have significant associated injuries may be candidates for coronary angiography and subsequent procedures to improve coronary blood flow such as transluminal angioplasty, coronary artery stents, or urgent coronary artery bypass grafting.

■ Septic Shock (Vasodilatory Shock) A multidisciplinary consensus has established some useful definitions for the patient with an inflammatory response and sepsis.118 First, the systemic inflammatory response syndrome (SIRS) occurs as a response to a wide variety of physiologic insults, and is defined as the presence of two or more of the following conditions: temperature 38°C or 36°C, pulse rate 90 beats/min, respiratory rate 20 breaths/min or PaCO2 32 mm Hg, white blood cell count 12,000/mm3 or 4000/mm3, or 10% immature (band) forms. Sepsis is defined as the systemic inflammatory response to infection. In association with infection, manifestations of sepsis are the same as those previously defined for SIRS. Severe sepsis occurs when sepsis is associated with hypoperfusion and organ dysfunction. Perfusion abnormalities may be manifested by lactic acidosis, oliguria, or an acute alteration in mental status. Septic shock is a subset of severe sepsis and is defined as sepsis-induced hypotension despite adequate fluid resuscitation along with the presence of perfusion abnormalities that may include, but are not limited to, lactic acidosis, oliguria, or an acute alteration in mental status. Patients who require inotropic or vasopressor agents may no longer be hypotensive by the time they manifest hypoperfusion abnormalities or organ dysfunction, yet they would still be considered to have septic shock.119 Septic shock is a clinical syndrome that occurs as part of the body’s immune and inflammatory response to invasive or severe localized infection, typically from bacterial or fungal pathogens. In its attempt to eradicate the pathogens, the reticuloendothelial system elaborates a wide array of protein mediators (cytokines). These mediators enhance effector mechanisms for macrophage and neutrophil killing, increase procoagulant activity and fibroblast activity to localize the invaders, and increase microvascular blood flow to enhance delivery of killing forces to the area of invasion. When this response is overly exuberant or becomes systemic rather than localized, manifestations of sepsis may be evident. These findings include peripheral vasodilation, fever, leukocytosis, and tachycardia.120,121 Sepsis is an uncommon etiology for shock in the acute presentation of a trauma patient unless there has been a substantial delay between injury and presentation to the ED. Typically, invasive infection in the injured patient occurs days to weeks after injury and is prevalent in the severely injured patient who develops a nosocomial infection in the intensive care unit.

Management of Shock

Diagnosis

Treatment Obtunded patients may require intubation to protect their airway while patients whose work of breathing is excessive may require intubation and mechanical ventilation to prevent respiratory collapse. Since vasodilation and a decrease in total peripheral resistance may produce hypotension, restoration of circulatory volume is essential. Since the portal of entry of the offending organism and its identity may not be evident until culture data return or imaging studies are completed, empiric antibiotics that cover the most likely pathogens are chosen. The bacteriologic profile of infectious events in an individual intensive care unit can be obtained from the infection control department and may identify potential responsible organisms. Antibiotics should be tailored to cover the responsible organisms once culture data are available and, if appropriate, the spectrum of coverage narrowed. Long-term empiric use of broad-spectrum antibiotics should be minimized to reduce the development of resistant organisms and avoid the potential complications of fungal overgrowth and antibiotic-associated colitis from Clostridium difficile.122

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Attempts to standardize terminology have led to the establishment of criteria for the diagnosis of sepsis in the hospitalized adult. These criteria include manifestations of the host response to infection (fever, leukocytosis, mental contusion, tachypnea, tachycardia, hypotension, oliguria), as well as identification of an offending organism.118 Septic shock requires the presence of these conditions associated with evidence of tissue hypoperfusion. Recognizing septic shock in the trauma patient begins with defining high-risk groups as follows: critically ill patients in the intensive care unit where nosocomial infection rates are high, patients who have suffered injuries associated with significant contamination (colorectal wounds with fecal spillage, soft tissue wounds embedded with soil or dirt), patients with injuries that may be associated with persistent devitalized tissue (crush injuries), patients whose wounds put them at risk for complications (anastomotic disruption, pancreatic leak), or patients with missed injuries. The clinical manifestations of septic shock should prompt the initiation of treatment before bacteriologic confirmation of an organism or source of active infection is identified. An aggressive search for the source of the infection includes a thorough physical exam, inspection of all wounds, evaluation of intravascular catheters or other foreign bodies, sampling of appropriate body fluids for culture, and adjunctive imaging studies as needed. The hemodynamic parameters characteristic of septic shock include peripheral vasodilatation with resultant decrease in systemic vascular resistance. Initially, there is a decrease in a cardiac output; however, after volume resuscitation the cardiac output will actually be elevated. Changes in cardiac preload and filling pressures will likewise reflect the volume status of the patient. It is unusual to require placement of a pulmonary arterial catheter to guide therapy in patients with septic shock. Most of these patients can be resuscitated according to central venous pressure, ScvO2, and serum lactate.

In the trauma patient, intravenous antibiotics will frequently be insufficient to adequately treat the infection. Source control, that is, drainage of infected fluid collections, removal of infected foreign bodies, and debridement of devitalized tissue are essential to eradicate the infection. This process may require multiple operations. For patients who manifest symptoms of septic shock early in their hospitalization, consideration of the possibility of a missed injury to a hollow viscus should be entertained. Missed abdominal injuries represent a significant source of sepsis and the septic response leading to MODS.123,124 Vasopressor therapy may be required as a supportive measure when hypotension is refractory to volume infusion in patients in septic shock. α-Adrenergic agents promote peripheral vasoconstriction, improve systemic blood pressure, and can be titrated by continuous infusion to target an adequate mean arterial pressure. Unfortunately, high doses of α-adrenergic agents can be associated with tachyarrhythmias, ischemia of the midgut, gangrene of the digits, or the development of hyposensitivity requiring increasing doses to achieve the desired goals. As previously noted, vasopressin has been utilized as an adjunct for the treatment of vasodilatory shock in some centers and may be associated with a decreased need for α-adrenergic agents.125 High doses of vasopressin should be avoided so as to decrease adverse gastrointestinal and cardiovascular side effects. In 2008 the multidisciplinary Surviving Sepsis Campaign published international guidelines for the management of severe sepsis and septic shock.119 These recommendations include the early goal-directed resuscitation of the septic patient during the first 6 hours after recognition, obtaining blood cultures before initiation of antibiotic therapy, prompt performance of imaging to identify the source of infection, the administration of broad-spectrum antibiotic therapy within 1 hour of diagnosis of septic shock, subsequent narrowing antibiotic coverage after microbiologic data are obtained, source control, and administration of crystalloid or colloids for fluid resuscitation. Furthermore, volume resuscitation should be guided by blood pressure, cardiac filling pressures, lactate, and ScvO2. After appropriate filling pressures have been achieved, persistent hypotension should be treated with norepinephrine or dopamine to maintain a target mean arterial pressure 65 mm Hg. Inotropic support with dobutamine should be instituted when cardiac output or ScvO2 remains low despite these maneuvers. Stress-dose glucocorticoid therapy should only be given to patients with septic shock if hypotension is poorly responsive to fluid and vasopressor therapy. Treatment with human recombinant activated protein C should be reserved for patients with severe sepsis and high risk of mortality, with caution for its use in surgical patients or other patients at risk for bleeding. In addition, in the absence of active coronary artery disease or acute hemorrhage, a target hemoglobin of 7–9 g/dL is appropriate. Patients with acute lung injury or ARDS should undergo mechanical ventilation with low tidal volumes (6 mL/kg) and maintaining plateau airway pressures 30 cm H2O. Much controversy has existed regarding tight glycemic control in the septic patient; the most recent large randomized control trials suggest that the complications of tight glycemic control may outweigh the

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benefits,126–128 and therefore maintaining blood glucose 150 mg/dL appears to be a reasonable target. Strategies for immune modulation have been developed for the treatment of septic shock. These include the use of antiendotoxin antibodies, anticytokine antibodies, cytokine receptor antagonists, immune enhancers, anti–nitric oxide compounds, and oxygen radical scavangers.129–135 Each of these compounds is designed to alter some aspect of the host immune response to shock. Most of these strategies, however, have failed to demonstrate efficacy in patients despite utility in well-controlled animal experiments. It is unclear whether the failure of these compounds is due to poorly designed clinical trials, inadequate understanding of the interactions of the complex immune response to injury and infection, or animal models of shock that poorly represent human disease. Recent trials have demonstrated the efficacy of activated protein C in improving mortality from sepsis.136 Subgroup analysis of patients with sepsis, but at low risk of death, did, however, document an increased risk of bleeding complications associated with therapy without a substantial improvement in survival.137 Sepsis and nosocomial infections in critically ill patients continue to represent significant sources of morbidity and consume substantial health care resources. Despite advances in critical care, the mortality rate for severe sepsis remains at 30–50%. In United States, 750,000 cases of sepsis occur annually, one third of which are fatal.138

■ Obstructive Shock Hypoperfusion can be due to mechanical obstruction of the circulation impeding venous return to the heart or preventing cardiac filling. The end result of either of these two events is decreased cardiac output leading to decreased peripheral perfusion. Most commonly, mechanical obstruction is due to the presence of a tension pneumothorax or cardiac tamponade. With either condition, there is decreased cardiac output associated with increased central venous pressure.

Diagnosis and Treatment The manifestations of a tension pneumothorax are the presence of shock in the context of diminished breath sounds over one hemithorax, hyperresonance to percussion, jugular venous distension, and shift of mediastinal structures to the unaffected side. Unfortunately, not all of the clinical manifestations of tension pneumothorax may be evident on physical examination. Hyperresonance may be difficult to appreciate in a noisy resuscitation area. Jugular venous distension or tracheal deviation may be obscured by a cervical collar in the multiply injured patient and not seen unless specifically sought. Furthermore, hypovolemia from concurrent bleeding may diminish central venous pressure and prevent jugular venous distension even when increased pleural or pericardial pressure restricts flow. For the multiply injured patient with hypotension, the placement of bilateral chest tubes may be both diagnostic and therapeutic in this situation. In these circumstances, a chest x-ray is both unnecessary and potentially a dangerous waste of time. When a chest tube cannot be immediately inserted, such as in the prehospital setting, the pleural

space can be decompressed with a large caliber needle inserted in the second interspace at the midclavicular line, or in the fourth or fifth intercostal space at the anterior axillary line. Immediate return of air and rapid resolution of hypotension suggest strongly that a tension pneumothorax was present. Due the immediate threat to life, the diagnosis of tension pneumothorax should be a clinical one. If obtained (which would mean the diagnosis was missed on clinical examination), the typical findings on a chest x-ray include deviation of mediastinal structures, depression of the hemidiaphragm, and hypo-opacification with absent lung markings. Cardiac tamponade results from the accumulation of blood within the pericardial sac and most commonly occurs from penetrating trauma. While precordial wounds are most likely to injure the heart and produce tamponade, any projectile or wounding agent that passes in proximity to the mediastinum can potentially produce tamponade. Blunt rupture of the heart is fortunately rare, but the diagnosis is aided by the FAST exam that is performed immediately on all patients at risk. The manifestations of cardiac tamponade may be as catastrophic as total circulatory collapse and cardiac arrest or they may be more subtle. A high index of suspicion is warranted to make a rapid diagnosis. Patients who present with circulatory arrest due to cardiac tamponade from a precordial penetrating wound require emergency pericardial decompression through a left anterolateral thoracotomy, and the indications for this maneuver are discussed in Chapter 14. Cardiac tamponade may also be associated with tachycardia, muffled heart tones, jugular venous distension, and elevated central venous pressure. Absence of these clinical findings, however, may not be sufficient to exclude cardiac injury and cardiac tamponade. Muffled heart tones may be difficult to appreciate in a busy trauma center and jugular venous distension and central venous pressure may be diminished by coexistent bleeding and hypovolemia. Therefore, patients at risk for cardiac tamponade whose hemodynamic status permits should undergo additional diagnostic tests. Invasive hemodynamic monitoring may support the diagnosis of cardiac tamponade if elevated central venous pressure, pulsus paradoxus (decreased systemic arterial pressure with inspiration), or elevated right atrial and right ventricular pressure by pulmonary artery catheter is present. These hemodynamic profiles suffer from lack of specificity, the time required to obtain them, and their inability to exclude cardiac injury in the absence of tamponade. Chest radiographs may provide information on the possible trajectory of a projectile, but are rarely diagnostic since the acutely filled pericardium distends poorly. Pericardial ultrasound as part of a surgeonperformed FAST examination, through either the subxiphoid or transthoracic approach, is practiced routinely at many trauma centers. Excellent results in detecting pericardial fluid have been reported.114,115 The yield in identifying pericardial fluid obviously depends on the skill and experience of the ultrasonographer, body habitus of the patient, and absence of wounds that preclude visualization of the pericardium. Standard two-dimensional transthoracic or TEE to evaluate the pericardium for fluid is typically performed by cardiologists or anesthesiologists skilled at evaluating ventricular function, valvular abnormalities, and integrity of the proximal thoracic

Management of Shock

■ Traumatic Shock Some authors consider traumatic shock a separate clinical entity.60 The term is used to represent a combination of several insults after injury that, by themselves, may be insufficient to induce shock, but produce profound hypoperfusion when combined. Hypoperfusion from relatively modest loss of volume can be magnified by the proinflammatory activation that occurs following injury or shock. The systemic response after trauma, combining the effects of soft tissue injury, long bone fractures, and blood loss, is clearly a different physiologic insult than simple hemorrhagic shock alone. In addition to ischemia or ischemia/reperfusion, simple hemorrhage induces proinflammatory activation and causes many of the cellular changes typically attributed previously only to septic shock.23,27 Examples of traumatic shock might include small-volume hemorrhage accompanied by injury to soft tissue (femur fracture, crush injury) or any combination of hypovolemic, neurogenic, cardiogenic, and obstructive shock that induces rapidly progressive activation of proinflammatory cytokines. MOF, including ARDS, develops relatively often in the blunt trauma patient, but rarely after pure hemorrhagic shock alone. The hypoperfusion deficit in traumatic shock is magnified by the proinflammatory activation that occurs following the induction of shock. At a cellular level, the pathophysiology of traumatic shock may be attributable to the release of cellular products termed damage-associated molecular patterns (DAMPs, i.e., ribonucleic acid, uric acid, and high mobility group box 1) that activate

the same set of cell surface receptors as bacterial products, initiating similar cell signaling.143 The receptors are termed pattern recognition receptors (PRPs) and include the toll-like receptor (TLR) family of proteins. In laboratory models of traumatic shock, the addition of a soft tissue or long bone injury to the hemorrhage produces lethality with significantly less blood loss than when the animals are stressed by hemorrhage alone. Therapy for this form of shock is focused on correction of the individual elements to diminish the cascade of proinflammatory activation contributing to its existence. Therapeutic maneuvers include prompt control of hemorrhage, adequate volume resuscitation to correct oxygen debt, debridement of nonviable tissue, stabilization of bony injuries, and appropriate treatment of soft tissue wounds.

END POINTS IN RESUSCITATION OF THE TRAUMA PATIENT There is still significant controversy as to how to best determine the effects of the magnitude of shock, specifically, to be able to identify quantitative determinants that are truly indicators of the depth and the duration of shock. If such parameters would be easily measurable, then they would be the ideal end points of resuscitation. Clearly, routinely measured vital signs are not adequate and complex devices used to calculate oxygen delivery are not practical especially early in the resuscitation. Porter and Ivatury performed an extensive review of the data regarding end points for the resuscitation of trauma patients.144 Most clinicians would agree that heart rate, systemic arterial blood pressure, skin temperature, and urine flow provide relatively little information about the adequacy of oxygen delivery to tissues. Accordingly, reliance on these simple indices of perfusion may result in failure to recognize occult or compensated shock. Physiologically, shock begins when oxygen delivery (DO2) falls below the tissue oxygen consumption (VO2) requirements. A persistent mismatch between the DO2 and VO2 has been associated with progressive multiple organ dysfunction. Unfortunately, there are several limitations in our ability to assess perfusion status. Due to these limitations, it is necessary to use surrogates of tissue hypoxia. During anaerobic metabolism, large quantities of pyruvate are converted to lactate rather than entering the tricarboxylic acid cycle. Meanwhile, because of the stoichiometry of substrate-level (as contrasted with oxidative) phosphorylation of ADP to ATP, there is a net accumulation of protons.145 Accordingly, increases in arterial BD or blood lactate concentration are evidence of an increase in the rate of anaerobic metabolism. Numerous studies have documented that high blood lactate levels portend an unfavorable outcome in patients with shock,146 but it has not been proven that survival is improved when therapy is titrated using blood lactate concentration as an end point. BD is the amount of base (in millimoles) required to titrate 1 L of whole blood back to a pH of 7.40 with the sample maintained at 37°C and fully saturated with oxygen

CHAPTER 12

aorta. These skilled examiners are usually not immediately available at all hours and waiting for this test may result in inappropriate delays. In addition, while both ultrasound techniques may demonstrate the presence of fluid or characteristic findings of tamponade (large volume of pericardial fluid, right atrial collapse, poor distensibility of the right ventricle), they do not exclude cardiac injury per se,139,140 and their utility will be discussed in greater detail in Chapter 15. Pericardiocentesis to diagnose pericardial blood and potentially relieve tamponade has a long history in the evaluation of the trauma patient. Its inability to evacuate clotted blood and potential to produce cardiac injury make it a poor alternative in most busy trauma centers. Diagnostic pericardial window represents the most direct method to determine the presence of blood within the pericardium. It can be performed through either the subxiphoid or transdiaphragmatic approach.141,142 Some authors report performing this technique using local infiltrative anesthesia. However, the ability to achieve satisfactory safety and visualization in the trauma victim who may be intoxicated, in pain, or anxious from hypoperfusion usually mandates the use of general anesthesia. Once the pericardium is opened and tamponade relieved, hemodynamics usually improve dramatically and formal pericardial exploration can be performed. Exposure of the heart can be achieved by extending the incision to a formal sternotomy, performing a left anterolateral thoracotomy, or performing bilateral anterior thoracotomies (“clamshell”) as discussed in Chapters 14 and 24.

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and equilibrated with an atmosphere containing carbon dioxide at a PCO2 of 40 mm Hg. In practice, BD is calculated by arterial blood gas analyzers using the nomogram developed by Astrup et al.147 BD has been shown to have prognostic value in patients with shock.148 Although intuitively reasonable, it remains to be proven that titrating therapy to a BD end point improves survival. Until recently, BD was more quickly and easily measured than lactate concentration; however, point-of-care portable lactate assays are now available and used in settings such as during transport in the helicopter or in the prehospital scenario. Preliminary data of prehospital lactate suggest that these values are highly predictive of outcome.149 Few published data have shown that using a monitoring tool to guide resuscitation can improve outcome in critically ill patients.150 Subsequently, Rivers et al. published results from randomized trial of goal-directed therapy for septic shock initiated in the emergency room.151 An algorithm was developed to adjust central venous pressure to 8–12 mm Hg, mean arterial pressure to 65–90 mm Hg, and central venous oxygen saturation to a value greater than 70%. In this study a central venous oximetry catheter was used to titrate resuscitation with the idea of balancing systemic oxygen supply with oxygen demand. The authors found that early institution of goal-directed hemodynamic support prevented cardiovascular collapse in high-risk patients and reduced hospital mortality from 46.5% to 30.5% (P . 009). Recent reviews suggest that our lack of understanding of the effects of shock and resuscitation stem from a discrepancy between the need to identify effective strategies aimed at restoring normal oxygen delivery and the fact that most resuscitation research is aimed at controlling inflammation and coagulopathy. The degree of activation of the inflammatory mechanisms and coagulation derangements are directly related to the magnitude of the hypoxia-induced tissue injury. It is naïve to believe that simply correcting oxygen delivery or modulating a specific pathway would prevent the ensuing of multiple organ dysfunction.152 Until more practical and quantitative methods are introduced to measure the accumulative effect of the oxygen deficit, it is likely that we will continue to use a combination of surrogates of tissue perfusion. We can estimate the magnitude of the systemic insult by assessing the BD or lactic acid at the time of initiating resuscitation and follow how these parameters respond to our interventions. In addition to theses parameters, we can also use noninvasive methods to quantitatively assess the extent of regional ischemia, and we could build a more complete picture of the patient’s magnitude of injury and response to resuscitation. Perhaps the most studied method to measure the adequacy of regional tissue perfusion relies on the application of nearinfrared spectroscopy (NIRS). The introduction of more quantitative and reproducible methods coupled with reliable and practical devices has generated a plethora of clinical studies demonstrating the use of parameters such as tissue oxygen saturation as well as other parameters measured based on optical determinations.

■ Near-Infrared Spectroscopy Introduction NIRS offers a technique for continuous, noninvasive, bedside monitoring of tissue oxygenation. It measures oxygenation in the tissue’s microvasculature and, thus, not only examines the adequacy of tissue perfusion but also provides a potential window to noninvasively study tissue metabolism. In the clinical setting, NIRS has been used for continuous monitoring of metabolic variables including tissue O2 availability,153 tissue O2 consumption, tissue O2 saturation (StO2),154 and changes of rate of StO2 decrease due to vascular occlusion,155,156 in diverse populations of patients (trauma,148,157 sepsis,158 and heart failure) with promising results. However, it is early in the history of this “new” technology and many questions remain unanswered.

NIRS-Derived StO2 is Not Pulse Oximetry NIRS uses the same principles of light transmission and absorption as pulse oximetry to measure StO2. However, StO2 measurements differ in several important ways from the SpO2 measurements provided by pulse oximetry. Importantly, NIRS measurements do not require the arterial pulsatile component on which pulse oximetry relies to derive its estimation. This also means that the saturation of oxygen measured by StO2 belongs not to the arterial compartment as is the pulse oximetry–derived SpO2, but to a different compartment. In fact, the deeper transillumination provided by StO2 allows the assessment of oxygenation in small vascular compartments within the muscle. Given that only 20% of blood volume is stored in the arterial circuit, StO2 is primarily indicative of the venous oxyhemoglobin concentration. Consequently, as opposed to SpO2, StO2 is a measure of the microvasculature, and as such its estimation represents local rather than systemic conditions. Finally, the fact that no oxygen exchange takes place between the thick arterial walls and tissues allows SpO2 to remain fairly constant regardless of whether the measurement is done in the earlobe, fingers, or toes. On the other hand, StO2 may vary depending on the site where the probe is placed.

How does it Work? At physiologic concentrations the molecules that absorb most light are hemoglobin, myoglobin, cytochromes, melanins, carotenes, and bilirubin. These substances can be quantified and measured in intact tissues using simple optical methods. Only three compounds change their spectra when oxygenated: cytochrome aa3, myoglobin, and hemoglobin. Therefore, the assessment of tissue oxygenation by NIRS is based on the specific absorption spectrum of hemoglobin, myoglobin, and cytochrome aa3. The NIRS sensor consists of an emission probe and a detection probe. The interface between the patient and the NIR spectroscope is only this sensor on the distal tip of the NIRS optical cable. The sensor conducts the optical signal to the patient and back to the monitor.

Management of Shock

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FIGURE 12-6 Histogram of StO2 in healthy volunteers. (Reproduced with permission from Crookes BA, Cohn SM, Bloch S, et al. Can nearinfrared spectroscopy identify the severity of shock in trauma patients? J Trauma. 2005;58:806.)

The spacing between the illumination fibers and detection fibers determines the tissue penetration and thus the type of tissue sampled. The NIRS sensors can be used to monitor tissue oxygenation in different tissues as well as different depths within the same tissue. For this purpose, various types of sensors are available, with the only difference being the distance between emission and detection probes. In clinical setting, measuring oxygenation of the thenar muscle is now the most common use. The thenar eminence is said to be the optimal solution because it is easily accessible, has thin subcutaneous tissue, withholds fairly low amounts of fluid during edematous conditions compared to other sites, and provides consistent results among healthy volunteers.157 Crookes et al.157 studied the StO2 in 707 healthy volunteers, and found a mean StO2 of 86 6%. Fig. 12-6 shows a histogram of the thenar StO2 values in 707 healthy human volunteers. Near-infrared light can propagate through tissues and, at particular wavelengths, is differentially absorbed by the oxygenated and deoxygenated forms of hemoglobin, myoglobin, and cytochrome aa3. They all absorb light at 800 nm, whereas at 760 nm absorption is primarily by the deoxygenated forms. These absorption spectra of oxygenated and deoxygenated hemoglobin provide a means to calculate the ratio of oxygenated hemoglobin to total hemoglobin. When measured in the microcirculation of a volume of tissue, this is expressed as percent tissue oxygen saturation (StO2): StO2 

HbO2 HbO2  Hb

Because Mb, Hb, and cytaa3 absorption spectra overlap, they are indistinguishable with NIRS. In muscle tissue, myoglobin accounts for approximately 10% of the NIRS light absorption signal159 and cytaa3 for 2–5%.153 However, the NIRS signal is minimally influenced by myoglobin or cytaa3 oxygen saturation. Changes in muscle blood flow affect the absorption of 760- to 800-nm light and NIRS has the ability to detect significant fluctuations in localized tissue oxygenation secondary

to these flow changes.159 Besides that, NIRS rapidly changes in response to progressive oxygen deprivation and correlates with changes in blood flow and oxygen consumption in skeletal muscle.159,160

NIRS in Hemorrhagic Shock Adequate resuscitation of patients from hemorrhagic shock depends on restoration of oxygen delivery (DO2) to tissues. This process may be monitored in several ways. Traditionally, resuscitation has been monitored indirectly by examination of highly dependent end-organ functions, such as blood pressure, heart rate, urine output, and mental status. Direct measurement of DO2 during shock states requires invasive techniques such as pulmonary artery catheterization. The ideal device for monitoring the adequacy of resuscitation in the trauma patient would have two basic characteristics. It would be noninvasive and it would provide the clinician with an objective parameter that measures oxygenation at the tissue level in end organs. Changes in StO2 induced by experimental hemorrhagic shock are not as profound as those seen in systemic DO2. However, Beilman et al.161 found that skeletal muscle and gastric StO2 measured by noninvasive NIRS strongly correlates with DO2. Changes in the liver StO2 were less correlated, likely reflecting a protected circulation to the hepatic parenchyma. Rhee et al.162 found similar results, but the decrease in liver was larger. McKinley et al.163 compared subcutaneous and skeletal muscle StO2 to invasive DO2 measurements. The correlation of the subcutaneous StO2 was different from skeletal muscle StO2. The authors found that skeletal muscle StO2 correlates well with systemic oxygen delivery. Subcutaneous tissue, as a tissue with primary functions of energy storage and insulation, had lower O2 consumption requirement and less perfusion per unit than other tissues. The lower O2 consumption resulted in extracting less O2 and maintenance of higher StO2. Taylor et al.154 evaluated the utility of NIRS for early determination or irreversibility of hemorrhagic shock. They used skeletal muscle StO2 measurements to study this differentiation.

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FIGURE 12-7 ROC curves of StO2 for prediction of MODS development and mortality. (From Crookes BA, Cohn SM, Bloch S, et al. Can near-infrared spectroscopy identify the severity of shock in trauma patients? J Trauma. 2005;58:806.)

NIRS monitoring provided a means for early differentiation between resuscitatable and nonresuscitatable animals after a period of hemorrhagic shock. Recently, Cohn et al.148 did a prospective multicenter study on 383 traumatic shock patients. They compared the sensitivity and specificity of NIRS StO2 measurements in the first hour after arrival at the emergency room in predicting MODS and death to measurements of maximum BDs and minimum blood pressure. When using a cutoff point StO2 of 75% (StO2 minimum 75% in first hour at ER), they found a sensitivity and specificity of 78% and 39% to predict MODS and 91% and 31% to predict death. Crookes et al.157 studied StO2 in trauma patients. They found that StO2 at admission predicted the development of multiple organ dysfunction and death (Fig. 12-7). They also showed that StO2 absolute values were able to differentiate patients with moderate to severe shock from healthy volunteers. However, StO2 failed to discriminate between healthy volunteers and trauma patients with no shock or with mild shock.

The use of NIRS measurement of cytochrome aa3 redox state in hemorrhagic shock has also been studied. Cytaa3 is the terminal electron carrier in the mitochondrial electron transport chain, and it is rapidly reduced when local tissue oxygen demand exceeds supply. Therefore, during hypoxemia, cytaa3 would remain in a reduced state, reflecting a cellular shift to anaerobic metabolism. However, the cytaa3 contribution to the NIRS light attenuation is very small (about 2–5%). Controversy exists regarding whether NIRS can be used as a valid tool to measure changes in cytochrome oxidase since the influence of Hb is so dominant. Cairns et al.164 studied cytaa3 redox state in trauma patients and found a direct impairment in mitochondrial oxidative function in severely injured patients who later developed MOF. Rhee et al.162 compared conventional parameters of resuscitation with NIRS cytaa3 measurements in a hemorrhagic shock model. They found significant correlations between mitochondrial cytaa3 redox state and DO2 throughout shock and resuscitation, but resuscitation did not uniformly restore cellular

Management of Shock

Muscle Oxidative Metabolism Measured with NIRS The signal obtained by NIRS reflects the state of hemoglobin, myoglobin, and cytaa3 oxygenation, thereby representing the balance between the oxygen supply and consumption. Several groups studied the possibility to dissociate O2 consumption from O2 supply by arterial occlusion with a tourniquet, which is called the ischemic challenge. Hampson and Piantadosi160 were the first to study the skeletal muscle oxygenation in human. They measured the NIRS cytaa3 redox state during forearm tourniquet ischemia in healthy volunteers and reported a significant decrease in muscle oxygenation level in ischemia. By adding exercise at various intensities, these exercise intensities would indicate muscle metabolism. In this way, NIRS-O2 could be a quantitative measure of muscle oxidative metabolism. Hamaoka et al.166 used these exercise theory and compared the NIRS measurements of muscle O2 consumption to 31P magnetic resonance spectroscopy. Their results confirm that the decline rate in NIRS-O2 during arterial occlusion is a quantity of muscle oxidative rate (r  0.98). Boushel et al.167 compared values of muscle oxygen saturation and consumption derived from measurements of NIRS, SvO2 with 31P magnetic resonance spectroscopy. Their results showed that the NIRS-O2 closely reflected the exercise intensity and correlated highly with the MRS-determined metabolic rate in the muscle. In the former studies, the flow to the muscle was not monitored. However, a decrease in oxygen delivery in critically ill patients often involves a combination of decreased flow and decreased saturation.

Guery et al.168 used an isolated perfused pig hind limb to produce an experimental model of controlled hypoxemia and ischemia, allowing to detect the influence of flow on NIRS measurements. In both types of hypoxia they found a high correlation of the cytaa3 redox state and DO2 (r 2  0.90 and 0.87 for, respectively, the ischemic and hypoxic groups). This illustrates that NIRS measurements are well related to DO2 in either ischemic or hypoxic hypoxia. Gomez et al.169 evaluated the deoxygenation and recovery slopes of StO2 after performing a vascular occlusion test (VOT) in healthy volunteers (Fig. 12-8). This was first done at rest and subsequently during exercise. Presumably, the rate of StO2 decline depends on the specific tissue metabolic rate, the volume of microvasculature screened, redistribution phenomena, and hemoglobin concentration. However, VOT should rapidly stop blood flow fixing the total amount of blood in the tissues during the ischemic phase making vascular blood volume constant while eliminating flow. Ischemia-induced changes in vasomotor tone may account for subtle redistribution within the extremity. Nevertheless, such volume shifts should be small owing to the low blood volume. This suggest that, although the absolute StO2 value reflects a balance between three components (hemoglobin flow, relative weights of vascular beds, and metabolic rate), the deoxygenation slope after VOT must represent only the metabolic rate as flow has ceased and redistribution is minimal. By the same token, the recovery slope after VOT release is a function of the local cardiovascular reserve, defined as the tissue’s ability to reoxygenate. In this case, the slope of recovery is influenced by the ischemic level reached prior to release, arterial oxygen saturation (SaO2), local blood flow (which depends on capillary integrity, local blood volume, and local vasomotor tone), perfusion pressure, and local hemoglobin.169 If the level of ischemia and the perfusion pressure are kept constant between repeated measures, then changes in the recovery slope will be a function of changes in cardiovascular reserve, systemic hemoglobin, and SaO2. Also, changes in microvascular integrity, smooth muscle response, or vasomotor tone will modify the recovery slope. Thus, this parameter is a sensitive, but not specific marker of local cardiovascular reserve. The results of this study showed that the deoxygenation slope was faster during exercise when compared to rest, whereas the recovery slope did not change. Furthermore, it was identified that unstable trauma patients had a slower recovery slope than healthy volunteers (2.88 1.71 vs. 5.20 1.19, P . 05). Creteur et al.170 had similar findings regarding the recovery slope, but in patients with septic shock. In addition, this group found that the recovery slope had the ability to predict MODS development and mortality. In summary, the measurement of the redox state of the cytaa3 as well as the estimation of the deoxygenation and recovery slopes has the potential advantage over absolute StO2 measurement, of assessing the oxidative metabolism during ischemia and exercise. This suggests a potential role in noninvasive assessment of metabolism during hypoperfusion states. Nonetheless, there are still questions regarding how these parameters vary according to different resuscitation strategies and also whether it has the potential to guide therapy.

CHAPTER 12

oxygenation in all tissue beds. Despite the normalization of traditional resuscitation parameters, the postresuscitative NIRS values in the gastric and muscular beds were low. NIRS may be useful in identifying regional areas of dysoxia. NIRS has also been used to measure pH, by observing spectral changes in the bond energy of the imidazole ring of histidine residue within hemoglobin. Puyana et al.165 examined NIRS measurements of small bowel pH during hemorrhagic shock. NIRS pH represented an accurate measurement of splanchnic mucosal pH. These findings suggest that NIRS may be useful in measuring not only StO2 but also other important components of tissue metabolism. Furthermore, it may be able to identify at an early stage those patients destined to development of MOF later in their disease. Finally, it may be a useful monitor of differential organ perfusion after resuscitation. In summary, despite some limitations, StO2 measurement seems to be a useful parameter when determining perfusion status and, probably, in predicting the course of disease. The supporting evidence, although favorable, is still scarce as to fully understand the meaning of its measurements and, thus, to recommend its systematic use. Potentially, additional studies will help clarify its strengths and weaknesses and hopefully will continue to endorse the already suggested utility.

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SECTION 2 FIGURE 12-8 Measurement of StO2 during a VOT. Baseline is stable; the forearm cuff is inflated. StO2 is allowed to fall to 40%. The cuff is deflated, and StO2 returns to baseline and overshoots. Deoxygenation and recovery slopes are marked in the figure. (Reproduced from Gomez H, Torres A, Polanco P, et al. Use of non-invasive NIRS during a vascular occlusion test to assess dynamic tissue O-2 saturation response. Intensive Care Med. 2008;34:1600–1607.)

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Management of Shock 154. Taylor JH, Mulier KE, Myers DE, Beilman GJ. Use of near-infrared spectroscopy in early determination of irreversible hemorrhagic shock. J Trauma Inj Infect Crit Care. 2005;58:1119–1125. 155. Pareznik R, Knezevic R, Voga G, Podbregar M. Changes in muscle tissue oxygenation during stagnant ischemia in septic patients. Intensive Care Med. 2006;32:87–92. 156. Skarda DE, Mulier KE, Myers DE, Taylor JH, Beilman GJ. Dynamic near-infrared spectroscopy measurements in patients with severe sepsis. Shock. 2007;27:348–353. 157. Crookes BA, Cohn SM, Bloch S, et al. Can near-infrared spectroscopy identify the severity of shock in trauma patients? J Trauma. 2005;58: 806–816. 158. Podbregar M, Mozina H. Skeletal muscle oxygen saturation does not estimate mixed venous oxygen saturation in patients with severe left heart failure and additional severe sepsis or septic shock. Crit Care. 2007;11:R6. 159. Mancini DM, Bolinger L, Li H, Kendrick K, Chance B, Wilson JR. Validation of near-infrared spectroscopy in humans. J Appl Physiol. 1994;77:2740–2747. 160. Hampson NB, Piantadosi CA. Near-infrared monitoring of human skeletal muscle oxygenation during forearm ischemia. J Appl Physiol. 1988;64:2449–2457. 161. Beilman GJ, Groehler KE, Lazaron V, Ortner JP. Near-infrared spectroscopy measurement of regional tissue oxyhemoglobin saturation during hemorrhagic shock. Shock. 1999;12:196–200. 162. Rhee P, Langdale L, Mock C, Gentilello LM. Near-infrared spectroscopy: continuous measurement of cytochrome oxidation during hemorrhagic shock. Crit Care Med. 1997;25:166–170. 163. McKinley BA, Marvin RG, Cocanour CS, Moore FA. Tissue hemoglobin O-2 saturation during resuscitation of traumatic shock monitored using near infrared spectrometry. J Trauma Inj Infect Crit Care. 2000;48: 637–642. 164. Cairns CB, Moore FA, Haenel JB, et al. Evidence for early supply independent mitochondrial dysfunction in patients developing multiple organ failure after trauma. J Trauma Inj Infect Crit Care. 1997;42: 532–536. 165. Puyana JC, Soller BR, Zhang SB, Heard SO. Continuous measurement of gut pH with near-infrared spectroscopy during hemorrhagic shock. J Trauma Inj Infect Crit Care. 1999;46:9–14. 166. Hamaoka T, Iwane H, Shimomitsu T, et al. Noninvasive measures of oxidative metabolism on working human muscles by near-infrared spectroscopy. J Appl Physiol. 1996;81:1410–1417. 167. Boushel R, Pott F, Madsen P, et al. Muscle metabolism from near infrared spectroscopy during rhythmic handgrip in humans. Eur J Appl Physiol Occup Physiol. 1998;79:41–48. 168. Guery BPH, Mangalaboyi J, Menager P, Mordon S, Vallet B, Chopin C. Redox status of cytochrome a,a3: a noninvasive indicator of dysoxia in regional hypoxic or ischemic hypoxia. Crit Care Med. 1999;27:576–582. 169. Gomez H, Torres A, Polanco P, et al. Use of non-invasive NIRS during a vascular occlusion test to assess dynamic tissue O-2 saturation response. Intensive Care Med. 2008;34:1600–1607. 170. Creteur J, Carollo T, Soldati G, Buchele G, De Backer D, Vincent JL. The prognostic value of muscle StO(2) in septic patients. Intensive Care Med. 2007;33:1549–1556.

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136. Bernard GR, Vincent JL, Laterre P, et al. Efficacy and safety of recombinant human activated protein C for severe sepsis. N Engl J Med. 2001;344:699–709. 137. Abraham E, Laterre P, Garg R, et al. Drotrecogin alfa (activated) for adults with severe sepsis and a low risk of death. N Engl J Med. 2005;353: 1332–1341. 138. Angus DC, Linde-Zwirble WT, Lidicker J, Clermont G, Carcillo J, Pinsky MR. Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care. Crit Care Med. 2001; 29:1303–1310. 139. Bolton JWR, Bynoe RP, Lazar HL, Almond CH. 2-Dimensional echocardiography in the evaluation of penetrating intrapericardial injuries. Ann Thorac Surg. 1993;56:506–509. 140. Freshman SP, Wisner DH, Weber CJ. 2-D echocardiography: emergent use in the evaluation of penetrating precordial trauma. J Trauma. 1991;31:902. 141. Garrison RN, Richardson JD, Fry DE. Diagnostic transdiaphragmatic pericardiotomy in thoracoabdominal trauma. J Trauma. 1982;22:147. 142. Miller FB, Bond SJ, Shumate CR, Polk HC Jr, Richardson JD. Diagnostic pericardial window: a safe alternative to exploratory thoracotomy for suspended heart injuries. Arch Surg. 1987;122:605. 143. Mollen KP, Anand RJ, Tsung A, Prince JM, Levy RM, Billiar TR. Emerging paradigm: toll-like receptor 4—sentinel for the detection of tissue damage. Shock. 2006;26:430–437. 144. Porter JM, Ivatury RR. In search of the optimal endpoints of resuscitation. J Trauma. 1998;44:908–914. 145. Hochachka PW, Mommsen TP. Protons and anaerobiosis. Science. 1983;219:1391–1397. 146. Abramson D, Scalea TM, Hitchcock R, Trooskin SZ, Henry SM, Greenspan J. Lactate clearance and survival following injury. J Trauma Inj Infect Crit Care. 1993;35:584–589. 147. Astrup P, Engel K, Jorgensen K, Siggaard-Andersen O. Definitions and terminology in blood acid–base chemistry. Ann N Y Acad Sci. 1966; 133:59–65. 148. Cohn SM, Nathens AB, Moore FA, et al. Tissue oxygen saturation predicts the development of organ dysfunction during traumatic shock resuscitation. J Trauma Inj Infect Crit Care. 2007;62:44–54. 149. Guyette FX, Hostler D, Suffoletto B, et al. Feasibility of using noninvasive measurements of circulatory shock in critical care transport. Advanced Technology Applications for Combat Casualty Care (ATACCC); August 11–13, 2008; St. Pete’s Beach, FL (Poster presentation). 150. Gutierrez G, Palizas F, Doglio G, et al. Gastric intramucosal Ph as a therapeutic index of tissue oxygenation in critically ill patients. Lancet. 1992;339:195–199. 151. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345: 1368–1377. 152. Barbee RW, Reynolds PS, Ward KR. Assessing shock resuscitation strategies by oxygen debt repayment. Shock. 2010;33:113–122. 153. Boushel R, Langberg H, Olesen J, Gonzales-Alonzo J, Bülow J, Kjaer M. Monitoring tissue oxygen availability with near infrared spectroscopy (NIRS) in health and disease. Scand J Med Sci Sports. 2001;11: 213–222.

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Postinjury Hemotherapy and Hemostasis Fredric M. Pieracci, Jeffry L. Kashuk, and Ernest E. Moore

The ponderous literature on the subject of hemostasis could perhaps be considered a classical example of the infinite ability of the human mind for abstract speculation. For several years, the number of working theories of the hemostatic mechanism greatly exceeded and not always respected the confirmed experimental facts. In recent years, however, the revived interest in this field has led to an accumulation of new findings which has been almost too rapid for their orderly incorporation into a logical working pattern. As a result, we have rapidly gone from a state of “orderly ignorance” to one of “confused enlightenment,” from which we have not emerged as yet. Mario Stefanini, April 19541 The first recorded blood product transfusion to a human being occurred in 1667 in France and involved transfusion of approximately three tablespoons of whole blood from a calf to a man who was suffering from insanity.2 The physician performing the transfusion postulated that the calm temperament of the calf would transfer to the patient via its blood. The procedure was well tolerated, although the patient developed severe flank pain and tar-colored urine following the subsequent three transfusions: the first recorded evidence of immune-mediated hemolysis, albeit unbeknownst to the physician at the time. Although transfusion medicine has undergone enormous development since this sentinel event, as summarized by Stefanini, important gaps in scientific knowledge persist, and several fundamental issues involving hemotherapy following major trauma remain controversial. There has been an explosion in the science of hemostasis, with a resultant revolution in all aspects of the care of the coagulopathic trauma patient. Our understanding of the mechanisms of coagulation has shifted from that of a simple enzymatic cascade to a cell-based paradigm, in which endothelium, erythrocytes, leukocytes, and platelets interact to coordinate a delicate balance between thrombosis and fibrinolysis. Furthermore, both an early

postinjury endogenous coagulopathy associated with traumatic shock and a myriad of secondary factors that exacerbate this condition have been elucidated. Diagnosis of coagulopathy is shifting from the routine use of laboratory tests designed to monitor anticoagulation therapy toward point-of-care testing, which provides essential real-time clinical correlates. Treatment algorithms of traumatic coagulopathy have emphasized early replacement of both clotting factors and platelets with concomitant restraint of crystalloid administration (termed damage control resuscitation), as well as pharmacologic adjuncts that exploit the endogenous coagulation system. On the other hand, documentation of the deleterious effects of overzealous blood component replacement has led to a reevaluation of this strategy, in an attempt to reach a balance between abatement of coagulopathy and minimization of subsequent organ dysfunction. This chapter will attempt to synthesize recent developments in the complex management of the bleeding, coagulopathic trauma patient.

RED BLOOD CELL TRANSFUSION Red blood cell (RBC) transfusion is lifesaving in the face of critical anemia associated with hemorrhagic shock. However, the optimal target hematocrit during resuscitation remains unknown. Shock is defined broadly as the development of an oxygen debt due to impaired delivery, utilization, or both, with resultant anaerobic metabolism and organ dysfunction. Elimination of this oxygen debt involves optimization of oxygen delivery, which is the product of cardiac output and arterial oxygen content. The arterial oxygen content, in turn, is dependent primarily on the hemoglobin concentration and oxygen saturation. Oxygen consumption, defined as the product of the cardiac output and the difference between the arterial and venous oxygen content, represents a more specific marker of oxygen availability at the cellular level.

Postinjury Hemotherapy and Hemostasis need of resuscitation. However, these data are provocative, and future large-scale trials of lower transfusion triggers for the resuscitation of hemorrhagic shock are warranted in light of the accumulating evidence documenting the untoward effects of RBC transfusion. In addition to oxygen transport, RBCs play an important role in hemostasis. As the hematocrit rises, platelets are displaced laterally toward the vessel wall, placing them in contact with the injured endothelium; this phenomenon is referred to as margination. Platelet adhesion via margination appears optimal at a hematocrit of 40%.10 Erythrocytes are also involved in the biochemical and functional responsiveness of activated platelets. Specifically, RBCs increase platelet recruitment, production of thromboxane B2, and release of both ADP and P-thromboglobulin. Furthermore, RBCs participate in thrombin generation through exposure of procoagulant phospholipids. Interestingly, animal models suggest that a decrease of the platelet count of 50,000 is compensated for by a 10% increase in hematocrit.11 Despite these experimental observations, no prospective data exist detailing the relationship between hematocrit, coagulopathy, and survival among critically injured trauma patients. In summary, prior investigations into the ideal hematocrit for oxygen-carrying capacity during hemorrhagic shock are in large part irrelevant to modern-day resuscitation with allogeneic blood. Banked erythrocytes are subject to a time-dependent diminution of oxygen-carrying capacity, and the effect of blood transfusion on oxygen consumption, regardless of hematocrit, remains questionable. The CRIT trial suggested that patients in shock tolerate a hemoglobin concentration of 7.0 g/dL at least as well as 9.0 g/dL, although this hypothesis was not testing during the initial resuscitation of hemorrhagic shock specifically. Furthermore, the role of erythrocytes in hemostasis must be considered. In practice, clinical circumstance (e.g., ongoing hemorrhage with hemodynamic instability and coagulopathy), as opposed to an isolated laboratory measurement, should inform the decision to transfuse. However, until there is definitive evidence to challenge the CRIT data, a hemoglobin concentration of 7 g/dL should be considered the default transfusion trigger for resuscitation from shock.

POSTINJURY COAGULOPATHY PERSPECTIVE Uncontrolled hemorrhage is the leading cause of preventable morbidity and mortality following trauma. Hemorrhage is responsible for nearly one half of all trauma deaths, and is the second leading cause of early death, preceded only by central nervous system injury.12 Most hemorrhagic deaths occur within the first 6 hours postinjury, and require tremendous resource mobilization in terms of blood component therapy. Although most life-threatening hemorrhage originates as major vascular injury that is amenable to either surgical or angiographic control, a diffuse coagulopathy frequently supervenes. Originally described over 60 years ago,1 postinjury hemorrhage that persists despite control of surgical bleeding has been referred to by many names, including medical bleeding, diffuse bleeding diathesis, posttransfusion bleeding disorder, medical

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During resuscitation, a balance must occur between the competing goals of maximal oxygen content (hematocrit  100%) and minimal blood viscosity (hematocrit  0%). Furthermore, irrespective of hematocrit, the oxygen-carrying capacity of transfused allogeneic erythrocytes is impaired due to storage-induced changes in both deformability and hemoglobin oxygen affinity. Accordingly, although many studies have measured an increase in oxygen delivery following transfusion of allogeneic RBCs, almost none have reported an increase in oxygen consumption.3 Finally, beyond a role in oxygen delivery, erythrocytes are integral to hemostasis via their involvement in platelet adhesion and activation, as well as thrombin generation. The hematocrit is thus relevant to hemorrhagic shock as it relates to both oxygen availability and hemostatic integrity. Early canine models of hemorrhagic shock suggested that oxygen consumption is optimized at a relatively high hematocrit (range 35–42%).4 However, hematocrit variation was achieved via autotransfusion of the animal’s shed whole blood, eliminating the aforementioned limitations of allogeneic erythrocytes, and rendering the results inapplicable to modern resuscitation of hemorrhagic shock. Furthermore, acute normovolemic hemodilution of dogs to a hematocrit of 10% is well tolerated, with little decrement in oxygen delivery secondary to a compensatory increase in cardiac output.5 Retrospective observations among critically ill surgical patients in the 1970s suggested a hematocrit of 30% as optimal for both oxygen-carrying capacity and survival.6 Such studies formed the basis of the traditional recommendation to maintain the hematocrit 30%, although the marked limitations of this retrospective literature were recognized ultimately. As the deleterious effects of RBC transfusion became increasingly evident, renewed interest in the ideal transfusion trigger occurred. The Transfusion Requirements in Critical Care (TRICC) Trial, which compared restrictive (hemoglobin 7.0 g/dL) and liberal (hemoglobin 9.0 g/dL) transfusion triggers among 838 patients, provided the first level I evidence regarding RBC transfusion strategies among the critically ill.7 Although inclusion criteria did not specify ongoing resuscitation, 37% of patients were in shock at the time of enrollment as evidenced by the need for vasoactive drugs. No difference in 30-day mortality was observed between groups. However, in-hospital mortality, as well as mortality among less severely ill patients (Acute Physiology and Chronic Health Evaluation II score 20) and younger patients (age 55 years), was significantly lower in the restrictive transfusion group. Current evidence thus suggests that a hemoglobin concentration of 7 g/dL is at least as well tolerated as a hemoglobin concentration of 9 g/dL among critically ill patients. It is possible that hemoglobin concentrations below 7 g/dL are safe, particularly in younger patients. However, a hemoglobin concentration of 5 g/dL appears to be the threshold for critical anemia. Whereas hemodilution of healthy volunteers as low as a hemoglobin concentration of 5 g/dL is well tolerated,8 a study of postoperative patients who refused RBC transfusion reported a sharp increase in mortality below this same hemoglobin concentration.9 Such populations differ fundamentally from the multiply injured, exsanguinating patient in

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oozing, and disseminated intravascular coagulation (DIC). Clinically, the coagulopathy is manifest as nonsurgical bleeding from mucosal lesions, serosal surfaces, and wound and vascular access sites that continues after control of identifiable vascular bleeding. Although postinjury coagulopathy has long been recognized, several authors have struggled to elucidate both its predictors and mechanisms. Reporting on a large cohort of combat casualties, Simmons et al. appropriately identified the relationship between major trauma and coagulopathy, but were unable to predict coagulopathy using a myriad of both clinical and laboratory parameters.13 In 1982, our group described the “bloody vicious cycle,” in which the synergistic effects of acidosis, hypothermia, and coagulopathy combined to create an irreversible clinical deterioration among patients who had received large-volume blood transfusion, eventuating in death by exsanguination despite surgical control of bleeding.14 In the late 1980s, Lucas and coworkers from Wayne State University detailed the relationship among large-volume blood transfusion, decrement in clotting factor concentrations, and the corresponding prolongation of traditional measures of coagulopathy, such as the prothrombin time (PT) and activated partial thromboplastin time (aPTT).15 Development of coagulopathy following massive transfusion (MT), which was postulated to be secondary to both consumption and dilution of clotting factors, was similarly unable to be predicted by either clinical or laboratory parameters.16 Most recently, evidence of an endogenous coagulopathy associated with severe traumatic injury has emerged, which occurs early and is independent of the secondary effects of body temperature, acidosis, and clotting factor consumption or dilution.17 The burden of postinjury coagulopathy on the severely injured trauma patient is enormous. Overt coagulopathy affects at least one in four seriously injured patients and is associated independently with increased mortality.18 In a large series from our institution, over one half of deaths due to exsanguinations occurred after control of surgical bleeding and were thus due to coagulopathy.14 Persistent hemorrhage despite surgical control of bleeding remains the most common reason for abandonment of definitive repair of injuries (damage control surgery). Finally, patients who develop postinjury coagulopathy nearly universally require MT of blood products, placing an incalculable financial burden on both institutional and national health care delivery systems.

CELL-BASED COAGULATION CONSTRUCT Effective management of postinjury coagulopathy requires an understanding of the coagulation process. Hemostatic integrity involves an intricate balance between hemorrhage and thrombosis, achieved in concert by complex interactions between the anticoagulant, procoagulant, and fibrinolytic systems. The inciting event for thrombosis following injury is the exposure of tissue factor (from both the subendothelium and mononuclear cells) to circulating clotting factors. From this point forward, multiple enzymatic cascades, orchestrated by a myriad of cells, direct the balance of thrombosis and hemorrhage based on both substrate availability and the status of global tissue perfusion (i.e., shock). Whereas clotting factors

exist in concentrations sufficient to maintain hemostasis in health, major trauma overwhelms the capacity of the coagulation system, with resultant systemic thrombosis and hemorrhage. For example, an isolated lobar pulmonary contusion may involve a surface area large enough to exhaust the body’s endogenous fibrinogen and platelet reserves. Major proteins involved in the procoagulant, anticoagulant, and fibrinolytic systems are listed in Table 13-1. The coagulation process has been considered traditionally a cascade of proteolytic reactions occurring in isolation. In this classic view of hemostasis (extrinsic and intrinsic pathways), the cell surface serves primarily to provide an anionic phospholipid region for procoagulant complex assembly. Whereas this model is supported by traditional laboratory tests of isolated coagulation in a test tube, it does not correlate with current concepts of hemostasis occurring in vivo. This antiquated model has been supplanted by the cellbased model (CBM) of coagulation. This model recognizes the important interactions of the cellular and plasma components to clot formation, as opposed to the more simplistic schema of the classic view. The CBM suggests that procoagulant properties result from expression of a variety of cell-based features, originating at the endothelial level, including protein receptors, which activate components of the coagulation system at specific cell surfaces. Furthermore, this model allows for improved understanding and potential mechanistic links with cross-talk between inflammation and coagulation components. In addition, platelet receptors, endothelial cells, proteases, cytokines, and phospholipids have important roles in coagulation. This model also incorporates RBCs and their aforementioned interactions with the hemostatic process. The CBM occurs in three overlapping phases: initiation (which occurs on tissue factor–bearing cells), amplification, and propagation. Amplification and propagation involve platelet and cofactor activation eventuating in the generation of massive amounts of thrombin, known as the thrombin burst. Both amplification and propagation occur on the cell surface of platelets, underscoring the central role of the platelet in the hemostatic process. In summary, the CBM represents a major paradigm shift from a theory that views coagulation as being controlled by concentrations and kinetics of coagulation proteins to one that considers the process to be driven by diverse cellular interactions. Coagulation factors work as enzyme/cofactor/substrate complexes on the surface of activated cells, and hemostasis requires the interaction of endothelium, plasma proteins, platelets, and RBCs.

HEMOSTASIS MANAGEMENT CONTROVERSIES ■ Acute Coagulopathy of Trauma Coagulation disturbances following trauma follow a trimodal pattern, with an immediate hypercoagulable state, followed quickly by a hypocoagulable state, and ending with a return to a hypercoagulable state.19 Conceptualization of the early hypocoagulable state has changed markedly over the last 10 years. Trauma-induced coagulopathy was considered traditionally to

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TABLE 13-1 Proteins Involved in Coagulation, Anticoagulation, and Fibrinolysis Source

Activated By

Function

Exposure to circulating platelets

Complexes with VII to initiate clot formation

Fibrinogen (factor I) Factor V

Subendothelium, monocytes in response to IL-6 Activated platelets Activated platelets

Thrombin Thrombin

Factor VII rVIIa

Liver N/A

Thrombin, Xa, XIa, XIIa N/A

Factor Factor Factor Factor Factor

Endothelial cell, liver Liver Liver Liver Liver

Thrombin Factor XI Factors VIII and IX Thrombin Thrombin

Clot formation Cofactor that accelerates conversion of prothrombin to thrombin; Leiden mutation renders it resistant to inactivation by APC Complexes with TF to convert X to Xa Complexes with TF → activates X Binds to activated PLTs → activates X (bypassing VIII and IX) Activates TAFI Cofactor, activates factor X Cofactor, activates factor X Converts ∼ prothrombin to thrombin Activates IX Cross-links fibrin

Endothelial cells Liver Liver

Ischemia, hypoxia Thrombin Thrombin, TM, EPCR complex

VIII IX X XI XIII

Anticoagulants Heparin sulfates Antithrombin III Protein C Protein S Thrombomodulin (TM)

Liver Endothelial cell

Endothelial protein C receptor (EPCR) Tissue factor pathway inhibitor (TFPI)

Endothelial cell

Tissue hypoperfusion (shock) Thrombin N/A

Liver

Thrombin

Fibrinolytic system Plasminogen tPA

Eosinophiles Endothelial cell

PAI-1

Endothelium

tPA Ischemia, hypoxia, thrombin inflammation

Protein C

Liver

Thrombin activatable fibrinolysis inhibitor (TAFI)

Liver

Platelet activators/inhibitors vWF Subendothelium, platelets NO Endothelial cells Prostacyclin Endothelial cells

Thrombin:thrombomodulin complex Thrombin:thrombomodulin complex

Platelets, collagen Ischemia Ischemia

Activation of ATIII Inhibition of thrombin, Xa, XIa, XIIa Irreversibly inactivates Va and VIIIa Cofactor for protein C Complexes with thrombin to activate protein C; reduces thrombin’s procoagulant activity Inhibits TAFI, leading to fibrinolysis Complexes with thrombin and TM to activate protein C Inhibits TF–VII complex from converting X → Xa, thereby inhibiting coagulation cascade Converted to plasmin, leading to fibrinolysis Converts plasminogen to plasmin Inhibits tPA, resulting in inhibition of fibrinolysis Inhibits PAI-1, leading to fibrinolysis Inhibits fibrinolysis

Binds to PLT surface protein Ib–V–IX to cause adhesion Inhibits platelet activation Inhibits platelet activation

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Protein Procoagulant Tissue factor

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be the consequence of clotting factor depletion (via both hemorrhage and consumption), dilution (secondary to massive resuscitation), and dysfunction (due to both acidosis and hypothermia). However, several recent reports have detailed that many trauma patients present with a coagulopathy prior to fluid resuscitation and in the absence of the aforementioned parameters.17,18,20 In a study by Brohi et al., clotting factor concentrations on emergency department entry were correlated with both hypoperfusion (measured by the base deficit) and coagulopathy (measured by both the PT and PTT) for 208 trauma activations from 2003 to 2004.17 Coagulopathy was observed only in the presence of hypoperfusion (base deficit 6) and was not related to clotting factor consumption as measured by prothrombin fragment concentrations. Similarly, in a review of trauma patients from our institution who required at least one transfusion, we noted that early (1 hour postinjury) fibrinolysis occurred frequently among the most severely injured, and correlated significantly with markers of hypoperfusion, such as presenting systolic blood pressure, arterial pH, and base deficit.21 Such studies provide evidence of what we have termed an “acute endogenous coagulopathy of trauma,” which occurs early after injury, is independent of traditional mechanisms of coagulopathy, and is correlated closely with hypoperfusion. Such a mechanism may have evolved to protect hypoperfused vascular beds from thrombosis in the event of ischemia, but is clearly pathologic in the setting of diffuse tissue injury with resultant hemorrhagic shock. Trauma patients who present with this endogenous coagulopathy incur a 4-fold increase in mortality as compared to those patients who do not develop the coagulopathy.22 Furthermore, these patients are eight times more likely to die in first 24 hours,20 and have an increased incidence of multiple organ failure (MOF), transfusion requirements, intensive care unit (ICU) length of stay, and mortality.22 Although the existence of an endogenous coagulopathy of trauma has been well documented, potential mechanistic links to this process remain elusive. Brohi et al. noted in their study that an increasing base deficit was significantly and directly correlated with thrombomodulin concentration (an auto-anticoagulant protein expressed by the endothelium in response to ischemia [Table 13-1]), and inversely correlated to protein C concentration.17 Moreover, a decreased concentration of protein C was correlated with a prolongation of the PTT, suggesting increased activation of protein C via thrombomodulin upregulation as a possible mechanism. Activated protein C (APC), in turn, both inhibits the coagulation cascade via inhibition of factors Va and VIIIa and promotes fibrinolysis via irreversible inhibition of plasminogen activator inhibitor (PAI). A decreased concentration of protein C also correlated with a decrease in the concentration of PAI, an increase in tissue plasminogen activator (tPA) concentration, and an increase in D-dimers. This final observation suggested that protein C–mediated hyperfibrinolysis via consumption of PAI may contribute to traumatic coagulopathy. Further associations between the endogenous coagulopathy of trauma and the APC pathway have since been described in both animals23 and humans.22 Using a mouse model of

hemorrhagic shock, Chesebro et al. documented an association between coagulopathy and an elevated APC concentration (as opposed to the surrogate protein C concentration utilized in the study of Brohi et al.17).23 Inhibition of APC with mAb1591 prevented coagulopathy associated with traumatic hemorrhage (as measured by the PTT). However, complete inhibition of APC caused universal death at 45 minutes due to thrombosis and perivascular hemorrhage, underscoring the delicate balance between hemorrhage and thrombosis. Others have argued that the early coagulopathic changes following severe injury simply reflect the traditional concepts of DIC.24 Specifically, the hematologic consequences following injury may be considered to represent a generic coagulopathic response to any insult that induces widespread inflammation (e.g., trauma, infection, ischemia/reperfusion). The release of proinflammatory cytokines, in turn, has two main effects on the coagulation system: (1) release of tissue factor with subsequent clotting factor consumption and massive thrombin generation and (2) hyperfibrinolysis due to upregulation of tPA. In favor of this argument is the long-standing documentation of diffuse intravascular thrombi in multiple, uninjured organs of victims of hemorrhagic shock.25 Furthermore, the cytokine elaboration patterns of both trauma and septic patients are nearly identical, suggesting a potential common pathophysiologic mechanism.26 However, this argument is limited by the aforementioned finding that clotting factor levels are relatively preserved in trauma patients following shock.17 Furthermore, fibrinogen levels are inconsistently depressed in patients with acute traumatic coagulopathy. Moreover, the degree of fibrinolysis, when present, appears substantially higher in the endogenous coagulopathy of trauma as compared to DIC.21 Lastly, DIC occurs classically in the setting of an underlying hypercoagulable state (e.g., malignancy, septic shock) and is associated with an upregulation of PAI-1,27 as opposed to the early hypocoagulable state observed in the bleeding trauma patient, which reflects a predominance of both t-PA upregulation and PAI-1 inhibition. Our current conceptualization of the acute endogenous coagulopathy of trauma emphasizes the integral role of fibrinolysis. Specifically, diffuse endothelial injury leads to both massive thrombin generation and systemic hypoperfusion. These changes, in turn, result in the widespread release of tPA, leading to fibrinolysis. Both injury and ischemia are wellknown stimulants of tPA release,28 and we have observed a strong correlation between hypoperfusion, fibrinolysis, hemorrhage, and mortality among injured patients who require transfusion.21 The various proposed pathways involved in the endogenous coagulopathy of trauma are depicted in Fig. 13-1. Regardless of the inciting mechanism, elucidation of an endogenous coagulopathy of trauma has important therapeutic implications. Given that the driving force of early coagulopathy appears mediated initially by hypoperfusion as opposed to clotting factor consumption, replacement of clotting factors at this time would be ineffective. In fact, early clotting factor replacement in the face of ongoing hypoperfusion may serve to exacerbate coagulopathy via generation of additional thrombin substrate for thrombomodulin. For this reason, we have noted the endogenous coagulopathy of trauma to be “fresh frozen

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Hemorrhagic shock

Massive thrombin generation

tPA

Fibrin deposition

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Hypoperfusion

thrombomodulin

thrombomodulin/ thrombin complex protein C

tPA

APC PAI

Fibrinolysis

Va & VIIIa

Anti-coagulation

FIGURE 13-1 Proposed pathways for the acute endogenous coagulopathy of trauma. Note the prominent role of fibrinolysis via multiple mechanisms, the necessary thrombin substrate, and the positive feedback cycle that perpetuates the coagulopathy. tPA, tissue plasminogen activator; APC, activated protein C; PAI, plasminogen activator inhibitor.

plasma (FFP) resistant.” By contrast, the development of a secondary coagulopathy due to the complications of massive resuscitation renders the patient clotting factor deficient and thus “FFP responsive.” Elucidation of the integral role of fibrinolysis also raises the possibility of mitigation of the coagulopathy via early administration of antifibrinolytic drugs (discussed below). Refinement of the mechanisms underlying the endogenous coagulopathy of trauma represents one future goal within the area of postinjury coagulopathy research. Currently, neither a standardized definition nor diagnostic criteria for the endogenous coagulopathy of trauma exist. Furthermore, little is known about the initiators of both upregulation and eventual downregulation of thrombomodulin during traumatic shock. Overexpression of APC has been inferred in humans from a decreased concentration of protein C rather than direct measurement of the APC concentration. Finally, although a correlation between markers of shock and clotting factor expression profiles has been documented, causality remains to be proven. Despite these limitations, description of the endogenous coagulopathy of trauma represents a major turning point in our understanding of the hemostatic derangements following injury. Although the endogenous coagulopathy of trauma results in an immediate hypocoagulable state among shocked patients following injury, several secondary conditions may develop, which exacerbate this preexisting coagulopathy. Such conditions are, in large part, due to the complications of massive fluid resuscitation, and include clotting factor dilution, clotting factor consumption, hypothermia, and acidosis. Although these factors were considered traditionally as the driving force of traumatic coagulopathy, recent evidence suggests that their effect may have been overestimated.

The positive interaction between hypothermia, acidosis, and coagulopathy has been termed both the “bloody vicious cycle” and “lethal triad of death,” which we proposed at the 40th annual meeting of the American Association for the Surgery of Trauma in 1981.14 Each of these three factors exacerbates the others, eventuating in uncontrolled hemorrhage and exsanguination. Many causes of hypothermia exist for the trauma patient, including altered central thermoregulation, prolonged exposure to low ambient temperature, decreased heat production due to shock, and resuscitation with inadequately warmed fluids. The enzymatic reactions of the coagulation cascade are temperature dependent and function optimally at 37°C; a temperature 34°C is associated independently with coagulopathy following trauma.29 However, both experimental and clinical evidence suggest that the effect of hypothermia is modest at best, with each 1° corresponding to a decrease in clotting factor activity of approximately 10%.30 When defined using an elevation of the PT 18 seconds, hypothermia did not correlate with coagulopathy among a large cohort of trauma patients.22 Thrombin generation was also not effected by hypothermia (T 35°C). Coagulopathy may be relevant clinically in severe hypothermia (T 32°C),31 but this condition is present in less than 5% of trauma patients. Furthermore, it is unclear if the increased mortality observed in severely hypothermic patients is causal or merely circumstantial. Hypothermia also affects both platelet function32 and fibrinolysis33; however, pronounced platelet dysfunction is only observed below 30°C, and clinical data correlating platelet dysfunction secondary to severe hypothermia and adverse outcomes are lacking. Thus, although severe hypothermia exacerbates coagulopathy, advances in resuscitation of the trauma patient have minimized the risk of this degree of hypothermia, thereby limiting its relevance. By contrast,

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isolated hypothermia likely has minimal clinical impact on hemostasis within the temperature range commonly seen in trauma patients (33–36°C). Clotting factor activity is also pH dependent, with 90% inhibition occurring at pH 6.8.34 Coagulopathy secondary to acidosis is apparent clinically below a pH of 7.2. Because hypoperfusion results in anaerobic metabolism and acid production, it is difficult to discern the independent effect of acidosis on hemostatic integrity. A recent study adjusted the pH of blood samples from healthy volunteers using hydrochloric acid.35 Using thrombelastography (TEG), a significant correlation was observed between pH and clot-forming time over the pH range of 6.8–7.4. However, no difference was found in either clotting time (a measurement of the time to initiation of a clot) or maximum clot firmness over the range of pH, with the possible exception of a pH equal to 6.8. Similarly, Brohi et al. found that although thrombin generation increased with increasing injury severity, there was no relationship between degree of acidosis (as measured by the base deficit) and either thrombin generation or factor VII concentration.22 Finally, conflicting evidence exists regarding the ability of correction of acidosis via buffer to reverse coagulation disturbances.35,36 Although the independent effect of acidosis on hemostatic integrity remains unclear, correction of acidosis via resuscitation remains a valuable therapeutic end point in terms of minimizing the aforementioned hypoperfusion-induced endogenous coagulopathy of trauma. Furthermore, mainte-

nance of the arterial pH 7.20 during resuscitation of shock (with bicarbonate, if necessary) maximizes the efficacy of both endogenous and exogenous vasoactive drugs. Finally, although both consumption and dilution of clotting factors have been implicated in postinjury coagulopathy, there is little experimental evidence to support this theory. The amount of thrombin generated is not related to coagulopathy in patients without shock,17 and there is no effect of dilution on coagulopathy either in vitro37 or in healthy volunteers.38 In summary, an endogenous coagulopathy occurs following trauma among patients sustaining shock, and does not appear to be secondary to coagulation factor consumption or dysfunction. Rather, current evidence suggests that it is due to ischemia-induced both anticoagulation and hyperfibrinolysis, and is resistant to clotting factor replacement. Although the hematologic changes observed following severe trauma demonstrate many characteristics of DIC with a fibrinolytic phenotype, clotting factor consumption does not appear integral. During this time frame, therapy should focus on definitive hemorrhage control, timely restoration of tissue perfusion, and point-of-care monitoring in an effort to identify fibrinolysis. Following restoration of tissue perfusion, an “FFP-sensitive” pathway may emerge, which is characterized by coagulopathy due to traditional factors, such as acidosis, hypothermia, consumption, and dilution. Recognition of the transition from the “FFP-resistant” to the “FFP-sensitive” pathway is a critical objective of current research. Fig. 13-2 depicts our “updated”

Life-threatening trauma

Immuno activation

Blood loss

Tissue injury

Activation and consumption of the complement system

Iatrogenic factors Core hypothermia

Metabolic acidosis Hypocalcaemia

FFP

resi

Massive RBC transfusion

Cellular shock

stan

t

Pre-existing diseases

FFP sensitive Clotting factor deficiencies

FIGURE 13-2 Updated bloody vicious cycle. It incorporates both the early acute endogenous coagulopathy of trauma, which is resistant to clotting factor replacement with fresh frozen plasma (FFP resistant), and a subsequent secondary coagulopathy that may be due to hypothermia, acidosis, clotting factor deficiency (FFP sensitive), or any combination thereof.

Postinjury Hemotherapy and Hemostasis

■ Hypotensive Resuscitation Permissive hypotension involves deliberate tolerance of lower mean arterial pressures in the face of uncontrolled hemorrhagic shock in order to minimize further bleeding. This strategy is based on the notion that decreasing perfusion pressure will maximize success of the body’s natural mechanisms for hemostasis, such as arteriolar vasoconstriction, increased blood viscosity, and in situ thrombus formation. Animal models of uncontrolled hemorrhage have revealed that crystalloid resuscitation to either replace three times the lost blood volume39 or maintain 100% of pre-injury cardiac output40 exacerbates bleeding39,40 and increases mortality39 as compared to more limited fluid resuscitation. Randomized clinical trials (RCTs) that compare fluid management strategies prior to control of hemorrhage among human subjects are limited. In the first large-scale trial, Bickell et al. randomized 598 patients in hemorrhagic shock (systolic blood pressure 90 mm Hg) who had sustained penetrating torso trauma to either crystalloid resuscitation or no resuscitation prior to operative intervention.41 Prespecified hemodynamic targets were not used. Mean systolic arterial blood pressure was significantly decreased on arrival to the emergency department for the delayed resuscitation group as compared to the immediate resuscitation group (72 mm Hg vs. 79 mm Hg, respectively, P  .02) with a corresponding increase in survival (70% vs. 62%, respectively, P  .04). A trend toward a decreased incidence of postoperative complications was also observed for the delayed resuscitation group. However, a subsequent subgroup analysis documented that these benefits occurred only among patients who had cardiac injury with tamponade.42 Two recent trials have failed to replicate these findings. Turner et al. randomized 1,306 trauma patients with highly diverse injury patterns and levels of stability to receive early versus delayed or no fluid resuscitation.43 Although no mortality difference was observed (10.4% for the immediate resuscitation group versus 9.8% for the delayed/no resuscitation group), protocol compliance was poor (31% for the early group and 80% for the delayed/no resuscitation group), limiting interpretability. Most recently, Dutton et al. randomized 110 trauma patients presenting in hemorrhagic shock (systolic blood pressure 90 mm Hg) to receive crystalloid resuscitation to a systolic blood pressure of 70 mm Hg versus 100 mm Hg.44 Randomization occurred following presentation to the emergency department. Not all patients required operation, and hemorrhage control was determined at the discretion of the trauma surgeon or anesthesiologist. Although there was a significant difference in mean blood pressure during bleeding between the conventional and low groups (114 mm Hg vs. 110 mm Hg, respectively, P  .01), the mean blood pressure was substantially higher than intended ( 70 mm

Hg) for the low group, and the absolute difference between groups was likely insignificant clinically. Mortality was infrequent and did not vary by resuscitation arm (7.3% for each group). Methodological variability between these trials has precluded a meaningful meta-analysis,45 and may help to explain the discrepant mortality findings. It is clear that the degree of hemorrhagic shock was most pronounced in the study of Bickell et al., as evidenced by the lowest presenting systolic blood pressure as well as the highest mortality. Furthermore, randomization was accomplished in the prehospital setting, and all patients required operative intervention. By contrast, mortality was infrequent in the study of Dutton et al., and the target systolic blood pressure of 70 mm Hg in the “low” group was, on average, not achieved. Thus, at present, it is possible to conclude that limited volume resuscitation prior to operative intervention may be of benefit among patients with penetrating trauma resulting in cardiac injury, although the optimum level of permissive hypotension remains unknown. The benefit of such therapy among a more diverse cohort of patients in hemorrhagic shock, with a low associated risk of death, is not clear. Finally, regardless of therapeutic benefit, reliable achievement of permissive hypotension appears challenging once hospital care has begun.

■ Preemptive Blood Components The widespread replacement of whole blood by component therapy in the early 1980s allowed for improved specificity of therapy, increased storage time of individual components, and decreased transmission of infectious disease. However, the relative amounts (if any) of components indicated for resuscitation of the exsanguinating trauma patient were not addressed, and remain debated approximately 30 years later. Traditional doctrine, as espoused by Advanced Trauma Life Support training, calls for 2 L of crystalloid followed by RBCs in the case of persistent hemodynamic instability; clotting factor and platelet replacement are indicated only in the presence of laboratory derangements (PT and platelet count, respectively).46 Although this approach is reasonable for patients who have sustained relatively minor hemorrhage (20% of circulating blood volume), replacement of lost blood with isolated erythrocytes becomes problematic in the face of ongoing hemorrhagic shock requiring a large volume of blood transfusion. In this case, replacement of shed blood with isolated RBCs will result in a dilutional coagulopathy. Several authors have attempted to quantify the amount of RBCs transfused for which dilutional coagulopathy mandates concomitant component replacement therapy, with definitions ranging from loss of one blood volume to the need for greater than 10 U of RBCs in the first 24 hours following injury. The latter criterion is the most commonly accepted definition of MT, and is the time period on which most studies of empiric component replacement therapy are based. However, because over 80% of blood component therapy transfused to patients who require MT is administered within the first 6 hours of injury,47 we believe this to be a more appropriate time period for

CHAPTER 13

bloody vicious cycle, which incorporates both the acute endogenous coagulopathy of trauma and the aforementioned secondary factors. Finally, a hypercoagulable state supervenes following restoration of tissue perfusion, usually within 72 hours of injury.

223

224

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SECTION 2

analysis. Thus, the focus on preemptive blood components should shift to the first 6 hours postinjury. The debate regarding preemptive blood components began with platelets during the time of whole blood resuscitation.48 Recognition of the dangers of isolated RBC therapy during MT followed shortly after the widespread institution of component therapy in the early 1980s. Our group and others noted that mortality among massively transfused patients was reduced when increased amounts of both plasma and platelets were administered empirically. Specifically, when introducing the concept of RBC:FFP ratios, we reported increased mortality among a cohort of patients with major vascular trauma associated with RBC:FFP ratios greater than 5:1, with overt coagulopathy observed nearly universally with ratios exceeding 8:1.14 In 2007, Borgman et al. published a series of 254 massively transfused US soldiers in Iraq and Afghanistan, reporting markedly improved survival among those transfused with an RBC:FFP ratio in the range of 1.5:1, as compared to higher ratios.49 This ratio appeared appealing intuitively as it most closely resembled that of whole blood, although a 1:1 formulation is actually both anemic (hematocrit 27%) and clotting factor deficient (65% activity) as compared to fresh whole blood.50 Several subsequent studies, in both the military and civilian settings, have corroborated the findings of Borgman et al.51–53 An association between early, aggressive FFP administration and improved survival has also been documented among trauma patients who underwent sub-MT.54 These data have given rise to the concept of damage control resuscitation, which involves early transfusion of increased amounts of both clotting factors and platelets, in addition to minimization of crystalloid resuscitation in patients who are expected to require MT. Currently, in the absence of routine point-ofcare assessment of coagulopathy, many trauma centers advocate preemptive transfusion of RBC:FFP using a target ratio of 1:1 for such patients. Unfortunately, the literature addressing component transfusion ratios during MT suffers from substantial methodological limitations (Table 13-2). Despite a myriad of retrospective data, mathematical models,55 and expert opinion, there remains no prospective evidence to support an empiric transfusion ratio. A major limitation of the retrospective literature involves survival bias. Specifically, it remains unclear if increased FFP transfusion improves survival or if patients

TABLE 13-2 Methodological Limitations of the Literature Addressing FFP:RBC Ratios During Massive Transfusion Lack of mechanistic link Survival bias Extended period after which cumulative ratios are calculated Confounding Inconsistent benefit across mechanism of injury Lowest ratios approximate 1.5:1 as opposed to 1:1

who survive simply live long enough to receive more FFP. Indeed, patients who are bleeding faster get less plasma as the trauma team and blood bank struggle to keep up. Related intimately to the issue of survival bias is that of the time period over which the RBC:FFP ratio is calculated. Although over 80% of RBC transfusions are administered within 6 hours of injury, most studies have reported the cumulative RBC:FFP ratio as calculated at 24 hours. Such a strategy exacerbates survival bias, as the RBC:FFP ratio is known to decrease over time. Accounting for the time-dependent nature of the RBC:FFP transfusion ratio eliminated any association with survival in one recent report.56 Furthermore, when the cumulative RBC:FFP ratio was analyzed at 6 hours as opposed to 24 hours, our group identified a ratio in the range of 2:1 to 3:1, as opposed to 1:1, as associated with the lowest predicted mortality.47 The next major limitation involves the lack of a mechanistic link between a lower RBC:FFP ratio and improved survival. The clinical efficacy of FFP remains largely unproven,57 and no study has documented an association between a lower RBC:FFP ratio and fewer total blood products administered. Moreover, differences in laboratory markers of coagulopathy (e.g., PT, TEG) have not been demonstrated between groups of varying RBC:FFP ratios. In fact, a canine model showed no benefit to adding FFP following MT in terms of changes in coagulation protein levels or clotting times.58 The benefit of a 1:1 RBC:FFP ratio has also not been consistent across various mechanisms of injury.59 Finally, early, aggressive FFP administration may serve to exacerbate the endogenous coagulopathy of trauma by generating large amounts of thrombin that, in the setting of ischemia-induced endothelial thrombomodulin overexpression, may perpetuate a hypocoagulable state via continued activation of protein C. Although many experts advocate an RBC:FFP transfusion ratio of 1:1 during MT, the lowest ratio achieved in most studies approaches 1.5:1. While moving from an RBC:FFP ratio of 2:1 to 1:1 may appear trivial, such a paradigm shift represents a 100% increase in FFP utilization. An increase of this magnitude would place tremendous strain on the marginal FFP donor pool, as well as increase exponentially blood bank labor, likely to the point of nonsustainability in the event of a mass casualty. Finally, unbridled FFP administrated must be viewed with caution in light of the accumulating evidence detailing the immunomodulatory properties of such therapy (discussed below). The trigger for empiric platelet replacement during MT remains equally controversial. Both thrombocytopenia60 and thrombocytopathy (qualitative platelet dysfunction)61 have long been implicated in the coagulopathy of trauma. Nearly all massively transfused patients develop thrombocytopenia,60 and the bleeding time is universally prolonged in these patients. Interestingly, thrombocytopenia develops following MT even when the lost blood volume is replaced as whole blood, suggesting a mechanism independent of thrombodilution. By contrast, platelet dysfunction following transfusion of less than 10 U of pRBC appears rare.61 This is likely due to the fact that platelets are both stored in the reticuloendothelial system and sequestered

Postinjury Hemotherapy and Hemostasis In summary, the literature involving empiric component therapy suffers from several methodological limitations. Currently, the optimal empiric RBC:FFP ratio for resuscitation of patients who require MT appears to be in the range of 1:2 to 1:3. Furthermore, although no absolute numerical trigger for platelet transfusion exists, it appears reasonable to transfuse platelets following the 10th unit of pRBCs. However, whenever possible, component replacement should be both individualized and goal directed, such that overzealous clotting factor and platelet replacement and the complications thereof are minimized.

■ Goal-Directed Hemostasis Lack of an accurate tool to identify and track coagulopathy remains a major limitation of the literature surrounding both postinjury hemostatic derangements and empiric blood component replacement therapy. Classic laboratory tests of coagulation function, such as PT and PTT, were described originally for the assessment of anticoagulation function in hemophiliacs, and are based on the interaction of the coagulation factors in isolation.63 To date, not surprisingly, the performance characteristics of these tests in the trauma patient remain unproven. Furthermore, a prohibitive amount of time (approximately 45 minutes) is required to conduct these assays. Because both the PT and PTT are performed on platelet-poor plasma, they are sensitive only to the earliest initiation of clot formation. However, greater than 95% of thrombin generation occurs after the initial polymerization of fibrinogen. Hence, monitoring of platelet function appears essential for accurate measurement of clot strength. Finally, these tests are performed in an artificial environment, irrespective of the patient’s core body temperature and pH. Measurements of individual clotting proteins, such as protein C and thrombomodulin, are both costly and time consuming. Diagnosis of fibrinolysis is also problematic. The euglobulin lysis time is a complex and time-consuming procedure that can take more than 180 minutes. Other techniques used to identify hyperfibrinolysis, such as plasmin–antiplasmin complex, PAI-1, thrombin activatable fibrinolysis inhibitor, and D-dimers, suffer from the same limitations. Thus, all major aspects of the hemostatic system are measured inadequately using conventional laboratory testing of trauma patients. The limitations of these tests in the trauma setting have been validated repeatedly.64,65 In response to the shortcomings of conventional measurements of coagulopathy, point-of-care, rapid TEG (R-TEG) is emerging as the standard of care for both the diagnosis and treatment of postinjury coagulopathy at many trauma centers. TEG provides a rapid, comprehensive assessment of in vivo coagulation status. The TEG analyzer is composed of two mechanical parts separated by a blood specimen: a plastic cup or cuvette, into which a 0.36-mL blood specimen is pipetted, and a plastic pin attached to a torsion wire and suspended within the specimen (Fig. 13-3). Once the sample within the cuvette is placed on the TEG analyzer, the temperature is adjusted to that of the patient. The cup then oscillates slowly through an angle of 4°45′. Initially, movement of the cuvette does not affect the

CHAPTER 13

on endothelium. These observations have led to the traditional recommendation of empiric platelet transfusion following each 10 U of pRBCs. However, despite the high prevalence of thrombocytopenia following MT, the platelet count itself has not been found to predict coagulopathy. Harrigan et al. studied platelet function in 22 patients in hemorrhagic shock who had received at least 10 U of RBC (mean 21 U, range 10–80 U) but no platelet replacement therapy.48 Both the platelet count and markers of platelet function, including the bleeding time and aggregation to ADP, were depressed. However, no patient developed clinically apparent coagulopathy. Phillips et al. were similarly unable to predict postoperative coagulopathy based on the lowest platelet count among a cohort of patients who required more than 20 U of RBC in 24 hours.16 One half of patients with a platelet count 50,000 did not appear to have coagulopathy. An absolute platelet transfusion trigger thus does not exist for the trauma patient requiring MT. Many investigators have similarly attempted to identify an ideal ratio of RBC:platelets for preemptive platelet administration during MT. Only one group has studied the impact of prophylactic platelet administration in a randomized fashion.62 Reed et al. randomized 33 patients who required MT, defined as 12 U of modified whole blood within 12 hours of presentation, to receive either 6 U of platelets or 2 U of FFP for every 12 U of modified whole blood transfused. The primary outcome was the development of microvascular, nonmechanical bleeding, determined subjectively by the surgical team. Three patients in each group developed clinical coagulopathy (approximately 18% per group), and the platelet counts were no different between groups at any time point. The authors concluded that prophylactic platelet administration during MT was not warranted. However, apart from small sample size and subjective outcome, this study both employed a relatively low RBC:platelet ratio (12:1) and occurred with modified whole blood, limiting its contemporary relevance. More recent retrospective investigations into empiric platelet administration during MT are limited by the same problems inherent to the RBC:FFP ratio data. Specifically, several authors have shown that a decreased RBC:platelet ratio is associated with improved survival, with the lowest mortality observed in the range of 1:2 to 1:5.52 These data have been extrapolated to recommend empiric therapy with a ratio of 1:1. However, this so-called 1:1 is actually 1:0.2 as it is based on random donor units of platelets (5.5  1010) rather than apheresis units (3.0  1011).50 Regardless of the specific ratio, a causal relationship to these data is lacking, and confounding, survival bias, and lack of a mechanistic link render these data difficult to interpret. The overall poor quality of evidence supporting a low RBC:platelet ratio, as well as the morbidity associated with increased platelet transfusion, disfavors this strategy. Our current policy is to transfuse platelets based on point-of-care evidence of dysfunction as determined by TEG, or following the 10th unit of RBC transfusion, regardless of laboratory evidence of platelet dysfunction.

225

226

Generalized Approaches to the Traumatized Patient TEG tracing

TEG instrument Coagulation

Fibrinolysis

SECTION 2

Torsion wire

Pin Cup Heating element, sensor and controller

.36 ml whole blood (clotted)

MA R

EPL

K

4˚45

FIGURE 13-3 Thrombelastography instrument and tracing. The instrument diagram depicts the cuvette where a whole blood sample is placed, and the pin attached to a torsion wire. Once the assay is initiated, a tracing is produced and an initial linear segment (zone of precoagulation) extends from the beginning of the test to the formation of the first fibrin strand, causing the tracing to split (split point). The progressive divergence of the tracing reflects the formation of the clot. (Image of the TEG® Thromboelastograph® instrument and hemostasis tracing is used by permission of Haemonetics Corporation.)

pin, but as clot develops, resistance from the developing fibrin strands couples the pin to the motion of the cuvette. In turn, the torsion wire generates a signal that is amplified and records the characteristic tracing seen in Fig. 13-3. In earlier iterations, this tracing was recorded on heat-sensitive paper moving at a rate of 2 mm/min. More recent computer technology has allowed for automatic calculation of TEG variables. At our institution, a dynamic TEG tracing is transmitted directly to the operating room or ICU via computer within minutes, enabling prompt interpretation. The various components of the TEG tracing are depicted in Fig. 13-3. The split point (SP, minutes) is a measure of the time to initial clot formation, interpreted from the earliest resistance detected by the TEG analyzer causing the tracing to split; this is the point at which all other platelet-poor plasma clotting assays (e.g., PT and PTT) fail to progress. The reaction time (R, minutes) is defined as the time elapsed from the initiation of the test to the point where the onset of clotting provides enough resistance to produce a 2-mm amplitude reading on the TEG tracing. Of note, in the R-TEG assay (discussed below), due to the acceleration of clotting initiation, the R time is represented by a TEG-derived activated clotting time (TEGACT). The R time and TEG-ACT are most representative of the initiation phase of enzymatic clotting factors. Whereas a prolonged R time or TEG-ACT is diagnostic of hypocoagulability, decreased values may suggest hypercoagulability. The coagulation time (K, minutes) is a measurement of the time interval from the R time to the point where fibrin cross-linking provides enough clot resistance to produce a 20-mm amplitude reading. The alpha-angle (α, degrees) is the angle formed by the slope of a tangent line traced from the R to the K time measured in degrees. Both the K time and the alpha-angle denote the rate at which the clot strengthens and are most representative of thrombin’s cleaving of available fibrinogen into fibrin. The maximum amplitude (MA, millimeters) indicates the point at which clot strength reaches its maximum measure in millimeters on the TEG tracing, and reflects the end result of maximal

platelet–fibrin interaction via GPIIb–IIIa receptors. The clot strength (G, dynes/cm2) is a calculated measure derived from amplitude (A, mm); G  (5,000  A)/(100  A). Due to its exponential relationship with A, G appears to be the best measure of overall clot strength. Finally, the estimated percentage lysis (EPL, %) corresponds to the percentage of the clot that has lysed at a given time point (e.g., 5 minutes). The various TEG parameters and their significance are summarized in Table 13-3. Blood coagulation as measured by TEG is initiated by addition of an activating solution consisting of kaolin, phospholipids, and buffered stabilizers, which requires an activation phase of several minutes before coagulation starts. To expedite time to generate results (e.g., in the setting of hemorrhagic shock), clotting initiation can be further prompted by addition of tissue factor. This permits the earliest tracings via R-TEG to be viewed within 10 minutes. Fig. 13-4 depicts deranged TEG profiles characteristic of specific coagulation abnormalities along with a normal TEG tracing (tracing A). Anticoagulation causes enzymatic inhibition of coagulation factors and produces a prolonged R time due to delayed initiation of clot formation, along with normal fibrinogen (normal K time and alpha-angle) and platelet function (normal MA) (tracing B). Platelet dysfunction is noted by a tracing with a normal R time and a primarily decreased MA, as seen in tracing C. We have defined clinically significant fibrinolysis when EPL values exceed 15%,21 resulting in a characteristic tapering of the TEG tracing immediately after the MA is reached (tracing D). Tracing E is characteristic of hypercoagulability, identifiable by decreased R and K times along with an elevated alpha-angle and MA. Recent data suggest the superiority of TEG as compared to both aPTT and PT/INR for assessment of the acute coagulopathy of trauma. Kheirabadi et al. showed in a rabbit model that TEG is a more sensitive indicator of dilutional hypothermic coagulopathy than PT.66 A recent clinical study of trauma patients surviving the first 24 hours reported that TEG

Postinjury Hemotherapy and Hemostasis

227

TABLE 13-3 TEG Parameters

R time K time Alpha-angle

MA

G

EPL

Significance Earliest activity of enzymatic factors, causing tracing to split Initiation phase of enzymatic factor activity Potentiation phase of enzymatic factors yielding clot strengthening Rate of clot strengthening through polymerization of available fibrinogen Platelet functional contribution to clot strength through IIB–IIIa receptor interaction with fibrin Overall total clot strength resulting from all coagulation interactions, calculated from amplitude (A), G  (5,000  A)/(100  A) Fibrinolytic activity, derived from percent decrease in clot strength after MA is reached

A B C D E

SP  split point, minutes; R  reaction time, minutes; K  coagulation time, minutes; alpha-angle, degrees; MA  maximum amplitude, millimeters; G  clot strength, dynes/cm2; EPL  estimated percent lysis, %.

FIGURE 13-4 Characteristic thrombelastographic tracings observed in the trauma patient. (A) Normal tracing; (B) prolonged R time seen with coagulation factor deficiency or inhibition by anticoagulation; (C) decreased maximum amplitude (MA), seen during platelet dysfunction or pharmacologic inhibition; (D) hyperfibrinolysis; (E) decreased R and K times, elevated alphaangle, and increased MA represent a hypercoagulable state. (Image of the TEG® Thromboelastograph® hemostasis tracings is used by permission of Haemonetics Corporation.)

detected hypercoagulability (by an increased MA and G), whereas the PT and aPTT did not.67 In a retrospective review of penetrating injuries, Plotkin et al. demonstrated hypocoagulation based on delayed propagation of the clot (increased K time and reduced alpha-angle) and decreased clot strength (reduced MA), where MA correlated with blood product use (r  0.57, P  .01).68 These findings emphasize the limitations of classic coagulation tests and their lack of efficacy particularly in postinjury coagulopathy. Goal-directed transfusion therapy guided by TEG tailors blood product administration to the pathophysiologic state of the individual patient. At our institution, this approach has become an integral part of resuscitation. Importantly, empiric blood component replacement using an RBC:FFP ratio of approximately 2:1 is initiated prior to attainment of the first TEG tracing; this time period, however, rarely exceeds 10 minutes. An initial hemostatic assessment with R-TEG identifies patients at risk for postinjury coagulopathy on arrival. Following interpretation of the initial tracing, blood component therapy is then tailored to address each deranged phase of clotting in a specific manner, while subsequent reassessment allows the evaluation of response, until a set threshold is reached. This strategy also permits improved communication with the blood bank; based on initial assessment and response to component therapy, more accurate estimations of component requirements can be made using real-time data.

Our current goal-directed approach to coagulopathy is depicted in Fig. 13-5. Reflecting the initiation phase of enzymatic factor activity, a prolonged TEG-ACT value is the earliest indicator of coagulopathy; when the value is above threshold, FFP is administered. K time and alpha-angle are most dependent on the availability of fibrinogen to be cleaved into fibrin while in the presence of thrombin. If indicated by K and alpha-angle, cryoprecipitate is administered, providing a concentrated form of fibrinogen. The MA demonstrates the relationship between fibrin generated during the initial phases of hemostasis and platelets via IIb–IIIa receptor interaction. Platelets are administered based on an MA 50 mm, which reflects the platelets’ functional contribution to clot formation. Of note, in this protocol, platelet transfusion is not based on platelet count but on functional contribution to clotting, reflected by the MA. Finally, antifibrinolytics are administered for an EPL 15%. Importantly, interpretation of the various TEG parameters occurs in parallel, rather than in series, such that multiple coagulation derangements are corrected simultaneously. In summary, TEG offers the following major advantages over traditional coagulation status testing: (1) rapid, pointof-care testing, (2) assessment of the spectrum of coagulation function, including fibrinolysis and thrombocytopathy, (3) reflection of in vivo clotting activity, and (4) serial graphical representations of goal-directed response to therapy. Implementation of a goal-directed approach to postinjury coagulopathy may reduce transfusion volumes, attain earlier

CHAPTER 13

Parameter SP time

228

Generalized Approaches to the Traumatized Patient

Rapid TEG SECTION 2

ACT > 100 sec

Angle < 60˚

MA < 50 mm

EPL > 15%

FFP

CRYO

Platelets

ACA

Rapid TEG FIGURE 13-5 Goal-directed hemostatic resuscitation via thrombelastography. Using point-of-care rapid thrombelastography (TEG), all components of the coagulation system of the bleeding trauma patient are both accessed and treated in parallel. Following goal-directed therapy based on the initial TEG tracing, coagulation status is reaccessed using serial rapid TEG determinations, until correction of each coagulation derangement is achieved. ACT, activated clotting time; MA, maximum amplitude; EPL, estimated percentage fibrinolysis; FFP, fresh frozen plasma; CRYO, cryoprecipitate; ACA, α-aminocaproic acid.

correction of coagulation abnormalities, improve survival in the acute hemorrhagic phase due to improved hemostasis from correction of coagulopathy, and improve outcomes in the later phase due to attenuation of the complications of overzealous blood product administration. Preliminary validation studies of these potential benefits have been encouraging. Retrospective data and pilot studies support a reduction in MT rates, decreased need for multiple and repeated classic coagulation tests, and decreased morbidity and mortality after implementation of TEG in trauma care.69,70 Our group recently compared pre-TEG to post-TEG outcomes of patients at risk of postinjury coagulopathy admitted to our trauma center.71 The TEG G value was significantly associated with survival (P  .03), whereas PT/INR and PTT did not discriminate between survivors and nonsurvivors. Further validation studies are ongoing at our institution as well as other trauma centers and will be necessary before supporting widespread application of this technology.

HEMOSTASIS ADJUNCTS ■ Recombinant Factor VIIa Treatment of postinjury coagulopathy with supraphysiologic doses of recombinant factor VIIa (rVIIa) is believed to amplify coagulation through generation of a thrombin burst in the presence of both tissue factor and functional platelets, and in the absence of either hypothermia or acidosis. Although the drug was developed originally for use in patients with hemophilia A,72 several case reports of successful off-label use in patients with postinjury coagulopathy raised enthusiasm for a formal indication in this setting. Commonly prescribed doses

(range 50–200 μg/kg) for this indication are estimated to be greater than 100 times physiologic. In 2004, the Maryland Shock Trauma Center reported a case series detailing outcomes of rVIIa use in 81 trauma patients who had undergone MT (defined in this series as 10 U RBC, 8 U FFP, and 1 U platelets).73 A standard dose of 100 μg/kg was used, and 80% of patients received the medication within 24 hours of injury. Coagulopathy, as measured by the PT, improved following administration of rVIIa in all patients, and no thrombotic events were observed. Furthermore, 61 of 81 (75.3%) patients were considered “responders” based on a subjective improvement in hemostasis noted by the trauma team. However, when rVIIa patients were compared to matched coagulopathic registry patients who had not received rVIIa, mortality was equivalent (50% vs. 44%, respectively, P  .60). Due to continued concerns over both efficacy and thrombotic risk, two parallel randomized controlled trials, one of penetrating and one of blunt trauma patients, were conducted among 32 international institutions (exclusive of the United States) from 2003 to 2004.74 Eligibility criteria mandated transfusion of 6 U RBC in 4 hours. Subjects were randomized to receive either placebo or three doses of rVIIa, 200, 100, and 100 μg/kg, with the first dose given after the eighth unit of RBC transfused, and the second and third doses 1 and 3 hours following. The primary end point was the number of RBC transfusions in the 48 hours following the first dose, although no standard transfusion trigger was specified. The trials were powered to detect a clinically relevant reduction in transfusion requirement of 2.6 U. A reduction in RBC transfusion requirement for both blunt (median 7.0 vs. 7.5, P  .02) and penetrating (3.9 vs. 4.2, P  .10) groups was observed among those alive 48 hours after the first dose of the study drug. However, these relatively small differences were eliminated

Postinjury Hemotherapy and Hemostasis 1 hour of injury, and correlated significantly with all traditional parameters of shock, MT, and mortality.21 Furthermore, our identification of lower levels of fibrinolysis in patients with less severe injury supports current theories suggesting a mechanism based on varying concentrations of tPA and PAI, and implicates fibrinolysis as an integral component of the endogenous coagulopathy of trauma. Antifibrinolytic agents are employed commonly for hyperfibrinolysis associated with elective (predominantly cardiac) surgery, with favorable efficacy and safety profiles.78 Such agents include the competitive plasmin inhibitors α-aminocaproic acid (Amicar) (dosing  150 mg/kg followed by 15 mg/h) and tranexamic acid (dosing 10 mg/kg, followed by 1 mg/(kg h)), as well as the direct plasmin inhibitor aprotinin (dosing 280 mg, followed by 70 mg/h). In addition to plasmin, aprotinin inhibits tissue kallikrein, trypsin, and factor XIIa. Because use of aprotinin (currently unavailable) is limited due to the need for a test dose, expense, and increased risk of both renal and thrombotic complications, we prefer α-aminocaproic acid. The evidence for efficacy of antifibrinolytics in the treatment of postinjury coagulopathy is less clear, and no agent currently carries FDA approval for this indication. Two previous trials have attempted to evaluate the benefit of aprotinin in a randomized fashion.79,80 However, small samples, imprecise outcome reporting, and interval advancements in the care of the bleeding trauma patients all limit the applicability of these trials.81 The results of a third RCT addressing the efficacy of antifibrinolytics in the trauma setting, entitled the Clinical Randomization of an Antifibrinolytic in Significant Hemorrhage (CRASH) II study, were published recently.82 The trial randomized 20,127 adult trauma patients with significant hemorrhage (defined as systolic blood pressure 90 mm Hg, pulse 110 beats/min, or both) from 274 collaborating hospitals in 40 countries to receive tranexamic acid (1 g over 10 minutes load followed by an additional gram over 8 hours) or placebo within 8 hours of injury. A small but significant reduction in both all-cause mortality (14.5% vs. 16.0%, respectively, P  .004) and death due to hemorrhage (4.9% vs. 5.7%, respectively, P  .008) was observed for the tranexamic acid as compared to the placebo group. One important limitation of this study involved the lack of point-of-care diagnosis of fibrinolysis as an inclusion criterion. Our data suggest that although approximately two thirds of patients who require MT demonstrate evidence of fibrinolysis, only one third demonstrate clinically significant fibrinolysis (TEG EPL 15%).21 Therefore, analysis of all trauma patients in the CRASH-II study may have diluted any survival benefit for the subgroup of patients with significant fibrinolysis. Our current standard is to treat bleeding trauma patients who demonstrate evidence of clinically significant hyperfibrinolysis on a TEG tracing (EPL 15%) with α-aminocaproic acid.

■ Antifibrinolytics

■ Factor XIIIa

All current theories of the acute endogenous coagulopathy of trauma implicate hyperfibrinolysis. Our recent report showed that fibrinolysis was identified via point-of-care TEG within

Factor XIII acts to stabilize the fibrin clot once formed, and a clear relationship between XIII concentration and maximal clot firmness as demonstrated by TEG has been demonstrated.83

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when the analysis was expanded to include patients who had died within the first 48 hours of injury, a subgroup of clear importance. A significant difference in the need for MT, defined as 20 total U RBC, was also eliminated after accounting for these early deaths. Although a significant difference in the incidence of ARDS was noted between the rVIIa and placebo groups among blunt trauma patients (4% vs. 16%, respectively, P  .03) (again only among those alive at 48 hours), no difference in length of stay, ventilator days, or mortality was observed in any analysis. A subsequent subgroup analysis of 136 patients with coagulopathy reported decreases in both RBC and FFP transfusion requirements at 48 hours among the rVIIa patients as compared to controls (delta  2.6 U and 600 mL, respectively).75 Importantly, these analyses were not limited to 48-hour survivors. However, mortality remained equivalent. Again, no standardized transfusion practice was followed, and the definition of coagulopathy was determined subjectively as an FFP:RBC transfusion ratio 1:4, or any transfusion of either platelets or cryoprecipitate. Thus, the only level I evidence regarding use of rVIIa in the trauma setting is hindered by both methodological limitations, such as a lack of power and standardized transfusion policy, and a failure to demonstrate an improvement in either coagulopathy (which was not measured) or survival. Most recently, Knudson et al. compared patients from a multicenter rVIIa registry to patients in a multicenter MT study who had not received rVIIa.76 Patients who had received rVIIa had higher mortality and increased death due to hemorrhage. Thus, at present, the initial enthusiasm for rVIIa in the trauma setting has been curtailed by a lack of data documenting efficacy, prohibitive cost, and continued concerns for increased thrombotic risk.77 If rVIIa therapy is contemplated, several pharmacokinetic properties of the drug warrant consideration. The activity of rVIIa is both pH and temperature dependent, with a 60% decrement at a pH of 7.20 and a 20% decrement at a temperature of 33°C.34 Furthermore, physiologic concentrations of calcium, fibrinogen, and platelets are required, such that replacement of these clotting factors is mandatory prior to rVIIa administration. Dosages range from 50 to 200 μg/kg, with redosing required in the face of continued coagulopathy beyond the half-life of 2 hours. As the technology for diagnosing coagulopathy improves, further indications for treatment with rVIIa may emerge. For example, our group has observed a postfibrinolysis consumptive coagulopathy, which is characterized by serial TEG tracings documenting diffuse clotting factor deficiency secondary to massive consumption after fibrinolysis. The resulting severe thrombin deficiency may respond to rVIIa, and we have noted anecdotally rapid improvement with normalization of TEG patterns after such treatment.

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Early depletion of the limited endogenous XIII stores has been documented following major hemorrhage, and is believed to contribute to coagulopathy.84 Although prospective data are lacking, empiric therapy with rXIIIa should be considered in postinjury coagulopathy that is refractory to conventional factor replacement therapy.

■ Prothrombin Complex Concentrate Prothrombin complex concentrate (PCC) contains the vitamin K–dependent coagulation factors II, VII, IX, and X, as well as the anticoagulants protein C and protein S. As such, its main indication involves rapid reversal of the anticoagulant effects of warfarin in bleeding patients. Importantly, PCC provides these factors in a concentrated form as compared to FFP (approximately 50 mL vs. 300 mL, respectively). The efficacy of PCC for urgent reversal of warfarin reversal in the perioperative period has been well documented85; use of PCC in this setting has been recommended by expert panels in both the United States and Europe.86 Although RCTs in head-injured, warfarinized patients are lacking, it seems reasonable to use PCC in this setting as well, particularly when concern for volume overload is high. Kalina et al. reported decreased time to normalization of the INR and operative intervention using PCC as compared to a combination of vitamin K and FFP in a review of warfarinized patients with intracranial hemorrhage (ICH).87 The role of PCC in the nonwarfarinized patient continues to evolve. Bruce and Nokes reported favorable outcomes following PCC administration for uncontrolled hemorrhage following cardiac surgery, exclusive of warfarin use.88 The benefit of PCC over traditional therapies for the treatment of postinjury coagulopathy remains unproven. Several recent animal studies of hemodilutional coagulopathy have reported superior achievement of hemostatic resuscitation using PCC as compared to both FFP89 and rVIIa.90 However, although the reduced time and volume necessary to achieve coagulation factor replacement are appealing, transfusion of PCC likely carries the same immunomodulatory risks as those of FFP. Furthermore, the cost of PCC is currently prohibitive at many trauma centers. Controlled trials in humans are necessary prior to definitive recommendations.

PRE-INJURY ANTITHROMBOTIC AGENTS ■ Warfarin Warfarin is an oral anticoagulant that inhibits synthesis of the vitamin K–dependent clotting factors II, VII, IX, and X, as well as the anticoagulant protein C and protein S. It is the most common drug prescribed to achieve chronic anticoagulation; 1% of the world’s population uses warfarin currently.91 As the elderly demographic continues to expand exponentially, warfarin use will only increase. Several studies have documented an increased likelihood of traumatic ICH, as well as severity of injury and mortality, among trauma patients using warfarin as compared to nonwarfarinized patients.92–94 Importantly, the increased

likelihood of adverse outcomes is observed only among patients who have achieved therapeutic anticoagulation (INR 2), negating the possibility of underlying demographic differences between warfarin and nonwarfarin patients.92 Rapid identification of the warfarinized patient at risk for traumatic ICH, as well as reversal of anticoagulation, is paramount to minimizing hemorrhage progression with resultant irreversible neurologic devastation. Most authors advocate empiric transfusion of FFP prior to laboratory documentation of therapeutic anticoagulation in the warfaranized patient at risk for head injury, arguing that the morbidity of a delay in reversal of patients with a supratherapeutic INR outweighs that of unnecessary factor administration to patients with a subtherapeutic INR. Although up to one half of warfaranized trauma patients present with a subtherapeutic INR,92 the morbidity of an expanding ICH renders this argument reasonable. However, a striking amount of variability exists among trauma surgeons as to the INR above which reversal of anticoagulation should be implemented, the rapidity with which the PT is normalized, or the target INR following reversal.95 Ivascu et al. developed a protocol in which warfarin anticoagulated trauma patients suspected to have ICH underwent rapid triage and computed tomography.96 In the case of positive imaging, 2 U of universal donor, prethawed FFP, and 10 mg vitamin K were administered. Protocol subjects were compared to historical controls. The authors observed a decreased time to evaluation, diagnostic imaging, and full anticoagulation reversal (INR 2.0). Furthermore, the time to initiation of treatment decreased from 4 to 2 hours. The percentage of patients whose hemorrhage progressed decreased from 40% to 11%, with an associated mortality decrease from 50% to 10%. Reversal of warfarin-induced anticoagulation using either PCC or rVIIa may be particularly beneficial in patients at high risk for cardiopulmonary complications secondary to largevolume clotting factor concentrate administration. Although case series have documented efficacy without thrombotic morbidity,87,97 prospective, controlled data are lacking. The risk of warfarin anticoagulation in the non-head-injured trauma patient is less clear. Ott et al. studied 212 blunt trauma patients of age 60 years who sustained trauma to the abdomen or thorax in the absence of intracranial injury.98 No outcome differences between warfarinized patients (mean INR 2.1) and nonwarfarinized patients were observed.

■ Antiplatelet Therapy Antiplatelet therapies, which consist predominantly of acetylsalicyclic acid (ASA) and clopidogrel, have revolutionized the care of patients with atherosclerotic cardiovascular disease. Although via independent mechanisms, both ASA and clopidogrel inhibit irreversibly platelet aggregation. The average lifespan of a platelet is 7–10 days, such that patients using antiplatelet therapies possess some degree of platelet dysfunction throughout this time period. However, platelet function recovers gradually during this time period, as the bone marrow generates approximately 20,000 platelets per day.

Postinjury Hemotherapy and Hemostasis

COMPLICATIONS OF BLOOD COMPONENTS Modern-day transfusion practice has minimized substantially the risk of both infectious disease transmission and blood group compatibility mismatch. Consequently, the current major morbidities of blood product transfusion involve immunomodulation with resultant organ failure, storage-related rheologic changes, and cardiovascular compromise secondary to both volume overload and increased vascular resistance. The immunomodulatory properties of RBC transfusion were first noted as a correlation between transfusion and graft survival following solid organ transplantation.103 The observation that tumor recurrence was associated with RBC transfusion soon followed.104 It is now appreciated that RBC transfusion both impairs humoral immunity and causes elaboration of proinflammatory cytokines. These phenomena are dependent on both transfusion dose and storage time. There appear to be at least two important mechanisms resulting in immunomodulation. The first involves passive transfer of antileukocyte and anti-HLA antibodies from alloimmunized donors. Passenger leukocytes accompanying RBCs in storage result in the sustained generation of proinflammatory cytokines. Substantial quantities of additional inflammatory mediators such as activated complement, fibrin

degradation products, and arachidonic acid are present in both FFP and platelets. Second, proinflammatory compounds present in donor blood (e.g., phospholipids presumably generated from degradation of the RBC membrane with storage) incite the recipient’s immune system, thereby exacerbating inflammation. Clinically, this immune activation is manifest as a dosedependent increased risk of organ failure associated with transfusion. The most common and well-delineated organ system affected is the lung. Several reports of critically ill patients, including trauma patients, have detailed a strong correlation between blood product transfusion and the development of acute lung injury, ARDS, and death, even after adjusting for the fact that patients who receive transfusions are, in general, sicker than those who do not.105,106 Additional deleterious effects of RBC transfusion include storage time–dependent degradation with resultant entrapment in the microcirculation, resulting in obstruction and eventual ischemia.107 Moreover, transfused blood exerts a number of negative effects on cardiodynamics, including increased pulmonary vascular resistance, depletion of endogenous nitric oxide stores, and both regional and systemic vasoconstriction. Finally, large-volume blood product transfusion results in a massive oncotic load, eventuating in organ system edema and the consequences thereof. Numerous clinical studies have documented an independent association between RBC transfusion and mortality following MT.105,108 Importantly, current evidence suggests that sub-MT also imparts an increased risk of morbidity. In fact, a clear dose– response relationship between blood transfusion and organ dysfunction, as well as death, has been documented repeatedly among trauma patients, such that even a single transfusion worsens outcome.109 In a study of trauma patients who developed ARDS, this dose–response relationship followed an exponential function, with a 60% likelihood of ARDS among patients who received 10 U RBC.110 The risks of transfusion extend beyond the initial resuscitation period. In a recent study of trauma patients who did not receive their first blood transfusion until at least 48 hours after injury, each transfusion was independently associated with an increased likelihood of developing ventilatorassociated pneumonia, ARDS, and death.111 Transfusion of both FFP and platelets appears equally deleterious. In a single institution study of 841 critically ill medical patients, RBC transfusion, FFP transfusion, and platelet transfusion each independently increased the likelihood of either ALI or ARDS.112 In a multivariable logistic regression model that adjusted for the probability of transfusion and other ALI risk factors, any RBC transfusion increased the likelihood of lung injury by 39%, FFP transfusion by 248%, and platelet transfusion by 389%. Watson et al. investigated the relationship between platelet, FFP, and cryoprecipitate transfusion among 1,175 blunt trauma patients with hemorrhagic shock.113 Although no mortality differences were noted for either platelets or cryoprecipiate, each unit of FFP increased the risk of MOF by 2.1% and ARDS by 2.5%. Most recently, Inaba et al. documented a significant, independent correlation between units of FFP transfused and complications among a large cohort of trauma patients who had received sub-MT.114

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Data comparing the incidence of ICH between patients using antiplatelet therapy and controls are sparse. However, several matched case series of head-injured patients have documented an increased severity of hemorrhage, as well as mortality, among patients using antiplatelet therapy as compared to controls.99–101 These reports are limited primarily by confounding by comorbidity, as patients using antiplatelet therapies tend to be sicker than those who do not. Despite an apparent increased morbidity associated with pre-injury antiplatelet agents among head-injured patients, little data exist to support routine platelet transfusion in this setting. Neither Ivascu et al.100 nor Downey et al.102 documented a mortality difference associated with platelet transfusion among head-injured patients using antiplatelet therapies. However, platelet administration was at the discretion of the trauma team. Furthermore, data regarding the rapidity and effectiveness of transfusions were not available. Prospective, randomized data are necessary prior to recommending routine platelet administration in this cohort, preferably incorporating serial point-of-care assessment of platelet mapping, such as is possible with TEG. These studies are particularly timely as both the elderly demographic and prevalence of antiplatelet therapy are increasing exponentially. Pending these data, platelet transfusion may be based currently on expert opinion and clinical circumstance. Interestingly, the deleterious effects of antiplatelet therapy do not appear to extend to the non-head-injured trauma patient. In a recent report, no mortality difference was noted for patients using antiplatelet therapies as compared to controls among a cohort of trauma patients with no evidence of ICH on CT.98 However, injury severity was relatively low in this group. The effect of pre-injury antiplatelet therapy on trauma patients who require MT remains unknown.

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The incidence of ARDS was increased 12-fold in patients who had received 6 U of FFP as compared to those patients who had received 6 U. A major limitation of this retrospective literature involves confounding. Specifically, MT may serve simply as a marker for severe illness rather than a true causal parameter. However, the aforementioned CRIT trial, which remains the only randomized trial of blood transfusion triggers, demonstrated a significantly increased risk of ARDS with a liberal transfusion strategy.7 Furthermore, the persistent adverse relationship between transfusion and organ failure among less ill patients strengthens the argument for causality. In summary, abundant data now exist documenting the deleterious effects of blood product transfusion. One particularly morbid complication involves inflammationinduced organ failure. These data, in conjunction with the aforementioned limitations of the literature suggesting an empiric RBC:FFP:platelet transfusion ratio of 1:1:1, underscore the importance of minimizing unnecessary transfusions. Consequently, blood product replacement should be both restrictive and goal directed.

POSTINJURY HYPERCOAGULABILITY Trauma patients who survive their initial injury transition from a hypocoagulable to a hypercoagulable state as early as 24 hours following presentation.115 The etiology of this hypercoagulable state is likely multifactorial, involving endothelial injury, circulatory stasis, platelet activation, decreased levels of endogenous anticoagulants, and impaired fibrinolysis. Hypercoagulability predisposes the trauma patient to venous thromboembolism (VTE); large series among trauma patients have reported an incidence of deep vein thrombosis from 10% to 80%116 and pulmonary embolism from 2% to 22%.117 Pulmonary embolism is the third most common cause of death in trauma patients who survive the first 24 hours.117 Similar to the early coagulopathy of trauma, both diagnosis and treatment of hypercoagulability following injury are limited by lack of accurate laboratory testing. Conventional tests used to monitor coagulation status such as the aPTT and PT/INR are neither able to diagnose hypercoagulability nor delineate the relative contributions of enzymatic and platelet components. Previous prospective trials addressing the benefit of various mechanical and pharmacoprophylactic regimens among injured patients have thus neither documented hypercoagulability nor monitored the efficacy of prophylaxis. Furthermore, current guidelines do not address the contribution of platelets to hypercoagulability, nor do they recommend prescription of antiplatelet drugs as part of standard pharmcoprophylactic regimens.118 This last issue is of particular concern as a growing body of evidence has implicated platelet activation in the development and propagation of VTE.119 In light of these limitations, it is not surprising that most VTEs among trauma patients occur because of prophylaxis failure rather than failure to provide prophylaxis.120 In addition to its usefulness in the management of the coagulopathic, bleeding trauma patient, point-of-care TEG offers many advantages for the treatment of postinjury hyper-

coagulability. An increased G, decreased R time, increased alpha-angle, and increased MA are all suggestive of hypercoagulability (Fig. 13-4E), and our group recently documented a strong correlation between hypercoagulability as evidenced by the aforementioned TEG parameters and subsequent VTE.69 Furthermore, despite standard chemoprophylaxis, 60% of patients displayed evidence of hypercoagulability. Additional advantages of TEG in this setting include differentiation of enzymatic from platelet hypercoagulability, as well as monitoring of the effect of both enzymatic and platelet inhibitors via platelet mapping. Despite the many theoretical advantages of TEG-driven chemoprophylaxis protocols, prospective data remain sparse. Our institution is currently conducting an RCT comparing conventional pharmacoprophylaxis to TEG-guided therapy among trauma patients. Outcomes will include the incidence of VTE, as well as the efficacy of both enzymatic and platelet inhibition. We hope that these data will inform future clinical practice guidelines, as well as provide insight into whom, when, and how to prophylaxis adequately against VTE.

CONCLUSION Postinjury coagulopathy remains a major cause of both morbidity and mortality. Major advances in the care of the coagulopathy trauma patient include the elucidation of the endogenous coagulopathy of trauma, conceptualization of damage control resuscitation, and the application of point-ofcare TEG to the trauma setting. Limitations of the retrospective literature addressing blood component ratios for empiric replacement, as well as continued evidence documenting the adverse effects of blood component transfusion, have led the pendulum to swing away from a “1:1:1” ratio of RBC:FFP:platelets. Current evidence supports an empiric FFP:RBC ratio of 1:2 to 1:3, with early platelet and cryoprecipitate replacement based on goal-directed monitoring. Future directions in the field of postinjury coagulopathy involve continued elucidation of the mechanisms of the endogenous coagulopathy of trauma (including therapeutic targets), rigorous research of hemostatic adjuncts, and dissemination of the technology of TEG to trauma physicians.

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Postinjury Hemotherapy and Hemostasis 35. Engstrom M, Schott U, Romner B, Reinstrup P. Acidosis impairs the coagulation: a thromboelastographic study. J Trauma. 2006;61: 624–628. 36. Martini WZ, Dubick MA, Pusateri AE, Park MS, Ryan KL, Holcomb JB. Does bicarbonate correct coagulation function impaired by acidosis in swine? J Trauma. 2006;61:99–106. 37. Brazil EV, Coats TJ. Sonoclot coagulation analysis of in-vitro haemodilution with resuscitation solutions. J R Soc Med. 2000;93: 507–510. 38. Coats TJ, Brazil E, Heron M, MacCallum PK. Impairment of coagulation by commonly used resuscitation fluids in human volunteers. Emerg Med J. 2006;23:846–849. 39. Bickell WH, Bruttig SP, Millnamow GA, O’Benar J, Wade CE. The detrimental effects of intravenous crystalloid after aortotomy in swine. Surgery. 1991;110:529–536. 40. Owens TM, Watson WC, Prough DS, Uchida T, Kramer GC. Limiting initial resuscitation of uncontrolled hemorrhage reduces internal bleeding and subsequent volume requirements. J Trauma. 1995;39:200–207 [discussion 8–9]. 41. Bickell WH, Wall MJ Jr, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994;331:1105–1109. 42. Wall MJ, Granchi T, Liscum K, Aucar J, Mattox KL. Delayed vs. immediate fluid resuscitation in patients with penetrating trauma: subgroup analysis. J Trauma. 1995;39:173. 43. Turner J, Nicholl J, Webber L, Cox H, Dixon S, Yates D. A randomised controlled trial of prehospital intravenous fluid replacement therapy in serious trauma. Health Technol Assess. 2000;4:1–57. 44. Dutton RP, Mackenzie CF, Scalea TM. Hypotensive resuscitation during active hemorrhage: impact on in-hospital mortality. J Trauma. 2002;52:1141–1146. 45. Kwan I, Bunn F, Roberts I. Timing and volume of fluid administration for patients with bleeding. Cochrane Database Syst Rev. 2003:CD002245. 46. Advanced Trauma Life Support for Doctors. 2nd ed. Chicago, IL: American College of Surgeons; 1997. 47. Kashuk JL, Moore EE, Johnson JL, et al. Postinjury life threatening coagulopathy: is 1:1 fresh frozen plasma:packed red blood cells the answer? J Trauma. 2008;65:261–270 [discussion 70–71]. 48. Harrigan C, Lucas CE, Ledgerwood AM, Walz DA, Mammen EF. Serial changes in primary hemostasis after massive transfusion. Surgery. 1985;98:836–844. 49. Borgman MA, Spinella PC, Perkins JG, et al. The ratio of blood products transfused affects mortality in patients receiving massive transfusions at a combat support hospital. J Trauma. 2007;63: 805–813. 50. Armand R, Hess JR. Treating coagulopathy in trauma patients. Transfus Med Rev. 2003;17:223–231. 51. Duchesne JC, Hunt JP, Wahl G, et al. Review of current blood transfusions strategies in a mature level I trauma center: were we wrong for the last 60 years? J Trauma. 2008;65:272–276 [discussion 6–8]. 52. Holcomb JB, Wade CE, Michalek JE, et al. Increased plasma and platelet to red blood cell ratios improves outcome in 466 massively transfused civilian trauma patients. Ann Surg. 2008;248:447–458. 53. Teixeira PG, Inaba K, Shulman I, et al. Impact of plasma transfusion in massively transfused trauma patients. J Trauma. 2009;66:693–697. 54. Spinella PC, Perkins JG, Grathwohl KW, et al. Effect of plasma and red blood cell transfusions on survival in patients with combat related traumatic injuries. J Trauma. 2008;64:S69–S77 [discussion S77–78]. 55. Hirshberg A, Dugas M, Banez EI, Scott BG, Wall MJ Jr, Mattox KL. Minimizing dilutional coagulopathy in exsanguinating hemorrhage: a computer simulation. J Trauma. 2003;54:454–463. 56. Snyder CW, Weinberg JA, McGwin G Jr, et al. The relationship of blood product ratio to mortality: survival benefit or survival bias? J Trauma. 2009;66:358–362 [discussion 62–64]. 57. O’Shaughnessy DF, Atterbury C, Bolton Maggs P, et al. Guidelines for the use of fresh-frozen plasma, cryoprecipitate and cryosupernatant. Br J Haematol. 2004;126:11–28. 58. Martin DJ, Lucas CE, Ledgerwood AM, Hoschner J, McGonigal MD, Grabow D. Fresh frozen plasma supplement to massive red blood cell transfusion. Ann Surg. 1985;202:505–511. 59. Mace JE, White CE, Simmons JW. High plasma to RBC ratio improves survival based on mechanism of combat injury in massively transfused patients. J Am Coll Surg. 2009;209:S47. 60. Faringer PD, Mullins RJ, Johnson RL, Trunkey DD. Blood component supplementation during massive transfusion of AS-1 red cells in trauma patients. J Trauma. 1993;34:481–485 [discussion 5–7].

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8. Weiskopf RB, Viele MK, Feiner J, et al. Human cardiovascular and metabolic response to acute, severe isovolemic anemia. JAMA. 1998;279:217–221. 9. Carson JL, Noveck H, Berlin JA, Gould SA. Mortality and morbidity in patients with very low postoperative Hb levels who decline blood transfusion. Transfusion. 2002;42:812–818. 10. Goldsmith HL. The flow of model particles and blood cells and its relation to thrombogenesis. Prog Hemost Thromb. 1972;1:97–127. 11. Quaknine-Orlando B, Samama CM, Riou B, et al. Role of the hematocrit in a rabbit model of arterial thrombosis and bleeding. Anesthesiology. 1999;90:1454–1461. 12. Sauaia A, Moore FA, Moore EE, et al. Epidemiology of trauma deaths: a reassessment. J Trauma. 1995;38:185–193. 13. Simmons RL, Collins JA, Heisterkamp CA, Mills DE, Andren R, Phillips LL. Coagulation disorders in combat casualties. I. Acute changes after wounding. II. Effects of massive transfusion. 3. Post-resuscitative changes. Ann Surg. 1969;169:455–482. 14. Kashuk JL, Moore EE, Millikan JS, Moore JB. Major abdominal vascular trauma—a unified approach. J Trauma. 1982;22:672–679. 15. Harrigan C, Lucas CE, Ledgerwood AM. The effect of hemorrhagic shock on the clotting cascade in injured patients. J Trauma. 1989;29:1416–1421 [discussion 21–22]. 16. Phillips TF, Soulier G, Wilson RF. Outcome of massive transfusion exceeding two blood volumes in trauma and emergency surgery. J Trauma. 1987;27:903–910. 17. Brohi K, Cohen MJ, Ganter MT, Matthay MA, Mackersie RC, Pittet JF. Acute traumatic coagulopathy: initiated by hypoperfusion: modulated through the protein C pathway? Ann Surg. 2007;245:812–818. 18. MacLeod JB, Lynn M, McKenney MG, Cohn SM, Murtha M. Early coagulopathy predicts mortality in trauma. J Trauma. 2003;55:39–44. 19. Cannon WB, Fraser J, Cowell E. The preventive treatment of wound shock. JAMA. 1918;70:618–621. 20. Maegele M, Lefering R, Yucel N, et al. Early coagulopathy in multiple injury: an analysis from the German Trauma Registry on 8724 patients. Injury. 2007;38:298–304. 21. Kashuk JL, Moore EE, Sawyer M, et al. Primary fibrinolysis is integral in the pathogenesis of the acute coagulopathy of trauma. Ann Surg. 2010;252(3):434–442. 22. Brohi K, Cohen MJ, Ganter MT, et al. Acute coagulopathy of trauma: hypoperfusion induces systemic anticoagulation and hyperfibrinolysis. J Trauma. 2008;64:1211–1217 [discussion 7]. 23. Chesebro BB, Rahn P, Carles M, et al. Increase in activated protein C mediates acute traumatic coagulopathy in mice. Shock. 2009;32:659–665. 24. Gando S. Acute coagulopathy of trauma shock and coagulopathy of trauma: a rebuttal. You are now going down the wrong path. J Trauma. 2009;67:381–383. 25. Hardaway RM. The significance of coagulative and thrombotic changes after haemorrhage and injury. J Clin Pathol Suppl (R Coll Pathol). 1970; 4:110–120. 26. Gando S, Nakanishi Y, Tedo I. Cytokines and plasminogen activator inhibitor-1 in posttrauma disseminated intravascular coagulation: relationship to multiple organ dysfunction syndrome. Crit Care Med. 1995;23:1835–1842. 27. Levi M. Disseminated intravascular coagulation. Crit Care Med. 2007; 35:2191–2195. 28. Kooistra T, Schrauwen Y, Arts J, Emeis JJ. Regulation of endothelial cell t-PA synthesis and release. Int J Hematol. 1994;59:233–255. 29. Jurkovich GJ, Greiser WB, Luterman A, Curreri PW. Hypothermia in trauma victims: an ominous predictor of survival. J Trauma. 1987;27: 1019–1024. 30. Watts DD, Trask A, Soeken K, Perdue P, Dols S, Kaufmann C. Hypothermic coagulopathy in trauma: effect of varying levels of hypothermia on enzyme speed, platelet function, and fibrinolytic activity. J Trauma. 1998;44:846–854. 31. Wolberg AS, Meng ZH, Monroe DM 3rd, Hoffman M. A systematic evaluation of the effect of temperature on coagulation enzyme activity and platelet function. J Trauma. 2004;56:1221–1228. 32. Valeri CR, Feingold H, Cassidy G, Ragno G, Khuri S, Altschule MD. Hypothermia-induced reversible platelet dysfunction. Ann Surg. 1987; 205:175–181. 33. Yoshihara H, Yamamoto T, Mihara H. Changes in coagulation and fibrinolysis occurring in dogs during hypothermia. Thromb Res. 1985; 37:503–512. 34. Meng ZH, Wolberg AS, Monroe DM 3rd, Hoffman M. The effect of temperature and pH on the activity of factor VIIa: implications for the efficacy of high-dose factor VIIa in hypothermic and acidotic patients. J Trauma. 2003;55:886–891.

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61. Lim RC Jr, Olcott C 4th, Robinson AJ, Blaisdell FW. Platelet response and coagulation changes following massive blood replacement. J Trauma. 1973;13:577–582. 62. Reed RL 2nd, Ciavarella D, Heimbach DM, et al. Prophylactic platelet administration during massive transfusion. A prospective, randomized, double-blind clinical study. Ann Surg. 1986;203:40–48. 63. Bick RL, Kaplan H. Syndromes of thrombosis and hypercoagulability. Congenital and acquired causes of thrombosis. Med Clin North Am. 1998;82:409–458. 64. Counts RB, Haisch C, Simon TL, Maxwell NG, Heimbach DM, Carrico CJ. Hemostasis in massively transfused trauma patients. Ann Surg. 1979;190:91–99. 65. Lucas CE, Ledgerwood AM. Clinical significance of altered coagulation tests after massive transfusion for trauma. Am Surg. 1981;47:125–130. 66. Kheirabadi BS, Crissey JM, Deguzman R, Holcomb JB. In vivo bleeding time and in vitro thrombelastography measurements are better indicators of dilutional hypothermic coagulopathy than prothrombin time. J Trauma. 2007;62:1352–1359 [discussion 9–61]. 67. Park MS, Martini WZ, Dubick MA, et al. Thromboelastography as a better indicator of hypercoagulable state after injury than prothrombin time or activated partial thromboplastin time. J Trauma. 2009;67: 266–275 [discussion 75–76]. 68. Plotkin AJ, Wade CE, Jenkins DH, et al. A reduction in clot formation rate and strength assessed by thrombelastography is indicative of transfusion requirements in patients with penetrating injuries. J Trauma. 2008;64:S64–S68. 69. Kashuk JL, Moore EE, Sabel A, et al. Rapid thrombelastography (r-TEG) identifies hypercoagulability and predicts thromboembolic events in surgical patients. Surgery. 2009;146:764–772 [discussion 72–74]. 70. Gonzalez EA, Kashuk JL, Moore EE, Silliman CC. Differentiation of enzymatic from platelet hypercoagulability using the novel thrombelastography parameter delta. J Surg Res. 2010;163(1):96–101. 71. Kashuk JL, Moore EE, Wohlauer M. Point of care rapid thrombelastography improves management of life threatening postinjury coagulopathy. Presented at: American Association for the Surgery of Trauma Sixty-Eight Annual Meeting; October 2009; Pittsburgh, PA. 72. Hedner U, Kisiel W. Use of human factor VIIa in the treatment of two hemophilia A patients with high-titer inhibitors. J Clin Invest. 1983; 71:1836–1841. 73. Dutton RP, McCunn M, Hyder M, et al. Factor VIIa for correction of traumatic coagulopathy. J Trauma. 2004;57:709–718 [discussion 18–19]. 74. Boffard KD, Riou B, Warren B, et al. Recombinant factor VIIa as adjunctive therapy for bleeding control in severely injured trauma patients: two parallel randomized, placebo-controlled, double-blind clinical trials. J Trauma. 2005;59:8–15 [discussion 15–18]. 75. Rizoli SB, Boffard KD, Riou B, et al. Recombinant activated factor VII as an adjunctive therapy for bleeding control in severe trauma patients with coagulopathy: subgroup analysis from two randomized trials. Crit Care. 2006;10:R178. 76. Knudson MM, Cohen MJ, Reidy R, Jaegar S, Wade C, Holcomb JB. Trauma, transfusions, and recombinant activated factor VII: a multicenter analysis of 1,041 patients. Presented at: 68th Annual Meeting of the American Association for the Surgery of Trauma; 2009; Pittsburgh, PA. 77. Thomas GO, Dutton RP, Hemlock B, et al. Thromboembolic complications associated with factor VIIa administration. J Trauma. 2007;62:564–569. 78. Levi M, Cromheecke ME, de Jonge E, et al. Pharmacological strategies to decrease excessive blood loss in cardiac surgery: a meta-analysis of clinically relevant endpoints. Lancet. 1999;354:1940–1947. 79. Auer LM, Marth E, Heppner F, Holasek A. Proteolytic enzyme activity in patients with severe head injury and the effect of a proteinase inhibitor. Acta Neurochir (Wien). 1979;49:207–217. 80. McMichan JC, Rosengarten DS, Philipp E. Prophylaxis of posttraumatic pulmonary insufficiency by protease-inhibitor therapy with aprotinin: a clinical study. Circ Shock. 1982;9:107–116. 81. Coats T, Roberts I, Shakur H. Antifibrinolytic drugs for acute traumatic injury. Cochrane Database Syst Rev. 2004:CD004896. 82. CRASH-2 Trial Collaborators, Shakur H, Roberts I, et al. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial. Lancet. 2010;376:23–32. 83. Schroeder V, Chatterjee T, Kohler HP. Influence of blood coagulation factor XIII and FXIII Val34Leu on plasma clot formation measured by thrombelastography. Thromb Res. 2001;104:467–474.

84. Godje O, Haushofer M, Lamm P, Reichart B. The effect of factor XIII on bleeding in coronary surgery. Thorac Cardiovasc Surg. 1998;46: 263–267. 85. Lorenz R, Kienast J, Otto U, et al. Successful emergency reversal of phenprocoumon anticoagulation with prothrombin complex concentrate: a prospective clinical study. Blood Coagul Fibrinolysis. 2007;18:565–570. 86. Spahn DR, Cerny V, Coats TJ, et al. Management of bleeding following major trauma: a European guideline. Crit Care. 2007;11:R17. 87. Kalina M, Tinkoff G, Gbadebo A, Veneri P, Fulda G. A protocol for the rapid normalization of INR in trauma patients with intracranial hemorrhage on prescribed warfarin therapy. Am Surg. 2008;74: 858–861. 88. Bruce D, Nokes TJ. Prothrombin complex concentrate (Beriplex P/N) in severe bleeding: experience in a large tertiary hospital. Crit Care. 2008;12:R105. 89. Dickneite G, Pragst I. Prothrombin complex concentrate vs fresh frozen plasma for reversal of dilutional coagulopathy in a porcine trauma model. Br J Anaesth. 2009;102:345–354. 90. Dickneite G, Dorr B, Kaspereit F, Tanaka KA. Prothrombin complex concentrate versus recombinant factor VIIa for reversal of hemodilutional coagulopathy in a porcine trauma model. J Trauma. 2010;68: 1151–1157. 91. Tharmarajah P, Pusey J, Keeling D, Willett K. Efficacy of warfarin reversal in orthopedic trauma surgery patients. J Orthop Trauma. 2007;21:26–30. 92. Pieracci FM, Eachempati SR, Shou J, Hydo LJ, Barie PS. Degree of anticoagulation, but not warfarin use itself, predicts adverse outcomes after traumatic brain injury in elderly trauma patients. J Trauma. 2007;63:525–530. 93. Pieracci FM, Eachempati SR, Shou J, Hydo LJ, Barie PS. Use of longterm anticoagulation is associated with traumatic intracranial hemorrhage and subsequent mortality in elderly patients hospitalized after falls: analysis of the New York State Administrative Database. J Trauma. 2007;63:519–524. 94. Karni A, Holtzman R, Bass T, et al. Traumatic head injury in the anticoagulated elderly patient: a lethal combination. Am Surg. 2001;67:1098–1100. 95. Coimbra R, Hoyt DB, Anjaria DJ, Potenza BM, Fortlage D, Hollingsworth-Fridlund P. Reversal of anticoagulation in trauma: a North-American survey on clinical practices among trauma surgeons. J Trauma. 2005;59:375–382. 96. Ivascu FA, Howells GA, Junn FS, Bair HA, Bendick PJ, Janczyk RJ. Rapid warfarin reversal in anticoagulated patients with traumatic intracranial hemorrhage reduces hemorrhage progression and mortality. J Trauma. 2005;59:1131–1137 [discussion 7–9]. 97. Deveras RA, Kessler CM. Reversal of warfarin-induced excessive anticoagulation with recombinant human factor VIIa concentrate. Ann Intern Med. 2002;137:884–888. 98. Ott MM, Eriksson E, Vanderkolk W, Christianson D, Davis A, Scholten D. Antiplatelet and anticoagulation therapies do not increase mortality in the absence of traumatic brain injury. J Trauma. 2010;68:560–563. 99. Ohm C, Mina A, Howells G, Bair H, Bendick P. Effects of antiplatelet agents on outcomes for elderly patients with traumatic intracranial hemorrhage. J Trauma. 2005;58:518–522. 100. Ivascu FA, Howells GA, Junn FS, Bair HA, Bendick PJ, Janczyk RJ. Predictors of mortality in trauma patients with intracranial hemorrhage on preinjury aspirin or clopidogrel. J Trauma. 2008;65:785–788. 101. Wong DK, Lurie F, Wong LL. The effects of clopidogrel on elderly traumatic brain injured patients. J Trauma. 2008;65:1303–1308. 102. Downey DM, Monson B, Butler KL, et al. Does platelet administration affect mortality in elderly head-injured patients taking antiplatelet medications? Am Surg. 2009;75:1100–1103. 103. Opelz G, Terasaki PI. Improvement of kidney-graft survival with increased numbers of blood transfusions. N Engl J Med. 1978;299:799–803. 104. Gantt CL. Red blood cells for cancer patients. Lancet. 1981;2:363. 105. Malone DL, Dunne J, Tracy JK, Putnam AT, Scalea TM, Napolitano LM. Blood transfusion, independent of shock severity, is associated with worse outcome in trauma. J Trauma. 2003;54:898–905 [discussion 905–907]. 106. Napolitano LM, Corwin HL. Efficacy of red blood cell transfusion in the critically ill. Crit Care Clin. 2004;20:255–268. 107. Simchon S, Jan KM, Chien S. Influence of reduced red cell deformability on regional blood flow. Am J Physiol. 1987;253:H898–H903. 108. Zallen G, Offner PJ, Moore EE, et al. Age of transfused blood is an independent risk factor for postinjury multiple organ failure. Am J Surg. 1999;178:570–572.

Postinjury Hemotherapy and Hemostasis 115. Schreiber MA, Differding J, Thorborg P, Mayberry JC, Mullins RJ. Hypercoagulability is most prevalent early after injury and in female patients. J Trauma. 2005;58:475–480 [discussion 80–81]. 116. Attia J, Ray JG, Cook DJ, Douketis J, Ginsberg JS, Geerts WH. Deep vein thrombosis and its prevention in critically ill adults. Arch Intern Med. 2001;161:1268–1279. 117. O’Malley KF, Ross SE. Pulmonary embolism in major trauma patients. J Trauma. 1990;30:748–750. 118. Rogers FB, Cipolle MD, Velmahos G, Rozycki G, Luchette FA. Practice management guidelines for the prevention of venous thromboembolism in trauma patients: the EAST Practice Management Guidelines Work Group. J Trauma. 2002;53:142–164. 119. Kim Y, Nakase H, Nagata K, Sakaki T, Maeda M, Yamamoto K. Observation of arterial and venous thrombus formation by scanning and transmission electron microscopy. Acta Neurochir (Wien). 2004;146:45–51 [discussion 51]. 120. Patel R, Cook DJ, Meade MO, et al. Burden of illness in venous thromboembolism in critical care: a multicenter observational study. J Crit Care. 2005;20:341–347.

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109. Shapiro MJ, Gettinger A, Corwin HL, et al. Anemia and blood transfusion in trauma patients admitted to the intensive care unit. J Trauma. 2003;55:269–273 [discussion 73–74]. 110. Silverboard H, Aisiku I, Martin GS, Adams M, Rozycki G, Moss M. The role of acute blood transfusion in the development of acute respiratory distress syndrome in patients with severe trauma. J Trauma. 2005;59:717–723. 111. Croce MA, Tolley EA, Claridge JA, Fabian TC. Transfusions result in pulmonary morbidity and death after a moderate degree of injury. J Trauma. 2005;59:19–23 [discussion 23–24]. 112. Khan H, Belsher J, Yilmaz M, et al. Fresh-frozen plasma and platelet transfusions are associated with development of acute lung injury in critically ill medical patients. Chest. 2007;131:1308–1314. 113. Watson GA, Sperry JL, Rosengart MR, et al. Fresh frozen plasma is independently associated with a higher risk of multiple organ failure and acute respiratory distress syndrome. J Trauma. 2009;67:221–227 [discussion 8–30]. 114. Inaba K, Branco BC, Rhee P, et al. Impact of plasma transfusion in trauma patients who do not require massive transfusion. J Am Coll Surg. 2010;210:957–965.

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Emergency Department Thoracotomy Clay Cothren Burlew and Ernest E. Moore

The number of patients arriving at hospitals in extremis, rather than expiring in the prehospital setting, has increased due to the maturation of regionalized trauma systems (see Chapter 4). Salvage of individuals with imminent cardiac arrest or those already undergoing cardiopulmonary resuscitation (CPR) often requires immediate thoracotomy as an integral component of their initial resuscitation in the emergency department (ED). The optimal application of emergency department thoracotomy (EDT) requires a thorough understanding of its physiologic objectives, technical maneuvers, and the cardiovascular and metabolic consequences. This chapter reviews these features and highlights the specific clinical indications, all of which are essential for the appropriate use of this potentially life-saving yet costly procedure.

HISTORICAL PERSPECTIVE Emergent thoracotomy came into use for the treatment of heart wounds and anesthesia-induced cardiac arrest in the late 1800s and early 1900s.1 The concept of a thoracotomy as a resuscitative measure began with Schiff ’s promulgation of open cardiac massage in 1874.1 Block first suggested the potential application of this technique for penetrating chest wounds and heart lacerations in 1882.2 Following use of the technique in animal models, the first successful suture repair of a cardiac wound in a human was performed at the turn of the century.3 Subsequently, Igelsbrud described the successful resuscitation of a patient sustaining cardiac arrest during a surgical procedure using emergent thoracotomy with open cardiac massage.1 The utility of the emergent thoracotomy was beginning to be tested in a wide range of clinical scenarios in the early 1900s. With improvement in patient resuscitation and an ongoing evaluation of patient outcomes, the indications for emergent thoracotomy shifted. Initially, cardiovascular collapse from medical causes was the most common reason for thoracotomy in the early 1900s. The demonstrated efficacy of closed-chest

compression by Kouwenhoven et al.4 in 1960 and the introduction of external defibrillation in 1965 by Zoll et al.5 virtually eliminated the practice of open-chest resuscitation for medical cardiac arrest. Indications for emergent thoracotomy following trauma also became more limited. In 1943, Blalock and Ravitch advocated the use of pericardiocentesis rather than thoracotomy as the preferred treatment for postinjury cardiac tamponade.6 In the late 1960s, however, refinements in cardiothoracic surgical techniques reestablished the role of immediate thoracotomy for salvaging patients with life-threatening chest wounds.7 The use of temporary thoracic aortic occlusion in patients with exsanguinating abdominal hemorrhage further expanded the indications for emergent thoracotomy.8,9 In the past decade, critical analyses of patient outcomes following postinjury EDT has tempered the unbridled enthusiasm for this technique, allowing a more selective approach with clearly defined indications.10,11

DEFINITIONS The literature addressing EDT appears confusing, likely due to widely varying terminology. As a result, there is a lack of agreement among physicians regarding the specific indications for EDT as well as the definition of “signs of life.”12 In this chapter, EDT refers to a thoracotomy performed in the ED for patients arriving in extremis. At times, the term EDT is used interchangeably with the term resuscitative thoracotomy; however, this should not be confused with a thoracotomy that is performed in the operating room (OR) or intensive care unit (ICU) within hours after injury for delayed physiologic deterioration. The value of an indication for EDT for acute resuscitation may also be confusing because of the variety of indices used to characterize the patient’s physiologic status prior to thoracotomy. Because there have been a wide range of indications for which EDT has been performed in different trauma centers, comparisons in the literature are difficult. The authors

Emergency Department Thoracotomy

PHYSIOLOGIC RATIONALE FOR EDT The primary objectives of EDT are to (a) release pericardial tamponade, (b) control cardiac hemorrhage, (c) control intrathoracic bleeding, (d) evacuate massive air embolism, (e) perform open cardiac massage, and (f ) temporarily occlude the descending thoracic aorta. Combined, these objectives attempt to address the primary issue of cardiovascular collapse from mechanical sources or extreme hypovolemia.

■ Release Pericardial Tamponade and Control Cardiac Hemorrhage The highest survival rate following EDT is in patients with penetrating cardiac wounds, especially when associated with pericardial tamponade.7 Early recognition of cardiac tamponade, prompt pericardial decompression, and control of cardiac hemorrhage are the key components to successful EDT and patient survival following penetrating wounds to the heart (see Chapter 26).13 The egress of blood from the injured heart, regardless of mechanism, results in tamponade physiology. Rising intrapericardial pressure produces abnormalities in hemodynamic and cardiac perfusion that can be divided into three phases.14 Initially, increased pericardial pressure restricts ventricular diastolic filling and reduces subendocardial blood flow.15 Cardiac output under these conditions is maintained by compensatory tachycardia, increased systemic vascular resistance, and elevated central pressure (i.e., ventricular filling pressure). In the intermediate phase of tamponade, rising pericardial pressure further compromises diastolic filling, stroke volume, and coronary perfusion, resulting in diminished cardiac output. Although blood pressure may be maintained deceptively well, subtle signs of shock (e.g., anxiety, diaphoresis, and pallor) become evident. During the final phase of tamponade, compensatory mechanisms fail as the intrapericardial pressure approaches the ventricular filling pressure. Cardiac arrest ensues as profound coronary hypoperfusion occurs. The classic description of clinical findings, Beck’s triad, is rarely observed in the ED; therefore, a high index of suspicion in the at-risk patient sustaining penetrating torso trauma is crucial, with prompt intervention essential. In the first two phases of cardiac tamponade, patients may be aggressively managed with definitive airway control, volume resuscitation to increase preload, and pericardiocentesis. The patient in the third phase of tamponade, with profound hypotension (systolic blood pressure [SBP]  60 mm Hg), should undergo EDT rather than pericardiocentesis as the management for evacuation of pericardial blood.16,17 Following release of tamponade, the source of tamponade can be directly controlled with appropriate interventions based on the underlying injury (see Technical Details of EDT).

■ Control Intrathoracic Hemorrhage Life-threatening intrathoracic hemorrhage occurs in less than 5% of patients following penetrating injury presenting to the ED, and in even lower percentage of patients sustaining blunt trauma.18 The most common injuries include penetrating wounds to the pulmonary hilum and great vessels; less commonly seen are torn descending thoracic aortic injuries with frank rupture or penetrating cardiac wounds exsanguinating into the thorax through a traumatic pericardial window. There is a high mortality rate in injuries to the pulmonary or thoracic great-vessel lacerations due to the lack of hemorrhage containment by adjacent tissue tamponade or vessel spasm (see Chapters 25 and 26). Either hemithorax can rapidly accommodate more than half of a patient’s total blood volume before overt physical signs of hemorrhagic shock occur. Therefore, a high clinical suspicion is warranted in patients with penetrating torso trauma, particularly in those with hemodynamic decompensation. Patients with exsanguinating wounds require EDT with rapid control of the source of hemorrhage if they are to be salvaged.

■ Perform Open Cardiac Massage External chest compression provides approximately 20–25% of baseline cardiac output, with 10–20% of normal cerebral perfusion.19,20 This degree of vital organ perfusion can provide reasonable salvage rates for 15 minutes, but few normothermic patients survive 30 minutes of closed-chest compression. Moreover, in models of inadequate intravascular volume (hypovolemic shock) or restricted ventricular filling (pericardial tamponade), external chest compression fails to augment arterial pressure or provide adequate systemic perfusion; the associated low diastolic volume and pressure result in inadequate coronary perfusion.21 Therefore, closed cardiac massage is ineffective for postinjury cardiopulmonary arrest. The only potential to salvage the injured patient with ineffective circulatory status is immediate EDT.

■ Achieve Thoracic Aortic Cross-Clamping The rationale for temporary thoracic aortic occlusion in the patient with massive hemorrhage is 2-fold. First, in patients with hemorrhagic shock, aortic cross-clamping redistributes the patient’s limited blood volume to the myocardium and brain.9 Second, patients sustaining intra-abdominal injury may benefit from aortic cross-clamping due to reduction in subdiaphragmatic blood loss.8 Temporary thoracic aortic occlusion augments aortic diastolic and carotid SBP, enhancing coronary as well as cerebral perfusion.22,23 Canine studies have shown that the left ventricular stroke-work index and myocardial contractility increase in response to thoracic aortic occlusion during hypovolemic shock.24 These improvements in myocardial function occur without an increase in the pulmonary capillary wedge pressure or a significant change in systemic vascular resistance. Thus, improved coronary perfusion resulting from an increased aortic diastolic pressure presumably accounts for the observed enhancement in contractility.25

CHAPTER 14

define “no signs of life” as no detectable blood pressure, respiratory or motor effort, cardiac electrical activity, or pupillary activity (i.e., clinical death). Patients with “no vital signs” have no palpable blood pressure, but demonstrate electrical activity, respiratory effort, or pupillary reactivity.

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These experimental observations suggest that temporary aortic occlusion is valuable in patients with either shock due to nonthoracic trauma or continued shock following the repair of cardiac or other exsanguinating wounds. Indeed, occlusion of the descending thoracic aorta appears to increase the return of spontaneous circulation following CPR.26,27 Reports of successful resuscitation using EDT in patients in hemorrhagic shock and even sustaining cardiac arrest following extremity and cervical injuries exist.28 In these situations, EDT may be a temporizing measure until the patient’s circulating blood volume can be replaced by blood product transfusion. However, once the patient’s blood volume has been restored, the aortic cross-clamp should be removed. Thoracic cross-clamping in the normovolemic patient may be deleterious because of increased myocardial oxygen demands resulting from the increased systemic vascular resistance.29 Careful application of this technique is warranted as there is substantial metabolic cost and a finite risk of paraplegia associated with the procedure.30–32 However, in carefully selected patients, aortic cross-clamping may effectively redistribute the patient’s blood volume until external replacement and control of the hemorrhagic source is possible. Typically, complete removal of the aortic cross-clamp or replacement of the clamp below the renal vessel should be performed within 30 minutes; the gut’s tolerance to normothermic ischemia is 30–45 minutes.

■ Evacuate Bronchovenous Air Embolism Bronchovenous air embolism can be a subtle entity following thoracic trauma, and is likely to be much more common than is recognized.33–35 The clinical scenario typically involves a patient sustaining penetrating chest injury who precipitously develops profound hypotension or cardiac arrest following endotracheal intubation and positive-pressure ventilation. Traumatic alveolovenous communications produce air emboli that migrate to the coronary arterial systems; any impedance in coronary blood flow causes global myocardial ischemia and resultant shock. The production of air emboli is enhanced by the underlying physiology—there is relatively low intrinsic pulmonary venous pressure due to associated intrathoracic blood loss and high bronchoalveolar pressure from assisted positive-pressure ventilation. This combination increases the gradient for air transfer across bronchovenous channels.36 Although more often observed in penetrating trauma, a similar process may occur in patients with blunt lacerations of the lung parenchyma (see Chapter 25). Immediate thoracotomy with pulmonary hilar crossclamping prevents further propagation of pulmonary venous air embolism. Thoracotomy with opening of the pericardium also provides access to the cardiac ventricles; with the patient in the Trendelenburg’s position (done to trap to air in the apex of the ventricle), needle aspiration is performed to remove air from the cardiac chambers. Additionally, vigorous cardiac massage may promote dissolution of air already present in the coronary arteries.35 Aspiration of the aortic root is done to alleviate any accumulated air pocket, and direct needle aspiration of the right coronary artery may be attempted.

CLINICAL RESULTS FOLLOWING EDT The value of EDT in resuscitation of the patient in profound shock but not yet dead is unquestionable. Its indiscriminate use, however, renders it a low-yield and high-cost procedure.37–39 In the past three decades there has been a significant clinical shift in the performance of EDT, from a nearly obligatory procedure before declaring any trauma patient to very few patients undergoing EDT. During this swing of the pendulum, several groups have attempted to elucidate the clinical guidelines for EDT. In 1979, we conducted a critical analysis of 146 consecutive patients undergoing EDT and suggested a selected approach to its use in the moribund trauma patient, based on consideration of the following variables: (1) location and mechanism of injury, (2) signs of life at the scene and on admission to the ED, (3) cardiac electrical activity at thoracotomy, and (4) SBP response to thoracic aortic cross-clamping.39 To validate these clinical guidelines, we established a prospective study in which these data were carefully documented in all patients at the time of thoracotomy. In 1982, the first 400 patients were analyzed.38 A more recent review has summarized the data on 868 patients who have undergone EDT at the Denver Health Medical Center.40 Of these, 676 (78%) were dead in the ED, 128 (15%) died in the OR, and 23 (3%) succumbed to multiple organ failure in the surgical ICU. Ultimately, 41 (5%) patients survived, and 34 recovered fully without neurologic sequelae. Although this yield may seem low, it is important to emphasize that thoracotomy was done on virtually every trauma patient delivered to the ED. In fact, 624 (72%) were without vital signs in the field, and 708 patients (82%) had no vital signs at the time of presentation to the ED. In contrast, it is equally important to stress that patients without signs of life at the scene but who responded favorably to resuscitation were excluded from this analysis because they did not require EDT; these patients remind the practitioner that prehospital clinical assessments may not always be reliable in triaging these severely injured patients.43 Indeed, the authors have salvaged a number of individuals sustaining blunt and penetrating trauma who were assessed to have no signs of life at the scene of injury. The survival rate and percentage of neurologic impairment following EDT varies considerably, due to the heterogeneity of patient populations reported in the literature. As previously discussed, critical determinants of survival include the mechanism and location of injury and the patient’s physiologic condition at the time of thoracotomy.42,43 We have attempted to elucidate the impact of these factors in ascertaining the success rate of EDT by collating data from a number of clinical series reporting on 50 or more patients (Table 14-1). Unfortunately, inconsistencies in patient stratification and a paucity of clinical details limit objective analysis of these data. Although some reviews provide a specific breakdown of the injury mechanism and clinical status of patients presenting to the ED, others combine all injury mechanisms. We believe it is crucial to stratify patients according to the location and mechanism of injury as well as the status of signs of life (i.e., blood pressure, respiratory effort, cardiac electrical activity, and pupillary activity).

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TABLE 14-1 Outcome Following Emergency Department Thoracotomy in Adults

Penetrating Denver40 Detroit81 Houston86 Indianapolis87 Johannesburg82 Los Angeles83 New York88 Oakland89 San Francisco43 Seattle85 Washington90 Overall Blunt Denver40 Houston86 Johannesburg83 San Francisco43 Seattle91 Overall

Shock

No Vital Signs

No Signs of Life

Total

3/9 (33%) 9/42 (21%)

0/7 (0%) 3/110 (3%)

1/53 (2%)

2/5 (40%) 7/20 (35%) 18/37 (49%) 4/11 (36%) 43/124 (35%)

6/11 (55%) 18/53 (32%) 0/25 (0%) 11/47 (23%) 47/254 (19%)

2/55 (4%) 0/18 (0%)

4/69 (6%) 12/152 (8%) 13/108 (12%) 10/71 (14%) 24/91 (26%) 18/63 (29%) 15/58 (26%) 96/612 (16%)

19/78 (24%) 9/42 (21%) 14/156 (9%) 3/7 (43%) 31/413 (8%) 2/5 (40%) 8/32 (25%) 8/24 (33%)

14/399 (4%) 3/110 (3%) 18/162 (11%) 1/50 (2%) 10/149 (7%) 6/11 (55%) 8/77 (10%)

4/11 (36%) 7/13 (54%) 145/1007 (14%)

11/47 (23%) 3/47 (6%) 100/1252 (8%)

4/86 (5%) 0/42 (0%) 1/109 (1%)

4/311 (1%) 0/27 (0%) 0/39 (0%)

0/28 (0%)

5/237 (2%)

4/377 (1%)

0/28 (0%)

The data summarized to date confirm that EDT has the highest survival rate following isolated cardiac injury (Table 14-1). An average of 35% of adult patients presenting in shock, defined as an SBP 70 mm Hg, and 20% without vital signs were salvaged after isolated penetrating injury to the heart if EDT was performed. In contrast, only 1–3% of blunt trauma patients undergoing EDT survive, regardless of clinical status on presentation. Following penetrating torso injuries, 14% of patients requiring EDT are salvaged if they are hypotensive with detectable vital signs, whereas 8% of those who have no vital signs but have signs of life at presentation, and 1% of those without signs of life are salvaged. These findings are reiterated by a recent report incorporating all patients undergoing EDT for either blunt or penetrating mechanism from 24 separate studies42; survival rates for patients undergoing EDT for penetrating injuries was 8.8% and 1.4% for blunt mechanisms. Additionally, more patients survive EDT for isolated cardiac wounds (19.4%) followed by stab wounds (16.8%) and gunshot wounds (4.3%). Although there is a clear role for EDT in the patient presenting in shock but with measurable vital signs, there is

4/126 (3%)

0/80 (0%) 1/108 (1%) 2/55 (4%) 0/25 (0%) 2/228 (1%)

6/615 (1%)

33/477 (7%) 12/152 (8%) 32/318 (10%) 4/137 (3%) 42/670 (6%) 10/71 (14%) 16/134 (12%) 10/252 (4%) 32/198 (30%) 15/58 (25%) 10/60 (17%) 283/2986 (10%) 8/397 (2%) 0/69 (0%) 1/176 (1%) 1/60 (2%) 1/88 (1%) 11/790 (1.4%)

disagreement about its use in the patient population undergoing CPR prior to arrival in the ED. Although there have been multiple reports with low survival rates and dismal outcomes following prehospital CPR, termination of resuscitation in the field should not be performed in all patients.44 Our most recent evaluation, spanning 26 years of experience, indicates EDT does play a significant role in the critically injured patient undergoing prehospital CPR.10 The majority of patients arriving in extremis who survived to discharge sustained a stab wound to the torso, consistent with previous reports. Additionally, over 80% of patients were neurologically intact at discharge. In this study, clear guidelines for the use of EDT as a resuscitative measure to ensure that all potentially salvageable patients were proposed. EDT should be performed for blunt trauma and penetrating non-torso trauma with CPR less than 5 minutes, and in penetrating torso trauma if less than 15 minutes of CPR.10 To further define the limits of EDT, a prospective, multicenter trial was performed by the Western Trauma Association (WTA).45 The WTA data substantiate that injury mechanism alone is not a discriminator of futility. Specifically, with the

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Injury Pattern Cardiac Denver80 Detroit81 Johannesburg82 Los Angeles83 New York84 San Francisco43 Seattle85 Overall

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TABLE 14-2 Current Indications and Contraindications for Emergency Department Thoracotomy

SECTION 2

INDICATIONS: Salvageable postinjury cardiac arrest: Patients sustaining witnessed penetrating thoracic trauma with 15 min of prehospital CPR Patients sustaining witnessed penetrating nonthoracic trauma with 5 min of prehospital CPR. Patients sustaining witnessed blunt trauma with 10 min of prehospital CPR Persistent severe postinjury hypotension (SBP  60 mm Hg) due to: Cardiac tamponade Hemorrhage-intrathoracic, intra-abdominal, extremity, cervical Air embolism CONTRAINDICATIONS: CPR 15 min following penetrating injury and no signs of life (pupillary response, respiratory effort, or motor activity) CPR 10 min following blunt injury and no signs of life Asystole is the presenting rhythm and there is not pericardial tamponade CPR  cardiopulmonary resuscitation; SBP  systolic blood pressure.

exception of an overtly devastating head injury, blunt trauma does not prohibit meaningful survival, even with requirements for CPR. This multicenter experience suggests current indications for EDT (Table 14-2). Specifically, EDT is unlikely to yield productive survival when patients: (1) sustain blunt trauma and require 10 minutes of prehospital CPR, (2) have penetrating wounds and undergo 15 minutes of prehospital CPR, or (3) manifest asystole without pericardial tamponade. We recognize, however, that there will invariably be exceptions to the recorded literature.28,41,46,47 Emerging data indicate the clinical results in the pediatric population mirror that of the adult experience (Table 14-3). One might expect that children would have a more favorable outcome compared to adults, due to improved results following head injury (see Chapter 43); however, this has not been borne out in multiple studies.48–52 Beaver et al. reported no survivors among 27 patients, from 15 months to 14 years of age, undergoing postinjury EDT at Johns Hopkins Hospital.49 Powell et al., at the South Alabama Medical Center, described an overall survival of 20% (3 of 15 patients) in patients ranging from 4 to 18 years.52 In a study at Denver Health Medical Center, encompassing an 11-year experience with 689 consecutive EDT, we identified 83 patients (12%) who were under 18 years old.50 Survival by injury mechanism was 9% (1 of 11) for stab wounds, 4% (1 of 25) for gunshot wounds, and 2% (1 of 47 patients) for blunt trauma. Among 69 patients presenting to the ED without vital signs, only 1

patient (1%) survived (with a stab wound). This contrasted to a salvage of 2 (14%) among 14 patients with vital signs. The outcome in blunt trauma, the predominant mechanism of lethal injury in children, was disappointing, with only 2% salvage, and no survivors when vital signs were absent. Thus, as in adults, outcome following EDT in the pediatric population is largely determined by injury mechanism and physiologic status on presentation to the ED. In sum, overall analysis of the available literature indicates that the success of EDT approximates 35% in the patient arriving in shock with a penetrating cardiac wound, and 15% for all penetrating wounds. Patients undergoing CPR upon arrival to the ED should be stratified based upon injury and transport time to determine the utility of EDT. Conversely, patient outcome is relatively poor when EDT is done for blunt trauma; 2% survival in patients in shock and less than 1% survival with no vital signs.

INDICATIONS FOR EDT Based on our 26 successive years of EDT prospective analysis10 and the recent WTA multicenter trial,45 we propose current indications for EDT (Table 14-2). Clearly, the specific application of these guidelines must include consideration of the patient’s age, preexisting disease, signs of life, and mechanism of injury, as well as logistic issues such as the proximity of the ED to the OR, and qualified personnel. Our current decision algorithm for resuscitation of the moribund trauma patient and use of EDT was formulated and implemented as a key clinical pathway in the ED (Fig. 14-1). At the scene, patients in extremis without electrical cardiac activity are declared dead. Patients in extremis but with electrical cardiac activity are intubated, supported with cardiac compression, and rapidly transported to the ED. On arrival to the ED, the time from initiation of CPR is recorded; blunt trauma patients with greater than 10 minutes of prehospital CPR and no signs of life are declared, whereas penetrating trauma patients with greater than 15 minutes of prehospital CPR and no signs of life are pronounced. Patients within the time guidelines or those with signs of life trigger ongoing resuscitation and EDT. After performing a generous left anterior thoracotomy and subsequent pericardotomy, the patient’s intrinsic cardiac activity is evaluated. Patients in asystole without associated cardiac tamponade are declared. Patient’s with a cardiac wound, tamponade, and associated asystole are aggressively treated; the cardiac wound is repaired first followed by manual cardiac compressions and intracardiac injection of epinephrine. Following several minutes of such treatment and volume resuscitation, one should reassess salvageability, typically defined as the patient’s ability to generate a SBP 70 mm Hg. Patient’s with an intrinsic rhythm following EDT should be treated according to underlying pathology. Those with tamponade should undergo cardiac repair, either in the trauma bay or in the OR (see Chapter 26). Control of intrathoracic hemorrhage may entail hilar cross-clamping, digital occlusion of the direct injury, or even packing of the apices for subclavian injuries. Treatment of bronchovenous

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TABLE 14-3 Outcome Following Emergency Department Thoracotomy in Children

Blunt Baltimore49 Denver50 Mobile52 Sacramento51 Overall

Shock

No Vital Signs

1/3 0/1 1/4 2/8

0/2 (0%) 1/5 (20%) 3/9 (33%) 0/4 (0%) 4/20 (20%)

(33%) (0%) (25%) (25%)

1/11 (9%) 0/6 (0%) 1/17 (6%)

0/15 (0%) 0/6 (0%) 0/5 (0%) 0/9 (0%) 0/35 (0%)

air embolism includes cross-clamping of the hilum, putting the patient in Trendelenberg’s position, aspirating the left ventricle and aortic root, and massaging the coronaries. Finally, aortic cross-clamping is performed to decrease the required effective circulating volume, for either thoracic or abdominal sources of hemorrhage, and facilitate resuscitation. In all of these scenarios, reassessment of the patient following intervention and aggressive resuscitation efforts is performed, with the goal systolic pressure of 70 mm Hg used to define salvageability.

No Signs of Life

0/28 (0%)

0/28 (0%)

0/30 (0%)

0/30 (0%)

Total 0/2 (0%) 2/36 (6%) 3/10 (30%) 1/8 (13%) 6/56 (11%) 0/15 (0%) 1/47 (2%) 0/5 (0%) 0/15 (0%) 1/82 (1%)

TECHNICAL DETAILS OF EDT The optimal benefit of EDT is achieved by a surgeon experienced in the management of intrathoracic injuries. The emergency physician, however, should not hesitate to perform the procedure in the moribund patient with a penetrating chest wound when thoracotomy is the only means of salvage. The technical skills needed to perform the procedure include the ability to perform a rapid thoracotomy, pericardiotomy, cardiorrhaphy, and thoracic aortic cross-clamping; familiarity

FIGURE 14-1 Algorithm directing the use of EDT in the multiply injured trauma patient.

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Injury Pattern Penetrating Baltimore49 Denver50 Mobile52 Sacramento51 Overall

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SECTION 2

with vascular repair techniques and control of the pulmonary hilum are advantageous. Once life-threatening intrathoracic injuries are controlled or temporized, the major challenge is restoring the patient’s hemodynamic integrity and minimizing vital organ reperfusion injury.

■ Thoracic Incision A left anterolateral thoracotomy incision is preferred for EDT. Advantages of this incision in the critically injured patient include (a) rapid access with simple instruments, (b) the ability to perform this procedure on a patient in the supine position, and (c) easy extension into the right hemithorax, a clamshell thoracotomy, for exposure of both pleural spaces and anterior and posterior mediastinal structures. The key resuscitative maneuvers of EDT, namely, pericardiotomy, open cardiac massage, and thoracic aortic cross-clamping are readily accomplished via this approach. The initial execution of a clamshell thoracotomy should be done in hypotensive patients with penetrating wounds to the right chest. This provides immediate, direct access to a right-sided pulmonary or vascular injury while still allowing access to the pericardium from the left side for open cardiac massage. Clamshell thoracotomy may also be considered in patients with presumed air embolism, providing access to the cardiac chambers for aspiration, coronary vessels for massage, and bilateral lungs for obliteration of the source. Preparation for EDT should be performed well ahead of the patient’s arrival. Set-up should include a 10-blade scalpel, Finochietto’s chest retractor, toothed forceps, curved Mayo’s scissors, Satin-sky’s vascular clamps (large and small), long needle holder, Lebsche’s knife and mallet, and internal defibrillator paddles. Sterile suction, skin stapler, and access to a variety of sutures should be available (specifically 2-0 prolene on a CT-1 needle, 2-0 silk ties, and teflon pledgets). Upon patient arrival and determination of the need for EDT, the patient’s left arm should be placed above the head to provide unimpeded access to the left chest. The anterolateral thoracotomy is initiated with an incision at the level of the fifth intercostal space (Fig. 14-2). Clinically, this level for incision corresponds to the inferior border of the pectoralis major muscle, just below the patient’s nipple. In women, the breast should be retracted superiorly to gain access to this interspace, and the incision is made at the inframammary fold. The incision should start on the right side of the sternum; if sternal transection is required, this saves the time-consuming step of performing an additional skin incision. As the initial incision is carried transversely across the chest, and one passes beneath the nipple, a gentle curve in the incision toward the patient’s axilla rather than direct extension to the bed should be performed; this curvature in the skin correlates with the natural curvature of the rib cage. The skin, subcutaneous fat, and chest wall musculature are incised with a knife to expose the ribs and associated intercostal space. Intercostal muscles and the parietal pleura are then divided in one layer either with curved Mayo scissors or sharply with the scalpel; the intercostal muscle should be divided along the superior margin of the rib to avoid the intercostal neurovascular

A

B FIGURE 14-2 (A) and (B) The thoracotomy incision is performed through the fourth or fifth intercostal space; the incision should start to the right of the sternum, and begin curving into the axilla at the level of the left nipple. The Finochietto’s rib retractor is placed with the handle directed inferiorly toward the bed.

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A B FIGURE 14-3 (A) and (B) Transverse division of the sternum requires individual ligation of the internal mammary arteries.

bundle. Chest wall bleeding is minimal in these patients and should not be a concern at this point in the resuscitation. Once the incision is completed and the chest entered, a standard Finochietto’s rib retractor is inserted, with the handle directed inferiorly toward the axilla (Fig. 14-2). Placement of the handle toward the bed rather than the sternum allows extension of the left thoracotomy into a clamshell thoracotomy with crossing of the sternum without replacing the rib retractor. If the left anterolateral thoracotomy does not provide adequate exposure, several techniques may be employed. The sternum can be transected for additional exposure with a Lebsche’s knife; care must be taken to hold the Lebsche’s knife firmly against the underside of the sternum when using the mallet to forcefully transect the sternum, or the tip of the

A

instrument may deviate and result in an iatrogenic cardiac injury. If the sternum is divided transversely, the internal mammary vessels must be ligated when perfusion is restored; this may be performed using either a figure of eight suture with 2-0 silk or by clamping the vessel with a tonsil and individually ligating it with a 2-0 silk tie (Fig. 14-3). A concomitant right anterolateral thoracotomy produces a “clamshell” or “butterfly” incision, and achieves wide exposure to both pleural cavities and anterior and posterior mediastinal structures (Fig. 14-4). Once the right pleural space is opened, the rib retractor should be moved to more of a midline position to enhance separation of the chest wall for maximal exposure. When visualization of penetrating wounds in the aortic arch or major branches is needed, the superior sternum is additionally split in the midline.

B

FIGURE 14-4 (A) and (B) A bilateral anterolateral (“clamshell”) thoracotomy provides access to both thoracic cavities including the pulmonary hila, heart, and proximal great vessels.

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SECTION 2 A

B

FIGURE 14-5 (A) and (B) Pericardiotomy is done with toothed pickups and curved Mayo scissors; the incision begins at the cardiac apex, anterior to the phrenic nerve, and extends on the anterior surface of the heart toward the great vessels.

■ Pericardiotomy and Cardiac Hemorrhage Control The pericardium is incised widely, starting at the cardiac apex and extending toward the sternal notch, anterior and parallel to the phrenic nerve (Fig. 14-5). If the pericardium is not tense with blood it may be picked up at the apex with toothed forceps and sharply opened with scissors. If tense pericardial tamponade exists, a knife or the sharp point of a scissors is often required to initiate the pericardiotomy incision. Blood and blood clots should be completely evacuated from the pericardium. The heart should be delivered from the pericardium by placing the right hand through the pericardial incision, encircling the left side of the heart and pulling it into the left chest. This effectively places the left side of the pericardium behind the heart allowing access to the cardiac chambers for repair of cardiac wounds and access for effective open cardiac massage. Prompt hemorrhage control is paramount for a cardiac injury. In the beating heart, cardiac bleeding sites should be controlled immediately with digital pressure on the surface of the ventricle and partially occluding vascular clamps on the atrium or great vessels. Efforts at definitive cardiorrhaphy may be delayed until initial resuscitative measures have been completed. In the nonbeating heart, cardiac repair is done prior to defibrillation and cardiac massage. Cardiac wounds in the thin walled right ventricle are best repaired with 3-0 nonabsorbable running or horizontal mattress sutures. Buttressing the suture repair with Teflon pledgets is ideal for the thinner right ventricle, but not essential. When suturing a ventricular laceration, care must be taken not to incorporate a coronary vessel into the repair. In these instances, vertical mattress sutures

should be used to exclude the coronary and prevent cardiac ischemia. In the more muscular left ventricle, control of bleeding can occasionally be achieved with a skin-stapling device if the wound is a linear stabwound whose edges coapt in diastole. Low-pressure venous, atrial, and atrial appendage lacerations can be repaired with simple running or pursestring sutures. Posterior cardiac wounds may be particularly treacherous when they require elevation of the heart for their exposure; closure of these wounds is best accomplished in the OR with optimal lighting and equipment. For a destructive wound of the ventricle, or for inaccessible posterior wounds, temporary inflow occlusion of the superior and inferior vena cava may be employed to facilitate repair (see Chapter 26). BioGlue may be used as a hemostatic agent in such cases. Use of a Foley catheter for temporary occlusion of cardiac injuries has been suggested; in our experience this may inadvertently extend the injury due to traction forces.

■ Advanced Cardiac Life Support Interventions Including Cardiac Massage The restoration of organ and tissue perfusion may be facilitated by a number of interventions.53 First, a perfusing cardiac rhythm must be established. Early defibrillation for ventricular fibrillation or pulseless ventricular tachycardia has proven benefit, and evidence supports the use of amiodarone (with lidocaine as an alternative) following epinephrine in patients refractory to defibrillation. Magnesium may be beneficial for torsades de pointes; other dysrhythmias should be treated according to current guidelines.53 Internal defibrillation may also be required, with similar indications as closed-chest CPR.

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A

B

FIGURE 14-6 (A) and (B) Internal paddles for defibrillation are positioned on the anterior and posterior aspects of the heart.

Familiarity with the internal cardiac paddles and appropriate charging dosages in joules is required (Fig. 14-6). In the event of cardiac arrest, bimanual internal massage of the heart should be instituted promptly (Fig. 14-7). We prefer to do this with a hinged clapping motion of the hands, with the wrists apposed, sequentially closing from palms to fingers. The ventricular compression should proceed from the cardiac apex to the base of the heart. The two-handed technique is strongly recommended, as the one-handed massage technique poses the risk of myocardial perforation with the thumb. Pharmocologic adjuncts to increase coronary and cerebral perfusion pressure may be needed. The first agent in resuscitation at this juncture is intracardiac epinephrine. Epinephrine should be administered using a specialized syringe, which resembles a spinal needle, directly into the left ventricle. Typically, the heart is lifted up slightly to expose the more posterior left ventricle, and care is taken to avoid the circumflex coronary during injection. Although epinephrine continues to be advocated during resuscitation, there is a growing body of data suggesting that vasopressin may be superior to epinephrine in augmenting cerebral perfusion and other vital organ blood flow.54 Administration of calcium, while theoretically deleterious during reperfusion injury, increases cardiac contractility, and may be helpful in the setting of hypocalcemia produced by massive transfusion. Although metabolic acidosis is common following EDT and resuscitation, the mainstay of therapy is

provision of adequate alveolar ventilation and restoration of tissue perfusion. Sodium bicarbonate therapy has not been proven beneficial in facilitating defibrillation, restoring spontaneous circulation, or improving survival. It may be warranted following protracted arrest or resuscitation, because catecholamine receptors may be sensitized.

■ Thoracic Aortic Occlusion and Pulmonary Hilar Control Following thoracotomy and pericardiotomy with evaluation of the heart, the descending thoracic aorta should be occluded to maximize coronary perfusion if hypotension (SBP  70 mm Hg) persists. We prefer to cross-clamp the thoracic aorta inferior to the left pulmonary hilum (Fig. 14-8). Exposure of this area is best provided by elevating the left lung anteriorly and superiorly. Although some advocate taking down the inferior pulmonary ligament to better mobilize the lung, this is unnecessary and risks injury to the inferior pulmonary vein. Dissection of the thoracic aorta is optimally performed under direct vision by incising the mediastinal pleura and bluntly separating the aorta from the esophagus anteriorly and from the prevertebral fascia posteriorly. Care should be taken in dissecting the aorta, and completely encircling it may avulse thoracic and other small vascular branches. Alternatively, if excessive hemorrhage limits direct visualization, which is the more

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SECTION 2 A

B

FIGURE 14-7 (A) and (B) Open cardiac massage is performed with a two-handed hinged technique; the clapping motion sequentially closes the hands from palms to fingers.

A

B

FIGURE 14-8 (A) and (B) Aortic cross-clamp is applied with the left lung retracted superiorly, below the inferior pulmonary ligament, just above the diaphragm. The flaccid aorta is identified as the first structure encountered on top of the spine when approached from the left chest.

Emergency Department Thoracotomy

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realistic clinical scenario, blunt dissection with one’s thumb and fingertips can be done to isolate the descending aorta. Once identified and isolated, the thoracic aorta is occluded with a large Satinsky or DeBakey’s vascular clamp. If the aorta cannot be easily isolated from the surrounding tissue, digitally occlude the aorta against the spine to affect aortic occlusion. Although occlusion of the thoracic aorta is typically performed after pericardiotomy, this may be the first maneuver upon entry into the chest in patients sustaining extrathoracic injury and associated major blood loss. Control of the pulmonary hilum has two indications. First, if coronary or systemic air embolism is present, further embolism is prevented by placing a vascular clamp across the pulmonary hilum (Fig. 14-9). Associated maneuvers such as

X

X X

FIGURE 14-10 In cases of bronchovenous air embolism, sequential sites of aspiration include the left ventricle (1), the aortic root (2), and the right coronary artery (3).

vigorous cardiac massage to move air through the coronary arteries and needle aspiration of air from the left ventricular apex and the aortic root are also performed (Fig. 14-10). Second, if the patient has a pulmonary hilar injury or marked hemorrhage from the lung parenchyma, control of the hilum may prevent exsanguination. Hilar control can be performed by a Satinsky’s clamp, the pulmonary hilar twist, or temporarily with digital control (see Chapter 26).

A

COMPLICATIONS AND CONSEQUENCES OF EDT ■ Procedural Complications

B FIGURE 14-9 (A) and (B) A Satinsky clamp is used to clamp the pulmonary hilum for hemorrhage control or to prevent further bronchovenous air embolism.

247

Technical complications of EDT involve virtually every intrathoracic structure. The list of such misadventures included lacerations of the heart, coronary arteries, aorta, phrenic nerves, esophagus, and lungs, as well as avulsion of aortic branches to components of the mediastinum. Previous thoracotomy virtually assures technical problems from the presence of dense pleural adhesions and is therefore a relative contraindication to EDT. Additional postoperative morbidity among ultimate survivors of EDT includes recurrent chest bleeding; infection of the pericardium, pleural spaces, sternum, and chest wall; and postpericardiotomy syndrome. Importantly, there is a finite risk to the health care providers and trauma team performing an EDT.55 The use of EDT by necessity involves the rapid use of sharp surgical instruments and exposure to the patient’s blood. Even during elective procedures in the OR, the contact rate of patient’s blood with the surgeon’s skin can be as high as 50%, and the contact rate

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SECTION 2

of patients’ blood with health care workers’ blood as high as 60%. The overall seroprevalence rate of human immunodeficiency virus (HIV) among patients admitted to the ED for trauma is around 4%, but is much higher among the subgroup of patients most likely to require an EDT, for example, 14% of penetrating trauma victims and nearly 30% of intravenous drug abusers. Caplan et al.56 found that 26% of acutely injured patients had evidence of exposure to HIV (4%), hepatitis B (20%), or hepatitis C virus (14%); there was no difference in the incidence comparing blunt to penetrating trauma. Thus, the likelihood of a health care worker sustaining exposure to HIV or hepatitis in the ED is substantial. The risk of contagion from exposures to HIV and other blood-borne pathogens can be minimized by the use of appropriate barrier precautions and the selective use of EDT.

■ Hemodynamic and Metabolic Consequences of Aortic Cross-Clamping Aortic cross-clamping may be life saving during acute resuscitation, but there is a finite cost to the patient. Occlusion of the aorta results in an increase in blood pressure, but there is an associated 90% reduction in femoral artery SBP; in addition, abdominal visceral blood flow decreases to 2–8% of baseline values.31,32 Therefore, cross-clamping magnifies the metabolic cost of shock by reducing local blood flow to abdominal viscera even further. This results in tissue acidosis and increased oxygen debt, and may ultimately contribute to postischemic multiple organ failure.32 Additionally, return of aortic flow may not result in normalization of flow to vital organs; in animal models, blood flow to the kidneys remained at 50% of baseline despite a normal cardiac output. The metabolic penalty of aortic cross-clamping becomes exponential when the normothermia occlusion time exceeds 30 minutes, both in trauma and in elective thoracic aortic procedures.57–59 Hypoxia of distal organs, white blood cells, and endothelium induces the elaboration, expression, and activation of inflammatory cell adhesion molecules and inflammatory mediators; this systemic inflammatory response syndrome has been linked to impaired pulmonary function and multiple organ failure60 (see Chapter 61). Consequently, the aortic clamp should be removed as soon as effective cardiac function and adequate systemic arterial pressure have been achieved. Removal of aortic occlusion may result in further hemodynamic sequelae.61 Besides the abrupt reperfusion of the ischemic distal torso and washout of metabolic products and inflammatory mediators associated with aortic declamping, there are direct effects on the cardiopulmonary system. The return of large volumes of blood from the ischemic extremities, with its lower pH, elevated lactate, and other mediators may exert a cardiodepressant activity on myocardial contractility.62 Overzealous volume loading during aortic occlusion may also result in left ventricular strain, acute atrial and ventricular dilatation and, consequently, precipitous cardiac failure.32 Following release of aortic occlusion there is impaired left ventricular function, systemic oxygen utilization, and coronary perfusion pressure in the postresuscitation period.61,63 The

transient fall in coronary perfusion may not be clinically relevant in patients with efficient coronary autoregulation; however, in patients with coronary disease or underlying myocardial hypertrophy, this increase in cardiac work may result in clinically critical ischemia.63

OPTIMIZING OXYGEN TRANSPORT FOLLOWING EDT Following EDT, patients are frequently in a tenuous physiologic state. The combination of direct cardiac injury, ischemic myocardial insult, myocardial depressants, and pulmonary hypertension adversely impact postinjury cardiac function (see Chapter 56). Additionally, aortic occlusion induces profound anaerobic metabolism, secondary lactic academia, and release of other reperfusion-induced mediators. Consequently, once vital signs return, the resuscitation priorities shift to optimizing cardiac function and maximizing oxygen delivery to the tissues. The ultimate goal of resuscitation is adequately tissue oxygen delivery and cellular oxygen consumption (see Chapter 55). Circulating blood volume status is maintained at the optimal level of cardiac filling in order to optimize cardiac contractility, and the oxygen-carrying capacity of the blood is maximized by keeping the hemoglobin above 7–10 g/dL. If these measures fail to meet resuscitative goals64 (e.g., oxygen delivery 500 mL/min/,2 resolution of base deficit, or clearance of serum lactate), inotropic agents are added to enhance myocardial function.

FUTURE CONSIDERATIONS ■ Defining Nonsalvageability As clinicians faced with increasing scrutiny over appropriation of resources, it is critical to identify the patient who has permanent neurologic disability or death. Resuscitative efforts should not be abandoned prematurely in the potentially salvageable patient but field assessment of salvageability is unreliable.41,65–67 Our clinical pathway attempts to optimize resource utilization, but outcomes must continue to be evaluated, searching for more definitive predictors of neurologic outcome. For example, markers of brain metabolic activity such as increased serum neuron–specific enolase activity appear to have prognostic significance for irreversible brain damage.68 The use of more advanced monitoring devices in the ED, together with further elucidation of the characteristics of irreversible shock, may permit a more physiologic prediction of outcome for these critically injured patients in the future.

■ Temporary Physiologic Hibernation A potential adjunct in the care of traumatic arrest is the timely application of hypothermia. Recent randomized studies suggest the use of hypothermia for central nervous system protection after nontraumatic cardiac arrest.69,70 In these studies, patients randomized to a period of mild-to-moderate hypothermia (32–34°C) after cardiac arrest had improved neurologic outcomes compared to those kept normothermic. This

Emergency Department Thoracotomy

■ Temporary Mechanical Cardiac Support The concept of temporary mechanical cardiac support for the failing heart following injury is intuitively attractive. Unfortunately, experience with the intra-aortic balloon pump in this scenario has been unrewarding. The advent of centrifugal pumps (Bio-Medicus Pump; Bio-Medicus, Inc., Minneapolis, MN), that allow partial cardiac bypass without systemic anticoagulation, offers another potential means for increasing salvage of the moribund patient. Centrifugal pumps have become the standard approach to the torn descending thoracic aorta in the patient with associated myocardial contusion (see Chapter 26).75,76 The adjunctive use of extracorporeal membrane oxygenation may also play a critical role in supporting the patient with massive injuries or early multiple organ failure.77 Finally, hypothermia circulatory arrest may find utility in a broad spectrum of patients with injuries that are considered “irreparable.”78,79

REFERENCES 1. Hemreck AS. The history of cardiopulmonary resuscitation. Am J Surg. 1988;156:430. 2. Beck CS. Wounds of the heart. Arch Surg. 1926;13:205. 3. Blatchford JW III. Ludwig Rehn–the first successful cardiography. Ann Thorac Surg. 1985;39:492. 4. Kouwenhoven WB, Jude JR, Knickerbocker GG. Closed-chest cardiac massage. JAMA. 1960;173:1064. 5. Zoll PM, Linenthal AJ, Norman LR, et al. Treatment of unexpected cardiac arrest by external electric stimulation of the heart. N Engl J Med. 1956;254:541. 6. Blalock A, Ravitch MM. A consideration of the nonoperative treatment of cardiac tamponade resulting from wounds of the heart. Surgery. 1943;14:157. 7. Beall AC Jr, Diethrich EB, Crawford HW, et al. Surgical management of penetrating cardiac injuries. Am J Surg. 1966;112:686. 8. Ledgerwood AM, Kazmers M, Lucas CE. The role of thoracic aortic occlusion for massive hemoperitoneum. J Trauma. 1976;16:610. 9. Millikan JS, Moore EE. Outcome of resuscitative thoracotomy and descending aortic occlusion performed in the operating room. J Trauma. 1984;24:387. 10. Powell DW, Moore EE, Cothren CC, et al. Is emergency department resuscitative thoracotomy futile care for the critically injured patient requiring pre-hospital cardiopulmonary resuscitation? JACS. 2004; 199:211. 11. ACS-COT Subcommittee on Outcomes. Practice management guidelines for emergency department thoracotomy. JACS. 2001;193:303.

12. Miglietta MA, Robb TV, Eachempati SR et al. Current opinion regarding indications for emergency department thoracotomy. J Trauma. 2001;51:670. 13. Breaux EP, Dupont JB Jr, Albert HM, et al. Cardiac tamponade following penetrating mediastinal injuries: improved survival with early pericardiocentesis. J Trauma. 1979;19:461. 14. Shoemaker WC, Carey JS, Yao ST, et al. Hemodynamic alterations in acute cardiac tamponade after penetrating injuries to the heart. Surgery. 1970;67:754. 15. Wechsler AS, Auerbach BJ, Graham TC, et al. Distribution of intramyocardial blood flow during pericardial tamponade. J Thorac Cardiovasc Surg. 1974;68:847. 16. Mattox KL, Beall AC Jr, Jordon GL Jr, et al. Cardiorrhaphy in the emergency center. J Thorac Cardiovasc Surg. 1974;68:886. 17. Wall MJ Jr, Mattox KL, Chen CD, et al. Acute management of complex cardiac injuries. J Trauma. 1997;42:905. 18. Graham JM, Mattox KL, Beall AC Jr. Penetrating trauma of the lung. J Trauma. 1979;19:665. 19. Boczar ME, Howard MA, Rivers EP, et al. A technique revisited: hemodynamic comparison of closed- and open-chest cardiac massage during human cardiopulmonary resuscitation. Crit Care Med. 1995; 23:498. 20. Rubertsson S, Grenvik A, Wiklund L. Blood flow and perfusion pressure during open-chest versus closed-chest cardiopulmonary resuscitation in pigs. Crit Care Med. 1995;23:715. 21. Luna GK, Pavlin EG, Kirkman T, et al. Hemodynamic effects of external cardiac massage in trauma shock. J Trauma. 1989;29:1430. 22. Spence PA, Lust RM, Chitwood WR Jr, et al. Transfemoral balloon aortic occlusion during open cardiopulmonary resuscitation improves myocardial and cerebral blood flow. J Surg Res. 1990;49:217. 23. Wesley RC Jr, Morgan DB. Effect of continuous intra-aortic balloon inflation in canine open chest cardiopulmonary resuscitation. Crit Care Med. 1990;18:630. 24. Dunn EL, Moore EE, Moore JB. Hemodynamic effects of aortic occlusion during hemorrhagic shock. Ann Emerg Med. 1982;11:238. 25. Michel JB, Bardou A, Tedgui A, et al. Effect of descending thoracic aortic clamping and unclamping on phasic coronary blood flow. J Surg Res. 1984;36:17. 26. Gedeborg R, Rubertsson S, Wiklund L. Improved hemodynamics and restoration of spontaneous circulation with constant aortic occlusion during experimental cardiopulmonary resuscitation. Resuscitation. 1999;40:171. 27. Rubertsson S, Bircher NG, Alexander H. Effects of intra-aortic balloon occlusion on hemodynamics during, and survival after cardiopulmonary resuscitation in dogs. Crit Care Med. 1997;25:1003. 28. Sheppard FR, Cothren CC, Moore EE, et al. Emergency department resuscitative thoracotomy for non-torso injuries. Surgery. 2006; 139:574. 29. Kralovich KA, Morris DC, Dereczyk BE, et al. Hemodynamic effects of aortic occlusion during hemorrhagic shock and cardiac arrest. J Trauma. 1997;42:1023. 30. Connery C, Geller E, Dulchavsky S, et al. Paraparesis following emergency room thoracotomy: Case report. J Trauma. 1990;30:362. 31. Mitteldorf C, Poggetti RS, Zanoto A, et al. Is aortic occlusion advisable in the management of massive hemorrhage? Experimental study in dogs. Shock. 1998;10:141. 32. Oyama M, McNamara JJ, Suehiro GT, et al. The effects of thoracic aortic cross-clamping and declamping on visceral organ blood flow. Ann Surg. 1983;197:459. 33. King MW, Aitchison JM, Nel JP. Fatal air embolism following penetrating lung trauma: An autopsy study. J Trauma. 1984;24:753. 34. Thomas AN, Stephens BG. Air embolism: a cause of morbidity and death after penetrating chest trauma. J Trauma. 1974;14:633. 35. Yee ES, Verrier ED, Thomas AN. Management of air embolism in blunt and penetrating thoracic trauma. J Thorac Cardiovasc Surg. 1983;85:661. 36. Graham JM, Beall AC Jr, Mattox KL, et al. Systemic air embolism following penetrating trauma to the lung. Chest. 1977;72:449. 37. Baxter BT, Moore EE, Moore JB, et al. Emergency department thoracotomy following injury: critical determinants for patient salvage. World J Surg. 1988;12:671. 38. Cogbill TH, Moore EE, Millikan JS, et al. Rationale for selective application of emergency department thoracotomy in trauma. J Trauma. 1983;23:453. 39. Moore EE, Moore JB, Galloway AC, et al. Postinjury thoracotomy in the emergency department: a critical evaluation. Surgery. 1979;86:590. 40. Branney SW, Moore EE, Feldhaus KM, et al. Critical analysis of two decades of experience with postinjury emergency department thoracotomy in a regional trauma center. J Trauma. 1998;45:87.

CHAPTER 14

favorable effect was presumably due to a decrease in cerebral metabolic demand during hypothermia. In addition, hypothermia may reduce oxygen radical generation and inflammatory mediator production. By extension, then, if an injured patient in transport could be cooled to a minimal metabolic rate (i.e., suspended animation), one can posit that transfer to definitive care might be possible.71,72 Application of this principle to the multiply injured or bleeding patient, however, is problematic. Rapid cooling is not currently practical in the field, and there are legitimate concerns about the adverse effects of hypothermia on immune function and effective clot formation. Overall, while some73 preclinical work supports the application of hypothermia after resuscitation from hemorrhage, other investigators have reached the opposite conclusion.74

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41. Pickens JJ, Copass MK, Bulger EM. Trauma patients receiving CPR: predictors of survival. J Trauma. 2005;58:951. 42. Rhee PM, Acosta J, Bridgeman A, et al. Survival after emergency department thoracotomy: review of published data from the past 25 years. JACS. 2000;190:288. 43. Baker CC, Thomas AN, Trunkey DD. The role of emergency room thoracotomy in trauma. J Trauma. 1980;20:848. 44. Stockinger ZT, McSwain NE. Additional evidence in support of withholding or terminating cardiopulmonary resuscitation for trauma patients in the field. JACS. 2004;198:227. 45. Moore EE, Knudson MM, Burlew CC, et al. Defining the limits of resuscitative emergency department thoracotomy: a contemporary Western Trauma Association perspective. J Trauma. 2011;70:334–339. 46. Fialka C, Sebok C, Kemetzhofer P, et al. Open-chest cardiopulmonary resuscitation after cardiac arrest in cases of blunt chest or abdominal trauma: a consecutive series of 38 cases. J Trauma. 2004;57:809. 47. Seamon MJ, Fisher CA, Gaughan JP, et al. Emergency department thoracotomy: survival of the least expected. World J Surg. 2008;32:602. 48. Li G, Tang N, DiScala C, et al. Cardiopulmonary resuscitation in pediatric trauma patients: survival and functional outcome. J Trauma. 1999;47:1. 49. Beaver BL, Colombani PM, Buck JR. Efficacy of emergency room thoracotomy in pediatric trauma. J Pediatr Surg. 1987;22:19. 50. Rothenberg SS, Moore EE, Moore FA, et al. Emergency department thoracotomy in children: a critical analysis J Trauma. 1989;29:1322. 51. Sheikh AA, Culbertson CB. Emergency department thoracotomy in children: rationale for selective application. J Trauma. 1993;34:323. 52. Powell RW, Gill EA, Jurkovich GJ, et al. Resuscitative thoracotomy in children and adolescents. Am Surg. 1988;54:1988. 53. American Heart Association. Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2000;102:I1. 54. Nolan JP, de Latorre FJ, Steen PA, et al. Advanced life support drugs: do they really work? Curr Opin Crit Care. 2002;8:212. 55. Sikka R, Millham FH, Feldman JA. Analysis of occupational exposures associated with emergency department thoracotomy. J Trauma. 2004;56:867. 56. Caplan ES, Preas MA, Kerns T, et al. Seroprevalence of human immunodeficiency virus, hepatitis B virus, hepatitis C virus, and rapid plasma reagin in a trauma population. J Trauma. 1995;39:533. 57. Fabian TC, Richardson JD, Croce MA, et al. Prospective study of blunt aortic injury: Multicenter trial of the American Association for the Surgery of Trauma. J Trauma. 1997;42:374. 58. Gharagozloo F, Larson J, Dausmann MJ, et al. Spinal cord protection during surgical procedures on the descending thoracic and thoracoabdominal aorta. Chest. 1996;109:799. 59. Katz NM, Blackstone EH, Kirklin JW, et al. Incremental risk factors for spinal cord injury following operation for acute traumatic aortic transection. J Thorac Cardiovasc Surg. 1981;81:669. 60. Adembri C, Kastamoniti E, Bertolozzi I, et al. Pulmonary injury follows systemic inflammatory reaction in infrarenal aortic surgery. Crit Care Med. 2004;32:1170. 61. Kralovich KA, Morris DC, Dereczyk BE, et al. Hemodynamic effects of aortic occlusion during hemorrhagic shock and cardiac arrest. J Trauma. 1997;42:1023. 62. Perry MO. The hemodynamics of temporary abdominal aortic occlusion. Ann Surg. 1968;168:193. 63. Michel JB, Bardou A, Tedgui A, et al. Effect of descending thoracic aorta clamping and unclamping on phasic coronary blood flow. J Surg Res. 1984;36:17. 64. McKinley BA, Kozar RA, Cocanour CS, et al. Normal versus supranormal oxygen delivery goals in shock resuscitation: the response is the same. J Trauma. 2002;53:825. 65. Battistella FD, Nugent W, Owings JT, et al. Field triage of the pulseless trauma patient. Arch Surg. 1999;134:742. 66. Fulton RL, Voigt WJ, Hilakos AS. Confusion surrounding the treatment of traumatic cardiac arrest. J Am Coll Surg. 1995;181:209.

67. Stratton SJ, Brickett K, Crammer T. Prehospital pulseless, unconscious penetrating trauma victims: field assessments associated with survival. J Trauma. 1998;45:96. 68. Fogel W, Krieger D, Veith M, et al. Serum neuron-specific enolase as early predictor of outcome after cardiac arrest. Crit Care Med. 1997; 25:1133. 69. Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med. 2002;346:557. 70. The Hypothermia After Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med. 2002;346:549. 71. Rhee P, Talon E, Eifert S, et al. Induced hypothermia during emergency department thoracotomy: an animal model. J Trauma. 2000;48:439. 72. Safar P, Tisherman SA, Behringer W, et al. Suspended animation for delayed resuscitation from prolonged cardiac arrest that is unresuscitatable by standard cardiopulmonary-cerebral resuscitation. Crit Care Med. 2000;28:N214. 73. Prueckner S, Safar P, Kenter R, et al. Mild hypothermia increases survival from severe pressure-controlled hemorrhagic shock in rats. J Trauma. 2001;50:253. 74. Mizushima Y, Wang P, Cioffi WG, et al. Should normothermia be restored and maintained during resuscitation after trauma and hemorrhage? J Trauma. 2000;48:58. 75. Read RA, Moore EE, Moore FA, et al. Partial left heart bypass for thoracic aorta repair: survival without paraplegia. Arch Surg. 1993;128:746. 76. Szwerc MF, Benckart DH, Lin JC, et al. Recent clinical experience with left heart bypass using a centrifugal pump for repair of traumatic aortic transection. Ann Surg. 1999;230:484. 77. Perchinsky MJ, Long WB, Hill JG, et al. Extracorporeal cardiopulmonary life support with heparin-bonded circuitry in the resuscitation of massively injured trauma patients. Am J Surg. 1995;169:488. 78. Chughtai TS, Gilardino MS, Fleiszer DM, et al. An expanding role for cardiopulmonary bypass in trauma. Can J Surg. 2002;45:95. 79. Howells GA, Hernandez DA, Olt SL, et al. Blunt injury of the ascending aorta and aortic arch: repair with hypothermic circulatory arrest. J Trauma. 1998;44:716. 80. Moreno C, Moore EE, Majure JA, et al. Pericardial tamponade: a critical determinant for survival following penetrating cardiac wounds. J Trauma. 1986;26:821. 81. Tyburski JG, Astra L, Wilson RF, et al. Factors affecting prognosis with penetrating wounds of the heart. J Trauma. 2000;48:587. 82. Velhamos GC, Degiannis E, Souter I, et al. Outcome of a strict policy on emergency department thoracotomies. Arch Surg. 1995;130:774. 83. Asensio JA, Berne JD, Demetriades D, et al. One hundred five penetrating cardiac injuries: a 2-year prospective evaluation. J Trauma. 1998; 44:1073. 84. Rohman M, Ivatury RR, Steichen FM, et al. Emergency room thoracotomy for penetrating cardiac injuries. J Trauma. 1983;23:570. 85. Rhee PM, Foy H, Kaufmann C, et al. Penetrating cardiac injuries: a population-based study. J Trauma. 1998;45:366. 86. Durham LA, Richardson RJ, Wall MJ, et al. Emergency center thoracotomy: impact of prehospital resuscitation. J Trauma. 1992; 32:775. 87. Brown SE, Gomez GA, Jacobson LE, et al. Penetrating chest trauma: should indications for emergency room thoracotomy be limited? Am Surg. 1996;62:530. 88. Ivatury RR, Kazigo J, Rohman M, et al. “Directed” emergency room thoracotomy: a prognostic prerequisite for survival. J Trauma. 1991;31:1076. 89. Mazzorana V, Smith RS, Morabito DJ, et al. Limited utility of emergency department thoracotomy. Am Surg. 1994;60:516. 90. Danne PD, Finelli F, Champion HR: emergency bay thoracotomy. J Trauma. 1984;24:796. 91. Esposito TJ, Jurkovich GJ, Rice CL, et al. Reappraisal of emergency room thoracotomy in a changing environment. J Trauma. 1991;31:881.

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CHAPTER 15

Diagnostic and Interventional Radiology Salvatore J.A. Sclafani

Trauma imaging may be used to provide rapid and broad surveys when clinical evaluation is likely to be incomplete or unreliable or used to characterize recognized injuries as part of treatment planning. And it may be used to guide observational, operative, and minimally invasive decisions. Therefore, trauma imaging may inform clinical diagnosis and can guide, but not make, management decisions. Imaging strategies are affected by the proximity of available imaging technology to the resuscitation area, the capabilities of the imaging equipment, the experience and availability of radiology technologists performing emergent imaging procedures, and timely access to expert interpretation and reporting. The timing of diagnostic imaging should reflect the needs of individual patients and the local system. With some exceptions for image-guided endovascular hemostasis, hemodynamically unstable patients should be resuscitated prior to imaging according to accepted guidelines and recommendations. In order to enhance efficiency, triage priorities for imaging should be based on the acute needs for accurate information that can be used to direct treatment of the patient. Close cooperation and open communication between the emergency physicians, traumatologists, consultants, nurses, imaging technologists, and radiologists are always necessary to optimize any imaging assessment. One chapter cannot reasonably teach interpretation of diagnostic images. Therefore, a general approach to the role of imaging in the evaluation of selected clinical scenarios is presented, while pointing out the advantages and disadvantages of a given imaging strategy.

INITIAL IMAGING FOR THE ASSESSMENT OF BLUNT TRAUMA ■ Trauma Series As part of the secondary survey of victims of blunt trauma, an imaging survey of the chest (supine anteroposterior [AP] chest with 10° of caudal angulation of the central x-ray beam), pelvis (supine AP pelvis), and cervical spine (horizontal-beam, crosstable lateral cervical spine obtained with bilateral arm pull) may be performed, if clinical evaluation alone is deemed insufficient (Fig. 15-1). The goals of these initial imaging studies are to identify life-threatening, but clinically occult, injuries such as an unstable pelvic fracture, hemomediastinum, or instability of the cervical spine.1,2 The trauma resuscitation “ABCD” strategy may be extended to this “trauma series.” Verification of the integrity of the airway (and other tubes and lines) should be specifically made on the x-rays of both the chest and lateral cervical spine. Radiographic pulmonary opacities associated with hypoxemia include pulmonary contusions, aspiration pneumonitis, and atelectasis (including collapse due to aspirated dental or foreign debris). Tension pneumothorax and hemothorax are typically detected on clinical examination, while clinically occult pneumothoraces or hemothoraces are commonly shown by chest x-rays as a “deep sulcus” sign and generalized hemithoracic opacity, respectively. Other injuries, such as rupture of the hemidiaphragm, flail chest, pneumopericardium, and pneumomediastinum and hemomediastinum, are often diagnosed or suggested by initial conventional x-ray findings. Hemodynamic instability may be due to extraperitoneal hemorrhage from

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B

D

C FIGURE 15-1 Trauma series. This 27-year-old unrestrained left rear seat passenger sustained multiple injuries, superfluous in a high-speed side-impact crash. (A) Anteroposterior (AP) recumbent chest radiograph shows hyperexpanded and hyperlucent left hemithorax with “deep sulcus” sign (short white arrow) and rightward mediastinal shift (double-ended arrow) due to left tension pneumothorax. Short black arrows show multiple displaced rib fractures. Asterisk shows irregularity of left hemidiaphragm, which strongly suggests herniation of abdominal contents through left diaphragmatic laceration. (B) AP pelvis radiograph shows lateral-compression-type pelvic ring disruption consisting of bilateral iliopubic and ischiopubic ramus and left sacral fractures (long arrows) with sacroiliac joint disruptions (short arrow). (C) Cross-table lateral cervical spine radiograph is grossly normal to C5. Therefore, this constitutes a nondiagnostic study. Craniocervical alignment should be assessed and may be easily overlooked. Dens–basion distance (white double-ended arrow) is normally no greater than 12 mm. Posterior axial line represents cephalad extension of posterior cortex of C2 body (and is normally no more than 12 mm posterior or 4 mm anterior to basion) (black double-ended arrow). Anterior atlantodens interval is normally no greater than 3 mm in adults and 5 mm in children (8 years and younger). Laminar point of C2 (laminar points are most anterior extent of neural canal margin of lamina) should be within 1.5 mm of line connecting laminar points of C1 and C3. (D) Coronal image of right upper quadrant from focused abdominal sonography for trauma (FAST) shows free intraperitoneal fluid in anterior subhepatic (Morison’s) space (arrows), compatible with hemoperitoneum.

Diagnostic and Interventional Radiology

■ Focused Abdominal Sonography for Trauma (FAST) FAST is performed as part of the secondary survey in victims of torso trauma (see Chapter 16). It is a temporally (2–5 minutes) and anatomically limited real-time sonographic examination whose core components include a direct sonographic search for free fluid in the pericardial sac, both upper abdominal quadrants, and the intraperitoneal recesses adjacent to the urinary bladder. Scanning is optimally performed in two orthogonal planes (e.g., longitudinal and transverse), and intraparenchymal and retroperitoneal injuries are generally not sought but are sometimes seen. FAST may be extended to detect a hemothorax and pneumothorax. Commercially available, portable handheld real-time imaging devices are technically adequate to perform FAST. FAST is uniformly accurate for the detection of intraperitoneal fluid with moderately large volumes 400 cm3 (at smaller volumes, accuracy varies with user experience).3–5 Unfortunately, isolated hepatosplenic injuries with minimal or no hemoperitoneum represent as many as one third of solid organ injuries.6,7 Fortunately, small isolated intraparenchymal lesions with less than 250 mL of intraperitoneal blood rarely require endovascular or surgical intervention (liver 1%, spleen 5%).8 False-positive interpretation of FAST images can result from improper machine settings (gain), sonolucent perinephric fat (which is rarely sonolucent in both axial and coronal scanning planes), fluid-filled loops of bowel, bladder, various types of fluid-filled intra-abdominal cysts, and physiological or nontraumatic free fluid (ascites). FAST is widely available, inexpensive, and noninvasive, uses no ionizing radiation, and can be repeated serially. In the setting of patients admitted with severe hemodynamic compromise or obvious hemorrhagic shock, FAST can establish the abdomen as a source of hemorrhage within a few seconds. The FAST does, however, require operator training and experience for reliable performance and interpretation, and these can limit its value. In addition, FAST is not very valuable in patients with pelvic fractures as a hemoperitoneum may be present in the absence of visceral injury. Another important limitation of FAST is that isolated injuries to the bowel and retroperitoneal injuries are not reliably detected. While a systematic review of the literature would not support the use of FAST as a replacement for DPL and computed tomography (CT) in blunt abdominal trauma, many trained surgeonsonographers use it on a daily basis with great accuracy.9

Hemodynamically stable patients who have suffered blunt trauma with a clinical presentation suspicious for injury to the bowel (e.g., lap belt sign and associated Chance or flexion-distraction injury to the thoracolumbar spine) or hematuria (e.g., gross hematuria in all age groups, microscopic hematuria defined as 50 red blood cell count per high-power field in individuals 16 years old and younger, or in those older with at least one documented episode of hypotension) should undergo intravenous contrast-enhanced CT of the abdomen and pelvis.

COMPREHENSIVE IMAGING FOR BLUNT POLYTRAUMA Victims of blunt multiple trauma often receive portable imaging in the trauma suite and are then triaged based on their hemodynamic status to the operating room, intensive care unit, or angiography suite for ongoing resuscitation or remain in the trauma center for completion of secondary and tertiary surveys, including initial imaging. Typically, this consists of CT for clinically appropriate imaging (e.g., head, neck, chest, abdomen, and pelvis) for the most severely injured, but hemodynamically stable patients. Subsequently, conventional x-rays of the extremities and spine may be obtained. Less severely injured individuals may take a slightly different route with conventional x-rays preceding CT and directed at abnormalities found by clinical examination or prior imaging. There are some who advocate the “pan scan,” also known as the “head to toe” CT, as a method of detecting many injuries. This paradigm advocates utilization of high-resolution thin collimation image acquisition to include CT scanning of the head, face, soft tissue of the neck, the chest, the abdomen, and pelvis, including the acetabulum and the spine. While it does provide excellent coverage, it exposes patients to much radiation and is not recommended as a general rule. On the other hand, the “pan scan” has value in a high-volume facility with considerable imaging resources and the need for rapid screening.

■ Multidetector Computed Tomography (MDCT) MDCT scanners have changed the way CT is used in imaging trauma.10,11 MDCT scanners, with 16 or more detectors, can provide nearly equivalent resolution in any imaging plane with progressively shorter scan times. This greatly improves the quality of both two-dimensional (multiplanar) and threedimensional reformations. The rapidity of multidetector helical scanning and enormously improved designs of x-ray tubes allow for single-session scanning from cranial vertex to pelvic ischia in less than 90 seconds.12,13 This includes two- and threedimensional reformations of the thoracic and abdominal aorta, maxillofacial skeleton, cervical and thoracolumbar spines, and pelvis and acetabulae. With appropriate anticipation and proscription, scanning parameters allow raw axial data to be reconstructed using different thicknesses (e.g., 5-mm-thick slices for abdominal viscera and 2.5-mm-thick slices for CT aortography). Thus, individual thin-section imaging of parts of the body in addition to the CT survey is superfluous, increases ionizing radiation unnecessarily,

CHAPTER 15

disruption of the pelvic ring. Biomechanically unstable disruptions of the pelvic ring are almost always shown on AP radiographs and may be associated with injuries to the bladder and urethra. In addition, pelvic x-rays may show hip dislocations and fractures of the acetabulum and proximal femur. A technically adequate (C1–T1) lateral x-ray of the cervical spine provides a reasonable “screening” study to identify most unstable cervical injuries. It may provide important information regarding the best technique for airway control and may confirm that spinal shock from a vertebral fracture is the cause of unexplained hypotension.

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FIGURE 15-2 Epidural hematoma. Helmetless bicyclist in crash. (A) Lateral scout scanogram shows linear lucency compatible with fracture (arrows). (B) Axial computed tomography (CT) displayed at bone window shows minimally displaced right parietal skull fracture with overlying subgaleal hematoma. Fracture is marked by white arrow and barely visible hyperintensity of extra-axial blood collection by arrowheads. Bone windows are inadequate to identify intracranial hemorrhages. (C) Axial CT at brain windows shows epidural hematoma (arrowheads), associated midline shift (short arrow), and subgaleal hematoma (asterisk). (D) Axial CT at level of the suprasellar cistern, brain windows, shows epidural hematoma (black asterisk), asymmetric widening of perimesencephalic cistern (arrow), which suggests impending uncal herniation. (Reproduced with permission from D. K. Hallam.)

and increases time-out of the critical care area. This previous standard of detailed specialized imaging of the face and spine should be abandoned.

■ Computed Tomography of the Head Axial noncontrast CT scanning remains the reference standard in patients with acute craniocerebral trauma, guiding initial decisions regarding the clinical management.14,15 Indications for CT of the cranium include the following: (1) objective evidence of closed injury to the brain, including decreased level of

consciousness; (2) cranial or facial deformity; (3) hemotympanum; or (4) evidence for leakage of cerebrospinal fluid (Figs. 15-2 to 15-4). Clinical criteria reliably predict significant intracranial injury (ICI) and help determine which patients will require CT scanning of the head. In children,17 significant ICI is extremely unlikely in any child who does not exhibit at least one of the following high-risk criteria: (1) evidence of significant skull fracture; (2) altered level of alertness; (3) neurological deficit; (4) persisting vomiting; (5) scalp hematoma; (6) abnormal behavior; or (7) coagulopathy.16 More generically, minor trauma to the head may lead to surgically important injuries to

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FIGURE 15-3 Blunt head injury: Diffuse axonal injury. This 48-year-old helmeted female motorcyclist sustained diffuse axonal injury. (A) Axial computed tomography (CT) at level of lateral ventricles demonstrates intraventricular hemorrhage (asterisk), “tear” hemorrhage in posterior limb of internal capsule (white arrow). Black arrow denotes splenium of corpus callosum, which appeared normal by CT. (B) Axial magnetic resonance imaging (MRI) using FLAIR shows clot in right lateral ventricle as extended region of low signal (asterisk), edema associated with tear hemorrhage (white arrow), and splenium of corpus callosum (black arrow) to better advantage. (C) MRI gradient recalled echo (GRE) sequence shows low signal intensity of magnetic susceptibility due to hemorrhage in region of posterior horn of internal capsule (white arrow) and in right lateral ventricle (asterisk). Splenium of corpus callosum has region of mildly increased signal intensity compatible with edema (black arrow). In general, the more central findings of diffuse axonal injury, the greater the degree of neurological disability. (Reproduced with permission from W. A. Cohen.)

the brain, and liberal utilization of CT is appropriate among individuals who have sustained “high-risk” mechanisms. These clinical criteria are not as reliable in the elderly patient.17 Singlephoton emission CT (SPECT) may be helpful in initial diagnostic evaluation of patients with mild traumatic brain injury (MTBI), particularly for those with normal CT findings and associated post-traumatic amnesia (PTA), postconcussion syndrome (PCS), and loss of consciousness.18 Images are reconstructed using both bone and soft tissue algorithms and viewed at bone windows and two different soft tissue windows (“brain” and “blood”). CT scanning is highly sensitive for the detection of extraand intra-axial hemorrhage and mass effect, as well as for soft tissue injuries to the globe and paranasal sinuses. In patients with diffuse axonal injury, however, CT may even be normal and discordant between the severity of the clinical brain injury and radiographic findings. On a cautionary note, skull fractures aligned in the plane of scanning may be subtle, and review of the scout views used to plan the CT head study may alert the clinician to such fractures. Except for medicolegal imaging of nonaccidental trauma (child abuse), conventional x-rays of the skull are usually not necessary.19,20

■ Computed Tomography of the Maxillofacial Skeleton Indications for specific facial CT scans include the following: (1) deformity or instability of the maxillofacial structures found by physical examination; (2) deformity, opacification, or fracture of

the periorbital or paranasal sinus shown on head CT; and (3) clinical evidence for leakage of cerebrospinal fluid (Fig. 15-5). The mnemonic “LIPS-N” (lip lacerations, intraoral lacerations, periorbital contusions, subconjunctival hemorrhage, or nasal lacerations) provides a helpful tool during clinical examination of trauma patients, also, given the high association between any of LIPS-N lesions and facial fractures.21 Absence of opacification of a paranasal or periorbital sinus on CT generally excludes surgically important injury to the maxillofacial skeleton.22 Images need be acquired in only one plane, usually the axial, with reformations in the orthogonal plane, or as reconstruction from a CT of the cranium obtained from an appropriately prescribed study (i.e., 1.00- to 1.25-mm slice thickness). Spiral CT, and especially MDCT, can be reformatted into 2D reformations in the orthogonal planes (e.g., coronal, sagittal, oblique sagittal) and 3D reformations, using 1.0- to 1.25-mm thick sections in the axial plane, without loss of image quality and accuracy, stress on the neck, and further radiation. Primary axial images are obtained using 1.0- to 1.25-mm slice thickness from above the frontal sinus to the hard palate or maxillary alveolus. These are commonly extended to include the mandible to aid surgical diagnosis, especially in children, as fractures of the condyle of the mandible are the most commonly missed maxillofacial fractures in this age group.23–25 Reformations in the coronal and sagittal planes should be perfectly orthogonal to the axial images. Reformations in the sagittal plane may be performed either relative to the coronal plane or as sagittal oblique reformations parallel to the optic nerve, if evaluating for blowout fractures of the orbital floor.26

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FIGURE 15-4 Patterns of herniation. (A). Axial computed tomography (CT) at level of suprasellar cistern shows extensive subarachnoid hemorrhage extending from lateral aspect of suprasellar cistern (1), into the sylvian fissure (2), circumferentially about brainstem and perimesencephalic cistern (3), along tentorium (4), and interpedunculate cistern of mesencephalon (5). Entrapment of lateral ventricles is shown as dilatation of temporal horns (white arrows). Brainstem appears relatively lucent and heart shaped, with pointed inferior portion of heart due to “beaking” of mesencephalon due to upward herniation. (B) Subfalcine shift. Axial CT, at brain windows, at level of lateral ventricles shows marked rightward subfalcine shift (black arrow), quantified as distance from third ventricle to line connecting anterior and posterior portions of sagittal sinus (which tend not to shift due to their fixed relation to calvarium). Note extensive hemorrhage in left frontal parietal region extending into left ventricle. (Reproduced with permission from W. A. Cohen.) (C) Uncal herniation. Axial CT at level of middle cranial fossa shows large left temporal hematoma (black asterisk) associated with left uncal herniation (small white arrows). Enlargement of right temporal horn (large white arrow) is compatible with obstruction to cisternal system. (Reproduced with permission from A. B. Baxter.) (D) Combined upward and downward herniation. This is a 38-year-old with posterior leukoencephalopathy due to hypertension. Axial CT at level of suprasellar cistern shows enlargement of lateral ventricles and right temporal horn (long white arrows). Suprasellar cistern is poorly seen. Perimesencephalic cisterns are absent and posterior aspect is beaked, compatible with superior herniation from posterior fossa. Upward herniation is also shown by the cerebellar vermis filling the subtentorial cisternal space (multiple small arrows). (Reproduced with permission from W. A. Cohen.) (E) Same patient as in (D). Sagittal T1-weighted magnetic resonance imaging shows tonsillar herniation through the foramen magnum (arrowheads), as well as superior herniation of cerebellum and mesencephalon at level of tentorium (white arrow).

While CT is highly accurate at detecting and characterizing surgically important injuries, it does not show the magnitude of osseous fragmentation found at surgery in complex fractures. Orbital and maxillary fractures should heighten suspicion of more complex fractures. Although its incremental diagnostic value is small, 3D-CT reformation appears to be the best imaging method for the global portrayal of complex maxillofacial injury patterns such as Le Fort–type fractures. This technique provides valuable information on spatial

relationships and is particularly useful in planning operative treatment.27–30 On the other hand, axial and 2D reformations best portray defects in soft tissue, interposition of osseous fragments, and herniations of soft tissue (e.g., orbital floor blowout fractures) and are best for quantifying size of fractures.26,31 Maxillofacial CT delivers a significant radiation dose to the orbits and to the soft tissues of the neck (e.g., thyroid). This is an important consideration when imaging children.32

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FIGURE 15-5 Facial fracture: zygomaticomaxillary complex (ZMC) fracture with associated nasoethmoidal orbital complex fracture. This 54-year-old male sustained a blow to the face in a motorcycle crash. (A) Anteroposterior (AP) scanogram shows loss of symmetry to orbital volumes, with elliptoid enlargement of right orbit. Associated indistinctness of orbital floor and lateral maxillary sinus walls is also present. Opacification of right maxillar sinus is shown. (B) Axial computed tomography (CT) image at the level of zygomatic arches shows depression and overriding apposition of impacted zygomatic arch fracture (lateral white arrow), posterolateral maxillary sinus wall disruption (posterior arrow), and segmental comminuted fracture of anterior maxillary wall (anterior arrow). Medial to this anterior arrow is the base of the nasofrontal process of the maxilla with a fractured nasolacrimal duct just posterior to it. Internal rotation of the nasofrontal process of the maxiilla and associated fracture of the nasolacrimal duct are not portions of ZMC fracture and represent an associated nasoethmoidal orbital complex fracture. (C) Coronal CT reformations shows separation of right frontozygomatic suture (lateral and superior arrow), disruption of orbital floor (white arrow projected over orbit), and lateral maxillary wall (inferior white arrow). (D) Sagittal CT reformation shows associated vertical fracture of right ascending ramus of mandible, with anterior subluxation at temporomandibular joint (white and black arrows, respectively). (E) Three-dimensional CT reformation gives an overview of complex fracture of zygomaticomaxillary region and right mandibular fracture. It is important to note that spatial resolution is lost with threedimensional reformations, although spatial comprehension is often improved. (F) Three-dimensional CT reformation shows depression of right zygomatic arch and loss of projection of the right zygoma (flat cheek).

■ Imaging for Soft Tissue Injuries of the Neck Clinical findings for blunt injury to the aerodigestive tract include subcutaneous crepitus, hemoptysis, hoarseness, neck pain, and abrasions or hematomas (e.g., from the shoulder harness of a three-point restraint; Figs. 15-6 and 15-7). In the absence of a pneumothorax, x-ray findings that suggest injury

to the aerodigestive tract include parapharyngeal or precervical emphysema, soft tissue swelling, or fracture of the larynx or hyoid bone on the lateral image of the cervical spine. X-rays of the neck for the soft tissues, however, are superfluous as the image resolution is inferior and the imaging findings are not substantive. CT is the standard of care for imaging this area.

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FIGURE 15-6 Soft tissue neck injury. This is a 15-year-old male motorcyclist with “clothesline injury,” causing tracheal and esophageal transection. (A) Lateral view of cervical spine shows extensive subcutaneous emphysema (white arrows). Endotracheal cuff balloon is abnormally large (diameter 3 cm), compatible with soft tissue injury, abnormal airway, or tracheomalacia. In general, the presence of precervical or parapharyngeal emphysema in neck without pneumothorax should raise question of airway or digestive tract injury. (B) Axial computed tomography (CT), lung windows. Cervical tracheal disruption is shown between two short white arrows at posterior and left side of trachea. Extensive parapharyngeal and precervical emphysema is present (long arrows). (C) A different 27-year-old man sustained thyroid cartilage fracture in strangulation. Axial CT at level of thyroid cartilage, soft tissue windows. White arrow points to paramedian thyroid cartilage fracture. Thyroid cartilage fractures typically occur within 2 or 3 mm of anterior junction of the lamina of the thyroid cartilage and are thought to be due to wishbone-like spreading of thyroid cartilage as it is driven against the vertebrae. Overriding apposition of fracture fragments shortens the vocal cord on the affected side, causing hoarseness and lower voice.

B

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FIGURE 15-7 Esophageal injuries. (A) Gunshot wound in Zone II of the neck of a teenager. Barium extravasation directly enters the airway from a high laryngoesophageal fistula (circled). (B) Gunshot wound traversing Zone I into the right chest. Barium swallow shows leak on both the left side of the cervical esophagus (curved arrows) and the right thoracic esophagus (straight arrow). (C) A 27-year-old male sustained a low transverse mediastinal gunshot wound entering left, exiting right. Gastrografin esophagram shows leak into the right chest (straight right arrow) and into the peritoneal cavity (curved black arrow). A

Diagnostic and Interventional Radiology

IMAGING FOR VASCULAR INJURIES OF THE NECK Blunt carotid and vertebral injury (BCVI) (Fig. 15-8A) is now known to be much more common than previously appreciated. Vascular imaging of the neck is warranted in injury patterns associated with a high risk of blunt injury to the carotid and vertebral arteries, including the following: fracture of the cervical spine (especially involving C1–C3, involving the transverse foramina or extension into foramen magnum), neurological deficits not explained by findings at brain imaging, new-onset Horner’s syndrome, high-energy facial fractures (Le Fort II or III), fracture of the skull base involving the foramen lacerum, or soft tissue injury in the neck (neck belt sign and “hangings” sufficient to cause central anoxia).33,34 Catheter angiography is indicated emergently in patients with an expanding cervical hematoma, active extravasation from nose, mouth, or ears, or a cervical bruit in individuals younger than 50 years old.35 Angiography is the primary diagnostic tool in symptomatic BCVI because it allows for rapid utilization of endovascular therapy for bleeding and identifies patients at risk for embolic stroke.33,36 The sensitivity of duplex Doppler US is inadequately low (38.5%) for directly depicting BCVI. Therefore, CT angiography using MDCT, with a sensitivity of 90–100%, is the imaging test of choice in patients with less obvious signs of vascular injury because it allows rapid acquisition of a vascular assessment without delaying a rapid trauma workup.37–39 CT arteriography of the neck is obtained following a timing bolus performed at the C6 level using 20 mL of contrast at 3 mL and a slice thickness of 5 mm. Based on the timing bolus, the CT arteriogram of the neck is acquired. Reformations, including those that are three-dimensional, performed as multiplanar volume reformations (MPVR) with maximum-intensity projections, are obtained.

PENETRATING VASCULAR INJURIES OF THE NECK The imaging algorithm used to evaluate penetrating neck trauma is very complex. It depends on the mechanism of injury, the locations of entry and exit wounds, the hemodynamic and neurological assessment, and the likelihood of injury. Gunshot wounds may cause a blast injury involving intima, and shards and fragments of bone and metal can cause artifacts in the area that make interpreting a CT difficult. Catheter-based arteriography is advised for such wounds. When the likelihood of asymptomatic injury is low, CT arteriography may play a role in management of such patients. Location of penetration is a key driver of the imaging workup for a suspected vascular injury. Zone III, above the angle of the mandible, is difficult to assess clinically and to explore operatively. There are extensive vessels at risk, including the internal carotid artery, the external carotid artery and branches, the vertebral artery, and the accompanying veins. Thus, imaging plays a vital role in these patients. Selective internal and external carotid arteriography, vertebral

CHAPTER 15

Noncontrast MDCT of the neck to visualize the larynx requires thin-section axial imaging from the hyoid bone to the sternal notch. Images are reconstructed using both bone and standard (soft tissue) algorithms and portrayed at bone and soft tissue windows, respectively. CT is often most helpful in the evaluation of laryngotracheal injuries when deformed anatomy or extensive hemorrhage makes direct or indirect endoscopy more difficult. A careful search for open injuries (e.g., air adjacent to cartilaginous fractures) guides the need for intervention for debridement and mucosal closure. CT can assist in the grading of laryngotracheal injuries, but tends to understage compared to endoscopy or open exploration. The search should begin in the region of the valleculae and extend anteriorly along the larynx and trachea. The most common injuries are those to the thyroid cartilage. Fractures of the thyroid cartilage typically occur within 2–3 mm of the anterior crest of the two lateral laminae. Comminuted fractures of the laminae generally result from higher energy and direct impact injuries to the larynx, and are more commonly associated with thyrocricoid dislocation. Also, CT can demonstrate subluxations and dislocations of the arytenoid cartilage. Most tracheal disruptions are in the membranous portion of the trachea and will heal with conservative therapy. Soft tissue emphysema immediately adjacent to the trachea suggests an injury in this location. A search for a fracture of a tracheal ring is often fruitless unless the fracture is displaced. Coronal reformations through the trachea may show separation (vertical diastasis between tracheal rings) of the trachea compatible with more serious grades of injury. A blunt injury to the esophagus is uncommon. It generally occurs in the proximal third, especially in the cervical esophagus. On the other hand, a penetrating injury to the esophagus is more common and may involve any portion of the esophagus. A definitive diagnosis requires contrast esophagography or endoscopy or both, because neither is sufficiently accurate to exclude injuries, especially in patients who are intubated or unconscious. Barium sulfate is the contrast agent of choice for suspected esophageal injuries at or above the carina where aspiration is a concern. Water-soluble contrast media are less accurate in identifying leakage and are inflammatory when aspirated into the airway. Gastrografin should be avoided because it is hypertonic and results in pulmonary edema if aspirated into the airway. When there is concern of an injury to the distal esophagus or stomach, barium should be avoided because it can result in granulomas and peritonitis. Therefore, water-soluble contrast media should be used first when peritoneal contamination is a concern. Rapid filming is necessary. In all but the most cooperative patients, the author injects thin barium through a feeding tube or a nasogastric tube to obtain full distention of the esophagus. The patient is placed in an oblique projection with a feeding tube or nasogastric tube positioned at the region of penetration. To obtain full distention, 50 mL contrast agent is rapidly injected, during which time fluoroscopic cineradiographs are obtained at 2–3 frames/s.

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SECTION 2 A FIGURE 15-8 Blunt carotid and vertebral injury. (A) This 40-yearold lawyer complained of severe chronic unrelenting headaches. Prior history included a whiplash injury as a driver. Vertebral arteriogram shows fusiform dilatation of the vertebral artery at the level of the skull base (circled in white). This likely represents long-term effect of BCVI. A 2.8 French microcatheter was negotiated through the tortuous vertebral artery. Then coils were placed proximal and distal to the fusiform aneurysm with relief of headaches. (B) A 22-year-old man sustained a gunshot wound of Zone III of the neck and face. He was exsanguinating. Internal carotid arteriogram showed transection of the internal carotid artery high near the skull base and well above the angle of the mandible (arrow) with active oral hemorrhage (circled). The internal carotid artery was embolized with coils and patient made full neurological recovery. B

arteriography, and four-vessel intracranial arteriography all play important roles in detecting and evaluating such injuries. Indeed, arteriography is so valuable for the evaluation and treatment of bleeding in this zone that aggressive steps to resuscitate the unstable patient and control bleeding by packing are warranted to allow angiography to proceed. Most vascular injuries in Zone III are best managed by the interventional radiology service (Fig. 15-8B). Zone II, between the inferior margin of the mandible and the manubrium/clavicles, is evaluated easily by a physical examination. If the common carotid artery or the internal jugular vein require repair, operative exposure is relatively simple and unobstructed. Thus, little imaging is necessary after penetration when “hard” signs of a vascular injury (see Chapter 41) are present. Treatment of asymptomatic patients is more controversial. In Zone I, the area inferior to the manubrium/clavicles, the brachiocephalic vessels, trachea, or esophagus may be injured, and rapid exsanguination may occur. As a result, symptomatic patients may undergo urgent exploration without imaging. When patients are stable or asymptomatic, immediate angiography has great value in excluding injury, in detecting vascular injuries that can be treated nonoperatively by embolization or insertion of a stent or stent graft, and in facilitating surgical exploration. CT angiography can be considered as a screening test because it often determines trajectory and the presence of hemorrhage. Penetrating injuries to Zones I and III

of the neck are best evaluated with catheter-based imaging in the hemodynamically stable patient. CT of the neck and chest may allow analysis to determine whether penetration is in proximity to the great vessels or even whether vessels are injured. Unfortunately, artifacts are often present when bullets are adjacent to the area or the contrast medium is administered from the arm. As intimal injuries to the great vessels may be lifethreatening, these artifacts limit the usefulness of CTA in Zone I and, possibly, in Zone III.

■ Computed Tomography of the Cervical Spine In adults and older children (10 years old), validated clinical prediction rules (i.e., National Emergency X-Radiography Utilization Study Group [NEXUS] and the Canadian Cervical Spine Rule) can reliably determine those trauma victims who need imaging of the cervical spine. Another clinical prediction rule helps determine which imaging modality is most costeffective. Specifically, Blackmore et al.40 developed a clinical prediction rule to determine pre-imaging risk of fracture in select patients about to undergo a helical CT to survey the cervical spine for fracture and soft tissue injuries (Figs. 15-9 to 15-12). For the application of this clinical prediction rule, it is assumed that the patient will already be undergoing CT of the cranium. Any one of three mechanisms of injury or any one of

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C D C FIGURE 15-9 Upper cervical spine, coronal reformations from computed tomography (CT). (A) Coronal reformation of craniocervical junction CT shows pathological widening of right lateral atlantoaxial interval (double-ended arrow), widening of left occipital condyle–C1 lateral mass interval, and bony flake due to left type 1 dens fracture (long arrow). These findings are compatible with atlanto-occipital dissociation. (B) Coronal reformation of the craniocervical junction shows transverse type 2 dens fracture (white arrow). Black arrow marks tubercle on C1 for the insertion of transverse atlantal ligament. Asterisk marks osteophyte at superior margin of C1 portion of anterior atlantodens articulation, a common finding in older patients. (C) Coronal reformations in a patient who sustained high-energy trauma show type 3 dens fracture (white arrows), which is minimally distracted. (D) Coronal reformations from survey CT of cervical spine focused at craniocervical junction. Black arrow demonstrates displaced type 2 dens fracture. White arrows show a right lateral mass fracture of C1. Intra-articular (lateral mass) fractures of C1 less often have involvement of transverse atlantal ligament unlike Jefferson burst fractures, which are more commonly extra-articular or minimally intra-articular.

three clinical findings puts the patient at a pretest risk of greater than 5% of harboring an injury in the cervical spine. High-risk mechanisms of injury include the following: a high-speed motor vehicle crash 35 mph or 50 km/h combined impact, motor vehicle crash with a death at the scene, or a fall from a height of 10 ft or 3 m. Clinical parameters suggesting an increased risk for injury to the cervical spine that are associated with a high-risk mechanism include the following: a significant closed injury to the brain (or intracranial hemorrhage shown by CT of the cranium), acute neurological deficits referable to the cervical spine (acute myelopathy or radiculopathy), or either pelvic fracture or multiple extremity fractures. Hanson et al.41 validated the clinical prediction rule prospectively and showed its application by separating victims of blunt trauma into a high-risk group (12% prevalence of acute injury to the cervical spine) and a low-risk group (0.2% prevalence of injury to the cervical spine). In infants (1-year old) and younger children (9 years old) no validated rule exists. In general, patients with greater severities of injury (ISS 25) have an elevated risk of injury to the cervical spine. Conventional x-rays will depict

essentially all clinically important fractures and dislocations in patients aged 9 years and younger. CT is not indicated in younger children and infants to screen the cervical spine, nor in search for other occult injuries causing neurological deficits.42,43 CT should be reserved as a staging/treatment planning procedure among patients with a known bony abnormality. Axial slices of thickness of 1.25–3.0 mm are obtained from the skull base through the T4 vertebral body. Images are typically reconstructed at half the slice thickness interval for creation of parasagittal and coronal reformations. Reformations are typically contiguous 2.5- to 3.0-mm thick images and can be reconstructed using either a bone or soft tissue algorithm, but evaluated using bone windows. Generally, the information gathered from these reformations is sufficient and makes plain x-rays unnecessary. Since helical CT produces large numbers of axial images, the review of the examination is substantially facilitated by use of picture archiving and communication systems (PACS) workstations and the so-called scroll functions. In addition, use of cross-referencing tools on the PACS workstation facilitates identification of specific vertebral levels.

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FIGURE 15-10 Upper cervical spine, sagittal reformations from computed tomography (CT). (A) Left parasagittal CT reformation. This 3-year-old was run over by a trailer. The upper, long, white arrow shows a vertically and coronally oriented fracture of occipital condyle. The two lower arrows show superior articular surface of C1 lateral mass, with anterior subluxation of head. (B) Midline sagittal reformation shows hyperextension teardrop fracture at C2 (white arrows) in a 20-year-old man. (C) Midline sagittal CT reformation shows a combination of anterior subluxation of C2 relative to C3 (white arrow), as well as posterior displacement of lamina of C2 relative to C1–C3 line as manifestation of hyperextension hangman’s fracture of C2. (D) Sagittal mid-plane CT reformation shows diastasis of type 2 dens fracture (double-ended arrow). Distraction of >3 mm is commonly associated with disruption of anterior and posterior longitudinal ligaments.

In many ways, the coronal reformations may be viewed using the same approach as standard frontal x-rays such as the open mouth views of the craniocervical junction and the AP view of the cervical spine, while viewing of the sagittal reformations can be performed with guidelines used for the lateral cervical spine. Particular attention in parasagittal images to the alignment at C0–C1 will avoid missing a subtle incongruity of this typically perfectly matched joint, a finding suggestive of atlanto-occipital instability. Similarly, careful evaluation of sagittal reformations will avoid oversight of “in-plane” (axial

plane) fractures, such as type II fractures of the dens and fractures of the horizontal spinous process/lamina. Nonetheless, careful attention to axial images is necessary to detect fractures involving the craniocervical junction,44 transverse processes (potential vertebral artery injury), margins of vertebral bodies, pedicles, lateral mass, or lamina and spinous processes. The sensitivity of this survey CT for acute bony injuries to the cervical spine is above 95% with specificity around 95%. Although CT does not directly show soft tissue injuries to the spine, focal kyphosis, focal lordosis, and widening of the disk

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FIGURE 15-11 Lower cervical spine, sagittal reformations from computed tomography (CT). (A) This 84-year-old woman sustained C5 hyperextension injury in a fall. Lateral cervical spine shows extensive spondylosis but no obvious fracture to vertebral bodies. However, white Xs mark laminar points and show definite retrolisthesis of C5 on C6. Careful attention to laminae, particularly in the elderly, is good practice in detecting translational abnormalities. (B) Same patient as in (A). Sagittal reformation in midline from CT shows complex fracture of C6 with marked neurocanal narrowing at C5 body–C6 laminar level. Disruption of flowing osteophytosis of anterior longitudinal ligament (ALL), seen in diffuse idiopathic skeletal hyperostosis, should be presumed grossly unstable. Extent of anterior, appositional osteophytes is marked by “W” and is fairly typical of diffuse idiopathic skeletal hyperostosis. (C) Midline sagittal CT reformation shows flexion teardrop fracture of C6 in a 79-year-old man. Mechanistic classification of these fractures is based on relation of height relative to width of avulsed fragment (H and W). Teardrop fracture (black arrow) separates anterior inferior corner of C6 vertebral body from its corpus. In this case, H is greater than W, compatible with hyperflexion injury. In lower cervical spine, hyperextension injuries tend to have greater width than height of their corner fragments and can be from anteroinferior or anterosuperior corner. Note this relation is different at C2, where hyperextension fragments typically have greater height than width, due to peculiar shape of anteroinferior corner of C2. (D) Parasagittal CT reformation shows oblique corner fracture through the C7 lateral mass, with anterior and inferior displacement of C6 lateral mass relative to inferior cervical spine (white arrow).

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FIGURE 15-12 Multimodality correlations: cervical spine. A patient with C6-7 fracture dislocation underwent pre-reduction lateral conventional radiograph (A), post-reduction sagittal reformation (B) from axial computed tomography (CT), and MRI of the spine and cord (C) and (D). (A) White Xs mark laminar points and connecting them shows disruption of spinolaminar line at C6–C7. Arrow points to fractures of inferior articular process of C6. Sagittal CT reformation (B) shows improved alignment of vertebral bodies but persistent encroachment of neural canal from bony fragments from body and posterior elements (arrow). (C and D) Sagittal magnetic resonance imaging performed using short tau inversion recovery (STIR) and gradient recalled echo (GRE) sequences following reduction of C6–C7 fracture dislocation. Single asterisk shows precervical edema and double asterisk edema in posterior spinal musculature. Long white arrow shows a region of cord swelling with heterogeneous signal, suggesting cord transection at C6 level. Short arrow shows abnormal signal within C6–C7 disk space. GRE sequences (D) show decreased signal at C6 level within the center of the cord that is compatible with hemorrhage (white square), which portends poorer neurological prognosis than edema alone.

Diagnostic and Interventional Radiology

■ Conventional X-Rays of the Spine Clinical decision rules and expert recommendations provide guidelines as to who does not require an image survey of the cervical spine.46-49 Basically, oriented asymptomatic individuals without findings on a physical examination following trauma do not require subsequent imaging. Imaging of the thoracic and lumbar spine following blunt trauma is indicated when patients present with one or more of the following: (1) signs or symptoms of local injury (pain, tenderness, interspinous stepoff ); (2) depressed level of consciousness, including intoxication; (3) acute myelopathy or radiculopathy referable to the thoracolumbar spine; and (4) major distracting injury, including concomitant injuries to the cervical spine.50,51 Given the differences in the incidence of injury to the cervical spine in children and the differences in their distribution (far more common in the upper cervical spine) relative to adults, an examination limited to frontal and lateral views is acceptable.52 In infants 0–4 years of age and in children 5–9 years of age, AP, lateral, and open mouth views are satisfactory. All patients aged 10 and over require a minimum of three views to as many as five or six views to adequately survey the cervical spine. The minimum views include an AP view of the craniocervical junction (open mouth view), an AP view of the subdental cervical spine, and a lateral view of the cervical spine that extends down to the C7–T1 interspace. To supplement these three views, bilateral trauma oblique views and a swimmer’s lateral are often used. These views of the lower cervical spine including the cervicothoracic junction are intended to be more conclusive, but are of limited resolution. Trauma oblique views are obtained without moving the patient. The imaging cassette is placed on the surface of the table or gurney on which the patient is lying and positioned such that its leading edge is near the patient’s midline and its inferior edge is beneath a portion of the patient’s shoulder girdle. The x-ray beam is angled at 45° to the plate with the central beam centered on the anterior aspect of the patient’s neck, with approximately 10–15° of cranial angulation. Trauma oblique projections obtained in this fashion show the posterior elements and the end plates of the vertebral body. Films of the thoracic and lumbar spine are usually obtained as separate sets of frontal and lateral projections. The upper thoracic spine may require the addition of a swimmer’s lateral view, if one has not been previously obtained as part of a cervical spine series, to show the cervicothoracic junction and upper thoracic spine. In general, if pathology is identified, the authors recommend “coned” views of the affected vertebral body. This represents more collimated images centered on the level of abnormality. When examinations of the cervical or thoracic spine are technically inadequate, it is almost always due to the inability to adequately visualize the cervicothoracic junction and the upper thoracic spine. Swimmer’s lateral views are generally

obtained with one arm elevated above the head and the other arm in caudal traction. Obviously, when there are fractures of the upper extremity, it may be either difficult or impossible to humanely obtain such studies in a conscious patient. It is possible for experienced observers to substitute carefully evaluated trauma oblique views for swimmer’s views; however, most centers would use CT in a targeted fashion when the conventional x-rays are inadequate to view this area. To reinforce the point, it is necessary to see the top of T1 on the cervical spine and the bottom of C7 on radiographs of the thoracic spine. One of the common errors made in evaluating the cervical spine is mistaking developmental variations for pathology (Fig. 15-11). Common variations at the craniocervical junction include the following: fusion of C1 to the occiput, which may be partial or complete; failure of fusion or development of the posterior elements of C1; pseudospreading of C1 relative to C2, which may mimic Jefferson burst fractures (most common in the 0- to 4-year age range, but may be seen up through puberty); pseudosubluxation of C2 on C3 in pediatric patients, which can be recognized as normal by a normal C1–C3 spinolaminar line; and os odontoideum (an anomalous bone that replaces all or part of the dens axis and is not attached to the atlas). In the thoracic and lumbar spine, the authors recommend a careful count of the vertebral bodies on the frontal examination to establish the correct levels, based on the number of ribbearing (thoracic) and non-rib-bearing (lumbar) vertebrae. On the lateral view, it is important to look at the corners of the vertebral bodies, especially the anterior superior corner, which is affected in approximately 90% of all vertebral body fractures. On the frontal view, it is most important to evaluate the adjacent end plates for continuity, the lateral margins of the vertebrae, the posterior elements for pathological interspinous and interpediculate widening, and horizontal lucencies that would suggest horizontal soft tissue and/or osseous disruption of a flexion-distraction-type injury. Once an abnormality is identified on conventional x-rays, CT and/or MRI may be used to further characterize the injury for planning of treatment and provide information on the patient’s prognosis.

■ Computed Tomography of the Thoracolumbar Spine Among patients undergoing CT of the chest and/or abdomen, a review of axial images in bone algorithm and bone windows, sagittal reformations, or lateral and AP scanograms (topograms) may be used in lieu of conventional x-rays to study the thoracic and lumbar spine.53 Liberal use of CT for the further evaluation of vertebral body deformities that are thought to be related to trauma based on conventional x-rays is highly recommended. In addition, patients with high-risk mechanisms and impressive signs or symptoms without abnormal x-rays (e.g., a palpable step-off suggesting disruption of the posterior elements) should undergo a thoracolumbar CT to detect occult minimal burst fractures or Chance or flexion-distraction-type injuries. A 2.5–3.0-mm axial slice thickness is used to acquire images from two vertebral body levels above an abnormality through two vertebral body levels below. Images are reconstructed using

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space can be used as with conventional x-rays to suggest associated injuries to soft tissue. Some authors feel that clinically important injuries to soft tissue causing biomechanical instability are almost always evident on technically adequate CTs of the cervical spine (especially on the sagittal and parasagittal reformations).45

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both bone and soft tissue algorithms; however, acquisition of the entire thoracic or lumbar spine is advised as it allows more accurate determination of the location of injury. Sagittal reformations are made in both algorithms and viewed at bone and soft tissue windows, respectively. In the thoracic or lumbar spine, it is important to have some reference to the scanogram or to the reformations to allow accurate assessment of the vertebral levels imaged. In addition to careful evaluation of the vertebral elements, some attention should be paid to possible injuries to ribs, aorta, sternomanubrial junction, and the kidneys. If flexion-distraction or Chance fractures are detected, careful attention should be directed to the abdominal aorta, bowel, and retroperitoneal structures, including the ureteropelvic junction.

■ Magnetic Resonance Imaging of the Spine The principal indications for MRI are to characterize soft tissue injuries associated with fractures and luxations of vertebral bodies and to assess the neural elements (Fig. 15-12). An MRI is indicated in individuals who have no conventional x-rays or CT abnormality, but who have an acute myelopathy or radiculopathy (spinal cord injury without radiographic abnormality [SCIWORA]). The use of MRI is frequently controversial in the setting of dislocation of bilateral or unilateral facets (see Chapter 23). Some advocate initial reduction followed by MRI, but this is a practice that varies from institution to institution. In general, urgent MRI is appropriate when there is an evolving neurological deficit or neurological deficits without explanation. Edema of the spinal cord has a much better prognosis than hemorrhage into the cord, and MRI in the subacute setting can

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help make this distinction, as well as detect epidural hematomas that may require decompression. Evaluations of the disk spaces, ligaments, and facet joints, including the cranio-occipital articulation, are best made with MRI. Sagittal and axial T1-weighted and fluid-sensitive sequences (e.g., T2-weighted STIR) are standard. Gradient echo sequences are useful in detecting an artifact of magnetic susceptibility, a finding in the acute and subacute setting that allows more reliable assignment of a fluid collection to being blood. When assessing the transverse atlantal ligament, images should be obtained in the axial plane parallel to Ranawat’s line (a line from the anteriormost portion of the anterior tubercle of C1 to the most posterior aspect of the posterior arch of C1). MRIs have been used to “clear” the cervical spine in obtunded or unexaminable patients with otherwise normal imaging (CT or high-quality conventional radiographs).54,55 The absence of abnormal high signal intensity in ligaments and discs effectively excludes biomechanically significant injuries; however, an abnormal signal does not imply instability. At this time, MRI has not been shown to accurately grade injuries to the posterior longitudinal ligament (PLL) or anterior longitudinal ligament (ALL).

■ Flexion and Extension X-Rays of the Cervical Spine Among individuals who are completely alert and who have normal x-rays and tenderness at the posterior midline, flexion and extension radiographs may be used to assess ligamentous stability (Fig. 15-13). Some centers have recommended the use of passive (guided by the physician) flexion and extension studies using fluoroscopy. While this may be appropriate in very

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FIGURE 15-13 Flexion–extension radiograph: cervical spine showing subtle instability at C2–C3. This 24-year-old male bicyclist was struck by a car from behind and posterior midline tenderness of upper cervical spine was palpated. (A) Upright lateral out-of-collar radiograph shows loss of usual cervical lordosis without focal kyphosis or translation. Precervical soft tissues are normal. (B) Upright lateral flexion radiograph of cervical spine shows no gross interspinous widening or loss of parallelism of facet joint. Reference lines are drawn from posteroinferior corner of C3 to most inferior aspect of C3 spinous process. Perpendicular to that line from posteroinferior corner, a line is used as a reference for translation of C2 relative of C3, as demonstrated by double-arrowed line. (C) Upright lateral extension radiograph of cervical spine again shows no gross widening of anterior disk space. Using same reference for translation of C2 on C3, 2.5 mm of difference at C2–C3 disk space is demonstrated between flexion and extension, compatible with partial, dynamic instability.

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■ Computed Tomography of the Chest Chest CT is generally performed to evaluate adult victims of high-energy blunt trauma (especially those with chest pain, deformity, or hypoxia),56 with particular attention to the mediastinal contents (Figs. 15-14 to 15-18). Children presenting with hypotension, elevated respiratory rate, abnormal physical examination, depressed consciousness, and femur fractures after blunt trauma are at a substantially increased risk for an intrathoracic injury.57 In this setting, CT provides significant information about the lungs, pleural cavities, and chest wall. Indications for evaluating the mediastinum are principally to exclude injury to the intrathoracic aorta and great vessels (sensitivity 97–99%58). The role of MDCT in the diagnosis of acute traumatic aortic injury has been evolving, and it is believed to be most cost-effective in the following circumstances: when patients are already undergoing another CT examination (e.g., CT of the head, abdomen, and pelvis); are at risk for injury to the thoracic aorta because of high-energy mechanism, associated injuries, or age (50 years old); or have a previously abnormal study (chest x-ray). A decision rule has been proposed by Blackmore et al.59 in which individuals with two or more of the following are at high risk for aortic injury: age 50, unrestrained occupant in motor vehicle crash, hypotension, thoracic injury (rib fracture, pneumothorax, pulmonary contusion, or laceration), abdominopelvic injury (fracture of lumbar spine or pelvic ring, injury requiring laparotomy), fractures of appendicular skeleton, or injury to the brain. Axial images are obtained with a slice thickness of 2.5 mm from the thoracic inlet to at least the bifurcation of the abdominal aorta and through the perineum if there is a known fracture of the pelvic ring. The 2.5-mm images are reconstructed at 1.25-mm intervals for the purposes of developing the

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FIGURE 15-14 (A–C) Blunt traumatic rupture of the thoracic aorta in a 47-year-old driver. (A) Noncontrast CT of the chest showed evidence of periaortic hemorrhage (white circles). (B) Axial CTA of the chest clearly shows disruption of the descending aorta at the aortic isthmus (arrow). (C) Catheter aortography adds little in this case: increased opacity at the area just distal to the left subclavian origin may represent contrast extravasation posteriorly.

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limited circumstances in the hands of physicians of considerable experience, the published data are not sufficiently strong to warrant generalization. A qualified physician should be in attendance if the examination is performed shortly after injury (hours vs. days), and the patient needs to be completely alert and able to assume an upright posture and precisely follow commands. An initial x-ray is obtained with the patient upright and with the cervical spine in a neutral position. This examination is reviewed by the physician overseeing the examination. If this examination is normal, the patient is asked to actively extend to the maximum and an x-ray is obtained. The patient’s cervical spine is then returned to a neutral position. This extension x-ray is evaluated in a manner similar to that taken with the cervical spine in a neutral position. If normal, the examination is repeated with maximum effort at flexion, and an x-ray is obtained. Standards for an adequate examination vary from a range of motion of 30° to 90°. The test is intended to study the capacity of the spine to resist physiological stresses, however, and the mean normal range of motion in adults is approximately 90°. If the patient’s midline tenderness is in the upper or mid-cervical spine, it is not critical to see the C7–T1 interspace. If the discomfort is in the lower cervical spine or more diffuse, the entire area of abnormality needs to be visualized. Evaluation of cranio-occipital stability by conventional x-rays is based on the detection of translation and distraction between the basion and the cervical spine. If the flexion– extension x-rays are abnormal in the acute or subacute setting, MRI is pursued. If the examination does not show an adequate range of motion, the patient’s spine is immobilized (hard collar) and the examination is repeated in 2 weeks (if the patient remains symptomatic).

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FIGURE 15-15 (A–C) Aortic injury. Subtle CTA and obvious catheter aortogram. A 71-year-old male was involved in a high-speed crash. (A) Composite of CTA shows relatively subtle extravasation from descending aorta (arrows). (B) Catheter aortography shows medial and lateral bulges (arrows). (C) This injury was treated by stent graft. C

multiplanar volume-rendered reformations and three-dimensional reformations useful for portraying the anatomy of the aorta and great vessels. Reconstructing the images at 5 and 2.5 mm can be used for evaluating the chest and abdomen, and thoracolumbar spine, respectively, at bone and soft tissue algorithms and windows. In patients unable to receive contrast, noncontrast CT can be effective in detecting a mediastinal hematoma (Fig. 15-17A) and guiding the patient to evaluations such as transesophageal echocardiography, magnetic resonance angiography, etc. CT is generally the most cost-effective survey study for patients at modest to moderate risk for injury to the thoracic aorta. The role of CT aortography is evolving, and this technique has mostly replaced that previously held by catheter angiography. Findings on CT can be divided into direct and

indirect. Direct findings are visualization of pseudoaneurysms, intimal flaps, and pseudocoarctation (due to subadventitial dissection). A mediastinal hematoma, however, is an indirect finding. To suggest an aortic injury, a mediastinal hematoma should be contiguous with the aortic wall and should not be separated from the aorta by a rim of fat (Fig. 15-17B). Thus, in very thin patients or in patients with extensive edema and pleural or parenchymal opacification, determination of whether or not a mediastinal hematoma has obliterated juxtaaortic fat can be difficult. Complex atheromatous disease can make interpretation of the examination difficult, particularly for more subtle injuries. Finally, artifacts of the technique, including aortic pulsations and beam hardening due to dense contrast in adjacent venous structures, may make interpretation difficult.

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FIGURE 15-16 (A–E) Gunshot injury of the aortic arch not detected on catheter aortography. A 24-year-old male sustained a gunshot wound of the back with mediastinal traverse. He was hemodynamically stable but paraplegic. (A) Portable chest radiography showed hemothorax and a very wide indistinct mediastinum with a bullet in the mediastinum. (B and C) Right and left anteroposterior catheter aortograms did not show any evidence of an injury. (D) However, suspicion of an aortic injury persisted. Therefore, a CT arteriogram was performed. This shows that the bullet had traversed the spine and fragmented into parts that went to the right and the left (dashed arrows). The left fragments penetrated the posterior arch and exited the anterior arch of the aorta (arrows). (E) Surface-rendered reformations clearly show the path of the bullet. E

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FIGURE 15-17 Mediastinal hematoma caused by nonaortic injury. (A) This 75-year-old man was injured in high-speed motor vehicle crash with sternal fracture. Anteroposterior (AP) recumbent chest shows widening of right paratracheal stripe (H), with maintenance of normal para-aortic arch and aortopulmonary window (#1 and 2, respectively). (B) Same patient as in (A), axial computed tomography (CT) shows anterior mediastinal hematoma (asterisk). Note maintenance of normal fat surrounding descending aorta (arrow). (C) AP chest radiograph performed on 19-year-old unrestrained driver in head-on motor vehicle crash shows multiple injuries, including T6 and left shoulder fractures. Widening of right paratracheal stripe (H), obscuration of aortic arch (black arrow), and abnormal right paraspinal line (white arrows) suggest mediastinal hematoma. In absence of osteophytes, right paratracheal stripes are not typically seen in young adults and their presence locally should direct search for underlying pathology. Left paraspinal line is typically seen due to descending aorta and should not be seen as continuous line between the lower chest and the apex of lung. Continuous left paraspinal line from apex to diaphragm is pathognomonic for mediastinal collection, such as hematoma in setting of trauma. (D) Same patient as in (C); axial CT following intravenous contrast shows extensive posterior mediastinal hematoma (asterisks). Note inset showing sagittal plane translational fracture-dislocation of T6.

It is particularly important in the presence of an abnormal examination to delineate the anatomy of interest to the trauma surgeon, such as the distance from the most proximal point of injury to the takeoff of the left subclavian artery or any anomalous branches. This information is readily provided by CT, particularly with three-dimensional and multiplanar reformations. These capabilities have begun to alter the role of angiography from its traditional role of diagnosis, staging, and pretreatment planning to one more often used for resolving diagnostic conun-

drums raised by CT or transesophageal echocardiography, or as part of treatment (e.g., placement of aortic stent grafts). CT is the most sensitive diagnostic method for detection of acute blood in the pericardium.60 It is also among the most sensitive methods for detection of injuries to the chest wall, pleural cavities, or lungs. It is less sensitive in the detection of injuries to the hemidiaphragm (sensitivity is 65–70%) or the tracheobronchial tree. For suspected diaphragmatic injuries, especially herniations through a diaphragmatic tear, coronal

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FIGURE 15-18 Pulmonary contusion (A and B) and laceration (C and D) due to blunt-force injury. (A) This 22-year-old woman was in a high-speed motor vehicle crash. Anteroposterior (AP) recumbent chest shows peripheral nonanatomic patchy opacity (bracketed arrows). Pulmonary contusions are typically present by the time patient presents to the hospital and may evolve for 48–72 hours. Progression thereafter should be considered a complication, such as pneumonia or adult respiratory distress syndrome. Typically, pulmonary contusions resolve within 1 week. (B) Same patient as in (A); contrast-enhanced axial CT shows subpleural location of patchy opacities compatible with contusion against rib cage (arrows). Atelectasis is seen in right posterior hemithorax. (C) This 22-year-old male passenger was involved in a side-impact crash with significant intrusion into passenger compartment. AP recumbent chest shows extensive pulmonary opacities, with mixed lucency seen in left mid-lung (arrow) and multiple displaced rib fractures (arrowheads). Mediastinal contours are also abnormal with obscuration of aortic arch, aortopulmonary window, and widening of right paratracheal stripe. (D) Contrast-enhanced axial computed tomography in same patient as (C) shows large anterior pneumothorax (asterisk), dense opacification throughout left lung compatible with contusions, and air-fluid level within cystic structure compatible with lacerations (arrow). Post-traumatic pulmonary opacities associated with pneumothorax should properly be called lacerations.

and sagittal multiplanar reformations are useful, as they better display characteristic findings.

■ Computed Tomography of Abdomen and Pelvis Abdominopelvic CT is one of many adjunctive tests to assist the trauma surgeon in the evaluation of otherwise occult intraabdominal injury or to aid in characterization of injuries previously detected by other diagnostic tests (e.g., DPL or FAST;

Figs. 15-19 to 15-24). Usual indications include abdominal signs (e.g., lap belt sign) or symptoms (e.g., pain and tenderness) following high-energy trauma. The combination of left costal margin and pleuritic chest pain is an independent predictor of splenic injury and warrants diagnostic evaluation.61 Among patients with distracting injuries (e.g., femur or pelvic ring fractures), physical examination may lead to an underdiagnosis of surgically important intra-abdominal injuries in up to 15%. In addition, abdominopelvic CT is the principal means of both detection and characterization of renal injuries

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FIGURE 15-19 (A–C) Three examples of diaphragmatic rupture seen on three modalities. (A) Portable chest film on admission demonstrates an elevated left hemidiaphragm. There is compression of the gastric air in the fundus, consistent with compression as the stomach traverses the diaphragm. (B) Upper gastrointestinal imaging demonstrates a narrow area of barium entering the chest. Note again the compression. (C) Scout film after embolization of a ruptured spleen shows similar compression of the gastric shadow as seen in (A). Patient was explored, the hernia reduced, and the diaphragm repaired. A Grade IV nonbleeding lacerated spleen was left undisturbed. C

among adults with gross hematuria, children with microscopic hematuria (50 red blood cell count per high-power field), or microscopic hematuria among adults who have had one or more episodes of systolic hypotension. Indications for CT cystography include hematuria and fracture of either the pelvic ring or acetabulum or hematuria and free intraperitoneal fluid. In the absence of hematuria, cystography is not necessary. A “dual-phase” intravenous contrast-enhanced study is used to acquire 5-mm slice thickness from the lower chest to the bifurcation of the abdominal aorta during the mid-portal venous phase and from the iliac crest to the perineum following a brief delay to avoid “outrunning” the intravenous bolus and to allow opacification of the distal ureters. Images are reconstructed using a standard algorithm and viewed at soft tissue and bone windows. In those patients whose arterial or parenchymal phase images demonstrate a renal injury, a series of images through the upper urinary tract is repeated after a 10-minute delay using 5-mm slice thickness to detect and quantify the extravasation of urine. CT cystography typically is performed prior to the administration of intravenous contrast (Fig. 15-25). Two techniques are applicable. The first utilizes the CT scanograms in the frontal

and lateral views as “scout films.” The bladder is then distended with 400 mL of 30% contrast media after which frontal and lateral scanograms are repeated looking for extravasation. If none is seen, the bladder is emptied and additional frontal and lateral scanogram images are performed to look for subtle leakage. In the second method, 100 mL of 5% iodinated contrast is instilled. If this shows no extravasation, additional contrast is instilled into the urinary bladder until 40 cm of water pressure is achieved and 2.5-mm axial images are obtained through the bony pelvis. No postdrainage scanning is obtained. Images are reconstructed using a soft tissue algorithm and reviewed at soft tissue and bone windows. This author prefers the first method as evacuation of the contrast before axial imaging enables better detection of subtle pelvic intraperitoneal hemorrhage. The arterial-weighted parenchymal phase images are particularly useful for the detection of extravasation, especially if a pseudoaneurysm or arteriovenous fistula is present. Extravasation of venous contrast is seen in 5–10% of victims of high-energy blunt trauma. Splenic hemorrhage is the most commonly appreciated area of isolated extravasation; however, fractures of the pelvic ring are most commonly associated with multiple sites of extravasation.62 The amount of hematoma associated with disruptions of the pelvic ring directly correlates with the

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FIGURE 15-20 Examples of contrast extravasation in the abdomen. (A) Laceration of the left lobe of the liver with arterial extravasation exiting the liver and spreading in the peritoneum. Note that the extravasation is as dense as the aorta and denser than the stomach. This enables differentiation of GI contrast and vascular contrast. Sometimes a bone “window” allows better discrimination by widening the gray scale. (B) Extravasation posterior to the stomach (arrow) in the lesser sac represents GI extravasation from the duodenum at the ligament of Treitz. (C) Extravasation mixed with air indicated bowel perforation. (D) Extravasation (black arrow) adjacent to thick-walled (white dots) colon indicates colonic perforation by gunshot wound. (E) Contrast extravasated within the perinephric space indicates urinary leakage. (F) Extravasation in the mesentery is of similar density to the aorta and vena cava. It represents a mesenteric tear with active bleeding.

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FIGURE 15-21 Patterns of injury: “the central package.” This 54-year-old male motorcyclist sustained multiple injuries, including laceration of horseshoe kidney, duodenal contusion, bladder rupture, and anteroposterior (AP) compression fracture of pelvic ring. (A) AP radiograph of pelvis. Greater than 2.5 cm diastasis of pubic symphysis is compatible with disruption of sacrospinous, sacrotuberous, and anterior capsular ligaments of sacroiliac joints. Appearance supports AP compression mechanism and is associated with increased risk for intra-abdominal, intrathoracic, and head injuries. (B) Axial computed tomography (CT) abdomen at L3–L4 level in the arterial phase. White arrow shows median fracture of horseshoe kidney with posterior perinephric hematoma (asterisks). This is arterial phase image because there is dense opacification of aorta directly posterior to neck of horseshoe kidney without opacification of the inferior vena cava immediately to its right. Arterial phase images best demonstrate active extravasation and pseudoaneurysms. (C) Axial CT at level of third portion of duodenum shows paraduodenal hematoma (asterisk), suggestive of duodenal injury. (D) Axial CT at level of right acetabulum shows widening of symphysis and extraperitoneal bladder laceration as contrast in anterior abdominal wall (asterisk). Posterior wall of bladder is irregular with double densities within urine contrast compatible with hematoma (arrowheads).

likelihood of an angiographically demonstrable arterial injury (200 cm3, 5% arterial injury; more than 500 cm3, approximately 50% arterial injury)63 (Figs. 15-30 and 15-31). Nonetheless, otherwise unexplained continued hemodynamic instability in patients with blunt pelvic fractures warrants angiographic evaluation, even if the initial CT showed no extraperitoneal hematoma (Figs. 15-26 and 15-27).64 Regarding splenic (Fig. 15-28) and hepatic lacerations, detection of extravasation is a more powerful guide to the

need of intervention than is grading of the organ injury. The detection of lacerations that extend to the hepatic veins is of particular importance in the liver, as these have a strong predictive value for failure of nonoperative management when associated with large (10 cm) hypoperfused regions.65 Adrenal hemorrhage is relatively common, particularly on the right. In general, it is not of clinical importance unless bilateral, and even then, post-traumatic hypoadrenalism is rare.

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FIGURE 15-22 Patterns of injury: “the left package.” This 22-year-old male driver was injured in a side-impact crash with substantial intrusion to driver’s side of car. Multiple injuries sustained. (A) Anteroposterior (AP) scanogram from computed tomography (CT) of chest, abdomen, and pelvis shows extensive opacity of left mid- and lower lung fields compatible with contusion, a deep sulcus (arrow) at left costophrenic angle compatible with left pneumothorax, and multiple left-sided rib fractures (arrowhead). Patient is intubated, and there is right upper lobe collapse. (B) Axial CT of upper abdomen during parenchymal phase shows injury of the anterior portion of left kidney (medial arrow) and splenic laceration with sentinel clot (black and white arrows, respectively). Although rib fractures are not shown on current image, subcutaneous emphysema in left chest wall and distal extent of small pneumothorax are shown. (C) Oblique sagittal reformation from CT aortography shows complex segmental intimal injury to proximal descending aorta in the typical location (arrows) and pseudoaneurysm formation due to acute traumatic aortic injury. Air-fluid levels (arrowheads) are compatible with pulmonary lacerations.

CT is relatively insensitive to the detection of isolated injury to the bowel. Findings may include thickened bowel wall, asymmetric mural enhancement, and free fluid not explained by other injuries (Figs. 15-29 and 15-30). Nonetheless, when interloop fluid is present, this is very suspicious for a transmural injury to the bowel even in the presence of injury to a solid organ and even

immediately following DPL (Fig. 15-20F). One note of caution regarding free intraperitoneal fluid is that women of childbearing age have small amounts of fluid (50 mL) in their pelvis. Patients who have been vigorously resuscitated (especially if they are 24 hours from their injury) may have ascites and interloop fluid present due to a capillary leak syndrome. Acute and

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FIGURE 15-23 Patterns of injury: “The right package.” This 22-year-old unrestrained passenger was ejected from car in sideimpact high-speed crash. (A) Anteroposterior (AP) view of pelvis shows bilateral iliopubic and ischiopubic ramus fractures (white arrows) and disruption of right sacral arcuate lines (arrowheads); findings are compatible with lateral compression fracture due to right lateral impact. (B) Axial contrast-enhanced abdominal CT shows free intraperitoneal fluid (asterisks) due to complex collection of liver lacerations (arrow) extending to the intrahepatic inferior vena cava. The relatively uniform enhancement of hepatic parenchyma suggests that the hepatic veins are not occluded. (C) Axial computed tomography through S1, bone windows, shows through-and-through fracture of S1 ala, which traverses S1 neuroforamina (white arrows). Such through-and-through fractures are typically associated with biomechanical instability. C

subacute hemorrhage typically measures 40–70 Hounsfield units (H), while urine, bowel contents, and ascites measure closer to water (e.g., 0–30 H). CT performs slightly better at detection of diaphragmatic ruptures than conventional x-rays, with a sensitivity of 60%. A normal contour of the diaphragm and no pleural collections or adjacent airspace disease effectively exclude injury to the diaphragm. Another pitfall in the search for diaphragmatic injuries is the increasing prevalence of fibrous replacement of diaphragmatic muscle among older (65 years old) individuals, which may mimic the so-called discontinuous diaphragm sign of a ruptured diaphragm.66,67

■ Computed Tomography of the Pelvis and Acetabulum CT is generally indicated for unstable fractures of the pelvic ring, as determined by physical examination or appearances on conventional x-rays (simultaneous anterior and posterior displacement of fractured pelvic ring) (Figs. 15-31 to 15-35). Acetabular CT is indicated following reduction of hip dislocations

to detect entrapped intra-articular debris and for the evaluation of unstable fractures. Finally, individuals who sustain bilateral sacral fractures benefit from a sacral CT obtained with coronal imaging of S1–S3 and sagittal reformations. The general goal of imaging for unstable fractures of the pelvic ring and acetabulum is to aid in surgical planning. CT scans of acetabular fractures are performed for the assessment of fracture types,68 secondary congruence of the hip (e.g., are the fracture fragments symmetrically oriented about the intact femoral head?), evidence for marginal impaction (e.g., subarticular bone depressed or impacted, and not showing secondary congruence), detection of a fracture of the femoral head, and detecting intra-articular debris. There is approximately a 15% concurrent rate for fractures of the pelvic ring and acetabulum. CT of the pelvis typically uses a slice thickness of 2.5–5 mm in the axial plane from the level of the L5 transverse processes to the ischia. Images are reconstructed using a bone algorithm and reviewed at bone and soft tissue windows. If using an MDCT scanner, 5-mm thicknesses can be obtained by coupling two contiguous 2.5-mm channels and thus allow scanning of the

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FIGURE 15-24 Grade IV renal laceration. This 14-year-old sustained an injury in a fall from a dirt bicycle while jumping. (A) Contrastenhanced axial CT scan, soft tissue windows, performed in parenchymal phase shows perinephric hematoma on left (asterisk) adjacent to laceration that extends into renal hilum (arrows). Right kidney shows normal pyelographic phase. Free intra-abdominal fluid is due to Grade III splenic laceration (not shown). (B) Contrast-enhanced axial computed tomography (CT) obtained in arterial phase shows wedge-shaped defect in left kidney (arrowheads) compatible with laceration and infarct extending to capsule secondary to segmental arterial occlusion. (C) Contrast-enhanced axial CT at level of kidneys shows thrombus within collecting system (black arrows), perinephric hematoma, and contusion of posterior aspect of kidney, just below laceration seen on image (A). Perinephric hematoma surrounds kidney. (D) In such complicated cases, delayed images (10 minutes) are highly valuable in assessing associated urinary leakage. Ten-minute delayed images show a type III extravasation of contrast-enhanced urine from anterior and medial pole of kidney into the perinephric space (black arrow). Striated nephrogram is present posteriorly (white arrow), compatible with contusion adjacent to laceration.

acetabulum without additional radiation. Similarly, 2.5-mm slice thicknesses obtained from multidetector scanning may be reconstructed at 1.25-mm intervals when bilateral sacral fractures are present to obtain oblique coronal (in plane of S1–S3 sacral promontory) and sagittal reformations of diagnostic quality. Acetabular CTs are usually performed using a slice thickness of 2.5–3.0 mm in the axial plane through the acetabulae, with 5-mm slick thickness in the remainder of the bony pelvis. Occasionally, sagittal and coronal reformations may be helpful in better depicting anatomy. In assessing CT for a disruption of the pelvic ring, it is important to correlate with at least an AP x-ray of the pelvis. A top to bottom, posterior to anterior approach of reviewing

images is recommended, such that the review is initiated at the level of L5 looking for avulsions of the transverse processes due to the iliolumbar ligament and the posterior superior iliac spine due to the strong posterior sacroiliac ligaments. The sacroiliac joints are subsequently assessed for their side-to-side symmetry and integrity of their subchondral white lines. The anterior surface of the sacrum is carefully evaluated for “buckle” fractures due to internal rotation of the hemipelvis as seen with the most common fracture mechanism, internal rotation of the hemipelvis due to a lateral impact (lateral compression mechanism). Fractures of the sacrum are assessed relative to the neural canals, particularly at S1 and S2, the neural foramina from S1 to S5, and the origins of the sacrospinous and the sacrotuberous

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FIGURE 15-25 (A–D) Lower genitourinary injuries. (A) A 38-yearold male was hit by car leaving a bar. Retrograde cystography shows streaky contained contrast media on the left side of the bladder. (B) CT scan of the pelvis in a woman who was struck by a car shows streaky contained extravasation surrounding the bladder and extending into the obturator spaces. Streaky contained contrast medium indicates retroperitoneal extravasation and is consistent with tears of the retroperitoneal surfaces of the bladder. (C) Retrograde cystogram shows contrast media extending into the left subphrenic space (asterisk) and the left paracolic gutter (curved arrow). Note how the contrast surrounds loops of bowel in pelvis (arrows). This is consistent with tear of the dome of the bladder and free spillage into the peritoneal cavity. (D) A 25-year-old male motorcyclist sustained pelvic fractures. Retrograde urethral injection of contrast media clearly shows extravasation extending up into the pelvis from a posterior urethral injury above the urogenital diaphragm. D

ligaments. Fractures of the iliopubic and ischiopubic rami are assessed for their orientation (lateral compression fractures typically show orientation in the axial plane or coronal plane, while AP compression and vertical shear fractures will show orientation in the sagittal plane). The normal pubic symphysis is never more than 1 cm in width in normal subjects, regardless of age. When the pubic symphysis is traumatically wider than 2.5 cm, disruptions of both sacrospinous and sacrotuberous ligaments

are assumed. In the posterior ilium, it is important to look for avulsion fractures of the posterior superior iliac spine, so-called crescent fractures, as these are strongly associated with biomechanically unstable fractures in the presence of disruption of the anterior pelvic ring. The axial images give good evaluation of the amount of internal or external rotation, but underestimate the amount of flexion or extension of a hemipelvis relative to the intact pelvis. Furthermore, evaluation of the amount of pelvic

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FIGURE 15-26 Fatal bleed from internal iliac arteries: 28-year-old female hit by bus. AP pelvic digital subtraction angiogram shows exsanguinating hemorrhage from the internal iliac arteries bilaterally. This was treated with placement of a distal aortic occlusion balloon prior to emergent surgery. Note the small size of the iliac arteries due to spasm and profound hypovolemic shock.

FIGURE 15-27 Left superior gluteal artery bleed. Left posterior oblique (LPO) digital subtraction pelvic angiogram in this 56-year-old male post-motorcycle accident and pelvic fracture reveals a large active bleed from a left superior gluteal artery transection. Such injuries often require occlusion by coil embolization because the bleeding comes from the trunk of the superior gluteal artery.

FIGURE 15-28 Splenic laceration and active extravasation: 43-year-old-male post-MVC. Contrast-enhanced axial CT abdomen shows anterior splenic laceration with active focal extravasation (long arrow).

hematoma may be helpful in determining the need for angiography for embolization. Localization of these hematomas is a good predictor of associated pelvic vascular injuries. Pelvic CT is not a dynamic study, and the assessment of biomechanical instability may be difficult. Certainly, the combination of a crescent fracture from the posterior superior iliac spine and displaced, anterior pelvic ring fractures will be unstable under anesthesia. The stability of other patterns, however, is not so predictable, even though CT images provide a

FIGURE 15-29 Small bowel perforation: 14-year-old-boy, unhelmeted bicycle rider hit by car, sustained small bowel perforation. Intravenous contrast-enhanced axial CT shows three findings consistent with small bowel (jejunal) injury: (1) diffusely enhancing and thickened jejunum loops within the left side of the abdomen, with a focal hypoenhancing segment compatible with at least partial transmural injury (short arrow); (2) high-density interloop fluid within the mesentery adjacent to abnormal bowel (arrowhead) strongly suggests transmural bowel laceration; (3) small amount of pneumoperitoneum (long arrow) collecting within mesentery. Extra-alimentary air almost always correlates with transmural laceration of bowel.

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FIGURE 15-30 Shock-bowel syndrome: 11-year-oldgirl sustained fall from height. Intravenous contrastenhanced axial CT abdomen shows flat (slit-like) IVC, diffusely dilated small bowel loops with slightly thickened and enhancing walls, and extensive mesenteric and retroperitoneal edema. Reduced splanchnic blood flow due to underresuscitation results in capillary leak and prolonged transit time for intravenous contrast. This constellation of findings is consistent with shock bowel. Also note moderate intraperitoneal fluid from DPL.

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FIGURE 15-31 Pelvic ring fracture: lateral compression type. This 36-year-old unrestrained woman in rollover motor vehicle crash sustained injuries to right upper and lower extremities. (A) Anteroposterior (AP) conventional radiograph of pelvis shows disruption of rightsided arcuate lines at S1 and S2 (black arrows), left iliopubic ramus at pubis (white arrow), and right ischial pubic ramus near synchondrotic scar (black arrowhead). (B) Inlet view of pelvis better shows the disruption of anterior sacrum at right alae (black arrows), left pubic (white arrow), and right ischial pubic ramus (black arrowhead). (C) Axial computed tomography (CT) shows impacted fracture of right S1 ala, lateral to neuroforamen (arrow). Frequency of injury to sacral nerve roots is greatest when fractures involve medial aspect of the neural canal (Denis zone 3), lowest when lateral to the neuroforamen (Denis zone 1), and intermediate when involving neuroforamen (Denis zone 2). (D) Axial CT image at superior margin of symphysis pubis demonstrates an impacted fracture of posterior margin of left pubis (arrow).

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FIGURE 15-32 Pelvic ring fracture: anteroposterior (AP) compression type. This 55-year-old male sustained an injury during a 7-m fall onto concrete. (A) AP radiograph of pelvis shows symphyseal diastasis (double-ended arrow); right ischiopubic ramus fracture, which is minimally displaced (arrowhead); and disruption of right sacral arcuate lines (black arrows). Right femur is abducted (white arrow), a finding that is common with fractures of femoral shaft that this patient also sustained. (B) Inlet view of pelvis (obtained with 45° angulation caudally) better shows disruption of arcuate lines (white arrows) and again shows pubic symphyseal diastasis. (C) Axial CT at the lumbosacral junction shows through-and-through fracture (arrows) of right lateral mass of S1 with 6 mm of lateral and 8 mm of anterior translation. (D) Axial CT image at ischial tuberosities shows oblique sagittal fracture through right ischial pubic ramus (white arrows). Orientation of ischial fractures often reflects mechanism injury (sagittal plane fractures due to AP compression or vertical shear; transverse or axial plane fractures due to lateral compression).

great deal of anatomic and conceptual (injury pattern) information. Therefore, conventional x-rays are necessary as guides to intraoperative reduction. Evaluation of the acetabulum with CT is usually accomplished by an initial rapid survey, in which obvious fractures are ignored and the observer completes the general survey. If fractures involve the acetabulum, the goal is to determine what remains attached to the intact hemipelvis and describe and characterize the major fracture fragments and their relation to each other and the femoral head. Initiating the search at the

anterior surface of the sacrum, evaluating symmetry of the sacroiliac joint, and following along the cortical margin of the sciatic buttress to the tectum provide an anatomic approach that extends from the intact hemipelvis toward the fracture. Assessment of the posterior through anterior walls, the ischium for the posterior column, the pubis and symphysis for evaluation of the anterior column, the iliac wing for superior extension, and the secondary congruence between the femoral head and tectum allows for a more complete recognition of fracture fragments.

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FIGURE 15-33 Vertical shear injury with unstable sacral fracture. An “H”-shaped sacral fracture was sustained in 40-ft fall. This was associated with right calcaneus and T12 compression fractures. (A) Anteroposterior (AP) pelvis CT scout shows disruption of arcuate lines bilaterally (arrows). Such finding requires excellent lateral view of sacrum to exclude transverse components of the fracture to create either “H”- or “U”-shaped sacral fractures, which are typically biomechanically unstable. This can rarely be obtained. Computed tomography (CT) better evaluates this area as coronal reformations of thin-section axial CT. (B) Axial CT shows bilateral through-andthrough sacral fractures (arrows) that are transforaminal in their course. At this level, no transverse fracture is appreciated. (C) Coronal oblique CT reformation shows bilateral lateral mass fractures (arrows), as well as a portion of transverse fracture (arrowhead). (D) Sagittal CT reformation clearly shows transverse fracture (arrow).

APPENDICULAR SKELETON ■ Conventional Radiography Conventional radiography is for evaluation of long bones showing obvious deformity, instability, palpable crepitus, pain, and swelling. For periarticular regions, conventional x-rays are indicated for deformity, instability, decreased range of motion, pain, and swelling. The Ottawa ankle and knee clinical prediction rules add considerable precision to specificity.69–71 For long bones (Fig. 15-36), two orthogonal views are obtained, including an AP view and lateral projection centered at the midshaft. Projections should include the joint above and the joint below the long bone, or the end of the bone. Periarticular regions (joints) (Figs. 15-37 to 15-41) should have two orthogonal views and one or two oblique views, centered at the midportion of the articulation. Analysis of the long bone should allow assessment of the direction of the force that created the fracture pattern (e.g.,

twisting injuries result in spiral fractures; bending injuries result in wedge fractures). In general, higher-energy injuries tend to be more comminuted and displaced. If there is a mismatch between the apparent amount of comminution and the reported energy of the injury, osteoporosis or otherwise pathological bone should be suspected. For periarticular regions, subluxations are suggested by partial or complete loss of congruity of the joint, the appearance of a so-called white line due to overlapping of bones, and disruption of expected alignment of adjacent articulating structures. Careful attention to soft tissues (e.g., focal swelling, obliteration of normal fat pads, joint effusions) is helpful for subtle or otherwise occult fractures (e.g., elbow, knee, and wrist).

■ Computed Tomography of Appendicular Joints CT of appendicular joints (e.g., shoulder, supracondylar femur, tibial plateau, pilon, and calcaneus) is indicated for “displaced”

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C FIGURE 15-34 Acetabulum: transverse acetabular fracture with associated posterior wall fracture. This 25-year-old unrestrained male backseat passenger partially ejected in high-speed motor vehicle crash. (A) Anteroposterior (AP) view of pelvis shows disruption of iliopectineal and ischiopubic lines adjacent to acetabulum, with medial and proximal displacement of distal fragment (white arrow). Note that no fracture involving obturator foramen is evident, and no supraacetabular extension fracture is shown to suggest a column fracture. Black arrow shows concentric-shaped region of radiodensity due to overlap of tectum and femoral head, characteristic of dislocation. Position of femur in adduction and internal rotation is characteristic for posterior dislocation. Asterisk shows eyebrow-shaped radiopacity of displaced posterior wall fragment. (B) Left obturator oblique again shows transverse fracture (black arrow) and posterior wall fragment (asterisk), following relocation of posterior hip dislocation. Careful attention to shape of femoral head allows detection of subtle fractures associated with dislocation. Femoral head fractures may be either shear injuries or impaction fractures (the latter, similar to Hill-Sachs fractures associated with anterior shoulder dislocations). (C) Left iliac oblique shows location of posterior wall fragment (asterisk) and better shows transverse fracture course through anterior wall. (D) Axial computed tomography (CT) image at the level of tectum shows a sagittal plane fracture (arrows) characteristic of transverse fractures of acetabulum. Transverse fractures typically divide acetabulum into superior and lateral moiety, which maintains its connection to the intact hemipelvis, and a medial and inferior moiety in continuity with ischium. In this case, CT was obtained prior to reduction, and femoral head (H) is posterior to tectum (circular radiodensity just anterior to dislocated femoral head). The most inferior portion of posterior wall fracture fragment (PW) is also shown.

intra-articular fractures (e.g., 1–2 mm at the wrist or scapula, and glenoid, 5–10 mm at the tibial plateau) or unstable fracture patterns (Figs. 15-37 to 15-41). CT may be very helpful in presurgical planning and in the detection of otherwise occult fractures. In most patients, CT should be performed after provisional placement of traction or reduction. Slice thicknesses of

0.5–1.25 mm in the axial plane may be used in all appendicular joints to acquire raw data and may be reconstructed using bone algorithms. Initial reformations are usually obtained perpendicular to the joint of interest and orthogonal to source data and initial reformation planes. Three-dimensional volumerendered reformations should be made from reconstructions

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FIGURE 15-35 Acetabulum: both column fractures. This 63-year-old man sustained left acetabular fracture in 12-ft fall onto concrete. (A) Anteroposterior (AP) conventional radiograph of pelvis shows disruption of both iliopectineal and ischiopubic line on left, and disruption of left ischiopubic ramus. (B) Left obturator oblique view shows so-called spur sign, characteristic of both column fractures. Spur (arrow) represents intact iliac bone connected to sacroiliac joint, exposed due to medial migration of unstable anterior hemipelvis. Judet obliques are named for affected side, such that when obturator foramen is visible en face, image is termed an obturator oblique, and when iliac wing is imaged en face with foreshortening of obturator foramen, the view is termed iliac oblique. Oblique views give best conventional film representation of acetabular anatomy. (C) Axial computed tomography (CT) image obtained just above tectum shows comminuted coronal plane fracture of left acetabulum. White arrow marks intact supraacetabular ileum and is piece of bone that accounts for “spur” seen on obturator oblique views of affected hip (B). On CT, column fractures, whether anterior, posterior, or both columns, are typically shown as coronal plane fractures. (D) Sagittal CT reformation shows separation of acetabular roof from intact hemipelvis, characteristic of both column acetabular fractures. (E) Oblique coronal plane reformation from axial CT shows good secondary congruence between femoral head and free-floating tectum. Disruptions of medial acetabular wall, as well as supra-acetabular wall, are demonstrated.

Diagnostic and Interventional Radiology

CATHETER ANGIOGRAPHY Catheter angiography is the definitive method of evaluating arterial blood vessels for injury and of identifying active arterial hemorrhage. While CT angiography is frequently favored for imaging of many traumatic conditions, it has rarely been validated against the “Gold Standard” of catheter angiography. A notable exception is the screening of traumatic injury of the thoracic aorta that has replaced catheter angiography for many patients. Advantages of catheter angiography are many. It allows simultaneous detection and treatment of a wide variety of traumatic vascular injuries. It is a very specific method of identifying bleeding at the submillimeter diameter of vessel. It can evaluate many sites of bleeding simultaneously. It has an excellent safety record, especially when using iso-osmolar nonionic contrast agents, coaxial micropuncture access, digital subtraction techniques, coaxial microcatheters, and steerable guidewires. Disadvantages are cost, the delay necessary to assemble the team of radiologists, technologists, and nurses, the lack of suitability as a screening test, and the risks of radiation exposure. Technical expertise is limited to predominantly subspecialtytrained interventional radiologists (although endovascular surgeons and cardiologists may develop this expertise on an individual basis). These disadvantages are magnified when the likelihood of injury is low. Thus, noninvasive vascular techniques such as CT angiography should be explored under controlled studies to further assess their accuracy and appropriateness in such situations.

■ Transcatheter Endovascular Therapies FIGURE 15-36 Long-bone fracture: Monteggia. Lateral view of proximal forearm shows anterior convex angulation of midshaft fracture of ulna. Anterior dislocation of radius at radiocapitellar articulation is present. While Monteggia and Galeazzi fractures are well-known long-bone fractures with associated dislocations at adjacent joint, the evaluation of any long-bone fractures should include careful evaluation of adjacent joints. (Reproduced with permission from CC Blackmore.)

created using standard (soft tissue) algorithms and variable (user-defined) opaqueness. Use of traction prior to imaging allows ligamentotaxis to indirectly reduce fracture fragments and support indirect assessment of the integrity of soft tissue attachments to major bony fragments. Specifically, bone fragments that do not move or reduce on stretch are presumed to be no longer attached to soft tissue and may require debridement or direct repositioning. In addition, CT facilitates the assessment of intact bone and the integrity of subchondral bone (e.g., need for bone grafting).

Endovascular techniques have become a broadly accepted way of controlling traumatic hemorrhage for a variety of reasons. Catheter-based hemostasis allows precise control from a remote site that avoids exacerbation of venous hemorrhage, introduction of pathogens, and hypothermia that may result from open exposure. It is especially valuable for hemorrhage that is remote or hidden from view and requires laborious time-consuming exposures or that is the result of multiple small bleeding sites that are not easily detected or controlled during operative exploration. Endovascular techniques include embolization, stenting, stent grafting, and temporary balloon occlusion. They may be definitive or an adjunct to operative exposure. The methods of embolization include particulate or microcoil embolization of small vessels, proximal and distal large vessel isolation of a bleeding vessel, and conduit coil occlusion to cause selective temporary hypotension of the bleeding zone. Stenting, which facilitates blood flow beyond an injury, has largely been replaced by covered stent grafts that exclude lacerations, transections, and arteriovenous fistulae while maintaining flow through the conduit. Endografts are made of a

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CT for injuries to the scapula allows for the assessment of intra-articular step-offs, displacement of 1–2 mm or more, and the determination of stability of shoulder projection (which is determined by an intact clavicle, acromion, basiacromion, and glenoid neck). In addition, function of the supraspinatus and infraspinatus muscles may be disrupted in the presence of scapular spine fractures that are displaced for 10 mm or more.

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FIGURE 15-37 Periarticular fracture: coronoid process fracture of elbow. (A) Anteroposterior (AP) radiograph of left elbow shows displaced coronoid process (arrow). Elsewhere, joint appears congruent. (B) Lateral view of left elbow shows tip of coronoid process fracture (arrow). Coronoid process fractures can be graded by amount of coronoid process involved, such that larger coronoid process fracture fragments are more likely to result in elbow instability. (C) Axial computed tomography (CT) obtained because mismatch between radiographic and clinical findings of instability shows highly comminuted fracture of coronoid process (arrows). Radial head (R) and olecranon process (O) appear normal. (D) Sagittal CT reformation shows nearly all the coronoid process is involved in fracture. Secondary congruence between trochlea and olecranon–coronoid process is fair. (E and F) Three-dimensional “surface-rendered” CT reformations more graphically demonstrate transverse and distal extent and displacement of coronoid process fracture.

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FIGURE 15-38 Periarticular injury: shoulder dislocation. (A–C) Anterior dislocation sustained by a 52-year-old struck by falling tree on his back. (A) An anteroposterior (AP) radiograph with medial location of humeral head relative to glenoid (circle). (B) Postero-oblique radiograph of humeral head and glenoid (dotted line). Note that amount of overlap of scapula is less on this posterior oblique view than it is on anterior view (A), characteristic of anterior dislocation. (C) An axillary view; shows anterior location of humeral head relative to glenoid (upward pointing arrow and circle, respectively) on axillary lateral view. (D and E) Posterior dislocation sustained in a 42-yearold man who fell during a seizure. Posterior oblique radiograph (D) shows overlap of glenoid (circle) and medial aspect of humeral head (dotted line). (E) An axillary projection that shows the location of the humeral head posterior to glenoid (oval). Posterior margin of the head is denoted by downward pointing black arrow. Three downward pointing white arrows show impaction on anterior margin of humeral head, so-called trough fracture or reverse Hill–Sachs deformity.

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FIGURE 15-39 Periarticular fractures: intra-articular intercondylar distal femur fracture. This 20-year-old man was involved in a highspeed motor vehicle crash as a belted driver. (A) Anteroposterior (AP) radiograph of knee shows transverse T-type fracture of distal supracondylar femur, with intra-articular extension into intercondylar notch (arrows). (B) Lateral radiograph of knee shows transverse supracondylar component (arrow), from which femoral condyles have dissociated. In addition, lateral femoral condyle shows coronal plane, comminuted fracture of posterior aspect of condyle (arrowheads). In up to 40% of intra-articular intracondylar fractures caused by high-energy mechanisms, such coronal plane fractures (Hoffa’s fracture) may be overlooked. (C) Axial computed tomography (CT) shows a sagittal plane fracture extending into midportion of trochlea of the patellofemoral joint and a comminuted coronal plane fracture of posterior aspect of lateral femoral condyle (arrow). (D) Coronal plane reformation from axial CT shows T-type intra-articular fracture with dissociation of medial and lateral femoral condyles (white lines). Asterisk marks developmental variant, nonossifying fibroma. (E) Sagittal reformation from axial CT in central portion of lateral knee joint compartment shows coronal plane fracture of posterior femoral condyle (Hoffa’s fracture) as marked by arrow. Asterisk notes nonossifying fibroma, a benign developmental variant.

variety of porous materials such as expanded polytetrafluoroethylene and are reinforced by a metallic skeleton that apposes the stent graft to the native artery. Reports of midterm patency, while limited at this time, are beginning to show that these are durable options to vascular repairs.

Contraindications to endovascular techniques are highly dependent on skills, teamwork, and hemodynamics; however, there are some injuries that are difficult for rapid surgical control and endovascular techniques have a role, even in the unstable patient.

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FIGURE 15-40 Periarticular fractures: tibial plateau fracture (Schatzker 2). This 46-year-old man fell on the stairs. (A) Anteroposterior (AP) radiograph of knee shows valgus angulation due to collapse of lateral femoral condyle into a split depressed fracture of tibial plateau (arrows). (B) Axial image from computed tomography (CT) shows depressed left (asterisk) and split (arrows) portions of split depressed fracture. Note extension of comminuted fracture lines into medial tibial plateau across posterior aspect of proximal tibia and into intercondylar eminences, where anterior eminence (A) is minimally displaced. (C) Coronal reformation from axial CT shows split (arrow) and depressed (asterisk) portions of Schatzker type 2 fracture. Also note apparent elevation of anterior tibial eminence (A), on which anterior cruciate ligament inserts. Less striking step-off is seen in central portion of medial tibial plateau. (D) Three-dimensional CT reformation graphically demonstrates depression and lateral displacement of articular surface and lateral rim of tibial plateau, respectively. Also shown on this view is fracture of proximal fibula.

■ Arch Angiography for Acute Blunt-Force Traumatic Aortic Injury Blackmore et al.59 have published a clinical prediction rule as an aid to determine which patients should be screened for traumatic aortic injury. Usual indications are either direct (pseudo-

aneurysm, intimal flap) (Fig. 15-42) or indirect (juxta-aortic hematoma) CT findings, especially if the abnormality involves the ascending aorta. If patients are going directly to angiography for evaluation of disruptions of the pelvic ring and the mediastinum is not normal on a chest x-ray, catheter arch angiography is the preferred “screening” modality; otherwise,

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FIGURE 15-41 Periarticular fractures: calcaneus and Lisfranc fractures of midfoot. This 51-year-old restrained driver in a high-speed motor vehicle crash sustained multiple extremity and torso injuries. (A) Lateral conventional radiograph shows intra-articular fracture of calcaneus (upward pointing arrow denotes primary fracture plane; asterisk shows double density of central lateral fragment of posterior subtalar joint of calcaneus). Downward pointing arrow shows displacement of one of the metatarsal bases with an adjacent cuneiform fracture. (B) Axial computed tomography (CT) image at level of base of sustentaculum tali shows varus deformity through primary fracture (arrow). Secondary fracture plane extends toward anterior process (bracket). It is important to note continuity of cortex of medial wall of anterior process, as it influences distal extent of necessary fixation. (C) Sagittal reformation from axial CT shows primary fracture plane (upward arrow) with centrolateral fragment rotated into its superior extent. (D) Coronal reformation shows comminuted fracture of posterior facet of calcaneus due to bursting of body by lateral process (LP) of the talus. Centrolateral fragment is shown by asterisk. White arrow denotes lateral dislocation of peroneal tendons from peroneal groove in posterior fibula. (E) Axial CT at level of sinus tarsi, soft tissue window, shows lateral and anterior dislocation of peroneal tendons surrounded by hemorrhage and edema (white arrow). (F) Three-dimensional reformation from axial CT, medial oblique projection, shows divergent dislocations of great toe and third to fifth metatarsal bases (arrows).

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FIGURE 15-42 Traumatic aortic pseudoaneurysm. A 30-year-oldmale following high-speed motor vehicle accident. Left anterior oblique (LAO) digital subtraction arch aortogram shows traumatic aortic pseudoaneurysm extending proximal to the left subclavian artery. Of note, the aortic diameter and the distance from the left subclavian artery are important when considering endovascular therapy.

CT is the preferred modality for patients at 0.5% risk for aortic injury.72 Modern CT angiographic techniques are quite exquisite in demonstrating aortic injuries as well as providing coronal and sagittal reformations that can illustrate the important relationships and variants necessary for surgeons to create a treatment plan. Among selected patients sustaining aortic injury who are not operative candidates, endovascular stent grafts have been advocated as either temporizing or definitive therapy. Typically, a 5 French pigtail catheter is guided to the ascending aorta via a femoral arterial approach. Patients are positioned and imaged in both 35° right anterior oblique (RAO) and left anterior oblique (LAO) projections, using injection rates of approximately 25–30 mL/s for 40–60 mL volume (depending on hemodynamic status) and positioning to include the great vessels and diaphragm. The arteriographic appearance is classical. Linear filling defects indicate torn and ruffled intimal lining; expansion of the lumen, typically at the ligamentum arteriosum, indicates the presence of a pseudoaneurysm. This is sometimes associated with distal narrowing of the contrast column. Associated injuries should also be identified. Injuries of the brachiocephalic branches may occur instead of or in association with aortic injury. Bleeding from the internal mammary or the intercostal arteries is easily overlooked without diligence.

B FIGURE 15-43 Liver laceration. (A) CT of the upper abdomen reveals a Grade V liver laceration with pseudoaneurysm of the right hepatic lobe in this 18-year-old male status post-high-speed MVA. (B) Right hepatic angiogram identified the pseudoaneurysm. Note the size of the feeding vessel in relation to the 5 French diagnostic catheter. Selective coil embolization was performed through a microcatheter. When selective catheterization is not possible, the liver is quite tolerant of wide arterial embolization due to the dual blood supply provided the portal veins are patent.

■ Hepatic Angiography for Blunt-Force Lacerations Visceral catheter angiography is appropriate to evaluate hepatic lacerations (Fig. 15-43), especially in patients with a labile hemodynamic status or those with active extravasation or vascular abnormalities on a contrast-enhanced CT. Gross hemodynamic instability and profound shock, however, usually mandate urgent celiotomy. Of course, angiography may have a role after a “damage control” operation. Hepatic fracture lines seen on CT that traverse the hepatic triad more often result in bleeding than those fractures that are parallel to the triad. Extravasation of CT contrast tends to be

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associated with a positive arteriogram, but the decision to use angiography should primarily be based on clinical status rather than the CT appearance. Lack of enhancement of segments of the liver on CT is a very important finding. It represents a large hematoma in the liver, occlusion of the portal triad, or injury of the hepatic outflow from that segment. It is vital to distinguish nonenhancement from a hematoma. A large hepatic hematoma pushes the hepatic fragments away from each other, and unopacified or opacified hepatic vessels are not seen in a hematoma. If the area of nonenhancement has vessels running through it, it suggests an occlusion of the portal vein and hepatic artery or injury to a hepatic vein. Therefore, CT nonenhancement of the liver is a clear indication for urgent angiography if at all possible to confirm such injuries and to control arterial hemorrhage. As surgical exploration of damaged hepatic veins may be quite difficult, hepatic embolization and observation of a nonbleeding hepatic venous injury can be lifesaving. And, as noted above, hepatic angiography has an important role in the management of penetrating liver injuries that are isolated to the liver, as well as a secondary procedure. Selective catheterization of both the celiac trunk and the superior mesenteric artery (SMA) is essential due to the high rate of hepatic vascular variants, particularly the aberrant replaced right hepatic artery from the SMA. Imaging should be continued through the late portal venous phase. Moreover, it is important to determine whether there is patency of portal flow prior to embolization of the hepatic artery. Critical findings include arterial extravasation, spasm and occlusion, or shunting and fistula to portal or hepatic venous structures. Embolization of discretely abnormal vessels can be performed using a number of methods. A diffusely abnormal parenchymal injury with arterial bleeding may be safely embolized with Gelfoam due to the dual blood supply of the liver (hepatic arterial and portal venous). Embolization of hepatic arteries in the absence of portal flow increases the risk of developing an infarction or abscess. Depending on the location of bleeding and on the difficulty with catheterization, particulate embolization is the fastest technique; however, single microcoil embolization is preferred if time and circumstances allow. While formation of a postprocedure abscess is a complication of embolization, outcomes are favorable by integrating percutaneous image-guided drainage into the scheme.

author and his surgical colleagues observe (i.e., bed rest) most Grade I injuries, but advocate liberal use of angiography for triage of most other CT-diagnosed splenic injuries, especially in those patients with a significant hemoperitoneum or transient hypotension. Patients with high-grade injuries on CT should be imaged by angiography early to avoid transfusion or delayed rupture. The absence of arteriographic extravasation is a highly reliable predictor of successful nonoperative therapy regardless of grade. Identification of active arterial extravasation is the standard indication for endovascular treatment. Diagnostic angiography of the celiac trunk is followed by selective splenic artery catheterization with a 5 French catheter. If splenic artery anatomy permits, and a solitary pseudoaneurysm or focus of extravasation is seen, distal coil embolization at the site of injury can be attempted. This is especially true in a patient in whom the extravasation extends beyond the splenic capsule into the peritoneal cavity. It should be remembered that distal superselective embolization is associated with the development of more postprocedure splenic infarctions and abscess, though these are uncommon. Finally, most patients have tortuous splenic arteries and most extravasations are multiple. Diffuse intrasplenic extravasation is far more common, and superselective occlusion of these multiple sites would be very time consuming and less effective. Also, the splenic tortuosity that results from medial displacement of the spleen by the perisplenic hematoma often prevents rapid catheterization (Fig. 15-44). In such cases, embolization of the proximal splenic artery by coils placed distal to the dorsal pancreatic branch and proximal to the pancreatic magna branches is advocated to reduce the arterial pressure head at the injury site while allowing perfusion through collateral vessels. Such collaterals prevent splenic infarction by maintaining splenic perfusion through connections between the left gastric and the short gastric arteries, between the dorsal pancreatic artery and the pancreatica magna branches, between the right and left gastroepiploic vessels, and others (Fig. 15-45). Complications are uncommon when proximal splenic artery embolization is performed. A poorly selected coil size may result in hilar occlusion if the selected coil is too small and migrates distally. Too large coils may migrate proximally to occlude the celiac axis or embolize into the aorta. As noted above, distal microembolization bypasses the collateral circulation and results in more loss of immune function.

■ Splenic Arteriography for Blunt-Force Lacerations

■ Interventions for Renal Trauma

A patient who is hemodynamically unstable is not a candidate for angiography and embolization. Other patients who have an injury of the spleen diagnosed on CT are candidates for nonoperative therapy with good results. CT is not a reliable predictor, however, of which patients are best managed by bed rest compared to those patients who require hemostasis. When a CT demonstrates active arterial extravasation or a parenchymal vascular abnormality, one should consider angiography. Unfortunately, there is not good correlation between the CT grading system and outcome of treatment. Many Grade IV injuries can be observed and some Grade I injuries become worse, rebleed, and require definitive procedural therapy. The

Low-grade renal injuries are usually well tolerated and do not require angiography, especially when caused by blunt trauma. Initial nonoperative management of blunt renal injuries with an intact pedicle is the common practice. High-grade injuries that result in massive hemorrhage are usually managed by nephrectomy. In other patients who are hemodynamically stabilized, angiography with intent to embolize bleeding is appropriate. Angiography is recommended for patients with CT evidence of a major renal injury and ongoing blood loss or persistent gross hematuria. Areas of nonenhancement on CT suggest a renal vascular injury, such as a polar avulsion or intimal stretch of the main renal artery with distal platelet embolization.

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FIGURE 15-44 Splenic intraparenchymal false aneurysms. Digital subtraction angiogram of the splenic artery reveals multiple focal extravasations in this 56-year-old male status post-MVA. Selective embolization is not desirable because so many vessels are injured and selective catheterization would be difficult due to splenic artery tortuosity. In such cases proximal splenic artery coil embolization proximal to the pancreatic magna branch is usually successful in controlling this hemorrhage.

Penetrating renal injuries are more aggressively approached by angiography if nonoperative management is undertaken. Large perinephric hematomas, areas of nonenhancement, and extravasations on CT warrant angiography. Aortography is helpful to assess injury of the origin of the renal artery, to exclude renal parenchymal injury perfused by accessory renal arteries, and to look for associated intraperitoneal and retroperitoneal bleeding sites. A selective renal arteriogram using a 5 French catheter is then performed. Most injuries will require use of a coaxial microcatheter and embolization of small branches. Coils are preferred as they can be carefully placed to prevent infarction of adjacent noninjured renal tissue, but surgical gelatin pledgets can be used, as well. Because renal branches are end vessels with little collateralization, infarction is likely, and the goal is to reduce these infarctions to a minimum. The treatment of vascular injury in the renal pedicle continues to be a vexing problem, especially since delays in revascularization usually result in a renal infarction. Partial wall injuries that result in a pseudoaneurysm, false aneurysm, and segmental infarction often went unrecognized prior to the use of CT. Such injuries are detected currently before complete arterial thrombosis and renal infarction occurs. Therefore, arteriography is indicated when an injury in the renal artery is suspected. When such injuries are detected, treatment options are many, including operative revascularization, antiplatelet therapy and observation, and the application of covered stent grafts. Stent grafts can effectively seal full thickness injuries and

FIGURE 15-45 Demonstration of long-term follow-up of splenic artery embolization. A 40-year-old female pedestrian sustained blunt splenic injury after being struck by a motor vehicle 10 years ago. She was treated by coil occlusion of the proximal splenic artery with good results. During admission 10 years later for stab wound to the neck, the coils were detected. Splenic arteriography was performed. This demonstrated marked enlargement of the pancreatic collaterals that bridged the occlusion. Flow was rapid through these very large collaterals.

cover exposed media that results in embolic infarctions. While long-term follow-up of series of these patients is lacking, the midterm (1–5 years) patency of stent grafts throughout the body remains high (Fig. 15-46).

■ Pelvic Hemorrhage Blunt Pelvic Fractures Blunt pelvic fractures with crushing or shearing tear the small branches of the internal iliac artery that accompany ligaments, muscles, and tendons. Injuries tend to be multiple and bilateral, and from several branches. In addition, bony fragments can penetrate or perforate vascular structures. Examples include a fracture of the superior pubic ramus injuring the internal pudendal or obturator artery, a fracture of the iliac wing through the sciatic notch injuring the superior gluteal artery, and disruption of the sacroiliac joints injuring the lateral sacral arteries. Pelvic fractures are potentially life-threatening injuries that are caused by high-energy impact trauma and account for about 3% of skeletal injuries. They are the third most common lethal injury after motor vehicle crashes. The majority of patients with pelvic fractures do not require massive transfusion (greater than 6 U) as bleeding in most cases is likely to be venous or osseous in nature and is self-limited. Radiological intervention is not commonly needed in patients with routine pelvic fractures. Severe hemorrhage, however, occurs in 3–10% of patients, and mortality rates may be as high as 50% in patients with unstable pelvic fractures. Thus, the use of angiography in patients with pelvic fractures is highly dependent on the hemodynamic status, the type of fracture pattern, the transfusion requirements, and the presence or absence of hemoperitoneum.

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SECTION 2 A

C

B

D

FIGURE 15-46 (A–D) Renal artery injury. A 56-year-old man fell from a height of about 10 m. (A) During CT evaluation inhomogeneous enhancement of the spleen was detected. Central perinephric hemorrhage (asterisks) and irregularity of the renal artery (arrow) were seen. (B) Coronal reformation shows irregularity of the renal artery and thickening of its wall. (C) Aortography showed irregular enlargement of the proximal renal artery near the ostium (circled). Slight extravasation was seen on the later images. (D) Therefore, a stent graft was placed over the area of injury. The vessel wall was then smooth, and no extravasation was seen. Two-year follow-up arteriography showed continued patency and no stenosis.

Most of the indications for angiography in blunt pelvic trauma have remained the same for more than 30 years and are listed as follows: 1. Hemodynamic instability in a patient with a pelvic fracture with no or little hemoperitoneum detected by FAST or diagnostic peritoneal lavage 2. Pelvic fracture and transfusion requirement of greater than 4 U in 24 hours 3. Pelvic fracture and transfusion requirement of greater than 6 U in 48 hours 4. Pelvic fracture and a large or expanding hematoma identified during celiotomy 5. CT evidence of large retroperitoneal hematoma with extravasation of contrast 6. Need for detection and treatment of other injuries during angiography

With MDCT the detection of extravasation of contrast has been used as an indication for follow-up pelvic angiography. Of course, CT is not as reliable as clinical signs as extravasation may be venous in origin and not correlate with massive arterial hemorrhage. Although it should not delay angiography that is already indicated for pelvic hemorrhage, CT is helpful in localizing the vessels likely to be bleeding and in excluding associated abdominal and cerebrospinal injuries. Correlations of location of the hematoma and site of vascular injury include obturator space and obturator artery, presacral space and lateral sacral artery, space of Retzius and internal pudendal artery, and buttock and gluteal artery. Femoral access is the preferred approach; however, catheterization may be difficult because of hypotension, tachycardia, and difficulty in palpating the vessels as the pelvic hematoma expands. Ultrasound or fluoroscopic guidance is very helpful in these situations. A 5 French aortic flush catheter is used for flush abdominopelvic aortography. This is valuable to screen

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the abdominal viscera and mesentery, to exclude aortoiliac and other retroperitoneal bleeding sources, and as a road map of the pelvic vessels. Bilateral internal iliac arteriography is mandatory to exclude bleeding sites since aortography may not identify all bleeding. From one access, both internal iliac arteries are sequentially catheterized and opacified. Then, external iliac arteriography is used to evaluate the external pudendal and external obturator vessels. Multiple areas of extravasation are often identified. These may be bilateral and may involve multiple vascular beds. Extravasation is often punctate, but can be large, coarse, and extensive, also. The size of such extravasations may not correlate with the degree of blood loss. Vascular occlusions are common, as well. These can be due to thrombosis or vasospasm that often cannot be differentiated. Failure to treat these occlusions may result in recurrent hemorrhage when vasospasm resolves. Arteriovenous fistulas can occur, but are more common in penetrating trauma. Because bleeding is usually multifocal and originates from multiple small blood vessels, embolization requires small particulate embolization. Large coil occlusion is as ineffective as surgical ligation of the internal iliac artery because bleeding soon resumes through numerous collateral circuits. Surgical gelatin pledgets are ideal because they are inexpensive, readily available, and often temporary lasting only a few weeks and allowing reestablishment of normal blood flow after the tissue has healed (Fig. 15-47A and B). Permanent particulate emboli, however, are often used because of their ease of use through a microcatheter (Fig. 15-48A and B). Embolization is technically successful in more than 90% of patients, and hemorrhage control is highly effective. Survival depends on many other factors including associated injuries, the presence of an open fracture, transfusion requirements, and delays to embolization.

A

Penetrating Pelvic Trauma Penetrating trauma is an uncommon indication for pelvic angiography as most patients are hemodynamically unstable or have clear indications for exploratory celiotomy. Moreover, they are more likely to sustain injuries to large vessels. Because the retroperitoneum has been exposed by a penetrating wound, intraperitoneal bleeding is likely and direct exploration is warranted. Occasionally, angiography is valuable when operative control cannot be initially accomplished and damage control has been performed. Angiography and embolization prior to unpacking will avoid additional blood loss at a reoperation. Large vessel conduit injuries require a very different endovascular strategy. When an injury to a noncritical internal iliac artery or branch has been missed at operation, but detected on postoperative angiography, coil occlusion of both the proximal and, whenever possible, the distal end of the vessel is the standard treatment.

■ Peripheral Vascular Injuries A discussion of the use of interventional radiology in the treatment of extremity injuries must be preceded by a discussion of the use of imaging in the diagnostic workup of suspected vascular trauma in the extremities. The indications and

295

B FIGURE 15-47 (A and B) Multiple bleeds from pelvic fractures: 48-year-old male driver in a motor crash sustained pelvic fractures requiring transfusions. (A) Circles surround multiple bleeding sites from the region of the sacroiliac joint; from the pelvic side wall on the right hemipelvis emanate anterior and posterior branches of the right internal iliac artery and in the region (B) multiple points of extravasation were detected (circle). They are emanating from the left lateral sacral artery. Such diffuse hemorrhage is not amenable to superselective embolization because it would be too time consuming. Pledgets of surgical gelatin, 2–3 mm in size, can occlude these vessels effectively.

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SECTION 2 A

B FIGURE 15-48 (A and B) A 26-year-old motorcyclist sustained unstable pelvic fractures during a crash. He developed expanding perineal and scrotal hematomas requiring red cell transfusion. (A) Left internal iliac arteriogram reveals a source of bleeding from the left internal pudendal artery (curved arrow). The more medial contrast stain (straight arrow) is a normal finding. It represents the blush of the perineal body and root of the ischiocavernosa muscle that is frequently seen on internal iliac arteriography of mails. (B) Because this was focal hemorrhage, selective embolization via 2.8 French catheter placed coaxially through the 5 French catheter was attempted and successfully achieved hemostasis.

contraindications depend on a variety of factors that are primarily related to clinical presentation and hospital course, and also to associated injuries, mechanism of injury, and signs of circulatory shock. Vigorous or pulsatile external active hemorrhage, a rapidly expanding hematoma, or loss of pulses at the wrist or ankle mandates emergent operative exploration. Other patients with proximity wounds and stable hematomas, diminished pulses, or signs of an arteriovenous fistula may benefit from arteriography. The availability of stent grafts has also increased the utilization of angiography as a prelude to nonoperative management of some clinically significant vascular injuries. While debatable to some, “proximity” angiography has value in asymptomatic patients with penetration that has passed close to the estimated path of major vessels. Vascular injuries occur in 3–8% of asymptomatic patients. Failure to diagnose arterial injuries may result in delayed hemorrhage or chronic arteriovenous fistulas with claudication, venous insufficiency, and congestive heart failure. Exclusion angiography avoids the time and effort needed to keep track of patients who are often negligent in their own follow-up. The indications for the use of angiography in patients who have sustained fractures and dislocations are a more complicated matter. Vascular injuries resulting from fractures and dislocations are uncommon. Clinical evaluation is often difficult as the hematoma from a fracture may be quite large and indistinguishable from one associated with a vascular injury. Crush wounds, angulation deformities, and fracture hematomas may cause a pulse deficit by kinking, entrapping the vessel, or inducing spasm without an intrinsic vascular injury. A laceration into muscle may result in external blood loss without major vascular injury. Finally, a compartment syndrome may result in tissue ischemia without loss of pulses. Almost all peripheral vascular injuries can be reached using a 5 French catheter from femoral access provided a long enough catheter is available. Angiography should be done in multiple projections with opaque marking of the entry and exit wounds demonstrating that the entire course of the wounding agent is within the field of view. Iso-osmolar nonionic contrast medium is the optimal agent for visualization. Multiple images in the arterial, capillary, and venous phases are necessary. The imaging signs of vascular injury include luminal narrowing, arterial extravasation, bulge of the wall, intraluminal filling defects, occlusions, and arteriovenous fistulas. The imaging signs are in some cases quite nonspecific. Luminal narrowing can result from spasm, mural thrombus, intramural hematoma, and extrinsic compression, while dilatation can result from a traumatic true aneurysm, traumatic false aneurysm (“pseudoaneurysm”), or arteriovenous fistula. Finally, occlusion can be caused by thrombosis or vasospasm. The natural history of many injuries cannot be predicted by the angiographic appearance. Therefore, observation of some injuries is warranted. Equivocal findings such as luminal narrowing can be assessed by repeating angiography after infusion of an intra-arterial vasodilator, on a subsequent day. Small irregularities and intimal tears that are not flow restricting may be treated by antiplatelet therapy and will heal (Fig. 15-49A–D).

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A

B

C

D

FIGURE 15-49 “Minimal injury” of the popliteal artery. Pedestrian who was struck by a motor vehicle sustained comminuted tibial plateau fracture of the left knee. Pulses were diminished and angiography was sought after incomplete reduction. (A and B) Initial popliteal arteriogram showed numerous filling defects consistent with intimal tears (white arrows). Patient was treated with aspirin. (C and D) Arteriogram 1 week later showed healing of the intimal tears.

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SECTION 2 FIGURE 15-50 Thrombosis of popliteal artery with endovascular repair. A 46-year-old morbidly obese woman sustained comminuted tibial plateau fractures after a fall from curb. Pulses were absent. (A) Popliteal arteriogram shows complete occlusion of the mid-popliteal artery. (B) The catheter was quickly advanced to a location just above the occlusion and a guidewire advanced easily into the posterior tibial artery. An ePTFE reinforced stent graft was deployed between proximal and distal extent of the occlusion. (C) Follow-up popliteal arteriogram showed restoration of direct line flow. The entire procedure took less than 1.5 hours.

A

B

FIGURE 15-51 Example of vascular isolation by proximal and distal coil occlusion. A 22-year-old male sustained a single stab wound of the upper left chest resulting in very large hemothorax. (A) Subclavian arteriogram shows that there is active arterial hemorrhage from a lacerated fourth anterior intercostal branch of the left internal mammary artery. (B) Because there was continuity between anterior and posterior intercostals, it was necessary to advance a 2.8-French microcatheter across the laceration into the distal segment to deliver a coil distally before withdrawing the catheter and delivering a coil proximally.

Diagnostic and Interventional Radiology

REFERENCES 1. Blackwood GA, Blackmore CC, Mann FA, et al. The importance of trauma series radiographs: have we forgotten the ABC’s? In: 13th Annual Scientific Meeting of the American Society of Emergency Radiology, 2002. 2. Bushberg JT, Seibert SJ, Leidholdt EMJ, et al. The Essential Physics of Medical Imaging. 2nd ed. Williams and Wilkins: Philadelphia; 2001. 3. Stengel D, Bauwens K, Sehouli J, et al. Systematic review and metaanalysis of emergency ultrasonography for blunt abdominal trauma. Br J Surg. 2001;88:901.

4. Davis DP, Campbell CJ, Poste JC, et al. The association between operator confidence and accuracy of ultrasonography performed by novice emergency physicians. J Emerg Med. 2005;29:259. 5. Branney SW, Wolfe RE, Moore EE, et al. Quantitative sensitivity of ultrasound in detecting free intraperitoneal fluid. J Trauma. 1995;39:375. 6. Chiu WC, Cushing BM, Rodriguez A, et al. Abdominal injuries without hemoperitoneum: a potential limitation of focused abdominal sonography for trauma (FAST). J Trauma. 1997;42:617 [discussion 623]. 7. Poletti PA, Wintermark M, Schnyder P, et al. Traumatic injuries: role of imaging in the management of the polytrauma victim (conservative expectation). Eur Radiol. 2002;12:969. 8. Ballard RB, Rozycki GS, Knudson MM, et al. The surgeon’s use of ultrasound in the acute setting. Surg Clin North Am. 1998;78:337. 9. Stengel D, Bauwens K, Sehouli J, et al. Emergency ultrasound-based algorithms for diagnosing blunt abdominal trauma. Cochrane Database Syst Rev. 2005:CD004446. 10. Becker CD, Poletti PA. The trauma concept: the role of MDCT in the diagnosis and management of visceral injuries. Eur Radiol. 2005;15:D105. 11. Fang JF, Wong YC, Lin BC, et al. Usefulness of multidetector computed tomography for the initial assessment of blunt abdominal trauma patients. World J Surg. 2006;30:176. 12. Linsenmaier U, Krotz M, Hauser H, et al. Whole-body computed tomography in polytrauma: techniques and management. Eur Radiol. 2002;12:1728. 13. Novelline RA, Rhea JT, Rao PM, et al. Helical CT in emergency radiology. Radiology. 1999;213:321. 14. Toyama Y, Kobayashi T, Nishiyama Y, et al. CT for acute stage of closed head injury. Radiat Med. 2005;23:309. 15. Parizel PM, Van Goethem JW, Ozsarlak O, et al. New developments in the neuroradiological diagnosis of craniocerebral trauma. Eur Radiol. 2005;15:569. 16. Oman JA, Cooper RJ, Holmes JF, et al. Performance of a decision rule to predict need for computed tomography among children with blunt head trauma. Pediatrics. 2006;117:e238. 17. Mower WR, Hoffman JR, Herbert M, et al. Developing a decision instrument to guide computed tomographic imaging of blunt head injury patients. J Trauma. 2005;59:954. 18. Gowda NK, Agrawal D, Bal C, et al. Technetium Tc-99m ethyl cysteinate dimer brain single-photon emission CT in mild traumatic brain injury: a prospective study. AJNR Am J Neuroradiol. 2006;27:447. 19. de Lacey G, McCabe M, Constant O, et al. Testing a policy for skull radiography (and admission) following mild head injury. Br J Radiol. 1990;63:14. 20. Masters SJ, McClean PM, Arcarese JS, et al. Skull x-ray examinations after head trauma. Recommendations by a multidisciplinary panel and validation study. N Engl J Med. 1987;316:84. 21. Holmgren EP, Dierks EJ, Assael LA, et al. Facial soft tissue injuries as an aid to ordering a combination head and facial computed tomography in trauma patients. J Oral Maxillofac Surg. 2005;63:651. 22. Lambert DM, Mirvis SE, Shanmuganathan K, et al. Computed tomography exclusion of osseous paranasal sinus injury in blunt trauma patients: the “clear sinus” sign. J Oral Maxillofac Surg. 1997;55:1207 [discussion 1210]. 23. Manson P. Organization of treatment in panfacial fractures. In: Rein PJ, ed. Manual of Internal Fixation in the Cranio-Facial Skeleton. Berlin: Springer Verlag; 1998:95. 24. Stanley R. Maxillofacial trauma. In: Cummings CW, Fredrickson JM, Harker LA, et al., eds. Otolaryngology: Head and Neck Surgery. 3rd ed. St. Louis: Mosby-Year Book; 1998:453. 25. Schuknecht B, Graetz K. Radiologic assessment of maxillofacial, mandibular, and skull base trauma. Eur Radiol. 2005;15:560. 26. Rake PA, Rake SA, Swift JQ, et al. A single reformatted oblique sagittal view as an adjunct to coronal computed tomography for the evaluation of orbital floor fractures. J Oral Maxillofac Surg. 2004;62:456. 27. Dos Santos DT, Costa e Silva AP, Vannier MW, et al. Validity of multislice computerized tomography for diagnosis of maxillofacial fractures using an independent workstation. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2004;98:715. 28. Klenk G, Kovacs A. Do we need three-dimensional computed tomography in maxillofacial surgery? J Craniofac Surg. 2004;15:842 [discussion 850]. 29. Saigal K, Winokur RS, Finden S, et al. Use of three-dimensional computerized tomography reconstruction in complex facial trauma. Facial Plast Surg. 2005;21:214. 30. Chen WJ, Yang YJ, Fang YM, et al. Identification and classification in le fort type fractures by using 2D and 3D computed tomography. Chin J Traumatol. 2006;9:59.

CHAPTER 15

Treatment of angiographically diagnosed vascular injuries is based on the criticality of the bleeding vessel, its size, location, and accessibility, the hemodynamic condition of the patient, and the type of lesion. Small vessels that are not essential for tissue perfusion can be treated by small particle embolization, using surgical gelatin pledgets or more permanent smaller agents. Permanent agents have no advantage, but in some instances are more easily administered through microcatheters than surgical gelatin. These agents are delivered by flow direction toward the path of least resistance, which is usually toward the bleeding site. Microcoils can be utilized for injury to a small vessel provided they can be delivered near enough to the injury site to avoid collateral recruitment that permits continued bleeding. Examples of vessels that can be treated by embolization of small particles include hemorrhage from a pelvic fracture, multifocal hepatic arterial hemorrhage, and injuries to small muscular branches in the extremities. Injury to larger vessels such as those greater than 3 mm in diameter requires two techniques, one for essential vessels and one for expendable vessels. The treatment of essential vessels requires repair of the bleeding site while allowing continued blood flow. Thus, stent grafts can be deployed to cover the injured segment while allowing prograde flow (Fig. 15-50). Nonessential conduits, such as branches of the profunda femoris artery or the brachial artery, or one of the arteries in the shank, can be safely embolized. Particulate embolization will flow past the injury and penetrate deep into the vascular bed. When conduits are injured, this insult to the vascular bed is unnecessary. Therefore, large vessel agents are used to occlude the damaged segment of the conduit while the vascular bed is perfused through collaterals (Fig. 15-51). Coils in various sizes, some containing threads or fibers to accelerate thrombosis, are the most common devices used to occlude a large vessel. A coil is sized to have a diameter large enough to prevent distal migration, but not too large to end up recoiling into a parent, nontarget vessel. The technique of conduit isolation attempts to occlude both the proximal and distal vessels around the area of injury by coiling (Fig. 15-51). The goal is to exclude the vascular defect and prevent rebleeding through collateral vessels. This is highly desirable in most circumstances, but mandatory when treating arteriovenous fistulas. The guidewire is carefully maneuvered distal to the injured segment, but proximal to any branches, and coils are delivered. The catheter is then withdrawn, and coils are placed in the proximal segment.

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31. Ploder O, Klug C, Voracek M, et al. Evaluation of computer-based area and volume measurement from coronal computed tomography scans in isolated blowout fractures of the orbital floor. J Oral Maxillofac Surg. 2002;60:1267 [discussion 1273]. 32. Brenner D, Elliston C, Hall E, Berdon W. Estimated risks of radiationinduced fatal cancer from pediatric CT. AJR Am J Roentgenol. 2001;176:289. 33. Biffl WL. Diagnosis of blunt cerebrovascular injuries. Curr Opin Crit Care. 2003;9:530. 34. Miller PR, Fabian TC, Croce MA, et al. Prospective screening for blunt cerebrovascular injuries: analysis of diagnostic modalities and outcomes. Ann Surg. 2002;236:386 [discussion 393]. 35. Biffl WL, Egglin T, Benedetto B, et al. Sixteen-slice computed tomographic angiography is a reliable noninvasive screening test for clinically significant blunt cerebrovascular injuries. J Trauma. 2006;60:745 [discussion 751]. 36. Cothren CC, Moore EE, Ray CE Jr, et al. Carotid artery stents for blunt cerebrovascular injury: risks exceed benefits. Arch Surg. 2005;140:480 [discussion 485]. 37. Mutze S, Rademacher G, Matthes G, et al. Blunt cerebrovascular injury in patients with blunt multiple trauma: diagnostic accuracy of duplex Doppler US and early CT angiography. Radiology. 2005;237:884. 38. LeBlang SD, Nunez DB Jr. Noninvasive imaging of cervical vascular injuries. AJR Am J Roentgenol. 2000;174:1269. 39. Bub LD, Hollingworth W, Jarvik JG, et al. Screening for blunt cerebrovascular injury: evaluating the accuracy of multidetector computed tomographic angiography. J Trauma. 2005;59:691. 40. Blackmore CC, Emerson SS, Mann FA, et al. Cervical spine imaging in patients with trauma: determination of fracture risk to optimize use. Radiology. 1999;211:759. 41. Hanson JA, Blackmore CC, Mann FA, et al. Cervical spine injury: a clinical decision rule to identify high-risk patients for helical CT screening. AJR Am J Roentgenol. 2000;174:713. 42. Adelgais KM, Grossman DC, Langer SG, et al. Use of helical computed tomography for imaging the pediatric cervical spine. Acad Emerg Med. 2004;11:228. 43. Hernandez JA, Chupik C, Swischuk LE. Cervical spine trauma in children under 5 years: productivity of CT. Emerg Radiol. 2004;10:176. 44. Aulino JM, Tutt LK, Kaye JJ, et al. Occipital condyle fractures: clinical presentation and imaging findings in 76 patients. Emerg Radiol. 2005;11:342. 45. Van Goethem JW, Maes M, Ozsarlak O, et al. Imaging in spinal trauma. Eur Radiol. 2005;15:582. 46. Marion D, Domeier R, Dunham CM, et al. Determination of cervical spine stability in trauma patients. Chicago, IL: Eastern Association for the Surgery of Trauma (EAST); 2000. 47. Mower WR, Hoffman JR, Pollack CV Jr, et al. Use of plain radiography to screen for cervical spine injuries. Ann Emerg Med. 2001;38:1. 48. Stiell IG, Wells GA, Vandemheen KL, et al. The Canadian C-spine rule for radiography in alert and stable trauma patients. JAMA. 2001; 286:1841. 49. Hoffman JR, Wolfson AB, Todd K, et al. Selective cervical spine radiography in blunt trauma: methodology of the National Emergency X-Radiography Utilization Study (NEXUS). Ann Emerg Med. 1998;32:461. 50. Holmes JF, Panacek EA, Miller PQ, et al. Prospective evaluation of criteria for obtaining thoracolumbar radiographs in trauma patients. J Emerg Med. 2003;24:1. 51. Hsu JM, Joseph T, Ellis AM. Thoracolumbar fracture in blunt trauma patients: guidelines for diagnosis and imaging. Injury. 2003;34:426.

52. Kuhns L. Imaging of Spinal Trauma in Children. Hamilton, Ontario: BC Decker Inc; 1998. 53. Roos JE, Hilfiker P, Platz A, et al. MDCT in emergency radiology: is a standardized chest or abdominal protocol sufficient for evaluation of thoracic and lumbar spine trauma? AJR Am J Roentgenol. 2004; 183:959. 54. Richards PJ. Cervical spine clearance: a review. Injury. 2005;36:248 [discussion 270]. 55. Sliker CW, Mirvis SE, Shanmuganathan K. Assessing cervical spine stability in obtunded blunt trauma patients: review of medical literature. Radiology. 2005;234:733. 56. Rodriguez RM, Hendey GW, Marek G, et al. A pilot study to derive clinical variables for selective chest radiography in blunt trauma patients. Ann Emerg Med. 2006;47:415. 57. Holmes JF, Sokolove PE, Brant WE, et al. A clinical decision rule for identifying children with thoracic injuries after blunt torso trauma. Ann Emerg Med. 2002;39:492. 58. Mirvis SE, Shanmuganathan K, Miller BH, et al. Traumatic aortic injury: diagnosis with contrast-enhanced thoracic CT—five-year experience at a major trauma center. Radiology. 1996;200:413. 59. Blackmore CC, Zweibel A, Mann FA. Determining risk of traumatic aortic injury: how to optimize imaging strategy. AJR Am J Roentgenol. 2000;174:343. 60. Omert L, Yeaney WW, Protetch J. Efficacy of thoracic computerized tomography in blunt chest trauma. Am Surg. 2001;67:660. 61. Holmes JF, Ngyuen H, Jacoby RC, et al. Do all patients with left costal margin injuries require radiographic evaluation for intraabdominal injury? Ann Emerg Med. 2005;46:232. 62. Ryan MF, Hamilton PA, Chu P, et al. Active extravasation of arterial contrast agent on post-traumatic abdominal computed tomography. Can Assoc Radiol J. 2004;55:160. 63. Sheridan MK, Blackmore CC, Linnau KF, et al. Can CT predict the source of arterial hemorrhage in patients with pelvic fractures? Emerg Radiol. 2002;9:188. 64. Brown CV, Kasotakis G, Wilcox A, et al. Does pelvic hematoma on admission computed tomography predict active bleeding at angiography for pelvic fracture? Am Surg. 205;71:759. 65. Poletti PA, Mirvis SE, Shanmuganathan K, et al. CT criteria for management of blunt liver trauma: correlation with angiographic and surgical findings. Radiology. 2000;216:418. 66. Killeen KL, Shanmuganathan K, Mirvis SE. Imaging of traumatic diaphragmatic injuries. Semin Ultrasound CT MR. 2002;23:184. 67. Patselas TN, Gallagher EG. The diagnostic dilemma of diaphragm injury. Am Surg. 2002;68:633. 68. Hunter JC, Brandser EA, Tran KA. Pelvic and acetabular trauma. Radiol Clin North Am. 1997;35:559. 69. Stiell IG, Greenberg GH, McKnight RD, et al. Decision rules for the use of radiography in acute ankle injuries. Refinement and prospective validation. JAMA. 1993;269:1127. 70. Stiell IG, Greenberg GH, Wells GA, et al. Prospective validation of a decision rule for the use of radiography in acute knee injuries. JAMA. 1996;275:611. 71. Stiell IG, Wells GA, Hoag RH, et al. Implementation of the Ottawa knee rule for the use of radiography in acute knee injuries. JAMA. 1997; 278:2075. 72. Ouwendijk R, Kock MC, Visser K, et al. Interobserver agreement for the interpretation of contrast-enhanced 3D MR angiography and MDCT angiography in peripheral arterial disease. AJR Am J Roentgenol. 2005;185:1261.

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Surgeon-Performed Ultrasound in Acute Care Surgery Christopher J. Dente and Grace S. Rozycki

INTRODUCTION For nearly two decades, acute care surgeons have successfully performed, interpreted, and taught bedside ultrasound examinations of patients who are injured or critically ill.1–13 Real-time imaging allows the surgeon to receive instantaneous information about the clinical condition of the patient and, therefore, helps to expedite the patient’s management, which is important in patients with time-sensitive diagnoses. In many centers, ultrasound machines are owned by surgeons or surgical departments and are part of the standard equipment in the trauma resuscitation area as well as in the intensive care unit (ICU). While diagnostic peritoneal lavage (DPL) and computed tomography (CT) scanning are still valuable diagnostic tests for the detection of intraabdominal injury in patients, ultrasound is not only faster but also noninvasive and painless. As an extension of the physical examination, acute care surgeons routinely use ultrasound in the trauma setting to augment their physical examination in patients with suspected torso and extremity trauma, not only within the standard hospital resuscitation area but also in a variety of other locales. Additionally, ultrasound may be used to supplement the history and physical examination of nontrauma patients presenting with acute abdominal pain and a variety of other time-sensitive diagnoses in the emergency department. Finally, ultrasound may be used in the ICU in a variety of ways to facilitate procedures, detect complications, and augment a surgeon’s physical examination. As such, this chapter begins with a basic introduction to select principles of ultrasound physics and then covers the components, indications, and pitfalls of the common, focused ultrasound examinations used by acute care surgeons who are evaluating trauma patients, nontrauma patients presenting

with acute symptoms, and, finally, critically ill patients in the ICU.

ULTRASOUND PHYSICS Ultrasonography is operator dependent and, therefore, an understanding of select principles of ultrasound imaging is necessary so that images may be acquired rapidly and interpreted correctly. Knowledge of some of these basic principles enables the acute care surgeon to select the appropriate transducer, optimize resolution of the image, and recognize artifacts. Some basic terms and principles of physics relative to ultrasound imaging in the acute setting are defined in Tables 16-1 to 16-3. In general, an ultrasound system includes the following components: (1) a transmitter that controls electrical signals sent to the transducer; (2) a receiver or image processor that admits the electrical signal; (3) a transducer containing piezoelectric crystals to interconvert electrical and acoustic energy; (4) a monitor to display the ultrasound image; and (5) an image recorder or printer.14,15 The ultrasound images that are obtained depend on the orientation of the transducer or probe relative to the structure or organ being imaged, with each transducer having an indicator that directs its orientation to the screen. The indicators on most probes are oriented such that placing the indicator cephalad in a coronal or sagittal plane or to the left in the transverse plane will orient the image correctly left to right. As the image may be purposefully reversed by a machine adjustment, the surgeon should confirm the orientation of the probe by adding ultrasound gel to the probe’s footprint and gently rubbing it to visualize where the motion is detected on the screen. This should allow the surgeon to determine how the indicator will orient the image. The orientations or scanning planes are described in Table 16-4 and the projected

SECTION 2 Frequency Propagation speed

Definition High-frequency (20 kHz) mechanical radiant energy transmitted through a medium Number of cycles/s (106 cycles/s  1 MHz) Speed with which wave travels through soft tissue (1,540 m/s). Propagation speed (determined by density and stiffness of medium) is greater in solids than in liquids and greater in liquids than in gases Gas

Acoustic impedance

Liquid

Solid

Significance Diagnostic ultrasound: 1–30 MHz Medical diagnostic ultrasound: 2.5–10 MHz Increasing frequency improves resolution Higher-frequency transducers (e.g., 7.5 MHz) provide better resolution of tissues To image an organ, the ultrasound wave must be emitted from the transducer, travel through a medium (soft tissue or liquid), strike the organ, and bounce back to the transducer. It is the reflected wave that forms the ultrasound image. Ultrasound waves travel better through solids and liquids (molecules are more compact, less interference) than through gas. Therefore, ultrasound waves do not travel well through air-filled structures (e.g., lungs or bowel). These organs are visualized, however, when they are surrounded by fluid that acts as an acoustic window and allows the through transmission of waves The formation of a good ultrasound image depends on two principles of physics: (1) how well sound waves are transmitted through the tissue (acoustic impedance, which equals the density of the material times the speed of sound through the material) and (2) the amount of sound waves reflected once they hit a target organ. A good ultrasound image, therefore, is formed when sound waves travel well through tissues of higher and similar density, such as the liver and kidney In the presence of subcutaneous emphysema, a large impedance mismatch exists because of the difference in densities between the air-filled tissue and the soft tissue (liver). As a result, the waves travel poorly through the air-filled tissue and not enough of them are reflected back to the transducer to form a good image The air-filled lung is not normally visualized because the air within the lung reflects the sound waves too strongly and, therefore, no image is formed. When a hemothorax or pleural effusion is present, the differences in tissue acoustic impedance between fluid and the lung allow the lung to be visualized Acoustic impedance  density of tissue times the speed of sound in tissue (sound velocity) The strength of the returning wave depends on difference in density between two organs imaged. Structures of different acoustic impedance (e.g., bile and gallstone) are relatively easy to distinguish from one another. Those of similar acoustic impedance (e.g., spleen and kidney) are more difficult to distinguish, although Gerota’s fascia has a higher tissue acoustic impedance (more dense) and, therefore, allows the spleen and kidney to be visualized as two distinct organs

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Term Ultrasound

302

TABLE 16-1 Ultrasound Physics Terminology Relevant to Ultrasound Imaging

Amplitude

Strength or height of wave

Attenuation

Decrease in amplitude and intensity of wave as it travels through a medium; attenuation is affected by absorption, scattering, and reflection Conversion of sound energy into heat Redirection of wave as it strikes a rough or small boundary Return of wave toward transducer Error in imaging. Features on the ultrasound image that do not have precise correspondence to the image being scanned

Absorption Scattering Reflection Artifact

Amplitude and intensity are reduced (attenuated) as waves travel through tissue. The higher the frequency, the more the wave is attenuated. Therefore, higher-frequency transducers cannot visualize deep structures well. Increasing the gain setting on the machine enhances the amplitude of the returning or reflected ultrasound waves. If the gain setting is too high, echo amplification is too strong and the image appears too bright

Liver Kidney Mirror image

kHz  kilohertz; MHz  megahertz.

Surgeon-Performed Ultrasound in Acute Care Surgery

Examples include shadowing (gallstones), reverberation (comet tail, metallic fragment), and mirror image (diaphragm as strong reflector). In the normal sagittal ultrasound image of the lower thoracic cavity, the supradiaphragmatic area (lung) appears to have a similar echogenicity to the liver because of a mirror image artifact. This artifact occurs because the diaphragm acts as a strong reflector of the ultrasound waves, sending them back to the transducer and then re-reflecting them again as they return to the interface of the diaphragm and the liver. (It should be recalled that it is the returning or reflected wave that forms the ultrasound image on the screen.) These re-reflected or smaller waves return to the transducer after the original reflected waves and, therefore, “create” an image that appears to be deeper than the liver and diaphragm, hence the “mirror image”76

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TABLE 16-2 Essential Principles of Ultrasound

SECTION 2

Principle Piezoelectric effect Pulse-echo principle

Explanation Piezoelectric crystals expand and contract to interconvert electrical and mechanical energy When ultrasound waves contact an organ, some are reflected and some are transmitted through the organ or tissue. Reflected waves return to the transducer and generate electrical impulses that are converted to the image seen on the monitor Bound energy

Electrical energy

Tissue Plezoelectric crystals within transducer Ultrasound machine

patient positions on the ultrasound monitor are shown in Fig. 16-1.16 Although diagnostic ultrasound uses transducer frequencies ranging from 1 MHz (megahertz  1 million cycles/s) to 30 MHz, medical diagnostic imaging most often uses frequencies between 2.5 and 10 MHz (Table 16-5). Accordingly, transducers are chosen on the basis of the depth of the structure or organ to be imaged. High-frequency transducers (5 MHz) provide excellent resolution for imaging superficial structures such as an abscess in the soft tissue of an extremity. Lowerfrequency transducers emit waves that penetrate deeply into the tissue and, therefore, are preferred for visualizing organs such as the liver or spleen.14,17,18 Tips to maximize accuracy and quality of ultrasound imaging relative to the above-mentioned physics principles are listed in Table 16-6.

TABLE 16-3 Terminology Used in Interpretation of Ultrasound Images Term Echogenicity

Anechoic Isoechoic Hypoechoic Hyperechoic

Definition Degree to which tissue echoes the ultrasonic waves (generally reflected in ultrasound image as degree of brightness) Showing no internal echoes, appearing dark or black Having appearance similar to that of surrounding tissue Less echoic or darker than surrounding tissue More echoic or brighter than surrounding tissue

Adapted from Hedrick WR, Hykes L, Starchman DE. Glossary. In: Ultrasound Physics and Instrumentation. 3rd ed. St. Louis, MO: Mosby; 1995:355.

SURGEON-PERFORMED ULTRASOUND IN TRAUMA ■ FAST Developed for the evaluation of injured patients, the Focused Assessment for the Sonographic Examination of the Trauma Patient (FAST) is a rapid diagnostic examination to assess patients with potential injuries to the torso. The test sequentially surveys for the presence or absence of fluid in the pericardial sac and in the dependent abdominal regions, including

TABLE 16-4 Scanning Planes Used in Ultrasound Imaging16 Scanning Plane (Fig. 16-2) Sagittal

Transverse

Coronal

Definition Divides body into right and left sections parallel to long axis Divides body into superior and inferior sections perpendicular to long axis Divides body into anterior and posterior sections perpendicular to sagittal and parallel to long axis

Transducer Orientation Transducer indicator points toward patient’s head Transducer indicator points toward patient’s right side Transducer indicator points toward patient’s head when imaging exteriorly

Adapted from Tempkin BB. Scanning planes and methods. In: Tempkin BB, ed. Ultrasound Scanning: Principles and Protocols. Philadelphia, PA: WB Saunders Company; 1993:7.

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Sagittal

Coronal

Transverse

FIGURE 16-1 Scanning planes used in ultrasound imaging. (Adapted with permission from Tempkins BB. Scanning Planes and Methods. Ultrasound Scanning: Principles and Protocols. Philadelphia, PA: WB Saunders Company; 1993, © Elsevier.)

Morison’s pouch region in the right upper quadrant (RUQ), the left upper quadrant (LUQ) behind the spleen and between the spleen and kidney, and the pelvis posterior to the bladder. Surgeons can perform the FAST during the primary or secondary survey of the American College of Surgeons Advanced Trauma Life Support19 algorithm and, although minimal patient preparation is needed, a full urinary bladder is ideal to provide an acoustic window for visualization of blood in the pelvis. Blood, as any fluid, will accumulate in dependent regions of the abdomen.20 In the supine position, this corresponds to Morison’s pouch, the splenorenal recess, and above the spleen

TABLE 16-5 Clinical Applications of Selected Transducer Frequencies Frequency (MHz) 2.5–3.5

5.0

7.5

Applications General abdominal FAST Transvaginal Pediatric abdominal Testicular Vascular Soft tissue Thyroid Pneumothorax

MHz  megahertz; FAST  Focused Assessment for the Sonographic Examination of the Trauma Patient.

as well as in the pelvis posterior to the bladder. All these regions may be visualized rapidly and dependably with the FAST. Furthermore, ultrasound is an excellent modality for the detection of intra-abdominal fluid, having been shown to detect ascites in small amounts.21,22 Although the exact minimum amount of intraperitoneal fluid that can be detected by ultrasound is not known,23 most authors agree that it is a sensitive modality. The FAST is performed in a specific sequence for several reasons. The pericardial area is visualized first so that blood within the heart can be used as a standard to set the gain (Table 16-1). Most modern ultrasound machines have presets so that the gain does not need to be reset each time the machine is turned on. Occasionally, if multiple types of examinations are performed with different transducers, the gain should be checked to ensure that intracardiac blood appears anechoic. This maneuver ensures that a hemoperitoneum will also appear anechoic and will be readily detected on the ultrasound image. The abdominal part of the FAST begins with a survey of the RUQ that is the location within the peritoneal cavity where blood most often accumulates and is most readily detected with the FAST. Indeed, investigators from four Level I trauma centers examined true-positive ultrasound images of 275 patients who sustained either blunt (#220) or penetrating (#55) injuries.24 They found that regardless of the injured organ (with the exception of those patients who had an isolated perforated viscus), blood was most often identified on the RUQ image of the FAST. This can be a time-saving measure because when hemoperitoneum is identified on the FAST examination of a hemodynamically unstable patient, that image alone, in combination with the patient’s clinical picture, is

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TABLE 16-6 Maximizing Accuracy in Ultrasound Imaging

SECTION 2

1. Proper maintenance of the ultrasound machine as per the guidelines of the institution’s department of biomedical engineering is recommended 2. Apply liberal amounts of gel to the area being examined. The gel acts as an acoustic coupling agent to help transmit the ultrasound waves and reduce the amount of reflection 3. Manipulate the transducer only slightly (not wide sweeps) and apply gentle pressure initially. This is particularly helpful when imaging soft tissue as too much pressure will compress the area and distort the image 4. Perform an ultrasound examination of normal tissue first, before examining the area in question. For example, when trying to assess an abscess or deep vein thrombosis in an extremity, inspect the normal extremity first so that you can see the normal tissue. This will help distinguish subtle pathologic changes in the abnormal tissue 5. If the left upper quadrant of the abdomen is difficult to visualize, insert a nasogastric tube to decompress the stomach and minimize air so that it does not interfere with the transmission of the ultrasound waves 6. A full bladder is needed to act as an acoustic window so that pelvic structures can be visualized. If the bladder is not full enough because a urinary catheter has already been inserted, clamping the urinary catheter will allow the bladder to fill and the examination can be repeated. A full bladder compressed in the “oval shape” and surrounded by hematoma may be an indirect sign of a pelvic fracture 7. Blood vessels are usually identified with only B-mode ultrasound but occasionally differentiating the artery from the vein may be difficult because of transmitted pulsations from the artery. Application of the Doppler mode, compression of the vessel (veins compress very easily), or having the patient perform the Valsalva maneuver can help differentiate arterial and venous anatomy

FIGURE 16-2 Schematic diagram of transducer positions for FAST: pericardial, right upper quadrant, left upper quadrant, and pelvis.

identify the heart and to examine for blood in the pericardial sac. The normal and abnormal views of the pericardial area are shown in Fig. 16-3. The subxiphoid image is usually not difficult to obtain, but a severe injury to the chest wall, a very narrow subcostal area, subcutaneous emphysema, or morbid obesity can prevent a satisfactory examination.25 Both of the latter conditions are associated with poor imaging because air and fat reflect the wave too strongly and prevent penetration into the target organ.14 If the subcostal pericardial image cannot be obtained or is suboptimal, a parasternal ultrasound view of the heart should be performed (Figs. 16-4 and 16-5). Next, the transducer is placed in the right anterior or midaxillary line between the 11th and 12th ribs to obtain sagittal images of the liver, kidney, and diaphragm (Fig. 16-6) and determine the presence or absence of blood in Morison’s pouch and in the right subphrenic space. Next, attention is

Abnormal

Normal Blood

sufficient to justify an immediate abdominal operation.24 In a stable patient, following the exam of the RUQ, the LUQ and pelvis are visualized as discussed below.

Technique Ultrasound transmission gel is applied on four areas of the thoracoabdomen, and the examination is conducted in the following sequence: the pericardial area, RUQ, LUQ, and the pelvis (Fig. 16-2). A 3.5-MHz convex transducer is oriented for sagittal or longitudinal views and positioned in the subxiphoid region to

FIGURE 16-3 (Left) Sagittal view of pericardial area showing pericardium as single echogenic line (normal). (Right) Sagittal view of pericardial area showing separation of visceral and parietal areas of pericardium with blood (arrow) that appears anechoic.

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A FIGURE 16-4 Transducer position for left parasternal view of heart.

Normal turned to the LUQ. With the transducer positioned in the left posterior axillary line between the 10th and 11th ribs, the spleen and left kidney are visualized and the presence or absence of blood between the two organs and in the left subphrenic space is determined (Fig. 16-7). The splenic window is often the most difficult window to adequately visualize and the probe should be placed significantly more posterior (posterior axillary line) and superior (one to two rib spaces higher) than with the RUQ window. Finally, the transducer is directed for a transverse view and placed about 4 cm superior to the symphysis pubis. It is slowly swept inferiorly to obtain a coronal view of the full bladder and the pelvis examining for the presence or absence of blood (Fig. 16-8).

Accuracy of the FAST Improper technique, inexperience of the examiner, and inappropriate use of ultrasound have long been known to adversely impact the accuracy of ultrasound imaging. More recently, the etiology of injury, the presence of hypotension on admission, and select associated injuries have also been shown to influence the accuracy of this modality.2,3,8 Failure to consider these factors has led to inaccurate assessments of the accuracy of the FAST by comparing it inappropriately to a CT scan and

Abnormal

Normal Blood

FIGURE 16-5 Normal (left) and abnormal (right) heart, parasternal view.

Abnormal

Blood

B FIGURE 16-6 (A) Normal sagittal view of liver, kidney, and diaphragm. Note Gerota’s fascia is hyperechoic. (B) Abnormal sagittal view of liver, kidney, and diaphragm. Note fluid (blood) in between liver and kidney (arrows).

not recognizing its role in the evaluation of patients with penetrating torso trauma.26,27 Both false-positive and -negative pericardial ultrasound examinations have been reported to occur in the presence of a massive hemothorax or mediastinal blood.4,8,10,28 Repeating the FAST after the insertion of a tube thoracostomy improves the visualization of the pericardial area and decreases the number of false-positive and -negative studies. While false studies may occur, a rapid focused ultrasound survey of the subcostal pericardial area is a very accurate method to detect hemopericardium in most patients with penetrating wounds in the “cardiac box.”4,10 In a large study of patients who sustained either blunt or penetrating injuries, the FAST was 100% sensitive and 99.3% specific for detecting hemopericardium in patients with precordial or transthoracic wounds. Furthermore, the use of pericardial ultrasound has been shown to be especially helpful in the evaluation of patients who have no overt signs of pericardial tamponade. This was highlighted in a study in which 10 of 22 patients with precordial wounds and a hemopericardium on an ultrasound examination had admission systolic blood pressures 110 mm Hg and were relatively asymptomatic. Based on these signs and the lack of symptoms, it is unlikely that the presence of cardiac wounds would have been strongly suspected in these patients and, therefore, this rapid ultrasound

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SECTION 2

Normal

Abnormal Blood

Blood

FIGURE 16-7 (Left) Normal sagittal view of spleen, kidney, and diaphragm. (Right) Abnormal sagittal view of spleen, kidney, and diaphragm with fluid (blood) in between spleen and kidney and above the spleen in the subphrenic space.

examination provided an early diagnosis of hemopericardium before the patients underwent physiologic deterioration. The FAST is also very accurate when it is used to evaluate hypotensive patients who present with blunt abdominal trauma. In this scenario, ultrasound is so accurate that when the FAST is positive, an immediate operation is justified.4,8,10,29 Because the FAST is a focused examination for the detection of blood in dependent areas of the abdomen, its results should not be compared to those of a CT scan because the FAST does not readily identify intraparenchymal or retroperitoneal injuries. Therefore, select hemodynamically stable patients considered to be at high risk for occult intra-abdominal injury should undergo a CT scan of the abdomen regardless of

Normal

Abnormal

Blood

FIGURE 16-8 (Left) Normal coronal view of full urinary bladder. (Right) Abnormal coronal view of full bladder with fluid in pelvis. (Note the bowel floating in fluid.)

the results of the FAST examination. These patients include those with fractures of the pelvis or thoracolumbar spine, major thoracic trauma (pulmonary contusion, lower rib fractures), and hematuria. These recommendations were based on the results of two studies by Chiu et al. in 199730 and Ballard et al. in 1999.31 Chiu et al. reviewed their data on 772 patients who underwent FAST examinations after sustaining blunt torso injury. Of the 772 patients, 52 had intra-abdominal injury but 15 (15/52  29%) of them had no hemoperitoneum on the admitting FAST examination or on the CT scan of the abdomen. In other work conducted by Ballard et al. at Grady Memorial Hospital, an algorithm was developed and tested over a 3.5-year period to identify patients who were at high risk for occult intra-abdominal injuries after sustaining blunt thoracoabdominal trauma.31 Of the 1,490 patients admitted with severe blunt trauma, there were 102 (70 with pelvic fractures, 32 with spine injuries) who were considered to be at high risk for occult intra-abdominal injuries. Although there was only 1 false-negative FAST examination in the 32 patients who had spine injuries, there were 13 false negatives in those with pelvic fractures. Based on these data, the authors concluded that patients with pelvic fractures should have a CT scan of the abdomen regardless of the result of the FAST examination. The lower accuracy of the FAST in patients with pelvic fractures was again noted in a recent series published by Friese et al., in which an initial FAST examination had an 85% positive predictive value but only a 63% negative predictive value in 146 patients with pelvic fractures.32 These studies have helped provide guidelines to decrease the number of false-negative FAST studies, but, as with the use of any diagnostic modality, it is important to correlate the results of the test with the patient’s clinical picture. Suggested

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BAT

US

US

POS

POS

Equivocal

NEG

OR

OR (pericardial window)

Observation

A

Equivocal

Stable

Unstable

CT

OR

Stable

CT

DPL

NEG

Repeat US

Unstable DPL or OR

POS*

NEG*

B

FIGURE 16-9 (A) Algorithm for the use of ultrasound in patients with penetrating chest wounds. (B) Algorithm for the use of ultrasound in patients with blunt abdominal trauma.

algorithms for the use of FAST are depicted in Fig. 16-9A and B. Indeed, the FAST exam has been included in the most recently published evidence-based guidelines for the evaluation of patients with blunt abdominal trauma from the Eastern Association for the Surgery of Trauma (EAST) with reported accuracy rates of 96–98%.33

Quantification of Blood The amount of blood detected on the abdominal CT scan34 or in the DPL aspirate (or effluent) has been shown to predict the need for operative intervention.35 Similarly, the quantity of blood that is detected with ultrasound may be predictive of a therapeutic operation.36,37 Huang et al. developed a scoring system based on the identification of hemoperitoneum in specific areas such as Morison’s pouch or the perisplenic space.36 Each abdominal area was assigned a number from 0 to 3, and the authors found that a total score of 3 corresponded to more than 1 L of hemoperitoneum. This scoring system had a sensitivity of 84% for determining the need for an immediate abdominal operation. Another scoring system developed and prospectively validated by McKenney et al. examined the patient’s admission blood pressure, base deficit, and the amount of hemoperitoneum present on the ultrasound examinations of 100 patients.37 The hemoperitoneum was categorized by its measurement and its distribution in the peritoneal cavity, so that a score of 1 was considered a minimal amount of hemoperitoneum but a score of 3 signified a large hemoperitoneum. Forty-six of the 100 patients had a score 3, and 40 (87%) of them underwent a therapeutic abdominal operation. This scoring system had a sensitivity, specificity, and accuracy of 83%, 87%, and 85%, respectively. The authors concluded that an ultrasound score of 3 is statistically more accurate than a combination of the initial systolic blood pressure and base deficit for determining which patients will undergo a therapeutic abdominal operation. Although the quantification of hemoperitoneum is not exact, it can provide valuable information about the need for an abdominal operation as well as its potential to be therapeutic.

Recent Advances and Organ Specificity As surgeons have become more facile with ultrasound exams and as technology has improved, extensions of the FAST exam have been described. Again, it is noted that the standard FAST exam is designed to accurately answer two simple questions: Is there fluid in the peritoneal cavity and is their fluid in the pericardial sac? The use of ultrasound for more complex diagnostic interventions is described below, but these areas are less well studied and beyond the purview of the traditional FAST exam. A more recent prospective, multicenter trial conducted by the Western Trauma Association reported on the use of ultrasound to serially evaluate patients with documented solid organ injuries (SOI) after trauma.38 The so-called BOAST exam, or the bedside organ assessment with sonography after trauma, was performed by a limited number of experienced surgeon sonographers in 126 patients with 135 SOI in 4 American trauma centers. This study, performed over nearly 2 years, was designed to be a more thorough abdominal ultrasound examination with multiple views obtained of each solid organ (kidneys, liver, and spleen). Criteria for enrollment included normal hemodynamics, absence of peritonitis or other need for urgent laparotomy, and lack of excessive blood transfusion in the attending physician’s judgment. All patients were victims of blunt trauma with a mean Injury Severity Score (ISS) of nearly 15. Overall, only 34% of injuries to solid organs were seen with BOAST yielding an error rate of 66%. None of the 34 grade I injuries were identified and only 13 (31%) of the grade II injuries were identified. Sensitivities for grade III and IV injuries ranged from 25% to 75% and only one grade V injury (to the liver) was examined and positively identified. Eleven patients developed 16 intra-abdominal complications (8 pseudoaneurysms, 4 bilomas, 3 abscesses, and 1 necrotic organ), and 13 (81%) were identified by the sonographers. This study emphasizes that ultrasound, in most surgeons’ hands, should not be considered a reliable modality for diagnosis and grading of SOI although it may be acceptably accurate in the diagnosis of post-traumatic abdominal complications in patients with SOI managed nonoperatively.

CHAPTER 16

Penetrating chest wound

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In Europe, preliminary work using Power Doppler ultrasonography to identify specific organ injuries has been published in recent years.39,40 Many of these exams include the use of a sonographic contrast agent injected peripherally during the scan. In one study, the authors were able to document extravasation of contrast in 20 of 153 patients (13%). Extravasation was seen not only from the spleen, liver, and kidney after trauma but also in postoperative patients (aortic aneurysm repair, postsplenectomy) and in a patient with a ruptured aortic aneurysm. In 9 of 20 patients, CT scan was performed and all 9 confirmed extravasation of contrast. In the 133 patients without extravasation, the absence of active bleeding was inferred by a subsequent CT scan in 82 patients, surgical data in 13 patients, and clinical follow-up in 38 patients, with no cases of active bleeding missed by ultrasound. Thus, the addition of an ultrasonic contrast agent and Power Doppler may be of some benefit in the diagnosis of specific injuries. It should be emphasized, however, that the FAST exam in most American trauma centers is used simply as a screening tool to identify the presence or absence of hemoperitoneum or hemopericardium in a trauma patient.

FIGURE 16-10 Transducer positions for thoracic ultrasound examination (detection of hemothorax).

A focused thoracic ultrasound examination was developed by surgeons to rapidly detect the presence or absence of a traumatic hemothorax in patients during the ATLS secondary survey.9 This focused thoracic ultrasound examination employs the ultrasound physics principles of the mirror image artifact and tissue acoustic impedance as presented in Table 16-1. A test that promptly detects a traumatic effusion or hemothorax is worthwhile because it dramatically shortens the interval from the admission of the patient with hemothorax to the insertion of a thoracostomy tube.

and also uses the same type and frequency transducer. In point of fact, it is performed one to two rib spaces higher than the RUQ and LUQ FAST views using the same probe. Ultrasound transmission gel is applied to the right and left lower thoracic areas in the midaxillary to posterior axillary line between the 9th and 10th intercostal spaces (Fig. 16-10). The transducer is slowly advanced cephalad to identify the hyperechoic diaphragm and to interrogate the supradiaphragmatic space for the presence or absence of fluid (Fig. 16-11A and B) that appears anechoic. In the positive thoracic ultrasound examination, the hypoechoic lung can be seen “floating” amidst the fluid. The same technique can be used to evaluate a critically ill patient for a pleural effusion as discussed earlier.

Technique

Accuracy

The technique for this examination is similar to that used to interrogate the upper quadrants of the abdomen in the FAST

One of the earliest reports on the use of ultrasound for the evaluation of fluid collections in the pleural space was described

■ Traumatic Hemothorax

Blood Diaphragm Lung Blood

A

B

FIGURE 16-11 (A) Sagittal view of liver, kidney, and diaphragm. Note supradiaphragmatic (lung) area but absence of pleural effusion. (B) Sagittal view of right supradiaphragmatic space. The right hemithorax contains fluid (blood) that appears anechoic.

Surgeon-Performed Ultrasound in Acute Care Surgery

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by Joyner et al. in 1967.41 Later, Gryminski et al. documented the superiority of ultrasound over standard radiography for the detection of pleural fluid.42 In that study, they reported that ultrasound detected even small amounts of pleural fluid in 74 (93%) of 80 patients, whereas plain radiography detected pleural fluid in only 66 (83%) of these patients. Surgeons at Emory University have also examined the accuracy of this examination in 360 patients with blunt and penetrating torso injuries.9 They compared the time and accuracy of ultrasound with that of the supine portable chest x-ray and found both to be very similar with 97.4% sensitivity and 99.7% specificity observed for thoracic ultrasound versus 92.5% sensitivity and 99.7% specificity for the portable chest x-ray. Performance times, however, for the thoracic ultrasound examinations were statistically much faster (P  .0001) than those for the portable chest x-ray. Although it is not recommended that the thoracic ultrasound examination replace the chest x-ray, its use can expedite treatment in many patients and decrease the number of chest radiographs obtained.

■ Pneumothorax The use of ultrasound for the detection of a traumatic pneumothorax is not a new diagnostic test, having been reported by numerous acute care surgeons dating back to the early 1990s.43–47 This examination is useful to the surgeon to evaluate a patient for a potential pneumothorax in the following circumstances: (1) bulky radiology equipment is not readily available; (2) inordinate delays for obtaining a chest x-ray are anticipated; or (3) numerous injured patients (mass casualty situation) must be rapidly assessed and triaged.48,49 Although useful in the trauma resuscitation area, surgeons may also find this examination helpful to detect a pneumothorax in a critically ill patient who is on a ventilator, after a thoracentesis procedure, or, potentially, after discontinuing the suction on an underwater seal device.

Technique A 5.0- to 7.5-MHz linear array transducer is used to evaluate a patient for the presence of a pneumothorax. The examination may be performed while the patient is in the erect or the supine position. Ultrasound transmission gel is applied to the right and left upper thoracic areas at about the third to fourth intercostal space in the midclavicular line and the presumed unaffected thoracic cavity is examined first. The transducer is oriented for longitudinal imaging, is placed perpendicular to the ribs, and is slowly advanced medially toward the sternum and then laterally toward the anterior axillary line. The normal examination of the thoracic cavity identifies the rib (seen as black on the ultrasound image because it is a refraction artifact), pleural sliding, and a comet tail artifact (Table 16-1). Pleural sliding is the identification of the visceral and parietal layers of the lung seen as hyperechoic superimposed pleural lines. When a pneumothorax is present, air becomes trapped between the visceral and parietal pleura and does not allow for the transmission of the ultrasound waves. Therefore, the

311

FIGURE 16-12 Comet tail artifact (arrow).

visceral pleura is not imaged and pleural sliding is not observed. The comet tail artifact is generated because of the interaction of two highly reflective opposing interfaces, that is, air and pleura (Fig. 16-12). When air separates the visceral and parietal pleurae, the comet tail artifact is not visualized. If desired, the examination may be repeated with the transducer oriented for transverse views, with images obtained with the probe parallel to the ribs.

Accuracy Several studies have documented excellent sensitivity and specificity of ultrasound for the detection of a pneumothorax in the resuscitation area.43,45,46,50 Dulchavsky et al. from Detroit Receiving Hospital, Wayne State University, showed that ultrasound can be successfully used by surgeons to detect a pneumothorax in injured patients.51 Of the 382 patients (364 trauma; 18 spontaneous) evaluated with ultrasound, 39 had pneumothoraces and ultrasound successfully detected 37 of them, yielding a 95% sensitivity. Not unexpectedly, pneumothoraces in two patients could not be detected because of the presence of significant subcutaneous emphysema. The authors recommended that when a portable chest x-ray cannot be readily obtained, the use of this bedside ultrasound examination for the identification of a pneumothorax can expedite the patient’s management. One study, published in 2006, however, documents significant loss of accuracy of an ultrasound examination starting about 24 hours after chest tube insertion.52 This study documents the hospital course of 14 patients with tube thoracostomies undergoing 126 ultrasound examinations over

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their hospital course. While ultrasound detection of pleural sliding in uninstrumented pleural cavities remained 100% accurate over time, the accuracy of ultrasound examination after chest instrumentation fell to 65% after 24 hours.52 It was theorized that adhesion formation led to false-positive examinations, in that normal pleural sliding was unable to be appreciated in patients with lung adhesions. This point illustrates the subtle difference in the usefulness of the ultrasound examination for pneumothorax: a “positive” examination is related to the absence of a normal finding (pleural sliding) rather than the presence of abnormal finding (i.e., fluid within the peritoneal cavity after blunt abdominal trauma). Thus, other causes of the loss of sliding (i.e., adhesion formation) can cause a false-positive and misleading examination. Indeed, a review of the literature revealed studies in animal models in which significant adhesion formation occurred as early 24 hours after thoracotomy.53 This same study also noted that the rapidity and degree of adhesion formation not only was variable based on the type and degree of injury but also varied within animals with similar injuries.53 Thus, one should be cautious when interpreting ultrasound examinations in patients with acute or chronic evidence of chest manipulation as false-positive studies may occur.52

■ Sternal Fracture Fractures of the sternum are visualized on a lateral x-ray view of the chest, but this film may be difficult to obtain in a patient with multiple injuries. For this reason, an ultrasound examination of the sternum can rapidly detect a fracture while the patient is still in the supine position and, therefore, avoid the need to obtain a lateral x-ray.54

Technique The ultrasound examination of the sternum is performed using a high-frequency (5.0 MHz) linear array transducer that is oriented for sagittal (longitudinal) views. Ultrasound transmission gel is applied over the sternal area while the patient is in the supine position. Beginning at the suprasternal notch, the transducer is slowly advanced in a caudad direction to interrogate the bone for a fracture. The examination is then repeated with the transducer oriented for transverse views. The examination of the intact sternum is shown in Fig. 16-13. A sternal fracture is identified on the ultrasound examination as a disruption of the cortical reflex (Fig. 16-14). Investigators have found that the use of ultrasound for this diagnosis is more accurate (and much more rapid) than a lateral x-ray view of the chest.54

■ Special Situations

Skin

Normal sternum

FIGURE 16-13 Sagittal view of sternum. Normal findings.

nized abdominal trauma is a major problem in the pregnant trauma patient.19 Concerns over changes in abdominal anatomy leading to difficulty in obtaining images have not borne out in objective evaluations. Goodwin et al.55 reported on their 8-year experience with the FAST exam in 127 pregnant patients, including 5 of 6 patients with hemoperitoneum who were found to have fluid on the FAST exam (sensitivity 83%). Of the 120 without abdominal injury, 117 had a truenegative FAST (specificity 98%), with three false-positive exams due to serous intraperitoneal fluid. Furthermore, Brown et al.56 reported on their experience with a more extensive ultrasound exam in 101 stable, pregnant patients with suspected blunt abdominal trauma. Median gestational age was just over 24 weeks, and these patients underwent an official abdominal ultrasound by a certified technician to include images of the fetus and placenta. The sensitivity was 80% (four of five patients had correct identification of injuries) with one missed placental hematoma that required an emergent cesarean delivery for fetal distress. Injuries identified included one placental abruption, two splenic lacerations, one hepatic laceration, and one renal injury. None of the 96 patients with a negative ultrasound had injuries dis-

Skin

Fractured sternum

Ultrasound in the Pregnant Trauma Patient Ultrasound would seem to be an ideal method of evaluating a pregnant patient with suspected blunt abdominal trauma as it is portable, noninvasive, and free of ionizing radiation. The Advanced Trauma Life Support course teaches that unrecog-

FIGURE 16-14 Sagittal view of sternum illustrating fracture (interruption of hyperechoic line).

Surgeon-Performed Ultrasound in Acute Care Surgery

Ultrasound in Penetrating Trauma Ultrasound for the diagnosis of injuries after penetrating trauma has been studied much less extensively than ultrasound used after blunt trauma. Several of the larger, well-known series4,9,10 have included patients with penetrating trauma and, as stated previously, ultrasound of the pericardium has been shown to be accurate for diagnosis of injury in patients with penetrating injury to the “cardiac box.”9 In a recent study of 32 patients with penetrating anterior chest trauma, ultrasound was used to diagnose 8 pericardial effusions with a reported 100% accuracy (8 true-positive and 24 true-negative exams).57 Eight other patients were noted to have intraperitoneal fluid and underwent therapeutic exploration including repair of five diaphragmatic injuries, three hepatic lacerations, three splenic lacerations, three gastric injuries, two injuries to the small bowel, and one injury to the adrenal gland. No false-positive or false-negative examinations of the peritoneum were reported. Other studies have shown that the accuracy of FAST after penetrating trauma is somewhat less with one study reporting a sensitivity for abdominal injury after penetrating trauma as low as 67%.58 A recent report by Murphy et al. looked at the utility of ultrasound to diagnose fascial penetration after anterior abdominal stab wounds.59 In this study, 35 patients underwent ultrasonic evaluation of their anterior abdominal fascia with an 8.0-MHz linear array probe followed by a local wound exploration. While ultrasound had only a 59% sensitivity (13/22 patients), it did have a 100% specificity with no falsepositive studies. Thus, if fascial penetration is noted on ultrasound, a more invasive wound exploration is probably not needed; however, a negative ultrasound evaluation is clearly less helpful and does not preclude peritoneal penetration.

Ultrasound in Pediatric Trauma Patients Ultrasound as a modality would seem to be attractive for use in a pediatric population for many of the same reasons that have already been elaborated upon, including the lack of radiation exposure and the noninvasive nature of the examination. Many of the early studies in the pediatric literature regarding the use of ultrasound after trauma involved studies performed by radiologists or sonographers.27,60,61 However, there are now several studies of surgeon-performed FAST examinations that show similar sensitivities, specificities, and accuracies as in the adult population.62–64 For example, in a series by Soundappan et al.,64 FAST examination had a sensitivity of 81%, a specificity of 100%, and an accuracy of 97% in a group of 85 pediatric patients who were victims of blunt abdominal trauma. Thus, while the literature is not as robust as in the adult population, the use of surgeon-performed ultrasound in the pediatric trauma bay is becoming much more widespread.

■ Ultrasound in Austere Settings Ultrasound on Deployment The portability of ultrasound makes it ideal for use in forward settings. Training courses are in place to teach the use of the FAST exam to military surgeons, and handheld ultrasound is now routinely deployed within the British Defence Medical Services.65 Indeed, in a survey of surgeons reviewing potential preventable casualties in Vietnam, ultrasound was the fourth most commonly mentioned advancement in technology (behind modern ventilators, CT scanners, and modern antibiotics) that may have assisted in better patient salvage.66 Although up to 90% of war wounds are penetrating, ultrasound may allow quicker, more accurate triage decisions as patients with penetrating abdominal trauma with no or minimal hemoperitoneum may be transferred to the next echelon where the study may be repeated or additional diagnostic maneuvers undertaken.67 In a study from the Croatian conflict in 1999, FAST was shown to have a sensitivity of 86%, a specificity of 100%, and an accuracy of 97% when applied to 94 casualties evaluated over a 72-hour period. This was comparable to the accuracy achieved by the authors in their civilian experience with FAST in more than 1,000 patients over the 3 years prior to the conflict. In a somewhat recent small series,67 FAST was used with excellent results in a British military hospital in Iraq. Fifteen casualties were evaluated with serial FAST exams, and 14 had negative exams at admission and again at 6 hours. One patient underwent laparotomy based on trajectory and had no intraperitoneal fluid but two small holes were discovered in the cecum that required repair. The other 13 patients recovered without sequelae. One exam was positive and led to immediate laparotomy in a patient with a grade V liver injury after a motor vehicle collision. Because ultrasound is portable enough to use in active combat situations, research is ongoing to evaluate the best method to teletransmit images obtained in the field. Several different satellite transmission systems have been evaluated, and high-quality images were able to be obtained in the majority of cases; however, the balance between the weight of the system and the minimum image quality has still not been completely achieved.67 It has been noted that images can be transmitted from up to 1,500 ft from the antennae without significant degradation.68 As technology advances, one would expect imaging systems to continue to become smaller and lighter with improved image quality, making ultrasound even more appealing as a modality for use in the forward setting.

Ultrasound in Space Many of the same qualities that make ultrasound appealing for use in combat make it equally appealing as a diagnostic modality in space, where an injury might mandate abortion of a multimillion dollar mission. Indeed, ultrasound is one of the only feasible diagnostic modalities on space missions, given size and weight restrictions. Also, ultrasound examinations are easily taught and images can be relayed with minimal delay to physicians on the ground. ATLS procedures are also feasible

CHAPTER 16

covered later in their hospital course (specificity 100%). Thus, it would seem that ultrasound remains a good screening tool for the pregnant patient with blunt abdominal trauma and has the advantages of repeatability and a lack of radiation exposure.

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in space,69 and lifesaving procedures could be performed based on ultrasound findings. Ultrasound has been used in space for several decades. Indeed, it has been ultrasound technology that has taught us much about the physiologic effects of microgravity, especially the fluid shifts associated with space travel.70 As early as 1982, cardiac ultrasound was used to evaluate left ventricular systolic function and cardiac chamber size in cosmonauts. The first American ultrasound system in space was the American flight echograph from Advanced Technology Laboratories (Bothel, WA) that first flew in 1984 and eventually was capable of threedimensional images using a tilt frame device. Currently, the Human Research Facility aboard the International Space Station is equipped with a state-of-the-art Philips HDI 5000 (Philips Medical, Bothel, WA).70 Because surface tension and capillary action are the principal physical forces in space, scientists questioned whether images obtained on the standard FAST exam would be useful in microgravity. There are now several published studies of ultrasounds performed on parabolic flights in the NASA Microgravity Research Facility, a KC-135 aircraft. This aircraft can generate 25- to 30-second intervals of weightlessness using serial parabolic trajectories. A porcine model of intra-abdominal hemorrhage was created on the ground and studied during parabolic flights.71 Over 2,000 ultrasound segments were recorded with 80% of these considered feasible for diagnosis of the presence or absence of abdominal fluid. The sonographers felt the exam was no more difficult than one done on the ground as long as the sonographer and patient were adequately restrained. For the intraperitoneal portion of the exam, a fourth view (the midline “abdominal sweep”) was added and, with this addition, the FAST exam was able to reliably detect even relatively small amounts of intraperitoneal fluid. The Morison’s pouch view remained the most sensitive window for fluid detection.71 Further study using a similar model revealed that ultrasound can also reliably detect both hemothorax and pneumothorax in microgravity.72 Recently, astronauts aboard the International Space Station performed FAST ultrasounds that were transmitted with a 2-second satellite delay to directors on the ground, who were able to provide them with real-time instructions for probe position and system adjustments. Exams were able to be completed in roughly 5 minutes with adequate images obtained in all views.73 Astronauts have also been able to perform comprehensive ocular ultrasounds with the same real-time feedback.74 In summary, ultrasound fulfills all the necessary criteria for a diagnostic modality in space. It is sufficiently portable, teletransmittable, teachable, and accurate. It will likely continue to be the only feasible technology to assist with medical diagnoses on space missions in the near future.

SURGEON-PERFORMED ULTRASOUND IN ACUTE SURGICAL DISORDERS Given the acceptance of surgeon-performed ultrasound in the trauma setting, as described above, it is only logical for surgeons to build on their experience and extend the use to other aspects

of acute care surgery, including the evaluation of the stable and unstable patients with acute abdominal pain.

■ Evaluation of the Stable Patient with Acute Abdominal Pain While there remains no substitute for an adequate and accurate history and physical examination, an ultrasound examination may provide additional information that helps a surgeon determine the patient’s need for urgent intervention. While ultrasound imaging has several uses in the stable patient with abdominal pain, it is likely most useful for the assessment of patients with RUQ pain. In a patient with RUQ pain, ultrasound can demonstrate the presence or absence of gallstones, an abnormally thickened gallbladder wall, sludge within the gallbladder, or a dilated common bile duct. The presence of these sonographic signs of gallbladder disease, combined with the patient’s clinical condition, provides the surgeon with immediate information that may narrow the differential diagnosis and expedite the patient’s treatment. In an older series, Laing et al. studied the usefulness of ultrasound imaging in 52 patients with acute RUQ pain. The 52 patients were able to be accurately triaged into one of three approximately equal groups: those with acute cholecystitis (18/52), those with chronic cholecystitis (17/52), or those with nonbiliary conditions (17/52).75 In the acute cholecystitis group, there was one false-negative and five false-positive examinations yielding a sensitivity of 94% and a specificity of 85%. In the chronic cholecystitis group, the sensitivity and specificity were 71% and 97%, respectively.75 In a more recent European study, the use of ultrasound as an adjunct to initial evaluation of a general group of patients with abdominal pain was shown to increase a surgeon’s diagnostic accuracy by about 10%. It was helpful in confirming a correct diagnosis in roughly 25% of evaluations and was helpful in ruling out specific causes in roughly another 25%, being noncontributory in nearly 40% of cases.76 Another randomized study published by the same authors noted that the use of surgeon-performed ultrasound allowed for significantly fewer subsequent studies, a lower “admission for observation” rate, and a higher proportion of patients submitted directly to surgery from the emergency department.77 Finally, a recent study showed a higher self-rated patient satisfaction rating on emergency department discharge in a group of patients receiving a surgeon-performed ultrasound over patients evaluated by the same surgeons without an ultrasound examination, although there was no noted change in patient mortality or other outcome.78

■ Evaluation of the Unstable Patient with Acute Abdominal Pain Surgeons are often asked to evaluate a hypotensive patient with abdominal pain who is unable to provide an adequate history due to his or her existing shock state. In addition to resuscitation, the surgeon must quickly initiate an evaluation aimed at defining the cause of the abdominal catastrophe. Ultrasound imaging can be very helpful in this clinical scenario to identify

Surgeon-Performed Ultrasound in Acute Care Surgery

■ Dehiscence and Soft Tissue Infections Soft tissue infections may be difficult to assess by physical examination because the signs of infection may only be superficial and may not reflect the status of the entire wound. With the ultrasound transducer in hand, the surgeon can assess the presence, depth, and extent of an abscess at the patient’s bedside and determine the appropriate treatment. Furthermore, the collection can be localized to ensure its complete drainage, especially if it is loculated. In the postoperative period, wounds can be imaged to examine for hematomas or seromas. Furthermore, because the fascia can be precisely delineated with ultrasound, a fascial dehiscence (Fig. 16-15) can be diagnosed at an earlier stage. Foreign bodies can be the cause of recurrent soft tissue infections and, therefore, removal is often recommended. Several studies have confirmed the value of ultrasound in the detection of radiolucent foreign bodies in human tissue.85–88

Technique The ultrasound examination of soft tissue is performed using a 5.0- to 8.0-MHz linear array transducer. The area of inflammation is scanned in both the transverse and longitudinal views to accurately assess the depth and extent of the fluid collection. The depth should be measured so that the appropriate length of the needle is chosen. Once the fluid collection is assessed, an ultrasound-guided needle aspiration may be performed. Aspiration of the collection is performed after the planned point of needle insertion is marked with a felt-tipped pen. The field is prepped and draped, and an 18or 20-gauge needle attached to a 10- or 12-cm3 syringe is inserted into the tissue at the marked site. An alternate method involves using real-time ultrasound imaging with sterile transmission gel and a sterile plastic cover for the transducer. The ultrasound transducer is held in the nondominant hand and the area is imaged as the needle is

CHAPTER 16

the pathologic process, exclude a suspected diagnosis, or assist with percutaneous aspiration of intra-abdominal fluid. For example, aneurismal disease of the abdominal aorta has been estimated to occur in 5–10% of the geriatric population with associated hypertension or vascular disease.79 Furthermore, nearly 11,000 deaths occur annually in the United States as a result of abdominal aortic aneurysm, and almost 80% of these are from rupture.80 The diagnosis of rupture remains a challenge because the sensitivity of physical examination in stable patients ranges from 50% to 65% and its accuracy in patients with disrupted aneurysms is unknown.81 Also, these patients are generally too unstable to undergo CT scan. For detection of abdominal aortic aneurismal disease, ultrasound has been shown to have a sensitivity approaching 100% in several series.82,83 A Swiss series of 132 patients who were treated over a 5-year period found that ultrasound assisted in 22% of the diagnoses.84 Furthermore, a negative ultrasound examination of the abdominal aorta in a patient with abdominal or back pain can reliably direct a surgeon to other possible causes for the patient’s shock state.

315

FIGURE 16-15 Fascial dehiscence (arrow).

directed into the fluid collection. The advantage of this method is that the surgeon visualizes the active drainage of the entire fluid collection and collapse of the cavity.

SURGEON-PERFORMED ULTRASOUND IN THE INTENSIVE CARE UNIT The surgeons’ use of ultrasound is particularly applicable to the evaluation of critically ill patients in the ICU for the following reasons: (1) many patients have a depressed mental status making it difficult to elicit pertinent signs of infection; (2) physical examination is hampered by tubes, drains, and monitoring devices; (3) the clinical picture often changes necessitating frequent reassessments; (4) transportation to other areas of the hospital is not without inherent risks89; and (5) these patients frequently develop complications, which if diagnosed and treated early, may lessen their morbidity and length of stay in the ICU.90 Indeed, both diagnostic and therapeutic ultrasound examinations can be performed by the surgeon without disrupting rounds in the ICU. These focused examinations should be performed with a specific purpose and as an extension of the physical examination, not as its replacement.12 Several retrospective studies have documented the utility of portable ultrasound examinations performed in diverse groups of critically ill patients.91,92 In these studies, evaluation for sepsis of unknown origin, suspected gallbladder pathology, and renal dysfunction were the most common indications for the examinations. Slasky et al. reported their findings on the ultrasound evaluations of 107 patients in the ICU.92 The sonographic results of their examinations supported the suspected diagnosis in 29 (27%) patients and excluded the initial diagnosis in

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78 (73%) patients. There were no false-negative studies in this series. Additionally, 22 of the ultrasound examinations showed unsuspected abnormalities, although only 5 patients had their management altered based on these findings. In another study, however, Lichtenstein and Axler prospectively performed ultrasound examinations in 150 consecutive patients admitted to the medical ICU.91 They examined the pleural cavity, abdomen, and the femoral veins of critically ill patients and found that information derived from their sonographic examinations directly contributed to a change in the management of 33 (22%) patients. Other investigators have reported similar results and further suggest that critically ill patients most likely to benefit from a bedside ultrasound examination are those with occult hemorrhage, sepsis of unknown origin,93 and pleural effusion.12 Surgeons most commonly use bedside ultrasound examination for the evaluation of patients in the ICU to detect pleural effusions, intra-abdominal and soft tissue fluid collections, hemoperitoneum, and femoral vein thrombosis, and as a guide for the cannulation of central veins in patients with difficult access. Before introducing specific ultrasound techniques and procedures, some basic principles of interventional ultrasound will be discussed.94,95 Advantages of interventional ultrasound as used by the surgeon in the ICU include the following: (1) visualization in real-time imaging to allow direct placement of a catheter and confirmation of complete drainage of a fluid collection; (2) performance at the patient’s bedside to avoid transport; and (3) ultrasound being safe, minimally invasive, and repeatable, if necessary. Contraindications to the performance of an ultrasound-guided interventional procedure include the lack of a safe pathway, presence of a coagulopathy, and an uncooperative patient. Larger needles and those that are Teflon coated produce more echogenicity and are easier to visualize with ultrasound.96 But, when performing a transabdominal procedure, an 18-gauge (or smaller) needle is probably preferred to avoid large injuries to the bowel. Although minor procedures may be done with minimal preparation, basic principles of sterility should be followed for major interventional procedures.

■ Pleural Effusions The use of ultrasound for the detection of a pleural effusion is similar to that described earlier in this chapter for the detection of a traumatic hemothorax.12 Although the technique for the focused thoracic ultrasound examination has already been described, the following is the technique used for an ultrasound-guided thoracentesis.

Technique The head of the bed is elevated to a 45–60° angle (if the patient’s spine is not injured), or the patient may be supine if spinal precautions are needed. A 3.5- or 5.0-MHz convex array transducer is oriented for sagittal views and placed in the midaxillary line at the sixth or seventh intercostal space. The liver (or spleen) and diaphragm are identified, and then the tho-

racic cavity is interrogated for the presence of pleural fluid. After the fluid is localized, the area adjacent to the transducer is marked using a felt-tipped pen and the chest is prepped and draped. A local anesthetic is injected into the skin near the mark and infiltrated into the underlying subcutaneous tissue and parietal pleura. The pleural space is entered with an 18-gauge needle obtained from a central line kit, and the fluid from the pleural space is aspirated in its entirety. For large effusions, a guidewire is passed through the needle into the pleural cavity using the Seldinger technique. A small skin incision is made around the guidewire and, if necessary, the stiff dilator is passed just through the dermis to allow easy passage of the catheter but minimize the risk of a pneumothorax. A standard central line catheter is placed into the pleural space and a three-way stopcock is connected to the port so that the pleural fluid can be aspirated entirely and collected into a separate container. The central line catheter is removed from the pleural space while applying constant suction with a syringe, and an occlusive dressing is placed over the small incision. Real-time ultrasound imaging can also be used for the detection and aspiration of small or loculated fluid collections because the needle is observed as it enters the collection and collapse of the space confirms that the fluid is entirely removed.

■ Intraperitoneal Fluid/Blood A sudden decrease in a patient’s blood pressure or persistent metabolic acidosis despite continued resuscitation is a common indication to reassess the peritoneal cavity as the source of hemorrhage. The FAST examination can be performed as needed at the patient’s bedside to exclude hemoperitoneum as a potential source of hypotension. This may be applied to a critically ill patient who has multisystem injuries or one receiving anticoagulation therapy. Ultrasound is also used to evaluate a patient with cirrhosis who has abdominal pain. An ultrasound-guided aspiration of ascites can also be performed, minimizing the risk of injury to the bowel.

■ Insertion of a Central Venous Catheter The placement of a central venous catheter is a commonly performed procedure in critically ill patients. Although surgical residents are generally adept at the insertion of central lines, ultrasound-guided procedures may be helpful when the resident is initially learning the technique or when the patency of a vessel is uncertain. Ultrasound-guided central line insertions are especially useful in patients with anasarca or morbid obesity and for the immobilized patient with a potential injury to the cervical spine.97,98 In the past decade, several studies have evaluated the use of ultrasound as an aid for central line placement in order to reduce the risk of complications.98–104 For example, Fry et al. successfully used ultrasound-guided central venous access in 52 patients and, with the exception of a pneumothorax that occurred in 1 patient, no other complications were noted.103 These studies suggested that the use of ultrasound results in a decreased number of cannulation attempts and complications for inser-

Surgeon-Performed Ultrasound in Acute Care Surgery

Artery

Vein

Technique The central veins in the cervical and upper thoracic region are imaged with a 7.5-MHz linear transducer. The skin insertion site may be marked prior to creating a sterile field, or the procedure may be performed with real-time imaging. Cannulation of the subclavian vein is slightly more difficult because of its location beneath the clavicle and, therefore, color-flow duplex and Doppler may be helpful to identify the vein prior to cannulation. Gualtieri et al.101 suggest identification of the axillary vein and artery just inferior to the lateral aspect of the clavicle. Patency of the vein is determined by its ability to be easily compressed with the ultrasound transducer. The vein is then imaged about 2–3 cm medial to the point of the planned insertion site. The transducer should be held in the nondominant hand and the cannulating needle is followed during real-time imaging as it traverses the soft tissue toward the vein. Once the vein is cannulated, the remainder of the procedure is completed using the standard Seldinger technique.

■ Thrombosis of the Common Femoral Vein Despite the administration of prophylactic agents and routine screening by duplex imaging, deep venous thrombosis (DVT) still occurs in high-risk patients. The characteristics of venous thrombosis as seen on the duplex imaging study include the following: dilation, incompressibility, echogenic material within the lumen, absence or decreased spontaneous flow, and loss of phasic flow with respiration. Although each ultrasound characteristic of a thrombosed vein is important in making the diagnosis of DVT, loss of compressibility of a thrombus-filled vein is the most useful with the other criteria considered supportive of the diagnosis.105–108 A focused ultrasound examination of the femoral veins is based on the following principles: (1) most lethal pulmonary emboli originate from the iliofemoral veins;109 (2) the common femoral artery is identified as a pulsatile vessel lateral to the common femoral vein on brightness-mode (B-mode) ultrasound and provides a consistent anatomic landmark; (3) B-mode ultrasound can be used to evaluate for incompressibility of the vein, echogenic material (thrombus) within the lumen of the vein, and dilation of the vein; and (4) surgeons are familiar with B-mode ultrasound because it is frequently used to detect hemopericardium, hemoperitoneum, and pleural effusion/traumatic hemothorax in critically ill patients, hence enhancing its practical applicability in this setting.

Right common femoral vessels

FIGURE 16-16 Transducer position for the evaluation of femoral vein.

array transducer is used to examine the common femoral veins according to the following protocol as described by Lensing et al.:105 1. The transducer is oriented for transverse imaging, and the right common femoral vein and artery are visualized (Fig. 16-16). 2. The vein is examined for the presence or absence of intraluminal echogenicity (consistent with thrombus) (Fig. 16-17) and for ease of compressibility. 3. The transducer is positioned for sagittal images, and a view of the common femoral vein is identified. The vein is inspected for intraluminal thrombus (Fig. 16-18) and adequate compressibility. The diameter of the vein is measured just distal to the saphenofemoral junction. 4. The same examination (1–3) is then conducted on the left lower extremity. A positive study is defined as dilation of the common femoral vein (more than 10% increase) when compared to the same

Artery

Vein

Technique The focused ultrasound examination of the common femoral veins is performed with the patient in the supine position as an extension of the physical examination. A 7.5-MHz linear

FIGURE 16-17 Transverse ultrasound image of right common femoral vein and artery.

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tion of subclavian and internal jugular venous catheters. A recent study reported similar excellent results with ultrasoundguided percutaneous access of the cephalic vein in the deltopectoral groove.104

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SECTION 2 Deep venous thrombosis

the right atrium. A 10-MHz IVUS catheter is aligned tip-to-tip with the filter deployment sheath. The IVUS catheter is then marked at the level of the deployment sheath hub. The IVUS images of the vena cava from the right atrium to the iliac confluence are obtained. The IVC is measured and a point 1 cm below the lowest renal vein is determined. The reference mark on the IVUS is transferred to the patient’s thigh, and the IVUS is removed. The introducer sheath is exchanged for the deployment sheath that is advanced to the correct depth and deployed. A follow-up abdominal x-ray confirms proper position of the filter.

EDUCATION OF SURGEONS IN ULTRASOUND FIGURE 16-18 Sagittal ultrasound image of right common femoral vein with thrombus.

vein in the opposite extremity,110 incompressibility of the vein, and/or the presence of echogenic foci consistent with an intraluminal thrombus. A negative study is the presence of a normal-caliber vein with good compressibility and the absence of an echogenic intraluminal thrombus.

■ Insertion of Inferior Vena Caval Filters Because critically ill surgical patients are at significant risk for DVT and because many have contraindications to anticoagulation, therapeutic and prophylactic inferior venal caval filters (IVCF) are being used more and more frequently. Indeed, while the topic is quite controversial, one author recommends prophylactic insertion of an IVCF within 48 hours in critically ill patients who are at high risk for DVT and have a contraindication to anticoagulation.111 While many other authors are less apt to be this aggressive, enough critically ill surgical patients require this procedure that a bedside technique for insertion would be ideal. In fact, with improvements in technology and the advent of intravascular ultrasound (IVUS), bedside insertion of IVCF is now possible. Indeed both transabdominal duplex ultrasonography112,113 and IVUS114,115 have been used to insert vena caval filters successfully and safely at the bedside. Ashley et al.115 reported on their experience with bedside insertion of 29 IVCF using IVUS in the trauma ICU. All patients were able to have their vena caval diameter measured and renal veins located. All filters were successfully deployed in good position without complication. Follow-up CT scans in 27 of the 29 patients were available that indicated proper placement (in reference to the renal veins) in all 27 patients. A much larger experience with bedside IVCF insertion was recently published with similarly excellent results.116

Technique After preparing the right groin and right thigh, a 9 French introducer sheath is placed in the right common femoral vein using a Seldinger technique. The stiff guidewire is passed into

Although many approaches have been shown to be effective in teaching these focused ultrasound examinations, surgeons should have a solid understanding of the physics principles of ultrasound imaging as an integral part of that education process. Furthermore, these principles should be emphasized each time the examinations are taught. The first educational model for how surgeons can learn ultrasound was published by Han et al. from Emory University.7 Incoming interns took a pretest and then attended a lecture and videotape about the FAST examination. After completion of the ATLS laboratory session, three swine had DPL catheters reinserted to infuse fluid and produce “positive” ultrasound examinations. Two other fresh swine were “negatives.” All five swine were draped similarly to disguise interventions. Incoming interns were tested individually by surgeon sonographers to determine whether the ultrasound image was “positive” or “negative.” The interns completed a posttest that showed a statistically significant improvement from the pretest (P  .001). The authors concluded that incoming interns could learn the essential ultrasound principles of the FAST and that swine are feasible models for learning it. In another study using pretesting and posttesting, Ali et al. showed how a workshop in ultrasound consisting of didactics, videotapes, and hands-on demonstrations improved the ultrasound skills of nonradiologists.117 Other paradigms that have been used as educational models include cadavers whose peritoneal cavities were instilled with saline118 and simulators that had data stored in threedimensional images.119 In the latter study, Knudson and Sisley conducted a prospective cohort study involving residents from two university trauma centers. They compared the posttest results between residents trained on a real-time ultrasound simulator and those trained in a traditional hands-on format. The main outcome measured was the residents’ performance on a standardized posttest, which included interpretation of ultrasound cases recorded on videotape. They determined no significant difference between those residents trained on the simulator and those trained on models or patients. From their study, the authors concluded that the use of a simulator is a convenient and objective method of introducing ultrasound to surgery residents. Another issue is that of the learning curve. One of the best studies to address this issue for the FAST was conducted by

Surgeon-Performed Ultrasound in Acute Care Surgery

SUMMARY As the role of the general surgeon continues to evolve, the surgeon’s use of ultrasound will surely influence practice patterns, particularly for the evaluation of patients in the acute setting. With the use of real-time imaging, the surgeon receives

“instantaneous” information to augment the physical examination, narrow the differential diagnosis, or initiate an intervention. The advantages of ultrasound are easily seen in each of the following clinical scenarios. As a noninvasive modality, ultrasound can be used to evaluate the injured pregnant patient and simultaneously identify the fetal heart so that its rate can be recorded. For the patient with multiple fractures who is in traction, the portable machine is wheeled to the patient’s bedside and the FAST is performed without having to move the patient. If hypotension or an unexpected decrease in hematocrit occurs, an ultrasound examination can be easily repeated to exclude hemoperitoneum as the source of hypotension. When several patients with penetrating thoracoabdominal injuries present simultaneously to the emergency department, a rapid FAST examination with thoracic views can assess for pericardial effusion, massive hemothorax, or hemoperitoneum within seconds. This information helps the surgeon to prioritize resources and triage patients. Finally, ultrasound may be suitable for the initial assessment of the injured child. This painless noninvasive modality is well accepted by children because it is performed at the bedside and is not intimidating. As surgeons become more facile with ultrasound, it is anticipated that other uses will develop to further enhance its value for the assessment of patients in the acute setting.

REFERENCES 1. Tso P, Rodriguez A, Cooper C, et al. Sonography in blunt abdominal trauma: a preliminary progress report. J Trauma. 1992;33:39–44. 2. Rozycki GS, Ochsner MG, Jaffin JH, et al. Prospective evaluation of surgeons’ use of ultrasound in the evaluation of trauma patients. J Trauma. 1993;34:516–527. 3. Rozycki GS, Ochsner MG, Schmidt JA, et al. A prospective study of surgeon-performed ultrasound as the primary adjuvant modality for injured patient assessment. J Trauma. 1995;39:492–500. 4. Rozycki GS, Feliciano DV, Schmidt JA, et al. The role of surgeonperformed ultrasound in patients with possible cardiac wounds. Ann Surg. 1996;223:737–746. 5. McKenney MG, Martin L, Lentz K, et al. 1000 consecutive ultrasounds for blunt abdominal trauma. J Trauma. 1996;40:607–612. 6. Boulanger BR, McLellan BA, Brenneman FD, et al. Emergent abdominal sonography as a screening test in a new diagnostic algorithm for blunt trauma. J Trauma. 1996;40:867–874. 7. Han DC, Rozycki GS, Schmidt JA, et al. Ultrasound training during ATLS: an early start for surgical interns. J Trauma. 1996;41:208–213. 8. Rozycki GS, Ballard RB, Feliciano DV, et al. Surgeon-performed ultrasound for the assessment of truncal injuries: lessons learned from 1,540 patients. Ann Surg. 1998;228:557–567. 9. Sisley AC, Rozycki GS, Ballard RB, et al. Rapid detection of traumatic effusion using surgeon-performed ultrasound. J Trauma. 1998;44: 291–297. 10. Rozycki GS, Feliciano DV, Ochsner MG, et al. The role of ultrasound in patients with possible penetrating cardiac wounds: a prospective multicenter study. J Trauma. 1999;46:543–552. 11. Shackford SR, Rogers FB, Osler TM, et al. Focused abdominal sonogram for trauma: the learning curve of nonradiologist clinicians in detecting hemoperitoneum. J Trauma. 1999;46:553–564. 12. Rozycki GS, Pennington SD. Surgeon-performed ultrasound in the critical care setting: its use as an extension of the physical examination to detect pleural effusion. J Trauma. 2001;50:636–641. 13. Dolich M, McKenney MG, Varela J, et al. 2,576 ultrasounds for blunt abdominal trauma. J Trauma. 2001;50:108–112. 14. Edelman SK, ed. Understanding Ultrasound Physics, Fundamentals and Exam Review. 2nd ed. College Station, TX: Tops Printing Inc; 1997.

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Shackford et al. from the University of Vermont.11 In this study, the authors questioned the recommendations that various numbers of ultrasound examinations should be done under supervision before a surgeon is considered qualified to perform them. The authors calculated the primary and adjusted error rates and then determined the potential clinical utility of the FAST. They found that although the clinician’s (nonradiologists) initial error rate was 17%, it fell to 5% after the clinicians performed 10 examinations. Additionally, in that study, the authors proposed the following recommendations for credentialing: (1) The process for credentialing of surgeons in the use of ultrasound should occur within the Department of Surgery by either surgeons or a committee composed of surgeons and nonsurgeons that reports to the Chairperson of the Department of Surgery. (2) A formal course with 4 hours of didactic and 4 hours of “hands-on” training is adequate. The curriculum for the performance of ultrasound in trauma, recently developed by the American College of Surgeons, is strongly recommended. (3) Competency for performance of the FAST exam should be determined based on error rate with respect to the prevalence of the target disease in the series. (4) “Control” or repeat scans should be allowed during the proctored experience. (5) After completion of proctoring, an ongoing monitoring process of error rates and causes of indeterminate studies using the Department of Surgery’s quality improvement program is essential.11 The teaching of surgeon-performed ultrasound is now an integral part of the American College of Surgeons’ educational program. Modular courses begin with an ultrasound basics course, which is now available on compact disc. Advanced courses in many topics, including an “Acute/ Trauma” module, are taught at the College meetings and across the country each year. A recent survey of surgeons participating in these courses shows that they have been a tremendous success.120 Experience with ultrasound is now a mandated part of residency training in general surgery. In a published survey, 95% of all residency programs are teaching ultrasonography, in either a didactic or clinic form.121 FAST, general abdominal, and breast ultrasound were all being taught in both academic and community-based programs. Academic centers additionally reported significant resident experience with IVUS, laparoscopic, and endocrine ultrasound.121 Finally, a recent study documented that surgical residents could diagnose hypertrophic pyloric stenosis with 100% accuracy using ultrasound examinations.122 These data suggest that ultrasound is being incorporated to a larger and larger extent in surgical training programs.

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Surgeon-Performed Ultrasound in Acute Care Surgery 98. Gilbert TB, Seneff MG, Becker RB. Facilitation of internal jugular venous cannulation using an audio-guided Doppler ultrasound vascular access device: results from a prospective, dual-center, randomized, crossover clinical study. Crit Care Med. 1995;23:60–65. 99. Mallory DL, McGee WT, Shawker TH, et al. Ultrasound guidance improves the success rate of internal jugular vein cannulation. A prospective, randomized trial. Chest. 1990;98:157–160. 100. Gratz I, Afshar M, Kidwell P, et al. Doppler-guided cannulation of the internal jugular vein: a prospective, randomized trial. J Clin Monit. 1994; 10:185–188. 101. Gualtieri E, Deppe SA, Sipperly ME, et al. Subclavian venous catheterization: greater success rate for less experienced operators using ultrasound guidance. Crit Care Med. 1995;23:692–697. 102. Leger D, Nugent M. Doppler localization of the internal jugular vein facilitates central venous cannulation. Anesthesiology. 1984;60:481–482. 103. Fry WR, Clagett GC, and O’Rourke PT. Ultrasound guided central venous access. Arch Surg. 1999;134:738–740. 104. LeDonne J. Percutaneous cephalic vein cannulation (in the deltopectoral groove), with ultrasound guidance. J Am Coll Surg. 2005;200: 810–811. 105. Lensing AW, Prandoni P, Brandjes D, et al. Detection of deep-vein thrombosis by real-time B-mode ultrasonography. N Engl J Med. 1989; 320:342–345. 106. Appleton PT, De Jong TE, Lampmann LE. Deep venous thrombosis of the leg: US findings. Radiology. 1987;163:743–746. 107. Polak JF, Culter SS, O’Leary DH. Deep veins of the calf: assessment with color Doppler flow imaging. Radiology. 1989;171:481–485. 108. Vogel P, Laing FC, Jeffrey RB Jr, et al. Deep venous thrombosis of the lower extremity: US evaluation. Radiology. 1987;163:747–751. 109. Wheeler HB, Anderson FA Jr. Can noninvasive tests be used as the basis for treatment of deep vein thrombosis. In: Bernstein EF, ed. Noninvasive Diagnostic Techniques in Vascular Disease. 3rd ed. St. Louis, MO: Mosby; 1985:805–818. 110. Effeney DJ, Friedman MB, Gooding GA. Iliofemoral venous thrombosis: real-time ultrasound diagnosis, normal criteria, and clinical application. Radiology. 1984;150:787–792. 111. Carlin AM, Tyburski JG, Wilson RF, et al. Prophylactic and therapeutic inferior vena cava filters to prevent pulmonary emboli in trauma patients. Arch Surg. 2002;137:521–527. 112. Corriere MA, Passman MA, Guzman RJ, et al. Comparison of bedside transabdominal duplex ultrasound versus contrast venography for inferior vena cava filter placement: what is the best imaging modality? Ann Vasc Surg. 2005;19:229–234. 113. Conners MS, Becker S, Guzman RJ, et al. Duplex scan-directed placement of inferior vena cava filters: a five-year institutional experience. J Vasc Surg. 2002;35:286–291. 114. Gamblin TC, Ashley DW, Burch S, et al. A prospective evaluation of a bedside technique for placement of inferior vena cava filters: accuracy and limitations of intravascular ultrasound. Am Surg. 2003;69: 382–386. 115. Ashley DW, Gamblin TC, McCampbell BL, et al. Bedside insertion of vena cava filters in the intensive care unit using intravascular ultrasound to locate renal veins. J Trauma. 2004;57:26–31. 116. Passman MA, Dattilo JB, Guzman RJ, et al. Bedside placement of inferior vena cava filters by using transabdominal duplex ultrasonography and intravascular ultrasound imaging. J Vasc Surg. 2005;42: 1027–1032. 117. Ali J, Rozycki GS, Campbell JP, et al. Trauma ultrasound workshop improves physician detection of peritoneal and pericardial fluid. J Clin Res. 1996;63:275. 118. Frezza EE, Solis RL, Silich RJ, et al. Competency-based instruction to improve the surgical resident technique and accuracy of the trauma ultrasound. Am Surg. 1999;65:884–888. 119. Knudson MM, Sisley AC. Training residents using simulation technology: experience with ultrasound for trauma. J Trauma. 2000;48:659–665. 120. Staren ED, Knudson MM, Rozycki GS, et al. An evaluation of the American College of Surgeons’ ultrasound education program. Am J Surg. 2006;191:489–496. 121. Freitas ML, Frangos SG, Frankel HL. The status of ultrasonography training and use in general surgery residency programs. J Am Coll Surg. 2006;202:453–458. 122. McVay MR, Copeland DR, McMahon LE, et al. Surgeon-performed ultrasound for the diagnosis of pyloric stenosis is accurate, reproducible, and clinically valuable. J Pediatr Surg. 2009;44:169–172.

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70. Martin DS, South DA, Garcia KM, et al. Ultrasound in space. Ultrasound Med Biol. 2003;29:1–12. 71. Kirkpatrick AW, Hamilton DR, Nicolaou S, et al. Focused assessment with sonography for trauma in weightlessness: a feasibility study. J Am Coll Surg. 2003;196:833–844. 72. Hamilton DR, Sargsyan AE, Kirkpatrick AW, et al. Sonographic detection of pneumothorax and hemothorax in microgravity. Aviat Space Environ Med. 2004;75:272–277. 73. Sargsyan AE, Hamilton DR, Jones JA, et al. FAST at MACH 20: clinical ultrasound aboard the International Space Station. J Trauma. 2005; 58:35–39. 74. Chiao L, Sharipov S, Sargsyan AE, et al. Ocular examination for trauma; clinical ultrasound aboard the International Space Station. J Trauma. 2005;58:885–889. 75. Laing FC, Federle MP, Jeffrey RB. Ultrasonic evaluation of patients with acute right upper quadrant pain. Radiology. 1981;140:449–455. 76. Lindelius A, Torngren S, Pettersson H, et al. Role of surgeon-performed ultrasound on further management of patients with acute abdominal pain: a randomized controlled clinical trial. Emerg Med J. 2009;26:561– 566. 77. Lindelius A, Torngren S, Sonden A, et al. Impact of surgeon-performed ultrasound on diagnosis of abdominal pain. Emerg Med J. 2008;25: 486–491. 78. Lindelius A, Torngren S, Nilsson L, et al. Randomized clinical trial of bedside ultrasound among patients with abdominal pain in the emergency department: impact on patient satisfaction and health care consumption. Scand J Trauma Resusc Emerg Med. 2009;17:60–68. 79. Thurmond AS, Semler HJ. Abdominal aortic aneurysm: incidence in a population risk. J Cardiovasc Surg. 1986;27:457–460. 80. Cabellon S, Moncrief CL, Pierre DR, et al. Incidence of abdominal aortic aneurysms in patients with atheromatous arterial disease. Radiology. 1983;146:575–576. 81. Lederle FA, Walker JM, Reinke DB. Selective screening for abdominal aortic aneurysms with physical examination and ultrasound. Arch Intern Med. 1988;148:1753–1756. 82. Maloney JD, Pairolero PC, Smith BF, et al. Ultrasound evaluation of abdominal aortic aneurysms. Circulation. 1977;56:1180–1185. 83. Nusbaum JW, Fremanis AK, Thomford NR. Echography in the diagnosis of abdominal aortic aneurysm. Arch Surg. 1971;102:385–388. 84. Weber EE, Egloff L, Turnia M. Ruptured aneurysm of the abdominal aorta and iliac arteries: an analysis of 132 cases. J Suisse Med. 1988;118: 227–232. 85. Fry WR, Smith RS, Schneider JJ, et al. Ultrasonographic examination of wound tracts. Arch Surg. 1995;130:605–608. 86. Fornage BD, Schernberg FL. Sonographic diagnosis of foreign bodies of the distal extremities. AJR. 1986;147:567–569. 87. Banerjee B, Das RK. Songraphic detection of foreign bodies of the extremities. Br J Radiol. 1991;64:107–112. 88. Hill R, Conron R, Greissinger P, et al. Ultrasound for the detection of foreign bodies in human tissue. Ann Emerg Med. 1997;29:353–356. 89. Braxton CC, Reilly P, Schwab CW. The Traveling Intensive Care Unit Patient: Road Trips. Vol. 80. No. 3. Philadelphia, PA: WB Saunders; 2000:949–956. 90. Ballard RB, Rozycki GS, Knudson MM, et al. The surgeon’s use of ultrasound in the acute setting. In: Rozycki GS, ed. Surgeon-Performed Ultrasound. Philadelphia, PA: WB Saunders Co; 1998:337–364. 91. Lichtenstein D, Axler O. Intensive use of general ultrasound in the intensive care unit. Prospective study of 150 consecutive patients. Intensive Care Med. 1993;19:353–355. 92. Slasky BS, Auerbach D, Skolnick ML. Value of portable real-time ultrasound in the ICU. Crit Care Med. 1983;11:160–164. 93. Lerch MM, Riehl J, Buechsel R, et al. Bedside ultrasound in decision making for emergency surgery: its role in medical intensive care patients. Am J Emerg Med. 1992;10:35–38. 94. Staren ED, Torp-Pedersen S. General interventional ultrasound. In: Staren ED, ed. Ultrasound for the Surgeon. Philadelphia, PA: LippincottRaven; 1997:137–160. 95. Holm HH, Skjoldbye B. Interventional ultrasound. Ultrasound Med Biol. 1996;22:773–789. 96. Staren ED, ed. Ultrasound for the Surgeon. Philadelphia, PA: LippincottRaven; 1997. 97. Mansfield PF, Hohn DC, Fornage BD, et al. Complications and failures of subclavian-vein catheterization. N Engl J Med. 1994;331: 1735–1738.

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Principles of Anesthesia and Pain Management Dirk Younker

Providing an anesthetic for the trauma victim is among the greatest challenges for an anesthesiologist. In many cases, care must be rendered to a patient about whom one knows very little, who may be physiologically unstable, who may possess obvious comorbidities that increase anesthetic risk, and for whom one has very little time to prepare. Additionally, necessity may demand that an anesthetic be provided with nothing more than basic monitoring modalities, using the simplest of anesthetic techniques. Consequently, it is helpful for the surgical practitioner to possess a basic working knowledge of anesthetic principles and practice.

AN OVERVIEW OF THE ANESTHETIC PLAN The anesthetic plan must encompass preoperative, intraoperative, and postoperative care. During the preoperative phase, the fitness of the patient for the intended anesthetic and surgical procedure is determined; the urgency of surgery determines much of the time devoted to this phase. The postoperative period includes monitoring the recovery of the patient from the anesthetic, maintaining an attitude of vigilance in respect to the development of postoperative complications and managing postoperative pain. The American Society of Anesthesiologists has published specific guidelines that outline the provision of care during these periods, which can be modified as circumstances demand. The responsibility for the preoperative and postoperative care of a patient is shared by nursing personnel, surgeons, and anesthesiologists, who work together for the benefit of their patient. In contrast, the intraoperative phase of the anesthetic care plan is the realm of the anesthesia professional. It has three components: induction, maintenance, and emergence. An anesthetic plan of action arises from the needs of the patient, the experience of the anesthesiologist and the constraints placed upon both by the proposed surgical procedure. In particular, a trauma anesthetic needs to be dynamic and responsive to rapid changes in patient condition. The

design of such a plan is aided through the employment of a decision tree, which is constructed by answering three questions: “why,” “what else,” and “what if.” The “Why?” Question One seeks the answers to any number of questions, from “How did the injury occur?” to “Why are these lab values abnormal?” to “Is my plan still what this patient needs—and if not, why not?” The “What else?” Question Questions posed include, but are not limited to, those such as “If general anesthesia is not an option, what else can I do” or “If succinylcholine is contraindicated, what else can I use?” or “If my patient gets nauseated when he gets opiates, what else can I do for his pain?” The “What if?” Question Of course, the classic question is “What if I can’t intubate the patient?”, and there are innumerable others, including “What if my block fails,” “What if he arrests when the aortic clamp comes off,” and “What if he develops malignant hyperthermia?” The successful execution of the plan requires vigilance, adaptability, and a thorough understanding of the basic principles pharmacology, physiology, and monitoring modalities, as applied to the victim of trauma.

BASIC ANESTHETIC PHARMACOLOGY The goals of an anesthetic plan may include some or all of the following: anxiolysis, analgesia, amnesia, unconsciousness, control of sympathetic reflexes, maintenance of homeostasis, and muscle relaxation. The anesthesia professional achieves these goals through pharmacologic manipulation of basic physiologic processes. The drugs employed to accomplish are divided into two general categories: anesthetic agents and anesthetic adjuvants. Anesthetic agents include general and local anesthetic agents; anesthetic adjuvants include sedatives, narcotics, and muscle relaxants. General Anesthetic Agents These include volatile inhalational (halothane, enflurane, isoflurane, sevoflurane, desflurane) and

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TABLE 17-1 General Anesthetic Agents Delivered by Inhalation Properties Compressed liquid

Metabolites Almost none

Isoflurane Sevoflurane

Ether bond Ether bond

Desflurane

Ether bond Evaporates at atmospheric pressure

Almost none [F ] Hexaflouro-isopropanol Almost none

intravenous (thiopental, methohexital, propofol, etomidate, ketamine) agents. The volatile agents possess simple halogenated alkane or ether structures. Nitrous oxide is usually considered an adjuvant to general inhalational techniques because it can produce surgical anesthesia only under hyperbaric conditions. All of these drugs share the ability to inhibit spinal and supraspinal neural transmission through either the activation or the inhibition of specific receptors. With the exception of ketamine, they are able to produce suppression of cortical electrical activity and inhibition of spinal reflexes. Burst suppression on the electroencephalogram may be achieved in clinically useful doses, and isoelectricity (and cardiovascular depression) may result if these doses are exceeded. The effects of these drugs usually dissipate following their metabolism and excretion. In the case of volatile inhalational agents, this is very rapid because they are, in general, metabolically inert and are removed by reversing their concentration gradients. The majority of intravenous anesthetic agents follow time-dependent pathways of metabolism through the liver and kidneys. The mechanism of action of general anesthetic agents is not uniform and is the subject of intense study.1,2 Pertinent physicochemical characteristics are summarized in Tables 17-1 and 17-2.

Side Effects Megaloblastic anemia Expands air-filled cavities Coughing CO Compound A Coughing Laryngospasm

Local Anesthetic Agents These include the amino-amide (lidocaine, mepivacaine, bupivacaine, ropivacaine) and aminoester (cocaine, tetracaine, benzocaine) local anesthetic agents. They are used to produce topical anesthesia of mucous membranes, infiltration anesthesia of superficial skin wounds, blockade of the neuraxis using the spinal or epidural approach, and peripheral nerve blockade. Appropriately administered neuraxial or peripheral nerve blockade generally produces surgical anesthesia to the target dermatomes. Their mechanism of action is thought to involve inhibition of sodium conductance in excitable membranes, which suppresses the transmission of neural impulses. Amino-amide local anesthetic agents are metabolized in the liver and excreted by the kidneys; aminoester agents are inactivated by plasma cholinesterase. Unintentional intravenous injection or overdosage generally results in seizure activity, cardiovascular collapse and, in the case of bupivacaine or ropivacaine, a particularly malignant form of torsade de pointes. Intravenous intralipid administration may be helpful in treating this dysrhythmia, should it occur in the setting of toxicity involving these two agents.3,4 Excessive doses of benzocaine are well known to produce methemoglobinemia, a side effect that may be avoided through careful attention to dosing requirements. Cocaine inhibits the reuptake

TABLE 17-2 General Anesthetic Agents Administered Intravenously Agent Barbiturates

Properties Barbituric acid ring

Metabolism/Excretion Liver/kidneys

Etomidate

Imidazole

Liver/kidneys

Propofol

Substituted phenol

Liver/kidneys

Ketamine

Cyclohexanone

Liver/kidneys

Side Effects Histamine release Apnea Contraindicated in porphyria Venoirritation Myoclonus Adrenal suppression Venoirritation Apnea Pediatric “Propofol Infusion Syndrome” Hallucinations Salivation Laryngospasm

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TABLE 17-3 Local Anesthetic Agents

SECTION 2

Agent Benzocaine

Properties Aminoester

Metabolism/Excretion Plasma cholinesterase

Lidocaine

Aminoamide

Liver/kidneys

Bupivicaine

Aminoamide

Liver/kidneys

Ropivicaine

Aminoamide

Liver/kidneys

of catecholamines at noradrenergic nerve terminals; therefore, adrenergic agents must be administered with caution in its presence. Interestingly, the concept of regional anesthesia is expanding outside the immediate intraoperative period to include techniques suitable for postoperative pain control. This is a particularly attractive concept for many trauma patients. Pertinent physicochemical characteristics are summarized in Table 17-3. Sedative-Hypnotic Agents Although almost any intravenous or inhalational agent may be administered in very low doses to produce sedation or hypnosis, it is the benzodiazepine class of minor tranquilizers that are most commonly used for this purpose. They produce reliable amnesia and anxiolysis; they have no analgesic potency. In combination with an opiate, benzodiazepines (most commonly midazolam) are the linchpins of the technique of conscious sedation. Intense amnesia can be achieved with the co-administration of small doses of a benzodiazepine and ketamine, with the ketamine providing additional, substantial analgesia. These drugs are reliable anticonvulsants and should be at hand whenever local anesthetic agents are being administered. Midazolam has a relatively short duration of action, although its effects can be prolonged in the presence of hepatorenal impairment or systemic acidosis. In large doses, it is possible to achieve a plane of relatively deep general anesthesia with benzodiazepines. Flumazenil is considered to be a specific benzodiazepine antagonist; its duration of activity, however, is much shorter than that of most benzodiazepines and it should be administered with careful attention to this limitation. Neuromuscular Blocking Agents There are two broad categories of muscle relaxants: those that produce competitive inhibition of impulse transmission at the junctional endplate and those that do not. Competitive inhibitors of neuromuscular transmission are further subdivided into two groups, which are distinguished by their chemical structures. These groups are the benzylisoquinoline curariform alkaloids (curare, atracurium, mivacurium, cis-atracurium) and the 4-aminosterol compounds (pancuronium, vercuronium, rocuronium). The sole noncompetitive inhibitor of neuromuscular transmission in contemporary clinical use is succinylcholine. All of these

Side Effects Possible allergic reaction from benzoic acid moiety Methemoglobinemia Seizures Cardiac arrest Seizures Cardiac arrest torsade de pointes Seizures Cardiac arrest

drugs are generally used to facilitate endotracheal intubation and to enhance the muscle relaxation produced by general anesthetics. Plasma cholinesterase rapidly cleaves the succinylcholine molecule and terminates its activity; its duration of action may be prolonged in the rare patient who possesses a genetic deficiency of this enzyme. Terminating the activity of competitive neuromuscular blocking agents is more complex. Curare and each of the 4-amino sterol compounds must first be displaced from the junctional endplate by acetylcholine and then be transported in the plasma to the liver for metabolism and excretion, usually by the kidneys. Plasma cholinesterase assists in terminating the activity of mivacurium. A complex, pHdependent process known as “Hoffmann degradation” assists the inactivation of atracurium and its isomer cis-atracurium. No similar assistive processes exist for terminating the activity of the 4-aminosterol compounds. With competitive inhibitors, these time-dependent processes of inactivation may be hastened by transiently increasing the concentration of acetylcholine at the junctional endplate, which through mass effect displaces a greater amount of relaxant and makes it available for metabolism and excretion. This displacement is usually produced by the simultaneous administration of a cholinesterase inhibitor and an anticholinergic agent; neostigmine and glycopyrrolate are generally used to accomplish this objective. This practice is commonly known as “reversal,” which is a misleading term, because it is more precisely an example of time-dependent pharmacologic antagonism. The duration of activity of most cholinesterase inhibitors is relatively brief and their effect may dissipate prior to complete termination of a profound neuromuscular block. If this should occur, re-paralysis of the patient may ensue. The mechanism of action of sugammadex represents a novel approach to the concept of antagonism; however, its efficacy is greatest only for rocuronium, and it is currently not available in the United States.5,6 Neuromuscular blockade monitors (“twitch monitors”) are routinely used to assess the depth of paralysis and the efficacy of antagonism. It should be clear by now that these complex drugs are potentially lethal and that their effects

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TABLE 17-4 Neuromuscular Blocking Agents

Atracurium cis-Atracurium Pancuronium Vecuronium Rocuronium

Properties Noncompetitive Looks like acetylcholine Competitive Looks like curare Competitive Looks like curare Competitive Looks like steroid Competitive Looks like steroid Competitive Looks like steroid

Metabolism/Excretion Plasma cholinesterase Liver and Hoffman degradation/ kidneys Liver and Hoffman degradation/ kidneys Liver/kidneys

Duration (min) 10 May be longer if abnormal cholinesterase 30 45 90

Liver/kidneys

60

Liver/kidneys

60

must be carefully monitored. Pertinent physicochemical characteristics are summarized in Table 17-4. Analgesic Agents Drugs commonly employed to facilitate analgesia fall into two general categories: those that stimulate inhibitory opiate receptors and those that block excitatory N-methyl-D-aspartate (NMDA) receptors. Nonsteroidal antiinflammatory drugs are also used, as are nerve blocks produced by local anesthetics. Stimulation of the inhibitory, G-protein– linked opiate receptor is accomplished with agents possessing either a morphinan nucleus (morphine, codeine, hydromorphone, hydrocodone, oxycodone) or a phenylpiperidine nucleus (meperidine, fentanyl, sufentanil). Blockade of the excitatory NMDA receptor is achieved with ketamine, dextromethorphan, or nitrous oxide. Methadone constitutes a special case: broadly speaking, it is a phenylpiperidine derivative and its racemic mixture has activity at both opiate and NMDA receptors. Its potency and duration of activity make it a very useful analgesic; however, recent reports of its association with a drug-induced prolonged QT syndrome are troubling.7–10 Most analgesic agents are dependent upon hepatic metabolism and renal excretion for the termination of their effects; dosages must be adjusted for the extremes of age or in the presence of hepatorenal impairment. Morphine and meperidine may also accumulate potent active metabolites in the presence of renal insufficiency. Opiate agonists are notorious for producing an array of side effects, such as meiosis, respiratory depression, constipation, dysphoria, urinary retention, and generalized pruritus. The side effects of the NMDA antagonist ketamine include agitation, hallucinosis, hypersalivation, and sympathetic stimulation. There is a “ceiling effect” to the analgesia produced by both classes of drugs, and there is no point in their further administration if side effects are developing. Smaller doses of both classes of drugs, for example morphine and ketamine, may be given together to provide a synergistic response characterized by intense analgesia with less frequent side effects.11,12

Naloxone produces reliable antagonism of the narcosis and respiratory depression produced by opiate agonists. However, it is a very short-acting drug and care must be taken not to antagonize the analgesic effects of the opiate agonist. A massive sympathetic discharge producing cardiac arrest may ensue if a patient abruptly awakens from an opiate-induced narcosis and has the sudden perception of extreme pain. There is no reliable antagonist for ketamine.

AN INTRODUCTION TO ANESTHESIA MACHINES AND MONITORS Anesthesia Machines Anesthesia delivery systems range from the simple (an open drop ether cone) to the complex (the modern electronic anesthesia machine); however, all incorporate certain basic features. These include a means to supply calibrated flows of gases such as oxygen, air, or nitrous oxide (flow meters); a mechanism for the vaporization and controlled delivery of volatile anesthetic agents (vaporizers); devices to monitor the concentrations of inspired oxygen and expired carbon dioxide; an absorber to remove carbon dioxide from exhaled gases; and a method to support ventilation of the lungs. They are constructed with one-way valves, which inhibit re-breathing of carbon dioxide, and they have internal cutoff failsafe valves, which are designed to prevent the delivery of a hypoxic mixture to the patient. They possess distinctive, audible warning alarms. Cylinders of compressed oxygen, air and nitrous oxide are present; these are used to maintain essential gas flows in the event of pipeline failure. Contemporary anesthesia machines contain complex electronic circuitry and substantial amounts of ferrous metal, which render them useless in an MRI suite; anesthetics in this hostile environment are conducted using specially constructed machines and shielded monitors. The American Society of Anesthesiologists has published guidelines for the appropriate daily checkout and maintenance of contemporary anesthesia machines.13 Rugged, reliable anesthesia machines, stripped

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SECTION 2

down to their essential components, are available for use in the field. A brief review of any of these will provide the nonanesthesiologist with a more complete idea of what an anesthesia machine is meant to accomplish.14 Monitoring Systems The American Society of Anesthesiologists has published specific minimum requirements for the monitoring of patients who receive anesthetic care. These include, but are not limited to, methods of assessing the adequacy of oxygenation, ventilation, and circulation. These requirements are normally interpreted to mean the routine use of a blood pressure cuff, electrocardiography, stethoscope, temperature probe, pulse oximetry, and capnography on all patients. Extended monitoring includes the use of invasive hemodynamic monitoring, transesophageal echocardiography, and monitors of neuromuscular or cerebral function. The routine use of cerebral function monitors (“processed EEGs”) is controversial; however, they may be helpful in identifying those trauma patients at risk for intraoperative awareness.15 Also, it is difficult to accurately place their electrodes in the face of traumatic intracranial procedures. In addition, the administration of ketamine will reduce the reliability of the signal. Transesophageal echocardiography is very useful in the detection and monitoring of traumatic injuries to the heart and great vessels;16 nonetheless, both its institution and the accurate interpretation acquired images may require the presence of an additional, experienced anesthesia caregiver.

AREAS OF SPECIFIC CONCERN TO THE ANESTHESIOLOGIST The Full Stomach Trauma patients rarely, if ever, enjoy the luxury of an overnight fast; therefore, pulmonary aspiration of gastric contents presents a very real risk for them. In addition, the stress of trauma or the administration of opiate analgesics will profoundly inhibit gastric emptying. Induction of general anesthesia in these cases is usually accomplished with a “rapid sequence” technique and the use of Sellick’s maneuver (“cricoid pressure”).17,18 This induction sequence is performed with airway rescue devices at hand and the “difficult airway algorithm,” developed by the American Society of Anesthesiologists, is invoked if it fails.19 Institution of regional anesthesia in a trauma patient does not remove the risk of pulmonary aspiration; the patient may aspirate at any time if he loses consciousness and his protective airway reflexes become obtunded. Rapid Sequence Induction and the Suspected Cervical Spine Injury Virtually every experienced trauma anesthesiologist has his own “tried and true” method of securing the airway in these patients, many of whom present for intubation in the emergency room.20 Common characteristics of emergent orotracheal intubation include Sellick’s maneuver, maintenance of the neck of the patient in the neutral position and removal of the anterior portion of the cervical collar in order to facilitate laryngoscopy. Airway rescue devices are usually at hand, as should be the resources needed to perform a tracheotomy.

The Field Intubation Many trauma anesthesiologists will confirm the appropriate position of an endotracheal tube, which they themselves have not inserted, using one or more of the following techniques: auscultation of breath sounds, capnography, repeat direct laryngoscopy, or fiberoptic bronchoscopy. The desire to immediately reintubate a patient with a functioning esophageal obturator already in place must be tempered by the knowledge that its insertion may have produced substantial upper airway trauma. If possible, any exchange of airway devices may best be reserved for the formal operating room environment. The Extremes of Age Pediatric and geriatric patients possess substantial deviations from what is considered “normal adult” cardiovascular, pulmonary, hepatic, and renal physiology. They may respond to volume depletion with precipitate hypotension, apnea may be poorly tolerated and drug clearance may be unpredictable (it is generally reduced) in the presence of immature or senescent hepatorenal function. They share an inability to maintain normal body temperature under conditions of stress and an impressive coagulopathy may develop in the presence of hypothermia. The Morbidly Obese Patient Even under optimal circumstances, the anesthetic care of the morbidly obese patient presents many challenges. At the top of the list are airway considerations: obese patients may be difficult to ventilate, difficult to intubate, and may possess a markedly reduced functional residual capacity, resulting in rapid arterial desaturation in the presence of ineffective ventilation of the lungs. Their body habitus may make effective arterial or venous access very difficult to achieve. They may present with numerous medical comorbidities, including hypertension, coronary artery disease, congestive heart failure, obstructive or restrictive lung disease, diabetes mellitus, deep vein thrombosis, and hepatic steatosis; these may be in varying states of compensation at the time of injury. Considerations such as these accompany the patient into the postoperative period, complicating the recovery phase. The Pregnant Patient Unique physiologic changes complicate the care of the pregnant trauma patient. Circulating progesterone relaxes the lower esophageal sphincter, allowing free reflux of gastric contents into the hypopharynx; even in the absence of traumatic injury, a rapid sequence induction with Sellick’s maneuver is essential in order to prevent massive aspiration. Circulating plasma volume is increased, producing an edematous upper airway and extremities; intubation may be difficult and reliable vascular access may be a challenge to secure. Tracheotomy may be rendered hazardous by an enlarged, hypervascular thyroid gland. Also, the gravid uterus exerts upward pressure on the bases of the lungs, reducing functional residual capacity; this results in rapid arterial desaturation if ventilation is ineffective. In addition, when the patient is supine, the gravid uterus rests upon her aorta and inferior vena cava, reducing venous return to the heart. Therefore, profound hypotension and fetal asphyxia may occur if she is not positioned on her side, or at least with the left hip elevated, for transport, induction and surgery itself. Of course, not all pregnant trauma victims are healthy prior to injury: gestational diabetes mellitus, pregnancy-induced hypertension, seizure disorders, gestational asthma, deep vein

Principles of Anesthesia and Pain Management will avoid the administration of triggering agents to these individuals.22 Malignant hyperthermia presents with a spectrum of reactions, ranging from mild to severe, and it is treated by immediately discontinuing any inhaled anesthetics or succinylcholine and by administering dantrolene sodium. The Joint Commission for the Accreditation of Hospital Organizations requires that a supply of dantrolene sodium be present in every surgical suite. Supportive measures include cooling the patient, hydration, and the treatment of acid–base disturbances. Other genetic disorders that are associated with malignant hyperthermia include hypokalemic periodic paralysis, central core disease, multiminicore disease, and Duchenne’s muscular dystrophy. Treatment protocols and resources for patients may be quickly accessed on the website of The Malignant Hyperthermia Association of the United States.23 Drug Intoxications Many trauma victims present with a documented history of substance abuse. Common intoxicants include ethanol, cocaine, marijuana, phencyclidine, ketamine, opiates, and any one of a number of amphetamine compounds. Of compelling concern to the anesthesiologist are the pulmonary and cardiovascular effects of central nervous system stimulants, in particular, when they are inhaled. The inhalation of “crack cocaine” or “crystal meth” can produce pulmonary thermal injury, abrupt hypertension, myocardial ischemia, and malignant ventricular dysrhythmias.24 Also, chronic abuse of “crystal meth” has been linked to the development of a severe dilated cardiomyopathy, thought to be the result of continual catcholamine elevation.25 In addition, severe intoxication with cocaine, amphetamines and certain major tranquilizers may produce muscle rigidity and an elevation of core body temperature; these signs and symptoms may be confused with malignant hyperthermia.26 In most of these clinical situations, the administration of dantrolene sodium is generally ineffective. Laparoscopic Procedures The course of an anesthetic for a “screening laparoscopy” in a healthy, stable trauma patient is generally uneventful. However, the associated pneumoperitoneum may be poorly tolerated in patients with limited myocardial or pulmonary reserve: abrupt hypotension, hypoxemia, or both may develop, and may not resolve until deflation of the abdomen.27 The institution of invasive monitoring or the use of transesophageal echocardiography may be helpful if pneumoperitoneum cannot be avoided. The Prone Position Most healthy, stable trauma patients will compensate for the reductions in cardiac output and functional residual capacity that occur during movement from the supine to the prone position.28 However, patients with limited myocardial or pulmonary reserve may develop abrupt, profound hypotension, or hypoxemia, or both, after prone positioning; this is particularly evident in the morbidly obese patient. In addition, the obese patient may become very difficult to ventilate because of increases in intra-abdominal and intrathoracic pressure. The simplest remedy is to avoid the prone position in an unstable patient and to use the lateral position, if at all possible. If the prone position is essential for surgical access, one may consider the use of an operating table that does not inhibit the free excursion of thorax and abdomen; an example of this is the orthopedic spine table.

CHAPTER 17

thrombosis, various coagulation abnormalities, and morbid obesity may be present, with all of their medical, surgical, and anesthetic implications. Also, one must remember that there are two patients who require attention: the mother and the fetus. Emergent evacuation of the uterus should always be anticipated and may be necessary in the event of maternal arrest. The fetus cannot survive in the absence of effective uteroplacental perfusion and the mother cannot be effectively resuscitated as long as the gravid uterus reduces venous return to the heart. Traumatic Brain Injury Open or closed brain trauma may occur as an isolated finding or as one of several injuries in a victim of multiple trauma. In most of these patients, the bloodbrain barrier is disrupted and cerebral edema is present. Many of these patients will be obtunded, lack protective airway reflexes and possess ineffective spontaneous ventilation. The resulting hypoxemia and hypercarbia will increase intracranial pressure and will have detrimental effects on the viability of injured neural tissue. They are also clearly at risk for pulmonary aspiration of gastric contents. Consequently, emergent endotracheal intubation is usually indicated in order to protect the airway and to control oxygenation and ventilation. Since the salvage of cells within the ischemic penumbra of injured neural tissue is of paramount importance, maintenance of a normal perfusion pressure and oxygen carrying capacity in the blood essential. The institution of hyperventilation in indicated for the control of intracranial hypertension, if present, as is the administration of osmotic diuretics. These considerations should be kept in mind from the time of initial intubation in the emergency room, through the period of diagnostic imaging, into the operating room and in the postoperative recovery phase. Acute Spinal Cord Injury Many of the considerations for traumatic brain injury also are present in the patient with acute spinal cord injury. Succinylcholine may be used to facilitate emergent intubation in these patients at the time of their initial presentation; however, its administration is contraindicated later in their hospital course due to the risk of abrupt, fatal hyperkalemia. The Open Globe The administration of succinylcholine to the patient with an open globe injury is now considered by many to be safe.21 Used to facilitate endotracheal intubation, it does not result in the extrusion of vitreous humor and it is the muscle relaxant of choice if the patient requires a rapid sequence induction. Patient movement or “bucking” during the course of the anesthetic, however, will place the patient at risk for this complication and it must be avoided. Malignant Hyperthermia Patients with this disease may develop fatal hyperthermia, skeletal muscle rigidity, rhabdomyolysis, and dysrhythmias when exposed to inhaled anesthetic agents or succinylcholine. The disease is caused by inherited or spontaneous mutations of the RYR1 or CAC1NAS genes, which regulate calcium ion transport in the sarcoplasmic reticulum. Definitive diagnosis is made by subjecting biopsied muscle to the halothane- or caffeine-contracture test. Most anesthesiologists will consider any member of a kindred afflicted with malignant hyperthermia to be at risk for developing the reaction, even in the absence of a personal history, and

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SECTION 2

Ophthalmic complications may occur following the use of the prone position for surgery. Postoperative blindness is the most devastating of these; it may be caused by central retinal artery occlusion, ischemic optic neuropathy and rarely, ischemia of the visual cortex. Its incidence has increased as the number of lengthy spine procedures has increased.29,30 Associated factors include intraoperative anemia or hypotension, operative procedures of long duration, diabetic or hypertensive retinal vascular disease, excessive in fluid administration, and pressure on the globe. A national registry exists, the purpose of which is to monitor the incidence of this complication.31 Single-lung Ventilation The use of single lung ventilation delivered by a double lumen tube will facilitate surgery on the thoracic aorta. These large endotracheal tubes are relatively inflexible and intubation with this airway device requires an experienced anesthesiologist. Experience is particularly important should the patient also possess an associated injury to the cervical spine or be at risk for aspiration of gastric contents. Fiberoptic bronchoscopy is essential for the confirmation of appropriate endotracheal tube placement following initial intubation. It is also helpful in repositioning a tube that has slipped out of position during the course of surgery. Patients with traumatic injuries to the thoracic aorta may also have associated pulmonary contusions; if substantial injury to the nonoperative lung is present, it may be impossible to effectively oxygenate or ventilate the patient once the operative lung is deflated. This may be detected prior to positioning and the initiation of surgery by simply collapsing the operative lung and observing the oximeter for signs of arterial desaturation. Mass Casualties and Disasters The administration of anesthesia in the face of mass casualties presents any number of logistic and medical challenges. Supplies may be limited, standard equipment or facilities poorly functional and conventional anesthetic techniques impossible to institute. Recent eyewitness reports from medical volunteers in Haiti illustrate these problems.32 If general inhalation anesthesia cannot be administered, continuous infusions of etomidate or ketamine produce relatively reliable hemodynamic stability and are the cornerstones of total intravenous anesthesia delivered under extreme conditions.33 Etomidate lacks analgesic potency and does not produce muscle relaxation; analgesics and adjuvant muscle relaxation must be administered if it is used. Adrenocortical suppression may also occur if large doses are given over a long period of time. Ketamine infusions produce reliable anesthesia, amnesia, analgesia and modest muscle relaxation. However, in anesthetic doses the drug produces an increase in intracranial and intraocular pressure and should be used with caution, if at all, in the presence of head trauma or an open globe injury. Also, large doses of ketamine may produce a prolonged emergence from general anesthesia, accompanied by impressive psychomimetic side effects. With both of these drugs, the airway should be secured with a cuffed endotracheal tube should the patient be at risk for aspiration of gastric contents. If resources are limited, regional anesthesia may present as the only safe option for anesthetic care.34 Neuraxial anesthesia and simple peripheral nerve blocks may be employed to produce surgical anesthesia; however, careful patient selection

for these techniques in this setting is of paramount importance.35,36 Contraindications to the use of regional anesthesia in the extreme trauma setting include hemodynamic instability, infection at the site of needle insertion, sepsis, abnormal coagulation, and known allergy to the proposed local anesthetic agent.

AN OVERVIEW OF ACUTE PAIN MANAGEMENT In the presence of traumatic injury, the primitive protective pain reflex is activated, which results in both the cognitive perception of pain and a well-defined neuroendocrine physiologic response. Thickly myelinated Aδ and nonmyelinated C-fibers carry afferent impulses from the peripheral tissues to synapses in the spinal cord and brain. Aδ fibers form the fast response and C-fibers form the slow response limbs of this feedback loop. The neurotransmitters involved in initiating, transmitting, and modulating this reflex include endogenous opiates, NMDA, and substance P. For purposes of pain management, these neurotransmitters are present in peripheral tissues (substance P), the substantia gelatinosa of the spinal cord (endogenous opiates), the nucleus proprius of the spinal cord (NMDA receptors), and in the limbic system, hypothalamus, and floor of the fourth ventricle in the brain. Stimulation of opiate receptors and blockade of NMDA receptors will tend to suppress transmission of pain impulses. Local anesthetic agents, delivered by a number of regional anesthetic techniques, will block the afferent limb of the pain loop, thereby inhibiting the transmission of pain impulses. Therefore, the pain reflex may be manipulated in the periphery, spinal cord, and brain through the stimulation or blockade of any number of receptors. Early and aggressive pain management, beginning in the preoperative period, will assist in controlling both the neuroendocrine responses to pain and the development of debilitating posttraumatic chronic pain syndromes. The most rational approach to the management of acute traumatic pain involves the utilization of nonsteroidal antiinflammatory agents, opiates, NMDA-receptor antagonists, anticonvulsants, antidepressants, and local anesthetics, which are then employed according to a plan that is tailored to specific patient needs.37,38 Targeted blockade of the neuraxis or peripheral nerves has long been used to provide surgical anesthesia as well as lingering postoperative analgesia. In this sense, the development of ultrasound-guided, indwelling continuous catheter techniques for regional anesthesia and analgesia has revolutionized the management of pain in trauma patients and their postoperative rehabilitation.36,39 Both “single shot” and continuous catheter techniques have been designed to access the thoracic epidural and paravertebral spaces, the lumbar paravertebral space, the sheath of the brachial plexus, the femoral sheath, and the sheath that surrounds the sciatic and popliteal nerves. With catheter-based techniques, analgesia is provided by the continuous infusion of dilute concentrations of local anesthetic agent, which may be supplemented by the admixture of small-dose opiates or ketamine.

Principles of Anesthesia and Pain Management

REFERENCES

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1. Campagna JA, Miller KW, Forman SA. Mechanisms of actions of inhaled anesthetics. N Engl J Med. 2003;348:2110–2124. 2. Nemergut EC, Lynch C. Mechanisms of general anesthetic action. Adv Anesth. 2003;21:115–161. 3. Leskiw U, Weinberg GL. Lipid resuscitation for local anesthetic toxicity: is it really lifesaving? Curr Opin Anaesthesiol. 2009;22(5):667–671. 4. Weinberg G. Lipid rescue resuscitation from local anaesthetic cardiac toxicity. Toxicol Rev. 2006;25(3):139–145. 5. Yang LP, Keam SJ. Sugammadex: a review of its use in anaesthetic practice. Drugs. 2009;69(7):919–942. 6. Abrishami A, Ho J, Wong J, et al. Sugammadex, a selective reversal medication for preventing postoperative residual neuromuscular blockade. Cochrane Databse Syst Rev. 2009;(4):CD007362. 7. Gupta A, Lawrence AT, Krishnan K, et al. Current concepts in the mechanisms and management of drug-induced QT prolongation and torsade de pointes. Am Heart J. 2007;153(6):891–899. 8. Ehret GB, Desmeules JA, Broers B. Methadone-associated long QT syndrome: improving pharmacotherapy for dependence on illegal opioids and lessons learned for pharmacology. Expert Opin Drug Saf. 2007;6(3): 289–303. 9. Andrews CM, Krantz MJ, Wedam EF, et al. Methadone-induced mortality in the treatment of chronic pain: role of QT prolongation. Cardiol J. 2009;16(3):210–217. 10. Fredheim OM, Moksnes K, Borchgrevink PC, et al. Clinical pharmacology of methadone for pain. Acta Anaesthesiol Scand. 2008;52(7):879–889. 11. Berti M, Baciarello M, Troglio R, et al. Clinical uses of low-dose ketamine in patients undergoing surgery. Curr Drug Targets. 2009;10(8):707–715. 12. Bell RF, Dahl JB, Moore RA, et al. Perioperative ketamine for acute postoperative pain. Cochrane Databse Syst Rev. 2009;(3):CD004603. 13. Guidelines for effective anesthesia apparatus checkout recommendations. Available at: http://www.asawebapps.org/docs/checkout%20Design%20 guidelines.pdf. Park Ridge, IL. Accessed February 21, 2010. 14. Petty WC. Military anesthesia machines. In: Zajtchuk R, Grande CM, eds. Textbook of Military Medicine: Anesthesia and Perioperative Care of the Combat Casualty. Washington, DC: Office of the Surgeon General, Borden Institute, Walter Reed Army Medical Center; 1995:141–174. 15. American Society of Anesthesiologists Task Force on Intraoperative Awareness. Practice advisory for intraoperative awareness and brain function monitoring: a report by the American Society of Anesthesiologists Task Force on Intraoperative Awareness. Anesthesiology. 2006;104: 847–864. 16. American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists Task Force on Transesophgeal Echocardiography. Practice guidelines for perioperative transesophageal echocardiography: a report by the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists Task Force on Transesophgeal Echocardiography. Anesthesiology. 1996;84(4):986–1006. 17. Rice MJ, Mancuso AA, Gibbs C, et al. Cricoid pressure results in compression of the postcricoid hypopharynx: the esophageal position is irrelevant. Anesth Analg. 2009;109(5):1546–1552. 18. Ovassapian A, Salem MR. Sellick’s maneuver: to do nor not do. Anesth Analg. 2009;109(5):1360–1362. 19. American Society of Anesthesiolgists Task Force on Management of the Difficult Airway. Practice guidelines for management of the difficult airway: an updated report by the American Society of Anesthesiolgists Task Force on Management of the Difficult Airway. Anesthesiology. 2003;98:1269–1277.

20. Bonhomme V, Hans P. Management of the unstable cervical spine: elective versus emergent cases. Curr Opin Anaesthesiol. 2009;22: 579–585. 21. Vachon CA, Warner DO, Bacon DR. Succinylcholine and the open globe: tracing the teaching. Anesthesiology 2003;99:220–223. 22. Larach MG, Gronert GA, Allen GC, et al. Clinical presentation, treatment, and complications of malignant hyperthermia in North America from 19887 to 2006. Anesth Analg. 2010;110:498–507. 23. The Malignant Hyperthermia Association of the United States. Available at: http://www.mhaus.org. Accessed February 21, 2010. 24. Devlin RJ, Henry JA. Clinical review: major consequences of illicit drug consumption. Critical Care. 2008;12:202–209. 25. Yeo KK, Wijetunga M, Ito H, et al. The association of methamphetamine use and cardiomyopathy in young patients. Am J Med. 2007;120(2): 165–171. 26. Altman CS, Jahangiri MF. Serotonin syndrome in the perioperative period. Anesth Analg. 2010;110:526–528. 27. Hirvonen EA, Poikolainen EO, Paakkonen ME, et al. The adverse hemodynamic effects of anesthesia, head-up tilt, and carbon dioxide pneumoperitoneum during laparoscopic cholecystectomy. Surg Endosc. 2000;14:272–277. 28. Edgcombe H, Carter K, Yarrow S. Anaesthesia in the prone position. Br J Anaesth. 2008;100(2):165–183. 29. Chang S-H, Miller NR. The incidence of vision loss due to perioperative ischemic optic neuropathy associated with spine surgery. Spine. 2005;30(11):1299–1302. 30. Newman NJ. Perioperative visual loss after nonocular surgeries. Am J Ophthalmol. 2008;145:604–610. 31. Practice advisory for the perioperative visual loss associated with spine surgery: a report by the American Society of Anesthesiolgists Task Force on Perioperative Blindness. Anesthesiology. 2006;104:1319–1328. 32. Sontag S. Foreign doctors are haunted by Haitians they couldn’t aid. The New York Times. 2010;159(54950):A1,A8. 33. Fox DJ, Saunders LD, Menk EJ, et al. Intravenous anesthesia. In: Zajtchuk R, Grande CM, eds. Textbook of Military Medicine: Anesthesia and Perioperative Care of the Combat Casualty. Washington, DC: Office of the Surgeon General, Borden Institute, Walter Reed Army Medical Center; 1995:211–233. 34. Bruckenmaier CC, McKnight GM, Winkley JV, et al. Continuous peripheral nerve block for battlefield anesthesia and evacuation. Reg Anesth Pain Med. 2005;30:202–205. 35. The Defense & Veterans Pain Management Initiative. Available at: http:// www.arapmi.org/initiatives.html. Washington, DC. Accessed February 21, 2010. 36. The Defense & Veterans Pain Management Initiative: MARAA Book Project. Available at: http://www.arapmi.org/maraa-book-project.html. Washington, DC. Accessed February 21, 2010. 37. Buvanendran A, Kroin JS. Multimodal analgesia for controlling acute postoperative pain. Curr Opin Anaesthesiol. 2009;22:588–593. 38. Heitz JW, Witkowski TA, Viscusi ER. New and emerging analgesics and analgesic technologies for acute pain management. Curr Opin Anaesthesiol. 2009;22:608–617. 39. Clark L, Varbanova M. Regional anesthesia in trauma. Adv Anesth. 2009:27:191–222.

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CHAPTER 18

Infections Michael A. West and Daniel Dante Yeh

INTRODUCTION Death after traumatic injury has been described in terms of a trimodal distribution. Immediate and acute (24 hours) deaths usually result from uncontrolled hemorrhage, but infections and multiple organ dysfunction syndrome, which often arise from infection, are responsible for a significant proportion of late deaths. Indeed, infection is responsible for most deaths in patients who survive longer than 48 hours after trauma.1 Trauma-related infections are generally divided into those that result directly from the injury (e.g., due to contamination that occurs in conjunction with the traumatic injury) and nosocomial infections that arise in the health care setting, secondary to treatment of the injury. The pathogens involved can be exogenous or endogenous bacteria, depending on the mechanism of injury and/or the iatrogenic cause. Most post-traumatic infections are polymicrobial and involve a mixture of aerobic and anaerobic organisms.2 In one series, 37–45% of all trauma patients experienced infectious complications during their initial hospitalization. Furthermore, in the same study, 80% of trauma patients staying at least 7 days in the intensive care unit met systemic inflammatory response syndrome (SIRS) criteria.3 Therefore, it is important that all caregivers understand the principles of surgical infections in the context of trauma patients. This chapter discusses the following: factors that normally prevent infection, how trauma disrupts or overwhelms normal host defenses, how to recognize and treat the most common infectious complications after traumatic injury, principles that can be employed to prevent infection, and how those principles can be applied chronologically during the treatment of trauma patients.

PATHOGENESIS OF INFECTION Humans have evolved mechanisms to avoid infection despite the ubiquitous presence of bacteria in our environment and throughout our bodies. Under normal circumstances there is a

balance between bacteria, intact environmental barriers, and host defenses (see Fig. 18-1). With surgery in general, and trauma in particular, there is a disruption in this balance that significantly increases the probability of developing an infection (Fig. 18-2). Bacteria are abundant on the surface of the skin, within the oral cavity, and present in increasing numbers down the length of the gastrointestinal tract. Bacterial numbers differ at various locations, and the pathogenic species and their respective numbers at different anatomic sites are summarized in Table 18-1. Trauma disrupts the environmental barriers that prevent bacteria from gaining access to normally sterile regions of the body. When inoculation of bacteria into normally sterile sites occurs, infection will ensue if bacteria can proliferate faster than the host defense mechanisms can eradicate them. Furthermore, there is potential for much greater disruption of normal barriers with trauma than occurs with elective surgery as there is often concomitant hypoperfusion (shock), devitalized tissue, and retained foreign bodies.

■ Environmental Barriers Normally, entry of microbes is limited by the integrity of environmental barriers. These environmental barriers include intact skin, respiratory, gastrointestinal, and genitourinary tracts.4 The importance of intact skin is clearly evident when one considers the potential for microbial infection seen in burn patients or in patients with toxic epidermal necrolysis.2 Many traumatic injuries are associated with an alteration in the integrity of the skin. Even minor lacerations and abrasions have the potential to disrupt crucial environmental barriers. Interventions that are made in the process of caring for trauma patients, such as insertion of intravenous or urinary catheters, tube thoracostomy, etc., disrupt the integument and may provide skin bacteria access to sterile sites. Furthermore, the quantitative number of microbes required to produce clinical infection is significantly decreased in the presence of foreign bodies, blood, or devitalized tissue.2

Infections

Host defense

Environmental factors

FIGURE 18-1 Under normal circumstances the determinants of infection, microbial factors, environmental factors, and host defenses interact such that there is no infection. (Adapted with permission from Meakins JL, et al. Host defenses. In: Howard RJ, Simmons RL, eds. Surgical Infectious Diseases. 2nd ed. Norwalk, CT: Appleton & Lange; 1988. Copyright © The McGraw-Hill Companies, Inc.)

■ Microbial Factors The bacteria that are responsible for clinical infections in surgery or trauma patients constitute a minority of the skin or gastrointestinal flora and they generally possess one or more virulence

A

B

Microbial factors

Host defense

Environmental factors

Environmental factors

C

Microbial factors

Host defense

Microbial factors

D Host defense

Environmental factors

Microbial factors

Host defense

Environmental factors

FIGURE 18-2 (A) Under circumstances in which there is excessive microbial contamination, (B) serious disruption of environmental barrier, (C) impaired host defenses, or (D) all factors that ensure there will be an increased likelihood of developing infection (shaded intersection of determinants of infection).

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Microbial factors

factors that facilitate infection and increase their pathogenicity. In contrast, the vast majority of endogenous and environmental bacteria are relatively nonpathogenic. For example, more than 99% of the colonic flora is nonpathogenic anaerobes that never cause clinical infections. Similarly, most skin bacteria are lactobacilli, which do not cause clinical infection either. In contrast, Staphylococcus aureus, the most common pathogen associated with surgical site infections (SSI), has numerous virulence factors that facilitate invasion and thwart host defenses. In the abdominal cavity, Escherichia coli and Bacteroides fragilis are the prototypical organisms associated with intra-abdominal infection, yet they account for only 0.01% and 1% of colonic bacteria, respectively. Indeed, to some extent the normal presence of overwhelming numbers of nonpathogenic bacteria constitutes a defense against infection. That is, infection is proportionately less likely if 99% of the inoculum is incapable of producing infection. This concept of adherent resident bacteria preventing invasion has been termed colonization resistance.4 This is an important point as skin and gastrointestinal flora changes considerably when trauma patients are hospitalized, both in terms of number and proportion of virulent bacteria and in terms of susceptibility to antibiotics, should an infection develop. Skin flora is relatively homogeneous, although bacterial numbers are higher in the axilla and groin areas. The endogenous skin bacteria are predominately gram-positive aerobic Staphylococcus and Streptococcus species, along with Corynebacterium and Propionibacterium.4 As noted above, S. aureus is the most common pathogen present on the skin. Most recently an increasing number of S. aureus isolates from trauma patients and other

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TABLE 18-1 Pathogenic Microorganisms Present at Various Anatomic Sites

SECTION 2

Region Skin (all areas) Skin (infraumbilical)

Oropharynx

Stomach Proximal small intestine Distal ileum and colon

Microbes Staphylococcus aureus and S. epidermidis Streptococcus (non-Enterococcal) Streptococcus faecalis and Streptococcus faecium Escherichia coli Staphylococcus aureus and S. epidermidis Streptococcus (non-Enterococcal) Bacteroides (non-fragilis) Fusobacterium Haemophilus Peptostreptococcus Staphylococcus aureus and S. epidermidis Streptococcus (non-Enterococcal) Streptococcus (non-Enterococcal) Candida Bacteroides fragilis and other Escherichia coli and other Enterobacteriaceae Bacteroides (fragilis and other spp.) Escherichia coli and other Enterobacteriaceae Streptococcus faecalis and S. faecium

Quantity 102 to 103 102 to 105

109 to 1011

102 to 103 103 to 107 105 to 1010

From Dunn DL. Diagnosis and treatment of infection. In: Norton JA, Barie PS, Bollinger RR et al, eds. Surgery: Basic Science and Clinical Evidence. 2nd ed. New York: Springer-Verlag; 2008:212. With kind permission from Springer+Science Business Media.

community-acquired infections have been methicillin resistant (MRSA).5,6 This fact, along with knowledge of the local incidence of MRSA, needs to be taken into account in terms of appropriate empiric or prophylactic antibiotic selection for these patients.6 The oral and nasopharynx harbor large numbers of bacteria, with streptococcal species being most frequently present. Much smaller numbers of bacteria, typically 102–103 CFU/ mL, are present in the normal stomach, because the normally acid pH of the stomach inhibits bacterial growth. Gastric bacterial numbers increase in the absence of gastric acid as in patients on proton pump inhibitors. Bacterial numbers are much higher in the small intestine, and the density of bacteria increases further as chyme progresses from the duodenum to the terminal ileum. Bacterial counts in the proximal gastrointestinal tract are in the range of 104–105 CFU/mL, whereas numbers in the terminal ileum are close to colonic densities (108–1010 CFU/mL). Bacterial numbers in the colon are even higher, with approximately 1011–1012 CFU/mL of stool, although many of these colonic bacteria are nonpathogenic. These large numbers are also associated with very low oxygen tension, and 99.9% of bacteria present are anaerobes. The urogenital, biliary, pancreatic ductal, and distal respiratory tracts do not possess resident microflora in healthy individuals.4

■ Host Defense Mechanisms Host defense refers to endogenous factors that counteract microbial invasion. In addition to the environmental factors and colonization resistance described above, humoral and cellular host

defense mechanisms that are crucial to eliminate bacteria within a sterile space exist. Initially, several primitive and relatively nonspecific host defenses including proteins such as lactoferrin, fibrinogen, and complement begin to act against invading microbes. Lactoferrin sequesters the critical microbial growth factor iron, thereby limiting microbial growth. Fibrinogen within the inflammatory fluid has the ability to trap large numbers of microbes during the process in which it polymerizes into fibrin.4 Complement is activated on contact with bacteria and viruses, from tissue damage, or when IgG/IgM antibodies recognize microbial agents. Activation of complement releases C3a and C5a, which are potent chemotaxins that result in recruitment of neutrophils and macrophages. These components enhance endothelial adhesiveness and increase vascular permeability. Complement activation can directly destroy microbial agents via formation of a membrane attack complex (composed of complement proteins C5–C9) and enhance microbial phagocytosis by way of C1q and C3bi subunits. In vitro studies have shown that 50–70% of a moderate inoculum is eliminated prior to the influx of phagocytic host cells. Many different tissues also contain resident innate immune cells. These include macrophages, dendritic cells, Kupffer cells, glial cells, mesangial cells, and alveolar macrophages.7 These innate immune cells express a wide variety of pathogen-associated molecular pattern (PAMP) receptors on their surface.8–10 The best known examples of PAMPs are the toll-like receptors (TLRs) of which there are now more than 10 well-described receptor molecules.10 TLRs bind to ligands on bacteria (or damaged host tissue), and TLR binding results in activation of these

Infections

MODS

Re

sol

CHAPTER 18

Inflammatory

2˚ SIRS; Second hit Response

utio

n

Innate immune response 14 d

Counterinflammatory

7d Adaptive immune response

n

utio

sol

Re CARS; Increased risk of infection

FIGURE 18-3 Schematic depiction of how acute injury simultaneously initiates the proinflammatory systemic inflammatory response syndrome (SIRS) and the anti-inflammatory compensatory anti-inflammatory response syndrome (CARS). Under normal circumstances there is a defined temporal period in which these initial responses surge and resolve. When a second or subsequent insult (“hit”) is imposed on this response, it may lead to multiple organ dysfunction syndrome (MODS) and death in a significant subset of patients. (Reproduced with permission from Ni Choileain N, Redmond HP: Cell response to surgery. Arch Surg. 2006;141(11):1132–1140. Copyright © 2006 American Medical Association. All rights reserved.)

cells. Activated macrophages secrete a wide array of substances in response leading to amplification and regulation of the acute proinflammatory response (Fig. 18-3). Sequential release of protein cytokines, including tumor necrosis factor-alpha (TNFalpha), interleukin-1 (IL-1), IL-6, IL-8, and interferon-gamma (INF-γ), follows. These mediators produce the signs and symptoms (fever, tachycardia, tachypnea, leukocytosis, etc.) that we associate with infection. IL-8 is a very potent chemoattractant for neutrophils, which are primarily responsible for ongoing microbial phagocytosis and intracellular microbial killing. Unfortunately, the same process that recruits neutrophils and stimulates phagocytosis and oxidative killing may also be responsible for damage to host tissues. Simultaneous with the innate immune proinflammatory response there is production of anti-inflammatory mediators, such as IL-10, also.11 Some of these mediators may contribute to the immune hyporesponsiveness of trauma over the ensuing days (Table 18-2). Particular anatomic locations have additional unique factors that defend against infection.13 For example, the peritoneal cavity has lymphatic channels on the undersurface of the diaphragm that facilitate removal of bacteria.14 The subdiaphragmatic surface is a lower-pressure area, due to the effect of respiratory excursion, and this serves to move free fluid within the peritoneal cavity to this location. Movement of the diaphragm “pumps” this fluid into the thoracic duct and from there it gains rapid access to the systemic circulation. Experimental studies show that labeled bacteria inoculated into the peritoneal cavity appear in the thoracic duct within 6 minutes and in the bloodstream within 12 minutes.13 The respiratory tract has unique host defenses that help to ensure the sterility of the lung parenchyma as well. Goblet cells within the respiratory mucosa secrete mucin

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that helps to traps bacteria. Ciliated respiratory epithelial cells move the mucus centrally where it, and the bacteria trapped within it, can be expectorated by coughing. The presence of endotracheal tubes, smoking, inhaled toxins, and some anesthetic agents interfere with mucociliary clearance mechanisms, and this may predispose to pneumonia. Bacteria or other microbes that gain access to the alveoli are normally phagocytosed by alveolar macrophages, although the macrophage activation that may accompany this process has been proposed as one possible pathogenetic mechanism for acute lung injury (ALI) or adult respiratory distress syndrome (ARDS).15–17

MICROBIOLOGY To a very large extent the microbial agents responsible for infections or infectious complications after trauma are the same agents that cause most other surgical or ICU-associated infections. Table 18-1 shows the most common infectious agents that cause trauma-associated infections at various anatomic sites. Generally, Staphylococcus spp. and Streptococcus spp. are the most common pathogens responsible for infections in which the traumatic injury or operative intervention needed to treat the injury did not transgress a mucosal surface. For traumatic injuries that involve the aerodigestive tract the most common isolates are E. coli (43.4%), S. aureus (18.9%), Klebsiella pneumoniae (14.4%), and Entercoccus faecalis (5.6%).1 Hospitalized trauma patients develop nosocomial bacterial infections from the usual ICU-associated pathogens (Table 18-3). There are a few important infectious agents that can be associated with trauma, that are seldom encountered in other settings including rabies virus, Clostridium tetani, and Vibrio spp.

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SECTION 2

TABLE 18-2 Immunologic Defects Associated with Traumatic Injuries

TABLE 18-3 ICU Pathogens Isolated from Patients with Ventilator-Associated Pneumonia

Type of Cell and Action

Change from Normal

Organism/Class

T and B lymphocytes CD4 /CD8 ratio TGF-β production Th17 phenotype Immunosuppressive Treg phenotype

Decreased Increased Increased Increased

Monocytes/macrophages Immunocompetent activation HLA-DR expression Antigen-presenting capability PGE2 production IL-12 production IFN-γ release

Decreased Decreased Decreased Increased Decreased Decreased

Common characteristics of T cells and monocytes Proportion of Th2 phenotype Increased Trauma-induced apoptosis Increased Polymorphonuclear neutrophils (PMN) Chemotaxis Decreased Phagocytic capacity Decreased Release of elastase Increased O2 radical release Increased β-Integrin expression Decreased Leukotriene B4 production Decreased Apoptosis Delayed Adapted with permission from Tschoeke and Ertel,12 © Elsevier.

■ Rabies Rabies is a rare, but potentially fatal, clinical disease caused by the rabies virus. It is an RNA virus that is present in the saliva of mammals and transmission to humans generally occurs following a bite from a rabid animal. Prior to the development of a vaccine by Louis Pasteur, bites from a rabid animal were uniformly fatal. In North America, raccoons, skunks, bats, foxes, coyotes, and bobcats are the primary reservoirs. Most human rabies cases have no documented exposure to a rabid animal and the majority of these cases are associated with bat bites. Many victims underestimate the importance of a bat bite and a substantial portion do not even recall being bitten. Bats (Carnivora and Chiroptera) represent the ultimate zoonotic reservoir for the virus, as well. The rabies virus is highly labile and can be inactivated readily by ultraviolet radiation, heat, desiccation, and other environmental factors. The word “rabies” derives from the Latin rabere meaning “to rage” and refers to the clinical manifestations of the disease that include hyperactivity, disorientation, hallucinations, and bizarre behavior. The rabies virus is neurotropic and causes an acute encephalitis. Other hallmarks of the disease include hydropho-

Total (%)

Lactose-fermenting gram-negative bacillus Escherichia coli 8.1 Klebsiella sp. 11.1 7.6 Enterobacter sp. Morganella sp. 0.5 Citrobacter sp. 1.0 Serratia sp. 1.5 Lactose-nonfermenting gram-negative bacillus Stenotrophomonas sp. 2.0 Acinetobacter sp. 8.6 Pseudomonas sp. 13.6 Staphylococcus aureus 31.8 total 22.2 Methicillin sensitive 9.6 Methicillin resistant Community pathogens Streptococcus pneumoniae Haemophilus sp.

2.0 3.0

Other pathogens Polymicrobial species Fungus

3.0 1.5

Adapted from Eachempati et al.18

bia and aerophobia, as these stimuli tend to cause intense laryngeal and pharyngeal spasm. Once the patient begins manifesting symptoms, death is nearly certain. With increased vaccination and postexposure prophylaxis (PEP) over the past 50 years, the clinical disease is becoming increasingly uncommon, with only 32 cases of human rabies reported in the United States between 1980 and 1998. That said, it is important for the practitioner of emergency medicine/surgery to be knowledgeable about rabies since animal bites are encountered frequently in clinical practice. Humans are not routinely vaccinated against rabies. Rather, domestic animals receive routine rabies vaccinations. If a human is bitten by a rabid animal, rabies can be prevented by PEP before the virus enters the central nervous system during the incubation period. The diagnosis of rabies can be made rapidly by identification of rabies virus in the brain of a potentially infected animal. This procedure can be performed in a timely manner, but requires euthanizing the suspected animal. The incidence of positive rabies tests ranges from as high as 6–10% in wild animals down to levels of ∼1% in domestic pets. If the rabies test is negative, then no postexposure vaccination or prophylaxis is needed. An acceptable alternative approach, if the suspected source is a domestic pet (dog, cat, ferret, etc.), is that the offending animal be quarantined and observed for 10 days. If the animal exhibits signs of rabies, the exposed person should begin PEP immediately and the animal should

Infections

■ Tetanus Tetanus is a rare, life-threatening condition that is caused by toxins produced by C. tetani, a spore-forming, gram-positive bacillus.20 Clostridial spores can survive indefinitely, and they are ubiquitous in soil and feces. Under anaerobic conditions the spores can germinate into mature bacilli, which elaborate the neurotoxins tetanospasmin and tetanolysin. Tetanospasmin is the toxin that produces most clinical symptoms by interfering with motor neuron release of the inhibitory neurotransmitters gamma-aminobutyric acid (GABA) and glycine. This loss of inhibition results in muscle spasm (usually spasm of the masseter muscle) and severe autonomic overactivity manifested by high fever, tachycardia, and hypertension. Historically, tetanus was highly fatal, but intensive medical therapy with neuromuscular blockade, mechanical ventilation, and ICU monitoring has lowered the case fatality rate to 11–28%. Since the mid1970s there have been 100 tetanus cases reported annually in the United States. Even so, clinicians and trauma surgeons must remain alert for the potential of clostridial contamination and provide tetanus prophylaxis.20 The diagnosis of tetanus is made on clinical grounds alone, as there are no laboratory tests that can diagnose the condition or rule it out. Tetanus immunization is accomplished as a component of standard early childhood immunizations (diphtheria– pertussis–tetanus [DPT]), with administration of tetanus toxoid (TT) every 5–10 years to maintain immune memory. There have been no deaths reported in individuals who have been fully immunized. The CDC recommendations for tetanus prophylaxis depend on the wound characteristics and the prior immunization status of the patient. A wound with extensive contamination, one that is poorly vascularized, or with extensive soft tissue trauma is considered to be a tetanus-prone

wound. A tetanus booster should be administered to patients who have received primary immunization, but who have not received TT during the past 10 years, or the past 5 years for tetanus-prone wounds.19 In patients who have never undergone primary immunization, human tetanus immune globulin (HTIG) should be administered along with TT at a different site. Antitetanus antibody binds to exotoxins and neutralizes their toxicity. High-risk groups such as the elderly, human immunodeficiency virus (HIV)–infected individuals, and intravenous drug users (IVDU) who had received primary vaccination may not have tetanus antibodies and more liberal use of HTIG should be considered in these groups.19

■ Infections Associated with Marine Trauma Vibrio vulnificus is a gram-negative rod present in seawater that can result in atypical, necrotizing soft tissue infections when traumatic injuries occur in the ocean.21–23 V. vulnificus is common in warm seawater and thrives in water temperatures greater than 68°F (20°C). The organism is not associated with pollution or fecal waste. Approximately 25% of V. vulnificus infections are caused by direct exposure of an open wound to warm seawater containing the organism. Exposure typically occurs when the patient is participating in water activities such as boating, fishing, or swimming. Infections are occasionally attributed to contact with raw seafood or marine wildlife. The risk of developing Vibrio infection is much higher in immunocompromised patients or patients with preexisting hepatic disease or diabetes mellitus.22 Established infection with V. vulnificus can be highly invasive with mortality rates of 30–40% and a mortality greater than 50% in immunocompromised patients. A recent published report documented a 37% mortality rate even after implementation of a specific treatment guideline for necrotizing Vibrio infections.21 Patients with wound infections caused by V. vulnificus develop painful cellulitis that progresses rapidly.22–24 Physical examination will often reveal marked swelling and painful, hemorrhagic bullae surrounding traumatic wounds. In some cases, there can be rapid progression and associated systemic symptoms. Marked local tissue swelling with hemorrhagic bullae is characteristic. Systemic symptoms include fever and chills, and bacteria are present in the bloodstream in more than 50% of patients. Hypotension or septic shock may be an early symptom and alterations in mental status occur in approximately one third of patients. Table 18-4 summarizes clinical symptoms present in patients with Vibrio infection. It is important for trauma surgeons to be aware of the potential for Vibrio infections in the appropriate clinical setting, because antibiotic treatment is distinctly different from the agents typically employed for trauma patients. Aggressive surgical debridement, incision and drainage of purulent collections, and even amputation may be crucial adjuncts for management of occasionally severe soft tissue infections.22 A recent experience in 30 patients found that fasciotomy was needed in all patients, and 17% required amputation.21 Recommended antibiotics include doxycycline (100 mg iv/po bid), ceftazidime (2 g q 8 hours), cefotaxime (2 g q 8 hours), or ciprofloxacin (750 mg po bid or 400 mg iv q 12 hours).22,25

CHAPTER 18

be euthanized and its brain tissue tested for rabies. If the animal is confirmed to have rabies, PEP should be completed. When the test results are negative, PEP can cease. Immediate measures that should be taken to decrease the risk of rabies transmission include thorough washing of bite and scratch wounds with soap and water, followed by application of povidone–iodine or alcohol. Human rabies immune globulin (HRIG) and rabies vaccine should be given in all cases except in persons who have been immunized previously.19 Immune globulin should never be delivered in the same syringe as the vaccine, as this will cause precipitation. The Advisory Committee on Immunization Practices (ACIP) of the Centers for Disease Control and Prevention (CDC) and the American Academy of Pediatrics recommend a single dose (20 IU/kg) of HRIG be given to provide protection for the first 2 weeks until the vaccine elicits an antibody response. Detailed and up-todate information for rabies exposure is available on the CDC’s Web site (http://www.cdc.gov/RABIES/), and this site should be consulted for the latest information. The ACIP recommends a regimen of human diploid cell vaccine (Imovax®) for PEP on days 0, 3, 7, 14, and 28 along with a single dose of HRIG on day 0. Once initiated, rabies prophylaxis should not be interrupted or discontinued because of local or mild systemic reactions to the vaccine.

335

336

Generalized Approaches to the Traumatized Patient

TABLE 18-4 Clinical Characteristics Associated with Vibrio vulnificus Wound Infections

SECTION 2

Characteristic Cellulitis at wound site Skin bullae Fever (37.8°C) Chills Ecchymosis Obtundation, disorientation, or lethargy Hypotension (90 mm Hg) Vomiting Diarrhea

Patients (%) 88 88 65 29 18 18 12 6 6

Adapted from Klontz et al.23

Traumatic injuries that occur in freshwater conditions may develop infections from Aeromonas hydrophila.24 A. hydrophila is a gram-negative anaerobic rod that is a common pathogen of fish and amphibians. Cutaneous inoculation of the organism can result in cellulitis, abscesses, and, occasionally, necrotizing soft tissue infections. Like the situation with Vibrio infections, patients with hepatic disease and immunocompromised patients have a greater risk of developing generalized disease. A. hydrophila can be recovered from the bloodstream in a significant proportion of patients and this fact, along with a history of injury in fresh water, will aid in alerting clinicians to the correct diagnosis. Antibiotic agents active against A. hydrophila include third-generation cephalosporins, fluoroquinolones, doxycycline, or trimethoprim–sulfamethoxazole.24

PREVENTION OF INFECTIONS ■ General Principles As in all other aspects of surgical care, it is preferable to try to prevent infections wherever possible. A number of interventions and practices have been demonstrated to be highly effective in preventing infections after elective operations, and many of those techniques have specific application in the care of injured patients. In this section, the current evidence-based interventions to prevent infection that are applicable to trauma patients are discussed.

■ Prophylactic Antibiotics Prophylactic antibiotics are intended to prevent development of infection. The concept of prophylaxis presupposes that infection is not present at the time. The decision to use prophylactic antibiotics and the choice of agents are based on the risk of developing SSI. There are very good data regarding SSI rates for elective surgery and the incidence of SSI by wound class for elective operations is shown in Table 18-5. Traditionally, Class I or clean wounds are those that do not violate the respiratory, alimentary, or genitourinary tracts. The wound infection rate is approximately 2%. Class II, or clean-contaminated wounds, refers to elective operations on potentially contaminated organs, such as the gastrointestinal tract, genitourinary tract, and respiratory tree (the procedure will violate a mucosal surface, which can never be completely sterile). The usual incidence of infection for these types of wounds is 5–10%. Contaminated wounds (Class III) differ from Class II wounds by the degree of spillage, with an incidence of infection of 15–30%. Finally, Class IV or dirty-infected wounds are

TABLE 18-5 Classification of Surgical Woundsa Wound Class Clean

Characteristics Uninfected, no inflammation, no mucosal surface transected

Clean/contaminated

Uninfected, no inflammation, mucosal surface transected

Contaminated

Open accidental wounds, break in sterile conditions, spillage, stomas

Dirty/infectedb

Infection, perforation, devitalized tissue

a

Adapted from Nichols.26

b

Dirty wounds: infection antibiotics indicated as therapy.

Examples Mastectomy Thyroidectomy Vascular bypass CABG Colectomy Cholecystectomy Laryngectomy Urologic procedures Pulmonary lobectomy Appendicitis Diverticulitis Small bowel GSW Incise and drain abscess Peritonitis Enteric fistulas Remove infected implant

SSI Rate (%) 2

5–15

15–30 30

Infections a prophylactic antibiotic has been linked to increased rates of subsequent nosocomial infections with resistant organisms.41 To maintain adequate tissue and serum levels of antibiotics in the face of ongoing hemorrhage and vasoconstriction, the administered dose may be increased 2- or 3-fold and repeated after every 10th unit of blood product transfusion, although there is not strong evidence to support this practice.

■ Surgical Scrub Until recently, povidone–iodine scrub has been the standard disinfectant used for surgical prep and scrub. This supremacy has been challenged by several well-designed studies performed in elective surgery showing significantly lower SSI rates with the use of chlorhexidine–alcohol compared with iodine (9.5% vs. 16.1%).42 The fact that chlorhexidine–alcohol begins bacterial killing immediately on contact and does not require drying for antimicrobial effectiveness makes it potentially attractive for use in emergent surgery. One caveat regarding use of alcoholbased disinfectants is that it is imperative that the solutions be dry if electrocautery is used during surgical procedures to avoid intraoperative fires.

■ Double Gloving Glove perforation is an underappreciated phenomenon that may adversely impact the sterility of an operative procedure. Microperforation rates as high as 16% have been reported.43 When two pairs of gloves are used, inner glove perforation rate is substantially lower. In addition to patient outcome, the

TABLE 18-6 Evidence-Based Recommendations for Antibiotic Prophylaxis for Specific Interventions or Injuries Intervention/Injury Chest tube Intraventricular pressure monitor

Basilar skull fractures Burns Hand/tendon repairs Mandibular fractures Open globe injuries Penetrating brain injury Closed fractures Open fractures

Agent/Route/Duration First-generation cephalosporin prior to chest tube insertion. 24-h duration of antibiotic First-generation cephalosporin prior to insertion. Data unclear regarding duration of prophylaxis and impact on development of ventriculomeningitis. Prophylaxis may be continued in presence of CSF leak or concurrent extracranial infection Evidence does not support prophylactic antibiotics to decrease risk of meningitis in presence of rhinorrhea or otorrhea Prophylactic systemic parenteral antibiotics are strongly discouraged Single dose of first-generation cephalosporin may be beneficial. No evidence to support 24-h duration No benefit to prolonged postoperative antibiotics Recommendation to administer intravitreal and intravenous antibiotics to reduce endophthalmitis at the discretion of clinician First-generation cephalosporin for 5 days First-generation cephalosporin at time of ORIF, if needed, for no longer than 24 h Timing of debridement does not impact incidence of infection First-generation cephalosporin for 72 or 24 h after wound closed Consider addition of gram-negative antimicrobial coverage for Grade III fractures No benefit to routine use of antibiotic beads

References 29,30

31,32

33

34 35

36 117

37 38

109 39 82

82

CHAPTER 18

characterized by frank pus or extensive and prolonged contamination. These wounds are characterized by an infection rate of 30% if primary closure is attempted.27 Emergent operative interventions increase the wound class by one step, so it is clear that higher wound infection rates will be encountered in dealing with patients who have acute traumatic injuries that require operative intervention. In trauma surgery, the majority of wounds encountered will be Class III or IV, and the luxury of a preinoculation dose of antibiotics, as recommended by the Surgical Care Improvement Project (SCIP), is usually unavailable.28 With this in mind, it is prudent to administer a single dose of an agent with activity against community-acquired aerobic and anaerobic pathogens as soon as possible for all patients requiring operation in the thorax or abdomen. Evidence-based guidelines for antibiotic prophylaxis of other surgical interventions or different anatomic sites are summarized in Table 18-6. The issue of postoperative continuation of prophylactic antibiotics in penetrating abdominal trauma has been investigated extensively. The Eastern Association for the Surgery of Trauma (EAST) has published guidelines derived from an evidence-based review.40 A single preoperative dose of prophylactic antibiotics with broad-spectrum aerobic and anaerobic coverage is recommended for trauma patients sustaining penetrating abdominal wounds. Absence of a hollow viscus injury requires no further administration. If, however, a hollow viscus injury is present, there are sufficient Class I and Class II data to recommend continuation of prophylactic antibiotics for only 24 hours. Timely discontinuation of prophylactic antibiotics is important because the practice of prolonged administration of

337

338

Generalized Approaches to the Traumatized Patient

SECTION 2

surgeon must consider personal safety. Epidemiologic studies report that the prevalence of HIV or hepatitis C is as high as 20–65% and 10–45%, respectively, in an urban university hospital population for patients undergoing lymph node biopsy or drainage of a soft tissue infection.44 More recently, Brady et al.45 reported that the seroprevalence of undiagnosed hepatitis C virus (HCV) infection was 7.9% with another 7.8% of the population having preexisting HCV infection.

■ Temperature Control Hypothermia has been shown to be a strong prognostic indicator of poor outcome when considered in the context of the “triad of death” (hypothermia, acidosis, coagulopathy).46 In addition to inducing an acquired coagulopathy, hypothermia has profound adverse effects on SSI rates. In elective colorectal surgery a prospective, randomized study compared a group in whom intraoperative normothermia (36.6°C) was maintained to a control group with mild hypothermia (34.7°C). The normothermic group had a significantly lower rate of SSI (6% vs. 19%) and a 20% shorter hospital stay.47 The precise mechanism for the beneficial effects of normothermia remains unclear, but may relate to tissue perfusion and improved host defense. Therefore, every reasonable effort should be made to maintain normothermia.

■ Supplemental Oxygen The role of oxygen in development of SSI was examined in another prospective randomized study in patients undergoing elective colorectal operations. The authors observed a significantly lower SSI rate when 80% versus 30% inspired oxygen was delivered during the operation.48 It is noteworthy that other studies have failed to replicate these results49 and that this intervention has never been studied in a trauma population; however, an alternative interpretation of this study in elective patients is that it is best to avoid lower intraoperative FiO2.

■ Suture Material There has recently been an extensive marketing effort advocating the use of antibiotic-coated sutures to decrease SSI. Several anecdotal reports describe impressive decreases in the incidence of wound infections (4.9% down from 10.8%) when the authors switched to antibiotic-coated suture.50 Sutures decrease the inoculum of bacteria needed to establish infection and can serve as a foreign body within potentially infected wounds. So while it is clear that studies to specifically compare the efficacy of antibiotic-coated sutures with regular sutures are needed before strong recommendations can be made, there is a sound physiologic basis for a potential benefit. An additional consideration, however, is whether this intervention, like many others, is cost-effective.

■ Blood Transfusion Autologous blood transfusion can be lifesaving for an exsanguinating patient, but numerous authors have reported worse

infectious complications with increased blood utilization both in the immediate resuscitation51–54 and when used in a delayed fashion.55–57 Transfusion results in a multitude of immunosuppressive effects, including: (1) decreased CD3 , CD4 and CD8 cells; (2) overall reduced T-cell proliferation to mitogenic stimuli; (3) decreased natural killer cell activity; (4) defective antigen presentation; and (5) impaired cell-mediated immunity.58 The increased risk of infection associated with blood transfusion appears to be dose dependent57,59 and logistic regression analyses report that the risk of infection increases 13% per unit transfused.60 Taylor et al.61 report that for each unit of packed red blood cells (PRBCs) transfused, the odds of developing a nosocomial infection were increased by a factor of 1.5. The age of the transfused blood is an additional risk factor for infectious complications.62–64 As blood ages in the blood bank, it undergoes predictable changes that affect its ability to deliver oxygen. This “storage lesion” includes the following: (1) an increased affinity of hemoglobin for oxygen and reduced oxygen release to tissues; (2) depletion of 2,3-diphosphoglyerate (2,3-DPG) with resultant inadequacy of oxygen transport by red blood cells; (3) reduction in deformability, altered adhesiveness, and aggregability; and (4) accumulation of bioactive compounds with proinflammatory effects. In trauma patients, Offner and coworkers64 estimated that each transfused unit of RBC older than 14 days increased the risk of major infection by 13%. To minimize infectious risk, one should limit blood transfusion in nonbleeding patients. A large multicenter randomized study reported the safety of a restrictive transfusion strategy (trigger of 7.0 g/dL hemoglobin) compared to a liberal strategy with a trigger of 10.0 g/dL. In fact, patients who were younger (age 55) and less sick (APACHE 20) had over double mortality rates when liberally transfused. When the subgroup of trauma patients (n  203) was reviewed in a secondary analysis, McIntyre et al.65 confirmed the safety of the restrictive strategy. Additionally, practices to be avoided include transfusing multiple units of blood in stable nonbleeding patients, using blood as a volume expander, and transfusing blood preemptively in anticipation of future operative blood loss. Advanced age should not be used as a sole criterion to transfuse a patient. Several recent guidelines describe transfusion of autologous RBCs in trauma patients in the postresuscitation period.66,67

■ Nutritional Support The timing, adequacy, and route of administration of nutrition to trauma patients have definite implications for infectious complications. Adequate nutrition is essential for patient recovery and healing of traumatic wounds. This is because trauma causes increased metabolism and protein turnover, and this results in a catabolic state characterized by skeletal muscle breakdown, impaired healing, and immunosuppression. After resuscitation is complete nutritional support should be instituted and the enteral route is preferred. Numerous trials have compared enteral nutrition (EN) with parenteral nutrition (PN). Advantages of the enteral route include lower cost, maintenance of function of the gut mucosal barrier, and more

Infections

339

TABLE 18-7 Recommendations for Antibiotic Choice and Duration for Different Anatomic Regions and Mechanisms of Injury

Open fractures Closed fractures

Agent Cephalosporina Agent with activity against aerobic and anaerobic bacteria First-generation cephalosporina Cephalosporina

Duration (h) 24 24 24 24

References 80 118

82 38

a

Appropriate substitution should be made in patients who are cephalosporin allergic.

physiologic delivery of nutrients while the advantages of PN are primarily related to the consistency of adequate calorie provision. Based on the available high-quality studies, the evidence strongly favors the use of EN over PN in regards to infectious complications.68–70 Traditional markers of nutrition (albumin, transferrin, and retinal-binding protein) are restored better using EN.69 An additional factor that has been implicated in infectious complications is the issue of glycemic control. Current recommendations relating to glycemic control71 are in flux, but it appears clear that results are improved when high levels of glucose are avoided. Enthusiasm for “very tight” glucose control has waned after several studies showed no benefit and increased complications with attempts to maintain blood glucose 110 mg/dL.72–74

■ Tracheostomy Although several studies comparing early and late tracheostomy have been performed, there is still no consensus regarding whether earlier tracheostomy impacts development of ventilator-associated pneumonia (VAP).75–77 The current EAST recommendations (Level 3) are that early tracheostomy be considered in trauma patients anticipated to require mechanical ventilation of 7 days.78 The decision to perform tracheostomy is often institution and surgeon specific. A recent meta-analysis identified high-risk groups that were likely to benefit from early (72 hours) tracheostomy.75

TRAUMA-RELATED INFECTIONS ■ Diagnosis of Infection Almost by definition, infectious problems are never the presenting complaint of a patient who has sustained an acute traumatic injury; however, recognition of an infection in a patient recovering from traumatic injuries is a common, and sometimes challenging, clinical problem. Several of the signs and symptoms that we commonly associate with infections are frequently present in trauma patients. The immediate physiologic and immunologic response to tissue injury is initiation of the inflammatory response. Acute traumatic injuries cause the cardinal signs of inflammation including pain (dolor), edema (turgor), heat (calor), redness (rubor), and loss of function (functio laesa). Furthermore, trauma victims will often have

several of the SIRS criteria (e.g., tachycardia, elevated temperature, elevated WBC) in the setting of a clinical context in which they are at increased risk for infection.79 Diagnosis of infection requires a high clinical suspicion, tempered by knowledge of the most likely infectious complications at various time points after injury. Finally, this is filtered by experience with caring for patients with similar injuries. As discussed in the earlier section on “Prevention of Infections,” the preferred management of infections is to prevent their occurrence. When prevention measures have been ineffective, the diagnosis of infection is based on clinical, laboratory, and radiologic methods. Most trauma patients, especially those requiring operative interventions, those with open fractures, or those who have sustained penetrating trauma, will be treated with a course of empiric antibiotics (Table 18-7). The choice of specific antimicrobial agents is determined by the endogenous pathogens or likely exogenous contamination (e.g., exposure to Vibrio spp. with marine trauma, exposure to Clostridium sp. with farm injury) that would be present at the anatomic site of injury. Hospitalized patients are at risk for development of nosocomial infections and diagnosis is made on the basis of a high suspicion with laboratory and/or radiologic confirmation. In most cases, bacterial culture constitutes the “gold standard” for diagnosis of infection, although at times it can be impractical or impossible to obtain adequate samples. The most specific culture information, if available, is obtained with quantitative or semiquantitative methods (e.g., burn wound biopsy, bronchoscopic alveolar lavage [BAL], or non-BAL). In cases where cultures cannot be obtained, empiric treatment is initiated based on the most likely pathogenic organisms and adjusted based on clinical response. Evidence-based recommendations have been developed for diagnosis and antimicrobial treatment of most hospital-acquired infections,81–86 albeit not specifically addressing trauma patients. The trauma glue grant (www.gluegrant.org) has proposed a standard operating procedure (SOP) to go about identifying the source of infection in critically ill trauma patients (Fig. 18-4).88 This SOP emphasizes and prioritizes the most likely infections and suggests acceptable antimicrobial agents that are otherwise consistent with evidence-based guidelines from infectious disease specialty societies for a wide range of different infections. Diagnostic imaging, particularly crosssectional imaging, and/or ultrasound, can be helpful to

CHAPTER 18

Region/Mechanism Chest trauma Penetrating abdominal

340

Generalized Approaches to the Traumatized Patient Glue Grant SOP for antibiotic administration in critically ill patients with severe injury*

SECTION 2

Clinical Dx requiring treat with antibiotics1

Empiric Broad Spectrum Rx2: Coverage for Gm+ and Gm- aerobes and anaerobes. Consider origin of infection (community vs. hospital), site, suspected pathogens, and local sensitivity Empiric Rx: pip/tazo + vanco, imipenem + vanco, cefipime + flagyl + vanco

Site infection identified?1 NO Yes

Yes > 4 day admit? resist org?

Skin/skin structure infection? (SSSI)

Pneumonia? (+Quant Bact.) NO VAP, HAP, HCAP Yes

Intraabdominal source? NO (IAI)

> 4 day admit? resist org?

NO

Cover Gm- aerobes & anaerobes. Empiric Rx: pip/tazo. carbapenam, or tigecycline. (? ± anti-fungal)

Yes

Nec. Fasc.? Severe SSSI? NO

NO

Yes

Cover Gm- and Gm+ aerobes. (MRSA, VRE), Pseudomonas, and Acinetobacter Empiric Rx: vanco or linezolid plus pip/tazo, carbapenam aminoglycoside, or cefepime

Cover Gm- aerobes & anaerobes. Empiric Rx: unasyn, ertapenem, moxifloxacin, or cipro/levaquin + metronidazole

NO

Yes

Yes

Yes

Central venous catheter infection? (CVCI)

Cover Gm+ aerobes. MSSA, MRSA. Staph epi. Empiric Rx: vanco, linezolid

Cover Gm+ & Gm- aerobes, & anaerobes. Strep, Staph sp. Empiric Rx: PCN, vanco, pip/tazo, [Note: may add clinda inhibit toxin production.]

Cover Gm- aerobe & anaerobes. Empiric Rx: unasyn, cefoxitin, ertapenem, moxifloxacin, or cipro/levaquin + metronidazole

Cover Gm+ (& Gm-) aerobes. Empiric Rx: cefazolin, ertapenem, moxifloxacin

Follow clinical response to Rx4 Adjust ABX per culture results

Glue Grant SOP for antibiotic administration in critically ill patients with severe injury* Adjust Rx per cultures3

Yes

Fungal infection? multiple sites (+), (+) blood culture abscess (+)

NO

Yes Add fluconazole, voriconazole, caspofungin, or Ampho B

Culture + for enterococcus? compromised Pt, (+) blood culture abscess (+)

NO

Yes Add vanco, linezolid or tigecycline if primary pathogen or resistant to current Rx

C. difficile? watery diarrhea C. diff. toxin (+) Procto/Bx (+)

NO

Follow exam and response to Rx4

Yes oral or iv metronidazole, ? Oral vanco

1 Important to try, whenever possible, to obtain cultures from suspected sites of infection prior to initiating antimicrobial therapy. 2 Empiric choice should include ≥ 1 antibiotic with activity directed against the likely pathogens. 3 Adjust antibiotics with eye toward appropriate “de-escalation” of therapy based on culture results, response to therapy and clinical condition. 4 Always reassess antimicrobials after 48–73 hr based on micro and clinical data. There is no evidence that combination Rx is more effective than mono Rx if microorganisms are sensitive to agent. Duration of Rx should typically be 7–10 days. * Individual antibiotic choices will be heavily influenced by local ID restrictions and /or formulary choices. This guideline is intended to highlight parameters that need to be considered in choice of agents.

FIGURE 18-4 Diagnostic approach to identify and treat postinjury infections in critically ill trauma patients. (Figure from West et al.88 Used with permission.)

identify and access potentially infected fluid collections in deep locations. Percutaneous aspiration and/or drainage has largely replaced the need for operative management of deep infections and abscesses.89,90

■ Intra-Abdominal Infections Intra-abdominal infections, particularly an abscess, represent relatively common infectious complications of both blunt and penetrating abdominal trauma. The presence of very high

Infections

341

TABLE 18-8 SIS/IDSA Evidence-Based Guidelines for Antibiotic Choices for Community-Acquired Intra-Abdominal Infections

Combination therapy (two agent)b

Mild–Moderate Severity Cefoxitin Ertapenem Moxifloxacina Tigecycline Ticarcillin–clavulanate Cefazolin Cefuroxime Cetriaxone Cefotaxime, ciprofloxacina Levofloxacina plus metrinidazole

Levofloxacina plus metronidazole

Children Severe or High-Risk Patients Ertapenem Meropenem Imipenem–cilastatin Ticarcillin–clavulanate Pipericillin–tazobactam Cetriaxone Cefotaxime Cefepime Ceftazidine plus metronidazole Gentamicin Tobramycin plus metronidazole or clindamycin  ampicillin

Adapted from Solomkin et al.92 E. coli resistance to fluroquinolones is increasingly reported, so local sensitivity information should be consulted. b With combination regimens acceptable agents with activity against aerobic gram-negative bacteria are listed first, followed by agents directed against anaerobes. A single agent with aerobic activity should be paired (combined) with an antianaerobic drug. a

numbers of bacteria within the gut coupled with the impaired perfusion present in shock states and the immune alterations associated with trauma results in a 10–25% incidence of intraabdominal infection. Appropriate resuscitation and empiric antibiotics, along with sound intraoperative decision making, minimize the risk for infectious complications. Primary control of the source (see section on Operating Room) is crucial to limit the likelihood for postoperative infections. Primary infection is relatively rare, but may be the presenting complaint in patients in whom a hollow viscus injury has not been recognized. Clinical examination may provide sufficient information to warrant abdominal exploration, and the presence of peritoneal signs or other signs of an acute abdomen should not be ignored in trauma patients. Peritonitis and acute abdominal signs may develop if bacterial contamination has been present for 12 hours. More often, even acutely, diagnostic studies such as an abdominal CT scan will suggest the diagnosis (e.g., unexplained free fluid or free intra-abdominal air is highly suspicious for injury to a hollow viscus). Diagnostic imaging is much more important to identify postoperative abdominal infections, since physical examination may be equivocal in awake patients and it may be impossible to adequately examine sedated trauma victims in the ICU. Intra-abdominal infections that are identified later in the hospital course are much more likely to be caused by hospitalassociated, rather than community-associated, organisms. This is because most patients will have received one or several doses of antibiotics (frequently relatively broad-spectrum antibiotics) that will have altered the remaining bacterial flora.88 Late intraabdominal infections may grow Pseudomonas spp., Serratia spp.,

or Candida spp. Percutaneous aspiration and/or drainage has become the mainstay for treatment of late intra-abdominal abscesses and fluid collections. Whenever possible, material from intra-abdominal collections should be sent for Gram stain, culture, and sensitivity determination because of the high incidence of resistant bacteria that are encountered in recent series.91 The Surgical Infection Society and the Infectious Disease Society of American recently published updated evidence-based guidelines to inform antibiotic choices for abdominal infection.92 These guidelines differentiate between community- and hospital-acquired infections (Tables 18-8 and 18-9). As a general rule, antimicrobial coverage directed against community abdominal pathogens may be given within the first 3 days after injury, whereas antibiotic choices 4 days after injury should anticipate hospital organisms.

■ Empyema Under normal circumstances the pleural cavity has a net negative pressure and a very small (20 mL) volume of fluid.93 The present understanding of fluid flux within the pleural cavity implicates the lymphatics in the parietal pleural as the main route through which fluid is removed.94 Pleural fluid normally turns over at a rate of ∼0.15 mL/(kg h) (10–12 mL/h for a 70-kg individual), and the maximum capacity for lymphatic drainage is estimated to be ∼700 mL per day (∼30 mL/h). If there is increased production or decreased clearance of pleural fluid, a pleural effusion will develop. Pleural effusions are frequently associated with fluid overload, but can also arise in the setting of acute inflammatory processes of the lung including

CHAPTER 18

Monotherapy (single agent)

Adults Severe or High-Risk Patients Imipenem–cilastatin Meropenem Doripenem Pipericillin–tazobactam Cefepime Ceftazidine Ciprofloxacina

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TABLE 18-9 SIS/IDSA Evidence-Based Guidelines for Initial Adult Antibiotic Dosing in IntraAbdominal Infections

SECTION 2

Antibiotic

Adult Dosage

β-Lactam/β-lactamase inhibitor combination Piperacillin– 3.375 g q 6 h (Note: increase dose tazobactam to 3.375 g q 4 h or 4.5 g q 6 h for Pseudomonas infections) Ticarcillin– 3.1 g q 6 h (FDA labeling indicates 200 mg/kg per day in divided clavulanic acid doses q 6 h for moderate infection and 300 mg/kg per day in divided doses q 4 h for severe infection) Carbapenems Doripenem Ertapenem Imipenem– cilastatin Meropenem Cephalosporins Cefazolin Cefepime Cefotaxime Cefoxitin Ceftazidime Ceftriaxone Cefuroxime Tigecycline Fluoroquinolones Ciprofloxacin Levofloxacin Moxifloxacin Metronidazole Aminoglycosides Gentamicin or tobramycin Amikacin Aztreonam Vancomycin

500 mg q 8 h 1 g q 24 h 500 mg q 6 h or 1 g q 8 h 1gq8h 1–2 g q 8 h 2 g q 8–12 h 1–2 g q 6–8 h 2gq6h 2gq8h 1–2 g q 12–24 h 1.5 g q 8 h 100 mg initial dose, and then 50 mg q 12 h 400 mg q 12 h 750 mg q 24 h 400 mg q 24 h 500 mg q 8–12 h or 1,500 mg q 24 h 5–7 mg/kg q 24 h (based on adjusted body weight) 15–20 mg/kg q 24 h (based on adjusted body weight) 1–2 g q 6–8 h 15–20 mg/kg q 8–12 h (based on total body weight)

Adapted from Solomkin et al.92

pneumonia (parapnemonic effusion), ALI, or ARDS. Chest trauma, both blunt and penetrating, can induce alterations within the pleural cavity, with loss of negative pressure (traumatic pneumothorax), accumulation of blood (hemothorax), or a combination of both (hemopneumothorax). Treatment of a hemothorax or pneumothorax generally requires inserting a

TABLE 18-10 Bacteriology of Post-Traumatic Empyema (N  37) Organism S. aureus MRSA P. aeruginosa S. pneumoniae Mixed No growth

N (%) 20 (54) 7 (19) 2 (6) 1 (3) 4 (11) 10 (27)

Adapted from Hoth et al.97

thoracostomy tube, and this intervention introduces the possibility of bacterial contamination of the fluid or blood present within the pleural cavity. In addition, since lymphatic stomata of the parietal pleural are the means by which blood and/or fluid is normally reabsorbed, the presence of fibrin clot obstructs this route of egress and contributes to persistence of fluid within the chest cavity. As discussed in Section “Prevention of Infections,” the presence of bacteria, blood, foreign bodies, and unexpanded lung can predispose to infection within the pleural cavity or what is recognized clinically as an empyema. The diagnosis of empyema requires sampling of fluid or tissue from the pleural space.95 Analysis of pleural fluid will demonstrate a pH 7.20, glucose 40, the presence of bacteria on Gram stain, or a positive culture in the presence of empyema.96 Table 18-10 shows the most common bacterial isolates from post-traumatic empyema, although it is worth noting that some obviously purulent collections may fail to have positive cultures. It is now generally understood that post-traumatic empyema arises from exogenous contamination of the pleural cavity. This was demonstrated clearly by Hoth et al.97 who obtained simultaneous bronchoalveolar lavage and pleural cultures and noted that there was minimal correlation between pleural cultures and BAL samples. Recognition that skin flora is associated with empyema underscores the importance of using sterile technique during insertion of a thoracostomy tube. Studies examining risk factors for development of empyema have identified the duration of drainage through a chest tube and incomplete evacuation of hemothorax as two of the leading factors.98 Retained hemothorax and empyema complicate about 4% of patients with a hemothorax that was treated with a thoracostomy tube.99 Several modalities have been employed to treat empyema.96 Complete evacuation of a hemothorax and reexpansion of the lung at the time the initial chest tube is inserted are important to prevent empyema. Chest CT scans showing pleural thickening or incomplete evacuation may be important adjuncts in managing patients with thoracic trauma. Instillation of fibrinolytic agents has been demonstrated to aid in the evacuation of a retained hemothorax; however, this may be dangerous in the presence of intrathoracic injury. There is now considerable enthusiasm for early use of videoassisted thoracoscopy (VATS), which has proven to be safe and more cost-effective than a second thoracostomy tube.99,100

Infections

TABLE 18-12 Selected Virulence Determinants for S. aureus Bone and Joint Infections

Bacteria isolated from joint infections Staphylococcus aureus Streptococcus pyogenes Streptococcus pneumoniae Escherichia coli Pseudomonas aeruginosa Serratia marcescens Salmonella species Neisseria species Aerobacter species Bacteroides species

Bacterial Determinant Collagen-binding protein Protein A

Bacteria isolated from bone infections Staphylococcus aureus Staphylococcus epidermidis Streptococcus species Haemophilus influenzae Escherichia coli Pseudomonas aeruginosa Salmonella species Mycobacterium species Adapted from Wright and Nair.104

Ideally, VATS should be performed within 7 days of injury, as the rates of empyema and conversion to thoracotomy are increased after 1 week.101

■ Osteomyelitis/Septic Arthritis Trauma-related osteomyelitis and septic arthritis represent not uncommon complications of musculoskeletal injury.102 While hematogenous dissemination of bacteria is involved in most nontraumatic bone and joint infections, post-traumatic musculoskeletal infections generally arise from bacteria introduced exogenously, either at the time of injury or during operative repair. Although a variety of bacterial species have been isolated from post-traumatic osteomyelitis and septic arthritis (see Table 18-11), Staphylococcus species are far and away the most common isolates.103,104 S. aureus and S. epidermidis have a number of virulence factors that provide a particular predilection to bone tissue.104 These virulence factors are summarized in Table 18-12, but include adhesive properties and exotoxins and enzymes that facilitate invasion. Another property that has recently been recognized as being etiologically important to the development and persistence of osteomyelitis is a small colony variant (SCV) phenotype that grows more slowly and has increased resistance to aminoglycosides and decreased hemolytic activity. Clinical use of aminoglycoside beads and broaderspectrum antibiotics may select for these more resilient SCV phenotypes in vivo. The presence of contaminating bacteria at the site of a bone or joint injury incites a vigorous local inflammatory response.

Polysaccharide capsule Enterotoxins A, B, C, and D TSST-1 Alpha-, beta-, and gamma-toxin agr sar CpG motifs

Putative Function Adhesin for collagen Interferes with opsonization and phagocytosis Resists phagocytosis and bacterial killing Superantigens Superantigen Cytolytic toxins Gene regulator Gene regulator DNA, TLR9-dependent release of proinflammatory cytokines

Adapted from Mandal et al.103

The local source of the inflammatory cytokines TNF, IL-1, and IL-6 is not entirely clear, but osteoblasts may contribute. In any case, high local levels of proinflammatory cytokines have dramatic effects on bone turnover and new bone formation. TNF and IL-1 induce increased maturation of osteoclasts and enhance osteoclastic activity.105 At the same time these mediators inhibit mesenchymal cell differentiation into osteoblasts. Similar processes contribute to cartilage and bone destruction in chronic arthritides. In such settings anti-TNF and anti-IL-1 therapies have been very successful in preventing inflammation.106 The net impact of increased osteoclast and decreased osteoblast activity is either bone destruction or inhibition of bone healing. Furthermore, contact between osteoblasts and S. aureus can induce TNF-related apoptosis-inducing ligand (TRAIL), which, in the presence of Fas-associated death domain (FADD), commits cells to apoptotic cell death. There are several unique factors associated with bone infection that underscore the importance of evidence-based recommendations that emphasize early and continuing aggressive debridement of orthopedic injuries, particularly those associated with open or contaminated wounds. At sites of bone or joint injury local blood supply to fragments may be interrupted predisposing to bone necrosis. Lack of blood supply also precludes delivery of systemic antibiotics, host inflammatory cells, and the molecular oxygen needed for oxygen-dependent bactericidal activity of such cells. It is axiomatic that all dead bone must be removed to minimize the risk of bone infection. In addition, many orthopedic injuries require the presence of plates, rods, or other foreign bodies to stabilize fractures. Only very low levels of bacteria are needed experimentally to produce infection in the presence of a foreign body. If there is extensive local bony destruction and/or contamination, many orthopedic surgeons will utilize external fixation devices to minimize, but not eliminate, the risk of infection and nonunion.

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TABLE 18-11 Bacteria Isolated from Septic Joints and Osteomyelitic Bone Infections

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■ Occupational Exposure to Environmental Pathogens SECTION 2

It is an unfortunate reality that health care workers in general and surgeons in particular, are exposed to blood-borne occupational hazards, including hepatitis B virus (HBV), HCV, and HIV. Body fluids considered potentially infectious include blood, cerebrospinal fluid, synovial fluid, pleural fluid, peritoneal fluid, pericardial fluid, and amniotic fluid. Conversely, exposures to nonbloody feces, nasal secretions, saliva, sputum, sweat, tears, urine, and vomitus are not considered potentially infectious as the risk for transmission of HBV, HCV, and HIV infection from these fluids is extremely low.107 Personal protective measures that have been demonstrated to be effective include double gloving, using blunt needles for fascial closure, protective eye shields, impervious surgical gowns, and routine implementation of universal precautions. While prevention is obviously the best course of action, certain measures taken after an exposure can decrease the risk of seroconversion. The first step involves treatment of the exposure site. Wounds and skin sites should be washed with soap and water and mucous membranes flushed with water. There is no evidence to support applying antiseptics to the wound or expressing fluid to reduce the risk of transmitting a blood-borne pathogen. The CDC strongly discourages the application of caustic agents (e.g., bleach) or the injection of antiseptics or disinfectants into the wound. Second, the exposure source should be evaluated for HBV, HCV, and HIV status. If the status is unknown, the patient should be informed of the incident. The health care practitioner must be aware of applicable state and local laws regarding informed consent for serologic testing. Testing of needles or other sharp instruments involved in the exposure is not acceptable as a replacement or complement to testing the source patient. Additional up-to-date resources and recommendations are available via the National Clinician’s Postexposure Prophylaxis Hotline (PEPline, 888-448-4911 or via http://www.nccc. ucsf.edu/). When an exposure to HBV occurs, the risk of seroconversion is dependent on the degree of contact (i.e., size of the inoculum) and the hepatitis B e-antigen (HBeAg) status of the source. For example, if the patient is HBeAg positive, the risk of developing HBV infection is about 50%, compared to 25% if the patient is HBeAg negative. PEP includes hepatitis B immune globulin (HBIG) and, possibly, the hepatitis B vaccination series, depending on the hepatitis B antigen status of the patient and the antibody status of the at-risk health care worker. If indicated, HBIG should be given as soon as possible, since early administration after exposure to hepatitis B surface antigen–positive blood can provide an estimated 75% protection from HB infection.107 In contrast to HBV, HCV is not efficiently transmitted via occupational exposure. It is estimated that HCV seroconversion after accidental percutaneous exposure from an HCVpositive source occurs 1.8% of the time, and some have suggested that transmission occurs only from puncture by hollow-bore needles. Transmission has never been reported after intact or nonintact skin exposure to blood and only rarely

occurs after exposure of mucous membranes to blood. Currently, intravenous immune globulin (IVIG) is not recommended after occupational HCV exposure. The rationale is based on several clinical observations including the following: (1) HCV infection does not incite a protective antibody response; (2) studies of IVIG use for PEP in HAV and HBV cannot be extrapolated to HCV; and (3) HCV IVIG use in chimpanzees has failed to prevent HCV seroconversion after exposure.107 There is no evidence that the administration of INF-α or antiviral agents prevents HCV infection after occupational exposure and their use is not currently recommended. The exposed health care worker should be tested for baseline HCV viral status and continue close follow-up for 12 months for the purpose of early identification should seroconversion occur. Additionally, the health care worker should contact the CDC Hepatitis Information Line (888) 443-7232 or http://www. cdc.gov/hepatitis.107 Like HCV, transmission of HIV occurs rarely after occupational exposure. The CDC estimates that the risk of seroconversion is approximately 0.3% following a percutaneous exposure to HIV-infected blood and 0.09% after exposure of a mucous membrane. For exposure to fluids or tissues other than HIVinfected blood, the risk of transmission has not been quantified, but is probably much lower. The U.S. Public Health Service (PHS) guidelines recommend a combination of zidovudine (ZDV) and lamivudine (3TC) as the first choice for PEP regimens. To maximize the possibility of protection, PEP should be initiated as soon as possible and the health care worker exposed to HIV should be evaluated within hours. A baseline HIV test should be performed and HIV antibody testing should be performed for at least 6 months postexposure (at 6 weeks, 12 weeks, and 6 months). Currently, a 4-week regimen is advised for most HIV exposures and an expanded regimen including a third drug may be added for exposures that pose an increased risk for HIV transmission. If the source person’s virus is known to be resistant to the routine PEP regimen, selection of an alternate regimen is highly recommended.107

CHRONOLOGIC APPROACH TO PREVENTION, RECOGNITION, AND TREATMENT OF INFECTIONS IN TRAUMA PATIENTS ■ Resuscitation Bay Efforts to minimize infection must be initiated as soon as the patient arrives in the trauma bay. Although the initial focus will appropriately center on control of hemorrhage and initiation of resuscitation, these efforts will have beneficial impacts on reducing the risk of infection, as well. Restoration of adequate blood flow and oxygen delivery is the first step in reducing the incidence of infection. It has been clearly shown that the incidence of infection from invasive procedures in the ICU such as insertion of a central venous line or chest tube can be dramatically decreased by employing full-barrier precautions.108 Fullbarrier precautions may not always be practical in severely injured victims, but suspension of proven infection control measures and sterile technique for invasive procedures should

Infections

■ Operating Room The conduct of operative interventions, if needed, can also significantly impact the likelihood for postoperative infectious complications. The primary factor(s) determining the risk for infection is the nature and magnitude of the traumatic injury requiring surgical intervention. Furthermore, it is crucial that the operating surgeon keep in mind that the highest priority during an exploratory laparotomy for hemorrhagic shock is control of bleeding. For example, if a patient sustained abdominal gunshot wounds with multiple enterotomies and an injury to the inferior vena cava and right renal hilum, it is highly likely that the surgeon would encounter blood and massive intestinal contamination on entering the abdomen. The initial focus must be on controlling hemorrhage, and this may require resisting the usual surgical impulse to stop enteric leakage. The analogy is similar to the principle applied to prioritization of exsanguinating abdominal hemorrhage, in a patient with a severe traumatic brain injury. The best way to save the brain (or to minimize infection) is to control the hemorrhage! Once hemorrhage is controlled, it is appropriate to stop ongoing leakage from the bowel and to try to remove most gross contamination. In addition to the bacterial contamination arising from enteric leakage, disruption of gastrointestinal integrity also releases foreign bodies (e.g., undigested food particles), mucin, and bile. Any or all of these so-called adjuvant substances have been shown to significantly decrease the inoculum of bacteria needed to establish infection. Adjuvant substances enhance bacterial infectivity via two mechanisms. First, some adjuvant substances augment bacterial growth or stimulate bacteria to express virulence factors.110 The second mechanism involves interference with host defense mechanisms such as the function of innate immune cells.14 For example, bile’s detergent

activity can result in lysis of polymorphonuclear leukocytes and macrophages. Blood and devitalized tissue are two additional adjuvant factors that are frequently present. Blood (specifically hemoglobin) can be metabolized into a leukotoxin by some species of enteric bacteria.111 Fibrin clots sequester bacteria and make them inaccessible to host phagocytes, and this action may predispose to late development of intra-abdominal abscesses.112,113 Devitalized, ischemic, or necrotic tissue is a potent source of damage/danger signals that can activate host immune cells and exacerbate acute inflammation, while at the same time interfere with phagocytosis and oxidative killing mechanisms of the host defense cells.8,114 Thus, it is desirable to remove most blood and blood clot from the peritoneal cavity to the extent possible. This can be accomplished by irrigating the peritoneal cavity with a goal of removing the obvious contamination, foreign material, and blood. It is worth noting that a prospective randomized study showed no benefit to formal meticulous debridement to remove fibrinous debris from the peritoneal cavity in established peritonitis.115 While it is a popular aphorism that “the solution to pollution is dilution,” there is scant evidence to back up this bias. Experimentally, the best approach involves the least amount of irrigation that will remove gross contamination and adjuvant material. Evidence-based guidelines for antimicrobial prophylaxis of trauma recommend broad-spectrum agents with activity against the anticipated pathogens that are likely to be encountered at the anatomic area of injury.116 The guidelines are predicated on the principle that it is always the best course to anticipate the worst case scenario. In terms of infectious risk for blunt or penetrating abdominal injury, this requires coverage against colonic bacterial flora. Therefore, agents with activity against aerobic and anaerobic bacteria are recommended in the case of abdominal trauma.116–118 With injuries to the extremities the most likely pathogens will be aerobic gram-positive bacteria, particularly Staphylococcus species. Injury to maxillofacial structures requires antibiotic prophylaxis with activity against normal oral flora, and neurosurgical procedures most often employ agents similar to those used for the extremities. Little is known about the pharmacology of antibiotics in the acute resuscitative phase of trauma. Most of the available data are derived from healthy individuals and, therefore, cannot be applied to injured patients. Buijk et al.119 described a cohort of 89 critically ill patients who received aminoglycosides. In these septic patients, the volume of distribution was significantly higher than in those without septic shock, and the maximum concentration of antibiotic achieved was significantly lower. In a study of patients who required significant resuscitation with fluids and blood during a laparotomy, the volume of distribution was significantly expanded and correlated with the degree of fluid resuscitation. Additionally, antibiotic elimination was more rapid in these injured patients when compared with normal estimates.120 With massive blood loss antibiotic prophylaxis will require frequent redosing to maintain plasma and tissue levels above the mean inhibitory concentration (MIC). Animal models of experimental infection after hemorrhagic shock report better prophylaxis with increasing doses of appropriate intraoperative antibiotics.121 Large volume resuscitation and altered

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be the rare exception, rather than the rule. Maintenance of normothermia likewise represents optimal treatment for the trauma patient and has the additional benefit that it will decrease the likelihood for development of infectious complications.47 Contaminated wounds should be cleaned and/or formally debrided in an urgent time frame, although more recent reviews of experience in high-energy orthopedic injuries have downplayed the importance of time to debridement as an important factor in development of osteomyelitis.109 TT booster should be administered to all patients, unless it is known that they have received a booster dose within 5 years. Prophylactic or empiric antibiotics should be initiated in the trauma bay, if they are indicated. Antibiotics should be started in all patients with penetrating injuries, with open fractures, and in any patient in whom there is a high likelihood of injury to a hollow viscus. Due to the hostile environment in which military injuries occur, current recommendations are that injured soldiers start oral or parenteral antibiotics as soon as possible if there is trauma involving any break in the skin. Patients with blunt mechanisms who require operative interventions should receive perioperative antibiotic prophylaxis according to the established, evidence-based guidelines. Antibiotic choices for different anatomic regions are compiled in Table 18-7.

345

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SECTION 2

endothelial permeability with trauma or burns result in an expanded volume of distribution. Renal dysfunction from hypovolemia, myoglobinuria, or radiologic contrast often accompanies severe injury, but the potential risk of nephropathy has no impact on acute antibiotic dosing. The greatest risk for subsequent infectious complications arises from underdosing rather than overdosing in acute trauma. The conduct of the operation itself significantly impacts the chances for survival and the risk of infection. Abundant data from elective surgery underscore the importance of maintaining normothermia, avoiding shock, and minimizing use of blood transfusion.47,55,57,122 Damage control surgery, with an emphasis on acute management of immediate life-threatening injuries, has the collateral benefit of positively impacting the incidence of postoperative infectious complications.123 In most cases with a damage control approach, vascular reconstruction and bowel anastomoses, if needed, will be delayed until the patient is warm, adequately resuscitated, and hemodynamically stable. While the emphasis is not on infection control, but rather on acute management of life-threatening injuries, this approach has been shown to decrease the incidence of intra-abdominal complications. Most surgeons continue empiric prophylactic antibiotics while the wound is temporarily closed, although this approach has not been formally evaluated for efficacy. There is insufficient evidence to recommend for or against the use of prophylactic antibiotics in the management of an open abdomen. If the patient is hemodynamically stable, euvolemic, and normothermic, then there is no adverse impact to definitively managing abdominal, vascular, neurosurgical, or orthopedic injuries during the first operation. In a grossly contaminated wound, primary closure is associated with an unacceptably high wound infection rate. Delayed primary closure (DPC), a practice dating back to Ambrose Pare, was advocated by surgical pioneer John Hunter in the 1700s and popularized during World War I.124 It is based on the normal development of fine granulations within the wound prior to definitive closure. Thus, DPC combines the infective resistance of healing by secondary intention with the cosmesis and patient satisfaction of primary closure. Randomized prospective trials have reported significantly lower rates of wound infections when compared with primary closure in the management of grossly contaminated wounds.125–127 The management of penetrating wounds to the colon has evolved since World War II, when the diverting ostomy reduced mortality rates to about 30% in the preantibiotic era. With improvements in trauma resuscitation and accumulating experience with antibiotics, investigators began to question whether fecal diversion was necessary after colonic repair. Initially, Stone and Fabian128 published the first prospective randomized trial of colostomy versus primary repair. They excluded patients with “high-risk” criteria such as shock, hemorrhage, greater than two organs injured, gross contamination, operative delay greater than 8 hours, injury requiring resection, and loss of the abdominal wall. Subsequent investigations have reported that primary colon repair, even in the face of “high-risk” criteria, is associated with a decreased incidence of infectious complications when compared with diverting ostomy.129–131 .

Open pelvic fractures are associated with extremely high morbidity and mortality, mostly from septic complications. Diverting colostomies are often placed in such patients, but the evidence supporting this approach is weak and is generally derived from small retrospective studies. One systematic review found no difference in the overall infection rate with or without colostomy, with the exception of a lower complication rate when colostomy was used for perineal/rectal wounds.132 More studies are required to provide definitive recommendations. Recommendations for management of extremity fractures continue to evolve. A recent large study found that the most important factor in outcome was early transfer to a trauma center for definitive management.109 Specifically, this study called into question the benefit of early operative debridement of open fractures, inasmuch as time to operative debridement did not confer a statistically significant benefit. The concept of damage control has also been applied to orthopedic injuries.133 Recent military experiences also underscore the utility of this concept, coupled with more liberal use of external fixation devices to minimize infectious complications in this hostile environment.134 With proper debridement and acute management of the fracture, it is interesting to note that bacteria inoculated into fractures at the time of injury are rarely isolated from postoperative infections. Rather, hospital-acquired flora are almost universally responsible for infections in fractures.82

■ ICU and Early Postoperative Period Infectious complications are commonly encountered in the early postoperative period and are even more likely to be seen in patients who require ongoing critical care (Table 18-13). Clinicians should have a high index of suspicion and consider

TABLE 18-13 Nosocomial Infections in the Surgical/ Trauma Intensive Care Unit Pneumonia Community-acquired pneumonia (CAP) Health care–associated pneumonia (HCAP) Ventilator-associated pneumonia (VAP) Catheter-associated infections Central venous catheter infections (CVC) Catheter-related bloodstream infections (CRBSI) Intra-abdominal infections (IAI) Intra-abdominal abscess Secondary peritonitis Tertiary peritonitis Urinary tract infections Skin and soft tissue infections Superficial surgical site Infections (SSI) Decubitus ulcers Burn wound sepsis Empyema Sinusitis Antibiotic/C. Difficile Associated Colitis

Infections

347

TABLE 18-14 Surviving Sepsis Guidelines for Initial Resuscitation and Infection Control Priorities for Septic Shock and Severe Sepsis

Diagnosis of infection Obtain appropriate cultures prior to start antibiotics (but do not delay antibiotic administration) (1C) 2 blood culture samples, 1 blood percutaneous culture, culture all vascular access devices present 48 h, and other sites as indicated Perform imaging studies promptly to identify source of infection, if safe (1C) Antibiotic therapy Begin iv antibiotics ASAP and always 1 h after recognition of severe sepsis (1D) and septic shock (1B) Broad-spectrum activity, 1 agent active against likely pathogens (1B), and good penetration for presumed source (1B) Reassess antibiotic regimen daily (1C) Duration of therapy typically 7–10 days (1D) Stop antimicrobial therapy if noninfectious cause (1D) Infection source identification and control Establish anatomic site of infection ASAP (1C) and 6 h of presentation (1D) Evaluate patient for focus of infection amenable to source control (1C) Implement source control measures ASAP after successful initial resuscitation (1C) Source control choice to maximize efficacy and minimize physiologic upset (1D) Remove intravascular access devices if potentially infected (1C) GRADE criteria139 in parentheses reflect strength of recommendation and quality of evidence. Adapted with permission from Dellinger et al.86

potential sources of infection in the context of the injuries, the characteristics of the patient, the likely offending organisms, and the length of hospital stay. The immediate postoperative course of a severely injured patient is characterized by a vigorous SIRS response.79 Clinical signs such as mild to moderate fever and tachycardia are almost universal. Furthermore, it is now known that danger signals released from injured tissue activate innate immune responses via the same TLR pathways stimulated by bacterial infection. Leukocytosis is a common manifestation of the SIRS response and there is little utility in monitoring the white blood cell count immediately after injury. It is useful to keep the overall trajectory of the patient in mind before automatically initiating a series of expensive and low yield investigations (e.g., blood cultures, urinalysis, x-rays). Identifying infection is particularly difficult in the ICU setting.86,135 Injured patients are at increased risk for development of nosocomial infections such as pneumonia, catheterrelated bloodstream infections (CRBSI), urinary tract infections (UTI), antibiotic-associated colitis, and SSI; however, critically ill trauma victims are susceptible to severe sepsis and septic

shock, as well. The Surviving Sepsis Campaign has emphasized the importance of prompt recognition, aggressive resuscitation, and early institution of broad-spectrum antimicrobial agents in their recently updated evidence-based guidelines (Table 18-14).86 In the sections that follow we discuss the diagnosis and treatment of common postinjury/postoperative infections that are frequently encountered in trauma patients.

Ventilator-Associated Pneumonia In a broad sense, pneumonia can be divided into communityacquired pneumonia (CAP) and hospital- or health care– associated pneumonia (HCAP), the former being present on admission and the latter manifesting later in the hospital course. HCAP can further be divided into early (4 days) and late (4 days). These distinctions are more than merely pedantic, as the most likely responsible organisms are different and require different spectrums of antibiotic coverage. All postoperative patients are at risk for pulmonary complications and, therefore, aggressive mobilization and pulmonary toilet should be employed

CHAPTER 18

Initial resuscitation (first 6 h) Begin immediately if systolic BP 90 or serum lactate 4 mmol/L (1C) Resuscitation goals (1C) CVP 8–12 mm Hg MAP 65 mm Hg Urine output 0.5 mL/(kg h) SsvcO2 70% or SvO2 65% If venous oxygen saturation target not achieved (2C) Consider further fluid; transfuse PRBC to Hct 30% and/or dobutamine infusion

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SECTION 2

when possible. Unfortunately, injuries such as rib fractures that interfere with coughing and deep breathing, orthopedic injuries that limit mobility, or traumatic brain injuries result in an altered mental status, and complicate pulmonary toilet. CAP should be treated in accordance with local prevalence patterns, most commonly with ceftraixone and azithromycin, as the most common microbes are Haemophilus influenzae and Streptococcus pneumoniae. Early HCAP is initially treated with vancomycin (for MRSA coverage) and ceftraixone.137 Within the broader category of HCAP an important subgroup is patients who develop pneumonia on mechanical ventilation. VAP is a leading cause of morbidity and mortality in the injured population and remains a daunting diagnostic challenge.138,139 In the intensive care unit there are abundant data focusing on the utility of measures designed to prevent VAP.140 Simple measures such as routine hand hygiene and elevation (30–45°) of the head of bed to decrease the likelihood of reflux have resulted in dramatic decreases in VAP rates. Reverse Trendelenberg positioning is an acceptable alternative in patients who must remain supine. Subglottic suctioning and chlorhexidine oral hygiene have been shown to be effective though to a lesser degree, and all of these measures have been incorporated into “ventilator bundles.”140 The duration of mechanical ventilation is the greatest risk factor for development of VAP, with an estimated incidence of 1.2–3.5% risk of developing pneumonia per day of mechanical ventilation.141 Every effort should be made to achieve liberation from the ventilator as soon as possible. Patients should be assessed daily for a trial of spontaneous breathing and extubation should occur if the patient successfully passes the trial.139,142,143 The diagnosis of pneumonia can be challenging in critically ill trauma patients because physical examination is often limited in the obtunded or sedated patient. In addition, lung contusions or atelectasis complicate interpretation of chest x-rays and bacterial colonization of the endotracheal tube and trachea is universal after a few days of mechanical ventilation. There is value in using the clinical pulmonary infection score (CPIS, see Table 18-15) initially described by Pugin to compare invasive and noninvasive pulmonary sampling techniques for VAP.145 Subsequent trials have shown that CPIS alone is not sufficiently accurate to diagnose or rule out VAP.146 In the authors’ hands the CPIS is useful in that a low initial CPIS can direct the team to search for an extrapulmonic source of infection and a day 3 improvement in an initial high CPIS may alter the duration of antibiotic therapy. Diagnostic sampling of the respiratory tract will greatly assist in differentiating tracheal colonization from true infection and in guiding antibiotic therapy. Three modalities of diagnostic sampling of the lower respiratory tree, BAL, bronchoscopic protected specimen brushing, and blind “mini-BAL,” are currently employed and the specimens are sent for quantitative or semiquantitative microbiologic culture.147 Some controversy remains as to the optimal mode for sampling and the quantitative criteria differ depending on the diagnostic method of diagnosis. A positive confirmatory culture is defined as a BAL or mini-BAL culture 104 CFU/mL or protected specimen brush 103 CFU/mL. A true pneumonia will also manifest as a new radiographic infiltrate, increased oxygen requirements, and the

TABLE 18-15 Clinical Pulmonary Infection Score (CPIS) Clinical Parameter (a) Temperature

(b) WBC

(c) Tracheal secretions

(d) Oxygenation (PaO2/FiO2)

(e) Pulmonary radiography

(f) Progression of pulmonary infiltrate (g) Culture of tracheal aspirate

Value 36.5°C to 38.4°C 38.5°C to 38.9°C 39°C or 36°C 4,000 to 11,000 4,000 or 11,000 4,000 or 11,000 and 50% bands None or scant Presence of nonpurulent secretions Presence of purulent secretions 240, presence of ARDS or contussion 240 and no ARDS (Note: ARDS defined as PaO2/ FiO2 200, PCWP 18 mm Hg, and acute bilateral infiltrates) No infiltrate Diffuse (or patchy) infiltrate Localized infiltrate No infiltrate Radiographic progression (after excluding CHF and ARDS) No growth or light growth of pathogenic bacteria Pathogenic bacteria in moderate to heavy growth

Points 0 1 2 0 1 2 0 1 2 0 2

0 1 2 0 2

0 1

Scoring: Add points in each category (a)–(g) to obtain total CPIS score. CPIS 6: consistent with pneumonia. CPIS 6: pneumonia is unlikely; consider other sources of infection. Adapted from Singh et al.144 Reproduced with permission from Pugin J, et al. Diagnosis of ventilator-associated pneumonia by bacteriologic analysis of bronchoscopic and nonbronchoscopic “blind” bronchoalveolar lavage fluid. Am Rev Respir Dis. 1991;143:1121–1129. Copyright © American Thoracic Society.

presence of thick, copious secretions. These diagnostic criteria must be satisfied within a 48-hour period. When pneumonia is identified, it is important to institute therapy as soon as possible. Current recommendations for antimicrobial coverage for pneumonia, and especially VAP, emphasize beginning with broad-spectrum coverage and then de-escalating or narrowing the coverage once culture results are

Infections

Urinary Tract Infections UTI is the most common hospital-acquired infection and is almost universally associated with an indwelling urinary catheter.152–154 Most injured patients in the ICU require urinary drainage and differentiation between urinary colonization and infection can be difficult. The diagnosis of UTI requires a quantitative urine culture with 105 CFU/mL along with at least one of the following clinical criteria: (1) temperature 38.5°C, (2) WBC 10K or 3K, and (3) urinary urgency, dysuria, or suprapubic tenderness. Additionally, these factors must be present within a contiguous 48-hour period. A recent study of trauma patients in an ICU setting suggested that early (within 14 days of admission) UTI were an infrequent source of sepsis and, when present, were seldom associated with fever or leukocytosis. Clinically significant urinary infections usually occur in the setting of urinary trauma and/or repair. Responsible organisms in hospitalized patients include E. coli, Pseudomonas, Proteus, Enterobacter, Serratia, and Citrobacter.155 Gram-negative coverage is indicated. Fortunately, many systemic antibiotics are excreted via the kidney and will achieve urinary levels that far exceed the MICs for most of these pathogens.

Catheter-Related Bloodstream Infection While decreasing in incidence in recent years, CRBSI remains a source of serious morbidity, increased hospital and ICU stay, increased costs, and potential death.156,157 The decision to insert a central line should not be taken lightly. Indications for central access include poor peripheral access, administration of TPN, and administration of high-dose vasoactive medications. A large-bore introducer is commonly inserted in the acute resuscitation of an unstable patient. Often, the clinician is faced with the difficult decision to remove necessary central access or maintain the catheter in the face of potential line sepsis. In trauma patients whose catheters were placed emergently using nonsterile technique, the lines should be removed and

replaced, if needed, with aseptically inserted catheters at new sites. Femoral venous catheters are associated with unacceptably high rates of both infection and deep vein thrombosis and catheters at these sites should be removed as soon as possible. The use of peripherally inserted central catheters (PICC) is associated with a lower incidence of CRBSI. Routine guidewire exchange at predefined intervals does not decrease the rate of CRBSI and may even increase the incidence. Using an evidence-based approach Pronovost et al.158 reported a 66% sustained reduction in the incidence of CRBSI by removing unnecessary catheters, avoiding the femoral site, using fullbarrier precautions during insertion, hand washing, and cleaning the skin with chlorhexidine. When presented with a possible CRBSI, remember that this is a diagnosis of exclusion and requires the presence of bacteremia or fungemia in a patient in whom there is no alternate source of infection. Without local signs of infection (i.e., redness and purulence), a search for other infectious etiologies should always be performed first. As a caveat, infected catheters are frequently thrombogenic and the first sign of infection may be an inability to aspirate blood through the port. In addition to meeting SIRS criteria, the patient must have microbiologic evidence of catheter infection as follows: (1) positive semiquantitative culture (15 CFU/cm catheter segment); (2) quantitative (103 CFU/cm catheter segment) culture with the same organism isolated from blood cultures; and (3) simultaneous quantitative blood cultures with a 5:1 CVC to blood ratio of the same bacterial species.

Surgical Site Infections SSI are infections arising at the site of a previous surgical procedure, defined as a location in which an incision had been made or a procedure performed.159,160 Classification of SSI is based on the anatomic depth of the infection and whether the infection is present in the wound or within an organ space. Superficial and deep incisional SSI are differentiated based on whether the infection extends below the fascial layers (deep SSI). By convention, SSI are infections identified within 30 days of the initial surgical procedure. Superficial SSI are not infrequent in trauma patients based on the wound classification, disruption of environmental barriers, bacterial inoculation at the time of injury, and dysfunction of host defenses seen with injury. Diagnosis of a superficial SSI is determined by the presence of at least one of the following clinical criteria at the site of a surgical procedure: (1) purulent drainage from the surgical incision; (2) culture of organisms from an aseptically obtained fluid or tissue sample from the incision; (3) clinical signs or symptoms of infection; or (4) clinical diagnosis of infection by the surgeon (e.g., the need to open wound). Conditions such as stitch abscesses and erythema or serous drainage at external fixator pin sites do not constitute superficial SSI. In contrast to superficial SSI, a deep SSI involves the deeper soft tissues (e.g., fascial and muscle layers) at the site of the surgical incision and 1 of the following: (a) purulent drainage deep to the fascia or muscle layers; (b) spontaneous fascial dehiscence; or (c) identification of a deep abscess on direct examination, during reoperation, or radiologic examination. Finally, an organ

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obtained. Inadequate initial antibiotic therapy has repeatedly been shown to be associated with worse outcomes and increased mortality.86,148–150 Beyond 5 days after hospital admission, the patient is at risk for infection by resistant organisms such as Pseudomonas, Acinetobacter, and extended-spectrum beta-lactamase producers such as Klebsiella and E. coli, especially if previously exposed to antibiotics. Gram-negative coverage should include piperacillin/tazobactam, cefepime, imipenem, or meropenem. The addition of an aminoglycoside for “synergistic effect” against Pseudomonas is not supported by current guidelines. With the increasing prevalence of MRSA, vancomycin should always be included as initial empiric coverage. Once pneumonia has been diagnosed and therapy initiated, the next question is the appropriate duration of therapy. An oft-quoted study by Chastre et al.151 reported that an 8-day antibiotic course was equivalent to 15-day therapy for VAP. The foremost consideration should be the clinical status of the patient, with a good response consisting of resolution of elevated temperature, resolving leukocytosis, decreased respiratory secretions, and improved oxygenation. Radiographic resolution often lags behind clinical improvement.

349

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space SSI involves anatomic structures (e.g., organs or spaces) that were manipulated during the surgical procedure. In addition, diagnosis of an organ space SSI is based on at least one of the following: (1) purulent drainage from a drain placed into the organ or space (either incisional or percutaneously drained); (2) culture-positive fluid or tissue; or (3) the presence of an abscess during reoperation or radiologic evaluation. Treatment of SSI depends on the location and depth of infection.88,92,161 Superficial SSI are treated by opening of the surgical incision followed by local wound care. There is no demonstrated benefit to systemic antibiotic treatment for superficial SSI in the absence of systemic symptoms. For deep SSI and organ space infections, it is advisable to try to obtain cultures of any purulent drainage, since prior antibiotic selection pressure and the increasing incidence of resistant strains within hospitals makes it difficult to predict antimicrobial responses.88 In the face of negative cultures, a not infrequent occurrence, clinicians should base antibiotic choices on the anticipated pathogens at the anatomic site. It is well to keep in mind that infections that arise after treatment with a longer course of antibiotics will almost certainly be resistant or, at best, only partially sensitive to the initial agent used. Thus, while awaiting culture and sensitivity results, it is wise to employ a different antibiotic agent or even class.

TABLE 18-16 Recommendations for Postsplenectomy Vaccinationsa ●

●

●

●

●

●

●

The 23-valent polysaccharide pneumococcal vaccine is recommended for persons 2–64 years old with functional or anatomic asplenia High-risk individuals should be considered for vaccination with H. influenza type B conjugate vaccine Meningococcal vaccine should be administered to all asplenic patients Vaccines should be administered 14 days prior to elective splenectomy to maximize the antibody against T-cell-dependent immunogens Patients who undergo emergent or unanticipated splenectomy should receive vaccinations 14 days postoperatively A single revaccination with the 23-valent polysaccharide pneumococcal vaccine should be given 5 years after the initial vaccination. No additional subsequent redosing is recommended No current recommendations to redose H. influenza or meningococcal vaccines

a

Adapted from Surgical Infection Society guidelines.19

Clostridium difficile Diarrhea C. difficile is a gram-positive anaerobic bacterium that is a frequent cause of infectious colitis.162,163 It is a part of the normal colonic flora in 2–5% of the healthy population and is normally nonpathogenic. The incidence in the trauma population has been reported to be 3%.164 Disruption of the colonic flora by antibiotics causes relative overgrowth of this organism. Although the occurrence has been reported with all antibiotics, the association is highest with clindamycin and third-generation cephalosporins. The organism reproduces via spore formation and should be considered highly contagious, as the spores are heat resistant and stomach acid resistant. Additionally, alcohol-based hand sanitizers are ineffective in eradicating the spores. Soap and water hand washing is mandatory after contact with a contagious patient. Since 2001, there has been a significant increase in the incidence of C. difficile infection to approximately 84 per 100,000, and this has coincided with an increased number of serious or fatal infections. The higher failure rates being reported (18.2%) with metronidazole therapy have prompted several professional societies to recommend vancomycin as a first-line agent for patients with severe infection (at a dose of 125 mg four times per day, per os). Vancomycin can also be administered per rectum by enema (500 mg four times daily). For milder infections, oral metronidazole remains the preferred treatment because of its lower cost. For both severe and mild infections, intravenous or oral metronidazole (500 mg four times daily) may be given. After initial treatment, recurrence rates after treatment with metronidazole or vancomycin are 20% and may be a result of reinfection with a different strain of C. difficile or persistence of the initial strain. If it is the latter, the recurrent episode may be treated with the same agent used to treat the initial episode. After the first recurrence, the risk of a second recurrence is 40%

and 60% after two or more recurrences. There are no standard recommendations for treatment of multiple recurrences; however, a recently completed multicenter, randomized, doubleblind placebo-controlled trial of monoclonal antibodies to C. difficile toxins A and B reported significantly lower recurrence rates among the treatment arm when compared with placebo (7% vs. 25%, P  .001).165

Postsplenectomy Vaccinations The optimal timing of administration of vaccines after traumatic splenectomy is unknown, but data suggest an increasing trend for elevated functional antibody activity with a delay in vaccination and improved immune antibody response to vaccination at 14 days after surgery.166 The ACIP recommends the use of the 23-valent polysaccharide pneumococcal vaccine for persons 2–64 years of age who have functional or anatomic asplenia. The CDC suggests a single booster dose for those older than 2 years of age who are at high risk for serious pneumococcal infection and those most likely to have a rapid decline in antibody titers. A single revaccination should be given at least 5 years after the first dose, with further dosing not recommended routinely. H. influenzae vaccination with ActHIB conjugate vaccine is recommended. The available meningococcal vaccine protects against serotypes A, C, Y, and W-135 of Neisseria meningitidis.19 There currently is no recommendation to revaccinate for H. influenza type b or meningococcus. Most trauma patients will be discharged from the hospital much earlier, and given that the population of trauma patients is characterized by poor follow-up, it is probably best to vaccinate the patient prior to discharge rather than wait 14 days (Table 18-16).

Infections

■ Late Infectious Complications Overwhelming Postsplenectomy Infection (OPSI)

Surgical Site Infection after Discharge In the modern health care environment there is increased pressure for earlier hospital discharge. While this practice is reported to be safe and clearly decreases costs, it complicates identification of SSI. In a prospective study of 268 patients, 33% of all patients with SSI were diagnosed after hospital discharge.170 Trauma caregivers should educate patients about signs and symptoms of SSI at the time of discharge and request that they be notified if infections are identified. In the future it is conceivable that shared electronic health records may aid in identification of late SSI.

REFERENCES 1. Morales CH, Villegas MI, Villavicencio R, et al. Intra-abdominal infection in patients with abdominal trauma. Arch Surg. 2004;139(12): 1278–1285 [discussion 1285]. 2. West MA. Contemporary Guide to Surgical Infections. Newtown, PA: Handbooks in Health care Co; 2008. 3. Claridge JA, Golob JF Jr, Leukhardt WH, et al. The “fever workup” and respiratory culture practice in critically ill trauma patients. J Crit Care. 2010;25:493–500. 4. Dunn DL, Bellman JG. Surgical infections. In: Brunicardi FC, Andersen DK, Billiar TR, Dunn DL, Hunter JG, Pollock RE, eds. Schwartz’s Principles of Surgery. New York: McGraw-Hill; 2005:chap 5. 5. McManus AT, Mason AD Jr, McManus WF, Pruitt BA Jr. What’s in a name? Is methicillin-resistant Staphylococcus aureus just another S aureus when treated with vancomycin? Arch Surg. 1989;124(12):1456–1459. 6. Bratzler DW, Houck PM, for the Surgical Infection Prevention Guidelines Writers Workgroup. Antimicrobial prophylaxis for surgery: an advisory statement from the National Surgical Infection Prevention Project. Clin Infect Dis. 2004;38:1706–1715. 7. Shasby DM, McCray P. Sepsis and innate immunity. Am J Respir Crit Care Med. 2004;169(2):144–145.

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Historically, the spleen was considered expendable and the prevailing opinion was that it could be removed with relative impunity. Our current understanding is that the spleen plays an important role in the production of immune mediators that aid in the clearance of bacteria and viruses. Splenic mediators (opsonins) coat circulating bacteria and viruses and convert them into immune complexes, facilitating clearance.167,168 It is difficult to estimate the current incidence of OPSI, as most of the published data on OPSI antedate the widespread availability of the pneumococcal and H. influenzae vaccines. The time since splenectomy is an important risk factor as 50–70% of admissions to the hospital for serious infections occur within the first 2 years. In a review of articles published between 1966 and 1996, Bisharat et al.169 identified almost 20,000 patients who had undergone splenectomy with a median follow-up of 6.9 years. The overall incidence of postsplenectomy infection was 3.2%, with a 1.4% mortality rate. The incidence of infection and mortality were marginally lower (2.3% and 1.1%, respectively) in the 920 trauma patients included in the study. Interestingly, among the trauma patients the mean interval between splenectomy and infection was 49.7 months. Pneumococcal infections account for the majority of reported cases while H. influenzae type b, N. meningitides, and Group A Streptococcus account for an additional 25%.167

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83. Render ML, Brungs S, Kotagal U, et al. Evidence-based practice to reduce central line infections. Jt Comm J Qual Patient Saf. 2006;32(5): 253–260. 84. Schunemann HJ, Jaeschke R, Cook DJ, et al. An official ATS statement: grading the quality of evidence and strength of recommendations in ATS guidelines and recommendations. Am J Respir Crit Care Med. 2006; 174(5):605–614. 85. Pronovost P. Interventions to decrease catheter-related bloodstream infections in the ICU: the Keystone Intensive Care Unit Project. Am J Infect Control. 2008;36(10):S171.e1– S171.e5. 86. Dellinger RP, Levy MM, Carlet JM, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008. Crit Care Med. 2008;36(1):296–327. 87. Ni Choileain N, Redmond HP. Cell response to surgery. Arch Surg. 2006;141(11):1132–1140. 88. West MA, Moore EE, Shapiro MB, et al. Inflammation and the host response to injury, a large-scale collaborative project: patient-oriented research core—standard operating procedures for clinical care VII— guidelines for antibiotic administration in severely injured patients. J Trauma. 2008;65(6):1511–1519. 89. Marshall JC, Innes M. Intensive care unit management of intraabdominal infection. Crit Care Med. 2003;31(8):2228–2237. 90. Jaffe TA, Nelson RC, Delong DM, Paulson EK. Practice patterns in percutaneous image-guided intraabdominal abscess drainage: survey of academic and private practice centers. Radiology. 2004;233(3): 750–756. 91. Nathens AB. Relevance and utility of peritoneal cultures in patients with peritonitis. Surg Infect (Larchmt). 2001;2(2):153–160 [discussion 160–162]. 92. Solomkin JS, Mazuski JE, Bradley JS, et al. Diagnosis and management of complicated intra-abdominal infection in adults and children: guidelines by the Surgical Infection Society and the Infectious Diseases Society of America. Surg Infect (Larchmt). 2010;11(1):79–109. 93. Miserocchi G. Physiology and pathophysiology of pleural fluid turnover. Eur Respir J. 1997;10(1):219–225. 94. Zocchi L. Physiology and pathophysiology of pleural fluid turnover. Eur Respir J. 2002;20(6):1545–1558. 95. Evans HL, Cuschieri J, Moore EE, et al. Inflammation and the host response to injury, a Large-Scale Collaborative Project: patient-oriented research core standard operating procedures for clinical care IX. Definitions for complications of clinical care of critically injured patients. J Trauma. 2009;67(2):384–388. 96. Lee SF, Lawrence D, Booth H, et al. Thoracic empyema: current opinions in medical and surgical management. Curr Opin Pulm Med. 2010;16(3):194–200. 97. Hoth JJ, Burch PT, Bullock TK, et al. Pathogenesis of posttraumatic empyema: the impact of pneumonia on pleural space infections. Surg Infect (Larchmt). 2003;4(1):29–35. 98. Karmy-Jones R, Holevar M, Sullivan RJ, et al. Residual hemothorax after chest tube placement correlates with increased risk of empyema following traumatic injury. Can Respir J. 2008;15(5):255–258. 99. Meyer DM, Jessen ME, Wait MA, Estrera AS. Early evacuation of traumatic retained hemothoraces using thoracoscopy: a prospective, randomized trial. Ann Thorac Surg. 1997;64(5):1396–1400 [discussion 1400–1401]. 100. Heniford BT, Carrillo EH, Spain DA, et al. The role of thoracoscopy in the management of retained thoracic collections after trauma. Ann Thorac Surg. 1997;63(4):940–943. 101. Carrillo EH, Richardson JD. Thoracoscopy in the management of hemothorax and retained blood after trauma. Curr Opin Pulm Med. 1998;4(4):243–246. 102. Lew DP, Waldvogel FA. Osteomyelitis. N Engl J Med. 1997;336(14): 999–1007. 103. Mandal S, Berendt AR, Peacock SJ. Staphylococcus aureus bone and joint infection. J Infect. 2002;44(3):143–151. 104. Wright JA, Nair SP. Interaction of staphylococci with bone. Int J Med Microbiol. 2010;300(2–3):193–204. 105. Tokukoda Y, Takata S, Kaji H, et al. Interleukin-1beta stimulates transendothelial mobilization of human peripheral blood mononuclear cells with a potential to differentiate into osteoclasts in the presence of osteoblasts. Endocr J. 2001;48(4):443–452. 106. Takayanagi H. Osteoimmunology and the effects of the immune system on bone. Nat Rev Rheumatol. 2009;5(12):667–676. 107. U.S. Public Health Service. Updated U.S. Public Health Service guidelines for the management of occupational exposures to HBV, HCV, and HIV and recommendations for postexposure prophylaxis. MMWR Recomm Rep. 2001;50(RR-11):1–52.

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136. Schunemann HJ, Oxman AD, Brozek J, et al. Grading quality of evidence and strength of recommendations for diagnostic tests and strategies. BMJ. 2008;336(7653):1106–1110. 137. Arroll B. Antibiotics for upper respiratory tract infections: an overview of Cochrane reviews. Respir Med. 2005;99(3):255–261. 138. Shorr AF, Kollef MH. Ventilator-associated pneumonia: insights from recent clinical trials. Chest. 2005;128(5 suppl 2):583S–591S. 139. Isakow W, Kollef MH. Preventing ventilator-associated pneumonia: an evidence-based approach of modifiable risk factors. Semin Respir Crit Care Med. 2006;27(1):5–17. 140. Dodek P, Keenan S, Cook D, et al. Evidence-based clinical practice guideline for the prevention of ventilator-associated pneumonia. Ann Intern Med. 2004;141(4):305–313. 141. Cook DJ, Walter SD, Cook RJ, et al. Incidence of and risk factors for ventilator-associated pneumonia in critically ill patients. Ann Intern Med. 1998;129(6):433–440. 142. Epstein SK. Weaning from ventilatory support. Curr Opin Crit Care. 2009;15:36–43. 143. Nathens AB, Johnson JL, Minei JP, et al. Inflammation and the host response to injury, a large-scale collaborative project: patient-oriented research core—standard operating procedures for clinical care. I. Guidelines for mechanical ventilation of the trauma patient. J Trauma. 2005;59(3): 764–769. 144. Singh N, Rogers P, Atwood CW, et al. Short-course empiric antibiotic therapy for patients with pulmonary infiltrates in the intensive care unit. A proposed solution for indiscriminate antibiotic prescription. Am J Respir Crit Care Med. 2000;162(2 pt 1):505–511. 145. Pugin J. Clinical signs and scores for the diagnosis of ventilatorassociated pneumonia. Minerva Anestesiol. 2002;68(4):261–265. 146. Rosbolt MB, Sterling ES, Fahy BG. The utility of the clinical pulmonary infection score. J Intensive Care Med. 2009;24(1):26–34. 147. Minei JP, Nathens AB, West M, et al. Inflammation and the Host Response to Injury, a Large-Scale Collaborative Project: patient-oriented research core—standard operating procedures for clinical care. II. Guidelines for prevention, diagnosis and treatment of ventilatorassociated pneumonia (VAP) in the trauma patient. J Trauma. 2006; 60(5):1106–1113 [discussion 1113]. 148. Kollef MH, Ward S, Sherman G, et al. Inadequate treatment of nosocomial infections is associated with certain empiric antibiotic choices. Crit Care Med. 2000;28(10):3456–3464. 149. Alvarez-Lerma F, Alvarez B, Luque P, et al. Empiric broad-spectrum antibiotic therapy of nosocomial pneumonia in the intensive care unit: a prospective observational study. Crit Care. 2006;10(3):R78. 150. Dupont H, Mentec H, Sollet JP, Bleichner G. Impact of appropriateness of initial antibiotic therapy on the outcome of ventilator-associated pneumonia. Intensive Care Med. 2001;27:355–362. 151. Chastre J, Wolff M, Fagon JY, et al. Comparison of 8 vs 15 days of antibiotic therapy for ventilator-associated pneumonia in adults: a randomized trial. JAMA. 2003;290(19):2588–2598. 152. Richards MJ, Edwards JR, Culver DH, Gaynes RP. Nosocomial infections in combined medical-surgical intensive care units in the United States. Infect Control Hosp Epidemiol. 2000;21(8):510–515.

153. Trautner BW, Darouiche RO. Prevention of urinary tract infection in patients with spinal cord injury. J Spinal Cord Med. 2002;25(4): 277–283. 154. Trautner BW. Management of catheter-associated urinary tract infection. Curr Opin Infect Dis. 2010;23(1):76–82. 155. Liu H, Mulholland SG. Appropriate antibiotic treatment of genitourinary infections in hospitalized patients. Am J Med. 2005;118(suppl 7A): 14S–20S. 156. Pelletier SJ, Crabtree TD, Gleason TG, et al. Bacteremia associated with central venous catheter infection is not an independent predictor of outcomes. J Am Coll Surg. 2000;190(6):671–680 [discussion 680–681]. 157. Smith RL 2nd, Sawyer RG, Pruett TL. Hospital-acquired infections in the surgical intensive care: epidemiology and prevention. Zentralbl Chir. 2003;128(12):1047–1061. 158. Pronovost P, Needham D, Berenholtz S, et al. An intervention to decrease catheter-related bloodstream infections in the ICU. N Engl J Med. 2006;355(26):2725–2732. 159. Horan TC, Gaynes RP. Surveillance of nosocomial infections. In: Mayhall CG, ed. Hospital Epidemiology and Infection Control. Philadelphia: Lippincott Williams & Wilkins; 2004:1659–1702. 160. Mangram AJ, Horan TC, Pearson ML, et al. Guideline for prevention of surgical site infection, 1999. Hospital Infection Control Practices Advisory Committee. Infect Control Hosp Epidemiol. 1999;20(4): 250–278 [quiz 279–280]. 161. May AK, Stafford RE, Bulger EM, et al. Treatment of complicated skin and soft tissue infections. Surg Infect (Larchmt). 2009;10(5):467–499. 162. Hull MW, Beck PL. Clostridium difficile-associated colitis. Can Fam Physician. 2004;50:1536–1540, 1543–1545. 163. Kyne L. Clostridium difficile—beyond antibiotics. N Engl J Med. 2010; 362(3):264–265. 164. Lumpkins K, Bochicchio GV, Joshi M, et al. Clostridium difficile infection in critically injured trauma patients. Surg Infect (Larchmt). 2008;9(5): 497–501. 165. Lowy I, Molrine DC, Leav BA, et al. Treatment with monoclonal antibodies against Clostridium difficile toxins. N Engl J Med. 2010;362(3): 197–205. 166. Shatz DV, Schinsky MF, Pais LB, et al. Immune responses of splenectomized trauma patients to the 23-valent pneumococcal polysaccharide vaccine at 1 versus 7 versus 14 days after splenectomy. J Trauma. 1998;44(5):760–765 [discussion 765–766]. 167. Brigden ML, Pattullo AL. Prevention and management of overwhelming postsplenectomy infection—an update. Crit Care Med. 1999;27(4): 836–842. 168. Okabayashi T, Hanazaki K. Overwhelming postsplenectomy infection syndrome in adults—a clinically preventable disease. World J Gastroenterol. 2008;14(2):176–179. 169. Bisharat N, Omari H, Lavi I, Raz R. Risk of infection and death among post-splenectomy patients. J Infect. 2001;43(3):182–186. 170. McIntyre L, Warner K, Nester T, Nathens A. The incidence of postdischarge surgical site infection in the injured patient. J Trauma. 2009;66:407–410.

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MANAGEMENT OF SPECIFIC INJURIES

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CHAPTER 19

Injury to the Brain Alexander F. Post, Thomas Boro, and James M. Ecklund

INTRODUCTION Traumatic brain injury (TBI) is a disruption or alteration of brain function due to external forces. The disruption of function may be transient or long lasting and may vary in severity. The external forces creating the injury may be the result of a variety of insults including acceleration or deceleration, direct compression, penetrating objects, combined effects, and complex mechanisms such as in blast. It may produce subtle effects not discernible on radiological imaging, focal injuries such as fractures, contusion, subarachnoid hemorrhage (SAH), subdural hemorrhage (SDH), epidural hemorrhage (EDH), or intraparenchymal hemorrhage (IPH), or more widespread damage such as diffuse axonal injury (DAI). All injuries and symptoms, even if apparently minor on initial presentation, should be taken seriously since injuries may rapidly progress and become life-threatening.

EPIDEMIOLOGY The exact number of people suffering TBI is unknown since many individuals suffering mild or moderate TBI do not seek medical attention, and some who suffer severe traumatic injuries do not survive to receive medical attention. Of those who do receive medical attention in an emergency department, approximately 1.4 million people per year suffer TBI. Of these patients, approximately 1.1 million are treated and released, 240,000 are hospitalized, and 50,000 die.1 Common causes for TBI are falls (28%), motor vehicle accidents (20%), pedestrian impact (19%), and assault (11%). TBI has a bimodal age distribution with the greatest risk in 0–4 and 15- to 19-year-olds. Males have 1.5 times the risk of females. The younger group is often the victim of abuse and cannot protect itself. The older group practices greater risk-taking behavior, and includes the population of new drivers and

teenagers exposed to drugs and alcohol. Military personnel comprise a statistically small number of the overall TBI injuries per year, but have a higher incidence of penetrating and blast injuries resulting from combat operations.

PATHOPHYSIOLOGY TBI is a dynamic process and management must be tailored throughout the patient’s course. Primary injuries of the brain result from the forces imparted at the time of the accident. This includes disruption of scalp (lacerations), bone (cranial vault, skull base, facial bones), vasculature (SDH/EDH/IPH/intraventricular hemorrhage [IVH], traumatic aneurysm), or brain parenchyma (contusion, DAI). Secondary injuries occur after the initial impact and may be more insidious and more difficult to control. They are often due to failure of autoregulation and loss of normal homeostasis. These injuries include hypoxemia, ischemia, initial hyperemia, cerebral edema, and expansion of hemorrhages leading to increased intracranial pressure (ICP), seizures, metabolic abnormalities, and systemic insults.

GENERAL PRINCIPLES ■ Systemic Evaluation and Resuscitation Assessment and treatment of head-injured patients often begins in the prehospital setting with family, bystanders, and off-duty medical personnel. Care continues with the primary care physician or emergency medical technician (EMT), transfers to the physician in the emergency department, and eventually involves the trauma team, neurologist, neurosurgeon, and neurointensivist. Treatments may be started at any point along the patient’s journey based on recognition of neurological signs and availability of appropriate medication, equipment, and personnel.

Injury to the Brain

■ Neurological Examination An accurate neurological examination is essential to determine diagnosis, treatment strategies, and prognosis in TBI patients. The exam may be limited due to the patient’s age, level of education, native language, presence of sedative or paralytic medication, illicit drugs, hypotension, hypoxia, hypothermia, or hypoglycemia. Examination of the pediatric patient may include further limitations due to overall neural development and degrees of myelination, inability to visualize the pupils or fundi of the premature or newborn infant, and limited cooperation. It is critical to monitor the overall trend of the neurological examination over time. It must be understood that these examinations can and will fluctuate based on the patient’s improving or declining condition, the evolution of disease processes, and the ability of medical personnel to minimize or eliminate factors that confound an accurate neurological assessment. In the uncooperative patient or unconscious patient with severe TBI, the exam may be limited to the Glasgow Coma Scale (GCS), pupillary reactivity, and testing of various reflex actions (Table 19-1). As the patient becomes more alert and cooperative, a more complete neurological examination will provide greater sensitivity for assessment of neurological change. The extent of the examination must be tailored to each patient’s neurological ability.

■ Pupillary Response The parasympathetic, pupilloconstrictor, and light reflex (pupillary reflex) can be easily and rapidly assessed in the unconscious patient. Damage to the Edinger–Westphal nucleus or uncal compression of CN III at the tentorial notch will result in pupillary dilatation (4 mm). If severe enough (i.e., cerebral herniation), the pupil will be fixed in this dilated position and

TABLE 19-1 Neurological Examination for Trauma Level of consciousness Cranial nerve

Motor

Sensory

Reflex

Uncooperative Patient Glasgow Coma Scale

Pupil reactivity (ambient and bright light) Look for afferent papillary defect Facial asymmetry Movement to central and peripheral noxious stimuli (differentiate from flexion withdrawal spinal reflex) Resting tone of anal sphincter Grimace/grunt/withdrawal to noxious stimulus Deep tendon reflex Plantar reflex (Babinski), clonus Anal wink, bulbocavernosus reflex

Cooperative Patient Orientation Comprehension, verbalization Fluency of language Visual acuity/visual fields Funduscopic exam (papilledema, detached retina) Complete CN exam Strength assessment of all muscle groups in four extremities Tone of voluntary anal sphincter contraction Detailed exam to light touch and pinprick in major dermatomes (C4, C6, C7, C8, T4, T6, T10, L2, L4, L5, S1) Joint position sense (posterior column function)

CHAPTER CHAPTER 19 X

The nervous system does not exist in a vacuum and patients with TBI may have additional injuries. Treatments specific to TBI are often complementary or adjunctive to the treatment of the trauma patient without neurological injury. The basic principles of trauma resuscitation should be adhered to and include rapid assessment and maintenance of an airway, breathing, and circulation. A detailed medical and surgical history should be obtained including the events preceding a trauma, a description of the accident scene, accurate description of the patient’s neurological baseline, and any subsequent changes to the neurological status. Chronic medications and medications given in the prehospital setting should be determined. Special attention should be paid to medications with the ability to alter the neurological examination including sedatives or psychopharmacologics (to restrain the altered patient), paralytics (for intubation or transportation), atropine (for cardiac resuscitation), and other mydriatics (for evaluation of ocular trauma). Primary and secondary surveys should evaluate for systemic injuries including discrete injuries to the head and cervical spine. Open lacerations and vigorous scalp hemorrhage may lead to hypovolemia. In the newborn or premature infant, cephalohematoma may allow enough displacement of blood to produce hemodynamic instability. Raccoon’s eyes (periorbital ecchymosis), Battle’s sign (postauricular ecchymosis), and otorrhea/rhinorrhea suggest a basilar skull fracture. Palpable fractures or depressions may indicate bony injury with a higher likelihood of underlying hemorrhage or parenchymal injury. Periorbital edema or proptosis may suggest local ocular or orbital trauma. Puncture wounds may indicate a more serious, penetrating injury to the brain, spinal cord, sympathetic plexus, or vasculature. Bruits of the carotid artery or globe of the eye may represent carotid dissection or carotid-cavernous fistula, respectively. Multiple areas of swelling or bruising may indicate prior seizure activity.

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TABLE 19-2 Glasgow Coma Scale (Recommended for Age 4)

SECTION 3 X

6 5 4 3

2

1

Best Motor Obeys Localizes to pain Withdraws to pain Decorticate posturing (flexor) Decerebrate posturing (extensor) None

Best Verbal

Best Eye Opening

Oriented Confused (fluent speech) Inappropriate (words)

Spontaneously

Incomprehensible (sounds/ grunts) None

To pain

To speech

None

is unresponsive to a light stimulus. Direct orbital trauma can also result in pupillary dilation/fixation in the absence of temporal lobe herniation or intracranial hypertension (IC-HTN). It should be considered (quickly) before assuming that a dilated pupil is due to brainstem compression. In cases of orbital or periorbital trauma, facial fractures, or abnormal eye movement, ophthalmology may examine the patient and wish to instill mydriatics. To avoid confusion, this should only be permitted after concerns regarding elevated ICP have been addressed. Clear notation should be made, in the chart and at the bedside, as to when mydriatics have been used and for how long they will last.

■ Glasgow Coma Scale The GCS has become the standard for objective measurement of TBI severity.2 The patient is assessed in three parameters (best motor function [M], best verbalization [V], and best eye opening [E]) and the summation of these individual scores represents their overall GCS score (Table 19-2). A neurologically intact patient can achieve a maximum of 15 points and the most severely injured patient achieves a total of 3 points. If the patient is intubated, he or she receives a score of 1 for the verbal component and the overall scored is annotated with a

“T.” For example, an intubated patient with eye opening to pain and extremity withdrawal to pain would have a GCS score of M4/VT/E2  4 1 2  7T. The same GCS score can be derived from different values of the motor, verbal, and eye components. Therefore, it is beneficial for practitioners to denote each of the subscores and not just the overall number. The GCS allows practitioners to communicate quickly and reliably regarding a patient’s general condition. The postresuscitation GCS is also effective in stratifying patients into groups for definition of injury severity and overall prognosis. Patients with GCS  13–15 are defined as having mild TBI, are usually awake, and have no focal deficits. Patients with GCS  9–12 have moderate TBI and usually have altered sensorium and may have focal deficits. GCS  3–8 have severe TBI, and usually will not follow commands and meet the generally accepted definition of patients in a comatose state. As with all neurological assessments, confounding factors must be investigated and eliminated. Paralytics are used for patient transport, restraint, or cardiopulmonary stabilization and will limit the motor exam. Similarly, unrecognized spinal cord injury can produce a lower motor component score of the GCS and should be sought if suggested by the mechanism of injury. Hearing deficits, lack of hearing aids, or impairment of language function may limit the verbal component score. Finally, the pediatric population represents a special subset where modifications to the verbal component score better reflect the limited language skills of the young child3 (Table 19-3).

RADIOGRAPHIC EVALUATION FOR TRAUMA ■ Plain X-Rays Plain x-rays are most useful in the trauma setting for evaluating and clearing the cervical spine. The spine is imaged from the occiput to T1 and a C-collar is maintained until instability has been ruled out. In the C-spine AP, lateral and odontoid views are the most useful; T- and L-spine films are obtained based on mechanism of injury, degree of neurological deficits, and pain. Additionally, if CT or MRI scans are unavailable, plain x-rays can be used to determine pneumocephalus, skull fractures, and the tract of penetrating objects. It must be remembered that intracranial ricochets of projectiles may occur, and CT is the imaging modality of choice.

TABLE 19-3 Glasgow Coma Scale for Children (Recommended for Age 4) 6 5

4 3 2 1

Best Motor Obeys Localizes to pain

Withdraws to pain Decorticate posturing (flexor) Decerebrate posturing (extensor) None

Best Verbal

Best Eye Opening

Smiles, oriented to sound, follows objects, interacts Crying

Interaction

Consolable Inconsistently consolable Inconsolable None

Inappropriate Moaning Restless

Spontaneously To speech To pain None

Injury to the Brain

359

■ CT Scan CHAPTER CHAPTER 19 X

Overwhelmingly, the CT scan has become the initial study of patients presenting after head trauma, or with a new neurological deficit. In a single, rapid pass, without patient repositioning, scans of the head, neck, chest, abdomen, and pelvis can be performed. From these, cervical, thoracic, and lumbar spine images can be reconstructed without additional radiation. Administration of contrast allows for CT angiogram reconstruction to evaluate vasculature of the head and neck and be used for diagnosis and operative planning. CT scan findings after trauma include SDH, EDH, SAH, IPH, and IVH, contusions, hydrocephalus, cerebral edema or anoxia, skull fractures, ischemic infarction (if 12 hours old), mass effect, or midline shift. Indications for an initial post-traumatic CT scan include GCS 14, unresponsiveness, focal deficit, amnesia for the injury, altered mental status, and signs of basilar skull fracture.

■ MRI MRI scans have better parenchymal resolution and can evaluate infarction, ischemia, edema, and DAI. MRI is also helpful to determine ligamentous injury of the spine or traumatic cord injury. It is generally performed after the initial trauma evaluation and resuscitation have been completed. MRIs have limited availability, slower image acquisition time, and increased cost. Their use in the initial assessment of trauma is not routinely recommended since intracranial surgical lesions seen on MRI are also identified on CT scan.4

■ Angiography In penetrating trauma when the tract of injury is near a known vessel distribution or when a delayed intracerebral hemorrhage occurs, angiograms are used to look for direct vessel injury or pseudoaneurysms. When CT or MRI scans are unavailable, angiograms may be used to look for mild vessel shift indicative of compressive mass lesions (e.g., SDH, EDH, IPH). More significant vessel shift may be indicative of transtentorial or subfalcine herniation and suggest the need for more rapid treatment.

CLASSIFICATION AND SURGICAL MANAGEMENT OF SPECIFIC INJURIES ■ Skull Fractures Skull fractures can be described by the state of the overlying scalp (closed or open), the number of bone fragments (simple or compound), the relationship of bone fragments to each other (depressed or nondepressed), whether the fracture enters or widens an existing cranial suture (diastatic, more common in children), and whether it involves the cranial vault or skull base. In general, lower force impacts (falls from standing) will create fractures that are more linear, closed, and without dural laceration. Higher force impacts (MVA, falls from heights, penetrating trauma) will produce compound, open fractures with a greater likelihood of underlying dural or cerebral injury.

FIGURE 19-1 CT bone windows showing ping-pong skull fracture. The multiple nondisplaced linear lucencies are normal sutures.

“Ping-pong” fractures are greenstick-type fractures usually seen in newborns due to the plasticity of the skull (Fig. 19-1). They show a local concavity of the skull, without sharp edges, and usually do not require intervention as the skull remodels during growth and smooths out the cosmetic deformity.5 Associated clinical signs suggestive of calvarial skull fractures include gross deformity and palpable skull fracture in patients with open scalp lacerations. Basilar skull fractures may show postauricular or periorbital ecchymosis, hemotympanum or laceration of the external auditory canal, and CSF rhinorrhea or otorrhea. Cranial nerve injuries may be seen with fractures of the cribriform plate (CN I, anosmia), optic canal (CN II, visual deficit), and temporal bone (CN VII, facial weakness; or CN VIII, hearing loss). Severe basilar skull fractures may result in pituitary gland injury and resultant endocrinopathies. Direct injury to vasculature that penetrates the skull base may result in arterial dissection, traumatic aneurysm formation, or traumatic carotid-cavernous sinus fistula with symptoms of cranial neuropathies, chemosis, bruits, and strokes. Fractures of air sinuses or mastoid air cells may rarely present with meningitis, even years after the initial event.

Radiographic Diagnosis Skull fractures can be discovered on isolated plain x-rays or as part of a skeletal survey for abuse. They can be differentiated from vascular grooves or normal cranial sutures by characteristics listed in Table 19-4.6 Most skull fractures are discovered by CT scan due to its overwhelming use in the initial evaluation of trauma patients. Plain films may be superior to CT scan in discovering linear calvarial fractures parallel to the skull base (in the plane of CT

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Management of Specific Injuries

TABLE 19-4 Differential Diagnosis of Fractures on Skull X-Rays

SECTION 3 X

Density Course Branches Width

Linear Skull Fracture Black Straight Usually none Very thin

Vascular Groove Gray Curving Often branching Thicker than fracture

Suture Line Gray Follows known suture course Joins other suture lines Jagged, wide

slice acquisition). CT scans provide better visualization of facial and orbital fractures, temporal bone fractures, and pneumocephalus, and better evaluation of air sinuses and mastoid air cells containing air fluid levels and varying degrees of opacification. Thin cut bone windows can be reconstructed in coronal or sagittal planes or 3D surface modeling to aid in fracture identification and surgical planning. CT angiograms/venograms are useful for assessing fractures involving skull base foramen containing vasculature (e.g., carotid canal, foramen magnum) or fractures that cross major venous sinuses (superior sagittal or transverse sinuses, jugular foramen). All fractures must be assessed and treated in concert with the underlying brain. The following discussion of skull fracture treatment assumes that the underlying brain has been evaluated for subdural or epidural hematomas, parenchymal hemorrhages, or contusions and cerebral edema and that clinical criteria do not separately mandate operative decompression. Closed, nondisplaced fractures do not require immediate intervention. Open skull fractures should be debrided and carefully inspected and all should receive antibiotics. Those with obvious underlying dural laceration, CSF leakage, or visible brain should be surgically repaired in layers to reduce the risks of meningitis or brain herniation through a dural defect. In the pediatric population laceration of the underlying dura can rarely lead to a growing skull fracture (leptomeningeal cyst) seen in 0.05–0.6% of skull fractures.7 Pulsations of the underlying rapidly growing brain widen the dural laceration and fracture line over time (Fig. 19-2). These are most common in children under 1 year and over 90% occur in children under 3 years old.8 Surgical repair includes wide bony exposure to repair the dural edges that retract beyond the limits of the visible fracture. Relative indications for surgical elevation of a depressed skull fracture include depression of more than 8–10 mm or more than the thickness of the skull (Fig. 19-3), a focal neurological deficit clearly attributable to compressed underlying brain, significant intraparenchymal bone fragments (implying dural laceration), and persistent cosmetic deformity after all swelling has subsided. There is no evidence that post-traumatic seizure (PTS) risk is improved by elevation of a simple, depressed skull fracture.9 For children, the growing brain

FIGURE 19-2 CT revealing growing skull fracture from leptomeningeal cyst in child. Note displaced bone and expansion of CSF-filled soft tissue.

induces remodeling of the overlying skull. If there is no dural violation, there is no difference in seizure risk, neurological outcome, or cosmesis afforded by elevation of a simple depressed skull fracture.10 Fractures that cross a major dural venous sinus may warrant a more conservative approach given

FIGURE 19-3 CT bone windows showing a depressed skull fracture that required surgical elevation and dural repair. The patient also had an underlying brain contusion and presented with a receptive aphasia.

Injury to the Brain

■ Focal Cerebral Injuries Trauma patients, and their injuries, are hardly uniform. During a single traumatic event, patients may be subjected to forces of different magnitude, direction, and duration. The following injuries are presented as separate discussions for the sake of clarity. It must be remembered that more than one injury type may, and often does, occur in the same patient.

Cerebral Contusion Cerebral contusions are injuries to the superficial gray matter of the brain caused by a focal force. External forces striking the head cause acceleration of the intact skull or fractured skull fragments toward the brain surface. Conversely, during a motor vehicle accident, the brain continues to move toward the rapidly decelerating skull and dural folds of the falx or tentorium. “Coup” lesions are ipsilateral to the impact site and can be associated with adjacent calvarial fractures. “Contrecoup” lesions are opposite the coup lesion and result from gyral crests of the rebounding brain striking the inner table of the skull. Fifty percent of contusions involve the temporal lobes with the temporal pole striking the sphenoid wing. Thirty-three percent involve the frontal lobes with impact of the frontal pole or abrasions of the inferior frontal lobes on the rough floor of the anterior cranial fossa. Twenty-five percent are parasagittal, “gliding” contusions caused by abrasions of the cerebral hemispheres along the fixed falx or tentorium cerebelli. Less likely locations include parietal and occipital lobes, cerebellar vermis, brainstem, and cerebellar tonsils. Ninety percent of cases show multiple or bilateral contusions.12 On CT scans, contusions are patchy, hyperdense lesions with a hypodense background. They are best appreciated on MRI where FLAIR imaging shows the hyperintense edematous background and associated SAH and gradient echo (GRE) series show “blooming” of hemorrhagic foci. Contusions may coalesce or enlarge within the first 12 hours and the associated edema will often worsen over the first several days. Vigilant monitoring of the patient with a contusion is essential, and repeat CT scanning is frequently required.

Intraparenchymal Hemorrhage IPH or traumatic intracerebral hemorrhage (TICH) is seen in up to 8.2% of all TBI and up to 35% of severe TBI cases. Similar to contusions, TICH and associated edema may

increase over time and produce increasing mass effect and neurological deterioration. Delayed traumatic intracerebral hemorrhage (DTICH) will appear in approximately 20% of cases and most occur within 72 hours of the initial trauma.13 If patients develop neurological decline referable to the TICH lesion such as IC-HTN refractory to medical treatment or increasing mass effect with impending herniation, surgical decompression is warranted. Investigation of patient subtypes has shown that surgical decompression is often necessary in patients with TICH 50 cm3, or patients with GCS  6–8 who have frontal or temporal contusions 20 cm3 with midline shift 5 mm and/or cisternal compression on CT scan.11 Surgical procedures range from localized frontal or temporal craniotomy with resection of underlying focal clot to more extensive craniectomies with duraplasty, evacuation of severely contused brain, or temporal lobectomy.

Epidural Hemorrhage EDH occurs when blood collects in the potential space between the dura and inner table of the skull. It is seen in 1% of all head trauma admissions and in 5–15% of patients with fatal head injuries. It is more common in males (M:F  4:1), usually occurs in young adults, and is rarely seen in ages 2 or 60 since the dura is more adherent to the inner table of the skull in these groups. Ninety percent of EDHs are due to arterial bleeding that is often due to a fracture at the middle meningeal artery groove, and 10% are due to venous bleeding, usually associated with violation of a venous sinus by an occipital, parietal, or sphenoid wing fracture. EDHs are usually located at the site of impact over the lateral convexity of a cerebral hemisphere (70%), frontal (5–10%), parieto-occipital (5–10%), or posterior fossa locations (5–10%). On CT scan, EDHs usually appear as a hyperdense, biconvex (lenticular) mass adjacent to the inner table of the skull (Fig. 19-4). This classic description occurs 84% of the time with the medial edge being straight 11% of the time and crescentic (resembling an SDH) 5% of the time.14 Unless there is sutural diastasis, the EDH is externally bounded by cranial sutures, and may cross the falx or tentorium. Additional associated findings include SDHs and cerebral contusions. Of those managed nonsurgically, 23% showed an increase in size, usually in the first 36 hours, with a mean enlargement of 7 mm. Up to 10% of EDHs are not seen on the initial CT scan and present in delayed fashion.15 The classic clinical presentation of an EDH is a brief posttraumatic loss of consciousness (LOC) followed by a lucid interval, of varying duration, proceeding to obtundation, contralateral hemiparesis, and ipsilateral pupillary dilatation. Interestingly, this only occurs in 27–50% of cases.16 LOC is seen in only 40% of cases, a lucid interval is seen in 80% of cases, a dilated pupil is seen in 60% of cases, and only 85% of these dilated pupils are ipsilateral. Kernohan’s phenomenon (a false localizing sign) occurs when some cases of EDH produce local hemispheric mass effect with compression of the contralateral brainstem against the tentorial notch and ipsilateral hemiparesis.

CHAPTER CHAPTER 19 X

the increased risk of bleeding and air embolus that may be incurred during surgical repair. Current recommendations support surgical repair of open fractures depressed greater than the thickness of the cranium and nonoperative management of open depressed cranial fractures if there is no evidence of dural penetration. Surgery is also supported in cases of significant intracranial hematoma, depression 1 cm, frontal sinus involvement, gross cosmetic deformity, wound infection, pneumocephalus, or gross wound contamination. If there is no gross wound contamination, primary bone fragments may be replaced without excessive infection risk.11

361

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Management of Specific Injuries examinations, CT scans, and a low threshold for surgical intervention.

SECTION 3 X

Subdural Hemorrhage

FIGURE 19-4 CT showing epidural hemorrhage. Note the biconvex- or lenticular-shaped hemorrhage. On the bone windows this was adjacent to a diastatic left lambdoid suture.

Overall mortality is 5–12%17 with a unilateral EDH but is increased in cases of bilateral EDH (15–20% mortality), no lucid interval (20% mortality), posterior fossa location (25% mortality), and concurrent acute SDH (25–90% mortality, seen at autopsy in 20% of patients with EDH). Rapid diagnosis and intervention when indicated is paramount to optimize the outcome. Surgical guidelines suggest that EDH of 30 cm3 should be evacuated regardless of GCS score. EDH of 30 cm3 and 15 mm of thickness and 5 mm midline shift may be treated conservatively at a neurosurgical center with frequent neurological examinations and serial CT scanning.11 Relative indications exist for resection of EDHs that are neurologically symptomatic or have a maximal thickness 1 cm. Patients with acute EDH in coma (GCS 8) and anisocoria should undergo surgical evacuation as soon as possible.11 Most surgeons favor craniotomy for complete clot evacuation with meticulous hemostasis and use of tack-up sutures to decrease the potential epidural space. Posterior fossa injury is rare, comprising 3% of head injuries; however, the majority of these lesions are EDHs. The limited space of the posterior fossa and the potential compromise of the brainstem and CSF pathways underscore the importance of rapid evacuation via suboccipital craniectomy.11 Patients without signs of mass effect or neurological deterioration may be watched conservatively with serial neurological

SDH occurs when blood collects between the arachnoid and inner dural layer and is usually divided into hyperacute (6 hours), acute (6 hours to 3 days), subacute (3 days to 3 weeks), and chronic (3 weeks to 3 months) variants. It is usually due to traumatic stretching and tearing of cortical bridging veins that cross the subdural space and drain into a dural sinus. The force may be direct (impact) or indirect (nonimpact) and may involve linear or rotational motion. Less common etiologies include coagulopathy, subdural dissection of IPH, and rupture of a vascular anomaly (AVM, aneurysm, cavernoma, dural AV fistula) into the subdural space. Patients with cerebral atrophy, cranial CSF shunts, and large arachnoid cysts (usually in the middle fossa) are predisposed to SDH given the increased traction on cortical veins. Following craniocerebral trauma, SDHs are found in 10–20% of all imaged patients and 30% of autopsies. Over 70% of patients with acute SDHs have other significant associated lesions. SDHs are commonly located over the hemispheric convexities and may cover part or all of a hemisphere (holoconvexity SDH). Classically, they are crescent shaped, cross suture lines, and layer along the falx or tentorium (Fig. 19-5). Patients present with symptoms of mass effect or more diffuse brain injury. Chronic SDH may present with headaches and/ or focal deficits.

FIGURE 19-5 CT showing an acute subdural hemorrhage. Note that crescentic hemorrhage crosses under the right coronal suture.

Injury to the Brain

TABLE 19-5 Appearance of SDH on CT and MRI

Early subacute (4–7 days) Late subacute (1–3 weeks) Chronic (3 weeks to 3 months)

MRI T2 ↑ ↓

↑

↓

—

↑

↑

↓

↓

↓

↑/—/↓, hyperdense/isodense/hypodense to brain (CT) or hyperintense/isointense/hypointense (MRI).

The appearance of SDHs changes with time. On CT, acute SDHs are hyperdense (60%, homogenous) or of mixed density (40%, may show “swirl sign” of active bleeding), subacute SDHs are isodense with brain, and chronic SDHs become hypodense. Some SDHs may be isodense acutely if there is coagulopathy, significant anemia, or an admixture of blood and CSF. There is inward displacement of the gray/ white cortical ribbon and cortical vessels on contrast-enhanced CT. Subdural membranes may appear starting at 4 days and enhance with contrast administration.18 MRI shows varying intensities based on the age of the SDH that is, in turn, based on degradation of blood products from oxyhemoglobin to deoxyhemoglobin to methemoglobin to hemosiderin (Table 19-5). SDHs often have worse outcomes when compared to EDHs of similar size/shape. EDHs require force directed toward the skull and epidural vessels (i.e., middle meningeal artery), are usually of arterial origin, and present with symptoms quickly allowing for rapid diagnosis and treatment. It is postulated that SDHs have greater force and impart greater damage to the underlying brain and cortical vessels, have slower onset from venous sources, and have symptoms due to primary brain injury in addition to the midline shift and brainstem compression. Guidelines suggest that an acute SDH with thickness 1 cm or a midline shift 5 mm should be evacuated regardless of GCS score. Patients with acute SDH 1 cm thick and midline shift 5 mm and in coma (GCS 8) should undergo SDH evacuation if the GCS decreases by 2 points between the time of injury and hospital admission, if they present with pupils that are asymmetric or fixed/dilated, or if the ICP 20 mm Hg.11 A craniotomy to evacuate an acute clot should be performed as soon as possible, and may require craniectomy and duraplasty for ICP control. A larger craniotomy flap is needed for acute clot that has a texture of thick jam. As the clot breaks down, passing through subacute to chronic stages, it liquefies and may require smaller craniotomies or even burr hole access for appropriate drainage.

Subarachnoid Hemorrhage SAH is blood located between the pial and arachnoid membranes. Traumatic subarachnoid hemorrhage (tSAH) results from venous tears in the subarachnoid space. tSAH is seen in 33% of patients with moderate head injury and is found in nearly 100% of trauma patients at autopsy. It can be seen as a sulcal hyperdensity on CT scan (Fig. 19-6) and as a FLAIR hyperintensity on MRI. It may be confused with FLAIR hyperintensities from 100% FiO2, inflammation, or propofol use. It is often seen embedded in convexity sulci or adjacent to contusions, SDH, or fractures. It may mimic aneurysmal SAH, present in the interpeduncular or other basal cisterns or layers on the tentorium. Patients may complain of headache, emesis, and lethargy and treatment is largely supportive using IV fluids, anticonvulsants, and nimodipine, a Ca2 channel blocker, to prevent vasospasm. Vasospasm involves narrowing or closure of a vessel with subsequent ischemia or infarct in the vascular territory it supplies. It occurs in 2–41% of trauma cases with tSAH, may occur as early as 2–3 days post-trauma, has heightened incidence from days 3 to 14, and may last up to 2–3 weeks after injury.

FIGURE 19-6 CT with arrow pointing to a small traumatic subarachnoid hemorrhage in left central sulcus.

CHAPTER CHAPTER 19 X

Hyperacute (6 h) Acute (6 h to 3 days)

MRI T1 — —

CT Density ↓ ↑/swirl/iso if coagulopathy —

Mortality ranges from 50% to 90% and may be related more to the underlying injury rather than the SDH itself. It is increased in the elderly and in patients on anticoagulants.19 Outcome is improved in patients operated on in less 4 four hours with mortality improvements from 66–90% down to 30–59%.20,21

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■ Diffuse Cerebral Injuries Concussion

SECTION 3 X

A concussion, or mild traumatic brain injury (MTBI), is defined as an alteration of consciousness resulting from nonpenetrating injury to the brain. Classic symptoms of concussion include headache, confusion, amnesia, and sometimes LOC. Additional symptoms include deficits of motor function (incoordination, stumbling), speech (slowed, slurred, incoherent), memory or processing (amnesia, short-term memory loss, difficulty concentrating or focusing, inattention, perseveration, easy distractibility), and orientation (vacant stare, “glassy eyed,” unable to orient to time/date), and presence of irritability. When present, LOC is usually brief. The two most common grading systems for concussion are from Cantu22 and the American Academy of Neurology (AAN)23 and are shown in (Table 19-6).6 Physiological responses to concussion include a transient increase in cerebral blood volume due to loss of vascular autoregulation. In mild cases, this may result in mild cerebral swelling, or hyperemia. In more severe cases, malignant cerebral edema24 may occur with elevated ICPs refractory to nearly all measures and 50–100% mortality. This is the presumed cause of “second impact syndrome”25,26 seen in child and teenage athletes who suffer a second concussion before fully recovering from their first one. Classically, the athlete walks off the field, suffers LOC in 1–5 minutes, and develops vascular engorgement with further neurological deterioration, cerebral herniation, and death. CT findings may be subtle or nonexistent and include mild diffuse swelling secondary to hyperemia. Being more sensitive, MRI may show positive findings in up to 25% of cases where CT scans are normal.27 Pathologic specimens show no gross or microscopic parenchymal abnormalities in patients who have suffered a single concussion. TABLE 19-6 Concussion Grading Grade 1 (mild)

Cantu System 1. PTA 30 min 2. No LOC

AAN System 1. Transient confusion 2. No LOC 3. Symptoms resolve in 15 min

2 (moderate)

1. LOC 5 min, or 2. PTA 30 min

1. Transient confusion 2. No LOC 3. Symptoms last 15 min (PTA common)

3 (severe)

1. LOC 5 min, or 2. PTA 24 h

Any LOC (brief or prolonged)

Reproduced with permission from Greenberg MS. Handbook of Neurosurgery. 7th ed. New York, NY: Thieme Medical Publishers; 2010:851. Copyright © Greenberg Graphics.

Most important for the treatment of concussion is the recognition of injury. Many concussions occur during athletic endeavors and more subtle signs of concussion might not prompt the layperson to seek medical attention. It is the responsibility of the athlete, coach, team doctor, teacher, EMT, or other medical professional to understand the nature of concussions, prompt the patient to seek medical attention, and initiate restriction of further head-injury-prone activities until the patient has fully recovered. All experts agree that a symptomatic player should not return to play. According to one publication contraindications for return to contact sports28 include persistent postconcussive symptoms, permanent neurological symptoms, hydrocephalus, spontaneous SAH, and symptomatic abnormalities at the foramen magnum (e.g., Chiari malformation). If none of the above contraindications apply, then various suggestions exist regarding the timing of return to play after evaluation by a medical professional. AAN management options for a single sports-related concussion23 are listed in (Table 19-7)6 and recommendations for multiple sports-related concussions in the same season29 are listed in (Table 19-8).6

Diffuse Axonal Injury DAI is a traumatic axonal stretch injury caused by overlying cerebral cortex and underlying deep brain structures moving at different relative speeds. Mild cases result in axonal stretching and transient neuronal dysfunction while more severe cases cause axonal shearing and permanent neuronal damage. DAI does not require head impact and may be caused by rapid acceleration or deceleration in a linear or rotational fashion.30 Eighty percent of DAI are microscopic and nonhemorrhagic with impaired axonal transport and delayed axonal swelling. When hemorrhagic DAI, the most severe form, is visible on CT/MRI, it must be assumed that it is the tip of the iceberg and that more widespread DAI exists. It should be readily investigated in cases where the degree of neurological injury exceeds what initial imaging would suggest. DAI represents 50% of all primary intra-axial TBI lesions and is found in 80–100% of autopsy patients in fatal injuries. CT scans may be normal (50–80%) or may show hyperdense petechial hemorrhage (20–50%). MRI scans show multifocal hyperintense T2 signal at gray matter/white matter interfaces, especially in frontal lobes (67%), the corpus callosum (20%), and brainstem (10%). Injury severity parallels the amount of force required to create DAI lesions and prognosis worsens with increasing number of lesions or as lesion depth progresses from the cortex to corpus callosum to brainstem. Prognosis is variable but generally related to the patient’s age, presenting neurological status, and trajectory of neurological improvement.

Penetrating Nonmissile Injury Penetrating injuries to the brain and spinal cord may be caused by lower-velocity objects (knives, arrows, lawn darts, ice pick) and by higher-velocity missile-type projectiles. If the object is still embedded, and protruding, great care should be taken to stabilize the object during transport and evaluation. External

Injury to the Brain

365

TABLE 19-7 Recommendations for a Single Sports-Related Concussion Management Options 1. Remove from contest 2. Examine q 5 min for amnesia or postconcussive symptomsa 3. May return to contest if symptoms clear within 15 min

2 (moderate)

1. 2. 3. 4. 5. 6.

3 (severe)

1. Ambulance transport from field to E/R if still unconscious or for concerning signs (C-spine precautions if indicated) 2. Emergent neurological exam. Neuroimaging as appropriate 3. May go home with head injury instructions if normal findings at time of initial neurological exam 4. Admit to hospital for any signs of pathology or for continued abnormal mental status 5. Assess neurological status daily until all symptoms have stabilized or resolved 6. Prolonged unconsciousness, persistent mental status alterations, worsening postconcussion symptoms, or abnormalities on neurological exam → urgent neurosurgical evaluation or transfer to a trauma center 7. After brief (1 min) grade 3 concussion, do not return to practice until asymptomatic for 1 full weeka 8. After prolonged (1 min) grade 3 concussion, return to practice only after 2 full weeks without symptomsa,c 9. CT or MRI if H/A or other symptoms worsen or last 1 weekb

Remove from contest Disallow return that day Examine on-site frequently for signs of evolving intracranial pathology Reexamination the next day by a trained individual CT or MRI if H/A or other symptoms worsen or last 1 weekb Return to practice after 1 full week without symptomsa

a

Evaluation at rest and with exertion. Season is terminated for that player if CT/MRI shows edema, contusion, or other acute intracranial pathology. Return to play in any contact sports in the future should be seriously discouraged. b

c

Some experts require a normal CT scan. Reproduced with permission from Greenberg MS. Handbook of Neurosurgery. 7th ed. New York, NY: Thieme Medical Publishers; 2010:851. Copyright © Greenberg Graphics.

TABLE 19-8 Recommendations for Multiple Sports-Related Concussions in the Same Season No. 2

Concussion Severity Mild

3

Moderate/ severe Mild

2

Moderate Severe

Guidelines to be Met Before Return to Competition 1 week without symptoms at rest or on exertion 1 month without symptoms (as above) normal CT/MRI Season-ending injury, evaluate with CT/MRI Season-ending injury, consider ending all participation in contact sports

Reproduced with permission from Greenberg MS. Handbook of Neurosurgery. 7th ed. New York, NY: Thieme Medical Publishers; 2010:851. Copyright © Greenberg Graphics.

examinations should describe entry and exit wounds if present. Scalp shaving may be required as well as control of vigorous scalp hemorrhage. CT should be performed to localize the precise location of the foreign body or injury. Catheter angiography should be performed if the foreign body passes through the territory of any major vessels. All radiographic evaluation, planning, and operative setup should be performed with the foreign body still embedded and removal should only proceed in the OR (Fig. 19-7). To help plan the removal, a similar or identical object may be useful to have as a reference. Broad-spectrum antibiotics should be administered and cultures may be taken at the time of surgery.

Penetrating Missile Injury Gunshot wounds to the head (GSWH) represent the majority of penetrating cranial injuries and account for 35% of brain injury deaths in patients 45 years old. In civilian GSWH, approximately 66% of people die at the accident scene and the GSWH is the cause of death in 90% of victims.31

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AAN Grade 1 (mild)

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SECTION 3 X FIGURE 19-7 Intraoperative picture of a penetrating nail-gun injury into the brain. The bone flap has been removed and the dura is open showing the nail entering the brain parenchyma.

Traditionally, GSW have been divided into those from high muzzle velocity rounds (approximately 750–1,000 m/s, hunting rifles, military weapons) and those from low muzzle velocity rounds (approximately 200–500 m/s, most handguns). With escalating civilian firepower, however, these distinctions are becoming more blurred. The above velocities are taken as the projectile leaves the barrel of the weapon. As the bullet covers aerial distance, ricochets off objects, or passes through objects, it loses velocity and kinetic energy. Primary injuries from gunshot wounds include direct injuries to face and scalp, pressure waves of gas combustion from the weapon (if touching or fired at close range), coup/ contrecoup contusion injuries from missile impact, and destruction of brain or bone along the primary path of the original bullet or paths created by fragments of bullets and bone. Highvelocity projectiles also create secondary cavitation that pushes tissue away from the bullet in a cone of injury many times wider than the projectile itself. The vacuum that follows the cavitation may pull surface debris into the wound and may serve as a nidus for infection. Some specially designed bullets mushroom, fragment, or tumble in order to increase the width of the destructive path. Projectiles can also careen around or ricochet off the inner table of the skull. Secondary injuries from GSWs mimic those seen in other types of head trauma and include edema, enlarging contusions, DAI, loss of autoregulation, DIC and hemorrhage from vessel disruption, ischemia, infarction, and herniation. Late complications include abscess or traumatic aneurysm formation, seizures, and migration of embedded fragments of bone or debris. Surgery must be quickly, and carefully, contemplated in patients with GSWs to the head since many of these patients

have devastating and irrecoverable injuries that will not benefit from surgery. The most critical information to accurately triage a GSW patient is the postresuscitative GCS and the CT findings. Patients with GCS 3–5 without a large intracerebral hemorrhage to explain the exam generally have a poor outcome, and consideration for limited treatment is reasonable. Suicide, bilateral fixed and dilated pupils, and coagulopathy are poor prognostic factors. Poor prognosis and high mortality is also associated when bullets cross midline, pass through the geographic center of the brain, traverse the ventricles, or pass through more than one cerebral lobe. One study showed a 94% mortality among patients with GSWH who had GCS 8 and flaccid or decorticate/decerebrate posturing, and half of the survivors were severely disabled.32 When surgery is performed for GSWs, all attempts should be made to evacuate hematomas causing mass effect (SDH/ EDH/IPH), obtain meticulous hemostasis and reduce infection through debridement of devitalized tissue and foreign debris, and obtain a watertight closure to prevent CSF leaks. A “chain of evidence” (for forensics) should be maintained when bullet fragments are removed. When the trajectory is near a known vascular territory, an angiogram should be performed.

Blast Traumatic Brain Injury Although it may be seen in the civilian population, the military combatant is especially at risk for explosive blast traumatic brain injury (bTBI). Head injury accounts for approximately 20% of all combat-related injuries in recent modern wars33,34 including Operation Enduring Freedom in Afghanistan and Operation Iraqi Freedom. In these two conflicts, explosive bTBI frequently results from the use of improvised explosive devices (IEDs). Modern helmets, body armor, rapid transport of injured personnel, and forward-based field hospitals have provided unprecedented rates of warfighter survival and have allowed for a better understanding of the effects of bTBI. bTBI may be composed of four distinct types of injuries that can occur separately, or in concert, to varying degrees. Primary blast injury occurs from overpressure. This has long been known to contribute to injuries in air-filled organs such as the lungs, GI tract, and middle ear. Possible contribution of overpressure to brain injury is currently the focus of much study. Secondary blast injury results from penetrating objects that are energized by the explosive. Tertiary blast injury results from the patient being thrown and striking the ground or other object. Quaternary blast injury results from additional factors not included above (e.g., thermal, toxic, hypoxia). Blast injuries in an enclosed space produce an enhanced and complex wave pattern as forces reflect off walls and various objects to impact the head at multiples angles and to multiple degrees. A blast-induced TBI often includes closed and penetrating TBI components, and many of these patients also have additional serious injuries such as traumatic limb amputations or hemorrhagic shock. The combination of these factors makes it difficult to assess the true contribution of primary or quaternary blast effects on patients with TBI after a blast-induced injury. In milder cases combatants may not recognize that they

Injury to the Brain

Extracranial Vascular Injury Post-traumatic intracranial strokes may result from injuries to the internal carotid artery (ICA), common carotid artery (CCA), or vertebral artery (VA) in the neck. Rarely, the injury is due to penetrating trauma with direct ICA, CCA, or VA injury. More often, vessel dissection is sustained in motor vehicle accidents, falls, neck rotation, spine fracture, or iatrogenic injury (surgery, chiropractic maneuvers). Traumatic dissection is more common in the ICA, occurs in 0.08–0.4% of blunt trauma patients, and runs from a few centimeters above the carotid bifurcation to the skull base. Less common is VA dissection that is usually at the C1–C2 level. Vessel dissection allows blood to collect between the adventitia and media (pseudoaneurysm formation) or between the intima and media of the vessel wall (luminal stenosis). This intramural hematoma may expand or may propagate with distal propagation being more common. Spontaneous dissections occur in younger to middle-aged adults with 70% between 35 and 50 years old. Seven percent occur in adolescents, and spontaneous dissection is rare in children. Sixty to 90% of patients present with headache and neck pain that is often unrelenting. Symptoms and diagnosis may occur hours to weeks after the initial trauma and include TIAs or strokes, Horner’s syndrome, and, less often, carotid bruits, pulsatile tinnitus, and lower cranial nerve palsies (CN 9–12). On CT, injuries are seen as a linear lucency within an enhancing vessel and represent the flap separating the true and false vessel lumens. MRI shows a crescentic band surrounding the native flow void and ultrasound shows an echogenic intimal flap. Twenty percent of cases have an associated injury such as cervical spine injury or silent dissection of another vessel. Treatment consists of heparin followed by Coumadin anticoagulation with balloon angioplasty in select cases.

Child Abuse/Nonaccidental Trauma Nonaccidental trauma (NAT) is traumatic injury deliberately inflicted on infants and children. The concept was first described as an injury triad in infants consisting of long bone metaphyseal fractures, SDHs, and retinal hemorrhages36 and has become known in common parlance as “whiplash shaken infant syndrome” or “shaken baby syndrome.”37 It is almost

certainly underreported and represents the primary etiology of brain injury death in children 2 years old. Some medical professionals find the cases difficult due to awkward discussions with the child’s parents, an emotional attachment to the child, frequent lack of accurate information, rare confessions from perpetrators, and the medicolegal implications of child abuse accusations. A heightened level of suspicion must be maintained since missed recognition of NAT returns the child to a harmful environment, almost always results in continuation or escalation of the abuse, and may result in the patient’s death. The two most common histories are no trauma and trivial blunt trauma such as a short-height fall from bed/low surface. Except for the rare EDH with middle meningeal arterial bleeding, low-height falls (household falls, head to impact distance 3 ft) do not result in life-threatening brain injuries.38,39 With no trauma history, the only indicators of NAT may be feeding difficulty, emesis, lethargy, irritability, abnormal movements, seizures, unresponsiveness, or apnea. Radiologically, NAT shows multiple brain injuries that are more severe than expected given the reported history. Impact injuries include skull fractures, superficial scalp lacerations or swelling, and injuries to the underlying brain and have a high association with other organ injuries. Historically, some fracture patterns have been incorrectly considered more suspicious for child abuse. Fractures that are multiple, compound, diastatic, midline, or nonparietal or that cross suture lines (multiple bones) may denote a greater degree of imparted force but are not pathognomonic for NAT. A shaking mechanism can result in injuries of differing ages and diffusely distributed SDH. The most frequent hemorrhagic finding is a combination of convexity and interhemispheric SDH (often posterior). Some experts believe interhemispheric SDH has highest specificity for abuse of any intracranial injury. SDH, SAH, and retinal hemorrhages are far more commonly seen in abused children than in nonabused children. EDHs can occur but are much more commonly accidental. Retinal hemorrhages are seen in 65–95% of children with inflicted head injuries and may be unilateral or bilateral. However, severe bilateral retinal hemorrhages are occasionally seen in accidental trauma and usually have a well-defined mechanism of action with major application of force (e.g., MVA). Given the right circumstances, practically any pattern of hemorrhage or fracture can result from either accidental or inflicted trauma. However, inflicted injury is the only known illness or condition with the combination of acute SDH, skeletal fractures, and severe bilateral retinal hemorrhages. Finally, the severity of injury is staggering with 15–38% overall mortality and 60% mortality if the patient is comatose on presentation. Survivors face a 60–70% likelihood of significant neurological handicap.

■ Medical Management of Traumatic Brain Injury There are multiple treatments for TBI that may be used in series or parallel. Although a dedicated discussion of prehospital care is beyond the scope of this chapter, some treatments can be

CHAPTER CHAPTER 19 X

suffer delayed effects of bTBI or knowingly hide their deficits to remain with their combat unit. Mild and moderate bTBI can cause concussion symptoms including headache, confusion, amnesia, and altered mental status. Postconcussive symptoms (difficulty concentrating, sleep disturbance, and mood alteration) also can be difficult to differentiate from post-traumatic stress disorder that may also be involved. Patients with more severe bTBI may have hyperemia and severe cerebral edema early in their course requiring decompressive craniectomy. Higher rates of traumatic pseudoaneurysm and vasospasm are also seen, versus similar civilian closed and penetrating TBI patients, and may require more frequent endovascular or open vascular repair.35

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started in the field and others may be added as more advanced equipment or qualified personnel are available in the emergency department, neuroscience floor, intensive care unit, or operating room. Basic measures should be implemented in all patients undergoing monitoring and management of TBI. They should be in an ICU setting with frequent monitoring of vital signs, fluid intake, and output and neurological examinations (as permitted). Appropriate monitoring may require multiple invasive lines for blood pressure (arterial line), volume assessment (Swan–Ganz), administration of fluids, medication, or nutrition (central venous catheter), urine output or temperature (Foley catheter), ICP, cerebral tissue oxygenation, or cerebral blood flow (CBF). Patients should be kept normothermic and euvolemic with isotonic fluids (i.e., NS 20 mEq KCl/L). They should have GI prophylaxis against Cushing’s (stress) ulcers that are frequently seen in severe head injury and cases of elevated ICP. The head of bed should be elevated to 30–45°, the neck should be kept midline, and the fit of the patient’s cervical collar and endotracheal tube stabilizer should be assessed to prevent compression of the jugular veins and promote venous outflow from the head. Most important is frequent assessment of the patient’s condition, determination of response to therapies implemented, and willingness to adjust care strategies in a fluid manner for optimal outcome. Over the past two decades, it has become clear that systematic treatment of TBI patients by dedicated neurologists, neurosurgeons, neurointensivists, and surgical trauma and critical care teams has resulted in marked improvement in patient survival and outcome.40 Central to this effort has been the creation, implementation, and refinement of Guidelines for the Management of Severe Traumatic Brain Injury41 with companion guidelines for prehospital management of TBI,42 pediatric TBI,43 surgical management of TBI,11 penetrating TBI,44 and field management of combat-related head trauma.45 These guidelines have undertaken a critical evaluation of the available literature and we readily refer the reader to these excellent works for further detail into the creation of current recommendations.

Blood Pressure and Oxygenation TBI results from primary injury at the time of impact followed by secondary injury in the minutes, hours, and days that follow. While the medical practitioner cannot “take back” the events of the primary injury, every effort must be made to mitigate or eliminate the secondary injuries that are often more severe. Prior to, or during, transport to a hospital setting, a significant portion of patients may experience periods of hypoxemia or hypotension.46 A single episode of hypoxemia (apnea, cyanosis or O2 saturation 90% in the field, or PaO2 60 mm Hg) or hypotension (SBP 90) is an independent predictor of worse outcome in TBI.47–50 Oxygen saturation and blood pressure monitoring should start in the field and continue in the hospital setting with the goal of identifying, avoiding, and rapidly correcting hypoxemia or hypotension, as described above. Empiric oxygen administration

should start as early as possible and endotracheal intubation may be required. Similarly, isotonic or hypotonic saline, plasma, colloid, blood, or intravenous pressors may be required to avoid hypotension.41

■ Intracranial Pressure Assessment To understand the rationale behind ICP management, one must start with understanding how pressure in the intracranial space differs from that in other body compartments. If a patient sustains an injury to his or her arm or leg, the surrounding soft tissue has a significant ability to expand outwards from the humerus or femur. By contrast, in cases of TBI, the brain is unable to expand because of the rigid skull. A useful concept is the modified Monro–Kellie hypothesis, first proposed by Monro51 and verified by Kellie.52 Assuming that the skull is completely inelastic, that the ventricular space is confluent, and that pressures are equally and readily transmitted throughout the intracranial space, the hypothesis states that there is a balance between the brain, blood volume, and CSF contained in the intracranial space. Increases in the volume of one constituent (e.g., cerebral edema, hyperemia) or addition of new components (e.g., tumor, hemorrhage) mandate compensatory decreases in other constituents to maintain the same ICP. Mildly increased, localized pressure in the brain causes neurological dysfunction of the immediate area. More severe pressure increases cause local tissue compression, shift of intracranial structures, subfalcine and transtentorial herniation, and both local and distant neurological dysfunctions. In the most severe cases, herniation causes compression at the level of the brainstem with direct tissue damage to the pons and medulla, occlusion of brainstem vasculature, infarction, and death.

ICP Monitoring Normal ICPs vary by age and are considered to be 10–15 mm Hg in adults and older children, 3–7 mm Hg in children, 1.5–6 mm Hg in infants, and may be subatmospheric in the neonates. IC-HTN is seen in 13% of trauma patients with a normal head CT, 60% of patients with an abnormal head CT (hemorrhage, contusion, edema, herniation, or compressed basal cisterns), and ∼60% of patients with a normal head CT plus two or more of the following select criteria on motor examination: age 40, SBP 90 mm Hg, and unilateral or bilateral abnormal posturing (decorticate or decerebrate).53 Therefore, ICP monitoring is recommended in patients with severe TBI (GCS  3–8) and an abnormal CT scan or with severe TBI, a normal CT scan, and two or more of the select criteria listed above. ICP monitoring may also be considered in patients without an accurate neurological examination due to sedatives, paralytics, or general anesthesia required for other reasons (e.g., difficult ventilator management, agitation, need for additional non-neurological surgery). Higher mortality and worse outcomes are seen in patients with ICP persistently above 20 mm Hg.54 Therefore, most centers consider IC-HTN to be defined as ICP  20 –25 mm Hg. ICP reduction measures are recommended when ICP thresholds exceed 20 mm Hg.41

Injury to the Brain

Cerebral Perfusion Pressure The post-traumatic brain is at risk for local ischemia in the region of defined traumatic lesions, as well as global ischemia from a more diffuse loss of cerebral autoregulation. Neurological dysfunction may come from direct tissue injury or may come from impaired function of structurally intact neural tissue. For neural tissue to function, it must have adequate CBF to meet the metabolic demand. CBF depends on cerebral perfusion pressure (CPP), which is MAP – ICP. Studies have shown that the injured adult brain is more susceptible to ischemia if the CPP trends below 50 mm Hg.55 Similar studies in children have shown improved survival in those patients who sustain CPP  40 mm Hg.56 Studies in the adult population have shown that keeping the CPP 70 results in unacceptably higher rates of adult respiratory distress syndrome (ARDS) without significantly improved outcome.57,58 There is likely an age-dependent continuum of optimal CPP measurements. Current recommendations support avoidance of CPP 40 in children, 50 in adults, and 70 in either population.41

Cerebral Blood Flow and Metabolism CT perfusion can provide measure of CBF at a single point in time. It measures the relative cerebral blood volume, CBF, and mean transit time after injection of iodinated contrast. It has been used extensively in stroke patients and has been investigated in TBI patients to determine the potential viability of contusional and pericontusional tissue, and to help guide other therapeutic strategies such as optimized hyperventilation (HPV). Intermittent measurements of the jugular venous oxygen saturation (SjvO2) in the bulb of the jugular vein can also be used to assess cerebral perfusion. Normal venous saturation of oxygen is approximately 50–69% and studies have shown that multiple episodes of venous desaturation (50%) or sustained and profound desaturations are associated with poor outcome.59 In addition, excessively high SjvO2 (75%) is associated with poor outcome and may indicate hyperemia or significant areas of infarction that will not extract oxygen. The arterial–jugular venous oxygen content difference (AJdO2) may also be calculated.

More focal measurements of CBF include transcranial Doppler (TCD) ultrasonography and parenchymal CBF probes. Thermal diffusion probes provide local CBF measurements based on the thermal temperature difference between microprobes and the relative conductive properties of cerebral tissue and convective properties of blood flow. Probes are often placed in penumbral tissue that is thought to be “at risk” but still salvageable. Cerebral microdialysis involves placement of a microprobe into penumbral tissue, and measurement of neurochemicals that diffuse into a dialysate through a semipermeable membrane. Neurochemical changes indicative of primary and secondary brain injury are seen in penumbral tissue and TBI patients with poor clinical outcome have been shown to have elevated levels of neurotransmitters, elevated lactate/pyruvate ratios, and abnormal lactate and glutamate levels.60 Brain tissue oxygen tension (PbtO2) monitoring allows direct measurement of focal tissue oxygen tension in a specific region of the brain. Probes are placed in a penumbral area of white matter and allow measurement of local oxygen content or delivery. Normal PbtO2 is approximately 32 mm Hg and studies have shown that patients with multiple or prolonged episodes of PbtO2 10–15 mm Hg have increased morbidity and mortality.61 Current recommendations suggest that SjvO2 and PbtO2 may be monitored as adjuncts to ICP and CPP and therapies should be targeted to keep SjvO2 50% and PbtO2 15 mm Hg.41

■ Intracranial Pressure Management A ventricular catheter, as mentioned previously, is an excellent method to measure ICP because it facilitates CSF drainage, which is a powerful tool to control ICP. Additional methods follow in this section.

Analgesics and Sedatives TBI patients, by definition, have suffered trauma and will have increased levels of stress, agitation, and, possibly, discomfort. Patients may suffer discomfort or anxiety from their initial traumatic injury, invasive monitoring, the ICU environment, and procedures. They may be disoriented and/or agitated due to neurological injury or prescribed medication. Pain and agitation can cause increased sympathetic tone, increased temperature, and hypertension. Left unopposed, they can lead to increased venous and ICP, increased metabolic demand, and resistance to controlled ventilation. Patients may require sedatives or psychotropic medication to prevent self-injurious behavior and dislodgement of airway, vascular lines, or monitoring equipment. Patients on ventilators may require sedatives or paralytics to allow appropriate lung excursion or timing of breath patterns. The medications used to treat pain and agitation, and the doses used, must be carefully monitored and administered so that a balance is achieved between their beneficial effect in reducing pain and anxiety and their side effects of hypotension, alteration or obliteration of the neurological examination, and rebound ICP elevation. Initially, haloperidol may be useful for agitation given its relatively nonsedating quality. If further sedatives or paralytics are

CHAPTER CHAPTER 19 X

The most accurate, low-cost, and reliable ICP technology is the fluid-coupled ventriculostomy catheter, or external ventriculostomy drain (EVD), connected to an external strain gauge.41 Another advantage to ventriculostomy placement is that CSF drainage can be performed as a therapeutic measure to control ICP. Other ventricular catheters using fiber-optic or microstrain gauge transduction are more costly and roughly as accurate. Parenchymal ICP monitors require less tissue penetration and do not require the ability to localize the ventricle. However, they cannot be recalibrated in situ and may be subject to measurement drift. Parenchymal monitors are diagnostic (able to measure ICP) while ventricular catheters have the added benefit of being therapeutic (able to drain CSF). Subarachnoid, subdural, and epidural monitors tend to be less accurate.

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needed and a neurological examination becomes unobtainable, an ICP monitor should be placed. Short-acting agents are preferred in order to facilitate frequent, intermittent neurological examination. Continuous infusion administration may be preferable to bolus administering as this avoids the potential for transient ICP increases seen with some analgesics. Increasingly, fentanyl and its related derivatives (remifentanil, sufentanil) are becoming the agents of choice for acute and longer-term analgesia. They are short acting, reversible, and conducive to administration by continuous infusion. Midazolam and propofol are two commonly used agents for sedation. Midazolam is a short-acting benzodiazepine that is also effective for sedation of the ventilated TBI patient. Propofol is a hypnotic anesthetic commonly used for treatment of TBI patients with rapid onset and a very short half-life that facilitates rapid neurological assessment. It also reduces cerebral metabolism and oxygen consumption and exerts a neuroprotective effect. Propofol use should be limited in both concentration and duration to avoid propofol infusion syndrome.62 First described in children, and later in adults, excessively high doses or extensive durations of propofol use can result in hyperkalemia, hepatomegaly, metabolic acidosis, rhabdomyolysis, renal failure, and death. Caution should be used if doses exceed 5 mg/(kg h) or 48 hours of therapy in adults. Although the use of analgesics or sedatives has not shown an independent improvement on neurological outcome, their effectiveness in ICP reduction ensures that they will be used for the foreseeable future.

Hyperosmolar Therapy While the exact mechanism by which mannitol provides beneficial outcome is unclear, two primary methods are postulated. In the first few minutes, it produces immediate plasma expansion with reduced hematocrit and blood viscosity, improved rheology, and increased CBF and O2 delivery. This reduces ICP and is most notable in patients with CPP 70 mm Hg.63,64 Over the next 15–30 minutes, and lasting 1.5–6 hours, mannitol produces an osmotic effect with increased serum tonicity and withdrawal of edema fluid from the cerebral parenchyma. When given as a bolus, the ICP reduction is evident at 1–5 minutes and peaks at 20–60 minutes. The initial bolus of mannitol, for acute ICP reduction in cases of neurological worsening or herniation, should be dosed at 1 g/kg with subsequent administration at smaller doses and longer intervals (i.e., 0.25–0.5 g/kg Q 6 hours). Mannitol opens the blood–brain barrier (BBB) and may cross the BBB itself, drawing water into the brain and transiently exacerbating vasogenic cerebral edema. Furosemide may also be used synergistically with mannitol65 to reduce cerebral edema through increased serum tonicity and reduced CSF production. There has been concern that continuous mannitol infusions lead to elevated serum levels of mannitol, sequestering of mannitol within brain tissue, rebound shifts of water back into the brain, and worsening outcomes. It was thought that bolus administration reduced this effect and was more effective than mannitol infusions for ICP reduction66 with an added benefit

of maximized rheologic increase in CBF. More recent data suggest that there are no significant data to support this.67 The significant water shifts employed by the use of mannitol mandate accurate measurement of urine output and fluid replacement to maintain euvolemia. Accurate diagnosis of diabetes insipidus (DI) may be precluded in the presence of mannitol. Acute tubular necrosis (renal failure) may be seen when mannitol is used in high doses, in patients with preexisting renal disease, or with other nephrotoxic drugs. Serum osmolality should be monitored and use of mannitol should be restricted when serum osmolality is 320 mOsm/L.68 It is imperative to follow urine output to allow replacement of urinary electrolyte loss and continued avoidance of hypotension and hypovolemia. Although TBI patients usually get mannitol in conjunction with ICP monitoring, some patients may benefit from high-level empiric dosing.42 No strong evidence supports empiric prehospital administration of mannitol to TBI patients69 but mannitol may be of benefit in patients with acute mass lesions and may be used as a bridge toward definitive therapy such as operative evacuation of mass lesions. Comatose patients acutely presenting with operative subdural hematomas or with operative intraparenchymal temporal lobe hemorrhages and abnormal pupillary dilatation demonstrated improved clinical outcomes when treated preoperatively with large doses of mannitol, approximately 1.4 g/kg.70,71

Hypertonic Saline As with mannitol, hypertonic saline (HS) is thought to lower ICP through two mechanisms. First, an oncotic pressure gradient, across the BBB, results in mobilization of water from brain tissue and hypernatremia. Second, rapid plasma dilution and volume expansion, endothelial cell and erythrocyte dehydration, and increased erythrocyte deformability lead to improvements in rheology, CBF, and oxygen delivery. HS is often administered as a continuous infusion of 25–50 mL/h of 3% saline (replacing the patient’s isotonic IV fluid) or bolus infusions of 10–30 mL of 7.2%, 10%, or 23.4% saline solution. Onset of clinical response can be within minutes and may last for hours making HS a candidate for use in cases of severe ICP elevation or acute herniation syndrome. A serum sodium goal of 145–160 mEq/L is frequently used although higher serum sodium levels may be necessary to achieve clinical goals. Serum sodium and osmolality levels should be aggressively followed as excessively rapid increases in sodium, seen during HS administration, may result in central pontine myelinolysis. This occurrence is most often seen in patients with preexisting, chronic hyponatremia and is rarely seen in the chronically normonatremic patient treated with HS. HS may also induce or exacerbate pulmonary edema in patients with underlying cardiac or pulmonary deficits.

Hyperventilation HPV lowers PCO2 with subsequent vasoconstriction, reduction of cerebral volume, and reduction in ICP. Time of onset ranges from 30 seconds to 1 hour; peak effect may be seen at 8 minutes and may last up to 15–20 minutes. This rapid onset

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of action makes HPV particularly effective in the treatment of an IC-HTN crisis and as a bridge to more definitive therapy (i.e., surgical decompression) or while other ICP reduction measures take effect. Although HPV was once used as a first-line therapy, concern has grown regarding prophylactic or prolonged use in TBI patients. During the first 24 hours after injury, patients with severe TBI show CBF reduction of at least 50%.72 Forced vasoconstriction, through HPV, can lower this further. Depending on the degree of functional autoregulation, there may be increases in the oxygen extraction fraction or shunting of blood to ischemic areas with widening of the total ischemic territory. Severe TBI patients should aim to be normocarbic (PCO2  35–40). HPV should be avoided during the first 24 hours postinjury when CBF is most reduced. If HPV is necessary after the first 24 hours, short-term, mild HPV (PCO2  30–35) can be effective for ICP control necessary to implement other treatment strategies. Further, moderate HPV produces even further reductions in CBF,73 and should be avoided except for very brief periods while other therapies are prepared. Prophylactic HPV (PCO2 25) is contraindicated as it is associated with increased ischemia and worse outcomes.74 When HPV is used, further monitoring should be considered to monitor oxygen delivery and may include jugular venous saturation or PbtO2 monitors.

FIGURE 19-8 CT of a bilateral hemispheric decompressive craniectomy performed in a patient with severe edema from a likely second impact syndrome.

Decompressive Craniectomy When the above therapies fail to provide adequate control of ICP, other second-tier therapies can be considered. These include decompressive craniectomy, temporal lobectomy, optimized HPV, barbiturate coma, and hypothermia. Some cases of TBI require acute craniotomies to address focal lesions (e.g., SDH, EDH, IPH). The bone is removed, the lesion is resected, and the dura and bone are replaced. More severe cases of TBI may develop diffuse cerebral edema, contusions of large size in eloquent areas, or multiple, coalesced contusions. In these cases, it may be preferable to leave the bone flap off. Additionally, when ICP is refractory to the previously mentioned techniques, a decompressive craniectomy effectively expands the intracranial space to lower the ICP. The most common decompressive craniectomy is unilateral hemispheric. Bifrontal and bilateral hemispheric craniectomies (Fig. 19-8) have also been described and are based on the location and severity of the underlying lesion(s). In decompressive craniectomies the dura is opened widely and areas of noneloquent contused and devitalized brain can be removed if required. In the hemispheric technique at least a 12-cm cranial flap is removed. The brain is then contained only by the augmented dural covering and the more compliant scalp. While decompressive craniectomy has been shown to be effective in reducing ICPs, many studies are observational or case series, lack appropriate control subjects, or do not achieve statistical significance with regard to all end points.75–78 As a result this procedure has not yet been definitively proven to improve outcomes in the trauma patient. Two international trials are currently ongoing (DECRA and RESCUEicp) to address this question.

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Decompressive craniectomy is most commonly used as a second-tier option for patients with IC-HTN refractory to maximal medical management and success is dependent on patient selection.79 Ideally, operative intervention should occur within 48 hours of the initial injury and before ICP has surpassed 40 mm Hg for sustained periods of time. Outcomes tend to be more favorable in younger patients with diffuse injury and limited secondary injury. Regardless of the preoperative indications or patient profile, continuing postoperative IC-HTN greater than 35 mm Hg has been associated with 100% mortality.80 Early decompressive craniectomy, as a primary treatment, has the advantage of rapid control of IC-HTN11,81; however, there are a number of potential complications. These include infection, subdural hygromas, hydrocephalus, syndrome of the trephined, perfusion breakthrough, and cerebral infarction. Early surgical intervention may be an option for patients presenting with severe unilateral or bilateral cerebral edema, parenchymal lesions resistant to initial medical management of ICP, or other injuries whose management conflicts with standard ICP control measures (e.g., patients with acute respiratory distress syndrome requiring elevated ventilatory pressures).

Barbiturates Barbiturates benefit TBI patients by decreasing metabolic demand for oxygen (CMRO2), decreasing free radicals and intracellular calcium, and lowering ICPs. Side effects such as immunosuppression and hypotension from reduced sympathetic tone and mild cardiodepression often limit their use. TBI patients in coma (GCS 8) receiving barbiturate therapy have infection

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and respiratory complication rates in excess of 50%80 and significant systemic hypotension is present in 25% of patients82 despite adequate intravascular volume and pressor therapy. Patients with hemodynamic instability, sepsis, respiratory infection, or cardiac risk factors are excluded from this therapy and those receiving barbiturates should be closely monitored for signs of cardiac compromise or infection with cessation of therapy if systemic effects of the treatment become significant and unmanageable. A pretherapy echocardiogram and intratherapy use of a Swan–Ganz catheter should be considered. Barbiturates clearly reduce ICP but studies have shown both improved and worsened outcomes for TBI patients receiving barbiturate therapy. There is no role for prophylactic barbiturate therapy in TBI patients, as it increases hypotension without significantly improving outcome,83,84 and it is to be used only as a second-line therapy when other treatment measures have failed. A typical pentobarbital regimen is a loading dose of 10 mg/kg over 30 minutes followed by a 5 mg/(kg h) infusion for 3 hours. A maintenance dose of 1 mg/(kg h) should then be started.41 Serum barbiturate levels of 3–4 mg% should be maintained, although poor correlation exists between serum level, therapeutic benefit, and systemic complications. Continuous electroencephalographic evaluation is more reliable and dosing to the point of EEG burst suppression produces near-maximal reductions of CMRO2 and CBF.

Hypothermia Induced prophylactic hypothermia attempts to improve outcome in patients with severe TBI through reduction of cerebral metabolism, ICP, inflammation, lipid peroxidation, excitotoxicity, cell death, and seizures. Side effects of hypothermia include decreased cardiac function, thrombocytopenia, elevated creatinine clearance, pancreatitis, and shivering with associated elevations in ICP. Initial interest for induced hypothermia stemmed from anecdotes (e.g., a child trapped in a frozen lake), single-center clinical trials, and four meta-analyses.85–89 Although its use has been adopted by some trauma centers and there is level 1 evidence for its use in V-fib or V-tach MI, initial literature had not shown statistically significant improvements in mortality directly attributable to induced hypothermia for the trauma patient. Meta-analyses of more recent data and subsequent guidelines from the Brain Trauma Foundation41 note a nonstatistically significant trend toward mortality reduction (compared to normothermic controls) when target temperatures were maintained for greater than 48 hours. Hypothermia-treated patients also had significantly higher Glasgow Outcome Scale scores. Additionally, it was found that patients who were hypothermic on admission had improved outcomes when hypothermia was maintained. Results are limited, however, by the small sample sizes and potential confounding factors of each study in the meta-analyses. Hypothermic therapy is an option in the patient with severe TBI. Selected patients should be cooled relatively early in their care or maintained in a cooled state if hypothermic on arrival. A target temperature of 32–33°C should be achieved and, if

possible, maintained for greater than 48 hours. These patients should be closely monitored for the untoward effects of hypothermia such as electrolyte abnormalities, hypocoagulability, and cardiac rhythm alterations.90 Rewarming of these patients should be very slow, generally not exceeding more than 1° per 24 hours.

Steroids Glucocorticoids are not recommended for improving outcome or reducing ICP in TBI.41,91,92 Side effects of steroid use include coagulopathies, hyperglycemia, and increased infection and are reflected in poor outcomes.

Antiseizure Prophylaxis PTSs are deleterious in the TBI patient for many reasons including elevated metabolic demand that exacerbates ischemia and increased ICP. TBI patients at increased risk for PTS include those with GCS 10, depressed skull fractures, cortical contusions or hemorrhage (SDH, EDH, IPH), and penetrating hemorrhage or seizure within 24 hours of head injury.93 Anticonvulsants have been shown to effectively reduce the risk of early PTS (7 days postinjury) but not late PTS (7 days postinjury)94 and the prophylactic administration of phenytoin or carbamazepine is indicated for the prevention of early PTS only41 (i.e., 7 days after injury). Despite no controlled study showing an equivalent efficacy for early PTS prevention, many centers are now using levetiracetam (Keppra®) because of reduced side effects and ease of administration.

■ Specific System Considerations Nutrition At rest, all patients have basal energy expenditure (BEE) dependent on their sex, age, height, and weight. All injured patients show an increase in BEE regardless of neurological course. Patients who are sedated and paralyzed may show BEE increases to 120–130% of baseline.97 Comatose patients (GCS 8) with isolated head injury have BEE approximately 140% (range 120–250%).96,97 Mortality is reduced in patients who receive full caloric replacement by 1 week postinjury98 and at least 15% of calories should be supplied as protein. Since it may take 2–3 days to ramp up feedings, nutritional replacement should start by 72 hours postinjury. Enteral feeding is preferred over parenteral nutrition as it provides enhanced immunocompetence and a reduced risk profile.99 If the patient has diminished gastric motility, a jejunal feeding tube can be placed since patients with severe TBI can tolerate early jejunal feeding even in the presence of gastric dysfunction and absent small bowel activity.100 Total parenteral nutrition should be started if enteral feeding is not possible or if higher nitrogen intake is required.

Infection Trauma patients may incur infection as part of their initial injury from gross wound contamination or immunosuppression, or iatrogenically from open surgical procedures, intubation for mechanical ventilation, and invasive monitoring equipment.

Injury to the Brain

Coagulopathy and DVT Prophylaxis Patients suffering head trauma often develop or present with coagulopathy even without medical comorbidities or medications. Most critically ill trauma patients will have decreased levels of plasma antithrombin (AT) activity. Head-injured patients, however, tend to have increased rates of coagulopathy with supranormal AT activity that can progress to disseminated intravascular coagulation and fibrinolysis (DICF), and expansion of existing contusions and delayed development of additional hemorrhages.102,103 Coagulopathy is especially prevalent in penetrating brain injury. For all trauma patients, the patients’ medical history and review of systems should specifically address coagulopathic medical disorders, prior episodes of trauma, bleeding or clot formation, use of specific antiplatelet or anticoagulant medication (aspirin, warfarin, low-molecular-weight heparin), and medications that have antiplatelet compounds as a component. Laboratory studies should be performed including measurements of prothrombin time (PT), activated partial thromboplastin time (aPTT), international normalized ratio (INR), platelet count (plt), and bleeding time or platelet function assay (when necessary). Coagulopathies should be rapidly and aggressively treated until the patient achieves a normal coagulation profile. Effects of warfarin anticoagulation may be reversed by administration of vitamin K, fresh frozen plasma (FFP), or prothrombin complex concentrate; effects of heparin may be reversed with protamine sulfate; and thrombocytopenia or platelet deactivation may be treated with donor platelet transfusion. Unfortunately, patients may have life-threatening intracranial hemorrhage or developing cerebral edema with rising ICPs and these treatments require time for transfusion. Recombinant activated coagulation factor VII (rFVIIa) rapidly forms a complex with tissue factor to produce thrombin and, separately, converts factor X to its active form, factor Xa, resulting in a “thrombin burst” at the site of tissue damage.104 It is FDA approved for use in hemophiliacs and patients with antibodies to factor VIII or IX, and has been studied off-label in cases of ICH and trauma patients requiring rapid craniotomy in the face of coagulopathy. Its effects on neurological outcome and mortality, as well as its cost burden (∼$10,000/dose), are currently under investigation and have not been fully defined.105,106 Trauma patients, in general, and head-injured patients, in particular, are at risk for venous thromboembolism (VTE) such

as deep venous thrombosis (DVT) and pulmonary embolus (PE). Neurological risk factors for DVT and PE include stroke or spinal cord injury, need for prolonged surgery or prolonged bed rest, SAH or head injury causing altered coagulation or dehydration, and increased blood viscosity from cerebral salt wasting and treatment of cerebral edema.107,108 The incidence of DVTs in neurosurgical patients ranges from 19% to 50%. Lowrisk, prophylactic measures against DVTs include passive range of motion, early ambulation, rotating beds, and electrical stimulation of calf muscles. If DVTs are not already present, pneumatic compression boots (PCBs) and sequential compression devices may be safely used and can reduce the incidence of DVTs to 1.7–2.3% and PEs to 1.5–1.8%.109 Active, pharmacologic anticoagulation can increase the effectiveness of DVT prophylaxis with the risk of additional hemorrhagic complications. Low-molecular-weight heparins have a higher ratio of anti–factor Xa to anti–factor IIa activity, versus unfractionated heparin, have greater bioavailability after subcutaneous injection, and have more predictable plasma levels. They can be added to PCBs without significantly increased risk of hemorrhage,110 and their use is recommended in postoperative neurosurgery patients.41 There are no universally accepted recommendations for the method and timing of postoperative anticoagulation and this should be tailored to each patient. One study has shown no increased incidence of hemorrhagic complications once full anticoagulation was resumed 3 days after craniotomy.19

OUTCOME ■ Prognosis To interpret and compare the effectiveness of various treatments, common end points are necessary for communication between practitioners or comparison of studies. The Glasgow Outcome Scale111 (Table 19-9) is a widely used outcome grading scale with many studies separating patients into those with good outcome (GOS  4 or 5), those with poor outcome (GOS  2 or 3), and those who are dead (GOS  1). Although its separation of patient categories is relatively coarse and may not identify the subtleties of recovering TBI patients, it remains a useful tool for describing patient outcome just as the GCS is a useful tool for measuring a patient’s neurological examination. The medical practitioner is often called upon to make predictions of outcome based on limited information early on in the patient’s course. The patient’s ultimate neurological outcome may not be fully evident until weeks or months of treatment have taken place in hospitals, rehabilitation centers, and at home. Various studies and meta-analyses112–114 show that worse prognosis is seen in patients with bilaterally dilated ( 4 mm) or absent pupillary light reflexes, absent oculocephalic or oculovestibular reflexes, increased injury severity scale ( 40), advanced age ( 60 and possibly  2), hypotension (SBP  90, worse with concomitant hypoxemia), abnormal CT scan (extensive tSAH, compression or obliteration of basal cisterns), persistent ICP 20 mm Hg, elevated ICP during the first

CHAPTER CHAPTER 19 X

In general, antibiotic coverage should be targeted toward specific organisms and removed as soon as possible to decrease drug-resistant strains of bacteria or alterations in normal floral patterns and bacterial overgrowth (i.e., C. difficile colitis). Perioperative antibiotics are generally only recommended for the first 24 hours. Routine flushing or exchange of ventricular catheters is not recommended.41 Conflicting evidence precludes recommendations for periprocedural antibiotics during EVD placement, although one study has shown that use of rifampin-impregnated ventriculostomy catheters resulted in an overall decrease in infection rates with a concomitant increase in rifampin-resistant organisms.101

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TABLE 19-9 Glasgow Outcome Score

SECTION 3 X

Score 5—good recovery

Meaning Resumption of normal life

4—moderate disability

Disabled but independent

3—severe disability

Conscious but disabled

2—persistent vegetative state

Unresponsive, speechless

1—death

Dead

Notes May have minor deficits,  return to work Exceeds ADLs, can use public transportation, work in sheltered environment Dependent for daily support,  needs institutionalization May achieve sleep/ wake cycles and open eyes after 2–3 weeks Most deaths due to primary head injury occur within 48 h

24 hours, or presence of apolipoprotein E allele. There is a stepwise, increasing probability of poor outcome with worsening initial total GCS scores (especially GCS 9) and some studies show worse prognosis based on lower GCS subscores (motor 3, eye opening 2, verbal response 2).

■ Brain Death Determination and Organ Donation “Brain death” denotes the absence of any observable neurological activity in the brain and the irreversibility of cessation of the cardiopulmonary system or the entire brain. It must be explained to patients’ families that brain death is a legally binding death and a true clinical death. The requirements of a brain death examination may vary slightly between states or medical facilities but retain similar core elements. There must be no complicating conditions (hypothermia 32.2°C, hypotension [SBP 90], exogenous sedatives, paralytics, drug/alcohol, hepatic encephalopathy, hyperosmolar coma, atropine, recent CPR/shock/anoxia) to confuse the neurological exam. Patients have fixed, dilated pupils and no observable corneal, oculocephalic, oculovestibular, gag, or cough reflexes. There is no movement to deep central or peripheral pain and no spontaneous breathing is seen on disconnection from the ventilator with PaCO2 60 mm Hg (i.e., apnea test). If the patient is unable to tolerate an apnea test or if parts of the brain death protocol are equivocal, secondary tests may be used to confirm or augment the above information. Most commonly used are cerebral angiography to show absence of

intracranial flow and cerebral radionuclide angiogram to show absent uptake in brain parenchyma. Head-injured patients who progress to brain death may be candidates for organ donation. Specialized organ procurement organizations are present in most states and represent a party separate from the treating team and with no conflict of interest regarding the patient’s care. Although the patient’s death is unfortunate, organ donation can provide family members with a slightly more positive conclusion to a series of unfortunate events.

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100. Grahm TW, Zadrozny DB, Harrington T. The benefits of early jejunal hyperalimentation in the head-injured patient. Neurosurgery. 1989; 25:729–735. 101. Zabramski JM, Whiting D, Darouiche RO, et al. Efficacy of antimicrobialimpregnated external ventricular drain catheters: a prospective, randomized, controlled trial. Neurosurgery. 2003;98:725–730. 102. Owings JT, Bagley M, Gosselin R, et al. Effect of critical injury on plasma antithrombin activity: low antithrombin levels are associated with thromboembolic complications. J Trauma. 1996;41:396–405. 103. Kaufman HH, Moake JL, Olson JD, et al. Delayed and recurrent intracranial hematomas related to disseminated intravascular clotting and fibrinolysis in head injury. Neurosurgery. 1980;7:445–449. 104. Hoffman M, Monroe DM 3rd. A cell-based model of hemostasis. Thromb Haemost. 2001;85(6):958–965. 105. McQuay N Jr, Cipolla J, Franges EZ, et al. The use of recombinant activated factor VIIa in coagulopathic traumatic brain injuries requiring emergent craniotomy: is it beneficial? J Neurosurg. 2009;111(4): 666–671. 106. Brown CV, Foulkrod KH, Lopez D, et al. Recombinant factor VIIa for the correction of coagulopathy before emergent craniotomy in blunt trauma patients. J Trauma. 2010;68(2):348–352. 107. Hamilton MG, Hull RD, Pineo GF. Venous thromboembolism in neurosurgery and neurology patients: a review. Neurosurgery. 1994;34:280–296. 108. Olson JD, Kaufman HH, Moake J, et al. The incidence and significance of hemostatic abnormalities in patients with head injuries. Neurosurgery. 1989;24:825–832. 109. Black PM, Baker MF, Snook CP. Experience with pneumatic calf compression in neurology and neurosurgery. Neurosurgery. 1986;18: 440–444. 110. Frim DM, Barker FG 2nd, Poletti CE, et al. Postoperative low-dose heparin decreases thromboembolic complications in neurosurgical patients. Neurosurgery. 1992;30:830–832. 111. Jennett B, Bond M. Assessment of outcome after severe brain damage: a practical scale. Lancet. 1975;1:480–484. 112. Zink BJ. Traumatic brain injury outcome: concepts for emergency care. Ann Emerg Med. 2001;37:318–332. 113. Miller JD, Butterworth JF, Gudeman SK, et al. Further experience in the management of severe head injury. J Neurosurg. 1981;56: 650–659. 114. Chesnut RM, Ghajar J, Maas AIR, et al. Early Indicators of Prognosis in Severe Traumatic Brain Injury. New York, NY: Brain Trauma Foundation. Available at: https://www.braintrauma.org/coma-guidelines/. Accessed April 2, 2010.

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CHAPTER 20

Eye Petros E. Carvounis and Yvonne I. Chu

EPIDEMIOLOGY OF EYE TRAUMA Worldwide 1.6 million people are estimated to be blind from ocular trauma and another 19 million people suffer from severely impaired vision in one eye due to trauma.1 Published literature from England looking at 15 years of more than 39,000 patients treated for major trauma found that 2.3% of patients had associated ocular injuries. Given that the eyes represent only 0.27% of the total body area, it is a curious phenomenon that the eyes are affected so often. In this series, the most common injuries involved the cornea, optic nerve, conjunctiva, and sclera.2 Men are reported to be four times more likely to suffer from ocular trauma compared to women and in the same series from England, 75.1% of major trauma patients with ocular injuries were men. While ocular trauma most commonly results from motor vehicle accidents, workplace injuries and recreational injuries are also very commonly seen. Most injuries were resulting from sharp objects (54.1%), followed by blunt objects (34.4%), and chemical injuries accounted for 11.5% of ocular injuries.3

EYE TRAUMA TERMINOLOGY AND CLASSIFICATION Eye trauma is divided first by etiology into mechanical, chemical, thermal, and electric. Thermal (e.g., corneal burn from curling iron) and electric (e.g., lightning) eye traumas are very uncommon and treatment of complications will be by an ophthalmologist in an outpatient setting after discharge from the emergency room/urgent care setting. Chemical injury (alkali and acid burns) is not uncommon and its management will be discussed in detail as immediate intervention by first responders and emergency room physicians can be sight-saving. Mechanical eye trauma is the most common form of eye injury. It is divided into open globe injury, where the sclera

and/or cornea (eyewall) have a full-thickness wound, and closed globe injury where the eyewall does not have a full-thickness wound (Fig. 20-1).4–6 Closed globe injuries are further subdivided into contusion injuries, lamellar laceration (i.e., partial thickness laceration), and superficial foreign body (i.e., foreign body lodged on cornea, conjunctiva, or under the conjunctiva but without full-thickness wound of the eyewall).6 Open globe injuries are further divided into ruptured globes and globe lacerations.4,5 Ruptured globes result from blunt trauma, due to an extreme elevation of intraocular pressure on the moment of impact causing a rupture of the eyewall at the weakest site of the globe (force from inside out), usually away from the site of impact and frequently with significant herniation of intraocular contents.4–6 Globe lacerations result from sharp trauma (usually) due to the direct impact on the eyewall (force from outside inwards).4,5 Perforating injury is a specific type of globe laceration in which the projectile or sharp object has caused an entry as well as an exit full-thickness eyewall wound.4,5 In a penetrating injury only a single full-thickness eyewall wound is present per projectile/object (there is no exit wound).4,5 Finally, an intraocular foreign body (IOFB) is a type of penetrating laceration in which the foreign object is retained within the globe.4–6 The above classification is not simply an academic exercise. It provides an effective means of communication between treating physicians but even more importantly the exact type of injury has specific implications to management and prognosis.4–6 Specifically, an open globe needs urgent operative repair, whereas a closed globe typically does not. Among open globes, globe rupture portends a poorer prognosis for final visual outcome than globe laceration.7,8 Finally, an IOFB is usually best removed by a vitreoretinal surgeon and may require vitrectomy (sometimes not available in general ophthalmology operating rooms), whereas a penetrating or perforating injury can be managed by any ophthalmologist in an operating room with an ophthalmic operating microscope. Certainly in needed circumstances, primary closure

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Management of Specific Injuries

Mechanical Eye Injury SECTION 3 X

Open globe injury Eye wall has full-thickness wound

Closed globe injury No full-thickness eye wall wound

Globe rupture Increased pressure within the eye causes full-thickness wound

Contusion

Lamellar laceration Laceration Full-thickness wound caused by direct impact of usually sharp object

Penetrating: Single laceration

Superficial foreign body

Intraocular foreign body: Retained foreign object causing laceration

Perforating: Two lacerations (exit and entry) wound FIGURE 20-1 Injury classification.

can be achieved and the patient can be referred to a retina specialist for removal of an IOFB at a second procedure.

CLINICAL APPROACH TO EYE TRAUMA It is imperative that concomitant nonocular injuries be evaluated and assessed on presentation to the emergency room. Involvement of the ophthalmologist in a timely manner and in the absence of life-threatening injury before transfer to the operating room is important. Sight-threatening injury needs to be recognized and treated within an appropriate time interval.

■ History Every effort should be made to take a focused history—if not from the patient (if he or she is unconscious, distracted by other severe injuries, or under the influence of alcohol or drugs), then from relatives, bystanders, or first responders. In the setting of trauma, being time efficient is obviously of the utmost importance. The most important aspect of the history is the mechanism of injury, as specific mechanisms suggest specific injuries that must be assessed for and treated. For example, hammering is associated with intraocular metallic foreign bodies, while fireworks injury is commonly associated with chemical injury that must be treated emergently (as well as contusion injury—rarely open globe). Injury to the forehead as a result of a bicycle accident followed by loss of consciousness is a common scenario in which traumatic optic neuropathy may develop, while injuries from BB guns are associated with globe lacerations with

particularly poor prognosis. Additionally, it is important to elucidate the setting of the injury: penetrating injuries in a rural setting are associated with higher rates of endophthalmitis. Documenting whether protective eyewear was worn at the time of the injury is important for medicolegal reasons. Patient symptoms are also important: floaters and a visual field defect are highly suggestive of a retinal detachment, while pain with sensitivity to light without compromise in the vision suggests a traumatic iritis (although a globe laceration and even an IOFB remain a possibility). Past ocular history is important for two reasons. First, it may modify the effects of trauma, for example, in the case of a patient who has previously had a corneal transplant an open globe due to dehiscence of the graft will occur with much less force than normally expected. Similarly, in patients with previous cataract or glaucoma or radial keratotomy surgery the globe ruptures at the site of the previous wound. Second, past ocular history is important as preexisting pathology may dictate different treatment decisions following trauma. For example, the threshold for surgical evacuation of a hyphema would be much lower in a patient with advanced glaucomatous optic neuropathy than in a patient with healthy optic nerves. Past medical history is similarly important as it can modify treatment decisions. For example, hyphema is managed differently in patients with sickle cell disease. Another example would be patients with pseudoxanthoma elasticum who invariably have angioid streaks and have a much higher risk of choroidal rupture. There are also several systemic conditions that result in eye conditions unrelated to trauma, an obvious example being diabetes mellitus causing diabetic retinopathy that can cause nontraumatic vitreous hemorrhage.

Eye

■ Clinical Examination Clinical examination can be challenging due to pain or poor patient cooperation due to the influence of alcohol, drugs, or severe eyelid swelling; yet it is essential for proper diagnosis and management of ophthalmic trauma. The basic tool kit needed for rudimentary eye examination includes: penlight, near vision card, eyelid retractor/speculum, topical anesthetic, fluorescein strip, and eye wash.

Visual Acuity It is no exaggeration to state that failure to document the visual acuity is inexcusable and akin to failure to document the pulse! Measuring visual acuity is crucial for three reasons. First, a specific level of vision prompts the examining physician to search for a diagnosis explaining it. For example, vision of hand motions only (HM) is not explained by a subconjunctival hemorrhage and requires the examiner to carefully examine for the other signs of a scleral rupture. Another example would be the patient who had trauma 3 days previously and presents to the emergency room with photosensitivity, mild lid edema, and vision of 20/400: before knowing this level of vision, traumatic iritis could have been contemplated but with vision of 20/400 endophthalmitis with a self-sealed corneal or scleral laceration becomes a strong possibility. The second reason it is important to measure the visual acuity is to document a baseline so that later in the course it can be established whether there is improvement or deterioration. For example, a patient with a vitreous hemorrhage and vision of HM is seen by a vitreoretinal surgeon for examination to rule out retinal tears and detachment; if a week later the vision is 20/200 (and there are no retinal tears or detachment), further observation is reasonable as it appears that the vitreous hemorrhage is spontaneously resolving. In contrast, if a week later the vision is light perception, this suggests that a retinal detachment has occurred due to an undetected retinal tear. The final reason why it is important to measure visual acuity is that visual acuity at presentation is a strong predictor for final visual outcome.7,8 Therefore, having an initial visual acuity is essential if discussing the prognosis of the injury with the patient. Measuring visual acuity is relatively easy. Obviously each eye is tested separately by covering the other eye with an occluder (or the patient’s hand if there is no occluder available). The goal is to determine whether the patient has no light perception (NLP— cannot even see the light from a strong pen torch right in front of the injured eye with the room darkened), light perception only (LPO—can see the light but no hand movements), HM (can see

hand movements but cannot count fingers), or vision between 1/200 and 20/20. When trying to measure vision between 1/200 and 20/20, the patient should be wearing his or her spectacles (if these are available). Counting fingers at a distance x is equivalent to x/200 (e.g., counting fingers at 2 ft is vision of 2/200). For vision better than 5/200 a Rosenbaum reading card or a Snellen or ETDRS visual acuity chart can be used. If none of these are available, documentation of ability to read the newspaper title (approximately 20/200) or the normal magazine print (approximately 20/40) is still extremely helpful.

Pupillary Examination (Shape, Reaction, and Relative Afferent Pupillary Defect) The pupil may be peaked if there the iris is sealing (plugging) a corneal or anterior scleral laceration. The pupil may also be irregular if there has been injury to the iris sphincter muscle (typically a result of blunt trauma, commonly associated with hyphema). The pupil will be dilated and not react to light if there is compression or damage to the third cranial nerve intracranially (following head trauma); if this is suspected, urgent neurosurgical consultation and computed tomography (CT) imaging is required. Additionally, an orbital compartment syndrome (due to retrobulbar hemorrhage or any cause for swelling within the orbit) may cause compression of the third nerve (and all the other nerves) and result in a fixed dilated pupil. Finally, if there has been damage or ischemia of the iris sphincter (very elevated intraocular pressure or torn iris sphincter), the pupil will not react to light. A relative afferent pupillary defect (RAPD) is important to document for two reasons: first, its presence means that there is injury to the retina or optic nerve. This is important as it prompts the examiner to carefully consider the diagnoses that may be affecting the retina and optic nerve and not satisfy himself or herself with a diagnosis involving the anterior segment only. Second, the absence of an RAPD is a strong predictor of visual survival, with only 97% of eyes without an RAPD maintaining some vision.9 Measuring an RAPD is by alternately shining a strong light to each eye. At least 2 seconds should be spent shining each eye with 1 second in transit. When the pupils dilate when the light is shone into one of the eyes, it is said that an RAPD is present in that eye. It is important to note that it is the first movement of the pupil when the light is shone into it that matters. From the above, it should be obvious that even in a patient with a pupil that is immobile in the injured eye determination of the presence or absence of an RAPD in that eye is possible since the contralateral pupil movement can be observed while shining the light into the injured eye.

Motility Examination of motility is important to rule out cranial nerve 3–6 injury in head trauma and also to detect muscle entrapment following an orbital fracture (typically inferior rectus muscle entrapment causing a deficit in elevation following an orbital floor fracture—in children this can be associated with severe, even life-threatening bradycardia due to the oculocardiac reflex).

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Important aspect of the drug history is whether the patient is on anticoagulants or antiplatelet agents as this will complicate operative repair. Additionally, determining allergies to medications is critical. Review of systems must assess for the patient’s ability to survive anesthesia and surgical repair. Patients who cannot undergo surgery safely may be better managed medically even though the risk of losing their sight in one eye is evitable rather than dying from complications of anesthesia.

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SECTION 3 X

Examination of motility is by asking the patient to follow an extended second digit or pen in all directions of gaze. It is important to ascertain whether the patient has diplopia when looking at any of these directions.

the case of a corneal laceration with extrusion of ocular contents or in the case of rupture at the site of prior cataract surgery with extrusion of the intraocular implant), whether it is subluxed, whether there is an intralenticular foreign body, or whether cataractous changes have developed.

External and Ocular Adnexal Examination Examination of the ocular adnexa involves looking at the eyelid position with eyes both open and closed, contour, and evidence of laceration. It is important to also evaluate for proptosis and in patients with proptosis, testing for resistance to retropulsion may point toward elevated intraocular pressure and congested orbital compartment. As part of the routine external examination, the examiner should palpate the orbital rim for “step off ” in cases of suspected orbital fractures. In cases of suspected orbital floor fractures, testing sensation along the distribution of cranial nerve V on either cheek can be an early sign.

Slit Lamp Biomicroscopy The slit lamp biomicroscope is the ideal instrument to examine the anterior segment. Portable versions exist for patients who cannot sit up to be examined with the regular slit lamp. If not even a portable slit lamp is available, a direct ophthalmoscope offers high magnification and can be used, and if even this is unavailable, a penlight with a blue filter and a magnifying lens can be used. Throughout the examination of the anterior segment it is important to remember that pressure should not be exerted on the globe (as it may be open and it is uncomfortable to the patient)— rather the lids should be lifted and held up by applying pressure against the orbital rim. Examination of the anterior segment starts with inspection of the conjunctiva and sclera. Subconjunctival hemorrhage is a common finding sometimes even after trivial trauma, but can be a sign of an open globe; therefore, the other signs of an open globe should be sought. Additionally, a subconjunctival hemorrhage can be a sign of a retrobulbar hemorrhage, especially if its posterior margin cannot be defined; therefore, the other signs of this condition should also be sought. Uveal tissue, vitreous gel, or even retina is sometimes evident on or under the conjunctiva in cases of scleral rupture or laceration. Inspection of the cornea should be performed actively searching for a corneal laceration, a corneal foreign body, a corneal abrasion, and a corneal concussive injury to the endothelium (appears as opacity on the endothelium). A corneal abrasion may be more easily seen by applying fluorescein drops or a fluorescein strip in the tear lake and using the cobalt blue filter. Examination of the anterior chamber should be performed looking for hyphema, hypopyon (layering of white cells inferiorly diagnostic of endophthalmitis in the setting of trauma), a shallow anterior chamber suggestive of open globe, an anterior chamber foreign body, and anterior chamber cell (white cells in the anterior chamber—are seen in endophthalmitis or traumatic iritis). Examination of the iris should be performed looking for iris tears or iris dialyses. Finally, examination of the lens should be performed to determine whether it is present or not (it may have been lost in

Intraocular Pressure There is no need to check the intraocular pressure if the globe is obviously open, but if not, measurement of the intraocular pressure is mandatory. Intraocular pressure is best measured using a Goldmann applanation device used with the slit lamp, but a Tono-Pen is a convenient device for use in the emergency room setting. A high pressure can be seen with hyphema or with a retrobulbar hemorrhage (due to transmission of the elevated intraorbital pressure), while a low pressure is seen with an open globe or severe intraocular inflammation. It should be noted, however, that the intraocular pressure may on occasion be normal (rarely high) with an open globe.

Dilated Fundoscopy Dilated fundoscopy is best performed using indirect ophthalmoscopy, a skill beyond the remit of a trauma surgeon. However, a direct ophthalmoscope can establish whether the view is clear or not (if not, either there is a problem with the cornea, anterior chamber, or lens or there is a vitreous hemorrhage), can detect a choroidal rupture and commotio retinae, or can document a normal posterior pole examination. Any patient with a vitreous hemorrhage needs indirect ophthalmoscopy for detection of retinal tears or peripheral retinal detachment.

■ Ancillary Studies B-mode ultrasonography is very useful for examination of the posterior segment in the presence of media opacities not allowing ophthalmoscopy. Retinal tears, detachments, and IOFBs can be detected. It should be noted that the investigation is strongly operator dependent and that even in experienced hands severe vitreous hemorrhage cannot be reliably distinguished from a retinal detachment.10 CT imaging is important in evaluating for orbital fractures, orbital foreign bodies, and IOFBs, especially metallic. An orbital CT scan with thin slices should be ordered. Note that the dimensions of foreign bodies are commonly exaggerated on CT images.10 It should also be noted that vegetable matter (such as wood) in the orbit is not well imaged by CT.

■ Initial Management of the Patient with Ocular Trauma After the patient is stabilized (i.e., life-threatening injuries have been stabilized) other organ-threatening injuries need to be managed in parallel to evaluating the injured eye. The following are priorities when managing the injured eye: 1. Rule out a chemical injury by history (splash of liquid into the eye, explosion at chemical facility, firework injury).

Eye

PROGNOSIS OF EYE TRAUMA Prognosis of eye trauma involves discussion of three entities: whether the patient is going to retain his or her globe, what the patient may expect his or her vision to be in the long term, and finally whether this will affect the uninjured eye (see discussion on sympathetic ophthalmia below). Whether a patient is going to retain his or her globe depends on the specifics of the traumatic injury. It is rare that enucleation will be required for an eye sustaining an injury other than an open globe. Primary enucleation is rare (0.17% of open globes) and reserved for eyes where the sclera and cornea have been injured so severely that they cannot be sutured back together (usually due to a blast injury where the eye has been

blown away or a gunshot injury directly to the eye).11 Secondary enucleation (reported in 6–20% of open globes) is much more common for ruptures than lacerations and is usually performed for a blind (NLP), painful eye.7,9,11,12 An RAPD, NLP or LPO, visible uveal tissue, and concomitant eyelid laceration at presentation are risk factors for enucleation.7,11,12 Enucleation to prevent sympathetic ophthalmia is also sometimes performed, although it is controversial (see below). The best system that predicts long-term visual outcome (after appropriate management including surgical treatment) is the ocular trauma score (OTS).8,13 In the OTS a functional outcome (initial visual acuity) and five signs or diagnoses (rupture, endophthalmitis, relative afferent papillary defect, retinal detachment, perforating injury) are used to estimate the likely visual outcome (Table 20-1).8 Many patients worry that a poorly seeing eye will cause “straining” of the other eye—this is unequivocally nonsense. However, the uninjured eye may develop sympathetic ophthalmia, a rare (incidence 0.03/100,000 per year),14 bilateral uveitis that may occur 2 weeks to 50 years usually following eye trauma or surgery.15,16 While originally described as a consequence of trauma, currently it is more common following eye surgery.14 This is a consequence of improved management of ocular trauma, including prompt primary repair. Indeed, most cases with sympathetic ophthalmia following eye trauma present to the ophthalmologist several weeks after the initial trauma when the vision in the second eye is affected.17 Tellingly, since World War II there had been no cases of sympathetic ophthalmia reported in any military conflict until a single case in the recent war in Iraq.15 With current treatments, eyes affected with sympathetic ophthalmia commonly maintain functional vision with the majority maintaining reading vision.18 While removing the injured eye (when the vision is NLP) may decrease the rates of sympathetic ophthalmia, this is quite controversial given that sympathetic ophthalmia is rare (especially with appropriate management of the injured eye) and treatable.

SPECIFIC INJURIES AND THEIR MANAGEMENT ■ Chemical Injury Chemical injuries to the eye are true ocular emergencies and time is of essence when treating acute chemical exposure. They represent 7.7–18% of ocular trauma.19–21 Immediate and copious irrigation is vital to limiting the extent of damage to the ocular surface. Alkaline agents tend to penetrate the eye more rapidly due to saponification of cell membranes and lead to liquefactive necrosis. Acidic agents cause coagulative necrosis with protein precipitation within the tissue; thus, acidic injuries tend to cause less severe injury compared to alkali agents due to less penetrative damaging effects.22 The nature of the toxic agent should be identified and brought into the emergency center if possible so that pH can be tested. Following toxic chemical exposure to the ocular surface, irrigation should begin immediately with water, saline, or any commercially available eyewash with a neutral pH, and continued if possible while en route to the nearest emergency center.

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If there is suspicion of a chemical injury, a pH strip should be checked (from the fornix) and irrigation should be started at once (see Section “Chemical Injury”). 2. Rule out an open globe if possible: look for the specific signs (corneal/scleral laceration, prolapse of uveal tissue, hemorrhagic chemosis of the conjunctiva, low intraocular pressure, asymmetry in anterior chamber depth, vitreous hemorrhage). If there is reasonable suspicion of an open globe, exploration in the operating room should still be carried out (such as appendectomy; while one endeavors to reduce the rate of negative exploration, it is better to have a negative exploration than to miss the diagnosis). If there is an open globe or an open globe is suspected: a. The patient needs urgent (as soon as possible and certainly within 12 hours) repair in the operating room by an ophthalmologist—the necessary arrangements need to be made (this may include transfer to a center with an operating microscope and available ophthalmologist, ophthalmology consult, etc.). Certainly a nil per os (NPO) order needs to be written and intravenous fluids started. b. Place a shield to cover the eye and instruct the patient not to squeeze his or her lids or strain as this may cause further extrusion of intraocular contents; if a metal shield is not available, a cut Styrofoam cup may be taped over the eye. When taping the shield, it is important that the edge of the shield is secure over the orbital rim (i.e., make sure it is not pressing against the globe). c. Order a CT scan to rule out an IOFB if the mechanism of injury suggests this is a possibility. d. Administer tetanus toxoid. e. Intravenous fluoroquinolone antibiotic (moxifloxacin, levofloxacin, or ciprofloxacin) needs to be considered in penetrating injury, especially when this occurred in a rural setting or if an IOFB is present. f. Repair of lid lacerations or orbital fractures should never be undertaken before an open globe has been ruled out or repaired. 3. Identify other orbital or ocular injuries and treat accordingly (see Section “Specific Injuries and their Management”).

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TABLE 20-1 Determination of Ocular Trauma Score

SECTION 3 X

Determination of OTS Vision

Variable No light perception (NLP) Light perception only (LP) or hand motions only (HM) 1/200 to 19/200 20/200 to 20/50 20/40

Raw Score 60 70 80 90 100

Diagnoses

Globe rupture Endophthalmitis Perforating injury Retinal detachment

–23 –17 –14 –11

Sign

Relative afferent pupillary defect

–10

Probability of a Given Visual Outcome Given OTS Score Score

OTS

NLP (%)

LP/HM (%)

1/200 to 19/200 (%)

20/200 to 20/50 (%)

20/40 (%)

0–44 45–65 66–80 81–91

1 2 3 4

74 27 2 1

15 26 11 2

7 18 15 3

3 15 31 22

1 15 41 73

On arrival to the emergency center, an initial pH should be taken by placing pH testing paper in the inferior fornix. Irrigation should continue until the measured pH is neutral (7.2–7.4) for at least 5 minutes after irrigation has stopped. It is important to note that irrigation can last up to an hour or more depending on the severity of the splash injury in order for the eye’s pH to normalize. Irrigation can be performed by directly pouring saline from intravenous tubing to the surface of the eye. Placing one drop of topical ophthalmic anesthetic such as proparacaine may help the patient to keep the affected eye open. Caution should be exercised when placing irrigation lenses such as a Morgan lens since retained particulate matter or foreign body can be trapped in the fornices of the eye. If an irrigation lens is to be used, the superior eyelid should be everted to look for embedded foreign body and both the superior and inferior fornices should be swept clean with a moist cotton swab to remove any particulate matter. Chemical injuries are classified using the Roper-Hall classification system (Table 20-2). The size of the corneal epithelial defect and the clock hours of limbal ischemia should be documented after cessation of irrigation by drawing a circle to represent the cornea. Corneal epithelial defects can be easily detected using topical fluorescein staining, such as a moistened fluorescein strip or manufactured combination of fluorescein and topical anesthetic eye drops. Limbal ischemia appears as blanching of normal conjunctival and limbus blood vessels. Hyperemia in the setting of chemical injury presents better prognosis than a white eye. Successful management of chemical ocular injury is to stop ongoing tissue degradation, promote reepithelialization of the surface, minimize inflammation, and prevent infection. For

grade 1 damage, the patient can be treated with an antibiotic (e.g., erythromycin) or antibiotic/steroid mixed combination eye ointment (e.g., dexamethazone/polymyxin/neomycin) four times a day to the affected eye and a topical cycloplegic agent (e.g., atropine) to decrease ciliary spasm and decrease formation of posterior synechiae.22 For grade 2, topical steroid eye drops may need to be added to the regimen to decrease the inflammatory response for the first 1–2 weeks postinjury. In grades 3 and 4, high-dose vitamin C, 10 ascorbate eye drops, and 10% citrate eye drops have been associated with more rapid recovery and

TABLE 20-2 Classification of Severity of Ocular Surface Burns by Roper-Hall Grade Prognosis I Good II

Good

III

Guarded

IV

Poor

Cornea Corneal epithelial damage/loss Corneal haze, iris details visible Total epithelial loss, stromal haze, iris details obscured but visible Cornea opaque, iris and pupil obscured

Conjunctiva/ Limbus No limbal ischemia 1/3 limbal ischemia 1/3 to 1/2 limbal ischemia 1/2 limbal ischemia

Eye

MECHANICAL INJURY ■ Subconjunctival Hemorrhage Subconjunctival hemorrhage is a very common condition that presents as an ocular emergency. Clinically, subconjunctival hemorrhages appear as flat, bright red blood noted under the bulbar conjunctiva (Fig. 20-2). It can be alarming in appearance and although severity can be variable, in general, it is rather benign and poses no threat to vision. Spontaneous subconjunctival hemorrhage can be due to Valsalva maneuvers, coughing, sneezing, vomiting, or heavy lifting. Minor trauma such as excessive eye rubbing can also cause subconjunctival hemorrhages. Often, no specific etiology can be found. When subconjunctival hemorrhage is noted with other signs of facial or ocular trauma, one must rule out occult globe injury. Obtaining a good history is vitally important to determining if further workup is needed. A history of blunt trauma may present with subconjunctival hemorrhage but the patient may also have orbital fractures that need to be evaluated. Patients who present with complete 360° of subconjunctival hemorrhage from blunt trauma should be examined by an ophthalmologist to rule out possible occult scleral rupture or open globe injury. Clues that may indicate occult open globe injury include: peaked pupil, asymmetric anterior chamber depth, asymmetrically low intraocular pressure, and subconjunctival pigment. In cases of isolated subconjunctival hemorrhage, no treatment is needed. The hemorrhage will usually resolve spontaneously

FIGURE 20-2 Subconjunctival hemorrhage.

in a few weeks. Patients need to be informed that the hemorrhage will change color over the next few days and may expand as the bruising process evolves. These patients typically do not require ophthalmic follow-up.

■ Conjunctival Lacerations Conjunctival lacerations may present in isolation or in combination with damage to deeper layers of the eyewall and the sclera. Isolated conjunctival lacerations do not require surgical repair unless they are large (e.g., 2 cm) or lie over an extraocular muscle insertion. Often it is difficult to assess if the sclera is involved without manipulation using a cotton tip swab to gently push away the conjunctiva exploring the scleral wall beneath. For large conjunctival lacerations or those that may involve the sclera, ophthalmic consultation is warranted. Scleral penetration can be associated with vitreous hemorrhage and if the scleral defect is large enough, vitreous prolapse can be seen as well. If there is vitreous hemorrhage, the patient’s vision may be compromised. It is important to not engage the vitreous prolapsed through a scleral defect since traction on the vitreous strands can lead to retinal tears leading to rhegmatogenous retinal detachments.

Corneal Abrasion Patients with corneal abrasions typically present with intense pain and photophobia. Trauma to the cornea from a fingernail, paper cut, thrown objects, and contusive injury (e.g., air bag) can result in the superficial corneal epithelium being stripped away from the underlying stroma. Simple corneal abrasions can be one of the most painful injuries that patients experience because beneath the corneal epithelium lies an extensive plexus of sensory nerves from the ophthalmic division of the trigeminal nerve and when they become exposed, severe pain results. Corneal abrasions can be diagnosed clinically when topical fluorescein dye is taken up by the area devoid of epithelium and turns bright green viewed with a cobalt blue light. The size and location of the abrasion can be documented using a circle to represent the cornea. Traditional teaching advocated patching for corneal abrasions in the past. Currently, evidence shows that patients heal faster without patching, and also with patching, there is no benefit with regards to pain reduction. Small corneal abrasions without concomitant ocular injury can be managed and treated with antibiotic ophthalmic ointment, topical cycloplegic agent, and topical ophthalmic NSAID (e.g., ketorolac or diclofenac). Although there is no good evidence that topical ophthalmic antibiotic is indicated in cases where there was no recent history of contact lens wear and the injury with organic material, given the devastating sequela of corneal infection and scarring, use of a topical ophthalmic antibiotic is not unreasonable.26–33 History of contact lens wear or injury with organic material raises the risk of infection. These patients should never be patched given the elevated risk of infection, and referred for ophthalmic consultation. Patients with large corneal abrasions may benefit from bandage soft contact lens placed by an eye

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better vision.23 Oral doxycycline is a collagenase inhibitor and may reduce the risk of corneal thinning and perforation in severely burned eyes.24,25 Consultation with an ophthalmologist is necessary for follow-up and ensuring that the treatment regimen is leading to clinical improvement. Rarely is immediate surgical intervention needed in chemical injury patients.

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Management of Specific Injuries care professional for comfort. If the affected eye is patched, the patient should follow up next day with an eye care professional to monitor healing and assess for early signs of infection.

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Corneal Foreign Bodies Corneal foreign bodies are one of the most common forms of ocular trauma presenting second in frequency only to corneal abrasions in emergency centers.34 Most patients present with small superficial corneal foreign body with good or mildly affected vision. Individuals can have debris blown into the eye while walking outdoors or while performing high-risk activities such as grinding, drilling, hammering, and using a leaf blower. There are many causes for corneal foreign body, but lack of protective eyewear contributes to increased risk. Specific questions regarding hammering metal on metal or grinding metal need to be asked and a detailed history regarding exactly the mechanism of injury helps to highlight patients at increased risk for penetrating ocular injury or IOFB. An initial exam should include looking at the corneal surface with magnification; if slit lamp is not readily available, surgical loupes can offer a better exam rather than the naked eye. Often a superficial corneal foreign body will be obvious, but it is important to evert and inspect under the upper eyelid and to look in the inferior fornix as well. After a penetrating injury has been ruled out, superficial corneal foreign bodies can sometimes be easily removed with a moist cotton swab. Instill a topical ophthalmic anesthetic and moisten a sterile cotton swab with anesthetic, and then gently roll across the surface of the cornea and the foreign body may stick to the cotton tip. Irrigation with eyewash can also be utilized to loosen and remove the foreign body. If these maneuvers fail, ophthalmic consultation should be considered. Those foreign bodies that are moderately embedded in the anterior one third of the cornea can be removed at the slit lamp with a TB syringe or 25-gauge needle. Care must be exercised to not go too deep into the corneal tissue. The average central corneal thickness measures only 550 μm. After removal of the corneal foreign body, start treatment as a corneal abrasion with ophthalmic ointment, cycloplegic agent, and topical antibiotic. Follow up with eye care provider to access if further debridement is indicated and to look for early signs of infection.

prognosis.37 Endophthalmitis is a major concern following penetrating injuries. An IOFB also needs to be ruled out. A corneal laceration is evident on examination with a slit lamp biomicroscope although it can be usually seen by oblique illumination with a penlight. It is important to realize that smaller corneal lacerations can self-seal or be plugged by iris (which can result in a peaked pupil), allowing normal vision and a formed anterior chamber with normal or near-normal intraocular pressure. It is critically important to realize that eyes that have sustained a self-sealing laceration are first still at risk of endophthalmitis particularly if there is an IOFB and second are at risk for further extrusion of intraocular contents/low intraocular pressure if the patient applies pressure at immediately behind the laceration—say by rubbing the eye. Sadly, we have seen several eyes with undiagnosed self-sealed lacerations that developed endophthalmitis that was erroneously treated as traumatic iritis with steroids by unsuspecting emergency room physicians or pediatricians (with disastrous effects for the eye). Corneal lacerations can be full thickness or partial thickness (lamellar laceration). A full-thickness laceration is classified under the general diagnosis of open globe. With lamellar or partial thickness lacerations, the globe is considered closed. The diagnosis of a full-thickness corneal laceration is often easy to recognize when there is protruding iris or uveal tissue (Fig. 20-3). In these cases, the anterior chamber may also be shallow or flat, which can be seen when shining a penlight from the lateral or temporal side of the eye. Some corneal lacerations may be combined and encompass the limbus and extend into sclera (aka corneal–scleral laceration). As with all open globe injuries, extreme care must be taken to prevent any direct pressure on the eye that may result in extrusion of intraocular contents. If corneal laceration is suspected, a metal shield (aka Fox shield) should be placed over the affected eye. The goal is to prevent any direct pressure or contact on the globe; soft eye patch should be avoided. For partial thickness lacerations, depending on the size and depth of the laceration, simple observation with topical antibiotic prophylaxis up to suturing the partial thickness flap may be warranted. Due to the expertise needed to evaluate the depth of

Corneal Lacerations Corneal rupture is unusual unless the patient has had previous penetrating keratoplasty (corneal graft) or radial keratotomy. In the former case, dehiscence at the junction of the graft with the host cornea is common. In the latter, rupture occurs along the keratotomy as the cornea is very thin in that location. Loss of the crystalline lens or intraocular implant through the rupture site is sometimes observed. Management is by emergent operative repair, by closing the rupture site with 10-0 nylon sutures. Corneal and/or scleral lacerations have better prognosis than ruptures with about 50% retaining vision of 20/40 or better (driving vision).35,36 Scleral/corneal lacerations limited in location to being anterior to the insertion of the recti muscles and those having a length 10 mm are associated with a better

FIGURE 20-3 Corneal laceration with protrusion of iris.

Eye the laceration with a slit lamp, ophthalmic consultation should be sought in corneal lacerations.

Scleral rupture occurs in about 3.5% of eyes with severe blunt trauma.38 It most commonly involves the sclera immediately posterior to the recti muscle insertion (about 6–7 mm posterior to the limbus) as the sclera is thinnest at that location; in patients who have had previous surgery involving the sclera (most commonly a glaucoma filtration surgery) rupture at the site of the previous scleral wound may also occur. Scleral rupture is invariably accompanied by rupture of the highly vascular choroid or ciliary body. As a result, hemorrhagic chemosis, hyphema, vitreous hemorrhage, or a combination of these is invariably present.38 Prolapsed uveal tissue appears dark brown or black while prolapsed vitreous gel appears as a transparent or blood-tinged blob of gel; since the mechanism of scleral rupture is due to an extreme elevation of intraocular pressure at the moment of blunt impact, the force causing the rupture is from the inside—prolapse of intraocular contents is therefore not uncommon, although it can be difficult to discern clinically as it may be covered by the hemorrhagic chemosis of the conjunctiva. Signs with the greatest specificity are a low intraocular pressure (6 mm Hg), anterior chamber depth asymmetry (can be abnormally shallow or deep compared to fellow eye), and vision poorer than hand motions.35,38 Scleral rupture generally has poor outcomes with only 30–35% of eyes regaining ambulatory vision (i.e., vision that allows getting around without a guide).36 Moreover, scleral rupture is a risk factor for enucleation with up to 40% of eyes with scleral rupture being enucleated.7,12,35,36 Particularly poor predictors are scleral rupture greater than 11 mm, golf ball injury, and presenting vision of hand motions or worse.12,35 Treatment is by operative repair for scleral ruptures anterior to the equator that consists of excising necrotic uveal tissue, repositing viable uveal tissue and retina into the globe, and approximating the scleral edges using 8-0 nylon sutures. Posterior scleral ruptures are not accessible for repair (to access the posterior sclera, one would have to disinsert one or more of the recti muscles and pull to turn the eye that would cause further extrusion of intraocular contents making matters worse) and are allowed to heal by secondary intention.

■ Traumatic Hyphema Hyphema is when blood accumulates in the anterior chamber (Fig. 20-4). It can present even after minor trauma in patients with impaired coagulation either idiopathic or medically induced. The presentation includes pain, photophobia, and decreased vision and on further examination with a penlight, a reddish pool of blood can be seen layered toward the inferior half of the anterior chamber due to gravity. If a patient has been recumbent, due to gravity, the hyphema may be layered over the pupil precluding a clear view to the posterior segment. The estimated annual incidence of hyphema is 17 patients in 100,000. The mean age of presentation is 25 years old with a higher prevalence in men over women. A hyphema does not rule out an open globe injury and up to one third of patients with traumatic hyphema can have concomitant open globe

Special Situation: Trauma in LASIK Patients In 2007, more than 800,000 Americans underwent LaserAssisted In Situ Keratomileusis (LASIK) vision correction surgery.39 The first clinical trial for LASIK refractive surgery was performed in 1995 and it has been a growing surgical procedure for the past 10 years. To perform LASIK, a thin corneal flap is first made and folded back to allow for laser remodeling of the corneal stroma. The flap is most commonly hinged either superiorly or nasally and floated back into position once laser remodeling is completed without any need for suturing. Since this is commonly done as an outpatient procedure in an ophthalmologist’s office or laser center, most patients do not consider this a significant part of their medical history.

FIGURE 20-4 Hyphema.

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Sclera Laceration or Rupture

It is important to recognize that both early and late traumatic flap dislocation and amputation have been reported in the literature. There are case reports of LASIK flap complications up to 7 years postsurgery. Minor blunt traumas with fingernail or sports-related injuries have been the reported cause of flap dislocation and amputation.40–42 Patients with LASIK flap dislocation and amputation will typically present with decreased vision and pain, and a very similar history to simple traumatic corneal abrasion patients. In fact, a complete amputation of the LASIK flap can look very much like a large corneal abrasion with fluorescein staining since the corneal epithelium is lost with the flap. LASIK flap dislocation and amputations are treated very differently than a simple traumatic corneal abrasion and patients will need consultation with an ophthalmologist, preferably a corneal-refractive surgeon. Prognosis for early flap dislocation has generally been good and with later flap dislocation, vision recovery is generally acceptable. For patients with flap amputation, prognosis is poor due to development of irregular astigmatism and corneal haze and scarring. Given the large number of patients who have undergone this very popular procedure over the past 15 years, it is crucial to always ask specifically regarding prior history of refractive or LASIK surgery.

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affected eye to protect from further injury. Depending on the interval until the patient is seen by an ophthalmologist, routine treatment for hyphema can be initiated with topical steroid eye drops (i.e., prednisolone acetate 1%) four times a day and a topical cycloplegic agent (i.e., 1% atropine) twice a day.

Traumatic Iritis/Mydriasis/ Iris Sphincter Tears/Iridodialysis

FIGURE 20-5 Hyphema and lid lac.

injury.43 Patients can also present with eyelid injuries or orbital fractures concurrently with hyphema (Fig. 20-5). Concussive injury causes equatorial expansion of the eyeball with resulting damage to the iris, ciliary body, and major arterial circle of the anterior segment. Depending on the level of force exerted, differing levels of bleeding can be seen. Some patients may only have a microhyphema where a very small amount of red blood cells circulates in the anterior chamber but not enough blood is present to collect in the inferior part of the anterior chamber. These patients generally have very mild symptoms and can be managed similarly to traumatic iritis patients. For patients who suffer more severe bleeding, the hyphema may completely fill the anterior chamber, also known as an “eight-ball” hyphema obscuring all anterior chamber details. Typically, the grading scale for hyphema is described by using an estimated percent layered in the anterior chamber. For example, a hyphema reaching mid-pupil level could be described as “50%” layered hyphema. At the initial encounter, visual acuity, intraocular pressure, and grading of the hyphema severity should be documented. For patients of African American descent and others with known risk factors for hemoglobinopathies, a sickle cell prep or hemoglobin electrophoresis should be ordered along with other initial laboratory workup. This will provide important information for intraocular pressure management. For individuals with sickling hemoglobinopathies, carbonic anhydrase inhibitors are contraindicated and, thus, those who have elevated intraocular pressures may need surgical intervention. For any patient with a layered hyphema regardless of percentage, an ophthalmic consultation is warranted since these patients will need close follow-up for the first 5 days after initial injury when the risk of rebleeding is highest. Also, patients who suffer concussive injury great enough to cause a layered hyphema are likely to have concomitant injury to other intraocular structures and have an increased risk of traumatic glaucoma resulting in permanent blindness in the future. For patients who will need to be transferred for ophthalmic consultation, a clear or metal eye shield should be placed on the

With minimal blunt trauma to the eye, patients may suffer a mild inflammatory reaction known as traumatic anterior uveitis or traumatic iritis. Patients generally present with mild blurry vision, eye pain, and light sensitivity or photophobia. The symptoms can be immediate or delayed for 24–48 hours and examination often will reveal nothing more than mildly red eyes or conjunctival injection. However, if a slit lamp examination is done, an inflammatory reaction with circulating cells and flare can be seen in the anterior chamber. Most cases will resolve within 1–2 weeks with topical steroid eye drop (1% prednisolone acetate, four times a day) and topical cycloplegic agent (1% atropine, twice a day). When prescribing cycloplegic agents, it is important to inform the patient that objects at near will be blurry in the treated eye due to the loss of accommodation from pharmacologic dilation. In patients who have long-standing anterior uveitis from any etiology, posterior synechiae or iris–lens adhesions can form. The use of a topical cycloplegic agent is not only for patient comfort but also as a preventative measure against formation of posterior synechiae (Fig. 20-6). With more forceful blunt trauma, patients may suffer direct damage to the iris sphincter causing tears or traumatic mydriasis (seen near the pupil) or to the iris base causing iridodialysis (seen near the limbus). On initial examination, patients with traumatic mydriasis (dilation) or iris sphincter tears will have unequal pupil size and contour. Most patients may not complain acutely of symptoms but some will note the difference between the affected and unaffected eye in a mirror and question the etiology. There is no acute treatment for sphincter tears and traumatic mydriasis other than to treat the associated traumatic iritis.

FIGURE 20-6 Posterior synechiae.

Eye intraoperative risks, modern techniques for cataract removal are quite successful and yield excellent vision provided there are no retinal or optic nerve abnormalities.

Lenticular Foreign Body Lenticular foreign body refers to the unusual occurrence of a small foreign body, usually metallic, being retained within the crystalline lens.44–46 On many occasions these have been well tolerated for many years without adverse effect as the anterior capsule heals over the site of entry into the crystalline lens. Indeed, toxicity would be expected to manifest by cataract formation and then prompt surgical removal by phacoemulsification would be advised.

■ Vitreous Hemorrhage ■ Traumatic Lens Injury Lens Dislocation/Subluxation The lens is suspended like a hammock behind the iris by fibers called zonules that attach to the ciliary body and to the equator of the lens capsule. The lens is part of the total visual system and helps with vision and accommodation. Without the natural lens in position, patients would need a contact lens or intraocular lens placed to help visual rehabilitation. Thus, patients who suffer from lens dislocation will complain of decreased vision as well. Three major traumatic injuries to the lens are lens dislocation/subluxation, traumatic cataract, and intralenticular foreign body. With blunt trauma, the zonules may break and cause the lens to dislocate either partially or completely depending on the amount of support remaining. A sign of zonular fiber loss may be seen at the slit lamp as iridodonesis, where the iris “jiggles” with rapid eye movements, or phacodonesis, where the lens shakes or moves with rapid eye movements. Typically, emergent intervention is not needed for lens subluxation or dislocation unless the lens is dislocated into the anterior chamber causing pupillary block, where the lens is obstructing aqueous flow from behind the pupil, or corneal endothelial decompensation, where the lens is in contact with the corneal endothelium. Patients who have a history of prior cataract surgery with artificial intraocular lens placement can also experience artificial lens dislocation. They will also experience a decrease in vision since the artificial lens acts as a substitute for the natural lens and is part of the total visual system. Surgical intervention can usually be done to reposition or replace the intraocular lens as an outpatient on an elective basis.

Traumatic Cataract Traumatic cataracts are generally seen months to years after the acute episode. They can result from blunt trauma, penetrating trauma, electrical shock, and ionizing radiation. Unilateral vision loss in young adults is most commonly due to unilateral traumatic cataract, most likely due to not only accidental trauma but also sports-related activities that routinely have associated blunt trauma such as boxing, soccer, and martial arts. Although traumatic cataracts may pose additional

Vitreous hemorrhage occurs in 30% of eyes with serious trauma. Its presence attests to the severity of the injury and is a marker for concomitant injury that is harder to detect due to its presence. Vitreous hemorrhage is invariably present in eyes with scleral rupture and may be present in penetrating injuries. In closed globe injury, it may be associated with iris sphincter tears, hyphema, and lens dislocation, while in the posterior segment associated findings include retina tear/detachment, traumatic macular hole, choroidal rupture, and traumatic optic neuropathy.47 Eyes with vitreous hemorrhage need to be examined carefully to rule out occult scleral rupture or laceration and concurrent retinal tears or detachment. If the severity of the vitreous hemorrhage does not allow sufficient visualization of the retina, B-mode ocular echography to detect retinal tears or detachment can be utilized as an acceptable alternative to direct visualization. It should be noted that when the vitreous hemorrhage is very severe, it is impossible to reliably detect a retinal detachment. In the case of closed globe injury, management includes observation for 4–6 weeks as spontaneous resolution is common, with vitrectomy if faster visual rehabilitation is desired. Recently it has been suggested that early vitrectomy can prevent retinal complications, although convincing evidence for this is lacking thus far.

Intraocular Foreign Body IOFBs are present in 30–40% of open globe injuries.48–50 In the vast majority (85%) the patient is male.48,50–52 The IOFB is typically metallic (90%), usually iron, and results from hammering (60–70%) or use of a high-speed rotary tool.49,51,52 Glass foreign bodies can be found after car accidents, explosive blast injuries typically associated with terrorism, or assault with beer bottle.53 Stone and concrete represent less than 2% of IOFB, except in combat trauma where they are common after eye injury following explosion of roadside improvised explosive devices (IEDs).49–51 The majority of IOFBs are in the posterior segment (75%).52 Patient symptoms are dictated by the possible concomitant injury or complication (corneal laceration, scleral laceration, cataract, vitreous hemorrhage, endophthalmitis, retinal detachment). In every case of corneal or scleral laceration, even when self-sealing

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With significant blunt force trauma, the longitudinal and radial fibers of the iris root can be torn apart at the ciliary body causing an iridodialysis. The diagnosis can easily be made with a penlight exam. The separation can occur at any clock hour and often will look as though a second pupil has been formed near the limbus. Sometimes, patients with large iridodialysis will complain of diplopia (seeing double) in the affected eye due to images being projected through the pupil and also simultaneously, the new iris defect. Patients who suffer iris trauma need to be followed up with an ophthalmologist to monitor resolution of the inflammatory reaction and intraocular pressure, and assess potential damage to other anterior segment structures. For some patients with extensive iris damage, reconstructive anterior segment surgery may be warranted.

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(i.e., not requiring operative repair), it is critically important to rule out IOFB by helical CT of the orbits. Additionally, any time a patient presents with ocular pain after hammering and subconjunctival hemorrhage, CT is essential to rule out IOFB as a scleral laceration may be present under the hemorrhage. IOFBs are associated with an increased incidence of endophthalmitis that results in poorer visual outcomes after penetrating injury.54,55 Additionally, copper foreign bodies may incite severe inflammation and in the long term retained IOFBs may lead to retinal toxicity (e.g., iron IOFBs lead to ocular siderosis which among other effects leads to loss of vision due to retinal toxicity).56 While there is agreement that primary repair of open globe injury should be undertaken emergently, the timing of IOFB removal is controversial.52,54,57–59 IOFB removal from the posterior segment is usually performed by pars plana vitrectomy although for ferromagnetic IOFBs an external magnet can be used for smaller IOFBs if the requisite expertise for performing pars plana vitrectomy is not available.58–60

Retinal Contusion Commotio retinae (Berlin’s edema) is the term used to describe the opacified retina observed as a result of closed globe contusion injury to the retina. If the macula is involved, the vision will be affected. Spontaneous resolution is the rule with the long-term prognosis determined by concomitant retinal pigment epithelium injury. Contusion of the retinal pigment epithelium is infrequently described, yet it is a common sequela of closed globe injury characterized by atrophic changes and mottling of the retinal pigment epithelium in the long term. It is an important cause of limited vision following such injury.61

Retinal Detachment Retinal tears/dialyses and detachment may arise following closed or open globe injury. The difference between retinal tears and dialyses is beyond the scope of this text but is significant when considering surgical repair of a detachment. Following closed globe injury, the sudden expansion of the equatorial region of the eye results in the forced separation of the vitreous from the retina; in young individuals the vitreous may adhere strongly to the retina and its forced separation may result in tears in the retina or retinal dialysis. Usually vitreous hemorrhage (which can be very minor) occurs concomitantly due to bleeding from the vascular retina. In about 85% of patients with retinal tears or dialyses fluid passes under the tear/ dialysis causing the retina to float away from the choroid, which is a retinal detachment.62 Patients with retinal tears may report floaters (black dots or “spider”-like opacities in their vision that move as the eye moves), while patients with a retinal detachment report a visual field defect (“dark area” or “curtain” in the vision, “like seeing underwater”). If the retinal detachment advances to include the fovea, patients will also report blurred vision. Timely treatment of retinal tears with laser retinopexy (or cryopexy) to reinforce the adhesion between retina and retinal pigment epithelium will prevent retinal detachment. Given that most traumas

involve young individuals whose vitreous is more gel than fluid, only 12–30% of traumatic retinal detachments present immediately after trauma while 20% present more than 1 year after trauma.62–64 There is therefore ample opportunity to prevent retinal detachment after closed globe injury and it is imperative that a thorough examination of the fundus by indirect ophthalmoscopy by an experienced ophthalmologist is performed within a few days after such injury. If a retinal detachment occurs, timely treatment (before the fovea is involved) can lead to preservation of excellent vision— therefore, a retinal detachment not involving the fovea needs to be repaired within 24 hours. Once the fovea is involved, the vision will never be normal; patients presenting with fovea-involving retinal detachments need to undergo repair within 1 week of presentation. When retinal detachments are not treated promptly, proliferative vitreoretinopathy (a process of scar formation in the vitreous cavity) supervenes and surgical outcomes are poorer (both anatomic and visual outcomes) and there is a greater risk of phthisis bulbi (globe becoming shrunk with opacification of the cornea). Treatment of retinal detachments is by scleral buckling if the cause is a dialysis, pars plana vitrectomy if there is a giant retinal tear, and pars plana vitrectomy or scleral buckling if the cause is a retinal tear.65,66 In open globe injury retinal tears commonly arise by the same mechanisms as in closed globe injury but may also be the direct result of the penetrating or perforating injury (e.g., a sharp projectile penetrating the eyewall and the choroid and retina causing a retinal tear); IOFBs may cause further retinal tears at the site of internal impact on the retina. Moreover, a hemorrhagic retinal detachment may arise from bleeding under the retina. Retinal detachment occurs in approximately 20% of open globe injuries.67 Treatment is by pars plana vitrectomy.

Traumatic Macular Hole Traumatic macular holes usually arise as a consequence of blunt ocular trauma, typically from a fist or finger, a champagne cork, a ball (baseball, softball, soccer ball, tennis ball usually), or rubber band.68–70 The typical symptom is a blurring of the central vision. It should be noted that development of a traumatic macular hole may be delayed by a few days or weeks following trauma. Anatomic closure occurs spontaneously in 44–64% within the first 4–6 months.71,72 Pars plana vitrectomy with lifting of posterior hyaloid face and gas endotamponade successfully closes macular holes in up to 96% of patients and is indicated after a period of observation for spontaneous closure, 3–4 months.68–70 Improvement in vision usually accompanies anatomic closure but may be limited by RPE mottling/atrophic changes due to RPE concussive injury.

Chorioretinitis Sclopetaria Chorioretinitis sclopetaria is a rare type of closed globe contusion injury due to a high-velocity projectile grazing the globe without penetrating it. Ophthalmoscopically there is a white area as sclera is visible surrounded by hyperpigmentation adjacent to the path of the projectile while remote to the path of the projectile is an area of hyperpigmentation and RPE atrophic

Eye

changes with a characteristic severe epiretinal membrane, usually at the macular area.73,74 These appearances become apparent several weeks after the injury while immediately they are typically obscured by vitreous hemorrhage.73,74

Endophthalmitis Endophthalmitis is a devastating complication of ocular trauma occurring in 1–11% open globes,52,55,75–78 with a higher incidence (4–30%) when IOFBs are present.52,54,76 Delayed primary closure, presence of IOFB, disruption of the lens capsule, rural setting of injury, and possibly posterior segment involvement increase the risk of endophthalmitis.54,55,75,78 Common microorganisms are streptococci, staphylococci (especially with IOFBs), and Bacillus cereus, while gram-negative organisms occur in about 10% and fungi in fewer than 5% of injuries.54,77–79 Symptoms include severe to extreme pain, sensitivity to light, and decreased vision. Hypopyon (white blood cells/pus collection in the anterior chamber), fibrin in the anterior chamber (Fig. 20-7), vitreous inflammation, and sheathing of vessels are characteristic.78 Other signs commonly present are chemosis and erythema of the conjunctiva (which can be severe), severe tenderness, and lid edema. Sadly, we have seen several patients over the years misdiagnosed as having only traumatic iritis, which rarely would present with hypopyon or severe tenderness. Endophthalmitis is a true ophthalmic emergency and in the case of virulent microorganisms such as Bacillus a few hours can make the difference between retaining the globe and losing it to phthisis. Suspicion of endophthalmitis should prompt an emergent ophthalmology consult and institution of systemic treatment with a fluoroquinolone (ideally fourth generation) as fluoroquinolones have excellent penetration into the vitreous and they are effective against B. cereus.80 Definitive management is by injection of intravitreous antibiotics with vitrectomy for selected cases.

■ Choroidal Rupture Rupture of the choroid accompanies closed globe trauma more often than open globe trauma and is usually a consequence of

■ Traumatic Optic Neuropathy Sharp objects, projectiles, or bone fragments may directly damage the optic nerve (direct traumatic optic neuropathy). Direct optic neuropathy is associated with severe loss of vision with little prospect of improvement. If suspected, imaging of the optic nerve (orbital CT) is recommended to detect the rare case where surgical relief of impingement of the optic nerve may improve vision. More commonly, however, traumatic optic neuropathy results from concussive head injury, especially involving impact to the forehead (indirect traumatic optic neuropathy). In indirect optic neuropathy, impact forces are transmitted from the frontal bone to the orbital bones and concentrated in the area of the optic canal causing a shearing injury to neuronal axons of the intracanalicular portion of the optic nerve.85,86 Patients with indirect traumatic optic neuropathy are usually young, male (85%), have commonly lost consciousness, and have typically sustained their injury as a result of involvement in a motor vehicle or bicycle accident (about 50%), fall, or assault.87,88 Patients notice a typically unilateral decrease in vision immediately or after regaining consciousness.87,88 The severity of visual loss is often dramatic (40% have NLP and a further 23% only have light perception or hand motions vision). In cases with less dramatic visual loss, symptoms may include visual field defects and abnormalities of color vision.87,88 On examination an RAPD is present but the fundoscopic examination is normal until several weeks after the injury when optic nerve pallor/atrophy becomes apparent. Spontaneous improvement has been reported in up to 57% of patients with indirect traumatic optic neuropathy.87,88 The regimen employed in the Second National Acute Spinal Cord Injury Study (NASCIS) of an initial dose of 30 mg/kg methylprednisolone followed by continuous infusion of 5.4 mg/(kg h) for 24–48 hours has been used for the treatment of traumatic optic neuropathy despite lack of evidence for efficacy in this condition.87–92 Indeed, several comparative studies have failed to show benefit from the use of megadose or high-dose

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FIGURE 20-7 Hypopyon in an eye with corneal laceration and iris protrusion.

injury with a ball (soccer ball), other large projectile (rock, shoe, etc.), or fist.81,82 The choroidal rupture appears as a white crescent, typically concentric to the optic nerve and within the macula (70%).81,82 Vision immediately following injury may be limited if the choroidal rupture is through or adjacent to the fovea or from associated subretinal hemorrhage (which resolves). A treatable, long-term complication of choroidal ruptures in the macula, especially in older individuals, is choroidal neovascular membranes (CNVM: growth of new vessels from the choroid under the retina which tend to leak fluid or cause hemorrhage). Off-label intravitreous injection of bevacizumab or photodynamic therapy for CNVM due to choroidal rupture may lead to excellent visual outcomes if the patient presents early.83,84 Therefore, it is critically important to educate patients with choroidal rupture at risk of developing CNVM that if they develop a sudden change in vision or metamorphopsia (distortion in vision so that straight lines appear curved), they should see an ophthalmologist at once.

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corticosteroids over placebo for indirect traumatic optic neuropathy.87,88,93 Moreover, recently the CRASH study demonstrated excess mortality for patients with significant closed head injury who were given corticosteroids compared to placebo.94 Therefore, the role, if any, of megadose steroids in the treatment of this condition is controversial. Finally, surgical decompression has been performed with encouraging results in several case series but with no evidence that results are superior to observation.95

Optic Nerve Avulsion Optic nerve avulsion is a specific type of indirect traumatic optic neuropathy with a distinct pathogenesis. In optic nerve avulsion a blunt object (typically a finger, unusually a snooker cue or golf club) is inserted between the globe and orbit and causes abrupt rotation of the globe as well as a sudden increase in intraocular pressure resulting in retraction of the optic nerve within its dural sheath. The clinical appearance is striking once the accompanying hyphema or vitreous/subhyaloid hemorrhage clears: there is a hole or cavity where the optic disc has retracted within its dural sheath.96,97 Prognosis is guarded, with limited potential for spontaneous improvement and no effective treatment.

■ Eyelid Lacerations The approach to a patient with eyelid trauma must be systematic and take into account a detailed history to rule out open globe injuries that may preclude repair of the eyelid until the globe can be surgically closed. There are multiple types of eyelid injury and a patient can have more than one type depending on the mechanism of injury. These include: 1. Contusion: blunt impact injury with superficial soft tissue swelling and ecchymoses 2. Abrasion: scraping causing superficial epithelial skin loss 3. Avulsion: shearing or tearing away of tissue 4. Puncture: defect through multiple tissue planes caused usually by sharp objects 5. Laceration: cut tissue can be superficial or deep, usually caused by sharp objects For patients with isolated eyelid contusion and abrasion, conservative medical management with ice packs and antibiotic ointment is usually all that is required. Given time, the healing and reepithelialization of the skin gives good results. For eyelid avulsion, puncture, and laceration, surgical repair is generally needed. Depending on the patient’s age, mental status, and size of injury, repair may be done at the bedside with local anesthesia, preferably with 2% lidocaine with epinephrine for better hemostasis. Deeper tissue involvement, full thickness, marginal, or lacrimal duct involvement will generally require involvement of an ophthalmologist or oculoplastic surgeon to repair. Signs that may clue into deeper tissue involvement include orbital fat prolapse, exposed sclera under the laceration, and medial canthal involvement. Once an eyelid laceration is suspected, a plan to explore the extent of the injury needs to be formulated. Since soft tissue swelling can distort the natural anatomy and create the

FIGURE 20-8 Lid lac.

false impression of missing tissue due to excessive tension when approximating tissue margins, ice packs applied to the wound can help to decrease swelling before manipulation. Importance is given to be sure that an occult open globe injury has been ruled out before exploration of the eyelid laceration (Fig. 20-8). When exploring an eyelid laceration, anesthetize the tissues prior to cleansing and gently pull lacerated tissues apart during your inspection as fibrin tends to hold these lacerated edges together giving an inaccurate impression on the level of deep tissue involved. It is important to reapproximate the deep tissue layers to avoid undue excess tension on the superficial layers. The timing of eyelid laceration repair is more forgiving than most other ocular injuries due to the well-vascularized tissues of the eyelid. In some cases of extensive swelling, waiting 24–72 for eyelid repair can give a better anatomic and cosmetic result. For subcutaneous closure, an absorbable suture is preferred such as 5-0 polyglactic acid (Vicryl®, Ethicon, Somerville, NJ) on a spatulated needle to close deeper tissues. This same suture size can be used above and below the brow or to secure tissue to the periosteum. For skin closure, nylon suture is preferred because it creates the least amount of inflammation, but if follow-up for removal of the sutures in 7–10 days cannot be assured, it is better to use an absorbable suture. 6-0 sutures can be used for closure above and below the brow; some oculoplastic surgeons advocate using a smaller suture size such as 7-0 for closure below the brow.

■ Orbital Fractures Patients with orbital injuries such as orbital wall and floor fractures typically will have concomitantly significant facial trauma. These patients will need to be simultaneously managed with head and neck, oral maxillofacial, or plastic surgeons. An orbital CT scan should be obtained to optimally diagnose and manage orbital injuries. Many times, specific orbital cuts can be added to a standard face CT scan protocol when initially ordered to evaluate the patient with facial trauma. Neurosurgery consultation may be necessary for patients with orbital roof fractures, which can happen after significant

Eye

Intraorbital Foreign Bodies Intraorbital foreign bodies can result from both blunt and sharp objects, usually as a result of assault, industrial accidents, accidents at home, or recreational activities. They can cause vision loss if the globe is involved, or in case of neurologic damage from intracranial extensions. A high index of suspicion is important in evaluating patients with recent or remote history with persistent periocular inflammation. Signs and symptoms of retained intraorbital foreign bodies include: 1. Orbital mass 2. Proptosis 3. Painful or restricted eye movements

4. 5. 6. 7. 8. 9.

Diplopia Ptosis Lagophthalmos Orbital cellulitis Draining sinus tract Gaze-evoked amaurosis (transient loss of vision)

An orbital CT scan is the preferred imaging modality since metallic foreign bodies are contraindicated for MRI scan; once a metallic foreign body is ruled out, an MRI scan may be better at detecting organic matter such as wood. Depending on the size and extension of the foreign body, neurosurgery and/or otorhinolaryngology consultation may be necessary to safely remove the foreign body. Not all orbital foreign bodies need to be removed. Certain inert metals, glass, plastic, and silicone can be left in place as long as there is no optic nerve impingement. Foreign bodies made from iron should be removed since long-term toxicity can occur leading to vision loss and retinal damage from siderosis.

Orbital Compartment Syndrome The orbit is susceptible to compartment syndrome due to its small size and the bony walls of the orbit lacking the ability to stretch or flex. The normal orbital volume is 30 cm3. Trauma directly to the orbit or to other regions of the face resulting in fractures can cause bleeding into retrobulbar, subperiosteal, extraconal, and/or intraconal spaces of the orbit with rapid expansion in orbital distention. Rapid escalation in orbital compartmental pressure can cause ischemia of the orbital tissues and increased intraocular pressure can lead to damage and permanent vision loss. Patients with large orbital floor and wall fractures have less risk for developing orbital compartment syndrome since the orbital contents can be decompressed into the sinuses. Proptosis and taut orbital content or increased resistance to retropulsion on examination is always seen in orbital compartment syndrome. Depending on the extent of orbital congestion, patients with mild compartment syndrome have only mildly elevated intraocular pressures without visual compromise, and can be treated with glaucoma agents topically or orally. Once intraocular pressures exceed 40 mm Hg despite antiglaucoma therapy in an orbital compartment syndrome patient, close monitoring of vision and pupillary response will help guide need for lateral canthotomy and cantholysis. On the rare occasion, a patient may have bleeding into the optic nerve sheath causing direct impingement and compression of the optic nerve, or a bony fragment from posterior fractures can compress on the optic nerve causing an RAPD. Thus, reviewing the orbital imaging is important to rule out such cases that will need to be referred to an oculoplastic surgeon for urgent optic nerve sheath fenestration. Patients with mild compartment syndrome should not have any signs of optic nerve compromise and a patient with an RAPD and decreased vision may need urgent decompression with emergent canthotomy and cantholysis of the lateral canthal tendon performed at the bedside. This works to allow the taut orbital content to prolapse anteriorly out of the orbit.

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trauma, usually from motor vehicle accidents or falls from heights. These fractures can often include complications of CSF leaks due to dural tears, intracranial hemorrhage, traumatic encephalocele, and brain abscesses or meningitis. The orbit is comprised of many bony structures with the purpose of protecting the globe. The orbital roof and lateral wall have the thickest walls. The thinnest wall is the medial wall comprised of the ethmoidal bone, also known as the lamina papyracea, and the orbital floor medal to the infraorbital groove. Contusive orbital injuries can lead to a “blowout” fracture of these thin areas. The quality of the thin bones in orbital blowout fractures actually provides a protective feature, where a large area of the orbital floor and medial wall has given way allowing for decompression of the orbital contents. This expanded volume into the sinuses allows for decreased congestion in the orbital space. A pure blowout fracture does not include fracturing of the orbital rim. When evaluating a patient with potential orbital fracture, one of the clues to diagnosing an orbital floor fracture is decreased skin sensation on the cheek of the affected side. The infraorbital nerve, a branch of the trigeminal nerve, travels through the infraorbital canal and within the floor to exit just under the inferior orbital rim at the infraorbital foramen. This nerve is often affected when traumatized by orbital floor fractures and presenting with hypoesthesia of the cheek. Another clue can be subcutaneous emphysema that often results from the patient blowing his or her nose forcing air into the tissues. Since up to one third of patients with orbital blowout fractures will have other accompanying ocular injuries, such as corneal abrasion, iritis, hyphema, ruptured globe, retinal detachment, and retinal hemorrhage, it is important to examine these patients systematically with the eight-point eye exam to diagnose correctly and treat more sight-threatening conditions first. Once an orbital wall or floor fracture has been diagnosed, patients must be given instructions to not blow their nose since this can cause further expansion of air into the orbital tissue and can lead to a tight orbit and elevated intraocular pressure. Patients can use ice packs during the first 48 hours to help with reduction of the soft tissue swelling and for patients who need surgical repair, this is usually done in the next 1–2 weeks. Management and treatment of orbital floor fractures will be discussed in Chapter 21.

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Success is measured by improved vision, lower intraocular pressure, and reversal of optic nerve compromise or RAPD. If the orbital compartment syndrome is not decompressed adequately with a lateral canthotomy and cantholysis, consultation with an oculoplastic surgeon is warranted to decompress the orbit via bony decompression. Steps to perform a lateral canthotomy and inferior cantholysis are as follows: 1. Obtain informed consent if patient is able to cooperate. 2. Prep and drape the affected eye. 3. Anesthetize with 2% lidocaine with epinephrine in the lateral canthal region. Make sure to infiltrate subcutaneously and subconjunctivally. 4. Allow the anesthetic to take effect and clamp a hemostat over the lateral canthus vertically; this will help direct the cut in the next step. 5. Using Steven scissors, place one blade on the conjuntival side of the later canthus and the other blade on the skin surface, and then cut the lateral corner of the eyelid while applying lateral pressure. 6. The inferior crus of the lateral canthal tendon will need to be cut to release the lower eyelid from the lateral orbital wall. Taking the scissors with blades closed, strum the inferior tendon inside the cut canthotomy wound. The attachment should feel like a firm, tense cord. Now, open the blades of the scissors and cut the cordlike structure until the lower eyelid becomes freely mobile. 7. Hemostasis can be achieved with pressure or the use of handheld cautery if available.

WHEN TO OBTAIN CONSULTATION WITH AN OPHTHALMOLOGIST While some cases will be grossly evident in need of a consultation with ophthalmology (Fig. 20-9), others may be more subtle, such as an occult scleral laceration or open globe injury from a full-thickness eyelid laceration (Fig. 20-10). The key in successfully managing patients with ocular injury is to perform

FIGURE 20-9 Intraocular foreign body.

FIGURE 20-10 Open globe.

a systematic exam and use a common vocabulary to communicate those findings with the consultant. The role of the emergency care provider or trauma surgeon with regards to ocular trauma is to recognize common traumatic eye injuries that can be managed immediately and be able to refer sight-threatening conditions appropriately for ophthalmic follow-up. While there are a few true ophthalmic emergencies—open globe, chemical injury, endophthalmitis, and orbital compartment syndrome—many isolated ocular injuries in an otherwise healthy individual can often be managed outside of the emergency room setting. Like injury to any other organ system, potential long-term complications require follow-up with specialists.

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14. Kilmartin DJ, Dick AD, Forrester JV. Prospective surveillance of sympathetic ophthalmia in the UK and Republic of Ireland. Br J Ophthalmol. 2000;84:259–263. 15. Castiblanco CP, Adelman RA. Sympathetic ophthalmia. Graefes Arch Clin Exp Ophthalmol. 2009;247:289–302. 16. Sen HN, Nussenblatt RB. Sympathetic ophthalmia: what have we learned? Am J Ophthalmol. 2009;148:632–633. 17. du Toit N, Motala MI, Richards J, et al. The risk of sympathetic ophthalmia following evisceration for penetrating injuries at Groote Schuur Hospital. Br J Ophthalmol. 2008;92:61–63. 18. Galor A, Davis JL, Flynn HW, et al. Sympathetic ophthalmia: incidence of ocular complications and vision loss in the sympathizing eye. Am J Ophthalmol. 2009;148:704–710. 19. Jones NP, Hayward JM, Khaw PT, et al. Function of an ophthalmic accident and emergency department: results of a six month survey. Br Med J. 1986;292:188. 20. Pfister RR. Chemical injury of the eye. Ophthalmology. 1983;90:1246. 21. Liggett P. Ocular trauma in an urban population. Ophthalmology. 1989;97:581. 22. Yu JS, Ralph RA, Rubenstein JB. Ocular burns. In: MacCumber MW, ed. Management of Ocular Injuries and Emergencies. Philadelphia: LippincottRaven; 1998:163–171. 23. Brodovsky SC, McCarty CA, Snibson G, et al. Management of alkali burns: an 11 year retrospective review. Ophthalmology. 2000;107(10): 1829. 24. Perry HD, Hodes LW, Seedor JA, et al. Effect of doxycycline hyclate on cornel epithelial wound healing in the rabbit alkali-burn model: preliminary observation. Cornea. 1993;12(5):379. 25. Ralph RA. Tetracyclines and the treatment of corneal stromal ulceration: a review. Cornea. 2000;19:274. 26. Patterson J, Fetzer D, Krau J, et al. Eye patch treatment for the pain of corneal abrasion. South Med J. 1996;89:227. 27. Hart A, White S, Conboy P, et al. The management of corneal abrasion in accident and emergency. Injury. 1997;28:527. 28. Arbour JD, Brunette I, Boisjoly HM, et al. Should we patch corneal erosions? Arch Ophthalmol. 1997;115:313. 29. Solomon A, Halpert M, Frucht-Perry T. The use of topical indomethacin and eye patching for minor corneal trauma. Arch Ophthalmol. 2000;32:316. 30. Kaiser PK, Pineda R. A study of topical non-steroidal anti-inflammatory drops and no pressure patching in the treatment of corneal abrasions. Corneal Abrasion Patching Study Group. Ophthalmology. 1997;104:1353. 31. May DR, Kuhn FP, Morris RE, et al. The epidemiology of serious eye injuries from the United States Eye Injury Registry. Graefes Arch Clin Exp Ophthalmol. 2000;238:153. 32. Xiang H, Stallones L, Guanmin C, et al. Work-related eye injuries treated in hospital emergency departments in the U.S. Am J Ind Med. 2005;48:57. 33. Hemady RK. Ocular injury from violence treated at city hospital. J Trauma. 1994;37:5. 34. Hamill MB. Corneal injury. In: Brachmer JH, Mannus MJ, Holland EJ, eds. Cornea: Fundamentals of Cornea and External Disease. Vol. 2. St. Louis: Mosby; 1997:1416–1419. 35. Russell SR, Olsen KR, Folk JC. Predictors of scleral rupture and the role of vitrectomy in severe blunt ocular trauma. Am J Ophthalmol. 1988;105:253–257. 36. Pieramici DJ, MacCumber MW, Humayun MU, et al. Open-globe injury update on types of injuries and visual outcomes. Ophthalmology. 1996;103:1798–1803. 37. Sternburg P, De Juan E, Michels RG, Auer C. Multivariate analysis of prognostic factors in penetrating ocular injuries. Am J Ophthalmol. 1984;98:467–472. 38. Klystra JA, Lamkin JC, Runyan DK. Clinical predictors of scleral rupture after blunt ocular trauma. Am J Ophthalmol. 1993;115:530–535. 39. LASIK eye surgery. New York Times. Available at: http://www.nytimes. com. Accessed April 24, 2008. 40. Tetz M, Werner L, Muller M, et al. Late traumatic LASIK flap loss during contact sport. J Refract Surg. 2007;33:1332–1335. 41. Srinivasan M, Prasad S, Prajna P. Late dislocation of Lasik flap following fingernail injury. Indian J Ophthalmol. 2004;52:327–328. 42. Cheng AC, Rao SK, Leung GY, et al. Late traumatic flap dislocations after LASIK. J Refract Surg. 2006;22(5):500–504. 43. Walton W, Von Hagen S, Grigorian R, et al. Management of traumatic hyphema. Surv Ophthalmol. 2002;47(4):297–334. 44. Cazabon W, Dabbs TR. Intralenticular metallic foreign body. J Cataract Refract Surg. 2002;28:2233–2234.

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75. Duch-Samper AM, Menezo JL, Hurtado-Sarrio M. Endophthalmitis following penetrating eye injuries. Acta Ophthalmol Scand. 1997;75: 104–106. 76. Verbraeken H, Rysselaere M. Post-traumatic endophthalmitis. Eur J Ophthalmol. 1994;4:1–5. 77. Chhabra S, Kunimoto DY, Kazi L, et al. Endophthalmitis after open globe injury: microbiologic spectrum and susceptibilities. Am J Ophthalmol. 2006;143:852–856. 78. Zhang Y, Zhang MN, Jiang CH, et al. Endophthalmitis after open globe injury. Br J Ophthalmol. 2010;94:111–114. 79. Lieb DF, Scott IU, Flynn HW, et al. Open globe injuries with positive intraocular cultures. Ophthalmology. 2003;110;1560–1566. 80. Cebulla CM, Flynn HW. Endophthalmitis after open globe injuries. Am J Ophthalmol. 2009;147:568–569. 81. Shortsleeve Ament C, Zacks DN, Lane AM, et al. Predictors of visual outcome and choroidal neovascular membrane formation after traumatic choroidal rupture. Arch Ophthalmol. 2006;124:957–966. 82. Wyszynski RE, Grossniklaus HE, Frank KE. Indirect choroidal rupture secondary to blunt ocular trauma. Retina. 1988;8:237–243. 83. Artunay O, Rasier R, Yuzbasioglu E, et al. Intravitreal bevacizumab injection in patients with choroidal neovascularization due to choroid rupture after blunt-head trauma. Int Ophthalmol. 2009;29: 289–291. 84. Harissi-Dagher M, Sebag M, Gauthier D, et al. Photodynamic therapy in young patients with choroidal neovascularization following traumatic choroidal rupture. Am J Ophthalmol. 2005;139:726–728. 85. Anderson RL, Panje WR, Gross CE. Optic nerve blindness following blunt forehead trauma. Ophthalmology. 1992;89:445–455. 86. Gross CE, DeKock JR, Panje WR, Hershkowitz N, Newman J. Evidence for orbital deformation that may contribute to monocular blindness following minor frontal head trauma. J Neurosurg. 1981;55: 963–966.

87. Levin LA, Beck RW, Joseph MP, et al. The treatment of traumatic optic neuropathy. The International Optic Nerve Trauma Study. Ophthalmology. 1999;106:1268–1277. 88. Lessell S. Indirect optic nerve trauma. Arch Ophthalmol. 1989;107: 382–386. 89. Wolin MJ, Lavin, PJM. Spontaneous visual recovery from traumatic optic neuropathy after blunt head injury. Am J Ophthalmol. 1990;109: 430–435. 90. Wu N, Yin ZQ, Wang Y. Traumatic optic neuropathy therapy: an update of clinical and experimental studies. J Int Med Res. 2008;36:883–889. 91. Bracken MB, Shepard MJ, Collins WF, et al. A randomized, controlled trial of methylprednisone or naloxone in the treatment of acute spinalcord injury. Results of the Second National Acute Spinal Cord Injury Study. N Engl J Med. 1990;322:1405–1411. 92. Steinsapir KD. Treatment of traumatic optic neuropathy with high-dose corticosteroid. J Neuroophthalmol. 2006;26:65–67. 93. Entezari M, Rajavi Z, Sedighi N, et al. High-dose intravenous methylprednisone in recent traumatic optic neuropathy; a randomized double-masked placebo-controlled clinical trial. Graefes Arch Clin Exp Ophthalmol. 2007;245:1267–1271. 94. CRASH Trial Collaborators. Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASH trial): randomised placebo-controlled trial. Lancet. 2004;364:1321–1328. 95. Yu-Wai-Man P, Griffiths PG. Surgery for traumatic optic neuropathy. Cochrane Database Syst Rev. 2005;(4):CD005024. DOI: 10.1002/ 14651858.CD005024.pub2. 96. Foster BS, March GA, Lucarelli MJ, et al. Optic nerve avulsion. Arch Ophthalmol. 1997;115:623–630. 97. Cirovic S, Bhola RM, Hose DR, et al. Computer modeling study of the mechanism of optic nerve injury in blunt trauma. Br J Ophthalmol. 2006;90:778–783.

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CHAPTER 21

Face Robert M. Kellman

INTRODUCTION Facial structures participate in essential functions of human life, including respiration, mastication, deglutition, vision, and the expression of both verbal and nonverbal communication. The face is the focal point of human social interaction.1 Thus, to restore facial form and function is to restore much of a patient’s opportunity to live a normal life. In order to effectively manage facial trauma, the surgeon must understand care in the emergency room; the anatomy, evaluation, and management of injuries to the soft tissue, visceral, and bony components of the face; and the management of secondary deformities and complications. In this manner, not only is a broad discussion of facial trauma achieved, but the reader is also made aware of the place occupied by facial trauma within advanced trauma life support (ATLS) (see Chapter 10) and subsequent management.

EMERGENCY DEPARTMENT CARE ■ Primary Survey of the Face Care of facial trauma in the emergent setting, as in the management of any trauma, is initially focused on the “ABCs.” The adequacy of airway, breathing, and circulation are determined, and the appropriate ATLS algorithms are instituted. In addition to airway and circulation or bleeding issues, the cervical spine must be appropriately managed, and it adds potential difficulty to management of the airway.

retrodisplacement of these structures, which may cause compromise of the airway. Trauma to the airway itself or neurologic injury can cause direct airway obstruction or loss of vocal cord function. Airway compromise may be rapidly lethal and is assessed first. The reader is cautioned that significant obstruction of the airway, even impending loss of the airway, may be accompanied by normal or near-normal oximetry. The Glasgow Coma Scale (GCS) is used to rapidly assess for neurologic impairment that may lead to centrally based loss of airway protection. Subcutaneous emphysema may suggest pharyngeal, laryngeal, or tracheal disruption. Stridor (the sound of breathing through a partially obstructed airway) suggests airway narrowing and possible impending obstruction. If time permits, flexible fiberoptic nasopharyngolaryngoscopy allows rapid and definitive evaluation of the potentially compromised hypopharyngeal and laryngeal airway. Foreign material in the airway may be manually evacuated, and blood and secretions are suctioned from the oral cavity and pharynx. A “jaw thrust,” even in the setting of mandibular trauma, and bag-valve mask (BVM) assistance may allow oxygenation, especially in the setting of injury to the brain or spinal cord. The compromised airway can then be secured via rapid sequence orotracheal or nasotracheal intubation. Orotracheal intubation is preferred in the setting of possible midface fractures, though nasal intubation can be accomplished with care and a thorough knowledge of the anatomy of the nose and skull base anatomy.2–4 If necessary, the airway should be accessed through an emergent tracheotomy or cricothyrotomy.

Airway Injuries to the upper aerodigestive tract and craniofacial skeleton may result in airway obstruction from tissue trauma and edema, foreign debris, or bleeding. The natural mechanisms of airway protection rely on functioning oropharyngeal structures supported by an intact facial skeleton. Injuries may lead to

Bleeding After management of the airway, any brisk bleeding should be controlled. The face is very well vascularized, and soft tissue injuries may result in profuse hemorrhage. The scalp bleeds profusely because large vessels are located near the surface and

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the tissue is relatively inelastic.5 Intraoral and pharyngeal bleeding may be due to injury to the carotid artery or internal jugular vein or their branches and may result in compromise of the airway. After securing the airway, the throat may be packed in order to control pharyngeal bleeding, the source of which may be difficult to determine initially. Injuries to the carotid artery and/or jugular vein may also occur with coincident trauma to the neck. A neck hematoma may threaten the airway via extrinsic compression. Bullet wounds involving the parapharyngeal and retropharyngeal spaces, the nasopharynx, and the infratemporal fossa carry the risk of injury to the internal carotid artery, and emergent angiography may be indicated. Massive, high-energy wounds to the face may present with massive bleeding. Direct pressure and pressure dressings are applied. A pressure dressing secured to the face with a clear synthetic full-face wrap after airway diversion through a tracheostomy or cricothyrotomy has been described.2–4

Cervical Spine Facial injuries may also be associated with trauma to the cervical spine and brain. In order to minimize further damage, any patient with suspected injury to the cervical spine should be immobilized on a backboard with a rigid cervical collar until definitive evaluation can be completed.2 Most notably, cervical spine precautions are maintained during intubation or emergent tracheostomy by maintaining a neutral position of the head via inline traction and minimal extension. Various techniques are available to make intubation safer and more dependable.3,4

Disability Finally, assessment of the patient’s level of consciousness and neurologic function is summarized by the Glasgow Coma Scale score (GCS). Up to 15 points are allocated based on a patient’s motor, verbal, and eye-opening performance. Computed tomography (CT) scan of the head and brain and neurosurgical consultation are indicated with a GCS 14.2

■ Secondary Survey With the airway, breathing, hemodynamics, and cervical spine stabilized, the remainder of the trauma survey is undertaken. At this time, facial and craniomaxillofacial injuries are also identified. The need for imaging should be determined, since radiographic studies are often readily available in the emergency department. With new fast CT scanners in use, the maxillofacial structures can be included in the initial screening scans. If the patient is stable, the input of consultants who care for craniofacial and associated wounds is sought. This may include otolaryngology/facial plastic surgery, plastic surgery, oral and maxillofacial surgery, ophthalmology, and neurosurgery.

NORMAL ANATOMY In order to make an accurate assessment of craniofacial injuries and to effect an adequate reconstruction, an understanding of the normal anatomy is required.

■ Soft Tissue The scalp covers the entire cranial vault and extends over the upper face. It consists of five layers including skin, subcutaneous fat, galea aponeurosis (including the frontalis muscle in the forehead), loose areolar tissue, and periosteum of the skull known as the pericranium. In the inferior aspect of the temporal scalp, the temporal branch of the facial nerve runs over the superficial surface of the temporalis investing fascia to innervate the frontalis muscle (Fig. 21-1). The supratrochlear and supraorbital neurovascular bundles emanate from notches or foramina in the superior orbital rims and penetrate the frontalis muscle 2–4 cm above the rim. Therefore, subperiosteal dissection of the 3–4 cm above the supraorbital rims ensures protection of these structures until they are encountered at the orbital rim itself. The eyelid is a trilamellar structure (Fig. 21-2). The anterior lamella consists of skin and the sphincteric orbicularis muscle and the posterior lamella consists of the conjunctiva. The tarsal plates comprise the middle layer, and they are attached at their transverse extents to the medial and lateral orbital rims by the medial and lateral canthal tendons, respectively. The orbital septum extends from the tarsus to the orbital rim and separates the orbicularis from the orbital fat. Levator and depressor muscles insert on the superior and inferior margins of the upper and lower lid tarsal plates, respectively, and open the eyelids upon stimulation by the third cranial nerve. The orbicularis closes the lids and is innervated by the facial nerve. The conjunctiva, or posterior lamella, covers the inner surface of the lid and extends over the anterior aspect of the globe itself. The medial canthal tendon (MCT) is derived from the orbicularis oculi muscle, which divides into anterior and posterior slips (Fig. 21-3). These fuse, forming the common anterior and posterior limbs of the MCT, which inserts on the anterior and posterior lacrimal crests, respectively. A third slip of the tendon also attaches more superiorly. Together, these structures surround the lacrimal sac within the lacrimal fossa. Tears enter the lacrimal canaliculi through the puncti of the upper and lower lids and flow into the lacrimal sac. With blinking, the components of the MCT squeeze the sac and force tears into the nasolacrimal duct. The lateral canthal tendon inserts on Whitnall’s tubercle, which is located 2-mm posterior to the lateral orbital rim and 9-mm inferior to the zygomaticofrontal (ZF) suture. The external ear projects 15–25° from the parasagittal plane. The cartilaginous framework defines ridges and hollows covered by perichondrium and skin with no subcutaneous fat. It has a complex anatomical structure and can be challenging to reconstruct. The nose consists of nine aesthetic subunits and comprises a bony and cartilaginous framework with an overlying skin–soft tissue envelope. These subunits include the midline dorsum, paired sidewalls, the midline tip, and columella, as well as the paired lateral sidewalls, soft triangles or facets, and alae. The lower third is analogous to a tripod consisting of the septum and the paired lower lateral cartilages.6 Like the eyelids, the lips consist of a sphincteric muscle, the orbicularis oris, levator and depressor muscles, and tendonous support in the form of the modiolus. Loss of muscular

Face

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FIGURE 21-1 The fascial planes of the temporal scalp and underlying temporalis muscle. The frontal branch of the facial nerve located on or within the superficial layer of deep temporalis fascia. (Reproduced with permission from Kellman RM, Marentette LJ. Atlas of Craniomaxillofacial Fixation. Raven Press: New York; 1995:97.)

attachment to the modiolus may result in rounding of the commissure and oral incompetence. The lip margins consist of vermillion, a thin nonkeratinizing squamous epithelium overlying rich capillary beds. The junction of the vermillion and lip skin is called the white roll, and the junction of

vermillion and mucosa is known as the wet line. The philtrum is found in the central aspect of the upper lip, extending vertically from the columella to the vermillion. The cheeks comprise the lateral aspect of the face. The key aesthetic point of the cheek is the malar prominence. Most of

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Fat Septum Orbicularis oculi muscle

Müller’s muscle Superior rectus muscle

Levator aponeurosis

Tarsus Skin Conjunctiva

Tarsus Inferior rectus muscle Inferior oblique muscle

Capsulopalpebral fascia Müller’s muscle Fat Septum Orbicularis oculi muscle

FIGURE 21-2 Cross section of eyelids and schematized globe. (Reproduced with permission from Wobig J. Eyelid Anatomy. In: Putterman AM, ed. Cosmetic Oculoplastic Surgery. 2nd ed. Philadelphia: WB Saunders; 1993:73. © Elsevier.)

the muscles of facial expression lie within a fibrofatty fascial layer of the cheek known as the superficial muscular aponeurotic system.

■ Visceral The deep aspect of the cheek contains the parotid gland and facial nerve. The parotid duct crosses the lateral surface of the masseter and enters the mouth through an orifice in the buccal mucosa lateral to the second maxillary molar. The duct is intimately associated with the buccal branches of the facial nerve. The facial nerve exits the stylomastoid foramen of the temporal bone and immediately enters the posterior aspect of the parotid gland. The nerve divides into a superior and inferior divisions and then ramifies further creating five divisions as follows: the frontal, the zygomatic, the buccal, the marginal

mandibular, and the cervical. The frontal branch crosses the midpoint of the zygomatic arch. The zygomatic branch travels inferior to the zygomatic arch until it inserts on the deep surface of the orbicularis oculi. The buccal division consists of multiple anastomotic branches that course over the masseter muscle to innervate the buccinator and upper lip and nasal muscles. The marginal mandibular branch innervates the depressor anguli oris and lower aspect of the orbicularis. The cervical branch innervates the platysma muscle. Sensory innervation of the face is supplied primarily by the divisions of the fifth cranial nerve, though the great auricular nerve contributes some as well. The contents of the orbit include the globe, the extraocular muscles, the terminal branches of the second, third, fourth, and sixth cranial nerves, as well as terminal branches of the internal carotid arterial system.

Face

■ Bony The upper face (the forehead) is supported by the paired, broad, flat frontal bones that articulate inferiorly with the nasal bone and frontal process of the maxilla medially and with the

1

2 3

A

B

C

FIGURE 21-4 (A) Classic medial (1), lateral (2), and posterior (3) vertical maxillary buttresses and the infraorbital horizontal buttress. (B) Lines of the classic Le Fort fractures of the midface. (C) Comminuted midface fractures, including right Le Fort III, bilateral Le Fort II, and left Le Fort I fractures as well as frontal sinus, orbital, and palatal fractures, demonstrating the complex pathology commonly resulting from high-speed blunt force trauma. (A) (Reproduced with permission from Forrest CR, Phillips JH, Prein J. Craniofacial Fractures, Le Fort I-III Fractures. In: Prein J, ed. Manual of Internal Fixation in the Cranio-Facial Skeleton. Berlin Heidelberg: SpringerVerlag; 1998:109.) (B) (Reproduced with permission from Ducic Y, Hamlar DD. Fractures of the Midface. Facial Plast Surg Clin North Am. 1998;6:471. © Elsevier.)

CHAPTER CHAPTER 21 X

FIGURE 21-3 The components of the medial canthal tendon are represented by arrows. The resultant vector is best reconstructed by placing the tendon or a canthopexy stitch in a posterior– superior position, at the point X. (Reproduced with permission from Rodriguez L, Zide B. Reconstruction of the Medial Canthus. Clin Plastic Surg. 1988;15:257. © Elsevier.)

frontal process of the zygoma laterally. Posterior to the lateral orbital rims, the frontal bone articulates with the greater wing of the sphenoid. Inferiorly, the frontal sinus communicates with the nasal passage through the paired nasofrontal ducts (NFDs) that penetrate the sinus floor medially. The midface includes the paired maxillae, zygomas, and nasal bones. It articulates deeply with the orbital walls and ethmoid structures. Thickened regions of these structures comprise the medial, lateral, and posterior “vertical buttresses” as well as the “horizontal beams”—lines of thickened cortical bone that withstand greater loads than the intervening regions of thin, weak bone (Fig. 21-4). This lattice-like arrangement of the midface is suspended from the orbital bar and is projected from the skull base via its articulations with the ethmoid, pterygoid, and temporal bones. The vertical buttresses resist the forces of mastication and include the paired nasomaxillary (medial), zygomaticomaxillary (ZM) (lateral), and pterygomaxillary (posterior) struts. The ZM extends from the maxillary alveolus above the first molar, across the ZM suture and the ZF suture in the lateral orbital rim to the suprorbital bar. The nasomaxillary buttress ascends from the canine fossa into the lateral wall of the piriform aperture and superiorly along the nasomaxillary junction to the glabella. The pterygomaxillary buttress comprises thickened bone at the junction of the posterior maxillary sinus and the takeoff of the pterygoid plates.7 The horizontal stabilizers are less robust and include the maxillary alveolar bone, the infraorbital rims, and the supraorbital rims (frontal bone). In addition, the orientation of medial and

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lateral pterygoid plates provides horizontal stabilization for the posterior buttress. In the anterior/posterior (AP) direction, the zygomatic arches determine the AP position of the midface.7 The lateral orbital wall consists of the greater wing of the sphenoid and the zygoma anteriorly. The orbital floor is predominately formed by the orbital plate of the maxilla, and the zygoma makes a contribution laterally. Vertical processes of the palatine bones also contribute to the medial orbital walls. Posteriorly, the orbital plate of the maxilla sweeps medially and superiorly to meet the lamina papyracea. The orbital roof and floor are mostly concave anteriorly, but the floor is convex anteromedially. Thus, an anteromedial fracture that eliminates this convexity will significantly enlarge the orbital volume and result in enophthalmos. The zygoma is the keystone structure of the midfacial buttress system. The infraorbital rim and lateral buttress intersect in the body of the zygoma. Thus, the zygoma and maxilla in this region are considered together as a zygomaticomaxillary complex (ZMC) (Fig. 21-5). The mandible is the primary component of the lower third of the face. The mandibular alveolus is the arch of toothbearing bone that extends anteriorly from the angle. As might be expected, the bone is thickest in the tooth-bearing areas. The vertical rami extend from the angles to the temporal bones at the temporomandibular joint. The inferior alveolar nerve enters the lingual side of the ramus and runs through the mandibular body to exit as the mental nerve.

EVALUATION ■ Soft Tissue Soft tissue injuries are generally obvious on initial physical examination; however, all soft tissue wounds must be accurately evaluated and documented. After adequate local anesthesia, wounds should be carefully probed and examined to determine depth, extent and involvement of visceral structures.

A

The severity of the injury depends upon the amount of energy transferred to the wound. Close-range ballistic wounds may cause severe tissue damage, and they can be classified according to the region of tissue loss. Shotgun wounds are commonly inflicted from close range and impart energy to an even wider field of tissue. Suicide attempts represent the most common shotgun wounds, and these usually direct energy to the lower face and midface from below.8 Skin does not respond to blunt trauma randomly. Lee et al.9 determined that blunt trauma results in repeatable patterns of soft tissue wounding. In a study of blunt wounds to cadaver heads, they found that in approximately 80% of wounds the skin broke along cleavage planes as previously defined by others. These cleavage planes resemble the relaxed skin tension lines along which wrinkles occur.

■ Visceral High-energy cause, deep soft tissue wounds, craniofacial fractures, and multiorgan trauma suggest the possibility of an intracranial injury. The neurologic examination should be repeated, and a head CT should be obtained routinely. Ophthalmologic examination should be performed and repeated, and injury to the lacrimal drainage system must be considered. The loss of facial sensation may suggest the depth or extent of injury. Facial paralysis must be identified, since primary facial nerve anastamosis should be attempted during primary repair of a facial wound. Wounds to the cheek or submental region that injure the salivary glands or ducts should be identified.

■ Bony Most often, craniofacial fractures occur along well-recognized lines of weakness in the midfacial skeleton and in repeated patterns in the mandible. Clinical evaluation is directed by knowledge of these typical fractures.

B

C

FIGURE 21-5 (A) The vertical and horizontal arcs created by the zygomaticomaxillary (ZMC) complex. (B) Axial computed tomography image of left ZMC fracture demonstrates loss of malar projection. (C) Schematic illustration of use of the bone hook to mobilize the ZMC complex. (A) (Reproduced with permission from Stanley R. The zygomatic arch as a guide to reconstruction of comminuted malar fractures. Arch Otolaryngol: Head Neck Surg. 1989;115:1459. Copyright © 1989 American Medical Association. All rights reserved.) (C) (Reproduced with permission from Markowitz BL, Manson PN. Craniofacial Fractures, Zygomatic Complex Fractures. In: Prein J, ed. Manual of Internal Fixation in the Cranio-Facial Skeleton. Berlin: Springer-Verlag; 1998:133.)

Face

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Upper Face

CHAPTER CHAPTER 21 X

A laceration of the forehead skin and depression of the forehead suggest a possible fracture of the frontal sinus. The presence of an anterior table fracture associated with mental status changes or cerebrospinal fluid (CSF) rhinorrhea should alert the surgeon to possible posterior table involvement, a dural tear, or a traumatic brain injury.

Midface The lattice system of medial and lateral buttresses usually prevents random fractures through the midface.10 Instead, the midface most commonly fractures along the classic weak lines described by Rene Le Fort in 1901, although variations in the pattern and in the combination of Le Fort fractures are the rule11 (Fig. 21-4). A Le Fort I fracture separates the maxillary alveolus and palate from the upper midface. Horizontal impact of the upper midface usually results in Le Fort II fracture line, which crosses from the nasal dorsum, ascending process of the maxillae, and lacrimal bones into the orbit. In the orbit, the fracture line descends through the floor and infraorbital rim into the anterior and lateral antral walls, and through the pterygoid plates. This separates a pyramidal central midfacial and alveolar segment from the zygomas and pterygoid plates. In contrast, downward, oblique impact separates the facial skeleton from the skull base (“craniofacial disjunction”) via fractures across the nasofrontal suture, the lacrimal and ethmoid bones, and into the orbital floor. At the inferior orbital groove, the fracture trifurcates, extending across the ZF suture, the zygomatic arch, and the pterygoid plates. Clinical examination of the vertical and horizontal buttresses involves inspection and palpation. Mobility of the midface relative to the skull base suggests a Le Fort fracture. Palatal fractures in the sagittal plane are suggested by palatal lacerations, widening of the dental arch, and abrupt changes in the vertical level of dentition. Step-off deformities of the infraorbital rims may be palpated. The upper midface fractures classically cause the face to recede posteroinferiorly, creating a flat or “dish-face” appearance. This commonly results in early posterior contact and anterior open-bite. The zygomatic fracture typically results in loss of the anterior, lateral, and vertical position of the malar eminence. Despite varying degrees of edema, malar flattening is evident from the vertex or basal perspective. Fractures of the weak, central compartment of the midface result in characteristic naso-orbital ethmoid (NOE) injuries. The sine qua non of the NOE fracture is telecanthus. Disruption of the bony attachment of the medial canthi can be determined through inspection and palpation. The nasal root will appear broad and flat, and the canthus will appear rounded and lateralized, and it may be displaced inferiorly. The central bony fragments may be easily mobilized, and the canthal tendons may give easily with gentle lateral tugging. The canthi should be no further apart than the alar base of the nose and should be roughly one half of the interpupillary distance. In general, an intercanthal distance of greater than 35 mm is suggestive of telecanthus, and greater than 45 mm is usually definitive.12

FIGURE 21-6 Coronal computed tomography image of orbital blowout fracture with disruption of the orbital floor and medial orbital wall. Entrapment of the medial rectus muscle is also seen.

Orbit Isolated orbital blowout fractures (fractures of the orbital walls without associated fractures through the orbital rims) occur when blunt force is applied directly to the orbital contents and transmitted to the walls. Intraorbital volume is increased and the globe recedes posteriorly (known as “enophthalmos”). Diplopia is readily recognized by the patient. Enophthalmos is often evident on the basal or vertex view of the patient, although orbital and periorbital edema may fill the enlarged orbital volume, temporarily preventing recession of the globe. Orbital wall fractures may also result in herniation and entrapment, most commonly of the inferior or medial rectus muscles, restricting extraocular movements (Fig. 21-6). Chemosis, scleral injection, periorbital ecchymosis, and diplopia suggest orbital fractures.

Mandible Clinical evaluation can be directed by knowledge of the mechanism of injury. In addition, gingival lacerations, ecchymoses, and bleeding are signs of underlying fracture. Malocclusion, facial asymmetry, stepoff deformities of the dental arch, mobility of the arch with palpation (performed gently), pain, and trismus (restricted mandibular movement) are obvious indications for radiographic imaging.

Radiographic Evaluation CT scanning has essentially replaced plain film radiography for evaluation of craniofacial fractures. Studies have shown that CT evaluation of the mandible will reveal fractures not visible on plain and panoramic radiographs, though orthopantomograms are still helpful for following mandible fractures.13 Perhaps the most significant advancement in imaging is the three-dimensional (3D) reconstruction of axial CT sections (Fig. 21-7). Three-dimensional CT images can be rotated 180 or 360° on a

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B

FIGURE 21-7 (A) Three-dimensional computed tomography scan of the mandible demonstrates the ease with which the special orientation of the segments of this subcondylar and ramus fracture are visualized. (B) Three-dimensional computed tomography scan of the same patient with mandible in situ. Evident are the cross bite and anterior open bite as well the facial asymmetry that results from vertical shortening of the left ramus.

variable axis and clearly reveal fracture lines as well as the relations of small bony fragments. With multiple complex fractures, 3D images facilitate surgical planning; however, it must be kept in mind that the computer algorithms that create the 3D images do create some inaccuracies, so that careful analysis of directly obtained CT images remains essential.14

MANAGEMENT ■ Soft Tissue Low-energy Wounds Careful written and photographic documentation of injuries and their repair may be useful in counseling patients and in interacting with the legal system, which may be necessary. Most soft tissue wounds are then managed at the bedside using local anesthesia. After local anesthesia is achieved, wounds are debrided and cleansed. Contamination and foreign material are sources of deep tissue infection, and granules of foreign material embedded in the skin can cause permanent tattooing. Copious saline irrigation is commonly performed, although one group found that irrigation does not significantly reduce the risk of infection or improve the cosmetic outcome in facial wounds that are superficial, minimally contaminated, and less than 6 hours old.15 They suggest that irrigation may damage tissue and that such wounds are amenable to cleansing with saline and gauze. Debridement is limited to frankly necrotic soft tissue. Given the abundant vascularity of the face, tissue that appears compromised, but not necrotic, is likely to survive. The following general principles may then be applied to the closure of soft tissue wounds of the face. First, with adequate debridement and irrigation, the robust vascularity of the face supports primary closure of almost all facial wounds. With proper antimicrobial therapy, the incidence of secondary

infection is low, even in the setting of bite wounds less than 24 hours old. Closure of facial wounds by secondary intention typically results in unacceptable scars. Second, wounds should be closed in a layered fashion. Mucosa is closed with interrupted absorbable sutures, whereas muscle should be reapproximated with braided, absorbable suture. Failure to reapproximate muscular layers can result in loss of function and facial deformity, as well as depressed and excessively wide scars. Skin closure is accomplished with interrupted absorbable polyglycan 4-0 dermal stitches (except in the thin skin of the nose, eyelids, and ear) followed by 5-0, or 6-0 monofilament sutures in the epidermis. In small children, where suture removal presents an additional challenge, 6-0 fast absorbing gut may be used. Every attempt is made to achieve eversion of wound edges. Where tissue is lost via avulsion, undermining the skin up to 2–4 cm from the wound edge will often allow primary closure. Undermining is usually accomplished in the subcutaneous plane, although the forehead and scalp are undermined in the subgaleal plane, and nasal skin is undermined in the submuscular plane. In larger avulsions, local or regional flaps may be needed. Alternatively, a skin graft can be used in the acute setting, and definitive closure can be achieved in the future when the full range of reconstructive techniques may be more available. Facial sutures should be removed early, often at 4–5 days and certainly within 1 week, in order to prevent “railroad track” scars.

Lips The mucosa, the orbicularis, and the skin are closed in discrete layers. The primary aim is reapproximation of the white roll and the vermillion margin, as well as the wet line and the orbicularis. Great care is taken to precisely reapproximate the vermillion-cutaneous junction, and the authors commonly begin lip closures with a single interrupted skin suture at the vermillion-cutaneous border followed by a muscular stitch that also contributes to precise alignment. Next, the mucosa is

Face

Eyelids Similar to lip repair, eyelid closure involves layered closure of the lamellae, as well as careful reconstruction of the lateral supporting structures, in this case the canthal tendons. The tarsus is reapproximated with interrupted absorbable 6-0 stitches; however, the levator aponeurosis must be repaired to prevent lid ptosis. The grey line is reapproximated with 6-0 silk suture. The conjunctiva may be closed with interrupted, absorbable sutures, though it is not always necessary. Finally, the skin and orbicularis may be closed as a single flap. The canthal tendons must be repaired if torn or if displaced from the orbital rims. There is a common misconception that the lateral canthus attaches more superiorly than the medial canthus; however, recent analyses have revealed that these attachments are actually along a horizontal line.17 Repair of the MCT is covered below in a discussion of nasal orbital ethmoid complex fractures. The medial canthal ligament is repaired by fixing it to the lacrimal bone, usually with a transnasal suture or wire.

Nose The principles of augmentive rhinoplasty and of nasal reconstruction of skin cancer defects are utilized in repairing soft tissue trauma of the nose. Superficial lacerations can often be closed primarily. The relatively inelastic nasal skin is, however, prone to scar contracture, trapdoor deformity, and scar depression. Therefore, wound edges are everted via submuscular undermining, deep sutures are used to reapproximate wound margins, and skin closure is with vertical mattress sutures. Small areas (1 cm) of skin loss located in concavities of the nasal surface (such as the nasofacial or alar facial sulci) can be left to granulate, as these tend to heal nicely by secondary intention.18 Lacerated cartilages should be reapproximated with interrupted 4-0 polydioxanone sutures. The alar rims, especially in the soft triangles, are especially prone to notching as a result of scar contracture. Here, eversion of wound edges is essential, and skin is supported with underlying cartilage batten grafts harvested from the septum or auricular conchae. For extensive tissue loss, the principles of cancer reconstruction are applied. These involve reconstruction of all affected layers, including mucosa, cartilage framework and skin, utilizing a variety of available grafts or flaps, including free tissue transfer when indicated.18 The septum must be examined. Hematomas must be aspirated or drained via incision and drainage to prevent cartilage loss and resultant late saddle nose deformity. A quilting stitch or a nasal pack is placed in order to coapt the cartilage and mucoperichondrium to prevent reaccumulation.

Ear As with the nose, ear skin is inelastic and supported by a cartilaginous framework. Lacerations of skin and cartilage must be meticulously repaired. Auricular cartilage is directly repaired

and/or the anterior and posterior perichondrium are reapproximated, and, where the cartilaginous support is absent, supporting cartilaginous grafts may be introduced and wound edges everted in order to prevent notching. Analogous to the septal hematoma, an auricular hematoma separates the skin from the underlying cartilage and must be evacuated. A hematoma may be removed through needle aspiration or a small stab incision, and a bolster is then sewn to the ear. Significant tissue loss requires grafting of cartilage, often taken from the contralateral concha, and soft tissue coverage. For large defects, pedicled, staged soft tissue flaps provide coverage. Postauricular skin flaps cover the helix and antihelix well, and the temporoparietal fascial flap covered by a skin graft is useful for larger defects. For complete or near-complete avulsion, primary reattachment of the auricle, two-stage postauricular skin flap coverage of the auricle, and microvascular reanastomosis may be used, though simply sewing the avulsed segment into place is unlikely to succeed. In this case, the cartilage may be denuded of all skin and perichondrium and buried in a subcutaneous pocket for later reconstruction. Complete reconstruction using carved rib cartilage may be used as well.

■ Visceral Injuries to the cheek involving deep tissue must be explored for possible trauma to the parotid gland and duct. Laceration of the gland itself is often not reparable, although an attempt at closure of the parotidomasseteric fascia may be made. Injury to the parotid gland may result in a salivary-cutaneous fistula or sialocele. It is important to assess for a possible injury to Stensen’s duct. Treatment options for ductal injuries include primary anastomosis, creation of an oral fistula, ductal ligation, and conservative nonoperative measures. Repair requires cannulation and microsurgical anastomosis. Some authors favor conservative management.19,20 When the duct is not repaired, antisialogogues are useful to reduce salivary output and pain.21 Salivary cutaneous fistula and sialoceles may result from injury to the gland, an unrecognized ductal laceration, or intentionally conservative management of parotid injury. Sialoceles should be aspirated in serial fashion, and a pressure dressing may be applied. Most will resolve, though more aggressive measures may be required. Injury to facial nerve branches often accompanies injury to the parotid gland. If evidence of paralysis in one or more regions of the seventh nerve is found on physical examination, an attempt at primary microsurgical reanastomosis should be made at the time of initial wound repair.

■ Facial Skeleton Approaches If facial lacerations exist, they may provide adequate exposure with minimal extension. Otherwise, the principles of soft tissue approaches include minimizing (and avoiding) incisions in facial skin and protecting neurovascular structures while achieving maximal exposure.

CHAPTER CHAPTER 21 X

closed with interrupted absorbable sutures. The remainder of the muscle and skin is then closed. Multiple algorithms exist for the reconstruction of fullthickness lip defects, and these are handled in the same fashion as lip reconstruction after tumor resection.16

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The coronal approach exposes the entire upper face down to the nasal bones as well as the anterior calvarium, lateral orbital rims, and zygomas.22,23 The scalp is incised in serpentine, geometric, or gently curved (Soutar) fashion from the root of one auricular helix to the other. A scalp flap is raised anteriorly in either the subgaleal or the subperiosteal plane between the temporal lines. If a pericranial flap will be harvested, the subgaleal plane is often followed, leaving a healthy layer of loose areolar tissue down on the pericranium. Alternatively, the pericranium can be raised with the scalp and harvested from the scalp flap secondarily. Extreme care is required to avoid injury to the temporal branches of the facial nerve. Dissection over the temporal fat pads can be performed either just over the deep temporal fascia, hugging the fascia to avoid nerve injury, or, to be safer, the deep fascia can be incised where it divides into two layers, and the dissection can be continued inferiorly just over the fat (Fig. 21-1 and Fig. 21-8A). The dissection can then be carried forward to the superior and lateral orbital rims and inferiorly to the zygomatic arches. Supratrochlear and supraorbital neurovascular bundles are carefully protected. Scalp closure is achieved in layers. A wide scar is prevented by taking particular care to reapproximate the galea. The skin may be sutured or stapled. Exposure of the midface is obtained through either a sublabial or a midface degloving approach (Fig. 21-8B). After an incision in the superior oral vestibule is made perpendicular to mucosa and then deepened perpendicular to bone, a subperiosteal dissection over the face of the maxilla is performed, using care to avoid the infraorbital nerve. When greater exposure is required, a bilateral sublabial approach may be converted to a midface degloving approach.24 Subperiosteal dissection is extended into the floor of the piriform aperture and into the nose. The nasal vestibule is incised circumferentially, connecting the nasal floor, membranous septum and intercartilagenous region. Thus, the lower one third of the nose is raised with the flap. The orbits are directly approached through modified brow and blepharoplasty incisions.22,24 Although the brow incision for access to the lateral superior orbit and lateral orbital rim has been advocated for years, many surgeons have abandoned it in favor of the upper lid blepharoplasty incision.22 Lower lid blepharoplasty incisions provide the best direct exposure of the orbital floor and inferior, medial, and lateral walls. In the lower lid, a subciliary skin incision can provide access to the inferior rim and floor, but it does produce a facial scar (even though fine) and does carry greater risk of lid retraction than does an approach through the conjunctiva. The transconjunctival approach may include a lateral extension, which requires a canthotomy and inferior cantholysis. In this case, it is initiated with the lateral incision and canthotomy. Otherwise, only the conjunctival incision is used. The surgeon develops either a preor post-septal plane and carries the dissection to the inferior rim (Fig. 21-8C). The conjunctiva may be left open or is closed with a 6-0 fast absorbing gut suture. The inferior oral vestibular approach exposes the mandibular symphysis and body. Subperiosteal dissection exposes the

mental nerves and the anterior two thirds of the mandible. Closure is water-tight, and the soft tissue of the mentum must be resuspended from the skeleton. An incision along the anterior border of the ramus is used to expose the vertical mandibular structures, including the coronoid process, the sigmoid notch, and the condylar neck. This ramus approach combined with a transbuccal stab incision is usually adequate for reduction of a subcondylar, ramus, or angle fracture. Occasionally, the mandible may be approached through external skin incisions. These are positioned in appropriate skin creases (relaxed skin tension lines), and care is taken to avoid branches of the facial nerve.

Fundamentals of Rigid Fixation Skeletal support for the soft tissue and visceral structures of the face must be reconstituted. The surgeon reduces and fixates fractured skeletal elements in order to restore proper form and function and to optimize bony healing.22,25–27 Interfragmentary motion prevents the formation of the delicate vascular support of growing bone, thereby preventing osteoblastic bone formation and the development of a stable population of osteocytes. Rigid fixation not only maintains alignment of bone segments, it also eliminates motion in the fracture gap.25 Lack of adequate fixation increases the chance of device failure and nonunion as well as wound infection and osteomyelitis.22,26,27 Traditional fixation for most of the 20th century was performed by wiring the teeth in occlusion using maxillomandibular fixation (MMF), frequently in combination with interosseous wiring. In the 1970s and 1980s, rigid fixation of the facial skeleton with plates and screws began to gain popularity, and these techniques now predominate. Rigid fixation, as the name suggests, involves properly applying fixation devices to bone so that the dynamic forces of distraction in function are overcome. When properly adapted to bone using screws, a plate provides immobilization and strong, rigid splinting. Multiple plating strategies have been developed. Compression plates take advantage of eccentric, ramped screw holes that force the turning screw to slide down the shoulders of the screw hole, thereby bringing a bone fragment with it and compressing it against an opposing bone fragment (Fig. 21-9).22 Recently however, compression plates have fallen out of favor, not because they are ineffective, but as a result of comparably high success rates with the technically easier and more tolerant miniplate approaches. Miniplate technology reliably achieves complete healing with comparable success rates.28 The newer “locking plates” add a margin of safety by fixing the screw heads to the plate itself. The heads of locking screws thread-lock to the plate hole, and functions more like an external fixator. Therefore, it requires less precision in adapting the plate.29 Compression fixation is also achieved with lag screws— either alone or in combination with a plate (Fig. 21-10). Lag screws can be used whenever bone fragments overlap or meet in a way that allows fixation of the screw in the second cortex.30

Face

CHAPTER CHAPTER 21 X

Cut edge of superficial layer of deep temporal fascia

N.-superficial to plane of dissection

Middle temporal a. deep to fat pad Cut edge of zygomatic arch periosteum

Segment of zygomatic arch to expose

A

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C

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FIGURE 21-8 Surgical approaches. (A) The left half of a coronal approach. The plane of dissection is carried deep to the superficial layer of deep temporal fascia thereby protecting the facial nerve. (B) The transconjunctival approach with the preseptal plane of dissection demonstrated. (C) The midface degloving approach combines bilateral sublabial approaches and circumferential incisions in the nasal vestibule, permitting access to nearly the entire midface. (Reproduced with permission from Kellman RM, Marentette LJ. Atlas of Craniomaxillofacial Fixation. New York: Raven Press; 1995: 98, 113, 116.)

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Management of Specific Injuries

SECTION 3 X FIGURE 21-9 Compression plate fixation demonstrated. As the screw is driven against the ramped screw hole, the plate and bone are displaced in opposite directions, resulting in axial compression of the fracture segments. (Reproduced with permission from Kellman RM, Marentette LJ. Atlas of Craniomaxillofacial Fixation. New York: Raven Press; 1995:63.)

Titanium is currently the metal of choice for nearly all metal craniofacial plates. Titanium does not corrode and does not interfere with imaging, and it seems to “integrate” with bone, with osteocytes adhering directly to the material without a fibrous interface.31

Mandibular Repair The goals of treatment are restoration of form, manifested by normal occlusion, and restoration of function, or the capacity to bear the load of mastication. Although many fractures could heal solely through the application of MMF, there is increased

Face

407

CHAPTER CHAPTER 21 X

FIGURE 21-10 Lag screw fixation of a manibular angle fracture through an inferior oral vestibular approach. Note that the proximal segment is overdrilled and that a countersink is created in its cortical surface. (Reproduced with permission from Kellman RM, Marentette LJ. Atlas of Craniomaxillofacial Fixation. New York: Raven Press; 1995:238.)

risk of malunion due to less dependability of maintenance of position and increased risk of nonunion due to lack of adequate stabilization. Therefore, most fractures are treated with open reduction and internal fixation (ORIF) so that healing is accelerated and patient comfort and safety are improved. Interestingly, there is even a recent trend toward completely avoiding the application of arch bars and proceeding directly to rigid fixation of the fracture fragments, though this approach remains quite controversial. It is certainly agreed, however, that there are benefits of avoiding postoperative MMF, particularly in the patient with a traumatic brain injury or one who is seizure prone. Still, most maxillofacial repair is started with application of arch bars and wires. As noted above, the goal of rigid fixation is to overcome the forces that will tend to distract the fracture fragments. To accomplish this, Champy et al.32 proposed “ideal lines” of osteosynthesis, along which miniplates should be placed (Fig. 21-11). With tension at the superior border and compressive forces at the inferior border of symphysis, parasymphsysis, and body fractures, Champy demonstrated the mechanical advantage of placing a “tension band” plate across the superior border. For fractures of the symphysis and parasymphysis, Champy proposed a second plate, placed inferiorly to overcome any rotational forces. Champy’s technique also suggests that a single miniplate along the ideal line will stabilize a body or angle fracture of the mandible, though several groups have demonstrated better outcomes when two miniplates are fixed at the angle.33,34 Increasingly sophisticated techniques, including computer modeling, have demonstrated the differential loads

borne by discrete areas of the mandible relative to the placement of fracture lines and bite force.35 Management of condylar and subcondylar fractures remains controversial. Although it is widely agreed that fractures of the condyle and the subcondylar region may cause a significant

FIGURE 21-11 Dotted lines represent “Champy’s Ideal Line of Osteosynthesis” as defined by Professor Maxime Champy. Miniplate fixation along these lines counteracts the predominant forces acting in each region. (Reproduced with permission from Kellman RM, Marentette LJ. Atlas of Craniomaxillofacial Fixation. New York: Raven Press; 1995:43.)

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Management of Specific Injuries

SECTION 3 X

disturbance of masticatory movement, the patient’s ability to adapt to such a disturbance may be great.36 Furthermore, there has been great concern about the risk of facial nerve injury when open reduction of these fractures is performed. This has led to decreased use of open reduction, a choice made more acceptable by the tolerable results seen with closed treatment. It should be noted, however, that closed approaches do not reduce these fractures, so that the term “closed reduction” should be removed from the lexicon. Instead, it should be called “closed management,” with the realization that management of the occlusion is a form of “forced adaptation” of the occlusion to a less than ideal anatomic position of the underlying bone. Furthermore, despite the development of a “functional occlusion” in most cases, this result is achieved at the expense of physiologic adaptation, including altered kinematics of the jaw while chewing37 and possible foreshortening of the mandi-

ble on the fractured side. This may produce significant facial asymmetry at rest and with mouth opening.36,38,39 Moreover, some patients may not be capable of adaptation, and altered jaw movement may result in chronic pain or trismus.36,37 Recently, a randomized, prospective, multiinstitutional study in Europe has demonstrated a fairly clear advantage to open reduction of subcondylar fractures of the mandible. It is an excellent study, and the reader is referred to the original publication for further elaboration.40 The introduction of the endoscope into the armamentarium of the maxillofacial trauma surgeon may minimize the main concern associated with open reduction of subcondylar fractures of the mandible.39,41 The endoscope allows for an intraoral approach and has been shown to reduce the risk of injury to the facial nerve and to eliminate facial scarring while effecting excellent results in selected patients39,41,42 (Fig. 21-12).

A

B

C

D

E

F

G

H

I

J

FIGURE 21-12 Endoscopic subcondylar fracture repair. (A) Frame of a coronal computed tomographic scan demonstrating a right subcondylar fracture with lateral overlap of the proximal fragment. (B) Lateral overlap of the proximal fragment as seen through the endoscope. (C) Artist’s depiction of B. (D) Wire through the angle of the mandible. Inset, inferior traction on the distal fragment allows the proximal fragment to fall into a reduced position. (E) Proximal fragment falling into place as inferior traction is applied. (F) Artist’s depiction of E. (G) Threaded fragment manipulator being passed through the right cheek. (H) The manipulator in position over the proximal fragment. (I) Artist’s depiction of the manipulator passing through the proximal plate hole into the proximal bone fragment. (J) Endoscopic view of the reduced fracture after plate placement is complete. (Reproduced with permission from Kellman RM. Endoscopically assisted repair of subcondylar fractures of the mandible: an evolving technique. Arch Facial Plast Surg. 2003;5:244. Copyright © 2003 American Medical Association. All rights reserved.)

Face

CHAPTER CHAPTER 21 X

Note that when a segment of mandible is severely injured with comminution or bone loss, miniplate fixation cannot provide adequate stability. A mandibular reconstruction plate is fixated to adequate proximal and distal bone stock, incorporating the comminuted fragments between.11,22 The reconstruction plate is a large plate fixed with multiple fixation points, so that it can provide a “replacement” for bone that is either missing or unable to provide support. Comminuted fragments may be fixed to one another with miniplates or wires or lagged to the reconstruction plate. Note, however, that not only is bending a heavy reconstruction plate more difficult than bending a miniplate, greater precision in adapting reconstruction plates is required to avoid creating an uncorrectable malocclusion.

Midface The forces acting across midface fractures are far less than those found in mandibular fractures. Occlusal forces impart only compressive forces to the medial and lateral buttress, and the masseter muscle imparts only mild-to-moderate amounts of shearing and rotation to a fractured zygoma.22 Thus, repair considerations focus less on the fixation strategy than on the realignment of skeletal elements so that the buttresses are restored and soft tissue and visceral structures are properly supported. In general, single miniplate fixation of buttresses and microplate fixation of intervening segments are sufficient. Repair of lower midface or Le Fort I fractures involves exposure of the bones, disimpaction of the midface, realignment of fracture segments, and plating of the vertical buttresses. Primary principles are the restoration of occlusion and vertical facial height. After reduction, the bones are secured in position with small plates and screws, and MMF is then released. Comminution complicates repair, and gaps should be spanned by bone grafts from the calvarium, rib, or iliac crest.43 Upper midface (middle third) fractures include buttress fractures in the Le Fort II and III pattern, as well as fractures through the orbital walls and zygomatic articulations. The maxillary vestibular approach is again utilized to approach the upper midface in combination with the transconjuntival approach to the orbital rims and floor. The buttresses are reduced and plated. Nasal root exposure may sometimes be required, as well. The midface may also transmit force to the deeper skeletal elements of the orbit. Therefore, after the lateral buttress and orbital rims are approached and repaired, the orbital walls, especially the floor, are explored when necessary, and reconstructed with an appropriate alloplastic or autogenous material. Le Fort II and III fractures also imply disruption of the nasal pyramid. The medial buttress is plated superiorly, reestablishing the frontal process of the maxilla and the medial orbital rim. A strong tendency for posterior rotation of the lower facial skeleton, hinged at the nasal root, is an indication for plating nasal fractures, and stabilizing the nasal root to the frontal bone. Defects in the nasal dorsum may be repaired with a free bone graft cantilevered from the glabella.22 Most recently, endoscopic repair of the orbital floor and medial wall fractures has been described. The floor is approached through the maxillary vestibular incision and an anterior maxillotomy. This approach avoids possible complications of eyelid

409

FIGURE 21-13 Orbital floor repair using autogenous bone graft. The graft is fixed to the inferior orbital rim. Multiple pieces may be plated or wired together in order to account for defects with complex shapes. (Reproduced with permission from Kellman RM, Marentette LJ. Atlas of Craniomaxillofacial Fixation. New York: Raven Press; 1995:293.)

incisions and may afford better visualization of the posterior orbital floor. The orbital contents are reduced and the floor is grafted44 (Fig. 21-13). There is a risk, however, of inadvertently pushing bone fragments into the orbit from below. Endoscopic approaches to medial orbital fractures has also been recently advocated.45,46 These are performed through the nose by exposing the fractures through the ethmoid sinus. Forces directed at the nasal root may lead to telescoping inward of the strong nasal bone as the weaker laminae of the medial orbital walls give way, allowing the lacrimal bones to splay, thereby causing telecanthus (pseudohypertelorism). This is the NOE fracture. For the purpose of repair, NOE fractures are categorized as types I, II, and III, depending on the severity of disruption of the medial canthal ligaments47 (Fig. 21-14). Type I injuries result in a large central fragment with the medial canthal ligament attached to it. Fixing this fragment above and below will stabilize the ligament in place as well. Type II fractures involve comminution of the central fragment without avulsion of the medial canthal ligament. Therefore, fixation should be augmented by transnasal fixation of the medial canthi with 28 gauge wire or 2-0 permanent suture.47 Type III injuries involve severe comminution of the NOE complex and avulsion of the medial canthus. In this case, the stumps of the canthi are approximated with a wire or permanent suture that crosses the nasal septum. Comminuted fragments are microplated or free bone grafts are used to span any gap between the medial buttress and the frontal bone.48 Often severe NOE injuries involve the lacrimal system, which should be probed and stented.

410

Management of Specific Injuries Zygoma fractures may be isolated to the arch or may involve the entire “ZMC” or “tripod.” Simple, nondisplaced fractures of the arch may be treated with observation. Displacement, however, may result in impingement of the temporalis muscle and dimpling of the cheek and should be reduced. Classically, this is accomplished via an external, Gilles incision in the temporal hair tuft or a sublabial incision. The fracture is reduced with an elevator. Most displaced ZMC fractures require ORIF. Nondisplaced fractures may be observed and, since many displaced fractures result only in cosmetic rather than functional deficits, patients may decline surgical repair. The central principle of repair is fracture realignment and fixation to reestablish the malar prominence. Although the zygomaticosphenoid (ZS) suture may be overlooked, it often provides the key information in determining final ZMC reduction. In addition, malalignment of the ZS articulation can result in a significant step-off in the lateral orbital wall and change in the orbital volume. Upper facial fractures consist of either anterior cranial vault fractures, beyond the scope of this chapter, or frontal sinus fractures and the occasional superior orbital rim fracture. Frontal sinus fractures may be isolated, but often occur in the setting of upper midface fractures including Le Fort II and III and NOE injuries (Fig. 21-15). Multiple algorithms for the evaluation and repair of frontal sinus injuries are described.48,49 The principles of treatment include reestablishing an aesthetic anterior wall, ensuring the function of the frontal sinus should it be preserved, and safe management of a possible leak of CSF or exposure of the brain. Despite minor variations, the authors agree that the following distinctions determine the treatment needed to achieve those principles: (1) site of fracture—anterior versus posterior table; (2) degree of fracture displacement in either the anterior or the posterior

Type I Fracture

SECTION 3 X Type II Fracture

Type III Fracture

FIGURE 21-14 Naso-orbito-ethmoid fracture classification.

A

B

FIGURE 21-15 Variation in severe panfacial fractures. (A) Coronal computed tomography (CT) demonstrating left Le Fort III, frontal sinus, naso-orbital ethmoid (NOE), and bilateral Le Fort I fractures as well as a split palate. (B) Three-dimensional CT demonstrating severely comminuted frontal sinus, bilateral Le Fort III, left Le Fort II, NOE, and bilateral high Le Fort I fractures. Both injuries resulted from highspeed motor vehicle accidents.

Face

FIGURE 21-16 An approach to maxillofacial and mandibular injury.

mandates increasingly aggressive treatment. Fractures that traverse the floor of the sinus, especially medially, are likely to produce dysfunction of the NFD. Possible sequelae include frontal sinusitis, mucocele, and mucopyocele. Thus, involvement of the NFD in anterior or posterior table fractures requires more aggressive management. Minimal or questionable fractures through the sinus floor or posterior table can be further assessed via endoscopy for the presence of CSF leak or obstruction of the NFD. Management options include observation, observation with medical management including antibiotic coverage, ORIF, sinus and duct obliteration, and sinus cranialization with duct obliteration. In reality, upper face and midface fractures most commonly occur in combination as the result of high-speed motor vehicle

CHAPTER CHAPTER 21 X

wall; (3) the presence of fractures through the NFD, and (4) the presence of possible CSF leak. Nondisplaced fractures of the anterior table can be observed. Anterior table fractures with significant depression or displacement should be repaired for cosmetic reasons, though the patient may opt for observation, utilizing delayed repair if a significant cosmetic deformity develops. Nondisplaced fractures of the posterior wall can also be observed. Classically, displacement of posterior table fractures greater than the width of the posterior table itself has been used as an indication for exploration. The fear is communication between the frontal sinus and the intracranial compartment with increased risk of dural tear, CSF leak, and meningitis.48,49 In reality, any displacement suggests these risks, though obviously, increasing severity of a posterior table fracture including the presence of CSF leak

411

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Management of Specific Injuries

SECTION 3 X

accidents and may also present with lower facial injuries. Although such “pan-facial” fractures represent daunting challenges to the surgeon, the authors and others espouse a “subunit” approach, by which complex fractures are repaired sequentially, thereby creating less complexity with each step of the repair.7,22 Classical approaches have been described as either “outside-in” or “inside out”; that is, from the periphery toward the center or vice versa. The authors use somewhat of a combined approach, first stabilizing the occlusion and then proceeding from the periphery toward the center (“outside-in”). The central midface is the most dependent portion of the craniofacial skeleton, providing the least in terms of native strength. Facial height and projection is, therefore, established through reconstitution of the mandible and the maxillary alveolus below and the cranial vault and upper midface above. The zygomatic arches relate the upper midface to the cranial base posteriorly. The vertical and horizontal buttresses are then reconstituted, and the upper and lower halves of the craniofacial skeleton are thus linked, with occlusion as the primary determinant of the final position. The central midface is addressed last, repairing telecanthus and restoring projection of the nasal root. Proper reduction of the mandibular arch is key.11 If the mandible is incompletely reduced and then used to set the midfacial width, height, and projection via occlusal relationships, a wide and insufficiently projected midface results. Finally, fractures of the frontal sinus and the upper midface, especially the NOE complex, may well result in disruption of the anterior skull base. Severely comminuted fractures of the frontal sinus, suspected dural lacerations, or impingement on the optic nerve suggest fractures of the anterior skull base. In this case, the authors perform a subcranial approach to the anterior skull base. This involves temporary removal of the nasoglabellar complex and a variable extent of the superior orbital rims and frontal calvarium.50 This approach affords superior exposure of the frontal lobe dura and anterior skull base with minimal retraction of the brain. The medial canthi are also directly exposed, simplifying telecanthus repair.50

MASSIVE WOUNDS High-energy insults resulting in massive full-thickness wounds to the face deserve particular attention. These include both high-speed motor vehicular trauma and close-range gunshot injuries. Management of such wounds is complex; however, primary principles and treatment approaches that maximize success have been be identified (Fig. 21-16).8,51,52 Blast wounds to the face require immediate stabilization of remaining skeletal elements, especially the mandible and midfacial buttresses, and closure of overlying soft tissue. Delay results in severe retraction of soft tissue and devitalization of the underlying skeleton. Large bony defects should be spanned by reconstruction plates in the mandible or by miniplates and bone grafts in the midface and cranial vault. Debridement in the zone of injury is repeated over the first several days until further tissue loss is not encountered. Early reconstruction utilizing local and regional tissue provides an aesthetic outcome far superior to that obtained by delayed secondary

repair including free tissue transfer.8,52 Where free tissue transfer is needed, one should expect that more than one flap will be needed. Finally, Clark et al.8 suggest that lack of lining tissue in the oral cavity and sinuses is an underappreciated cause of infection and failure of bone grafting.

REFERENCES 1. Holt G. Acute soft tissue injuries. In: Papel I, ed. Facial Plastic and Reconstructive Surgery. New York, NY: Theime; 2002:689–696. 2. Trauma TACoSCo. Advanced Trauma Life Support for Doctors. 2nd ed., Vol. 1. Chicago, IL: American College of Surgeons; 1999. 3. Kellman RM. The cervical spine in maxillofacial trauma: assessment and airway management. Otolaryngol Clin North Am. 1991;24:1. 4. Kellman RM, Losquadro WD. Comprehensive airway management of patients with maxillofacial trauma. Craniomaxillofac Trauma Reconstr. 2008;1:39–47. 5. Hoffmann J. Management of facial soft-tissue injuries. Facial Plast Surg Clin North Am. 1998;6:407–429. 6. Johnson CM, Toriumi DM. Open Structure Rhinoplasty. Philadelphia: W.B. Saunders; 1990:516. 7. Manson PN, Clark N, Robertson B, et al. Subunit principles in midface fractures: the importance of sagittal buttresses, soft-tissue reductions, and sequencing treatment of segmental fractures. Plast Reconstr Surg. 1999; 103:1287–1306, quiz 1307. 8. Clark N, Birely B, Manson PN, et al. High-energy ballistic and avulsive facial injuries: classification, patterns, and an algorithm for primary reconstruction. Plast Reconstr Surg. 1996;98:583–601. 9. Lee RH, Gamble WB, Mayer MH, et al. Patterns of facial laceration from blunt trauma. Plast Reconstr Surg. 1997;99:1544–1554. 10. Stanley R, Nowack G. Midfacial fractures: importance of angle of impact to horizontal craniofacial buttresses. Otolaryngol Head Neck Surg. 1985; 93:186–192. 11. Prein J, Assael LA. Arbeitsgemeinschaft fèur Osteosynthesefragen. Manual of Internal Fixation in the Cranio-Facial Skeleton: Techniques Recommended by the AO/ASIF-Maxillofacial Group. Berlin, New York: Springer; 1998:227. 12. Stranc MF. Primary treatment of naso-ethmoid injuries with increased intercanthal distance. Br J Plast Surg. 1970;23:8–25. 13. Gear AJ, Apasova E, Schmitz JP, et al. Treatment modalities for mandibular angle fractures. J Oral Maxillofac Surg. 2005;63:655–663. 14. Levy RA, Rosenbaum AE, Kellman RM, et al. Assessing whether the plane of section on CT affects accuracy in demonstrating facial fractures in 3-D reconstruction when using a dried skull. AJNR Am J Neuroradiol. 1991;12:861–866. 15. Hollander JE, Richman PB, Werblud M, et al. Irrigation in facial and scalp lacerations: does it alter outcome? Ann Emerg Med. 1998;31:73–77. 16. Baker SR, Swanson NA. Local Flaps in Facial Reconstruction. St. Louis: Mosby; 1995:606. 17. Rosenstein T, Talebzadeh N, Pogrel MA. Anatomy of the lateral canthal tendon. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2000; 89:24–28. 18. Baker SR, Naficy S. Principles of Nasal Reconstruction. St. Louis: Mosby; 2002:301. 19. Lewis G, Knottenbelt JD. Parotid duct injury: is immediate surgical repair necessary? Injury. 1991;22:407–409. 20. Parekh D, Glezerson G, Stewart M, et al. Post-traumatic parotid fistulae and sialoceles. A prospective study of conservative management in 51 cases. Ann Surg. 1989;209:105–111. 21. Lapid O, Kreiger Y, Sagi A. Transdermal scopolamine use for postrhytidectomy sialocele. Aesthetic Plast Surg. 2004;28:24–28. 22. Kellman RM, Marentette LJ. Atlas of Craniomaxillofacial Fixation. New York: Raven Press; 1995:337. 23. Frodel JL, Marentette LJ. The coronal approach. Anatomic and technical considerations and morbidity. Arch Otolaryngol Head Neck Surg. 1993;119:201–207, discussion 140. 24. Ellis E, Zide MF. Surgical Approaches to the Facial Skeleton. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 2006. 25. Greenberg AM, Prein J. Craniomaxillofacial Reconstructive and Corrective Bone Surgery: Principles of Internal Fixation Using AO/ASIF Technique. New York: Springer; 2002:784. 26. Kellman RM, Tatum SA. Internal fixation of maxillofacial fractures: Indications and current implant technologies and materials. Facial Plast Surg. 1998;14:3–9.

Face 40. Eckelt U, Schneider M, Erasmus F, et al. Open versus closed treatment of fractures of the mandibular condylar process—a prospective randomized multi-centre study. J Cranio-Maxillofac Surg. 2006;34:306–314. 41. Kellman RM, Cienfuegos R. Endoscopic approaches to subcondylar fractures of the mandible. Facial Plastic Surg. 2009;25:23–28. 42. Schon R, Gutwald R, Schramm A, et al. Endoscopy-assisted open treatment of condylar fractures of the mandible: extraoral vs intraoral approach. Int J Oral Maxillofac Surg. 2002;31:237–243. 43. Phillips JH, Forrest CR, Gruss JS. Current concepts in the use of bone grafts in facial fractures. Basic science considerations. Clin Plast Surg. 1992;19:41–58. 44. Farwell DG, Strong EB. Endoscopic repair of orbital floor fractures. Facial Plast Surg Clin North Am. 2006;14:11–16. 45. Ballin CR, Sava LC, Maeda CAS, et al. Endoscopic transnasal approach for treatment of the medial orbital blowout fracture using nasal septum graft. Facial Plastic Surg. 2009;25:3–7. 46. Hinohira Y, Takahashi H, Komori M, Shiraishi, A. Endoscopic endonasal management of medial orbital blowout fractures. Facial Plastic Surg. 2009;25:17–22. 47. Markowitz BL, Manson PN, Sargent L, et al. Management of the medial canthal tendon in nasoethmoid orbital fractures: the importance of the central fragment in classification and treatment. Plast Reconstr Surg. 1991;87:843–853. 48. Strong E, Sykes J. Frontal sinus and nasoorbitoethmoid complex fractures. In: Papel I, ed. Facial Plastic and Reconstructive Surgery. New York, NY: Theime Medical; 2002:747–758. 49. Yavuzer R, Sari A, Kelly CP, et al. Management of frontal sinus fractures. Plast Reconstr Surg. 2005;115:79e–93e, discussion 94e. 50. Kellman R. Use of the subcranial approach in maxillofacial trauma. Facial Plast Surg Clin North Am. 1998;6:507–510. 51. Taher AA. Management of weapon injuries to the craniofacial skeleton. J Craniofac Surg. 1998;9:371–382. 52. Yuksel F, Celikoz B, Ergun O, et al. Management of maxillofacial problems in self-inflicted rifle wounds. Ann Plast Surg. 2004;53:111–117.

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27. Kellman R. Clinical applications of bone plating systems to facial fractures. In: Papel I, ed. Facial Plastic and Reconstructive Surgery. New York, NY: Thieme Medical; 2002:720–737. 28. Winzenburg SaIM. Mandible fractures. Facial Plast Surg Clin North Am. 1998;6:445–466. 29. Haug RH, Street CC, Goltz M. Does plate adaptation affect stability? A bio-mechanical comparison of locking and nonlocking plates. J Oral Maxillofac Surg. 2002;60:1319–1326. 30. Frodel JL Jr, Marentette LJ. Lag screw fixation in the upper craniomaxillofacial skeleton. Arch Otolaryngol Head Neck Surg. 1993; 119:297–304. 31. Steinemann SG. Titanium–the material of choice? Periodontology. 2000, 1998;17:7–21. 32. Champy M, Lodde JP, Schmitt R, et al. Mandibular osteosynthesis by miniature screwed plates via a buccal approach. J Maxillofac Surg. 1978;6:14–21. 33. Fox AJ, Kellman RM. Mandibular angle fractures: two-miniplate fixation and complications. Arch Facial Plast Surg. 2003;5:464–469. 34. Levy FE, Smith RW, Odland RM, et al. Monocortical miniplate fixation of mandibular angle fractures. Arch Otolaryngol Head Neck Surg. 1991;117:149–154. 35. Tams J, van Loon JP, Rozema FR, et al. A three-dimensional study of loads across the fracture for different fracture sites of the mandible. Br J Oral Maxillofac Surg. 1996;34:400–405. 36. Ellis E, Throckmorton GS. Treatment of mandibular condylar process fractures: biological considerations. J Oral Maxillofac Surg. 2005; 63:115–134. 37. Throckmorton GS, Ellis E III, Hayasaki H. Jaw kinematics during mastication after unilateral fractures of the mandibular condylar process. Am J Orthod Dentofacial Orthop. 2003;124:695–707. 38. Miloro M. Considerations in subcondylar fracture management. Arch Otolaryngol Head Neck Surg. 2004;130:1231–1232. 39. Kellman RM. Endoscopically assisted repair of subcondylar fractures of the mandible: an evolving technique. Arch Facial Plast Surg. 2003;5:244–250.

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CHAPTER 22

Neck David V. Feliciano and Gary A. Vercruysse

INTRODUCTION One of the first reported cases of cervical trauma was in Homer’s Iliad when Achilles delivered a fatal lance blow to Hector’s neck, “where the clavicle marks the boundary between the neck and thorax.” This was portrayed by Peter Paul Rubens in about 1631 and hangs in the Museum Boymans-van Beuningen in Rotterdam, the Netherlands.1 Treatment was first described by Ambrose Pare in the mid 16th century when he ligated the right carotid artery and jugular vein of a solider who suffered a bayonet wound. The patient survived, but was aphasic and developed a dense, left-sided hemiplegia.2 The first successful treatment of a major cervical vascular injury did not occur until 1803 when Fleming aboard the HMS Tonnant ligated the common carotid artery of a sailor after a suicide attempt while at sea. The sailor made a prolonged, but complete recovery.3,4 A similar case was reported by Eves of Cheltenham, England, in 1849.5

ANATOMY Knowledge of the surface landmarks of the neck is important for optimal evaluation and management of cervical injuries.6 The defining borders of the neck encompass the area between the lower margin of the mandible and the superior nuchal line of the occipital bone and the suprasternal notch and the upper borders of the clavicles. Palpable structures from the upper to lower border of the neck include the symphysis menti, which is where the two halves of the body of the mandible unite in the midline. The submental triangle, located between the symphysis menti and the body of the hyoid bone, is bounded anteriorly by the midline of the neck. Laterally, it is bounded by the anterior belly of the digastric muscle, and the mylohyoid muscle forms the floor. The body of the hyoid bone lies opposite the third cervical vertebra. The area between the hyoid bone and the thyroid

cartilage is the thyrohyoid membrane, while the notched upper border of the thyroid cartilage is at the level of the fourth cervical vertebra. The cricothyroid ligament or membrane occupies the space between the thyroid cartilage and the cricoid cartilage, which lies at the level of the sixth cervical vertebra and the junction of the pharynx with the esophagus. The interval between the cricoid cartilage and the first tracheal ring is filled by the cricotracheal ligament. Moving inferiorly, the isthmus of the thyroid gland is at the level of the second, third, and fourth tracheal rings. The suprasternal notch can be palpated between the clavicular heads and lies opposite the lower border of the body of the second thoracic vertebra. The sternocleidomastoid muscles, which divide the sides of the neck into anterior and posterior triangles, can be palpated from sternum and clavicle to the mastoid process. The borders of the posterior triangle are the body of the mandible, the sternocleidomastoid muscle anteriorly, and the border of the trapezius muscle posteriorly, along with the clavicle inferiorly. Posteriorly, the structures of the neck that can be palpated in the midline are the external occipital protuberance, the nuchal groove, and the spinous process of the seventh cervical vertebra (cervical spines 1–6 are covered by the ligamentum nuchae). The platysma, a thin muscular sheet, is enclosed by the superficial fascia. Its origin is from the deep fascia that covers the upper part of the pectoralis major and deltoid muscles, and it inserts into the lower margin of the body of the mandible. It is the anatomic landmark that is often cited when determining whether a penetrating wound of the neck is superficial or deep. The potential for injury to a vital structure exists when this structure is penetrated. Beneath the superficial sternocleidomastoid, strap, and trapezius muscles that envelop much of the neck, there are eight body systems that lie within or pass through the neck. Included among these are the following: (1) skeletal system (seventh cervical vertebra, hyoid bone); (2) nervous system (spinal cord and the glossopharyngeal [IX], vagus [X], spinal accessory [XI], and

Neck

ZONES Penetrating wounds to the neck, particularly those that might involve cervical vascular structures, have been grouped into three separate zones since the original description by Monson et al. in 19697 (Fig. 22-1). A minor modification suggested by Roon and Christensen in 1979 is not of clinical significance.8 Zone I is inferior to the clavicles and manubrium sterni and encompasses all structures in the thoracic outlet. Structures in this zone include the proximal common carotid arteries, vertebral arteries, right and left extrathoracic subclavian arteries, jugulo-subclavian venous junctions, crossover left innominate vein, thoracic duct, trachea, esophagus, spinal cord, proximal brachial plexus, and the vagus nerve. Operative exposure for injuries in Zone I mandates a median sternotomy with cervical extensions, high anterolateral thoracotomy, or a supraclavicular incision with claviculotomy or partial excision of the clavicle, so strong clinical evidence of vascular or visceral injury must be present prior to operation. Zone II is between the thoracic outlet and the angle of the mandible. Structures in this zone include the common carotid arteries and bifurcations, vertebral arteries, internal jugular veins, larynx and cervical trachea, cervical esophagus, spinal cord, and the vagus, spinal accessory, and hypoglossal nerves. Operative exposure for injuries in Zone II mandates an ipsilateral oblique incision along the anterior border of the sternocleidomastoid muscle or a high anterior cervical incision with oblique extensions for possible bilateral injuries. Zone III is between the angle of the mandible and the base of the skull. Structures in this zone include the internal carotid arteries, vertebral arteries, internal jugular veins, pharynx, spinal cord, and the facial,

glossopharyngeal, vagus, spinal accessory, and hypoglossal nerves. Operative exposure for injuries in Zone III mandates subluxation of the temporomandibular joint with interdental wiring or vertical ramus mandibulotomy (to be discussed).

PRESENTATION Patients with penetrating or blunt trauma to the neck present with overt symptoms and/or signs, moderate or modest symptoms and/or signs, or they are asymptomatic without signs of aerodigestive or vascular injury. The presentation of a patient with overt symptoms or signs will vary depending on the zone of the neck involved. In Zone I a vascular injury from a penetrating wound may cause external hemorrhage from the thoracic outlet or intrapleural exsanguination. A penetrating wound in Zone II or blunt disruption of the cricotracheal junction secondary to a “clothesline” injury may lead to loss of the airway and early asphyxiation. Loss of the airway can occur secondary to the presence of a large hematoma from an injury to the carotid artery, as well. Active hemorrhage from either the carotid artery or internal jugular vein in Zone II can be external and lead to exsanguination or internal bleeding into an associated injury to the trachea, leading to aspiration and asphyxiation. While injures in Zone III are uncommon, exsanguination can occur from an injury to the internal carotid artery at the base of the skull. Patients with modest or moderate symptoms or signs may present with complaints of hoarseness, dysphagia, or odynophagia and palpable crepitus suggestive of injury to the larynx, trachea, or esophagus. The other presentations in this group are proximity of penetrating wound or blunt contusion to the carotid sheath and/or a stable hematoma suggestive of injury to the carotid artery or internal jugular vein. An asymptomatic patient will have penetration of the platysma muscle by a gunshot or knife wound or bruising or contusion after blunt trauma, but have no symptoms or signs of injury to the aerodigestive tracts, cervical vessels, the spine, or the spinal cord. Management of the patient depends on presentation. Overtly symptomatic patients have “A, B, or C” problems on the primary survey as taught in the Advanced Trauma Life Support course, and immediate resuscitation is performed in the emergency center or operating room (see below). Patients with modest or moderate symptoms or signs undergo a diagnostic evaluation referable to the suspected system injured or one that encompasses the aerodigestive and arterial systems. Asymptomatic patients are discharged, admitted for observation, or, in some centers, undergo a limited radiologic evaluation (i.e., cervical computed tomography [CT]).

MANAGEMENT OF PATIENTS WITH OVERT SYMPTOMS OR SIGNS

FIGURE 22-1 Zones of the neck. (From Monson DO, Saletta JD, Freeark RJ. Carotid vertebral trauma. J Trauma. 1969;9:987. Used with permission.)

In patients with exsanguinating external hemorrhage from the thoracic outlet or the lower anterior neck, usually from a penetrating wound, blind finger compression of the bleeding vessel through the skin defect is appropriate in the emergency center (Fig. 22-2). If this is unsuccessful, rapid enlargement of

CHAPTER CHAPTER 22 X

hypoglossal [XII] cranial nerves); (3) respiratory system (oropharynx, larynx, cervical trachea); (4) gastrointestinal system (oropharynx, cervical esophagus); (5) vascular system (common, internal, and external carotid arteries, vertebral arteries, internal and external jugular veins); (6) lymphatic system (thoracic duct); (7) endocrine system (thyroid and parathyroid glands); and (8) immune system (cervical extensions of the thymus).

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Management of Specific Injuries

FIGURE 22-2 Algorithm for management of patients with overt symptoms or signs.

Neck

FIGURE 22-3 Endotracheal intubation into the distal trachea in a patient with a slash wound to Zone II.

CHAPTER CHAPTER 22 X

the skin defect with or without local anesthesia is performed. Once again, an attempt is made to compress the bleeding vessel with two or three fingers inserted through the enlarged skin defect. An unsuccessful attempt is followed by tight packing of the area using 3- or 4-in gauze and rapid transport to the operating room. The operative incision will depend on the track of the wound, whether or not manual compression or packing has controlled the bleeding, and the patient’s hemodynamic status. For example, a wound thought to involve the proximal common carotid artery at the base of the neck rather than more proximally in the mediastinum is exposed with the standard anterior oblique invasion on the side of injury. An unstable patient with continuing hemorrhage from the outlet or presumed intrapleural exsanguination should undergo a high anterolateral thoracotomy (fourth intercostal space above the male nipple) on the side of the injury to allow for direct proximal clamping or pack compression of the injured vessel in the thoracic outlet. If the wound is on the right side of the thoracic outlet and the patient is profoundly hypotensive, the sternum is divided transversely and a standard (below the nipple) left anterolateral thoracotomy is performed, as well. This will allow for cross-clamping of the descending thoracic aorta to increase perfusion to the coronary and carotid arteries as resuscitation and vascular repair or ligation are accomplished. In Zone II a penetrating wound may cause impending asphyxiation from a major injury to the trachea (suggested by a continuing air leak from the entrance site). The skin defect is rapidly enlarged with or without local anesthesia, and an endotracheal tube is inserted through the enlarged track following the air bubbles into the distal end of the trachea once it is visualized (Fig. 22-3). The aforementioned “clothesline” injury from blunt trauma may cause cricotracheal separation. Even with impending asphyxiation there should only be one attempt at standard rapid sequence endotracheal intubation.9,10 If this is unsuccessful, a rapid standard tracheostomy is performed between the second and third tracheal rings below the area of injury. Should there be bruising and palpable crepitus over the thyroid cartilage suggestive of an injury to the larynx itself, once again there should only be one attempt at standard

417

FIGURE 22-4 Significant Zone II hematoma secondary to gunshot wound of carotid artery. (From Brown MF, Graham JM, Feliciano DV, et al. Carotid artery injuries. Am J Surg. 1982;144: 748–753. Used with permission, © Elsevier.)

endotracheal intubation. Failure to complete this is followed by a rapid standard tracheostomy much as with cricotracheal separation. Loss of the airway in Zone II may occur secondary to tracheal deviation or compression from a hematoma resulting from injury to the carotid artery or internal jugular vein, also (Fig. 22-4). With impending asphyxiation, the patient is rapidly moved to the operating room for an attempt at endotracheal intubation over a fiber-optic bronchoscope. If this fails or if the patient is unable to move air when first seen, a cricothyroidotomy is performed rapidly as its high limited central incision (as compared to a standard tracheostomy) avoids the lateral hematoma from the vascular injury. With external hemorrhage from a penetrating wound in Zone II, direct compression with a finger or fist on the entrance site is performed in the emergency center and en route to the operating room. The decision on where to make the incision can be made in the operating room after endotracheal intubation has been performed. On rare occasions, there may be internal hemorrhage into the airway when there are adjacent injuries to the carotid artery and trachea. While compression is placed on the carotid artery at the entrance site or at the base of the neck, a cricothyroidotomy is performed. As aspiration is likely to have occurred, fiber-optic bronchoscopy is performed once the injury to the carotid artery has been repaired. There are two options when exsanguinating hemorrhage occurs from a penetrating wound to the internal carotid artery at the base of the skull in Zone III.11 Finger compression is often only partially successful in this location as the internal carotid artery is deep to the mandible. The quickest option is to maintain manual compression as the patient is moved rapidly to the operating room. Once the patient is intubated and the neck is draped, a #3 or #4 Fogarty balloon catheter is inserted into the wound, advanced 2 cm, and the balloon is inflated12,13 (Fig. 22-5). If hemorrhage continues, the balloon is deflated and advanced 1 cm at a time and inflated till balloon tamponade controls the hemorrhage. The catheter is then sutured to the skin and the balloon left inflated for 24 hours.

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saturation level. An intracranial pressure monitor is appropriate, as well, so that treatment can be initiated when ischemic edema occurs. When the baseline EEG is abnormal and the contralateral carotid arteriogram documents inadequate crossover flow, cerebral ischemia is occurring. This is expected in patients who have had a period of significant hypotension secondary to exsanguination prior to inflation of the balloon. In the past, it was recommended that a patient with ipsilateral cerebral ischemia undergo a saphenous vein bypass from the cervical internal carotid artery to the petrous portion through a small temporal craniotomy.14 Currently, deflation of the balloon(s) and rapid insertion of an endovascular stent into the high internal carotid artery would be the procedure of choice.15,16

EVALUATION OF PATIENTS WITH MODEST OR MODERATE SYMPTOMS OR SIGNS OR ASYMPTOMATIC PATIENTS (FIG. 22-6) ■ Zone I

FIGURE 22-5 A Fogarty balloon catheter was inserted into a high cervical stab wound to control exsanguinating hemorrhage. Deflation of the balloon and removal of the catheter were performed on the fourth day after insertion. (From Feliciano DV. Management of penetrating injuries to carotid artery. World J Surg. 2001;25:1028–1035. Used with permission.)

When external passage of the balloon catheter is partially successful or unsuccessful, a Foley balloon catheter is passed as it has a larger balloon. If this is unsuccessful, as well, the catheter is removed and manual compression is applied once again. A standard oblique cervical incision on the anterior border of the sternocleidomastoid muscle is made, the internal carotid artery is exposed, and a small arteriotomy is made in the middle of a 6-0 polypropylene purse-string suture. Once again, a #3 or #4 Fogarty balloon catheter is passed through the arteriotomy and inflated sequentially until balloon tamponade is successful. On rare occasions, it may be necessary to pass balloon catheters through the entrance site and through the internal carotid artery simultaneously. A baseline EEG is performed at this time. This is followed by a contralateral carotid arteriogram to evaluate the extent of crossover flow to the side of the brain that has been rendered possibly ischemic by balloon occlusion of the internal carotid artery. Even in the patient with adequate crossover flow, every attempt should be made to keep the patient normotensive with a 100% oxygen

Hemodynamically stable patients with penetrating wounds in proximity to the thoracic outlet should undergo surgeonperformed ultrasound and a chest x-ray. The ultrasound will rule out an associated cardiac injury and document the presence of a hemothorax or pneumothorax. The chest x-ray will aid in tracking the course of the missile and in documenting the presence of a hematoma in the superior mediastinum, base of the neck, or supraclavicular area. There have been several retrospective studies that have documented that a normal physical examination and chest x-ray virtually exclude a vascular injury at the thoracic outlet.17,18 Even so, certain trauma centers will use a screening CT as an added study to determine the track of a penetrating wound in this area.19 When the track of a missile or knife wound is in proximity to vessels at the thoracic outlet and there is an adjacent hematoma on the chest x-ray, digital subtraction arteriography (DSA) of the carotid, vertebral, and subclavian arteries or a CT arteriogram (CTA) is performed. This will document the presence and location of a vascular injury and allow for the choice of an appropriate operative incision. There are symptoms (hoarseness, dysphagia, odynophagia), signs (palpable crepitus, continuing air leak through the wound), or findings on a cervical or chest x-ray (cervical or mediastinal air) that suggest a possible injury to the trachea or esophagus. The diagnostic workup is described in Section “Zone II.”

■ Zone II The approach to possible injuries in this zone has varied considerably over the past 55 years. Based on the report by Fogelman and Stewart20 at Parkland Memorial Hospital in 1956, mandatory exploration for wounds penetrating the platysma muscle was recommended. This recommendation was based on a mortality rate of 6% in patients undergoing early operation versus 35% in those undergoing delayed operation.

Neck

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FIGURE 22-6 Evaluation of patients with modest or moderate symptoms or signs or an asymptomatic patient.

It quickly became obvious, however, that cervical explorations in all patients (overtly symptomatic, modestly or moderately symptomatic, asymptomatic) with penetration of the platysma muscle in Zone II resulted in a “negative” exploration rate of approximately 50%.21 A more selective approach to operation based on symptoms and signs as described above was then adopted by many centers. One review article in 1991 comparing the two approaches noted that mandatory cervical exploration for platysma penetration had a mortality rate of 5.8% versus 3.7% for a selective approach.22 Of interest, a negative or nontherapeutic cervical operation occurred in 46.2% of patients treated with mandatory exploration. When patients with modest or moderate symptoms or signs or those who are asymptomatic are managed with a selective approach, only 55–65% eventually come to operation. Numerous large studies subsequently verified the safety of a selective approach in the 1980s and 1990s.23–33

endoscopy, serial examinations of the patient’s neck every 6–8 hours for 24–36 hours are appropriate.

Computed Tomography CT has been used as an adjunct to physical examination over the past decade in selected centers.19,36,37 In asymptomatic patients with a normal physical examination after a penetrating wound in Zone II, it “contributes minimally” to the sensitivity of physical examination.37 When patients have no “hard signs” of vascular injury in Zone II, but are “at risk for injury to vital structures within the neck,” CT can demonstrate a trajectory away from these structures.19 With such a trajectomy, “invasive studies can often be eliminated from the diagnostic algorithm.”19 A more recent study using multislice helical computed tomography/angiography (MCTA) documented a “100% sensitivity and 95.5% specificity in detecting all vascular and aerodigestive injuries sustained.”38

Physical Examination Physical examination alone is highly accurate in evaluating an asymptomatic patient with a penetrating (through the platysma muscle) stab wound in Zone II. This is true for patients with gunshot wounds in Zone II, as well, as long as the track is tangential or away from the vascular (lateral) or aerodigestive tract (central).33–35 With platysma penetration, but without further evaluation by CT, CT angiography, duplex ultrasonography, or

Arteriography, Duplex Ultrasonography, Color Flow Doppler, CTA Patients with “hard” signs of a vascular injury in Zone II present with external bleeding, bleeding into the trachea or esophagus, an expanding or stable large hematoma, and/or an audible bruit/palpable thrill. Patients with bleeding or an expanding or large stable hematoma undergo an emergency

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cervical exploration. A patient with a likely arteriovenous fistula should have some type of vascular diagnostic study performed. Should a fistula between the internal carotid artery and jugular vein be present, an endovascular stent rather than cervical exploration may be chosen. In patients with “soft” signs (modest or moderate signs) of a vascular injury in Zone II such as a history of bleeding at the scene, proximity of a stab, missile, or pellet track, or a small nonexpanding hematoma, the role of arterial diagnostic studies remains controversial. As noted above, physical examination alone is highly accurate in ruling out an arterial injury in the asymptomatic patient. Much as in evaluating possible peripheral arterial injuries, however, there is at least a 3–5% chance of a surgically reparable arterial lesion in a patient who presents with a cervical vascular “soft sign.” And it is likely that a combination of “soft signs” (i.e., proximity of wound and small hematoma) will increase the need for surgical intervention. Therefore, some type of diagnostic study is performed in patients with “soft signs” in most centers (Fig. 22-7). Four-vessel cerebral arteriography was the longtime standard of care for evaluating the carotid and vertebral arteries. The technique is highly accurate in diagnosing arterial injuries, eliminating nontherapeutic explorations, and allowing for transcatheter embolization when indicated.39,40 The disadvantages include the time required to allow the interventional radiology team to return to the hospital at night, the dye load required, and the low yield when all asymptomatic or modestly symptomatic patients are studied.41 Duplex ultrasonography, a combination of real-time brightness (B)–mode imaging and pulsed Doppler velocimetry, has been used in the diagnosis of atherosclerotic occlusive decrease of the carotid artery for 35 years.41–43 Basically, the technology produces images that define anatomy and a spectral

profile that documents flow through the vessel. Numerous reports during the 1990s documented the ease and accuracy of the technique when applied to patients with penetrating wounds in Zone II.44–47 It was suggested that duplex replace conventional arteriography because of ease of performance and the significant cost-savings that would result.46–48 This did not happen over time in most trauma centers as the technique can be performed only by a registered vascular technologist or experienced vascular surgeon trained in duplex. A related technique of “color flow Doppler” has been used to evaluate the carotid arteries after penetrating trauma to Zone II, as well.49,50 In this technique, flow to and from the point of the Doppler examination is represented on a color scale. Several studies in the 1990s documented that the combination of a careful physical examination and color flow Doppler was a safe alternative to routine contrast angiography.49,50 For the past 15 years there have been ongoing studies to determine the accuracy of CTA, particularly in patients with possible blunt cerebrovascular injuries (BCVI; to be discussed). Penetrating cervical injuries have been studied, as well, with early reports coming from the Hospital Universitario San Vicente de Paul in Medellin, Colombia.51,52 Based on the ease and speed of obtaining accurate images reconstructed at 1-mm intervals, the authors from this well-known trauma center concluded that “helical CT can replace conventional angiography in this setting” (penetrating injuries to the neck).52 Another early report from 2005, before the current generation of 32- and 64-slice detectors, documented that the use of CTA significantly decreased the number of conventional arteriograms required and negative cervical explorations performed.53 The enthusiasm for using CTA is tempered, of course, by continuing concerns about its accuracy in evaluating possible BCVI.54 But the aforementioned 2006 study with a 100% sensitivity in evaluating patients with penetrating cervical wounds is certainly reassuring.38 Based on available data, it appears that multidetector helical CTA is slowly replacing conventional arteriography as a rapid screening modality to evaluate possible arterial injuries in Zone II after penetrating trauma. An equivocal screening study or one in which the anatomic area of interest is obscured by artifacts created by adjacent metallic fragments should be followed by a conventional arteriogram.

Esophagogram/Esophagoscopy/CT

FIGURE 22-7 Pellet wound in an asymptomatic patient caused 30% transection of left common carotid artery in Zone II. Arteriogram performed secondary to traverse of missile through Zone II.

Patients with modest or moderate symptoms of an esophageal injury present with complaints of deep cervical pain, dysphagia, odynophagia, or hematemesis. On examination, palpable crepitus and deep cervical tenderness may be present. An x-ray of the neck will usually demonstrate retropharyngeal or retroesophageal air in the soft tissues, while a pneumomediastinum will be present on a chest x-ray if there has been a delay in the patient’s arrival in the trauma center. Historically, the time-honored “sip test” was performed in such patients in centers with limited resources.30 A patient who was able to swallow a mouthful of water without severe discomfort was felt to have only a small injury or no injury of the cervical esophagus and was admitted for observation only. The patient who had severe pain with swallowing would then

Neck Fiber-optic tracheoscopy and bronchoscopy is used to evaluate stable patients with suspected injuries to the trachea and major bronchi.65,66 The technique allows for placement of an endotracheal tube over the fiber-optic bronchoscope in patients with impending airway distress and for detection of penetrating or blunt perforations. Of interest, the aforementioned study using multidetector CT (MCT) in penetrating wounds of the neck documented the presence of 6 tracheal injuries in the 12 patients with positive MCT studies.38 Larger studies will be necessary to confirm the diagnostic accuracy of MCT in detecting laryngeal and tracheal injuries.

■ Zone III Historically, conventional arteriography was recommended for all stable patients with penetrating wounds in Zone III.67 Much as with mandatory diagnostic studies and/or operation in all patients with penetrating wounds of the neck, the approach to wounds in Zone III is now more selective.68 As with the other zones of the neck, patients with hard signs of an arterial injury in Zone III have a greater than 90% chance of having a positive cervical exploration. Patients without hard signs, however, rarely have an arterial injury on conventional arteriography that will require surgical intervention.68–70 Of course, arteriography or CTA will be of value in a select number of stable patients with hard signs not including bleeding or a combination of soft signs such as a history of bleeding, proximity of wound, and/or a nonexpanding hematoma in this location. When a limited arterial injury is diagnosed on one of these studies, observation or endovascular therapy would be appropriate (to be discussed).

Laryngoscopy/Fiber-Optic Bronchoscopy/CT Patients with modest or moderate symptoms of an injury to the larynx or cervical trachea present with hoarseness, stridor, or hemoptysis. On examination, contusions over the larynx or cervical trachea, palpable crepitus, deep cervical tenderness and bubbling, or an ongoing leak of air from a penetrating wound may be present. As with injuries of the cervical esophagus, paratracheal air or a pneumomediastinum will usually be present on cervical and chest x-rays. In asymptomatic patients with air in the soft tissues of the neck or those with a combination of modest/moderate symptoms and signs of a tracheal injury, the traditional diagnostic evaluation includes laryngoscopy and fiber-optic tracheoscopy and bronchoscopy. Laryngoscopy will diagnose and localize an injury to the supraglottic, glottic, or subglottic larynx.6 A vertical fracture of the thyroid cartilage with rupture of the thyroepiglottic ligament is an example of a supraglottic injury and results in retraction of the epiglottis. A fracture of the thyroid cartilage with an associated rupture of the thyroarytenoid muscles extending into the true vocal cords and aryepiglottic folds is an example of a glottic injury and results in hoarseness or stridor. As previously described, a significant injury to the lower thyroid cartilage and cricoid cartilage with separation from the trachea would result in acute respiratory distress long before a laryngoscopy could be performed.64

EVALUATION AND TREATMENT OF PATIENTS WITH POSSIBLE BLUNT CEREBROVASCULAR INJURIES While BCVI were first described in 1872, knowledge about pathophysiology, screening, diagnosis, and treatment has mainly accumulated over the past 30 years.71–74 The unique relationship of the carotid and vertebral arteries and the skull and cervical vertebrae is a causative factor for these injuries. The common carotid artery bifurcates into the internal and external carotid arteries at the level of the fourth cervical vertebra. The internal carotid artery passes upward and is then fixated in the carotid canal of the petrous portion of the temporal bone until it reaches the foramen lacerum. Most blunt injuries occur in the internal carotid artery below this fixed area in the skull. In a similar fashion, the second portion of the vertebral artery passes through the transverse foramina (foramina transversaria) of the cervical vertebrae C2–C6 before curving behind the lateral mass of the atlas. The mechanism of blunt injury to the internal carotid artery can be a direct cervical blow, a basilar skull fracture involving the carotid canal, or a fracture of the petrous portion of the temporal bone. Most authors, however, feel that the most common mechanism is a cervical hyperflexion/hyperextension injury with stretching of the vessel over the bodies of cervical

CHAPTER CHAPTER 22 X

undergo standard diagnostic testing to evaluate for the presence of an esophageal injury. While CT has now been widely applied in the diagnostic evaluation of patients with penetrating and blunt cervical trauma as previously noted, its accuracy in detecting an injury of the cervical esophagus is unclear. This is because several of the reports in which CT has been evaluated do not include any patients with esophageal injuries.36,38 For this reason, asymptomatic patients with air in the soft tissues of the neck after trauma, those with a positive “sip” test, or those with a combination of modest/moderate symptoms and signs of an esophageal injury undergo the standard diagnostic evaluation using a contrast esophagogram and endoscopy.55–57 While there is a risk of secondary necrotizing pneumonitis and pulmonary edema if the contrast agent Gastrografin (meglumine sodium) is aspirated, it remains the initial contrast agent of choice for esophagograms in most centers.56 The accuracy of detecting an injury to the cervical esophagus with this agent is 57–80%.57–60 A “thin” barium study follows a negative Gastrografin swallow or has been used as the primary contrast agent in some centers.56,57 As contrast esophagograms with either Gastrografin or thin barium have a less than 100% sensitivity in diagnosis, flexible esophagoscopy is next performed in the at-risk patient with a negative contrast study. It has long been known that the combination of a contrast study and esophagoscopy has an accuracy of nearly 100% in patients with esophageal injuries in Zone II.61 In two studies describing the results of flexible esophagoscopy specifically over the past 16 years, sensitivity was 98.5–100%, specificity 96–100%, and accuracy 97–99.3%.62,63

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vertebrae C1–C3.75 The hyperflexion/hyperextension injury is a presumed sequela of the use of shoulder harness restraints in the modern car. Prior to the use of these, many frontseat victims of head-on motor vehicle crashes sustained hyperextension injuries only on impact with the windshield. The hyperflexion–hyperextension injury to the internal carotid artery may be compounded by lateral rotation of the neck away from the side of the shoulder restraint.75,76 The mechanism of blunt injury to the vertebral artery may be a fracture of one of the foramina transversaria or a subluxation-type injury in the cervical spine with a locked facet, destroyed facet, or dislocation with instability. Depending on the cause, direct trauma to the vertebral artery (i.e., a fracture) or distraction of the foramina with secondary stretching of the artery (i.e., dislocated facet) will result.

■ Incidence/Screening As the recent incidence of BCVI is only 0.58–1.03% of all admissions for blunt trauma, there has been long-term interest in developing and analyzing screening criteria to increase the yield of diagnostic studies.77–83 There is, however, no current consensus on which risk factors mandate screening for BCVI. The group at Denver Health Medical Center, University of Colorado, has described liberal screening criteria that include symptoms/signs of BCVI and associated injuries from a “highenergy” mechanism80 (Table 22-1). A more discrete list of criteria from the University of Tennessee Health Science Center, Memphis, includes the following: (1) neurological exam not explained by brain imaging; (2) skull base fractures involving the foramen lacerum; (3) Horner’s syndrome; (4) LeFort II or III facial fractures; (5) cervical spine fracture; and (6) soft tissue injury in the neck (e.g., seatbelt injury or hanging).54,79,84 Using these criteria for screening documented an overall incidence of BCVI of 0.58% and an incidence of BCVI in the screened patients (748/20,049  3.7%) of 16%.54 In another recent study using similar criteria in 9,935 patients from the East Texas Medical Center in Tyler, the incidence of a carotid artery BCVI was 0.43% and vertebral artery BCVI was 0.59%.82 When evaluating the yield of individual criteria, the Memphis group noted that the incidence of BCVI when only

TABLE 22-1 Screening Criteria for BCVI

one criterion was present ranged from 6% to 17%.54 When similar criteria were analyzed at the University of Cincinnati in 2009, the respective incidences of BCVI varied widely. For example, skull base fractures through or near the carotid canal had a BCVI incidence of 16.9%, midface fracture or fracture dislocation of the cervical spine had an incidence of 38.8/30.7%, and Raeder or Horner’s syndrome had an incidence of 80%.81 Of interest, a recent report based on an analysis of 1,398,310 patients with blunt trauma in the National Trauma Data Bank of the American College of Surgeons (BCVI incidence  0.15%) noted that BCVI was “poorly predicted by modeling with other injuries.”83

■ Imaging for Screening With the availability of CTA over the past decade, there has been increasing enthusiasm for using this modality rather than digital subtraction cerebral arteriography to screen for BCVI. There have been numerous studies suggesting that 16-slice multidetector CTA is a very accurate modality when screening for BCVI. In one study by Berne et al.85 in which four-vessel cerebral arteriography was performed if a 16-slice CTA was positive or equivocal for BCVI, no patient with a negative CTA subsequently developed neurological symptoms. Eastman et al.86 described 146 patients who had both a 16-slice CTA and cerebral arteriography and noted a 97.7% sensitivity, 100% specificity, and 99.3% accuracy for CTA. In the study by Biffl et al.87 in which 331 patients had a 16-slice CTA and abnormal studies were followed by a conventional arteriogram, no patient with a negative CTA developed a BCVI. Much as with the lack of consensus regarding screening criteria, there are numerous studies that question the accuracy of CTA in detecting BCVI. Goodwin et al.88 performed CTA with a 16- or 64-slice scanner followed by conventional angiography 24–48 hours later in 158 patients. The combined results of CTA with 16- or 64-slice scanner were sensitivity and specificity of 97% and 41%, respectively. Similar unacceptable sensitivities have been noted in other recent studies, as well.89,90 Also, only a limited number of patients with possible BCVI have been studied with magnetic resonance angiography at this time.91 Therefore, this study cannot be recommended.

■ Types of Injuries

Cervical spine fracture Neurological exam not explained by brain imaging Horner’s syndrome LeFort II or III facial fractures Skull base fractures involving the foramen lacerum Neck soft tissue injury (e.g., seatbelt injury or hanging)

Most centers use the blunt carotid arterial injury grading scale developed at Denver Health Medical Center by Biffl et al. in 1999.92 This grading scale is described as follows: Grade I, luminal irregularity or dissection with a 25% narrowing; Grade II, dissection or intraluminal hematoma with  25% luminal narrowing, intraluminal thrombus, or raised intimal flap; Grade III, pseudoaneurysm; Grade IV, occlusion; and Grade V, transection with free extravasation.

From Miller PR, Fabian TC, Croce MA, et al. Prospective screening for blunt cerebrovascular injuries. Analysis of diagnostic modalities and outcomes. Ann Surg. 2002;236:386–395. Used with permission.

■ Management Only observation without the administration of anticoagulants is appropriate temporarily in patients with a Grade I–IV injury

Neck

OPERATIVE MANAGEMENT ■ General Principles/Incisions Once an airway has been established using the emergency techniques previously described or with standard endotracheal intubation, a rolled sheet is placed transversely under the shoulders to hyperextend the neck. The patient is then placed in a sitting position to bring the operative field closer to the surgical team. With a unilateral track of penetrating wound or with any aerodigestive injury below the larynx in Zone II, an ipsilateral oblique incision is made along the anterior border of the sternocleidomastoid muscle. The length depends on the location of the known or presumed injury, the likelihood of a significant vascular injury, and the experience of the surgeon. For

example, a patient with a large unilateral hematoma in Zone II overlying a presumed injury to the carotid artery or internal jugular vein should have an incision extending from the sternum inferiorly to the mastoid process superiorly. Such an extensive incision will allow for proximal and distal vascular control around the injury before entering the hematoma. In contrast, a patient without symptoms and signs of a vascular injury despite a deep stab wound in Zone II may be explored through a more limited oblique incision by an experienced surgeon. When the track of a missile is through Zone II bilaterally, a high anterior collar incision at the level of the track is appropriate. Depending on the patient’s hemodynamic status, superior and inferior subplatysma flaps are raised before the midline raphe of the sternohyoid muscles is opened longitudinally or the sternohyoid muscles are separated from the sternocleidomastoid muscles laterally. An injury on either side of the neck that is higher than expected can be exposed through an oblique extension of one side of the collar incision. The appropriate incision for probable or documented injury in Zone I will depend on the likely injury, the patient’s hemodynamic status, and the experience of the surgeon. A profoundly hypotensive patient with active intrapleural hemorrhage from an injury to a great vessel in the superior mediastinum or a subclavian vessel behind the clavicle should have an ipsilateral high (above the nipple) anterolateral thoracotomy. If the injury is on the right side, a trans-sternal extension and left anterolateral thoracotomy (above or below the nipple) is added to allow for cross-clamping of the descending thoracic aorta as part of resuscitation. Vascular control is then obtained with pack compression or direct clamping. When the patient is modestly hypotensive (systolic blood pressure 90–120 mm Hg) and there is a hematoma in the superior mediastinum, a median sternotomy with a cervical or supraclavicular extension is appropriate. In the stable patient with a localized vascular injury on a CTA or conventional arteriogram, a median sternotomy or supraclavicular incision is chosen depending on which vessel is injured. In the rare patient with hemorrhage from a penetrating wound to the internal carotid artery at the base of the skull in Zone III, a balloon catheter is passed through the entrance site as previously noted. Inadequate vascular control with the balloon inflated should prompt an ipsilateral oblique cervical incision to allow for exposure of the internal carotid artery and transarterial passage of a Fogarty balloon catheter for internal tamponade.106

■ Injury to the Carotid Artery Patients with “hard” signs of an arterial injury such as external hemorrhage from Zone II, internal hemorrhage into the trachea or esophagus, or the presence of a pulsating/expanding hematoma in the anterior triangle of the neck should undergo immediate cervical exploration. In patients with loss of the carotid pulse, but no neurological deficit, many centers choose to perform a CTA or conventional arteriogram to verify thrombosis of the internal carotid artery. Management of a documented thrombosis from a penetrating wound in the asymptomatic patient (observation vs. revascularization) is controversial. The

CHAPTER CHAPTER 22 X

and an associated traumatic brain injury or solid organ injury. The timing of initiation of anticoagulant therapy in the described patient groups is unclear at this time. It should, however, be based on the presence or absence of neurological findings, the magnitude of the BCVI, and the magnitude of the associated injuries. The use of anticoagulants in this situation is somewhat analogous to the use of the same for prophylaxis against deep venous thrombosis in patients with traumatic brain injuries. In one recent study using early enoxaparin in selected patients with traumatic brain injuries, but without CT exclusion criteria, the safety of this approach was demonstrated.93 Early heparinization with a continuous dosage of 10 U/(kg h) of heparin to a target partial thromboplastin time of 40–50 seconds is appropriate for patients with BCVI Grade I–IV injuries.84,94 If necessary, antiplatelet therapy may be substituted when heparin is contraindicated.95 Depending on the rate of hemorrhage, a Grade V injury is treated with surgery after subluxation of the temporomandibular joint with interdental wiring or vertical ramus osteotomy as previously noted or insertion of an endovascular stent with insertion of extraluminal coils as needed. The early enthusiasm for endovascular stenting for primarily Grade III injuries92,96–99 was tempered somewhat by the followup report from the Denver group in 2005 in which carotid stents had an occlusion rate of 45%.100 Subsequent reports, however, have demonstrated a much lower occlusion rate.101–104 In Memphis, a patient with a blunt dissection (Grade I or II) or traumatic aneurysm (Grade III) on the original CTA or conventional arteriogram is placed on anticoagulants for 1–2 weeks. Three days prior to a repeat imaging study, the patient is placed on aspirin and clopidogrel bisulfate. Should the repeat imaging study document progression of the dissection or worsening of the traumatic aneurysm, an endovascular stent is placed. Persistence of a traumatic false aneurysm outside the stent is followed by placement of a coil through the stent. The patient then continues on long-term aspirin and clopidogrel bisulfate (Timothy C. Fabian, MD, personal communication). When endovascular and operative therapies were compared in 842 patients with blunt injuries of the carotid arteries in the National Trauma Data Bank, there was no functional or survival advantage for either group.105

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presence of a suspected carotid artery–internal jugular vein fistula, particularly in high Zone II or in Zone III, should prompt a CTA or conventional arteriogram, as well. Depending on local expertise, a documented arteriovenous fistula may be treated with an endovascular stent or an open repair. As previously noted, patients with “soft” signs of an arterial injury still undergo a diagnostic workup in many centers. Included would be patients with a history of bleeding at the scene or in transit, a gunshot wound passing through Zone II, a stable hematoma, or a neurological deficit such as hoarseness from an injury to the vagus nerve proximal to the origin of the recurrent laryngeal nerve. Management will vary depending on the magnitude of any injury to the carotid artery documented on a CTA, conventional arteriogram, duplex ultrasonography, or color flow Doppler examination. In general, extravasation, the presence of an early, pulsatile pseudoaneurysm, significant disruption of the intima, or significant disruption of flow to the brain mandates ipsilateral cervical exploration and repair of the common or internal carotid artery.

Patient with an Associated Neurological Deficit A neurological deficit in a patient with a penetrating wound to the common or internal carotid artery may be due to cerebral ischemia from the injury itself, hypotension from hemorrhage, acute alcoholic intoxication, or the use of illicit drugs. In patients with any neurological deficit short of coma (GCS  8), immediate repair of the carotid artery is indicated as the etiology of the deficit may be unknown.106–112 The often-quoted review article by Liekweg and Greenfield in 1978 documented that a “favorable outcome” occurred in only 27% of patients undergoing carotid revascularization versus 25% undergoing ligation when “coma” was the presentation.106

Exposure of Zone III Injuries When stenting is not appropriate for an injury to the internal carotid artery in Zone III (i.e., active hemorrhage, pseudoaneurysm has failed stenting with trans-stent coil, internal carotid artery very small), an operative approach is indicated. Exposure of the distal internal carotid artery at the base of the skull is obtained by a “stepladder” mandibulotomy,113 subluxation of the temporomandibular joint with interdental wiring114–116 or with monocortical screws and steel wiring,117 or a vertical ramus osteotomy.118

Repair In the absence of other significant injuries, systematic heparinization (100 U/kg) is used when any repair more complex than lateral arteriorrhaphy is needed (Table 22-2). Repairs of the carotid artery are accomplished using standard techniques including the following: (1) minimal debridement and lateral arteriorrhaphy with interrupted 6-0 polypropylene sutures for a lateral defect; (2) patch angioplasty with saphenous vein, thin-walled polytetrafluoroethylene, or bovine pericardium for loss of one wall; (3) segmental resection and end-to-end anastomosis for through-and-through injuries or segmental disruption; and (4) segmental resection and insertion of a saphenous vein or polytetrafluoroethylene interposition graft.11,108,110 On

TABLE 22-2 Principles of Repair of the Carotid Artery ●

●

●

●

Systemic heparinization (100 U/kg) if complex repair (resection with end-to-end anastomosis or interposition graft) or repair at base of skull will be necessary No intraluminal shunt unless inadequate backbleeding or prolonged repair at base of skull will be necessary Interrupted 6-0 polypropylene suture repair in children or in internal carotid artery in all patients Flushing sequence after verifying back-bleeding is externally, and then into external carotid artery, and, finally, flow is reestablished into internal carotid artery

rare occasions, an injury to the proximal internal carotid artery may be repaired by ligating and dividing the distal external carotid artery and using the proximal segment as a transposition graft. In a young patient with excellent back-bleeding from the internal carotid or common carotid artery after distal vascular control has been attained, an intraluminal shunt is not indicated as the repair is completed. With a rare distal injury in the internal carotid artery in upper Zone II or in Zone III, insertion of a graft may take longer than 30 minutes. In this situation, a temporary intraluminal shunt should be considered as the repair is completed. As cross-clamping of the common or internal carotid artery after a period of hypotension and during a period of repair may result in ipsilateral cerebral ischemia, postoperative care is critical.119 The possibility of an ischemia–reperfusion injury with secondary ipsilateral cerebral edema mandates avoiding hypotension and hypoxemia as well as performing serial careful postoperative neurological examinations. Should the patient have no improvement of preoperative neurological symptoms or develops neurological deterioration in the early postoperative period, an emergency CT of the brain is performed. Ipsilateral cerebral edema is treated with the insertion of an intracranial pressure monitor as well as standard drainage and medications such as mannitol. In one older series, the survival rate for all 129 patients undergoing operation on an injured carotid artery was 75%.108 When patients failing resuscitation were excluded, the survival rate was 85%.108

Injury to the Vertebral Artery An injury to the vertebral artery such as dissection from blunt trauma or intimal disruption, a pseudoaneurysm, arteriovenous fistula, or active hemorrhage from a penetrating wound is usually diagnosed on a CTA or other imaging study in the hemodynamically stable patient. Appropriate treatment is the placement of an endovascular stent for a pseudoaneurysm or intimal lesion and acute balloon occlusion, if needed, followed by coil embolization of an arteriovenous fistula or active hemorrhage.120,121

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■ Injury to the Internal Jugular Vein Lateral venorrhaphy is appropriate for wall defects, while more extensive injuries are treated with ligation. As bilateral ligation of the internal jugular veins may result in pseudotumor cerebri, every effort should be made to repair one internal jugular vein when bilateral injuries are present.

■ Injury to the Esophagus The simplest technique to expose the cervical esophagus is to dissect down to the cervical vertebral bodies and then lift the posterior wall of the esophagus off them by stripping with a finger (Table 22-3). Exposure of the anterior esophagus requires some care, as the recurrent laryngeal nerves are located in the tracheoesophageal groove at the lower cervical level. Once the esophagus has been dissected circumferentially, it can be looped with a finger or Penrose drain and carefully inspected by pulling it toward the operating surgeon. Any area

TABLE 22-3 Principles of Repair of the Esophagus ●

●

●

Either one- or two-layer repair with absorbable sutures is acceptable, preferably in a transverse direction Loss of portion of the wall in Zone II and some patients with a delayed diagnosis of perforation should be treated with a loop esophagostomy over a rod rather than an acute tenuous repair that is likely to dehisce Combined injuries with the trachea or carotid artery mandate a vascularized muscle buttress/separator such as the sternocleidomastoid muscle

of hematoma staining should be gently explored with a scissor to see if the mucosa underneath has been perforated. If the mucosa is intact, the esophageal muscle is reapproximated with several simple interrupted sutures of 3-0 absorbable material. On occasion, it may be necessary to have the anesthesiologist help make the diagnosis of a small occult perforation in the cervical esophagus. One technique is to compress the distal esophagus at the thoracic inlet and to fill the proximal esophagus with 30–50 mL of methylene blue dye in saline (one ampule in 200 mL). Full-thickness staining of dye at any location suggests that a perforation is present. Another technique is to place the tip of a nasogastric tube in the midcervical esophagus, compress the distal esophagus with a finger or noncrushing clamp, and have the anesthesiologist inject 30–50 mL of air into the proximal esophagus through the nasogastric tube. By filling the operative field with saline solution, any air leak from an occult perforation would be seen as bubbling into the saline. With a limited injury from a stab or gunshot wound, minimal debridement is performed. A two-layer repair starts with a continuous 3-0 absorbable suture closure of the mucosa, preferably in a transverse direction. The repair is completed by placing interrupted 3-0 absorbable sutures through the muscularis layer of the esophagus. As there is a 5–25% leak from repairs of the cervical esophagus historically, a small Penrose drain or closed suction drain is placed adjacent to the repair before closure of the incision.126–129 This drain is brought anteriorly so as not to cause erosion of the carotid artery laterally. When there has been a loss of tissue from one wall or the diagnosis of a perforated cervical esophagus has been delayed, a simple lateral suture repair or end-to-end anastomosis is not appropriate. A lateral blowhole esophagostomy at the site of the defect is placed over a red Robinson catheter (like a rod under a loop colostomy) located in the incision or lateral to it.130,131 Whether a tie of absorbable suture material should be placed around the distal side of the elevated loop remains controversial.131,132 Keeping the esophagus in continuity, even with a large defect, will avoid the need for a colon interposition or free jejunal graft in the future. Conversion to a loop esophagostomy rather than performing a tenuous repair avoids the complication of a large esophagocutaneous fistula with secondary problems such as tracheoesophageal fistula, carotid artery blowout, or wound infection in the postoperative period. The esophagostomy has a tendency to shrink and to pull to the posterior midline over time, and delayed closure is often much easier than expected (Fig. 22-8).

■ Injury to the Trachea Anterior or lateral perforations are not debrided and are closed with interrupted full-thickness 3-0 absorbable sutures to create an airtight seal (Table 22-4).66,132 When there is tissue loss in the anterior or lateral trachea, a tracheostomy tube can be placed into the defect until a decision is reached on use of a vascularized muscle patch or formal reconstruction. Should the large defect be in the proximal trachea, the sternal head of the sternocleidomastoid muscle is detached, rotated medially, and sewn directly to the defect to create an airtight seal after

CHAPTER CHAPTER 22 X

In patients undergoing a cervical exploration for hemorrhage or a suspected injury to the aerodigestive systems, active hemorrhage originating from the posterolateral neck adjacent to the spinal transverse processes is likely from an injured vertebral artery. While detailed descriptions of operative approaches to the different levels of the vertebral artery are available, they are almost never utilized in the modern era.122–124 As proximal ligation of the ipsilateral vertebral artery originating from the second portion of the subclavian artery is unlikely to stop the hemorrhage, packing with bone wax or gauze is commonly utilized and is always successful. Many surgeons leave the bone wax in place, while the gauze pack will need to be removed at a reoperation. With occlusion of the vertebral artery by the trauma itself or by operative ligation or coil embolization, antegrade thrombosis is a risk in the postoperative/postprocedure period. For this reason, anticoagulation with heparin is appropriate before discharge. Whether long-term anticoagulation is necessary is unclear. When unilateral vertebral artery ligation, packing, or coil occlusion is performed, a mortality of 5–15% expected.122,125 Deaths are invariably due to prehospital exsanguination or an associated injury to the brain.

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■ Combined Injuries to the Trachea– Esophagus, Trachea–Carotid Artery, or Esophagus–Carotid Artery SECTION 3 X FIGURE 22-8 Closure of loop cervical esophagostomy was a relatively easy procedure in this patient who had esophagogastrectomy after a distal esophageal repair leaked.

removal of the tracheostomy tube. Resection of a large defect, mobilization of both ends of the trachea, and an end-to-end anastomosis have never been performed at a first operation in the senior author’s experience. When there is a large defect in the membranous portion of the cervical trachea, a three-sided longitudinal anterior pericardial flap based superiorly is created after a median sternotomy is performed. The pericardial flap is then sewn to the defect in the membranous trachea to create an airtight seal. Late reconstruction of a previously injured trachea with a segmental partial loss of tissue is best performed by a thoracic surgeon with experience in tracheal resection and reconstruction. Dissection should be limited at the 3 and 9 o’clock areas of the trachea to avoid devascularizing the ends. Both laryngeal lowering and bilateral lung elevating procedures may be necessary with gaps in the trachea exceeding 5–6 cm.133 Repair is accomplished with interrupted 3-0 absorbable sutures, no protective tracheostomy is performed, and a sternocleidomastoid muscle flap may be used to buttress the suture line (see below).

A postoperative complication rate of 74% was reported in one older series of 23 combined tracheoesophageal injuries.134 Analysis of the complications documented that the majority were due to leaks from the esophageal repair. This led to wound infections, tracheoesophageal fistulas, secondary pneumonias, and blowouts of adjacent repairs of the carotid artery. With adjacent repairs of the trachea and esophagus, trachea and carotid artery, or esophagus and carotid artery, a vascularized sternocleidomastoid muscle flap should be wrapped around the visceral repair135 (Fig. 22-9). This should lower the incidence of a leak from the visceral repair and, if a leak occurs, protect the adjacent arterial repair. The sternocleidomastoid muscle has a tripartite blood supply that includes the thyrocervical trunk, superior thyroid artery, and occipital artery. Therefore, it can be detached from the sternum and clavicle inferiorly or the mastoid process superiorly and rotated to cover the repair of the trachea or esophagus and act as a vascularized buttress. With combined injuries of the trachea, esophagus, and/or carotid artery at the upper or mid-area of Zone II, the first step is detaching the sternal head of the sternocleidomastoid muscle from the sternum if the muscle is bulky. If it is not, both the sternal and clavicular attachments are divided. Either the detached sternal end or the entire muscle is then mobilized and rotated medially to buttress the tracheal or esophageal repair and separate it from the repair in the carotid artery. The mobilized muscle is sewn in place with multiple interrupted sutures of 3-0 absorbable material. Any esophageal repair is drained anteriorly with the drain and drain track away from the repair in the carotid artery.

SUMMARY Patients with penetrating or blunt injuries to the three zones of the neck present with overt symptoms or signs, moderate or modest symptoms or signs, or they are asymptomatic without signs of aerodigestive or vascular injury. When overt symptoms

TABLE 22-4 Principles of Repair of the Trachea ● ●

●

●

No debridement is necessary One-layer repair with absorbable suture if small or moderate-sized hole When there is loss of a portion of the anterior or lateral wall, a tracheostomy tube is inserted into the defect. The sternocleidomastoid muscle is then detached inferiorly, mobilized, and sewn in an airtight fashion to the defect after the tracheostomy tube is removed When there is loss of a portion of the membranous trachea, a three-sided rectangular longitudinal flap of pericardium based superiorly is sewn to the defect to create an airtight seal

FIGURE 22-9 The sternal head of the left sternocleidomastoid muscle was interposed between tracheal and esophageal repairs after a gunshot wound in Zone II.

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REFERENCES 1. Breasted JH. The Edwin Smith Surgical Papyrus. Chicago: University of Chicago Press; 1930. 2. Key G, ed. The Apologie and Treatise of Ambroise Pare containing the Ayages made into Divers Places with Many Writings upon Surgery. London: Falcon Education Books; 1957. 3. Fleming D. Case of rupture of the carotid artery; the wounds of several of its branches, successfully treated by tying the common trunk of the carotid itself. Med Chir J Rev. 1817;3:2. 4. Keevil JJ. David Fleming and the operation for ligation of the carotid artery. Br J Surg. 1949;37:92. 5. Eves A. Report of a case of suicidal wound of the throat with profuse haemorrhage successfully treated by ligature of the common carotid artery. Lancet. 1849;1:556. 6. Britt LD, Weireter LJ Jr, Cole FJ Jr. Management of acute neck injuries. In: Feliciano DV, Mattox KL, Moore EE, eds. Trauma. 6th ed. New York, NY: McGraw-Hill; 2008:467–476. 7. Monson DO, Saletta JD, Freeark RJ. Carotid vertebral trauma. J Trauma. 1969;9:987. 8. Roon AJ, Christensen N. Evaluation and treatment of penetrating cervical injuries. J Trauma. 1979;19:391. 9. Shearer VE, Giesecke AH. Airway management for patients with penetrating neck trauma: a retrospective study. Anesth Analg. 1993;77:1135. 10. Mandavia DP, Qualls S, Rokos I. Emergency airway management in penetrating neck trauma. Ann Emerg Med. 2000;35:221.

11. Feliciano DV. Management of penetrating injuries to carotid artery. World J Surg. 2001;25:1028. 12. Feliciano DV, Burch JM, Mattox KL, et al. Balloon catheter tamponade in cardiovascular wounds. Am J Surg. 1990;160:583. 13. Ball CG, Wyrzykowski AD, Nicholas JM, et al. A decade’s experience with balloon catheter tamponade for the control of hemorrhage. J Trauma. 2011;70:330. 14. Rostomily RC, Newell DW, Grady MS, et al. Gunshot wounds of the internal carotid artery at the skull base: management with vein bypass grafts and a review of the literature. J Trauma. 1997;42:123. 15. Cox MW, Whittaker DR, Martinez C, et al. Traumatic pseudoaneurysms of the head and neck: early endovascular intervention. J Vasc Surg. 2007;46:1227. 16. Herrera DA, Vargas SA, Dublin AB. Endovascular treatment of penetrating traumatic injuries of the extracranial carotid artery. J Vasc Interv Radiol. 2011;22:28. 17. Eddy VA. Is routine arteriography mandatory for penetrating injuries to Zone 1 of the neck? J Trauma. 2000;48:208. 18. Gasparri MG, Lorelli DR, Kralovich KA, et al. Physical examination plus chest radiology in penetrating periclavicular trauma: the appropriate trigger for angiography. J Trauma. 2000;49:1029. 19. Gracias VH, Reilly PM, Philpott J, et al. Computed tomography in the evaluation of penetrating neck trauma. A preliminary study. Arch Surg. 2001;136:1231. 20. Fogelman MJ, Stewart RD. Penetrating wounds of the neck. Am J Surg. 1956;91:581. 21. Bishara RA, Pasch AR, Douglas DD. The necessity of mandatory exploration of penetrating zone II neck injuries. Surgery. 1986;100:655. 22. Asensio JA, Valenziano CP, Falcone RE, et al. Management of penetrating neck injuries. The controversy surrounding zone II injuries. Surg Clin North Am. 1991;71:267. 23. Rao PM, Bhatti MF, Gaudino J, et al. Penetrating injuries of the neck: criteria for exploration. J Trauma. 1983;23:47. 24. Dunbar LL, Adkins RB, Waterhouse G. Penetrating injuries to the neck. Selective management. Am Surg. 1984;50:198. 25. Narrod JA, Moore EE. Selective management of penetrating neck injuries. A prospective study. Arch Surg. 1984;119:574. 26. Ayuyao AM, Kaledzi YL, Parsa MH, et al. Penetrating neck wounds. Mandatory versus selective exploration. Ann Surg. 1985;202:563. 27. Cohen ES, Breaux CW, Johnson PN, et al. Penetrating neck injuries: experience with selective exploration. South Med J. 1987;80:26. 28. Wood J, Fabian TC, Mangiante EC. Penetrating neck injuries: recommendations for selective management. J Trauma. 1989;29:602. 29. Gerst PH, Sharma SK, Sharma PK. Selective management of penetrating neck trauma. Am Surg. 1990;56:553. 30. Ngakane H, Muckart DJJ, Luvuno FM. Penetrating visceral injuries of the neck: results of a conservative management policy. Br J Surg. 1990; 77:908. 31. Mansour MA, Moore EE, Moore FA, et al. Validating the selective management of penetrating neck wounds. Am J Surg. 1991;162:517. 32. Demetriades D, Charalambides D, Lakhoo M. Physical examination and selective conservative management in patients with penetrating injuries of the neck. Surgery. 1993;80:1534. 33. Atteberry LR, Dennis JW, Menawat SS, et al. Physical examination alone is safe and accurate for evaluation of vascular injuries in penetrating zone II neck trauma. J Am Coll Surg. 1994;179:657. 34. Sekharan J, Dennis JW, Veldenz HC. Continued experience with physical examination alone for evaluation and management of penetrating zone 2 neck injuries: results of 145 cases. J Vasc Surg. 2000;32:483. 35. Azuaje RE, Jacobson LE, Glover J, et al. Reliability of physical examination as a predictor of vascular injury after penetrating neck trauma. Am Surg. 2003;69:804. 36. Mazolewski PJ, Curry JD, Browder T, et al. Computed tomography scan can be used for surgical decision making in zone II penetrating neck injuries. J Trauma. 2001;51:315. 37. Gonzalez RP, Falimirski M, Holevar MR, et al. Penetrating zone II neck injury: does dynamic computed tomographic scan contribute to the diagnostic sensitivity of a physical examination for surgically significant injury? A prospective blinded study. J Trauma. 2003;54:61. 38. Inaba K, Munera F, McKenney M, et al. Prospective evaluation of screening multislice helical computed tomographic angiography in the initial evaluation of penetrating neck injuries. J Trauma. 2006;61:144. 39. Sclafani SJ, Cavaliere G, Atweh N, et al. The role of angiography in penetrating neck trauma. J Trauma. 1991;31:557. 40. North CM, Ahmad J, Segall HD, et al. Penetrating vascular injuries of the face and neck: clinical and angiographic correlation. AJNR Am J Neuroradiol. 1986;7:855.

CHAPTER CHAPTER 22 X

and/or signs are present, standard “ABC” resuscitation as described in the ATLS manual is performed. With moderate or modest symptoms or signs, a variety of diagnostic tests including cervical CT, conventional arteriography, duplex ultrasonography, color flow Doppler, CTA, esophagography, and fiber-optic esophagoscopy, tracheoscopy, and bronchoscopy are used to determine whether an injury to the carotid artery system, vertebral arteries, esophagus, or trachea is present. When a BCVI is diagnosed, heparinization for Grade I–IV injuries and endovascular stenting, balloon occlusion, or operation for Grade V injuries are indicated. Prior to repeat imaging (CTA) in patients with Grade I–III injuries, aspirin and clopidogrel bisulfate are administered in anticipation of the need for an endovascular stent. Basic principles and techniques of arterial repair are used when penetrating carotid artery injuries are present. Temporary intraluminal shunts are only indicated if distal backflow is poor or if a prolonged complex repair is anticipated in Zone III. Penetrating unilateral vertebral artery injuries with hemorrhage are managed with packing, temporary balloon, or permanent occlusion or proximal and distal ligation. Simple esophageal perforations are repaired with one or two layers of absorbable sutures. When there is a loss of esophageal tissue from one wall or a delay in diagnosis of an esophageal injury, a cervical loop esophagostomy is occasionally necessary. Tracheal repairs for routine perforations are performed with one layer of absorbable sutures. A more significant anterior defect is managed with a tracheostomy at the first operation. When there is loss of the membranous trachea, a three-sided pericardial flap that is rotated superiorly will be necessary. Diagnostic approaches and operative techniques have been refined significantly over the past 60 years, and this has resulted in a significant decrease in unnecessary operations and better outcomes after indicated operations.

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41. Menawat SS, Dennis JW, Laneve LM, et al. Are arteriograms necessary in penetrating zone II neck injuries? J Vasc Surg. 1992;16:397. 42. Blackshear WM, Phillips DJ, Thiele BL, et al. Detection of carotid occlusive disease by ultrasonic imaging and pulsed Doppler spectrum analysis. Surgery. 1979;86:698. 43. Strandress DE Jr. History of ultrasonic duplex scanning. Cardiovasc Surg. 1996;4:273. 44. Meissner M, Paun M, Johansen K. Duplex scanning for arterial trauma. Am J Surg. 1991;161:552. 45. Bynoe RP, Miles WS, Bell RM, et al. Noninvasive diagnosis of vascular trauma by duplex ultrasonography. J Vasc Surg. 1991;14:346. 46. Fry WR, Dort JA, Smith RS, et al. Duplex scanning replaces arteriography and operative exploration in the diagnosis of potential cervical vascular injury. Am J Surg. 1994;168:693. 47. Ginzburg E, Montalvo B, LeBlang S, et al. The use of duplex ultrasonography in penetrating neck trauma. Arch Surg. 1996;131:691. 48. Kuzniec A, Kaufman P, Molnar LJ, et al. Diagnosis of limbs and neck arterial trauma using duplex ultrasonography. Cardiovasc Surg. 1998;6:358. 49. Demetriades D, Theodorou D, Cornwell E III, et al. Penetrating injuries of the neck in patients in stable condition. Physical examination, angiography, or color flow Doppler imaging. Arch Surg. 1995;130:971. 50. Demetriades D, Theodorou D, Cornwell E, et al. Evaluation of penetrating injuries of the neck: prospective study of 223 patients. World J Surg. 1997;21:41. 51. Munera F, Soto JA, Palacio D, et al. Diagnosis of arterial injuries caused by penetrating trauma to the neck: comparison of helical CT angiography and conventional angiography. Radiology. 2000;216:356. 52. Munera F, Soto JA, Palacio DM, et al. Penetrating neck injuries: helical CT angiography for initial evaluation. Radiology. 2002;224:366. 53. Woo K, Magner DP, Wilson MT, et al. CT angiography in penetrating neck trauma reduces the need for operative neck exploration. Am Surg. 2005;71:754. 54. Emmett KP, Fabian TC, DiCocco JM, et al. Improving the screening criteria for blunt cerebrovascular injury: the appropriate role for computed tomography angiography. J Trauma. 2011;70:1058. 55. Bagheri SC, Khan HA, Bell RB. Penetrating neck injuries. Oral Maxillofac Surg Clin North Am. 2008;20:393. 56. Bryant AS, Cerfolio RJ. Esophageal trauma. Thorac Surg Clin. 2007;17:63. 57. Wu JT, Mattox KL, Wall MJ. Esophageal perforations: new perspectives and treatment paradigms. J Trauma. 2007;63:1173. 58. Defore WW Jr, Mattox KL, Hansen HA, et al. Surgical management of penetrating injuries of the esophagus. Am J Surg. 1977;134:734. 59. Symbas PN, Hatcher CR Jr, Vlasis SE. Esophageal gunshot wounds. Ann Surg. 1980;191:703. 60. Armstrong WB, Detar TR, Stanley RB. Diagnosis and management of external penetrating esophageal injuries. Ann Otol Rhinol Laryngol. 1994;103:868. 61. Weigelt JA, Thal ER, Snyder WH, et al. Diagnosis of penetrating cervical esophageal injuries. Am J Surg. 1987;154:619. 62. Flowers JL, Graham SM, Ugarte MA, et al. Flexible endoscopy for the diagnosis of esophageal trauma. J Trauma. 1996;40:261. 63. Arantes V, Campolina C, Valerio SH, et al. Flexible esophagoscopy as a diagnostic tool for traumatic esophageal injuries. J Trauma. 2009; 66:1677. 64. Hermon A, Segal K, Har-el G, et al. Complete cricotracheal separation following blunt trauma to the neck. J Trauma. 1987;27:1365. 65. Grover FL, Ellestad C, Arom KV, et al. Diagnosis and management of major tracheobronchial injuries. Ann Thorac Surg. 1979;28:384. 66. Lyons JD, Feliciano DV, Wyrzykowski AD, et al. Modern management of penetrating tracheal injuries. Am Surg. In press. 67. Scalfani SJ, Panetta T, Goldstein AS, et al. The management of arterial injuries caused by penetration of zone III of the neck. J Trauma. 1985;25:871. 68. Ferguson E, Dennis JW, Vu JH, et al. Redefining the role of arterial imaging in the management of penetrating zone 3 neck injuries. Vascular. 2005;13:158. 69. Biffl WL, Moore EE, Rehse DH, et al. Selective management of penetrating neck trauma based on cervical level of injury. Am J Surg. 1997;174:678. 70. Rivers SP, Patel Y, Delany HM, et al. Limited role of arteriography in penetrating neck trauma. J Vasc Surg. 1988;8:112. 71. Mulloy JP, Flick PA, Gold RE. Blunt carotid injury: a review. Radiology. 1998;207:571. 72. Verneuil M. Contusions multiples: delire violent; hemiplegie a droite, signes decompression cerebrale. Bull Acad Natl Med (Paris). 1872;36:46 [cited in Ref.71].

73. Welling RE, Saul TG, Tew JM Jr, et al. Management of blunt injury to the internal carotid artery. J Trauma. 1987;27:1221. 74. Davis JW, Holbrook TL, Hoyt DB, et al. Blunt carotid artery dissection: incidence, associated injuries, screening, and treatment. J Trauma. 1990; 30:1514. 75. Biffl WL, Moore EE, Elliott JP, et al. Blunt cerebrovascular injuries. Curr Probl Surg. 1999;36:505. 76. Feliciano DV. Patterns of injury. In: Feliciano DV, Moore EE, Mattox KL, eds. Trauma. 3rd ed. Stamford, CT: Appleton & Lange; 1996: 85–103. 77. Kerwin AJ, Bynoe RP, Murray J, et al. Liberalized screening for blunt carotid and vertebral artery injuries is justified. J Trauma. 2001;51:308. 78. Berne JD, Norwood SH, McAuley CE, et al. The high morbidity of blunt cerebrovascular injury in an unscreened population: more evidence of the need for mandatory screening protocols. J Am Coll Surg. 2001; 192:314. 79. Miller PR, Fabian TC, Croce MA, et al. Prospective screening for blunt cerebrovascular injuries. Analysis of diagnostic modalities and outcomes. Ann Surg. 2002;236:386. 80. Cothren CC, Moore EE, Ray CE, et al. Screening for blunt cerebrovascular injuries is cost-effective. Am J Surg. 2005;190:845. 81. Ringer AJ, Matern E, Parikh S, et al. Screening for blunt cerebrovascular injury: selection criteria for use of angiography. J Neurosurg. 2010; 112:1146. 82. Berne JD, Cook A, Rowe SA, et al. A multivariate logistic regression and analysis of risk factors for blunt cerebrovascular injury. J Vasc Surg. 2010; 51:57. 83. Cook A, Osler T, Gaudet M, et al. Blunt cerebrovascular injury is poorly predicted by modeling with other injuries: analysis of NTDB data. J Trauma. 2011;71:114. 84. Fabian, TC, Patton JH Jr, Croce MA, et al. Blunt carotid injury. Importance of early diagnosis and anticoagulant therapy. Ann Surg. 1996;223:513. 85. Berne JD, Reuland KS, Villarreal DH, et al. Sixteen-slice multi-detector computed tomographic angiography improves the accuracy of screening for blunt cerebrovascular injury. J Trauma. 2006;60:1204. 86. Eastman AL, Chason DP, Perez CL, et al. Computed tomographic angiography for the diagnosis of blunt cervical vascular injury: is it ready for primetime? J Trauma. 2006;60:925. 87. Biffl WL, Egglin T, Benedetto B, et al. Sixteen-slice computed tomographic angiography is a reliable noninvasive screening test for clinically significant blunt cerebrovascular injuries. J Trauma. 2006; 60:745. 88. Goodwin RB, Beery PR II, Dorbish RJ, et al. Computed tomographic angiography versus conventional angiography for the diagnosis of blunt cerebrovascular injury in trauma patients. J Trauma. 2009;67:1046. 89. Sliker CW, Shanmuganathan K, Mirvis SE. Diagnosis of blunt cerebrovascular injuries with 16-MDCT: accuracy of whole-body MDCT compared with neck MDCT angiography. AJR Am J Roentgenol. 2008;190:790. 90. DiCocco JM, Emmett KP, Fabian TC, et al. Blunt cerebrovascular injury screening with 32-channel multidetector computed tomography: more slices still don’t cut it. Ann Surg. 2011;253:444. 91. Ren X, Wang W, Zhang X, et al. Clinical study and comparison of magnetic resonance angiography (MRA) and angiography diagnosis of blunt vertebral artery injury. J Trauma. 2007;63:1249. 92. Biffl WL, Moore EE, Offner PJ, et al. Blunt carotid arterial injuries: implications of a new grading scale. J Trauma. 1999;47:845. 93. Norwood SH, Berne JD, Rowe SA, et al. Early venous thromboembolism prophylaxis with enoxaparin in patients with blunt traumatic brain injury. J Trauma. 2008;65:1021. 94. Cothren CC, Moore EE, Biffl WL, et al. Anticoagulation is the gold standard therapy for blunt carotid injuries to reduce stroke rate. Arch Surg. 2004;139:540. 95. Wahl WL, Brandt MM, Thompson BG, et al. Antiplatelet therapy: an alternative to heparin for blunt cardiac injury. J Trauma. 2002; 52:896. 96. Kerby, JD, May AK, Gomez CR, et al. Treatment of bilateral blunt carotid injury using percutaneous angioplasty and stenting: case report and review of the literature. J Trauma. 2000;49:784. 97. Brandt MM, Kazanjian S, Wahl WL. The utility of endovascular stents in the treatment of blunt arterial injuries. J Trauma. 2001;51:901. 98. Duane TM, Parker F, Stokes GK, et al. Endovascular carotid stenting after trauma. J Trauma. 2002;52:149. 99. Diaz-Daza O, Arraiza FJ, Barkley JM, et al. Endovascular therapy of traumatic vascular lesions of the head and neck. Cardiovasc Intervent Radiol. 2003;26:213.

Neck 117. Jaspers GW, Witjes MJ, van den Dungen JJ, et al. Mandibular subluxation for distal internal carotid artery exposure in edentulous patients. J Vasc Surg. 2009;50:1519. 118. Kumins NH, Tober JC, Larsen PE, et al. Vertical ramus osteotomy allows exposure of the distal internal carotid artery to the base of the skull. Ann Vasc Surg. 2001;15:25. 119. Bradley EL III. Management of penetrating carotid injuries: an alternative approach. J Trauma. 1973;13:248. 120. Waldman DL, Barquist E, Poynton FG, et al. Stent graft of a traumatic vertebral artery injury: case report. J Trauma. 1998;44:1094. 121. Albuquerque FC, Javedan SP, McDougall CG. Endovascular management of penetrating vertebral artery injuries. J Trauma. 2002;53:574. 122. Meier DE, Brink BE, Fry WJ. Vertebral artery trauma: acute recognition and treatment. Arch Surg. 1981;116:236. 123. Golueke P, Sclafani S, Phillips T, et al. Vertebral artery injury—diagnosis and management. J Trauma. 1987;27:856. 124. Reid JDS, Weigelt JA. Forty-three cases of vertebral artery trauma. J Trauma. 1988;28:1007. 125. Blickenstaff KL, Weaver FA, Yellin AE, et al. Trends in the management of traumatic vertebral artery injuries. Am J Surg. 1989;158:101. 126. Popovsky J, Lee YC, Berk JL. Gunshot wounds of the esophagus. J Thorac Cardiovasc Surg. 1976;72:609. 127. Cheadle W, Richardson JD. Options in management of trauma to the esophagus. Surg Gynecol Obstet. 1982;155:380. 128. Winter RP, Weigelt JA. Cervical esophageal trauma. Arch Surg. 1990; 125:849. 129. Asensio JA, Chahwan S, Forno W, et al. Penetrating esophageal injuries: multicenter study of the American Association for the Surgery of Trauma. J Trauma. 2001;50:289. 130. Rigberg DA, Centeno JM, Blinman TA, et al. Two decades of cervical esophagostomy: indications and outcomes. Am Surg. 1998;64:939. 131. Koniaris LG, Spector SA, Staveley-O’Carroll KF. Complete esophageal diversion: a simplified, easily reversible technique. J Am Coll Surg. 2004;199:991. 132. Symbas PN, Hatcher CR, Boehm GAW. Acute penetrating tracheal trauma. Ann Thorac Surg. 1976;22:473. 133. Montgomery WW. Suprahyoid release for tracheal anastomosis. Arch Otolaryngol. 1974;99:255. 134. Feliciano DV, Bitondo CG, Mattox KL, et al. Combined tracheoesophageal injuries. Am J Surg. 1985;150:710. 135. Losken A, Rozycki GS, Feliciano DV. The use of the sternocleidomastoid muscle flap in combined injuries to the esophagus and carotid artery or trachea. J Trauma. 2000;49:815.

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100. Cothren CC, Moore EE, Ray CE, et al. Carotid artery stents for blunt cerebrovascular injury. Risks exceed benefits. Arch Surg. 2005;140:480. 101. Joo JY, Ahn JY, Chung YS, et al. Therapeutic endovascular treatments for traumatic carotid artery injuries. J Trauma. 2005;58:1159. 102. Cohen JE, Ben-Hur T, Rajz G, et al. Endovascular stent-assisted angioplasty in the management of traumatic internal carotid artery dissections. Stroke. 2005;36:45. 103. Edwards NM, Fabian TC, Claridge JA, et al. Antithrombotic therapy and endovascular stents are effective treatment for blunt carotid injuries: results from longterm followup. J Am Coll Surg. 2007;204:1007. 104. DuBose J, Recinos G, Teixeira PGR, et al. Endovascular stenting for the treatment of traumatic internal carotid injuries: expanding experience. J Trauma. 2008;65:1561. 105. Li W, D’Ayala M, Hirshberg A, et al. Comparison of conservative and operative treatment for blunt carotid injuries: analysis of the national trauma data bank. J Vasc Surg. 2010;51:593. 106. Liekweg WG Jr, Greenfield LJ. Management of penetrating carotid arterial injury. Ann Surg. 1978;188:587. 107. Ledgerwood AM, Mullins RJ, Lucas CE. Primary repair vs. ligation for carotid artery injuries. Arch Surg. 1980;115:488. 108. Brown MF, Graham JM, Feliciano DV, et al. Carotid artery injuries. Am J Surg. 1982;144:748. 109. Weaver FA, Yellin AE, Wagner WH, et al. The role of arterial reconstruction in penetrating carotid injuries. Arch Surg. 1988; 123:1106. 110. Feliciano DV. A new look at penetrating carotid artery injuries. In: Maull KI, Cleveland HC, Feliciano DV, et al., eds. Advances in Trauma and Critical Care. Vol. 9. St. Louis, MO: Mosby-Year Book; 1994:319–345. 111. Ramadan F, Rutledge R, Oller D, et al. Carotid artery trauma: a review of contemporary trauma center experiences. J Vasc Surg. 1995;21:46. 112. Teehan EP, Padberg FT Jr, Thompson PN, et al. Carotid arterial trauma: assessment with the Glasgow Coma Scale (GCS) as a guide to surgical management. Cardiovasc Surg. 1997;5:196. 113. Dichtel WJ, Miller RH, Woodson GE, et al. Lateral mandibulotomy: a technique of exposure of penetrating injuries of the internal carotid artery at the base of the skull. Laryngoscope. 1984;94:1140. 114. Fisher DF Jr, Clagett GP, Parker JI, et al. Mandibular subluxation for high carotid exposure. J Vasc Surg. 1984;1:727. 115. Dossa C, Shepard AD, Wolford DG, et al. Distal internal carotid exposure: a simplified technique for temporary mandibular subluxation. J Vasc Surg. 1990;12:319. 116. Simonian GT, Pappas RJ, Padberg FT Jr, et al. Mandibular subluxation for distal internal carotid exposure: technical considerations. J Vasc Surg. 1999;30:1116.

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CHAPTER 23

Vertebrae and Spinal Cord Maneesh Bawa and Reginald Fayssoux

INTRODUCTION Injuries to the spine are common in trauma patients. The morbidity associated with these injuries can be significant and lifechanging, and some injuries can be life-threatening. Because polytrauma patients are initially seen in urgent circumstances, many fractures may be overlooked. In addition, the diversity of injury patterns and the potential for neurologic compromise make the evaluation and treatment of spinal trauma complex. Failure to recognize these injuries or to properly manage known injuries can have catastrophic consequences. In this chapter, the epidemiology of injuries to the spinal column, the anatomy, biomechanics, and physiology of the spine and spinal cord, the acute management and evaluation of trauma patients with suspected spinal injury, and the management of specific injuries and situations will be reviewed.

EPIDEMIOLOGY To date, the bulk of the literature on the epidemiology of spinal injury in North America has focused on patients sustaining spinal cord injury (SCI), while the epidemiology concerning patients with spinal column injuries without SCI has been less studied. There is currently only one population-based study that has been conducted on spinal column injuries.1 This 1996 study by Hu et al.1 reviewed spinal injuries within the Canadian province of Manitoba in the early 1980s. More recent studies that have attempted to define the epidemiology of spinal injury have relied on the review of patients with blunt trauma presenting to emergency rooms.2,3 While these are perhaps a less accurate reflection of the true incidence, they provide a useful estimation of the scope of the problem. In the United States, the incidence of spinal fractures has been estimated to be greater than 50,000 injuries per year. Hu et al.1 reported an annual incidence rate of spinal fractures to be 64 per 100,000 in Manitoba. In the United States, with

a population of just over 300 million, this would translate to over 192,000 injuries per year. In patients with blunt trauma, the reported incidence of spinal injury is between 3% and 4% in the cervical spine and approximately 6% in the thoracolumbar spine.2,3 Demographically, young men and elderly women are most commonly involved. Although the incidence of females sustaining spinal injury has increased in recent years, males continue to account for the majority of all patients with injury to the spine (52–70%). The most common mechanism of injury is motor vehicle crashes, followed by falls, acts of violence (gunshots, stab wounds), and sports. In certain urban regions, assaults and gunshot wounds (GSWs) may surpass falls as the principal mechanism of spinal injury (Fig. 23-1). Data regarding the epidemiology of SCI are much more robust as a result of the vast amount of time, effort, and research that has been undertaken to improve outcomes with these devastating injuries. The National Spinal Cord Injury Statistical Center (NSCISC), established at the University of Alabama in Birmingham, supervises and directs the collection, management, and analysis of data from a network of 16 federally sponsored regional centers for SCI throughout the United States. Over the past 30 years in North America, the incidence of SCI has remained relatively stable and is currently estimated to be approximately 40 cases per million population (excluding lethal cases).4,5 In the United States, this translates to over 12,000 new disabled patients each year. Currently, approximately 260,000 Americans live with an SCI. The average age at injury is 40.2 years and has been increasing over the past three decades as a result of the increasing proportion of elderly individuals affected. The mode age (i.e., the most common age at injury), however, has remained relatively consistent at 19 years. Males account for 80% of patients with SCI, blacks are at higher risk than whites, and the percentage of cases occurring among blacks has been increasing in recent years. Median hospitalization days in the acute setting has declined from 24 days from 1973 to 1979 to 12 days from 2005 to 2009.5

Vertebrae and Spinal Cord

Other/Unkn, 8.5% Vehicular, 41.3%

Violence, 15.0%

Falls, 27.3%

FIGURE 23-1 Causes of SCI since 2005. (Reproduced with permission from National Spinal Injury Statistical Center (NSCISC).)

The etiologies of SCIs are not significantly different from the etiologies of injuries to the spinal column. Motor vehicle crashes are the most common cause of SCIs, comprising approximately 41% of all injuries with rollovers accounting for 70% of these.5 Ejections occurred in 39% of those injured, and only 25% reported using seatbelts. The next most common etiology is falls (27%), followed by violence (15%), sports/recreation (8%), and other causes (9%) (Fig. 23-1). A complex interplay of social issues and advances in regulatory oversight have influenced trends in spinal injury. Improvements in emergency medical services systems, the development of safer automobiles, legislation requiring safety measures such as seatbelts, more occupational safety standards, and better regulation of contact sports have resulted in more individuals with SCI surviving the prehospitalization phase of injury and having better outcomes in survivors. As evidence of this, 38% of individuals with SCIs in 1970 died before hospitalization. In 2000, this figure had decreased to 15.8%.6 The proportion of injuries that are due to violent acts has varied over time as well, reflecting variation in national crime rates. Violent acts caused 13% of SCIs prior to 1980 and then peaked at 25% from 1990 to 1999 before declining to only 15% from 2005 to 2009.4,5 In Canada, violent acts are less common and caused only approximately 4% of all cases of SCI between 1997 and 2001.6 Falls are responsible for an increasing proportion of injuries due to the aging of the population and continue to be a major public health concern.7 Prevention and appropriate medical treatment of osteoporosis may help mitigate this trend. The assessment of comorbidities is integral to outcome following traumatic injury to the spine in these patients. The implementation of injury prevention programs developed through an understanding of injury mechanisms in national injury tracking registries and other observational studies has caused a decrease in sport-related SCIs. Previously, diving accounted for a large majority of sport-related SCIs, but the incidence of dive-related injuries has steadily decreased as a result of prevention programs. The majority of these now occur in unsupervised recreational settings.4 American football still accounts for a significant number of catastrophic spinal injuries in the United States, but the incidence of these has also decreased as a result of rule changes banning spear tackling (tackling maneuver using the crown of the head to “spear” an opposing player).8 Extreme sports such as snowboarding and mountain biking now account for an increasing percentage of SCIs. Incomplete quadriplegia is the most frequent neurologic category of SCI (38%), followed by complete paraplegia

ANATOMY AND BIOMECHANICS OF THE SPINAL COLUMN The spine functions to allow spinal motion while protecting the enclosed neural elements from injury. The spinal column is composed of 7 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 4–5 coccygeal vertebral segments and forms the foundation of the axial skeleton of the body, extending from the base of the skull to the pelvis with articulations to the rib cage. Each vertebra has an opening that contributes to the anatomy of the spinal central canal as well as multiple processes that serve as lever arms for the ligamentous and muscular attachments (e.g., spinous process, transverse process). The normal spine in the uninjured state positions the head directly over the pelvis in the coronal and sagittal planes (i.e., coronal and sagittal balance). In the coronal plane the spine is straight, while, in the sagittal plane, the cervical and lumbar spines are lordotic and the thoracic spine is kyphotic. These sagittal curvatures in conjunction with the intervertebral discs provide resiliency to applied loads. The unique, highly specialized anatomy of the upper cervical spine allows weight transfer between the head and neck,

CHAPTER CHAPTER 23 X

Sports, 7.9%

(23%), incomplete paraplegia (22%), and complete quadriplegia (17%). Over the past 15 years, the proportion of persons with incomplete paraplegia has increased with a concomitant decrease in the proportion of persons with complete paraplegia and quadriplegia. Improved survival after occipitocervical and upper cervical injuries as a result of improvements in EMS and direct medical care has likely contributed to an increase in ventilator-dependent discharges in the last 30 years (2.3–6.8%).4 The overall impact of an SCI on the individual patient, family, and society remains staggering. Few conditions aside from SCI result so abruptly in such a degree of permanent disability. The young and highly functional individuals that SCI so typically affects (recall the mode age of 19 years) face the severe challenge of reintegrating into society after injury. The patient has suffered a devastating transformation in quality of life and loss of independence, and the injury will have a profound impact on his or her lifestyle, personal goals, economic security, and interpersonal relationships. Data from the NSCISC have shown that only one third of persons with paraplegia and about one fourth of those with quadriplegia were employed at postinjury year 8.5 Among those who were married at the time of injury, as well as those who marry after injury, the likelihood of their marriage remaining intact is much lower when compared to the general population.5 Also, less than 5% of patients with SCI will marry following their injury. In addition, the economic burden of all persons living with SCIs in the United States has been estimated to approach $10 billion per year.5 The lifetime costs for health care and living expenses vary depending on severity of injury and age at the time of injury. Estimates for these lifetime costs (in 2009 dollars) range from $750,000 for a 50-year-old patient with paraplegia to $3.3 million for a 25-year-old individual with high quadriplegia (C1–C4). Note that these are the direct costs and do not account for the indirect costs associated with lost wages and productivity.

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Management of Specific Injuries

SECTION 3 X

Basion Anterior atlantooccipital membrane

Vertebral artery

Apical ligament of dens

Posterior arch of atlas Superior longitudinal band of cruciate ligament

Anterior acrh of atlas Dens Inferior longitudinal band of cruciate ligament

Tectorial membrane Ligamentum flavum

Anterior longitudinal ligament Posterior longitudinal ligament A

AP

AP

AL

AC

TR

B

C

FIGURE 23-2 (A) Midsagittal section of the upper cervical spine. Note the tectorial membrane as the cranial continuation of the posterior longitudinal ligament (PLL). (B) Posterior view of the cruciate ligament composed of a transverse atlantal ligament (TR) with superior and inferior longitudinal bands. The strong transverse atlantal ligament (TR) is important for preventing atlantoaxial subluxation. Note the apical (AP) and alar (AL) ligaments just anterior to the cruciate ligament. (C) Anterior view of the apical and alar ligamentous attachments. (Reproduced with permission from Jackson RS, Banit DM, Rhyne AL, Darden B V. Upper cervical spine injuries. J Am Acad Orthop Surg. 2002;10:271. Copyright 2002 by the American Academy of Orthopaedic Surgeons.)

facilitates neck motion, and protects the neurovascular elements from injury (Fig. 23-2). The occiput articulates with the atlas through paired synovial joints formed between the convex occipital condyles located at the lateral margins of the foramen magnum and the concave facets of the atlantal lateral masses. The occipitoatlantal articulation is responsible for 50% of the normal flexion–extension arc. The atlas itself is composed of two lateral masses connected by anterior and posterior arches that serve as attachment points for controlling and stabilizing ligamentous and muscular insertions. Grooves on the superior surface of the posterior arch accept the paired vertebral arteries after they pass through the paired transverse foramina. The odontoid process, or dens, extends rostrally from the body of the axis to articulate with the posterior aspect of the anterior arch of the atlas. Embryologically, the odontoid is the former centrum of the atlas that separates during gestation and fuses with the centrum of the axis. These three atlantoaxial synovial articulations allow rotational motion to occur and are responsible for 50% of the normal rotational range of motion (ROM). The spinous process of the axis is generally large and bifid due to the multiple insertions it accommodates.

The motion afforded to the upper cervical spine by this complex osseous anatomy requires stabilizing ligamentous restraints to prevent damage to the enclosed neural elements. This reliance on ligamentous structures for stability is important, and proper evaluation of the stability of the upper cervical spine requires an assessment of the integrity of these ligamentous structures (i.e., dynamic radiography, magnetic resonance imaging, etc.). Multiple ligaments stabilize the upper cervical articulations, and these can be divided into intrinsic and extrinsic ligaments. The intrinsic ligaments, located within the spinal canal, are the most important contributors to stability of the upper cervical articulations. They form three layers anterior to the dura and include, from dorsal to ventral, the tectorial membrane, the cruciate ligament, and the odontoid ligaments. The tectorial membrane is the cranial continuation of the posterior longitudinal ligament connecting the posterior body of the axis with the anterior margin of the foramen magnum. The cruciate ligaments lie just ventral to the tectorial membrane where they stabilize the odontoid articulation with the anterior arch of the atlas. The transverse atlantal ligament (TAL) is the strongest component of the cruciate ligament. Injury to it can result in instability of the

Vertebrae and Spinal Cord

CHAPTER CHAPTER 23 X

Superior view

Posterior view

Lateral view

Anterior view

FIGURE 23-3 Cervical vertebrae. Front, back, side, and axial views.

atlantoaxial articulation. The odontoid ligaments are the furthest ventral and include the apical and paired alar ligaments. The smaller and less structurally important apical ligament connects the tip of the odontoid process with the anterior margin of the foramen magnum. The much stronger paired alar ligaments connect the odontoid to the occipital condyles. Extrinsic stability is provided by the ligamentum nuchae, which extends from the external occipital protuberance to the posterior arch of the atlas and the tips of the cervical spinous processes as well as the paired occipitoatlantal and atlantoaxial joint capsules. In the upper cervical spine, flexion is limited by the bony anatomy, while extension is limited by the tectorial membrane. Rotation and lateral bending are restricted by the contralateral alar ligaments. The cruciate ligaments restrict potentially dangerous anterior translation during flexion, while still allowing torsion around the dens. Distraction 2 mm is prevented by the tectorial membrane and alar ligaments. Translation is limited by the facet joints when the tectorial membrane and alar ligaments are intact. The apical ligament has a negligible effect on restricting motion between the occiput and C2. The remaining vertebrae of the subaxial cervical spine (C3–C7) more closely resemble the vertebrae of the thoracic and lumbar spines (Fig. 23-3). Vertebral bodies are separated by intervertebral disks. The posterior elements are composed of paired pedicles, lateral masses, facet joints, laminae, transverse processes, and a single spinous process. The transverse process contains the transverse foramen, through which the vertebral artery (the first major branch of the subclavian artery) passes. The motion segments are stabilized by three structures as follows: (1) the anterior longitudinal ligament running on the ventral aspect of the vertebral bodies from the foramen magnum to the sacrum; (2) the posterior longitudinal ligament running

on the dorsal aspect of the vertebral bodies from the foramen magnum to the sacrum (its cranial extent between C2 and the occiput is referred to as the tectorial membrane); (3) and the posterior ligamentous complex (PLC). The anatomical structures of the PLC include the supraspinous ligament, interspinous ligament, ligamentum flavum, and facet joint capsules (Fig. 23-4). The PLC plays a critical role in protecting the spine and spinal cord against excessive flexion, rotation, translation, and distraction. Some have likened it to a posterior tension band that restricts excessive motion. Once disrupted, the ligamentous

Posterior longitudinal ligament

433

Lamina

Superior articular process Spinous process Supraspinal ligament

Body Inter vertebral fibrocartilage

Ligamenta flava

Anterior longitudinal ligament

Inter-spinal ligament

Basivertebral vein Pedicle

Capsular ligament

FIGURE 23-4 Midsagittal section of the lumbar spine detailing the components of the posterior ligamentous complex (PLC). This important posterior tension band is composed of the facet capsules, ligamentum flavum, and the interspinous and supraspinous ligaments.

434

Management of Specific Injuries

SECTION 3 X

Superior view

Posterior view

Lateral view

Posterior view

FIGURE 23-5 Lumbar vertebrae. Front, back, side, and axial views.

structures demonstrate poor healing and the need for adjunctive surgical stabilization of the involved vertebrae to prevent progressive kyphotic collapse. The PLC plays an important role in spinal stability in the thoracic and lumbar spines, as well. Thoracic vertebrae are similar in structure to the cervical, but they are larger, lack transverse foramina, and have larger transverse and spinous processes. There is much more inherent stability of the thoracic spine compared with the cervical and lumbar regions due to the stabilizing effects of the rib cage and sternum. The thoracolumbar junction is a transition zone between the relatively rigid thoracic spine and the more flexible lumbar segments. The lumbar vertebrae are the most stout as they must carry more body weight than their cervical and thoracic counterparts (Fig. 23-5). An important stabilizing ligament is the iliolumbar ligament, between the L5 transverse process and the ilium, which can be injured with spinal or pelvic trauma. The sacrum forms the base of the spinal column and also functions as the keystone of the pelvic ring. There are no true intervertebral disks within the sacrum though occasionally a rudimentary disk may be noted in the presence of transitional lumbosacral anomalies. These anomalies are important to recognize because they affect the numbering of vertebrae. In these situations, numbering from the sacrum up may not match up with the numbering when counting down from the last thoracic rib. This can result in confusion between caregivers and has been shown to contribute to wrong-level surgery. The sacral nerve roots lie within intraosseous sacral foramina. The S1 and S2 nerve roots are larger and take up more room within their foramina in contrast to the S3 and S4 nerve roots and are more susceptible to injury.

ANATOMY AND PHYSIOLOGY OF THE SPINAL CORD The spinal cord represents the caudal continuation of the brain and brainstem, extending from the brainstem at the level of the foramen magnum through the spinal canal to T12–L1 where it terminates as the conus medullaris. A collection of lumbosacral nerve roots continues from the conus medullaris forming the cauda equina. At each intervertebral space, the ventral and dorsal roots join to form a nerve root that exits the spinal canal through the neural foramen. The central nervous system is invested by three layers of meninges from superficial to deep including the dura, arachnoid, and pia mater. The spinal cord and intraspinous portions of the nerve roots are contained within dura mater, the thickest of the meningeal layers. Between the arachnoid and the pia mater lies the subarachnoid space. Cerebrospinal fluid within the subarachnoid space surrounds the spinal cord providing a mechanical buffer to injury (i.e., shock absorber) and also allows for homeostatic regulation of the distribution of neuroendocrine factors. The neural elements within the spinal cord itself are arranged geographically. The long neural tracts extending to and from the brain are arranged peripherally and are composed primarily of white matter. The more central gray matter contains the cell bodies of the lower motor neurons. The main descending motor pathway is the lateral corticospinal tract. The upper motor neuron originates in the contralateral cerebral cortex, decussates in the midbrain, and descends on the ipsilateral periphery of the spinal cord. The upper motor neuron then synapses with its corresponding

Vertebrae and Spinal Cord

Posterior spinal arteries Penetrating arteries Sulcal arteries Radiculomedulary artery of Adamkiewicz Anterior spinal artery Radicular artery

Segmental artery

Aorta

FIGURE 23-6 Blood supply of the spinal cord. (Reproduced, with permission, from Prasad P, Price RS, Kranick SM, Woo JH, Hurst RW, Galetta S. Clinical reasoning: a 59-year-old woman with acute paraplegia. Neurology. 2007;69:E41–E47.)

NEUROLOGIC INJURY ■ Location of SCI The cervical region and thoracolumbar junction are the most frequent sites of injury in patients with SCI. Cervical spine injuries can occasionally be lethal, especially when the upper cervical cord is involved because it is critical for respiratory drive. Fracture–dislocations and subluxations of the cervical spine are most common at the level of the C5–C6 vertebrae. Thoracic fractures are less common than cervical, and most of these involve the vertebrae of the thoracolumbar junction (T10–12). These injuries are typically caused by crushing or extreme flexion of the spine in motor vehicle crashes or falls. Injuries involving the lumbar spine can damage the conus or the cauda equina depending on the level of injury.

■ Primary and Secondary Spinal Cord Injury Primary SCI results from direct mechanical forces such as shear, laceration, distraction, and compression that cause structural disruption of neural and vascular structures with abrupt and indiscriminate cell death. Persistent pressure on the cord by space occupying bone, ligaments, or a disc can potentiate mechanical damage to the cord after the primary injury. As a response to the initial mechanical insult, hemorrhage, edema, and ischemia rapidly follow, extending to contiguous areas of neural tissue. A subsequent biochemical cascade of events that involves a variety of complex chemical pathways leads to delayed or secondary cell death that evolves over a period of days to weeks. These “secondary injury” mechanisms result in the death of a population of neural cells that otherwise would have survived the initial insult. Thus, except for petechial hemorrhage, the human spinal cord may show no significant macroscopic or histopathologic changes until 6–24 hours after trauma.9 Although the exact mechanism of secondary spinal cord damage is not well understood, various functional hypotheses are proposed. After the initial hemorrhage, inflammation proceeds in the central gray matter. On a systemic level, hypotension, either from hypovolemia or from autonomic dysfunction with neurogenic shock, contributes to impaired perfusion of the spinal cord and ischemia. Experimental studies in animal models of SCI have shown an increase in products of anoxic metabolism in neural tissue. Multiple other theoretical mechanisms could potentially contribute to the pathophysiology of secondary injury; however, a synergistic effect of several of these mechanisms is most likely responsible. In the inflammatory theory, increased activity of cyclooxygenase and lipoxygenase results in accumulation of inflammatory mediators (i.e., prostaglandins, leukotrienes, platelet-activating factor, serotonin) that produce secondary neuronal damage.10 The effect of inflammatory mediators seems to be potentiated in anoxic conditions with diminished tissue perfusion.11 The neurotransmitter theory posits that increased levels of excitatory amino acid neurotransmitters such as glutamate and aspartate are released as a result of primary SCI and may cause secondary neuronal injury.12 Evidence to support this theory includes the experimentally induced neurologic dysfunction that occurs

CHAPTER CHAPTER 23 X

lower motor neurons in the anterior horn of the gray matter. The lateral corticospinal tract has traditionally been thought to be arranged with the tracts subserving function of the upper extremity more centrally located and the tracts subserving function of the lower extremity and sacral roots more peripherally located. This has been proposed as the reason for the disproportionately greater motor impairment in upper compared to lower extremities in patients with central cord syndrome; however, whether this lamination truly exists is controversial. The major ascending sensory pathways include the posterior column tracts (fasciculus gracilis, fasciculus cuneatus) and the more ventrally located lateral spinothalamic tracts. Sensory input from the periphery synapses at the neuronal cell bodies located in the dorsal root ganglion and then enters the posterior horn of the gray matter. Pain and temperature input cross immediately to the opposite side of the spinal cord and ascend in the contralateral lateral spinothalamic tract. Proprioception and vibratory sensation ascend ipsilaterally in the posterior column of the spinal cord and decussate at the level of the brainstem. Similar to the lateral corticospinal tract, the dorsal columns are arranged such that tracts subserving function of the upper extremity are more centrally located and tracts subserving function of the lower extremity and sacral roots are more peripheral. The major vessels (i.e., aorta and vena cava) lie anterior to the thoracic and lumbar vertebral bodies. Segmental branches arising from the aorta and iliac arteries course around the lateral edge of the vertebral bodies where they enter the vertebral foramina to form the anterior and paired posterior spinal arteries, the main blood supply to the spinal cord (Fig. 23-6).

435

Management of Specific Injuries of opiate antagonists such as naloxone has improved neurologic recovery in experimental models.15

■ Classification All spinal cord lesions can be classified as neurologically complete or incomplete using the American Spinal Injury Association (ASIA) Scale16 (Fig. 23-7). This distinction is important prognostically since incomplete injuries have a chance at neurologic recovery, whereas motor recovery is achieved in only 3% of patients with complete injury during the first 24 hours and never after 24–48 hours.17,18 Patients with complete cord injury have no motor or sensory function caudal to the level of the injury. Although the ASIA classification requires a patient to have sacral sparing in order to be classified as incomplete, any sensory or motor function caudal to the level of injury is sufficient to designate a patient as incomplete because this signifies at least partial continuity of the long white-matter tracts (i.e., corticospinal and spinothalamic) from the cerebral cortex to the conus medullaris. During the initial evaluation of a patient with SCI, sacral root sparing may be the only neurologic function

STANDARD NEUROLOGICAL CLASSIFICATION OF SPINAL CORD INJURY LIGHT TOUCH

MOTOR R

L

C2 C3 C4 C5 C6 C7 C8 T1 T2 T3 T4 T5 T6 T7 T8 T9 T10 T11 T12 L1 L2 L3 L4 L5 S1 S2 S3 S4-5

TOTALS

KEY MUSCLES

L

R

SENSORY

+

=

MOTOR SCORE (100)

NEUROLOGICAL R SENSORY LEVEL The most caudal segment MOTOR

TOTALS

0 = absent 1 = impaired 2 = normal NT = not testable

C3 C4

C2 C3 C4 T2

S3

T1 C6

S4-5

T2

T3 T4 T5 T6 T7 T8 T9

C5

C5

T1 C6

T10 T11 T12

Palm L 2 L 3

S2

L1

L1

L2

L2

Palm

L 2 L 3

S2

L3

L3

Dorsum L 4 S1 L5

Dorsum

L 4

L4 S1

L4 L5

L5

L5

Key Sensory Points S1

S1 S1

Any anal sensation (Yes/No) + +

(MAXIMUM) (56) (56)

L

C2

KEY SENSORY POINTS

L

C2 C3 C4 Elbow flexors C5 Wrist extensors C6 C7 Elbow extensors Finger flexors (distal phalanx of middle finger) C8 Finger abductors (little finger) T1 T2 0 = total paralysis T3 1 = palpable or visible contraction T4 2 = active movement, T5 gravity eliminated T6 3 = active movement, T7 against gravity T8 4 = active movement, T9 against some resistance T10 5 = active movement, T11 against full resistance T12 NT = not testable L1 Hip flexors L2 Knee extensors L3 Ankle dorsiflexors L4 Long toe extensors L5 S1 Ankle plantar flexors S2 S3 Voluntary anal contraction (Yes/No) S4-5

(MAXIMUM) (50) (50)

with normal function

R

PIN PRICK

C7 C8

SECTION 3 X

when the cord is exposed to excitatory amino acids, as well as the reduction in the extent of functional deficits with pretreatment using amino acid antagonists.13 The free-radical theory suggests that free radicals accumulate in the injured neural tissue and damage nucleic acids within the cell as well as lipids and proteins that comprise the cell membrane. Inability to maintain the integrity of the cell membrane results in neuronal death due to uncontrolled influx of ions and unbalanced osmotic pressure. The calcium ion theory implicates the influx of extracellular calcium ions into nerve cells as the cause of secondary injury since intracellular accumulation of calcium with efflux of potassium has been observed in experimental SCI.14 An excess of calcium ions activates phospholipases, proteases, and phosphatases that in turn lead to interruption of mitochondrial activity and disruption of the cell membrane. Initial neuronal swelling is related to sodium influx, whereas subsequent neuronal disintegration results from calcium influx. Both competitive and noncompetitive calcium channel blockers have been demonstrated experimentally to reduce secondary neurologic injury.15 Another theory postulates the involvement of endogenous opioids such as peptides, dynorphin, endorphin, and enkephalins, because timedependent injuries can be related to dynorphin. Also, application

C7 C8 C6

436

= =

PIN PRICK SCORE LIGHT TOUCH SCORE

(max: 112) (max: 112)

(56) (56)

COMPLETE OR INCOMPLETE? Incomplete = Any sensory or motor function in S4-S5

ASIA IMPAIRMENT SCALE

ZONE OF PARTIAL R PRESERVATION SENSORY Partially innervated segments MOTOR

FIGURE 23-7 The ASIA classification of neurologic deficit following spine injury. (This form may be copied freely but should not be altered without permission from the American Spinal Injury Association.)

L

Vertebrae and Spinal Cord

CHAPTER CHAPTER 23 X

present to differentiate incomplete from complete SCI. Evaluation for sacral sparing consists of perianal sensation to light touch and pinprick, rectal tone, and voluntary contraction of the external anal sphincter. Spinal shock can complicate this assessment. It is a temporary state of spinal cord dysfunction associated with complete areflexia that usually resolves 24–48 hours after the time of injury. Until spinal shock has resolved, the completeness of the neurologic injury cannot be determined. Return of the bulbocavernosus reflex heralds the end of spinal shock. This clinical test assesses the integrity of the local S3–S4 reflex arc and is performed by squeezing the glans penis, placing pressure on the clitoris, or tugging on a Foley catheter while performing a rectal exam. An intact reflex will result in contraction of the anal sphincter. If there continues to be no distal sensory or motor recovery at the point the bulbocavernosus reflex has returned, the injury is designated as complete and no further significant neurologic improvement can be expected.

Anterior Spinal Cord Syndrome

■ Neurologic Syndromes Anterior Cord Syndrome This incomplete SCI results classically from vascular injury, resulting in anterior spinal artery insufficiency and ischemic injury to the anterior two thirds of the cord, but can also occur after blunt trauma to the anterior spinal cord (Fig. 23-8). Clinically, patients present with loss of motor function and pain and temperature sensation below the level of injury from involvement of the ventrally located lateral corticospinal and spinothalamic tracts. They do, however, retain proprioception and the ability to sense vibration and deep pressure from preservation of the posterior columns. Because ischemic neural tissue has a poor prognosis for recovery, the chance of meaningful clinical recovery in anterior cord syndromes is poor.

Central Spinal Cord Syndrome

Brown-Séquard Syndrome

Central Cord Syndrome Classically, central cord syndrome results from a hyperextension injury in an older patient with preexisting cervical spondylosis. It can, however, arise from a variety of different mechanisms. Clinically, the upper extremities are more involved than the lower extremities, due to the more central location of the upper extremity axons within the spinal cord tracts. Patients typically regain the ability to walk, but have more limited return of upper extremity function.

Brown-Séquard Syndrome This incomplete cord syndrome can result from hemitransection of the spinal cord with unilateral damage to the corticospinal tract, spinothalamic tract, and dorsal columns. Patients present with loss of ipsilateral light touch sensation, proprioception, and motor function and contralateral loss of pain and temperature sensation. The prognosis is generally good.

Posterior Spinal Cord Syndrome

FIGURE 23-8 The most common patterns of incomplete spinal cord injury.

with many patients experiencing difficulty walking due to the deficit in proprioceptive sensation.

Cervical Root Syndrome Posterior Cord Syndrome This syndrome is rare and results from involvement of the dorsal columns with subsequent loss of proprioception and vibration and preserved motor function. The prognosis is variable

437

This represents an isolated nerve root injury that causes a deficit in sensation and motor function. This injury can be associated with an acute disc herniation or facet fracture, subluxation, or dislocation.

438

Management of Specific Injuries

Conus Medullaris Syndrome

SECTION 3 X

The conus medullaris is typically located at the level of the L1–L2 intervertebral space. Injury can produce mixed upper and lower motor neuron findings. Isolated injury to the conus may result in loss of bowel and bladder control (no sacral sparing), and the prognosis for recovery is poor.

Cauda Equina Syndrome The cauda equina extends distal to the conus and is composed of the lumbar and sacral nerve roots. Injury results in lower motor neuron findings with sensory loss and motor dysfunction. Involvement of the lower sacral roots can result in bladder and bowel dysfunction. Urgent decompression (within 72 hours) optimizes outcomes, and the prognosis for motor recovery is moderate.

PREHOSPITAL CARE Advances in prehospital screening and transport have helped reduce the chance of missing a significant spinal injury.19 Field evaluation of patients with suspected spinal injury begins with the primary and secondary surveys as detailed by the American College of Surgeons Advanced Trauma Life Support (ATLS) course. The primary survey begins with evaluation of the airway, breathing, and circulation, followed by assessment of disability and exposure (ABCDE). All patients are considered to have a spinal injury until proven otherwise. If lack of significant spinal injury cannot be ruled out at presentation, then immediate institution of spinal precautions is necessary. The cervical spine can be immobilized with a rigid cervical collar, but this is not a substitute for careful handling of the patient. With complete ligamentous disruption, the collar provides minimal stabilization. Manual stabilization of the spine is much more important and effective in restricting motion during patient transfers than any external orthosis.20 The thoracic and lumbar spines can be immobilized with a backboard at the time of injury. Recently, considerable attention has been directed toward the role of immobilization at the scene of injury since uniform application of spinal immobilization to all trauma patients may be unnecessary (e.g., patient with GSW to torso).21 If it becomes necessary to secure an airway, care is required during intubation to prevent hyperextension of the neck that might cause an iatrogenic injury to the cervical spine or spinal cord. Therefore, intubation should be performed with in-line cervical traction, a cervical collar in place, or fiber-optic assistance. Maintenance of oxygenation and hemodynamic stability with supplemental oxygen, blood pressure support, and early use of blood products may minimize the potential for secondary ischemic injury in patients with a suspected SCI. Patients who present with hypotension and shock usually have hypovolemia from hemorrhage and should be aggressively treated with fluid resuscitation and blood products. In patients with an injury to the spinal cord, however, hypotension may result from neurogenic shock, which is due to disruption of sympathetic output to the heart and peripheral vasculature. Neurogenic shock is distinguished by bradycardia, instead of tachycardia, in

the presence of hypotension. These patients typically require the use of inotropic and chronotropic support to maintain adequate systolic blood pressures. Aggressive fluid resuscitation in patients with neurogenic shock risks fluid overload, pulmonary edema, and heart failure. The secondary survey consists of a thorough head to toe evaluation of the patient, and a complete neurologic exam should be obtained. Details of the injury and the past medical history of the patient should be obtained from the patient, family members, and bystanders and relayed to the treating team. Knowledge of the mechanism of injury is important for the caregivers because associated injuries can then be predicted. Any transient neurologic symptoms noted after the traumatic event should be reported to the trauma team in the emergency department because such findings after trauma, even transient ones, suggest spinal instability. Disease states that may predispose patients to spinal injury should be asked about, as well. Included would be diseases that affect the structural integrity of the vertebrae (e.g., osteoporosis, metastatic disease), those that may be associated with instability (e.g., rheumatoid arthritis, trisomy 13, skeletal dysplasias), and those that result in a stiff spinal column (e.g., ankylosing spondylitis [AS], diffuse idiopathic skeletal hyperostosis [DISH], Klippel–Feil syndrome). Also, preexisting stenosis of the spinal canal may predispose to acute SCI. Urgent transport to centers with the appropriate resources should follow initial stabilization in the field. Ideally, patients with SCI should be transferred directly to a facility experienced in the care of these patients (i.e., regional SCI center). If immediate transport is not possible, provisions should be made for early transfer once the patient is stabilized.

EVALUATION IN THE EMERGENCY ROOM On arrival in the emergency room, the primary and secondary surveys are repeated. In obvious cases of cervical SCI, the need for ventilatory assistance should be determined in patients with paradoxical abdominal movement with respirations. A patient with an SCI above C5 and complete neurologic lesion is more likely to require intubation. As oxygenation and hemodynamic parameters are maintained, the patient should be examined for signs of injury and a repeat neurologic examination should be performed. During inspection of the face and trunk, it is important to keep in mind that certain injuries can be associated with significant visceral and axial skeletal injuries. Facial trauma should alert the examining physician to the possibility of an injury to the cervical spine. An abrasion under the strap of a restraint can be associated with significant injuries to the cervical spine and cervicothoracic junction. Lap belt contusions should heighten suspicion for flexion–distraction injuries to the thoracolumbar spine. These can be associated with visceral injury, as well. Calcaneal fractures from significant decelerations (e.g., falls, motor vehicle crashes) are associated with fractures of the thoracolumbar and lumbar spines. The unstable spine is at risk for injury from careless manipulation. Therefore, strict logrolling is the preferred method for evaluation of the back of the patient with a suspected spinal injury. The paraspinal soft tissues should be inspected for

Vertebrae and Spinal Cord

439

Basilar line of Wackenheim

10mm

Chamberlain McGregor Redlund–Johnell

4mm

not <13mm

4–5mm

not >3mm

15mm

FIGURE 23-9 Analyzing a lateral cervical spine x-ray. The anterior vertebral line, posterior vertebral line, and the spinolaminar line should be smooth, collinear curves. An adequate study should visualize the entire cervical spine to the C7–T1 junction. The retropharyngeal soft tissue shadow can suggest the presence of injury when its thickness exceeds 6 mm at C2 and 2 cm (i.e., 20 mm) at C6 (“6 at 2 and 2 at 6”).

evidence of swelling, malalignment, or bruising. Systematic palpation of the spinous processes of the entire spinal column can help to identify and localize a spinal injury as significant gapping between processes can occur from flexion–distraction and fracture–dislocation mechanisms. Following a systematic inspection, a complete neurologic examination that includes assessment of light touch and pinprick, graded motor examination, and reflexes is performed. In the appropriate settings, examination of sacral root function can be critically important though spinal shock can complicate this assessment. In patients with SCI, the ASIA Impariment Scale is useful for the characterization of residual function below the level of the SCI. The goal of the secondary assessment is to identify and provide initial treatment of potentially unstable spinal fractures from both a mechanical and a neurologic basis. All clinical examinations of the spine should follow a consistent and repeated pattern. This pattern allows for comparison of neurologic status on a longitudinal basis, thus avoiding potential confusion about a progressive neurologic deficit.

IMAGING Clinicians should have a low threshold for obtaining appropriate x-rays in the polytrauma patient because missed spinal injuries complicated by a progressive neurologic deficit most commonly result from insufficient imaging studies. Two factors

associated with missed injuries in at least one study were traumatic brain injuries and AS.22 Plain x-rays are useful screening tools and are good for assessing overall alignment, though they have largely been replaced by computed tomographic (CT) imaging when evaluating the cervical spine. This is because a cervical CT is quicker to perform, more accurate, and cost-effective. The major difficulty with plain x-rays is obtaining technically adequate studies that are orthogonal and visualize the cervicothoracic junction. The lateral view of the cervical spine is still commonly obtained in the setting of an unstable polytrauma victim, however, because it can provide sufficient information to the surgical team to allow the patient to proceed to the operating room (Fig. 23-9). While plain radiographs of the thoracic and lumbar spines are useful for screening, it is difficult to obtain technically adequate films, especially in bedridden patients. CT allows for better visualization of bony detail and is especially useful for visualizing the occipitocervical and cervicothoracic junctions. During preoperative planning, it can assist the surgeon in appreciating fracture planes and the degree of compromise of the spinal canal. Subtle translations evident on CT may suggest soft tissue disruptions that can be further evaluated with MRI. In cases with known spinal injury, it is a rapid means of screening for noncontiguous injury that can be present in 15–20% of patients.23 It bears repeating that, in patients with an identified spinal injury, an aggressive search for noncontiguous injury should be undertaken as this is a common cause for iatrogenic morbidity.

CHAPTER CHAPTER 23 X

McRae

440

Management of Specific Injuries

SECTION 3 X

Magnetic resonance imaging allows for a detailed assessment of the soft tissues and is especially helpful for identifying pathology of the neural elements, intervertebral disks, and ligaments. It is not routinely used in the evaluation of the polytrauma patient because of the time required to perform a technically adequate scan. MRI is useful in the following patients: (1) when radiographic imaging is inconsistent with a patient’s neurologic presentation; (2) in the determination of ligamentous disruption when evaluating for spinal instability; and (3) prior to reduction maneuvers to exclude the presence of extruded intervertebral disks that could potentially be displaced dorsally into the thecal sac.

■ Ankylosing Spondylitis Patients with AS or other conditions that result in long fused spinal segments (e.g., DISH, extensive degenerative disease) deserve special mention in terms of their evaluation. These patients are particularly susceptible to fracture, even with lowenergy mechanisms, because their spine functions as a long bone with no intervertebral motion to absorb energy. Patients with AS may present with relatively benign complaints. During their evaluation, careful attention should be paid to the position of their cervical spine. Because these patients typically have significant thoracic kyphosis, allowing their head to rest on the bed may result in excessive hyperextension, potentially through an unstable fracture (Fig. 23-10). Their head should be propped up so that the cervical spine assumes its normal configuration with the thorax. It is imperative that the entire spine is thoroughly imaged as noncontiguous injuries are common. Also, these patients have an increased incidence of epidural hematoma, so close serial neurologic examinations are mandatory.

■ Clearing the Cervical Spine Historically, nearly one third of patients with injuries to the cervical spine had a delay in diagnosis or treatment due to inappropriate assessment.17 Of these patients with “missed injuries,” up to 5% may experience neurologic deterioration. Thus, early recognition of these injuries may prevent or limit neurologic compromise. While making sure injuries are not missed is essential, equally important is timely clearance in the absence of significant injury. This is because protracted evaluations may prolong immobilization, inhibit or restrict the thorough assessment of other organ systems, and complicate or delay recovery. Unfortunately, issues surrounding access and cost containment do not allow for the indiscriminant use of medical imaging on every trauma patient. For these reasons algorithms have been developed to identify patients who would benefit most from selected imaging studies. Within the context of these algorithms, imaging of the cervical spine in patients with minor trauma and in obtunded patients generates the most controversy. As noted above, CT of the cervical spine is the current imaging of choice.24,25 Anderson et al.26 have described a useful algorithm for clearance of the cervical spine whereby patients are classified into four groups as follows: asymptomatic, temporarily nonassessable secondary to distracting injuries or intoxication, symptomatic,

The NEXUS Low-Risk Criteria.* Cervical-spine radiography is indicated for patients with trauma unless they meet all of the following criteria: No posterior midline cervical-spine tenderness,† No evidence of intoxication,‡ A normal level of alertness,§ No focal neurologic deficit,¶ and No painful distracting injuries. * Criteria are from Hoffman and colleagues. † Midline posterior bony cervical-spinetenderness is present if the patient reports pain on palpation of the posterior midline neck from the nuchal ridge to the prominence of the first thoracic vertebra, or if the patient evinces pain with direct palpation of any cervical spinous process. ‡ Patients should be considered intoxicated if they have either of the following: a recent history provided by the patient or an observer of intoxication or intoxicating ingestion, or evidence of intoxication on physical examination such as an odor of alcohol, slurred speech, ataxia, dysmetria, or other cerebellar findings, or any behavior consistent with intoxication. Patients may also be considered to be intoxicated if tests of bodily secretions are positive for alcohol or drugs that affect the level of alertness. An altered level of alertness can include any of the following: a Glasgow Coma Scale score of 14 or less; disorientation to person, place, time, or events; an inability to remember three objects at five minutes; a delayed or inappropriate response to external stimuli; or other findings. ¶ A focal neurologic deficit is any focal neurologic finding on motor or sensory examination. No precise definition of a painful distracting injury is possible. This category includes any condition thought by the clinician to be producing pain sufficient to distract the patient from a second (neck) injury. Such injuries may include, but are not limited to, any long-bone fracture; a visceral injury requiring surgical consultation; a large laceration, degloving injury, or crush injury; large burns; or any other injury causing acute functional impairment. Physicians may also classify any injury as distracting if it is thought to have the potential to impair the patient's ability to appreciate other injuries.

FIGURE 23-10 NEXUS Low-Risk Criteria for clearance of the cervical spine. (Reproduced with permission from Stiell IG, Clement CM, McKnight RD, et al. The Canadian C-spine rule versus the NEXUS low-risk criteria in patients with trauma. N Engl J Med. 2003;349:2510. Copyright © 2003 Massachusetts Medical Society. All rights reserved.)

and obtunded. Asymptomatic patients can be cleared on clinical grounds without imaging. Current ATLS recommendations advocate immediate removal of a cervical collar in the awake, alert, sober, and neurologically normal patient who has no tenderness to palpation in the cervical spine and who exhibits full, pain-free ROM. Two relevant algorithms include the NEXUS Low-Risk Criteria and the Canadian C-Spine Rules (Figs. 23-10 and 23-11), and the latter has better sensitivity and specificity.27 Temporarily nonassessable patients can be reassessed within 24–48 hours after return of mentation or following treatment of painful injuries. In urgent situations, the evaluation is the same as that of the obtunded patient. Symptomatic patients require advanced imaging studies including adequate cervical x-rays and CT. The clearance of obtunded patients is controversial and, unfortunately, no clear standard has emerged despite extensive recent research. These patients should be evaluated in an expeditious manner to minimize the restrictions and sequelae of continued immobilization. Some major trauma centers have started clearing the cervical spine in obtunded patients if there is a normal CT scan. Advocates of the use of CT as a single modality argue that MRI may detect additional abnormalities (20–30%), but most of these are false positives and require no further treatment.28,29 Another option is to obtain an MRI if the CT is normal. Studies in favor of the use of MRI after a normal CT point to the high incidence of

Vertebrae and Spinal Cord

Imaging (required)

MDCT reformations

Negative

Option 1: Clear cervical spine Discontinue collar and restrictions

Positive

Option 2: MRI

Spine consultation Collar immobilization Activity restrictions

MRI (fat suppression or STIR)

Negative

Clear cervical spine Discontinue collar and restrictions

Positive

Spine consultation Collar immobilization Activity restrictions

FIGURE 23-11 Canadian Cervical Spine Rules for clearance of the cervical spine. (Reproduced with permission from Anderson PA, Gugala Z, Lindsey RW, et al. Clearing the cervical spine in the blunt trauma patient. J Am Acad Orthop Surg. 2010;18:149. © 2010 by the American Academy of Orthopaedic Surgeons.)

new abnormalities and an occasional unstable injury detected.30,31 Currently, both options can be supported in the literature.

PROPHYLAXIS AGAINST DEEP VEIN THROMBOSIS Prophylaxis against deep vein thrombosis (DVT) and venous thromboembolism (VTE) is an important consideration in patients with trauma to the spine. The incidence of VTE in trauma patients (with and without spinal trauma) varies from 0.36% to 30% within the literature.32,33 In patients with spinal trauma with no or a minimal neurologic deficit, studies suggest that the rate is low (0–2.1%).34 In contrast, one clinical study of patients with SCI using venography showed rates of DVT in the calf approaching 80% when no prophylaxis was used.35 Symptomatic VTE has been reported to occur in 4–10% of patients with SCI.36 Risk factors for DVT and VTE in trauma patients include the following: ventilator dependency 3 days, age 40 years, fracture in the lower extremity, major traumatic

brain injury, venous injury, major surgical procedure, blood transfusion, and SCI.33 General patient risk factors include the following: older age, male patients, tobacco usage, diabetes mellitus, cancer, and obesity. Specific risk factors associated with spine surgery include the following: prolonged procedures, prone positioning, and anterior exposures to the lumbar spine (because of retraction of the great vessels). All patients sustaining spinal trauma, especially those with an associated SCI, should have mechanical prophylaxis instituted as soon as possible with graduated compression stockings, sequential compression devices, or both. Pharmacologic prophylaxis (e.g., unfractionated heparin [UH] or low-molecular-weight heparin [LMWH]) is an additional consideration, but the benefit obtained in terms of reduction of DVT and VTE must be weighed against the risk of bleeding complications (e.g., spinal epidural hematoma). LMWH appears to be more effective for the prevention of DVT with fewer bleeding complications than UH.37 Patients at low risk (e.g., ambulatory patient with an isolated stable thoracolumbar compression fracture) do not need pharmacologic prophylaxis. Patients falling into the large “gray zone” between these two extremes must be considered on a case-by-case basis. In high-risk patients with spinal injuries amenable to nonoperative management, it is prudent to delay the start of pharmacologic DVT prophylaxis 24–48 hours to allow time for organization of any associated hematomas. In patients undergoing spinal surgery, pharmacologic DVT prophylaxis should be delayed until 24–48 hours after surgery to minimize the risk of wound problems and epidural hematoma. If pharmacologic prophylaxis is used in a patient who is scheduled for spinal surgery, it should be stopped an appropriate amount of time prior to surgery to allow the drug to clear the system as this minimizes the chances of bleeding complications (e.g., 12 hours prior to the procedure for LMWH). In patients who are poor candidates for pharmacologic prophylaxis (i.e., at high risk for bleeding complications), placement of a removable filter is another treatment option to be considered. The duration of pharmacologic prophylaxis should be based on the patient’s mobility in spinal trauma without SCI, while patients with SCI should be treated for at least 6 weeks.

THERAPEUTIC INTERVENTION WHEN AN SCI IS PRESENT Once the diagnosis of an SCI has been established, prevention of decubiti, maintenance of adequate oxygenation and hemodynamic parameters, the role of pharmacologic and cellular interventions, and timing of surgical decompression must be considered (Table 23-1).

■ Prevention of Decubitus Ulcer In the insensate patient, it is important to limit the time on a spine board (ideally, less than 2 hours) to avoid the development of ischemia of soft tissue. In patients with SCI, 8 hours on a backboard has been associated with a 95% likelihood that a decubitus ulcer will form.38 Although the damage is done in

CHAPTER CHAPTER 23 X

Altered mental status Prolonged intubation Psychiatric disturbance Unable to cooperate

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Management of Specific Injuries

TABLE 23-1 SCI Protocol for Initial Evaluation and Treatment

SECTION 3 X

ATLS protocol ABC’s Establish large bore intravenous access Expose patient and perform secondary survey Radiographs of the neck, chest, and pelvis Bladder catheterization Initial blood and urine laboratory analysis Cervical stabilization Cervical radiographs/computed tomography for diagnosis of injuries Maintain neck in cervical collar Subaxial cervical injury—5 lb of traction (rule out distraction injury) Methylprednisolone protocol Case-by-case basis GI prophylaxis with antacids, H2 blockers, or proton pump inhibitors DVT prophylaxis Sequential compression devices Consider pharmacologic DVT prophylaxis after 24–48 h postinjury/postsurgery Skin integrity Early removal from backboard Placement in skin pressure prevention bed (e.g., KCI RotoRest) Appropriate rolling side to side Attention to posterior aspect of cervical collar Blood pressure support Fluid or vasopressor agents to maintain mean arterial pressure at 90 mm Hg

the acute setting, the decubitus may not become evident for several days. Patients who cannot be mobilized immediately can be temorized in a rotating bed. These beds provide continuous mobilization (rotation of the bed along its longitudinal axis), improve drainage of lung secretions and ventilation, and reduce the risk of DVT and VTE.

■ Maintenance of Oxygenation and Hemodynamic Parameters Maintenance of adequate arterial oxygenation and blood pressure is critical as ischemia, whether as a result of hypoxia or decreased perfusion, may potentiate secondary injury of the spinal cord. Patients should be placed in intensive care during the acute phase of care to ensure these parameters are optimized. Central venous and indwelling arterial catheters can be used to monitor hemodynamic parameters and responses to therapy, and a Swan–Ganz catheter may be necessary. Current treatment guidelines for patients with SCI

recommend maintenance of systolic blood pressure 90 mm Hg and mean arterial blood pressure between 85 and 90 mm Hg for the first week after injury.39 Although there are limited data, volume resuscitation supplemented by inotropic or chronotropic support as needed to maintain these parameters has been shown to improve neurologic outcomes.

■ Pharmacologic and Cellular Interventions Neuroprotective interventions aim to attenuate the effects of secondary injury. How much secondary injury mechanisms contribute to overall neurologic deficit in patients with acute SCI is unknown. Atomic absorption spectroscopy suggests that secondary injury mechanisms may only account for 10% of the total pathology after SCI; however, the relative benefit of this small amount of preserved neural tissue may be significant. The administration of high-dose methylprednisolone (30 mg/kg bolus followed by a 5.4 mg/kg infusion), in accordance with the findings of the second and third National Acute Spinal Cord Injury Studies (NASCIS), had been the standard of care at most North American institutions for over a decade.40 Steroids effectively limit the cellular and molecular events of the inflammatory cascade and are hypothesized to decrease the extent of secondary injury. The improvement in motor scores in the NASCIS trials, however, was minimal and, many have argued, not clinically significant. Recent criticism of the methodology (i.e., post hoc analysis) and interpretation of data from these trials has resulted in changing practice patterns, and currently, the use of methylprednisolone therapy is controversial.41–44 This is because the routine use of methylprednisolone has significant adverse side effects. In the NASCIS III trial, severe pneumonia affected twice as many patients and severe sepsis four times as many patients in the 48-hour steroid group compared with the 24-hour group. Six times as many patients died from respiratory complications in the 48-hour steroid group.40 Overall, the literature only, but not the ATLS course, supports the use of methylprednisolone within an acute time frame after injury (8 hours) and in adult patients with nonpenetrating injuries. Whether or not to administer steroids, however, should be individualized for each patient. The risk of infection in patients with certain comorbidities (e.g., diabetes mellitus, HIV infection) probably outweighs any potential improvement in the SCI. Additionally, patients with thoracic injuries are unlikely to improve with steroids. The ideal patient for steroid administration is young and healthy and has an incomplete injury to the cervical spinal cord. While technically not a “drug,” systemic hypothermia is relatively noninvasive, systemically applied proposed treatment for patients with SCI. Though its use in this application was studied in the early 1990s with little success, renewed interest has resulted from its well-publicized application in Kevin Everett, an NFL football player who sustained a cervical SCI in 2007.45 He had immediate immobilization, steroids, hypothermia, and urgent surgery, though it is impossible to say which one of these contributed to his neurologic improvement. Systemic hypothermia is hypothesized to reduce the effects of secondary injury mechanisms through attenuation of the

Vertebrae and Spinal Cord the transplantation of OECs into a completely transected spinal cord facilitated the long-distance regeneration of corticospinal, noradrenergic, and serotonergic fibers culminating in significant functional recovery.54 Prompted by these results, many SCI centers have initiated human trials that focus on the application of putative OECs. Uncommitted mesenchymal and hematopoietic cells in the bone marrow are particularly promising for spinal cord repair due to their apparent ability to transdifferentiate into neurons and glia without cell fusion.55 These cells have great appeal because they can be easily procured, expanded in culture, and delivered intravenously. Preclinical studies have supported the feasibility of this approach and have confirmed the ability of intravenously administered mesenchymal stem cells to target regions of intraspinal cavitation.56 Significant concerns, however, exist for the potential of developing cancer from uncontrolled differentiation of these stem cell populations in vivo. Experimental animal models of SCI have generated a number of promising experimental neuroprotective interventions, but have also exposed the overwhelming complexity of the neurobiological challenges. A greater understanding of this technology will be necessary for the further development of the optimal therapeutic approaches to the injured spinal cord.

TIMING OF SURGICAL DECOMPRESSION IN SCI There are currently no standards regarding the role and timing of surgical decompression in acute SCI. Animal studies have shown that neurologic recovery is enhanced by early decompression, but the time frame for intervention in these studies is on the order of minutes to several hours.57,58 While several human studies have found a modest neurologic benefit to decompression within several hours, none of these studies were prospective, randomized, or controlled.59,60 Vaccaro et al.61 have performed the only prospective, randomized controlled study looking at functional outcomes in patients undergoing early versus late surgery after an SCI. This study showed no significant difference in outcomes between early and late surgery when the cutoff was 72 hours.61 Thus, the neurologic benefit of emergent (less than 4–8 hours) surgical decompression remains unclear. A prospective study, the Surgical Timing in Acute Spinal Cord Injury Study (STASCIS), is attempting to better define the benefits of urgent decompression and stabilization. Studies have suggested that patients with SCI who undergo “early surgery” have significant benefits in terms of more rapid rehabilitation, decreased incidence of pneumonia, decreased length of stay in the intensive care unit, and decreased hospital costs.62 The most recent recommendations suggest that there is good evidence that early (24 hours) surgical decompression can be performed safely and that urgent decompression (24 hours) is recommended following isolated acute cervical SCI provided hemodynamic stability is maintained.63 In addition, urgent closed reduction of unilateral or bilateral facet dislocations in patients with incomplete quadriplegia and urgent decompression in a patient with neurologic deterioration following an SCI are advocated in the literature.

CHAPTER CHAPTER 23 X

inflammatory cascade, but animal studies have had mixed results. Human clinical trials have not shown a consistent benefit, and, therefore, systemic hypothermia cannot be considered the standard of care. Other agents under investigation such as GM1 ganglioside, naloxone, thyrotropin-releasing hormone, nimodipine, and tirilazad mesylate have proven promising in animal studies, also, but have not demonstrated sufficient efficacy in clinical trails. Minocycline, erythropoietin, neurotrophic growth factors, and cellular therapies are promising neuroprotective agents and are being investigated. Minocycline, a tetracycline derivative, exhibits its neuroprotective properties by inhibiting matrix metalloproteinases, microglial activation (both are present during neuroinflammation), and preventing cell apoptosis.46 The administration of minocycline shortly after an experimentally induced SCI increased axonal sparing, reduced the apoptotic demise of oligodendrocytes, diminished axonal death, and culminated in improved locomotor and behavioral outcomes in animals.47 Erythropoietin, a hormone produced primarily by the kidney in response to hypoxia, has proven to be especially capable of minimizing SCI in ischemic models based on aortic occlusion.48 It has prevented motor neuron apoptosis and promoted motor functional recovery in animal models of SCI. Interestingly, erythropoietin reduced lipid peroxidation at the site of injury to a greater extent than methylprednisolone at the doses recommended in the Second National Acute Spinal Cord Injury Study (NASCIS II). Recently, there has been a renewed interest in applying neurotrophic factors, growth factors, cytokines, and various forms of cell therapies in the treatment of SCI. Neurite outgrowth at the site of injury can be inhibited by myelin, myelin-associated protein (MAG), and Nogo protein.49 The application of specific Nogo receptor blockers facilitates axonal sprouting and enhanced functional recovery in rats. Both brain-derived neurotrophic factor (BDNF) and glial-derived neurotrophic factors (GDNF) increase the levels of cyclic adenosine monophosphate (cAMP) in neurons and promote axonal regeneration over the long distances relevant for functional recovery of the spinal cord.50 In addition, several types of bone morphogenetic proteins (BMPs) and interleukin-6 (IL-6) are being actively investigated to elucidate their roles in triggering reparative cascades in the injured spinal cord.51 Cellular therapies aim to deliver committed or uncommitted cells locally to the injury site in an effort to restore a functionally competent cellular environment to the injured cord. The primary cell types used in this approach include Schwann cells, olfactory ensheathing cells (OECs), and uncommitted stems cells. Schwann cells have been recognized as the key cellular constituent for peripheral nerve regeneration. Several animal studies have demonstrated that transected spinal cords can be bridged with Schwann cells delivered to the site of injury where they function as chaperones, guiding the sprouting axons.52 OECs are distinct glial cells that guide the growing axons and play a crucial role in the renewal of sensory neurons within the olfactory epithelium. Unlike Schwann cells, OECs have demonstrated the unique ability to extend across glial scar within the transected cord.53 In animal models,

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MANAGEMENT OF SPINAL INJURIES SECTION 3 X

Traditionally, injuries of the spine have been treated nonoperatively but, over the past century, surgical indications have been continuously redefined as surgical techniques have improved and an evidentiary basis for intervention has been developed. Optimal management must weigh the risk and benefit of interventions against the goals of early mobilization, timely treatment of neurologic deficits, and maintenance of acceptable spinal alignment and stability in the context of the polytraumatized patient. To this end, communication between the trauma team and the spine surgeon is essential.

■ Spinal Stability One of the most important tasks for the treating spine surgeon is the determination of spinal stability. Most spine surgeons agree with the general definition that spinal stability refers to the ability of the spine to maintain its alignment and protect the neural structures during normal physiologic loads. Biomechanically, and in the laboratory, spinal instability refers to an abnormal response to applied loads and can be characterized by motion in spinal segments beyond the normal constraints. Clinically, this situation risks progressive deformity, neurologic compromise, or both and, therefore, is an indication for operative stabilization. In clinical practice, however, the quantitative assessment of spinal stability is challenging. Most classification systems of spinal trauma provide a descriptive analysis of various fracture patterns, and the extent to which these injuries reflect spinal stability remains controversial. One of the early classification systems proposed to aid in the assessment of spinal stability was region-specific parameter checklists, developed by White and Panjabi64 (Tables 23-2 and 23-3). This system assigns points based on a combination

TABLE 23-2 Checklist for the Diagnosis of Clinical Instability of the Thoracic and Thoracolumbar Spine (Total 5 Points  Unstable) Element Anterior elements destroyed or unable to function Posterior elements destroyed or unable to function Radiographic criteria (A) Sagittal displacement 2.5 mm (B) Relative sagittal angulation 5° Spinal cord or cauda equina damage Disruption of costovertebral articulations Dangerous loading anticipated

Total

Points 2 2 4

2 2 2 1 2

Adapted from White AA, Panjabi MM. Clinical Biomechanics of the Spine. Philadelphia: JB Lippincott; 1978:236–251.

TABLE 23-3 Checklist for the Diagnosis of Clinical Instability of the Lumbosacral Spine (Total 5 Points  Unstable) Element Anterior elements destroyed or unable to function Posterior elements destroyed or unable to function Radiographic criteria (A) Flexion–extension radiographs 1. Sagittal translation 4.5 mm or 15% 2. Sagittal rotation 15° at L1–L2, L2–L3, L3–L4 20° at L4–L5 25° at L5–S1 (B) Resting radiographs 1. Sagittal displacement 4.5 mm or 15% 2. Relative sagittal angulation 22° Cauda equina damage Dangerous loading anticipated

Total

Points 2 2 4

2

2 2 2

2 2 3 1

Adapted from White AA, Panjabi MM. Clinical Biomechanics of the Spine. Philadelphia: JB Lippincott: 1978:236–251.

of radiographic findings, neurologic examination, and the anticipated biomechanical demands of the patient. Scores above a certain cutoff (e.g., 5) suggest an unstable spine. Neurologic findings were considered important because these implied the spinal column had at some point failed in its ability to protect its enclosed neural elements and could, therefore, be considered unstable. In practice, most spine surgeons would agree that spine fractures associated with significant neurologic injury are unstable, except for those injuries secondary to penetrating trauma (i.e., gunshot, stab). While these systems have been in use for years, some of the parameters are difficult to define clinically. For example, it is difficult to determine whether anterior or posterior elements are “destroyed or unable to function” and what the definition of “dangerous loading anticipated” should be. Mechanistically, cervical spine fractures and dislocations have been most comprehensively classified by Allen et al.65 (Fig. 23-12). In this system, injury patterns are described according to the position of the neck at the time of the injury and the direction of the injuring force. The six most common patterns of cervical injuries are as follows: (1) flexion–compression; (2) vertical compression; (3) compression–extension; (4) flexion–distraction; (5) extension–distraction; and (6) lateral flexion injuries. Each injury pattern is graded in terms of the degree of injury to the involved motion segment and a higher stage denotes a more complex injury.

Vertebrae and Spinal Cord

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CHAPTER CHAPTER 23 X

FIGURE 23-12 Patterns of subaxial cervical spine injuries based on the injury mechanism. (Reproduced with permission from McAfee P. Cervical spine trauma. In: Frymoyer JW, ed. Adult Spine. New York: Raven Press; 1991:1080.)

More recently, evidence-based guidelines have been developed for the classification of subaxial spinal injuries. The Subaxial Injury Classification (SLIC) Scale proposes a scoring system using three major injury characteristics to help direct the management of subaxial injuries66 (Table 23-4). In addition to the morphologic fracture pattern considered with the earlier systems, the neurologic status of the patient and the integrity of the discoligamentous complex (DLC) that stabilizes the spine (i.e., the intervertebral disk, the facet joint capsule, the ligamentum flavum, the interspinous and supraspinous ligaments) are taken into consideration. The SLIC scoring system can be used to direct treatment into the broad categories of either surgical or nonsurgical by summing the points in each of the three categories. Injuries that score 5 or more points are treated surgically, whereas those scoring 3 or less are treated nonsurgically. A score of 4 is considered equivocal.

In the SLIC, injury morphology is divided into the following three categories based on the relationship of the vertebral bodies to each other (anterior support structures): (1) compression; (2) distraction; and (3) translation or rotation. The DLC is graded as disrupted, intact, or indeterminate. The integrity of these soft tissue constraints directly relates to spinal stability. Neurologic status is graded as intact, root injury, complete injury, and incomplete injury in increasing order of point value. An additional point is given if there is continuous neural compression in the setting of a neurologic deficit. In this system, the presence of an incomplete neurologic injury, particularly in the presence of ongoing root or cord compression, leads to the highest point score as these would tend to benefit most from operative stabilization. The management of thoracolumbar fractures has improved due to imaging techniques such as CT and MRI that better

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Management of Specific Injuries

TABLE 23-4 Subaxial Injury Classification (SLIC) Scale Points

SECTION 3 X

Morphology No abnormality Compression Burst Distraction (e.g., facet perch, hyperextension) Rotation/translation (e.g., facet dislocation, unstable teardrop, or advanced-stage flexion–compression injury) Discoligamentous complex (DLC) Intact Indeterminate (e.g., isolated interspinous widening, MRI signal change only) Disrupted (e.g., widening of disk space, facet perch or dislocation, kyphotic deformity) Neurologic Status Intact Root injury Complete cord injury Incomplete cord injury Continuous cord compression (in setting of a neurologic deficit)

0 1

1  2 3 4

0 1 2 0 1 2 2 3

1

4 points, nonoperative; 4 points, operative; 4 points, indeterminate.

delineate fracture patterns, associated injury to soft tissue, and compromise of the neural canal allowing a more complete understanding of these injuries. A number of classification systems have been developed to determine stability. Holdsworth67 introduced the concept of dividing the thoracolumbar spine into two structural columns. The anterior column consisted of the anterior longitudinal ligament, vertebral body, intervertebral disc, and the posterior longitudinal ligament. The posterior column consisted of the remaining osteoligamentous structures. According to Holdsworth’s model, instability occurs when both columns have been compromised. Denis68 developed the three-column classification system, separating Holdsworth’s anterior column into the anterior and middle columns. Compression fractures involved the anterior column, burst fractures the anterior and middle columns, flexion–distraction injuries all three columns, and fracture– dislocation injuries all three columns, as well. According to this model, involvement of at least two of the three columns results in spinal instability. Panjabi et al.69 tested an ex vivo cadaveric burst fracture model and validated the three-column theory. In this study the middle column proved to be the principal determinant of stability of the thoracolumbar spine. Magerl et al.70 described a comprehensive classification of thoracolumbar injuries that defined compression, distraction, and torsion as the three mechanisms. These 3 categories were divided into

53 specific subtypes altogether.70 Unfortunately, all these systems have deficiencies as they are cumbersome to use and they do not always predict the best clinical practice. For example, the Denis system defines burst fractures as unstable (i.e., require surgical stabilization) because of involvement of the anterior and middle columns. More recent studies have shown that many burst fractures are stable and amenable to nonoperative management. Recently, the Thoracolumbar Injury Classification and Severity Score (TLICS) has been introduced based on an extensive review of the literature as well as consensus opinion from an international group of spinal trauma surgeons. The goal is to simplify injury classification and facilitate decision making for treatment.71 Similar to the SLIC, the three major injury characteristics are defined as injury morphology, neurologic status, and integrity of the PLC. Point values are assigned to each major category based on injury severity (Table 23-5). The sum of these points represents the TLICS severity score, which may be used to guide treatment. Injuries with a score 4 are treated surgically because of significant instability, whereas injuries with a score 4 are treated nonsurgically. A score of 4 is considered equivocal. In the setting of multiple fractures, management is determined based on the injury with the greatest TLICS severity score. For noncontiguous fractures, the severity score of each injury may be used. Of note, there have been no systems used to define instability in the upper cervical spine where the integrity of the ligamentous restraints is the most important. Disruption of the facet capsules, tectorial membrane, alar ligament, and TAL have all been associated with significant clinical instability of the upper cervical spine.

TABLE 23-5 Thoracolumbar Injury Classification and Severity Score (TLICS) Points Morphology No abnormality Compression Burst Rotation/translation Distraction

0 1

1  2 3 4

Posterior ligamentous complex (PLC) Intact Indeterminate/injury suspected Injured

0 2 3

Neurologic status Intact Root injury Complete cord/conus medullaris injury Incomplete cord/conus medullaris injury Cauda equina

0 2 2 3 4

4 points, nonoperative; 4 points, operative; 4 points, indeterminate.

Vertebrae and Spinal Cord

NONOPERATIVE MANAGEMENT OF SPINAL INJURIES

■ Spinal Orthotics Spinal orthoses are external devices that can restrict the motion of the spine by acting indirectly through the intervening soft tissue. Despite the heterogeneity of designs, the theoretical functions of all spinal braces are similar and include restriction of spinal movement, maintenance of spinal alignment, reduction of pain, and support of the trunk musculature. Also, spinal braces act psychologically as proprioceptive reminders for the patient to restrict spinal motion. The immobilizing effectiveness of spine braces is dependent on the mobility and anatomical features of the spine to be stabilized, injury biomechanics, length and rigidity of the orthosis, thickness of the intervening soft tissues, and patient’s compliance with the orthosis. Although spinal braces are generally applied to stabilize a specific motion segment, their immobilization properties typically affect the entire spinal region (i.e., cervical, thoracic, or lumbar). Cervical spine bracing is particularly challenging due to the wide range of normal spinal motion. Due to the inability of the vital structures in the neck to withstand prolonged compression, cervical braces utilize the cranium and thorax as fixation points. Cervical orthoses can be used as a definitive treatment for some spinal injuries or as temporary immobilizers for postinjury transport or during the early hospital diagnostic process. These braces can generally be divided into soft collars, short cervicothoracic orthoses (CTOs), and long CTOs. Soft collars are basically foam cylinders that encircle the neck. The mechanical function of soft collars is negligible, and their effectiveness relates more to the psychological effect of wearing an orthosis. Soft collars are indicated for mild cervical sprains or to provide postoperative comfort following stable internal fixation. Short CTOs have molded occipital–mandibular supports that extend not lower than the level of the sternal notch anteriorly and the T3 spinous process posteriorly. These collars limit cervical

■ Halo The halo fixator consists of a ring attached to the skull via pins that in turn is connected via upright longitudinal struts to either a detachable vest or thoracic cast that can be applied with local or general anesthesia. The ring is positioned below the cranial brim similar to tongs, and the pins are inserted with approximately 6–8 in lb of torque. Anteriorly, pins should be placed 1 cm above the lateral one third of the eyebrow to avoid the temporalis fossa and the supraorbital and supratrochlear nerves medially (Fig. 23-13). The cast or vest must be well fitted to the iliac crest to prevent vertical toggle of the apparatus.

CHAPTER CHAPTER 23 X

The nonoperative management of spine fractures consists of spinal immobilization with an orthotic brace that restricts motion to an extent that allows healing of the injury while permitting mobilization of the patient. The success of nonoperative treatment is dependent on proper patient selection and on the physician’s understanding of the spinal injury. Most stable injuries without a neurologic deficit are managed nonoperatively with the orthotic brace used to minimize the risk of progressive collapse. Most bony injuries have the potential to heal with this approach, while healing of ligamentous injuries is less predictable and commonly requires spinal fusion. For patients in whom nonoperative management of their spinal injuries is chosen, continual reassessment of neurologic status and spinal stability is essential. Serial neurologic examinations are essential to monitor for progressive neurologic dysfunction. When the patient is able to be upright, repeat x-rays with the patient standing should be obtained. This will ensure that the initial assessment of spinal stability was accurate and that the spine is not progressively deforming with applied load due to collapse of the anterior column or insufficiency of the posterior ligaments.

motion to a much greater degree than soft collars, but still restrict motion only 50–80%.72 They control motion best in the sagittal plane. While certain collars restrict motion best among the aforementioned examples, they exert relatively high skin pressures and should be used only on a short-term basis. Long CTOs attach to the cranium at the occiput and mandible and extend to the lower thorax below the sternal notch and T3 spinous process. All of these braces provide better fixation to the head and trunk than short CTOs and, therefore, constitute the most effective of all cervical braces; however, they are cumbersome and the least well tolerated by patients. The major difference between short and long CTOs is the ability of the latter to provide better control of spinal rotation and sagittal motion in the middle and lower cervical spine. The thoracic spine (T1–10) is unique among spinal regions in terms of its inherent rigidity and location between highly mobile adjacent cervical and lumber segments. Stable injuries above T6 are not typically braced because of the stabilizing effects of the rib cage, sternum, and shoulder girdle and the poor compliance and unclear benefit of long cervicothoracic bracing. In addition, traditional thoracolumbosacral orthoses (TLSOs) do not effectively stabilize this region even with proximal extension of the brace to the armpits. Injuries below T7 may be amenable to bracing with a standard TLSO, but achieving significant restriction of movement in the unstable thoracic spine can be difficult. This is because rotation, the principal motion of the thoracic spine, is much more difficult to control than flexion and extension. The thoracolumbar region is the region best controlled by traditional TLSO bracing. The goal of thoracolumbar bracing is to support the spine by limiting overall motion of the trunk, decreasing muscular activity, increasing the intra-abdominal pressure, reducing spinal loads, and limiting spinal motion. Interestingly, interim analysis of a recent multicenter randomized trial found that thoracolumbar burst fractures without an associated injury to the PLC were successfully treated without a brace due to the inherent stability of fractures in this region.73 The lower lumbar spine (L4–L5) is difficult to brace due to the limited caudal fixation points and its physiologic hypermobility. Typically, adequate stabilization requires that the brace extend as much as four or five vertebral levels proximal and distal to the unstable segment. Even when the brace includes a hip spica component, hip flexion is not adequately controlled, resulting in inadequate lumbar protection. Current available orthoses include lumbosacral corsets, braces, and full-contact custom-molded orthoses.

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Management of Specific Injuries Supraorbital n.

Frontal sinus

Supratrochlear n.

SECTION 3 X

Safe zone

Equator

Temporalis m.

A

B

FIGURE 23-13 (A and B) Halo pin placement.

bending.74 Despite the fact that halos restrict cervical motion to a significant degree, they do not necessarily prevent progression of unstable injuries. Therefore, the decision to use a halo for definitive management should be carefully made. Halos are poorly tolerated in elderly patients and potentially increase the risk of injury due to falls as the device shifts the center of gravity upward and makes patients “top-heavy.”75 In patients with SCI, halo fixation can be problematic. Loss of protective sensation over the trunk can lead to formation of a decubitus ulcer. Restriction of expansion of the chest wall can lead to pulmonary complications in the patient with already compromised

Despite adequate fit, the halo vest does not guarantee complete spinal stabilization, especially when the patient is upright. The halo may be used to temporarily stabilize injuries prior to surgery or to definitively treat certain injuries. In comparison to other options for bracing of the cervical spine, halos are the best means of restricting upper cervical motion and, in addition, are superior to other options in the ability to restrict motion in all planes (Fig. 23-14). In a study of normal subjects, the halo fixator allowed only 4% of cervical sagittal motion compared with 13% for a rigid cervical collar and 74% for a soft collar and only 1% of lateral rotation and 4% of lateral

Stabilizer with open back rings To adjust flexion-extension

Anterior pin Lengthening or shortening along upright struts Adjustable strap

Wheel nut

Lengthening or shortening along upright struts

Upright strut To adjust anterior length

A FIGURE 23-14 (A and B) Halo ring apparatus.

Xiphoid process

To adjust posterior length

B

Vertebrae and Spinal Cord respiratory function. Furthermore, the bulk of the halo can hinder nursing care and mobilization.

Cervical traction is often indicated in the management of injury to the cervical spine to reduce bony deformity, indirectly decompress neural elements, and provide stability. The utilization of traction is helpful in the management of injury to the cervical spine because it is simple to apply and has low morbidity when applied properly. Use of this technique requires an awake and alert patient (i.e., cannot be intoxicated). Cervical traction can be applied with tongs or a halo ring, and the use of CT- and MRI-compatible materials is preferred. Traction tongs achieve fixation into the bony skull through two pins oriented 180° from each other. These pins have pointed tips that abruptly flare out to allow for fixation into the outer cortical table of the skull while preventing inner cortical penetration. These pins are placed in line with the external auditory meatus below the cranial brim or the widest diameter of the skull. Pins must be positioned posterior to the temporalis muscle since placement here can become symptomatic due to the thin bone in this region or from muscle irritation during mastication. The pins are tightened to 6–8 in lb torque and require repeat tightening within 24 hours to maintain the applied load. If the pins loosen again, they can be retightened and, if loosening continues to recur, the pins should be moved. Traction tongs control motion in a single plane through the application of longitudinal traction and are associated with a greater incidence of loosening than halo rings. They are indicated when the need for longitudinal traction is temporary or when the patient is bedridden. Use of a halo ring achieves better skeletal fixation due to its multipin circumferential application and is able to withstand higher loads for a longer period of time. Once a set of tongs or a halo ring has been applied, cervical traction can begin with approximately 10–15 lb. This is followed by immediate evaluation by x-rays to assess for overdistraction and to rule out occipitoatlantal injuries. The traction weight can then be increased by 5- to 10-lb increments with serial neurologic examinations and lateral x-rays obtained at approximately 10- to 15-minute intervals after each weight increase. The patient must be completely relaxed, and analgesia or muscle relaxants are often required to relieve muscle spasms or tension. The head of the bed should be elevated to provide bodyweight resistance to the traction, and the shoulder portion should be depressed to optimize visualization of the cervicothoracic region. The maximum amount of weight that can be safely applied for closed traction reduction of the cervical spine is controversial. Some authors recommend a maximum of 5 lb per level of cervical injury, beginning with 10 lb for the head. This would limit the weight applied to a C5–C6 facet dislocation to 35 lb. Other authors have supported a more rapid incremental increase in load, applying weights up to 150 lb without any adverse effects. Typically, the maximum weight tolerated is limited by the skeletal fixation utilized, and, for cranial tongs, this limit is up to 100 lb. Most injuries to the cervical spine can be reduced with only

OPERATIVE MANAGEMENT OF SPINAL INJURY Operative management requires a thorough understanding of the anatomy, biomechanics, and physiology of the injury as well as knowledge of the surgical strategies to achieve adequate spinal alignment, spinal stability, and neurologic decompression.

■ Perioperative Considerations A decision to proceed with surgery should include consideration of perioperative strategies to minimize the chances of untoward events. In general, patients should be moved with strict spinal precautions that include some form of immobilization if the cervical spine has not yet been cleared, logrolling of the patient for turns, and use of a backboard for transfers. It is important to remember that manual immobilization of the cervical spine restricts motion better than any orthosis. If the cervical spine has not yet been cleared, the neck must be carefully manipulated during intubation. Intubation with in-line cervical traction may be acceptable in more stable injuries. Consideration can be given to fiber-optic intubation, nasal intubation, or awake intubations in patients with less stable injuries. Oxygenation and blood pressure (mean arterial pressure 85–90 mm) should be supported during the procedure, especially in patients with unstable injuries or frank SCI. Intraoperative neurophysiologic monitoring may add a measure of protection against iatrogenic neurologic injury.

■ Goals of Operative Management Only spinal injuries that are unstable with or without neurologic involvement require surgical treatment. Surgical objectives include the correction of spinal alignment, the restoration and maintenance of spinal stability with instrumentation, and decompression of compromised neural elements to permit maximal functional recovery. Modern anterior and posterior surgical fixation devices provide stabilization while limiting the

CHAPTER CHAPTER 23 X

■ Cervical Traction

longitudinal traction, but small changes in the vector of traction (i.e., slightly more flexion or more extension) are necessary in some cases. The urgency of the reduction is based on animal studies of SCI that suggest a window of 6–8 hours during which decompression may reverse neurologic deficits.57,58 Pretraction MRI may be obtained to identify the presence of herniation of an intervertebral disc, but this is controversial.76,77 A recent survey of fellowship-trained spine surgeons found the timing and utilization of MRI for patients with a traumatic dislocation of a cervical facet to be variable.77 Early closed reduction in awake and alert patients presenting with significant motor deficits (e.g., complete SCI) without prior MRI appears reasonable because the benefit of early reduction appears to outweigh the risk of neurologic deterioration. In patients without a neurologic deficit or those unable to participate in a neurologic examination (e.g., obtunded patients), the risk of iatrogenic neurologic injury probably outweighs the benefit of early reduction.

449

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number of motion segments included in the construct in comparison to older devices. Finally, the injury type and the time to surgical intervention determine the most appropriate type of decompression. Neural decompression can be performed anteriorly, posteriorly, and/or indirectly (via restoration of spinal alignment). The literature suggests that the results of anterior direct versus posterior indirect spinal canal decompression are similar for patients with incomplete neurologic deficits.78 The absolute indications for anterior decompression would include the neurologically incomplete patient with greater than 50% canal compromise, greater than 72 hours postinjury, a failed attempt at posterior reduction, or significant loss of anterior and middle column (vertebral body) support despite posterior reduction.

SPECIFIC MANAGEMENT OF INJURIES OF THE UPPER CERVICAL SPINE

■ Timing of Stabilization of Spinal Fractures The optimal timing of stabilization following spinal injury is controversial. Some insist that surgery be performed as soon as possible as stabilization and mobilization of patients with SCI has been found to reduce the incidence of complications such as adult respiratory distress syndrome and DVT.79,80 Others advocate a delay of surgery to allow for cardiopulmonary optimization and to minimize the risk of bleeding. The indications for immediate surgery are progressive neurologic deterioration and fracture–dislocations associated with incomplete or no neurologic deficit. In the absence of a neurologic deficit, it is reasonable to delay surgery to facilitate surgical planning and to allow for edema of the spinal cord and nerve roots to resolve. Furthermore, organization of a hematoma occurs at about 48 hours after the injury and decreases intraoperative blood loss. An excessive delay to surgery may adversely affect the clinician’s ability to reduce the fracture and achieve clearance of the canal. Reports have shown that optimum clearance of the spinal canal is most effective if surgery is ideally performed within 4 days and certainly no later than 7–10 days from the time of injury.81,82 Management of the polytrauma patient with an associated spinal injury is a particularly difficult problem. In several studies examining the effects of early versus late stabilization of spinal fractures in such patients, surgery performed within 72 hours on patients with Injury Severity Scores (ISS) greater than 18 consistently and significantly decreased morbidity

Type I

and length of stay without significant differences in the rate of perioperative complications.83 Recently, with the development of less invasive spinal interventions, there has been growing interest in the application of “damage control” principles to spinal trauma. Because the morbidity of spinal surgery may not be tolerated in the acutely injured patients, less invasive techniques may find a role in the timely stabilization of injuries to allow for early mobilization of the patient. While the theoretical benefit of applying these techniques in the trauma population is sound, there are currently insufficient data from which to draw firm conclusions as to whether these techniques are associated with superior outcomes.

■ Occipital Condyle Injuries Fractures of the occipital condyles typically occur through an axial loading mechanism. They can be associated with significant occipitocervical instability and should be evaluated carefully. The integrity of the restraining ligaments is key in the assessment of stability. Anderson and Montesano84 described a classification system that evaluates the potential for instability based on CT patterns of bony injury and the presumed associated ligamentous injuries (Fig. 23-15). Type I fractures are comminuted (impaction fractures of the condyles) and are generally stable as the ligaments are typically intact. Type II fractures of the condyles are associated with a basilar skull fracture. These are stable unless the entire condyle is separated from the occiput (i.e., “floating” condyle). Both type I and type II fractures can be treated with a cervical orthosis. Type III fractures are avulsions of the insertion of the alar ligament into the occipital condyle. These have the greatest potential for instability and have been found to occur in 30–50% of patients with occipitocervical dislocations. For type III fractures, stable fracture patterns can typically be treated in a rigid collar for 6–8 weeks. Less stable (e.g., displaced) variants may benefit from halo immobilization for 8–12 weeks. Unstable patterns (e.g., significant translation, joint incongruity, or diastasis) typically require occiput to C2 fusion.

Type II

Type III

FIGURE 23-15 Classification of occipital condyle injuries. (Reproduced with permission from Anderson PA. Injuries to the occipital cervical articulation. In: Clark CR, ed. The Cervical Spine. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 1998:391.)

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FIGURE 23-16 The Rule of 12’s. The basion–atlantal interval (BAI) and the basion–dens interval (BDI) measure less than 12 mm in the uninjured state.

■ Acute Occipitocervical Instability

■ Fractures of the Atlas

Occipitocervical injuries are rare and usually fatal, but may be increasing because of better automobile restraints, improved prehospital care, and more thorough imaging techniques. These injuries consist of subluxations or dislocations and can include fractures of the occipital condyles. The most popular methods to describe the relationships between the occiput, atlas, and axis in the setting of trauma are the basion–dental interval (BDI) and the basion–posterior axial line interval (BAI).85 As values greater than 12 mm are associated with occipitoatlantal subluxation or dislocation, these measurements have been referred to as the “Rule of 12’s” (Fig. 23-16). The Power’s ratio can be used, as well; however, this is only useful for detecting anterior occipitocervical subluxations/dislocations (Fig. 23-17). Injuries are classified as type I (anterior displacement of the occiput on the atlas), type II (longitudinal facet distraction injury with diastasis of the occiput from the atlas), and type III (posterior displacement of the occiput on the atlas).86 Traction should be avoided in these injuries in favor of gentle manipulation, and reduction is achieved by either extension or flexion of the occiput. Occipitocervical subluxations/dislocations are extremely unstable and require operative stabilization and fusion. Halo immobilization is used for temporary urgent stabilization prior to definitive treatment.

Fractures of the atlas rarely cause a neurologic deficit, but are painful and compromise mobility of the neck. Fractures can consist of bone disruption without instability or bony and ligamentous injuries with subsequent displacement of the articulation of the lateral mass. The three common types of atlas fractures are as follows: (1) posterior arch fractures, in which the lateral atlantal masses do not spread; (2) burst or Jefferson fractures, in which the lateral masses will spread and displace laterally; and (3) lateral mass fractures, in which lateral displacement of the lateral mass will occur only on the fractured side (Fig. 23-18). Stable fractures with an intact transverse ligament and simple posterior arch fracture can be treated with a brace. For Jefferson fractures, combined overhang of the lateral mass greater than 7 mm (rule of Spence) on an open mouth odontoid x-ray can be associated with disruption of the TAL and instability.87 Unstable, displaced fractures in which the transverse ligament is disrupted require traction initially to reduce the displaced lateral masses and then can be placed in a halo vest. Fractures of the atlas with significant displacement can require traction for up to 6–8 weeks before a halo vest can be applied. Surgery is usually not required acutely, but is reserved for those patients who develop a symptomatic nonunion or late instability.

■ Acute Atlantoaxial Instability

FIGURE 23-17 Power’s ratio.

Atlantoaxial subluxation occurs when TAL insufficiency results in abnormal translation or rotation of the atlas with respect to the odontoid. TAL insufficiency can result from isolated rupture or avulsions of the TAL or, more commonly, from burst fractures of C1. On lateral cervical imaging, subluxation can be quantified by an increase in the anterior atlantodens interval (Fig. 23-19). CT is necessary to appropriately characterize these injuries. MRI is useful to evaluate the integrity of the soft tissue restraints, including the TAL. Because these injuries are extremely unstable, there is a high risk for neurologic deficit. Cervical traction with tongs is appropriate initially to achieve reduction. Definitive treatment consists of a posterior cervical fusion of C1–C2. Rotary subluxations of C1–C2 clinically present with torticollis. Subluxation will usually reduce with traction and requires only brace support or application of a halo vest. Irreducible

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Posterior arch fracture

Burst fracture

Lateral mass fracture

FIGURE 23-18 Atlas fractures. (Reproduced with permission from Jackson RS, Banit DM, Rhyne AL, Darden BV. Upper cervical spine injuries. J Am Acad Orthop Surg. 2002;10:271. Copyright 2002 by the American Academy of Orthopaedic Surgeons.)

subluxations require open reduction and C1–C2 fusion, but may occasionally require occiput to C2 fusion depending on the extent of injury.

■ Fractures of the Odontoid Odontoid fractures have been classified by Anderson and D’Alonzo88 according to the anatomical level of the fracture (Fig. 23-20). Type I fractures consist of avulsion injuries of the apical ligament that are essentially stable and require limited, if any, external support. Type II odontoid injuries occur at the waist of the odontoid, a watershed area for fracture healing, and have the potential for poor healing. Type III fractures extend below the waist of the odontoid into the body of C2 and usually result in uneventful bony union when treated with halo immobilization. Odontoid fractures can be visualized on lateral

and open mouth x-rays, but are best visualized on CT. Nonoperative treatment of type II injuries is associated with an up to 15% incidence of nonunion, although not all of these are symptomatic. Type II odontoid fractures are the most challenging since these require reduction of both translation and angulation and

Type I

Type II

Type III

FIGURE 23-19 Atlantoaxial subluxation. Note the increased anterior atlantodens interval (normal 4 mm).

FIGURE 23-20 Classification of odontoid fractures. (Reproduced with permission from Jackson RS, Banit DM, Rhyne AL, Darden BV. Upper cervical spine injuries. J Am Acad Orthop Surg. 2002;10:271. Copyright 2002 by the American Academy of Orthopaedic Surgeons. Adapted with permission from Anderson LD, D’Alonzo RT. Fractures of the odontoid process of the axis. J Bone Joint Surg Am. 1974;56:1663.)

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Type I

Type IA

Type II

Type IIA

Type III

FIGURE 23-21 Classification of traumatic spondylolisthesis of the atlas (Hangman’s fracture). (Reproduced with permission from Jackson RS, Banit DM, Rhyne AL, Darden BV. Upper cervical spine injuries. J Am Acad Orthop Surg. 2002;10:271. Copyright 2002 by the American Academy of Orthopaedic Surgeons. Adapted with permission from Levine AM, Edwards CC. The management of traumatic spondylolisthesis of the axis. J Bone Joint Surg Am. 1985;67:217.)

maintenance of fracture stability. Risk factors for nonunion include osteoporosis, rheumatoid arthritis, and diabetes mellitus. Significant displacement (10° of angulation, 5 mm displacement) and posterior displacement are radiologic risk factors for nonunion or malunion. Odontoid fractures should be reduced in traction prior to definitive management. After an adequate reduction has been achieved, treatment options include immobilization in a halo vest, anterior screw osteosynthesis, and posterior C1–C2 fusion.

■ Traumatic Spondylolisthesis of the Axis C2 pedicle or pars interarticularis fracture (Hangman’s fracture) results from hyperextension with an axial load. These fractures are rarely associated with a neurologic injury as separation of the fracture fragments decompresses the spinal canal. They can be detected on lateral x-rays, but are best visualized on CT. MRI is useful to assess the integrity of the associated DLC. These injuries have been classified by Levine and Edwards89 based on the extent of fracture displacement and angulation (Fig. 23-21). The treatment is dependent on the extent of associated injury to the disc and ligament. In the minimally displaced (3 mm) type I fracture, a rigid collar is sufficient treatment. In type II fractures, the C2–C3 disk and posterior longitudinal ligament are disrupted resulting in 3 mm of translation and significant angulation. These can be treated with gentle traction and reduction with extension followed by immobilization in a halo device. Type IIA fractures are a less common variant with minimal translation, but significant angulation. These have a more oblique fracture line and are thought to occur from a flexion–distraction-type mechanism. It is imperative to recognize these injuries as traction will worsen the deformity and potentially cause an SCI. Such injuries require reduction in extension with axial load followed by immobilization in a halo device. C2–C3 fusion is indicated for II or IIA injuries if reduction cannot be maintained. It is important to recognize an “atypical” Hangman’s fracture because these are associated with an increased risk of a neurologic injury.90 In this pattern, the fracture line extends further anteriorly into the body of the axis. Separation of the major fragments in this instance can result in spinal cord compression

by the posterior part of the body. C2 pars fractures with facet dislocation (type III) are uncommon. Nonoperative management is ineffective due to the disrupted continuity between the C2 body and the posterior elements, and open reduction and fusion are required.

■ Injuries of the Subaxial Cervical Spine (C3–C7) Subaxial cervical injuries can consist of fractures, dislocations, subluxation, or a combination of these injuries. The assessment of instability is essential to designing appropriate treatment strategies. Recently the SLIC score has been validated to assist in this determination.

■ Burst Fractures Burst fractures occur as a result of pure axial load applied to the injured vertebrae and are characterized by disruption of the anterior and middle columns of the spine with some degree of compromise of the spinal canal from retropulsed bony fragments. As in all of these spinal fractures, CT is helpful to delineate the bony injury. MRI is useful to assess the integrity of the soft tissue restraints and the degree of neurologic compromise. Appropriate treatment is determined by the presence of a neurologic deficit, degree of malalignment, and the extent of instability. Neurologic compromise is a clear indication for anterior decompression and instrumented fusion to provide stability. In the absence of a neurologic defect, the degree of instability becomes the most important factor guiding treatment. More stable variants may be treated with immobilization in a halo vest. Less stable fracture patterns (e.g., significant translation, kyphosis, loss of vertebral height) benefit from stabilization to prevent a neurologic injury and progressive kyphosis.

■ Flexion–Compression Fractures These occur from a combination of axial load and forward flexion resulting in compressive failure of the anterior vertebral body and tensile failure of the PLC. A teardrop-shaped avulsion of the anteroinferior tip of the more cranial vertebra is common

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SECTION 3 X FIGURE 23-22 Flexion–distraction subaxial cervical spine injury (i.e., jumped facets).

and responsible for the commonly associated eponym, “teardrop fracture.” These injuries are often complicated by significant neurologic compromise. The algorithm for treatment is similar to that of burst fractures as these fractures are typically very unstable and require stabilization.

■ Facet Fracture and Dislocation These injuries have a wide spectrum of presentation from isolated nondisplaced facet fractures to bilaterally jumped facets with SCI. They occur from a flexion–distraction mechanism often with some element of rotation. Facets may be fractured, subluxed, or dislocated, and this may be unilateral or bilateral (Fig. 23-22). These injuries typically require advanced imaging. As unilateral or bilateral facet injuries progress from subluxation to perched facets and then to dislocation, the extent of malalignment of the cervical spine provides a good indication of the degree of disruption of the facet capsule and posterior ligaments. An associated neurologic deficit can present as a radiculopathy with unilateral facet injuries, while compression of the spinal cord frequently occurs with bilateral injuries. Both unilateral and bilateral facet disruptions should be initially treated with closed traction. If the facet is locked in a dislocated position, open reduction and fusion is indicated as it is an unstable injury. Subluxations and

dislocations may benefit from traction with a cranial tong to reduce the deformity followed by operative stabilization. In irreducible situations, posterior approaches to the cervical spine allow access to the facets where direct reduction maneuvers can be performed. There is controversy over whether an MRI is indicated prior to attempts at reduction to determine whether a herniated disk that could potentially retropulse into the canal during reduction is present.76,77 In awake and alert patients able to participate in a neurologic exam, reduction can be attempted immediately without the delay in obtaining an MRI. Rapid intervention without MRI may be of some benefit in patients with SCI as more rapid decompression is associated with better outcomes in animal studies. In intact patients, the delay in getting an MRI is reasonable. Patients who are unable to participate in an exam require an MRI prior to reduction attempts. Minimally displaced facet fractures often result from a rotational mechanism of injury with variable involvement of the rest of the DLC. Neurologic injury is rare and, when present, is typically in the form of a root level injury. Associated pedicle and laminar fractures are common and can complicate the assessment of stability. Injury of the intervening intervertebral disk is possible and would lead to increased instability. Sometimes the instability is rotational that is difficult to identify on imaging studies, so a careful review of CT and MRI imaging is essential. Nondisplaced facet fractures can be treated in a rigid collar, but must be followed closely for rotational displacement. Displaced fractures require an overall assessment of stability to determine treatment.

■ Extension–Distraction Injuries These injuries occur from a hyperextension mechanism and are particularly common in the elderly after a fall with impact on their forehead. In the setting of spondylosis this mechanism can result in a central cord syndrome without bony and ligamentous instability. Typically, spinal instability is less of a concern in these injury patterns, and the decision centers on the timing of surgical decompression for patients with neurologic compromise.

■ Other Fractures Fractures of cervical spinous processes are not always benign and can be associated with significant ligamentous injury. Fracture lines that extend toward the ligamentum flavum and those that occur in association with other fractures should be carefully evaluated with CT and MRI. These studies would rule out potentially unstable injuries that could displace, causing delayed neurologic deficits.

SPECIFIC MANAGEMENT OF INJURIES OF THE THORACIC SPINE (T1–T9) The thoracic spine is inherently stable due to the rigid structural configuration of the sternum and rib cage. Injuries from a low-energy mechanism (e.g., compression fractures) can occur

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in patients with osteoporosis, but more commonly occur in the thoracolumbar spine. Compression fractures are uncommon in the upper thoracic spine (i.e., above T6), so their occurrence should raise the concern for a pathologic fracture from metastatic disease. Significant injuries to the thoracic spine usually result from a high-energy mechanism. Although stable injuries rarely involve neurologic compromise, profound neurologic deficits typically occur in the more unstable patterns. This high risk for neurologic injury is due to the small size of the neural canal, the tenuous arterial blood supply to the thoracic spinal cord, and the high energy required to inflict injury. Associated injuries occur in approximately 75% of all patients with injuries to the thoracic spine and can include rib fractures, pulmonary contusions, pneumothoraces, cardiac contusions, or vascular injuries. Associated sternal fractures (especially transverse patterns at the same level as the associated thoracic fracture) cause the entire chest cavity to be unstable. Stable fractures of the thoracic spine with an intact neurologic status can usually be treated nonoperatively. These fractures often consist of compression or burst fractures without significant flexion, rotation, or translation. A brace is rarely needed as the thoracic rib cage functions as an internal brace. Unstable fractures of the thoracic spine typically need operative stabilization since bracing is ineffective in this region. Instrumentation with a posterior pedicle screw is the most commonly employed method to regain stability. Fractures associated with significant ventral compression of the spinal cord may need decompression through an anterior thoracic exposure.

SPECIFIC MANAGEMENT OF INJURIES OF THE THORACOLUMBAR SPINE Fractures of the thoracolumbar spine are second only to injuries of the cervical spine in frequency. Because this region is the transition between the stiff thoracic spine and the mobile lumbar spine, it is highly susceptible to injury. Injuries in this location include compression fractures, burst fractures, flexion–distraction injuries, and fracture–dislocations. As in the cervical spine, the assessment of instability is essential for designing appropriate treatment strategies. Recently the TLICS score has been validated to assist in this determination.71

■ Compression Fractures Compression fractures involve the anterior column and typically occur as a result of an axial loading mechanism. They are the most frequent of all fractures of the thoracolumbar spine and are especially common in elderly patients with osteoporosis. These fractures are typically stable and are rarely associated with a neurologic deficit. Stable fractures can be treated in a brace, but recent interim analysis from a multicenter, randomized clinical trial suggests that treatment without bracing may have equivalent outcomes. Fractures with greater than 50% loss of anterior body height or more than 30° of angulation are considered unstable and may require surgical stabilization. Compression fractures that displace or become kyphotic may need surgical stabilization, as well.

455

FIGURE 23-23 Burst fracture of the thoracolumbar spine.

■ Burst Fractures Burst fractures involve the anterior and middle columns and typically occur through an axial loading mechanism (Fig. 23-23). There can be a component of flexion with the rotation centered on the PLL (the junction between the middle and posterior columns) and, therefore, the PLC can fail in tension. The involved middle column characteristically retropulses bony fragments into the canal that can result in a neurologic deficit. On imaging, burst fractures display loss of height of both the anterior and middle columns. They may have an associated vertical laminar fracture from splaying of the posterior elements, and this fracture can be associated with a dural tear and/or entrapment of a nerve root. Retropulsed bony fragments from the middle column may not be evident on plain x-rays, so CT imaging is necessary for full evaluation. Radiographic criteria for a stable burst fracture include less than 50% decrease in body height, less than 25° of angulation,

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and less than 50% compromise of the spinal canal. Burst fractures with greater than 50% decrease of body height, greater than 25° of angulation, and greater than 50% compromise of the spinal canal and those associated with neurologic deficit are potentially unstable. The most important criterion in determining if a burst fracture requires surgery is the neurologic status of the patient. Stable fractures that occur in neurologically intact patients can be treated nonoperatively even in the presence of significant compromise of the canal because the retropulsed fragments resorb over time.91 Historically, treatment consisted of immobilization with a TLSO with close follow-up to ensure maintenance of spinal alignment. Bailey et al.73 recently found that in adults less than 60 years with no neurologic deficit and kyphosis 35°, thoracolumbar burst fractures could be successfully treated without bracing. With unstable burst fractures or in the presence of significant neurologic deficits, surgery (instrumented posterior spinal fusion) is indicated. If the neural elements are not able to be adequately decompressed with indirect reduction methods (i.e., fracture reduction), direct decompression is necessary. The approach to directly decompressing the neurologic structures depends on the level of the fracture. At the level of the spinal cord and conus medullaris (T10–L1 or L2), retraction of the neural elements is risky. Therefore, an anterolateral approach is preferred for direct decompression of the retropulsed fragments to relieve compression of the ventral thecal sac. Below the level of the conus, the thecal sac can be retracted allowing the protruding bone fragments to be tamped ventrally through a posterior transpedicular approach.

■ Flexion–Distraction Injuries Flexion–distraction injuries, also known as Chance injuries and seatbelt injuries, involve the middle and posterior columns. The center of rotation for these injuries is at the anterior longitudinal ligament or anterior to the vertebral body. Therefore, the posterior elements (i.e., posterior column) fail in tension. Consequently, care must be taken to avoid traction/distraction maneuvers during the initial stabilization of this injury. Because of the mechanism of injury, abdominal viscera may be injured. On imaging, these fractures can look similar to burst fractures, but they are distinguished by a middle column that has failed in tension resulting in a gain in height of the posterior aspect of the vertebral body (i.e., middle column). Associated laminar fractures are horizontal in contrast to the vertical fracture orientation in burst fractures. These spinal column injuries can fail through bone, through the soft tissues (intervertebral disk and the PLC), or through a combination of the two. Consequently, CT and MRI are necessary to evaluate the degree of involvement of osseous and soft tissue. Closed reduction and bracing is appropriate in those injuries involving bone with less than 30° angulation because fractures tend to heal with appropriate bony apposition. Surgical reduction and fixation is indicated for flexion–distraction injuries that are primarily ligamentous (i.e., with poor healing potential) or have more than 30° angulation.

■ Fracture–Dislocations Fracture–dislocations are extremely unstable injuries that involve all three columns of the spine (Fig. 23-23 and Fig. 23-24A, B). These occur through some combination of rotation, flexion, and translation and usually result in a neurologic deficit, of which half are complete lesions. Nonoperative treatment is never appropriate. Incomplete injuries benefit from early surgical reduction, decompression, and stabilization. Complete injuries or intact patients will require surgical stabilization to facilitate early mobilization and rehabilitation.

■ Other Injuries Isolated injuries to posterior bony elements (e.g., lamina fractures, avulsions of spinous process tips, transverse process fractures) are typically stable injuries restricted to the posterior column of the spine with a few exceptions. Fractures of the L5 transverse processes are typically nonoperative spinal injuries; however, these can be associated with pelvic ring disruptions and warrant dedicated pelvic imaging.

SPECIFIC MANAGEMENT OF INJURIES OF THE SACRUM Sacral trauma comprises a complex constellation of injuries that includes associated disruptions of the pelvic ring and injuries to the nerve roots, cauda equina, and the spinal segments. These can be divided into injuries resulting from disruption of the pelvic ring, injuries intrinsic to the sacrum, and injuries involving the lumbosacral articulation. In general, the same principles previously described with regard to management of spinal instability and neurologic deficits apply to the management of sacral injuries. Restoration of spinal alignment and stability and neurologic decompression remain the treatment goals. There are, however, several additional considerations. Associated hemodynamic instability merits consideration for angiographic embolization of bleeding vessels in the pelvis. Also, it is important to rule out open fractures, especially in significantly displaced patterns, by rectal and vaginal examination. Finally, evaluation of pelvic ring stability is necessary, though this is typically done in conjunction with a consulting orthopedic surgeon familiar with the evaluation and treatment of pelvic ring disruptions. Intrinsic sacral fractures rarely compromise the stability of the sacrum or the lumbosacral articulations. They can be associated with neurologic deficits and occasionally require surgical decompression. The Denis classification system classifies intrinsic sacral fractures based on the relationship of the fracture line to the sacral neuroforamina and is useful for predicting neurologic deficits.92 Zone I fractures are lateral to the foramina and have a 6% chance of root involvement. Zone II fractures enter the foramina and have a 28% chance of root involvement. Because the upper sacral roots are larger, there is less room in their respective foramina and they are more prone to injury than the lower sacral roots. Type III fractures enter the central canal and are associated with a risk approaching

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FIGURE 23-25 CT of lumbosacral dissociation injury.

A

60%. Management of these injuries in the absence of an associated disruption of the pelvic ring is typically conservative and includes some degree of limitations on weight bearing. Associated disruptions of the pelvic ring require evaluation and treatment under the purview of a consulting orthopedic surgeon. Certain patterns of sacral injury can lead to instability. Vertically oriented transforaminal sacral fractures that extend proximally through or medial to the articular process of S1 can result in instability of the lumbosacral junction.93 Therefore, displaced transforaminal sacral fractures warrant close scrutiny of the lumbosacral junction with appropriate CT imaging. These injuries can be surgically stabilized (i.e., L5–S1 fusion) to minimize the sequelae of residual incongruence of the facets. Lumbosacral and lumbopelvic dissociation are rare and often fatal injuries that involve dissociation of the spine from the pelvis94 (Fig. 23-25). This can result from bilateral L5–S1 facet fracture/dislocation or a fracture line crossing the sacrum (e.g., U-type sacral fracture). These injuries can be missed as the patient is often in extremis. Surgical options include percutaneous screw techniques and lumbopelvic fixation. The latter is a stronger construct, but is a more invasive procedure.

GUNSHOT WOUNDS TO THE SPINE B FIGURE 23-24 (A and B) Fracture–dislocation of the thoracolumbar spine.

The incidence of civilian GSWs to the spine has been steadily increasing and is the second leading cause of SCI in many urban areas. As the wounding capacity of a GSW relates to its kinetic energy (KE  [1/2]mv2), the muzzle velocity has an exponential effect on the energy of the injury (see Chapter 1).

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Low-energy bullets travel less than 1,000–2,000 ft/s (e.g., handguns), while high-energy bullets travel at speeds greater than 2,000 ft/s (e.g., military assault rifles). Damage is created by several mechanisms, including the actual passage of the missile through tissue, a secondary shock wave, and cavitation. At impact, the bullet creates a temporary cavity at the entry site due to stretching forces and the vacuum created by its passing. The volume of this cavity and, consequently, the extent of tissue injury are proportional to the energy transferred by the missile. Neurologic injury can occur not only from direct contact but also from close passage of the bullet to the neurologic elements. Because of the low kinetic energy involved, civilian GSWs to the spine typically must traverse or remain inside the spinal canal to cause a neurologic deficit. All GSWs to the spine should be evaluated according to a routine management algorithm. A patient’s general medical condition should be addressed and stabilized prior to focusing on the spine. A detailed neurologic examination should be performed. Gunshot injuries to the neck may mandate routine angiography and panendoscopy to identify vascular and visceral injuries. Gunshot injuries to the thoracic spine may be associated with pulmonary or cardiac injuries, and those to the lumbar spine may involve abdominal viscera, genitourinary structures, or a major vessel. In particular, colonic perforations that occur before the bullet passes through the spine must be recognized because they are associated with an increased risk of infection if not appropriately treated with a course of broad-spectrum antibiotics. The spine should be routinely imaged with plain x-rays and CT to localize the level of injury and establish the extent of bony disruption. MRI is important to rule out an epidural hematoma as a cause for the neurologic deficit. Because most bullets are not ferromagnetic, MRI is rarely contraindicated except when the bullet is in the canal. Dynamic flexion– extension stress x-rays are rarely indicated in the acute setting, but can be considered in awake and alert patients or in a patient with suspected instability. Tetanus prophylaxis should be a consideration in all patients with gunshot injuries, and 24 hours of antibiotic coverage is prudent with the duration dictated by the extent of injury to soft tissue. Spinal injuries from transabdominal bullets that perforate a viscus prior to entering the spine have been associated with rates of spinal infection as high as 88% in the absence of appropriate antibiotic coverage.95 These patients should receive between 7 and 14 days of broad-spectrum antibiotic coverage, and surgical debridement has not been shown to be of benefit. The potential for spinal instability following low-energy GSWs is modest, and these patients rarely require bracing. The majority of reported cases of instability are iatrogenic resulting from ill-advised decompression.96 Isiklar and Lindsey97 reported on late spinal instability among patients with gunshot injuries treated nonoperatively. Of the instability cases identified, 75% occurred in the cervical spine. Therefore, the potential for spinal instability exists with a GSW and should always be considered, especially in the cervical spine. Neurologic recovery is usually limited after a GSW to the spine resulting in an SCI. In these situations, there is no role for

steroids. Surgical decompression of intracanal bullets may result in root level return in the cervical or lumbar spine, but there is no benefit in the thoracic spine.98 The increased risk of infection and cerebral spinal fluid fistula must be weighed against the potential benefit.96 Probably the strongest argument for removal of an intracanal bullet in these regions would be in the setting of an incomplete injury in the cervical spinal cord where the possibility of recovering a neurologic level may justify the increased risks of the procedure.

COMPLICATIONS The most devastating complication in patients with spinal trauma is neurologic deterioration. There are a variety of reasons a patient may decompensate neurologically. Evolution of a cranial bleed is an important consideration in patients with traumatic brain injuries. Inappropriate manipulation of the unstable spine during transfers can result in an iatrogenic injury, also. Intraoperatively, dural tears can expose sensitive neural tissues to inadvertent injury, and placement of hardware risks injury to the nerves and spinal cord. Epidural hematomas in preoperative and postoperative patients can expand, especially when pharmacologic anticoagulation is being used. Serial neurologic examinations in the preoperative and postoperative patients and neurophysiologic monitoring in the intraoperative setting may allow for the timely identification of neurologic deterioration and allow expedited intervention. Patients experiencing neurologic deterioration should be given supplemental oxygen to ensure adequate oxygenation and should have their hemodynamic parameters optimized. Prompt repeat imaging (i.e., MRI, CT, or CT myelogram) is then indicated to determine the etiology. Operative intervention may be indicated in the presence of a compressive lesion. Dural tears and leakage of cerebrospinal fluid are common complications of spinal trauma. Tears may occur at the time of injury and are frequently associated with laminar fractures. Alternatively, they can result during surgery. Significant leakage of cerebrospinal fluid in the patient with no plans for surgery in the near term may benefit from placement of a subarachnoid drain. In patients undergoing surgery, an attempt should be made to obtain a watertight seal of the durotomy through direct suture repair. If this is not possible, the dural defect may be patched with local fat, fascia, or synthetic patches with adjunctive use of dural sealants. For large, irreparable tears, a subarachnoid drain is required. Postoperative surgical site infections (SSIs) are unfortunately common in patients undergoing spinal surgery after trauma with an incidence of approximately 8%. This is higher than quoted rates for elective spinal surgery (1–2%) because of a variety of factors. These include injury to other organ systems, traumatized soft tissues, higher incidence of dural tears with leakage of cerebrospinal fluid, poor nutrition, and the lower socioeconomic strata of affected patients.99 In patients undergoing elective spinal surgery, Olsen et al.100 found diabetes mellitus was associated with the highest independent risk of SSI. Preoperative or postoperative hyperglycemia and obesity were other independently associated risk

Vertebrae and Spinal Cord

REFERENCES 1. Hu R, Mustard CA, Burns C. Epidemiology of incident spinal fracture in a complete population. Spine (Phila Pa 1976). 1996;21(4):492–499. 2. Holmes J, Miller P, Panacek E, et al. Epidemiology of thoracolumbar spine injury in blunt trauma. Acad Emerg Med. 2001;8:866. 3. Lowery DW, Wald MM, Browne BJ, et al. Epidemiology of cervical spine injury victims. Ann Emerg Med. 2001;38:12. 4. Jackson AB, Dijkers M, Devivo MJ, et al. A demographic profile of new traumatic spinal cord injuries: change and stability over 30 years. Arch Phys Med Rehabil. 2004;85:1740–1748. 5. National Spinal Cord Injury Statistical Center. Spinal Cord Injury Facts and Figures at a Glance. Available at: http://www.spinalcord.uab.edu. Accessed March 9, 2010. 6. Dryden DM, Saunders LD, Rowe BH, et al. The epidemiology of traumatic spinal cord injury in Alberta, Canada. Can J Neurol Sci. 2003;30:113–121. 7. Kannus P, Niemi S, Palvanen M, et al. Continuously increasing number and incidence of fall-induced, fracture-associated, spinal cord injuries in elderly persons. Arch Intern Med. 2000;160:2145–2149. 8. Torg JS, Guille JT, Jaffe S. Injuries to the cervical spine in American football players. J Bone Joint Surg Am. 2002;84-A(1):112–122. 9. Jellinger K. Pathology of spinal cord trauma. In: Errico TJ, Bauer RD, Waugh T, eds. Spinal Trauma. Baltimore, MD: Lippincott; 1990:455. 10. Anderson DK, Hall ED. Pathophysiology of spinal cord trauma. Ann Emerg Med. 1993;22:987. 11. Tempel GE, Martin HF. The beneficial effects of a thromboxane receptor antagonist on spinal cord perfusion following experimental cord injury. J Neurol Sci. 1992;109:162. 12. Liu D, Thangnipon W, McAdoo DJ. Excitatory amino acids rise to toxic levels upon impact injury to the rat spinal cord. Brain Res. 1991;547:344. 13. Wrathall JR, Teng YD, Choiniere D, et al. Evidence that local nonNMDA receptors contribute to functional deficits in contusive spinal cord injury. Brain Res. 1992;586:140. 14. Young W, Koren I. Potassium and calcium changes in injured spinal cords. Brain Res. 1986;365:42. 15. Gentile NT, McIntosh TK. Antagonists of excitatory amino acids and endogenous opioid peptides in the treatment of experimental central nervous system injury. Ann Emerg Med. 1993;22:1028. 16. American Spinal Injury Association. Standard Neurological Classification of Spinal Cord Injury Worksheet. Atlanta, GA: American Spinal Injury Association; 2006. 17. Bohlman HH. Acute fractures and dislocations of the cervical spine. An analysis of three hundred hospitalized patients and review of the literature. J Bone Joint Surg Am. 1979;61(8):1119–1142. 18. Stauffer ES. Neurologic recovery following injuries to the cervical spinal cord and nerve roots. Spine (Phila Pa 1976). 1984;9:532–534. 19. Toscano J. Prevention of neurological deterioration before admission to a spinal cord injury unit. Paraplegia. 1988;26:143–150. 20. Rechtine GR, Del Rossi G, Conrad BP, Horodyski M. Motion generated in the unstable spine during hospital bed transfers. J Trauma. 2004;57: 609–611. 21. Hauswald M, Braude D. Spinal immobilization in trauma patients: is it really necessary? Curr Opin Crit Care. 2002;8:566–570. 22. Levi AD, Hurlbert J, Anderson PA, et al. Neurologic deterioration secondary to unrecognized spinal instability following trauma—a multicenter study. Spine. 2006;31:451–458. 23. Vaccaro AR, An HS, Lin S, et al. Noncontiguous injuries of the spine. J Spinal Disord. 1992;5:320–329. 24. Brown CV, Antevil JL, Sise MJ, et al. Spiral computed tomography for the diagnosis of cervical, thoracic, and lumbar spine fractures: its time has come. J Trauma. 2005;58:890–895. 25. McCulloch PT, France J, Jones DL, et al. Helical computed tomography alone compared with plain radiographs with adjunct computed tomography to evaluate the cervical spine after high-energy trauma. J Bone Joint Surg Am. 2005;87:2388–2394. 26. Anderson PA, Gugala Z, Lindsey RW, et al. Clearing the cervical spine in the blunt trauma patient. J Am Acad Orthop Surg. 2010;18(3):149–159.

27. Stiell IG, Clement CM, McKnight RD, et al. The Canadian C-spine rule versus the NEXUS low-risk criteria in patients with trauma. N Engl J Med. 2003;349:2510–2518. 28. Harris TJ, Blackmore CC, Mirza SK, et al. Clearing the cervical spine in obtunded patients. Spine (Phila Pa 1976). 2008;33:1547–1553. 29. Tomycz ND, Chew BG, Chang YF, et al. MRI is unnecessary to clear the cervical spine in obtunded/comatose trauma patients: the four-year experience of a level I trauma center. J Trauma. 2008;64:1258–1263. 30. Stassen NA, Williams VA, Gestring ML, et al. Magnetic resonance imaging in combination with helical computed tomography provides a safe and efficient method of cervical spine clearance in the obtunded trauma patient. J Trauma. 2006;60:171–177. 31. Muchow RD, Resnick DK, Abdel MP, et al. Magnetic resonance imaging (MRI) in the clearance of the cervical spine in blunt trauma: a meta-analysis. J Trauma. 2008;64:179–189. 32. Meissner MH, Chandler WL, Elliott JS. Venous thromboembolism in trauma: a local manifestation of systemic hypercoagulability? J Trauma. 2003;54(2):224–231. 33. Knudson MM, Ikossi DG, Khaw L, et al. Thromboembolism after trauma: an analysis of 1602 episodes from the American College of Surgeons National Trauma Data Bank. Ann Surg. 2004;240(3):490–496 [discussion 496–498]. 34. Dai LY, Yao WF, Cui YM, et al. Thoracolumbar fractures in patients with multiple injuries: diagnosis and treatment—a review of 147 cases. J Trauma. 2004;56(2):348–355. 35. Geerts WH, Code KI, Jay RM, et al. A prospective study of venous thromboembolism after major trauma. N Engl J Med. 1994;331(24): 1601–1606. 36. Jones T, Ugalde V, Franks P, et al. Venous thromboembolism after spinal cord injury: incidence, time course, and associated risk factors in 16,240 adults and children. Arch Phys Med Rehabil. 2005;86(12):2240–2247. 37. Ploumis A, Ponnappan RK, Maltenfort MG, et al. Thromboprophylaxis in patients with acute spinal injuries: an evidence-based analysis. J Bone Joint Surg Am. 2009;91(11):2568–2576. 38. Curry K, Casady L. The relationship between extended periods of immobility and decubitus ulcer formation in the acutely spinal cordinjured individual. J Neurosci Nurs. 1992;24:185–189. 39. Hadley MN, Walters BC, Grabb PA, et al. Blood pressure management after acute spinal cord injury. Neurosurgery. 2002;50(suppl):58–62. 40. Bracken MB, Shepard MJ, Holford TR, et al. Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury. JAMA. 1997;277:1597–1604. 41. Coleman WP, Benzel E, Cahill DW, et al. A critical appraisal of the reporting of the National Acute Spinal Cord Injury Studies (II and III) of methylprednisolone in acute spinal cord injury. J Spinal Disord. 2000;13:185–199. 42. Hurlbert RJ. Methylprednisolone for acute spinal cord injury: an inappropriate standard of care. J Neurosurg. 2000;93:1–7. 43. Short DJ, El Masry WS, Jones PW. High dose methylprednisolone in the management of acute spinal cord injury: a systematic review from a clinical perspective. Spinal Cord. 2000;38:273–286. 44. Hugenholtz H, Cass DE, Dvorak MF, et al. High-dose methylprednisolone for acute closed spinal cord injury—only a treatment option. Can J Neurol Sci. 2002;29(3):227–235. 45. Cappuccino A, Bisson LJ, Carpenter B, et al. The use of systemic hypothermia for the treatment of an acute cervical spinal cord injury in a professional football player. Spine (Phila Pa 1976). 2010;35(2): E57–E62. 46. Zemke D, Majid A. The potential of minocycline for neuroprotection in human neurologic disease. Clin Neuropharmacol. 2004;27:293. 47. Stirling DP, Khodarahmi K, Liu J, et al. Minocycline treatment reduces delayed oligodendrocyte death, attenuates axonal dieback, and improves functional outcome after spinal cord injury. J Neurosci. 2004;24:2182. 48. Gorio A, Gokmen N, Erbayraktar S, et al. Recombinant human erythropoietin counteracts secondary injury and markedly enhances neurological recovery from experimental spinal cord trauma. Proc Natl Acad Sci U S A. 2002;99:9450. 49. Li S, Liu BP, Budel S, et al. Blockade of Nogo-66, myelin-associated glycoprotein, and oligodendrocyte myelin glycoprotein by soluble Nogo66 receptor promotes axonal sprouting and recovery after spinal injury. J Neurosci. 2004;24:10511. 50. Qiu J, Cai D, Dai H, et al. Spinal axon regeneration induced by elevation of cyclic AMP. Neuron. 2002;34:895. 51. Kwon BK, Fisher CG, Dvorak MF, et al. Strategies to promote neural repair and regeneration after spinal cord injury. Spine. 2005;30:S3. 52. Cheng H, Cao Y, Olson L. Spinal cord repair in adult paraplegic rats: partial restoration of hind limb function. Science. 1996;273:510.

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factors. Administration of prophylactic antibiotics within 1 hour before the skin incision and adjustment in antibiotic dosages for obesity are thought to be important strategies to decrease the risk of SSI.

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53. Ruitenberg MJ, Vukovic J, Sarich J, et al. Olfactory ensheathing cells: characteristics, genetic engineering, and therapeutic potential. J Neurotrauma. 2006;23:468. 54. Barnett SC, Riddell JS. Olfactory ensheathing cells (OECs) and the treatment of CNS injury: advantages and possible caveats. J Anat. 2004;204:57. 55. Camargo FD, Chambers SM, Goodell MA. Stem cell plasticity from transdifferentiation to macrophage fusion. Cell Prolif. 2004;37:55. 56. Sykova E, Jendelova P, Glogarova K, et al. Bone marrow stromal cells—a promising tool for therapy of brain and spinal cord injury. Exp Neurol. 2004;187:220. 57. Delamarter RB, Sherman J, Carr JB. Pathophysiology of spinal cord injury: recovery after immediate and delayed compression. J Bone Joint Surg Am. 1995;77:1042–1049. 58. Carlson GD, Gorden CD, Oliff HS, et al. Sustained spinal cord compression: part I: time-dependent effect on long-term pathophysiology. J Bone Joint Surg Am. 2003;85:86–94. 59. La Rosa G, Conti A, Cardali S, et al. Does early decompression improve neurological outcome of spinal cord injured patients? Appraisal of the literature using a meta-analytical approach. Spinal Cord. 2004;42: 503–512. 60. Papadopoulos SM, Selden NR, Quint DJ, et al. Immediate spinal cord decompression for cervical spinal cord injury: feasibility and outcome. J Trauma. 2002;52:323–332. 61. Vaccaro AR, Daugherty RJ, Sheehan TP, et al. Neurologic outcome of early versus late surgery for cervical spinal cord injury. Spine (Phila Pa 1976). 1997;22(22):2609–2613. 62. McKinley W, Meade MA, Kirshblum S, et al. Outcomes of early surgical management versus late or no surgical intervention after acute spinal cord injury. Arch Phys Med Rehabil. 2004;85:1818–1825. 63. Fehlings MG, Perrin RG. The timing of surgical intervention in the treatment of spinal cord injury: a systematic review of recent clinical evidence. Spine (Phila Pa 1976). 2006;31(11 suppl):S28–S35 [discussion S36]. 64. White AA, Panjabi MM. The problem of clinical instability in the human spine: a systematic approach. In: White AA, Panjabi MM, eds. Clinical Biomechanics of the Spine. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 1990:277–378. 65. Allen BL, Ferguson RL, Lehmann TR, et al. A mechanistic classification of closed, indirect fractures and dislocations of the lower cervical spine. Spine. 1982;7:1. 66. Vaccaro AR, Hulbert RJ, Patel AA, et al. Spine Trauma Study Group. The subaxial cervical spine injury classification system: a novel approach to recognize the importance of morphology, neurology, and integrity of the disco-ligamentous complex. Spine (Phila Pa 1976). 2007;32(21): 2365–2374. 67. Holdsworth F. Fractures, dislocations, and fracture–dislocations of the spine. J Bone Joint Surg. 1970;52A:1534. 68. Denis F. The three column spine and its significance in the classification of acute thoracolumbar spinal injuries. Spine (Phila Pa 1976). 1983;8(8):817–831. 69. Panjabi MM, Oxland TR, Kifune M, et al. Validity of the three-column theory of thoracolumbar fractures: a biomechanic investigation. Spine. 1995;20:1122. 70. Magerl F, Aebi M, Gertzbein SD, et al. A comprehensive classification of thoracic and lumbar injuries. Eur Spine J. 1994;3:184. 71. Vaccaro AR, Lehman RA Jr, Hurlbert RJ, et al. A new classification of thoracolumbar injuries: the importance of injury morphology, the integrity of the posterior ligamentous complex, and neurologic status. Spine (Phila Pa 1976). 2005;30(20):2325–2333. 72. Anderson DG, Vaccaro AR, Gavin KF. Cervical orthoses and cranioskeletal traction. In: Clark CR, ed. The Cervical Spine. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2005:110–121 [Table 7.1]. 73. Bailey CS, Dvorak MF, Thomas KC, et al. Comparison of thoracolumbosacral orthosis and no orthosis for the treatment of thoracolumbar burst fractures: interim analysis of a multicenter randomized clinical equivalence trial. J Neurosurg Spine. 2009;11(3):295–303. 74. Johnson RM, Hart DL, Simmons EF, et al. Cervical orthoses: a study comparing their effectiveness in restricting cervical motion in normal subjects. J Bone Joint Surg Am. 1977;59:332–339.

75. Majercik S, Tashijan RZ, Biffl WL, et al. Halo vest immobilization in the elderly: a death sentence? J Trauma. 2005;59:350–356. 76. Eismont FJ, Arena MJ, Green BA. Extrusion of an intervertebral disc associated with traumatic subluxation or dislocation of cervical facets. Case report. J Bone Joint Surg. 1991;73A:1555. 77. Grauer JN, Vaccaro AR, Lee JY, et al. The timing and influence of MRI on the management of patients with cervical facet dislocations remains highly variable: a survey of members of the Spine Trauma Study Group. J Spinal Disord Tech. 2009;22(2):96–99. 78. Hu SS, Capen DA, Rimoldi RL, et al. The effect of surgical decompression on neurologic outcome after lumbar fracture. Clin Orthop. 1993;288:166. 79. Fellrath RF, Hanley EN. Multitrauma and thoracolumbar fractures. Semin Spine Surg. 1995;7:103. 80. Ahn JH, Ragnarsson KT, Gordon WA, et al. Current trends in stabilizing high thoracic and thoracolumbar spinal fractures. Arch Phys Med Rehabil. 1984;65:366–369. 81. Willen J, Lindahl S, Irstam L, et al. Unstable thoracolumbar fractures: a study by CT and conventional roentgenology of the reduction effect of Harrington instrumentation. Spine. 1984;9:215. 82. Yazici M, Gulman B, Sen S, et al. Sagittal contour restoration and canal clearance in burst fractures of the thoracolumbar junction (T12–L1): the efficacy of timing of the surgery. J Orthop Trauma. 1995;9(6):491–498. 83. Campagnolo DI, Esquieres RE, Kopacz KJ. Effect of stabilization on length of stay and medical complications following spinal cord injury. J Spinal Cord Med. 1997;20:331. 84. Anderson PA, Montesano PX. Morphology and treatment of occipital condyle fractures. Spine. 1988;13:731–736. 85. Harris JH Jr, Carson GC, Wagner LK, et al. Radiologic diagnosis of traumatic occipitovertebral dissociation: 2. Comparison of three methods of detecting occipitovertebral relationships on lateral radiographs of supine subjects. AJR Am J Roentgenol. 1994;162:887–892. 86. Traynelis VC, Marano GD, Dunker RO, et al. Traumatic atlantooccipital dislocation: case report. J Neurosurg. 1986;65:863–870. 87. Spence KF Jr, Decker S, Sell KW. Bursting atlantal fracture associated with rupture of the transverse ligament. J Bone Joint Surg Am. 1970;52: 543–549. 88. Anderson LD, D’Alonzo RT. Fractures of the odontoid process of the axis. J Bone Joint Surg Am. 1974;56:1663–1674. 89. Levine AM, Edwards CC. The management of traumatic spondylolisthesis of the axis. J Bone Joint Surg Am. 1985;67(2):217–226. 90. Starr JK, Eismont FJ. Atypical Hangman’s fractures. Spine (Phila Pa 1976). 1993;18(14):1954–1957. 91. Wood K, Buttermann G, Mehbod A, et al. Operative compared with nonoperative treatment of a thoracolumbar burst fracture without neurological deficit. A prospective, randomized study. J Bone Joint Surg Am. 2003;85-A(5):773–781 [Erratum in J Bone Joint Surg Am. 2004; 86-A(6):1283]. 92. Denis F, Davis S, Comfort T. Sacral fractures: an important problem. Retrospective analysis of 236 cases. Clin Orthop Relat Res. 1988;227: 67–81. 93. Isler B. Lumbosacral lesions associated with pelvic ring injuries. J Orthop Trauma. 1990;4:1–6. 94. Vialle R, Wolff S, Pauthier F, et al. Traumatic lumbosacral dislocation: four cases and review of literature. Clin Orthop Relat Res. 2004;419: 91–97. 95. Romanick P, Smith T, Kopaniky D, et al. Infection about the spine associated with low-velocity missile injury to the abdomen. J Bone Joint Surg. 1985;67:1195–1201. 96. Stauffer ES, Wood RW, Kelly EG. Gunshot wounds of the spine: the effects of laminectomy. J Bone Joint Surg. 1979;61A:389. 97. Isiklar ZU, Lindsey RW. Low velocity civilian gunshot wounds of the spine. Orthopedics. 1997;20:967. 98. Waters R, Adkins R. The effects of removal of bullet fragment retained in the spinal canal. A collaborative study by the National Spinal Cord Injury Model Systems. Spine. 1991;16:934–939. 99. Lim MR, Lee JY, Vaccaro AR. Surgical infections in the traumatized spine. Clin Orthop Relat Res. 2006;444:114–119. 100. Olsen MA, Nepple JJ, Riew KD, et al. Risk factors for surgical site infection following orthopaedic spinal operations. J Bone Joint Surg Am. 2008;90(1):62–69.

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CHAPTER 24

Trauma Thoracotomy: Principles and Techniques Kenneth L. Mattox, Matthew J. Wall, Jr., and Peter Tsai

Chest trauma was documented in the Edwin Smith Surgical Papyrus, written by Imhotep over 5000 years ago.1 The first recorded operation in the United States was removal of an arrowhead from an Indian’s chest by Cabeza de Vaca in 1635.2 The mortality from chest injury during war has ranged from 28.5% during the Crimean War (1853–1856) to a less than 5% today. Currently, in the United States more than 16,000 deaths occur annually as a direct result of thoracic trauma.3 The chest composes almost one fourth of the total body mass and is therefore often subjected to injury during trauma from any etiology. Regardless of etiology, a patient with thoracic trauma requires logical and sequential evaluation of the chest injury, followed by focused therapy, which, in some instances (less than 20% of the time), involves an operation. Those evaluating and treating must understand the anatomy, physiology, and function of each of the thoracic organs, as well as how each decision and treatment will affect outcome. The acute care surgeon must understand thoracic organ responses to and manifestations of various injuries, appropriate evaluation tools, which evaluations might be misleading, redundant, or unnecessary, and approaches to therapy. It is essential to be able to recognize when minor intervention or damage control should be applied to a chest injury condition verses when a formal surgical intervention is indicated. When surgery is performed the surgeon must also understand benefits and limitations of the various patient positions and incisions. Finally, as every evaluation and therapy has its potential hazard or contraindication, the acute care surgeon must understand traditional concepts that are either dated or currently considered controversial. Injury to the chest and its organs may be caused by penetration (from missiles, fragments, knives, needles, and other objects), blunt forces, iatrogenic misadventure, blasts, ingestion of toxic substances, and, indirectly, from abnormal medical conditions elsewhere in the body. Each of these etiologies has differing initial manifestations as well as evaluation and

treatment approaches.4–6 These differences are more specifically discussed elsewhere in this textbook. This overview chapter contains many cultural views, which have become doctrine and standard use by the authors, but, admittedly, based on Class 3 evidence, which might differ from the culture in other trauma centers.

THORACIC ANATOMY AND PHYSIOLOGY: RESPONSE TO TRAUMA The thoracic cavity is surrounded by a flexible boney cage, supported by respiratory and locomotive muscles. Three separate compartments house the two lungs with their five segments that are attached by vascular structures to the central cardiovascular compartment. In addition, the trachea and bronchus connect the lungs to the pharynx, and a series of nerves traverse the thoracic cavity. In the healthy patient, the lungs and heart are separated from their surrounding cavities by a smooth fibrous pleural lining. Following inflammation, fusion of these linings may alter some physiology and, consequently, some treatment options. Prior to any procedure following thoracic trauma, the surgeon is well advised to review the regional anatomy, determine position and incision options for a particular technique, and consider all approaches.

■ Evaluation technology Significant technology—from simple physical examination to extremely complex and sophisticated imaging and laboratory testing—exists to assist in the evaluation of a patient with pathology in the chest.7 Imaging may involve ultrasound, Doppler technology, classic radiologic tests, helical multidetection computerized technology (CT scans), magnetic resonance imaging (MRI), and others. Other tests available to the surgeon include cardiologic evaluation using EKG, echocardiogram, and even cardiac catheterization. Hematologic, clotting, and

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metabolic testing, as well as pulmonary function testing are other potentially helpful adjuncts. Endoscopic evaluation of the trachea and esophagus can supplement imaging modalities. In deciding which evaluation tools to use, first consider what you expect the test to demonstrate and, then, consider how the results will alter decision-making or treatment. Once these questions are considered and answered, the treating physician may well decide the tests are not needed. It is always helpful to have a progress note reflecting the decision-making process—tests ordered/why/why not—in the patient’s medical record.

Although many different injury patterns may occur in the chest and to its contents, indications for an acute formal thoracotomy follow both anatomic and physiologic parameters and include: • • • • • •

TUBE THORACOSTOMY Tube thoracostomy is both the most common procedure performed following chest trauma and also one of the most misunderstood and underrated operations in medicine. It is the only invasive procedure that most (85%) of patients with chest injury will require. Upward of 25% of patients with chest tubes will encounter some difficulty with malposition, connection problems, collection system difficulty, pressure abnormalities, or misperceptions and complications at the time of removal. Often, such difficulty can and does result in a clotted hemothorax that is not evacuated, a pleural space problem, a retained pneumothorax, or a recurrent pneumothorax. Far too often, second and multiple chest tubes are unnecessarily inserted as a result of a misunderstanding of the function and technique of tube thoracostomy. Tube thoracostomy following trauma should be accomplished in as pain and complication free manner as possible. Trocar-tipped chest tubes should be avoided. Chest tubes are best inserted in the area of the auscultatory triangle in the midaxillary line near the 4th or 5th intercostal space. Subcutaneous tissue and muscular dissection may be accomplished with clamps or dissecting scissors, but the pleura should be opened with an exploring finger, not a sharp instrument. Care is taken to avoid injury to the intercostal vessels and nerve on the under surface of each rib, as such injury can produce iatrogenic bleeding and pain. Following a gentle digital exploratory thoracotomy, an appropriately sized chest tube (32–36 French) is directed toward the back and apex of the pleural space and attached to an appropriate collection device. This insertion site overlies the major pulmonary fissure. Care must be taken to assure that the chest tube is not in this fissure, the exact relative location of which can often be ascertained by preinsertion digital exploration. One might consider antotransfusing fresh hemothorax blood using an appropriate device.

INDICATIONS FOR THORACOTOMY FOLLOWING TRAUMA Only approximately 15% of patients with chest injury require a formal thoracotomy. The indications for thoracotomy continue to change as newer, noninvasive therapies such as endovascular removal of intravascular foreign bodies and endovascular stent graft insertions become available.

• • • • • • • • • • •

Loss of chest wall substance (traumatic thoracotomy) Traumatic hemopericardium8 Evidence of free wall, septal, or valvular cardiac disruption8 Radiologic or endoscopic evidence of tracheal, bronchial, esophageal, or great vessel injury9,10 Greater than 1500 mL blood loss from the pleural cavity following the initial tube thoracostomy11 Greater than a sustained 200 mL continuing blood loss per hour from the tube thoracostomy Loss of cardiac function or proximal vascular control (resuscitative thoracotomy)9,12–15 Massive air leak Demonstrable thoracic tracheal or bronchus injury Uncontrolled hemorrhage in thoracic outlet major injury Mediastinal missile traverse with massive blood or air loss through the chest tube Removal of selective foreign bodies Massive air embolism, particularly systemic air embolism Retained clotted hemothorax (subacute and chronic indications)16 Posttraumatic contained empyema16 Cardiac herniation (ruptured pericardium)17 Cardiac septal or valve disruption

MINOR THERAPEUTIC INTERVENTIONS In addition to the routine basic maneuvers to stabilize the trauma patient, a number of minor therapeutic interventions are available. Some, such as needle decompression of the pleural cavity, pericardiocentesis, interosseous sternal fluid infusions, and subxyphoid pericardiotomy, have been controversial with regard to specific indications and the ultimate expected benefit. Specific, evidence-based data are not sufficient to recommend these maneuvers. Other minor thoracic maneuvers used by the surgeon include: • Endotracheal intubation (limiting the ventilatory pressures to less than 40 TORR in order to prevent systemic air embolism • Intercostal tube thoracostomy • Video-assisted thoracic surgery (VATS) • Intercostal and epidural block for pain control • Digital thoracotomy (gentle digital exploration to the extent of the inserted finger at the time of tube thoracostomy)

PATIENT POSITIONS/INCISIONS The supine position is the utility position for operations on thoracic trauma patients, as it allows for a variety of anterior incisions, including median sternotomy, right and or left anterolateral thoracotomy, transternal bilateral anterolateral thoracotomy, and partial anterior incisions (Fig. 24-1).

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A

D

B

E

C

© Baylor College of Medicine 1980

FIGURE 24-1 Thoracic incisions for trauma include (A) median sternotomy, (B) book thoracotomy, (C) posterolateral thoracotomy, (D) anterolateral thoracotomy, and (E) extension of an anterolateral thoracotomy across the sternum. (Reproduced with permission from Baylor College of Medicine.)

Approaches to the posterior mediastinum and, at times, the hilum of the lung following trauma are via either a right or left posterolateral thoracotomy through a carefully chosen interspace. This position and these incisions are best suited for injury to the descending thoracic aorta, esophagus, azygous vein, and the mediastinal trachea and bronchi. If, for whatever reason, the initial approach was via an anterior incision but a predominately posterior injury is found, the anterior incision should be closed, and the patient reopened via a position and incision that optimizes exposure and management of the injury (Figs. 24-2 and 24-3). In the past, one indication for thoracotomy following trauma was presence of a thoracoabdominal injury, and a thoracoabdominal incision across the costal margin was recommended. Neither this indication nor this incision is now considered standard and use creates more difficulty in exposure as well as complications than the more standard incisions.5,6 It is more appropriate to approach injuries in

multiple cavities as if an injury were isolated to only one cavity, and enter the cavity with the most apparent complex injury first.

THORACIC DAMAGE CONTROL Damage control tactics were among the most important advances in trauma management during the 1990s. Packing an area inside the chest does not have the same damage control utility as such tactics have in the abdomen. Damage control tactics for the patient with thoracic trauma will be cited in other chapters of this book and include: • • • • •

Emergency room thoracotomy and resuscitation9,12–15 Pulmonary tractotomy18 Pulmonary hilar twist19 Endovascular hemorrhage control (emerging)10 Temporary damage control thoracic closure

464

Management of Specific Injuries INCISION ALGORITHM

SECTION 3 X

EC Thoracotomy

Left Anterolateral Thoracotomy

Urgent

Extremis

Left Anterolateral Thoracotomy Consider Extension to right “clamshell” “Search and Rescue”

Posterior injury Likely lung/ intercostal vessel

Utility

Anterior Precordial Stab Wound

Consider Posterolateral Thoracotomy

Anterolateral Thoracotomy on side of injury

Median Sternotomy

FIGURE 24-2 Incision algorithm.

THORACIC TRAUMA CONTROVERSIES In evaluating and treating patients with thoracic trauma, it is important to recognize that some of the historic approaches are both controversial and lacking in scientific evidence, despite wide popular use.

■ Controversies in CT Scanning CT scanning has provided many areas of human pathology with a very focused specific image of altered anatomy and is widely used in trauma, particularly blunt trauma. As a screening modality, it joins the plain chest x-rays in assisting the clinician. For missile traverse of the mediastinum, the CT scan provides a trajectory tract to aid in determining the need for

other diagnostic tests. In vascular injury, the CT scan joins classic arteriography to demonstrate direct and indirect trauma. For some areas of vascular evaluation, the CT angiogram and the computerized reconstructions demonstrate both specific and nonspecific changes, but the CT scan and CTA have also caused confusion and often beg the need for additional more diagnostic tests, such as a classic arteriogram. As an example, most of the supportive literature on CT scanning for the thoracic aorta has been limited to the area of the proximal descending thoracic aorta. In addition, literature is emerging to raise concerns about the amount of radiation exposure for patients.20–22 Numerous different CT and CTA protocols exist, depending on the possible injury as well as the specific organ to be imaged. With the greater sophistication of CT and MR imaging, it becomes increasingly important for the clinician to

SPECIFIC INJURIES

Ascending aorta Innominate artery Right carotid/ Subclavian artery Left carotid artery

Left subclavian artery

Known descending thoracic aorta Intrathoracic left subclavian artery

Known intrathoracic trachea/esophagus injury

Clotted hemothorax VATS

Median sternotomy with neck/ supraclavicular extension

Third interspace anterolateral thoracotomy with supraclavicular incision

Left posterolateral thoracotomy

Posterolateral thoracotomy

Posterolateral thoracotomy

FIGURE 24-3 Specific injuries algorithm.

Trauma Thoracotomy: Principles and Techniques understand these differences. Because of motion artifact, CTA of the thoracic aorta is not well suited for the ascending aorta, unless the newer ECG-gated synchronization is available.

Virtually every resuscitation course teaches and recommends the technique of pericardiocentesis to relieve hemopericardium and cardiac tamponade following injury. Trauma surgeons routinely describe clotted blood between the pericardium and heart at emergency thoracotomy for hemopericardium. Pericardial fluid aspiration that is successful for nonclotting fluid has not been proven to be as successful during the acute time interval following injury. Additionally, surgeons often describe iatrogenic cardiac penetration following an attempted pericardiocentesis for acute trauma. Pericardiocentesis for acute hemopericardium has not been a beneficial procedure. For such cases, emergency thoracotomy, pericardiotomy, and cardiorrhaphy are indicated.

■ Subxyphoid Pericardiotomy A subxyphoid pericardiotomy, often performed in the emergency room or operating room to detect hemopericardium, was introduced as a technique prior to the wide adaptation of the Focused Abdominal Sonographic (examination) for Trauma (FAST), and CT scanning was widely accepted for the evaluation of patients who might have a hemopericardium. This rather small abdominal incision would allow for direct drainage of pericardiac blood but would allow for no focused cardiorrhaphy. With more precise diagnostic techniques for pericardial fluid, a directed thoracic incision could be used to expedite relief of pericardial tamponade and repair any cardiac injury. It is logical to apply a thoracic incision to a thoracic injury when an open procedure is indicated.

■ Needle Decompression of Pleural Cavity Historically, a tension pneumothorax following thoracic trauma was believed to account for significant numbers of deaths in both prehospital and emergency room phases of evaluation and treatment. Insertion of a “decompressing” needle into the pleural cavity has been recommended in many of the resuscitation courses, despite any controlled studies to demonstrate the exact frequency of tension pneumothorax or the specific benefit or utility of needle decompression. Furthermore, tension pneumothorax is undoubtedly more difficult to determine than has been presumed, particularly in a moving ambulance. In patients without a pneumothorax or with a pleural symphysis, insertion of a large-bore needle into the lung in an intubated patient can contribute to fatal systemic air embolism and also cause a pulmonary hematoma with subsequent pulmonary insufficiency.

■ Trocar Chest Tubes Up to 25% of the population has some degree of pleural symphysis between the visceral and parietal pleura secondary to some earlier infection or inflammation. Consequently, it is

■ Clamping of Chest Tubes Large-bore chest tubes enhance drainage of blood, fluids, air, purulent material, and the like from the pleural cavity. Chest tubes are widely used for both penetrating and blunt thoracic trauma with concomitant pneumothorax or hemothorax, or both. An appropriately placed chest tube often precludes the need for a formal thoracotomy and should prevent retained clotted hemothorax. The chest tube is connected to a pleural drainage system. Once the pathology that necessitated chest tube insertion has resolved, the tube is removed. With a clear understanding of pleural anatomy and physiology, complications at chest tube removal are rare. Some clinicians involved in the care of trauma patients recommend that chest tubes be clamped prior to removal to assure appropriate timing of removal. This recommendation falls more into the “urban legend” category than evidence-based good practice and is not recommended by these authors.

■ Pledgets in Cardiorrhaphy Cardiorrhaphy is routinely accomplished during cardiac surgery without the use of adjunctive pledgets in the suture line. Although often used during posttraumatic cardiorrhaphy, this practice is not supported by experience and introduces an unnecessary added step for the surgeon and operating room nurse.

■ Trap Door Thoracotomy This combined anterolateral, partial sternotomy, and supraclavicular (“trapdoor” or “book”) incision that was popular in the 1970s for injuries to the left thoracic outlet but offers little exposure advantage and is very morbid. In the current endovascular era, proximal vascular control can be obtained with an intravascular balloon, followed by either endovascular repair or open repair via a supraclavicular incision.

TIMING OF THORACOTOMY Timing of an acute thoracotomy is a function of the immediacy of the life-threatening condition.23 Following injury to the chest, potentially life-threatening conditions include acute pericardial tamponade, acute and massive blood loss, disruption of ventilatory function, and decreased cardiac output. These conditions are the basis for the traditional A-irway, B-reathing, C-irculation of resuscitation. Infection, sepsis, pulmonary insufficiency, and other functional impairments may occur secondarily, and any or all contribute to the decision to operate and when.

CHAPTER CHAPTER 24 X

■ Pericardiocentesis

recommended that following the skin and muscle incisions for a tube thoracostomy, the pleura be entered with the exploring finger rather than an instrument. If percutaneously inserted, the commercially available chest tube device with a Trocartipped metal rod in the middle of the chest tube has the potential for causing an iatrogenic injury (stab) to the lung or other thoracic or upper abdominal organs as it is forcefully pushed into the body.

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• Immediate and Emergent: Immediate thoracotomy is usually performed either in the emergency center or in an operating room immediately available to the emergency center. For an acute injury to the heart and immediate loss of cardiac output from reversible conditions of pericardial tamponade, cardiac herniation, cardiac rupture, or a posttraumatic cardiac arrhythmia, immediate thoracotomy is performed by a knowledgeable and qualified physician. Patients with posttraumatic prehospital external cardiac massage for more than 5-10 minutes are unlikely to be resuscitated in the hospital, even with an emergency center thoracotomy. However, when the team determines a need for an EC thoracotomy, such procedures can be individualized and tracked by the hospital’s quality review process. • Urgent: An urgent thoracotomy is performed minutes to hours after injury to control and manage a potentially lifethreatening condition or prevent the development of further deterioration, injury or infection. • Delayed: Delayed posttraumatic thoracotomy is performed for one of two conditions. In a patient with multisystem trauma, delayed repair of an injured but controlled aortic injury may occur to allow time for stabilization or treatment of a severe lung, pelvis, or head injury. Alternatively, thoracotomy for evacuation of a clotted hemothorax, management of a late presenting complication or previously missed injury may be delayed. In the chest, as elsewhere in the body, following significant trauma, staged procedures are part of current approach to management.

•

•

•

Tube thoracostomy is the most common procedure following thoracic injury. However, a clotted hemothorax is not always completely evacuated with a chest tube alone. When a clotted hemothorax persists, VATS or thoracotomy should be used to evacuate it as soon as possible, even within 2 days of discovery. Early evacuation reduces the incidence of posttraumatic empyema. Every hospital’s trauma program can profit from a protocol to address this common complication, and, as such, can be followed as a performance improvement indicator.

COMPLICATIONS OF THORACIC TRAUMA EVALUATION AND TREATMENT The heart, great vessels, pleural cavity, and lungs each have a limited number of ways to respond to under- and overtreatment and related complications. Many of these specific complications will be cited and discussed in the organ-specific injury chapters. For completeness, a few of these complications are briefly cited here. • Fluid Overload and ARDS: Recognized for decades but specifically codified during the Vietnam War, fluid overload and the resultant adult respiratory distress syndrome have been increasingly described and better understood during the past 20 years. The ability for various crystalloids to activate inflammatory mediators, as well as contribute to ARDS, is now well described, resulting in the current wave of crystalloid restriction during the

•

resuscitative phase of trauma. It is also well recognized that the contused lung is more prone to barotrauma, pneumonia, and fluid overload than is the uninjured lung. Barotrauma: Although “high” positive end-expiratory pressure (PEEP) was used for patients with posttraumatic respiratory insufficiency during the 1970s, it is now recognized that high inspiratory pressures and other ventilatory forces cause an undesirable constellation of volutrauma/barotrauma to both the bronchial lining and the interstitium. Systemic Air Embolism: Vascular air embolism can affect venous return to the heart and the right cardiac circulation, as well as cause pulmonary venous air embolism, which becomes systemic air embolism. Both are most often iatrogenic, with systemic air embolism being secondary to lung injury under conditions of increased endobronchial pressures greater than 40 TORR. With needle, bullet, knife, or Trocar injury to the lung in an intubated patient in an ambulance, EC, OR, or ICU, air may be forced at the area of the injury from bronchioles to the pulmonary venules. From there, air can go to the left atrium, producing systemic air embolism, seizures, and ventricular fibrillation because of air in the coronary and cerebral arteries. It is preventable, but when it does occur, it is almost always fatal. Aspiration: Although aspiration into the lung is not uncommon following trauma, many of the resuscitative efforts in the EMS, EC, Radiology, and the OR may contribute to aspiration and some of its more undesirable side effects. The insertion of a nasogastric or feeding tube into the pharynx of a fully awake patient with a stomach full of food is conducive to aspiration of vomited gastric contents. Aspiration of water-soluble contrast material, such as gastrograffin, into the lungs produces a chemical pneumonia much more severe than that produced by aspiration of a barium-based contrast material. The insertion of a feeding tube into the bronchus, lung substance, or even the pleural cavity, and then subsequent insertion of feeding material into the lung or pleura produces devastating results. Aspiration is best treated by bronchoscopy to remove solid particles. Radiation Exposure: Primary, emergency, trauma, and consulting physicians all have a growing appetite for ordering increasing numbers of complex imaging studies. Overutilization of CT scanning and vascular contrast material has resulted in significant doses of radiation, greater than during the acute evaluation of a trauma patient just two decades ago. Controversy persists on number of studies ordered, necessity, and duplication, as well as the maximum radiation dosages that patients can tolerate. Unfortunately, quality review of medical records rarely reveals a pre-imaging progress note indicating why the test was ordered, what the clinician wanted to learn from the study, or how results of image might alter decision-making. Such progress notes undoubtedly would be beneficial in defending excessive radiation, which might have resulted in a radiation associated problem, such as a lymphoma or leukemia.20–22

Trauma Thoracotomy: Principles and Techniques

REFERENCES

CHAPTER CHAPTER 24 X

1. Breasted JH. The Edwin Smith Surgical Papyrus. Vol. 1. Chicago: University of Chicago Press; 1930. 2. Sparkman RS, Nixon PL, Croswait RW, et al. In: Sparkman RS, ed. The Texas Surgical Society: The First Fifty Years. Dallas: Texas Surgical Society; 1965:3. 3. LoCicero J, Mattox KL. Epidemiology of chest trauma. Surg Clin North Am. 1989;69:15. 4. Bala M, Shussman N, Rivkind AI, Izhar U, Almogy G. The pattern of thoracic trauma after suicide terrorist bombing attacks. J Trauma. 2010;69(5):1022–1029. 5. Hirshberg A, Mattox KL, Wall MJ Jr. Double jeopardy: thoracoabdominal injuries requiring surgery in both chest and abdomen. J Trauma. 1995;39:225–229. 6. Hirshberg A, Wall MJ Jr, Mattox KL. Bullet trajectory predicts the need for “damage control”—an artificial neural network model. J Trauma. 2002;52:852–858. 7. Mattox KL, Hirshberg A. Access, control and repair techniques. Chapter 7. In: Rich N, Mattox KL, Hirshberg A, eds. Vascular Trauma. 2nd ed. Philadelphia, PA: Elsevier Saunders; 2004:137–164. 8. Wall MJ Jr, Mattox KL, Chen C, et al. Acute management of complex cardiac injuries. J Trauma. 1997;42:905. 9. Hunt PA, Greaves I, Owens WA. Emergency thoracotomy in thoracic trauma—a review. Injury. 2006;37(1):1–19. 10. Mattox KL. Management of injury to the aorta—strategies, pitfalls, & controversy. Chapter 42. In: Pearce WH, Matsumura JS, Yao JST, eds. Trends in Vascular Surgery. Evanston, IL: Greenwood Academic; 2005. 11. Wall MJ Jr, Mattox KL, DeBakey ME. Injuries of the azygous venous system. J Trauma. 2006;60:357.

12. Durham LA, Richardson R, Wall MJ Jr, et al. Emergency center thoracotomy: impact of prehospital resuscitation. J Trauma. 1992;32:775. 13. Hoth JJ, Scott MJ, Bullock TK, Stassen NA, Franklin GA, Richardson JD. Thoracotomy for blunt trauma: traditional indications may not apply. Am Surg. 2003;69(12):1108–1111. 14. Onat S, Ulku R, Avci A, Ates G, Ozcelik C. Urgent thoracotomy for penetrating chest trauma: analysis of 158 patients of a single center. Injury. 2010;41(7):876–880. 15. Seamon MJ, Goldberg AJ, Schwab CW. Emergency department thoracotomy for gunshot wounds of the heart and great vessels. J Trauma. 2010;68(6):1514–1515. 16. Coselli JS, Mattox KL, Beall AC Jr. Reevaluation of early evacuation of clotted hemothorax. Am J Surg. 1984;148:786. 17. Wall MJ Jr, Mattox KL, Wolf DA. The cardiac pendulum: blunt rupture of the pericardium with strangulation of the heart. J Trauma. 2005; 59:136. 18. Wall MJ Jr, Villavicencio RT, Miller CC, et al. Pulmonary tractotomy as an abbreviated thoracotomy technique. J Trauma. 1998;45:1015. 19. Wilson A, Wall MJ Jr, Maxson RT, et al. Pulmonary hilum twist as damage control procedure for severe lung injury. Am J Surg. 2003;86:49. 20. Brenner DJ, Hall EJ. Computed tomography--an increasing source of radiation exposure. N Engl J Med. 2007;357(22):2277–2284. 21. Smith-Bindman R. Is computer tomography safe? N Engl J Med. 2010;363:1. 22. Tsushima Y, Taketomi-Takahashi A, Takei H, Otake H, Endo K. Radiation exposure from CT examinations in Japan. BMC Med Imaging. 2010;10(1):24. 23. Karmy-Jones R, Jurkovich GJ, Nathens AB, et al. Timing of urgent thoracotomy for hemorrhage after trauma: a multicenter study. Arch Surg. 2001;136(5):513–518.

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CHAPTER 25

Lung, Trachea, and Esophagus Joseph A. DuBose, James V. O’Connor, and Thomas M. Scalea

INTRODUCTION Injuries to the chest are common after both blunt and penetrating trauma. Blunt thoracic injuries are responsible for approximately 8% of all trauma admissions in the United States, with motor vehicle crashes being the most common mechanism.1,2 In one recent report from the Los Angeles County Hospital, penetrating chest trauma accounted for 7% of all trauma admissions and 16% of all penetrating trauma admissions overall.3 A 1961 study described a 28% mortality with blunt chest injuries as compared to a 7% mortality following penetrating injury.4 Associated injures were common and were associated with a 42% mortality. These figures have not changed, as a more recent study described approximately a 25% fatality rate as a direct result of thoracic injury with chest trauma playing a contributing role in 50% of nonpenetrating injuries overall.5 Despite the prevalence of thoracic injury following trauma, the majority of patients can be managed nonoperatively. Between 18% and 40% of patients sustaining thoracic trauma can be treated with tube thoracostomy alone. A thoracotomy will be required for between 3% and 9% of patients. Even among those with penetrating trauma, only 14% of stab wounds and between 15% and 20% of gunshot wounds to the chest require thoracotomy.3 Operative mortality varies between 5% and 45%, with approximately 30% of patients requiring lung resection at the time of thoracotomy.4,5 This wide variability is almost certainly related to differences in mechanism of injury, inclusion of cardiac and major thoracic injury in some of the datasets, the extent of pulmonary resection needed, and concomitant extrathoracic injuries.4–13 The influence of thoracic trauma on mortality is particularly striking among patients who die within 1 hour of arriving to a trauma center. In those patients, thoracic trauma, especially thoracic vascular injury, is second only to central nervous system injury as the most common cause of death after hospital admission.

The determination of the optimal treatment for patients with thoracic injuries remains a challenge. Technological advances, particularly the evolution of sophisticated imaging, have allowed clinicians to make the diagnosis of major thoracic injury more quickly. Advances in critical care have made postoperative management more sophisticated. Improved approaches for nonoperative management may make the need for operative exploration even less frequent. Despite these advances, however, a modest number of patients still require thoracotomy. Thus, clinicians caring for injury must adequately appreciate the indications for operation and understand the treatment options in the emergency department as well as in the operating room. Thoughtful decision making based on a comprehensive appreciation of the anatomic relationships of the thoracic cavity and the physiologic principles that govern trauma is necessary to insure the highest survival and optimize functional recovery.

INJURY TO THE LUNGS The lungs sit in each hemithorax. While physiologically quite complicated, in fact, the lungs are anatomically simple, consisting of primarily alveoli and blood vessels. The lungs have a dual blood supply, with a relatively large pulmonary artery and vein delivering significant volumes of blood at low pressure. While the bronchial vascular bed is characterized by a more substantial systemic pressure, the vessels of this vascular tree are quite small. The intercostal vessels in the chest wall also have systemic pressure, but possess larger-diameter vessels than their bronchial counterparts. The bony thorax protects the lungs from injury. Thus, in adults, injury to the chest wall is a good marker for pulmonary injury following blunt trauma. The greater elasticity to the chest wall in children means that pulmonary injury can occur without evidence of injury to the chest wall. The anatomic simplicity of the lungs means that a response to injury is relatively limited regardless of the severity and

Lung, Trachea, and Esophagus

■ Presentation and Evaluation Any patient with blunt chest trauma or penetrating injury around the thoracic cavity is at risk for injury to the lung. The history may be provided by the patient, but often it is given by prehospital personnel. The mechanism of injury, time from injury, vital signs, and neurologic status at the scene and any changes during transport are critical components of an adequate history. With blunt injury specifics such as prolonged extrication, the location and degree of occupant compartment vehicle deformation may also provide useful information. With penetrating trauma, the specific details are usually vague and often unreliable. Physical exam can often help make the diagnosis of intrathoracic injury. The presence of distended neck veins, tracheal deviation, subcutaneous emphysema, chest wall instability, absent breath sounds, or muffled heart sounds may all provide crucial information. Likewise, the absence of an upper extremity pulse suggests a proximal arterial injury. Vital signs should be frequently monitored with careful observation of the work of breathing and arterial saturation. Findings of subcutaneous air or decreased breath sounds should alert the clinician to the possibility of pneumothorax and/or hemothorax. Prompt placement of a tube thoracostomy in an unstable patient is wise, particularly as radiographic confirmation takes too long. Penetrating thoracic trauma in a hemodynamically unstable patient warrants operative exploration. The decision regarding

surgical exposure may be problematic especially if there is concomitant abdominal injury. The hemodynamically stable patient with penetrating thoracic injury may benefit from additional imaging, especially chest computed tomography which provides more detailed and organ-specific information as well as information about vascular anatomy.14–17 Following blunt trauma, stable patients require timely determination of the studies required to identify and characterize potential thoracic injuries. An arterial blood gas should be sent with the initial laboratory studies, and an electrocardiogram performed as indicated. A Focused Abdominal Sonography for Trauma (FAST) including the precordium should be performed. A portable chest radiograph (CXR) is routinely obtained, although some authors question the utility of this study in stable patients with a normal chest examination.16 We believe a CXR can rapidly yield critical information such as the identification of pleural space abnormalities including pneumothorax and hemothorax. If indicated, additional imaging studies such as thoracic ultrasound, a CT scan, esophagoscopy, bronchoscopy, and echocardiography should be obtained. A CXR should make the diagnosis of any large hemothorax or pneumothorax. Since screening CXRs are usually performed supine, a hemothorax can be somewhat difficult to adequately diagnose. Haziness of one hemithorax when compared to the other may be the only real radiographic sign of blood in the pleural space. If this is of any substance, a chest tube should be placed. In addition, pure anterior or posterior pneumothoraces, even if they are large, may not be well seen on a CXR (Fig. 25-1). The CXR should be examined for a deep sulcus sign, displacement of the diaphragm inferiorly, which may be the only radiographic sign of a pneumothorax. A CXR will also allow the clinician to evaluate the mediastinum for the possibility of a traumatic aortic injury. In the days of liberal CT scanning, particularly in patients with blunt trauma, many more patients are undergoing either CT scan of the chest or a total-body CT screening. This allows for more precise evaluation of the aorta and also gives a threedimensional evaluation of the thorax.14,16,17 Pneumothoraces or

FIGURE 25-1 Sizeable anterior pneumothorax not visible on initial trauma chest x-ray. A substantial amount of air can be present either anterior or posterior to the lung and not be appreciated by initial plain film.

CHAPTER CHAPTER 25 X

mechanism. The alveoli can rupture, causing a pneumothorax, or the lungs and parenchyma can bleed causing a hemothorax. The chest wall also bleeds when injured. Any of these can range from relatively trivial to life-threatening. Very large pneumothoraces produce tension by shifting the mediastinal structures toward the contralateral side. In these situations, the anatomic distortion combined with the increase in intrathoracic pressure decreases cardiac output. If untreated, this can cause cardiac arrest. In contrast, large hemothoraces generally produce symptoms through the effects of hypovolemia. Very large hemothoraces, however, can also cause some degree of mediastinal anatomic distortion. Injury to the lung can also cause intraparenchymal damage, usually pulmonary contusions or lacerations. These often cause symptoms such as shortness of breath or hypoxia. Following blunt trauma, these are often associated with rib fractures. Penetrating injury causes direct parenchymal damage. Radiographic findings often lag behind the clinical presentation. The increased use of CT scanning following most penetrating trauma allows the clinician to make the diagnosis earlier. As with many other entities, CT scanning may be overly sensitive and identify pulmonary pathology that is clinically unimportant. Systemic air embolization, while rare, can also occur following direct pulmonary injury. This most often happens when patients are placed on positive pressure ventilation. If there is an injured bronchus adjacent to an injured blood vessel, air can be forced into the systemic circulation. This should be suspected when patients have sudden decompensation immediately after intubation.

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hemothoraces not seen on chest x-ray are often seen on CT. If they are small and patients are asymptomatic, prudent practice is to simply observe these patients. Even if they require operations for an associated injury or intubation for positive pressure ventilation, the chances that these very small pneumothoraces will become clinically significant is relatively small. A follow-up CXR may be useful, particularly in patients with small pneumothoraces. In general, patients found to have large pneumothoraces not seen on CXR are treated with tube thoracotomy, particularly in patients who are multiply injured. While it is possible that these can be treated without drainage, our belief has been that these patients may well become symptomatic and we prefer to treat these patients preemptively. In general, hemothoraces are treated similarly to pneumothoraces. If they are small, observation is generally successful. However, any moderate-sized or large hemothorax should be drained with a tube thoracostomy. Blood left within the pleural cavity will clot and will not be able to be evacuated with a chest tube. The lung will become trapped and this will produce a fibrothorax. Small hemothoraces should be followed with serial exams and a repeat CXR as they occasionally slowly expand. Early recognition and triage is the best idea in these cases. When placed, tube thoracotomies are generally connected to a pleurevac and the pleurevac is connected to suction. Repeat chest x-rays should be obtained to demonstrate good tube placement and to evaluate the possibility of either retained blood or air. Patients with significant lacerations to the lung will often have large air leaks or hemoptysis. Bronchoscopy can be helpful in such patients to evaluate the possibility of major airway injury, as well as to attempt to localize the injured lobe or segment; this can be especially important if there is significant injury to both hemithoraces. In these cases, bronchoscopy should be performed by a senior clinician. Blood within the airway must be suctioned clear to allow for good visualization of all of the lobar airway structures. Patients with large volumes of hemoptysis or significant air leaks who do not have major airway injury should be considered for thoracotomy and lung repair or lung resection. If the patient is stable, CT scanning can also be quite helpful in patients with hemoptysis (Fig. 25-2). CT scanning should be able to demonstrate the anatomy of the lung injury and help localize the lobe or lobes most likely to be producing the air leak or hemoptysis. CT may also be able to demonstrate intraparenchymal vascular injuries. The pulmonary vascular tree is a low-pressure system and radiographic vascular injuries do not carry the same prognosis as do arterial vascular injuries identified within solid viscera in the abdomen. If symptomatic, operative exploration is generally the best idea. In a very selective group of patients who are a poor operative risk, transcatheter embolization offers an alternative to thoracotomy. The majority of patients with injury to the lung can be managed nonoperatively. Simple tube thoracostomy evacuates accumulated air and blood, and the lung should be reexpanded up against the chest wall. Peripheral lung injuries generally seal once the lung is reexpanded. As pressures in pulmonary circulation are relatively low, coapting the lung up against the chest wall generally stops bleeding as well.

FIGURE 25-2 CXR and corresponding CT demonstrating right-sided pulmonary contusion. This patient had some minimal associate hemoptysis on presentation, which resolved.

A number of patients, however, will require thoracotomy for pulmonary and/or chest wall injury. Intercostal hemorrhage, particularly after penetrating trauma, usually continues even after evacuation of the associated hemothorax and/or pneumothorax. This may also be true for major chest wall injuries after blunt trauma where a number of intercostal vessels may be injured. Bleeding can be impressive from injured chest wall musculature as well. Major lung lacerations can produce symptoms by either a continued air leak or hemorrhage.

■ Indications for Operation While indications for thoracotomy will be covered in a different chapter, some brief comments here may be helpful. Massive hemothorax, generally defined as 1,500 cm3 of blood in the chest cavity or persistent chest tube output of 200– 250 cm3/h for 3 consecutive hours, is generally considered an indication for thoracotomy. In addition, a 24-hour chest tube output 1,500 cm3 is generally considered an indication for thoracic exploration. Hemodynamic instability that is thought

Lung, Trachea, and Esophagus

■ Surgical Exposure There are a number of ways to approach thoracic injury, each with advantages and disadvantages. It is imperative that the trauma surgeon be familiar with all of them. The clinical situation generally dictates which incision will be the best. Many patients have thoracotomy for a diagnosed condition such as a nonsealing air leak or a diagnosed tracheal or esophageal injury. In those cases, the incisions can be tailored to provide optimal exposure of the anatomic injury. However, many patients have true explorations for undiagnosed injuries such as in patients with a massive hemothorax or a large lung laceration that has not been localized. In those cases, the thoracic incision must be versatile and allow extension to provide greater exposure if that is necessary. Hemodynamically unstable patients may not tolerate being put up in the lateral position, as it will exacerbate hypotension. In addition, patients with significant hemoptysis often do not tolerate being up in the lateral position. This puts them at risk for aspirating blood into the uninjured lung, which is now in the dependent position. In addition, there is sometimes the possibility of injury to an adjacent body cavity such as the abdomen and neck that requires operative care. This is especially true with penetrating thoracic trauma. The incision should be able to be modified in order to provide adequate exposure. Commonly employed approaches are anterolateral, posterolateral, bilateral anterior thoracotomies (“clamshell”), and median sternotomy. The anterolateral approach is rapid and extending it across the midline affords excellent exposure to both pleural spaces and the anterior mediastinum. Likewise, the incision can be continued as a celiotomy for abdominal exploration, and is preferred over the posterolateral approach in the patient in shock. The main disadvantage of the anterolateral approach is the inability to provide optimal exposure of

CHAPTER CHAPTER 25 X

to be referable to thoracic injury should virtually always prompt emergent thoracic exploration. As there is a linear relationship between total amount of thoracic hemorrhage and mortality, the surgeon should not delay thoracotomy when indicated. Care must be exercised when measuring chest tube output. Chest tubes routinely become clotted and if poorly positioned, may not completely evacuate blood or air. Blood will then continue to accumulate within the thoracic cavity. A repeat CXR can be helpful in detecting a retained hemothorax. While a second chest tube may be helpful, patients with a large retained hemothorax should generally be explored and drained. A number of patients may not need emergent thoracotomy, but may require thoracic operation at a later date. Examples of this include retained hemothorax, persistent air leak, missed injury, and pleural space infections. Many of these nonemergent procedures can be performed using a thorascopic technique.18,19 In general, air leak 7 days should be treated with an operation. Early evacuation of retained hemothorax prevents the clot from becoming fibrotic and trapping the lungs. Proven empyema is almost always best treated with operation.

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FIGURE 25-3 Anterolateral thoracotomy incision. Placing a bump to elevate the chest and extending the arm provides improved thoracic exposure.

posterior thoracic structures. By extending the ipsilateral arm and placing a bump to elevate the thorax approximately 20°, the incision can be carried to the axilla improving posterior exposure (Fig. 25-3). The posterolateral thoracotomy affords optimal exposure of the hemithorax, especially the posterior structures, and is the standard incision for most elective thorax operations. Its lack of versatility limits the usefulness in trauma but is the preferred approach to repair intrathoracic tracheal and esophageal injuries. Median sternotomy provides excellent access to the heart, great vessels, and anterior mediastinum. It is versatile and can be extended as an abdominal, periclavicular, or neck incision (Fig. 25-4). Opening the pleura after sternotomy provides good access to either hemithorax. Depending on the surgeon’s experience, a lung resection can be performed. The “trapdoor” incision is rarely used since left-sided thoracic vessels can be approached via sternotomy with extension.20

■ Operative Techniques Regardless of the incision choice, patients who undergo emergency thoracic operations should first have a complete exploration. Once entering the chest, blood should be evacuated to allow the surgeons good visualization of the entire contents of the thoracic cavity. The lung should be mobilized by taking down the inferior pulmonary ligament. In patients with serious injury to the lung, temporary inflow occlusion can be obtained by compressing the hilum. There are a number of techniques for hilar compression. Simple finger occlusion will temporarily occlude both the pulmonary artery and vein. A vascular clamp can be placed across the hilum if a longer period of occlusion is necessary. In addition, the lung can simply be twisted on itself at the level of the hilum. This occludes both the pulmonary artery and vein as well as the main stem bronchus. Patients with very tenuous hemodynamics may decompensate when the hilum is

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Management of Specific Injuries

SECTION 3 X FIGURE 25-4 Tracheal intubation on the operative field. Partial sternotomy was chosen to obtain control of the great vessels.

occluded. This is associated with a rapid rise in pulmonary artery pressure, which can cause acute right heart dysfunction or failure. While a double-lumen endotracheal tube is often used in elective thoracic operations, it is virtually never used in trauma, especially for emergency thoracotomies. Use of a single-lumen

endotracheal tube can make visualizing the organs within the thorax more difficult and perpetuates any air leak that may be coming from the injured lung. Holding ventilation while localizing an air leak and/or repairing or resecting the lung can be a useful technique. However, if the patient’s respiratory status is tenuous, any extended interruption of ventilation will precipitate decompensation. Manual compression of the adjacent lung may sufficiently consolidate the tissue to facilitate surgery on the lung. There are a number of techniques for lung repair. Pneumonorrhaphy is the simplest technique and is generally used to treat superficial pulmonary lacerations. The laceration is simply closed with a running simple suture or mattress sutures. Between 20% and 30% of patients requiring emergency thoracic exploration will need a pulmonary resection. This can range from simple wedge resection to major anatomic resections. The widespread adoption of a variety of surgical staplers has increased the options for lung surgery following trauma. Peripheral lacerations not amenable to simple repair can be treated with a small wedge resection using any of the commercially available staplers. The lung parenchyma is generally retracted up to view using a lung clamp and the stapler is fired to excise the injured lung tissue. More significant lung injuries, particularly those from gunshot wounds, are often best treated with tractotomy21–24 (Fig. 25-5). This is performed by placing the jaws of the stapler through the tract of the injury and firing it. This opens the lung and exposes the bleeding vessels and injured airways. These can then be individually ligated. Tissue thickness will determine whether tractotomy is appropriate and the appropriate-sized staples to use. At times, the staple line may need to be oversewn with a running suture. In general, relatively peripheral tracts are best treated with tractotomy, if more simple maneuvers are not appropriate. Long central missile tracts are usually not amenable to tracheotomy. Serious lobar injuries that are not amenable to tractotomy are often best treated with formal lobectomy. The lungs should

FIGURE 25-5 Pulmonary tractotomy with ligation of exposed hemorrhage sources. (Reproduced with permission from Petrone P, Asensio JA. Surgical management of penetrating pulmonary injuries. Scand J Trauma Resusc Emerg Med. 2009 23;17(1):8.)

Lung, Trachea, and Esophagus which is admirable, as nearly 70% of patients are acidotic, hypothermic, or coagulopathic.29,30

■ Video-Assisted Thoracoscopic Surgery Increasing experience with thoracoscopy has contributed to enthusiasm for the use of video-assisted thoracoscopic surgery (VATS) techniques for a variety of sequela of trauma.18,19 As a diagnostic tool, VATS remains an acceptable alternative to laparoscopy in the identification of isolated diaphragmatic injuries particularly after penetrating trauma. It can also potentially be utilized to diagnose other minor injuries of the thoracic cavity not well visualized with traditional imaging, although these indications have not been well elucidated. Therapeutically, there are several promising potential applications for VATS. While significant thoracic hemorrhage, pulmonary trauma, and other more severe injuries of the thoracic cavity and mediastinum remain matters best addressed with traditional open techniques, described indications for VATS include: surgical resection of persistent pleural air leak sources in the peripheral lung, ligation of isolated intercostal artery injury, rib fracture reduction, and evacuation of empyema or persistent retained hemothoraces. The latter two indications remain among the most commonly described, with early operation proving to have the greatest success among published case series. Early VATS for retained hemothorax has proven to be the most successful utilization of the modality. There is, however, a relative paucity of literature on the topic, with the definition of “early” varying between described experiences. However, beyond 72 hours the degree of fibrotic change occurring within the thoracic cavity may preclude the safe conduct of VATS for the evacuation of blood or infectious collections. When treating retained hemothorax and/or empyema, the procedure consists of evacuation of fluid collections and clot followed by decortication of the parietal pleura as necessary. Air leaks are repaired or treated with small wedge resections. VATS is performed in the operating room under general anesthesia. Double-lumen endotracheal intubation or other lung isolation techniques should be utilized to collapse the lung in the operative hemithorax to permit better utilization of the chest and its contents. The procedure is ideally done with the patient in the full lateral decubitus position with the affected side up. The field should be appropriately draped to facilitate conversion to an open posteriolateral thoracotomy if VATS is not sufficient. The first port is placed along the fourth or fifth intercostal space in the midaxillary or anterior axillary line. The tip of the scapula serves as a nice landmark to facilitate appropriate positioning (Fig. 25-6). The lung is desufflated by anesthesia as the chest is entered and port placement completed. An angled thoracoscope is preferred for initial use, as it improves visualization of the pleural space recesses. An aspiration catheter can be placed coaxially to the optical port to facilitate the lavage and evacuation required for initial visualization. Additional ports can then be developed under direct visualization to address the pathology encountered. The instruments used for VATS are the same as used for laparoscopic procedures. Conventional open surgery forceps

CHAPTER CHAPTER 25 X

be fully mobilized and the extent of injury absolutely determined before making a decision to do a lobectomy. The hilar blood vessels must be dissected free and the blood supply to the injured lobe identified. These can then be stapled or ligated, generally using heavy nonabsorbable ties. The bronchus is generally divided using a stapler and the injured lobe then removed. Hilar injuries are a special problem and pose significant challenges. There are usually injuries to the major blood vessels as well as the proximal airways. Hemorrhagic shock is almost always present. In very proximal hilar injuries, inflow occlusion is virtually always necessary in order to gauge the extent of injury. Opening the pericardium and controlling the pulmonary artery and vein within the pericardium can be quite helpful in some patients. Often, after good exposure, and delineation of injuries, many hilar injuries can be treated with either lobectomy or bilobectomy. However, certain injuries require pneumonectomy. Mortality after pneumonectomy for patients in shock approaches 100%.25 Patients die of either uncontrolled hemorrhage or acute right heart failure. It is imperative to make the decision to proceed with pneumonectomy as early as possible. If a number of attempts are made at lung salvage, and the patient is in profound shock, survival after pneumonectomy is rare. The postoperative care after pneumonectomy is as important as early decision making. Virtually all short-term survivors develop right heart dysfunction and/or acute respiratory failure. Liberal use of transesophageal echocardiography can be very helpful in estimating volume status as well as function of both ventricles. Selective pulmonary artery vasodilation such as nitric oxide26 and sildenafil also improves cardiac function. Virtually all short-term survivors require inotropic support. Finally, use of sophisticated modes of ventilation support such as prone positioning and extracorporeal membrane oxygenation (ECMO) is often needed in the postoperative period. As bronchial stump leak is a devastating complication following either lobectomy or pneumonectomy, we prefer to cover the bronchial stump with some live tissue. Rotating an intercostal muscle preserving the blood supply to cover the bronchial stump is attractive. Other options include mobilizing a tongue of pericardium. If a bronchial stump leak occurs later in the postoperative period, covering the stump leak with a local muscle flap such as latissimus dorsi or the omentum is another option. The concept of damage control was originally described for abdominal trauma but is applicable in the chest as well. As in any damage control operation, control of hemorrhage is the primary concern. Thoracic packing to control nonmechanical bleeding can be quite helpful.27–30 It is important to be sure that the packs do not interfere with cardiac or pulmonary function. The chest is then temporarily closed and the patient is brought to the intensive care unit. We generally employ a suction dressing similar to what we use in the abdomen when doing thoracic damage control. When the patient is physiologically improved, the chest can be reexplored and closed. Very rarely, the chest cannot be closed at the time of the first operation and the chest retractor is left in place until the patient is more stable. Thoracic damage control has a 17% mortality,

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complications occurring in over half of the survivors.31 The need for laparotomy has also been shown to increase mortality among those with penetrating trauma requiring thoracotomy.4,11 Several studies have demonstrated an increase in mortality with the magnitude of the pulmonary resection. Comparing nonanatomic with anatomic resection, the mortality was 4% and 77%, respectively.10 This difference may not solely reflect the extent of resection since the severity of the lung trauma, the presence of a centrally located or hilar injury, more often requires an anatomic resection. The correlation of increased mortality with the extent of lung resection has been well documented.4,9 Again this finding may reflect the degree of the parenchymal injury that necessities a more extensive resection. Systolic blood pressure on arrival to the operating room is also associated with increased mortality.4,9

■ Complications of Injury to the Lung Pneumonia

FIGURE 25-6 Port placement for video-assisted thoracoscopic surgery (VATS) of the left hemithorax. The scapula and edge of the latissimus dorsi anteriorly are marked for reference.

can also be used. Cautery, however, should be utilized cautiously and in close coordination with anesthesia, as oxygenrich air leaks and cautery may interact to create a fire hazard within the patient’s thorax. On completion the chest is irrigated with normal saline or sterile water. Thoracostomy tubes can then be placed and positioned under direct visualization, utilizing the developed port sites, and the lung reexpanded prior to wound closure. Following the procedure a chest x-ray should be obtained and the thoracostomy tubes can be managed using the same principles utilized following open thoracic surgery.

Pneumonia is the most common complication of lung injury. The relative risk of developing pneumonia is closely linked to the need for subsequent mechanical ventilation. Patients requiring intubation are approximately seven times more likely to contract pneumonia than those who do not require mechanical ventilation after thoracic injury.1 Of all patients admitted with the diagnosis of pulmonary contusion (Fig. 25-5), nearly 50% will develop pneumonia, barotraumas, and/or major atelectasis, and one fourth will go on to develop acute respiratory distress syndrome (ARDS).1 For all patients with concomitant rib fractures, pain control remains of paramount importance to maintain good pulmonary mechanics unimpeded by splinting from pain. The resulting atelectasis and poor clearance of secretions creates a situation that increases the risk for subsequent pneumonia. For these patients, placement of a thoracic epidural should be strongly considered. A prospective, randomized trial by Bulger et al. found that epidural use for patients with pain due to multiple rib fractures resulted in significantly fewer ventilator days and decreased incidence of pneumonia.32 Intrapleural or extrapleural analgesic delivery systems also represent a promising potential pathway for pain control, but have been comparatively less well studied. For cases involving chest wall instability, it has also been suggested that operative chest wall stabilization may decrease ventilatory requirements and pain.

■ Outcomes

Retained Hemothorax

There is wide variably in reported mortality after thoracic injury. Blunt trauma results in mortality as high as 68%.1,2 This is probably related to higher ISS, lower GSC, and more associated nonthoracic injuries than those with penetrating injuries.4,6 There is also variation in the reported mortality with penetrating trauma. Cardiac and major vascular injuries and the percentage of major pulmonary resections all contribute to poorer outcomes.4,8 In a high-risk group of patients with penetrating injury requiring urgent lobectomy or pneumonectomy, the mortality was 38% and 66%, respectively, with pulmonary

It has been estimated that tube thoracostomy fails to evacuate hemothorax completely in over 5% of cases.33 While the natural history of these collections of undrained blood in a violated space remains unknown, known sequela of retained hemothorax include fibrothorax and lung entrapment. The most common and worrisome complication of retained hemothorax, however, is empyema. A retained hemothorax is a known independent risk factor for the development of an empyema.34 The diagnosis of retained hemothorax requires computed tomography of the chest, as plain radiography has been shown

Lung, Trachea, and Esophagus

Empyema Empyema is diagnosed via documentation of an exudative effusion or from positive culture of intrapleural fluid. In approximately 25–30% of cases, cultures will be negative due to suppression, but not eradication, of bacterial growth by antibiotics.38 The optimal treatment of empyema has not been definitively studied, but trauma patients are at higher risk of gram-positive multiloculated empyema less amenable to simple drainage due to the presence of hemothorax. Additionally, the robust inflammatory response associated with infections of this type in trauma patients commonly means that patients require decortication and evacuation to ensure full lung reexpansion. Empyema has been described as occurring in three “stages.” The first, typically within 1–7 days, is referred to as the “acute” or “serous” phase. During this phase, the likelihood of the process being treated successfully by tube thoracostomy is increased compared to more mature stages of infection. Vigorous inflammation in this early phase of infection, however, is sometimes associated with failure of simple drainage. Beyond the first 7 days, loculations and progressive pleural obliteration occur as the hallmarks of the second “subacute” and third “chronic” phases of empyema. In these latter stages of infection, effective drainage with a tube thoracostomy drainage alone is highly unlikely to effectively treat the process and thoracotomy with operative drainage and decortication is the mainstay of therapy.1,39

Persistent Air Leak and Bronchopleural Fistula Individuals sustaining thoracic trauma may develop air leaks from both the proximal airways and the lung parenchyma due to a variety of reasons. A true bronchopleural fistula is a centrally located communication between the pleural cavity and the lobar or segmental bronchi. These types of communications are uncommon following trauma, unless the patient has required a pulmonary resection during his or her care and has developed a leak from a closure of a proximal airway conduit. Most post-traumatic leaks are actually communications with the distal airway conduits and can be more accurately termed parenchymal–pleural or alveolar–pleural fistula.

Persistent air leaks of this type can be challenging entities to manage, as large leaks occurring in a patient requiring mechanical ventilation can contribute to loss of effective tidal volume, resulting in increased ventilation–perfusion mismatch and respiratory acidosis. The diagnosis in these patients is usually not a subtle event, with persistent air bubbling through the water-seal chamber of the thoracostomy tube collection system. For the most common peripheral leaks, care is primarily supportive. Methods that can be utilized to promote resolution of these leaks include minimizing transpulmonary pressures, especially end-inspiratory plateau pressure as tolerated if the patient is mechanically ventilated, as well as using the minimum chest tube suction necessary to keep the lung inflated. These measures will minimize the flow of gas across the fistula and promote healing. A few patients will still have a persistent air leak. We generally wait 5–7 days before considering operative exploration. In addition, we routinely obtain a CT before proceeding with operation. Some patients have residual pneumothorax that helps perpetuate the air leak. Inserting a pigtail catheter can be helpful to coapt the lung up against the chest wall to help seal the leak.

Pneumatocele/Intraparenchymal Hematoma Pneumatocele and hematoma of the parenchyma are sequela of lung lacerations. Not surprisingly, these are often more visible on computed tomography imaging than traditional plain radiographic exams. These lesions usually resolve over several weeks, although this period may prove variable depending on size and location. Uncommonly, pneumatoceles may become infected and should then be treated in a similar fashion as a lung abscess.

Lung Abscess Lung abscesses after trauma can occur as a result of aspiration, complications of severe or necrotizing pneumonia, retained foreign body, or infected traumatic injury. Initial therapy for these lesions consists of antibiotics, postural drainage, and bronchoscopy. Percutaneous drainage may be required in select cases, but can be associated with subsequent air leak and potential ventilation difficulties. This approach also liberates the infection into the pleural space, frequently necessitating the need for subsequent thoracotomy to relieve the resulting lung entrapment and to adequately clear infection. Ruptured abscesses, likewise, commonly require operative treatment via thoracotomy with resection of the abscess cavity if this can be accomplished safely. At the time of operation, the lung tissue surrounding abscess cavity is frequently exceptionally friable, necessitating great care with resection. In critically ill or tenuous patients, drainage with thoracostomy or percutaneous techniques alone may prove the most prudent and effective course of action, even if thoracotomy is needed later.40

Chylothorax Primary traumatic chylothorax is an uncommon occurrence after traumatic injury. This condition can manifest in a delayed fashion with recurrent effusions of persistent, milky, chest tube

CHAPTER CHAPTER 25 X

to be insufficient for this purpose.35 Once identified, the optimal evacuation method for retained blood within the chest after initial chest tube placement remains a matter that has not been well investigated. Observation, placement of an additional thoracostomy tube, the use of intrapleural thrombolytics, and VATS have all been proposed. VATS, particularly when utilized early in the course of retained hemothorax, has a high success rate and affords minimal risk to the patient.36 The initial choice of evacuation technique may prove important, as it has been shown that 17% of patients with retained hemothorax require subsequent thoracotomy after failure of less-invasive treatments.37 At present, a prospective, observational, multicenter trial on the management of retained hemothorax is being conducted by the American Association for the Surgery of Trauma. This study may provide considerable insight into the appropriate management of this sequela of thoracic trauma.

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output associated with oral diet. The diagnosis can be established by analyzing the content of the effusion and documenting the presence of fat (triglyceride levels greater than 110 mg/dL) with or without predominant lymphocytes in the effusion. The primary complication of chylothorax is nutritional deprivation and compromise of immune function.41 Treatment includes promotion of full lung expansion to promote tamponade and use of parenteral nutrition. The length of parenteral nutrition use that should be employed is not well established. Octreotide can also be utilized as an adjunct. If conservative treatment with pleural drainage, parenteral nutrition, and octreotide fails to promote resolution over several weeks, or if the patient continues to deteriorate nutritionally, interventional or operative occlusion should be undertaken.

TRACHEOBRONCHIAL INJURIES Tracheobronchial injuries are infrequent, but potentially lifethreatening consequences of trauma. These injuries are far more common in the neck, where the trachea does not have the protection of the bony thorax. Both mechanism and location are important factors to consider in managing these patients. The most common cause of blunt injuries is high-speed motor vehicle crashes.42 Penetrating injury, also more common in the neck, can occur after either stab or gunshot wounds. Iatrogenic injuries occurring during emergent airway procedures, while rare, represent another potential source of injury in the trauma population.43 The cervical trachea is more commonly injured from penetrating trauma and the distal trachea from blunt trauma.44–46 Most penetrating injury of the cervical trachea, while straightforward to repair, may be associated with injury to vessels, esophagus, thoracic duct, and nerves.47 Because of the large amount of energy needed to cause blunt tracheal injury, concomitant injuries in both the neck and other body regions are frequent.44 Laryngeal trauma is a specific subset that needs to be considered separately. The superficial location of the larynx increases its risk of injury from anterior blunt force trauma. The proximity of the laryngeal nerves places them in jeopardy as well. Minor injuries that will heal without complication can be managed nonoperatively. More severe laryngeal injuries will require surgical repair and a variety of techniques can be utilized including simple suture repair, external plate fixation, and internal stabilization with a T-tube.47–52 The operative management of the tracheobronchial tree, particularly within the thorax, requires expertise in a number of surgical approaches and various operative techniques that may be required for appropriate repair. Likewise, the perioperative management of these patients demands vigilance against the onset of pulmonary complications.

■ Presentation and Evaluation Cervical tracheal injuries are often obvious on physical exam. In the case of penetrating injury, there may be large volume of subcutaneous air and/or air exiting within the missile tract. This often fluctuates with the patient’s respiratory status. In the

FIGURE 25-7 Tracheal injury visualized with preoperative bronchoscopy.

case of blunt trauma, there is often massive subcutaneous emphysema in the neck. Patients often present with respiratory distress and require urgent airway stabilization. Patients with major airway injury within the thorax may not have such obvious signs on physical exam. The classic patient with an injury to the distal trachea or proximal major bronchial structure will present with a very large pneumothorax. When a chest tube is inserted, it usually has a very large air leak and the lung may not completely reexpand. In the case of penetrating injury, these findings may not be as dramatic. Hemoptysis may be present but is not a reliable finding. Patients with suspected tracheal or major airway injury should undergo emergent bronchoscopy (Fig. 25-7). Flexible fiber-optic bronchoscopy is the technique most often used. Common indications for bronchoscopy include a bullet trajectory in proximity to the airway or clinical signs raising the suspicion of an airway injury such as hemoptysis, hoarseness, subcutaneous emphysema, and/or suspicious findings on a CT scan. Flexible bronchoscopy has the advantages of being able to be performed in the emergency department. In the case of penetrating trauma, gunshot wounds are more likely to be associated with an abnormal bronchoscopy when compared to knife wounds. In these patients, the bronchoscopy must be performed carefully to avoid missing any injury. While some patients have obvious injury at the time of bronchoscopy, more often the findings are far more subtle. The entire circumference of the trachea must be examined. Mucous and blood must be suctioned clear to be sure the endoscopist is able to get a clear look of the entire distal tracheal surface. Each main stem bronchus must be suctioned clear and examined. If the cervical trachea is at risk and the patient is intubated, the endotracheal tube may well have been inserted distal to

Lung, Trachea, and Esophagus

■ Operative Techniques The management of a tracheobronchial injury must begin with two critical procedures. First, a secure airway must be established. An emergency airway is required in 29% and 43% of patients presenting with airway injury. Compared to a distal tracheal injury, an emergent airway is more frequently required for laryngotracheal trauma.44–46 Endotracheal intubation, establishing a surgical airway, and directly intubating the tracheal laceration are all acceptable techniques.45,46 The risk of converting a partial tracheal laceration into a complete disruption during intubation can be minimized by intubating over a flexible bronchoscope. Second, the location and extent of the airway injury must be completely characterized. The patient must be evaluated for esophageal, vascular, and concomitant cavitary injuries. The second issue is that of intraoperative management. Cooperation between the anesthesiologist and the surgeon cannot be overemphasized. A well-defined plan for intraoperative airway management and contingencies must be discussed between the surgeon and the anesthesiologist prior to the start of the operation. Most cases can be managed with a singlelumen endotracheal tube and a reinforced tube should be considered. If necessary, the airway can be intubated over the operative field (Fig. 25-4). Any potential advantage of a doublelumen tube is negated by possible complications in placing it, not the least of which is further airway trauma. The surgical repair is facilitated by keeping the mean airway pressure as low as possible while consistent with adequate oxygenation and ventilation. In selected instances high-frequency ventilation may provide a quieter operative field and improved surgical exposure.49,50 Cardiopulmonary bypass and/or ECMO are rarely needed but in selected cases can be lifesaving. Examples are patients with severe pulmonary contusions and/or ARDS requiring high driving pressure ventilation, intrathoracic tracheal injuries with concomitant great vessel injury or cardiac injury, and complex carinal disruption.53 Although operative repair is the mainstay of treatment for tracheobronchial injuries, in highly selected patients there is limited role for both stent placement and nonoperative management.53 Conservative management is reserved for small

(2 cm), nontransmural tears, especially in those who are severely injured.54,55 There are limited data on the use of stents in the treatment of traumatic airway injuries; therefore, this modality must be individualized and considered on a caseby-case basis.53,56–58 Since most tracheobronchial injuries are amenable to primary repair, there must be compelling reasons to choose an alternative option. Appropriate tracheal exposure is determined by the anatomic location of the airway injury. It is essential to precisely locate the injury and its extent by bronchoscopy. Arterial blood supply to the trachea is segmental in nature and arises from the inferior thyroid and bronchial vessels. The proximal half of the trachea can be exposed through a collar incision. Occasionally it is necessary to divide the manubrium to the level of the angle of Louis, which provides improved exposure of the mid-trachea and allows control of the great vessels. A full sternotomy offers no additional advantage unless there is a concomitant cardiac injury. The distal half of the trachea, the right main stem, and proximal left main stem bronchus are best approached through a right posterolateral thoracotomy. Widely opening the mediastinal pleura, and doubly ligating and dividing the azygous vein will provide superior tracheal exposure (Fig. 25-8). If an esophageal injury has been excluded, placing an esophageal bougie will facilitate the dissection between the esophagus and trachea. The distal left main stem bronchus is best approached through a left posterolateral thoracotomy (Fig. 25-9). Mobilization of the aortic arch will improve exposure especially if the injury extends more proximally on the main stem bronchus. The technical details of the tracheal repair, while straightforward, require attention to detail. Lacerations are repaired with interrupted absorbable sutures. If the injury is more severe but not a near or total transaction, debridement to healthy tissue is necessary. Following debridement the repair is performed as for a laceration. Extensive circumferential injures necessitate endto-end anastomosis preserving the blood supply to avoid suture line ischemia (Fig. 25-6). Rarely does a significant length of trachea need to be resected. If necessary, additional length can be achieved by mobilizing the trachea by blunt dissection in the avascular pretracheal plane.

FIGURE 25-8 Intraoperative photograph of a distal tracheal repair. The mediastinal pleura is widely opened and tacked with stay sutures. The endotracheal tube is visible through the tracheal defect.

CHAPTER CHAPTER 25 X

the area of suspected injury. In these cases, the endotracheal tube should be withdrawn using the bronchoscope as a guide. Ideally, the endotracheal tube should then be positioned at the level of the vocal cords. This allows the endoscopist to examine the proximal trachea. When the examination is complete, the endotracheal tube can be threaded distally over the bronchoscope and repositioned. As the CT scanning has evolved, it is now sometimes used in the evaluation of potential trachea injuries. In the case of penetrating injury, a trajectory that is clearly away from the trachea should effectively rule out the possibility of a tracheal injury. Signs such as edema within the tracheal wall should prompt further investigation. Three-dimensional reformatting of the images can sometimes demonstrate a tracheal injury, though a negative study does not effectively rule out the presence of an injury.

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1

3

FIGURE 25-9 Intraoperative airway management using a single-lumen endotracheal tube during repair of a ruptured main stem bronchus. (Reproduced with permission from Maurice Hood R, ed. Thoracic Surgery: Techniques in General Thoracic Surgery. Philadelphia: WB Saunders Company; 1985.)

Other maneuvers such as laryngeal release are rarely needed. In extreme circumstances approximately half of the trachea can be resected and a primary repair performed. Whichever method is chosen, precise mucosa to mucosa apposition and an airtight, tension-free repair are mandatory. When placing the sutures, care must be taken to avoid the endotracheal tube balloon. When placing some sutures, it may be necessary to deflate the balloon and temporality interrupt ventilation to protect the balloon. If there is a concomitant vascular or esophageal injury, the possibility of postoperative fistula formation increases and vascularized muscle should be interposed between the suture lines. The postoperative goal is early extubation except in complex repairs or in those with another reason for mechanical ventilation. If postoperative ventilation is required, the balloon cuff ideally should be positioned distal to the repair using the bronchoscope. Securing the endotracheal tube to the teeth with wire suture helps prevent migration. Early patient mobilization, aggressive chest physiotherapy, and humidified oxygen are all

important in the postoperative period. Approximately 1 week after surgery flexible bronchoscopy should be preformed to assess the repair, and can also be used as needed to aid in clearing secretions.

■ Outcomes Because of small sample size, mechanism, associated injuries, and need for emergent airway, the results among published reports vary. In a study of 57 patients with penetrating cervical airway injury, 81% had an isolated tracheal injury and the mortality was 3.5%.55 This compares favorably with a 5% operative mortality among 26 patients with penetrating trauma, half of whom had an associated esophageal injury.59 In a larger series of 71 patients, the mortality with a blunt mechanism was 63% and that for penetrating trauma was 13.5%.60 These authors concluded that blunt mechanism and the need for an emergency airway were independent predictors of mortality.

Lung, Trachea, and Esophagus

■ Complications of Tracheobronchial Injuries Tracheal Stenosis Tracheal stenosis is an uncommon but potentially devastating complication of injury to the airway. Promoted by inflammation, scar, and injury characteristics, tracheal stenosis may manifest subtly and requires a high index of suspicion for detection in the earliest stages. Initial symptoms may be missed, or attributed to reactive airway diseases such as asthma or chronic obstructive pulmonary disease. The diagnosis can be made with high-resolution CT or even with appropriate flow-volume loop assessments. However, direct bronchoscopic visualization remains the gold standard of evaluation. Once identified, initial treatment consists of insuring a secure airway for patients with high-grade lesions. Subsequent therapy consists of rigid or balloon dilational techniques that should be performed under direct visualization. Airway stents have been utilized for cases of stenosis due to malignancy, but are not as well described for use due to post-traumatic stenosis. Surgical treatment for airway obstruction is typically reserved for severe and relatively short lesions. The surgical treatment for post-traumatic stenosis varies by location of the stenosis, but most commonly consists of end-to-end anastomosis or tracheal sleeve resection. Even after resection, the anastomotic site is prone to recurrent stenosis and may necessitate multiple dilations, reoperation, or even permanent tracheostomy.64

INJURIES TO THE ESOPHAGUS Injuries to the esophagus are serious, but rare, sequela of trauma. As with tracheal injuries, esophageal injuries are more common in the neck than within the thorax due to the protection of the bony thorax. Blunt injuries to the esophagus are very rare, but can occur due to a direct blow against a hyperextended neck or less commonly due to rupture secondary to overpressure of the esophagus.1 The majority of esophageal injuries occur due to penetrating injuries, but these injuries are not commonplace even among busy urban trauma centers. The largest multicenter study of penetrating esophageal injuries to date was conducted by the American Association for the Surgery of Trauma and involved 34 trauma centers in the United States. Only 405 penetrating esophageal injuries were identified over a span of 10.5 years. The majority of these (88%) had associated injuries.59 Esophageal injuries are associated with both high mortality and morbidity rates. The diagnosis of these injuries must be rapid, as delay in identification of these injuries is associated

with increased risk of both esophageal-related and overall complications. Once identified, the definitive treatment of esophageal trauma requires a comprehensive understanding of appropriate surgical techniques and prompt intervention in order to optimize outcome.

■ Presentation and Evaluation Any patient with a trajectory adjacent to the esophagus requires evaluation. Physical exam may be helpful in patients at risk for cervical esophageal injury. It is far less helpful in excluding thoracic esophageal injury. Saliva exiting an entrance would seem to make the diagnosis of esophageal injury. Other than that, there are really no hard signs of cervical esophageal injury on physical exam. However, signs that should alert the clinician for the possibility of esophageal injury include painful swallowing, subcutaneous emphysema, and hematemesis. Unfortunately, these findings are relatively nonspecific and occur in less than one quarter of patients with penetrating injury to the neck. In addition, only 18% of patients who have these findings will have an esophageal injury identified.65 Patients with thoracic esophageal injury may present with concomitant pneumothorax or hemothorax from associated injury to the lung and/or vascular structures. A tube thoracostomy should then be placed. Patients with pure esophageal injury may have a hydrothorax, which will appear identical to a hemothorax on chest x-ray. The drainage in the chest tube should be examined. If it is obviously saliva or has food substance in it, an esophageal injury should be high on the list of possibilities. Confirmatory testing should be performed immediately. Contrast esophagography has traditionally been the test used to evaluate both the cervical and the thoracic esophagus. If performed with good technique, the entire esophagus should be able to be evaluated. In patients who are intubated, the contrast can be instilled via a nasogastric tube that is pulled back to the proximal esophagus. The ability to truly evaluate the proximal portion of the cervical esophagus using this technique is certainly not 100%. Other studies may be preferable. In one recent series, contrast esophagoscopy was used in 82% of patients with suspected esophageal injury, while esophagoscopy was used in the other 18%.66 Contrast studies may miss esophageal injuries. Even if films are performed in two planes, contrast studies do not provide a true three-dimensional evaluation of the esophagus. In one series, contrast esophagography missed one third of injuries in the esophagus later diagnosed with rigid esophagoscopy. Several techniques exist. Some advocate performing a flush study with water-soluble contrast. If no leak is identified, the study can be repeated using barium that should miss a smaller number of injuries. Others simply use barium. This should be safe as barium is relatively inert and extravasation into the mediastinum will not cause additional morbidity. Obtaining high-quality contrast studies may be difficult, particularly in off-hours. Esophagoscopy is certainly an alternative. Acute care surgeons should be trained in esophagoscopy and therefore able to perform these studies at any time. Flexible esophagoscopy is most often used. However, rigid esophagoscopy may be superior to flexible esophagoscopy and has been

CHAPTER CHAPTER 25 X

The influence of associated injuries on mortality is striking. In studies where over half of the patients had associated injuries, the mortality was as high as 21%, with almost all deaths secondary to the concomitant injury, especially vascular trauma.61–63 Morbidity can be as high as 19% and often results from an associated injury.62,63 Delay in diagnosis, missed esophageal injuries, and associated injuries all correlate with increased morbidity and mortality. Therefore, a thorough evaluation and expeditious exploration are imperative.

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advocated as the study of choice in some centers. Rigid esophagoscopy is no longer part of surgical training in most institutions. Flexible esophagoscopy does not require general anesthesia and can be done in the emergency department. It has a negative predictive value of 100% but a positive predictive value of only approximately 33%.67,68 It would seem reasonable that a combination of flexible esophagoscopy and a contrast study should be able to make the diagnosis of esophageal injury in virtually every patient. It is imperative that an esophagoscopy be done carefully. While a few patients will have obvious injury at the time of endoscopy, many patients will have much more subtle endoscopic findings such as hemorrhage in the mucosa. An esophageal wall defect may not necessarily be obvious. This may explain the relatively low positive predictive value that has been reported in literature. The entire circumference of the esophagus must be carefully evaluated. Those patients with concerning findings on esophagoscopy should undergo either an additional study or exploration. CT scanning has become more popular in the evaluation of penetrating injury to the mediastinum, including the esophagus. Following penetrating injury, CT can often define the trajectory of the missile and determine whether the esophagus is at risk or not. If oral contrast has been administered, CT may well be able to identify contrast pooling outside of the esophagus. The ability to get a three-dimensional evaluation of the mediastinum potentially makes CT more attractive than a simple contrast study. Three-dimensional reformatted images may allow the clinician to obtain a relatively sophisticated look at the esophagus. However, CT is a static exam and one cannot see contrast moving through the esophagus, as is possible with the more dynamic esophagography.

■ Operative Treatment The topic of esophageal injures often encompasses spontaneous rupture, iatrogenic and chemically induced perforations, and external trauma. Published reports frequently include most or all of these etiologies in their analysis and description of management, with external trauma usually the least frequently described.69–71 Because esophageal injury is uncommon, most studies are composed of small series,71 and this topic is further complicated by reports based on anatomic location or mechanism alone.70–72 Although many of the principles developed for the treatment of nontraumatic esophageal injury are applicable to the external esophageal trauma management, there are several important differences. Successful nonoperative treatment of specific iatrogenic injury has been described.69–71 While this approach may be appropriate in selected cervical injury, it must be utilized judiciously, as surgical repair remains the mainstay of treatment of esophageal injury resulting from external trauma. A brief description of esophageal anatomy and vascular supply is important to fully appreciate surgical exposure, mobilization, and repair. The esophageal wall is composed of inner and outer muscular layers but lacks a serosa. The cervical esophagus is predominantly a left-sided structure and as it descends into the thorax it courses to the right. The largest angulation occurs

at the esophagogastric junction as the esophagus passes through the diaphragm to lie left of the midline in the abdomen. Arterial supply to the cervical and a portion of proximal esophagus arises from the thyroidal vessels. The thoracic esophagus is supplied by multiple aortic branches and bronchial vessels, and blood supply to the distal esophagus is derived from the left gastric artery. The intramural vasculature courses longitudinally. Exposure of the cervical esophagus is achieved via the left neck. Mobilizing the cervical esophagus is accomplished by lateral retraction of the sternocleidomastoid and blunt dissection in the prevertebral plane. During this dissection care must be exercised to avoid injuring the recurrent laryngeal nerves that lie in the tracheoesophageal grove. If needed, a rubber drain can be passed around the esophagus to facilitate exposure. A fundamental principle in treating esophageal trauma is visualizing the entire extent of the mucosal injury. The defect in the muscular layer is almost always less extensive than that in the mucosa. The extent of the mucosal defect is exposed by incising the muscular layer until both ends of the mucosal tear are visualized. Esophageal repair is performed in two layers and must be tension free. The mucosa is approximated with interrupted sutures, either absorbable or nonabsorbable, and the muscular layer is closed with interrupted nonabsorbable sutures (Fig. 25-10). Some authors advocate use of a nasogastric tube or bougie to ensure a widely patent repair.69,70 Drains, while not uniformly used, are recommended. In the unusual circumstance where no injury is found at exploration, drainage and antibiotics usually suffice.71,72 Intrathoracic esophageal injuries present a more challenging problem due to the degree of initial mediastinal contamination and extent of the esophageal injury. In addition, an uncontrolled mediastinal leak is more serious than one arising from the cervical esophagus. Historically, time from injury to repair often influenced operative management. This concept has evolved and time, while important, is no longer the main factor. The degree of mediastinal contamination is the principal consideration in determining intraoperative management. The majority of intrathoracic esophageal injuries can be managed similar to those in the cervical region. The surgical approach is through a right thoracotomy. The azygous vein is divided and the lung is retracted. The mediastinal pleura widely opened to expose the esophagus. The esophagus is then mobilized by blunt dissection. Visualization is facilitated by placing a rubber drain around it. Care must be taken to avoid injury to the trachea or main stem bronchi. Devitalized mediastinal and esophageal tissues are debrided. Following the repair, several tissues can be used as a buttress for the repair. A pedicled intercostal muscle is often used since it is robust and easily harvested.63,69,70–72 (Fig. 25-11). Wide mediastinal drainage is mandatory. A contrast study is performed approximately 1 week postoperatively, and if no leak is noted, oral feedings can be started. There are several surgical approaches to the distal esophagus or esophagogastric junction including a sixth or seventh interspace left posterolateral thoracotomy, laparotomy, or a thoracoabdominal incision. Injuries to the distal intrathoracic esophagus are best approached via thoracotomy. Widely opening the mediastinal pleura and freely mobilizing the esophagus will

Lung, Trachea, and Esophagus Diaphragm

481

Pericardium

CHAPTER CHAPTER 25 X

A

Mediastinal pleura

Aorta

Esophagus B

Right mediastinal pleura

C

Mucosa Muscularis FIGURE 25-10 (A) Necrotic mediastinal pleura has been excised, and esophageal tear has been debrided. (B) Elevation of the esophagus on a rubber drain allows for debridement of the right mediastinal pleura if indicated. (C) Debridement of the esophageal rupture. Muscularis is incised superiorly and inferiorly to allow visualization of the extent of mucosal defect before two-layer closure of the perforation if possible. (Reproduced with permission from Alexander Patterson GA, ed. Pearson’s Thoracic and Esophageal Surgery. Vol. 2. 3rd ed. Philadelphia: Elsevier; 2008. © Elsevier.)

enhance exposure. The choice of incision to expose the esophagogastric junction is influenced by the exact location of the injury and associated injuries. If there are concomitant abdominal injuries, laparotomy alone may be sufficient, while associated intrathoracic injuries may be approached by thoracotomy or thoracoabdominal incision. The same principles and techniques are used as previously described. Distal esophageal injuries lend themselves to reinforcement with a fundal wrap. Regardless of the location, a primary repair buttressed with muscle and adequate mediastinal drainage is the best solution. Esophageal excision and resection with diversion should be avoided, and every effort made to preserve esophageal length. In rare circumstances, the magnitude of the esophageal injury or the patient’s clinical condition precludes definitive repair. In these instances a damage control procedure may be lifesaving. Creating a controlled esophageal fistula by using a T-tube is an effective procedure.69,70,73 This technique, combined with wide drainage, controls mediastinal contamination and preserves esophageal length. Devastating injury to the stomach and

esophagogastric junction presents a unique challenge. These are not amenable to T-tube drainage; however, retrograde esophageal drainage may prove useful. Continuity is reestablished by an esophagojejunostomy performed several months later.74

■ Outcomes Esophageal trauma results in significant morbidity and mortality. Mortality ranges from 0% to 22%.62,71,75,76 In the large AAST series, the mortality was 19%.59 Complications are common and are often subdivided into those that are esophageal related ranging between 38% and 66%.59,75 With respect to cervical injuries the most common complication is an esophageal fistula, most of which close spontaneously.72 Esophageal-specific complications occur in 29–38% of patients with postoperative leak and infection predominating.59,75 The most important risk factors are delayed operation, magnitude of the esophageal injury, and resection and diversion.59,75 Prompt diagnosis, consideration of a damage

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8th rib

Intercostal muscle

Periosteum

Neurovascular bundle Pleura

Fascia

SECTION 3 X Periosteum

8th rib

7th rib

A

Pleura B

FIGURE 25-11 Construction of intercostal musculopleural flap. (A) Periosteum of the rib inferior to thoracotomy incision is incised, and the subjacent pleura is mobilized. (B) The neurovascular bundle is divided anteriorly, and the flap is created. (Reproduced with permission from Alexander Patterson GA, ed. Pearson’s Thoracic and Esophageal Surgery. Vol. 2. 3rd ed. Philadelphia: Elsevier; 2008. © Elsevier.)

control procedure in dire circumstances, and a precise technical repair are the essentials for a satisfactory outcome.

■ Complications of Esophageal Injury Missed/Delayed Diagnosis The diagnosis of esophageal injury must be made rapidly after trauma, as any delay in diagnosis confers significant risk for morbidity and mortality. In the largest study to date of penetrating esophageal injuries, Asensio and colleagues found that patients subjected to lengthy evaluations had higher complication rates overall and esophageal-related complications specifically, compared to counterparts who proceeded directly

to operation for diagnosis and received operative treatment in an expedited fashion.59 In another recent study of esophageal perforations due to trauma, iatrogenic injuries, and other causes, Eroglu et al.78 found that survival was significantly influenced by a delay of more than 24 hours in the initiation of treatment. Suspicion for late esophageal injury must be high depending on the mechanism. In alert patients, pain will be the most common symptom.76,78–80 Other symptoms may include dyspnea, fever, or dysphagia. Subcutaneous emphysema, while not specific or particularly sensitive for injury, may develop early in the course of injury. Utilizing the principles and approaches outlined earlier in this chapter, every effort should be made to rule out definitively esophageal injury whenever it is suspected.

Lung, Trachea, and Esophagus

Tracheoesophageal Fistula

REFERENCES 1. Karmy-Jones R, Jurkovich GJ. Blunt chest trauma. Curr Probl Surg. 2004;41(3):211–380. 2. Calhoon JH, Trinkle JK. Pathophysiology of chest trauma. Chest Surg Clin N Am. 1997;7(2):199–211. 3. Demetriades D, Velmahos GC. Penetrating injuries of the chest: indications for operation. Scand J Surg. 2002;91(1):41–45. 4. Karmy-Jones R, Jurkovich GJ, Shatz DV, et al. Management of traumatic lung injury: a western trauma association multicenter review. J Trauma. 2001;51(6):1049–1053. 5. Schramel R, Kellum H, Creech O Jr. Analysis of factors affecting survival after chest injuries. J Trauma. 1961;1:600–607. 6. LoCicero J 3rd, Mattox KL. Epidemiology of chest trauma. Surg Clin North Am. 1989;69(1):15–19. 7. Kulshrestha P, Munshi I, Wait R. Profile of chest trauma in a level I trauma center. J Trauma. 2004;57(3):576–581. 8. Demirhan R, Onan B, Oz K, Halezeroglu S. Comprehensive analysis of 4205 patients with chest trauma: a 10-year experience. Interact Cardiovasc Thorac Surg. 2009;9(3):450–453. 9. Huh J, Wall MJ Jr, Estrera AL, Soltero ER, Mattox KL. Surgical management of traumatic pulmonary injury. Am J Surg. 2003;186(6): 620–624. 10. Cothren C, Moore EE, Biffl WL, Franciose RJ, Offner PJ, Burch JM. Lung-sparing techniques are associated with improved outcome compared with anatomic resection for severe lung injuries. J Trauma. 2002;53(3): 483–487.

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Tracheoesophageal fistula following trauma is, fortunately, exceptionally rare. Any appropriately located injury to the trachea and/or esophagus has the potential to lead to the formation of a fistulous connection between these two structures. In these clinical scenarios it is advisable, therefore, to complete initial tracheal or esophageal repairs with muscle flap coverage interposed between the repairs to protect them from subsequent compromise and fistulization. The presentation of these patients may be initially subtle. Recurrent pneumonia and persistent cough with unidentified cause alone warrants evaluation in the appropriate patient. The diagnosis can be made with a combination of endoscopy, bronchoscopy, and/or esophageal swallow contrast study. Once diagnosed, treatment most commonly entails surgical intervention and ligation of the fistula with repair of the respective defects and muscle flap coverage. The use of covered tracheal or esophageal stents has been described for patients who are not operative candidates, as has diversion. Given the anatomic proximity of these two structures, combined injury can occur. While tracheoesophageal injuries can happen anywhere along their course, they occur more frequently in the cervical region, as this is the site of most tracheal trauma. The management of combined tracheoesophageal trauma is essentially the management of each individual injury. Surgical exposure is identical to the approach described above. Technical details include tracheal repair with interrupted absorbable sutures, a two-layer esophageal closure, and muscle interposition.63,71,80 Two alternative techniques have been described, closing the esophagus through the tracheal laceration without interposing muscle and utilizing a tracheal flap to close the esophageal defect.78,81 Mortality has ranged from 0% to 21% and complications were common.63,71,81 While the benefit of muscle interposition had not been proven, it is prudent, adds little operating time, and is widely employed.59,63,71,81

11. Acosta JA, Yang JC, Winchell RJ, et al. Lethal injuries and time to death in a level I trauma center. J Am Coll Surg. 1998;186(5):528–533. 12. Peng RY, Bongard FS. Pedestrian versus motor vehicle accidents: an analysis of 5,000 patients. J Am Coll Surg. 1999;189(4):343–348. 13. Demetriades D, Murray J, Charalambides K, et al. Trauma fatalities: time and location of hospital deaths. J Am Coll Surg. 2004;198(1):20–26. 14. Mirvis SE. Imaging of acute thoracic injury: the advent of MDCT screening. Semin Ultrasound CT MR. 2005;26(5):305–331. 15. Wisbach GG, Sise MJ, Sack DI, et al. What is the role of chest X-ray in the initial assessment of stable trauma patients? J Trauma. 2007;62(1): 74–78 [discussion 78–79]. 16. Meredith JW, Hoth JJ. Thoracic trauma: when and how to intervene. Surg Clin North Am. 2007;87(1):95–118, vii. 17. O’Connor JV, Scalea TM. Penetrating thoracic great vessel injury: impact of admission hemodynamics and preoperative imaging. J Trauma. 2010;68(4):834–837. 18. Carrillo EH, Heniford BT, Etoch SW, et al. Video-assisted thoracic surgery in trauma patients. J Am Coll Surg. 1997;184(3):316–324. 19. Heniford BT, Carrillo EH, Spain DA, Sosa JL, Fulton RL, Richardson JD. The role of thoracoscopy in the management of retained thoracic collections after trauma. Ann Thorac Surg. 1997;63(4):940–943. 20. Hajarizadeh H, Rohrer MJ, Cutler BS. Surgical exposure of the left subclavian artery by median sternotomy and left supraclavicular extension. J Trauma. 1996;41(1):136–139. 21. Velmahos GC, Baker C, Demetriades D, Goodman J, Murray JA, Asensio JA. Lung-sparing surgery after penetrating trauma using tractotomy, partial lobectomy, and pneumonorrhaphy. Arch Surg. 1999;134(2): 186–189. 22. Wall MJ Jr, Villavicencio RT, Miller CC 3rd, et al. Pulmonary tractotomy as an abbreviated thoracotomy technique. J Trauma. 1998;45(6): 1015–1023. 23. Asensio JA, Demetriades D, Berne JD, et al. Stapled pulmonary tractotomy: a rapid way to control hemorrhage in penetrating pulmonary injuries. J Am Coll Surg. 1997;185(5):486–487. 24. Wall MJ Jr, Hirshberg A, Mattox KL. Pulmonary tractotomy with selective vascular ligation for penetrating injuries to the lung. Am J Surg. 1994;168(6):665–669. 25. Alfici R, Ashkenazi I, Kounavsky G, Kessel B. Total pulmonectomy in trauma: a still unresolved problem—our experience and review of the literature. Am Surg. 2007;73(4):381–384. 26. Nurozler F, Argenziano M, Ginsburg ME. Nitric oxide usage after posttraumatic pneumonectomy. Ann Thorac Surg. 2001;71(1):364–366. 27. Phelan HA, Patterson SG, Hassan MO, Gonzalez RP, Rodning CB. Thoracic damage-control operation: principles, techniques, and definitive repair. J Am Coll Surg. 2006;203(6):933–941. 28. Rotondo MF, Bard MR. Damage control surgery for thoracic injuries. Injury. 2004;35(7):649–654. 29. Caceres M, Buechter KJ, Tillou A, Shih JA, Liu D, Steeb G. Thoracic packing for uncontrolled bleeding in penetrating thoracic injuries. South Med J. 2004;97(7):637–641. 30. Vargo DJ, Battistella FD. Abbreviated thoracotomy and temporary chest closure: an application of damage control after thoracic trauma. Arch Surg. 2001;136(1):21–24. 31. Carrillo EH, Block EF, Zeppa R, Sosa JL. Urgent lobectomy and pneumonectomy. Eur J Emerg Med. 1994;1(3):126–130. 32. Bulger EM, Edwards T, Klotz P, Jurkovich GJ. Epidural analgesia improves outcome after multiple rib fractures. Surgery. 2004;136(2): 426–430. 33. Eddy AC, Luna GK, Copass M. Empyema thoracis in patients undergoing emergent closed tube thoracostomy for thoracic trauma. Am J Surg. 1989;157(5):494–497. 34. Aguilar MM, Battistella FD, Owings JT, Su T. Posttraumatic empyema. risk factor analysis. Arch Surg. 1997;132(6):647–650 [discussion 650–651]. 35. Velmahos GC, Demetriades D, Chan L, et al. Predicting the need for thoracoscopic evacuation of residual traumatic hemothorax: chest radiograph is insufficient. J Trauma. 1999;46(1):65–70. 36. Meyer DM, Jessen ME, Wait MA, Estrera AS. Early evacuation of traumatic retained hemothoraces using thoracoscopy: a prospective, randomized trial. Ann Thorac Surg. 1997;64(5):1396–1400 [discussion 1400–1401]. 37. Oguzkaya F, Akcali Y, Bilgin M. Videothoracoscopy versus intrapleural streptokinase for management of post traumatic retained haemothorax: a retrospective study of 65 cases. Injury. 2005;36(4):526–529. 38. Cuschieri J, Kralovich KA, Patton JH, Horst HM, Obeid FN, KarmyJones R. Anterior mediastinal abscess after closed sternal fracture. J Trauma. 1999;47(3):551–554.

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39. Lemmer JH, Botham MJ, Orringer MB. Modern management of adult thoracic empyema. J Thorac Cardiovasc Surg. 1985;90(6):849–855. 40. Hagan JL, Hardy JD. Lung abscess revisited. A survey of 184 cases. Ann Surg. 1983;197(6):755–762. 41. Vallieres E, Shamji FM, Todd TR. Postpneumonectomy chylothorax. Ann Thorac Surg. 1993;55(4):1006–1008. 42. Gomez-Caro A, Ausin P, Moradiellos FJ, et al. Role of conservative medical management of tracheobronchial injuries. J Trauma. 2006; 61(6):1426–1434 [discussion 1434–1435]. 43. Sakles JC, Deacon JM, Bair AE, Keim SM, Panacek EA. Delayed complications of emergency airway management: a study of 533 emergency department intubations. West J Emerg Med. 2008;9(4):190–194. 44. Vassiliu P, Baker J, Henderson S, Alo K, Velmahos G, Demetriades D. Aerodigestive injuries of the neck. Am Surg. 2001;67(1):75–79. 45. Kelly JP, Webb WR, Moulder PV, Everson C, Burch BH, Lindsey ES. Management of airway trauma. I: tracheobronchial injuries. Ann Thorac Surg. 1985;40(6):551–555. 46. Rossbach MM, Johnson SB, Gomez MA, Sako EY, Miller OL, Calhoon JH. Management of major tracheobronchial injuries: a 28-year experience. Ann Thorac Surg. 1998;65(1):182–186. 47. McClish A, Deslauriers J, Beaulieu M, et al. High-flow catheter ventilation during major tracheobronchial reconstruction. J Thorac Cardiovasc Surg. 1985;89(4):508–512. 48. Dreyfuss D, Saumon G. Ventilator-induced lung injury: lessons from experimental studies. Am J Respir Crit Care Med. 1998;157(1): 294–323. 49. Symbas PN, Justicz AG, Ricketts RR. Rupture of the airways from blunt trauma: treatment of complex injuries. Ann Thorac Surg. 1992;54(1): 177–183. 50. Kuhne CA, Kaiser GM, Flohe S, et al. Nonoperative management of tracheobronchial injuries in severely injured patients. Surg Today. 2005;35(7):518–523. 51. Huh J, Milliken JC, Chen JC. Management of tracheobronchial injuries following blunt and penetrating trauma. Am Surg. 1997;63(10): 896–899. 52. Gabor S, Renner H, Pinter H, et al. Indications for surgery in tracheobronchial ruptures. Eur J Cardiothorac Surg. 2001;20(2):399–404. 53. Madden BP, Datta S, Charokopos N. Experience with ultraflex expandable metallic stents in the management of endobronchial pathology. Ann Thorac Surg. 2002;73(3):938–944. 54. Grewal H, Rao PM, Mukerji S, Ivatury RR. Management of penetrating laryngotracheal injuries. Head Neck. 1995;17(6):494–502. 55. Schaefer SD. The acute management of external laryngeal trauma. A 27-year experience. Arch Otolaryngol Head Neck Surg. 1992;118(6): 598–604. 56. Fuhrman GM, Stieg FH 3rd, Buerk CA. Blunt laryngeal trauma: classification and management protocol. J Trauma. 1990;30(1):87–92. 57. Cooper JD, Todd TR, Ilves R, Pearson FG. Use of the silicone tracheal T-tube for the management of complex tracheal injuries. J Thorac Cardiovasc Surg. 1981;82(4):559–568. 58. Miller RP, Gray SD, Cotton RT, Myer CM 3rd. Airway reconstruction following laryngotracheal thermal trauma. Laryngoscope. 1988;98 (8 pt 1):826–829. 59. Asensio JA, Chahwan S, Forno W, et al. Penetrating esophageal injuries: multicenter study of the American Association for the Surgery of Trauma. J Trauma. 2001;50(2):289–296. 60. Bhojani RA, Rosenbaum DH, Dikmen E, et al. Contemporary assessment of laryngotracheal trauma. J Thorac Cardiovasc Surg. 2005;130(2): 426–432.

61. Flynn AE, Verrier ED, Way LW, Thomas AN, Pellegrini CA. Esophageal perforation. Arch Surg. 1989;124(10):1211–1214 [discussion 1214–1215]. 62. Balci AE, Eren N, Eren S, Ulku R. Surgical treatment of post-traumatic tracheobronchial injuries: 14-year experience. Eur J Cardiothorac Surg. 2002;22(6):984–989. 63. Kelly JP, Webb WR, Moulder PV, Moustouakas NM, Lirtzman M. Management of airway trauma. II: combined injuries of the trachea and esophagus. Ann Thorac Surg. 1987;43(2):160–163. 64. Wright CD, Grillo HC, Wain JC, et al. Anastomotic complications after tracheal resection: prognostic factors and management. J Thorac Cardiovasc Surg. 2004;128(5):731–739. 65. Port JL, Kent MS, Korst RJ, Bacchetta M, Altorki NK. Thoracic esophageal perforations: a decade of experience. Ann Thorac Surg. 2003; 75(4):1071–1074. 66. Demetriades D, Theodorou D, Cornwell E, et al. Evaluation of penetrating injuries of the neck: prospective study of 223 patients. World J Surg. 1997;21(1):41–47 [discussion 47–48]. 67. Srinivasan R, Haywood T, Horwitz B, Buckman RF, Fisher RS, Krevsky B. Role of flexible endoscopy in the evaluation of possible esophageal trauma after penetrating injuries. Am J Gastroenterol. 2000;95(7): 1725–1729. 68. Flowers JL, Graham SM, Ugarte MA, et al. Flexible endoscopy for the diagnosis of esophageal trauma. J Trauma. 1996;40(2):261–265 [discussion 265–266]. 69. Bufkin BL, Miller JI Jr, Mansour KA. Esophageal perforation: emphasis on management. Ann Thorac Surg. 1996;61(5):1447–1451 [discussion 1451–1452]. 70. Wu JT, Mattox KL, Wall MJ Jr. Esophageal perforations: new perspectives and treatment paradigms. J Trauma. 2007;63(5):1173–1184. 71. Weiman DS, Walker WA, Brosnan KM, Pate JW, Fabian TC. Noniatrogenic esophageal trauma. Ann Thorac Surg. 1995;59(4):845–849 [discussion 849–850]. 72. Winter RP, Weigelt JA. Cervical esophageal trauma. Incidence and cause of esophageal fistulas. Arch Surg. 1990;125(7):849–851 [discussion 851–852]. 73. Andrade-Alegre R. T-tube intubation in the management of late traumatic esophageal perforations: case report. J Trauma. 1994;37(1):131–132. 74. O’Connor JV, Scalea TM. Retrograde esophageal intubation. Am Surg. 2007;73(3):267–270. 75. Beal SL, Pottmeyer EW, Spisso JM. Esophageal perforation following external blunt trauma. J Trauma. 1988;28(10):1425–1432. 76. Ahmed N, Massier C, Tassie J, Whalen J, Chung R. Diagnosis of penetrating injuries of the pharynx and esophagus in the severely injured patient. J Trauma. 2009;67(1):152–154. 77. Linden PA, Bueno R, Mentzer SJ, et al. Modified T-tube repair of delayed esophageal perforation results in a low mortality rate similar to that seen with acute perforations. Ann Thorac Surg. 2007;83(3): 1129–1133. 78. Eroglu A, Can Kurkcuogu I, Karaoganogu N, Tekinbas C, Yimaz O, Basog M. Esophageal perforation: the importance of early diagnosis and primary repair. Dis Esophagus. 2004;17(1):91–94. 79. Feliciano DV, Bitondo CG, Mattox KL, et al. Combined tracheoesophageal injuries. Am J Surg. 1985;150(6):710–715. 80. Mohlala ML, Ramoroko SP, Ramasodi KP, Vucinic M, Gunning AJ. A technical approach to tracheal and oesophageal injuries. S Afr J Surg. 1994;32(3):114–116. 81. Sokolov VV, Bagirov MM. Reconstructive surgery for combined tracheoesophageal injuries and their sequelae. Eur J Cardiothorac Surg. 2001;20(5):1025–1029.

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CHAPTER 26

Heart and Thoracic Vascular Injuries Matthew J. Wall, Jr., Peter Tsai, and Kenneth L. Mattox

INTRODUCTION The heart and its tributaries are encased in the chest cavity, composed of the manubrium, sternum, clavicle, rib cage, and vertebral bodies. This rigid chassis, for the most part, provides adequate protection against small impacts/injuries. Severe trauma requiring intervention occurs by penetrating or blunt mechanisms. Firearms often result in direct injury to the heart and great vessels, in the path of destruction. The bony structures, interestingly, can also provide unique forms of injuries as they cause a ricocheting of bullets or alter vectors of the original direction of penetration. Blunt forces can lead to crushing, traction, and torsion injuries to the heart from deceleration forces. Penetrating trauma to the great vessels can lead to immediate exsanguination or pattern of injury similar to blunt trauma including pseudoaneurysm, partial transection with intimal flap, thrombosis, and propagation.

HEART INJURY ■ Incidence Cardiac injury may account for 10% of deaths from gunshot wounds.1 Penetrating cardiac trauma is a highly lethal injury, with relatively few victims surviving long enough to reach the hospital. In a series of 1,198 patients with penetrating cardiac injuries in South Africa, only 6% of patients reached the hospital with any signs of life.2 With improvements in organized emergency medical transport systems, up to 45% of those who sustain significant heart injury may reach the emergency department with signs of life. It is somewhat frustrating however to note the overall mortality for penetrating trauma has not changed much even in the major trauma centers.3 Blunt cardiac injuries have been reported less frequently than penetrating injuries.1 The actual incidence of cardiac injury is unknown because of the diverse causes and classifications.

Thoracic trauma is responsible for 25% of the deaths from vehicular accidents of which 10–70% of this subgroup may have been the result of blunt cardiac rupture. There continues to be tremendous confusion as the term blunt cardiac injury/ cardiac contusion is applied to a wide spectrum of pathology.

■ Mechanism Penetrating Cardiac Injury Penetrating trauma is a common mechanism for cardiac injury, with the predominant etiology being from firearms and knives4 (Table 26-1). The location of injury to the heart is associated with the location of injury on the chest wall. Because of an anterior location, the cardiac chambers at greatest risk for injury are the right and left ventricles. In a review of 711 patients with penetrating cardiac trauma, this series noted 54% sustained stab wounds and 42% had gunshot wounds. The right ventricle was injured in 40% of the cases, the left ventricle in 40%, the right atrium in 24%, and the left atrium in 3%. The overall mortality was 47%. This series noted one third of cardiac injuries involved multiple cardiac structures.4 More complicated intracardiac injuries involved the coronary arteries, valvular apparatus, and intracardiac fistulas (such as ventricular septal defects). Only 2% of patients surviving the initial injury required reoperation for a residual defect. The majority of these repairs were performed on a semielective basis.4 Thus, the majority of injuries are to the myocardium, and are readily managed by the general/trauma or acute care surgeon. Intrapericardial and intracardiac foreign bodies can cause complications of acute suppurative pericarditis, chronic constrictive pericarditis, foreign body reaction, and hemopericardium.5 Needles and other foreign bodies have been noted after deliberate insertion by patients with psychiatric diagnoses. A report by LeMaire et al.5 recommended removal of intrapericardial foreign

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Management of Specific Injuries

bodies that are greater than 1 cm in size, that are contaminated, or that produce symptoms. Intracardiac missiles are embedded in the myocardium, retained in the trabeculations of the endocardial surface, or free in a cardiac chamber. These result from direct penetrating thoracic injury or injury to a peripheral venous structure with embolization to the heart. Observation might be considered when the missile is small, right sided, embedded completely in the wall, contained within a fibrous covering, not contaminated, and producing no symptoms. Right-sided missiles can embolize to the pulmonary artery, where they can be removed if large. In rare cases they can embolize through a patent foramen ovale or atrial septal defect. Left-sided missiles can manifest as systemic embolization shortly after the initial injury.

as a spectrum of free septal rupture, free wall rupture, coronary artery thrombosis, cardiac failure, complex and simple dysrhythmias, and rupture of chordae tendineae or papillary muscles.5 The specific mechanisms include motor vehicle accidents, vehicular–pedestrian accidents, falls, crush injuries, blast/explosion, assaults, CPR, and recreational events. Blunt injury may be associated with sternal or rib fractures. In one report a fatal cardiac dysrhythmia occurred when the sternum was struck by a baseball, which may be a form of commotio cordis.6 True cardiac rupture carries a significant risk of mortality. The biomechanics of this injury include (1) direct transmission of increased intrathoracic pressure to the chambers of the heart; (2) a hydraulic effect from a large force applied to the abdominal or extremity veins, causing the force to be transmitted to the right atrium; (3) a decelerating force between fixed and mobile areas, explaining atriocaval tears; (4) a direct force causing myocardial contusion, necrosis, and delayed rupture; and (5) penetration from a broken rib or fractured sternum.1 From autopsy data, blunt cardiac trauma with chamber rupture occurs most often to the left ventricle. In contrast, in patients who arrive alive to the hospital, right atrial disruption is more common. These are seen at the SVC–atrial junction, IVC–atrial junction, or the right atrial appendage. Blunt rupture of the cardiac septum occurs most frequently near the apex of the heart. Multiple ruptures as well as disruption of the conduction system have been reported. Injury to only the membranous portion of the septum is the least common blunt VSD. Traumatic rupture of the thoracic aorta is also associated with lethal cardiac rupture in almost 25% of cases. Pericardial tears secondary to increased intra-abdominal pressure or lateral decelerative forces can occur. These can occur on the left side, usually parallel to the phrenic nerve; to the right side of the pericardium; to the diaphragmatic surface of the pericardium; and finally to the mediastinum. Cardiac herniation with cardiac dysfunction can occur in conjunction with these tears. The heart may be displaced into either pleural cavity or even the abdomen depending on the tear. In the circumstance of right pericardial rupture, the heart can become twisted, leading to the surprising discovery of an “empty” pericardial cavity at resuscitative left anterolateral thoracotomy. With a left-sided cardiac herniation through a pericardial tear, a trapped apex of the heart prevents the heart from returning to the pericardium and the term strangulated heart has been applied. Unless the heart is returned to its normal position, hypotension and cardiac arrest can occur.7 One clue to the presence of cardiac herniation in a patient with blunt thoracic injury is sudden loss of pulse when the patient is repositioned, such as when moved or placed on a stretcher.

Blunt Cardiac Injury

Iatrogenic Cardiac Injury

Blunt cardiac trauma has replaced the term “cardiac contusion” and describes injury ranging from insignificant bruises of the myocardium to cardiac rupture. Pathology can be caused by direct energy transfer to the heart or by a mechanism of compression of the heart between the sternum and the vertebral column at the time of the accident. Cardiac rupture during external cardiac massage as part of cardiopulmonary resuscitation (CPR) can occur. Blunt cardiac injuries can thus manifest

Iatrogenic cardiac injury can occur with central venous catheter insertion, cardiac catheterization procedures, endovascular interventions, and pericardiocentesis. Cardiac injuries caused by central venous catheter placement usually occur with insertion from either the left subclavian or the left internal jugular vein.8 Perforation causing tamponade has also been reported with a right internal jugular introducer sheath for transjugular intrahepatic portocaval shunts. Insertion of left-sided central lines,

TABLE 26-1 Etiology of Traumatic Heart Diseases

SECTION 3 X

I. Penetrating (A) Low entry 1. Stab wounds—knives, swords, ice picks, fence posts, wire, sports (B) High entry 2. Gunshot wounds—handguns, rifles, nail guns, lawnmower projectiles 3. Shotgun wounds—close range versus distant 4. Blast—fragments II. Nonpenetrating (blunt) (A) Motor vehicle accident (B) Vehicular–pedestrian accident (C) Falls from height (D) Crush—industrial accident (E) Blast—explosives, fragments, improvised explosive devices (F) Assault (G) Sternal or rib fractures (H) Recreational—sporting events, rodeo, baseball III. Iatrogenic (A) Catheter induced (B) Pericardiocentesis induced (C) Percutaneous interventions IV. Others (A) Electrical (B) Embolic—missiles (C) Factitious—needles, foreign bodies

Heart and Thoracic Vascular Injuries

Electrical Injury Cardiac complications after electrical injury include immediate cardiac arrest; acute myocardial necrosis with or without ventricular failure; myocardial ischemia; dysrhythmias; conduction abnormalities; acute hypertension with peripheral vasospasm; and asymptomatic, nonspecific abnormalities evident on an electrocardiogram (ECG). Damage from electrical injury is due to direct effects on the excitable tissues, heat generated from the electrical current, and accompanying associated injuries (e.g., falls, explosions, fires).11

■ Clinical Presentation

of acute trauma patients. Pulsus paradoxus (a substantial fall in systolic blood pressure during inspiration) and Kussmaul’s sign (increase in jugular venous distention on inspiration) may be present but are also not reliable signs. A more valuable and reproducible sign of pericardial tamponade is narrowing of the pulse pressure. An elevation of the central venous pressure often accompanies overaggressive cyclic hyperresuscitation with crystalloid solutions, but in such instances a widening of the pulse pressure occurs. Gunshot wounds to the heart are more frequently associated with hemorrhage than with tamponade. The kinetic energy is greater with firearms, and the wounds to the heart and pericardium are usually more extensive. Thus, these patients present with exsanguination into a pleural cavity more often.

Blunt Cardiac Injury Clinically significant blunt cardiac injuries include cardiac rupture (ventricular or atrial), septal rupture, valvular dysfunction, coronary thrombosis, and caval avulsion. These injuries manifest as tamponade, hemorrhage, or severe cardiac dysfunction. Septal rupture and valvular dysfunction (leaflet tear, papillary muscle, or chordal rupture) can initially appear without symptoms but later demonstrate the delayed sequela of heart failure.1 Blunt cardiac injury can also present as a dysrhythmia, most commonly premature ventricular contractions, the precise mechanism of which is unknown. Ventricular tachycardia, ventricular fibrillation, and supraventricular tachyarrhythmias can also occur. These symptoms usually occur within the first 24–48 hours after injury. A major difficulty in managing blunt cardiac injury relates to definitions. “Cardiac contusion” is a nonspecific term, which should likely be abandoned. It is best to describe these injuries as “blunt cardiac trauma with”—followed by the clinical manifestation such as dysrhythmia or heart failure.12

Penetrating Cardiac Injury Wounds involving the epigastrium and precordium can raise clinical suspicion for cardiac injury. Patients with cardiac injury can present with a clinical spectrum from full cardiac arrest to asymptomatic with normal vital signs. Up to 80% of stab wounds that injure the heart eventually manifest tamponade. Rapid bleeding into the pericardium favors clotting rather than defibrination.1 As pericardial fluid accumulates, a decrease in ventricular filling occurs, leading to a decrease in stroke volume. A compensatory rise in catecholamines leads to tachycardia and increased right heart filling pressures. The limits of right-sided distensibility are reached as the pericardium fills with blood, and the septum shifts toward the left side, further compromising left ventricular function. As little as 60–100 mL of blood in the pericardial sac can produce the clinical picture of tamponade.1 The rate of accumulation depends on the location of the wound. Because it has a thicker wall, wounds to the ventricle seal themselves more readily than wounds to the atrium. Patients with freely bleeding injuries to the coronary arteries present with rapid onset of tamponade combined with cardiac ischemia. The classic findings of Beck’s triad (muffled heart sounds, hypotension, and distended neck veins) are seen in a minority

Pericardial Injury Traumatic pericardial rupture is rare. Most patients with pericardial rupture do not survive transport to the hospital due to other associated injuries. The overall mortality of those who are treated at trauma centers with such injury remains as high as 64%.13 An overwhelming majority of these cases are diagnosed either intraoperatively or on autopsy.7 The clinical presentation of pericardial rupture, with cardiac herniation, can mimic that of pericardial tamponade with low cardiac output due to impaired venous return. When the heart returns to its normal position in the pericardium, venous return resumes. Positional hypotension is the hallmark of cardiac herniation due to pericardial rupture,7 whereas pericardial tamponade is associated with persistent hypotension until the pericardium is decompressed. Therefore, a high index of suspicion is helpful when evaluating polytrauma patients with unexplained positional hypotension.

■ Evaluation The diagnosis of heart injury requires a high index of suspicion. On initial presentation to the emergency center, airway, breathing, and circulation under the Advanced Trauma Life Support

CHAPTER CHAPTER 26 X

especially during dilation of the line tract, can lead to SVC and atrial perforations. Even optimal technique carries a discrete rate of iatrogenic injury secondary to central venous catheterization. Common sites of injury include the superior vena caval– atrial junction and the superior vena cava–innominate vein junction. These small perforations sometimes lead to a compensated cardiac tamponade. Drainage by pericardiocentesis is often unsuccessful, and evacuation via subxiphoid pericardial window or full median sternotomy is sometimes required. At operation, when the pericardium is opened, the site of injury has sometimes sealed and may be difficult to find. Complications from coronary catheterization including perforation of the coronary arteries, cardiac perforation, and aortic dissection can be catastrophic and require emergency surgical intervention.9 Other iatrogenic potential causes of cardiac injury include external and internal cardiac massage, and right ventricular injury during pericardiocentesis, endovascular interventions, transthoracic percutaneous interventions, and intracardiac injections.10

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Management of Specific Injuries

SECTION 3 X

protocol are evaluated and established.14 Two large-bore intravenous catheters are inserted, and blood is typed and crossmatched. The patient can be examined for Beck’s triad of muffled heart sounds, hypotension, and distended neck veins, as well as for pulsus paradoxus and Kussmaul’s sign. These findings suggest cardiac injury but are present in only 10% of patients with cardiac tamponade. The patient undergoes focused assessment with sonography for trauma (FAST). If the FAST demonstrates pericardial fluid in an unstable patient (systemic blood pressure 90 mm Hg), transfer to the operating room can then occur. Patients in extremis can require emergency department thoracotomy for resuscitation. The clear indications for emergency department thoracotomy by surgical personnel include the following:15

fluid.17 Ultrasonography in this setting is not intended to reach the precision of studies performed in the radiology or cardiology suite but is merely intended to determine the presence of abnormal fluid collections, which aids in surgical decision making.18 Ultrasonography is safe, portable, and expeditious and can be repeated as indicated. If performed by a trained surgeon, the FAST examination has a sensitivity of nearly 100% and a specificity of 97.3%.17 As the use of FAST evolves, and highspeed abdominal CT scans are readily available, the most universally agreed-upon indication for its use is evaluation for pericardial blood. To evaluate more subtle findings of blunt cardiac injury, such as wall motion, valvular, or septal abnormalities in the stable patient, formal transthoracic echocardiography (TTE) or transesophageal echocardiography (TEE) can be obtained.

1. Salvageable postinjury cardiac arrest (e.g., patients who have witnessed cardiac arrest with high likelihood of intrathoracic injury, particularly penetrating cardiac wounds) 2. Severe postinjury hypotension (i.e., systolic blood pressure 60 mm Hg) due to cardiac tamponade, air embolism, or thoracic hemorrhage

Echocardiography

If, after resuscitative thoracotomy, vital signs are regained, the patient is transferred to the operating room for definitive repair. Chest radiography is nonspecific, but can identify hemothorax or pneumothorax. Other potentially indicated examinations include computed tomography (CT) scan for trajectory and laparoscopy for diaphragm injury.

TTE can have a limited use in evaluating blunt cardiac trauma because most patients also have significant chest wall injury, thus rendering the test technically difficult to perform. Its major use is in diagnosing intrapericardial blood and tamponade physiology. In stable patients, TEE can be used to evaluate blunt cardiac injury. Cardiac septal defects and valvular insufficiency are readily diagnosed with TEE. Ventricular dysfunction can often mimic cardiac tamponade in its clinical presentation. Echocardiography is particularly useful in older patients with preexisting ventricular dysfunction. However, most blunt cardiac injuries identified by echocardiography rarely require acute treatment.

Subxiphoid Pericardial Window Electrocardiography In cases of blunt cardiac injury, conduction disturbances can occur. Sinus tachycardia is the most common rhythm disturbance seen. Other common disturbances include T wave and ST segment changes, sinus bradycardia, first- and seconddegree atrioventricular block, right bundle branch block, right bundle branch block with hemiblock, third-degree block, atrial fibrillation, premature ventricular contractions, ventricular tachycardia, and ventricular fibrillation. Thus, a screening 12-lead ECG can be helpful for evaluation.

Cardiac Enzymes Much has been written about the use of cardiac enzyme determinations in evaluating blunt cardiac injury. However, no relationship among serum assays and identification and prognosis of injury has been demonstrated with blunt cardiac injury.16 Therefore, cardiac enzyme assays are unhelpful unless one is evaluating concomitant coronary artery disease.16

Focused Assessment with Sonography for Trauma (FAST) Surgeons are increasingly performing ultrasonography for thoracic trauma. The FAST examination evaluates four anatomic windows for the presence of intra-abdominal or pericardial

Subxiphoid pericardial window has been performed both in the emergency department and in the operating room with the patient under either general or local anesthesia. In a prospective study, Meyer et al.19 compared the subxiphoid pericardial window with echocardiography in cases of penetrating heart injury and reported that the sensitivity and specificity of subxiphoid pericardial window were 100% and 92%, respectively, compared with 56% and 93% with echocardiography. They suggested that the difference in sensitivity may have been due to the presence of hemothorax, which can be confused with pericardial blood, or due to the fact that the blood had drained into the pleura.19 Although there has been significant controversy in the past with regard to the indication for subxiphoid pericardial window, recent enthusiasm for ultrasonographic evaluation has almost eliminated the role of subxiphoid pericardial window in the evaluation of cardiac trauma. It is almost never needed in the ED. Pericardiocentesis has had significant historical support, especially when the majority of penetrating cardiac wounds were produced by ice picks and the (surviving) patients arrived several hours and/or days after injury. In such instances there was a natural triage of the more severe cardiac injuries and the intrapericardial blood had become defibrinated and was easy to remove. Currently, many trauma surgeons discourage pericardiocentesis for acute trauma.10

Heart and Thoracic Vascular Injuries

489

■ Treatment Penetrating Injury

There are probably more injuries from pericardiocentesis than diagnoses acutely. Indications for use of pericardiocentesis may apply in the case of iatrogenic injury caused by cardiac catheterization, at which time immediate decompression of the tamponade may be lifesaving, or in the trauma setting when a surgeon is not available. For the most part, as a diagnostic tool it has been replaced by the FAST examination. Pericardial exploration is sometimes used via a transdiaphragmatic route during laparotomy to evaluate the pericardium (Fig. 26-1).

FIGURE 26-2 Left anterior thoracotomy (extension across the sternum if required). (Copyright © Baylor College of Medicine, 2005.)

CHAPTER CHAPTER 26 X

FIGURE 26-1 Transdiaphragmatic exploration of the pericardium during laparotomy. (Copyright © Baylor College of Medicine.)

Only a small subset of patients with significant cardiac injury reaches the emergency department, and expeditious transport to an appropriate facility is important to survival. Transport times of less than 5 minutes and successful endotracheal intubation are positive factors for survival when the patient suffers a pulseless cardiac injury.20 Definitive treatment involves surgical exposure through an anterior thoracotomy (Fig. 26-2) or median sternotomy. The mainstays of treatment are relief of tamponade and hemorrhage control. Then reestablishment of effective coronary perfusion is pursued by appropriate resuscitation. Exposure of the heart is accomplished via a left anterolateral thoracotomy, which allows access to the pericardium and heart and exposure for aortic cross-clamping if necessary. This incision can be extended across the sternum to gain access to the right side of the chest and for better exposure of the right atrium. Manual access to the right hemithorax from the left side of the chest can be achieved via the anterior mediastinum by blunt dissection. This allows rapid evaluation of the right side of the chest for major injuries without transecting the sternum or placing a separate chest tube. Once the left pleural space is entered, the lung can be retracted to allow clamping of the descending thoracic aorta. The amount of blood present in the left chest suggests whether hemorrhage or tamponade is the primary issue. The pericardium anterior to the phrenic nerve is opened, injuries are identified, and repair is performed. In selected cases, particularly for small stab wounds to the precordium, median sternotomy can be used. This allows exposure of the anterior structures of the heart, but limits access

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Management of Specific Injuries

SECTION 3 X A

C

B

D

FIGURE 26-3 Temporary techniques to control bleeding. (A) Finger occlusion; (B) partial occluding clamp; (C) Foley balloon catheter; (D) skin staples. (Copyright © Baylor College of Medicine, 2005.)

to the posterior mediastinal structures and descending thoracic aorta for cross-clamping. Cardiorrhaphy should be carefully performed. Poor technique can result in enlargement of the lacerations or injury to the coronary arteries. If the initial treating physician is uncomfortable with the suturing technique, digital pressure can be applied until an experienced surgeon arrives. Other techniques that have been described include the use of a Foley balloon catheter or a skin stapler (Fig. 26-3). Injuries adjacent to coronary arteries can be managed by placing the sutures deep to the artery (Fig. 26-4). Mechanical support or cardiopulmonary bypass is very uncommonly required in the acute setting.4 For multiple fragments in stable patients, diagnosis in the past was pursued with radiographs in two projections, fluoroscopy, angiography, or echocardiography. Recently, the

multidetector CT scan can be used to diagnose and locate these fragments. The full-body topogram scan can identify all missiles, and then the cross-sectional images can be directed to precisely locate them. Trajectories can be ascertained. Treatment of retained missiles is individualized. Removal is recommended for intracardiac missiles that are left sided, larger than 1–2 cm, rough in shape, or that produce symptoms. Although a direct approach, either with or without cardiopulmonary bypass, has been advocated, a large percentage of right-sided foreign bodies can now be removed by endovascular techniques.

Blunt Cardiac Injury Much debate and discussion has occurred about the clinical relevance of “cardiac contusion.” Most trauma surgeons suggest

Heart and Thoracic Vascular Injuries

that this diagnosis should be eliminated because it does not affect treatment strategies. The majority of these patients seen are normotensive patients with normal initial ECG and suspected blunt cardiac injury. These cases are managed in observation units, with no expected clinical significance. Patients with an abnormal ECG are admitted for monitoring and treated accordingly. Patients who present in cardiogenic shock are evaluated for a structural injury, which is then addressed.12

■ Results Many factors determine survival in patients with traumatic cardiac injury including mechanism of injury, location of injury, associated injuries, coronary artery and valvular involvement, presence of tamponade, length of prehospital transport, requirement for resuscitative thoracotomy, and experience of the trauma team. The overall hospital survival rate for patients with penetrating heart injuries ranges from 30% to 90%. The survival rate for patients with stab wounds is 70–80%, whereas survival after gunshot wounds ranges between 30% and 40%. Cardiac rupture has a worse prognosis than penetrating injuries to the heart, with a survival rate of approximately 20%.

Complex Cardiac Injuries Complex cardiac injuries include coronary artery injury, valvular apparatus injury (annulus, papillary muscles, and chordae tendineae), intracardiac fistulas, and delayed tamponade. These delayed sequelae have been reported to have a broad incidence (4–56%), depending on the definition. Coronary artery injury is a rare injury, occurring in 5–9% of patients with cardiac

TABLE 26-2 Dysrhythmias Associated with Cardiac Injury Penetrating cardiac injury Sinus/supraventricular tachycardia ST segment changes associated with ischemia Supraventricular tachycardia Ventricular tachycardia/fibrillation Blunt cardiac injury Sinus tachycardia ST segment, T wave abnormalities Atrioventricular conduction defects, bradycardia Ventricular tachycardia/fibrillation Electrical injury Sinus tachycardia ST segment, T wave abnormalities Conduction/bundle branch delay Axis deviation Prolonged QT intervals Paroxysmal supraventricular tachycardia Atrial fibrillation Ventricular tachycardia, fibrillation Asystole (lightning strike)

CHAPTER CHAPTER 26 X

FIGURE 26-4 Injuries adjacent to coronary arteries can be addressed by placing sutures deep, avoiding injury to the artery. (Copyright © Baylor College of Medicine, 2005.)

injuries, with a 69% mortality rate.4 A coronary artery injury is most often controlled by simple ligation, but bypass grafting using a saphenous vein may be required for proximal left anterior descending or right coronary artery injuries (with cardiopulmonary bypass).4 Off-pump bypass can theoretically be used for cases of these injuries in the highly unlikely event that the patient is hemodynamically stable. Valvular apparatus injury is rare (0.2–9%) and can occur with both blunt and penetrating trauma.4,5 The aortic valve is most frequently injured, followed by the mitral and tricuspid valves, though most victims of aortic valve injuries likely die at the scene. These injuries are usually identified postoperatively after the initial cardiorrhaphy and resuscitation have been performed. Timing of repair depends on the patient’s condition. If severe cardiac dysfunction exists at the time of the initial operation, and valvular injury is identified, immediate valve repair or replacement may be required; otherwise, delayed repair is more commonly advised.8 Intracardiac fistulas include ventricular septal defects, atrial septal defects, and atrioventricular fistulas, with an incidence of 1.9% among cardiac injuries. The management depends on symptoms and degree of cardiac dysfunction, with only a minority of these patients requiring repair.4 These injuries are also usually identified after primary repair is accomplished, and they can be repaired after the patient has recovered from the original and associated injuries. Echocardiography should be obtained before repair so that specific anatomic sites of injury and incision planning can be accomplished. Dysrhythmias can occur as a result of blunt injury, ischemia, or electrolyte abnormalities and are addressed according to the injury (Table 26-2). Delayed pericardial tamponade is rare. It can occur as early as 1 hour after initial operation and to days after the injury.

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■ Follow-Up SECTION 3 X

As discussed above, secondary sequelae in survivors of cardiac trauma include valvular abnormalities and intracardiac fistulas.4,19,21 Early postoperative clinical examination and ECG findings are unreliable.4,21 Thus, echocardiography is recommended during the initial hospitalization in all patients to identify occult injury and establish a baseline study. Because the incidence of late sequelae can be as high as 56%, follow-up echocardiography 3–4 weeks after injury has been recommended by some.19,21

THORACIC GREAT VESSEL INJURY Injuries to the thoracic great vessels—the aorta and its brachiocephalic branches, the pulmonary arteries and veins, the superior and intrathoracic inferior vena cava, and the innominate and azygos veins—occur following both blunt and penetrating trauma. Exsanguinating hemorrhage, the primary acute manifestation, also occurs in the chronic setting when the injured great vessel forms a fistula involving an adjacent structure or when a post-traumatic pseudoaneurysm ruptures. Current knowledge regarding the treatment of injured thoracic great vessels has been derived primarily from experience with civilian injuries. Great vessel injuries have been repaired with increasing frequency, a phenomenon that has paralleled the development of techniques for elective surgery of the thoracic aorta and its major branches. A detailed understanding of normal and variant anatomy and structural relationships is important for the surgeon and any one who is a consultant to the surgeon in the evaluation of imaging studies. Venous anomalies are infrequent with the most common being absence of the left innominate vein and persistent left superior vena cava. Thoracic aortic arch anomalies are relatively common (Table 26-3). Knowledge of such anomalies is essential for both open and catheter-based therapies.

TABLE 26-3 Thoracic Aortic Anomalies Common origin of innominate and left carotid arteries (“bovine arch”) Ductus diverticulum Persistent left ductus arteriosus Aberrant takeoff of the right subclavian artery from the descending thoracic aorta Dextroposition of the thoracic aorta Coarctation of the thoracic aorta Origin of left vertebral artery off the aortic arch Pseudocoarction of the thoracic aorta (“kinked aorta”) Double aortic arch Right ductus arteriosus Persistent truncus arteriosus Cervical aortic arch (persistent complete third aortic arch) Absence of the internal carotid artery Cardio-aortic fistula

ETIOLOGY AND PATHOPHYSIOLOGY More than 90% of thoracic great vessel injuries are due to penetrating trauma: gunshot, fragments, and stab wounds or therapeutic misadventures.22 Iatrogenic lacerations of various thoracic great vessels, including the arch of the aorta, are reported complications of percutaneous central venous catheter placement. The percutaneous placement of “trocar” chest tubes has caused injuries to the intercostal arteries and major pulmonary and mediastinal vessels. Intra-aortic cardiac assist balloons can produce injury to the thoracic aorta. During emergency center resuscitative thoracotomy, the aorta may be injured during clamping if a crushing (nonvascular) clamp is used. Overinflation or migration of the Swan–Ganz balloon has produced iatrogenic injuries to pulmonary artery branches with resultant fatal hemoptysis; therefore, once a linear relationship has been established between the pulmonary artery diastolic pressure and the pulmonary capillary wedge pressure, further “wedging” may be unnecessary. Self-expanding metal stents have recently produced perforations of the aorta and innominate artery following placement into the esophagus and trachea, respectively.23 The great vessels particularly susceptible to injury from blunt trauma include the innominate artery origin, pulmonary veins, vena cava, and, most commonly, the descending thoracic aorta.24 Aortic injuries have caused or contributed to 10–15% of deaths following motor vehicle accidents for nearly 50 years. These injuries usually involve the proximal descending aorta (54–65% of cases), but often involve other segments—that is, the ascending aorta or transverse aortic arch (10–14%), the mid- or distal descending thoracic aorta (12%), or multiple sites (13–18%). The postulated mechanisms of blunt great vessel injury include (1) shear forces caused by relative mobility of a portion of the vessel adjacent to a fixed portion, (2) compression of the vessel between bony structures, and (3) profound intraluminal hypertension during the traumatic event. The atrial attachments of the pulmonary veins and vena cava and the fixation of the descending thoracic aorta at the ligamentum arteriosum and diaphragm enhance their susceptibility to blunt rupture by the first mechanism. At its origin, the innominate artery may be “pinched” between the sternum and the vertebrae during sternal impact. Blunt aortic injuries may be partial thickness—histologically similar to the intimal tear in aortic dissection—but most commonly are full thickness and therefore equivalent to a ruptured aortic aneurysm that is contained by surrounding tissues. The histopathological similarities between aortic injuries and nontraumatic aortic catastrophes suggest that similar therapeutic approaches be employed. Therefore, in hemodynamically stable patients with blunt aortic injuries, the concepts of permissive hypovolemia and minimization of arterial pressure impulse (dP/dT)—which are widely accepted in the treatment of aortic dissection and aneurysm rupture—should be considered. In opposition to patients with aortic intimal disease where the adventitia is the restraining barrier, with blunt injury to the descending thoracic aorta, it is the intact parietal pleura (not the adventitia) that contains the hematoma and prevents a massive hemothorax. True traumatic aortic dissection, with a longitudinal separation of the media extending along the length of the aorta, is extremely rare.25 The use of the term “dissection” in the setting

Heart and Thoracic Vascular Injuries

493

TABLE 26-4 Groups of Patients with Thoracic Aortic Injury

3

Description Dead/dying at scene Unstable during transport Stable

Time to Diagnosis 60 min 1–6 h

Location of Death Scene/EMS EMS/EC

Mortality (%) 100 96

Cause of Death Bleeding Multisystem trauma

4–18 h

ICU

5–30

CNS injury

of aortic trauma should be equally rare, being used only in a few appropriate cases. Similarly, the terms “aortic transection” and “blunt aortic rupture” should be used only when describing specific injuries, that is, full-thickness lacerations involving either the entire or partial circumference, respectively. Increasingly, patients with thoracic great vessel injury have associated head, abdominal, and extremity injury. Often preexisting medical conditions are present, such as diabetes, hypertension, coronary artery disease, or cirrhosis. These patients are also on a large variety of medications, often aspirin, warfarin, or other platelet inhibitors. These interfere with the clotting mechanism and adaptations in treatment must be made.

PATIENT CLASSIFICATION Three distinctly different groups of patients with thoracic aortic trauma exist (Table 26-4). The epidemiology of aortic injury is changing, due to rapid accident notification and emergency medical system (EMS) transport. The mortality statistics reveal that those whose cause of death is exsanguinating hemorrhage almost all die within the first 0–2 hours of injury. Those who die in the emergency department, operating room, or intensive care unit (ICU) within 2–4 hours of injury often have extensive multisystem injury with hemorrhage often being from sites other than the thoracic aorta. Hemodynamically stable patients who are subsequently found to have aortic injury but who die most often have central nervous system injury as the cause of their injury. It is this later group in whom the diagnosis is made by the trauma team, and therefore amenable to appropriate screening, diagnostic, and therapeutic considerations.

INITIAL EVALUATION ■ Prehospital Management Interventions often performed by paramedics during transport include judicious intravenous fluid administration and endotracheal intubation when indicated.26 Though seldom seen, pneumatic anti-shock garment (PAST) application in patients with thoracic great vessel injuries statistically increases the chance of death in both adult and pediatric populations.27 The PAST elevate blood pressure by increasing afterload and are equivalent to placing a cross-clamp distal to the potential injury—a clearly counterproductive maneuver. Similarly, in patients with acute thoracic great vessel injuries, excessive fluid resuscitation with the goal of increasing blood pressure to

normal or supernormal levels increases the incidence of mortality, ARDS, and other postoperative complications.28

■ Emergency Center Evaluation History In cases of penetrating thoracic trauma, information regarding the length of a knife, the firearm type and number of rounds fired, and the patient’s distance from the firearm is sought from the patient or accompanying persons. Unfortunately, this is frequently unavailable and unreliable. Although the head-on motor vehicle collision is often considered the typical mechanism for blunt aortic injury, recent epidemiological data reveal that up to 50% of cases occur following side-impact collisions. Blunt aortic injuries have also been reported following equestrian accidents, blast injuries, auto-pedestrian accidents, crush injuries, and falls from heights of 30 ft or more.29 In addition to information involving the mechanism of injury, the emergency transport personnel can provide medical information important in evaluating the potential for a thoracic great vessel injury, such as the amount of hemorrhage at the scene, the extent and location of damage to the vehicle, any history of intermittent paralysis following the accident, and hemodynamic instability during transport.

Physical Examination On arrival to the emergency center, each patient is given a rapid, thorough examination. External signs of penetrating or blunt trauma are noted. With an intrapericardial vascular injury, the classic signs of pericardial tamponade (distended neck veins, pulsus paradoxus, muffled heart sounds, elevated central venous pressure) may be present but not uniformly. Clinical findings associated with thoracic great vessel injury include: 1. Hypotension 2. Upper extremity hypertension 3. Unequal blood pressures or pulses in the extremities (upper extremity from innominate or subclavian injury, or lower extremity from pseudocoarctation syndrome) 4. External evidence of major chest trauma (e.g., steering wheel imprint on chest) 5. Expanding hematoma at the thoracic outlet 6. Intrascapular murmur 7. Palpable fracture of the sternum 8. Palpable fracture of the thoracic spine 9. Left flail chest

CHAPTER CHAPTER 26 X

Group 1 2

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Management of Specific Injuries

Chest Radiography

SECTION 3 X

On arrival, a supine anteroposterior 36-in chest radiograph should be performed, ideally in the emergency center and not in a distant radiologic suite. Emergency physicians, radiologists, and surgeons should develop diagnostic experience viewing supine portable chest x-rays as many trauma patients are hemodynamically unstable or have suspected spinal injuries, making an “upright” 72-in posterior–anterior chest radiograph unsafe to obtain. In many cases of great vessel injury, the radiologic findings are sufficient to warrant immediate arteriography or direct transport to the operating room. For penetrating injuries, it is helpful to place radiopaque markers to identify the entrance and exit sites. Radiographic findings that suggest penetrating thoracic great vessel injury include: 1. Large hemothorax 2. Foreign bodies (bullets or shrapnel) or their trajectories in proximity to the great vessels 3. A foreign body out of focus with respect to the remaining radiograph, which may indicate its intracardiac location (Fig. 26-5)

4. A trajectory with a confusing course, which may indicate a migrating intravascular bullet (Fig. 26-6) 5. “A missing” missile in a patient with a gunshot wound to the chest, suggesting distal embolization in the arterial tree Several radiographic findings have been associated with blunt injuries of the descending thoracic aorta (Table 26-5). The most reliable of these signs is the loss or “double shadowing” of the aortic knob contour, creating a “funny-looking mediastinum.” Mediastinal widening at the thoracic outlet and leftward tracheal deviation are suggestive of innominate artery injury. These signs are secondary to a mediastinal hematoma, which is an indirect sign of thoracic great vessel injury. The presence of any of these signs is a positive screening test and not a diagnosis. Missile wounds that appear to traverse the mediastinum create concern regarding injury to the heart, esophagus, trachea, spinal cord, or major vasculature. Should cardiac or vascular injury occur, tamponade or major hemorrhage is usually obvious. The newer multidetector CT is often used to demonstrate missile trajectory and aid the surgeon in a decision regarding directed thoracotomy or endoscopy.

■ Initial Treatment and Screening Emergency Center Thoracotomy Emergency center thoracotomy in patients presenting with signs of life and hemodynamic collapse may reveal injuries to major thoracic vessels. These injuries require temporizing maneuvers that gain rapid control of bleeding, allowing resuscitation, and subsequent transfer to the operating room for definitive repair.30 Subclavian vessel injuries, for example, can be controlled by packing, clamping at the thoracic apex, or inserting intravascular balloon catheters. Major hemorrhage from the pulmonary hilum can be temporally managed by cross-clamping the entire hilum proximally or twisting the lung 180° after releasing the inferior pulmonary ligament.

Tube Thoracostomy When the chest radiograph indicates a significant hemothorax, the chest tube can be connected to a repository for autotransfusion. An initial “rush” of a large volume of blood (1,500 mL) or significant ongoing hemorrhage (200–250 mL/h) may indicate great vessel injury, and is considered an indication for urgent thoracotomy.

Intravenous Access and Fluid Administration

FIGURE 26-5 Lateral chest x-ray demonstrating an “out of focus” bullet over the cardiac silhouette. The bullet was lodged in the wall of the right ventricle.

Currently, unless a patient is in extremis, large-bore intravenous portals are obtained but high-volume resuscitation avoided, until the time of an operation. If a subclavian venous catheter is required in a patient with a suspected subclavian vascular injury, the contralateral side should be used for cannulation. The treatment of severe shock should include blood transfusion. However, rapid infusions of excessive volumes of either blood or crystalloid solutions prior to operation may increase the blood pressure to a point that a protective soft perivascular

Heart and Thoracic Vascular Injuries

495

CHAPTER CHAPTER 26 X

FIGURE 26-6 Series of x-rays demonstrating the entrance site of a bullet in the left groin. The bullet embolized to the right pulmonary artery, as confirmed by arteriography.

TABLE 26-5 Radiographic Clues that should Prompt Suspicion of a Thoracic Great Vessel Injury Fractures • Sternum • Scapula • Multiple left ribs • Clavicle in multisystem injured patients • (?) First ribs Mediastinal clues • Obliteration/double shadow of aortic knob contour • Widening of the mediastinum 8 cm • Depression of the left mainstem bronchus 140° from trachea • Loss of perivertebral pleural stripe • Calcium layering at aortic knob • “Funny-looking” mediastinum • Deviation of nasogastric tube in the esophagus • Lateral displacement of the trachea Lateral chest x-ray • Anterior displacement of the trachea • Loss of the aortic/pulmonary window Other findings • Apical pleural hematoma • Massive left hemothorax • Obvious blunt injury to the diaphragm

clot is “blown out” and fatal exsanguinating hemorrhage ensues. The principles of permitting moderate hypotension (systolic blood pressure of 60–90 mm Hg) and limiting fluid administration until achieving operative control of bleeding are cornerstones in the management of rupturing abdominal aortic aneurysms and equally apply to acute thoracic great vessel injury. Aggressive preoperative fluid resuscitation increases postoperative respiratory complications and may contribute to an increased mortality when compared to fluid restriction.28 With both penetrating and blunt chest trauma, associated pulmonary contusions are common and provide an additional rationale for limiting the infusion of preoperative crystalloid solutions.

Impulse Therapy/Beta-Blockade The pharmacological reduction of dP/dT has remained a critical component of the treatment of aortic dissection since its original description by Wheat et al. in 1965.31 Based on the similarity between aortic dissection and blunt aortic injury, this principle was first applied to dP/dT reduction to patients with blunt aortic injury in 1970. Subsequent reports have described using beta-blockers in hemodynamically stable patients who had proven blunt aortic injuries but required a delay in definitive operative treatment.32 Some centers routinely begin betablockade therapy as soon as an aortic injury is suspected—prior to obtaining diagnostic studies as an attempt to reduce the risk of fatal rupture during the interval between presentation and confirmation of the diagnosis. While retrospective studies

496

Management of Specific Injuries suggest that it is safe, no prospective studies have demonstrated either the safety or efficacy of such treatment.

SECTION 3 X

Screening/Planning CT Scan for Thoracic Vascular Injury Multidetector CT scan of the chest is recommended by many radiologists as a screening test for mediastinal hematoma usually associated with aortic injury.33 In addition, various other aortic wall and intraluminal findings suggest aortic injury on the CT scan. Very often, the initial chest x-ray has already demonstrated findings suggestive of mediastinal hematoma. Some clinicians require the additional screening CT scan to substantiate a request for a diagnostic arteriogram. Although an increasing number of surgeons and radiologists have developed a “skill” and comfort level in performing an operation based on the CT findings alone, many surgeons use the arteriographic roadmap to determine the specific injury and any unexpected vascular anomalies. This also occurs when a confirmatory aortogram is obtained prior to thoracic endograft deployment. It is interesting to thus note in a 2008 report by Demetriades et al. of a multicenter study on blunt aorta injuries that CT was used as the primary “diagnostic” modality in 93% of patients, but as the majority of patients underwent endograft repair an aortogram was usually obtained.34 As resolution and experience in using CT to plan operations increases, it is important to assure that the same information regarding extent of injury, anatomy, and aberrant branches, as well as location of injury, is obtainable. Even when radiologists and surgeons have utilized CT scans as a diagnostic test, this test has primarily been used for injuries of the proximal descending thoracic aorta. Motion artifact in the proximal ascending aorta can be difficult to interpret on CT. CT scan gated to cardiac motion may better delineate the ascending aorta and provide increased resolution.35 The diagnostic controversy regarding CT for thoracic injuries may lie in the technology. CT scan technology has evolved at a very rapid rate. It is important to understand that a 4-channel 16-detector machine has different capabilities than a 64-channel/detector machine. With increasing technical complexity, the protocols for obtaining the CT examination such as number and spacing of detectors, channels, pitch, slice thickness, contrast injection, and timing can significantly alter the information obtained. The raw CT data are then manipulated in a “postprocessing” function to deliver the final images. The previous static CT film images are now read on digital displays where a knowledgeable observer can further manipulate the image. Three-dimensional reconstructions, while impressive to view, take a lot of processing resources and have not added a lot to the evaluation of blunt aortic injuries (Fig. 26-7). Multiplanar reformatting is a postprocessing mode where the CT slice can be angled and positioned to best display the pathology. This is most useful for the evaluation of blunt aortic injury when the CT slice/virtual gantry is aligned with the curvature of the ascending/arch/descending thoracic aorta and the slices can traverse through the aorta (Fig. 26-8). This is very helpful not only for diagnosis but also for planning, selecting device,

FIGURE 26-7 A three-dimensional reconstruction of the CT in a patient with an injury to the aortic isthmus showing the thoracic endograft deployed.

and evaluating landing/seal zones for the device. Centerline flow analysis displays the aorta as a straight line along its center allowing precise measurements of diameter and accurate measurements of seal zones/landing zones for planning (Fig. 26-9). It is our observation and a local postulate that as

FIGURE 26-8 Multiplanar reformatting display of a typical injury through the descending thoracic aorta distal to the left subclavian artery. This allows the viewer to align the slice along the axis of the aorta. The small cube in the lower right corner represents the orientation.

Heart and Thoracic Vascular Injuries

497

CHAPTER CHAPTER 26 X FIGURE 26-9 Centerline flow analysis of a patient with injury at the aortic isthmus. This view electronically straightens the aorta along the centerline axis of flow allowing accurate measurements regarding landing zones/seal areas and the device length to the determined. This analysis shows that by covering the left subclavian artery, a 15- to 16-mm proximal seal area is available and a 35-mm area will need to be covered. This display also shows the average aortic diameter to be 19 mm. This can be useful to plan difficult cases for which the landing zones/seal areas are difficult to precisely determine.

the technology progresses, if the clinician directly caring for the patient cannot manipulate and interpret the images himself or herself, much useful information as well as artifacts may not be appreciated. This may explain a lot of the confusion regarding multiple conflicting reports and opinions on the utility of CT for screening or diagnosis. With appropriate scanners, protocols, processing, display, and experience, CT potentially could yield more information than catheter angiography.

If a mediastinal hematoma is visualized on CT, formal aortography is usually obtained to specifically determine the site(s) of the injury(s) and to identify any vascular anomalies that require modifications in the operative approach. This is also uniformly done as part of the process immediately prior to placing an aortic endograft. Decision trees can be constructed to aid the surgeon in reaching a diagnosis and treating a patient with aortic injury (Fig. 26-10). As experience is developed with catheter-based methods, however, the CT scan is also helpful for

498

Management of Specific Injuries A

Major Thoracic Injury Potential Thoracic Vascular Injury

SECTION 3 X

Screening Techniques (History, Physical Examination, Chest X-Ray, FAST, Chest CT)

Patient in Extremis

Hypotensive (Unstable)

Normotensive (Stable)

Diagnostic Techniques (Tube thoracostomy, FAST, Arteriogram) Vascular Injury

Massive Hemothorax

Hemopericardium

Immediate Thoracotomy

Plan Therapy Endovascular Plan position, access, imaging, control and devices

Open Procedure Plan Position & Incision Reconstruct

B

Blunt Chest Injury Potential for Thoracic Aortic Injury Suggestive History or Physical Examination Afterload reduction (unless low BP or patient “unstable”) SCREENING Chest X-Ray/CT with appropriate protocol “Normal”

Strongly Suggestive/Equivocal

Treat Other Injuries AORTOGRAPHY

Positive

Negative

Trivial

Treatment

Treat Other Injuries

Timely Repeated Studies

Immediate Open

Delayed

Endovascular

FIGURE 26-10 (A) Algorithm for an approach to patients with suspected thoracic vascular injury. (B) Algorithm for the evaluation and treatment of a patient suspected of having a blunt injury to the thoracic aorta.

Heart and Thoracic Vascular Injuries

■ Diagnostic Studies Catheter Arteriography In penetrating thoracic trauma, catheter angiography is indicated for suspected aortic, innominate, carotid, or subclavian arterial injuries. Different thoracic incisions are required for

proximal and distal control of each of these vessels. Arteriography, therefore, is essential for localizing the injury and planning the appropriate incision. Proximity of a missile trajectory to the brachiocephalic vessels, even without any physical findings of vascular injury, can be an indication for arteriography. Although aortography may also be useful in hemodynamically stable patients with suspected penetrating aortic injuries, its limitations in this setting must be recognized. A “negative” aortogram may convey a false sense of security if the laceration has temporarily “sealed off ” or if the column of aortic contrast overlies a small area of extravasation (Fig. 26-11). Therefore, an effort must be made to obtain views tangential to possible injuries (Figs. 26-12 and 26-13).

E

A A

B B B

C

D D

FIGURE 26-11 Misdiagnosis by aortography. (A) Chest radiograph of a patient with a tiny puncture wound from a Philips screwdriver at the left sternal border in the second intercostal space. The patient arrived in the emergency room 30 minutes after being wounded and had stable vital signs for the following 48 hours. (B) Anteroposterior projection of the aortogram was interpreted as showing no injury. (C) Left anterior oblique projection of the aortogram was also interpreted as showing no injury. (D) Near-lateral projection of the aortogram was also read as normal by staff radiologist. (E) Subtraction aortography in the lateral projection demonstrates tiny outpouching of the thoracic aorta anteriorly at the base of the innominate artery and posteriorly on the undersurface of the transverse aortic arch (arrows). Penetrating injury of the transverse aortic arch was confirmed intraoperatively. (Reproduced with permission from Mattox KL. Approaches to trauma involving the major vessels of the thorax. Surg Clin North Am. 1989;69:83. © Elsevier.)

CHAPTER CHAPTER 26 X

preoperative planning for stent graft repair and evaluation for access. TEE has added little in the screening or diagnosis of thoracic aortic injury. Magnetic resonance angiography (MRI) can generate similarly detailed information; however, its application in these potentially unstable trauma patients is not currently practical.

499

500

Management of Specific Injuries

SECTION 3 X

seemingly innocuous mechanisms—including low-speed automobile crashes (10 mph) with airbag deployment and intrascapular back blows used to dislodge an esophageal foreign body—have been reported. Additionally, 50% of patients with thoracic vascular injuries from blunt trauma present without any external physical signs of injury, and 7% of patients with blunt injury to the aorta and brachiocephalic arteries have a normalappearing mediastinum on admission chest radiography.

TREATMENT OPTIONS ■ Nonoperative Management Nonoperative management of blunt aortic injuries should be considered in patients who are unlikely to benefit from an immediate repair:

FIGURE 26-12 Plain chest x-ray of a patient with a penetrating wound of the ascending aorta.

Following blunt trauma, the potential for thoracic great vessel injury—and, therefore, the need to proceed with aortography—is determined based on (1) the mechanism of injury, (2) physical examination, (3) the standard chest radiograph, or (4) a screening CT scan. As each of these factors has inherent limitations, all must be considered in concert. Traumatic aortic ruptures following

1. Severe head injury 2. Risk factors for infection: • Major burns • Sepsis • Heavily contaminated wounds 3. Severe multisystem trauma with hemodynamic instability and/or poor physiologic reserve In such instances, nonoperative management is actually a purposeful delay in operation that attempts to achieve physiologic optimization and improve the outcome of repair. Nonoperative management has also been used successfully in cases of “nonthreatening” aortic lesions, for example, minor intimal defects and small pseudoaneurysms. Close observation without operation is similarly reasonable for small intimal flaps involving the brachiocephalic arteries in asymptomatic patients, as many such lesions will heal spontaneously. With the increased use of endograft repair, as well as patients with increasing number of associated injuries, blunt aortic injuries are often definitively repaired greater than 24 hours after presentation when the patient is optimized. In a report by Demetriades et al. of a multicenter study, delayed repair (24 hours) of stable blunt thoracic aortic injury was associated with improved survival, but also a longer length of ICU stay and a higher complication rate.32 Although apparent minor vascular injuries may resolve or stabilize, their long-term natural history remains uncertain. Life-threatening complications of great vessel injuries—including rupture and fistulization with severe hemorrhage—occurring more than 20 years after injury are not uncommon.29 Therefore, careful follow-up, including serial imaging studies, is a critical component of nonoperative management. Avoiding hypertension and the use of impulse control agents are also recommended when patients with aortic injuries are treated nonoperatively.

■ Endograft Repair FIGURE 26-13 Aortogram of the patient in Fig. 26-9 demonstrating no apparent injury in the anteroposterior projection, but revealing a defect in the anterior aortic wall on the left anterior oblique projection (arrows).

From a technical standpoint, a chronic post-traumatic false aneurysm of the descending thoracic aorta should be a logical indication for placement of an aortic endograft. Beginning in the late 1990s, single case reports and small series of thoracic

Heart and Thoracic Vascular Injuries

TABLE 26-6 Comparison of Open Versus Endovascular Treatment of Blunt Thoracic Aortic Injury

Mortality (%) Average mortality (%) Paraplegia (%) Average paraplegia Complications

Open Operations 0–55 13

Endograft Repair 0–12 3.8

0–20 10%

1 1 out of 239 cases

ARDS CNS problems Neurologic

LSCA occlusion Graft compression Entry site problems

ARDS, adult respiratory distress syndrome; CNS, central nervous system; LSCA, left subclavian artery.

as available smaller sizes, conformation of the endograft to the curvature of the arch, tailored/branched grafts, and improved delivery systems. The short-term and midterm follow-up have seemed favorable for endovascular stenting.40 However, the long-term fate of the endograft as the aorta dilates with age is yet unanswered. With massive changes in the presenting patient population, technology related to diagnosis and imaging, and engineering improvements in endograft technology, the timing, diagnosis, and management of blunt aortic injuries have been dynamic. The report of Demetriades et al. of the AAST multicenter study with its two follow-up manuscripts documented a shift in original diagnostic modality to CT and a shift to endovascular repair with a decrease in mortality and paraplegia but an increase in device-related and access complications and concern for long-term sequelae.32,34,39 These reports have been the most comprehensive to date, and are a template to track results as the technology evolves. Studies documenting the rate of aortic dilation after endograft repair are being reported41 and will be important for assessing the long-term durability of endograft repair. The technology continues to evolve and improve on addressing the above-mentioned anatomic size challenges and capabilities of endografts available to treat acute injuries to the thoracic aorta. It is clear that the treatment for a specific patient will continue to be individualized, and multiple approaches (nonoperative/delayed/open/endograft) will continue to be needed.32,34,39

■ Surgical Repair Indications for urgent transfer to the operating room for thoracotomy include hemodynamic instability, significant hemorrhage from chest tubes, and radiographic evidence of a rapidly expanding mediastinal hematoma (Fig. 26-14). In the preoperative phase, whenever possible, patients and their families should be made aware of the potential for neurologic complications—paraplegia, stroke, and brachial plexus injuries—following surgical reconstruction of thoracic great

CHAPTER CHAPTER 26 X

endografting for acute transections of the proximal descending thoracic aorta were reported. These were often custom devices using aortic or iliac artery extenders.36 Not infrequently the left subclavian artery was occluded by the endograft, with subsequent left carotid–subclavian bypass in some cases. Iatrogenic injury to the access site of the femoral or iliac artery was occasionally reported. No reports exist for repair of thoracic ascending/arch/aortic injury and have focused on the proximal descending thoracic aorta. In the United States three commercial devices have been approved by the Food and Drug Administration for thoracic aortic aneurysms by the end of 2008. These devices are FDA approved for the treatment of thoracic aneurysms and are used off-label in patients with traumatic injuries to the descending thoracic aorta. The average diameter of the thoracic aorta among patients with aortic tears is 19.3 cm. The manufacturers recommend 15–20% oversizing. Thus, these thoracic devices need an aorta diameter of greater than 18 mm. Smaller aortas treated with endografts require custom or off-label abdominal devices. With greater oversizing, compression and infolding have been reported and infolding has resulted in a devastating thrombosis of the aorta. Over 85% of descending thoracic aortic tears are less than 1 cm from the orifice of the subclavian artery. A sealing distance on either side of the pathology of 2 cm is recommended. Additionally a young patient’s aorta has significant angulation in the potential proximal seal zone that can cause leading edge “beaking” and infolding. Thus, consideration for covering the left subclavian orifice occurs and can be influenced by the intracerebral and spinal circulation. Engineering challenges still exist regarding the existing approved thoracic aortic endografts when used in young trauma patients. Preoperative planning involves a carefully protocolized CT angiogram of chest/abdomen and pelvis, and delineating the size, tortuosity, and angulation of arterial vessels for determination of appropriateness or feasibility of introducer sheaths and devices capable of covering the aortic injury. Access can often be a problem in young patients, especially females, with small iliac/femoral arteries that prohibit safe introducer sheath placement due to small size mismatch. Currently the smallest commercially available thoracic endografts require a 7- to 8-mm external iliac artery. Direct introduction or sewing of an extra-anatomic graft to the common iliac artery or aorta to allow deployment of endovascular stent grafts may be necessary in such difficult cases. It should be noted that the majority of morbidity/mortality from thoracic endograft repair is from disruption of iliac vessels during endograft placement. In a composite report using a variety of approved and customized endografts, 239 patients have been reported to have been treated for blunt injury to the proximal descending thoracic aorta (Table 26-6).37 Many other small series or single case reports exist. Among the 239 cases there were 9 deaths (3.8%), and 1 paraplegia (0.5%). Even with potential selection bias, the lower mortality and almost nonexistent paraplegia rate make consideration for endovascular repair very compelling.38 The current trend in trauma is to favor delayed repair of stable patients.32,34,39 Yet to be answered are the engineering challenges of graft compression and infolding as well

501

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Management of Specific Injuries

SECTION 3 X FIGURE 26-14 Plain chest x-ray in a patient with a blunt injury to the descending thoracic aorta. Note the rightward deviation of both the trachea and nasogastric tube in the esophagus.

vessels. Careful documentation of preoperative neurologic status is important. With any suspicion of vascular injury, prophylactic antibiotics are administered preoperatively. In hemodynamically stable patients, fluid administration is limited until vascular control is achieved in the operating room. An autotransfusion device should be available. During the induction of anesthesia, wide swings in blood pressure should be avoided; while profound hypotension is clearly undesirable, hypertensive episodes can have equally catastrophic consequences. The operative approach to great vessel injury depends on both the overall patient assessment and the specific injury. The initial steps of patient positioning and incision selection (Table 26-7) are particularly important in surgery for great

vessel injuries, as adequate exposure is important for proximal and distal control. Prepping and draping of the patient should provide access from the neck to the knees to allow management of all contingencies. For the hypotensive patient with an undiagnosed injury, the mainstay of thoracic trauma surgery is the left anterolateral thoracotomy with the patient in the supine position. In stable patients, preoperative arteriography may dictate an operative approach by another incision. Appropriate graft materials should be available. While the failure mode of an infected prosthetic graft is a pseudoaneurysm, a saphenous vein graft is a devitalized collagen tube susceptible to bacterial collagenase, which may cause graft dissolution with acute rupture and uncontrolled hemorrhage. Therefore, for vessels larger than 5 mm, a prosthetic graft is the conduit of choice, especially in potentially contaminated wounds. However, due to patency considerations, a saphenous vein graft may need to be used when smaller grafts are required. For fragile vessels, such as the subclavian artery and the aorta in young people, a soft knitted Dacron graft is useful.

Damage Control Patients with severely compromised physiologic reserve often require damage control injury management to achieve survival. The two approaches to thoracic damage control are (1) definitive repair of injuries using quick and simple techniques that restore survivable physiology during a single operation and less commonly (2) abbreviated thoracotomy that restores survivable physiology and requires a planned reoperation for definitive repairs.30 Severe hilar vascular injuries can be quickly controlled by performing a pneumonectomy using stapling devices. Temporary vessel ligation or placement of intravascular shunts can control bleeding until the subsequent correction of acidosis, hypothermia, and coagulopathy allows the patient to be returned

TABLE 26-7 Recommended Incisions for Thoracic Great Vessel Injuries Injured Vessel Uncertain injury (hemodynamically unstable)

Ascending aorta Transverse aortic arch Descending thoracic aorta Innominate artery Right subclavian artery or vein Left common carotid artery Left subclavian artery or vein

Pulmonary artery Main/intrapericardial Right or left hilar Pulmonary vein Innominate vein Intrathoracic vena cava

Incision Left anterolateral thoracotomy  Transverse sternotomy  Right anterolateral thoracotomy (clamshell) Median sternotomy Median sternotomy  Neck extension Left posterolateral thoracotomy (fourth intercostal space) Median sternotomy with right cervical extension Median sternotomy with right cervical extension Median sternotomy with left cervical extension Left anterolateral thoracotomy (third or fourth intercostal space) with separate left supraclavicular incision  connecting vertical sternotomy (“book” thoracotomy) Median sternotomy Ipsilateral posterolateral thoracotomy Ipsilateral posterolateral thoracotomy Median sternotomy Median sternotomy

Heart and Thoracic Vascular Injuries

CHAPTER CHAPTER 26 X

to the operating room. En masse closure of a thoracotomy is more hemostatic than towel-clip closure. A “Bogotá bag” closure or “Vac Pack closure” can be used as a temporary closure of a median sternotomy in cases with associated cardiac dysfunction.

ARTERIAL INJURIES Ascending Aorta Patients with blunt ascending aortic injuries rarely survive transportation to the hospital. Operative repair usually requires use of total cardiopulmonary bypass and insertion of a Dacron graft. If the sinuses or valves are involved, aortic root replacement with reimplantation of the coronary ostia may be required.35 Penetrating injuries involving the ascending aorta are uncommon (Figs. 26-12 and 26-13). Survival rates approach 50% for patients having stable vital signs on arrival at a trauma center.42 Although primary repair of anterior lacerations can be accomplished without adjuncts, cardiopulmonary bypass may be required if there is an additional posterior injury. The possibility of a peripheral bullet embolus must be considered in these patients.

Transverse Aortic Arch When approaching an injury to the transverse aortic arch, extension of the median sternotomy to the neck is necessary to obtain exposure of the arch and brachiocephalic branches. If necessary, exposure can be further enhanced by division of the innominate vein. When hemorrhage limits exposure, the use of balloon tamponade is useful as a temporary measure. Simple lacerations may be repaired by lateral aortorrhaphy. With difficult lesions, such as posterior lacerations or those with concomitant pulmonary artery injuries, cardiopulmonary bypass can be used. As with injuries to the ascending thoracic aorta, survival rates approaching 50% are possible.42

FIGURE 26-15 Plain chest x-ray of a patient with a blunt injury of the innominate artery. Note that the hematoma is at the thoracic outlet rather than the aortic isthmus.

right subclavian and carotid arteries. Hypothermia, systemic anticoagulation, or shunting is not required. After the bypass is completed, the area of hematoma is entered, and the injury controlled with a partial occluding clamp (usually at the origin of the innominate artery) and oversewn. If concomitantly

Innominate Artery Median sternotomy is employed for access to innominate artery injuries. A right cervical extension can be used when necessary. Blunt injuries typically involve the proximal innominate artery (Figs. 26-15 and 26-16) and therefore actually represent aortic injuries and require obtaining proximal control at the transverse aortic arch. In contrast, penetrating injuries of the innominate artery may occur throughout its course. Exposure is enhanced by division of the innominate vein. In selected patients with penetrating injuries, a running lateral arteriorrhaphy using 4-0 polypropylene suture is occasionally possible. More often, injuries to the innominate artery require repair via the bypass exclusion technique (Fig. 26-17).43 Bypass grafting is performed from the ascending aorta to the distal innominate artery (immediately proximal to the bifurcation of the subclavian and right carotid arteries) using a Dacron tube graft. The area of injury is avoided until the areas for bypass insertion are exposed. A vascular clamp is placed proximal to the bifurcation of the innominate artery to allow collateral flow to the brain via the

503

FIGURE 26-16 Aortogram of the patient in Fig. 26-12 demonstrating the tear involving the proximal innominate artery.

504

Management of Specific Injuries

B

SECTION 3 X

A

C

FIGURE 26-17 (A–C) Drawing depicting the bypass exclusion technique employed in patients with innominate artery injuries. (Copyright © Baylor College of Medicine, 1981.)

hospital alive, the majority of blunt aortic injuries are located at the isthmus (Fig. 26-18). Patients presenting with an injury in the mid-descending thoracic aorta or distally, near the diaphragm, are far less common (Fig. 26-19). Multiple blunt aortic injuries are rare, but may occur. Injury to the descending thoracic aorta is often accompanied by other organ injuries. If the patient has a stable thoracic hematoma and concomitant abdominal injury, laparotomy should be the initial procedure. For the patient with a rapidly expanding hematoma, however, repair of the thoracic injury should be the primary therapeutic goal. Sequencing is driven by the lesion that is most likely to cause exsanguination. The current standard technique of repair involves clamping and direct reconstruction (Table 26-8). Three commonly employed adjuncts to this approach are (1) pharmacological agents, (2) temporary, passive bypass shunts, and (3) pumpassisted atriofemoral bypass or cardiopulmonary bypass. In the latter approach, two options exist: traditional pump bypass, which requires heparin, and use of centrifugal (heparinless) pump circuits. All three of these adjunctive approaches to the clamp and repair principle should be in the armamentarium of the surgeon, who must choose the approach most appropriate to the specific clinical situation. Injury to the descending thoracic aorta is approached via a posterolateral thoracotomy through the fourth intercostal space. The injury usually originates at the medial aspect of the

injured or previously divided, the innominate vein may be ligated with impunity. If the vein remains intact, a pedicled pericardial flap can be positioned between the vein and overlying graft to prevent erosion. The treatment of an iatrogenic tracheal-innominate artery fistula deserves special consideration. These fistulae are usually caused by the concave surface of a low riding tracheostomy tube eroding into the innominate artery. Sentinel bleeding through or around the tracheostomy tube should not be misinterpreted as “tracheitis.” Arteriography during a “stable interval” is generally not helpful in making a precise diagnosis; instead, the possibility of a tracheal-innominate fistula should be evaluated via bronchoscopy in the operating room. With massive bleeding, control is achieved by performing orotracheal intubation, removing the tracheostomy tube, and directly tamponading the bleeding digitally through the tracheotomy during transport to the operating room. Through a median sternotomy with a right neck extension, the innominate artery is ligated at its origin from the aorta and distally just before the division into the carotid and subclavian arteries. Despite a greater than 25% chance of neurologic complications, no attempt should be made at revascularization, since delayed graft infection with its dreaded complications inevitably occurs.

Descending Thoracic Aorta Prehospital mortality is 85% for patients with blunt injury to the descending thoracic aorta.44 In patients who arrive at the

FIGURE 26-18 Aortogram demonstrating the classic intimal tear and traumatic pseudoaneurysm of the descending thoracic aorta.

Heart and Thoracic Vascular Injuries

aorta at the level of the ligamentum arteriosum; however, one must take care to avoid missing a second injury (usually at the level of the diaphragm). The initial objective is proximal control; therefore, the transverse aortic arch is exposed, and umbilical tapes are passed around the arch between the left carotid and subclavian arteries. Similarly, the subclavian artery is encircled with umbilical tape. Care should be taken to avoid injuring the left recurrent laryngeal nerve though this is often difficult to visualize in the hematoma. If it is suspected that the tear extends to the aortic arch or ascending aorta, cardiopulmonary bypass should be available in the operating room. If the patient has had previous coronary artery bypass surgery with use of the left internal mammary artery as a conduit, repair may require cardiopulmonary bypass perhaps with profound hypothermic circulatory arrest to eliminate the need to clamp the left subclavian artery.

TABLE 26-8 Current Therapeutic Approaches to the Management of Thoracic Aortic Injuries 1. Surgical (clamp and direct reconstruction with or without an interposition graft) (a) Pharmacological control of proximal hypertension (b) Passive bypass shunts (c) Pump-assisted bypass • Traditional cardiopulmonary bypass (with total-body heparinization) • Atriofemoral bypass using centrifugal pump (with/without heparinization) 2. Nonoperative and/or purposeful delay of operation (with pharmacological treatment and close radiologic surveillance) 3. Endograft repair

CHAPTER CHAPTER 26 X

FIGURE 26-19 Aortogram in a patient with blunt chest trauma demonstrating an intimal tear of the descending thoracic aorta at the diaphragm.

Vascular clamps are applied to three locations: proximal aorta, distal aorta, and left subclavian artery. Close communication between anesthesiologist and surgeon is essential to maintain stability of hemodynamic parameters before, during, and after clamping. The use of vasodilators prevents cardiac strain during clamping. The hematoma is entered and back-bleeding from intercostal arteries is controlled. Care is taken to avoid indiscriminate ligation of intercostal vessels; only those required for adequate repair of the aorta should be ligated. The proximal and distal ends of the aorta are completely transected and dissected away from the esophagus; this maneuver allows fullthickness suturing while minimizing the risk of a secondary aortoesophageal fistula. The injury is then repaired by either end-to-end anastomosis or graft interposition. Graft interposition is utilized in more than 85% of reported cases. Prior to clamp removal, volumes of fluid (blood and crystalloid) may need to be administered to avoid clamp release hypotension. For patients undergoing repair of blunt descending thoracic aortic injury, the reported mortality ranges from 0% to 55% (average 13%).37,45 As expected in these victims of major blunt trauma, the mortality is primarily associated with multisystem trauma, and is ultimately due to head injury, infection, respiratory insufficiency, and renal insufficiency. The most feared complication of great vessel injury is paraplegia. Utilization of protective adjuncts when repairing descending thoracic aortic injuries remains a topic of considerable debate. There have been proponents of the use of passive shunts and cardiopulmonary bypass, with and without heparinization. The mortality rate with the use of routine cardiopulmonary bypass is probably secondary to the massive cerebral, abdominal, or fracture site hemorrhage that occurs in these victims of multisystem trauma. Recent experience using centrifugal pumps for left heart bypass without heparinization has provided an attractive alternative for those who wish to use controlled flow bypass without systemic anticoagulation. This also allows unloading of the left heart during clamping, which can be helpful in patients with cardiac disease. The use of bypass systems, however, is not without complications. In the trauma patient, difficulty inserting cannulae may occur due to patient position, the presence of periaortic hematoma, and time constraints imposed by an expanding, pulsatile, uncontrolled hematoma. Intraoperative and postoperative complications include bleeding at the cannulation sites and false aneurysm formation. Use of simple clamp and repair for injuries to the descending thoracic aorta (without the use of systemic anticoagulation or shunts) is a technique that continues to be used with excellent results. Sweeney in 1992 reported using simple clamp and repair in 75 patients, only 1 of whom developed postoperative paraplegia. Ultimately, the determinants of postoperative paraplegia are multifactorial (Table 26-9); therefore, the precise causes cannot be precisely identified in an individual patient. Paraplegia has been associated with perioperative hypotension, injury or ligation of the intercostal arteries, and duration of clamp occlusion during repair.46 However, there are reports of patients surviving surgery without paraplegia despite having long segments of aorta replaced and ligation of multiple intercostal arteries. The length

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Management of Specific Injuries

TABLE 26-9 Possible Contributing Factors Related to the Multifactorial Development of Paraplegia Following Operations for Thoracic Great Vessel Injury

SECTION 3 X

Injury factors

Direct segmental artery injury Direct radicular artery injury Direct spinal artery injury Spinal cord contusion/concussion Spinal canal compartment syndrome Severity of aortic injury Specific anatomic location of aortic injury

Patient factors

Location of arteri radicularis magna(?) Continuity of anterior spinal artery Caliber of individual segmental radicular arteries Congenital narrowing of spinal canal (?) Increased blood alcohol levels Total perispinal collateral blood supply

Operative factors

Required occlusion of segmental arteries Pharmacological agents required (?) Declamping hypotension (?) Required cross-clamp times (in combination with anatomic and injury factors cited in this table); length of required interposition grafting or required exclusion (?) Level of systolic (or mean) proximal aortic blood pressure (?) Level of distal aortic mean blood pressure (?) “Flow” in the aorta distal to clamp

Postoperative factors

Progressive swelling of the spinal cord Spinal canal compartment syndrome Delayed or secondary occlusion of injured or contused segmental, radicular, or spinal arteries Pharmacological induced spasm of spinal cord nutrient arteries

of cross-clamp time does not directly correlate with occurrence of paraplegia. A cross-clamp time under 30 minutes has been argued to provide a safe margin against paraplegia, and shunting techniques have been recommended when longer cross-clamp times are necessary.46 The use of a shunt, however, does not offer protection for the area of the spinal cord supplied by the arteries between the clamps. Furthermore, patients requiring longer clamp time or interposition grafts have more extensive injuries than those requiring shorter clamp times or end-to-end anastomoses. Thus, it is likely that an increased incidence of paraplegia associated with longer clamp times is secondary to more extensive disruption of intercostal arteries and other flow to the anterior spinal artery caused by the original injury. Various monitoring techniques are available to assess the effect of aortic occlusion on the spinal cord, including the measurement of somatosensory- and motor-evoked potentials. Although correlation appears to exist between loss of somatosensory-evoked potentials, duration of loss of conduction, and postoperative paraplegia, the use of this modality is not common to all trauma centers, the interpretation of results is still being debated, and actual positive applicability requires further delineation. Regardless of the technique used, paraplegia occurs in approximately 10% of these patients (range 0–22%).37,45 No

prospective, randomized trial has identified the superiority of any single method. Therefore, the choice of operative technique does not infer legal liability when paraplegia occurs. Even with potential selection bias in favor of endografts, the low mortality and almost nonexistent paraplegia rate make the use of endografting very compelling. The reported complications of graft migration, enfolding, compression, occlusion of the subclavian artery, and problems at the entry site are all technical and engineering challenges that may potentially be solved by new commercial devices.

Subclavian Artery Subclavian vascular injuries can involve any combination of the following regions: intrathoracic, thoracic outlet, cervical (zone 1), and upper extremity. Preoperative arteriography allows for planning appropriate incision(s) to obtain adequate exposure and control. A cervical extension of the median sternotomy is employed for exposure of right-sided subclavian injuries. For left subclavian artery injuries, proximal control is obtained through an anterolateral thoracotomy (above the nipple, second or third intercostal space), while a separate supraclavicular incision provides distal control. Although these incisions can be connected

Heart and Thoracic Vascular Injuries

Left Carotid Artery The operative approach for injuries of the left carotid artery mirrors that used for an innominate artery injury: a median sternotomy with a left cervical extension added when necessary. As with other great vessel injuries, neither shunts nor pumps are employed. With transection at the left carotid origin, bypass graft repair is preferred over end-to-end anastomosis. Intraoperatively, a carotid shunt can be used to temporize these until resources/assistants can be gathered in the OR.

Pulmonary Artery The intrapericardial pulmonary arteries are approached via median sternotomy. Minimal dissection is needed to expose the main and proximal left pulmonary arteries.49 Exposure of the intrapericardial right pulmonary artery is achieved by dissecting between the superior vena cava and ascending aorta. Although

anterior injuries can be repaired primarily without adjuncts, repair of a posterior injury usually requires cardiopulmonary bypass. Mortality rates for injury to the central pulmonary arteries or veins are greater than 70%.22 Distal pulmonary artery injuries present with massive hemothorax and are repaired through an ipsilateral posterolateral thoracotomy. When there is a major hilar injury, rapid pneumonectomy may be a lifesaving maneuver. The use of a large tamponading balloon catheter may control exsanguinating hemorrhage.

Internal Mammary Artery The internal mammary artery in a young patient is capable of flows in excess of 300 mL/min. Injuries to this artery can produce extensive hemothorax or even pericardial tamponade, simulating a cardiac injury. Such injuries are usually serendipitously discovered at the time of thoracotomy for suspected great vessel or heart injury.

Intercostal Arteries Persistent hemothorax can be caused by simple lacerations of the intercostal arteries. Because of difficulty in exposure, precise ligature can be difficult. At times, control must be achieved by circumferential ligatures around the rib on either side of the intercostal vessel injury.

■ Venous Injuries Thoracic Vena Cava Isolated injury to the suprahepatic inferior or superior vena cava is infrequently reported. Injury at either location has a high incidence of associated organ trauma and carries a mortality rate greater than 60%. Intrathoracic inferior vena cava injury produces hemopericardium and cardiac tamponade. Exposure of the thoracic inferior vena cava is extremely difficult unless the patient is placed on total cardiopulmonary bypass with the inferior cannula inserted via the groin in the abdominal inferior vena cava. Repair is exposed by a right atriotomy and intracaval balloon occlusion to prevent air entering the cannula and massive blood return to the heart except via the hepatic veins. Repair is achieved from inside the cava via the right atrium. Superior vena cava injuries are repaired by lateral venorrhaphy. At times, an intracaval shunt is necessary.50 For complex injuries a PTFE patch or Dacron interposition tube graft can be used and is more expedient than the time-consuming construction of saphenous vein panel grafts.

Pulmonary Veins Injury to the pulmonary veins is difficult to manage through an anterior incision. With major hemorrhage, temporary occlusion of the entire hilum may be necessary. If a pulmonary vein must be ligated, the appropriate lobe needs to be resected. Pulmonary vein injuries are often associated with concomitant injuries to the heart, pulmonary artery, aorta, and esophagus.

CHAPTER CHAPTER 26 X

to create a formal “book” thoracotomy, this results in a high incidence of postoperative “causalgia”-type neurologic complications and its use should be limited to highly selected leftsided subclavian artery injuries. In obtaining exposure, it is important to avoid injuring the phrenic nerve (anterior to the scalenus anticus muscle). In subclavian vascular trauma, a high associated rate of brachial plexus injury is seen; thus, documentation of preoperative neurologic status is important. Intraoperative iatrogenic injury to the brachial plexus should also be avoided. In most instances, repair requires either lateral arteriorrhaphy or graft interposition. It is unusual that an end-to-end anastomosis can be employed. Associated injuries to the lung should be managed with stapled wedge resection or pulmonary tractotomy.47 One pitfall in subclavian injuries is failure to anticipate the exposure necessary for proximal control. When approaching the subclavian artery via the deltopectoral groove without proximal control, exsanguination may occur. Resection of the clavicle may aid in proximal control. A combination of supraclavicular and infraclavicular incisions may be used to avoid the morbidity of clavicular resection. A mortality rate of 4.7% for patients with subclavian artery injuries has been reported, but death is often due to associated injuries. With the density of vascular structures in the thoracic outlet, and the morbidity of the thoracic incisions needed for proximal control, it would seem that endovascular techniques to address subclavian artery injuries would be advantageous. There are increasing reports of endovascular approaches to the subclavian artery in both stable and unstable patients.48 If diagnostic arteriography is performed in the OR, a balloon catheter can be left in the proximal left subclavian artery for proximal control. This is most applicable in centers where acute vascular imaging for trauma is available in the operating room and arteriography/covered stent placement can be performed by the trauma/cardiovascular surgeon. With a vascular imaging capable bed, a C-arm with vascular capability, and a simplified set of endovascular tools, even an unstable trauma patient can be brought to the operating room where he or she can be resuscitated, imaged/diagnosed, and bleeding controlled with both open and endovascular techniques.

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Subclavian Veins

SECTION 3 X

The operative exposure of the subclavian veins parallels that described for subclavian artery injuries: median sternotomy with cervical extension for right-sided injuries and left anterolateral thoracotomy with a separate supraclavicular incision for left-sided injuries. In most instances, repair requires either lateral venorrhaphy or ligation.

Azygos Vein The azygos vein is not usually classified as a thoracic great vessel, but because of its size and high flow, azygos vein injuries must be considered potentially fatal. Penetrating wounds of the thoracic outlet can produce combinations of injuries involving the azygos vein, innominate artery, trachea or bronchus, and superior vena cava. These complex injuries have a very high mortality rate, and are particularly difficult to control if approached through a median sternotomy. Combined incisions and approaches are frequently needed for successful repair. When injured, the azygous vein is best managed by suture ligature of both sides of the injury (Fig. 26-20). Concomitant injury to the esophagus and bronchus should be considered and ruled out.51

structures, mandatory exploration has been advocated in the past. The evaluation of stable patients using less invasive means—combined aortography, bronchoscopy, echocardiography, and esophagoscopy—has been described. A thoracic CT scan will often show the bullet trajectory and guide a need for surgery or additional diagnostic tests.

Thoracic Duct Injury Injuries to the thoracic great vessels may be complicated by concomitant thoracic duct injury, which, if unrecognized, may produce devastating morbidity due to marked nutritional depletion.52 Diagnosed by chylous material draining from the chest tube, this condition is usually treated medically. Continued chest tube drainage, coupled with a diet devoid of long-chain fatty acids, usually results in spontaneous closure in less than 1 month. Prolonged hyperalimentation beyond 3 weeks has not consistently resulted in spontaneous closure of thoracic duct fistula. If thoracotomy is required, a fatty meal or heavy cream to increase the chylous flow and facilitate identification of the fistula is given to the patient a few hours before surgery. The fistula is simply ligated with fine monofilament suture (6-0).

Systemic Air Embolism

■ Special Problems Mediastinal Traverse Injuries Because injuries from both stab and gunshot wounds that traverse the mediastinum are classically felt to have a high probability of injury to the thoracic great vessels and other critical

A fistula between a pulmonary vein and bronchiole due to a penetrating lung injury results in systemic air embolism. The fistula allows air bubbles to enter the left heart and embolize to the systemic circulation, including the coronary and cerebral arteries (Fig. 26-21). Intrabronchial pressure above 60 torr increases the incidence of this complication.53 Manifestations

©2005 Baylor College of Medicine

FIGURE 26-20 Injury to the azygos vein with control with lateral repair, ligation, division, and oversewing. (Copyright © Baylor College of Medicine, 2005.)

Heart and Thoracic Vascular Injuries

509

CHAPTER CHAPTER 26 X

Venule

Bronchiole

©Baylor College of Medicine 1979

100 mm Hg

Alveolus

FIGURE 26-21 Drawing depicting the mechanism of systemic air embolism following a penetrating lung injury. (Copyright © Baylor College of Medicine, 1979.)

include seizures and cardiac arrest. Resuscitation requires thoracotomy, clamping of the pulmonary hilum to prevent further air embolization, and aspiration of air from the left ventricle and ascending aorta. Cardiopulmonary bypass can be considered; however, very few survivors have been reported.

Foreign Body Embolism Because of their central location, the thoracic great vessels may serve as both an entry site and final resting place for intravascular bullet emboli.54 These migratory foreign bodies present a diagnostic and therapeutic dilemma. As the result of intravascular embolization, bullets may produce infection, ischemia, or injury to organs distant from the site of trauma. Bullets and catheters can embolize to the pulmonary vasculature; 25% of migratory bullets finally lodge in the pulmonary arteries (Fig. 26-6).54 Although small fragments, such as those the size of a BB, can probably be left in place without causing problems, catheter emboli and larger bullet emboli should be removed to prevent pulmonary thrombosis, sepsis, or other complications. Percutaneous retrieval of the foreign body using transvenous catheters and fluoroscopic guidance may obviate the need for thoracotomy.

■ Postoperative Management A significant portion of the in-hospital mortality associated with great vessel injury is secondary to the nature of the

multisystem trauma in this group of patients. The operating surgeon is best qualified to direct the patient’s postoperative management. Careful hemodynamic monitoring, with avoidance of both hypertension and hypotension, is critical. While urinary output is a generally a good indicator of cardiac function, for the patient with massive injuries, Swan–Ganz monitoring is often necessary to optimize hemodynamic parameters and manage fluids, pressors, and vasodilators. Various pulmonary problems—including atelectasis, respiratory insufficiency, pneumonia, and adult respiratory distress syndrome—represent the primary postoperative complications in this group of patients. The presence of pulmonary contusions and the potential for development of adult respiratory distress syndrome mandate that fluid administration be carefully monitored. Ventilatory strategies to address potential complications of these lung injuries can be used. Patient mobility is important, and adequate medication for pain relief results in fewer pulmonary complications. For the management of pain related to a thoracotomy or multiple rib fractures, postoperative thoracic epidural anesthesia can be considered in stable patients without spinal injuries; alternatively, intercostal nerve blocks can be performed intraoperatively and repeated in the ICU. Postoperative hemorrhage may be due to a technical problem, but is often the result of coagulopathy related to hypothermia, acidosis, and massive blood transfusion. Coagulation studies can be carefully monitored and corrected with

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Management of Specific Injuries

SECTION 3 X

administration of appropriate blood products. Blood draining via chest tubes can be collected and autotransfused. The presence of a prosthetic vascular graft requires special attention aimed at avoiding bacteremia. During the initial resuscitation of these critically injured patients, various intravascular lines are often rapidly placed at the expense of strict sterile technique; all such lines should be replaced after the patient has stabilized in the ICU. Antibiotic therapy should be continued into the postoperative period until potential sources of infection are eliminated. Patients are counseled regarding the necessity of antibiotic prophylaxis during invasive procedures, including dental manipulations. Most late complications are related to infections or sequelae from other injuries. Long-term complications specifically related to the vascular repair—including stenosis, thrombosis, arteriovenous fistula, graft infection, and pseudoaneurysm formation—are uncommon.

REFERENCES 1. Ivatury RR. Injury to the heart. In: Moore EE, Feliciano DV, Mattox KL, eds. Trauma. 5th ed. New York: McGraw-Hill; 2004. 2. Campbell NC, Thomsen SR, Murkart DJ, et al. Review of 1198 cases of penetrating cardiac trauma. Br J Surg. 1997;84:1737. 3. Thourani VH, Feliciano DV, Cooper WA, et al. Penetrating cardiac trauma at an urban trauma center: a 22 year perspective. Am Surg. 1999; 65:811. 4. Wall MJ Jr, Mattox KL, Chen CD, Baldwin JC. Acute management of complex cardiac injuries. J Trauma. 1997;42:905. 5. LeMaire SA, Wall MJ Jr, Mattox KL. Needle embolus causing cardiac puncture and chronic constrictive pericarditis. Ann Thorac Surg. 1998; 65:1786. 6. Maron BJ, Link MS, Wang PJ, et al. Clinical profile of commotio cordis: an underappreciated cause of sudden death in young during sports and other activities. J Cardiovasc Electrophysiol. 1999;10:114. 7. Wall MJ Jr, Mattox KL, Wolf DA. The cardiac pendulum—blunt rupture of the pericardium with strangulation of the heart. J Trauma. 2005; 59:136. 8. Baumgartner FJ, Rayhanabad J, Bongard FS, et al. Central venous injuries of the subclavian–jugular and innominate–caval confluences. Tex Heart Inst J. 1999;26:177. 9. Medizinische Klinik IV. Perforation und Ruptur Koronaryarterien. Herz. 1998;23:311. 10. Ivatury RR, Simon RJ, Rohman M. Cardiac complications. In: Mattox KL, ed. Complications of Trauma. New York: Churchill Livingstone; 1994:409–428. 11. Lee RC. Injury by electrical forces: pathophysiology, manifestations, and therapy. Curr Probl Surg. 1997;34:677. 12. Mattox KL, Flint LM, Carrico CJ, et al. Blunt cardiac injury (formerly termed “myocardial contusion”) [editorial]. J Trauma. 1992;31:653. 13. Galindo Gallego M, Lopez-Cambra MJ, Fernandez-Acenero MJ, et al. Traumatic rupture of the pericardium. Case report and literature review. J Cardiovasc Surg (Torino). 1996;37:187. 14. American College of Surgeons, Committee on Trauma. Advanced Trauma Life Support. Chicago: American College of Surgeons; 2008. 15. Biffl WD, Moore EE, Johnson JL. Emergency department thoracotomy. In: Moore EE, Feliciano DV, Mattox KL, eds. Trauma. 5th ed. New York: McGraw-Hill; 2004. 16. Bertinchant JP, Polge A, Mohty D, et al. Evaluation of incidence, clinical significance and prognostic value of circulating cardiac troponin I and T elevation in hemodynamically stable patients with suspected myocardial contusion after blunt chest trauma. J Trauma. 2000;48:924. 17. Rozycki GS, Schmidt JA, Oschner MG, et al. The role of surgeonperformed ultrasound in patients with possible penetrating wounds: a prospective multicenter study. J Trauma. 1998;45:190. 18. Mattox KL, Wall MJ Jr. Newer diagnostic measures and emergency management. Chest Surg Clin N Am. 1997;7:214. 19. Meyer DM, Jessen ME, Grayburn PA. Use of echocardiography to detect occult cardiac injury after penetrating thoracic trauma: a prospective study. J Trauma.1995; 39:902.

20. Durham LA, Richardson R, Wall MJ, et al. Emergency center thoracotomy: impact of prehospital resuscitation. J Trauma. 1992;32:779. 21. Mattox KL, Limacher MC, Feliciano DV, et al. Cardiac evaluation following heart injury. J Trauma. 1985;25:758. 22. Matttox KL, Feliciano DV, Beall AC Jr, et al. Five thousand seven hundred sixty cardiovascular injuries in 4459 patients. Epidemiologic evolution 1958–1988. Ann Surg. 1989;209:698. 23. Alfaro J, Varela G, De-Miguel E, de Nicilas M. Successful management of a tracheo-innominate artery fistula following placement of a wire selfexpandable tracheal Gianturco stent. Eur J Cardiothorac Surg. 1993; 7:615. 24. Horton TG, Cohn SM, Heid MP, et al. Identification of trauma patients at risk of thoracic aortic tear by mechanism of injury. J Trauma. 2000;48:1008. 25. Rogers FB, Osler TM, Shackford SR. Aortic dissection after trauma: case report and review of the literature. J Trauma. 1996;41:906. 26. Mattox KL. Prehospital management of thoracic injury. Surg Clin North Am. 1989;69:21. 27. Mattox KL, Bickell W, Pepe P, et al. Prospective MAST study in 911 patients. J Trauma. 1989;29:1104. 28. Bickell WH, Wall MJ, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994;331:1105. 29. McCollum CH, Graham JM, Noon GP, et al. Chronic traumatic aneurysms of the thoracic aorta: an analysis of 50 patients. J Trauma. 1979;19:248. 30. Wall MJ Jr, Soltero E. Damage control for thoracic injuries. Surg Clin North Am. 1997;77:863. 31. Wheat MW Jr, Palmer RF, Bartley TD, et al. Treatment of dissecting aneurysm of the aorta without surgery. J Thorac Cardiovasc Surg. 1965;50:364. 32. Demetriades D, Velmahos GC, Scalea TM, et al. Blunt traumatic thoracic aorta injuries: early or delayed repair—results of an American Association for the Surgery of Trauma prospective study. J Trauma. 2009;66:967–973. 33. Dyer DS, Moore EE, Ilke DN, et al. Thoracic aortic injury: how predictive is mechanism and is chest computed tomography a reliable screening tool? A prospective study in 1561 patients. J Trauma. 2000; 48:673. 34. Demetriades D, Velmahos GC, Scalea TM, et al. Diagnosis and treatment of blunt thoracic blunt thoracic aortic injuries: changing perspectives. J Trauma. 2008;64:1415–1419. 35. Wall MJ Jr, Tsai PI, Gilani R, et al. Challenges in the diagnosis of unusual presentations of blunt injury to the ascending aorta and aortic sinuses. J Surg Res. 2010;163:176–178 [Epub ahead of print]. 36. Tehrani HY, Peterson BG, Katariya K, et al. Endovascular repair of thoracic aortic tears. Ann Thorac Surg. 2006;82:873. 37. Mattox KL, Whigham C, Fisher RG, et al. Blunt trauma to the thoracic aorta: current challenges. In: Lumsden AB, Lin PH, Chen C, Parodi JC, eds. Advanced Endovascular Therapy of Aortic Disease. London: Blackwell Publishing; 2007. 38. Patel HJ, Williams DM, Upchruch GR, et al. A comparative analysis of open and endovascular repair for the ruptured descending thoracic aorta. J Vasc Surg. 2009;50:1265–1270. 39. Demetriades D, Velmahos GC, Scalea TM, et al. Operative repair or endovascular stent graft in blunt traumatic thoracic aortic injuries: results of an American Association for the Surgery of Trauma multicenter study. J Trauma. 2008;64:561–571. 40. Fernandez V, Mestres G, Maeso J, et al. Endovascular treatment of traumatic thoracic aortic injuries: short- and medium-term follow-up. Ann Vasc Surg. 2010;24:160–166. 41. Forbes TL, Harris JR, Lawlor K, et al. Aortic dilation after endovascular repair of blunt traumatic thoracic aortic injuries. J Vasc Surg. 2010;52: 45–48. 42. Pate JW, Cole FH, Walker WA, et al. Penetrating injuries of the aortic arch and its branches. Ann Thorac Surg. 1993;55:586. 43. Johnston RH Jr, Wall MJ, Mattox KL. Innominate artery trauma: a thirtyyear experience. J Vasc Surg. 1993;17:134. 44. Parmley LF, Mattingly TW, Marian WC, et al. Nonpenetrating traumatic injury of the aorta. Circulation. 1958;17:1086. 45. von Oppell UO, Dunne TT, De Groot MK, et al. Traumatic aortic rupture: twenty-year metaanalysis of mortality and risk of paraplegia. Ann Thorac Surg. 1994;58:585. 46. Mattox KL. Fact and fiction about management of aortic transection [editorial]. Ann Thorac Surg. 1989;48:1. 47. Wall MJ, Hirshberg A, Mattox KL. Pulmonary tractotomy with selective vascular ligation for penetrating injuries to the lung. Am J Surg. 1994;168:1.

Heart and Thoracic Vascular Injuries 51. Wall MJ Jr, Mattox KL, DeBakey ME. Injuries to the azygous venous system. J Trauma. 2006;60:357. 52. Dulchavsky SA, Ledgerwood AM, Lucas CE. Management of chylothorax after blunt chest trauma. J Trauma. 1988;28:1400. 53. Graham JM, Beall AC Jr, Mattox KL, et al. Systemic air embolism following penetrating trauma to the lung. Chest. 1977;72:449. 54. Mattox KL, Beall AC Jr, Ennix CL, et al. Intravascular migratory bullets. Am J Surg. 1979;137:192.

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48. Gilani R, Tsai P, Wall JR, Mattox KL, Lin P. Endovascular management of complex subclavian artery injuries. J Trauma. 2012 (in press). 49. Clements RH, Wagmeister LS, Carraway RP. Blunt intrapericardial rupture of the pulmonary artery in a surviving patient. Ann Thorac Surg. 1997;64:258. 50. DeBakey ME, Simeone FA. Battle injuries of arteries in World War II: an analysis of 2,471 cases. Ann Surg. 1946;123:534.

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CHAPTER 27

Trauma Laparotomy: Principles and Techniques Asher Hirshberg

INTRODUCTION Laparotomy is the most common operation performed for truncal trauma. It consists of a methodical sequence of steps that enable the surgeon to gain access to abdominal injuries, and identify and address them. These steps are guided by a series of priority-driven decisions that shape the operation.1 There are two modes of laparotomy for trauma, corresponding to the two major indications for the procedure: peritonitis and bleeding.2 The first mode is abdominal exploration in a hemodynamically stable patient with a tender abdomen. In these cases, the operation proceeds along the lines of an explorative laparotomy for an acute abdominal condition such as a hollow organ perforation: it is urgent but not hectic since there is no danger of imminent death. A less common but more dramatic mode is a crash laparotomy in a patient in shock with intra-abdominal hemorrhage.1 Here the patient’s life is in immediate jeopardy because on-table exsanguination is a real threat. Despite its hectic pace, a crash laparotomy is not merely an accelerated version of the first mode. Instead, it is a multidimensional effort that combines technical and team leadership skills. In a crash laparotomy, the surgeon has to calibrate the operative effort not only to the patient’s clinical condition but also to the capabilities of the surgical team and the available resources. A crash laparotomy requires therefore not only a more expedient technical approach to the task but also a different frame of mind. When operating for peritonitis in the stable patient, the focus is on reconstructing the anatomy. In a crash laparotomy, the focus is on rapid control of hemorrhage and preservation of the patient’s physiology. The anatomical integrity of the repair is less important, and is sometimes temporarily sacrificed to prevent an irreversible physiological insult. It is in these adverse circumstances that the special expertise of the trauma surgeon can make a difference.

This chapter provides an overview of laparotomy for trauma, with an emphasis on crash laparotomy in an unstable patient. The first part of the chapter describes the guiding principles of the procedure from the perspective of the trauma surgeon. This is followed by a detailed description of the technical steps and key maneuvers of a trauma laparotomy against the background of ongoing decision making. The final part of the chapter addresses special types of abdominal exploration in the injured patient such as urgent or planned reoperation after damage control surgery as well as bedside laparotomy and the current role of laparoscopy.

PRINCIPLES ■ The Core Mission In a trauma laparotomy, the core mission of the surgeon is to stop the bleeding. The success of the procedure hinges on the surgeon’s ability to rapidly reach the source of intra-abdominal hemorrhage and control it effectively. All else is of secondary importance simply because there is no alternative to achieving hemostasis. If the patient is not bleeding significantly, the mission then becomes to identify and repair other injuries (typically holes in the gut). The importance of remaining focused on the core mission cannot be overemphasized. The multitrauma patient often presents with a bewildering array of injuries surrounded by clouds of clinical, administrative, and medicolegal issues that easily divert attention from the uncontrolled bleeding in the abdomen. It is therefore crucial to keep in mind that once the indication for laparotomy has been established in a trauma patient in shock, nothing should stand in the way of a rapid organized effort to put the patient in the operating room (OR) and bring the surgeon face-to-face with the bleeder as quickly as possible.

Trauma Laparotomy: Principles and Techniques

■ The Surgeon’s Support Envelope

■ Preparation The less stable the patient, the less time should be spent on preoperative preparations. In the trauma resuscitation bay, in addition to the primary and secondary surveys and corresponding resuscitative maneuvers, it is very helpful (but not essential) to obtain chest and abdominal x-rays in patients with abdominal gunshot wounds. These x-rays help delineate the bullet trajectory and avoid missing injuries. This is especially important with multiple gunshot wounds. Some bullet trajectories carry special significance.3 A thoracoabdominal trajectory is associated with higher morbidity, and a trajectory across the abdominal midline (transabdominal) in a hypotensive patient is an early predictor of the need for damage control and a marker of high mortality. The arrival of the hemodynamically unstable patient to the OR is often hectic and disorganized. The surgeon and the OR team must then convert the scramble into a methodical effort and rapidly deploy the surgeon’s support envelope. This obligatory logistical interval from the patient’s entry into the OR to skin incision is known in the trauma surgery

TABLE 27-1 Anatomy of the Surgeon’s Support Envelope Support Tier Inner

Location In operative field

Key Resource Scrub nurse

Other Elements Assistant(s) Open instrument trays Other sterile technology

Middle

In OR

Circulating nurse

Anesthesia team Closed instrument trays Nonsterile technology

Outer

Outside OR

Circulating nurse

Additional help OR technology and devices Portable imaging Blood products supply chain SICU bed

CHAPTER CHAPTER 27 X

In the exsanguinating patient with a hole in the inferior vena cava, the goal of the entire team effort is to insert a vascular suture line into the wall of the injured vessel. The circulating nurse supplies the suture, the scrub nurse loads it on a needle driver, and the anesthesiologist transfuses and ventilates the patient—but it is the surgeon who will accomplish the goal on behalf of the entire team. The surgeon’s core mission cannot be accomplished without effective specialized support. Every trauma center therefore maintains a support envelope around the operating surgeon. The elements of this envelope are typically arranged in three tiers (Table 27-1). The inner tier is located inside the sterile field around the open abdomen and is immediately accessible to the surgeon. The middle tier is inside the OR but outside the sterile field, and the outer tier is outside the OR and consists of a wide array of assets and resources located at various distances from it. Some elements of the support envelope (especially in the inner and middle tiers) participate in the entire procedure, whereas others come into play at various stages. The single most important element in the support envelope and the engine that keeps it up and running is the circulating nurse. There is often a time lag between the decision to employ a specific element of the support envelope and its availability to the surgeon. This delay is inversely related to the tier in which the element is located. For example, there is no delay in getting hold of a Deaver retractor, but it takes at least a few minutes to bring a Rummel tourniquet into the operative field—and much longer than that to obtain a portable x-ray. It is sometimes difficult—but nevertheless essential—to think of a crash laparotomy in terms of resource allocation. Many elements in the surgeon’s support envelope are finite and precious resources that must not be wasted. Since the envelope responds to the surgeon’s requests, it becomes the surgeon’s responsibility to use those resources judiciously. A case in point is the circulating nurse, the most important resource not only in the middle tier but also in the entire support envelope. The

circulating nurse can propel the operation forward or slow it down to a crawl. Requesting a specific instrument from the OR storage area means that the circulating nurse will be temporarily unavailable for other tasks, some of which may be more important for the conduct of the operation. Similarly, there is little point in doing a 30-minute damage control laparotomy only to find on completion that mobilizing an SICU bed from the outer tier takes more time than the procedure itself. In using the resources of the support envelope, the surgeon must learn to be flexible and rapidly consider the cost of every request in terms of the precious time and attention of team members. The temptation to request “nice to have” items must be resisted for the sake of feasible solutions that move the operation forward. Close acquaintance with each of the three tiers and knowledge of the realistic capabilities of the key assets around the operative field are crucial to the smooth conduct of a trauma laparotomy.

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SECTION 3 X FIGURE 27-1 The wide operative field for torso trauma provides free access to the abdomen, chest, and groins. It reflects the principle of planning for unexpected obstacles during the procedure such as the need to extend the operation into another cavity to access the groins.

jargon as “the black hole.” During this interval, the patient is moved to the operating table, positioned, and prepared, but nothing is done to address the bleeding. The ability to minimize the duration of this interval is a measure of the efficiency of the OR team. Effective surgeons recognize the need to minimize the “black hole” interval and to start cutting as quickly as possible, but at the same time they are also aware of the importance of proper positioning and preparation. It is crucial that the surgeon share a brief outline of the operative plan with the OR team (e.g., “We are going to insert a right chest tube, and then do a laparotomy and possibly also a right thoracotomy”). Rather than delegate the preparatory steps to junior members of the team, effective surgeons minimize or eliminate their time at the scrub sink and remain with the patient throughout the “black hole” interval, orienting the team and coordinating the effort. The operative field for torso trauma extends from the chin to above the knees, between the posterior axillary lines and with

both arms fully abducted (Fig. 27-1). This wide sterile field provides free access to the abdomen and chest as well as both groins, while giving the anesthesia team access to both upper extremities and the head and neck. It reflects the underlying principle of preparing the operative field for a “worst case scenario” where the surgeon may have to enter other visceral compartments in mid-operation.4 As the surgical team defines, drapes, and prepares to work in the operative field, the inner and middle tiers of the surgeon’s support envelope organize and deploy. Before making the incision, the surgeon should take a moment to pause, look up from the operative field, take mental stock of the overall situation in the OR, and ascertain that everyone is ready.

■ The Operative Sequence Every trauma laparotomy follows a generic sequence of operative steps (Fig. 27-2).1 This sequence reflects the underlying logic and priorities of the procedure, but is often modified

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Decision

Access and exposure

Temporary bleeding control

Exploration

Damage control

FIGURE 27-2 A schematic depiction of the generic sequence of steps in a trauma laparotomy. This sequence reflects the global priorities but is frequently modified as needed. The key decision point is the choice of operative profile that shapes the rest of the procedure as well as the patient’s postoperative course.

according to the clinical circumstances and operative findings. For example, in the absence of significant bleeding there is no need to pack the abdomen for temporary hemostasis and the surgeon proceeds directly to exploration. If a major obvious bleeder (such as injury to an abdominal great vessel) is encountered shortly after entering the abdomen, temporary hemostasis often merges with a definitive vascular repair, and full exploration of the peritoneal cavity takes place later. Gaining access and exposure (a long midline incision and evisceration of the bowel) and gaining temporary hemostasis (by packing or manual pressure) are routine tasks that are rapidly accomplished with minimal support. Effective temporary hemostasis is a crucial early success because it gives the surgeon a first rough impression of the injuries, and provides a time window to pause, think, and plan ahead. The anesthesia team now has time to regroup and catch up on previous blood loss. Additional instruments (e.g., vascular tray), help (such as an experienced assistant), and technology (autotransfusion device) can be mobilized from the middle and outer support tiers. Failure to achieve early temporary hemostasis in the face of severe hemorrhage means that the surgeon and the team are denied all these advantages: the scramble continues (as does the bleeding) and can fatally derail the entire operation. Methodical exploration of the peritoneal cavity allows the surgeon to discover and define the injuries. However, in real life this methodical exploration may be interrupted by the urgent need to address another injury or enter another anatomical compartment (e.g., the chest). In other cases, the necessity to bail out to prevent an irreversible physiological insult (see below) may force the surgeon to abort the systematic exploration altogether, deferring it until reoperation. The most pivotal decision in the operative sequence is between definitive repair and damage control. By making this decision, the surgeon chooses an operative profile and shapes the remainder of the procedure. Definitive repair means repair or resection of the injured organs, reconstruction of the anatomy, and formal abdominal closure. This is the traditional trauma laparotomy and it applies to the great majority of cases.

Damage control (see Chapter 38) means a rapid bailout using temporary measures to control bleeding and spillage and temporary abdominal closure with the intention to return to abdomen in the next few days. Since damage control is associated with increased morbidity, it is used selectively in the most severely injured patients. A “forced bailout” is a situation where the patient’s physiology is so precarious that damage control remains the surgeon’s only feasible option. This occurs when the surgeon erroneously decides to proceed with definitive repair, having either underestimated the injuries or overestimated the capabilities of the surgical team. As the patient continues to bleed and becomes hypothermic, edematous, and coagulopathic, the surgeon is forced to pack the abdomen and bail out to avert an irreversible physiological insult. Similarly, ominous injury patterns such as multifocal or multicavitary exsanguination5 push the patient to the brink of death so quickly that a forced bailout is the only option if the surgeon managed to control the bleeding.

■ The Surgeon Effective surgeons always plan ahead. They conduct the operation with a clear sense of the core mission and how they plan to accomplish it. They anticipate difficulties and plan to avert or meet them. It is commonly said that an effective scrub tech must stay at least one step “ahead of the operation,” always preparing the instruments for the next step. In fact, this is only one example of dealing with the delays and time lags inherent in the structure of the surgeon’s support envelope. Obviously the elements of the middle and outer tiers must be even further ahead of the operation, with the circulator obtaining a device that will be needed in 5–10 minutes and the anesthesia team ordering blood products that will be used in half an hour or later. To confidently steer the operation in the right direction, the surgeon must therefore formulate a plan that extends well beyond the next few steps and has a clear end point (e.g., “We must pack the liver, tie off the bowel injuries and be in the SICU in less than an hour”).

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SECTION 3 X

Maintaining a continuous ongoing dialogue with the OR team is another hallmark of an effective surgeon. Amidst the drama of operating on a massively bleeding patient, it is sometimes easy to forget that team members outside the operative field cannot do their jobs intelligently without understanding at least the broad picture of what is being done and where the operation is heading. It is a sad fact that surgeons, anesthesiologists, and OR nurses spend their entire careers working as part of OR teams—yet train as individuals. Surgeons are taught to think of themselves as captains of the operative ship, yet are rarely, if ever, trained in collaborative teamwork.6,7 Team leadership in the OR is more about carefully listening to input from others and interacting with them than about making an endless stream of requests for esoteric instruments. A good example is communication with the anesthesia team who has crucial information that the surgeon simply cannot do without. Assessing the patient’s physiological reserves hinges on a set of variables such as core temperature and total blood loss, all of which are monitored by the anesthesia team but are also needed by the surgeon for an intelligent decision to bail out. The surgeon must also be acutely aware that the patient may be bleeding outside the operative field (e.g., into the pleural space) and the only clues that something is amiss in another visceral compartment will be noticed by the anesthesia team. Therefore, open communication lines and constant interaction between surgeon and anesthesiologist across the sterile drapes are absolutely essential for a safe laparotomy. Such a dialogue ensures that the anesthesiologist knows what the injuries are, understands the surgeon’s intentions, and tailors the anesthesia plan accordingly. One of the hallmarks of a crash laparotomy as compared to the more leisurely pace of laparotomy for peritonitis is the frequency of sudden changes in the operative plan. It is essential that the surgeon update the OR team of these changes directly and without delay. Trauma laparotomy is performed by general and trauma surgeons who vary widely in their trauma experience. From time to time, surgeons may face a technical challenge that they feel either is outside their comfort zone or requires more competent assistance. The correct thing to do is to get experienced help. There are several good “pause points” along the operative sequence where the surgeon can stop operating, assess the situation, and decide to summon help. For example, after obtaining effective temporary hemostasis, the surgeon may decide to pause the operation for a short time and recruit a better assistant from the outer support tier. Another valid “pause point” is at the end of exploration, where the surgeon may decide not to open a central retroperitoneal hematoma and instead summon a colleague with more vascular experience. This is certainly a wiser decision than plunging into the hematoma and losing control (and the patient). Pausing the operation with the situation temporarily at hand and seeking help is never a sign of weakness but rather a marker of sound judgment and of personal and professional maturity. Most trauma centers are also academic institutions where resident training closely follows patient care as a high priority.

Doing a crash laparotomy in a teaching setup is a special challenge because the surgeon must ensure that resident teaching does not interfere with the smooth and timely flow of the procedure. In other words, the teaching experience must be carefully tailored both to the specific situation in the operative field and to the resident’s capabilities. During a teaching-oriented crash laparotomy, the teacher does not actually hold the knife or needle driver but nevertheless maintains full control of all aspects of the operation, interacts with the team, and coordinates the support while the trainee focuses on the technical aspects of the operation. Making a crash laparotomy an educational experience for the resident without compromising patient safety is the hallmark of a true surgical educator.

TECHNIQUES AND MANEUVERS ■ Gaining Access and Exposure The most expedient access to the peritoneal cavity is through a long midline incision. Speed is especially important during a crash laparotomy when the patient is in shock. A bold xiphopubic skin incision skirting the umbilicus is rapidly followed by sharp division of the subcutaneous fat down to the fascia. The surgeon then “gains the midline” by identifying the decussating fibers of the anterior rectus sheath.8 Sharply dividing the linea alba with the scalpel exposes the preperitoneal fat throughout the entire length of the incision. In hypotensive patients, bleeding from the divided skin and subcutaneous fat is minimal due to peripheral vasoconstriction, and the entire incision can be completed with three long precise strokes of the scalpel. In most patients, the peritoneum just cranial to the umbilicus is very thin or has a defect, and is covered with scant preperitoneal fat. Poking a finger through this area (Fig. 27-3) is the quickest way to enter the peritoneal cavity. The hole is then enlarged by incising both the peritoneum and overlaying preperitoneal fat together to the full extent of the incision using Mayo scissors. Dividing the falciform ligament between clamps provides access to the right upper quadrant and completes the incision. When gaining rapid access to the peritoneal cavity, the major pitfall is iatrogenic injury. The left lateral lobe of the liver, transverse colon, and bladder are at risk in the upper, middle, and lower parts of the incision, respectively. In patients with a pelvic fracture, limiting the incision to the upper abdomen avoids entering a retroperitoneal hematoma that may extend into the preperitoneal space. In patients with previous laparotomy scars, the surgeon can either carefully reenter through the old scar or try to skirt around it. Most surgeons choose the former option, which entails carrying the skin incision beyond the previous scar into “virgin” territory. The peritoneal cavity is thus entered in an area where adhesions to the anterior abdominal wall are less likely, and the incision is gradually extended into the previous scar, carefully avoiding bowel loops that are often adherent to the undersurface of the scar. This process can be time consuming and frustrating in a hypotensive patient. The other option

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FIGURE 27-3 The quickest way to enter the peritoneal cavity is through the very thin (or absent) peritoneum immediately cranial to the umbilicus. After having divided the linea alba throughout the entire length of the incision, the surgeon can easily locate this area, bluntly poke a finger through it, and then incise the peritoneum and preperitoneal fat with heavy scissors.

is to bypass the troublesome area by making a completely new incision in a different orientation, such as a bilateral subcostal incision. The final and often neglected key maneuver that provides access to the abdominal cavity is complete evisceration of the small bowel (Fig. 27-4): gathering all the loops into a surgical towel outside the abdomen and to the patient’s right. This pivotal step converts the bloody mess inside the injured abdomen into an organized workspace.1

■ Achieving Temporary Hemostasis In blunt abdominal trauma, temporary bleeding control is typically achieved with empirical packing. Blindly shoving laparotomy pads into the abdomen without evisceration is not an effective way to achieve temporary hemostasis. After rapidly eviscerating the bowel and evacuating the blood from the peritoneal cavity using open laparotomy pads and suction, the surgeon proceeds to swiftly pack the abdomen without attempting to precisely identify the injuries (hence the term “empirical” packing). With the assistant elevating the corresponding portion of the abdominal wall using a large retractor, the surgeon places a hand over the dome of the liver, gently pulling it toward the

midline. Several laparotomy pads are then placed above and then below the liver, creating a hemostatic “sandwich” that approximates disrupted tissue planes. The same technique of packing over the surgeon’s hand and creating a “sandwich” is repeated above and below the spleen (Fig. 27-5). The paracolic gutters and pelvis are packed next. Empirical packing is especially useful in blunt trauma, since the most common sources of bleeding are the spleen, liver, and small bowel mesentery. Bleeding from the solid organs can often be temporarily controlled by packing (unless it is arterial), while mesenteric bleeders are immediately apparent in the eviscerated bowel and are easily accessible. In penetrating trauma, empirical packing is less useful. Knowing the presumed trajectory of the wounding agent allows the surgeon to focus on a specific quadrant or area of the abdomen. After evisceration, it is often possible to address the bleeder directly using atraumatic measures such as manual or digital pressure. Blind clamping in a pool of blood should be avoided because it is ineffective and dangerous. Packing can be used to temporarily control bleeding from an injured solid organ or a retroperitoneal hematoma. In a rapidly exsanguinating patient, most surgeons would consider supraceliac aortic clamping. This is a resuscitative maneuver, not a hemostatic technique. Instead of formally

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SECTION 3 X FIGURE 27-4 Complete evisceration of the small bowel immediately on entering the peritoneal cavity is a key maneuver that is often forgotten by the inexperienced. Gathering all bowel loops outside the abdomen and always to the patient’s right is a pivotal step in organizing the peritoneal cavity into a convenient workspace.

clamping the lowermost thoracic aorta through the crus of the diaphragm,9 which entails blind dissection through the crus and carries the risk of iatrogenic injury, it is safer to simply compress the supraceliac aorta manually through a hole in the lesser omentum. The aorta is identified by palpation as it emerges beneath the diaphragm immediately below and to the right of the abdominal esophagus, and is manually compressed against the spine.4 Successful temporary hemostasis is a pivotal moment in the operation because it has a significant psychological impact on the OR team. It lowers the sense of extreme urgency and turmoil that sometimes characterizes the previous steps. The unknowns in the abdomen are now at least partially known. Stress levels among team members are lower. The situation seems temporarily at hand. There is time to take a deep breath, think, and convert a frantic scramble into a disciplined procedure.

■ Exploring the Peritoneal Cavity The mesentery of the transverse colon divides the peritoneal cavity into a supramesocolic and an inframesocolic compartment, and each must be explored in turn using a consistent methodical sequence. Pulling the transverse colon cranially enables the surgeon and assistant to run the gut from the ligament of Treitz to the rectum, using two pairs of hands in a coordinated motion that flips each segment to inspect both sides of the bowel and mesentery. Spillage from holes in the gut is temporarily controlled using Babcock or Allis clamps. Colonic perforations can often be smelled before they are seen. Inspection of the bladder and the female reproductive organs concludes the exploration of the inframesocolic compartment. Pulling the transverse colon caudad allows the surgeon to explore the supramesocolic compartment from right to left.

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FIGURE 27-5 Empirical packing of the left upper quadrant to achieve temporary hemostasis. The surgeon uses one hand to pull the spleen medially and places laparotomy pads over that hand above and below the spleen to create a hemostatic “sandwich.” A similar technique is used in the right upper quadrant, both paracolic gutters, and the pelvis. Empirical packing is especially useful in blunt trauma.

The liver and gallbladder are inspected and palpated for injuries, followed by palpation of the right kidney. This is followed by inspection of the anterior stomach and proximal duodenum, and then palpation of the spleen and the left kidney. The surgeon then inspects each hemidiaphragm and notes if it is convex or is bulging into the abdomen. The posterior peritoneum is inspected for retroperitoneal hematoma. Entering the lesser sac is easiest through the left side of the greater omentum (which is typically thinner and less vascular). This provides a reasonable view of the posterior gastric wall and the body and tail of the pancreas. This exposure is good enough to inspect the lesser sac, but not to work in it. A wider

exposure can be achieved by taking down the entire length of the greater omentum from the transverse colon along the bloodless line. In patients with penetrating abdominal trauma, injuries tend to be missed at several less accessible locations, especially in obese patients (Table 27-2).10 The key to avoiding missed injuries during laparotomy for penetrating trauma hinges on two technical principles: • The surgeon must be able to reconstruct the path of the wounding missile, and the trajectory must be linear and make sense. Inability to “connect the dots” between different injuries is often a clue to a missed injury.

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TABLE 27-2 Common Locations of Missed Injuries in Penetrating Abdominal Trauma

SECTION 3 X

In the Peritoneal Cavity

In the Retroperitoneum

Esophagogastric junction Proximal jejunum (ligament of Treitz) Mesenteric border of small bowel Posterior wall of transverse colon

Retroperitoneal duodenum (DII, DIII, DIV) Ureters Extraperitoneal rectum and bladder

• Finding an odd number of perforations in a hollow organ is cause for concern and should prompt the surgeon for extra vigilance in looking for another missed hole. Since much of the colon is retroperitoneal and covered with omentum and pericolic fat, it is easy to miss small colonic perforations. Therefore, any seemingly superficial subserosal hematoma on the colon must always be carefully unroofed because it may hide a transmural injury. When the trajectory of the wounding agent passes anywhere near a ureter, the relevant side of the colon should be mobilized and the ureter fully visualized.

■ The Medial Visceral Rotations Rapid access to the abdominal great vessels (aorta and vena cava) and their major branches, as well as other retroperitoneal structures (such as the duodenum and kidneys), hinges on two maneuvers of medial visceral rotation. The Mattox maneuver and the Cattell–Braasch maneuver have become part of the folklore of trauma surgery, but there is still much confusion and misunderstanding regarding their proper use and precise anatomical details. Both maneuvers are based on the same anatomical principle of lifting the intraperitoneal viscera off the posterior abdominal wall and rolling them medially to expose the midline retroperitoneal structures. However, there are important differences in their utility. The Mattox maneuver is used for the specific purpose of gaining access to the suprarenal aorta, the most inaccessible segment of the abdominal aorta. The Cattell–Braasch maneuver provides access to the entire inframesocolic (or infrarenal) retroperitoneum and has therefore much wider use for different purposes and in various operative situations. The left-sided medial visceral rotation (Fig. 27-6) is known in trauma surgery as the Mattox maneuver.11 The surgeon begins the maneuver by mobilizing the lowermost descending colon. Incising the white line of Toldt enables the surgeon to bluntly dissect behind the left colon and rapidly mobilize it from below toward the splenic flexure. Continuing the blunt dissection in an upward and medial direction in the same avascular plane immediately anterior to the muscles of the posterior abdominal wall allows the surgeon to gradually rotate the left kidney spleen, pancreas, and stomach medially and expose the entire length of the abdominal aorta all the way

up to the diaphragmatic hiatus.4 In most situations requiring this maneuver, a large supramesocolic retroperitoneal hematoma greatly facilitates the dissection by lifting the peritoneal organs off the posterior abdominal wall. The surgeon can achieve proximal control of the supraceliac aorta immediately below the diaphragm. Another option is to incise the left diaphragmatic crus laterally, bluntly dissect around the aorta, and clamp it in the lower chest through the incised hole in the diaphragm. One crucial anatomical detail distinguishes the Mattox maneuver from the previously described left-sided medial visceral rotation used for aortic exposure in elective vascular surgery.12 The Mattox maneuver always includes the left kidney because leaving it in place interposes the anterior renal fascia between the plane of dissection and the aorta. This obscures the aorta and requires division of the fascia to get to it. Furthermore, by leaving the left kidney in place, the left renal vein restricts access to the anterior aspect of the aorta and the left ureter is vulnerable to injury. Splenic injury is by far the most common iatrogenic complication of left-sided medial visceral rotation,12 and is usually addressed by removing the injured spleen. Other sources of bleeding are avulsion of the descending lumbar vein from the left renal vein and clamp injury to the right lateral aortic wall when the aorta is clamped with insufficient circumferential dissection. Pancreatitis and gut ischemia related to retraction are rare and late complications that emphasize the need for gentle handling and protection of the rotated viscera. The right-sided medial visceral rotation consists of three successive steps4 (Fig. 27-7). The surgeon begins with a full Kocher maneuver, mobilizing the duodenal loop (and head of pancreas) from the common bile duct superiorly to the superior mesenteric vein inferiorly. This exposes the second part of the duodenum but does not provide free access to the underlying vascular structures (inferior vena cava and right renal hilum), which is so important in a trauma situation. The second step improves this limited exposure by carrying the incision in the posterior peritoneum caudad along the white line of Toldt and mobilizing the right colon.13 Reflecting the right colon medially provides wide exposure of the right-sided retroperitoneal organs, including the entire infrahepatic vena cava, the right kidney and renal vasculature, as well as the right iliac vessels. In fact, it is possible (but not convenient) to gain control of the suprarenal aorta and both renal arteries from the right side using this exposure.14 The third and final step of the right-sided medial visceral rotation is the complete Cattell–Braasch maneuver.15 Gathering the small bowel to the right enables the surgeon to clearly visualize and incise the avascular line of fusion of the small bowel mesentery to the posterior peritoneum. The incision is carried around the cecum and then all the way up along the “white line” between the cecum and the ligament of Treitz. This enables the surgeon to swing the small bowel and right colon out of the abdomen and onto the patient’s anterior chest, exposing the entire inframesocolic retroperitoneum (Fig. 27-8). Right-sided medial visceral rotation has fewer iatrogenic complications than its left-sided counterpart, the most serious

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© Kenneth L. Mattox, M.D.

FIGURE 27-6 The full left-sided medial visceral rotation for trauma (Mattox maneuver) always includes the left kidney. It provides access to the entire length of the abdominal aorta and is the only way to rapidly expose the suprarenal aortic segment in the presence of a central retroperitoneal hematoma. The inset shows the correct plane of dissection that is immediately on the muscles of the posterior abdominal wall. The presence of a large retroperitoneal hematoma greatly facilitates the maneuver. (Copyright © Kenneth L. Mattox, MD.)

being an injury to the superior mesenteric vein at the root of the mesentery. Once the right colon has been mobilized, it is hanging only by its mesentery and is vulnerable to avulsion of the middle colic vein off the superior mesenteric vein, resulting in unexpected fierce hemorrhage from the base of the mesentery. The ensuing rush to gain control may result in inadvertent clamping and division of the superior mesenteric vein. Originally described as a technique for exposing the third and fourth parts of the duodenum in nontrauma situations,15 the Cattell–Braasch maneuver has found many applications in abdominal surgery. The panoramic retroperitoneal exposure afforded by it is useful in a range of operative situations where wide access to the retroperitoneum can help the surgeon figure out a complex bullet trajectory, approach an inframesocolic or pelvic retroperitoneal hematoma, or expose inaccessible retroperitoneal structures. Mastering the medial visceral rotations adds very powerful weapons to the surgeon’s armamentarium. But they are precision weapons, not bludgeons. For example, the only indication to perform the Mattox maneuver is a central supramesocolic retroperitoneal hematoma. Yet the phrase “I Mattoxed the patient” is too often heard after a battle with abdominal bleeding

where there was no indication to use the maneuver. It is therefore crucial to gain ownership of these techniques by studying them in detail, and if possible practicing them in the lab. It is also equally important to fully understand the indications for and potential benefit of each medial visceral rotation.

■ Approach to Intra-Abdominal Bleeding The goal of a crash laparotomy is to achieve effective control of intra-abdominal bleeding before the patient exsanguinates or sustains an irreversible physiological insult (see the next section). A peritoneal cavity filled with blood or a large retroperitoneal hematoma can be an intimidating sight, but the surgeon must keep in mind that panic or reflexive action often leads to errors in bleeding control, failure to achieve hemostasis, and death on the operating table. The patient’s best chance is a cool-headed and systematic approach. The key to success is not technical brilliance but rather the ability to select effective techniques from a menu of hemostatic options and apply them in a methodical fashion until the bleeding stops. Full evisceration allows the surgeon to organize the abdominal cavity and gain a general impression of the source and magnitude of bleeding. The single crucial decision that the

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SECTION 3 X FIGURE 27-7 The three successive stages of the right-sided medial visceral rotation. The first step (Kocher maneuver) mobilizes the pancreaticoduodenal complex and is of limited utility in trauma. The second step (mobilization of the right colon) provides wide exposure of the inferior vena cava and right kidney and hilum. The third step (Cattell–Braasch maneuver) is completed by separating the small bowel mesentery from the posterior peritoneum.

surgeon must make during these first few hectic minutes inside the blood-filled abdomen is whether the bleeding problem is simple or complex, based on the bleeding rate and the accessibility of the bleeder. Simple bleeding problems are easy to solve because they are accessible and can be attacked directly. For example, even fierce hemorrhage from organs that have an accessible vascular pedicle (such as a shattered spleen or kidney) can be rapidly controlled by mobilizing the organ into the midline, controlling the pedicle, and then deciding whether to repair the injury or resect the organ. Bleeding from the majority of liver injuries stops either with packing or with lesser hemostatic options such as suture or electrocoagulation. A central retroperioneal hematoma is typically a manifestation of a major abdominal vascular injury and an example of a complex bleeding problem where a direct attack on the bleeder often proves a lethal mistake. Instead, the complex problem requires a disciplined approach consisting of proximal control,

exposure of the injury using the appropriate exposure maneuver, and a formal vascular repair. Other examples of complex hemostatic problems are bleeding from a high-grade liver injury that cannot be controlled with packing and simultaneous vigorous hemorrhage from several sites (also known as multifocal exsanguination). When addressing a complex bleeding problem, the surgeon must first achieve temporary hemostasis, and then pause the operation to mobilize the resources of the surgical support envelope and organize the attack on the injury. Pausing the operation at this point (sometimes for as long as 30 minutes or more) is absolutely vital because many resources that are required to successfully deal with a complex bleeding problem are located outside the OR, in the outer tiers of the support envelope. The surgeon may need another assistant or more experienced help, or may wish to use a special retraction system to better expose an inaccessible liver injury. The anesthesia team needs a stock of blood products in the room and an autotransfuser. The circulating nurse needs competent help and may decide that the situation also merits a more experienced scrub nurse in the operative field. Mobilizing all these resources takes time, but greatly improves the chances of success in accomplishing the core mission of the operation because it converts hectic fumbling into an organized, coordinated team effort. When facing a complex bleeding problem, the surgeon and team have only a narrow time window to achieve definitive hemostasis and conclude the operation with a live patient. Battle with an exsanguinating injury is surprisingly short. For example, when facing a high-grade liver injury, the surgeon has roughly 30–45 minutes and something in the order of 10–15 U of blood to achieve hemostasis and bail out of the abdomen before the patient develops severe hypothermia, coagulopathic bleeding, and an irreversible physiological insult. If more than one visceral compartment is open (e.g., abdomen and chest), the time window is even narrower because heat loss is accelerated. An effective operative support envelope may extend this window—but not by much, since even the best support cannot slow down heat loss from the open abdomen. However, a wellorganized attack has a higher chance of making effective use of the available time window.

■ Choosing an Operative Profile After having achieved definitive control of hemorrhage, the surgeon must decide how to proceed with the rest of the operation or, in other words, choose an operative profile. The options are either definitive repair of the injuries with formal abdominal closure (the correct choice for the majority of cases) or a rapid bailout using damage control techniques and temporary abdominal closure (see Chapter 38). Contrary to popular notions, the decision to use damage control does not rely on identifying the “lethal triad” of hypothermia, coagulopathy, and acidosis simply because by then it may be too late. Experienced surgeons decide to bail out early and preemptively,16 sometimes within minutes of entering the abdomen. They typically consider three factors (Table 27-3). The pattern of injury often dictates a damage control approach. For example, a packed liver will have to be revisited

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FIGURE 27-8 The full Cattell–Braasch maneuver provides panoramic exposure of the retroperitoneum. This maneuver is useful in a wide range of operative situations where wide exposure is needed to explore the retroperitoneum or access specific structures. The only two areas of the retroperitoneum that remain inaccessible are the retrohepatic vena cava and the suprarenal aorta. The latter is accessible with the Mattox maneuver.

and the combination of a major vascular trauma and hollow organ perforations will usually require a definitive repair for the former but a bailout solution for the latter. The patient’s overall trauma burden is another consideration. Serious injury to anatomical regions outside the operative field (e.g., ongoing bleeding from a chest tube) or even the clinical suspicion of such trauma (e.g., unequal pupils) is a strong

indication to abbreviate the laparotomy to address the other injuries as soon as possible. A realistic assessment of the OR system and circumstances may also point to damage control as the safest option. Working in a suboptimal environment (such as a small rural facility or a military forward surgery team), having limited trauma experience, or an inadequate support envelope are all situations where

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TABLE 27-3 Factors to Consider in Choosing an Operative Profile

SECTION 3 X

Early Decision (Preemptive Damage Control) Abdominal injury pattern Overall trauma burden OR system and circumstances

Late Decision (Forced Bailout) Physiological insult Perceptual cues in the operative field

a rapid bailout is often in the patient’s best interest. Damage control is rightfully known as the “great equalizer” of trauma surgery, allowing surgeons to successfully address complex lifethreatening injuries in austere conditions or with limited trauma experience. In gauging the magnitude of the physiological insult, the surgeon must focus on variables that reflect the cumulative insult over time rather than “snapshot” values of blood pressure or oxygen saturation. A realistic estimate of the overall blood volume lost, transfusion requirements, and the duration of hypotension are such cumulative variables. The degree of metabolic acidosis (pH 7.30) and hypothermia (35°C) are useful but late indicators, since the surgeon should ideally make the decision to bail out well before they occur. Occasionally, the surgeon proceeds with a definitive repair profile but recognizes at some point that the circumstances have changed and there is a need to abbreviate the operation. Subtle perceptual cues to make this switch are signs such as edema of the bowel wall, tissues cold to the touch, noncompliant and grossly edematous abdominal wall, and diffuse oozing from the surgical incision. Such a “forced” bailout actually means that the surgeon is trying to correct a previous error in judgment and should have bailed out long ago.

■ Temporary Abdominal Closure The goals of temporary abdominal closure at the end of a damage control laparotomy are to provide rapid atraumatic containment of the abdominal viscera, protect the bowel, and spare the fascia for the definitive closure. Effective temporary closure also reduces the catabolic effects of the open abdominal wound. The specific technique chosen is largely a matter of personal preference and is heavily influenced by institutional traditions and practices. The vacuum pack, introduced by Barker et al. in 1995, has revolutionized abdominal closure not only because it allowed rapid sutureless containment17 but also because it inadvertently modified the healing process of the abdominal wound. The vacuum pack is a sandwich of three layers. The visceral block is wrapped with a polyethylene sheet that is carefully tucked between the viscera and the abdominal wall all the way down into the paracolic gutters. The sheet is covered with a surgical towel to absorb peritoneal fluid. Two suction drains are placed on the surgical towel and brought out through the lower or upper corner of the abdominal wound. Their role is to evacuate the peritoneal fluid in a controlled fashion. The third and final layer is a large polyester adhesive drape that seals the sandwich.

The unexpected beneficial effect of the vacuum pack on the wound healing process of the open abdomen is brought about by the innermost layer of the sandwich, since the polyethylene sheet serves as a physical barrier between the visceral block and the abdominal wall. It prevents adhesion formation between the visceral block and the inner aspect of the abdominal wall, so that they granulate separately. As a result, the lateral mobility of the abdominal wall is preserved for much longer than the 10–14 days it takes the granulating bowel to adhere to the inner aspect of the wall with other temporary closure techniques. This, in turn, extends the window of opportunity to achieve delayed primary closure of the open abdomen to as much as a month after the initial operation.18 The popularization and commercial success of vacuumassisted wound management technology in the last decade rapidly led to its application to the open abdomen. Replacing the middle layer of the vacuum pack (the surgical towel that absorbs fluids) with a sponge has been advertised as facilitating wound healing and preventing lateral retraction of the fascia. While these claims have never been subject to a scientific comparison with the original vacuum pack, there is a growing number of reports that associate the use of vacuum-assisted wound management in the open abdomen with the formation of exposed (enteroatmospheric) fistulae,19 especially when there is a suture line in the bowel or if the gut is otherwise compromised. These have led to an FDA alert in November 2009 cautioning against using vacuum-assisted management systems in the open abdomen.

RELAPAROTOMY ■ Urgent Reoperation for Bleeding Reexploration of the injured abdomen for bleeding is a dramatic operation with high mortality: roughly one in four operations will end with a dead patient.20 The decision to operate may be difficult in critically injured patients since during the first few hours in the SICU they are often hemodynamically unstable and coagulopathic so a certain amount of postoperative bleeding and equilibration is to be expected. The surgeon must decide not whether the patient is bleeding but whether the amount or rate of hemorrhage exceeds what is expected in this specific clinical situation, representing a likely surgical bleeder. Most patients with ongoing postoperative bleeding are hemodynamically unstable and some of them also develop intra-abdominal hypertension and occasionally a full-blown abdominal compartment syndrome. The operative profile is therefore that of a crash laparotomy. Nowhere is the quality of the surgeon’s support envelope more important than during this high-stakes procedure where the patient’s physiology, already compromised by the original injury and laparotomy, is extremely shaky from the start. Reoperation for bleeding follows the same generic sequence described in the first part of this chapter. The only goal of the procedure is to achieve hemostasis and decompress the abdomen. All else is irrelevant. The patient’s only hope is a rapid focused effort to identify and control a surgical bleeder.

Trauma Laparotomy: Principles and Techniques

■ Urgent Laparotomy for Abdominal Infection Abdominal infection after laparotomy for trauma may be either controlled or uncontrolled. The former is more common and consists of single or multiple localized abscesses that can be drained percutaneously under CT guidance. Uncontrolled infection is much less frequent but more ominous, with an active ongoing source of infection that cannot simply be drained and therefore requires surgical control.21 Diffuse peritonitis from a duodenal missed injury, an exposed (enteroatmospheric) fistula draining through an open abdomen, and a septic dehiscence of the laparotomy wound due to a leaking colonic staple line are all examples of uncontrolled abdominal infection. Severe uncontrolled abdominal infection results in an extremely hostile peritoneal cavity: the bowel is edematous and very friable, the mesentery is foreshortened, and the abdominal wall is swollen and noncompliant. Granulation tissue and dense vascular adhesions fuse adjacent bowel loops and glue the visceral block to the abdominal wall, impeding access to the leak. The only goal of relaparotomy for abdominal infection is to achieve source control. The peritoneal cavity is typically entered through the previous incision, all purulent and necrotic material is removed, and the source of ongoing bacterial contamination is identified. Suture or staple lines created during the original operation are carefully inspected for leaks, and if none are found a diligent search is then undertaken for

TABLE 27-4 Technical Options for Source Control during Relaparotomy for Uncontrolled Abdominal Infection Technical Option Resection and anastomosis Resection and exteriorization Proximal diversion

Tube drainage Vacuum-assisted management

Comment Rarely feasible for early leaks Almost never feasible due to foreshortened mesentery Occasionally lifesaving (edematous abdominal wall is obstacle) Contraindicated Useful option for exposed fistula (caution if unprotected suture lines)

missed injuries along the presumed trajectory of the injuring missile and at locations prone to hide missed injuries (as described above). The technical options to achieve source control are given in Table 27-4. The simplest way is to resect or exteriorize the leaking segment.22 As a general rule, creating new unprotected suture lines in a hostile and severely inflamed peritoneal cavity is a hazardous undertaking even when dealing with “forgiving” viscera such as the stomach or the small bowel. When considering how to control the leak, the surgeon must take into account not only the local conditions in the abdomen but also the patient’s overall physiological reserves and ability to survive another leak. An example of this dilemma is the decision whether to perform a pyloric exclusion for a duodenal leak that is addressed in a delayed fashion in a severely inflamed abdomen. The benefits of the pyloric exclusion (as opposed to creating a tube duodenostomy and accepting a controlled side fistula) must be weighed against the added risk of another suture line failure in the hostile peritoneal cavity. When relaparotomy is delayed and the leaking bowel segment cannot be mobilized, exteriorized, or safely resected, the surgeon may still be able to achieve source control by proximal diversion, which can be lifesaving.22 Tube drainage alone typically does not provide effective source control since the leak continues around it, and the tube itself serves only to bore down and enlarge the hole in the gut. Vacuum-assisted wound management is an important adjunct that helps the surgeon achieve source control of exposed fistulae by continuous suction of the intestinal content. However, this modality must be used with caution in the presence of compromised bowel or intact suture lines in the gut as described above.23 Relaparotomy for uncontrolled abdominal infection usually commits the surgeon to a series of planned reoperations to wash out the abdomen, assess progress, optimize source control, and tailor the technical solutions (such as the size and shape of the vacuum-assisted dressing) to the granulating and gradually healing open abdominal wound.

CHAPTER CHAPTER 27 X

The abdomen is entered through the previous incision (or open wound). After rapid evisceration and evacuation of blood and clots, the surgeon proceeds to look for the source of bleeding. In roughly half the cases, the source of bleeding is incomplete (or failed) hemostasis at a site that was addressed during the original operation.20 This is most likely to occur in packed areas such as the liver and, less frequently, the retroperitoneum. Other sources of hemorrhage are missed injuries or iatrogenic damage (typically to the spleen). In reexploring the injured abdomen the surgeon must therefore be aware that the source of rebleeding is most likely found in the immediate vicinity of a previous repair or hemostatic effort. Not uncommonly, the surgeon faces a peritoneal cavity filled with blood and clots but cannot identify a discrete bleeder anywhere. The best option in this situation is to perform a full systematic exploration with emphasis on the location of previously addressed injuries, until the surgeon is satisfied that there is no active bleeder to address. The peritoneal cavity is irrigated with warm saline and a decision made whether to use temporary abdominal closure with a vacuum pack or to reclose the abdomen. Nothing is more frustrating than to find only diffuse oozing in the abdomen of a patient in extremis with no surgical bleeder. This situation is not amenable to surgical control and the reoperation only worsens the patient’s already precarious physiology. When encountered, diffuse coagulopathic oozing should be recognized early for what it is and the operation rapidly terminated. However, even with rapid packing and bailout, the survival after such procedures is very low.20

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■ Planned Reoperation SECTION 3 X

Planned relaparotomy after an initial damage control procedure is performed on a patient whose physiological envelope has been restored by rewarming and resuscitation. The patient often remains critically ill but is no longer facing imminent death from exsanguinations or irreversible shock. The operation is typically undertaken within 24–48 hours of the initial operation. The precise timing depends on clinical and logistical considerations. For example, the presence of a “closed loop” of bowel that has been stapled off at both ends is an argument for an earlier reoperation, while a high-grade liver injury that has been successfully packed will rarely be addressed before 48 hours, to allow the hemostatic clots time to stabilize and mature.21 Planned relaparotomy begins with meticulous exploration of the abdominal cavity. Significant injuries that have been overlooked or only partially defined in the heat of the original battle must now be identified and addressed. The next step is reconstruction. Major vascular reconstruction (e.g., replacing a temporary shunt in the common iliac artery with a synthetic graft) typically precedes GI tract repairs. The guiding principle for GI reconstructions during reoperation is to be conservative and avoid risky suture lines. Reconstructions that could have been considered safe during the original operation (such as a colocolostomy or pancreaticojejunostomy) may no longer be acceptable after 48 hours of an open abdomen in an edematous patient who will not tolerate a leak. The removal of packs and other temporary hemostatic devices (such as balloon catheter tamponade) is always the last step before abdominal closure, since there is always the risk that unpacking may result in recurrent bleeding and require repacking and another bailout. Packing should be removed after soaking the packs and the surrounding organs with saline and allowing time for the saline to soak through. Topical hemostatics and other adjuncts (such as an argon beam coagulator) should be ready to be applied to the unpacked areas, and a full set of vascular instruments should be available in case a major venous injury is uncovered under the packs. A safe technique for pack removal is to use a jet of water from a large bulb syringe directed at the interface between the packs and the tissue. The packs are then slowly removed. When bleeding is encountered, the surgeon stops unpacking to achieve hemostasis. The most common problem is slow persistent oozing from a raw surface, which is typically controlled by a combination of electrocoagulation, local hemostatic agents, and the application of gentle firm pressure. A key principle during any relaparotomy for trauma is that the surgeon must be mentally prepared to accept failure.21 When repeated attempts to achieve hemostasis fail and there is no indication for a formal vascular repair, admitting failure and rapidly repacking the area is a safer option than insisting on a definitive hemostatic solution. Formal abdominal closure, if feasible, is the last step in the reoperative sequence. Before closure, the surgeon should consider creating a route for early enteral feeding either via a nasojejunal tube passed by the anesthesiologist and guided by the surgeon past the pylorus or through a feeding jejunostomy.

TABLE 27-5 Technical Options for Delayed Abdominal Closure at Reoperation Primary Closure Feasible? Yes No

Preserved Peritoneal Space? Yes Yes

No

No

Technical Option Primary closure Components separation or biological prosthesis Planned ventral hernia

Simple delayed primary closure of the open abdomen may not be possible if the abdominal wall has retracted laterally, creating a large gap. In these situations, the surgeon’s technical options depend on whether the peritoneal space has been preserved, as explained above (Table 27-5). An obliterated peritoneal space means that the abdominal wound has granulated and healed by secondary intention. The wound edges therefore lack lateral-to-medial mobility and the fascia can neither be closed nor bridged. The only option is to cover the wound with a skin graft, accepting a giant planned ventral hernia that will be repaired many months later.24 With a preserved peritoneal space, the surgeon has two technical options to achieve delayed primary closure. The components separation technique25 achieves better long-term results, whereas the use of a biological prosthesis is technically more expedient but at the price of very high long-term failure rates.

BEDSIDE LAPAROTOMY Bedside laparotomy in the SICU was originally introduced as a practical solution for patients who needed a relaparotomy but were simply too unstable for even a short trip to the OR.21 The classic examples are the patient with full-blown abdominal compartment syndrome in need of immediate decompression,26 or the crashing patient with postoperative bleeding in the open abdomen. For these and other patients on very high ventilator settings and high-dose pressor support, the journey to the OR is much more perilous than the reoperation itself. At the other end of the severity spectrum is a hemodynamically stable (yet still critically ill) patient who needs a “routine washout” of the open abdomen but whose procedure is repeatedly postponed because of OR availability issues. As bedside laparotomy has gained popularity, the indications have expanded and also include planned and unplanned reoperation for abdominal infection (both controlled and uncontrolled) to drain infected fluid collections and optimize control of exposed fistulae. The great advantage of a bedside laparotomy is expediency. Since the abdomen is usually open, access is not an issue and the suboptimal sterility of the operative field is not a concern. The surgeon must, however, bear in mind the obvious limitations of a bedside laparotomy: working conditions (such as lighting and the physical distance of the surgeon from the abdominal wound) are inferior to those in the OR, the

Trauma Laparotomy: Principles and Techniques

FIGURE 27-9 Bedside laparotomy in the Surgical Intensive Care Unit. A scrub nurse and circulating nurse from the OR staff are preparing a sterile instrument tray (left) while a surgical resident is assigned to monitor the patient’s vital signs (right). Bedside laparotomy should be a protocol-driven routine activity that is ingrained in the culture of the trauma service and SICU.

course of action is to only evacuate the blood and rapidly pack the abdomen to achieve temporary hemostasis and then transfer the patient to the OR for a formal exploration and definitive hemostasis. Unless the source of bleeding is trivial and immediately accessible, definitive control of surgical bleeding should be done in the optimal work environment of the OR. In the patient with uncontrolled abdominal infection, bedside laparotomy can be used to search for an obvious source (such as a new hole in the gut or breakdown of an intestinal suture line), to ascertain bowel and stoma viability, and to optimize drainage by repositioning old drains or placing new ones. As a general rule, bowel resection and stoma formation should be done in the OR.

ROLE OF LAPAROSCOPY Following a brief period of initial enthusiasm, trauma surgeons were quick to discard laparoscopy as a useful modality in abdominal trauma roughly a decade ago. This was based on several retrospective studies from the early days of laparoscopy in general surgery that led to the perception that laparoscopy is not sensitive enough because it misses significant injuries, especially in patients with penetrating abdominal injuries.28 The inability to “run the bowel” properly was also often cited as a shortcoming of the technology. As a result, the current role of diagnostic laparoscopy in trauma is limited to ruling out diaphragmatic penetration in patients with asymptomatic left-sided thoracoabdominal stab wounds.29 Insufflating the abdomen and inserting a camera through a single umbilical port allows the surgeon to visualize the entire left hemidiaphragm and thus rule out a diaphragmatic penetration. If an injury is found, the procedure is typically converted to an open laparotomy since laparoscopy is considered unreliable in ruling out intra-abdominal visceral damage. Liberal use of laparoscopy led to the discovery of an occult diaphragmatic injury in roughly one in four of these patients. Another useful application of laparoscopy in trauma is as a useful adjunct to the conservative management of hepatic trauma.30 In some of these patients, bile leak combined with perihepatic hematoma leads to a septic clinical picture of smoldering bile peritonitis with a prominent systemic inflammatory response. In these situations, laparoscopic washout of the right upper quadrant is an elegant minimally invasive approach to the problem. Using the port arrangement of laparoscopic cholecystectomy, the surgeon can wash out the bile from the right upper quadrant, use the blunt dissector and suction irrigation to remove superficial fibrinous rinds on the liver capsule or infected clots around the liver, and place a suction drain in Morisson’s pouch under direct vision. The current very restricted role of laparoscopy in trauma does not do justice to the great potential of the technology. The early studies were done in an era of first-generation equipment and basic laparoscopic skills. Both have dramatically improved in the past decade. The technique for a detailed laparoscopic exploration of the abdominal cavity, including fully “running the bowel” using a four-port approach, has been published31 but has not caught on in the trauma community. Of the two modes of laparotomy in trauma described in Section

CHAPTER CHAPTER 27 X

surgeon’s support envelope is weaker, and the scope of the procedures that can be safely undertaken at the bedside is necessarily limited. Bedside laparotomy in the SICU cannot be improvised on a whim. It requires planning, a standardized institutional protocol, and clear understanding of what can or cannot be achieved at the bedside.27 Most importantly, the procedure must be ingrained in the institutional culture as a routine feature of SICU care rather than a rare dramatic occurrence. In other words, a large number of “routine washouts” performed regularly in the SICU are needed to develop and maintain the capability for an occasional dramatic save of a patient with intra-abdominal hemorrhage. Preparation for a bedside laparotomy consists of creating a sterile surgical perimeter on the patient’s bed as well as deploying a simplified support envelope around it. A basic laparotomy instrument tray and all necessary sterile adjuncts are brought in from the OR suite, including warm saline and a temporary abdominal closure device. A team member is assigned to continuously monitor the patient’s vital signs and lines throughout the procedure. In some institutions, OR nursing staff participates in bedside laparotomies as both scrub nurse and circulating nurse (Fig. 27-9). If this is not feasible, members of the SICU or trauma teams are assigned to fulfill these roles. The sequence of a bedside laparotomy is tailored to the specific clinical circumstances. In a routine washout, the surgeon removes the temporary abdominal closure device, performs a limited exploration of the peritoneal cavity, manually separates the granulating visceral block from the overlaying abdominal wall to preserve the peritoneal space, and ascertains that no undrained sources of sepsis are left behind. Copious irrigation of the peritoneal cavity with warm saline is then followed by rapid temporary reclosure with a new temporary device. An urgent bedside laparotomy for bleeding follows the same sequence as a similar procedure in the OR. However, the safe

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SECTION 3 X

“Introduction,” the procedure in a stable patient with a hole in the gut and limited or no bleeding is clearly suitable for at least a renewed evaluation of the role of laparoscopy. In an era when an increasing number of perforated gastric and duodenal ulcers are repaired laparoscopically, there is no good reason not to revisit the role of this technology in selected patients with abdominal trauma.

REFERENCES 1. Hirshberg A, Mattox KL. The crash laparotomy. In: Hirshberg A, Mattox KL, eds. Top Knife: The Art and Craft of Trauma Surgery. Shrewsbury: tfm Publishing; 2005:53–70:chap 4. 2. Como JJ, Bokhari F, Chiu WC, et al. Practice management guidelines for selective nonoperative management of penetrating abdominal trauma. J Trauma. 2010;68:721–733. 3. Hirshberg A, Wall MJ Jr, Mattox KL. Bullet trajectory predicts the need for “damage control”—an artificial neural network model. J Trauma. 2002;52:852–858. 4. Mattox KL, Hirshberg A. Access, control and repair techniques. In: Rich N, Mattox KL, Hirshberg A, eds. Vascular Trauma. 2nd ed. Philadelphia, PA: Elsevier Saunders; 2004:137–164:chap 7. 5. Rotondo MF, Zonies DH. The damage control sequence and underlying logic. Surg Clin North Am. 1997;77:761–777. 6. Hansen KS, Uggen PE, Brattebo G, et al. Team-oriented training for damage control surgery in rural trauma: a new paradigm. J Trauma. 2008;64:949–953. 7. Awad SS, Fagan SP, Bellows C, et al. Bridging the communication gap in the operating room with medical team training. Am J Surg. 2005;190: 770–774. 8. Chassin JL. Operative technique for midline incision. In: Chassin JL, ed. Operative Strategy in General Surgery: An Expositive Atlas. New York, NY: Springer-Verlag; 1980:40–43. 9. Veith FJ, Gupta S, Daly V. Technique for occluding the supraceliac aorta through the abdomen. Surg Gynecol Obstet. 1980;151:426–428. 10. Hirshberg A, Wall MJ Jr, Allen MK, et al. Causes and patterns of missed injuries in trauma. Am J Surg. 1994;168:299–303. 11. Mattox KL, McCollum WB, Beall AC, et al. Management of penetrating injuries of the suprarenal aorta. J Trauma. 1975;15:808–813. 12. Reilly LM, Ramos TK, Murray SP, et al. Optimal exposure of the proximal abdominal aorta: a critical appraisal of transabdominal medical visceral rotation. J Vasc Surg. 1994;19:375–390. 13. Buscaglia LC, Blaisdell FW, Lim RC. Penetrating abdominal vascular injuries. Arch Surg. 1969;99:764–769. 14. Lauter DM. Midline laparotomy and right retroperitoneal dissection is an alternative exposure for routine aortic surgery. Am J Surg. 2003;186:20–22.

15. Cattell RB, Braasch JW. A technique for the exposure of the third and fourth portions of the duodenum. Surg Gynecol Obstet. 1960;111: 378–379. 16. Hoey BA, Schwab CW. Damage control surgery. Scand J Surg. 2002;91: 92–103. 17. Barker DE, Kaufman HJ, Smith LA, et al. Vacuum pack technique of temporary abdominal closure: a 7-year experience with 112 patients. J Trauma. 2000;48:201–206. 18. Miller PR, Thompson JT, Faler BJ, et al. Late fascial closure in lieu of ventral hernia: the next step in open abdomen management. J Trauma. 2002;53:843–849. 19. Fischer JE. A cautionary note: the use of vacuum-assisted closure systems in the treatment of gastrointestinal cutaneous fistula may be associated with higher mortality from subsequent fistula development. Am J Surg. 2008;196:1–2. 20. Hirshberg A, Wall MJ Jr, Ramchandani MK, et al. Reoperation for bleeding in trauma. Arch Surg. 1993;128:1163–1167. 21. Hirshberg A, Stein M, Adar R. Reoperation: planned and unplanned. Surg Clin North Am. 1997;77:897–907. 22. Schein M, Decker GA. Gastrointestinal fistulas associated with large abdominal wall defects: experience with 43 patients. Br J Surg. 1990;77: 97–100. 23. Schecter WP, Hirshberg A, Chang DS, et al. Enteric fistulas: principles of management. J Am Coll Surg. 2009;209:484–489. 24. Jerrigan TW, Fabian TC, Croce MA, et al. Staged management of giant abdominal wall defects: acute and long-term results. Ann Surg. 2003; 238:349–357. 25. Shestak KC, Edington HJ, Johnson RR. The separation of anatomic components technique for the reconstruction of massive midline abdominal wall defects: anatomy, surgical technique, applications, and limitations revisited. Plast Reconstr Surg. 2000;105:731–738. 26. Morris JA Jr, Eddy VA, Blinman TA, et al. The staged celiotomy for trauma. Issues in unpacking and reconstruction. Ann Surg. 1993;217: 576–584. 27. Diaz JJ, Mejia V, Subhawong AP, et al. Protocol for bedside laparotomy in trauma and emergency general surgery: a low return to the operating room. Am Surg. 2005;71:986–991. 28. Villavicencio RT, Aucar JA. Analysis of laparoscopy in trauma. J Am Coll Surg. 1999;189:11–20. 29. Murray JA, Demetriades D, Asensio J, et al. Occult injuries to the diaphragm: prospective evaluation of laparoscopy in penetrating injuries to the left lower chest. J Am Coll Surg. 1998;187:626–630. 30. Franklin GA, Richardson JD, Brown AL, et al. Prevention of bile peritonitis by laparoscopic evacuation and lavage after nonoperative treatment of liver injuries. Am Surg. 2007;73:611–616. 31. Gorecki PJ, Cottam D, Angus LD, et al. Diagnostic and therapeutic laparoscopy for trauma: a technique for safe and systematic exploration. Surg Laparosc Endosc Percutan Tech. 2002;12:195–198.

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CHAPTER 28

Diaphragm Kevin M. Schuster and Kimberly A. Davis

INTRODUCTION The diaphragm, the most important muscle of respiration, separates the thorax and the abdomen. It can be injured in isolation or involved with injury in either body cavity, and the most challenging concern is the identification of injury. Initially the injury may be asymptomatic with later development of herniation and strangulation of the stomach or other viscera.

HISTORY Traumatic diaphragmatic rupture was first reported by Sennertus in 1541, and Ambroise Paré was the first to report a series of diaphragmatic perforations found at autopsy.1 Paré also described gastric and colonic incarceration in a ruptured diaphragm and the consequences.2 The diagnosis was made in an antemortem fashion for the first time by Bowditch in 1853,3 and it was not until 1886 that Riolfi was credited with the first successful repair.4 The first acute repair by Walker in 1899 was in a patient who had been struck by a falling tree.5 The largest early review of 378 diaphragmatic hernias was by Hedblom in 1925.4

ANATOMY The diaphragm is a dome-shaped musculofibrous septum separating the abdomen and thorax. It is bounded above by both pleural spaces and the pericardium, which is attached to the central tendon. Structures immediately adjacent to the inferior side of the diaphragm include the liver, spleen, stomach, and to varying degrees the colon, omentum, and small bowel. The origin of the diaphragm includes the lower sternum, lower six costal cartilages and adjacent ribs, and medial and lateral lumbocostal arches. The crura, two tendinous pillars, arise from the lumbar vertebrae. The insertion of the diaphragm is into the central tendon, an aponeurosis, located at the top of the dome,

oriented transversely, and separated into three segments. At rest the diaphragm rises to the level of the fourth intercostal space on the right and the fifth intercostal space on the left. At maximal contraction the diaphragm descends two rib spaces bilaterally. The aorta passes behind the diaphragm and between the crura where it has no attachments. Along with the aorta the thoracic duct and azygous vein pass through this opening. The esophagus traverses the esophageal hiatus mostly composed of the right crus along with the vagus nerves. The inferior vena cava passes through its hiatus at the junction of the right and middle leaflets of the central tendon to which it may be adherent (Fig. 28-1). The blood supply to the diaphragm is multiply redundant making necrosis extremely rare.6 The major source of blood supply to the abdominal side of the diaphragm is the inferior phrenic arteries, which are branches of the abdominal aorta or celiac trunk. Additional blood supply is from the superior phrenic, pericardiophrenic, musculophrenic, and the intercostal arteries. Lymphatic drainage is rich on both sides of the diaphragm with the peritoneal surface the major contributor to peritoneal lymphatic drainage. Innervation is principally through the phrenic nerves with some contribution of the sixth or seventh intercostal nerves to the costal region of the diaphragm. Both phrenic nerves enter the diaphragm near the anterior border of the central tendon. These nerves give branches along the thoracic surface of the diaphragm before penetrating it to spread branches in anterior, posterior, and lateral directions. The nerves are often buried deep in the muscle, and one should not rely on visualizing the nerves in order to choose incisions in the diaphragm. Safe diaphragm incisions that protect the phrenic nerves are depicted in Fig. 28-2.

PHYSIOLOGY The diaphragm is a vital muscle involved in the function of both the digestive and respiratory systems. It participates in breathing, swallowing, coughing, defecation, emesis, micturition,

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Management of Specific Injuries

SECTION 3 X FIGURE 28-1 View of the diaphragm from the abdomen including the aortic, esophageal, and caval hiatuses. IVC  inferior vena cava.

parturition, sneezing, and vocalization.7 In humans it is the most important muscle of inspiration and can independently generate negative intrapleural pressure sufficient for respiration.8 The innervation of the diaphragm is centrally unified in the spinal cord, and the entire diaphragm from the crura to the lateral margins has motor neuron origins intermingled within the spinal cord.9 The crural components, however, may have their function overridden through peripheral or central mechanisms related to function of the gastrointestinal tract.

Left hemidiaphragm

Right hemidiaphragm

2-3 cm

C A D B

FIGURE 28-2 Surgical incisions on the diaphragm. (A) An incision with a risk of total paralysis of the diaphragm. (B) A preferred incision with minimal risk of nerve injury. (C, D) Incisions in safe areas, but with small risk of nerve injury. (Reprinted from Anraku M, Shargall Y. Thoracic Surgical Clinics Vol. 19 Surgical conditions of the diaphragm: anatomy and physiology, Page 422., Copyright 2009, with permission from Elsevier.)

Perforation of the diaphragm can lead to acute changes in physiology. The displacement of intra-abdominal viscera into the chest under the influence of the pressure gradient between the abdomen and the chest may compromise both cardiac and respiratory function. Cardiac function can become deranged due to reduced ventricular filling leading to decreased cardiac output. Significant compression of the pulmonary parenchyma can lead to impaired ventilation on the ipsilateral side, and, if more severe, mediastinal shift and compression of the contralateral lung. As with any herniation of portions of the gastrointestinal tract, sequelae such as ischemia, necrosis, and perforation may develop. Unfortunately, there are no longterm outcome data that describe diaphragmatic function after repair for trauma. There are many reports of delayed repairs of diaphragmatic injuries, and this suggests that repair is durable and has little impact on either pulmonary or gastrointestinal tract function.

INCIDENCE The reported incidence of injuries to the diaphragm after blunt trauma ranges from less than 1 to 7% and from 10 to 15% in victims of penetrating trauma.10–12 This wide range stems from an inability to identify injuries treated at nontrauma centers, death prior to hospital admission, and missed injuries after admission to a trauma center despite complete evaluation. A query of the National Trauma Data Bank (NTDB) for the years 2002–2007 demonstrated an incidence of 0.43% or 10,128 injuries among 2,349,554 patients (Table 28-1).12 In a study at one center that included data from the medical examiner, survival to hospital admission was 87% indicating a relatively

Diaphragm

Mechanism Blunt Penetrating Other Unspecified Total

Number of Patients with Diaphragm Injury 3585 4788 99 1656 10128

Percent of Total NTDB Patients 0.15 0.20 0.00 0.07 0.43

From reference 12.

small fraction of patients are missed due to death.13 The highest rate of injury occurs in patients sustaining penetrating trauma to the thoracoabdominal region where the incidence of diaphragm injury has been reported to range as high as 42%.14 In one study of asymptomatic patients with penetrating thoracoabdominal trauma an injury rate of 24% was documented when mandatory laparoscopy was performed.15

MECHANISM OF INJURY AND PATHOPHYSIOLOGY Approximately 75% of diaphragmatic hernias occur on the left side.10 It has been postulated that this is secondary to a congenital weakness of the left side of the diaphragm.11 Many authors, however, have found no evidence for a congenital weakness of one side of the diaphragm and attribute the tendency for blunt rupture to occur on the left to protection of the right side by the liver.16 Others have reported no difference in incidence between the left and right sides in autopsy studies.17 Although less common, right-sided injuries are often associated with ipsilateral high energy impacts. Similarly the most common mechanism on the left is a left-sided impact though it is often of much lower energy.18 The higher energy impact necessary to cause right-sided rupture may explain the difference between the autopsy study and the clinical studies because high energy right-sided impacts would more commonly cause death. Similarly, penetrating injury to the diaphragm has a left-sided predilection secondary to prevalence of right-handed assailants.19,20 Penetrating wounds typically result in a smaller injury, but these injuries may enlarge over time and eventually cause acute incarceration and/or strangulation.19–21

PRESENTATION Grimes classified diaphragmatic injuries into the following three phases of presentation: acute, or during the period of recovery from injury; latent, an asymptomatic period; and obstructive, during which time herniation leads to cardiovascular compromise or gastrointestinal obstruction or perforation.22 Presentation in the acute phase is often dominated by

symptoms from concomitant injuries. Patients may have minimal signs of external injury or be experiencing severe shock and respiratory compromise that may or may not be directly related to the diaphragmatic injury. In the less severely injured, possible signs and symptoms include shoulder pain, epigastric pain, vomiting, dyspnea, absent breath sounds, or bowel sounds heard during auscultation of the chest.23 It is likely that the advent of routine helical computed tomography (CT) scanning has decreased the incidence of missed injuries after blunt trauma.24 Several case series have reported 3–15% of cases presenting in the late or obstructive phase.25,28 In the latent phase herniation may be discovered as an incidental finding on radiographic studies performed for other reasons. Symptomatic patients presenting in the obstructive phase often experience nausea, vomiting, early satiety, pain, dyspnea, postprandial pain, or generalized chest and abdominal pain. These symptoms may be intermittent or progressive. Patients may also present in extremis with signs and symptoms of septic shock due to ischemia or perforation related to strangulation of the stomach or colon or with cardiovascular collapse due to compression similar to a tension pneumothorax.21,26

ASSOCIATED INJURIES Blunt diaphragmatic injury typically involves high energy compression-type mechanisms, and associated injuries are common. Traumatic brain injury is present in half of the patients and is predictive of mortality.23 Other associated injuries include pelvic fractures, long bone fractures, and rib fractures. Intrathoracic injuries have included pneumothorax, pulmonary contusion, lung lacerations, blunt myocardial injury, and aortic rupture.16,23,27 Solid organ injuries are the most common associated intra-abdominal injuries.16,27,28 Penetrating injuries also have high rates of associated injuries, especially to intra-abdominal viscera, but including a hemothorax or pneumothorax, as well. Specific intra-abdominal organs typically injured with penetrating diaphragmatic injury include the upper abdominal organs.14,19,23,28 A list of associated injuries identified in patients with diaphragm injury in the NTDB is presented in Table 28-2.

DIAGNOSIS AND DIAGNOSTIC TESTS Diaphragmatic rupture is often asymptomatic, or the presentation is dominated by concomitant injury making an immediate diagnosis difficult. Information about the mechanism of injury should be obtained from prehospital personnel. In patients involved in motor vehicle crashes, information about the velocity and direction of impact, the severity of vehicular damage, the presence of passenger-compartment intrusion, and the presence or absence of deformity of the steering wheel will be helpful to indicate the severity of the crash. Injuries are graded according to the American Association for the Surgery of Trauma-Organ Injury Scale for Diaphragmatic Injuries (Table 28-3).29

CHAPTER CHAPTER 28 X

TABLE 28-1 Diaphragm Injury Statistics from the National Trauma Data Bank Years 2002 to 2007

531

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Management of Specific Injuries

TABLE 28-2 Injuries Associated with Diaphragmatic Injury from the National Trauma Data Bank Years 2002 to 2007

SECTION 3 X

Injuries Associated with Diaphragm Injuries Liver Hemo-/ pneumothorax Spleen Liver Rib fractures Bowel injury Extremity injury Renal injury Pelvic fracture Head injury Spinal cord injury Aortic injury Total

Number of Patients 4230 5210 3466 4230 475 3368 2700 1508 1533 1459 298 555 24838

Percent of Traumatic Diaphragm Injuries 41.8 51.4 34.2 41.8 4.7 33.3 26.7 14.9 15.1 14.8 2.9 5.5

From reference 12.

In penetrating trauma any injury to the thoracoabdominal area should raise suspicion for a potential diaphragmatic injury. Although most stab wounds that result in diaphragmatic injury will be in this region, gunshot wounds that injure the diaphragm may occur anywhere on the trunk.26 The initial diagnostic study for any patient where there is suspicion for injury to the diaphragm is a plain chest x-ray. Sensitivity of a chest x-ray for diaphragmatic injury has been reported to be in the range of 27–62% for left-sided injuries and 18–33% for right-sided injuries.30 The finding pathognomonic for blunt and some penetrating injuries of the hemidiaphragm is visualization of a hollow viscus above it with or without an area of constriction at the level of the diaphragm. Identification of the stomach above the diaphragm is often facilitated by the abnormal position of a nasogastric or orogastric tube (Fig. 28-3). Loss of a smooth

FIGURE 28-3 Chest radiograph demonstrating herniated stomach with gastric catheter in place.

contour, ipsilateral pleural effusion, ipsilateral elevated hemidiaphragm, and mediastinal shift represent nonspecific findings associated with diaphragmatic herniation. Contrast swallow studies and enemas as well as fluoroscopy have been used in the past and are potentially helpful (Fig. 28-4); however, their use has been largely supplanted by cross-sectional imaging techniques. Helical CT for the detection of blunt diaphragmatic disruption has a reported sensitivity of 71–100% and specificity of 75–100%, and sensitivity improves to 78–100% if only leftsided injuries are included.31 Multidetector CT (MDCT) scans with multiplanar reformatted images will likely improve

TABLE 28-3 Grading of Diaphragmatic Injuries Grade I II III IV V

Description of Injury Contusion Laceration 2 cm Laceration 2–10 cm Laceration 10 cm with tissue loss 25 cm2 Laceration with tissue loss 25 cm2

Reproduced with permission from Moore EE, Malangoni MA, Cogbill TH et al: Organ injury scaling IV: thoracic vascular, lung, cardiac and diaphragm. J Trauma. 1994;36(3):229–300.

FIGURE 28-4 Contrast enema with splenic flexure identified above the diaphragm.

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CHAPTER CHAPTER 28 X

A FIGURE 28-6 MRI with gastric herniation through diaphragmatic defect.

B FIGURE 28-5 CT scan demonstrating herniated viscus (A, B) and constriction or “collar sign” at the point of herniation (B).

diagnostic accuracy, though no large studies evaluating accuracy have been published. Findings consistent with diaphragmatic disruption include the following: direct visualization of the defect; segmental nonvisualization of the diaphragm; herniation of viscera; constriction of a herniated viscus or a “collar sign” (Fig. 28-5); dependent viscera sign or contact of intraabdominal organs with the posterior chest wall; thickening of the diaphragm; and active extravasation of contrast at the level of the diaphragm. MDCT has been evaluated in patients with penetrating trauma with a reported sensitivity and specificity of 87 and 72%, respectively, in one study.32 In addition to the signs above, contiguous visceral injuries on both sides of the diaphragm are an important potential finding in penetrating trauma. Magnetic resonance imaging (MRI) provides excellent resolution of the diaphragm and separates it from surrounding structures including the liver and atelectatic lung.31 In general, a distinct defect in the diaphragm can be visualized on MRI in addition to the other signs typically found on a CT scan

(Fig. 28-6). MRI is limited in application due to issues with the time required, location of scanners in most institutions, and poor access to the patient during the study. In the hemodynamically stable patient with equivocal CT findings, MRI may have a role, though there have not been any large studies examining its accuracy to date. Ultrasound has been reported in two case series to be capable of providing the diagnosis of diaphragmatic rupture after blunt abdominal trauma.33,34 Findings on ultrasound consistent with diaphragmatic rupture have included identification of viscera within the chest, visualization of the edge of the disruption, inability to visualize the diaphragm, and lack of diaphragmatic excursion in a spontaneously breathing patient. In patients with right-sided ruptures, a finding of liver sliding against the chest wall has also been reported.35 Although thoracoscopy and laparoscopy are invasive, they have been used as diagnostic modalities after penetrating thoracoabdominal injuries that may have injured the diaphragm.14,15,20 As the sensitivity of CT scanning improves, the need for thoracoscopy and laparoscopy may decline; however, none of the studies have compared the accuracy of CT scanning to that of laparoscopy.14,15,20 In one study 36% of patients with a penetrating thoracoabdominal injury and a normal chest x-ray were documented to have a diaphragmatic injury.14 Due to the high rate of associated intra-abdominal injuries, finding a penetrating diaphragmatic injury on laparoscopy mandates laparotomy unless the surgeon has the laparoscopic skills to comfortably exclude and treat an intra-abdominal injury. A potential diagnostic algorithm for identifying diaphragmatic injury is presented in Fig. 28-7.

REPAIR OF ACUTE DIAPHRAGMATIC INJURIES The two principles of repairing acute diaphragmatic hernias are complete reduction of the herniated organs back into the abdominal cavity and watertight closure of the defect to prevent

534

Management of Specific Injuries Diagnosis of Diaphragm Injury in Thoracoabdominal Trauma

SECTION 3 X

Blunt

Penetrating

Resuscitation

Insert NG (if no contraindications)

CXR

Abnormal

Normal

Nondiagnostic

Further imaging Diagnostic

Surgical intervention

- Helical CT - MRI - Contrast study - Laparoscopy (pentrating injury)

FIGURE 28-7 Diagnostic algorithm for identification of diaphragmatic injury.

recurrence. Given the high rate of associated abdominal injuries (generally 1.6 intra-abdominal injuries per patient on average), repair of the acutely injured diaphragm is best performed via an exploratory laparotomy.28,36,37 The right hemidiaphragm is best inspected after transection of the falciform ligament and downward traction of the liver. The left hemidiaphragm can be inspected by applying gentle downward retraction of the spleen and greater curvature of the stomach. The central tendon of the diaphragm should also be examined, along with the esophageal hiatus. Reduction of the intra-abdominal contents is generally not difficult in the period immediately following injury. If the herniated contents are difficult to reduce, the phrenotomy can be partially extended to facilitate reduction, with care taken to avoid injury to the phrenic nerve. It may be necessary to carefully debride the edges of a laceration if devitalized tissue is found, as with a high-velocity missile or close-range shotgun wound. The edges of the diaphragmatic laceration should then be grasped with Allis clamps, and the laceration spread apart to inspect the ipsilateral pleural

cavity. This allows for evaluation of ongoing hemorrhage from within the thoracic cavity, as well as the determination of the degree of contamination between the abdominal and thoracic cavities. Small diaphragmatic disruptions, commonly seen after penetrating trauma, can generally be repaired using interrupted nonabsorbable sutures. Larger defects, more likely associated with blunt trauma, may be repaired in a number of different ways, including interrupted figure of eight or horizontal mattress sutures, a running hemostatic suture line, or a double layer repair, using a combination of the two methods (Fig. 28-8). Generally, a # 0- or # 1-monofilament or braided nonabsorbable suture is used. The authors prefer a # 1-nonabsorbable monofilament placed in an interrupted fashion for the repair of traumatic diaphragmatic defects. In patients in whom a laceration through the central tendon exposes the inferior aspect of the heart, meticulous attention is given to the placement of the sutures to prevent inadvertent puncture or laceration of the myocardium. At the completion of the repair, the integrity of the suture line may be tested by increasing intrathoracic pressure with the administration of large tidal volumes and assessment of diaphragmatic motion. This maneuver is repeated with the field flooded with sterile saline to determine if there is escape of air through the suture line. In cases where there is concomitant injury to a hollow viscus in the abdomen, contamination of the chest will have occurred due to the pressure gradient between the positive pressure in the abdomen and the negative pressure in the thoracic cavity. In this event, careful irrigation of the thoracic cavity through the diaphragmatic disruption is necessary prior to diaphragmatic repair, as empyema is three times more prevalent when there is an associated injury to the bowel.28,38 Zellweger et al.39 studied the management of patients with penetrating thoracoabdominal wounds that injured the diaphragm and gastrointestinal tract and/or liver. He demonstrated that a transdiaphragmatic washout of the pleural cavity was an effective strategy to decrease thoracic contamination.39 At times, a thoracotomy is required for the management of a massive hemothorax, defined as greater that 1500 cc of blood on insertion of a chest tube or in the first 15–30 minutes or more than 200 cc of blood per hour for the first four hours after trauma.40 A laceration of the right hemidiaphragm with an associated laceration of the liver may present as a massive hemothorax, with the diagnosis made at the time of thoracotomy. In this scenario, the diaphragm may be repaired through the chest, but a formal laparotomy will be necessary for the operative management of the hepatic injury and to rule out other associated intra-abdominal injuries. Disruption of the diaphragm following high energy crushing injuries or major deceleration can result in avulsion of the diaphragm laterally from its chest wall attachments. Repair of this injury may require an ipsilateral thoracotomy, which allows horizontal mattress sutures to be placed around the ribs and secures the diaphragm into its normal anatomic position. In the presence of a flail segment of the ipsilateral chest wall, formal fixation of the ribs may be required to facilitate this complex repair of the diaphragm.23 Prosthetic material for diaphragmatic reconstruction in the acute setting is rarely indicated, as tissue retraction and loss has not occurred and concomitant

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CHAPTER CHAPTER 28 X

FIGURE 28-8 Technique for two layer repair of diaphragmatic defect. (Reproduced with permission from Juan A. Asensio, MD, FACS, FCCM and Demetrios Demetriades, MD, PhD, FACS.)

gastrointestinal injuries predispose theoretically to a high rate of postoperative infection. Massive diaphragmatic destruction such as that caused by thoracoabdominal shotgun injuries merits special mention. Bender and Lucas41 described the immediate reconstruction of the chest wall following this type of injury by first detaching the affected hemidiaphragm anteriorly, laterally, and posteriorly. The diaphragm was then translocated to a position above the full-thickness chest wall defect, which converted the defect functionally into an abdominal wall defect. The diaphragm was then resutured to the ribs at a higher intercostal space, while the abdominal wall defect was managed with local wound care in anticipation of reconstruction with either split-thickness skin grafts or myocutaneous flaps at a later date.41 Finally, a diaphragmatic injury diagnosed by laparoscopy in the absence of other injuries mandating laparotomy or thoracotomy can be repaired with this approach.42 Laparoscopic repairs of diaphragmatic injuries can be performed with sutures or staples.14,15

REPAIR OF CHRONIC DIAPHRAGMATIC INJURIES Patients who initially sustain small, undetected, diaphragmatic lacerations may remain asymptomatic or may experience a progressive increase in visceral herniation of the omentum or all or a portion of a hollow viscus.43,44 The diaphragm as a muscle is

quick to retract and atrophies. Therefore, tissue that could be approximated easily on the day of injury retracts in the latent or obstructive phase to the point where approximation is impossible at a late reoperation. Chronic diaphragmatic hernias can be repaired either transabdominally or transthoracically, with the choice generally determined by the subspecialization of the surgeon.45,46 The classical teaching, however, is that large chronic posttraumatic diaphragmatic hernias be approached using a thoracotomy to allow for lysis of intrathoracic adhesions. On occasion, a combined approach may be indicated to complete the procedure safely and effectively. The transthoracic approach offers several benefits including the direct visualization of intrathoracic adhesions, which may extend all the way to the apices of the pleural cavity, and avoidance of abdominal adhesions from the prior trauma.47–50 The thoracic approach has been performed successfully using both open and thoracoscopic techniques.51–53 The open procedure is generally performed through the seventh or eighth intercostal space using a posterolateral approach. Extension along the costal arch into a thoracoabdominal procedure allows access to the abdominal cavity if needed. As noted above, the transabdominal approach is often considered less attractive, due to the inherent difficulty of visualizing adhesions to the lung and other intrathoracic structures, and dealing with potential dense intra-abdominal adhesions from prior trauma and/or surgery. Additionally, if the

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Management of Specific Injuries

SECTION 3 X

procedure cannot be completed at laparotomy, the incision will need to be closed and the patient repositioned for a posterolateral thoracotomy. This is because it is difficult to visualize the posterior diaphragm from an anterolateral approach. Laparoscopy has been described for the reduction of chronic diaphragmatic hernias, as well, although problems with the iatrogenic pneumothorax have mandated the insertion of a thoracostomy tube.49,54–57 No matter which approach is used, current recommendations support the role of open surgery for patients with defects greater than 10 cm and for those extending to or through the esophageal hiatus.54 Careful dissection is required to free the entire diaphragm from its adhesions to surrounding tissues. Once mobilized, the edges should be brought together to evaluate for tension. If the edges can be approximated easily, the repair should be performed primarily as described in the section on acute diaphragmatic injuries. Generally, defects up to 8 cm can be closed primarily.58 Primary repair of larger defects in the diaphragm will cause unacceptable flattening of the diaphragm, and prosthetic material will be needed to reconstruct the diaphragm. Many different prostheses have been used, including mersilene, polytetrafluoroethylene (PTFE), polypropylene, and polydioxanone meshes.48,54,59–62 Recently, a 2-mm thick PTFE patch has been advocated as an excellent material for reconstructing the diaphragm as it provides the necessary strength and is watertight.58 Generally, the patch is sutured using a running 0-nonabsorbable suture around the edges of the defect, often starting medially (Fig. 28-9). The patch must be tailored to minimize laxity in the diaphragm. Full-thickness bites in the diaphragm are necessary, with care taken to avoid injury to underlying structures. For injuries extending laterally to the chest wall without adequate tissue for fixation, the prosthetic can be secured with interrupted sutures placed around the ribs, following the

natural course of the native diaphragm. Medially, the mesh can be secured either to pericardium or to the posterior crus if inadequate native diaphragmatic tissue exists.58 In contaminated fields, autologous tissue may be used instead of PTFE to reconstruct large diaphragmatic defects. Latissimus dorsi, rectus abdominis, external oblique, and transversus abdominis flaps have been described, mainly in pediatric populations.63–67 The benefit of autologous tissue in the pediatric population is that it allows for growth of the child. A surgical algorithm to approach diaphragmatic injuries is presented in Fig. 28-10.

OUTCOMES Mortality following diaphragmatic injury is dependent on the severity of the associated injuries.28 Mortality rates vary between 18 and 40%, depending on mechanism of injury (blunt versus penetrating).28,42 Recurrence rates of diaphragmatic hernias following repair are difficult to ascertain; however, it appears that the recurrence rate is higher when absorbable suture is used for the initial repair.28 Postoperative morbidity directly related to the acute surgical repair includes suture-line dehiscence, failure of diaphragmatic repair, hemidiaphragmatic paralysis secondary to iatrogenic injuries to the phrenic nerve, respiratory insufficiency, empyema, and subphrenic abscess. The complication rate after repair of a diaphragmatic injury has ranged from 30 to 68%.69,70 Atelectasis has been documented in 11–68% of patients, with pneumonia and pleural effusions reported in another 10–23%. Sepsis, multiorgan system failure, hepatic abscess, and empyema have been reported in 2–10% of patients.69,70 When complication rates were compared in blunt versus penetrating injuries of the diaphragm in one review, patients with blunt trauma had a 60% complication rate versus 40% complication rate in those with penetrating trauma.71 Most of the morbidity reported in these studies is clearly the result of the large number of associated injuries present in association with diaphragmatic injuries.69,71 Mortality following repair of a chronic diaphragmatic hernia depends entirely on the presence or absence of obstructive symptoms at the time of presentation. A mortality of less than 10% is expected in patients with asymptomatic diaphragmatic hernias, and this is related to the patient’s comorbidities and not to the repair.26,68 Patients presenting with gastrointestinal obstruction have a significantly higher morbidity (60%) and mortality (25–80%). This reinforces the need to pursue the diagnosis and surgical management of diaphragmatic injuries prior to the onset of obstructive symptoms with chronic hernias.19,26,37

PERICARDIO-DIAPHRAGMATIC RUPTURE

FIGURE 28-9 Technique for repair of the diaphragm using a prosthetic. (Reproduced with permission from Juan A. Asensio, MD, FACS, FCCM and Demetrios Demetriades, MD, PhD, FACS.)

Blunt ruptures of the central tendon of the diaphragm involving the pericardium are rare and may present as acute injuries or as chronic hernias following missed injuries. Most are caused by combined blunt trauma to the chest and abdomen; however, isolated trauma to either one of the cavities can also cause this entity. Simultaneous rupture of the pericardium into the left

Diaphragm

537

Treatment Diaphragm Injury

Laparoscopy

Laparotomy

Thoracotomy

Laparoscopy

Laparotomy

Reduce Hernia Debride devitalized tissue Evacuate blood/contaminants Reduce Hernia Evaluate size of hernia defect Evaluate diaphragmatic function

Repair

Simple repair Patch / autologous repair Tissue transposition

FIGURE 28-10 Algorithm for repair of an acute or chronic diaphragmatic defect.

and the right pleural spaces has also been described, as has herniation of the heart inferiorly into the peritoneal cavity.72 There is a high incidence of associated injuries including musculoskeletal injuries that occur predominantly on the left side of the body. The organs most frequently involved in pericardial herniation are the transverse colon, stomach, omentum, liver, and small bowel. Exploratory laparotomy is recommended as the preferred approach for the acute repair of these injuries.72

CONCLUSION Diaphragmatic injuries may be associated with other severe lifethreatening injuries as after blunt trauma or may be subtle in their presentation in a patient with a stab wound to the left thoracoabdominal area. In either situation a high index of suspicion is necessary to make the diagnosis. As modern imaging techniques improve, diagnosis may become less difficult. Once the diagnosis is made, repair in the acute phase can usually be accomplished using the surgical techniques described. In the latent or obstructive phases of presentation, repair or reconstruction of the diaphragm may be a surgical challenge. If gastrointestinal obstruction, perforation or ischemia occur with a chronic posttraumatic diaphragmatic hernia, postoperative morbidity and mortality are significant.

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Acute

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SECTION 3 X

16. Andrus CH, Morton JH. Rupture of the diaphragm after blunt trauma. Am J Surg. 1970;119:686–693. 17. Rashid F, Chakrabarty MM, Singh R, Iftikhar SY. A review on delayed presentation of diaphragmatic rupture. World J Emerg Surg. 2009;32:1–7. 18. Kearney PA, Rouhana SW, Burney RE. Blunt rupture of the diaphragm: mechanism, diagnosis, and treatment. Ann Emerg Med. 1989;18: 1326–1330. 19. Demetriades D, Kakoyiannis S, Parekh D, et al. Penetrating injuries of the diaphragm. Br J Surg. 1988;75:824–826. 20. Powell BS, Magnotti LJ, Schroeppel TJ, et al. Diagnostic laparoscopy for the evaluation of occult diaphragmatic injury following penetrating thoracoabdominal trauma. Injury. 2008;39:530–534. 21. Murray J, Demetriades D, Ashton K. Acute tension diaphragmatic herniation: case report. J Trauma. 1997;43:698–700. 22. Grimes O. Traumatic injuries to the diaphragm. Am J Surg. 1974;128: 175–181. 23. Hanna WC, Ferri LE. Acute traumatic diaphragmatic injury. Thorac Surg Clin. 2009;19:485–489. 24. Nchimi A, Szapiro D, Ghaye B, et al. Helical CT of blunt diaphragmatic rupture. AJR Am J Roentgenol. 2005;184:24–30. 25. Shah R, Sabanathan S, Mearns AJ, Choudhury AK. Traumatic rupture of diaphragm. Ann Thorac Surg. 1995;60:1444–1449. 26. Degiannis E, Levy RD, Sofianos C, et al. Diaphragmatic herniation after penetrating trauma Br J Surg. 1996;83:88–91. 27. Rodruguez-Morales G, Rodriguez A, Shatney CH. Acute rupture of the diaphragm in blunt trauma: analysis of 60 patients. J Trauma. 1986;26:438–444. 28. Hanna WC, Ferri LE, Fata P, Razek T, Mulder DS. The current status of traumatic diaphragmatic injury: lessons learned from 105 patients over 13 years. Ann Thorac Surg. 1995;60:1444–1449. 29. American Association for the Surgery of Trauma. Injury scoring scales. Available at: http://www.aast.org/library/traumatools/injuryscoringscales. aspx, Chicago, IL. Accessed February 25, 2010. 30. Mirvis SE, Shanmuganagthan K. Imaging hemidiaphragmatic injury. Eur Radiol. 2007;17:1411–1421. 31. Sliker CW. Imaging of diaphragmatic injuries. Radiol Clin North Am. 2005;44:199–211. 32. Bodanapally UK, Shanmuganathan K, Mirvis SE, et al. MDCT diagnosis of penetrating diaphragm injury Eur Radiol. 2009;19:1875–1881. 33. Kim HH, Shin YR, Kim KJ, et al. Blunt traumatic rupture of the diaphragm: sonography diagnosis. J Ultrasound Med. 1997;16:593–598. 34. Blaivas M, Brannam L, Hawkins M, Lyon M, Sriram K. Bedside emergency ultrasonographic diagnosis of diaphragmatic rupture in blunt abdominal trauma. Am J Emerg Med. 2004;22:601–604. 35. Kirkpatrick AW, Ball CG, Nicolaou S, Ledgerwood A, Lucas CE. Ultrasound detection of right-sided diaphragmatic injury; the “liver sliding” sign. Am J Emerg Med. 2006;24:251–252. 36. Hood RM. Traumatic diaphragmatic hernia [collective review]. Ann Thorac Surg. 1971;12:311–324. 37. Payne JH, Yellin AE. Traumatic diaphragmatic hernia. Arch Surg. 1982;117:18–24. 38. Eren S, Esme H, Sehitogullari A, et al. The risk factors and management of posttraumatic empyema in trauma patients. Injury. 2008;39:44–49. 39. Zellweger R, Navsaria PH, Hess F, et al. Trans-diaphragmatic pleural lavage in penetrating thoracoabdominal trauma. Br Jr of Surg. 2004;91:1619–1623. 40. American College of Surgeons. Advanced Trauma Life Support for Doctors. 8th ed. Chicago, IL: American College of Surgeons; 2008. 41. Bender JS, Lucas CE. Management of close-range shotgun injuries to the chest by diaphragmatic transposition: case reports. J Trauma. 1990;30:1581–1584. 42. Ochsner MG, Rozycki GS, Lucente F, et al. Prospective evaluation of thoracoscopy for diagnosing diaphragmatic injury in thoraco-abdominal trauma: a preliminary report. J Trauma. 1993;34:704–710. 43. Miller L, Bennett EV, Root HD, et al. Management of penetrating and blunt diaphragmatic injury. J Trauma. 1984;24:403–409.

44. Feliciano DV, Cruse PA, Mattox KL, et al. Delayed diagnosis of injuries to the diaphragm after penetrating wounds. J Trauma. 1988;28: 1135–1144. 45. Mihos P, Potaris K, Gakidis J, et al. Traumatic rupture of the diaphragm: experience with 65 patients. J Trauma. 2003;34:169–172. 46. Athanassiadi K, Kalavrouzlotis G, Athanassiou M, et al. Blunt diaphragmatic rupture. Eur J Cardiothorac Surg. 1999;15:469–474. 47. Matsevych OY. Blunt diaphragmatic rupture: four years’ experience. Hernia. 2008;12:73–78. 48. Sattler S, Canty TG Jr, Mulligan MS, et al. Chronic traumatic and congenital diaphragmatic hernias: presentation and surgical management. Can Respir J. 2002;9:135–149. 49. Murray JA, Weng J, Velmahos GC, et al. Abdominal approach to chronic diaphragmatic hernias: is it safe? Am Surg. 2004;70:897–900. 50. Kaw LL Jr, Potenza BM, Coimbra R, et al. Traumatic diaphragmatic hernia. J Am Coll Surg. 2004;198:668–669. 51. Kocher TM, Gurke L, Kuhrmeier A, et al. Misleading symptoms after minor chest trauma. Thoracoscopic treatment of diaphragmatic rupture. Surg Endosc. 1998;12:879–881. 52. Kurata K, Kubota K, Oosawa H, et al. Thoracoscopic repair of traumatic diaphragmatic rupture. Surg Endosc. 1996;10:850–851. 53. Koehler RM, Smith RS. Thoracoscopic repair of missed diaphragmatic injury in penetrating trauma: case report. J Trauma. 1994;36:424–427. 54. Matthews BD, Bui H, Harold KL, et al. Laparoscopic repair of traumatic diaphragmatic injuries. Surg Endosc. 2003;17:254–258. 55. Laws HL, Waldschmidt ML. Rupture of the diaphragm. JAMA. 1980;243:32. 56. Hutti TP, Lang R, Meyer G. Long-term results after laparoscopic repair of traumatic diaphragmatic hernias. J Trauma. 2002;52:562–566. 57. Meyer G, Hutti TP, Halz RA, et al. Laparoscopic repair of traumatic diaphragmatic hernias. Surg Endosc. 2000;14:1010–1014. 58. Finley DJ, Abu-Rustum NR, Chi DS, Flores R. Reconstructive techniques after diaphragmatic resection. Thorac Surg Clin. 2009;19:531–535. 59. Igai H, Yokomise H, Kumagai K, et al. Delayed hepatothorax due to right-sided traumatic diaphragmatic rupture. Gen Thorac Cardiovasc Surg. 2007;55:434–436. 60. Baldassarre E, Valenti G, Gambino M, et al. The role of laparoscopy in the diagnosis and treatment of missed diaphragmatic hernia after penetrating trauma. J Laparoendosc Adv Surg Tech A. 2007;17:302–306. 61. Matz A, Landau O, Alis M, et al. The role of laparoscopy in the diagnosis and treatment of missed diaphragmatic rupture. Surg Endosc. 2000;14: 537–539. 62. Slim K, Bousquet J, Chipponi J. Laparoscopic repair of missed blunt diaphragmatic rupture using a prosthesis. Surg Endosc. 1998;12: 1358–1360. 63. Bedini AV, Andreani SM, Muscolino G. Latissimus dorsi reverse flap to substitute the diaphragm after extrapleural pneumonectomy. Ann Thorac Surg. 2000;69:986–988. 64. McConkey MO, Temple CL, McFadden S, et al. Autologous diaphragm reconstruction with the pedicled latissimus dorsi flap. J Surg Oncol. 2006;94:248–251. 65. Hallock GG, Lutz DA. Turnover TRAM flap as a diaphragmatic patch. Ann Plast Surg. 2004;52:93–96. 66. Shimamura Y, Gunven P, Ishii M, et al. Repair of the diaphragm with an external oblique muscle flap. Surg Gynecol Obstet. 1989;169:159–160. 67. Simpson JS, Gossage JD. Use of abdominal wall muscle flap in repair of large congenital diaphragmatic hernia. J Pediatr Surg. 1971;6:42–44. 68. McElwee TB, Myers RT, Pennell TC. Diaphragmatic rupture from blunt trauma. Am Surg. 1984;50:143–149. 69. Wiencek RG, Wilson RF, Steiger Z. Acute injuries of the diaphragm: an analysis of 165 cases. J Thorac Cardiovasc Surg. 1986;92:989–993. 70. Beal SL, McKennan M. Blunt diaphragmatic rupture: a morbid injury. Arch Surg. 1988;123:828–832. 71. Meyers BF, McCabe CJ. Traumatic diaphragmatic hernia. Ann Surg. 1993;218:783–790. 72. Van Loenhout RMM, Schiphorst TJM, Wittens CHA, et al. Traumatic intrapericardial diaphragmatic hernia. J Trauma.1986;26:271–275.

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CHAPTER 29

Liver and Biliary Tract Timothy C. Fabian and Tiffany K. Bee

INTRODUCTION Liver injury occurs in approximately 5% of all trauma admissions.1 The liver’s size and anatomic location, directly under the right costal margin, make it the most susceptible organ for injury in blunt trauma and a frequently involved organ in penetrating trauma. The management of liver injury has evolved greatly over the last decade. There have been many technical advances in medicine, which now allow us to better diagnose and treat liver injuries both operatively and nonoperatively. However, the most severe liver parenchymal and venous injuries as well as those involving the portal triad continue to challenge even the most adept trauma or hepatobiliary surgeon and often lead to death. Therefore, despite our progress in liver injury management, many avenues for improvement remain to be explored.

HISTORY Liver injury management has been described in many of the early surgical textbooks. We consider nonoperative management of hepatic injury a modern approach; however, a 1905 surgical text states, “If the evidences of a rupture of the liver, such as the signs of shock and hemorrhage …. the continuous increase in pain, due to progressive abdominal distention, and muscular rigidity, are absent, no operative intervention can be considered.”2 Mortality from liver injury was as high as 62.5% in these early years.3 Pringle wrote a landmark paper examining the management of severe liver injury in 1908.4 Although many authors previous to this paper had described suturing methods of liver parenchyma as well as gauze packing into the liver laceration, Pringle described a maneuver of occluding the porta hepatis with the surgeon’s fingers and thus decreasing the amount of hemorrhage from a severely injured liver. This procedure continues to be a useful tool in the management of liver trauma.

During World War II, new ideas in the management of severe liver injury surfaced. Madding et al. used the principles of early laparotomy, drainage procedures, advances in anesthetic and aseptic care, as well as transfusion technology to improve mortality to 27.7%.5 The techniques of hemorrhage control adopted at that time incorporated parenchymal reapproximation with large blunt liver needles, resection, and direct vessel ligation. These methods prevailed until approximately 10 years ago. Trends in management have now led to an emphasis on nonoperative treatment for those patients who remain hemodynamically stable and liver packing with damage control for those who are unstable.

ANATOMY Comprehensive knowledge of hepatic anatomy is essential to the proper management of traumatic liver injuries. The understanding of the ligamentous attachments, parenchyma, and intraparenchymal and extraparenchymal vascularity of the liver is key to the effective application of methods for control and repair in liver injuries (Fig. 29-1).

■ Lobes Cantlie first described the lobar anatomy in 1898. The liver is divided into two lobes by a 75° angle traversing from the gallbladder fossa posteriorly to the left side of the inferior vena cava. This is the so-called line of Cantlie. Therefore, the left lobe includes the hepatic tissue to the left of the falciform ligament along with the quadrate and caudate lobes. The right lobe consists of the remaining parenchyma.

■ Functional Anatomy The functional anatomy of the liver separates the liver into segments pertinent to resection. In 1953, Couinaud provided the basis of modern resection planes by dividing the liver based on

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Management of Specific Injuries

SECTION 3 X FIGURE 29-1 Surgical anatomy of the liver: (1) inferior vena cava; (2) right hepatic vein; (3) middle hepatic vein; (4) left hepatic vein; (5) portal vein; (6) right branch portal vein; (7) left branch portal vein; (8) right triangular ligament; (9) coronary ligament; (10) left triangular ligament; (11) falciform ligament; (12) ligamentum teres.

the distribution of the hepatic veins and glissonian pedicles.6 The right hepatic vein traverses between the right posterolateral (VI and VII) and right anteromedial (V and VIII) segments. On the left, the left hepatic vein delineates the anterior (III and IV) and posterior (II) segments. The caudate lobe (I) drains directly into the inferior vena cava (Fig. 29-2).

■ Hepatic Artery The common hepatic artery branches from the celiac artery. This provides about 25% of the hepatic blood flow and 50% of hepatic oxygenation. The artery then branches into the gastroduodenal, right gastric, and proper hepatic. The proper hepatic is found in the porta hepatis usually to the left of the common bile duct and anterior to the portal vein. At the hilum of the liver, the artery bifurcates into a right (the longer branch) and a left hepatic artery. There are a number of anatomic variances. The most frequent (11%) is the aberrant superior mesenteric origin of the right hepatic artery traversing behind the duodenum. Other variants include a left hepatic artery origin from the left gastric artery (8%) and the left and right hepatic arteries arising from a superior mesenteric artery origin (9%). With these multiple variants, great care must be taken when controlling the traumatic hemorrhage.

Hepatic Veins The hepatic veins develop from within the hepatocytes’ central lobar veins. The superior, middle, and inferior vein branches originating from the right lobe form the right hepatic vein. The middle hepatic vein derives from the two veins arising from segments IV and V and frequently includes a branch from the posterior portion of segment VIII. In 90% of patients the middle hepatic vein joins the left hepatic vein just before draining into the inferior vena cava. The left hepatic vein is more variable in its segmental origin. Most important is the posterior positioning of

FIGURE 29-2 Functional division of the liver, according to Couinaud’s nomenclature. (Reproduced with permission from Blumgart LH, ed. Surgery of the Liver and Biliary Tract. New York: Churchill Livingstone; 1988. © Elsevier.)

the vein when dissecting the left coronary ligament; great caution must be used in this area to avoid inadvertent injury. The retrohepatic vena cava is about 8–10 cm in length. It receives the blood of the hepatic veins and also multiple small direct hepatic vessels. Exposure to this area can be very difficult, especially when an injury and accompanying hemorrhage make visualization very difficult.

Portal Vein The portal vein is formed from the confluence of the splenic and superior mesenteric veins directly behind the pancreatic head. It provides about 75% of hepatic blood flow and 50% of hepatic oxygen. The portal vein lies posteriorly to the hepatic artery and bile ducts as it ascends toward the liver. At the parenchyma, the portal vein divides into a short right and a longer left extrahepatic branch.

Ligaments When operating on the liver, it is crucial to understand the ligamentous attachments. The coronary ligaments attach the diaphragm to the parietal surface of the liver. The triangular ligaments are at the lateral extensions of the right and left coronary ligaments. The falciform ligament with the underlying ligamentum teres attaches to the anterior peritoneal cavity. The medial portion of the coronary ligaments is where the hepatic veins traverse and therefore dissection in this area must be done with caution.

LIVER INJURY INCIDENCE AND CLASSIFICATION Liver injury occurs in approximately 5% of all trauma admissions. Since the liver is the largest intra-abdominal organ, it is not surprising that the liver is the most commonly injured solid organ in blunt and penetrating injury. Data from the author’s institution

Liver and Biliary Tract

TABLE 29-1 Trauma Admissions, 2000 to May 2009 (N  39,722) Total 2,139 2,158 1,002 285 282 905

% Total 28 28 13 4 4 12

185 4,925

802 7,573

11 100

617 2,648

over the past 5 years illustrate the frequency of liver injury compared to other abdominal solid organ injury (Table 29-1). Motor vehicle collision is by far the most common etiology for a blunt liver injury. This is followed by pedestrian/car collisions, falls, assaults, and motorcycle crashes. Liver injury in penetrating trauma is also frequent, ranging from 13% to 35% of penetrating admissions, and is dependent on the weapon utilized. Uniform classification of liver injury is essential to compare the efficacy of management techniques (Fig. 29-3). The

FIGURE 29-3 Hepatic injury grading is important to compare outcome.

INITIAL MANAGEMENT Care for the patient with possible liver injury should proceed by the tenants of Advanced Trauma Life Support (ATLS). Of utmost importance is the initial evaluation, including attention to airway, breathing, and circulation (see Chapter 10). Other life-threatening injury may take precedence over possible internal injury in the primary survey. However, liver injury may indeed be a cause of hemorrhagic shock and cannot be overlooked. Resuscitation strategies are evolving in the care of trauma patients (see Chapter 12). The prospects of permissive hypotension, hypertonic saline resuscitation, and other strategies are the subject of many recent investigations. Physical exam of the patient remains a critical component of the initial evaluation. However, physical exam of a trauma patient may indeed miss significant internal injury. A study by Olsen et al. found that trauma patients with a “benign” physical exam had a 43% incidence of significant intra-abdominal injury.8 Therefore, it is justified that patients with benign physical exams are further evaluated by either serial exams or

CHAPTER CHAPTER 29 X

Organ Liver Spleen Kidney Pancreas Stomach Small bowel/ duodenum Colon/rectum Total

Mechanism of Injury Blunt Penetrating 1,554 585 1,996 162 761 241 174 111 22 260 233 672

American Association for the Surgery of Trauma established a detailed classification system that has been widely utilized7 (Table 29-2). This classification provides for uniform comparisons of both nonoperative and operatively managed hepatic injury.

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Management of Specific Injuries

TABLE 29-2 Liver Injury Scale (1994 Revision)

SECTION 3 X

Gradea I

Hematoma Laceration

II

Hematoma Laceration

III

Hematoma

Laceration IV

Hematoma Laceration

V

Laceration Vascular

VI a

Vascular

Injury Description Subcapsular, nonexpanding 10 cm surface area Capsular tear, nonbleeding. 1 cm parenchymal depth Subcapsular, nonexpanding, 10–50% surface area; intraparenchymal nonexpanding 10 in diameter Capsular tear, active bleeding; 1–3 cm parenchymal depth. 10 cm in length Subcapsular, 50% surface area or expanding; ruptured subcapsular hematoma with active bleeding; intraparenchymal hematoma 10 cm or expanding 3 cm parenchymal depth Ruptured intraparenchymal hematoma with active bleeding Parenchymal disruption involving 25–75% of hepatic lobe or 1–3 Couinaud’s segments within a single lobe Parenchymal disruption involving 75% of hepatic lobe or 3 Couinaud’s segments within a single lobe Juxtahepatic venous injuries (i.e., retrohepatic vena cava/ central major hepatic veins) Hepatic avulsion

ICD-9b 864.01 864.11 864.02 864.12 864.01 864.11 864.03 864.13

AIS90c 2 2 2 2 3

864.04 864.14

3 4

864.04

4

864.14

5 5 6

Advance one grade for multiple injuries, up to grade III.

b

International Classification of Diseases, 9th Revision. Abbreviated Injury Scale, 1990.

c

radiologic methods. Plain radiographs and ultrasound obtained in the trauma bay may give clues to possible liver injury if lower right rib fractures, hemothorax, hemoperitoneum, or a ruptured diaphragm is diagnosed. Although nonoperative management has become routine, a patient exhibiting clear peritoneal signs and instability requires immediate celiotomy. Important but often overlooked points include keeping the patient warm and collecting appropriate laboratory data. Hypothermia can have detrimental effects on coagulation and cardiac rhythm. Appropriate laboratory data should include type and cross, hematocrit, coagulation profile, amylase, and base deficit. Abnormalities can alert the clinician to possible internal injury and its severity.

DIAGNOSIS OF LIVER INJURY ■ Hemodynamically Unstable Patient After primary survey and resuscitation have been initiated, the patient may still be hemodynamically unstable. In these cases it is necessary to immediately determine the possible causes of the continued shock state. This can be difficult in patients with multiple injuries involving many organ systems.

Intra-abdominal injury can be an obvious cause of instability if physical exam reveals peritoneal signs, penetrating injury, or increasing distention. More often, a rapid diagnostic modality must be employed. The two most pertinent modalities for these situations are diagnostic peritoneal lavage (DPL) and focused abdominal sonography for trauma (FAST).

■ Diagnostic Peritoneal Lavage DPL is a very accurate method for determining the presence of intraperitoneal blood. Many reports have replicated the work of Root et al. that indicated up to a 98% accuracy of determining the presence of intra-abdominal blood.9 DPL is rapid and safe if performed with the semi-open or open technique. It remains a very useful tool in those patients who have altered sensorium and remain hemodynamically unstable. A positive DPL is defined as a gross aspiration of 10 mL of blood or greater than 100,000 RBC/mm3 in at least 300 mL of irrigant. A finding of gross blood in an unstable patient leads to immediate operative intervention. DPL does have limitations. It is not useful in determining the origin of the bloody aspirate and can actually be too sensitive since it is positive with minimal hemoperitoneum. Therefore, though it has its place in rapid determination

Liver and Biliary Tract

■ Focused Abdominal Sonography for Trauma The FAST exam has superseded DPL in many institutions for the determination of hemoperitoneum in the unstable bluntly injured patient (see Chapter 16). Surgeons have become very adept and familiar with this diagnostic modality. Richards et al. reported a 98% sensitivity of ultrasound for hemoperitoneum in grade III and higher liver injury.10 However, they were not able to identify the anatomic location of the hepatic parenchymal injury in 67% of these severely damaged livers. A multiinstitutional study by Rozycki et al. concluded that the RUQ area is the most common site of hemoperitoneum accumulation in blunt abdominal trauma.11 This information was reiterated in another study that discovered that the “two most common patterns of fluid accumulation after hepatic injuries were the RUQ only and the RUQ and lower recesses.”12 If the initial exam of the RUQ is negative, it is recommended that the pericardial, LUQ, and pelvic areas also be examined. The FAST exam is about 97% sensitive when 1 L of peritoneal fluid is present, but the examiner can rarely see volumes less than 400 mL with current technology.13 A repeat FAST exam can be beneficial after the initial resuscitation. Further resuscitation may promote further bleeding that then leads to more intraperitoneal blood on FAST exam. FAST exam is very beneficial in those unstable patients in whom the diagnosis of hemoperitoneum requires emergent surgery.

■ Hemodynamically Stable Patient Ultrasound and CT scanning are the mainstays of diagnosing hepatic injury in the hemodynamically stable but bluntly injured patient. Once the primary and secondary surveys have been completed, the patient at risk for intra-abdominal injury should undergo further radiologic evaluation for definitive diagnosis.

FAST FAST examination, as mentioned above, has proven to be a very good diagnostic tool in the evaluation of the blunt trauma patient. Some centers are using ultrasound for definitive diagnosis of intra-abdominal injury. Most examiners, though, are unable to distinguish between different grades of hepatic injury by ultrasound.10 Also, the source of free fluid in the peritoneal cavity is difficult to discern by ultrasound alone, especially if multiple injuries are present. A FAST exam has been reported to have a sensitivity as high as 83.3% and specificity of 99.7%.14 With these relatively low false-negative rates, some institutions are observing patients with negative FAST and not proceeding with CT scanning. However, Chiu et al. in 1997 reported a 29% incidence of abdominal injury following negative initial FAST.15 They reported confounding clinical factors including contusion, pain, pelvic fracture, and lower rib fractures that were present in many of the false-negative patients. Also, 27% of these negative FAST patients underwent laparotomy for

undetected splenic injury. A follow-up FAST exam was not performed on these patients prior to surgery and given the time for further hemoperitoneal fluid development these scans may now have been positive. Serial ultrasound exams are now used in many trauma centers if the initial scan is negative. Patients with pelvic ring-type fractures should undergo CT scan even if a negative FAST has been performed due to the more frequent occult injuries in these patients.16 Contrast-enhanced sonography shows some promise in the detection of liver injury. Contrast-enhanced ultrasound uses intravenously injected microbubbles containing gases other than air to produce the “contrasted” images. Valentino et al. reported a 100% sensitivity and specificity in seven liver injury patients with grade II–IV injuries.17 Similarly McGahan et al. reported 90% detection in liver injuries of the same grades.18 Another study described the ability of this modality to detect active extravasation from solid organs.19 With these advancements, patients may be subject to less risk from radiation or CT contrast. Also, this can be done at bedside instead of transporting a critical patient to a radiology suite. Overall, ultrasound is an excellent tool for the diagnosis of significant hepatic injury in the blunt trauma patient. FAST also has an expanding role in penetrating abdominal trauma with an institutional series sensitivity of 46% and specificity of 94% in penetrating injury,20 therefore concluding that FAST can be used to triage patients more directly to surgery. However, the limitations of FAST in penetrating trauma are significant. In a patient with a possible tangential wound, the question is often if the peritoneum has been penetrated. A finding of fluid in Morison’s pouch confirms penetration and will result in immediate surgical intervention. A negative fluid accumulation, however, does not definitively rule out penetration. These results have been validated.21 Two interesting studies have demonstrated that fascial penetration can be verified by ultrasound examination.22,23 Again, the sensitivity of this modality is low but the specificity is high. Ultrasound may be a good screening tool for finding fascial penetration and a positive result could alleviate the patient of a painful bedside wound exploration and also contribute to operative decision making. Future study in this area may develop greater uses for ultrasound in select penetrating injuries.

■ CT Scanning The advent of CT scanning and advances in that technology have resulted in tremendous changes in the management of liver injury. Since the first use of CT to diagnose intra-abdominal injury in the early 1980s, CT has become a routine part of the management of trauma patients.24 One recent study revealed that the specificity of the clinical examination with bedside radiologic investigations of plain x-ray and sonography in addition to laboratory values is not sufficient to preclude the blunt trauma patient from obtaining a CT scan for definitive diagnosis of injury.25 The advent of the helical CT scan has improved resolution as well as increased the speed of a head to pelvis scan to less than 10 minutes. Trauma surgeons now use CT scans for diagnosis and for management decisions in liver injuries. Being able to grade the extent of injury and to follow an existing

CHAPTER CHAPTER 29 X

of hemoperitoneum and subsequent immediate operative intervention, DPL has been replaced in most trauma centers by ultrasound and in more stable patients by computed tomography (CT) scanning.

543

544

Management of Specific Injuries

Nonoperative Management of Blunt Liver Injury

SECTION 3 X

Hemodynamic stability mandatory for nonoperative management

CT scan

Grades 1, 2, 3

Becomes unstable

Grades 4,5

Stable

Stable OR

Admit to floor, observe, AMHct

* ICU – serial Hct q6h, close observation

ICU* Abdominal pain, jaundice, unexplained signs of infection

Stable, improving

CT scan Pseudoaneurysm Abdominal fluid collection Angiography for embolization

DC from ICU Improved, unchanged

Search other sources Consider drainage

Outpatient management Grade 1,2,3

Grade 4,5

Repeat CT 1 month if pain or jaundice

Repeat CT 1 month

healed

Ad lib activity

Not healed

Light duty–repeat CT 1 month until healed

FIGURE 29-4 Algorithm for nonoperative management of blunt liver injury.

injury can determine if nonoperative management is possible and successful (Fig. 29-4). CT scanning is also being used in penetrating injury. Triplecontrast CT in back and flank wounds has been shown to have good sensitivity; however, the sensitivity for diaphragmatic and small bowel injury is poor.26 Therefore, a minor hepatic laceration can be evaluated and nonoperatively managed with CT guidance but continued frequent abdominal exam must also accompany this algorithm.

■ Laparoscopy Laparoscopy has been successfully used to diagnose peritoneal penetration of penetrating trauma, thus saving the patient from a nontherapeutic exploratory laparotomy.27 Repair of hepatic injury found at laparoscopy has also been reported.28,29 In

carefully selected patients, laparoscopy can be advantageous in the diagnosis and repair of hepatic injury.

MANAGEMENT OF LIVER TRAUMA Anatomic relationships are key to understanding the management of liver trauma. Blunt hepatic injury traverses almost exclusively along the segments of the liver. This most likely occurs due to the strength of the fibrous covering around the portal triad preventing injury from transecting these structures. However, the hepatic veins do not have a similar fibrous structure and therefore, having less resistance, are the primary structures injured in blunt trauma. Penetrating trauma, on the other hand, involves both venous and arterial injury with direct transection of any structure in the trajectory. These anatomic

Liver and Biliary Tract principles are key to understanding the rationale for making decisions in the management of liver trauma.

Nonoperative treatment of the hemodynamically stable patient with blunt injury has become the standard of care in most trauma centers (see Fig. 29-4). In 1995, Croce et al. published a prospective trial of nonoperative management of liver injury.1 In this study patients with all grades and volumes of hemoperitoneum were evaluated against operative controls. They found that they were able to successfully manage 89% of hemodynamically stable patients without celiotomy. Most blunt liver injuries produce hepatic venous injuries that are low pressure (3–5 cm H2O). Hence, hemorrhage usually stops once a clot forms on the area of disruption. Successful nonoperative therapy resulted in lower transfusion requirements, abdominal infections, and hospital lengths of stay. Hurtuk et al. have reported that indeed trauma surgeons “practice what they preach” in a recently published evaluation of the National Trauma Data Bank. They found that in the past 10 years there has been no effect on mortality in solid organ injury with prevalence of nonoperative management.30 Coimbra et al. reiterated these data by examining their experience in nonoperative treatment of grade III and IV hepatic injury.31 They reported no mortality in their nonoperatively managed patients and “discouraged” operative management of these injuries. Approximately 85% of patients with blunt liver trauma are stable. Once stability has been established, the patient must be carefully analyzed for the appropriateness of nonoperative care. The patient cannot exhibit signs of peritonitis and must continue to be hemodynamically stable without a significant transfusion requirement. The authors are generally comfortable in nonoperatively managing a stable patient with 3–5 U of blood in his or her abdomen. A contrast-enhanced helical CT scan should be obtained to evaluate injury grade, amount of hemoperitoneum, evidence for enteric injury, active extravasation of contrast, and presence of pseudoaneurysm (Fig. 29-5).

■ Complications of Nonoperative Blunt Hepatic Injury Management

FIGURE 29-5 CT scan demonstrating a “contrast blush,” indicative of active arterial bleeding in a patient with a grade IV blunt hepatic injury.

Most patients with blunt nonoperative liver injuries heal without complication. Follow-up CT scans generally show resolution of severe injuries within 4 months and about 15% show complete resolution at hospital discharge.1 However, complications can arise and management requires the surgeon to be prepared to deal with the possible adverse outcomes.37 A retrospective multi-institutional study included 553 patients with grade III–V injury.38 Of these patients, 12.6% developed hepatic complications that included bleeding, biliary problem, abdominal compartment syndrome, and infection. Significant coagulopathy and grade V injury were found to be predictors of complication. Therefore, with current nonoperative

CHAPTER CHAPTER 29 X

■ Hemodynamically Stable Patient with Blunt Injury

High-grade injury, large hemoperitoneum, contrast extravasation, and pseudoaneurysm are not contraindications for nonoperative management; however, these patients are at higher risk for nonoperative failure and may need a multimodality approach to stabilize their nonoperative injury. Stable patients with high-grade injury may be observed. However, Malhotra et al. noted that 14% of grade IV and 22.6% of grade V injuries fail nonoperative management, which was substantially higher than the 3–7.5% failure rate of more minor injuries.32 That same article reports large hemoperitoneum (blood around liver, pericolic gutter, and in the pelvis by CT) as a significant factor in failure of nonoperative management but that it could not predict which patients would ultimately fail nonoperative management. Richardson et al. speculated that many experienced trauma surgeons have taken stable but high-grade injury patients to the operating room only to find that “manipulation of venous injuries resulted in massive hemorrhage that resulted in the patient’s death.”33 They concluded that nonsurgical treatment has a “positive impact on survival.” A CT finding of contrast blush or extravasation has previously meant that patients were not candidates for nonoperative therapy. However, with the assistance of interventional radiology, some patients may be candidates for embolization and nonoperative treatment. Successful embolization of hepatic arterial injury in patients who are hemodynamically stable but with CT scans demonstrating intrahepatic contrast pooling was reported in 1996.34 Choosing the appropriate patient for embolization can be a challenge. One interesting study looked at 11 patients with hepatic injury and CT evidence of contrast extravasation who were stable “only with continuous resuscitation.”35 These patients were evaluated by hepatic angiography and seven patients were successfully treated with hepatic embolization. The other four patients had no active extravasation seen by angiography and became hemodynamically stable not requiring surgery. Misselbeck et al. reviewed their 8-year experience with hepatic angioembolization and found that hemodynamically stable patients with contrast extravasation on CT scan were 20 times more likely to require embolization than those without extravasation.36 Arterial extravasation with blunt liver injury is much less common than venous injury. However, many centers are anecdotally noting excellent results with a multimodality approach.

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management strategies, complications must be dealt with appropriately.

it seems that delayed hemorrhage is actually a rare and manageable complication.

Bile Leaks

Devascularization

One of the more frequent complications is bile leakage. Bilomas or bile leak can occur in 3–20% of nonoperatively managed patients.1 Hepatobiliary hydroxy iminodiacetic acid (HIDA) scan and MRCP have been used to localized bile leaks.39 Evidence of bile leak by HIDA scan does not mandate intervention. In fact, of the 14 patients found to have HIDA evidence of bile leak in a 1995 study, only 1 patient became symptomatic and required percutaneous drainage.1 Abnormal liver function tests, abdominal distention, and intolerance to feeding may all indicate a bile leak. CT scan evaluation with percutaneous drainage usually remedies the problem completely. However, large bile leaks can develop. Many authors have described management of bile peritonitis or large leaks not responsive to percutaneous drainage using percutaneous drainage techniques along with endoscopic retrograde cholangiography (ERC) and biliary stent placement.40 It has also been demonstrated that sphincterotomy can decrease the biliary pressure and allow healing of the bile leak.41 In some instances, actual stenting of a large ductal injury can be accomplished.42 Griffen et al. have reported success with a combined laparoscopic and ERC approach. They described patients with biliary ascitis taken to operating room for laparoscopic bile drainage and placement of drain near injury site with postoperative ERC and bile duct stenting. They report no septic complications and healing of the substantial biliary leaks.43 The authors have rarely experienced a persistent bile leak in the nonoperatively managed patient. Bile leaks or bilomas are drained percutaneously, sometimes for up to 4–6 weeks, and they nearly always resolved without ERC or other decompressive maneuvers.

Disruption of vascular inflow to a hepatic segment following trauma or post-angioembolization can lead to necrosis of that segment of liver. The consequences of necrosis may include elevation of liver transaminases, coagulopathy, bile leaks, abdominal pain, feeding intolerance, respiratory compromise, renal failure, and sepsis.45 Many studies suggest that patients with significant necrosis should undergo hepatic resection before complications arise.46,47 Devascularization can be identified by CT scan. It can be differentiated from intraparenchymal hemorrhage when follow-up CT scans reveal segments of liver that remain devascularized or have air within the devascularized area.45

Abscess Perihepatic abscesses have also been uncommonly encountered with nonoperative management. The patient may exhibit signs of sepsis, abnormal liver function tests, abdominal pain, or food intolerance. Abscesses, like biliary collections, can often be managed by CT-guided drainage catheters. However, if the patient fails to improve with drainage and antibiotics, wide surgical drainage should be performed. This may involve merely incision and adequate drainage of the cavity or it may involve extensive debridement of the hepatic parenchyma.

Hemorrhage Delayed hemorrhage after nonoperative management is a feared complication. Gates presented a review of the subject in 1994 and suggested an overall incidence of delayed hematoma rupture of 0–14%.44 The 14% figure is well above current reports. He discussed 13 publications and determined that 69% of these delayed hemorrhage cases could have been successfully treated nonsurgically. Using the same criteria that were originally utilized to manage these patients nonoperatively, namely, hemodynamic stability without ongoing blood loss, patients with delayed hemorrhage can undergo hepatic angiographic embolization and observation with success. Therefore,

Hemobilia Hemobilia can occur after blunt hepatic injury. In 1871, Quincke described the triad of right upper quadrant pain, jaundice, and upper GI bleeding that indicated hemobilia. This triad may not be evident in the trauma patients with hemobilia.48 In a 1994 study, three patients developed hemobilia with massive upper gastrointestinal hemorrhage following blunt hepatic injury.49 The authors concluded that hepatic artery pseudoaneurysm with hemobilia is predisposed by bile leak and that angiographic embolization was appropriate for patients without sepsis and with small cavities. However, formal hepatic resection or drainage, after angiographic vascular control, may be necessary for septic patients or those with large cavities. Hemobilia is much less common with the prevalence of nonoperative management. With operative interventions of the past including large parenchymal suturing and vessel ligation, communications between vessels and bile ducts often occurred iatrogenically. Now that nonoperative care is practiced, we rarely see hemobilia.

Systemic Inflammatory Response Nonoperatively treated patients with inadequately drained bile or blood collections may be susceptible to the development of a systemic inflammatory responses syndrome that may include respiratory distress. Recent articles from Franklin et al. and from Letoublon et al. advocate laparoscopic evacuation of undrained bile or hemoperitoneum at postinjury days 3–5.50,51 They report a marked decrease in the inflammatory response in many of these patients.

Unusual Complications Large subcapsular hematomas have been described to elevate intraparenchymal pressures high enough to cause segmental portal hypertension and hepatofugal flow.52 This “compartment syndrome of the liver” was described in a patient managed nonoperatively whose decreasing hematocrit and increasing liver function tests promoted angiographic examination revealing the hepatofugal flow in the right portal vein. After operative drainage of the tense hematoma, the patient did well with reversal of flow and viability of the right lobe liver tissue. This type of

Liver and Biliary Tract compressive complication has also been described causing a Budd–Chiari syndrome when hematoma results in intrahepatic vena cava compression or hepatic venous obstruction.53

Definitive data on the value of follow-up CT scanning of blunt hepatic injury are not available. Recent published reports suggest postobservation CT scans on those with more severe (grade III–V) injuries. Cuff et al. reported that of the 31 patients who received follow-up CT scans 3–8 days postinjury, only 3 patients’ scans affected future management.54 Additionally, the three scans that affected management were obtained due to a change in clinical picture and not merely routine. A 1996 report similarly concluded that follow-up CT did not change decision making in those with grade I–III injury.55 The authors’ institution concluded from their follow-up of 530 patients, including 89 grade IV or V, that follow-up CT scans are not indicated as part of the nonoperative management of blunt liver injuries.56 Follow-up CT scans are indicated only for those patients who develop signs or symptoms suggestive of hepatic abnormality. By scanning only those with clinical suspicion, there is a small inherent risk of missing unsuspected, possibly deleterious pseudoaneurysms that may result in delayed hemorrhage and require embolization. If a patient has had a follow-up CT that reveals significant healing, a postdischarge scan is not necessary. However, if significant healing has not occurred or if the patient had a grade IV or V injury, our practice is to obtain a postdischarge scan at 4–6 weeks after the injury.

■ Resumption of Activity No steadfast rules apply to activity resumption in patients with uncomplicated hospital courses following blunt hepatic injury. The practice of keeping a patient from activity for 4 months has been commonly employed. This practice most likely resulted from the observation that most hepatic injury seems to have resolved by CT in 4 months. A contrary approach to this practice can be based on some interesting animal studies. Dulchavsky et al. found in animal studies that hepatic wound burst strength at 3 weeks was as great or greater than uninjured hepatic parenchyma.57 This is most likely a result of fibrosis throughout the injured parenchyma and Glisson’s capsule. Therefore, activity can be resumed about 1 month after injury if a follow-up CT (in grade III–V) has shown significant healing.

■ Hemodynamically Stable Patient with Penetrating Injury Nonoperative Management of Penetrating Injury Peritoneal penetration has mandated operative exploration for many years. However, many trauma centers have adopted selective nonoperative management of knife stab wounds to the right upper quadrant. The work of Nance and Cohn in 1969 supported this nonoperative care in patients with stab wounds who were hemodynamically stable and had no evidence of peritoneal irritation.58 Since then, reports of successful nonoperative management of gunshot wounds (GSW) have been published.

■ Operative Management of Patients with Minor Liver Injury The decision for operative intervention of incidental liver injury may develop due to laparotomy for penetrating injury, patient instability, or concomitant internal injury. The incision of choice is the midline incision in a trauma patient. Not only will the operating surgeon be able to gain access to the hepatic region but the entire peritoneal cavity will also be able to be inspected and manipulated. On opening the peritoneal cavity, attention should first be focused on stopping uncontrolled hemorrhage. Laparotomy pads should be used to clear the peritoneal cavity of clot. In minor liver injury, the bleeding from the liver can initially be managed with packing of the hemorrhagic area. Before dealing with a minor liver injury, the remainder of the peritoneal cavity should be inspected for injury, including bowel injury and other solid organ injury. Many minor liver injuries do not require operative fixation and nonbleeding wounds should not be probed or otherwise manipulated. Small wounds of the liver parenchyma with minimal bleeding may be able to be controlled with electrocautery or argon beam coagulation. Small to moderate bleeding cavities may first be inspected for any obvious bleeding vessels that can be ligated. Next, packing a tongue of omentum, with its vascular supply intact, into the wound and securing it into

CHAPTER CHAPTER 29 X

■ Follow-Up CT Scanning of Blunt Hepatic Injury

Renz and Feliciano prospectively treated 13 patients with right thoracoabdominal GSW nonoperatively.59 The rationale behind this management is that these wounds of small caliber weapons may have injury to diaphragm and liver only, sparing any intestinal injury. The authors stressed the importance of serial abdominal exams and contrast CT scanning in their successful nonoperative management of penetrating injury. Other center experience has concurred with this selective nonoperative management.60,61 Demetriades et al. even reported successful nonoperative management of penetrating grade III and IV liver injuries that required angioembolization.62 The criteria for nonoperative management include those patients who are hemodynamically stable, have no peritoneal signs, and are not mentally impaired. These patients then undergo contrast-enhanced CT scan to rule out other abdominal visceral injury. Serial abdominal exams as well as close hemodynamic monitoring are also implemented. Triple-contrast CT of 86 abdominal GSW, as reported by Shanmuganathan et al., had a sensitivity and specificity of 97% and 98%, respectively.63 Velmahos et al. do not use triple-contrast CT at their center. They report a sensitivity and specificity of 90.5% and 96%, respectively, in diagnosing intraabdominal organ injuries requiring surgical intervention.64 All trauma surgeons do not accept nonoperative management of GSW. Missed or deliberate nonrepair of small diaphragmatic lesions may lead to long-term adverse sequelae, not only of diaphragmatic herniation but also of possible biliopleural fistula.65 Late intervention for other missed injury (e.g., duodenal injury) may also lead to substantial morbidity. Nonoperative management of RUQ penetrating trauma must be performed under the care of a center that has not only the capability of close continuous monitoring but also CT radiology accessibility and immediate operating room availability.

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SECTION 3 X FIGURE 29-6 Hepatic injury plugs may be useful for tamponading deep parenchymal wounds. FIGURE 29-7 Manual compression of major liver injury.

place halts most moderate bleeding. Stone and Lamb first described this technique in 1975.66 Wrapping a column of absorbable gelatin sponge with oxidized regenerated cellulose makes another beneficial device (Fig. 29-6). This is then inserted like a plug into deeper bleeding cavities. Omentum is often then brought up into the wound and secured to increase hemostasis. These maneuvers are very successful in the management of minor liver injury.

■ Operative Management of Patients with Major Liver Injury

triad occlusion can be accomplished with similar results. In one study describing the management of 1,000 cases of hepatic trauma, the Pringle maneuver was utilized for between 30 and 60 minutes in many of the high-grade injuries without adverse sequella.69 Pachter et al. managed 81 patients with the assistance of the Pringle maneuver for up to 75 minutes without any apparent morbidity from the procedure.70 Therefore, it seems that longer normothermic ischemic time can be used without added morbidity in the severely injured liver.

Initial Management Patients with major hepatic trauma may present with hemodynamic instability and are therefore taken urgently to the operating room. As in minor injury the most optimal incision for expected major liver injury is the midline incision. Once the peritoneum is entered in these patients, a large amount of blood may be evacuated, which decreases the natural tamponade of a large hemoperitoneum. Adequate resuscitation is the key at this time. Manual compression of obvious injury will decrease bleeding (Fig. 29-7). It is imperative that the anesthesia team is allowed to catch up with fluid loss prior to proceeding. Fluids should be warmed and coagulopathy corrected, keeping in mind current recommendations for coagulation products given with packed red blood cells (see Chapter 13). Once the patient has been adequately resuscitated, a more thorough exam of the peritoneal cavity must be completed. If indeed the bleeding source is localized to the liver and bleeding continues after manual compression is released, then the portal triad should be identified and a Pringle maneuver performed (Fig. 29-8). Much controversy has evolved around the normothermic ischemic time produced by the use of the Pringle maneuver. Many authors have advocated clamping for 20 minutes and then allowing reperfusion for 5 minutes.67,68 This practice has not been proven to be beneficial in traumatic liver injury. Multiple studies have emerged indicating that longer portal

FIGURE 29-8 The Pringle maneuver controls arterial and portal vein hemorrhage from the liver. Any hemorrhage that continues must come from the hepatic veins. (Reproduced with permission from Burch JM, Moore EE. Injuries to the liver, biliary tract, spleen, and diaphragm. In: Wilmore DW, ed. ACS Surgery: Principles & Practice. New York: WebMD Corporation; 2002.)

Liver and Biliary Tract

■ Hemostatic Maneuvers for Severe Parenchymal Injury Packing Perihepatic packing has become the most widely used and successful method for management of severe liver injury. Laparotomy pads are packed around the liver, thus compressing the wound between the anterior chest wall, diaphragm, and retroperitoneum. This “damage control” laparotomy provides hemostasis while the patient is able to be hemodynamically optimized in the intensive care unit (ICU) as well as provides pressure on the wound to achieve hemostasis. Beal reported an 86% survival rate in 35 patients in whom perihepatic packing was used.71 In order to provide the tamponade necessary for effective packing, the surgeon must mobilize the liver by taking down the right and left triangular, coronary, and falciform ligaments. If, however, there is obvious hematoma in a ligament, this area should not be entered. Hematoma in the ligament may indicate a vena caval or hepatic vein injury and mobilization may lead to rapid exsanguination. The decision to pack must be made early in the exploration, in order to provide the best chances for patient survival.72 Indeed, early packing is associated with the increased survival of liver trauma patients. Richardson et al. found that the death rate associated with packing significantly decreased after 1989 and was linked to less packing time, as was demonstrated by a decrease in the average blood loss despite the equal severity of injury.33 One of the difficulties with packing comes with removal. Often, the bare liver area that has become hemostatic is now adherent to the packs. Pulling off the packs can then cause further bleeding. Different solutions to this problem have been described from wetting the gauze with saline on removal to a more innovative technique described by Feliciano and Pachter.73 They suggest placing a nonadherent plastic drape directly on top of the hepatic surface and then placing the laparotomy pads above this plastic interface. An important issue regarding abdominal packing is abdominal closure. These patients will undoubtedly require significant resuscitation. Abdominal compartment syndrome diagnosed with elevated bladder pressure (above 25 mm Hg), increasing peak airway pressures, decreased urine output, and abdominal distention can be a life-threatening consequence of this resuscitation (see Chapter 38). Abdominal compartment syndrome can be avoided in these patients by leaving the fascia and skin edges open and placing a temporary closure device over the open abdomen. Packing is often useful in blunt, venous injury but cannot be expected to provide hemostasis in major arterial injury. Major arterial injury is often seen with penetrating trauma and therefore packing in penetrating bleeding may not be successful. The timing of packing removal continues to be the subject of debate. Correction of coagulopathy, acidosis, and hypothermia can almost always be accomplished within 24–48 hours of packing. Intra-abdominal sepsis is a risk of prolonged packing.

Krige et al. found that packs that remained for more than 3 days had an 83% incidence of developing perihepatic sepsis, whereas those left less than 3 days had a 27% chance of sepsis.74 A 1986 report found a 10.2% sepsis rate for patients who had packs removed within 24–48 hours along with complete clot evacuation and debridement of devitalized tissue.75 Caruso et al. advocate the removal of packs at 36–72 hours because they have experienced a higher rate of repacking for recurrent hemorrhage in the group of patients who had their packs removed earlier.72 Nicol et al. reported a significantly higher repacking rate in those hemodynamically stable patients whose packs were removed at 24 hours compared to those patients whose packs were removed after 48 hours.76 Overall, it seems that pack removal prior to 72 hours, effective residual peritoneal clot evacuation, and excision of devitalized tissue will provide the optimal circumstance for minimizing perihepatic sepsis.

Direct Suture Grade III and IV liver lacerations often do not respond to the more topical procedures listed for minor injury control. One of the oldest reported techniques to control deep parenchymal bleeding is direct suturing of the tissue with large, blunt-tipped 0-chromic suture. Utilizing a large blunt needle with 0 suture prevents the suture from tearing through Glisson’s capsule when tying. The stitches can be continuous or if a deeper laceration is encountered, a mattress configuration is preferred. This technique is most appropriate for lacerations less than 3 cm in depth. It is best to avoid the direct suture approach as blind passage of these large blunt needles may injure bile ducts and vascular structures thereby leading to possible intrahepatic hematomas or hemobilia.

Finger Fracture More severe parenchymal laceration may involve larger branches of the hepatic artery or portal system and will not respond to the attempted tamponade with large parenchymal suturing. In these cases some clinicians prefer the technique of finger fracture (Fig. 29-9).70 The utilization of this technique involves careful extension of the laceration using finger fracture until bleeding vessels can be identified and then controlled with clips, ligation, or direct repair. This technique can lead to extensive additional parenchymal bleeding while searching for the initially damaged vasculature.

Omental Packing Omental packing has been used successfully on its own as well as in conjunction with finger fracturing. It fills the potential dead space with viable tissue that also is a source of macrophage activity. Stone and Lamb original work was reinforced by Fabian and Stone when they managed to stop the venous hemorrhage of severe parenchymal laceration in 95% of patients with an 8% mortality.66,77 The technical aspects of this process include first mobilizing the greater omentum from the transverse mesocolon in the avascular plane. Next, the omentum is mobilized from the greater curvature preserving the usually right gastroepiploic vascular pedicle (Fig. 29-10). The tongue of omentum is then placed into the injury defect. The ability to achieve hemorrhage

CHAPTER CHAPTER 29 X

The Pringle maneuver often does not control all bleeding. It will control the inflow bleeding from the hepatic artery and portal vein but not the retrograde bleeding from the vena cava and hepatic veins.

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A

B

C

FIGURE 29-9 Hepatotomy with selective ligation is an important technique for controlling hemorrhage from deep (usually penetrating) lacerations. This technique includes finger fracture to extend the length and depth of the wound (A), division of vessels or ducts encountered (B), and repair of any injuries to major veins (C). (Reproduced with permission from Burch JM, Moore EE. Injuries to the liver, biliary tract, spleen, and diaphragm. In: Wilmore DW, ed. ACS Surgery: Principles & Practice. New York: WebMD Corporation; 2002.)

cessation with this method reiterates that most hepatic bleeding is venous. Tamponade with viable omental packing is superior to most of the direct techniques of hemorrhage control.

Penetrating Tract Penetrating tracts through the hepatic tissue provide another challenge for the surgeon. Often these are of great depth and length, therefore making visualization of the entire injury impossible. Management of these injuries has included the packing of omentum into the tract for hemostasis. Also, devices such as the rolled cellulose-covered gelatin sponge can be inserted into the tract for hemostasis. Poggetti et al. advocate the use of balloon tamponade of the tract.78 A Penrose drain is

placed over a hollow perforated tube and tied on both ends. The balloon is then placed into the tract and inflated with a contrast agent (Fig. 29-11). If successful tamponade has been achieved, the balloon is left in the abdomen and removed 24–48 hours later at a second laparotomy. A similar technique using a Foley balloon has been described.79 A size 16 Foley is inserted into the tract and inflated. If there is continued active bleeding, the catheter is moved back or forward and inflated again. If bleeding continues through the catheter but not out of tract, the balloon is proximal to the bleeder and needs to be repositioned deeper. If the bleeding continues from the tract orifice, then the balloon must be repositioned further out of the tract. Once the catheter is positioned, drains are placed in the area. The drains and catheter are brought out through the skin.

Liver and Biliary Tract

551

CHAPTER CHAPTER 29 X

FIGURE 29-10 Omental mobilization employed for liver packing.

The Foley can be removed after deflation produces no further signs of bleeding in 3–4 days or at the time of the next planned reexploration. Sengstaken–Blakemore tubes have also been used in these situations.80 Deep, small-diameter penetrating injury may continue to bleed from the depths of the wound. In these instances finger fracture of a significant liver segment may be necessary. Another alternative, considering institutional availability, may be angioembolization for these lesions.

FIGURE 29-11 A handmade balloon from a Robinson catheter and a Penrose drain may effectively control hemorrhage from a transhepatic penetrating wound. (Reproduced with permission from Burch JM, Moore EE. Injuries to the liver, biliary tract, spleen, and diaphragm. In: Wilmore DW, ed. ACS Surgery: Principles & Practice. New York: WebMD Corporation; 2002.)

Fibrin sealants have been a topic of much interest. Fibrin glue combines fibrinogen with thrombin, calcium chloride, and aprotinin to form a stable clot.81 However, difficulties have been found with the use of fibrin glue. Time required for preparing the glue, inability of the glue to stick to a bleeding surface, and hypotension with injection have led to minimal human use of the preparation. Fibrin sealants are currently undergoing clinical trials. The Modified Rapid Deployment Hemostat has been studied in trauma patients with severe liver injury. This device is made of a 1 cm layer of acetylated poly-N-acetyl glucosamine bonded to a 4  4 in gauze pad. Applying the bandage in direct contact with a bleeding vessel and placing direct pressure has been shown to decrease the bleeding substantially.82

resection may be necessary in 10% of liver injuries but more than half of these have a mortal wound.71 Another report from Australia and Hong Kong gave the results of resection in 37 patients with major liver injury.46 This article suggests that better resectional results occur when trained hepatobiliary surgeons perform the resection. However, the results are less than compelling when actual injury grade, the low number of resections during first laparotomy, and morbidity are taken into account. Better results have been reported by Polanco et al.84 They report on 56 patients who underwent hepatic resection during their initial operation with a morbidity of 30% and a mortality of 17.8%. They recommend hepatic resection in the following scenarios: patients with massive bleeding related to a hepatic venous injury that must be repaired directly, massive destruction of hepatic tissue, and finally patients with a major bile leak from a proximal main intrahepatic bile duct. Successful outcome by crushing the injured liver segment between two aortic clamps has also been reported.85 The hemostatic clamps are left in place and 36 hours later the patient is brought back to the operating room where the now necrotic segment is easily removed and the liver edge oversewn.

Resection

Hepatic Artery Ligation

Anatomic resections for severe hepatic trauma were often performed in the late 1960s and early 1970s. However, the 80% survival reported by McClelland and Shires has not been experienced in other reports.83 In fact, most series surmise that when anatomic resection is performed for massive bleeding, the mortality is prohibitively high. It has been stated that major lobar

Hepatic arterial ligation can be a useful maneuver either in the operating room or with the aid of angiography. Complete selective hepatic artery ligation is used in only about 1% of patients with severe hepatic trauma.33 If a patient has a noticeable decrease in bleeding after the Pringle maneuver has been performed, hepatic artery ligation should be considered. Such

Fibrin Sealants and Hemostatic Devices

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alternative for very few patients. The patient must have an overall excellent chance of survival with minimal concomitant injury, especially other intra-abdominal or neurologic injury. Also, if a trauma patient requires a transplant, it must be completed immediately; waiting for a donor organ to arrive is not an option. Case reports from Philadelphia and Miami describe successful transplantation.91,92 These cases present the requirements for possible transplantation as the patients had a single liver injury, no neurologic compromise, the achievement of hemodynamic stability, corrected coagulopathy, and the ability to obtain a donor organ within 36 hours of an anhepatic state.

instances occur in a scenario with a knife wound or small caliber missile wound with continued deep parenchymal bleeding. When the portal vein remains patent, the chance for severe hepatic dysfunction after hepatic artery ligation is minimal.86 However, with patients who have undergone significant hypoperfusion due to traumatic shock, hepatic artery ligation may produce enough further ischemia to produce necrosis or sepsis.87 One instance of hepatic failure following hepatic artery embolization resulted in the patient receiving an urgent liver transplant.88 Currently, most centers are advocating a multimodality approach to hepatic arterial bleeding. The role of interventional radiology has gained significant importance in the role of bleeding control after packing. Sclafani et al. in 1984 reported on the successful selective arterial embolization of severely injured liver parenchyma after packing.89 Angiography has become an important step in the management algorithm for severe liver injury. One report stated that an approach for high-grade liver injury includes “immediate surgery for control of life-threatening hemorrhage, the use of complex surgical techniques to address these injuries, the institution of early hepatic packing and immediate postoperative hepatic angiography and angioembolization.” In this report of 22 patients that had sustained grade IV and V injury, 15 underwent angiographic embolization (10 had been previously packed). All of these procedures were successful in arresting the continued bleeding.90 Therefore, it cannot be overemphasized that the care for severe hepatic parenchymal injury requires not only operative skill but also the judgment to determine the time for packing and collaboration with interventional radiology specialists (Fig. 29-12).

■ Retrohepatic Vena Cava/ Hepatic Vein Injury

Hepatic Transplantation

■ Direct Venous Repair

Hepatic transplantation has been successfully reported. This is assuredly a drastic approach to traumatic injury and is an

Direct venous repair without shunting has been advocated by Pachter and Feliciano. They describe occlusion of the portal

A

Severe hepatic trauma can injure the vena cava anywhere along its extraparenchymal course. Also, damage to the hepatic veins can be extraparenchymal or intraparenchymal. Life-threatening bleeding from these injuries occurs if the supporting structures, mainly the suspensory ligaments, diaphragm, or liver parenchyma, are disrupted. Therefore, the exposure of a major venous injury may release the tamponade and result in free bleeding and exsanguination. As Buckman et al. outlined, there are three main strategies described to deal with these mortal injuries. The first is to directly repair the venous injury with or without vascular isolation. The second is with a lobar resection. The third is by using a strategy of tamponade and containment of the venous bleeding.93

B

FIGURE 29-12 (A) Hepatic pseudoaneurysm. (B) Coiled hepatic pseudoaneurysm.

Liver and Biliary Tract

A

FIGURE 29-13 (A) A hole is cut in the right atrial appendage above a 2-0 silk purse-string suture. A Satinsky clamp maintains vascular control. (B) Final position of No. 36 chest tube acting as an atriocaval shunt. Note the extra hole cut in the chest tube at the level of the right atrium. All holes in the chest tube are outside the umbilical tapes, thereby forcing blood from the lower half of the body and the kidneys through the shunt. (Reproduced with permission from Feliciano DV, Pachter HL. Hepatic trauma revisited. Curr Probl Surg. 1989;26:499.)

triad for a significant time, mobilization of the liver with medial rotation, and efficient finger fracture to the site of injury.94 With these methods they reported a 43% (6/14) survival. Chen et al. have published similar results of a 50% survival.95 Various shunting maneuvers have been attempted for complete vascular control of the liver. Schrock et al. first introduced the atriocaval shunt in 196896 (Fig. 29-13). The goal is to shunt the blood from the infrahepatic vena cava, bypassing the retrohepatic cava, and directing flow into the atria. This, along with the Pringle maneuver, is theoretically used to create a bloodless field. Unfortunately, of the approximately 200 cases published using atriocaval shunting, only at best 10–30% survive their injury.33 The caveats of this maneuver include the need to plan for the procedure essentially before proceeding with the operation. All the equipment must be ready and a thorocoabdominal exposure is necessary. Shunting a patient cannot be successfully accomplished if the patient has already had major blood loss, becomes coagulopathic, and has inadequate operative incisional exposure. Shunting, in general, is not often used at present. The

■ Anatomic Resection As mentioned earlier, anatomic resection has resulted in a high mortality when carried out for traumatic bleeding. In certain circumstances when the dissection has already been done by the injury itself, resection for debridement may be indicated. However, current data do not promote anatomic resection for major venous injury unless direct repair is necessary.

■ Vena Cava Stenting Endoluminal stent grafts are now available for many uses. Reports of using the fenestrated graft in blunt trauma have been reported.103 The graft used by Watarida et al. was homemade and stayed patent at the 16-month follow-up. More successful reports of commercially available fenestrated grafts used in retrohepatic vena caval injuries are surfacing. These grafts are being placed both after “damage control” laparotomy and prior to laparotomy when the lesion is seen on CT.104,105 Hommes et al. report the survival of a patient with intraoperative placement of an endovascular stent graft into the IVC for a juxtahepatic IVC injury with parenchymal and packing.106 Though these grafting procedures are not yet commonplace, a significant future for their use is apparent.

■ Tamponade with Containment With the high mortality of direct venous repair and anatomic resection evident, the focus on severe vascular injury management has shifted to methods of tamponading and

CHAPTER CHAPTER 29 X

B

patients who require shunting often have catastrophic injury in which time is of the essence. Therefore, more often these patients are packed urgently and brought to angiography for embolization for any hope of true survival. Other shunting procedures have been utilized as well. Pilcher et al., in 1977, reported on a balloon shunt introduced through the saphenofemoral junction.97 This occlusive method has had some anecdotal success and avoids emergent thoracotomy without destruction of the surrounding ligamentous tamponade.98 The multi-institutional trial results in 1988 however did not show any survival benefit of the balloon shunt versus the atriocaval shunt.99 Venovenous bypass has been used in some institutions as well.100 Again this method requires considerable planning but obviates the hemodynamic instability of caval occlusion and ligamentous disruption. Direct clamping techniques have also been used in a small number of patients. Carrillo et al. had success with vascular clamps placed on hepatic vein injured ends, filling the laceration with viable omentum, and packing with planned reoperation.101 Nicoluzzi et al. report using hepatic vascular exclusion without aortic cross-clamping.102 After fluid loading, vascular clamps are placed on the porta, infrahepatic suprarenal inferior vena cava, and the suprahepatic inferior vena cava. Once clamping is tolerated, a direct vessel repair is accomplished. In general, direct approaches to vein repair are difficult and can often result in a profuse uncontrolled bleeding situation, especially since even the most veteran surgeon has little experience in these uncommon injuries.

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containing venous injury in addition to embolization of arterial bleeding. Many of the methods utilized for severe parenchymal injury are also effective for large venous injury. In Memphis, the mortality of patients with juxtahepatic venous injuries who were treated with omental packing was a low 20.5%.107 Another article emphasizing packing included 14 patients with hepatic vein injury and 6 patients with retrohepatic vena caval injury with an overall mortality of only 14%.71 Cue et al. depict four patients with retrohepatic vena cava, hepatic vein injury, or both who underwent initial packing and survived.108 At this time it seems that the most successful method of managing severe retrohepatic or hepatic venous injury is by using tamponade and containment. Direct repair of damaged vessels continues to have a very high morbidity even in the most experienced hands. Resection also has shown itself to be a morbid alternative with the survival data primarily being in the hands of experienced hepatobiliary surgeons in somewhat stable patients. Overall, the best approach to severe liver injury includes (a) expedient recognition and operative intervention of unstable hemorrhaging patients, (b) mobilization of the liver ligaments not directly involved with hematoma to better visualize the injury, (c) placement of a viable omental tongue into parenchymal defects, (d) rapid determination of the need for gauze packing when direct surgical maneuvers fail, and (e) angiographic embolization of hepatic arterial injured branches when ongoing hemorrhage or CT blush is seen.

■ Drains The use of closed-suction drains has clearly been proven to be superior over Penrose drain use in a number of publications. A 1991 study reported a perihepatic abscess rate of 6.7% with no drain, 3.5% with closed suction, and 13% with Penrose drainage.107 A study from Charity Hospital found an abscess rate of 1.8% in those with no drainage, 0% abscess rate in those with closed suction, and 8.3% abscess rate in those with open drains.109 Examination of these figures, however, indicates no significant difference in abscess rate between the no drainage group versus the closed-suction cohort. Indeed, in a review of 161 significant liver injuries, 78 patients underwent closed-suction drainage and 83 were left without a drain.110 The injury grade, blood loss, shock, specific injuries severity, and associated injuries were similar in the two groups. There was no difference in mortality, abscess formation, or biliary fistula between the two groups. Thereby, the study concluded that drainage should be done only in injuries with obvious bile leaks noted at the time of laparotomy. This viewpoint is reiterated in a 1988 article stating that the presence of hypotension and multiple transfusions are more predictive of abscess formation than drain placement.109 With the current use of interventional radiology techniques, routine drainage has become less of an issue. Most centers will treat patients expectantly and only place drains in patients with obvious bile leaks. If indeed a collection or abscess develops, many can be dealt with by percutaneous tube placement under radiologic guidance.

■ Complications of Operative Management Bleeding Postoperative hemorrhage is not a common occurrence. Most series quote a 2–7% hemorrhagic complication rate.73,99 Falling serial hematocrits, increasing abdominal distention, and episodes of hypotension or tachycardia mark continued bleeding. The inability to operatively control the bleeding is often confounded by hypothermia and coagulopathy. In the past these patients were urgently returned to the operating room after correction of their coagulopathy and rewarming. Currently, after resuscitation these patients can often be managed with angiographic localization of the bleeding source and embolization. Of course, unstable patients do need operative intervention and may in fact need reexploration of previously packed areas in order to specifically identify the bleeding source. The areas of bleeding must then be addressed by utilizing the previously discussed maneuvers of severe injury control.

Abdominal Compartment Syndrome Abdominal compartment syndrome may develop with packing and continued fluid requirements in these severely ill patients. Packing has been shown to even cause pulmonary embolism from venous stasis caused by infrahepatic vena caval compression.111 The physician must be vigilant in his or her care and resuscitation of these patients.

Hemobilia Immediate attention should be given to a patient who develops a significant upper gastrointestinal bleed following liver repair. Many times this is the only symptom that can point to the development of hemobilia. The often-mentioned signs and symptoms of hemobilia—jaundice, right upper quadrant pain, and falling hematocrit—are common occurrences in most patients after severe liver injury and therefore make the diagnosis of hemobilia difficult. The incidence of hemobilia ranges anywhere from 0.3% to 1.2%.49,112 The presentation may be days to weeks postinjury. Upper endoscopy and bleeding scans are generally unable to locate the source of bleeding. Angiography will frequently delineate a pseudoaneurysm and accomplish embolization of the damaged vessel.113,114 Operative debridement and drainage may be necessary if a large cavity has formed or sepsis is apparent.49

Bilhemia Biliovenous fistulas have also been described by Clemens and Wittrin in the literature but are quite rare.115 This entity occurs as the bilious venous blood dissolves in the bloodstream and is carried directly to the right heart. Therefore, one sees a patient with a drastically rising bilirubin with relatively normal liver function tests. Glaser et al. discussed three cases of bilhemia, which were identified by ERC.116 The management of these cases involved a left hemihepatectomy in the first, spontaneous resolution in the second, and controlled biliary fistula in the last. Another method of control included placement of a constant suction T-tube with subsequent resolution.117 Although spontaneous resolution has occurred, this entity can have a high mortality if left unaddressed.

Liver and Biliary Tract

Biliary Fistulae

Hepatic Necrosis Major hepatic necrosis can be a complication of the multimodality management of severe liver injury. Dabbs et al. found that 29 of 30 patients that they encountered with major hepatic necrosis underwent initial operative intervention.122 Many of the patients then had embolizations performed making their risk of major hepatic necrosis between 65% and 68%. A large number of these patients then required resection of their necrotic hepatic parenchyma.

Other Fistulae Problems Thoracobiliary fistulae are also encountered with traumatic liver injury. Though it is a rare complication, identification and management can prevent morbidity of progression to bronchobiliary fistula. Many of these injuries occur after thorocoabdominal penetrating injury. Often the patient does well initially with resolution of hemothorax, no evidence of jaundice, and stabilization

■ Traumatic Extrahepatic Biliary Tract Injury Overview Extrahepatic biliary and portal triad injuries make up only about 0.07–0.21% of all trauma admissions at Level I trauma centers.128,129 Though these injuries are rare, their evaluation and management prove difficult. Technical problems including continued hemorrhage, adjacent organ injury, and small duct size can prove insurmountable. A timely diagnosis and treatment method may prove to be the survival difference in patients with these severe injuries. In a Seattle paper, 38% were a result of blunt mechanisms, similar to the 31% with blunt mechanism quoted in a 1995 multi-institutional trial.128,129 Injury to this area carries an overall 50% mortality, with vascular injury (portal vein or hepatic artery) being the most morbid. When examining those with both portal vein and hepatic artery injury, the mortality is 99%. It is evident that the management of these injuries is a significant challenge (see Chapter 34). Most street weapons are now of high caliber and medium to high velocity. These weapons usually do not result in simple, single injury. Instead, multiple injuries to the liver, porta, vena cava, and surrounding viscera most often occur. Not only are these portal triad injuries difficult to manage, but also the specific injury cannot be identified preoperatively and, therefore, intraoperative decision making is crucial.

■ Injury Types and Diagnostics Gallbladder Gallbladder injury accounts for up to 66% of extrahepatic biliary tract injuries.128 Injury can be from either blunt or penetrating mechanisms. Blunt injury often involves avulsion, either partial or complete, contusion, or perforation. Penetrating injury has been seen involving everything from the body of the gallbladder down to the cystic duct. A review from 1995 warned that 100% of 22 cases of blunt gallbladder injuries were associated with other intra-abdominal trauma; however, this is

CHAPTER CHAPTER 29 X

Biliary fistulae are one of the complications that a surgeon is likely to encounter. Biliary fistula can account for up to 22.5% of traumatic liver management complications.90 Overall biliary fistulae seem to occur in about 4–6% of patients who undergo operative management of severe liver injury.118,119 Some bile duct injuries are obvious intraoperatively with significant bile staining and a visible disrupted bile duct. Many persistent fistulae may, however, manifest from smaller radicals, which retract into the liver parenchyma and are not visualized. Operative drain placement is advocated in liver injury with obvious bile staining. It is common for liver injuries to have transient early postoperative serosanguinous and bilious drainage. Bilious drainage of at least 50 mL per day that continues after 2 weeks is considered a biliary fistula.99 Also, persistent earlier drainage of over 300–400 mL of bile a day should be cause for further evaluation. The diagnosis of a biliary injury can be done by a fistulogram if a drain is in place, HIDA scan (though not anatomically exact), MRCP, or ERC. Major left or right bile duct injury often requires further intervention for closure. In the past the surgical approach was recommended with resection or Roux-en-Y procedures predominating. More recently, nonoperative approaches have proven successful. Percutaneous stenting of injuries and drainage of biloma collections has been utilized.120 Also, many reports are surfacing of management using ERC sphincterotomy with stenting and percutaneous drainage of biloma. One study described five patients with intrahepatic bile duct injuries.121 The injuries included left main hepatic duct, right second-order bile duct, and more peripheral lesions. All were successfully managed nonoperatively. Repeat ERC of these patients led the authors to conclude that “therapeutic ERC and percutaneous interventional radiology can both treat the complication of the ductal injury and allow healing of the ductal disruption.” Confirmation of healing of major ductal injury after ERC stenting and percutaneous drainage has been documented.90 For bile fistulae that do not involve a main bile duct, drainage alone will provide adequate treatment and other maneuvers are rarely necessary.

of liver injury only to become significantly tachypneic a week or more later. One report described the treatment of a thoracobiliary fistula with chest tube drainage and ERC.123 One patient returning for routine follow-up was operatively managed with thoracic and abdominal drains and diagnosed from an abnormal chest x-ray and subsequent CT. Rothberg et al. promote operative intervention in order to evaluate for significant diaphragmatic injury, liver necrosis, or lung necrosis with possible bronchial involvement.124 Penetrating injury can potentially provide a means for many severe fistula communications. Pleurocaval fistula may result from thorocoabdominal injury. This fistula may be the source of life-threatening air embolism.125 Arterioportal fistula are associated with initial hemorrhage and subsequent portal hypertension.126 One case report described a GSW that formed a left hepatic artery to portal vein fistula. This fistula was able to be successfully managed by interventional radiology embolization. Portosystemic venous shunts have also been reported in severe blunt liver injury.127

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cholangiogram through the gallbladder can be helpful.133 DPL has also shown a lack of specificity for biliary injury as duodenal, small bowel, and liver injuries may produce bile.134 Also, the small amount of bile may be obscured by the presence of blood in the peritoneum with the DPL. Late presenters of bile duct injury cannot be recognized until symptoms are apparent. At that time CT, ultrasound, or ERC can be used to visualize bile collections and localize injury.135

■ Management of Extrahepatic Biliary Injuries General Considerations FIGURE 29-14 CT scan revealing a distended gallbladder filled with blood (dark arrow) in a patient with blunt abdominal trauma and virtually no peritoneal signs.

not uniformly reported and isolated gallbladder injury is encountered.130 Therefore, though a patient may present with an isolated gallbladder injury, the surgeon must carefully rule out further intra-abdominal trauma. A trauma patient may also manifest a gallbladder injury as a result of a significant contusion. Blood in the gallbladder can cause stasis and blockage of the cystic duct, which may present as acute cholecystitis.131 Gallbladder injury is successfully evaluated by CT (Fig. 29-14). The findings of an ill-defined contour of the wall, collapse of the lumen, or intraluminal hemorrhage highly suggest blunt gallbladder injury.132 Patients may also present with bile peritonitis and right upper quadrant pain. Ultrasound examination in gallbladder injury has not been formally evaluated but intuitively should provide useful information about this injury. Despite these diagnostic methods, the diagnosis of gallbladder injury is most often secured at laparotomy.

Bile Duct Bile duct injury is most often encountered in penetrating injury.128 Blunt ductal injury is most likely to happen where the bile duct is fixed to its surroundings, for example, the pancreaticoduodenal junction.133 In a multi-institutional trial it was found that blunt injuries were predominately a complete transaction, whereas penetrating injuries were partial 75% of the time.128 Extrahepatic bile duct injuries are evident in two distinct settings: first, at the time of laparotomy for a patient in shock with other severe liver, vascular, pancreatic, or duodenum injury; second, in a late presentation often more than 24 hours and up to 6 weeks after the original injury time. The patients with late presentation may develop jaundice, abdominal distention and pain, intolerance to enteral feeding, fever, or worsening base deficit due to bilious ascitis or infection.129 Evaluation of the stable patient with CT scan or ultrasound in the acute setting will not be able to differentiate abdominal blood with biliary leak. There may be some indication of pancreatic head fullness, duodenal thickening, or portal edema but these are nonspecific findings. In the presence of bile staining during an operative procedure and no obvious injury, a

Patients with portal triad and extrahepatic biliary injuries usually arrive in shock. Therefore, the tenets described for major liver injury apply to portal injury as well. A midline incision should be made. Evacuation of blood clots and hemoperitoneum with urgent packing of the bleeding portions should be completed. The patient should be resuscitated and coagulopathy correction initiated by the anesthesia team. Hematoma or bleeding around or within the hepatoduodenal ligament or severe parenchymal injury leading to the porta hepatis should raise suspicion of a portal triad injury. Bile staining should also be fully investigated as 12% of bile duct injuries may be missed at the initial operation.133 The Pringle maneuver may be helpful in decreasing the inflow to a portal injury. In order to obtain adequate examination and exposure for repair, a wide Catell maneuver should be performed, which includes mobilizing the ascending and hepatic flexure areas of the colon, thus exposing the duodenum completely to the head of the pancreas and inferior vena cava.

Gallbladder Isolated gallbladder injury is most often managed with open cholecystectomy. However, there have been reports of laparoscopic cholecystectomy in penetrating trauma.136 This procedure should be done with great reserve since many gallbladder injuries are associated with other intra-abdominal injury in both penetrating and blunt trauma. Though the laparoscope can give a good superficial exam of the peritoneal cavity, visualization of the duodenum, pancreas, and porta is in most hands not sufficient. Minor gallbladder contusions can often be managed nonoperatively.137 This may lead to cholecystitis or delayed rupture if hematoma is present. Historically, it had been suggested that simple lacerations should undergo cholecystorraphy with absorbable suture.138 Cholecystorraphy, however, remains a rare procedure, as small gallbladder lacerations are rarely encountered and cholecystectomy can be rapidly performed. Cholecystectomy should also be performed on all patients with injury to the cystic duct or right hepatic artery that would eliminate the blood supply to the gallbladder.

Bile Duct Bile duct injury should be addressed after hemorrhage has been controlled. In the patient who remains in shock and coagulopathic, packing and placement of a Jackson-Pratt drain in the area of biliary injury is adequate until reexploration is performed.

Liver and Biliary Tract

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In the somewhat more stable patient who is becoming coagulopathic, a small T-tube placed in the injured duct will provide adequate drainage until a formal repair can be accomplished.139 With a partial transection of a right or left hepatic duct, insertion of a small T-tube into the common hepatic duct with a long limb traversing the partially transected area even without suturing may provide enough support for full healing.140 For the stable patient definitive repair is preferred at the first operation. Four broad categories of biliary duct injury have been described: (a) avulsion of cystic duct or small laceration, (b) transection without loss of tissue, (c) extensive defect in the wall, and (d) segmental loss of ductal tissue.140 Avulsions and small lacerations in the duct can be repaired primarily with 6-0 polyglycolic suture making sure not to narrow the lumen. A T-tube with a limb under the repair can be used; however, this may be difficult to insert in a patient with a normally small duct. The techniques used to place a T-tube may also devascularize an already compromised duct. Therefore, the authors will not place a T-tube in primary repair. For avulsions in which primary repair may narrow the lumen, a piece of the cystic duct or proximal gallbladder wall can be used for the repair.141 Penetrating injury very occasionally results in a transection of the bile duct without significant tissue loss. In these instances an end-to-end anastomosis can be performed. One must be sure to perform minimal dissection around the duct or the lacerated ends in order to maintain adequate blood supply for healing. Tension on the anastomosis will most certainly lead to stricture. Ivatury et al. reported a 55% stricture rate in the endto-end anastomosis that then required enteric conversion.142 Similarly, Stewart and Way had initial success in 67% of patients initially managed with Roux-en-Y for complete laceration following laparoscopic cholecystectomy with failure in all lacerations treated with end-to-end anastomosis.143 Extensive wall defects and segmental tissue loss require biliary-enteric anastomosis (Fig. 29-15). In the past many methods of “patching” were attempted. Saphenous vein grafts have had difficulties with shrinking and fibrosis, which then required stenting.144 Prosthetic patches and jejunal mucosal patches have also been tried with anecdotal success only.145 Deciding which type of biliary-enteric anastomosis to perform depends on the injury location, access, and size. Roux-en-Y hepaticojejunostomy with cholecystectomy and T-tube drainage is the most utilized approach to complex injury. The retrocolic Roux limb is at least 40 cm long and can be brought up to the common hepatic duct or even to the hilar plate similar to the Kasai procedure. An avulsion of the hepatic ducts at the bifurcation can be managed by suturing the ducts together medially before the end-to-side hepaticojejunostomy.146 If the distal common duct is not found due to its retraction behind the pancreas, drainage of the area may be all that is necessary.134 Roux-en-Y choledochojejunostomy with cholecystectomy and T-tube drainage is also useful for the management of common bile duct injury. However, the vascularity in this anastomosis is crucial and any sign of common bile duct vascular injury would lead the surgeon to construct an anastomosis closer to the common hepatic duct. Cholecystojejunostomy and ligation of the very distal common bile duct is a possibility if intraop-

557

FIGURE 29-15 Roux-en-Y choledochojejunostomy. Anastomosis is performed in a one-layer fashion. The T-tube is brought out through a separate proximal stab wound. The gallbladder has been removed.

erative cholangiography reveals a patent cystic duct. This is a viable option especially in patients with small caliber ducts or instability. Blunt distal hepatic duct injury is rare. However, the surgical treatment of these injuries must be individualized to each situation. Both the right and left hepatic duct injuries have been reported.147,148 Biliary-enteric anastomosis are sometimes possible right at the hilar plate; however, if the repair is difficult, ligation of a left or right duct has been reported to lead to atrophy of the involved lobe, not biliary cirrhosis.149 Stenting in biliary anastomosis is a controversial topic. Surgeons in favor of stenting report that stenting allows for decompression, when edema post-trauma may be significant, as well as allows access for cholangiography. T-tubes must exit the duct outside of the repair area or stricture will result. Enteric stents are not necessary and some surgeons feel comfortable without their use, stating that a foreign body in an already small duct may promote stricture or obstruction.150 Morbidity data cannot support a definitive answer for or against stenting and therefore a stent must be used at the discretion of the surgeon, taking each situation separately.

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When ampullary or intrapancreatic bile duct injury is discovered, a pancreaticoduodenectomy may be appropriate if duodenal and pancreatic injury is also seen. An isolated ampullary primary repair or reimplantation may be possible. The authors have repaired an ampullary injury by performing a transduodenal sphincteroplasty and primary repair of the ductal injury. Hepatic resection is necessary only in the case of combination injury to the liver parenchyma and hepatic duct traversing that segment.140 The major complications associated with biliary duct injury are fistula and stricture. A fistula may be able to be nonoperatively managed with drainage. Persistent fistula may require reexploration. Strictures may present with recurrent cholangitis or biliary cirrhosis. Stenting by endoscopists has become frequent; however, long-term results are not conclusive. A recent publication used an aggressive technique of placing an increasing number of stents until complete disappearance of the biliary stricture occurred. Though the authors did have a complication rate of 9%, their mean duration of treatment was 12 months with a 48.8-month stricture-free interval posttreatment thus far.151 Conversely, Johns Hopkins reported their experience with operative management of all postoperative bile duct strictures and had a 98% success rate.152

REFERENCES 1. Croce MA, Fabian TC, Menke PG. Nonoperative management of blunt hepatic trauma is the treatment of choice for hemodynamically stable patients. Results of a prospective trial. Ann Surg. 1995;221:744. 2. Moynihan BG. Abdominal Operations. Philadelphia: WB Saunders; 1905:473. 3. Tilton B. Some considerations regarding wounds of the liver. Ann Surg. 1905;41(1):27. 4. Pringle JH. Notes on the arrest of hepatic hemorrhage due to trauma. Ann Surg. 1908;48:541. 5. Madding GF, Lawrence KB, Kenney PA. Forward surgery of the severely injured. Second Aux Surg Group. 1942;1:307. 6. Couinaud C. Les envelopes vasculo-biliares de foie ou capsule de Glisson: leur interet dons la chirurgie vesiculaire, les resections hepatiqes et l’abord du hile du foie. Lyon Chir. 1954;49:589. 7. Moore EE, Cogbill TH, Jurkovitch GJ, et al. Organ injury scaling— spleen, liver (1994 revision). J Trauma. 1995;38:323. 8. Olsen WR, Redman HC, Hildreth DH. Quantitative peritoneal lavage in blunt abdominal trauma. Arch Surg. 1972;104:536. 9. Root HD, Hauser CW, McKinley CR, et al. Diagnostic peritoneal lavage. Surgery. 1965;57:633. 10. Richards JR, McGahan JP, Pali MJ, et al. Sonographic detection of blunt hepatic trauma: hemoperitoneum and parenchymal patterns of injury. J Trauma. 1999;47:1092. 11. Rozycki GS, Ochsner MG, Feliciano DV, et al. Early detection of hemoperitoneum by ultrasound examination of the right upper quadrant: a multicenter study. J Trauma. 1998;45:878. 12. Sirlin CB, Casola G, Brown MA, et al. Patterns of fluid accumulation on screening ultrasonography for blunt abdominal trauma. J Ultrasound Med. 2001;20:351. 13. Branney SW, Moore EE, Cantrill SV, et al. Ultrasound based key clinical pathway reduces the use of hospital resources for the evaluation of blunt abdominal trauma. J Trauma. 1997;42:1086. 14. Rozycki GS, Ballard RB, Feliciano DV, et al. Surgeon-performed ultrasound for the assessment of truncal injuries: lessons learned from 1540 patients. Ann Surg. 1998;228:557. 15. Chiu WC, Cushing BM, Rodriguez A, et al. Abdominal injuries without hemoperitoneum: a potential limitation of focused abdominal sonography for trauma. J Trauma. 1997;42:617. 16. Ballard RB, Rozycki GS, Newman PG, et al. An algorithm to reduce the incidence of false-negative FAST examinations in patients at high risk for occult injury. Focused Assessment for the Sonographic Examination of the Trauma patient. J Am Coll Surg. 1999;189:145.

17. Valentino M, Serra C, Zironi G, et al. Blunt abdominal trauma: emergency contrast-enhanced sonography for detection of solid organ injuries. Am J Roentgenol. 2006;186:1361. 18. McGahan JP, Horton S, Gerscovich EO, et al. Appearance of solid organ injury with contrast-enhanced sonography in blunt abdominal trauma: preliminary experience. Am J Roentgenol. 2006;187:658. 19. Catalano O, Sandomenico F, Raso MM, et al. Real-time, contrastenhanced sonography: a new tool for detecting active bleeding. J Trauma. 2005;59:933. 20. Udobe KF, Rodriguez A, Chiu WC, et al. Role of ultrasonography in penetrating abdominal trauma: a prospective clinical study. J Trauma. 2001;50:475. 21. Soffer D, McKenney MG, Cohn S, et al. A prospective evaluation of ultra-sonography for the diagnosis of penetrating torso injury. J Trauma. 2004;56:953. 22. Murphy JT, Hall J, Provost D. Fascial ultrasound for evaluation of anterior abdominal stab wound injury. J Trauma. 2005;59:843. 23. Bokhari F, Nagy K, Roberts R, et al. The ultrasound screen for penetrating truncal trauma. Am Surg. 2004;70:316. 24. Federle MP, Goldberg HI, Kaiser JA, et al. Evaluation of abdominal trauma by computed tomography. Radiology. 1981;138:637. 25. Poletti PA, Mirvis SE, Shanmuganathan K, et al. Blunt abdominal trauma patients: can organ injury be excluded without performing computed tomography? J Trauma. 2004;57:1072. 26. Phillips T, Sclafani SJ, Goldstein A, et al. Use of the contrast-enhanced CT enema in the management of penetrating trauma to the flank and back. J Trauma. 1986;26:593. 27. Fabian TC, Croce MA, Stewart RM, et al. A prospective analysis of diagnostic laparoscopy in trauma. Ann Surg. 1993;217:557. 28. Zantut LF, Ivatury RR, Smith RS, et al. Diagnostic and therapeutic laparoscopy for penetrating abdominal trauma: a multicenter experience. J Trauma. 1997;42:825. 29. Fabiani P, Iannelli A, Mazza D, et al. Diagnostic and therapeutic laparoscopy for stab wounds of the anterior abdomen. J Laparoendosc Adv Surg Tech A. 2003;13(5):309. 30. Hurtuk M, Reed RL, Esposito TJ, et al. Trauma surgeons practice what they preach: the NTDB story on solid organ injury management. J Trauma. 2006;61:243. 31. Coimbra R, Hoyt DB, Engelhart S, et al. Nonoperative management reduces the overall mortality of grades 3 and 4 blunt liver injuries. Int Surg. 2006;91(5):251. 32. Malhotra AK, Fabian TC, Croce MA, et al. Blunt hepatic injury: a paradigm shift from operative to nonoperative management in the 1990s. Ann Surg. 2000;231:804. 33. Richardson JD, Franklin GA, Lukan JK, et al. Evolution in the management of hepatic trauma: a 25-year perspective. Ann Surg. 2000;232:324. 34. Pachter HL, Knudson MM, Esrig B, et al. Status of nonoperative management of blunt hepatic injuries in 1995: a multicenter experience with 404 patients. J Trauma. 1996;40:31. 35. Ciraulo DL, Luk S, Palter M, et al. Selective hepatic arterial embolization of grade IV and V blunt hepatic injuries: an extension of resuscitation in the non-operative management of traumatic hepatic injuries. J Trauma. 1998;45:353. 36. Misselbeck TS, Teicher EJ, Cipolle MD, et al. Hepatic angioembolization in trauma patients: indications and complications. J Trauma. 2009;67:769. 37. Kozar RA, Moore JB, Niles SE, et al. Complications of nonoperative management of high-grade blunt hepatic injuries. J Trauma. 2005;59:1066. 38. Kozar RA, Moore FA, Cothren CC, et al. Hepatic-related morbidity associated with nonoperative management of complex blunt hepatic injuries: AAST multicenter trial. In: Sixty-Fourth Meeting of the American Association for the Surgery of Trauma; 2005; Atlanta, GA. 39. Kelly MD, Armstrong CP, Longstuff A. Characterization of biliary injury from blunt liver trauma by MRCP: case report. J Trauma. 2008;64:1363. 40. Bridges A, Wilcox MC, Varadarajulu S. Endoscopic management of traumatic bile leaks. Gastrointest Endosc. 2007;65:1081. 41. Marks JM, Ponsky JL, Shillingstad RB, et al. Biliary stenting is more effective than sphincterotomy in the resolution of biliary leaks. Surg Endosc. 1998;12:291. 42. Miyayama S, Matsui O, Taki K, et al. Bile duct disruption after blunt hepatic trauma: treatment with percutaneous repair. J Trauma. 2006;60:640. 43. Griffen M, Ochoa J, Boulanger BR. A minimally invasive approach to bile peritonitis after blunt liver injury. Am Surg. 2000;66:309.

Liver and Biliary Tract 73. Feliciano DV, Pachter HL. Hepatic trauma revisited. Curr Probl Surg. 1989;26:453. 74. Krige JE, Bornman PC, Terblanche J. Therapeutic perihepatic packing in complex liver trauma. Br J Surg. 1992;79:43. 75. Feliciano DV, Mattox KL, Birch JM. Packing for control of hepatic hemorrhage: 58 consecutive patients. J Trauma. 1986;26:738. 76. Nicol AJ, Hommes M, Primrose R, et al. Packing for control of hemorrhage in major liver trauma. World J Surg. 2007;31:569. 77. Fabian TC, Stone HH. Arrest of severe liver hemorrhage by an omental pack. South Med J. 1980;73:1487. 78. Poggetti RS, Moore EE, Moore FA, et al. Balloon tamponade for bilobar transfixing hepatic gunshot wounds. J Trauma. 1992;33:694. 79. Demetriades D. Balloon tamponade for bleeding control in penetrating liver injuries. J Trauma. 1998;44:538. 80. Ozdogan M, Ozdogan H. Balloon tamponade with Sengstaken– Blakemore tube for penetrating liver injury: case report. J Trauma. 2006;60:1122. 81. Kram HB, Reuben BI, Fleming AW, et al. Use of fibrin glue in hepatic trauma. J Trauma. 1988;28:1195. 82. King DR, Cohn SM, Proctor KG, et al. Modified rapid deployment hemostat bandage terminates bleeding in coagulopathic patients with severe visceral injuries. J Trauma. 2004;57:756. 83. McClelland RN, Shires T. Management of liver trauma in 259 consecutive patients. Ann Surg. 1965;161:248. 84. Polanco P, Leon S, Pineda J, et al. Hepatic resection in the management of complex injury to the liver. J Trauma. 2008;65:1264. 85. Ginzburg E, Klein Y, Sutherland M, et al. Prolonged clamping of the liver parenchyma: a salvage maneuver in exsanguinating liver injury. J Trauma. 2004;56:922. 86. Aaron WS, Fulton RL, Mays ET. Selective ligation of the hepatic artery for trauma of the liver. Surg Gynecol Obstet. 1975;141:187. 87. Lucas CE, Ledgerwood AM. Liver necrosis following hepatic artery transection due to trauma. Arch Surg. 1978;113:1107. 88. Anderson IB, Kortbeek JB, Al-Saghier M, et al. Liver transplantation in severe hepatic trauma after hepatic artery embolization. J Trauma. 2005;58:848. 89. Sclafani SJ, Shaftan GW, McAuley J, et al. Interventional radiology in the management of hepatic trauma. J Trauma. 1984;24:256. 90. Asensio JA, Demetriades D, Chahwan S, et al. Approach to the management of complex hepatic injuries. J Trauma. 2000;48:66. 91. Angstadt J, Jarrell B, Moritz M, et al. Surgical management of severe liver trauma: a role for liver transplantation. J Trauma. 1989;29:606. 92. Delis SG, Bakoyiannis A, Selvaggi G, et al. Liver transplantation for severe hepatic trauma: experience from a single center. World J Gastroenterol. 2009;15(13):1641. 93. Buckman RF, Miraliakbari R, Badellino MM. Juxtahepatic venous injuries: a critical review of reported management strategies. J Trauma. 2000;48:978. 94. Pachter HL, Feliciano DV. Complex hepatic trauma. Surg Clin North Am. 1996;76:763. 95. Chen RJ, Fang JF, Lin BC, et al. Surgical management of juxtahepatic venous injuries in blunt hepatic trauma. J Trauma. 1995;38:886. 96. Schrock T, Blaisdell W, Mathewson C. Management of blunt trauma to the liver and hepatic veins. Arch Surg. 1968;96:698. 97. Pilcher DB, Harman PK, Moore EE. Retrohepatic vena cava balloon shunt introduced via the sapheno-femoral junction. J Trauma. 1977;17:837. 98. McAnena OJ, Moore EE, Moore FA. Insertion of a retrohepatic vena cava balloon shunt through the saphenofemoral junction. Am J Surg. 1989;158:463. 99. Cogbill TH, Moore EE, Jurkovich GJ, et al. Severe hepatic trauma: a multicenter experience with 1,335 liver injuries. J Trauma. 1988;28:1433. 100. Baumgartner F, Scudamore C, Nair C, et al. Venovenous bypass for major hepatic and caval trauma. J Trauma. 1995;39:671. 101. Carrillo EH, Spain DA, Miller FB, et al. Intrahepatic vascular clamping in complex hepatic vein injuries. J Trauma. 1997;43:131. 102. Nicoluzzi JE, Von Bahten LC, Laux G. Hepatic vascular isolation in treatment of a complex hepatic vein injury. J Trauma. 2007;63:684. 103. Watarida S, Nishi T, Furukawa A, et al. Fenestrated stent-graft for traumatic juxtahepatic inferior vena cava injury. J Endovasc Ther. 2002;9:134. 104. Castelli P, Caronno R, Piffaretti G, et al. Emergency endovascular repair for traumatic injury of the inferior vena cava. Eur J Cardiothorac Surg. 2005;28:906. 105. Erzurum VZ, Shoup M, Borge M, et al. Inferior vena cava endograft to control surgically inaccessible hemorrhage. J Vasc Surg. 2003;38:1437.

CHAPTER CHAPTER 29 X

44. Gates JD. Delayed hemorrhage with free rupture complicating the nonsurgical management of blunt hepatic trauma: a case report and review of the literature. J Trauma. 1994;36:572. 45. Anderson IB, Al Saghier M, Kneteman NM, et al. Liver trauma: management of devascularization injuries. J Trauma. 2004;57:1099. 46. Strong RW, Lynch SV, Wall DR, et al. Anatomic resection for severe liver trauma. Surgery. 1998;123:251. 47. Smadja C, Traynor O, Blumgart LH. Delayed hepatic resection for major liver injury. Br J Surg. 1982;69:361. 48. Pollack CV. Hemobilia presenting as lower gastrointestinal hemorrhage without pain or jaundice: a case report. J Miss State Med Assoc. 1990; 31:1. 49. Croce MA, Fabian TC, Spiers JP, et al. Traumatic hepatic artery pseudoaneurysm with hemobilia. Am J Surg. 1994;168:235. 50. Franklin GA, Richardson JD, Brown AL, et al. Prevention of bile peritonitis by laparoscopic evacuation and lavage after nonoperative treatment of liver injuries. Am Surg. 2007;73:611. 51. Letoublon C, Chen Y, Arvieux C, et al. Delayed celiotomy or laparoscopy as part of the nonoperative management of blunt hepatic trauma. World J Surg. 2008;32:1189. 52. Pearl LB, Trunkey DD. Compartment syndrome of the liver. J Trauma. 1999;47:796. 53. Markert DJ, Shanmuganathan K, Mirvis SE, et al. Budd Chiari syndrome resulting from intrahepatic IVC compression secondary to blunt hepatic trauma. Clin Radiol. 1997;52:384. 54. Cuff RF, Cogbill TH, Lambert PJ. Nonoperative management of blunt liver trauma: the value of follow-up abdominal computed tomography scans. Am Surg. 2000;66:332. 55. Ciraulo DL, Nikkanen HE, Palter M, et al. Clinical analysis of the utility of repeat computed tomographic scan before discharge in blunt hepatic injury. J Trauma. 1996;41:821. 56. Cox JC, Fabian TC, Maish GO III, et al. Routine follow-up imaging is unnecessary in the management of blunt hepatic injury. J Trauma. 2005;59:1175. 57. Dulchavsky SA, Lucas CE, Ledgerwood AM, et al. Efficacy of liver wound healing by secondary intent. J Trauma. 1990;30:44. 58. Nance FC, Cohn I. Surgical judgement in the management of stab wounds of the abdomen: a retrospective and prospective analysis based on a study of 600 stabbed patients. Ann Surg. 1969;170:569. 59. Renz RM, Feliciano DV. Gunshot wounds to the liver. A prospective study of selective nonoperative management. J Med Assoc Ga. 1995;84:275. 60. Demetriades D, Gomez H, Chahwan S, et al. Gunshot injuries to the liver: the role of selective nonoperative management. J Am Coll Surg. 1998;188:343. 61. DuBose J, Inaba K, Teixeira PG, et al. Selective non-operative management of solid organ injury following abdominal gunshot wounds. Injury. 2007;38:1084. 62. Demetriades D, Hadjizacharia P, Constantinou C, et al. Selective nonoperative management of penetrating abdominal solid organ injuries. Ann Surg. 2006;244:620. 63. Shanmuganathan K, Mirvis SE, Chiu WC, et al. Penetrating torso trauma: triple-contrast helical CT in peritoneal violation and organ injury: a prospective study in 200 patients. Radiology. 2004;231:775. 64. Velmahos GC, Constantinou C, Tillou A, et al. Abdominal computed tomographic scan for patients with gunshot wounds to the abdomen selected for nonoperative management. J Trauma. 2005;59:1155. 65. Omoshoro-Jones JA, Nicol AJ, Navsaria PH, et al. Selective nonoperative management of liver gunshot injuries. Br J Surg. 2005;92:890. 66. Stone HH, Lamb JM. Use of pedicled omentum as an autogenous pack for control of hemorrhage in major injuries of the liver. Surg Gyn Obstet. 1975;141:92. 67. Sheldon G, Rutledge R. Hepatic trauma. Adv Surg. 1989;22:179. 68. Man K, Fan ST, Ng IO, et al. Prospective evaluation of Pringle maneuver in hepatectomy for liver tumors by a randomized study. Ann Surg. 1997;226:704. 69. Feliciano DV, Mattox KL, Jordan GL, et al. Management of 1000 consecutive cases of hepatic trauma (1979–1984). Ann Surg. 1986;204:438. 70. Pachter HL, Spencer FC, Hofstetter SR, et al. Significant trends in the treatment of hepatic trauma: experience with 411 injuries. Ann Surg. 1992;215:492. 71. Beal SL. Fatal hepatic hemorrhage: an unresolved problem in the management of complex liver injuries. J Trauma. 1990;30:163. 72. Caruso SM, Battistella FD, Owings JT, et al. Perihepatic packing of major liver injuries. Arch Surg. 1999;134:958.

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SECTION 3 X

106. Hommes M, Kazemier G, Van Dijk L, et al. Complex liver trauma with bilhemia treated with perihepatic packing and endovascular stent in the vena cava. J Trauma. 2009;67:E51. 107. Fabian TC, Croce MA, Stanford GG, et al. Factors affecting morbidity following hepatic trauma. A prospective analysis of 482 injuries. Ann Surg. 1991;213:540. 108. Cue JI, Cryer HG, Miller FB, et al. Packing and planned reexploration for hepatic and retroperitoneal hemorrhage: critical refinements of a useful technique. J Trauma. 1990;30:1007. 109. Noyes LD, Doyle DJ, McSwain NE. Septic complications associated with the use of peritoneal drains in liver trauma. J Trauma. 1988; 28:337. 110. Mullins RJ, Stone HH, Dunlop WE, et al. Hepatic trauma: evaluation of routine drainage. South Med J. 1985;78:259. 111. Waltensdorfer A, Mahla E, Zink M, et al. Central pulmonary artery embolism after perihepatic packing because of liver trauma. J Trauma. 2007;63:E81. 112. Walt AJ, Wilson RF. Management of Trauma: Pitfalls and Practice. Philadelphia: Lea and Febiger; 1975:348. 113. Cyret P, Baumer R, Roche A. Hepatic hemobilia of traumatic or iatrogenic origin. Recent advances of diagnosis and therapy. Review of the literature from 1976–1981. World J Surg. 1984;8:2. 114. Heimbach OM, Ferguson GS, Harley JD. Treatment of traumatic hemobilia with angiographic embolization. J Trauma. 1978;18:221. 115. Clemens M, Wittrin G. Bilhamie und hamobilie nach reitunfall. Vortrag 166. Hamburg: Tagung Nordwestdeutscher Chirurgen; 1975. 116. Glaser K, Wetscher G, Pointner R, et al. Traumatic bilhemia. Surgery. 1994;116:24. 117. Enneker C, Berens JP. Schwerste Leberruptur mit lebervenenabriss und massive bilhamie. Chirurg. 1978;49:311. 118. Hollands MJ, Little JM. Post-traumatic bile fistulae. J Trauma. 1991;31:117. 119. Howdieshell TR, Purvis J, Bates WB, et al. Biloma and biliary fistula following hepatorraphy for liver trauma: incidence, natural history, and management. Am Surg. 1995;61:165. 120. Dick R, Gilliams A, Dooley JS, et al. Stainless steel mesh stents for biliary stricture. J Intervent Radiol. 1989;4:95. 121. D’Amours SK, Simons RK, Scudamore DH, et al. Major intrahepatic bile duct injuries detected after laparotomy: selective nonoperative management. J Trauma. 2001;50:480. 122. Dabbs DN, Stein DM, Scalea TM. Major hepatic necrosis: a common complication after angioembolization for treatment of high-grade liver injuries. J Trauma. 2009;66:621. 123. Sheik-Gafoor MH, Singh B, Moodley J. Traumatic thoracobiliary fistula: report of a case successfully managed conservatively, with an overview of current diagnostic and therapeutic options. J Trauma. 1998;45:819. 124. Rothberg ML, Kilngman RR, Peetz D, et al. Traumatic thoracobiliary fistula. Ann Thorac Surg. 1994;57:472. 125. Danetz JS, Yelon JA, Fields CE, et al. Traumatic pleurocaval fistula: potential source of air embolism. J Trauma. 2001;50:551. 126. Eastridge BJ, Minei JP. Intrahepatic arterioportal fistula after hepatic gunshot wound: a case report and review of the literature. J Trauma. 1997;43:523. 127. Oppermann TE, Corcos AC, Jones LM, et al. Traumatic intrahepatic portosystemic venous shunt: a rare complication of grade V liver laceration. J Trauma. 2007;63:1230.

128. Jurkovich GJ, Hoyt DB, Moore FA, et al. Portal triad injuries—a multicenter study. J Trauma. 1995;39:426. 129. Dawson DL, Johansen KH, Jurkovich GJ. Injuries to the portal triad. Am J Surg. 1991;161:545. 130. Sharma O. Blunt gallbladder injuries: presentation of twenty-two cases with review of the literature. J Trauma. 1995;39:576. 131. Wilson RF, Walt AJ. Management of Trauma Pitfalls and Practice. 2nd ed. Baltimore: Williams and Wilkins; 1996:476. 132. Erb RE, Mirvis SE, Shanmuganathan K. Gallbladder injury secondary to blunt trauma: CT findings. J Comput Assist Tomogr. 1994;18:778. 133. Michelassi F, Ranson J. Bile duct disruption by blunt trauma. J Trauma. 1985;25:454. 134. Bourque M, Spigland N, Bensoussan A, et al. Isolated complete transection of the common bile duct due to blunt trauma in a child, and review of the literature. J Pediatr Surg. 1989;24:1068. 135. Jones KB, Thomas E. Traumatic rupture of the hepatic duct demonstrated by endoscopic retrograde cholangiography. J Trauma. 1985;25:448. 136. Velez SE, Llaryora RG, Lerda FA. Laparoscopic cholecystectomy in penetrating trauma. J Laparoendosc Adv Surg Tech A. 1999;9:291. 137. Soderstrom CA, Maika K, DuPriest RW. Gallbladder injuries resulting from blunt abdominal trauma. Ann Surg. 1981;193:60. 138. Smith SW, Hastings TN. Traumatic rupture of the gallbladder. Ann Surg. 1954;139:521. 139. Pachter HL, Liang HG, Hofstetter SR. Liver and biliary tract trauma. In: Trauma. 2nd ed. Norwalk, CT: Appleton and Lange; 1991:441. 140. Feliciano DV. Biliary injuries as a result of blunt and penetrating trauma. Surg Clin North Am. 1994;74:897. 141. Sandblom P, Tabrizian M, Rigo M, et al. Repair of common bile duct defects using the gallbladder or cystic duct as a pedicled graft. Surg Gynecol Obstet. 1975;140:425. 142. Ivatury RR, Rohman M, Nallathambi M, et al. The morbidity of injuries of the extrahepatic biliary system. J Trauma. 1985;25:967. 143. Stewart L, Way L. Bile duct injuries during laparoscopic cholecystectomy: factors that influence the results of treatment. In: Proceedings of the Pacific Coast Surgical Association, Seattle, WA, 19–21 February. 1995. 144. Monk JS, Church JS, Agarwal N. Repair of a traumatic noncircumferential hepatic bile duct defect using a vein patch: case report. J Trauma. 1991;31:1555. 145. Thomas JP, Metropol HJ, Myers RT. Teflon patch graft for reconstruction of the extrahepatic bile ducts. Ann Surg. 1964;160:967. 146. Voyles GR, Blumgart LH. A technique for the construction of high biliary-enteric anastomoses. Surg Gynecol Obstet. 1982;154:885. 147. Rodriguez-Montes JA, Rojo E, Martin LG. Complications following repair of extrahepatic bile duct injuries after blunt abdominal trauma. World J Surg. 2001;25:1313. 148. Eid A, Almogy G, Pikarsky AJ, et al. Conservative treatment of a traumatic tear of the left hepatic duct: case report. J Trauma. 1996;41:912. 149. Dawson DL, Jurkovich GJ. Hepatic duct disruption from blunt abdominal trauma: case report and literature review. J Trauma. 1991;31:1698. 150. Innes J, Ferrara J, Carey L. Biliary reconstruction without transanastamotic stent. Am Surg. 1988;54:27. 151. Costamagna G, Pandolfi M, Mutignani M, et al. Long-term results of endoscopic management of postoperative bile duct strictures with increasing numbers of stents. Gastrointest Endosc. 2001;54:162. 152. Lillemoe KD, Meltoon GB, Cameron JL, et al. Postoperative bile duct strictures: management and outcome in the 1990s. Ann Surg. 2000;232:430.

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CHAPTER 30

Injury to the Spleen David H. Wisner

The spleen is listed, along with the liver, as either the first or second most commonly injured solid viscus in the abdomen. Because splenic injuries have a tendency to demonstrate themselves clinically more often than do hepatic injuries, splenic injury was listed as the most commonly injured intraabdominal solid viscus prior to the advent of computed tomography (CT) scanning. After the advent of CT scanning and our ability to better diagnose clinically silent intra-abdominal injuries, it became apparent that the liver is also commonly injured. Therefore, some current series list hepatic injuries as more common than splenic injuries. During the past 50 years, there has been increasing interest in the notion that not all splenic injuries require splenectomy. Although evolution has steadily moved us away from routine aggressive operative management, it is important to always keep in mind that splenic injuries can be deadly and that patients with splenic injury can bleed to death.

HISTORICAL PERSPECTIVE The spleen has been subject to injury for as long as man has suffered trauma. In ancient India, where malaria was endemic and large and fragile spleens were commonplace, intentional injury of the spleen was a method of assassination (F. William Blaisdell, MD, Sacramento, CA, 1985, personal communication). Paid assassins called thuggee carried out their mission by delivering a blow to the left upper quadrant of the intended victim. They hoped to cause splenic rupture, for which there was no treatment at that time. If the rupture was severe enough, the victim would bleed to death. As we know from our current imaging capabilities and management protocols, the thuggees must have been frustrated on occasion by the lack of success of their attempted assassinations. The spleen was felt by the ancient Greeks and Romans to play a significant role in human physiology. Aristotle thought

that the spleen was on the left side of the body as a counterweight to the right-sided liver.1 He believed that the spleen was important in drawing off “residual humors” from the stomach. The close relation of the stomach and spleen and the presence of the short gastric vessels so important in present-day splenic mobilization likely encouraged this belief. The spleen was also felt to “hinder a man’s running,” and Pliny reportedly claimed that “professed runners in the race that bee troubled with the splene, have a devise to burne and waste it with a hot yron.”2 The exceptional speed of giraffes was felt to be related to the erroneous belief that giraffes were asplenic. Early references to removal of the spleen to increase speed make it apparent that it has long been known that the spleen is not absolutely necessary to sustain life. Paracelsus believed that the spleen could be removed and rejected the notion that it was important for the storage of “black bile.”3 In 1738, John Ferguson of Scotland removed a portion of the spleen through an open wound in the left side (Fig. 30-1).3 Once the era of abdominal surgery had begun, it was discovered that the spleen could be removed with what seemed like relative impunity. Mayo reported in 1910 that “the internal secretion of the spleen is not important, as splenectomy does not produce serious results.”4 Although some suggested that the spleen was important in some way for immune function and for the removal of senescent red blood cells, it was not felt that these functions were of great importance. Until several decades ago, this resulted in a philosophy in which any traumatic splenic injury, no matter how trivial, was treated with splenectomy.3,4 Even small iatrogenic injuries occurring during elective surgery were treated with splenic removal. There were some early thoughts that the spleen played a role in combating infection, but it only has been in the last century that our understanding of the role of the spleen in immune function has developed.5,6 The initial clinical impetus to more

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SPLENIC FUNCTION SECTION 3 X FIGURE 30-1 A depiction of the partial splenectomy done by John Ferguson of Scotland and reported in 1738. The operation actually had been done some years earlier. (Reproduced with permission from Hiatt JR, Phillips EH, Morgenstern L, eds. Surgical Diseases of the Spleen. New York: Springer-Verlag; 1997:6.)

closely examine the immunologic role of the spleen was based on the observation that neonates and infants who required splenectomy for hematologic disease suffered otherwise inexplicably high rates of postoperative mortality from overwhelming infection. Pneumonia and meningitis secondary to pneumococcus and other encapsulated organisms were particularly common. The dramatic consequences of splenectomy in this very specific group of patients led to the investigation of the effects of splenectomy in pediatric trauma patients. Although the evidence for severe immunologic consequences of splenectomy in this group was less convincing than in pediatric patients with hematologic disease, there was a strong inference that splenectomy for trauma would lead to an increased rate of overwhelming sepsis, just as occurred after splenectomy for hematologic disease. Cases of overwhelming postsplenectomy sepsis in adults who had undergone splenectomy for trauma were reported, also.7,8 Several other developments that paralleled our increased understanding of the importance of the spleen for immune function were the development of improved abdominal imaging and increasing questions about the safety of transfused blood. The advent of CT scanning of the abdomen and its continued improvement in quality markedly increased our ability to diagnose splenic injury nonoperatively, and it became apparent that clinically silent splenic injuries could occur. Concerns about the safety of stored blood transfusion with respect to hepatitis and human immunodeficiency virus, however, led to increasing questions about transfusions for patients with splenic injury. Most splenic injuries are obviously due to the same blunt and penetrating mechanisms that cause other traumatic injuries. Increased use of percutaneous procedures and abdominal ultrasound has revealed more obscure mechanisms such as colonoscopic manipulation and placement of a nephrostomy tube as potential causes of splenic injury.9,10

Histologically, the spleen is divided into what has been termed red pulp and white pulp.11 The red pulp is a series of large passageways that filter old red blood cells and trap bacteria, also. Filtering is important in removing poorly functioning senescent red blood cells from the bloodstream and keeping the hematocrit and blood viscosity within a normal range. The trapping of bacteria in the filters of the red pulp allows the antigens of the bacterial walls to be presented to the lymphocytes in the adjacent white pulp. The white pulp is filled largely with lymphocytes located such that they can be exposed to antigens either on microorganisms or circulating freely in the circulation. Lymphocyte exposure to antigens results in the production of immunoglobulins, the most common of which is IgM.11,12 Other potentially important functions of the white pulp are the production of opsonins such as tuftsin and properdin and complement activation in response to appropriate stimuli. All these functions of the spleen are, of course, lost after splenectomy. Collections of lymph tissue are also found in the liver, thymus, intestinal tract, and skin, and these areas may take over some of the functions of the spleen after splenectomy. In addition, some of the necessary functions of the spleen could conceivably be carried out by accessory spleens, but the removal of the spleen results in loss of most filtering and immune functions. How serious these losses are to normal function is a matter of debate. The loss of the filtering function of senescent red blood cells seems to be tolerated reasonably well. Although certain kinds of senescent red blood cells in the bloodstream are more pronounced after splenectomy, the normal production and removal of red blood cells seems, for the most part, to continue. The loss of splenic function has been the subject of a great deal of investigation. A study of isolated splenic injuries revealed an early postinjury infection rate of 9% in postsplenectomy patients as opposed to a rate of only 2% in patients successfully managed nonoperatively. There is also evidence of an increased incidence of overwhelming sepsis after splenectomy for trauma, but the precise incidence of such overwhelming infections, especially in adults, is so low that it is difficult to quantify.13 The possibility that small accessory spleens might provide residual splenic function raises the question of how much splenic mass is necessary for the filtering and immune functions of the spleen. This is a question of more than academic importance, in that a variety of techniques have been described for partial splenectomy or autotransplantation of the spleen after splenectomy.14,15 The exact amount of spleen to reimplant after splenectomy or leave behind after partial splenectomy is dependent on the minimum amount of splenic tissue necessary for normal function. How much spleen is necessary for normal function is not precisely known, but is thought to be between 30% and 50%.16

SPLENIC ANATOMY The spleen develops initially as a bulge on the left side of the dorsal mesogastrium and begins a gradual leftward migration to the left upper quadrant. It changes in relative size during maturation. In children, it is large because it is necessary for both

Injury to the Spleen important and prevalent pathology that can increase splenic vulnerability is portal venous hypertension. Usually such portal hypertension is secondary to cirrhosis of the liver and, when it is present, the spleen can become both enlarged and less firm in consistency. It is perhaps not intuitive from the anteroposterior views depicted in anatomy textbooks, but the spleen is normally located quite posteriorly in the upper abdomen (Fig. 30-2). It is covered by the peritoneum except at the hilum. Posteriorly and laterally the spleen is related to the left hemidiaphragm and the left posterior and posterolateral lower ribs. The lateral aspect of the spleen is attached to the posterior and lateral abdominal wall and the left hemidiaphragm (splenophrenic ligament) with a variable number of attachments that require division during mobilization of the spleen. The extent of these attachments is quite variable. Minimal attachments result in a fairly mobile spleen while thick attachments, when present, require sharp dissection. The lateral attachments tend to be smaller and less extensive in children than in adults. As the spleen lies adjacent to the posterior ribs on the left side, left posterior rib fractures should increase the index of suspicion for underlying splenic injury. Because of the close relation of the spleen to the diaphragm, simultaneous injuries to the two structures are not uncommon (see Chapter 28). After penetrating trauma, a knife or bullet can obviously injure both the left hemidiaphragm and the spleen. The diaphragm can also be

FIGURE 30-2 The spleen is located quite posteriorly in the left upper quadrant and is attached to surrounding structures by a variety of ligaments. (Reproduced with permission from Carrico CJ, Thal ER, Weigelt JA, eds. Operative Trauma Management: An Atlas. Norwalk, CT: Appleton & Lange; 1998. Copyright The McGraw-Hill Companies, Inc.)

CHAPTER CHAPTER 30 X

reticuloendothelial function and production of red blood cells. As the child’s bone marrow matures, the spleen becomes relatively less important and diminishes in size relative to the rest of the body. There are also some important differences between pediatric and adult spleens with respect to the splenic capsule and the consistency of the splenic parenchyma. The capsule in children is relatively thicker than it is in adults, and there is some evidence that the parenchyma is firmer in consistency in children than it is in adults, as well. These two differences have implications for the success of nonoperative management. A thicker capsule and tougher parenchymal consistency imply that pediatric spleens are more likely to survive an insult without major bleeding and the need for operative intervention. This is part of the explanation for why children are more often candidates for nonoperative management than are adults and why nonoperative management tends to be somewhat more successful in children than it is in adults. The normal adult spleen ranges in size from 100 to 250 g. A number of disease processes, however, can change both the size and consistency of the spleen. Malaria and its effects on the spleen with respect to enlargement and changes in consistency have already been referred to earlier. Hematologic diseases such as lymphoma and leukemia can also change both the size and consistency of the spleen and make it more susceptible to damage. Other more common diseases such as mononucleosis make the spleen more vulnerable to injury. An equally

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injured in blunt trauma, and the spleen, either injured or uninjured, can herniate through a diaphragmatic defect into the left pleural space. The diaphragm should always be closely inspected during surgery for splenic injury. Posteriorly, the spleen is related to the left iliopsoas muscle and the left adrenal gland. The left adrenal gland is usually fairly small and has a characteristic yellow-gold color. It tends to be related to the posterior aspect of the superior portion of the spleen and should be protected when seen during splenic mobilization. Posteriorly and medially, the spleen is related to the body and tail of the pancreas. Therefore, it is very helpful to mobilize the tail and body of the pancreas along with the spleen when elevating the spleen out of the left upper quadrant as this increases the extent to which the spleen can be mobilized. Medially and to some extent anteriorly, the spleen is related to the greater curvature of the stomach. This relation is important in that the spleen can receive a variable amount of blood supply from the greater curvature via short gastric branches from the left gastroepiploic artery. The short gastric vessels require division during full mobilization of the spleen. Posteriorly and inferiorly, the spleen is related to the left kidney. There are attachments between the spleen and left kidney (splenorenal ligament) that require division during mobilization of the spleen. The left kidney should be left in place while mobilizing the spleen and tail of the pancreas from lateral to medial. There are exceptions to leaving the kidney in place, most notably if the kidney also has been injured or if mobilization of the spleen is being done to provide exposure to the aorta from the left side (see Chapter 36). Finally, the spleen is related inferiorly to the distal transverse colon and splenic flexure. The lower pole of the spleen is attached to the colon (splenocolic ligament), and these attachments require division during splenic mobilization. The splenic artery, one of the major branches of the celiac axis, courses along the superior aspect of the body and tail of the pancreas toward the splenic hilum. Although generally located along the upper border of the body and tail of the pancreas, its course can be somewhat variable. The splenic artery is commonly quite tortuous, as well. It divides into a variable number of branches that provide a segmental blood supply to the spleen. Both the number of branches and the site at which the branching occurs are quite variable (Fig. 30-3). This variability is of surgical significance in that there is no absolute and dependable number of splenic artery branches that require division during splenectomy or segmental resection of the spleen. Most commonly, a number of separate splenic artery branches are ligated during splenectomy rather than a single ligation of the main splenic artery. It is possible to find the splenic artery along the superior margin of the body and tail of the pancreas if necessary, and sometimes it is helpful to ligate the artery at that location even after hilar branches have been ligated if the surgeon is interested in extra hemostasis. The other sources of arterial blood supply for the spleen are the short gastric vessels that connect the left gastroepiploic artery and the splenic circulation along the greater curvature of the stomach. There is an average of four to six short gastric

FIGURE 30-3 The arterial blood supply to the spleen can be quite variable. The most common configuration consists of two extraparenchymal divisions of the splenic artery (upper left figure).

arteries. As implied by their name, these branches off the greater curvature are generally fairly short and are easily injured during mobilization of the spleen. The venous drainage of the spleen, like the arterial inflow, is via two routes. The splenic vein drains the spleen via a number of branches that coalesce to form a single large vein that courses along the posterior aspect of the body and tail of the pancreas to its confluence with the superior mesenteric vein. Like venous anatomy elsewhere in the body, the location, size, and branches of the splenic view can be quite variable. The other route of splenic venous drainage is via short gastric veins that course adjacent to the short gastric arteries. They drain into the left gastroepiploic vein during its course along the greater curvature of the stomach.

PATHOPHYSIOLOGY OF INJURY Although nonoperative management is often appropriate after splenic injury, many patients with splenic injury still need emergency surgery to stop the bleeding. In a large multiinstitutional survey, approximately 45% of patients with splenic injury required emergency surgery.17 A study using rigid predefined criteria for nonoperative management revealed that 33% of isolated blunt splenic injuries require immediate operation and a further 23% treated with initial nonoperative management required operation, for an overall 56% operative rate.18 Overall operative rates vary depending on setting, with higher operative rates for rural and nonteaching hospitals.19 The higher operative rate in smaller hospitals may in part be due to different management philosophies. Also, it is related to the fact that large referral hospitals see a higher percentage of transferred patients who have already withstood the test of time and have proven themselves good candidates for nonoperative management. The rate also varies when comparing large multiinstitutional series with single institutional series. Regardless of the setting, however, it is clear that rapid operative intervention is sometimes necessary. This is particularly true when patients

Injury to the Spleen

INITIAL EVALUATION AND MANAGEMENT As with any other trauma patient, the initial management of the patient with splenic injury should follow the airway, breathing, and circulation (ABCs) of trauma evaluation and resuscitation (see Chapter 10). A particularly important general comment relative to initial resuscitation is that it is important to recognize refractory shock early and treat it with an appropriate operative response. There are some aspects of the initial evaluation, with respect to the spleen, that deserve special mention: 1. The possibility of an additional intra-abdominal injury in patients with splenic injury seen on CT scanning should be kept in mind. Injury to the gastrointestinal tract is of particular concern. 2. While operating on patients with splenic injury, it is important to look for associated injuries, particularly to the left hemidiaphragm and the pancreas. 3. When mobilizing the spleen, always mobilize the tail of the pancreas medially with the spleen to optimally expose

the splenic hilum and minimize risk to the spleen and pancreas. 4. Despite the fact that nonoperative management of splenic injury is a commonly successful strategy, patients can still bleed to death from splenic injury. Therefore, a significant percentage of patients still require surgical intervention and splenectomy. Elements of the history may be helpful in the diagnosis of splenic injury, and mechanism of injury is important. In patients injured in a motor vehicle crash, the position of the patient in the car can be of some importance in diagnosing splenic injury. Victims located on the left side of the car (drivers and left rear passengers) are perhaps slightly more susceptible to splenic injury because the left side of their torso abuts the left side of the car. This does not mean, however, that victims in other locations in a vehicle are not at risk. For patients who have suffered penetrating injury, the type and nature of the weapon is important. When possible, it is helpful to know the caliber of the gun or the length of the knife (see Chapter 1). In the initial history taking, it is important to note any previous operations the patient has undergone. Of particular importance are any operations that may have resulted in splenectomy (i.e., previous operations for hematologic disease or abdominal trauma). Any preexisting conditions that might predispose the spleen to enlargement or other abnormality should be asked about, as well. The patient or significant others should be asked about the presence of hepatic disease, ongoing anticoagulation, or recent usage of aspirin or nonsteroidal anti-inflammatory drugs, also. On physical examination, it is important to determine if the patient has left rib pain or tenderness. Left lower ribs are particularly important in that they overlie the spleen, especially posteriorly. Approximately 14% of patients with tenderness over the left lower ribs will have a splenic injury. Even with tenderness over the left lower ribs as their only indication of possible abdominal injury, 3% of patients will have a splenic injury.22 In children, the plasticity of the chest wall allows for severe underlying injury to the spleen without the presence of overlying rib fractures. Such a phenomenon is also possible in adults, but is less common than it is in children. The absence of tenderness over the left lower ribs does not preclude the presence of an underlying splenic injury and, in some cases, may be related to an altered level of consciousness from an associated traumatic brain injury or intoxication. In elderly patients, rib fractures may not manifest in a fashion similar to that seen in younger patients. Patients over the age of 55 may not describe lower rib pain and may not have particularly noteworthy findings on physical examination in spite of severe trauma to the chest wall and an underlying splenic injury. Another finding on physical examination that is occasionally helpful in the presence of a splenic injury is the presence of Kehr’s sign. Kehr’s sign is the symptom of pain near the tip of the left shoulder secondary to pathology below the left hemidiaphragm. There is minimal shoulder tenderness, and the patient typically does not have pain on range of motion of the left arm and shoulder unless there is an associated

CHAPTER CHAPTER 30 X

have a coagulopathy either from pre-injury anticoagulation or as a consequence of their injury. Bleeding can also be a problem on a delayed basis.20,21 The concept of “delayed rupture” of the spleen is in some ways a misnomer. The initial notion that the spleen could bleed on a delayed basis dates back to an era before abdominal CT scanning. In that era, it was observed that some patients who had suffered a traumatic injury did not manifest overt bleeding from their spleen for a number of days or sometimes even weeks or months after the traumatic event. With the advent of abdominal CT scanning, it became apparent that these were probably cases of “delayed bleeding” rather than that of delayed rupture. The distinction between these two entities is more than academic. If “delayed rupture” of the spleen can occur without much evidence of preexisting injury, CT scanning of the abdomen shortly after injury would be negative. In this case, there would be no good way to screen patients and make sure that they were not at risk for delayed splenic bleeding. In contrast, if what used to be called delayed rupture is actually just delayed bleeding, early diagnosis of the presence of the splenic injury should allow us to tailor our management such that the risk of the delayed bleeding is minimized. Penetrating injuries to the spleen are most commonly managed operatively, often because of concerns about associated intraperitoneal injuries. Concerns about injury to the diaphragm from the knife or bullet are a common rationale for operative intervention in patients with penetrating injury to the spleen, also. Operative intervention, of course, does not mandate splenectomy after penetrating injury any more than it does after blunt injury, although the risk of major arterial disruption after penetrating trauma is somewhat higher than after blunt trauma. Attempts at splenic salvage are appropriate after blunt or penetrating splenic injury, especially if the grade of injury is low and associated injuries are not particularly severe.

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musculoskeletal injury. Kehr’s sign after splenic injury is the result of irritation of the diaphragm by subphrenic blood. The innervation of the left hemidiaphragm comes from cervical roots 3, 4, and 5, the same cervical roots that innervate the tip of the shoulder, and referred pain from the diaphragmatic irritation causes the left shoulder pain. Although it is relatively uncommon, the presence of Kehr’s sign shortly after trauma should increase the index of suspicion for splenic injury. The physical examination of the abdomen sometimes demonstrates localized tenderness in the left upper quadrant or generalized abdominal tenderness, but not all patients with splenic injury will reliably manifest peritoneal or other findings on physical examination. Ecchymoses or abrasions in the left upper quadrant or left lower chest may be present, also. The unreliability of the physical examination of the abdomen is obvious in patients with an altered mental status and may be absent in patients with normal mentation, as well. As a consequence, imaging of the abdomen in hemodynamically stable patients has become an important element of diagnosis and management (see Chapter 15). There are no laboratory studies specific to patients with splenic injury, although a hematocrit and typing and crossmatching of blood are useful initial laboratory tests. Coagulation studies may be warranted if there is reason to believe that the patient is coagulopathic. As with all other early post-traumatic bleeding, bleeding from a splenic injury in the early postinjury period will not always cause a marked drop in hematocrit. An extremely low hematocrit on arrival of the patient in the resuscitation room, however, especially if the transport has been short and prehospital fluid resuscitation has been minimal, should alert the surgeon to the possibility of severe ongoing hemorrhage (see Chapter 10). Plain x-rays generally are not helpful in the diagnosis of splenic injury. Rupture of the left hemidiaphragm is sometimes apparent on an initial chest x-ray, however, and can suggest an associated splenic injury. A severe pelvic fracture on an anteroposterior pelvic film can sometimes be of importance in subsequent decision making about how to manage a splenic injury as the presence of simultaneous splenic and severe pelvic injuries often will dictate the removal of the spleen. When penetrating trauma is the mechanism of injury, an initial chest x-ray is important in ruling out associated thoracic injury and, in the case of gunshot wounds, helping to determine the path of a bullet and the location of a retained bullet or bullet fragments.

IMAGING AND DIAGNOSTIC PERITONEAL LAVAGE Diagnostic peritoneal lavage (DPL) is used much less frequently now. Its role as an initial diagnostic maneuver to dictate subsequent testing or operative intervention has been supplanted in many institutions by both ultrasonography and CT scanning of the abdomen (see Chapters 15 and 16). Peritoneal lavage remains useful when ultrasonography is not available, however, in that it is a quick way of determining whether or not a hemodynamically unstable patient is bleeding intraperitoneally. Although DPL is not specific for splenic injury, splenic injuries

with ongoing bleeding result in a positive peritoneal lavage most of the time that prompts timely operative intervention. When there is an associated diaphragmatic injury, however, DPL may not yield positive results. Because the instilled fluid may be retained in the pleural space, a diaphragmatic injury should be considered when the DPL yields little or no return of fluid. Ultrasound of the abdomen for free fluid, the so-called FAST exam, is being used increasingly as a means of diagnosing hemoperitoneum in patients with blunt trauma (see Chapter 16). Like DPL, it is most useful in unstable patients. Also, as with peritoneal lavage, the ability of ultrasound to determine exactly what is bleeding in the peritoneal cavity is limited. Small injuries and subcapsular hematomas of the spleen can also be missed by ultrasonography if they do not result in a significant hemoperitoneum. There have been attempts to use ultrasound not only to diagnose intraperitoneal fluid but also to diagnose specific injuries such as splenic injuries. Such attempts have met with limited success, and the most common method of using FAST exams is for detection of intraperitoneal fluid and as a determinant of the need for either further imaging of the abdomen or emergency surgery. CT scanning of the abdomen is the dominant means of nonoperative diagnosis of splenic injury. Patients are either sent directly for abdominal CT scanning after initial resuscitation or screened by abdominal ultrasonography as reasonable candidates for subsequent CT. When abdominal CT scanning is done, intravenous contrast is quite helpful in diagnosis. Oral contrast is much less helpful and does not increase the sensitivity of CT for detecting a splenic injury. Radiation exposure from CT, especially in children, has been raised as a potential concern and some selection should be used with respect to which patients with abdominal trauma should undergo scanning.23 Undue concern about radiation, however, should not put a patient at risk for a missed splenic injury and occult bleeding. The findings of splenic injury on CT scan are variable (Fig. 30-4). Hematomas and parenchymal disruption generally show up as hypodense areas. Free fluid can be seen either around the spleen or throughout the peritoneal and pelvic spaces. Locations where fluid frequently accumulates after splenic injury are Morison’s pouch, the paracolic gutters, and the pelvis. When a large amount of fluid is present in the peritoneal cavity, it can sometimes be seen between loops of small bowel as well as in the subphrenic spaces. When looking at CT scans of patients with splenic injury, it is also important to look at the adjacent left kidney and the distal pancreas. Injury to the spleen implies a blow to the left upper quadrant that can also injure the adjacent organs. The diagnosis of a pancreatic injury is particularly important in that this can significantly affect the patient’s subsequent course and prognosis. Also, it is important to remember that the presence of free fluid is not solely related to bleeding from a visible splenic injury in all cases. One of the pitfalls of CT diagnosis is that free fluid in the peritoneal cavity or in the pelvis may be attributed to a splenic injury when in fact the fluid is secondary to both a splenic injury and an associated injury to the mesentery or bowel.

Injury to the Spleen

Other than an obvious injury, the most important CT finding in the spleen is the presence in the disrupted splenic parenchyma of a “blush,” or hyperdense area with a concentration of contrast in it (Fig. 30-4). When seen, a blush is thought to represent ongoing bleeding with active extravasation of contrast. There is evidence that the presence of a blush correlates with an increased likelihood that continued or delayed bleeding will occur. A pseudoaneurysm of a branch of the splenic artery is evidence that the vessel has been damaged, as well. These arterial injuries need further assessment with either angiography or repeat CT scanning. In addition to the above findings, incidental findings such as cysts and granulomas are occasionally seen on CT. Primary cysts are parasitic (rare in the United States), congenital, or neoplastic. Secondary cysts (those without an epithelial lining) may result from trauma or infarction. A number of scoring systems have been devised to describe the degree of splenic injury seen on CT scanning.24–27 Some of these scoring systems will be described in further detail later. It is important to remember, however, that there is not a perfect correlation between the grade of splenic injury seen on CT scanning and the grade of splenic injury seen at the time of surgery in patients who require operative intervention. Also, it is important to remember that the CT grade of splenic injury and a patient’s subsequent clinical course are only roughly correlated. Magnetic resonance imaging (MRI) has been used sporadically in the diagnosis of splenic injury (see Chapter 15). The images obtained are sometimes quite impressive but, given that CT scanning has both a very high sensitivity and specificity for the presence of splenic injury (especially when newer-generation

GRADING SYSTEMS FOR SPLENIC INJURY A number of different grading systems have been devised to quantify the degree of injury in patients with ruptured spleens.24–27 These systems have been created based on both the computed tomographic appearance of ruptured spleens and the intraoperative appearance of the spleen. The best known splenic grading system is the one created by the American Association for the Surgery of Trauma (AAST) (Fig. 30-5; Table 30-1).24 As with all of the AAST grading systems except that used for hepatic injuries, it uses a scale of between I and V. The CT and intraoperative appearances of a splenic injury are often different from one another. Some of these differences might be because of evolution of the injury between the time of CT scanning and operation, but it is also likely that CT scanning is imperfect in describing the pathologic anatomy of a splenic rupture. Splenic injury scores based on CT scans can both overestimate and underestimate the degree of splenic injury seen at surgery. It is possible to have a CT appearance of fairly trivial injury, but find significant splenic disruption at surgery. Conversely, it is possible to see what looks like a major disruption of the spleen on CT scanning and not see the same kind of severity of injury at surgery. In general, the CT scan and associated scores tend, if anything, to underestimate the degree of splenic injury compared to what is seen at surgery.27,28 Additionally, interrater and intrarater agreement with respect to CT grading of splenic injury is only fair. A study comparing the CT interpretations of four experienced trauma radiologists revealed poor interrater reliability and also frequent “undergrading” of the degree of splenic injury when CT interpretations were compared with intraoperative findings.28

CHAPTER CHAPTER 30 X

FIGURE 30-4 Computed tomographic findings in a patient with a ruptured spleen. The splenic parenchyma is disrupted, and there is some blood and hematoma. There is also a splenic “blush” in the disrupted parenchyma.

multidetector scanners are used), MRI so far has not proven to be an obvious improvement. Furthermore, MRI is usually less available than is CT scanning, especially after hours. The logistical difficulties inherent in trying to obtain magnetic resonance images in a badly injured patient who requires close monitoring and possibly even mechanical ventilation make MRI even less helpful as a diagnostic modality. Continued improvements in MRI and our increasing ability to use it even for very sick patients could conceivably increase the role of MRI in the diagnosis of splenic injury in the future. Radioisotope scintigraphy was used in the diagnosis of splenic injury in the past. Most of the use of radioisotope scintigraphy occurred before the advent of widespread availability of CT scanning, and it is largely of historical interest at this point. Angiography is another test that has been used historically to diagnose splenic injury, but angiography for the diagnosis of splenic injury has largely been replaced by computerized tomography as described above. Angiography with embolization for bleeding does, however, have an important therapeutic role in the management of splenic injury. Laparoscopy has been tried as a means of diagnosing splenic injury, but is not a diagnostic improvement over CT scanning in patients with blunt trauma. After penetrating trauma, laparoscopy often misses associated bowel injuries. It may have some usefulness in diagnosis and treatment of injuries adjacent to the left hemidiaphragm (see Chapter 28).

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TABLE 30-1 The Splenic Organ in Jury Scaling System of the American Association for the Surgery of Trauma, 1994 Revision

SECTION 3 X

Gradea I

Hematoma Laceration

II

Hematoma Laceration

III

Hematoma

Laceration IV

Laceration

V

Laceration Vascular

Injury Description Subcapsular, 10% surface area Capsular tear, 1 cm parenchymal depth Subcapsular, 10–50% surface area, 5 cm in diameter 1–3 cm parenchymal depth that does not involve a trabecular vessel Subcapsular, 50% surface area or expanding; ruptured subcapsular or parenchymal hematoma; intraparenchymal hematoma 5 cm or expanding 3 cm parenchymal depth or involving trabecular vessels Laceration involving segmental or hilar vessels producing major devascularization (25% of spleen) Completely shattered spleen Hilar vascular injury that devascularizes spleen

a

Advance one grade for multiple injuries up to grade III.

FIGURE 30-5 Diagrammatic representation of the splenic organ injury scaling system of the American Association for the Surgery of Trauma. (Reproduced with permission from Carrico CJ, Thal ER, Weigelt JA, eds. Operative Trauma Management: An Atlas. Norwalk, CT: Appleton & Lange; 1998. Copyright The McGraw-Hill Companies, Inc.)

An important point about CT-based grading systems is that the patient’s subsequent clinical course does not correlate exactly with the degree of injury seen on CT. Although there is a rough correlation between the grade of splenic injury seen on CT scanning and the frequency of operative intervention, exceptions are common. It is possible to have what looks like a fairly trivial injury on CT scan turn out to require delayed operative intervention. In contrast, a patient with a “significant” splenic injury on CT scan quite often has a benign postinjury course with successful nonoperative management.

Probably the major usefulness of grading of a splenic injury, especially when the AAST Organ Injury Scale is used, is to allow for objective standardization of terminology and to ensure that individual injuries are described in precise terms understandable to others. Standardized organ injury scaling is useful in research, in describing populations of splenic injury patients, and in dictating treatment algorithms, as well (Fig. 30-6).

NONOPERATIVE MANAGEMENT Nonoperative management of splenic injury has become more common over time. Although approximately 40% of patients with splenic injury will require immediate operative intervention, nonoperative management is reasonable for hemodynamically stable patients.17,18,29

PATIENT SELECTION Appropriate patient selection is the most important element of nonoperative management. Determining which patients require emergency surgery and which can be initially managed

Injury to the Spleen

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Initial resuscitation and evaluation per ATLS guidelines

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Manage per management of penetrating abdominal trauma

Penetrating

Mechanism of injury Blunt

Hemodyn. Unstable

Yes

Positive

FAST exam or DPL Negative Search for other cause of hypotension. Eventual CT scan

No

Abdominal CT

No Splenic injury

Treat other injuries

Splenic injury

Yes

Contrast blush?

Angiography and embolization

Successful

No

Explore abdomen. Splenectomy vs. Splenorrhaphy

Yes

No Patient has multiple injuries or severe head injury?

Yes

Consider splenectomy

No Adequate resources exist for nonoperative management

No

Yes Monitor for hemodynamic instability, bleeding, increasing abdominal pain or tenderness

Present

Absent

Patients may be immunized immediately after diagnosis of splenic injury. Patients successfully managed for 24 hours may be allowed to eat. The risk of delayed splenic rupture decreases steadily over time and is extremely low by the 7th postoperative day.

FIGURE 30-6 Algorithm for the diagnosis and management of splenic injury.

nonoperatively is sometimes difficult, although hemodynamic status, age, grade of splenic injury, quantity of hemoperitoneum, and associated injuries have been shown to roughly correlate with the success or failure of nonoperative management.

Of paramount importance in the determination of the appropriateness of nonoperative management is the hemodynamic stability of the patient. Hemodynamic stability can be a somewhat illusory concept and one for which there is no

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consensus definition, but hypotension (systolic blood pressure 90 mm Hg in an adult) is generally considered to be worthy of concern. Hypotension in the prehospital period or emergency department is worrisome, and a high index of suspicion for ongoing hemorrhage should be maintained when either is present. Patients who have been hemodynamically unstable in the prehospital phase and remain hemodynamically unstable during their initial emergency department stay are, in most instances, inappropriate candidates for abdominal CT scanning. They require either a direct trip to the operating room (OR) or, more commonly, abdominal ultrasonography or DPL to help guide the initial decision-making process (see Chapters 10 and 16). Assuming hemodynamic stability, the other important prerequisite for consideration of nonoperative management is the patient’s abdominal examination. In patients who are awake and alert and can cooperate with a physical exam and provide feedback, it is important that they should not have diffuse peritonitis. Although patients with splenic injury will often have localized pain and tenderness in the left upper quadrant and abdominal findings secondary to intraperitoneal blood, obvious diffuse peritonitis can be a sign of intestinal injury and mandates an abdominal exploration. If a patient with a splenic injury is sent for CT scanning and subsequent nonoperative management, it is important to perform repeat physical examinations. If the examination worsens, the possibility of a blunt intestinal injury should be considered. The most common CT finding in patients with blunt intestinal injury is free fluid in the peritoneal cavity. As previously noted, the free fluid can be mistakenly attributed solely to the splenic injury, and the presence of an associated injury to the bowel can be missed. Repeated physical examinations are mandatory in such patients. The success rates of nonoperative management of splenic injury are very high in many of the published series. Reported success rates for nonoperative management are 95% or higher for pediatric patients and 80–94% in adults.30–34 These high success rates can be misleading, however, in that they apply only to the group of patients in whom nonoperative management was chosen rather than all patients with splenic injury. When patients undergoing immediate splenectomy are included, the overall splenic salvage rates tend to be 50–60% in adult patients. It is important to remember that these series generally do not include patients in whom the initial plan was for nonoperative management, but an emergency operation was necessary when the patient became hypotensive or developed peritonitis in the emergency department or in the CT scanner. The published series of nonoperatively managed spleens generally include only the selected patients who were stable enough to undergo CT scanning of the abdomen and in whom the CT scan showed a ruptured spleen. Patients who became unstable either before or during the scan and were taken emergently to surgery are usually not counted as patients who underwent “nonoperative” management. When these patients are reported at all, they are placed into the “operative” group rather than into the “failed nonoperative” group. Published series of splenic injuries, particularly in pediatric patients, are more likely to describe patients treated at referral

centers where there are large numbers of transfer patients who have already been triaged for stability prior to their arrival at the referral center. Finally, the literature on the success of nonoperative management of splenic injury should be interpreted with the awareness that publication bias tends to favor series in which success rates are high. Other important considerations beyond hemodynamic stability and abdominal findings in the determination of the appropriateness of nonoperative management have to do with the medical environment and some specific characteristics of the patient. Nonoperative management should only be undertaken if it will be possible to closely follow the patient. If close inpatient follow-up is simply not possible, abdominal exploration may be appropriate. Similarly, if rapid mobilization of the OR and quick operative intervention in the case of ongoing or delayed bleeding is not possible, early rather than emergent operative intervention may be appropriate. Finally, the patient’s circumstances after discharge occasionally may be important in the decision-making process. For patients who are to be discharged to a location remote from medical care, the consequences of delayed bleeding are greater in that they may not be close enough to a hospital that can perform an emergency operative procedure. In such circumstances, an otherwise reasonable candidate for nonoperative management might undergo operative intervention. For patients who are stable enough to undergo CT scanning and in whom a ruptured spleen is seen, nonoperative management is reasonable if they continue to remain stable. In addition to vital signs, one of the other commonly followed parameters in such patients is the hematocrit.35 A common practice is to determine a cutoff value below which the hematocrit will not be allowed to fall. If the hematocrit drops to that level or below, operative intervention is undertaken. Such an approach works best if there are no associated injuries; when associated injuries are present, it can be quite difficult to know if the spleen is continuing to bleed or if the fall in hematocrit is secondary to bleeding from other injuries. In general, there is consensus that hemodynamically stable patients without obvious or progressive peritoneal signs who can be followed closely are reasonable candidates for nonoperative management. There is some debate, however, about certain subgroups of patients and their appropriateness for nonoperative management.36 Pediatric patients are generally excellent candidates for nonoperative management as they have a low incidence of delayed bleeding after splenic injury.37 Because of the trauma mechanisms suffered by pediatric patients as opposed to adult patients, children are more likely to have isolated splenic injuries. As previously noted, the relative thickness of the splenic capsule is greater in children, perhaps conferring more structural integrity to the spleen. The spleen in children is more likely to fracture parallel to the splenic arterial blood supply rather than transverse to it, also38 (Fig. 30-7). This orientation of splenic injury tends to decrease the amount of blood loss from the splenic parenchyma. Children are more likely to have excellent physiologic reserve and minimal preexisting disease, as well. Finally, the risks of splenectomy with respect to immunologic consequences are greater in young children than they are in adults.5–7

Injury to the Spleen

571

Transverse T ransverse tear Trabe Trabeculae eculae

CHAPTER CHAPTER 30 X

Hilar vessel

Capsule Capsule

Spleni Splenic ic artery

FIGURE 30-8 A postembolization view of a patient with a splenic injury and contrast blush on CT after angiographic coil embolization (same patient as in Fig. 30-4). Trabeculae Tra ab beculae

FIGURE 30-7 Diagrammatic representation of a transverse laceration relative to the splenic vasculature in a pediatric patient. (Reproduced with permission from Upadhyaya P. Splenic trauma in children. Surg Gynecol Obstet. 1968;126:781, © Elsevier.)

There is some evidence that older patients might have a worse prognosis with respect to nonoperative management than do younger patients, and several series have reported that patients older than 55 are less likely to have successful nonoperative management.39 Other series examining the question of the threshold at 55 years of age and nonoperative management suggest the success of nonoperative management is no different in this group than it is in younger patients.40,41 Although the evidence in this area is somewhat conflicting and a large multicenter study found that older patients were more likely to fail nonoperative management, it is difficult to know to what extent this finding was self-fulfilling and related to preexisting surgeon bias.17 The presence of severe associated injuries, particularly a traumatic brain injury, has been suggested as another relative contraindication to nonoperative management of splenic injury. As has already been pointed out, following the hematocrit in a patient with severe associated injuries can be problematic. Furthermore, there are concerns about the effects of ongoing or delayed splenic bleeding on the prognosis of a severe traumatic brain injury (see Chapter 19). While these factors do not mandate operative intervention in all patients who fall into these groups, they should lower the threshold for operative intervention on an individual basis. There is little uniformity about what constitutes a “failed” attempt at nonoperative management. Different surgeons and different institutions have set different criteria for operative intervention, and much of the decision making is subjective. As has already been pointed out, there is no perfect relation between the severity of injury seen on CT scanning and a patient’s subsequent success or failure of nonoperative management. Some of this discrepancy is probably related to

the imperfect nature of the scoring systems and a lack of sensitivity of CT scanning. Also, it is likely that some of the differences are in the approach and thresholds for operative intervention. In some instances, concern about a “bad-looking” spleen on a CT scan might prompt more aggressive and quicker surgical intervention and make failed nonoperative management of severe splenic injuries a selffulfilling prophecy. An objective finding on CT scan that has proven useful as a prognostic sign with respect to nonoperative management is that of a blush in the injured splenic parenchyma as previously noted (Fig. 30-4).42,43 Such a blush is thought to represent ongoing bleeding when it is seen shortly after injury and a pseudoaneurysm when seen on later scans. There is evidence that when such a finding is present, the chances of subsequent successful nonoperative management are decreased. A contrast blush seen on initial CT scan should be evaluated with angiography and treated with embolization if ongoing bleeding is present and the patient is normotensive (Fig. 30-8). And a contrast blush is associated with a higher need for operative intervention (67% vs. 6% in adults; 22% vs. 4% in children).44,45 This approach seems reasonable as angiography with splenic embolization has improved success rates in patients managed nonoperatively. The most dramatic improvement is seen in patients with higher-grade splenic injuries. Available data suggest an improvement in nonoperative success rates from 67% to 83% in grade IV injuries and from 25% to 83% in grade V injuries.46 It is important to remember, however, that only highly selected patients with highgrade splenic injuries undergo angiographic embolization and that such patients are more likely to have complications after embolization.47 While most trauma centers practice selective angiography and embolization, a somewhat more extreme approach used by some is to have all patients with splenic injury, with or without a CT blush, undergo early angiography and embolization as necessary.48 Most centers do not treat splenic injury in this way, however, because the number of nontherapeutic angiograms with such an approach would be extremely high.

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TABLE 30-2 Proposed Guidelines for Resource Utilization in Children with Isolated Spleen or Liver Injury

SECTION 3 X

ICU stay (days) Hospital stay (days) Predischarge imaging Postdischarge imaging Activity restriction (weeks)a

I None 2 None

CT Grade II III None None 3 4 None None

IV 1 5 None

None

None

None

None

3

4

5

6

a

Return to full-contact, competitive sports (i.e., football, wrestling, hockey, lacrosse, mountain climbing) should be at the discretion of the individual pediatric trauma surgeon. The proposed guidelines for return to unrestricted activity include “normal” age-appropriate activities. From Stylianos S, the APSA Trauma Committee. Evidence-based guidelines for resource utilization in children with isolated spleen or liver injury. J Pediatr Surg. 2000;35:164–169, with permission, © Elsevier.

PATIENT MANAGEMENT After nonoperative management has been selected, the initial resuscitation should be continued and other diagnostic and therapeutic procedures carried out as necessary. There is little scientific evidence to dictate the specifics of how nonoperative management of splenic injury should be done, and most recommendations are simply matters of common sense and opinion.29 The most rigorous attempts to systematize recommendations for nonoperative management have been done in children (Table 30-2).49,50 Most patients should be admitted to an intensive care unit for their initial nonoperative management. This would include patients with grade II or above splenic injuries and patients with multiple associated injuries that make following serial hematocrit levels and physical examinations difficult. Even patients with grade I splenic injuries should be initially admitted to an intensive care unit if follow-up in a ward setting will be unreliable. During initial management patients should be kept with nothing by mouth in case they require rapid operative intervention. Nasogastric suction is not necessary unless needed for other reasons. Whether patients should be kept at bed rest or not is somewhat controversial. Although there are some theoretical reasons why bed rest might be a good idea, there is little empirical evidence that it makes a difference. The individual surgeon should choose the approach that works best in his or her practice. Patient’s vital signs and urine output should be monitored closely, serial physical examinations performed, and serial

hematocrits measured. As has been mentioned, changes in hematocrit can be influenced by bleeding from associated injuries as well as by bleeding from a splenic injury. This is important to take into account while following patients. As noted, many surgeons follow the practice of picking a specific hematocrit as a cutoff point below which they will not allow the patient to go without operative intervention. Vaccines to prevent streptococcal, meningococcal, and Hemophilus infections should be given while the patient is observed nonoperatively. There are some theoretical reasons to believe that the vaccinations are more effective if given while the spleen is still in situ. Therefore, it is preferable to vaccinate patients who are managed nonoperatively early in their course rather than waiting to vaccinate them after they have required splenectomy. The evidence to support such a practice is somewhat contradictory, and it is very difficult to study the effectiveness of vaccination timing in splenectomized patients because the incidence of overwhelming postsplenectomy infection is very low. How long a patient should remain in the intensive care unit is not clearly defined. Most centers keep patients with splenic injury in the intensive care unit for 24–72 hours and then transfer them to a ward bed if they have been stable and other injuries permit. It is generally at this point that patients are allowed to eat unless other injuries preclude oral intake. How long a patient should be kept in the hospital is poorly defined, also. There is no strong evidence supporting any particular approach, but a large multi-institutional study showed that most failures of nonoperative management occur within the first 6–8 days after injury.51 Our institutional approach is to keep patients in the hospital for an arbitrary 7 days. This approach has obvious financial and insurance implications, but will pick up most of the delayed bleeds while the patient is still an inpatient. How long to keep the patient depends to some extent on the nature of the splenic injury, also. Trivial injuries can be safely discharged earlier than more severe injuries. In many circumstances, associated injuries dictate the length of hospitalization more than does the splenic injury. Also, it is important to pay attention to where the patient lives and how close he or she will be to medical attention when deciding about timing of discharge. Patients who live far from medical attention may need to be kept in the hospital longer. Prophylaxis against deep venous thrombosis is a continuing problem in patients undergoing nonoperative management for a splenic injury. Sequential compression devices on the lower extremities should be used routinely. Early mobilization or range of motion exercises are important in minimizing thromboembolic complications, as well. Pharmacologic prophylaxis is more problematic because of concerns about bleeding from the injured spleen. After 24–48 hours of successful nonoperative management, it is reasonable, if necessary, to begin pharmacologic prophylaxis against deep venous thrombosis. If associated injuries require it, warfarin prophylaxis is also reasonable, beginning approximately 1 week after injury. These recommendations are based primarily on common sense rather than on solid data. Both the rate of clinically significant thromboembolic events in patients with

Injury to the Spleen

OPERATIVE MANAGEMENT In general, preoperative antibiotics should be given but do not need to be continued in the postoperative period unless dictated by associated injuries (see Chapter 18). A nasogastric tube is inserted to decrease the volume of the stomach and allow for easier visualization and mobilization of the spleen. A midline incision is the best incision for splenic surgery as well as most trauma operations on the abdomen. It is versatile, can be extended easily both superiorly and inferiorly, and is the quickest incision if speed of intervention is important, also. For operations on an injured spleen, it is often helpful to extend the incision superiorly and to the left of the xiphoid process. This maneuver improves exposure of the left upper quadrant, particularly in obese patients and those with a narrow costal angle. Transverse incisions in the left upper quadrant have occasionally been suggested for patients with a presumed isolated splenic injury. A midline incision is preferable because it is quicker and allows the surgeon to deal with a variety of different intra-abdominal findings. One situation in which a left

subcostal approach may be the incision of choice is when the patient is morbidly obese and preoperative CT scanning has suggested that an isolated splenic injury is present. As with all trauma celiotomies, it is important to rapidly examine all four quadrants of the abdomen in patients who are hemodynamically unstable. This initial investigation of the abdomen should not be definitive and should be used only for a quick look and for packing, especially of the upper quadrants. Definitive management of any injuries found should not be attempted until the entire abdomen has been inspected. While the quadrants are being inspected, it is helpful to look for clot. Clotting tends to localize to the site of injury, whereas defibrinated blood will spread diffusely in the abdomen. Clotted blood will often indicate the site of an injury and is helpful in determining where to direct definitive management after the abdomen has been packed. In patients who are thought to have an isolated splenic injury based on initial imaging or failed nonoperative management, direct attention can be turned sooner to the left upper quadrant. If viscera other than the spleen seem to be more badly injured and are bleeding more profusely than the spleen, the spleen should necessarily take second priority and be left packed until it is appropriate to attend to it. In comparison, a quick splenectomy is often a wise early move in a patient with multiple serious injuries in that it rapidly eliminates the spleen as a source of ongoing blood loss. Once attention has been directed to the left upper quadrant, all the structures in that quadrant should be inspected (Fig. 30-2). There should be an initial look at the greater curvature of the stomach and the left hemidiaphragm. If the spleen is mobilized, the left hemidiaphragm should be reinspected. If the left hemidiaphragm is ruptured in a patient with blunt trauma and the spleen is in the left side of the chest, it should be pulled down into the abdomen through the defect. The left lobe of the liver and left kidney should also be inspected as should the tail of the pancreas. If the spleen is to be mobilized, inspection of the tail of the pancreas is easier after mobilization has been accomplished. The anterior and anterolateral surfaces of the spleen can sometimes be seen fairly easily through the midline incision prior to any splenic mobilization, particularly if the patient is thin and there is a wide costal margin. If the patient is heavy and/or the costal margin is narrow, adequate inspection without some splenic mobilization may be very difficult. If the left upper quadrant is adequately inspected and there is no evidence of any bleeding or a splenic injury, the spleen does not require mobilization. If it is known that there is a small splenic injury, but it is not the primary reason for abdominal exploration or the spleen does not seem to be bleeding at the time of exploration, splenic mobilization is not always necessary. Mobilization of the spleen certainly provides better visualization of any injuries present, but is associated with the risk of worsening or “stirring up” the splenic injury. If the surgeon is in doubt about the need for mobilization, the best thing to do is to mobilize the spleen so that the full extent of injury is elucidated and the spleen can be repaired or removed as necessary. It is important to be as gentle as possible during mobilization of the spleen so that the splenic injury is not worsened.

CHAPTER CHAPTER 30 X

splenic injury and the rate of failure of nonoperative management in anticoagulated patients are quite low, making prospective study of the risks and benefits of anticoagulation prophylaxis in this patient population difficult to do in a prospective fashion. The issue of follow-up CT scans in patients with nonoperative management of splenic injuries is controversial, also.27,46,52–54 Most series indicate that they are not necessary or that the frequency with which they alter management is extremely low. A variety of different suggestions have been made in the literature about follow-up CT scans, ranging from no follow-ups at all to follow-ups at frequent intervals. A middle course is taken by some surgeons who only study the spleen with a follow-up CT scan when there is a high grade of injury or when they are contemplating allowing patients to return to contact sports or other activities. The author’s institutional policy is to study only patients who have persistent abdominal signs and symptoms after a week of observation. On occasion such patients have developed pseudoaneurysms of the spleen, even if the initial CT scan did not demonstrate a blush. It is difficult to know exactly what the natural history of these pseudoaneurysms would be if left untreated, but they can be impressive in appearance and are amenable to angiographic embolization. When patients are discharged, they should be counseled not to engage in contact sports or other activities where they might suffer a blow to the torso unless a follow-up CT scan has documented healing of the injured spleen. The best length of time to maintain this admonition is unknown, but typical recommendations range from 2 to 6 months. There is experimental evidence that most injured spleens have not recovered their normal integrity and strength until at least 6–8 weeks postinjury, so the recommendation to avoid contact sports for 2–6 months seems reasonable. Other than with respect to contact sports, there are no major restrictions for patients who have undergone successful nonoperative management.

573

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Management of Specific Injuries

SECTION 3 X FIGURE 30-9 Mobilization of the spleen is begun by early division of its lateral attachments.

Splenic mobilization should be done in a stepwise fashion. A stepwise approach helps in providing adequate mobilization while minimizing the chance of increased injury. Proper mobilization also allows for better visualization of the left kidney, the left hemidiaphragm, and the posterior aspects of the body and tail of the pancreas. The sequence of splenic mobilization is important in that it allows for splenic salvage and splenorrhaphy up until the final step of hilar ligation. In mobilizing the spleen, it is important to remember how posteriorly it is situated (Fig. 30-2). Also, it is important to remember that there is a great deal of variability in the length of the different ligaments around the spleen and in how mobile the spleen is before any dissection is done. If mobilization is done correctly, even spleens with fairly short surrounding ligaments and spleens in obese patients can be mobilized to a level at or above the anterior abdominal wall. The first step in mobilization of the spleen is to cut the splenophrenic and splenorenal ligaments laterally (Fig. 30-9). This step should be started with sharp dissection and can then be continued with a combination of blunt dissection and further sharp dissection. The dissection should be taken up to near the level of the esophageal hiatus so that all the lateral and superior attachments are cut. Cutting the lateral attachments is sometimes facilitated by putting a finger or clamp underneath them and then sharply developing the overlying plane. In obese patients and in those with a spleen that is very posterior, it may be necessary to do some of the dissection by feel. After the lateral attachments have been divided, the next step is to mobilize the spleen and tail of the pancreas as a unit from lateral to medial. One of the easier ways to do this is to place the back of the fingernails of the right hand underneath the spleen and tail of the pancreas so that they are adjacent to the underlying left kidney. The kidney can be palpated easily because it is quite hard and provides an excellent landmark for

the proper plane of dissection. A common error is to try to mobilize the spleen alone without the adjacent pancreas. Not mobilizing the pancreas with the spleen is easy to do if the surgeon is not posterior enough and is not in the plane between the tail of pancreas and kidney. If the tail of the pancreas is not mobilized with the spleen, the degree of splenic mobilization possible is much more limited and it is more difficult to avoid injury to the spleen. Injuries can occur during mobilization of the spleen. The splenic hilum can be damaged from behind as the surgeon’s fingers attempt mobilization from lateral to medial. The pancreas is more difficult to see if it is not mobilized with the spleen and can be damaged during hilar clamping if the spleen is to be removed. The pancreas is quite variable in length and requires varying degrees of mobilization. In patients with a very short pancreas, little pancreas, if any, requires mobilization to adequately mobilize the spleen. Conversely, if the pancreas is fairly long, a great deal of its body and tail will require mobilization in order to bring the spleen anteriorly and to the midline. After the spleen and pancreas have been mobilized as a unit, it is generally apparent that the next constraining attachments of the spleen are the short gastric vessels. Because of the dual blood supply of the spleen through its hilum and through the short gastric vessels, it is possible to divide the short gastric vessels without compromising splenic viability. The best way to divide the short gastric vessels is to have an assistant elevate the spleen and tail of the pancreas into the operative field and then to securely clamp the vessels starting proximally on the greater curvature of the stomach. The short gastric vessels should always be clamped and tied. They can be small and difficult to see, and it is tempting to simply divide the loose tissue between the spleen and stomach with the scissors or electrocautery. This should not be done as the short gastric vessels can then bleed either immediately or on a delayed basis. It is not uncommon to be concerned about a clamp on the gastric portion of a short gastric vessel including a small portion of stomach. In such cases, the tie on the stomach can necrose the wall, leading to a delayed gastric leak. This concern can be addressed by oversewing the short gastric tie on the stomach side with a series of Lembert sutures in the seromuscular layer of the stomach. The final step necessary for full mobilization of the spleen is division of the splenocolic ligament between the lower pole of the spleen and the distal transverse colon and splenic flexure. Obvious vessels in this ligament should be divided between clamps. During division of both the short gastric vessels and the splenocolic ligament, bleeding from the spleen can be controlled using digital compression of the hilum. If the patient is exsanguinating and the bleeding is massive, occasionally a clamp can be placed on the hilum during the later steps of mobilization. Mass clamping should only be done in extreme circumstances because it increases the chances of injury to the tail of the pancreas. After the spleen has been fully mobilized, it is possible to inspect it in its entirety. It is possible to examine the posterior aspect of the body and tail of the pancreas, as well. It is helpful after mobilization to pack the splenic fossa to tamponade any minor bleeding and to help keep the spleen and distal

Injury to the Spleen grades of injury (grade IV or V). Bleeding from the splenic parenchyma can be temporarily controlled with digital pressure on the hilum while the spleen is being mobilized. As previously noted, mass clamping of the hilum should be reserved for profoundly hypotensive patients in that it increases the risk of damage to the adjacent tail of the pancreas. If the decision has been made to remove the spleen, this is best done with serial dissection and division of the hilar structures after mobilization. Suture ligation should be used for large vessels, and it is desirable to ligate major arterial and venous branches separately to avoid creation of an arteriovenous fistula. As mentioned in Section “Splenic Anatomy,” a number of different splenic arterial and venous branches must be divided before removal of the spleen (Fig. 30-3). During the course of this dissection, it is common to encounter accessory spleens, in the hilum. If an accessory spleen is encountered, it should be left in place if possible. A special circumstance is the patient who has failed nonoperative management. The majority of these patients undergo splenectomy rather than splenorrhaphy.34,35,55 One reason is that the spleen is somewhat softer after a period of nonoperative management than it was before injury, and both mobilization of the spleen and splenorrhaphy are more difficult. Also, it is likely that splenic injuries that have failed nonoperative management are worse than injuries that do not fail nonoperative management. Another important factor is that the surgeon operating on a spleen that has failed nonoperative management has already decided that the spleen is a problem and is psychologically prepared for splenectomy at the time of operation. The worst-case scenario for such a surgeon is to perform splenorrhaphy after nonoperative management and have it fail, in which case the patient would require yet another trip to the OR. As has been mentioned earlier, it is helpful to pack the splenic bed during the latter stages of splenic mobilization and during splenectomy. After the spleen has been removed, the packs in the left upper quadrant should be removed and the splenic fossa reexamined. Inspection of the splenic fossa is facilitated by using a rolled up laparotomy pad. The laparotomy pad is placed deep in the splenic fossa and then rolled by the surgeon’s fingers up toward the cut vessels at the splenic hilum. During the course of this inspection, it is important to carefully visualize the splenic bed, stumps of the splenic vessels, and stumps of the short gastric vessels along the greater curvature of the stomach. This is because postoperative hemorrhage after splenectomy is most commonly related to bleeding from the cut ends of the short gastric vessels. Autotransplantation of splenic tissue that has been removed is a controversial topic. Splenic tissue has a remarkable ability to survive in ectopic locations even without a clearly identifiable blood supply. Greater or lesser degrees of spontaneous splenosis after splenectomy for trauma are quite common, and patients with splenosis demonstrate some degree of splenic function after splenectomy.60,61 The observation that accidentally seeded pieces of splenic tissue could survive and function led to the logical suggestion that portions of the spleen could be intentionally autotransplanted to ectopic sites after splenectomy. Several different methods for autotransplantation of the

CHAPTER CHAPTER 30 X

pancreas elevated into the field. During this packing maneuver, the left adrenal gland can be inspected and the left hemidiaphragm reexamined. Factors that figure into the decision about what to do with the injured spleen after mobilization include the degree of splenic injury, the overall condition of the patient, and the presence of any other intra-abdominal injuries. Obviously, if the spleen is not injured at all, it should be left in place. Similarly, if there is a trivial injury to the spleen and it is not bleeding, the spleen can be simply returned to the left upper quadrant and no further therapy is necessary. If there is a grade I injury of the spleen that is bleeding minimally or not bleeding at all, hemostatic agents can be used to stop the bleeding or prevent future bleeding. A variety of hemostatic agents are available. These include microfibrillar collagen, gelatin sponge, and fibrin glue. Whichever agent is chosen, the bleeding from the spleen should have ceased by the time the patient is closed. If the injury is more severe (grades II and III) and the patient’s overall condition is not too serious, splenorrhaphy can be done.55–57 Splenorrhaphy has become much less common with the increasing use of nonoperative management. Because we are no longer operating as much on the spleen, especially for lower grades of splenic injury, the number of splenic injuries found at surgical intervention that are amenable to splenorrhaphy has decreased along with experience with the techniques. The simplest version of splenorrhaphy has already been described earlier and is the placement of topical agents. Electrocautery of the spleen is only rarely helpful and has met with limited success, while argon beam coagulators may be helpful for hemostasis, especially of parenchyma that has been denuded of splenic capsule.58,59 The spleen can also be sutured, especially when there is an intact capsule, but it does not hold sutures particularly well. Therefore, it is often necessary to use pledget materials to bolster the repair. Several different methods for suturing the spleen have been described, and use of monofilament or chromic suture has some advantages in that either is less likely to cause injury while being placed through the splenic parenchyma. The splenic parenchyma is fairly soft even in the presence of an intact capsule, and it is easy to cinch sutures so tightly that the parenchyma is further disrupted. Partial splenectomy also has been described and is possible because of the segmental nature of the splenic blood supply. A pole or even half of the spleen can be removed, and the remaining spleen will survive provided that its hilar blood supply is left intact. One method of performing partial splenectomy is to ligate the blood supply to the damaged portion of the spleen and then observe the spleen for its demarcation into viable and nonviable portions. The damaged nonviable portion is removed, and the resultant cut splenic parenchyma is made hemostatic with the use of either mattress sutures or mesh wrapping. Wrapping of either all or part of an injured spleen with absorbable mesh has been used on occasion, as well. This technique is moderately time consuming, but reported success rates are high because of careful patient selection. Such an approach should be reserved for highly selected cases of isolated splenic injury in extremely stable patients. Splenectomy should be performed in patients who are unstable, have serious associated injuries, or have the higher

575

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Management of Specific Injuries

SECTION 3 X FIGURE 30-10 One described method for autotransplantation of splenic tissue is to place small pieces of the spleen into multiple pouches in the greater omentum. (Reproduced with permission from Millikan JS, Moore EE, Moore GE, et al. Alternatives to splenectomy in adults after trauma: repair, partial resection, and reimplantation of splenic tissue. Am J Surg. 1982;144:711, © Elsevier.)

spleen have been described (Fig. 30-10).14,15,62,63 One of the more common is to cut the spleen into pieces and place the pieces in omental pouches. Studies of autotransplantation in both animals and humans have demonstrated that some of the splenic tissue survives and has some level of function.64,65 Whether or not enough of it survives without attachment to the splenic artery in an adequately functioning form to provide adequate protection against postsplenectomy sepsis is an open question.66 Reports of overwhelming infection after autotransplantation suggest that autotransplantation is not universally successful in restoring normal immune function.67 Drains should not be routinely placed after either splenectomy or splenorrhaphy unless a coagulopathy is present as they may actually increase the rate of postoperative complications. Drainage is reasonable if there is an associated pancreatic injury or associated renal injury if there is concern about a postoperative urine leak.

COMPLICATIONS ■ Nonoperative Management The most common complication of nonoperative management of the spleen is continued bleeding. Many cases of the bleeding are probably just persistent bleeding that never stopped after the original injury. In these circumstances, there is hemodynamic instability or a progressive drop in hematocrit during the

first 24–48 hours after injury. Although about 60–70% of the failures of nonoperative management occur early after admission, many occur on a delayed basis and approximately 10% of the failures occur more than 1 week after injury.51 Early failures of nonoperative management can be determined by closely following the patient’s hemodynamic status, hematocrit, and physical examination. In many patients, a drop in hematocrit will be gradual and steady, but will ultimately dictate the need for surgical intervention. In other patients, especially those in whom the bleeding is delayed, bleeding can occur rather suddenly and be fairly dramatic. If an emergency operation is not performed in such cases, the patient is at risk for exsanguination. The pathophysiology of persistent bleeding after splenic injury and early failure of nonoperative management is fairly easy to understand. The pathophysiology of the more delayed bleeds is less obvious, and there are several hypotheses on why it occurs. One hypothesis is that as the blood in a subcapsular hematoma breaks down, increased osmotic forces pull water into the hematoma and expand the capsule. A similar pathophysiology has been described as an explanation for the increase in size of subdural hematomas. Another hypothesis for delayed bleeding from a splenic injury is the concept of “remodeling” of the clot in the splenic parenchyma. This hypothesis is based on the observation that the clot undergoes revision and degradation over time. It is possible that as this remodeling process occurs, the initial hemostasis of the splenic injury is lost. The observation that splenic injury can result in intraparenchymal pseudoaneurysms raises the possibility that delayed bleeding could also be the result of rupture of a pseudoaneurysm. Finally, it is simply possible that the damaged spleen, highly vulnerable to further injury, suffers what would otherwise be a minor second blow and starts to bleed again. The “failure” rate for nonoperative management varies from surgeon to surgeon and from institution to institution. The variability of these rates is due in part to the lack of a standardized definition of failure. Some surgeons and institutions have a low threshold for operative intervention after an attempt at nonoperative management, and some have a very high threshold. Interestingly, when studied prospectively with specific definitions for who will be initially managed nonoperatively and who will be deemed a failure of nonoperative management, the success rate for nonoperative management is considerably lower than that seen in retrospective studies.18 When nonoperative management has failed and the patient requires operative intervention, splenectomy is most often the appropriate operation unless there is minimal concern about subsequent bleeding.51 Another potential complication of nonoperative management of splenic injuries is that an associated intra-abdominal injury that requires operative intervention will be missed.68–70 This is most commonly a problem for missed injuries of the bowel and pancreas. Injury to the small bowel is particularly troublesome, as often free fluid is the only finding of blunt intestinal injury seen on CT of the abdomen. When splenic injury is present, it is easy to attribute the free fluid to bleeding from the spleen. If patients are good candidates for nonoperative management of their splenic injury, it is possible to miss the bowel injury and delay needed abdominal exploration.

Injury to the Spleen what to do. Anticoagulation of the patient puts the injured spleen at risk, while placement of a caval filter is invasive and expensive. Such patients should be managed on a case-by-case basis. Fortunately, these cases are rare in that most clinically obvious thromboembolic problems will not manifest themselves until after the major risk of bleeding from the injured spleen has passed. Patients who are managed nonoperatively often receive blood products, either because of their splenic injury or because of associated injuries, and there are risks associated with transfusion (see Chapter 13). These are well known and include the small risk of blood incompatibility, the risk of transmission of blood-borne diseases such as hepatitis, and the significant immunologic effects of transfusion, especially in critically ill and injured patients.72–74

■ Operative Management There is a risk of bleeding after splenectomy from the short gastric vessels or splenic bed and after splenorrhaphy from the splenic parenchyma. As after any operative procedure, it is important to closely follow the patient and to reexplore if postoperative bleeding is suspected. Patients with multiple associated injuries and a coagulopathy generally should have undergone splenectomy rather than splenorrhaphy. In these patients, the coagulopathy will be treated, but the possibility of surgical bleeding in the postoperative period should always be entertained when the patient has hemodynamic instability. In patients who have undergone splenorrhaphy, the risk of continued bleeding from the repaired spleen is only 2%. Gastric distention is a risk, and gastric decompression is reasonable for a short period of time after either splenectomy or splenorrhaphy. When the short gastric vessels have been cut and ligated, gastric distention can result in loss of a tie on the gastric end of a vessel and resultant bleeding. Even though this danger may be more theoretical than real, a short period of gastric decompression is probably reasonable. As previously noted, necrosis of a portion of the greater curvature of the stomach has been described, most commonly related to inclusion of a portion of the gastric wall in the ties placed on the gastric side of the cut short gastric vessels. The resultant gastric leak contaminates the abdomen, in particular the left upper quadrant, and can lead to the formation of a subphrenic abscess. Pancreatic injuries can be related either to the original trauma or to an iatrogenic injury during mobilization or removal of the spleen. A pancreatic injury will cause an increase in pancreatic enzymes, an ileus, and a generalized inflammatory state. The diagnosis is made from a combination of clinical and CT findings. The rare complication of an arteriovenous fistula in the ligated vessels in the hilum of the spleen has also been described as a risk of splenectomy. The best way to avoid such a complication is the aforementioned technique of ligating as many of the hilar vessels as possible and to avoid mass ligation of the hilar structures. Thrombocytosis is less common after a splenectomy for trauma than it is after a splenectomy for other diseases, and there is no solid evidence that splenectomy for trauma increases

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Pancreatic injuries are occasionally missed on initial CT scanning done shortly after injury and can result in serious morbidity or even mortality if not treated in an expeditious fashion (see Chapter 32). The proximity of the tail of the pancreas to the spleen makes the combination of injuries to the two organs a possibility. There is a 5–10% frequency of serious associated injuries being missed in patients who are good candidates for nonoperative management of the splenic injury, but this should decrease with improved CT technology. Repeated physical examinations, DPL, measurement of pancreatic enzymes, and repeat abdominal CT scanning are all helpful in minimizing the number of missed injuries to the small bowel and pancreas (see Chapters 31 and 32). Failure of nonoperative management is not without negative consequences. In a recent multicenter study, approximately 13% of the patients who failed nonoperative management died, with most of the deaths related to either hemorrhage from the injured spleen or a missed injury. A significant number of the cases of failed nonoperative management could be traced to an inappropriate initial decision to proceed with nonoperative management in hemodynamically unstable patients and/or when there was misinterpretation of the diagnostic imaging studies.71 A possible way of minimizing complications after nonoperative management is to obtain follow-up CT scans of the abdomen. A number of series have pointed out that the yield from such CT scans is extremely low and the patient can simply be followed clinically; however, other studies have shown that follow-up CT scans demonstrate pathology serious enough to require intervention in a small percentage of patients.53,54 The most commonly discovered pathology in such patients is pseudoaneurysm, the detection of which is of therapeutic importance because they are amenable to angiographic embolization42 (Figs. 30-4 and 30-8). The natural history of such pseudoaneurysms seen on a delayed basis is not known, but, as an extension of what is known about blushes and pseudoaneurysms seen in the early postinjury period, there is reason to be concerned about an increased risk of bleeding in such patients. Splenic cysts and abscesses are other pathologic entities sometimes seen on a follow-up CT scan.21,71 Cysts may not be apparent until a number of months after injury and are at risk for rupture with further trauma. Finally, routine CT scans done several months after injury are indicated for patients who desire to return to contact sports or some other activity that would put the spleen at risk. There are no other abdominal complications specific to nonoperative management of the spleen, but intrathoracic complications can occur. Associated pleural sympathetic effusions may result from blood and clot beneath the left hemidiaphragm, while a hemothorax may be caused by bleeding from associated fractured ribs. Deep venous thrombosis in the lower extremity is another potential complication after nonoperative management of a splenic injury because prophylaxis is usually delayed as previously described. Of interest, there is no firm evidence that the rate of thromboembolic complications is higher in patients with nonoperative management of a splenic injury. When a patient with a splenic injury develops a deep venous thrombosis or pulmonary embolism, it can be difficult to decide

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the risk of thromboembolic complications. As previously noted, appropriately timed prophylaxis again should be a standard measure in all injured patients and should cover whatever theoretical risks might be associated with the transient postsplenectomy thrombocytosis. There is some evidence that early postoperative complications are more common after splenectomy than they are in patients who do not have their spleens removed.35,75,76 Evidence is conflicting, however, and a difficulty in reviewing the literature on the subject is that it is hard to standardize the severity of injury in patients who have undergone splenectomy as compared to patients who have not undergone splenectomy. Some of the series that have suggested an increased risk of complications after splenectomy have noted that such patients were more severely injured than those who did not undergo a splenectomy.

OVERWHELMING POSTSPLENECTOMY INFECTION The first experimental evidence supporting the possibility that the spleen is of immunologic importance dates to 1919, but splenectomy remained the treatment of choice for both iatrogenic and traumatic splenic injuries until just several decades ago.77 In the early 1950s, it was noticed that neonates and young children (up to 6 months of age) with hematologic diseases who required a splenectomy had a high subsequent risk of serious infection.5 It became clear that an asplenic state in neonates and young children with hematologic diseases was a risk factor for overwhelming infection. From this observation, it was a logical next step to investigate the risk of overwhelming infection in both children and adults who had undergone splenectomy for trauma.78–81 Several studies suggested that the rate of overwhelming infection after splenectomy is increased when compared with a control population of patients who have not had their spleens removed. The actual rate at which overwhelming infection in asplenic patients occurs is unknown, but one estimate is a 0.026 lifetime risk for adults and a 0.052 lifetime risk for children, and all the estimates of risk tend to be very low.71 Not all studies have documented an increased risk of overwhelming life-threatening infection after splenectomy for trauma.82,83 Therefore, the risk of bleeding should always be weighed against the risk of overwhelming sepsis when considering the most appropriate treatment of an individual patient with a splenic injury. When infection does occur in the asplenic state, encapsulated organisms such as pneumococcus and meningococcus are the most common pathogens and pneumonia and meningitis are the most common infections.6 Because of the inference that overwhelming infection is more common after splenectomy, vaccines to prevent infection by pneumococcus, meningococcus, or Haemophilus organisms are recommended for splenectomized patients.83 There is empirical evidence in both animals and humans that the use of vaccines results in an antibody response; however, because the incidence of overwhelming infection after splenectomy is very low, it is difficult to prove that the vaccines actually have an impact on postsplenectomy infection and mortality. Nonetheless, they have become the standard of care in patients who have had a

splenectomy. In patients who have undergone splenectomy, the exact timing of vaccination is somewhat controversial.84–86 There is evidence that waiting several weeks after splenectomy to vaccinate the patient is appropriate.12 As with the question of the overall effectiveness of vaccines in preventing postsplenectomy infection, study of the optimal timing of vaccination is hampered by its low incidence. The most important principle of vaccination after splenectomy is to remember to perform it before discharge from the hospital in patients who are unlikely to return for postoperative follow-up. Whether or not patients should be revaccinated and when such revaccinations should be done remain open questions. One recommendation based on longitudinal antibody studies in a general group of patients (not just trauma postsplenectomy patients) is for revaccination every 6 years. Another measure that has been suggested for postsplenectomy patients is the continuous administration of antibiotics or the provision of a supply of antibiotics to be taken at the first sign of infection. When such measures have been tried, studies of patients’ compliance with the antibiotic regimen have been discouraging.87 The exact role of antibiotics in postsplenectomy patients is difficult to ascertain for the same reason that the effectiveness of the vaccines is difficult to prove.

REFERENCES 1. Aristotle. Parts of Animals. Peck AL, trans. London: Heinemann; 1955:261. 2. Krumbhaar EB. The history of extirpation of the spleen. N Y Med J. 1915;6:232. 3. Morgenstern L. A history of splenectomy. In: Hiatt JR, Phillips EH, Morgenstern L, eds. Surgical Diseases of the Spleen. New York: Springer; 1997. 4. Mayo WJ. Principles underlying surgery of the spleen. JAMA. 1910; 54:14. 5. King H, Shumacker HB. Splenic studies: I. Susceptibility to infection after splenectomy performed in infancy. Ann Surg. 1952;136:239. 6. Singer DB. Postsplenectomy sepsis. Perspect Pediatr Pathol. 1970;1:285. 7. Sherman R. Perspectives in management of trauma to the spleen: 1979 presidential address, American Association for the Surgery of Trauma. J Trauma. 1980;20:1. 8. Robinette CD, Fraumeni JF Jr. Splenectomy and subsequent mortality in veterans of the 1939–45 war. Lancet. 1977;2:127. 9. Saad A, Rex DK. Colonoscopy-induced splenic injury: report of 3 cases and literature review. Dig Dis Sci. 208;53:892–898. 10. Shah HN, Hegde SS, Mahajan AP, et al. Splenic injury: rare complication of percutaneous nephrolithotomy: report of two cases with review of literature. J Endourol. 2007;21:919–921. 11. Lynch AM, Kapila R. Overwhelming postsplenectomy infection. Infect Dis Clin North Am. 1996;10:693. 12. Shatz DV, Romero-Steiner S, Elie CM, et al. Antibody responses in postsplenectomy trauma patients receiving the 23-valent pneumococcal polysaccharide vaccine at 14 versus 28 days postoperatively. J Trauma. 2002;53:1037. 13. Malangoni MA, Dillon LD, Klamer TW, et al. Factors influencing the risk of early and late serious infection in adults after splenectomy for trauma. Surgery. 1984;96:775. 14. Moore FA, Moore EE, Moore GE, et al. Risk of splenic salvage after trauma. Analysis of 200 adults. Am J Surg. 1984;148:800. 15. Millikan JS, Moore EE, Moore GE, et al. Alternatives to splenectomy in adults after trauma. Repair, partial resection, and reimplantation of splenic tissue. Am J Surg. 1982;144:711. 16. Van Wyck DB, Wotte MH, Witte CL, et al. Critical splenic mass for survival from experimental pneumococcemia. J Surg Res. 1980;28:14. 17. Harbrecht BG, Peitzman AB, Rivera L, et al. Contribution of age and gender to outcome of blunt splenic injury in adults: multicenter study of the Eastern Association for the Surgery of Trauma. J Trauma. 2001;51:887.

Injury to the Spleen 46. Haan JM, Bochicchio GV, Kramer N, et al. Nonoperative management of blunt splenic injury: a 5-year experience. J Trauma. 2005;58:492. 47. Haan JM, Biffl W, Knudson M, et al. Splenic embolization revisited. J Trauma. 2004;56:542–547. 48. Sclafani SJ, Shaftan GW, Scalea TM, et al. Nonoperative salvage of computed tomography-diagnosed splenic injuries: utilization of angiography for triage and embolization for hemostasis. J Trauma. 1995; 39:818. 49. Stylianos S. Evidence-based guidelines for resource utilization in children with isolated spleen or liver injury. The APSA Trauma Committee. J Pediatr Surg. 2000;35:164–169. 50. Stylianos S. Compliance with evidence-based guidelines in children with isolated spleen or liver injury: a prospective study. J Pediatr Surg. 2002; 37:453–456. 51. Peitzman AB, Heil B, Rivera L, et al. Blunt splenic injury in adults: multiinstitutional study of the Eastern Association for the Surgery of Trauma. J Trauma. 2000;49:177. 52. Uecker J, Pickett C, Dunn E. The role of follow-up radiographic studies in nonoperative management of spleen trauma. Am Surg. 2001;67:22. 53. Allins A, Ho T, Nguyen TH, et al. Limited value of routine follow-up CT scans in nonoperative management of blunt liver and splenic injuries. Am Surg. 1996;62:883. 54. Thaemert BC, Cogbill TH, Lambert PJ. Nonoperative management of splenic injury: are follow-up computed tomographic scans of any value? J Trauma. 1997;43:748. 55. Cogbill TH, Moore EE, Jurkovich GJ, et al. Nonoperative management of blunt splenic trauma: a multicenter experience. J Trauma. 1989;29:1312. 56. Feliciano DV, Spjut-Patrinely V, Burch JM, et al. Splenorrhaphy. The alternative. Ann Surg. 1990;211:569. 57. Morgenstern L, Shapiro SJ. Techniques of splenic conservation. Arch Surg. 1979;114:449. 58. Go PM, Goodman GR, Bruhn EW, et al. The argon beam coagulator provides rapid hemostasis of experimental hepatic and splenic hemorrhage in anticoagulated dogs. J Trauma. 1991;31:1294. 59. Dunham CM, Cornwell EE III, Militello P. The role of the argon beam coagulator in splenic salvage. Surg Gynecol Obstet. 1991;173:179. 60. Pearson HA, Johnston D, Smith KA, et al. The born-again spleen. Return of splenic function after splenectomy for trauma. N Engl J Med. 1978; 298:1389. 61. Fremont RD, Rice TW. Splenosis: a review. South Med J. 2007;100: 589–593. 62. Mizrahi S, Bickel A, Haj M, et al. Posttraumatic autotransplantation of spleen tissue. Arch Surg. 1989;124:863. 63. Velcek FT, Jongco B, Shaftan GW, et al. Posttraumatic splenic replantation in children. J Pediatr Surg. 1982;17:879. 64. Leemans R, Manson W, Snijder JA, et al. Immune response capacity after human splenic autotransplantation: restoration of response to individual pneumococcal vaccine subtypes. Ann Surg. 1999;229:279. 65. Leemans R, Harms G, Rijkers GT, et al. Spleen autotransplantation provides restoration of functional splenic lymphoid compartments and improves the humoral immune response to pneumococcal polysaccharide vaccine. Clin Exp Immunol. 1999;117:596. 66. Zhao B, Moore WM, Lamb LS Jr, et al. Pneumococcal clearance function of the intact autotransplanted spleen. Arch Surg. 1995;130:946. 67. Moore GE, Stevens RE, Moore EE, et al. Failure of splenic implants to protect against fatal postsplenectomy infection. Am J Surg. 1983;146:413. 68. Buckman RF Jr, Piano G, Dunham CM, et al. Major bowel and diaphragmatic injuries associated with blunt spleen or liver rupture. J Trauma. 1988;28:1317. 69. Nance ML, Peden GW, Shapiro MB, et al. Solid viscus injury predicts major hollow viscus injury in blunt abdominal trauma. J Trauma. 1997;43:618. 70. Traub AC, Perry JF Jr. Injuries associated with splenic trauma. J Trauma. 1981;21:840. 71. Peitzman AB, Harbrecht BG, Rivera L, et al. Failure of observation of blunt splenic injury in adults: variability in practice and adverse consequences. J Am Coll Surg. 2005;201:179. 72. Robinson WP III, Ahn J, Stiffler A, et al. Blood transfusion is an independent predictor of increased mortality in nonoperatively managed blunt hepatic and splenic injuries. J Trauma. 2005;58:437. 73. Gunst MA, Minei JP. Transfusion of blood products and nosocomial infection in surgical patients. Curr Opin Crit Care. 2007;13: 428–432. 74. Shorr AF, Jackson WL. Transfusion practice and nosocomial infection: assessing the evidence. Curr Opin Crit Care. 2005;11:468–472. 75. Willis BK, Deitch EA, McDonald JC. The influence of trauma to the spleen on postoperative complications and mortality. J Trauma. 1986; 26:1073.

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18. Velmahos GC, Toutouzas KG, Radin R, et al. Nonoperative treatment of blunt injury to solid abdominal organs: a prospective study. Arch Surg. 2003;138:844. 19. Todd SR, Arthur M, Newgard C, et al. Hospital factors associated with splenectomy for splenic injury: a national perspective. J Trauma. 2004; 57:1065. 20. Kluger Y, Paul DB, Raves JJ, et al. Delayed rupture of the spleen—myths, facts, and their importance: case reports and literature review. J Trauma. 1994;36:568. 21. Cocanour CS, Moore FA, Ware DN, et al. Delayed complications of nonoperative management of blunt adult splenic trauma. Arch Surg. 1998;133:619. 22. Holmes JF, Nguyen H, Jacoby RC, et al. Do all patients with left costal margin injuries require radiographic evaluation for intra-abdominal injury? Ann Emerg Med. 2005;46:232–236. 23. Lynn KN, Werder GM, Callaghan RM, et al. Pediatric blunt splenic trauma: a comprehensive review. Pediatr Radiol. 2009;39:904–916. 24. Moore EE, Cogbill TH, Jurkovich GJ, et al. Organ injury scaling: spleen and liver (1994 revision). J Trauma. 1995;38:323. 25. Umlas S-L, Cronan JJ. Splenic trauma: can CT grading systems enable prediction of successful nonsurgical treatment? Radiology. 1991; 178:481. 26. Mirvis SE, Whitley NO, Gens DR. Blunt splenic trauma in adults: CT-based classification and correlation with prognosis and treatment. Radiology. 1989;171:33. 27. Shapiro MJ, Krausz C, Durham RM, et al. Overuse of splenic scoring and computed tomographic scans. J Trauma. 1999;47:651. 28. Barquist ES, Pizano LR, Feuer W, et al. Inter- and intrarater reliability in computed axial tomographic grading of splenic injury: why so many grading scales? J Trauma. 2004;56:334. 29. Alonso M, Brathwaite C, Garcia V, et al. Practice management guidelines for the nonoperative management of blunt injury to the liver and spleen. In: East Practice Management Guidelines. EAST Practice Parameter Workgroup For Solid Organ Injury Management; 2003:1. 30. Dent D, Alsabrook G, Erickson BA, et al. Blunt splenic injuries: high non-operative management rate can be achieved with selective embolization. J Trauma. 2004;56:1063. 31. Pearl RH, Wesson DE, Spence LJ, et al. Splenic injury: a 5-year update with improved results and changing criteria for conservative management. J Pediatr Surg. 1989;24:428. 32. Morse MA, Garcia VF. Selective nonoperative management of pediatric blunt splenic trauma: risk for missed associated injuries. J Pediatr Surg. 1994;29:23. 33. Schwartz MZ, Kangah R. Splenic injury in children after blunt trauma: blood transfusion requirements and length of hospitalization for laparotomy versus observation. J Pediatr Surg. 1994;29:596. 34. Oller B, Armengol M, Camps I, et al. Nonoperative management of splenic injuries. Am Surg. 1991;57:409. 35. Schweizer W, Bölen L, Dennison A, et al. Prospective study in adults of splenic preservation after traumatic rupture. Br J Surg. 1992;79:1330. 36. Velmahos GC, Chan LS, Kamel E, et al. Nonoperative management of splenic injuries: have we gone too far? Arch Surg. 2000;135:674. 37. Davies DA, Fecteau A, Himidan S, et al. What’s the incidence of delayed splenic bleeding in children after blunt trauma? An institutional experience and review of the literature. J Trauma. 2009;67:573–577. 38. Upadhyaya P, Simpson JS. Splenic trauma in children. J Am Coll Surg. 1968;126:781. 39. Smith JS, Wengrovitz MA, DeLong BS. Prospective validation of criteria, including age, for safe, nonsurgical management of the ruptured spleen. J Trauma. 1992;33:363. 40. Cocanour CS, Moore FA, Ware DN, et al. Age should not be a consideration for nonoperative management of blunt splenic injury. J Trauma. 2000;48:606. 41. Barone JE, Burns G, Svehlak SA, et al. Management of blunt splenic trauma in patients older than 55 years. J Trauma. 1999;46:87. 42. Davis KA, Fabian TC, Croce MA, et al. Improved success in nonoperative management of blunt splenic injuries: embolization of splenic artery pseudoaneurysms. J Trauma. 1998;44:1008. 43. Omert LA, Salyer D, Dunham CM, et al. Implications of the “contrast blush” finding on computed tomographic scan of the spleen in trauma. J Trauma. 2001;51:272. 44. Schurr MJ, Fabian TC, Gavant M, et al. Management of blunt splenic trauma: computed tomographic contrast blush predicts failure of nonoperative management. J Trauma. 1995;39:507. 45. Nwomeh BC, Nadler AP, Meza MP, et al. Contrast extravasation predicts the need for operative intervention in children with blunt splenic trauma. J Trauma. 2004;56:537.

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76. Wahlby L, Domellof L. Splenectomy after blunt abdominal trauma. A retrospective study of 413 children. Acta Chir Scand. 1981;147:131. 77. Morris DH, Bullock FD. The importance of the spleen in resistance to infection. Ann Surg. 1919;70:513–521. 78. Pimpl W, Dapunt O, Kaindl H, et al. Incidence of septic and thromboembolic-related deaths after splenectomy in adults. Br J Surg. 1989;76:517. 79. Sekikawa T, Shatney CH. Septic sequelae after splenectomy for trauma in adults. Am J Surg. 1983;145:667. 80. Gopal V, Bisno AL. Fulminant pneumococcal infections in “normal” asplenic hosts. Arch Intern Med. 1977;137:1526. 81. Green JB, Shackford SR, Sise MJ, et al. Late septic complications in adults following splenectomy for trauma: a prospective analysis in 144 patients. J Trauma. 1986;26:999. 82. Pringle KC, Rowley D, Burrington JD. Immunologic response in splenectomized and partially splenectomized rats. J Pediatr Surg. 1980; 15:531.

83. Schwartz PE, Sterioff S, Mucha P, et al. Postsplenectomy sepsis and mortality in adults. JAMA. 1982;248:2279. 84. Hutchison BG, Oxman AD, Shannon HS, et al. Clinical effectiveness of pneumococcal vaccine. Meta-analysis. Can Fam Physician. 1999; 45:2381. 85. Schreiber MA, Pusateri AE, Veit BC, et al. Timing of vaccination does not affect antibody response or survival after pneumococcal challenge in splenectomized rats. J Trauma. 1998;45:692. 86. Caplan ES, Boltansky H, Synder MJ, et al. Response of traumatized splenectomized patients to immediate vaccination with polyvalent pneumococcal vaccine. J Trauma. 1983;23:801. 87. Waghorn DJ, Mayon-White RT. A study of 42 episodes of overwhelming postsplenectomy infection: is current guidance for asplenic individuals being followed? J Infect. 1997;35:289.

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Stomach and Small Bowel Lawrence N. Diebel

INTRODUCTION Injuries to the stomach and small bowel are common in penetrating abdominal trauma. The incidence of gastrointestinal injury following gunshot wounds that penetrate the peritoneal cavity is over 80%. Thus, exploratory laparotomy is warranted on virtually all gunshot wounds that penetrate the peritoneal cavity. The incidence of hollow viscus injury (HVI) secondary to stab wounds that have penetrated the peritoneal cavity is much less, which in most series is about 30%. Thus, a selective approach to operative exploration has been advocated following stab wounds. Blunt injuries to the stomach and small bowel are much less common than penetrating injury, but collectively compromise the third most common type of blunt abdominal injury. The increasing use of computed tomography (CT) for diagnostic evaluation of the patient with blunt abdominal trauma and selective nonoperative management of solid organ injuries have contributed to some of the difficulties and controversies in the management of HVIs following blunt trauma. In contradistinction to some of the diagnostic difficulties with stomach and small bowel injuries, operative repair of stomach and small bowel injuries is relatively straightforward. The key to the successful management of stomach and small bowel injuries is prompt recognition and treatment, thus decreasing the likelihood of abdominal septic complications and subsequent late death.

HISTORICAL PERSPECTIVE Intestinal injuries were reported early in the medical literature (see Chapter 1). Small bowel perforation from blunt trauma was first recognized by Aristotle.1 Hippocrates was the first to report intestinal perforation from penetrating abdominal trauma. In 1275, Guillaume de Salicet described the successful suture repair of a tangential intestinal wound. Reports of

attempted surgical repair of gastric and intestinal wounds appeared in the literature with heightened interest and controversy during the American Civil War, the Spanish-American War, the Russo-Japanese War, and other military conflicts. However, the dismal results of surgical intervention lead to abandonment of laparotomy even with obvious intestinal injury during these military campaigns.2 By the late 19th century, improved surgical techniques led to renewed interest in laparotomy and repair of penetrating abdominal injuries. Theodore Kocher was the first surgeon to report successful repair of a gunshot wound of the stomach. Although still controversial, in 1901 President William McKinley, shot in the abdomen by an assassin, underwent expeditious transport and surgical repair of several gastric wounds. However, a wound to the pancreas was overlooked, and McKinley died 8 days later. A laparotomy for intestinal perforation at the start of World War I carried a mortality rate of 75–80%, almost equal to the mortality rate of nonoperative management. However, in the later part of World War I, operative management was recognized as the preferred management for penetrating abdominal trauma. In World War II, prompt evacuation, improvements in anesthesia, and better understanding and treatment of shock led to mortality rates of 13.9% for jejunal or ileal injuries and 36.3% if multiple injuries were present.3 Further improvements in mortality were noted during the Korean War and Vietnam conflicts. Lessons learned by military surgeons were quickly adopted by surgeons in civilian centers. However, the sheer volume of trauma in several major trauma centers dictated that patients with abdominal stab wounds be treated expectantly and operations performed on the basis of physical signs of peritonitis or hemodynamic instability. Based on this experience, it became obvious that stab wounds and/or low velocity gunshot wounds did not share the same risk as wounds from military weapons. Thus, selective management became a formal policy

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at larger experienced centers and soon included GSW that appeared tangential, or involved posterior, flank, or thoracoabdominal locations. Patients with gastrointestinal injuries under these circumstances may benefit from a staged operative approach for abdominal injuries. Simple repairs or temporizing measures aimed at controlling ongoing peritoneal contamination by gastrointestinal injuries are performed at the initial operation. Definitive repair for more complex gastrointestinal injuries is undertaken at a later operation after hemodynamic stabilization. Nonetheless, prompt recognition and repair of injuries are responsible for the low morbidity and mortality from isolated gastric and small bowel injuries. Associated injuries contribute significantly to morbidity and mortality in patients with gastric and small bowel injuries.

ANATOMY AND PHYSIOLOGY The stomach generally occupies the left upper quadrant of the abdomen. The nondistended stomach, especially in a supine individual, is located largely in the intrathoracic abdomen where it is offered some protection by the lower chest wall. The position of the stomach can be quite variable and in the erect individual may extend into the lower abdomen, particularly when distended with food or liquid. The stomach is fixed on its lesser curvature by the gastrohepatic ligament, cephalad by the gastrophrenic ligament, and distally by the retroperitoneal duodenum. The greater curvature of the stomach is loosely bound to the transverse colon via the greater omentum and to the spleen by the gastrosplenic ligament. The stomach enjoys a rich blood supply from the left and right gastric arteries, the left and right gastroepiploic arteries, and the short gastric arteries (Fig. 31-1). Venous drainage follows the arterial supply to the stomach for the most part. The normal stomach is relatively free of bacteria and other microorganisms because of the low intraluminal pH.4 However, up to 103 organisms/mL, including lactobacilli, aerobic streptococci, and even Candida, may be isolated. Low gastric acidity due to H2-receptor blockade or now proton pump inhibitors leads to increased bacterial concentrations in the stomach and proximal gastrointestinal tract, increasing the risk of peritoneal contamination with gastric perforation. Retained food in the stomach may also increase the risk of infection following gastric perforation. Factors include acid neutralization and increased luminal bacteria in the postabsorptive state as well as serving as an adjuvant in the event of peritoneal contamination. The small bowel distal to the ligament of Trietz is approximately 5–6 m in length in the adult. Protected anteriorly only by the abdominal wall musculature and occupying most of the true abdominal cavity, the small intestine is anatomically vulnerable to injury. The small intestine is suspended from the posterior abdominal wall by its mesentery, the base of which extends from the duodenal jejunal flexure, superior to inferior and left to right to the level of the right sacroiliac joint. The arterial supply to the small bowel is provided by the superior mesentery artery (SMA), which emerges from under the

pancreas and then courses anterior to the uncinate process of the pancreas to enter the root of the mesentery. The blood supply to the small bowel comes from the left side of the SMA via intestinal arteries (Fig. 31-2). The jejunal and ileal branches vary in number and supply all but the terminal part of the ileum. This is supplied by branches from the ileocolic artery. Numerous intestinal arcades form within the mesentery to assure excellent collateral blood supply to the small intestine. Venous return from the small intestine follows the arterial supply: the superior mesenteric vein joins the inferior mesenteric vein and splenic vein to form the portal vein. Although no clear distinction exists, the first 40% or so of the bowel is jejunum and the remainder is the ileum (Fig. 31-3). The jejunum has a larger diameter, more circular folds, and larger villi, but less lymphoid tissue than the ileum. The mesentery of the jejunum contains only a single arcade, whereas more than two or three sets of vascular arcades are present in the ileum. Mesenteric fat is also more prominent in the ileum than in the jejunum. The proximal jejunum is the primary site of carbohydrate, protein, and water-soluble vitamin absorption. Fat absorption occurs over a larger length of small bowel. The ileum is the primary site of carrier-mediated bile salt and vitamin B12 absorption. Loose intercellular junctions contribute to significantly greater water and sodium fluxes in the jejunum than in the ileum. Tighter intercellular junctions and active transport of sodium chloride allow for significant fluid reabsorption and concentration of luminal content in the ileum (and colon). However, distinctions between jejunum and ileum are of clinical importance only if a significant length of bowel is resected. The ileocecal valve is thought to act as a “break” to the delivery of small bowel content into the cecum. It may also be a barrier for reflux of colonic content into the small bowel. However, ileal peristalsis probably is the main factor in those functions. The luminal content of the proximal small bowel is of neutral pH and is relatively sterile, containing few bacteria. Most studies of the small bowel microflora have demonstrated increasing bacterial counts with distance away from the pylorus.5 The proximal small bowel flora resembles the gastric flora. The jejunum and proximal ileum contain gram-positive and gram-negative organisms at 104–105 cfu/mL. The bacterial concentration in the distal ileum rises to 105–108 in the ileum. There is also a higher number of anaerobic species in the ileum. This increase in bacterial load in the ileum is thought to contribute to an increased risk of infection with full-thickness injury in the distal small bowel versus the proximal small bowel.

■ Mechanism of Injury/Pathophysiology Blunt injuries to the stomach and small bowel are infrequently encountered. Injuries include contusions, intramural hematomas, lacerations, full-thickness perforations, and mesenteric avulsions. In the East Association for the Surgery of Trauma (EAST) multi-institutional study, HVI was noted in only 1.2% of over 225,000 admissions during the 2-year study period.6 Most HVIs in this study were hematomas and several tears. Perforated small bowel injury accounted for less than

Stomach and Small Bowel Left gastric artery

Esophageal branch

Celiac artery

583

Posterior gastric artery Splenic artery

Right and left branches

CHAPTER CHAPTER 31 X

Cystic artery Short gastric arteries

Hepatic artery proper Right gastric artery Common hepatic artery Gastroduodenal artery Supraduodenal artery

Left gastro-omental artery

Aorta Right gastro-omental artery

A. Anterior View Superior pancreaticoduodenal artery

Short gastric arteries

Spleen

Esophageal branch Left gastric artery

Splenic artery

Posterior gastric artery

Splenic artery Common hepatic artery

Celiac artery

Hepatic artery proper

Right gastric artery

Gastroduodenal artery

Supraduodenal artery Superior pancreaticoduodenal artery

Left gastro-omental (gastroepiploic) artery

Right gastro-omental artery

B. Anterior View

FIGURE 31-1 Blood supply to the stomach. An anomalous left hepatic artery can arise as a branch of the left gastric artery. This should be looked for when doing gastric resections. (Reproduced with permission from Agur AMR, Dalley AF, eds. Grant’s Atlas of Anatomy. 11th ed. Copyright Lippincott Williams & Wilkins; 2004.)

0.1% of blunt trauma admissions. Full-thickness perforations of the small bowel (unspecified site) and jejunum/ileum each accounted for 20–25% of all full-thickness HVIs. Gastric perforations following blunt trauma are rare and accounted for only 2.1% of the total HVI in the EAST study. Most gastric injuries are related to pedestrian motor vehicle or high-speed motor vehicle crashes. The stomach is thick walled and relatively resistant to a blunt injury. However, when

full after a recent meal, trauma to the left side of the body or inappropriate use of seat belts may contribute to rupture. Blunt gastric injuries include lacerations and full-thickness perforations, which most frequently involve the anterior gastric wall.7,8 Peritoneal signs and blood nasogastric tube aspirate are usually present and lead to early surgical intervention. Associated injuries are often severe because of the degree of force necessary to produce a gastric blowout.9 Associated

584

Management of Specific Injuries Transverse colon

SECTION 3 X

Omental appendix

Tenia coli

Sacculation

Middle colic artery

Jejunum

Vasa recta Right colic artery

Superior mesenteric artery

Anastomosis uncertain Ascending colon Ileocolic artery

Ileal branches

Cecum

Anterior View

Appendicular artery and appendix Ileum

FIGURE 31-2 Blood supply to the small bowel. Multiple branches to the jejunum and ileum originate directly from the superior mesenteric artery. The distal ileum is supplied via the ileocolic artery. (Reproduced with permission from Agur AMR, Dalley AF, eds. Grant’s Atlas of Anatomy. 11th ed. Copyright Lippincott Williams & Wilkins; 2004.)

injuries include liver, spleen, and pancreas, as well as injuries to the chest and head. Associated injuries are the main reason for the higher mortality rates for patients with blunt gastric rupture versus other HVIs.10–12 Small bowel perforation secondary to blunt abdominal trauma is uncommon, but thought to be increasing in incidence. Motor vehicle crashes are the most important mechanism for blunt intestinal trauma, followed by falls and bicycle accidents. Localized blows to the abdominal wall may also cause HVI. Mechanisms postulated for injury to the intestine to occur include: (1) crushing of bowel against the spine, (2) sheering of the bowel from its mesentery of a fixed point by sudden deceleration, and (3) bursting of a “pseudo-closed” loop of bowel owing to sudden increase in intraluminal

pressure. More recently Cripps and Cooper have demonstrated experimentally the potential for small intestinal injury in highvelocity, low-momentum impacts that do not greatly compress the abdominal cavity.13 Earlier series had described proximal jejunum and distal ileum as sites more prone to injury due to their relative immobility. More recent reports have not shown this to be the case, as mid-jejunal perforations have been increasingly reported. Although the use of seat belts alone or in combination with air bags is effective in reducing fatalities, there may be an increase in injuries associated with both proper and improper use of these devices. Garret and Brownstein first referred to the seat belt mark as ecchymoses across the abdominal wall that corresponds to the lap belt14 (Fig. 31-4). With the advent of the

Stomach and Small Bowel

585

CHAPTER CHAPTER 31 X

A

B

FIGURE 31-3 (A and B) The jejunum and ileum can be distinguished from one another by differences in luminal diameter, number of arterial arcades, and the presence or absence of fat encroaching on the gut wall. (Reproduced with permission from Agur AMR, Dalley AF, eds. Grant’s Atlas of Anatomy. 11th ed. Copyright Lippincott Williams & Wilkins; 2004.)

three-point restraint system, injuries may also involve the neck and chest. The “seat belt syndrome” now refers to intestinal injuries associated with lumbar fractures and abdominal or chest wall ecchymoses.14 Injury to other organs may occur and include the stomach and colon. Anderson et al. reported a 4.38-fold increase in risk of small bowel injuries with lap/shoulder restraint use and a more than 10-fold increase in risk with lap belts alone, compared with no restraint use.15 Chandler et al. reported 112 patients involved in motor vehicle crashes.16 Sixty percent of patients were wearing a seat belt, and the remainder were unrestrained. There was no difference in the overall incidence of abdominal injury between belted and unbelted patients (15% vs. 10%, respectively). However, the incidence of small bowel perforation was significantly increased in patients with a seat belt versus no belt (6% vs. 2.2%, respectively). The presence of a seat belt sign (SBS) was associated with an even greater likelihood of abdominal injuries and small bowel perforation (64% and 21%, respectively). More recently in the EAST multi-institutional study, the SBS was associated with a 4.7-fold increase in relative risk of

A

B

small bowel perforation in patients following motor vehicle crashes.17 The second highest relative risk of small bowel perforation was the use of a seat belt without evidence of an abdominal seat belt mark (2.4-fold increase in relative risk). Small bowel injuries noted with the use of seat belt use include small bowel transections (usually in the proximal jejunum) as a manifestation of a deceleration injury, sheering or crushing injuries usually involving the terminal ileum and associated mesentery, and (blowout) perforations on the antimesenteric aspect of the bowel. This latter injury is felt to be due to an acute sudden increase in intraluminal pressure in a functionally closed loop of bowel. It is believed that when air bags are deployed in combination with a properly placed seat belt, there is a decrease in the incidence of abdominal injuries. Children with an “SBS” may also have a higher rate of gastrointestinal injury. Sokolove et al. demonstrated that children with an SBS had a significantly greater risk of intra-abdominal injury, including gastrointestinal and pancreatic injuries.18 However, the increased risk of injury was only apparent in patients with abdominal pain or tenderness. In a study by Chidester et al., the SBS only had a sensitivity of 25% and a

C

FIGURE 31-4 Patients with blunt intestinal injury sometimes have ecchymoses of the abdominal wall caused by restraint devices. The findings may be relatively subtle (A) or more severe (B). The presence of such ecchymoses does not always signify underlying blunt intestinal injury. By the same token, many patients with blunt intestinal injury do not have abdominal wall ecchymoses. The patient in (A) had a grade II injury while a grade IV injury (C) occurred in patient (B).

586

Management of Specific Injuries

SECTION 3 X A

B

FIGURE 31-5 Some injuries to the lumbar spine are commonly caused by seat belts, and are frequently accompanied by associated blunt intestinal injury. Transversely oriented fractures through bone (A) are also sometimes known as Chance fractures. The mechanism of injury responsible for such fractures can cause soft-tissue disruption and dislocation in the same orientation as seen with Chance fracture (B).

specificity of 85% for abdominal injury.19 Similar to the study by Sokolove, the presence of SBS with abdominal tenderness was more predictive of abdominal injury. The association of a Chance-type fracture of the lumbar spine as a predictor of HVI is variably reported in the literature (Fig. 31-5). Anderson et al. reported 62.5% of 16 patients with Chance-type fractures had HVIs.15 Nine perforations occurred in the small bowel, and the remainder were in the colon. However, in the EAST multi-institutional trial with small bowel perforations there was no difference in incidence of Chance-type fracture in perforating or nonperforating small bowel injury patient groups versus patients without small bowel injury.17 The incidence of bowel perforations was quite low in all groups, and ranged between 2% and 3% of patients. In about 20% of patients with blunt intestinal perforations no other injuries are present. Other patients have significant extra-abdominal injuries with blunt injury as their sole intraabdominal injury. Approximately 25% of patients with blunt intestinal injury have more than one injury requiring surgical intervention.20–22 Thus, in patients undergoing laparotomy for blunt intestinal rupture a complete evaluation for other injuries and a thorough laparotomy are mandated. On rare occasions, patients may return to the hospital several days or weeks after blunt abdominal trauma with signs and symptoms of bowel obstruction. Contrast-enhanced CT of the abdomen performed at this time usually shows a thickened bowel loop, and narrowing of the lumen. This finding is due to intestinal stenosis resulting from mesenteric vascular injury. The stenosis is felt to be due to infarction resulting from the mesenteric injury rather then a direct injury to the intestine.23 Penetrating injuries to the stomach and small intestine are often more obvious. The anatomic location and space occupied by these organs make them the prime target following injury

due to knives, gunshot wounds, shotgun wounds, and other piercing instruments. Of those with peritoneal penetration only 30% of patients with knife wounds have significant injuries requiring operation, whereas over 80% of patients who suffer gunshot wounds have injuries requiring surgical repair. Thus, most institutions employ selective observation of patients with knife wounds even with peritoneal penetration. The decision for operation is based on clinical signs of peritonitis. Many institutions apply a selective approach to shotgun wounds.24 For non-close-range shotgun wounds, operative intervention is based on the range of the blast and pellet distribution as well as an estimate of the number of pellets penetrating the peritoneal cavity. Patients with shrapnel wounds to the abdominal region may also be managed selectively, depending on findings from the physical exam and imaging studies.25 Blast injuries to the GI tract are the result of a “multidimensional injury” as four separate mechanisms may play a role.26 The primary blast injury results from an overpressure wave induced by the blast itself. Although primary blast injuries to the GI tract more commonly occur in the colon, the small bowel may also be affected. Exposure to extreme blast overpressure (which is invariably fatal) results in immediate lacerations of the bowel. Nonfatal blast exposure may result in multiple contusions or intramural hematomas, which may evolve to full-thickness injury. The initial injury involves the mucosa–submucosa of the bowel wall; the presence of serosal injury is evidence of a transmural lesion at high risk of perforation. Because of the nature of this injury, there may be delay of 1–2 days, and rarely up to 14 days, before clinical symptoms occur. The overall incidence of bowel perforation is low (0.1–1.2%) but is increased with explosive amount, or when the victim is close to the center of the explosion or in an enclosed area.

Stomach and Small Bowel

DIAGNOSIS An accurate history of the traumatic event can help determine the potential for intra-abdominal injuries. In patients with a knife wound of the left thoracoabdominal region, diaphragmatic and gastric injuries are a primary concern. The small bowel is at risk of perforation following virtually any penetrating injury that violates the peritoneum. Evisceration of abdominal contents after abdominal stab wound is associated with significant intra-abdominal organ injury in 75% of patients even with no overt clinical signs that would mandate laparotomy. Certain patterns of blunt abdominal injury should alert the clinician as to the probability of gastric and small bowel perforations. Thus, a low threshold for laparotomy is appropriate in this setting. These include the use of seat belts, handle bar injury, and blows to the abdomen such as being kicked by a horse or other large animal. At the very minimum, individuals with an SBS should be admitted and observed with serial abdominal exams. The incidence of small bowel injury in patients diagnosed with solid organ injuries by CT is variable. Nance et al. in a review of 3,089 patients with solid organ injury from the Pennsylvania Trauma Systems Foundation found 296 patients who had an HVI (9.6%).22 The frequency of HVI increased with the number of solid organs injured: 7.3% with one solid organ injury, 15.4% with two solid organ injuries, and 34.4% with three solid organs injured. More recently, Miller et al. reviewed the Memphis experience with nonoperative management of 803 hemodynamically stable patients with blunt liver or spleen injuries.21 Overall, the incidence of associated intra-abdominal injury was higher in the patients with liver injury at 5% as compared with 1.7% of patients with isolated splenic injury. Bowel injury was discovered in 11% of liver injury patients and no patients with isolated splenic injury. It is believed that the blunt force capable of producing liver injuries or multiple solid organs places the small bowel at increased risk for perforation and should arouse clinical suspicion for bowel injury. Patients with penetrating gastric injuries usually present with significant peritoneal signs due to the peritoneal irritation from the intraperitoneal leakage of the low pH content of the stomach. Bloody nasogastric aspirate or free air demonstrated

on an upright chest x-ray may be indicative of gastric injury but is neither completely sensitive nor specific for the presence of gastric injury. In patients with obvious peritoneal penetration clinical findings following penetrating trauma to the small intestine may be minimal at first. This is because the luminal content of the small bowel has an almost neutral pH and is relatively sterile. Intestinal spill may also be relatively small, limiting the initial inflammatory response. In the East multi-institutional trial of blunt small bowel injury, 1.2% of 227,972 blunt trauma admits were found to have a hollow viscous injury.17 A total of 72.5% of patients with perforating small bowel injury had abdominal tenderness; however, only 33.5% had peritoneal signs. Nonetheless, a careful physical exam by an experienced surgeon may discern the likelihood of intestinal perforation. In patients with an SBS on the abdominal wall, tenderness or guarding away from the seat belt should heighten the concern for the possibility of perforated small bowel injuries. Perforations of the stomach and small bowel are recognized by signs of peritoneal irritation: tenderness with guarding and rebound. Sensitivity of clinical examination to identify patients in need of operation exceeds 95% for stab wounds and gunshot wounds. In other studies, clinical examination of the abdomen has been shown to be unreliable in approximately 50% of blunt abdominal trauma patients.17 Significant limitations include patients with head injury and altered level of consciousness, intoxication due to drugs or alcohol, and spinal cord injury. The variable effect of hemoperitoneum from associated solid organ injuries and the presence of distracting injuries (e.g., pelvic fracture) in the multi-injured patients may also limit the clinical reliability of the findings on physical exam. Laboratory studies including hematocrit, WBC, and serum amylase are not useful in the initial evaluation of patients with gastric and small intestinal injuries.17 In patients managed nonoperatively with solid organ injury or in patients with penetrating injuries undergoing serial clinical exams, unexplained tachycardia, hypotension, leucocytosis, an increase in serum amylase, or the development of a metabolic acidosis should arouse suspicion of a missed HVI. A variety of diagnostic tests have been used to further evaluate the abdomen following blunt and penetrating injuries (see Chapters 15 and 16). DPL is very sensitive in detecting intraperitoneal injury but is now infrequently used. The most common peritoneal lavage finding with bowel injuries is gross blood.28 However, this may be due to associated solid organ or mesenteric injuries. Peritoneal lavage with blood cell count has been used to diagnose HVI. However, Jacobs et al. found that a lavage white blood cell count 500/mm3 as the sole positive lavage criterion is a nonspecific indicator of intestinal perforation.29 It was suggested that sequential determinations of DPL and WBC may be useful in the diagnosis of intestinal perforation. Repeat lavage, diagnostic laparoscopy, or limited laparotomy in the patient already in the operating room for repair of other injuries may be prudent. DPL amylase and alkaline phosphatase levels may also be useful in identifying HVIs. Jaffin et al. found an alkaline

CHAPTER CHAPTER 31 X

Secondary blast injuries are caused by projectiles from the explosion that cause perforating injury to the victim. Tertiary blast injuries are the result of the generation of “blast winds” that propel the victim into rigid objects causing blunt injury. Quaternary injuries are the result of fire and heat generated by the explosion. Most injuries seen clinically are due to secondary or tertiary blast effects. Patients with penetrating torso injury or involving 4 body areas are at high risk for intraperitoneal injury.26 Patients with abdominal trauma after terror-related blast injury have a higher incidence of bowel injury (71.4%) and a lower incidence of solid organ injury (33%).26 Shrapnel is the leading cause of abdominal trauma in this setting.27 In the presence of peritoneal signs, the decision to perform surgery is easily made. Because bowel perforation may be delayed, careful observation is critical, even with negative initial image studies or diagnostic peritoneal lavage (DPL) results.

587

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Management of Specific Injuries

SECTION 3 X

phosphate level 10 IU in the DPL effluent to have a specificity of 99.8% and a sensitivity of 94.7% in detecting small bowel and colonic injury.30 McAnena et al. used lavage amylase 20 IU/L and lavage alkaline phosphatase levels 3 IU/L as predictors of HVIs following blunt penetrating trauma.31 These values had a sensitivity of 54%, specificity of 48%, and a positive predictive value of 88% for significant abdominal injury. The ability of DPL to detect hollow viscus perforation in the presence of hemoperitoneum secondary to solid organ injury may be improved by adjusting the positive criteria for WBC. Otomo et al. proposed a “positive” WBC criterion of WBC  RBC/150 when peritoneal lavage was positive for hemoperitoneum.32 These criteria had a sensitivity of 96.6% and a specificity of 99.4% for intestinal injury when performed more than 3 hours after injury. Fang et al. used a “cell count ratio” in diagnosing hollow viscus perforation.33 The cell count ratio was defined as the ratio between white blood cell count and red blood cell count in the lavage fluid divided by the ratio of the same parameters in the peripheral blood. A cell count ratio of 1 predicted hollow viscus perforation with a specificity of 97% and a sensitivity of 100% when performed before 1.5 and 5 hours from the time of injury. The “lag time” between intestinal perforation and peritoneal white cell response was felt to account for the reliability of the “corrected” peritoneal lavage white blood cell counts calculated in these later two studies to detect hollow viscus perforations. The Focused Assessment by Sonography for Trauma (FAST) has been a widely used test in the initial evaluation of suspected abdominal trauma. This is not as sensitive as DPL or CT in detecting stomach or small bowel injuries. This is most likely because of the relative inability of the FAST exam to pick up small amounts of free fluid typically found with isolated hollow viscus perforations. Rozycki et al. reported on 1,540 patients (1,227 with blunt injuries, 313 with penetrating injuries) who had FAST examinations performed as part of their initial assessment following injury.34 The sensitivity and specificity for detecting hemoperitoneum were 83.7% and 99.7%, respectively. However, there were 16 blunt abdominal trauma patients with false-negative ultrasound results. Three of these patients were subsequently found to have significant small bowel injuries. As an isolated finding, an additional patient had small bowel perforation and a ruptured bladder. Bowel injuries have been also missed by FAST examinations in patients with pelvic ring fractures. Detection of actual bowel injuries by FAST is unreliable. CT scan is the most commonly used diagnostic modality in evaluating the abdomen in hemodynamically stable blunt trauma victims. It is occasionally used in evaluating hemodynamically stable patients with penetrating injuries particularly to the back and flank areas. It is apparent that when blunt small bowel perforation is present, abdominal CT is usually abnormal.35–38 A number of CT findings are indicative or more often arouse suspicion for significant bowel and mesenteric blunt injuries. CT findings specific of bowel perforation include extraluminal oral contrast and discontinuity of hollow viscus wall. However, as oral contrast extravasation is noted in less than 10% of documented

FIGURE 31-6 This CT was obtained a few hours after injury. The findings were highly suspicious of oral contrast extravasation (arrows). The patient was found to have rupture of the small intestine at surgery.

cases of small bowel perforation, it is not advocated for routine care at most centers (Fig. 31-6). CT findings suggestive of bowel injury include pneumoperitoneum, gas bubbles close to the bowel wall, thickened (4–5 mm) bowel wall, bowel wall hematoma, and intraperitoneal free fluid without solid organ injury. Active contrast extravasation is a specific sign of mesenteric laceration, and mesenteric hematoma or fluid collection in the mesenteric folds is a CT finding suggestive of mesenteric injury (Fig. 31-7). Malhatra et al. reviewed the Presley Regional Trauma Center experience with screening helical CT evaluation of blunt bowel and mesenteric injuries.38 One hundred of 8,112 scans were suspicious of blunt bowel/mesenteric injuries. There were 53 patients with bowel/mesentery injuries (true positive) and 47 without (false positive). The most common finding in both true-positive and false-positive groups was unexplained intraperitoneal fluid

FIGURE 31-7 This CT was done shortly after injury. Multiple abnormalities are noted including thickened bowel and free fluid (arrows). However, a large amount of free air is the most notable finding. At operation a mid-jejunal perforation was found.

Stomach and Small Bowel necessary when used to evaluate patients with penetrating abdominal injuries.44 A recent meta-analysis by Goodman et al. demonstrated CT scanning in hemodynamically stable patients who had high (90%) specificity, negative predictive value, accuracy, and slight lower positive predictive value.45 Diagnostic laparoscopy is occasionally helpful in avoiding laparotomy in hemodynamically stable patients with penetrating thoracoabdominal trauma.46 Indications include penetrating left thoracoabdominal trauma with suspected diaphragmatic injuries. On some occasions small diaphragmatic tears and even gastric perforations may be repaired using laparoscopic techniques. Penetrating injuries to the anterior right thoracoabdominal area and tangential gunshot wounds to the abdomen may also be evaluated laparoscopically. Indications for diagnostic laparoscopy are less certain for patients with blunt intestinal trauma. A major limitation cited with diagnostic laparoscopy is in the relative inability to detect hollow viscus perforations. Earlier reports demonstrate an excessively high rate of missed injuries.46 Kawahara et al. recently demonstrated their experience in 75 hemodynamically stable patients with suspected abdominal injuries.47 Importantly, no small bowel injuries were missed, and unnecessary laparotomy was avoided in 73%. The reported accuracy was 98.66% with 97.61% sensitivity and 100% specificity. Obviously, advanced laparoscopic training is required, especially if therapeutic laparoscopy is attempted. Expertise in advanced laparoscopic surgical techniques is undoubtedly helpful in reliably excluding bowel injuries. A 30° angle laparoscope is used for abdominal exploration. Proper selection of sites for port placement is paramount for effective laparoscopic evaluation for bowel injury. Earlier recommendations include placement of the laparoscope through a 10-mm port 4 cm above the umbilicus, a second port in the suprapubic region, and a third port in a paramedian position at the level of the umbilicus on the side opposite the abdominal entrance wound. Currently, a supraumbilical port and two pararectus sites at the level of the umbilicus are advocated.47 After inspection for blood or bile, the bowel is examined from the ligament of Treitz to the ileocecal valve using atraumatic bowel graspers, and inspection of both sides of the bowel is required in sequential 10-cm segments. In patients found to have intestinal perforation, it is safest to convert to a laparotomy to properly address the bowel injury, as well as any additional injuries found on formal exploration.

C

OPERATIVE MANAGEMENT B A

A. Bullet entry through flank. B. Extraluminal air and fluid with injury to ileum and cecum. C. Soft tissue gas at exit site.

FIGURE 31-8 A single contact CT in a patient with tangential GSN shows the missile tract in close proximity to bowel with air around bowel loops.

After the initial evaluation and resuscitation of the injured patient, patients with suspected or recognized injury to the stomach or small bowel should undergo immediate operation. Under most circumstances the abdomen should be explored through a midline incision. Paraxyphoid extension is useful in the exposure of upper stomach or esophageal wounds. In patients with large traumatic abdominal wall defects (e.g., close-range shotgun wounds), the abdominal wall defect may be used for access to the peritoneal cavity. Usually, debridement with further surgical extension of the abdominal wall defect is necessary. Occasionally, stable patients with large

CHAPTER CHAPTER 31 X

present in 74% and 79% of scans, respectively. Pneumoperitoneum and bowel wall thickening were much more common in truepositive scans. Multiple findings suspicious for bowel/mesenteric injury were seen in 57% of the true-positive scans but in only 17% of false-positive scans. The overall sensitivity and specificity of CT for bowel/mesenteric injury were 88.3% and 99.4%, respectively. The positive and negative predictor values were 53.0% and 99.9%, respectively. In the EAST study, free fluid without solid organ injury had a 38.4% incidence of perforating small bowel injury.17 Even with the use of multidetector CT scans, free intraperitoneal fluid is the most common finding of blunt infected or mesenteric injury.36,39 It is important to semiquantify free fluid to help distinguish significance. Minimal fluid is defined as fluid in one anatomic region, and large amount of fluid is defined as fluid in multiple areas.40 Patients with minimal fluid can be followed by clinical exam or repeat CT imaging. Patients with larger amounts of fluid may be best served by DPL, diagnostic laparoscopy, or operative exploration. Of note, 12.2% of patients diagnosed with small bowel perforations in the EAST trial had a completely normal CT.17 Thus, if associated injuries do not mandate admission, a short period of observation may still be warranted, particularly if there is abdominal tenderness or the drug and/or alcohol screen is positive.41 In the initial report, Velmahos and colleagues demonstrated the safety of selective nonoperative management in over 1,800 patients with abdominal GSW.42 During observation, 80 of 792 patients selected for nonoperative management developed symptoms and underwent laparotomy, which was therapeutic in 57. In a follow-up study on 100 patients with nontangential abdominal GSW, the sensitivity and specificity of CT scanning were 70.5% and 90%, respectively.42 The two false-negative scans involved HVIs, which were repaired without complication. The most sensitive indicator for laparotomy for HVI from penetrating trauma is extension of the wound track, to or near a hollow viscus43 (Fig. 31-8). Therefore, oral or rectal contrast may not be

589

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Management of Specific Injuries

SECTION 3 X

defects and eviscerated bowel or omentum due to stab wounds may be explored through a surgical extension of the abdominal wall defect. After the initial control of significant hemorrhage, contamination from the GI tract is then addressed. In patients with ongoing hemorrhage temporized by packing, gastric and bowel perforations should then be rapidly controlled. Hemostasis and control of gastrointestinal spill is best obtained with a running Vicryl or Dexon suture closure of the perforation. This is particularly effective if there is significant bleeding from the lacerated stomach/intestine or adjacent mesentery. Alternatively, atraumatic clamps may be used to control spillage from the bowel. All injuries identified are then repaired as the next step. It is useful to grade stomach and small intestinal injuries according to their severity (Tables 31-1 and 31-2). In the patient who is hemodynamically stable, definitive repair of these injuries is relatively straightforward and based on their severity grade.

TABLE 31-2 Small Bowel Injury Scale Gradea I

Laceration

Mobilization of the stomach is essential for detection of gastric injuries. Exposure is generally easier if the stomach is decompressed first by a properly placed nasogastric tube. A bloody nasogastric return should arouse suspicion for a gastric injury. Certain areas of the stomach are more difficult to assess: the gastroesophageal junction, high in the gastric fundus, the lesser curvature, and the posterior wall. Division of the left triangular ligament and mobilization of the lateral

TABLE 31-1 Stomach Injury

II

III

IV

Description of Injury Contusion or hematoma Partial thickness laceration Laceration in GE junction or pylorus 2 cm In proximal one third of stomach 5 cm In distal two thirds of stomach 10 cm Laceration 2 cm in GE junction or pylorus In proximal one third of stomach 5 cm In distal two thirds of stomach 10 cm Tissue loss or devascularization  two thirds of stomach Tissue loss or devascularization  two thirds of stomach

AIS-90 2 2 3 3 3 3 3 3 4 4

GE  gastroesophageal. a

II

Laceration

III

Laceration

IV

Laceration

V

Laceration

Vascular

■ Stomach Injuries

Gradea I

Type of Injury Hematoma

Advance one grade for multiple lesions up to grade III.

Description of Injury AIS-90 Contusion or 2 hematoma without devascularization Partial thickness, no 2 perforation 3 Laceration 50% of circumference Laceration 50% 3 of circumference without transection Transection of the 4 small bowel Transection of the 4 small bowel with segmental tissue loss Devascularized segment 4

AIS  Abbreviated Injury Score. a

Advance one grade for multiple injuries up to grade III.

segment of the left lobe are helpful in exposing the gastroesophageal junction. A Bookwalter or Omni-Tract self-retaining retractor can greatly facilitate this exposure. In the hemodynamically stable patient, the reverse Trendelberg position can aid in exposure of this area and allow better visualization of associated diaphragmatic injuries. If the gastrohepatic ligament is divided, care must be taken to avoid injury to the vagus nerve or its branches or the occasional anomalous left hepatic artery. To visualize high in the gastric fundus, the short gastric vessels should be divided and ligated. Overzealous traction in this area may cause a tear of these vessels or of the splenic capsule leading to troublesome bleeding. The posterior wall of the stomach may be inspected by opening the avascular portion of the gastrocolic ligament along the greater curvature of the stomach. This may be extended up to the short gastric vessels to visualize areas high in the fundus if necessary. It is better to enter this space in the upper or mid portion of the greater curvature of the stomach to avoid making a rent in the transverse mesocolon and possibly causing injury to middle colic artery. When an anterior hole in the stomach is found, a diligent search for a second hole must be undertaken. This is usually relatively straightforward. However, there are several areas that can hide injuries and should be carefully inspected. These include the greater and lesser curvature of the stomach, the proximal posterior gastric wall, and fundus as well as the posterior cardia. If a suspicion still exists after the search for a second hole comes up empty, a useful diagnostic

Stomach and Small Bowel

■ Small Bowel Injuries Examination of the small intestine for injury is achieved by evisceration of the small bowel to the right and careful inspection of its entire length. The small bowel is examined loop by loop; no injuries are definitively repaired until the entire bowel is inspected. The decision to resect versus repair bowel is made only after careful assessment of the proximity of bowel perforations and the adequacy of the blood supply to the bowel in question. Mesenteric hematomas adjacent to the bowel wall following penetrating injury should be

carefully opened and the mesenteric aspect of the bowel inspected for injury. Other small nonexpanding mesenteric hematomas should be reassessed at intervals throughout the operative procedure to assure their stability. If significant bleeding from the mesentery is encountered, it should be controlled directly by either placement of clamps on the ends of the bleeding vessels followed by suture ligature or the accurate placement of sutures in a figure eight fashion. Mesenteric defects are closed later. Bleeding at the root of the mesentery requires extra caution in obtaining hemostasis because of the concern for compromising the blood supply to the bowel. Exposure and repair of proximal jejunal injuries may be facilitated by taking down the ligament of Trietz. The inferior mesenteric vein is at risk with injuries in this area. Occasionally division of this vein is necessary for exposure and repair of bowel injuries near the ligament of Trietz. Treatment of small bowel injury depends on its grade (Table 31-2). Obvious serosal tears should be closed with interrupted silk seromuscular sutures. Small serosal tears may be left alone if one is certain as to the depth of the intestinal wound. A grade I intramural hematoma can be safely inverted with 3-0 or 4-0 silk seromuscular sutures. Full-thickness small bowel perforations including less than 50% of the circumference (grade II) are repaired by careful debridement and primary closure (Fig. 31-9). The preferred method is to use a two-layer closure with a continuous Vicryl or Dexon suture for the inner layer and interrupted silk sutures for the outer layer. Alternatively, a single-layer closure with a running or interrupted suture can be used. A transverse closure is preferable because it assures the widest luminal opening. A transverse closure without tension may not always be possible, however, particularly with long lacerations along the antimesenteric border of bowel. A longitudinal single-layer closure may be preferable in this instance. Adjacent throughand-through wounds of the bowel are joined transversely using electrocautery and closed as a single defect. Multiple grade II injuries can usually be closed individually. Small bowel resection for multiple perforations is not recommended unless resection and anastomosis would take less time than closing the perforations individually and the amount of bowel sacrificed is minimal. An additional concern is the tendency to compromise the bowel lumen with closure of multiple perforations in a short segment. Concerns about the mesenteric circulation and residual luminal diameter dictate the treatment of grade III and IV injuries. Injuries to more than 50% of the small bowel circumference should usually be resected because of the high likelihood of luminal narrowing with primary closure (Fig. 31-10). However, grade III wounds that are oriented transversely or in the relative large proximal to mid jejunum may be primarily repaired provided that an adequate lumen (at least 30% of the circumference) is maintained. Complete transection of the bowel (grade IV) is treated by resection of the injured bowel and its adjacent blood supply followed by anastomosis (Fig. 31-11). Grade V injuries involve small bowel transections with segmental tissue loss or segmental devascularization and require resection with anastomosis (Fig. 31-12).

CHAPTER CHAPTER 31 X

adjunct is to have the anesthesiologist insufflate the stomach with air through the nasogastric tube. With the stomach submerged in saline, a telltale leakage of bubbles localizes any missed injury. Rarely, it may be necessary to enlarge the known injury so as to inspect the stomach from the inside in search of another injury to the stomach. A tangential wound to the stomach and bowel can occur but this is a diagnosis of exclusion. Gastric injuries thus identified are treated according to their severity (Table 31-1). Most intramural hematomas (grades I and II) are repaired with interrupted 3-0 silk seromuscular sutures after evacuation of the hematoma and hemostasis are obtained. Small grade I and II perforations can be closed primarily in one or two layers. Because the stomach is quite vascular and often bleeds profusely, we prefer a twolayer closure after hemostasis is achieved. A running locked absorbable suture should be used for the inner layer, and interrupted seromuscular sutures of 3.0 or 4.0 silk should be used for the outer layer. Large (grade III) injuries near the greater curvature can be closed by the same technique or by the use of a GIA stapler. Care must be taken to avoid stenosis in the gastroesophageal and pyloric area. A pyloric wound may be converted to a pyloroplasty to avoid possible stenosis in this area. Extensive wounds (grade IV) may be so destructive that either a proximal or a distal gastrectomy is required. Reconstruction with either a Billroth I or a Billroth II anastomosis is dictated by the presence or absence of an associated duodenal injury. In rare cases, a total gastrectomy and a Roux-en-Y esophagojejunostomy is necessary for severe injuries (grade V). If a diaphragm injury occurs in association with a gastric perforation, contamination of pleural cavity with gastric contents can be problematic. Under most circumstances it is sufficient to clear the pleural space through the diaphragmatic rent following closure of the gastric perforation. It may be necessary to enlarge the diaphragmatic injury to achieve complete evacuation of the pleural contamination. The powered irrigation system used in laparoscopic surgery may be an ideal method to clear the pleural cavity prior to chest tube insertion and closure of the diaphragm. The pleural contamination may be so severe, particularly if operation is delayed, that on rare occasions, a separate thoracotomy to provide adequate drainage of the pleural space is necessary. Thoracoscopic evacuation of the gastric contamination of the pleural space followed by chest tube placement is another option.

591

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Management of Specific Injuries 8-2 Grade I repair

SECTION 3 X

Inversion stitch

8-3a Grade II repair

8-3b

8-3c Grade II Multiple adjacent injuries 8-3d

FIGURE 31-9 Treatment of grade I and II small bowel injuries. Grade I injuries are treated by inversion with seromuscular sutures. Grade II injuries are treated by careful debridement and primary closure. Either a one- or two-layer closure may be used. Adjacent through-and-through perforations are treated as a single defect by dividing the bridge of tissue separating them with electrocautery. (Reproduced with permission from Carrico CJ, Thal ER, Weigelt JA, eds. Operative Trauma Management: An Atlas. Norwalk, CT: Appleton & Lange; 1998. Copyright The McGraw-Hill Companies, Inc.)

There remains some controversy as to the safety of stapled versus handsewn anastomoses for traumatic bowel injuries.48–52 Most of the available data are from retrospective studies with only one prospective study (Table 31-3). There are no controlled clinical trials comparing techniques for intestinal anastomosis following trauma. However, it is now the general consensus that the complication rate is similar for stapled and handsewn anastomoses. A handsewn anastomosis is the tried and true method to reestablish GI continuity. Techniques include a single- or twolayered anastomosis. Burch et al. conducted a prospective randomized study comparing a single-layer anastomosis with 3-0 polypropylene versus a two-layer anastomosis with running absorbable suture for the inner layer and 3-0 silk Lembert for the outer layer.53 One hundred and twenty-five patients were enrolled in the study of which only 31 were trauma patients. No differences in anastomotic leaks or intra-abdominal abscess between the two groups were noted. If a stapled anastomosis is

Second row: Interrupted Lembert 1st row 8-3e

performed, care should be taken if the enterotomy created for the GIA stapler is closed with a TA stapling device. The GIA staple line should be offset approximately 5 mm to avoid intersecting staple lines and potential tissue ischemia when using the TA stapler to close this defect. Regardless of the technique used, intestinal anastomotic healing is dependent on a good blood supply, a tension-free suture or staple line, an adequate lumen, a watertight closure, and no distal obstruction. The most appropriate factor in selecting the timing and technique of bowel anastomoses remains sound surgical judgment. There are several important tenants regarding intestinal anastomoses in the trauma setting. First, the surgeon should rely on techniques that he or she is most experienced with. Second, it may be preferable to hand sew, rather than staple, markedly thickened or edematous bowel. A staple line reinforcement with bioresorbable materials is another option. Third, certain circumstances make any anastomosis at risk for complications. These include shock with massive fluid and

Stomach and Small Bowel

8-4a

CHAPTER CHAPTER 31 X

Mesentery divided

8-4b

8-4c

8-4d 8-4e

Mesentery closed

FIGURE 31-11 Treatment of grade IV small bowel injuries requires resection of the injured bowel and its adjacent blood supply. Anastomosis may be performed using either suture or stapling techniques.

593

FIGURE 31-10 Grade III small bowel injuries are usually treated by resection and anastomoses. Proximal small bowel injuries or transversely oriented wounds may on occasion be primarily repaired. (Reproduced with permission from Carrico C, Thal ER, Weigelt JA, eds. Operative Trauma Management. 1st ed. Copyright McGraw-Hill Inc; 1998.)

FIGURE 31-12 Isolated mesenteric injury: Mesenteric injuries can be caused by both blunt and penetrating mechanisms. If the blood supply is disrupted enough to lead to questions about the viability of a short segment of small intestine, that segment should be resected.

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Management of Specific Injuries

TABLE 31-3 Small Bowel Injury: Handsewn versus Stapled Anastomoses

SECTION 3 X

Author Brundage et al.52

No. of Patients 84

Witzke et al.48

257

Brundage et al.49

199

Kirkpatrick et al.50

227

Site of Injury Small bowel (101) and colon (17)

Type of Small Bowel Anastomoses Handsewn Stapled 60 58

Small bowel only, but included primary repair (131) and resection/ anastomoses (144) Both small bowel (224) and colonic anastomoses (61)

34

110

84

140

Small bowel only; both primary repair (104) and resection with anastomoses (123)

24

52

blood administration, associated pancreatic injury, and the development of an abdominal compartment syndrome.51,54 Patients who incur significant bleeding during laparotomy may develop progressive acidosis, hypothermia, and coagulopathy. A damage control laparotomy should be considered and have bleeding controlled or temporized by packing and undergo further resuscitation before definitive repairs are performed. Only GI tract injuries that require simple repair should be definitively treated. More severe bowel injuries may be controlled by stapling of the bowel proximally and distally with resection of the injured part of the bowel. Anastomosis is performed in the operating room 24–48 hours later when the patient has been stabilized.55 If patients are returned to the operating room after more than 72 hours, great morbidity (abscess rate) and mortality have been reported.56 Bowel resection with anastomosis does not appear to place the anastomosis at risk of breakdown in the patient with an open abdomen if abdominal closure is achieved “early.”53,55 Two-hundred and four patients with enteric injuries and postinjury open abdomen were entered into the 2010 Western Trauma Association multi-institutional trial.57 Colonic

Results and Comments Retrospective single institutional study. Stapled anastomoses had significant increase in anastomotic leak requiring reoperation Retrospective single institution study showed no difference in rate of intra-abdominal abscess, fistula, an anastomotic leak, or postoperative bowel obstruction Retrospective study from five Level I trauma centers Higher leak rate and overall complication rate for stapled anastomoses Retrospective study from two institutions. No differences in anastomotic complication as related to technique used. Increased anastomotic complications associated with pancreaticoduodenal injury, or if done as part of a damage control procedure 47 anastomoses were done using suture/staples in a combined technique

anastomosis, particularly involving the left colon, had a greater leak rate than small bowel anastomosis. The leak risk was also higher in patients postinjury with ongoing hypoperfusion (indexed by 12-hour heart rate and base deficit). In particular, there was a four times greater likelihood of developing a leak if abdominal closure was not achieved until 7 days postinjury versus day 5 (3% vs. 12%). Protection of the bowel anastomosis with omental covering, gentle handling of the bowel on reoperation, and early facial closure are advised to prevent intestinal fistula formation.54,56 Anastomosis at a larger stage is facilitated by a decrease in bowel edema that may be significantly less at this time. Additionally, it allows reevaluation of bowel of questionable viability. Extensive destruction of the small bowel or its mesentery (grade V) necessitates resection and anastomosis. Treatment of isolated mesenteric injuries without bowel perforation is dependent on the viability of the bowel. Resection is required for devascularized bowel. If the involved bowel segment is short and there is doubt about the viability of the bowel, resection should be performed. Proximal injuries to the mesenteric blood vessels may result in large segments of questionable bowel viability.

Stomach and Small Bowel

POSTOPERATIVE MANAGEMENT The postoperative care of patients with gastric and small bowel injuries is usually relatively straightforward. Complications when they do arise are more often related to associated injuries or to delays in the operative management of the stomach and bowel injuries. Antibiotics are limited to a 24-hour course, usually of a single agent such as cefoxitin or ampicillin–sulbactam.58 However, appropriate dosing may be problematic in patients undergoing massive volume resuscitation with crystalloid and blood products. The advisability of routine nasogastric decompression following procedures involving an intestinal anastomosis is still controversial, despite prospective randomized controlled trials finding no advantage to this practice. A meta-analysis of selective versus routine nasogastric decompression after elective laparotomy was conducted by Cheatham et al. on 3,964 patients from 26 published trials.59 Routine nasogastric decompression was not supported by this meta-analysis of the literature. However, these studies did not involve trauma patients. The potential impact of other clinically important variables including the presence of multiple associated injuries, hemorrhagic shock, and postresuscitation bowel edema as well as an impaired sensorium from head injuries or drugs and alcohol may make nasogastric decompression the more prudent choice. It is our practice to continue nasogastric decompression, which was initiated during the initial resuscitation, until ileus resolves. It is also advisable to have a properly functioning nasogastric tube in place to decompress the proximal GI tract following a damage control laparotomy and planned reestablishment of gastrointestinal tract continuity. In patients in whom a jejunostomy is placed at laparotomy it is also useful to decompress the stomach and monitor gastric outputs as jejunal enteral feeds are initiated. Jejunal feeding may increase gastric output significantly that may lead to pulmonary aspiration in these patients.60 In uncomplicated cases involving stomach or small bowel injuries there is no evidence to support routine nutritional support of patients who were well nourished pre-injury. On the

other hand, in critically ill or injured patients it is prudent to start nutritional support early before hypermetabolism or sepsis intervenes.61 Available clinical evidence suggests that moderately to severely injured patients (ISS  16  25) should have enteral feedings started between 24 and 48 hours postinjury. Those with more severe injuries are more likely to have intolerance to enteral feedings. There is convincing evidence in the literature that patients with blunt and penetrating injuries sustain fewer septic complications when fed enterally as opposed to parenterally.62 However, total parenteral nutrition should be started by day 7 in severely injured patients who do not tolerate enteral feeding or fail to tolerate at least 50% of their goal rate of enteral feedings. There are conflicting data on the effects of enteral feeding on hepatosplenic circulation and metabolic demands.63,64 It is safest to start short enteral feedings at the end of active shock resuscitation. It appears that starting enteral feedings up to 36 hours postinjury and at a “trophic infusion rate” (15 mL/h) for up to 4 days is effective in decreasing pneumonia rates without untoward effects on the ICU course of patients with severe blunt abdominal trauma.65 There does not appear to be a clear advantage to postpyloric enteral feeding versus gastric feeding in trauma patients. Thus, with few exceptions (severe closed head injury, or severe pancreatic duodenal injury) surgical feeding jejunostomy (with the exception of a needle catheter jejunostomy) should not be routinely performed at the initial laparotomy. Further, bowel edema may make this simple procedure a far greater challenge than necessary. If patients do not tolerate intragastric feeds, it is far simpler to place a nasojejunal tube endoscopically at a later time. Immunomodulating (IMD) enteral formulas are enriched with glutamine, alone or in combination with arginine, nucleotides, and lipids, with high levels of omega-3 fatty acids.66 Other supplements include antioxidants and trace elements, including selenium. A meta-analysis conducted by Marik and Zaloga of 20 studies included 7 studies in trauma patients.67 They concluded that IMDs supplemented with arginine, with or without additional glutamine or omega-3 fats, did not appear to offer an advantage over standard enteral formulas in ICU, trauma, and burn patients (JSS  20, ATI  25). It is likely these IMDs may offer benefit only in the most severely injured patients when given early with adequate protein calorie support.66 There is some concern for initiating enteral feeds in the early (less than 24–48 hours) postinjury period. It is well known that gastrointestinal motility is adversely impaired following abdominal surgery. Bowel perforation requiring repair or resection and anastomosis is another confounding variable. A systemic review and meta-analysis evaluated early (within 24 hours of intestinal surgery) versus traditional management in patients following gastrointestinal surgery.68 Thirteen trials with a total of 1,173 patients were included in this analysis. Mortality was reduced with early postoperative feedings; however, the mechanism was not clear. Although early postoperative feeding increased vomiting, no obvious advantage in keeping patients NPO following gastrointestinal surgery could be demonstrated. Postoperative ileus (POI), an inevitable consequence of any laparotomy, may

CHAPTER CHAPTER 31 X

Clinical judgment about bowel viability has under the best circumstances only a 65% predictive value. Adjunctive techniques to access bowel viability such as intravenous fluorescein and bowel inspection using a Wood’s lamp, Doppler flow studies, and bowel surface oximetry may be useful. However, it is usually wiser to terminate the procedure, provide temporary abdominal closure, and perform a secondlook procedure in 24 hours after the patient is rewarmed and perfusion deficits corrected before deciding to perform an extensive bowel resection. Performing resection at this later time may allow preservation of bowel that was of questionable viability at the first operation. With massive bowel resections, it is important to note the location and length of the segment of the resected bowel. The most critical measurement is the length of the remaining small bowel. Preserving as much of the ileum as clinically possible and the ileocecal value, if feasible, may obviate the complications related to extensive bowel resections.

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hamper not only attempts at enteral feeding but also the timely recovery of the patient. There are multiple pathogenic mechanisms responsible for POI.69 Neural reflexes seem to be the most important, compounded by inflammatory mediators and the administration of opioids for pain control. Conventional treatments of POI include nasogastric suction, early ambulation, implementation of early enteral feeding, and the use of prokinetic drugs. Although nasogastric decompression and early ambulation are time-honored therapies for POI, neither method has ever been scientifically proven to speed the resolution of POI. Early enteral feeding most likely only has a modest effect on the resolution of POI, even though it is usually tolerated following injury. Enteral feeding tolerance is best achieved using a standardized protocol for initiating feeds and criteria for advancing the rate of infusion.70 Pharmacologic agents have been employed to improve enteral feeding tolerance and to relieve POI. The most commonly used agents include metoclopramide and erythromycin. Metoclopramide is a dopamine D2 receptor agonist, as well as a 5-HT3 receptor antagonist and a 5-HT4 receptor agonist. Its actions include increases in gastric motility, but only a modest effect on small bowel motility. Erythromycin stimulates GI motility by acting on motilin receptors located primarily in the proximal GI tract. A systemic evidence review by Booth et al. in 2002 concluded that these promotility agents improve gastric emptying and improve tolerance of enteral feedings.71 There was no effect on other important outcomes. Long-term use of erythromycin is limited by its antibacterial action and tachyphylaxis. The Cochrane review of systemic prokinetic pharmacologic treatment of POI following abdominal surgery in adults was reported in 2008.72 Thirty-nine randomized control trials were reviewed with a total of 4,615 patients. There were major flaws in most of the studies reviewed. There was insufficient evidence to recommend metoclopramide or erythromycin or other agents, except alvimopan, a peripheral μ-opioid receptor antagonist for POI. However, methodological concerns were raised concerning some of the studies supporting the effectiveness of alvimopan. As several mechanisms have been casually related to the development of POI, a multimodality approach for the management of POI would seem to be the most prudent. Complications directly related to gastric and small injuries include intra-abdominal septic complications and anastomotic disruption. An intra-abdominal septic complication most often presents as an intra-abdominal abscess. Anastomotic failures may present as peritonitis and/or the development of an external fistula. Infectious complications following gastric injury are most common following blunt trauma and if there is an associated colon injury. In these patients, ongoing fever and leukocytosis should mandate diagnostic imaging of both the chest and abdomen to look for foci of infection to drain. The most important etiologic factor relating stomach or small bowel injuries to intra-abdominal abscess formation is delayed recognition and surgical treatment.11,12 Diagnosis of blunt intestinal injury is especially problematic in the pediatric trauma population and may contribute to delays in operative treatments. Canty et al. suggested a delay of up to 24 hours after blunt intestinal trauma did not increase

mortality or morbidity.73 A delay in definitive repair over 24 hours was directly associated with increased morbidity but not mortality. Additionally, a multi-institutional retrospective study of 214 patients failed to demonstrate a correlation between time to surgery, complication rate, and hospital length of stay.74 The authors recommended serial examination rather than repeat abdominal CT to diagnose children with blunt intestinal injury after initial nondiagnostic imaging studies. Fang et al. retrospectively reviewed 111 consecutive blunt trauma patients with bowel injuries from a single institution.75 Delays in surgery for more than 24 hours did not significantly increase the mortality compared with when operations were performed within 4 hours of injury. However, intestinal-related complications including sepsis, wound infection, anastomotic failures, and intra-abdominal abscess formation increased dramatically. Fakhry et al. published a multicenter experience in 198 patients with blunt small bowel injuries.76 There were 21 deaths (10.6% of total) with 9 of these deaths attributable to delay in operation for small bowel injury. In patients in whom small bowel injury was the major injury, the incidence of mortality increased with time to operative intervention. Mortality rates were 2% if the patient was operated on within 8 hours, 9.1% if operated on between 8 and 16 hours, 16.7% if operated on between 16 and 24 hours, and 30.8% if operated on more than 24 hours after injury (P  .009). The incidence of bowel-related complications, especially intra-abdominal abscess formation, also increased significantly with time to operative intervention. Based on the available literature it seems advisable to determine the need for operation within 8 hours of injury and anticipate complications should operative intervention occur at a later time. Bleeding complications after gastric or small bowel trauma may present as bleeding into the peritoneal cavity or into the bowel lumen. Bleeding from the short gastric vessels or from a torn splenic capsule is a common iatrogenic source of bleeding in this area. Bleeding from the mesentery or lesser curvature of the stomach may not be apparent intraoperatively in the hypotensive patient. This may only become clinically apparent when the patient normalizes his or her blood pressure; continued bleeding postoperatively then manifests as hypotension and a falling hematocrit.77 After the patient is resuscitated, it is necessary to reoperate. Suture line bleeding can be troublesome and may manifest as bloody nasogastric secretions. Endoscopic hemostatic techniques may be carefully employed in this setting, particularly if the bleeding is from the stomach. Anastomotic leak following repair of gastric and small bowel injury can lead to significant morbidity and mortality. The definition of anastomotic leak is variable in both emergency and elective gastrointestinal reviews on the topic.78 These studies suggest, however, that an anastomotic leak occurs much later than previously thought. Anastomotic failure may present as a contained leak, diffuse peritonitis, or a gastrocutaneous or enterocutaneous fistula (ECF). Risk factors for breakdown of intestinal repair include resection and anastomosis rather than repair, massive perioperative blood and fluid administration, associated pancreatic injuries, and the development of the abdominal compartment syndrome.

Stomach and Small Bowel techniques to facilitate “early” fascial closure. Absorbable mesh materials and human acellular dermal materials (HADM) or other non-cross-linked biological materials may also be used to facilitate early abdominal closure.56 However, prolonged use of vacuum-assisted closure (VAC) of abdominal wounds and absorbable mesh materials may also contribute to the development of an EAF.80 A single institution review of the development of an ECF in the era of open abdomen management was published by Fischer et al.82 The overall incidence of ECF following trauma laparotomy was 1.9%. Patients with open abdomen had a higher ECF incidence (8% vs. 0.5%) and a lower rate of spontaneous closure (37% vs. 43%). The development of an ECF initiates the requirement for a prolonged ICU and hospital length of stay as well as the need for a team of dedicated and experienced nurses, wound care therapists, and surgeons. There are three phases in the management of an ECF.80 Phase 1 is the recognition of the fistula and patient stabilization. Initial clinical priorities include fluid and electrolyte imbalance, control of sepsis, nutrition, and wound care. The patient may present with enteric content coming from the wound or indolent sepsis and a leak eventually identified by imaging studies. External loss of intestinal fluids rich in electrolytes, minerals, and protein leads to fluid and electrolyte imbalances as well as eventual malnutrition. Identification of the fistula site and/or measurement of the electrolyte composition of the fistula effluent are sometimes helpful for fluid replacement (Table 31-4). However, in most cases, normal saline with 10–20 mEq of potassium is a suitable fluid to use for the initial intravenous fluid replacement. Patients with ECF may also develop significant calcium, magnesium, and phosphate deficits that should be corrected. Fistulas are classified as high output (500 mL per day), moderate output (200–500 mL per day), or low output (200 mL per day). This may be important to classify fistulas in this manner as it may allow anticipation of the method for nutritional support, and may be useful in predicting the likelihood of spontaneous closure and mortality.80 Control of sepsis may include image-guided or surgical drainage of intra-abdominal abscesses identified by CT. Empiric antibiotic should be started in septic patients and modified after relevant culture data are obtained. The presence of an ECF without clinical signs of sepsis does not warrant antibiotic therapy. The provision of adequate nutritional support is critical in the stabilization phase. Total parental nutrition has long been

TABLE 31-4 Composition and Volume of Gastrointestinal Secretions Type Salivary Stomach Duodenum Ileum Pancreas Bile

Volume (mL Per Day)

Na (mEq/L)

K (mEq/L)

Cl (mEq/L)

HCO3 (mEq/L)

1,500 1,500 2,000 3,000 800 800

10 60–100 130 140 140 145

26 10 5 5 5 5

15 100 90 100 75 100

50 0 0–10 15–30 70–115 15–35

CHAPTER CHAPTER 31 X

In patients with enteric injuries and managed with open abdomen technique, failure to obtain fascial closure after postinjury day 5 was found to increase leak rate in the Western Trauma Association multi-institutional study.57,79 Additional factors include evidence for ongoing hypoperfusion and the use of vasopressors during the initial resuscitation and in the early postinjury ICU management. CT is the best diagnostic imaging study to identify anastomotic leaks that are not clinically obvious. Therapeutic options include medical care only if there is a tiny radiographically evident but clinically insignificant leak. Reoperation is necessary with primary repair and drainage for a small leak discovered early postoperatively if there is minimal peritonitis in the otherwise stable patient. Percutaneous drainage is useful for a symptomatic leak presenting in a delayed fashion as an intraabdominal abscess. If there is complete disruption of an anastomosis with widespread peritoneal contamination, it is advisable to consider a proximal diverting enterostomy. Anastomotic leaks diagnosed in the immediate postoperative period may be surgically approached as the relevant tissue planes are amenable to surgical dissection. After 10 or 14 days, the inflammatory process makes dissection of bowel extremely difficult. In this case proximal diversion and/or controlled external drainage of the leak may be safer. An ECF is a dreaded complication following trauma laparotomy and may be the result of an anastomotic leak, missed injury, or complications with an open abdomen following a damage control laparotomy. An ECF developing with an open abdomen is referred to as an enteroatmospheric fistula (EAF) and is probably the most common type of ECF encountered by trauma surgeons.80,81 An EAF may result from anastomotic breakdown or de novo from exposed bowel in the open abdomen. Factors associated with the development of an EAF include deserolization and iatrogenic injury to the bowel in an open abdomen and dense granulation tissue with adhesion of bowel loops to the fascial rim or adjacent bowel loops.80 Excessive force on the bowel from coughing or even movement by the patient in this setting can lead to shearing of the bowel and bowel disruption. It is advisable to protect the bowel to avoid this complication. Measures include keeping omentum and/or nonadherent dressing materials over exposed bowel, gentle dressing changes by experienced caregivers, and aggressive attempts to obtain abdominal fascial closure as “early as possible.” Vacuum packs, vacuum-assisted wound management, and progressive closure with abdominal retention sutures are useful

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SECTION 3 X

recognized to be an important factor in the management of ECF. These patients are usually hypercatabolic and generally require 25–32 cal/kg per day in total calories with a calorie to nitrogen ratio of 150:1 and a protein intake of at least 1.5 g/kg per day. Attempts at enteral nutritional support may aggravate fluid and electrolyte imbalances in the early phase of ECF management. Adjuncts to control fistula drainage include nasogastric drainage, and acid suppression with H2-receptor antagonists or protein pump inhibitors. Fistula output can be reduced with somatostatin and octreotide. These agents reduce GI secretions and prolong transit times, thereby simplifying management of fistula output. However, no evidence exists that these agents increase spontaneous closure rates. Administration of somatostatin and its analog octreotide has been shown to have an inconsistent effect on fistula output and time to fistula closure. Furthermore, the use of these agents does not increase the rate of nonoperative closure of fistulas.83 If used, fistula output should be monitored before and after a trial with the use of these agents to determine efficacy. Protecting the integrity of the skin surrounding the fistulas will improve the quality of the surrounding tissues and decrease infectious complications. Low-output fistulas are usually managed with conventional measures. High-output fistulas or fistula(s) in the patient with an open abdomen may benefit by the use of the VAC system. These may be applied over the entire wound with the fistula or as a VAC dressing with openings for stoma pouches of the fistula openings.84,85 The main benefit of the use of the VAC system for ECF appears to be improved wound care before definitive surgery (Fig. 31-13). The second phase involves anatomic definition of the fistula. CT and/or fistulogram help define the anatomic details and any associated pathology that guide further interventions. Nutrition is continued by the parenteral route with attempts at the use of the enteral route. It is likely that at least 4 ft of functioning small bowel between the ligament of Treitz and the fistula is necessary for significant absorption of even low-residue formulas. However, recent reports have advocated that the provision of at least some of the caloric requirement should be by the enteral route. This may be helpful for “trophic” effects of enteral feedings on the intestine and, if tolerated, allow easier management in the outpatient setting. In patients with diversion of the proximal small bowel as an ostomy, reinfusion of the succus entericus into the distal GI tract may be helpful as well.86 Spontaneous closure of ECFs in patients provided adequate nutritional support and free of sepsis usually occurs within 4–6 weeks. Unfortunately spontaneous closure occurs only in about 30% of trauma patients.82 Definitive surgery (phase 3) in a patient with a persistent ECF is usually delayed 4–6 months following the initial operation. Failure to obtain spontaneous closure should not be a primary factor in the timing of operative intervention. But rather nutritional and wound status, as well as the overall clinical condition, of the patient should be optimal before embarking on an often long and difficult surgical procedure. The procedure should include complete lysis of adhesions to eliminate the possibility

FIGURE 31-13 Fistula VAC: the use of a VAC sponge is a valuable method for management of enteroatmospheric fistula. The VAC sponge is applied with polyurethane drape and negative pressure. The ostomy bag is adherent to the VAC drape collecting the enteric contents. (Reproduced with permission from Goverman J, Yelon JA, Platz JJ, Singson RC, Turcinovic M. The ‘fistula VAC,’ a technique for management of enterocutaneous fistulae arising within the open abdomen: report of 5 cases. J Trauma. 2006;60(2):428–431. Copyright © Wolters Kluwer Health.)

of distal obstruction as a contributing factor for the failure of spontaneous closure. Options include resection and reanastomoses of the involved bowel segments or oversewing or wedge resection of the fistula. Recurrence of an ECF is related to the method of surgical closure. In a study by Lynch et al., oversewing or wedge resection of the ECF was associated with 36% recurrence rate, while resection with reanastomoses had a 16% recurrence rate.87 After resection of the fistula and reestablishment of GI continuity, attention is then directed to closure of the abdominal wound. Closure with autologous tissue, often requiring a compound separation technique, is optimal.88 The use of HADM or a non-cross-linked biological material is a second option if closure with autologous tissue is not practical89 (Fig. 31-14). Absorbable mesh closure and acceptance of a later incisional hernia is another viable option. The use of other prosthetic materials, including cross-linked biological materials, is ill-advised due to concerns for the breakdown of intestinal anastomotic repair or the development of a de novo intestinal fistula.90,91

Stomach and Small Bowel

Ileostomy

A

B FIGURE 31-14 An enterocutaneous fistula that fails to close spontaneously should be managed operatively when the nutritional and wound statuses are optional (A). Closure with non-cross-linked biological materials may be used when autologous tissue is not available (B).

Small bowel obstruction (SBO) is a well-known complication following abdominal operation. Patients with nontherapeutic laparotomies for trauma had a 2.4% incidence of SBO in a report by Renz and Feliciano.92 The rate is higher if operative repair is required and may be up to 7.4% in patients with penetrating abdominal trauma and 10.8% in patients with small or large bowel injuries.93 However, trauma laparotomy

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Small bowel fistula

does not appear to have added risk versus that reported following elective colorectal and general surgery on the development of early SBO and need for operative management. CT imaging has superior sensitivity and specificity, compared with plain radiographs for making the diagnosis of mechanical SBO.94 The identification of a transition zone and “small bowel feces sign” on CT make the diagnosis of mechanical SBO more certain.94,95 However, the presence of radiographic transition zones does not increase the likelihood of need for operative intervention.96 CT findings suggestive of bowel ischemia include decreased bowel wall enhancement, mucal thickening, congestion of mesenteric veins, or ischemia. However, these findings could not discriminate between patients with strangulated and those with nonstrangulated SBO in a report by Rocha et al.94 The absence of these findings may be helpful in deciding on a course of conservative management for at least 10–14 days following initial laparotomy. Various clinicoradiological scores have been proposed to predict the risk for strangulated SBO.96,97 Fortunately, early postoperative SBO often resolves spontaneously. Thus, it may be initially treated expectantly with only a small risk of bowel strangulation.98 In patients reoperated for postoperative bowel obstruction or in patients who later require elective reestablishment of GI continuity, it may be prudent to attempt to minimize adhesion formation. A hyaluronic acid and carboxymethylcelloluse (HA/CMC) bioresorbable membrane (S) is the most common antiadhesive barrier used in general surgery. It is applied to potentially adhesiogenic tissues before closure of the abdomen. It adheres to moist tissue surfaces and is cleared from the body within 28 days of implantation. Initial clinical studies were promising. A multicenter trial by Fazio et al. compared HA/CMC application with no treatment in 1,701 patients who underwent intestinal resections.99 Although the overall bowel obstruction rate was unchanged, there was a significant reduction in the number of patients requiring reoperation for bowel obstruction. A more recent Cochrane systemic review of intraperitoneal agents for preventing adhesions and adhesive intestinal obstruction included six randomized trials involving the use of HA/ CMC.100 Although the use of HA/CMC reduced the incidence of adhesions, there was no reduction of intestinal obstruction needing surgical intervention. Resection of significant amounts of small bowel may lead to problems with malabsorption. In general, jejunal resections are better tolerated than ileal resections. Removal of significant portions of the jejunum may lead to lactose intolerance; however, this is usually self-limited. Resection of the distal ileum often leads to vitamin B12 deficiency as well as bile salt deficiencies, and subsequent fat malabsorption. Ileal resection also removes the “ileal breaking mechanism” that may cause decreased transit time throughout the gut. This may result in profuse diarrhea and significant fluid and electrolyte imbalances. The ileocecal valve also has an important role as it acts to decrease the volume of stool by slowing intestinal transit time. The short bowel syndrome may result from traumatic injury to the intestine and/or its blood supply. In a series of 196 adult

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patients evaluated at a single institution over 23 years, 8% of short bowel syndrome cases were secondary to traumatic injury.101 Eighty percent of trauma-related short bowel syndrome was due to mesenteric injuries. Clinical manifestations include malabsorption, diarrhea, steatorrhea, fluid and electrolyte disturbances, and malnutrition. Late complications include cholelithiasis and renal oxalate stones. Although resection of up to 100 cm of ileum causes diarrhea, short bowel syndrome is fully manifest when the remaining jejunum and ileum is less than 200 cm in length. Plasma citrulline may be a useful biomarker to index small bowel enterocyte mass.102 Physiologic adaptation of patients with short bowel syndrome follows three phases.103 The acute phase occurs during the immediate postoperative weeks and may last 1–3 months. This phase is marked by poor absorption of almost all macronutrients and micronutrients. Ostomies, if present, may have outputs exceeding 5 L per day during the first few days. Aggressive intravenous fluid and electrolyte replacement is necessary to prevent life-threatening dehydration and electrolyte imbalances. Gastric hypersecretion is frequent in this phase and may be treated with proton pump inhibitors. Loperamide, codeine, or diphenoxylate, or even tincture of opium, is used to slow gastric and intestinal transit to control diarrhea. Careful monitoring of fluid and electrolytes, particularly potassium, magnesium, and calcium, is critical. Fluid needs can be monitored by urinary and fistula output, as well as by urinary sodium and osmolarity. The primary route of nutrition is parenteral; however, enteral feeding should be slowly initiated later in this phase.103 Adaptation occurs during the subacute phase and enhances bowel absorption. This adaptive process in humans occurs over a period of months to 1–2 years and is due to dilation of the remaining bowel coupled with improved cell transport function and prolonged intestinal transit time. Intestinal adaptation may be mediated by growth factors and nutrients including human growth hormone (HGH), insulin-like growth factor, epidermal growth factor, transforming growth factor , and glucagen-like peptide 2 (GLP-2).104 Nutrients including glutamine and fatty acids may also act as growth factors in intestinal adaptation. The maintenance phase is characterized by achievement of maximal absorptive capacity. The goal of this phase is to achieve nutritional and metabolic homeostasis by primarily oral feeding. Enteral feeding to provide intraluminal nutrients to maintain gut mass is necessary for the adaptation response to occur. Thus, enteral nutrition remains the primary therapy in maximizing luminal nutrient absorption in the intestinal remnant. In a recent study the use of growth hormone, glutamine, and nutrients to facilitate bowel adaptation led to a significant reduction in the number of TPN-dependent adults with short bowel syndrome.105–107 The addition of GLP-2 may have a synergistic effect with HGH, glutamine, and optimal dietary management. A number of surgical techniques have been used in an attempt to slow transit time and/or increase functional bowel length. Most of these techniques have met with limited success and risk further bowel loss.108 Restoring the colonic remnant to the GI tract may be helpful as the colon takes on an absorptive

function by deriving energy from short-chain fatty acids and prolonging transit time, particularly if the ileocecal valve is intact. However, at least 3 ft of small intestine is required to prevent diarrhea and perianal complications. Surgical lengthening with the Bianchi procedure or serial transverse enteroplasty (STEP) may improve efficacy of enteral nutrition and reverse complications of TPN. The STEP is technically easier to perform than the Bianchi procedure. Both have been shown to improve absorption of nutrients by increasing the function of the remnant small bowel.108 Intestinal transplantation is reserved as a last alternative for patients unable to compensate and adapt following intestinal resection. It may also be offered to patients who require TPN to maintain body mass and have limited or no remaining venous access for parenteral nutrition, or parenteral nutrition– related liver disease. Trauma patients seem to have equivalent long-term survival rates as compared with nontrauma patients following intestinal transplantation.109 A multidisciplinary approach to the treatment of intestinal failure due to short bowel syndrome appears to be the best outcome for these patients.110

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CHAPTER 32

Duodenum and Pancreas Walter L. Biffl

INTRODUCTION Injuries to the pancreas and duodenum present a significant challenge, for a number of reasons. First, while the deep, central position of the pancreas and duodenum afford the organs some degree of protection, their retroperitoneal location confounds the clinical detection of injury. Second, the infrequency of these injuries has resulted in a lack of significant management experience among practicing trauma surgeons. Third, anatomic and physiologic factors contribute to a disturbingly high incidence of complications following injury; morbidity is exacerbated by delays in diagnosis and treatment. Consequently, trauma to the pancreas and duodenum is associated with relatively poor outcomes that have not improved significantly, despite advances in trauma and critical care management (see Tables 32-1 and 32-2).1–16

HISTORY Most early descriptions of duodenal and pancreatic injuries are isolated autopsy observations. The first acknowledged literature report of pancreatic trauma was published by Travers in 1827. By 1903, von Mikulicz-Radeck reported only 45 cases in the literature.17 Of note, 72% of operated patients survived, a success rate that rivals modern-day results. Many of the recommendations suggested in that early series still hold true today: thorough abdominal exploration, hemostasis, and drainage. A paucity of reports of injuries to the pancreas have emanated from wartime experiences. The first series of five patients from the American Civil War included one survivor, and a similar experience was described after World War I. World War II annals include 62 cases of pancreatic trauma, but only nine were reported from the Korean War. Although much sentinel work in trauma was done during the Vietnam War, virtually no reports of pancreatic or duodenal injuries are available except for a single report of two cases of pancreaticoduodenectomy.18

The first successful surgical repair of a duodenal rupture was published by Herczel in 1896. In 1904, Summers19 cautioned about the difficulty in diagnosis of a retroperitoneal perforation of the duodenum from a gunshot wound, and may have been the first to describe the potential application of the pyloric exclusion procedure. The earliest reported series of traumatic duodenal ruptures was that of Berry and Giuseppi20 from 10 London hospitals. There were 29 patients with duodenal injuries, all of whom died. In fact, the authors cited only one known survivor of duodenal trauma to that point in time. Cave, in a World War II experience, recorded 118 cases of duodenal injuries with a mortality of 57%, which is still the single largest military series of duodenal injuries.21

■ Recent Historical Trends Pancreatic and duodenal trauma remain uncommon, and no single institution has extensive experience. Trauma centers such as Ben Taub, Grady Memorial, UT-Southwestern, L.A. County, Detroit Receiving, Memphis, and Denver General Hospital saw only 10–20 duodenal and 10–20 pancreatic injuries per year in the 1960s–1980s.1–3,5,7–10,12,22,23 Recent series document incidences of 0.2–0.3% for duodenal injuries and 0.004–0.6% for pancreatic injuries.7,15,24,25 Duodenal or pancreatic injuries are found in 3–6% of patients undergoing laparotomy for trauma.7,26 The risk of pancreatic or duodenal injury is much higher in penetrating compared with blunt trauma, as suggested by the data in Tables 32-1 and 32-2.1–16,27 However, the most recent series have documented a reversal of this trend, consistent with decreasing urban violence over the past 15 years. The Harborview Hospital experience is comprised of 71% blunt trauma patients,15 and a recent survey of Level I Trauma Centers in New England found that 91% of pancreaticoduodenal injuries were caused by blunt trauma.16 The anatomic location of the pancreatic-duodenal axis, and its proximity to other vital structures, makes isolated injuries

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TABLE 32-1 Duodenal Trauma: Mortality by Mechanism of Injury in Large Series (100 Patients)

SECTION 3 X

Series Houston 19771 Atlanta 19792 Dallas 19803 New York 19854 Los Angeles 19875 WTA 19906 Detroit 20047 Overall

Total Patients (% Penetrating) 175 (87) 321 (92) 247 (78) 100 (100) 115 (82)b

Stab Wound Died/Total (%) 2/18 (11) 0/31 (0) 0/23 (0)a 5/30 (17) 0/42 (0)b

Gunshot Died/Total (%) 16/134 (12) 37/263 (14) 18/157 (11)a 20/70 (29) 4/52 (8)b

Penetrating Died/Total (%) 18/152 (12) 37/294 (13) 31/193 (16) 25/100 (25) 4/94 (4)b

Blunt Died/ Total (%) 6/23 (26) 4/27 (15) 12/54 (22) — 0/11 (0)b

Overall Died/Total (%) 24/175 (14) 41/321 (13) 43/247 (17) 25/100 (25) 14/115 (12)

164 (62) 222 (88) 1344 (85)

2/31 (6) 8/34 (24) 17/209 (8)

22/71 (31) 38/162 (23) 155/909 (17)

24/102 (24) 46/196 (23) 185/1131(16)a,b

6/62 (10) 4/26 (15) 32/203 (16)

30/164 (18) 50/222 (23) 227/1344 (17)

a

13 early deaths were due to penetrating trauma, but stab versus gunshot wound was not described. 10 patients died within 48 hours, and mechanism was not reported. Mortality figures for stab and gunshot reflect only delayed (48 hour) mortality. b

distinctly uncommon (Figs. 32-1 and 32-2). In virtually every large series, over 90% of pancreatic and duodenal injuries are associated with injuries to other organs.1–3,5–9,12,13,27 The common associated injuries and their frequencies are listed in Tables 32-3 and 32-4. On average, there are 2.5–4.6 associated injuries with each pancreatic or duodenal injury.7,27 Not surprisingly, complication rates are higher when there are associated injuries, and the mortality rate increases progressively with each associated injury.16 Notably, the combination of pancreatic and duodenal injuries doubles the mortality rate compared with that of either injury alone (Table 32-5). A survey of several large series over the past three decades demonstrates that stab victims do better than gunshot victims;

however, there is a consistent mortality rate of 16–17% for both pancreatic and duodenal injuries, whether blunt or penetrating (Tables 32-1 and 32-2). This reported rate has not changed significantly over time, but there appears to be a trend toward lower mortality rates. Current experience, with the routine use of sensitive diagnostic modalities, identifies more lowgrade injuries that may have previously escaped detection. In the series from Seattle15 and New England,16 for example, three quarters of the patients had grade I or II injuries (see Grading). This could explain decreased overall morbidity and mortality rates. Three quarters of patients who die from a pancreatic or duodenal injury do so within the first 48 hours, from

TABLE 32-2 Pancreatic Trauma: Mortality by Mechanism of Injury in Large Series (100 Patients)

Series Houston 19788 Atlanta 19819 Dallas 198510 New York 199011 Memphis 199112 Durban 199513 Memphis 199714 Seattle 200315 Boston 200916 Overall a

Total Patients (% Penetrating) 448 (78) 283 (79) 500 (72) 103 (100) 131 (76) 152 (85) 134 (81) 193 (39) 230 (9) 2174 (75)

Stab Wound Gunshot Died/Total Died/Total Penetrating Blunt Died/ Overall Died/ (%) (%) Died/Total (%) Total (%) Total (%) 5/75 (7) 53/273 (19) 58/348 (17) 73/448 (16) 15/100 (15) 2/32 (6) 27/192 (14) 29/224 (13) 39/283 (14) 10/59 (17) 4/76 (5) 74/286 (26) 78/362 (22) 104/500 (21) 26/138 (19) 7/32 (22)a 20/71 (28)a 33/103 (32)a 33/103 (32)a — 31b 68b 16/99 (16) 21/131 (16) 5/32 (16) 20/129 (16) 25/152 (16) 5/66 (8) 15/63 (24) 5/23 (22) 108c 17/134 (13) ?c ?c 26c 24/193 (12) 29c 47c 76c 117c 27/230 (12) ?c ?c ?c ?c 23/281 (8) 189/885 (21) 234/1265 (18) 61/352 (17) 363/2174 (17)

6 patients died after 48 hours, but stab versus gunshot wound was not described. Penetrating mechanism was not specified. c Data were not specified. b

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©Baylor College of Medicine 1988

©Baylor College of Medicine 1986

A

B

FIGURE 32-1 Anatomic relation of the pancreas and duodenum, emphasizing the proximity of major associated structures. (A) Relation to adjacent organs. (B) Important vascular structures in close proximity to the pancreas and duodenum.

exsanguinating hemorrhage in the setting of multiple associated injuries or from devastating neurologic injury (Table 32-6). Thus, predictors of survival include age, overall injury severity, indices of shock, and severe brain injury, rather than pancreatic or duodenal injury grade.7,15,26 Late deaths in cases of pancreatic and duodenal trauma are most often ascribed to sepsis and multiple organ failure, often provoked by complications related to the original pancreatic or duodenal injury. This underscores the importance of early and prompt diagnosis. One quarter to one half of patients who survive initial operation can be expected to develop a complication.15,16 Among those patients with a delay in the initial diagnosis of pancreaticoduodenal injury, morbidity and mortality rates are considerably higher.15,16

Gall bladder 9% Right kidney 21% Liver 38% Renal vessels 5% Transverse colon 30% Ureter 8%

ANATOMY AND PHYSIOLOGY The duodenum and pancreas are intimately associated with many vital structures in a deep and narrow region (Figs. 32-1 and 32-2). The name duodenum is derived from duodenum digitorum (“space of 12 digits”), from the Latin duodeni (“12 each”)— so named by Greek physician Herophilus for its length, approximately 12 finger-breadths. It extends about 30 cm, from the pyloric ring to the ligament of Treitz. Classically the duodenum is divided into four portions: superior or first, descending or second, transverse or third, and ascending or fourth portion. The first portion of the duodenum extends from the pylorus to the common bile duct (CBD)

Aorta 5% Vena cava 17% Common bile duct 5% Stomach 24% Pancreas 28% Small bowel 29% Superior mesenteric vessels 7%

Miscellaneous 17%

FIGURE 32-2 Drawing showing the incidence of injuries to nearby organs and vessels in patients with duodenal wounds. ( Reproduced with permission from Morton JR, Jordan GL Jr: Traumatic duodenal injuries: Review of 131 cases. J Trauma 8:127, 1968.)

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SECTION 3 X

TABLE 32-3 Associated Injuries in 1,234 Cases of Duodenal Trauma

TABLE 32-4 Associated Injuries in 1,086 Cases of Pancreatic Trauma

Organ Injury Major vascular Liver Colon Pancreas Small bowel Stomach Kidney Gallbladder/biliary tree Spleen

Organ Injury Liver Stomach Major vascular Spleen Kidney Colon Duodenum Small bowel Gallbladder/biliary tree

Patients (%) 596 (48) 543 (44) 378 (31) 368 (30) 363 (29) 279 (23) 237 (19) 176 (14) 41 (3)

Based on combined data from references 1–3, 5–7.

and gastroduodenal artery. The second portion extends from that point to the ampulla of Vater. The third portion extends from the ampulla of Vater to the superior mesenteric artery (SMA) and vein (SMV), which emerge from posterior to the pancreas and descend anteriorly over the duodenum. The fourth portion extends from the SMA and SMV to the point where the duodenum emerges from the retroperitoneum to join the jejunum, just to the left of the second lumbar vertebra, at the ligament of Treitz. Thus, the duodenum is almost entirely a retroperitoneal structure, with the exception of the anterior half circumference of the first portion of the duodenum and the most distal part of the fourth portion of the duodenum. The first portion, distal region of the third portion, and the fourth portion of the duodenum lie directly over the vertebral column. The psoas muscles, aorta, inferior vena cava, and right kidney complete the posterior boundaries of the duodenum. The liver and gallbladder overlie the first and second portions of the duodenum anteriorly; the second and third are bounded by the hepatic flexure and right transverse colon, and the fourth portion lies beneath the transverse colon, mesocolon, and stomach. The head of the pancreas is intimately associated within the C loop, or second portion. The pancreas is divided into the head, contained within the duodenal C-loop; the neck, which is the narrowest portion and overlies the SMA and SMV; the body, which is rather triangular

Patients (%) 500 (46) 449 (41) 300 (28) 277 (26) 240 (22) 189 (17) 173 (16) 165 (15) 46 (4)

Based on combined data from references 8,9,12,13,27.

in cross section and which extends to the left across the vertebral column; and the tail, which extends into the splenic hilum. In blunt force trauma, the vertebral column may act as a fulcrum and the pancreas may be transected. The root of the transverse mesocolon crosses the head anteriorly. Posteriorly, the head is separated from the body by the pancreatic incisure, where the superior mesenteric vessels lie. A part of the head, the uncinate process, extends to the left behind the SAM and SMV. The body of the pancreas extends laterally. The base of the transverse mesocolon is attached at the anterior margin, and is covered with peritoneum and forms the posterior wall of the omental bursa. The inferior surface of the pancreas is covered with peritoneum from the posterior mesocolon. The body of the pancreas rests on the aorta. The tail of the pancreas lies in front of the left kidney, in intimate proximity to the splenic flexure of the colon, often abutting the spleen via the lienorenal ligament. The splenic artery runs along the upper border of the gland, often crossing in front of the tail. The splenic vein lies in a groove behind the body and tail, usually on the inferior edge of the pancreas. The blood supply of the pancreas and duodenum comes from the gastroduodenal, SMA, and splenic arteries. There are numerous collateral vessels throughout the pancreas that protects it from ischemia, but also contributes to vigorous bleeding following injury. The second portion of the duodenum has a

TABLE 32-5 Combined Pancreaticoduodenal Trauma: Mortality by Mechanism of Injury in Large Series (100 Patients)

Series Los Angeles 19875 Detroit 20047 Atlanta 19819 Dallas 198510 Boston 200916 Overall

Total Patients 115 222 283 500 230

Duodenum Alone Died/Total (%) 10/89 (11) 26/147 (18) — — 4/60 (7) 40/296 (14)

Pancreas Alone Died/Total (%) — — 22/228 (10) 75/409 (18) 14/132 (11) 111/769 (14)

Combined Pancreaticoduodenal Died/Total (%) 4/26 (15) 24/75 (32) 17/55 (31) 29/91 (32) 9/38 (24) 83/285 (29)

Duodenum and Pancreas

607

TABLE 32-6 Timing of Death Following Pancreatic or Duodenal Trauma

Overall

Total Patients 164 131 134 72 193 222

Deaths (%) 30 (18) 21 (16) 17 (13) 12 (17) 24 (12) 50 (23)

Early Deaths Due to Hemorrhage/CNS (%) 22 (73) 14 (67) 11 (65) 8 (67) 18 (75) 40 (80)

916

154 (17)

113 (73)

unique blood supply that originates from both the gastroduodenal artery and the inferior pancreatoduodenal artery, a branch of the SMA. Both of these vessels divide into anterior and posterior branches that are located on the edge of the head of the pancreas and anastomose with each other anteriorly and posteriorly. The second portion of the duodenum receives radial branches from these vessels that comprise its only blood supply. Because the pancreatoduodenal vessels are located on the surface of the head of the pancreas, portions may be resected without causing necrosis of the second portion of the duodenum. If all of the pancreatoduodenal vessels are injured by trauma, a pancreatoduodenectomy will be necessary. The body and tail of the pancreas receive collateral circulation from the SMA and splenic artery. The third portion of the duodenum receives its blood supply from the notoriously short mesentery of the SMA. Although the arterial and venous supply as described is relatively constant, variations do exist and should be kept in mind during surgical exploration in this region. Origin of the common hepatic artery (5%) and a replaced right hepatic artery (15–20%) from the SMA are among the most frequent anomalous findings. In other instances, the right hepatic may arise from the aorta, gastroduodenal, or even left hepatic artery. In 4% of the population, the entire common or proper hepatic artery is aberrant, arising from the SMA, aorta, or left gastric artery. In addition, if the bifurcation of the proper hepatic artery is low, the right hepatic may lie in front of the CBD or cross in front of it as well as the cystic duct. Surgeons dealing with injuries to the duodenum and pancreas should be particularly well versed with the anatomic positions of the pancreatic and CBDs. The CBD descends from above to behind the first part of the duodenum, continuing downward on the posterior surface of the head of the pancreas where it is overlapped by lobules of pancreas obscuring its identification. In this region, the CBD curves to the right, and joins with the main pancreatic duct of Wirsung prior to entering the posteromedial wall of the second part of the duodenum as the ampulla of Vater. The main pancreatic duct usually traverses the entire length of the gland and is located posteriorly slightly above a line halfway between the superior and inferior edges of the pancreas. The accessory duct of Santorini typically branches out from the main duct near the neck and empties separately into the duodenum about

Late Deaths Due to Sepsis/MOF/Other (%) 8 (27) 7 (33) 6 (35) 4 (33) 6 (25) 10 (20) 41 (27)

2.5 cm proximal to the duodenal papilla. The CBD and main pancreatic duct may rarely enter the duodenum through separate openings. This is important to recognize when attempting cholangiopancreatography via the gallbladder or CBD. Partially digested chyle from the stomach and the proteolytic and lipolytic secretions of the biliary tract and pancreas mix in the duodenum. The powerful digestive enzymes commonly found in this location include lipase, trypsin, amylase, elastase, and peptidases. Approximately 10 L of fluid from the stomach, bile duct, and pancreas passes through the duodenum in a day. Under normal conditions, the small intestine absorbs more than 80% of this fluid, but following injury, this high volume and enzymatically charged flow accounts for the disastrous consequences of a lateral duodenal fistula and associated derangements in water and electrolyte homeostasis. The duodenum has several key roles in vitamin and mineral absorption as well as food processing. Vitamin B12 malabsorption may result from extensive duodenal resection. R protein is hydrolyzed by pancreatic enzymes in the duodenum to allow free cobalamin (B12) to bind to gastric parietal cell-derived intrinsic factor. The duodenum is the main site for transcellular transport of calcium. A key step in transport is mediated by calbindin, a calcium binding protein produced by enterocytes. Regulation of calbindin synthesis appears to be the main mechanism facilitating vitamin D regulated calcium absorption. The pancreas consists of both endocrine and exocrine cells. The endocrine cells are distributed throughout the substance of the gland, and the α-, β-, and δ-islet cells produce glucagon, insulin, and gastrin, respectively. The secretion of insulin and glucagon are responsive to blood glucose levels. Islet cell concentration is thought to be greater in the tail than the body and head of the gland, although it is generally held that approximately 10% of the gland remaining after resection may maintain normal hormonal balance. Both duct and acinar cells of the pancreas secrete between 500 and 800 mL/day of clear, alkaline, isosmotic fluid. In addition, the acinar cells produce amylase, proteases, and lipases. Pancreatic amylase is secreted in its active form and serves to hydrolyze starch and glycogen to glucose, maltose, maltotriose, and dextrins. Proteolytic enzymes produced by these cells include trypsinogen, which is converted to trypsin in the duodenal mucosa by enterokinase. Pancreatic lipase is secreted in an active form and hydrolyzes

CHAPTER CHAPTER 32 X

Series WTA 19906 Memphis 199112 Memphis 199714 Cleveland 199727 Seattle 200315 Detroit 20047

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SECTION 3 X

triglycerides to monoglycerides and fatty acids. The acinar and duct cells also secrete the water and electrolytes found in pancreatic juice. Bicarbonate secretion is directly related to the rate of pancreatic secretion; chloride secretion varies inversely with bicarbonate secretion so that the sum total of both remains constant. The hormone secretin, released from the duodenal mucosa, is the major stimulant for bicarbonate secretion, and serves to buffer the acidic fluid entering the duodenum from the stomach. Both endocrine and exocrine pancreatic functions are interdependent. Somatostatin, pancreatic polypeptides, and glucagons are all believed to have a role in inhibition of exocrine secretion. When pancreatic exocrine function is reduced to less than 10%, diarrhea and steatorrhea develop.

■ Diagnosis The approach to patients with abdominal trauma begins with an initial evaluation as described in the American College of Surgeons Advanced Trauma Life Support (ATLS) course.28 Many pancreatic and duodenal injuries are the result of penetrating trauma, and the injury is usually discovered during exploratory laparotomy. The hemodynamically unstable patient requires little preoperative evaluation other than expeditious transport to the operating room. Prior to exploring patients with gunshot wounds, plain x-rays of the chest, abdomen, and pelvis should be obtained if possible; information regarding potential trajectory and involvement of more than one body cavity is invaluable. Blood typing is performed in anticipation of potential transfusion, and antibiotics are administered. It is critical that thorough exploration and examination of the pancreas and duodenum are performed during trauma laparotomy, particularly when there is retroperitoneal hematoma, bile staining, fat necrosis, or edema in the supramesocolic region. Intraoperative evaluation of the duodenum and head of the pancreas begins with full mobilization achieved by the Kocher maneuver to the midline with coincident mobilization and medial rotation of the hepatic flexure of the colon. This provides exposure of the anterior and posterior surfaces of the second and third portions of the duodenum as well as the head and uncinate process of the pancreas. The body and tail of the pancreas are examined by division of the gastrocolic ligament and reflection of the stomach cephalad. Insertion of a curved retractor in the lesser sac allows full inspection of the anterior surface of the pancreas from the head to tail and from superior to inferior surfaces. In cases of active hemorrhage in the region of the neck of the pancreas suspected to originate from the juncture of the portal vein behind the pancreas, the pancreas should be divided without hesitation. A stapling device will allow for rapid exposure of the injured vessel and hemorrhage control of the pancreas. Further exposure of the posterior surface of the pancreas is accomplished by division of the retroperitoneal attachments along the inferior border of the pancreas and retraction of the pancreas cephalad. Additional mobilization of the spleen and reflection of the spleen and tail of the pancreas from the left to the midline is a useful technique for further evaluation of the remaining areas of the pancreas. Most

injuries sustained in penetrating trauma will be discovered with direct exploration. But in many cases, the integrity of the pancreatic duct remains in question. In these situations, it is crucial to assess the status of the main pancreatic duct (see below). Diagnosis of blunt injuries in hemodynamically stable patients is more challenging. A common mechanism in both duodenal and pancreatic injuries is blunt force to the epigastrium. Patients may have persistent abdominal pain and tenderness, but these findings may be elusive in the presence of intoxication, shock, brain injury, and severe associated injuries. Leukocytosis, unexplained metabolic acidosis, or fever may herald an occult injury. The utility of serum amylase— and more recently, lipase—assays has been debated. In 1943, Naffziger and colleagues suggested that amylase was of diagnostic value in the evaluation of patients with blunt abdominal trauma.29 Unfortunately, subsequent reports highlighted the poor sensitivity and specificity of the test. Bouwman et al.29 evaluated isoenzymes of amylase, with the same disappointing conclusion. Takishima et al.30 found that if the amylase level was measured more than 3 hours after trauma, it was most likely to reflect pancreatic injury. In sum, amylase levels should not be relied upon to either diagnose or exclude pancreatic injury. In a patient with persistent epigastric pain after blunt abdominal trauma, hyperamylasemia should prompt further diagnostic evaluation. On the other hand, a normal value in that setting may not be sufficient to avoid further work-up. Plain x-rays are of limited use in the diagnosis of blunt pancreatic or duodenal injuries. The Focused Abdominal Sonography for Trauma (FAST) is accurate in identifying hemoperitoneum, and is thus a useful tool to allow prompt transfer of unstable patients to the operating room, or to select stable patients for further evaluation. However, FAST does not evaluate the retroperitoneum reliably. Recently, contrastenhanced ultrasound has been reported to detect some pancreatic injuries.31 However, its role is poorly defined at this time. Diagnostic peritoneal lavage is not considered reliable for evaluation of the retroperitoneum, so it plays a limited role in diagnosing pancreaticoduodenal trauma. In the stable patient with suspicion of intraabdominal injury, computed tomography (CT) scanning is the primary diagnostic modality. Signs of duodenal perforation include free air and contrast extravasation. More subtle findings, such as edema, hematoma, or thickening of the bowel wall; surrounding fluid, hematoma, or fat stranding in the retroperitoneum; or intramural gas, should raise suspicion of duodenal injury (Fig. 32-3). It is critical to differentiate perforation from contusion or wall hematoma, as the former mandates laparotomy but the latter may be managed nonoperatively. Duodenography has been employed to help clarify the presence of perforation; however, its sensitivity is poor (54%) and thus it should not be considered an adjunct to CT.32 There are no specific data about the sensitivity and specificity of multidetector CT (MDCT), but accumulating experience suggests superior imaging with proper protocols.33 Equivocal studies may require repeat CT scanning with contrast in the duodenum. If there is any question, the most conservative approach is operative exploration to definitive diagnose or exclude injury, as delay in diagnosis is associated with morbidity.34

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FIGURE 32-3 Computed tomography (CT) finding of retroperitoneal duodenal perforation. CT scan shows poor definition of the structures in the region of the head of the pancreas (curved arrow) and diminished enhancement of the head compared to the body. A collection of extraluminal, retroperitoneal gas (straight arrow) lies immediately posterior to the second portion of the duodenum (d), consistent with a duodenal perforation. This patient is also depicted in Fig. 32-4. (Reproduced with permission from Smith DR, Stanley RJ, Rue LW III: Delayed diagnosis of pancreatic transection after blunt abdominal trauma. J Trauma 40:1009, 1996.)

The CT findings of pancreatic injury may be subtle, particularly when the imaging is performed within 12 hours of injury (Fig. 32-4). Specific signs of injury include fractures or lacerations of the pancreas (Fig. 32-5); active hemorrhage from the gland or blood between the pancreas and splenic vein; and edema or hematoma of the parenchyma.33 Contusions may

FIGURE 32-4 Computed tomography scan of pancreas, demonstrating subtle early signs of injury, including irregularity of the neck of the pancreas (arrow), peripancreatic fluid, and intrahepatic hematoma (H). (Reproduced with permission from Smith DR, Stanley RJ, Rue LW III: Delayed diagnosis of pancreatic transection after blunt abdominal trauma. J Trauma 40:1009, 1996.)

FIGURE 32-5 CT scan of pancreas, demonstrating midbody transection from a direct epigastric blow.

escape detection. The reported sensitivity and specificity of CT for pancreatic injuries is in the 80% range, but these data were based on earlier-generation scanners.33,35 It is believed that MDCT will improve on this. However, a recent American Association for the Surgery of Trauma (AAST) multicenter study looked at the accuracy of 16- and 64-detector row CT for detecting pancreatic injury in general, and pancreatic ductal injury specifically. Although specificity was better than 90%, the sensitivity of MDCT for either injury was only 47–60%.36 Ultimately, the accuracy of CT is dependent on not just the technology, but also the technique, the timing after injury, and the skills of the interpreting clinician. In the face of a normal initial CT, if a pancreatic injury is clinically suspected, CT should be repeated. The integrity of the main pancreatic duct is the most important determinant of prognosis, as most major morbidity is related to ductal disruption. Consequently, management is dependent on the status of the duct. As noted, CT scanning— even with MDCT—is not reliable for identifying ductal disruption. Evaluation of the duct can be accomplished in stable patients via endoscopic retrograde cholangiopancreatography (ERCP).37,38 This technique is particularly valuable in the trauma patient in whom there may be subtle changes on CT, and chemical evidence of pancreatitis but without overt clinical findings mandating laparotomy. In such cases, observation may be justified if a duct disruption can be excluded. An alternative technique that may be useful in a stable patient is magnetic resonance cholangiopancreatography (MRCP).39 Advantages of MRCP include its noninvasiveness and the ability to visualize not only the duct, but the pancreatic parenchyma and remainder of the abdomen.35 Delineation of ductal anatomy may be further enhanced by the administration of secretin, which increases pancreatic exocrine output and distends the pancreatic duct.40 Currently there are few series reporting the accuracy of MRCP, and it has not been prospectively compared with ERCP. However, it is considered an appropriate next step in evaluating a pancreatic duct whose integrity is questioned after CT scanning.

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SECTION 3 X FIGURE 32-7 Intraoperative cholangiogram obtained via duodenotomy and direct cannulation of the ampulla. Overly forceful injection resulted in contrast extravasation into the pancreatic head. Also note a distal pancreatic duct injury with contrast extravasation near the laparotomy pad marker. FIGURE 32-6 Intraoperative cholangiopancreatogram obtained via the gallbladder. Complete pancreatogram is obtained, depicting proximal pancreatic duct injury and extravasation of contrast.

Patients who are unstable, or who have pancreatic injury first diagnosed in the operating room, may require intraoperative pancreatography to assess the duct. Although intraoperative ERCP is an option, it may be difficult to mobilize a gastroenterology team rapidly, and the requisite bowel insufflation can interfere with abdominal closure. Alternatively, pancreatography may be performed by the surgeon.41 The simplest approach is to clamp the common hepatic duct and infuse contrast into the gallbladder for cholangiopancreatography (Fig. 32-6). If imaging is inadequate, a duodenotomy is then performed for identification and cannulation of the ampulla of Vater. A blunt-tipped probe can be passed, which may confirm the diagnosis of ductal disruption. If not, pancreatography is performed with 2–3 mL of water soluble contrast material under very low pressure with fluoroscopic imaging (Fig. 32-7). Some have recommended intraoperative pancreatography via transecting the tail of the pancreas and cannulation of the distal duct (Fig. 32-8). This technique has had inconsistent results; hence, transecting the pancreas to perform these evaluations appears ill-advised.

■ Grades I and II Duodenal intramural hematomas may be identified at the time of exploration, but are more often detected on CT scanning (Fig. 32-10). The clinical course is marked by progressive gastric outlet obstruction with or without bilious emesis. The lesion is more common in children, and there is a high frequency of nonaccidental trauma.43 Obstruction develops as fluid is sequestered into a hyperosmotic hematoma. If there are no other indications for laparotomy, treatment generally consists of IV hydration, parenteral nutrition, and nasogastric tube suction.44 Most duodenal hematomas will resolve spontaneously within 3 weeks. For patients who continue to manifest complete obstruction after 7–10 days, repeat CT scan should

■ Decision Making and Treatment Options Duodenum Treatment and decision making is perhaps best reviewed in light of injury severity. The classification system most commonly used for injury stratification is the AAST Organ Injury Scale (OIS) (Table 32-7 and Fig. 32-9).42 Injuries are graded on a I–V scale in ascending order of severity. Of note, this scale adds associated pancreatic injury as a major morbidity cofactor in duodenal injury.

FIGURE 32-8 Intraoperative proximal pancreatogram obtained via an injured mid-body pancreatic duct. Normal residual proximal duct is confirmed prior to performing distal pancreatectomy.

Duodenum and Pancreas

TABLE 32-7 AAST Duodenum Organ Injury Scale Hematoma

III

Laceration Hematoma Laceration Laceration

IV

Laceration

V

Laceration

II

Vascular

Injury Description Involving single portion of duodenum Partial thickness, no perforation Involving more than one portion Disruption 50% of circumference Disruption 50–75% circumference of D2 Disruption 50–100% circumference of D1, D3, D4 Disruption 75% circumference of D2 Involving ampulla or distal common bile duct Massive disruption of duodenopancreatic complex Devascularization of duodenum

Adapted from Moore EE, Cogbill TH, Malangoni MA, et al. Organ injury scaling II: Pancreas, duodenum, small bowel, colon, and rectum. J Trauma. 1990;30:1427–1429.42

be done to reevaluate the obstructive process, and operative management should be considered.45 Operative approaches for evacuation of the hematoma include open or laparoscopic drainage procedures. At exploration, the pancreas and duodenum must be thoroughly mobilized and examined. Duodenal

Patient has Urgent Indications for Laparotomy

Patient Requires Workup For Injury Assessment

• Hemodynamic Instability (+) Ultrasound • Peritonitis (+) CT (Free Air, Extravasation)

• CT with Suggestive Findings • Contrast Duodenography

Laparotomy Duodenal Hematoma

NG Suction TPN ? Late Decompression Grade I & II 1. Duodenal Hematoma • Small – observe • Med – NCJ • Large – Duodenotomy & Evacuation, NCJ 2. Laceration • Single Layer Repair, NCJ

Grade III

1. Primary Repair & Pyloric Exclusion & NCJ 2. Roux-en Y Jejunoduodenostomy

FIGURE 32-9 Algorithm I. Algorithm for duodenum injury.

Ascertain Ampulla Status

Grade IV & V • Damage Control Surgery • Reassess (? Whipple)

CHAPTER CHAPTER 32 X

Grade I

stricture or occult perforation or unsuspected injury to the head of the pancreas should be sought. Injuries can range from serosal staining to obstructing masses. Treatment is somewhat controversial. Opening of the hematoma at the time of initial operation is condoned by some authors, who favor tube decompression of the stomach and distal tube jejunostomy for postoperative enteral nutrition while the hematoma resolves. With patience, almost all hematomas resolve in this setting, and opening of the duodenum risks conversion of a closed to open injury. Our group favors a selective approach. We treat small hematomas with minimal luminal compromise with nasogastric suction and distal feeding tube jejunostomy, reserving incision and evacuation for larger hematomas with mass effect and luminal compromise (50%). In such situations, we perform meticulous hemostasis with closure of duodenum with running absorbable closure. Approximately 75% of duodenal lacerations occur as a result of penetrating trauma (Table 32-1). Exploratory laparotomy is performed via a midline incision. As described previously, standard trauma principles are employed for control of hemorrhage and enteric leaks. Exposure of the pancreas and duodenum is initiated with performance of the Kocher maneuver, which allows for evaluation of the head of the pancreas as well as the C-loop. The distal CBD and third portion of the duodenum are exposed by dissection of the overlying peritoneal attachments and fascia. By detaching the hepatic flexure of the colon from the second portion of the duodenum, evaluation of potential injury to the mesenteric vessels may be assessed. Full medial rotation of the right colon, cecum, and terminal ileum will allow complete evaluation of associated hepatic or vascular

611

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SECTION 3 X A

B

FIGURE 32-10 Diagnosing duodenal hematoma in a 30-year-old male. (A) Upper gastrointestinal radiograph showing narrowing of the second and third portions of the duodenum. (B) Computed tomography scan in the same patient, showing a giant hematoma of the transverse portion of the duodenum.

injuries in the right upper and middle abdomen. Incision in the right side of the root of the transverse colon will allow reflection of the small bowel superiorly for further exposure of the third part of the duodenum. After evaluation of the head of the pancreas, the neck, body, and tail are examined by opening the gastrocolic omentum from the left to the right. Adhesions to the stomach are taken down and the inferior border of the pancreas is visualized by incising the anterior reflection of the transverse mesocolon. Any evidence of blood, bile, or air in the retroperitoneum requires thorough exploration. Simple duodenal lacerations with limited injury or minimal tissue destruction often result from either stab wounds or small caliber gunshot wounds. The vast majority can be safely repaired primarily with a meticulous single layer closure if adequate blood supply is ensured.6 Duodenotomies can be repaired with running or interrupted sutures; a monofilament repair is preferred. Avoidance of tension is paramount. Repair in the direction in which the injury is formed is generally recommended. Although earlier reports advocated transverse repair of select longitudinal injuries to minimize luminal compromise, current use of single layer monofilament closure has eliminated this concern in most cases.46 In rare situations of laceration to the pancreatic side of the duodenum, mobilization may not be possible for repair. In such situations, an antimesenteric duodenotomy may be performed, with repair of the injury from the inside.

■ Grade III Some grade III lacerations may be repaired by simple duodenorrhaphy. Snyder et al.3 identified severity factors that were associated with morbidity and mortality, and often preclude primary duodenorrhaphy; blunt trauma or gunshot wound; involvement of 75% of the duodenal wall; injury in D1 or D2; an interval

from injury to repair 24 hours; and CBD injury. In those that are judged too extensive for primary repair after mobilization and debridement, other options must be considered. If a segment is removed and the ends can be mobilized without tension, end-to-end duodenoduodenostomy may be performed. Such a repair is rarely feasible in the second portion of the duodenum due to the intimate attachments to the pancreas and thus difficulty with mobilization. In this area, careful identification of the ampulla of Vater is essential to avoid injury at the time of repair. Injuries to the second portion of the duodenum distal to the ampulla can be repaired with division of the duodenum and end-to-end duodenojejunostomy using a Roux-en-y limb of jejunum passed through the transverse mesocolon. In these situations, the distal duodenal stump is oversewn and a distal jejunojejunostomy is created for intestinal continuity (Fig. 32-11). In the setting of extensive tissue loss but without the need for resection, the duodenum may be similarly reconstructed with a Roux-en-y duodenojejunostomy. Although jejunal mucosal patches and interposition grafts based on a vascular pedicle of the jejunal mesentery have been described, they are rarely used. Repair of injuries to the third and fourth portion of the duodenum may be compromised by the short mesentery, causing difficulty in mobilization and leading to ischemia. Resection and duodenoduodenal anastomosis in this setting is associated with a high rate of fistula formation. This is another role for resection and duodenojejunostomy. When confronted with a patient with an intermediate grade duodenal injury and associated pancreatic injury, the pyloric exclusion procedure as described by Vaughan et al.1 has been preferred (Fig. 32-12). This procedure is simpler than the original “diverticulization” technique described by Berne et al.47 The duodenal injury is repaired and is “protected” by gastric diversion. To accomplish this, a gastrotomy is created along the greater curve of the stomach adjacent to

Duodenum and Pancreas

■ Grades IV and V These injuries involve massive disruption or devascularization of the second portion of the duodenum with avulsion of the ampulla of Vater or distal CBD (grade IV) or massive disruption of the pancreaticoduodenal complex (grade V). In general, these injuries are caused by blunt trauma or large caliber/highvelocity gunshot wounds, and are associated with other significant injuries. In the face of significant hemorrhage, acidosis, hypothermia, and coagulopathy, a damage control approach is indicated. This entails hemostasis, debridement, and drainage, with subsequent definitive operative management after physiologic derangements are corrected.55 FIGURE 32-11 Roux-en-Y duodenojejunostomy is used to treat duodenal injuries between the papilla of Vater and superior mesenteric vessel when tissue loss precludes primary repair. (Reproduced with permission from Brunicardi FC et al. Schwartz’s Principles of Surgery, 8th ed. McGraw-Hill, Inc., 2005. Fig. 6-52, p. 168. © The McGraw-Hill Companies, Inc.)

the pylorus; the pylorus is oversewn from the inside with nonabsorbable monofilament suture; and a gastrojejunostomy is created with a loop of jejunum. A long jejunal limb should be used to prevent reflux of enteric contents to the duodenum. If a fistula develops, it is a functional end duodenal fistula, which is usually easier to manage than a higher output lateral fistula. A needle catheter jejunostomy is employed in this setting to ensure a route for enteral nutrition, and we have found this to be a safer method than standard jejunostomy.48,49 Even in the setting of an end fistula, the patient will often tolerate an oral diet after 10–14 days. The pylorus usually opens within 6–12 weeks; therefore, vagotomy is not usually performed. This procedure may also be employed as a protective adjunct for a tenuous duodenal repair. Other techniques that have been described include omental patch or jejunal patch with a loop of jejunum, although such procedures are unproven. As an alternative to pyloric exclusion and gastric diversion, Stone and Fabian2 advocated routine lateral tube duodenostomy or retrograde jejunostomy for decompression. However, this is no longer practiced. An interesting potential technique is bioprosthetic repair of complex duodenal defects. Primarily studied in preclinical models to date, there is a potential advantage of providing a durable repair more expediently.50 Although there are no randomized prospective studies to prove the benefit of any type of gastric diversion and drainage in severe injuries, several reports do support the use of

Pancreas The AAST OIS for pancreatic injury reflects the fact that the major determinant of morbidity following pancreatic trauma is the integrity of the main pancreatic duct (Table 32-8 and Fig. 32-13).42

■ Grades I and II With liberal application of sensitive MDCT imaging, many low-grade injuries are diagnosed in patients who have no other indications for laparotomy. Recognizing that most of the related morbidity is due to ductal disruption, nonoperative management has been suggested for low-grade injuries. This has been more widely practiced in children, with good results.56 There is not a great deal of literature in adults, but the approach appears safe. Duchesne et al.25 suggest that patients with apparent grade I or II injuries could be managed nonoperatively if ductal disruption is excluded by MRCP or ERCP. Of 35 patients managed in this way, 5 (14%) failed—three with pancreatic abscess, and 2 with missed bowel injuries. In the multicenter trial of New England trauma centers,16 69 (41%) of 170 patients with pancreatic or combined pancraticoduodenal injuries were managed nonoperatively, with 7 (10%) failing. The recurring themes in the reports of nonoperative management are that (a) it is safe to manage patients with grade I and grade II injuries nonoperatively; (b) it is important to exclude main pancreatic ductal disruption; and (c) main ductal disruptions may be best managed operatively, to avoid pancreatic duct-related complications (see below). More data are needed in this area. When grade I and grade II injuries are discovered intraoperatively, the vast majority can be treated with no more than surgical hemostasis and drainage.15,57 Even capsular tears that are not bleeding are not repaired and may be simply drained

CHAPTER CHAPTER 32 X

pyloric exclusion and gastrojejunostomy in selected cases, and particularly for intermediate- to high-grade duodenal injuries combined with pancreatic injuries.6,22,51,52 On the other hand, recent series have called the necessity of this adjunct into question, suggesting that patients may be managed safely with primary repair.53,54 Ultimately, the surgeon must exercise his or her judgment based on the patient’s overall condition and that of the duodenal tissue, and associated injuries.

613

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SECTION 3 X A

B

C FIGURE 32-12 (A) Pyloric exclusion is used to treat combined injuries of the duodenum and the head of the pancreas, as well as isolated duodenal injuries when the duodenal repair is less than optimal. (B) The pylorus is oversewn through a gastrotomy. The gastrotomy will subsequently be used to create a gastrojejunostomy. (C) These authors frequently employ needle-catheter jejunostomy tube feedings for these patients. (Reproduced with permission from Brunicardi FC, et al. Schwartz’s Principles of Surgery, 8th ed. McGraw-Hill, Inc., 2005. Fig. 6-53, p. 169. © The McGraw-Hill Companies, Inc.)

with closed suction drainage. Drainage is employed liberally as many minor appearing injuries will drain for several days. Unnecessary attempts at repair of lacerations without evidence of ductal disruption can result in late pseudocyst formation, whereas the vast majority of controlled, minor pancreatic fistulae are self-limited and easily managed with soft closed suction drains. The drains are usually removed within a few days, as long as the amylase concentration in the drain is less than that of serum. If amylase levels are elevated, drainage is continued until there is no further evidence of pancreatic leak. Prolonged gastric ileus is common with even minor pancreatic injuries, so distal enteral access with needle catheter jejunostomy should be considered in such cases. As the composition of most standard tube feeding increases the pancreatic effluent volume and amylase concentration, lower fat and higher pH (4.5) elemental diets are less stimulating to the pancreas and are particularly well suited for use in needle catheter jejunostomies.58

■ Grade III Distal transection or parenchymal injury with main pancreatic duct disruption generally requires surgical management in order to prevent pancreatic ascites or major fistula. Most ductal injuries can be identified either by preoperative studies in the stable patient or intraoperatively, as previously described. The

anatomic division between the head and body of the pancreas is the neck, where the SMA and SMV pass behind the pancreas. This anatomic division will provide an estimated 50% of pancreatic tissue. Management decisions are based upon the anatomic location of the parenchymal and duct injury (i.e., proximal vs. distal). Ductal injuries at or distal to the neck are treated definitively with distal pancreatectomy.14,59 In the vast majority of patients, distal resection should leave no concern for later pancreatic endocrine or exocrine function.60 If there is any concern for injury to the duct proximally in this setting (grade IV), a proximal pancreatogram can be performed through the end of the transected duct. In our experience, such situations are rarely encountered. The pancreas is divided at the injury location, and the proximal stump is closed. The optimal method of closure is debated. Roux-en-y pancreaticojejunosotmy does not appear to be justified. Alternatively, the parenchyma can be closed with nonabsorbable mattress sutures placed in a full-thickness noncrushing technique. The preference of many surgeons, however, is to perform a stapled resection using a TA-type stapler with 4.8-mm staples, which generally avoids excessively crushing the gland.61 In young trauma patients, the pancreatic duct is small but can usually be identified; it should be individually ligated at the time of pancreatic division.23 In the hemodynamically stable patient, the distal pancreatectomy can often be performed without

Duodenum and Pancreas

615

TABLE 32-8 AAST Pancreas Organ Injury Scale

III IV

Hematoma Laceration Hematoma Laceration Laceration Laceration

V

Laceration

II

Injury Description Major contusion without duct injury or tissue loss Major laceration without duct injury or tissue loss Involving more than one portion Disruption 50% of circumference Distal transection or parenchymal injury with duct injury Proximal (to right of superior mesenteric vein) transection or parenchymal injury Massive disruption of pancreatic head

a

Advance one grade for multiple injuries to the same organ. Adapted from Moore EE, Cogbill TH, Malangoni MA, et al. Organ injury scaling II: Pancreas, duodenum, small bowel, colon, and rectum. J Trauma. 1990;30:1427–1429.42

splenectomy.14,59 Efforts should be made to establish enteral access at the time of initial celiotomy in virtually all patients with grades III–V injuries to avoid the use of parenteral nutrition, with its attendant risks and complications.62 Verification of ductal injury will require laparotomy in most cases. To further refine decision making, Takishima et al.63 proposed a classification of pancreatic ductal injuries based on pancreatography. They suggested that class 1 (normal ducts) and 2a (branch injuries without extraparenchymal extravasation)

injuries could be managed nonoperatively; class 2b (branch injuries with leak into the retroperitoneum), 3a (main duct injuries in the body or tail), and 3b (main duct injuries in the head) injuries require surgical drainage. Although Takishima and colleagues did not address it, there have been several reports describing therapeutic applications of ERCP for acute trauma. Theoretically, performing sphincterotomy and/or placing stents would promote healing and eliminate leakage from traumatically disrupted ducts, just as is done for other

Patient Has Urgent indications for Laparotomy

Patient Requires Workup for Injury Assessment • Rising Serum Amylase • CT Scan – Findings of Pancreatic Injury

• Hemodynamic Instability (+) Ultrasound (Hemorrhage) • Peritonitis • CT Scan – Pancreatic Transection ERCP

Grade V Laparotomy • Damage Control Surgery • Staged Whipple Procedure

Grade I

Observe, No Drain Grade II Grade IV

Closed Suction Drainage

Grade III

Distal Pancreatectomy ( + ) Splenic Salvage (+) NCJ

FIGURE 32-13 Algorithm II. Algorithm for pancreatic trauma.

Wide drainage or Roux-en Y Jejunal limb to distal segment and oversewn proximal segment.

CHAPTER CHAPTER 32 X

Gradea I

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Management of Specific Injuries

SECTION 3 X

disorders.64,65 Although this seems an attractive minimally invasive alternative, results have been mixed. It has not been a panacea, and still is associated with complications. A prospective randomized clinical trial would help in determining the role of therapeutic ERCP in the management of acute pancreatic trauma. At this time, it is probably advisable only for select patients with minimal duct disruption.

■ Grade IV Trauma to the pancreatic head and neck represents the most challenging of pancreatic injuries. Careful assessment of the remaining pancreatic tissue and consideration of future function should be weighed when contemplating an extended distal pancreatectomy. Prior to embarking on such a procedure, one must carefully assess the status of the pancreatic duct and CBD (see above). If ductal status cannot be determined, wide external drainage and postoperative ERCP evaluation of the duct is recommended; stenting is reasonable if there is ductal disruption. Resection of greater than 85–90% is associated with a significant risk of pancreatic insufficiency.66 In the rare situation where resection will result in less than 20% of intact pancreatic tissue, the pancreas should be divided, the proximal segment closed, and the distal portion preserved with drainage into a Roux-en-Y pancreaticojejunostomy.60 Current trends emphasize the effectiveness of closed suction drainage alone even for extensive proximal gland injuries.14,67 However, the effectiveness of this technique with major ductal injury remains to be established.

■ Grade V Although rarely warranted, recent experience indicates that for devastating injury to the head of the pancreas, pancreaticoduodenectomy can be performed with acute outcomes similar to the elective setting.68–70 Indications for this procedure include massive pancreatic or retropancreatic hemorrhage; massive unreconstructable injury to the head of the pancreas, including the intrapancreatic bile duct and proximal main pancreatic duct; and avulsion of the ampulla of Vater from the duodenum with destruction of the second portion of the duodenum. As described above, these injuries are usually encountered with the patient in poor physiologic condition, so the principles of damage control apply (see above). As Seamons et al.71 recently reinforced the concept of pancreatic resection during damage control is ill-advised. Once the patient’s condition improves, the reconstruction is performed. In addition to improved physiologic status, there are tissue changes that facilitate reconstruction.72 Pancreatogastrostomy reconstruction may be preferable to pancreaticojejunostomy in these circumstances, for physiologic as well as anatomic reasons.69

Combined Pancreatic and Duodenal Injuries Combined pancreatic and duodenal injuries are quite common given their intimate anatomic relationship: 30% of duodenal and 16% of pancreatic injuries are combined (Tables 32-3 and 32-4). Such injuries are more common following penetrating trauma. The presence of both injuries significantly increases the

complication rates, with morbidity and mortality from combined pancreatoduodenal injury twice that observed from either injury alone (Table 32-5). Grades I–II duodenal lacerations with limited surrounding tissue damage, in combination with grades I–II pancreatic injuries, can be treated with primary duodenal repair and drainage. With higher grade duodenal or pancreatic injuries, the risk of duodenal suture line dehiscence is increased and pyloric exclusion should be considered. Grades IV–V injuries are discussed above. The basic principles of management include adequate debridement and drainage, duodenal diversion, and nutritional support.73–75

■ Complications of Pancreatic and Duodenal Trauma Three quarters of deaths associated with pancreatic and duodenal injuries occur in the first 48 hours (Table 32-6). The other deaths are generally due to late sepsis and multiple organ failure, often attributable at least in part to complications of the pancreatic or duodenal injury and/or repair. The morbidity related to duodenal injuries varies with the grade, ranging from 7 to 55%.6,7,16,24 The morbidity related to pancreatic injuries is consistently higher, ranging from 24 to 52%.14–16,59,67 Patients with combined pancreatoduodenal injuries have morbidity rates in the 21–36% range.16,75 The risk of complications can be predicted by the AAST injury grade, associated injuries, combined pancreatoduodenal injuries, hypothermia, and packing without drainage during initial damage control laparotomy.7,15,42,71

■ Hemorrhage Exsanguination is the most common cause of early death associated with pancreatic and duodenal injuries. Early application of damage control maneuvers is therefore necessary for successful management. Damage control techniques such as packing of hemorrhage and stapling or drainage of intestinal leaks will allow for deferred debridement and reconstruction. Correction of coagulopathy and hypothermia, and optimization of oxygen delivery may be life-saving, followed by definitive operative treatment upon return to the operating room.71 In our experience, this can usually be accomplished within 24–36 hours.55

■ Recurrent (Secondary) Hemorrhage Postoperative hemorrhage is a common concern after laparotomy for pancreatic and duodenal injuries, especially given the extent of associated injuries, which can be a source of bleeding. Approximately 10% of patients after pancreatic and duodenal trauma will sustain some degree of hemorrhage. Transfusion therapy should be guided by evaluation of the patient’s hemodynamic and coagulation status with attention to oxygen delivery.76 As in a patient presenting with initial trauma, it is important to resuscitate the patient with efforts to correct associated acidosis, coagulopathy, and hypothermia prior to embarking on a reexploration.55 In a stable patient with recurrent hemorrhage, angiography may identify the bleeding point for treatment with embolization. Other causes of postoperative hemorrhage late in the treatment course include progressive pancreatic necrosis or intra-abdominal infection/abscess. Serial

Duodenum and Pancreas

■ Pancreatic Fistula Pancreatic fistula is a significant complication, with an incidence in current series of 11–37%.14,15,67 A pancreatic fistula may be diagnosed in a patient with a measurable drain output with an amylase level greater than three times the serum level.77 A “benign” pancreatic fistula is defined as output less than 200 mL/day, and most will resolve spontaneously if adequate drainage without obstruction is established.78 High output lateral fistulae (greater than 700 mL/day) are rare. They are severe management challenges, and many will require long periods of drainage, nutritional support, or late surgical intervention.78 Early ERCP with sphincterotomy and/or stenting may accelerate resolution, but more data are needed to clarify its role.64 Stoma therapists can offer creative solutions for skin protection in these patients. Given the frequency of this complication, liberal enteral access is advised at the time of initial surgery (see above). The somatostatin analogue octreotide has shown some promise in treating patients with prolonged high-output fistulae.79 It has been shown to decrease the volume of fistulae drainage, but does not decrease the duration of the fistulae or increase the rate of spontaneous closure. There is a paucity of controlled data in trauma, but results have not supported routine use.80 In a multicenter review of distal pancreatectomy for trauma, the postoperative fistula rate was 14%; 89% closed within 8 weeks.59 Persistent pancreatic fistulae may require surgical treatment if not resolving. Of note, a recent review of posttraumatic biliary and pancreatic fistulae calculated that a pancreatic fistula was responsible for 27 additional hospital days and $191,000 in additional costs.78

■ Duodenal Fistula and Stricture Duodenal fistula generally results from failure of surgical repair due to suture line dehiscence, sometimes with distal duodenal obstruction from stricture. Patients with duodenal obstruction in the postoperative period should be evaluated with CT scan to rule out extrinsic compression from associated phlegmon or abscess. Avoidance of tension at the time of duodenal repair is essential to avoid subsequent stricture formation. With careful attention to these principles, duodenal stricture is rare. The incidence of duodenal fistula is generally less than 5%.59 However, it is still recommended to protect the surgical repair with pyloric exclusion in high-risk injuries. If a fistula develops, the diversion results in a less morbid end versus lateral fistula, and if a duodenal stricture or obstruction occurs, drainage is protected via the gastroenterostomy. Most such heal within several weeks. Once again, it is advisable to establish enteral access at the time of initial repair in high-risk injuries.

■ Abdominal Abscess Abscess formation should be considered in patients who develop sepsis after pancreatic or duodenal injury. The best predictors of postoperative abscesses are inadequate debridement or drainage during the initial operative management. Reexploration in this setting carries significant morbidity and mortality and should be avoided whenever possible. Imageguided drainage is preferable, and often is required more than once. Control of infections is important top avoid progression to multiple organ failure.

■ Pancreatic Pseudocyst and Pancreatitis Early pseudocyst formation may be indistinguishable from abscess; percutaneous aspiration may be helpful from both a diagnostic and therapeutic standpoint. Delayed pseudocysts may be managed surgically or endoscopically.81 In the setting of a pseudocyst, ERCP may be employed to evaluate the continuity of the pancreatic duct. If the duct is intact, percutaneous drainage will often resolve the problem. Endoscopic stenting has been described, but there is a paucity of data on late outcomes.64 Occasionally, pseudocyst formation is the presenting symptom of missed blunt pancreatic trauma. Transient hyperamylasemia is common in patients after laparotomy for pancreatic trauma; true acute pancreatitis with clinical abdominal pain is probably less frequent. A CT scan should be performed to rule out associated abscess, pseudocyst, or other complications. If the diagnosis is confirmed, treatment includes nasogastric suction, bowel rest, and nutritional support. Elemental enteral formulas appear to be tolerated well and should be employed with avoidance of total parenteral nutrition (TPN) and its associated complications. Most cases will resolve spontaneously. Chronic pancreatitis has been reported after pancreatic trauma; its treatment would follow the same principles as chronic pancreatitis due to other causes.82

■ Pancreatic Insufficiency This is a concern when resecting >80% of the pancreas, for grade IV or V injuries (see above). With careful attention to injury patterns as described, both exocrine and endocrine insufficiency should be rare after pancreatic trauma. In the trauma setting, it may be assumed that any resection distal to the mesenteric vessels will preserve adequate pancreas for normal function.59

REFERENCES 1. Vaughan GD III, Frazier OH, Graham DY, et al. The use of pyloric exclusion in the management of severe duodenal injuries. Am J Surg. 1977;134:785–790. 2. Stone HH, Fabian TC. Management of duodenal wounds. J Trauma. 1979;19:334–339. 3. Snyder WH III, Weigelt JA, Watkins WL, Bietz DA. The surgical management of duodenal trauma. Arch Surg. 1980;115:422–429. 4. Ivatury RR, Nallathambi M, Gaudino J, Rohman M, Stahl WM. Penetrating duodenal injuries: analysis of 100 consecutive cases. Ann Surg. 1985;202:153–158. 5. Shorr RM, Greaney GC, Donovan AJ. Injuries of the duodenum. Am J Surg. 1987;154:93–98.

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CT scan evaluation of pancreatic necrosis with aspiration and culture will predict the need for subsequent invasive radiological intervention and drainage. Many patients can be spared complicated and difficult reoperation with these techniques. Hemorrhagic pancreatitis is a rare complication, which may be indistinguishable from postoperative hemorrhage, and has a reported 75% mortality.8,10

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6. Cogbill TH, Moore EE, Feliciano DV, et al. Conservative management of duodenal trauma: a multicenter perspective. J Trauma. 1990;30: 1469–1475. 7. Blocksom JM, Tyburski JG, Sohn RL, et al. Prognostic determinants in duodenal injuries. Am Surg. 2004;70:248–255. 8. Graham JM, Mattox KL, Jordan GL Jr. Traumatic injuries of the pancreas. Am J Surg. 1978;136:744–748. 9. Stone HH, Fabian TC, Satiani B, Turkleson ML. Experiences in the management of pancreatic trauma. J Trauma. 1981;21:257–262. 10. Jones RC. Management of pancreatic trauma. Am J Surg. 1985;150: 698–704. 11. Ivatury RR, Nallathambi M, Rao P, Stahl WM. Penetrating pancreatic injuries. Analysis of 103 consecutive cases. Am Surg. 1990;56:90–95. 12. Voeller GR, Mangiante EC, Fabian TC. The effect of a trauma system on the outcome of patients with pancreatic trauma. Arch Surg. 1991;126: 578–580. 13. Madiba TE, Mokoena TR. Favourable prognosis after surgical drainage of gunshot, stab or blunt trauma of the pancreas. Br J Surg. 1995;82: 1236–1239. 14. Patton JH Jr, Lyden SP, Croce MA, et al. Pancreatic trauma: a simplified management guideline. J Trauma. 1997;43:234–241. 15. Kao LS, Bulger EM, Parks DL, Byrd GF, Jurkovich GJ. Patterns of morbidity after traumatic pancreatic injury. J Trauma. 2003;55:898–905. 16. Velmahos GC, Tabbara M, Gross R, et al. Blunt pancreatoduodenal injury: a multicenter study of the research consortium of New England centers for trauma (ReCONECT). Arch Surg. 2009;144:413–419. 17. von Mikulicz-Radecki J. Surgery of the pancreas. Ann Surg. 1903;38:1–8. 18. Halgrimson CG, Trimble C, Gale S, Waddell WR. Pancreaticoduodenectomy for traumatic lesions. Am J Surg. 1969;118: 877–882. 19. Summers JE. The treatment of posterior perforations of the fixed portions of the duodenum. Ann Surg. 1904;39:727–734. 20. Berry J, Giuseppi PL. Traumatic rupture of the intestine, with a case of recovery after operation and an analysis of the 132 cases that have occurred in ten London hospitals during the last fifteen years (1893– 1907). Proc Roy Soc Med. 1909;ii(Surg Sect):1–65. 21. Cave WH. Duodenal injuries. Am J Surg. 1946;72:26–31. 22. Kashuk JL, Moore EE, Cogbill TH. Management of the intermediate severity duodenal injury. Surgery. 1982;92:758–764. 23. Cogbill TH, Moore EE, Kashuk JL. Changing trends in the management of pancreatic trauma. Arch Surg. 1982;117:722–728. 24. Ballard RB, Badellino MM, Eynon CA, et al. Blunt duodenal rupture: a 6-year statewide experience. J Trauma. 1997;43:229–233. 25. Duchesne JC, Schmieg R, Islam S, Olivier J, McSwain N. Seelctive nonoperative management of low-grade blunt pancreatic injury: are we there yet? J Trauma. 2008;65:49–53. 26. Huerta S, Bui T, Porral D, Lush S, Cinat M. Predictors of morbidity and mortality in patients with traumatic duodenal injuries. Am Surg. 2005;71:763–767. 27. Akhrass R, Yaffe MB. Pancreatic trauma: a ten-year multi-institutional experience. Am Surg. 1997;63:598–605. 28. American College of Surgeons Committee on Trauma. Advanced Trauma Life Support for Doctors. 8th ed. Chicago, IL: American College of Surgeons; 2008. 29. Bouwman DL, Weaver DW, Walt AJ. Serum amylase and its isoenzymes: a clarification of their implications in trauma. J Trauma. 1984;24: 573–578. 30. Takishima T, Sugimoto K, Hirata M, et al. Serum amylase level on admission in the diagnosis of blunt injury to the pancreas: its significance and limitations. Ann Surg. 1997;226:70–76. 31. Valentino M, Serra C, Pavlica P, Barozzi L. Contrast-enhanced ultrasound for blunt abdominal trauma. Semin Ultrasound CT MRI. 2007;28:130–140. 32. Timaran CH, Daley BJ, Enderson BL. Role of duodenography in the diagnosis of blunt duodenal injuries. J Trauma. 2001;51:648–651. 33. Linsenmaier U, Wirth S, Reiser M, Korner M. Diagnosis and classification of pancreatic and duodenal injuries in emergency radiology. Radiographics. 2008;28:1591–1601. 34. Allen GS, Moore FA, Cox CS Jr, Mehall JR, Duke JH. Delayed diagnosis of blunt duodenal injury: an avoidable complication. J Am Coll Surg. 1998;187:393–399. 35. Rekhi S, Anderson SW, Rhea JT, Soto JA. Imaging of pancreatic trauma. Emerg Radiol. 2010;17:13–19. 36. Phelan HA, Velmahos GC, Jurkovich GJ, et al. An evaluation of multidetector computed tomography in detecting pancreatic injury: results of a multicenter AAST study. J Trauma 2009;66:641-647.

37. Barkin JS, Ferstenberg RM, Panullo W, et al. Endoscopic retrograde cholangiopancreatography in pancreatic trauma. Gastrointest Endosc. 1988;34:102–105. 38. Sugawa C, Lucas CE. The case for preoperative and intraoperative ERCP in trauma. Gastrointest Endosc. 1988;34:145-147. 39. Soto J, Alvarez O, Munera F, et al. Traumatic disruption of the pancreatic duct: diagnosis with MR pancreatography. AJR Am J Roentgenol. 2001;176:175. 40. Gillams AR, Kurzawinski T, Lees WR. Diagnosis of duct disruption and assessment of pancreatic leak with dynamic secretin-stimulated MR cholangiopancreatogrpahy. AJR Am J Roentgenol. 2006;186:499–506. 41. Berni GA, Bandyk DF, Oreskovich MR, Carrico CJ. Role of intraoperative pancreatography in patients with injury to the pancreas. Am J Surg. 1982;143:602–605. 42. Moore EE, Cogbill TH, Malangoni MA, et al. Organ injury scaling II: pancreas, duodenum, small bowel, colon, and rectum. J Trauma. 1990;30:1427–1429. 43. Clendenon JN, Meyers RL, Nance ML, Scaife ER. Management of duodenal injuries in children. J Pediatr Surg. 2004;39:964–968. 44. Jewett TC Jr, Caldarola V, Karp MP, Allen JE, Cooney DR. Intramural hematoma of the duodenum. Arch Surg. 1988;123:54–58. 45. Carrillo EH, Richardson JD, Miller FB. Evolution in the management of duodenal injuries. J Trauma. 1996;40:1037–1046. 46. Burch JM, Franciose RJ, Moore EE, Biffl WL, Offner PJ. Single-layer continuous versus two-layer interrupted intestinal anastomosis: a prospective randomized trial. Ann Surg. 2000;231:832–837. 47. Berne CJ, Donovan AJ, White EJ, Yellin AE. Duodenal “diverticulization” for duodenal and pancreatic injury. Am J Surg. 1974;127:503–507. 48. Moore EE, Dunn EL, Jones TN. Immediate jejunostomy feeding: its use after major abdominal trauma. Arch Surg. 1981;116:681–684. 49. Holmes JH IV, Brundage SI, Pak-cheun Y, et al. Complications of surgical feeding jejunostomy in trauma patients. J Trauma. 1999;47: 1009–1013. 50. Eckert MJ, Perry JT, Sohn VY, et al. Bioprosthetic repair of complex duodenal injury in a porcine model. J Trauma. 2009;66:103–109. 51. Martin TD, Feliciano DV, Mattox KL, Jordan GL Jr. Severe duodenal injuries: treatment with pyloric exclusion and gastrojejunostomy. Arch Surg. 1983;118:631–635. 52. Cone JB, Eidt JF. Delayed diagnosis of duodenal rupture. Am J Surg. 1994;168:676–679. 53. Velmahos GC, Constantinou C, Kasotakis G. Safety of repair for severe duodenal injuries. World J Surg. 2008;32:7–12. 54. Talving P, Nicol AJ, Navsaria PH. Civilian duodenal gunshot wounds: surgical management made simpler. World J Surg. 2006;30:488–494. 55. Moore EE, Burch JM, Franciose RJ, Offner PJ, Biffl WL. Staged physiologic restoration and damage control surgery. World J Surg. 1998;22:1184–1191. 56. Wood JH, Partrick DA, Bruny JL, Sauaia A, Moulton SL. Operative vs nonoperative management of blunt pancreatic trauma in children. J Pediatr Surg. 2010;45:401–406. 57. Fabian TC, Kudsk KA, Croce MA, et al. Superiority of closed suction drainage for pancreatic trauma: a randomized, prospective study. Ann Surg. 1990;211:724–730. 58. McArdle AH, Echave W, Brown RA, Thompson AG. Effect of elemental diet on pancreatic secretion. Am J Surg. 1974;128:690–692. 59. Cogbill TH, Moore EE, Morris JA Jr, et al. Distal pancreatectomy for trauma: a multicenter experience. J Trauma. 1991;31:1600–1606. 60. Yellin AE, Vecchione TR, Donovan AJ. Distal pancreatectomy for pancreatic trauma. Am J Surg. 1972;124:135–142. 61. Andersen DK, Bolman RM III, Moylan JA Jr. Management of penetrating pancreatic injuries: Subtotal pancreatectomy using the auto suture stapler. J Trauma. 1980;20:347–349. 62. Kudsk KA, Croce MA, Fabian TC, et al. Enteral versus parenteral feeding: effects on septic morbidity after blunt and penetrating abdominal trauma. Ann Surg. 1992;215:503–513. 63. Takishima T, Hirata M, Kataoka Y, et al. Pancreaticographic classification of pancreatic ductal injuries caused by blunt injury to the pancreas. J Trauma. 2000;48:745–752. 64. Bhasin DK, Rana SS, Rawal P. Endoscopic retrograde pancreatography in pancreatic trauma: need to break the mental barrier. J Gastroenterol Hepatol. 2009;24:720–728. 65. Rogers SJ, Cello JP, Schecter WP. Endoscopic retrograde cholangiopancreatography in patients with pancreatic trauma. J Trauma. 2010;68:538–544. 66. Dragstedt LR. Some physiologic problems in surgery of the pancreas. Ann Surg. 1943;118:576–589.

Duodenum and Pancreas 75. Lopez PR, Benjamin R, Cockburn M, et al. Recent trends in the management of combined pancreatoduodenal injuries. Am Surg. 2005;71:847–852. 76. Kashuk JL, Moore EE, Sawyer M, et al. Postinjury coagulopathy management: goal directed resuscitation via POC thromboelastography. Ann Surg. 2010; 251:604–614. 77. Bassi C, Dervenis C, Butturini G, et al. Postoperative pancreatic fistula: an international study group (ISGPF) definition. Surgery. 2005;138:8–13. 78. Vassiliu P, Toutouzas KG, Velmahos GC. A prospective study of posttraumatic biliary and pancreatic fistuli: the role of expectant management. Injury. 2004;35:223–227. 79. Martineau P, Shwed JA, Denis R. Is octreotide a new hope for enterocutaneous and external pancreatic fistulas closure? Am J Surg. 1996;172:386–395. 80. Nwariaku FE, Terracina A, Mileski WJ, Minei JP, Carrico CJ. Is octreotide beneficial following pancreatic injury? Am J Surg. 1995;170:582–585. 81. Buccimazza I, Thomson SR, Anderson F, Naidoo NM, Clarke DL. Isolated main pancreatic duct injuries: spectrum and management. Am J Surg. 2006;191:448–452. 82. Leppaniemi A, Haapiainen R, Kiviluoto T, Lempinen M. Pancreatic trauma: acute and late manifestations. Br J Surg. 1988;75:165–167.

CHAPTER CHAPTER 32 X

67. Vasquez JC, Coimbra R, Hoyt DB, Fortlage D. Management of penetrating pancreatic trauma: an 11-year experience of a level-1 trauma center. Injury. 2001;32:753–759. 68. Oreskovich MR, Carrico CJ. Pancreaticoduodenectomy for trauma: a viable option? Am J Surg. 1984;147:618–623. 69. Delcore R, Stauffer JS, Thomas JH, Pierce GE. The role of pancreatogastrostomy following pancreatoduodenectomy for trauma. J Trauma. 1994;37:395–400. 70. Asensio JA, Petrone P, Roldan G, Kuncir E, Demetriades D. Pancreaticoduodenectomy: a rare procedure for the management of complex pancreaticoduodenal injuries. J Am Coll Surg. 2003;197: 937–942. 71. Seamons MJ, Kim PK, Stawicki SP, et al. Pancreatic injury in damage control laparotomies: is pancreatic resection safe during the initial laparotomy? Injury. 2009;40:61–65. 72. Koniaris LG, Mandal AK, Genuit T, Cameron JL. Two-stage pancreaticoduodenectomy: delay facilitates anastomotic reconstruction. J Gastrointest Surg. 2000;4:366–369. 73. Feliciano DV, Martin TD, Cruse PA, et al. Management of combined pancreatoduodenal injuries, Ann Surg. 1987;205:673–680. 74. Mansour MA, Moore JB, Moore EE, Moore FA. Conservative management of combined pancreatoduodenal injuries. Am J Surg.1989;158:531–535.

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CHAPTER 33

Colon and Rectal Trauma Demetrios Demetriades and Kenji Inaba

COLON INJURIES ■ Introduction The management of colon injuries has undergone many radical changes in the last few decades, resulting in a dramatic reduction of colon-related mortality from about 60% during World War I to about 40% during World War II to about 10% during the Vietnam War and to lower than 3% in the last decade. However, the colon-related morbidity remains unacceptably high and in most prospective studies the abdominal sepsis rate is about 20% (Table 33-1).1–6 In patients with destructive colon injuries, high Penetrating Abdominal Trauma Index (PATI), or multiple blood transfusions the incidence of intraabdominal sepsis has been reported to be as high as 27%.7,8

■ Epidemiology In the United States, the vast majority of colon injuries are due to penetrating trauma, usually firearms. In abdominal gunshot wounds the colon is the second most commonly injured organ after the small bowel and it is involved in about 27% of cases undergoing laparotomy.8,9 In anterior abdominal stab wounds the colon is the third most commonly injured organ after the liver and small bowel and is found in about 18% of patients undergoing laparotomy. In posterior stab wounds the colon is the most commonly injured organ and is diagnosed in about 20% of patients undergoing laparotomy.10 The transverse colon is the most commonly injured segment after gunshot wounds and the left colon the most commonly injured segment after stab wounds. Stab wounds or low-velocity civilian gunshot wounds usually cause limited damage and most of them are amenable to debridement and primary repair (Fig. 33-1). High-velocity penetrating injuries, such as in war-related trauma, cause major tissue damage and almost always require colon resection (Fig. 33-2).

Blunt trauma to the colon is uncommon and occurs in about 0.5% of all major blunt trauma admissions or in 10.6% of patients undergoing laparotomy.11,12 Most of these injuries are superficial and only 3% of patients undergoing laparotomy have full-thickness colon perforations.11,13 Traffic trauma is the most common cause of blunt colon injury. The usual mechanism is rapid deceleration that may cause mesenteric tears and ischemic necrosis of the colon (Fig. 33-3). Another possible mechanism is the transient formation of a closed loop and blowout perforation. Seatbelt use increases the risk of hollow viscus perforations. The presence of a seatbelt mark sign should increase the index of suspicion for hollow viscus injury. In rare cases a colonic wall hematoma or contusion may result in delayed perforation several days after the injury. The left colon is the most commonly injured segment followed by the right colon and the transverse colon.11 In blast injuries such as in war or terror-related explosions, hollow viscera are more susceptible to injury than solid organs (Fig. 33-4). Often there is no evidence of major external abdominal trauma. The blast wave is more likely to cause colon rupture than any other intra-abdominal organ.14

■ Diagnosis The diagnosis of colon injury is almost always made intraoperatively. In patients with a penetrating abdominal trauma, selected for nonoperative management, the diagnosis is based on CT scan evaluation and serial clinical examinations. A rectal examination may show blood in the stool, especially in cases with distal colon or rectal injuries. The sensitivity and specificity of the intravenous contrast CT scan are about 90% and 96%, respectively.15 Other investigations, such as ultrasound, diagnostic peritoneal lavage, or laparoscopy, have little or no role in the evaluation of suspected colon injuries.

Colon and Rectal Trauma

Author George et al.1 Chappuis et al.2 Demetriades et al.3 Ivatury et al.4 Gonzalez et al.5 Demetriades et al.6 Overall

Number of Patients 102 56 100 252 114 297 921

CHAPTER 33 X CHAPTER

TABLE 33-1 Incidence of Abdominal Septic Complications in Colon Injuries (Prospective Studies) Abdominal Sepsis (%) 33 20 16 17 24 24 22

The preoperative diagnosis of colon injury following blunt trauma can be difficult, especially in unevaluable patients, due to severe associated head or spinal cord injuries. The diagnosis is often suspected by the presence of free gas, unexplained free peritoneal fluid, or thickened colonic wall on the routine abdominal CT scan (Fig. 33-5). Luminal contrast extravasation is an infrequent finding and its absence does not rule out an injury. In some cases the diagnosis may be delayed by many days with catastrophic consequences. Intraoperatively in penetrating trauma, every paracolic hematoma should be explored and the underlying colon should be evaluated carefully. Failure to adhere to this important surgical principle is a serious error with medical and legal implications. In blunt trauma there is no need for routine exploration of paracolic hematomas, unless there is a strong suspicion for an underlying perforation.

FIGURE 33-2 High-velocity destructive injury to the colon.

■ Operative Management Historical Perspective

The American Association for the Surgery of Trauma (AAST) developed a grading system for colon injuries that is useful in predicting complications and comparing therapeutic interventions. The AAST Colon Injury Scale is shown in Table 33-2.16

The first guidelines regarding the management of colon injuries were published by the US Surgeon General and mandated colostomy for all colon wounds. This unusual directive was initiated because of the very high mortality associated with colorectal injuries, in excess of 50%,17,18 during the early years of World War II. Although these guidelines were not based on any scientific evidence, they were credited for the improved outcomes in the last years of the war. However, during this period many other major advances such as faster evacuation from the battlefield, improved resuscitation, and introduction of penicillin and sulfadiazine could all have contributed to the reduction of mortality. The policy of mandatory colostomy remained the unchallenged standard of care until late 1970s. Stone and Fabian reported the first major scientific challenge of this policy in 1979.19 A prospective randomized study, which excluded patients with hypotension, multiple associated

FIGURE 33-1 Low-velocity gunshot wounds cause local damage to the colon.

FIGURE 33-3 High-speed motor vehicle injury with mesocolon avulsion and necrosis of the colon.

■ Colon Injury Scale

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Management of Specific Injuries

TABLE 33-2 AAST Colon Injury Scale

X SECTION 3

Grade I

II III IV V

Injury Description (a) Contusion or hematoma without devascularization (b) Partial thickness laceration Laceration 50% of circumference Laceration 50% of circumference Transection of the colon Transection of the colon with segmental tissue loss

Management of Nondestructive Colon Injuries FIGURE 33-4 Blast injury to the colon. (Courtesy of Captain P. Rhee.)

injuries, destructive colon injuries, and delayed operations, concluded that primary repair was associated with fewer complications than colostomy. The exclusion criteria were perceived as risk factors for anastomotic leak and were absolute indications for diversion. The validity of the “standard” contraindications for primary repair or resection and anastomosis was challenged in subsequent studies. New prospective randomized studies with no exclusion criteria demonstrated the safety of primary repair, at least in nondestructive colon injuries. An alternative to primary repair or colostomy was exteriorized repair, which was introduced in the 1970s. This technique included suturing and exteriorization of the colon. If the repair remained intact in the next 4–5 days, the colon was returned to the peritoneal cavity. If the repair broke down, it was converted to a loop colostomy.20,21 The enthusiasm for this approach waned in the 1980s due to the overwhelming evidence of the superiority of primary repair. In the 1990s and 2000s primary repair gained widespread acceptance and the role of colostomy was challenged, even in cases with perceived risk factors.

FIGURE 33-5 CT scan of a victim involved in a high-speed traffic injury. Note the thicken ascending colon wall (circle). The patient had rupture of the cecum.

Nondestructive injuries include those involving 50% of the bowel wall and without devascularization. There is now enough class I evidence supporting primary repair in all nondestructive colon injuries irrespective of risk factors. Chappuis et al.2 in a randomized study of 56 patients with no exclusionary criteria concluded that primary repair should be considered in all colon injuries irrespective of risk factors. In a subsequent study in 1995, Sasaki et al.22 randomized 71 patients with colon injuries to either primary repair or diversion, without any exclusionary criteria. The overall complication rate was 19% in the primary repair group and 36% in the diversion group. In addition, the complication rate for colostomy closure was 7%. The study concluded that primary repair should be performed in all civilian penetrating colon injuries irrespective of any associated risk factors. In another prospective randomized study in 1996, Gonzalez et al.5 randomized 109 patients with penetrating colon injuries to primary repair on diversion. The sepsis-related complication rate was 20% in the primary repair group and 25% in the diversion group. The authors continued their study and the series increased to 176 patients. They concluded again that all civilian penetrating colon injuries should be primarily repaired. Overall, collective review of all published prospective randomized studies identified 160 patients with primary repair and 143 patients treated with diversion. The abdominal sepsis complication rate was 13.1% and 21.7%, respectively (Table 33-3). In addition, numerous prospective observational studies (class II evidence) supported routine primary repair in nondestructive injuries.1,3,4,23 In conclusion, there are sufficient class I and II data to support routine primary repair of all nondestructive colon injuries, irrespective of risk factors. Despite the available scientific evidence, many surgeons still consider colostomy as the safest procedure in high-risk colon injuries. In a survey of 317 Canadian surgeons in 1996, 75% of them chose colostomy in low-velocity gunshot wounds to the colon.24 In another survey in 1998, of 342 American trauma surgeons, members of the AAST, a colostomy was the procedure of choice in 3% of injuries with minimal spillage, in 43% of injuries with gross spillage, in 18% of injuries involving 50% of the colon wall, and in 33% of cases with colon transection.25 It is obvious that old habits still play a significant role in modern surgical practice.

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TABLE 33-3 Primary Repair versus Diversion: Prospective Randomized Studies with No Exclusion Criteria

Management of Destructive Colon Injuries Destructive colon injuries include those with loss of more than 50% of the bowel wall circumference or with devascularization (Fig. 33-2) and require a segmental colonic resection. Destructive injuries were traditionally managed with diversion because of the perceived high risk for intra-abdominal sepsis. Small prospective studies in the 1990s suggested that primary anastomosis may be safe. Collectively, these studies included only 36 patients with colon resection and anastomosis. The incidence of anastomotic leak was 2.5% and no deaths occurred. These studies concluded that primary anastomosis is the procedure of choice irrespective of the presence of any risk factors for abdominal complications.2,22,23 However, another prospective observational study with 25 patients treated by resection and anastomosis and 2 patients treated by resection and colostomy reported two fatal anastomotic leaks (8%).7 The study concluded that some high-risk patients (PATI 25 or 6 U of blood transfusions or delayed operation) with destructive colon injuries might benefit from diversion. The study included only 2 patients with diversion, making any comparison with the primary anastomosis group impossible. There are two retrospective studies, which included only destructive colon injuries requiring resection. In an analysis of 43 patients who were managed by resection and anastomosis Stewart et al.26 reported an overall anastomotic leak rate of 14%. However, in the subgroup of patients with blood transfusion 6 U the leak rate was 33%. The study suggested that diversion should be considered in patients receiving massive blood transfusions or in the presence of underlying medical illness. In another retrospective study of 140 patients with destructive colon injuries requiring resection Murray et al.27 reported similar intra-abdominal sepsis rates with primary anastomosis or diversion. Univariate analysis identified Abdominal Trauma Index 25 or hypotension in the emergency room to be associated with increased risk of anastomotic leak. The study suggested that a diversion procedure should be considered in these high-risk subgroups of patients. In summary, the available prospective randomized studies, which include only a small number of cases, recommend resection with anastomosis irrespective of risk factors. Two larger retrospective studies suggest that diversion should be considered in selected patients with PATI 25, multiple blood transfusions, or associated medical illness.26,27 The guidelines of the

Diversion No. of Patients 28 28 87 143

Abdominal Complications 5 (17.9%) 8 (28.6%) 18 (21%) 31 (21.7%)

Eastern Association for the Surgery of Trauma (EAST) published in 199828 recommended that a diversion procedure should be considered in patients with shock, significant associated injuries, peritonitis, or underlying disease. However, these guidelines could not be supported by the literature and were based exclusively on class III evidence. There were only 40 patients in class I studies with resection and anastomosis and the anastomotic leak rate was 2.5% and without mortality. There were only 12 patients in class II studies who underwent anastomosis and the leak rate was 8.3% without mortality. In class III retrospective studies there were 303 patients with anastomosis with a leak rate of 5.2% and 3 deaths (1%) due to the leak. In order to address these limitations, the AAST sponsored a prospective multicenter study to evaluate the safety of primary anastomosis or diversion and identify independent risk factors for colon-related complications in patients with penetrating destructive colon injuries.6 The study included 297 patients with penetrating colon injuries requiring resection who survived at least 72 hours. Rectal injuries were excluded. The overall colon-related mortality was 1.3% (4 deaths) and all deaths occurred in the diversion group (P  .01). The most common abdominal complication was an intra-abdominal abscess (19% of patients) followed by fascia dehiscence (9%). The incidence of anastomotic leaks was 6.6% and no death occurred in these cases. Multivariate analysis identified severe fecal contamination, 4 U of blood transfusions within the first 24 hours, and inappropriate antibiotic prophylaxis as independent risk factors for abdominal complications. In the presence of all these three risk factors the incidence of abdominal complications was about 60%, in the presence of two factors the complication rate was 34%, in the presence of only one factor the rate was about 20%, and with no risk factors it was 13%. The method of colon management (anastomosis or diversion), delay of operation 6 hours, shock at admission, site of colon injury, PATI 25, ISS 20, or associated intraabdominal injuries were not found to be independent risk factors. In a second analysis, the study compared colon-related outcomes in high-risk groups (hypotension at admission, blood transfusions 6 U, delay of operation 6 hours, severe peritoneal contamination, or PATI 25) after primary anastomosis or colostomy. These risk factors have been suggested by many surgeons as indications for diversion. The colon-related

CHAPTER 33 X CHAPTER

Study Chappuis et al.2 Sasaki22 Gonzalez23 Total

Primary Repair Abdominal Septic No. of Patients Complications 28 4 (14.3%) 43 1 (2.3%) 89 16 (18%) 160 21 (13.1%)

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Management of Specific Injuries

TABLE 33-4 AAST Study of Destructive Colon Injuries: Comparison of Abdominal Complications Between Primary Anastomosis and Diversion in High- and Low-Risk Patients6

X SECTION 3

Patient Population (N ⴝ 297) All patients Low-risk patientsa High-risk patientsa

Abdominal Complications (%) Primary Anastomosis Diversion 22 27 13 8 28 30

Adjusted Relative Risk (95% CI) 0.81 (0.55–1.41) 1.26 (0.21–8.39) 0.90 (0.53–1.40)

P-value 0.69 0.82 0.67

High-risk patients were those with PATI 25 or severe fecal contamination or 6 hours from injury to operation or transfusion of 6 U of blood preoperative/intraoperative systolic blood pressure 90 mm Hg. Low-risk patients were those without any of the above risk factors. a

mortality in this high-risk group was 4.5% (4 of 88 patients) in the colostomy group and no deaths in the 121 patients who underwent primary anastomosis (P  .03). The adjusted relative risk of abdominal septic complications was similar with the two operative procedures, in both the low- and high-risk patients (Table 33-4). There was a trend toward longer ICU and hospital stay in the colostomy group. The study concluded that “In view of these findings and the fact that colon diversion is associated with worse quality of life and requires an additional operation for closure, colon injuries requiring resection should be managed by primary repair, irrespective of risk factors.”6 The optimal management of destructive colon injuries in patients undergoing damage control procedures is not clear, and the literature on this issue is scanty. It has been suggested that anastomosis may be safe because follow-up reexploration identifies any anastomotic problems and fecal diversion can be performed at this stage. There are some theoretical disadvantages of having a colostomy, because it is an open source of fecal material, near an open abdomen. In addition, the subsequent closure of the colostomy, especially end colostomy, might be a major technical challenge because of the hostile intra-abdominal environment. For those patients managed with stapling off of the injured colon as part of damage control, there is class III evidence that delayed primary anastomosis may be a safe option.29,30 This issue requires further investigation in larger and better controlled studies.

■ Risk Factors for Abdominal Complications after Colon Injuries The incidence of abdominal complications after colon injuries is very high, with a sepsis rate higher than 20% (Table 33-1). Various conditions have been suggested as possible risk factors for colon-related complications but most of them failed scientific scrutiny. (a) Left versus right colon injuries: For many years there was an anecdotal but widespread belief that left colon injuries are associated with a higher risk of anastomotic leaks and septic complications following repair or colocolostomy

than right colon injuries. This perception was based mainly on the anatomical differences between the two sides of the colon. This led to the practice of liberal primary repair in the right colon and colostomy in the left colon. However, no clinical or experimental study has ever demonstrated any healing differences between the two sides of the colon or any evidence that the two anatomical sides should be treated differently. Experimental work in baboons, which have anatomy and bacteriology very similar to those of humans, showed no difference of the healing properties between the right and left colon.31 The healing was evaluated clinically (anastomotic leak or abscess), biochemically (hydroxyproline concentrations), and mechanically (breaking strength of the anastomosis), in both normovolemic and hypovolemic conditions.31,32 However, there is strong evidence that ileocolostomy is associated with significantly fewer leaks than colocolostomy and it should be the procedure of choice in cases with right hemicolectomy.31,32 Good blood supply is the cornerstone of successful colon healing and this should be taken into account when repairing injuries in the watershed region of the splenic flexure. Associated abdominal injuries: Earlier retrospective studies suggested that multiple or severe associated intra-abdominal injuries (PATI 25) are associated with a high incidence of anastomotic leaks and therefore a colostomy should be performed, especially in patients with destructive colon injuries. However, class I and II studies have shown that although multiple associated intra-abdominal injuries are significant risk factors for intra-abdominal sepsis, the method of colon management does not affect the incidence of abdominal sepsis.3,5–7,33 Some studies have even suggested that the presence of a colostomy in these high-risk patients may independently contribute to abdominal sepsis.33 There is class II evidence that the presence of pancreatic or urine leaks is associated with increased risk of anastomotic failure.31,32 (b) Shock: There is now sufficient class I and II evidence that preoperative or intraoperative shock is neither an independent risk factor for abdominal sepsis nor a

Colon and Rectal Trauma

(d)

(e)

(f )

(g)

■ Colon Leaks The overall incidence of colon leaks after repair or anastomosis is fairly low. In a collective review of 35 prospective or retrospective studies with 2,964 primary repairs, there were 66 (2.2%) leaks.39 Review of the published prospective studies that included 534 patients with colon repair or resection and anastomosis showed 17 (3.2%) leaks.6,39 Resection and anastomosis is significantly more likely to leak than simple repairs. In

a collective review of 362 patients with resection and anastomosis the overall incidence of anastomotic leak was 5.5%.39 In a more recent multicenter prospective study of 197 patients with penetrating colon injuries who underwent resection and primary anastomosis, the leak rate was 6.6%.6 The risk factors for anastomotic leak are not well defined. Colocolostomies have been shown to be at a higher risk of anastomotic leaks than ileocolostomies. Murray et al. reported a leak rate of 4% in 56 patients with ileocolostomies and 13% in 56 colocolostomies.27 A multicenter prospective AAST study reported a leak rate of 4.2% for ileocolostomies and 8.9% for colocolostomies.6 Multiple blood transfusions, severe contamination, and multiple associated injuries were not identified as independent risk factors for anastomotic leak. The prognosis of colon leaks is usually good and most of the patients can safely be managed nonoperatively with adequate drainage and low-residue diet. However, in some patients the colonic leak may cause severe intra-abdominal sepsis and a proximal diversion procedure may be required. Curran and Borzotta reported no deaths in a collective series of 66 patients with repair leaks.39 However, Murray et al. reported 2 colonrelated deaths in a group of 10 patients with anastomotic leak.27 A multicenter AAST study reported no deaths in the 13 patients with anastomotic leaks. The overall mortality due to anastomotic leak-related complications in a collective review of 3,161 trauma patients treated with primary repair or resection and anastomosis was only 0.1%.6,39 In summary, colonic leaks occur more commonly in patients with colocolostomies than in patients with ileocolostomies. The majority of these leaks can safely be managed nonoperatively with adequate drainage and low-residue diet. Reexploration of the abdomen for wide drainage and fecal diversion or resection and reanastomosis should be reserved only for patients with generalized peritonitis or failed percutaneous drainage.

■ Technical Tips On entering the peritoneal cavity the first step is to control any bleeding. The extent of the colon injury is then assessed by adequate mobilization of the injured segment and careful inspection of the retroperitoneal wall. Any paracolic hematoma due to penetrating trauma should be explored to rule out any underlying perforation. Gentle squeezing of the suspected area may facilitate the diagnosis of any occult injuries by the manifestation of air or colonic content leak. The ureter should always be identified and examined in cases with injuries to the ascending or descending colon. The splenic flexure of the colon is the least accessible segment because of its anatomical location under the left hypochondrium. During its mobilization, caution should be exercised to avoid excessive downward traction of the colon, which may cause avulsion of the splenic capsule and troublesome bleeding (Fig. 33-6). In cases with multiple associated injuries and coagulopathy, many capsular tears may require a splenectomy, which increases the risk of postoperative complications. This iatrogenic complication can be avoided by placing three or four laparotomy pads under the diaphragm, above the spleen. This maneuver provides a good exposure and safe division of the splenocolic ligament.

CHAPTER 33 X CHAPTER

(c)

contraindication for primary colon repair or anastomosis.3,5,6 The duration and severity of hypotension might be important factors not taken into account in these studies. This is an area that needs further investigation. Blood transfusions: Multiple blood transfusions (4 U of blood within the first 24 hours) have been shown to be a major independent risk factor for abdominal septic complications.6,33 In a large prospective AAST study of 297 patients with penetrating destructive colon injuries multiple blood transfusions were the most important independent factor for abdominal sepsis. However, the method of colon management, primary anastomosis or colostomy, did not influence the complication rate in this group of patients.6 It is possible that massive transfusion might be an important risk factor for anastomotic failure and this possibility requires further investigation. Fecal contamination: Severe fecal spillage is a major independent risk factor for abdominal sepsis.1,6,11,27,33,34 This finding led some authors to suggest that this condition should be a contraindication for primary repair or anastomosis.1,11,34,35 However, all prospective randomized studies and recent large prospective observational studies have shown that the method of colon management does not influence the septic complication rate.2,5,6 Time from injury to operation: Although delays in the operative management of colon perforations increase the risk of septic complications, the length of delay over which the complication rate increases is not clear. Some studies suggest that this critical delay is 6 hours, while others extend it to 12 hours.7,27,36 It seems that the degree of contamination is much more important than the operative delay and the time delay in itself should not be used as an absolute criterion for primary repair or diversion. Retained missiles: There is no evidence that retained bullets, which passed through the colon, are associated with increased risk of local sepsis. Removal of the missiles does not reduce the risk of infection. In a study of 84 patients with gunshot wounds of the colon, the bullet remained in the body in 40 and was removed in 44. The incidence of local septic complications was 5% and 7%, respectively.37 Closure of the skin wound: Closure of the skin incision after colonic injuries, especially in the pressure of fecal spillage, is associated with a high incidence of wound infection that is often complicated by necrotizing fasciitis or fascia dehiscence.38 In these cases the skin should be left open and delayed closure should be performed a few days later.

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X SECTION 3

than 5% in recent reports. Similarly, the morbidity has been reduced from about 70% during the Vietnam War to less than 10% in recent studies.46 This improvement encouraged surgeons to challenge many practices that remained the cornerstone of therapy for many decades.

■ Anatomy The rectum is about 15 cm long and is only partially intraperitoneal. Only the upper two thirds anteriorly and the upper one third laterally are covered by peritoneum. The lower third of the rectum is completely extraperitoneal and makes exposure and repair of any injuries difficult. The rectum receives its blood supply from the superior rectal artery off the inferior mesenteric artery, the middle rectal artery off the internal iliac artery, and the inferior rectal artery off the internal pudendal artery.

■ Epidemiology

FIGURE 33-6 Excessive downward traction of the splenic flexure of the colon may cause avulsion of the capsule of the spleen and troublesome bleeding.

Adequate debridement of all penetrating wounds, especially gunshot wounds, is critical before any repair is performed. In destructive injuries the resection should ensure well-perfused and not contused edges and the anastomosis should be tension free. The role of local application of fibrin glue around the anastomosis is not clear. Although some experimental work suggested some protective benefits with fibrin glues,40 others failed to show any benefits.41 No clinical work has been published in this field. Further protection of the anastomosis with omental wrap is a common practice, although randomized studies in nontrauma colon operations failed to show any benefit.42 The method of anastomosis, handsewn or stapled, does not play any significant role in the incidence of anastomotic leaks. In a prospective AAST study of 207 patients with penetrating destructive injuries who underwent resection and anastomosis, 128 cases were managed by handsewn and 79 cases by stapled anastomosis. The incidence of anastomotic leak was 7.8% and 6.3%, respectively.43 Another debated technical issue is the role of one-layer versus two-layer anastomosis. Numerous studies in nontrauma operations have concluded that one-layer anastomosis is as safe as a two-layer anastomosis.44,45

RECTAL INJURIES ■ Introduction The management of rectal trauma has undergone many major changes over the last decades. The mortality related to rectal trauma has decreased from 67% during World War I to less

The majority of rectal injuries are due to penetrating trauma, usually firearms. In most series from American urban trauma centers gunshot wounds account for about 85% and stab wounds for about 5% of rectal injuries.47–49 Other causes of penetrating trauma include iatrogenic injuries from urologic and endoscopic procedures, sexual misadventure, and anorectal foreign bodies. Blunt trauma accounts for only 5–10% of injuries, and is usually the result of pelvic fractures or impalement.47–51

■ Rectal Organ Injury Scale The grading system developed by the AAST for rectal injuries is similar to that of colonic injuries (Table 33-5).

■ Diagnosis The clinical signs and diagnosis of intraperitoneal rectal injuries are the same as for colonic injuries. The majority of patients have signs of peritonitis and the diagnosis is almost always made intraoperatively. The diagnosis of extraperitoneal rectal injuries is more challenging because of the lack of peritoneal signs. The diagnosis is based on a high index of suspicion in the appropriate cases, a digital rectal examination, rigid proctosigmoidoscopy, and CT scan. In most series, the diagnostic

TABLE 33-5 AAST Rectal Organ Injury Scale Grade I

II III IV V

Injury Description (a) Contusion or hematoma without devascularization (b) Partial thickness laceration Laceration 50% of circumference Laceration 50% of circumference Full-thickness laceration with extension into the perineum Devascularized segment

Colon and Rectal Trauma they are too low for transabdominal repair and too high for transanal repair. These cases can safely be managed with a proximal diverting colostomy alone, without suturing of the perforation.53,62,63 A recent study from Cape Town, South Africa, reported that laparoscopic inspection to rule out intraperitoneal injuries followed by laparoscopic sigmoid loop colostomy was safe with a low rate of complications.62

■ Operative Management

Presacral Drainage. Presacral drainage was introduced in the management of extraperitoneal rectal injuries in World War II in an effort to decrease the pelvic sepsis rate. This approach has been challenged on the grounds that it may require extensive dissection of normal soft tissues in order to place the drain in the proximity of the rectal injury. Numerous studies, including a prospective randomized one, showed no benefit of routine presacral drainage.53,54,61,64 On the basis of the available evidence, routine use of presacral drains for extraperitoneal rectal injuries cannot be supported. Transabdominal presacral drainage may be useful in cases with posterior rectal injuries that have been repaired through a laparotomy.

Historical Perspective The history of the management of rectal trauma parallels that of colon trauma with many of the therapeutic principles evolving from lessons learned from wartime experiences. Mortality from rectal gunshot wounds was as high as more than 60% in the early part of World War II, until the Army Surgeon General mandated colostomy for all colon and rectal injuries.18 Presacral drainage was added in 1943, and appeared to further improve mortality. Shortly after World War II, distal rectal washout became part of the routine management. The triad of colostomy, presacral drainage, and rectal washout remained the standard of care of these injuries over the next several decades, despite the lack of any solid scientific evidence.47,52 The validity of these principles however was challenged in the 1990s with new studies suggesting that routine colostomy may not be necessary, presacral drain may have little or no value, and rectal washout may be harmful.46,53,57–62

Intraperitoneal Injuries There are no class I or class II data supporting any specific management algorithm for intraperitoneal rectal injuries. Because of the anatomical and clinical similarities between the intraperitoneal rectum and the distal left colon, intraperitoneal rectal injuries are managed like colon injuries, the vast majority amendable to primary repair.

Extraperitoneal Injuries As described above, on the basis of anecdotal recommendations, the cornerstone of extraperitoneal rectal injuries was based on a triad consisting of fecal diversion, presacral drainage, and distal rectal washout. This practice was challenged in the 1990s. Fecal Diversion or Primary Repair. Fecal diversion remains a useful and unchallenged therapeutic modality in selected cases with extraperitoneal rectal injuries where satisfactory repair cannot be performed because of anatomical location or because of the extent of the injury. A properly constructed loop colostomy may achieve complete fecal diversion, thus avoiding the complex reconstruction required after a Hartmann end colostomy. A loop ileostomy has been suggested as an option.29 The Hartmann’s procedure should be reserved for patients with extensive destruction of the rectum. The role of routine proximal colostomy in all cases with extraperitoneal rectal injury has been challenged in recent studies. It is now a common practice to perform primary repair without proximal fecal diversion in selected cases with small perforations.48,49,53,54 Some extraperitoneal injuries may be difficult to repair because

Distal Rectal Washout. Distal rectal irrigation was added to the management of rectal injuries during the Vietnam War, and was credited for reducing septic complications.65 However, there is no evidence that it is of any value in reducing morbidity. This parallels the data published in prospective randomized studies in nontraumatic colon and rectal operations that show no difference in infectious complications even with rigorous preoperative mechanical cleansing.59,60 It has been suggested that washout may liquefy the rectal contents and facilitate fecal spillage into the surrounding extrarectal soft tissues.

■ Technical Tips Patients with suspected extraperitoneal rectal injuries planned for operative management should be placed on the operating table in the lithotomy position for rigid sigmoidoscopy evaluation. In the hemodynamically unstable patients, due to associated intra-abdominal injuries, an exploratory laparotomy for bleeding control precedes the sigmoidoscopy. Low rectal injuries may be repaired transanally and high rectal injuries can be accessed transperitoneally after dissection of the peritoneum. In mid-rectal injuries, the exposure may be difficult, especially in males with a narrow pelvic inlet. In these cases a proximal diverting sigmoid loop colostomy should be considered without repairing the rectal perforation. It is not necessary to perform a Hartmann’s procedure or staple the distal limb of a loop colostomy in order to achieve complete fecal diversion. A properly constructed loop colostomy can achieve complete fecal diversion. A “bridge” can be created by a plastic rod placed through the mesocolon close to the distal loop of the colostomy. Alternatively, a heavy horizontal mattress suture (silk 1) through the aponeurosis of the external oblique muscle and the mesocolon can achieve an excellent fecal diversion (Fig. 33-7). To enhance the effectiveness of the diversion, a longitudinal colostomy is performed and the edge of the colon is sutured with the absorbable suture 3/0 to the skin incision (Figs. 33-7 and 33-8).

CHAPTER 33 X CHAPTER

accuracy of the digital rectal exam and rigid proctosigmoidoscopy ranges from 80% to 95%.46,47,49,52–54 However, the falsenegative rate of these two exams has been reported to be as high as 31%.55 CT scan with or without rectal contrast or a gastrografin enema study should be considered in selected cases with penetrating injuries to the buttocks.14,56

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X SECTION 3 FIGURE 33-7 A diverting loop colostomy can be achieved by a plastic rod or a heavy suture placed under the loop, through the mesocolon, close to the distal limb of the loop. Alternatively, a heavy horizontal mattress suture (silk 1) is placed through the aponeurosis of the external oblique muscle, mesocolon, contralateral aponeurosis, close to the distal limb of the loop. This creates a “bridge” that compresses the distal loop and achieves full fecal diversion. A longitudinal colostomy is performed and its edges are sutured to the edge of the skin, as shown in Fig. 33-8.

Associated bladder or iliac vessel injuries are commonly seen with rectal injuries and have been reported to occur in more than 50% of the cases.48,53 Every effort should be made to repair the rectal and any genitourinary injuries and separate the repairs with well-vascularized tissue such as omentum in order to reduce the risk of vascular graft infection or the formation of rectovesical fistula, which can occur in up to 24% of patients with combined bladder and rectal injuries52,66 (Fig. 33-9).

Complex anorectal injuries after open pelvic fractures pose a major management challenge. The cases should be managed with hemostasis, wound packing, and a sigmoid colostomy (Fig. 33-10). In rare cases with devastating anorectal injuries an early abdominoperineal resection may be the only option to control massive bleeding and prevent severe postoperative sepsis. Anorectal reconstruction is usually attempted electively or semielectively by an experienced colorectal surgeon.

WAR-RELATED COLORECTAL INJURIES

FIGURE 33-8 Completion of loop colostomy with complete diversion. Stoma inversion is achieved by placing three suture bites that include the edge of the colon, the colonic serosa about 1–2 cm below the edge of the colostomy, and the skin incision (D: Distal loop, P: Proximal loop).

The military surgical experience during the World War II played a major role in establishing protocols and standards of care in colorectal injuries.17,18 However, the recommendation for routine colostomy in all military colorectal injuries has recently been challenged, mainly on the basis of overwhelming evidence from civilian injuries supporting liberal primary repair or anastomosis. In a recent retrospective analysis of 65 war-related colon injuries, Vertrees et al.67 found no difference in outcomes between colostomy and primary repair. In addition, the study reported that damage control and delayed colon anastomosis is safe. In another retrospective analysis of 175 colorectal injuries (primary reconstruction in 53%, stoma in 33%, and damage control in 14%) Steele et al.68 reported that fecal diversion was associated with a decreased leak rate but had no impact on the incidence of sepsis or mortality. However, in a small retrospective of 23 colorectal injuries Duncan et al.69 suggested that colostomy should play a greater role in military casualties.

Colon and Rectal Trauma

For rectal injuries, the manual recommends the traditional 4 “D’s” in rectal injuries: diversion, debridement, distal washout, and presacral drainage. There is no doubt that battlefield injuries have many significant differences from civilian injuries: blast injuries or highvelocity bullet injuries are much more destructive than most civilian trauma; medical evacuation, long transportation times, and disruption of the continuity of postoperative care should be taken into account in deciding the method of operative management of the colon. Continuous and close postoperative monitoring for any signs of intra-abdominal sepsis is critical in the timely diagnosis and treatment of any leaks or abscesses. These differences require that each patient should be treated on a case-by-case basis. FIGURE 33-9 Gastrografin enema shows a rectovesical fistula following repair of a gunshot wound involving the rectum and the bladder. Every effort should be made to separate the two organs with vascularized tissue such as omentum, in order to reduce the risk of this complication.

The 2004 edition of Emergency War Surgery by the Department of Defense70 follows a conservative approach and makes the following recommendations for war-related colorectal injuries: (a) For simple, isolated colon injuries the surgeon is advised to perform debridement and a two-layer anastomosis or repair. The procedure should be clearly identified and

FIGURE 33-10 Open pelvic fracture with anorectal injury. This patient should be managed with hemostasis, packing of the wound, and diverting sigmoid colostomy.

WOUND MANAGEMENT Primary skin wound closure in colon or rectal injuries is an independent risk factor for wound sepsis and fascia dehiscence. In a prospective randomized study, primary wound closure doubled the risk of infection when compared with delayed primary closure.38 In the presence of fecal spillage these patients should be managed by delayed primary closure of the skin 3–5 days postoperatively.

ANTIBIOTIC PROPHYLAXIS In view of the high incidence of septic complications in patients with colon injuries, effective antibiotic prophylaxis is critical. A multicenter AAST study of destructive colon injuries identified inadequate empiric antibiotic coverage as an independent risk factor for abdominal sepsis.6 It is essential that any antibiotic regime covers against both aerobes and anaerobes, especially E. coli and B. fragilis. The role of enterococcus in early abdominal sepsis is controversial, although its pathogenicity in nosocomial abdominal infections is universally accepted. Most of the currently used prophylactic antibiotic regimes do not cover enterococcus, although some studies support enterococcal coverage.6,71 The issue is still unresolved and merits further investigation. Monotherapy is as effective as combination therapy72,73 and the specific antibiotic choice should be based on the individual hospital’s antibiogram. The duration of antibiotic prophylaxis has been a controversial issue. There is now class I evidence that 24-hour prophylaxis is at least as effective as prolonged prophylaxis for 3–5 days, even in the presence of major risk factors for abdominal sepsis, such as colon injury, multiple blood transfusions, and high Abdominal Trauma Index.74

CHAPTER 33 X CHAPTER

highlighted in cases planned for medical evacuation or change of the medical team taking care of the patient. (b) For complex injuries, especially in the presence of ongoing hypotension, hypoxia, massive blood transfusions, multiple associated injuries, high-velocity injuries, and extensive local tissue damage, a colostomy should be considered. (c) For indigent or enemy combatant victims who cannot be readily evacuated a colostomy is recommended.

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TRAUMA OSTOMY COMPLICATIONS X SECTION 3

There are numerous complications directly related to the creation of a colostomy or subsequent colostomy closure. The most common serious colostomy complications include necrosis, retraction, prolapse, parastomal abscess, and parastomal hernia. Other complications include troublesome skin irritation and difficulties in the application of the collection bag because of poor ostomy location. In a series of 528 trauma stomas Park et al. reported an incidence of 22% of severe or minor early complications and 3% of late complications.75 In a collective review of 1,085 colostomy closures the overall complication rate was 14.8%.76 Another single-center study of 110 colostomy closures reported an overall local complication rate of 14.5%, including 2.7% colon leaks.77

TIMING OF TRAUMA OSTOMY CLOSURE The optimal timing of colostomy closure is a debated issue. Traditionally, a minimum of 3 months from the original operation has been advocated in order to allow time for the colostomy to “mature.”78,79 Subsequent studies showed that closure of the stoma earlier than 3 months is safe and not associated with increased complication rates.77,80 More recent studies even recommended closure during the initial hospitalization, sometimes within 2 weeks of the colostomy creation.81,82 The optimal time for colostomy closure should be individualized, taking into account the nutritional recovery of the patient and complete healing of all the wounds. This might vary from a few weeks for some patients to many months in severe multitrauma patients.

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Colon and Rectal Trauma 62. Navsaria PH, Shaw JM, Zellweger R, Nicol AJ, Kahn D. Diagnostic laparoscopy and diverting sigmoid loop colostomy in the management of civilian extraperitoneal rectal gunshot injuries. Br J Surg. 2004;91(4): 460–464. 63. Navsaria PH, Graham R, Nicol A. A new approach to extraperitoneal rectal injuries: laparoscopy and diverting loop sigmoid colostomy. J Trauma. 2001;51(3):532–535. 64. Levy RD, Strauss P, Aladgem D, Degiannis E, Boffard KD, Saadia R. Extraperitoneal rectal gunshot injuries. J Trauma. 1995;38(2): 273–277. 65. Lavenson GS, Cohen A. Management of rectal injuries. Am J Surg. 1971; 122(2):226–230. 66. Franko ER, Ivatury RR, Schwalb DM. Combined penetrating rectal and genitourinary injuries: a challenge in management. J Trauma. 1993; 34(3):347–353. 67. Vertrees A, Wakefield M, Pickett C, et al. Outcomes of primary repair and primary anastomosis in war-related colon injuries. J Trauma. 2009; 66(5):1286–1291 [discussion 1291–1293]. 68. Steele SR, Wolcott KE, Mullenix PS, et al. Colon and rectal injuries during Operation Iraqi Freedom: are there any changing trends in management or outcome? Dis Colon Rectum. 2007;50(6):870–877. 69. Duncan JE, Corwin CH, Sweeney WB, et al. Management of colorectal injuries during Operation Iraqi Freedom: patterns of stoma usage. J Trauma. 2008;64(4):1043–1047. 70. Szul AC, Davis LB, eds. Emergency War Surgery: Third United States Revision. 3rd ed. Washington, DC: United States Department of Defense; 2004:13–14:chap 17. 71. Weigelt JA, Easley SM, Thal ER, Palmer LD, Newman VS. Abdominal surgical wound infection is lowered with improved perioperative enterococcus and bacteroides therapy. J Trauma. 1993;34(4): 579–584. 72. Hooker KD, DiPiro JT, Wynn JJ. Aminoglycoside combinations versus beta-lactams alone for penetrating abdominal trauma: a meta-analysis. J Trauma. 1991;31(8):1155–1160. 73. Sims EH, Thadepalli H, Ganesan K, Mandal AK. How many antibiotics are necessary to treat abdominal trauma victims? Am Surg. 1997;63(6): 525–535. 74. Cornwell EE 3rd, Dougherty WR, Berne TV, et al. Duration of antibiotic prophylaxis in high-risk patients with penetrating abdominal trauma: a prospective randomized trial. J Gastrointest Surg. 1999;3(6):648–653. 75. Park JJ, Del Pino A, Orsay CP, et al. Stoma complications: the Cook County Hospital experience. Dis Colon Rectum. 1999;42(12): 1575–1580. 76. Berne JD, Velmahos GC, Chan LS, Asensio JA, Demetriades D. The high morbidity of colostomy closure after trauma: further support for the primary repair of colon injuries. Surgery. 1998;123(2):157–164. 77. Demetriades D, Pezikis A, Melissas J, Parekh D, Pickles G. Factors influencing the morbidity of colostomy closure. Am J Surg. 1988; 155(4):594–596. 78. Freund HR, Raniel J, Muggia-Sulam M. Factors affecting the morbidity of colostomy closure: a retrospective study. Dis Colon Rectum. 1982;25(7):712–715. 79. Parks SE, Hastings PR. Complications of colostomy closure. Am J Surg. 1985;149(5):672–675. 80. Renz BM, Feliciano DV, Sherman R. Same admission colostomy closure (SACC). A new approach to rectal wounds: a prospective study. Ann Surg. 1993;218(3):279–292. 81. Velmahos GC, Degiannis E, Wells M, Souter I, Saadia R. Early closure of colostomies in trauma patients—a prospective randomized trial. Surgery. 1995;118(5):815–820. 82. Khalid MS, Moeen S, Khan AW, Arshad R, Khan AF. Same admission colostomy closure: a prospective, randomised study in selected patient groups. Surgeon. 2005;3(1):11–14.

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39. Curran TJ, Borzotta AP. Complications of primary repair of colon injury: literature review of 2,964 cases. Am J Surg. 1999;177(1):42–47. 40. Kanellos I, Mantzoros I, Demetriades H, et al. Healing of colon anastomoses covered with fibrin glue after immediate postoperative intraperitoneal administration of 5-fluorouracil. Dis Colon Rectum. 2004; 47(4):510–515. 41. van der Ham AC, Kort WJ, Weijma IM, van den Ingh HF, Jeekel J. Effect of fibrin sealant on the healing colonic anastomosis in the rat. Br J Surg. 1991;78(1):49–53. 42. Merad F, Hay JM, Fingerhut A, Flamant Y, Molkhou JM, Laborde Y. Omentoplasty in the prevention of anastomotic leakage after colonic or rectal resection: a prospective randomized study in 712 patients. French Associations for Surgical Research. Ann Surg. 1998;227(2):179–186. 43. Demetriades D, Murray JA, Chan LS, et al. Handsewn versus stapled anastomosis in penetrating colon injuries requiring resection: a multicenter study. J Trauma. 2002;52(1):117–121. 44. Burch JM, Franciose RJ, Moore EE, Biffl WL, Offner PJ. Single layer continuous versus two-layer interrupted intestinal anastamosis: a prospective study. Ann Surg. 2000;231:832–837. 45. Law WL, Bailey HR, Max E, et al. Single-layer continuous colon and rectal anastomosis using monofilament absorbable suture (Maxon): study of 500 cases. Dis Colon Rectum. 1999;42(6):736–740. 46. Morken JJ, Kraatz JJ, Balcos EG, et al. Civilian rectal trauma: a changing perspective. Surgery. 1999;126(4):693–698 [discussion 698–700]. 47. Burch JM, Feliciano DV, Mattox KL. Colostomy and drainage for civilian rectal injuries: is that all? Ann Surg. 1989;209(5):600–610 [discussion 610–611]. 48. Thomas DD, Levison MA, Dykstra BJ, Bender JS. Management of rectal injuries. Dogma versus practice. Am Surg. 1990;56(8):507–510. 49. Levine JH, Longo WE, Pruitt C, Mazuski JE, Shapiro MJ, Durham RM. Management of selected rectal injuries by primary repair. Am J Surg. 1996;172(5):575–578 [discussion 578–579]. DOI: 10.1016/S00029610(96)00244-9. 50. Tuggle D, Huber PJ Jr. Management of rectal trauma. Am J Surg. 1984;148(6):806–808. 51. Brunner RG, Shatney CH. Diagnostic and therapeutic aspects of rectal trauma. Blunt versus penetrating. Am Surg. 1987;53(4):215–219. 52. Ivatury RR, Licata J, Gunduz Y, Rao P, Stahl WM. Management options in penetrating rectal injuries. Am Surg. 1991;57(1):50–55. 53. Velmahos GC, Gomez H, Falabella A, Demetriades D. Operative management of civilian rectal gunshot wounds: simpler is better. World J Surg. 2000;24(1):114–118. 54. McGrath V, Fabian TC, Croce MA, Minard G, Pritchard FE. Rectal trauma: management based on anatomic distinctions. Am Surg. 1998; 64(12):1136–1141. 55. Grasberger RC, Hirsch EF. Rectal trauma. A retrospective analysis and guidelines for therapy. Am J Surg. 1983;145(6):795–799. 56. Anderson SW, Soto JA. Anorectal trauma: the use of computed tomography scan in diagnosis. Semin Ultrasound CT MR. 2008;29(6):472–482. 57. Steinig JP, Boyd CR. Presacral drainage in penetrating extraperitoneal rectal injuries: is it necessary? Am Surg. 1996;62(9):765–767. 58. Gonzalez RP, Falimirski ME, Holevar MR. The role of presacral drainage in the management of penetrating rectal injuries. J Trauma. 1998; 45(4):656–661. 59. Zmora O, Mahajna A, Bar-Zakai B, et al. Colon and rectal surgery without mechanical bowel preparation: a randomized prospective trial. Ann Surg. 2003;237(3):363–367. 60. Slim K, Vicaut E, Launay-Savary MV, Contant C, Chipponi J. Updated systematic review and meta-analysis of randomized clinical trials on the role of mechanical bowel preparation before colorectal surgery. Ann Surg. 2009;249(2):203–209. 61. Navsaria PH, Edu S, Nicol AJ. Civilian extraperitoneal rectal gunshot wounds: surgical management made simpler. World J Surg. 2007; 31(6):1345–1351.

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Abdominal Vascular Injury Christopher J. Dente and David V. Feliciano

The major sites of hemorrhage in patients sustaining blunt or penetrating abdominal trauma are the viscera, the mesentery, and the major abdominal vessels. The term abdominal vascular injury generally refers to injury to major intraperitoneal or retroperitoneal vessels and is generally classified into four zones described as follows and in Table 34-1: • Zone 1: midline retroperitoneum ❍ Supramesocolic region ❍ Inframesocolic region • Zone 2: upper lateral retroperitoneum • Zone 3: pelvic retroperitoneum • Porta hepatis/retrohepatic inferior vena cava As many of these vessels are somewhat difficult to quickly access via a midline laparotomy incision, a systematic operative approach is required to adequately diagnose and manage these potentially devastating injuries. A general discussion of epidemiology and methods of diagnosis, with subsequent descriptions of the operative management of abdominal vascular injuries within each region of the abdomen, follows.

EPIDEMIOLOGY In reviews of vascular injuries sustained in military conflicts, abdominal vascular injuries have been extraordinarily rare. For example, DeBakey and Simeone’s classic article on 2,471 arterial injuries during World War II included only 49 that occurred in the abdomen, an incidence of 2%.1 Reporting on 304 arterial injuries from the Korean conflict, Hughes noted that only 7, or 2.3%, occurred in the iliac arteries.2 In the review by Rich et al. of 1,000 arterial injuries in the Vietnam War, only 29, or 2.9%, involved abdominal vessels.3 Finally, a recent review of abdominal injuries during the Iraqi conflict documented only 4 injuries to major vessels in 145 patients undergoing laparotomy (2.8%).4

The data from civilian trauma centers are quite different. In 1979, 15% of patients with abdominal trauma treated at the Ben Taub General Hospital in Houston had injuries to major vascular structures.5 Also, abdominal vascular injury accounted for 27.5% of all arterial injuries treated over that same time period. A similar review from the same hospital in 1982 revealed that 31.9% of all vascular injuries occurred in the abdomen, including 18.5% of all arterial injuries and 47.5% of all venous injuries.6 Finally, a 30-year review (1958–1988) at the same hospital, published in 1989, documented that 33.8% of 5,760 cardiovascular injuries occurred in the abdomen.7 In the last 5 years of the period covered by the report (1984–1988), abdominal vascular injuries accounted for 27.3% of all cardiovascular injuries. Even with the recent decrease in the volume of penetrating trauma in some centers, many patients with abdominal vascular injuries continue to be treated. For example, there were 302 patients with 238 abdominal arterial and 266 abdominal venous injuries who underwent operative repair at the Los Angeles County Hospital (University of Southern California) from 1992 to 1997.8 Similarly, there were 300 patients with 205 abdominal arterial and 284 abdominal venous injuries who underwent operative repair at the Grady Memorial Hospital (Emory University) from 1989 to 1998.9 The significantly higher number of abdominal vascular injuries treated in civilian as opposed to military practice likely reflects the modest wounding capacity of many handguns when compared with military ordinance, as well as the shorter prehospital transit times in most urban areas of the United States. Advances in military armor and the changing tactics of modern warfare also have led to a shift in injuries to the extremities rather than the torso, although noncompressible (torso) hemorrhage remained the leading cause of combatant death from hemorrhage in a recent review.10 At present, the estimated incidence of injury to major abdominal vessels in patients sustaining blunt abdominal

Abdominal Vascular Injury

633

TABLE 34-1 Classification of Abdominal Vascular Injury Zone

1 (inframesocolic) 2 3

Porta hepatis

Operative Maneuversa Left medial visceral rotation Midline suprarenal aortic exposure

Renal artery

Infrahepatic inferior vena cava Renal vein

Common, external, and internal iliac arteries

Common, external, and internal iliac veins

Hepatic artery

Portal vein Retrohepatic vena cava

Right medial visceral rotation Midline infrarenal aortic exposure Midline control of the renal hilum Lateral control of the renal hilum Midline control of iliac arteries and veins Isolation and control of right common iliac vein/vena caval confluence Total pelvic isolation Portal exposure Exposure and control of retrohepatic inferior vena cava

a

Discussed in Sections “Exposure and Vascular Control.”

trauma is thought to be about 5–10%.11,12 This is compared with patients with penetrating stab wounds to the abdomen, who will sustain a major abdominal vascular injury approximately 10% of the time (V. Spjut-Patrinely, D. V. Feliciano, Data from Ben Taub General Hospital, Houston, Texas, July 1985 to June 1988, unpublished), and patients with gunshot wounds to the abdomen, who will have injury to a major vessel 20–25% of the time.13

PATHOPHYSIOLOGY ■ Blunt Trauma Rapid deceleration in motor vehicle crashes may cause two different types of vascular injuries in the abdomen. The first is avulsion of small branches from major vessels, with subsequent hemorrhage. A common example of this is the avulsion of intestinal branches from either the proximal or distal superior mesenteric artery at sites of fixation. A second type of vascular problem seen with deceleration injury is an intimal tear with secondary thrombosis of the lumen, such as is seen in patients with renal artery thrombosis, or a full-thickness tear with a secondary pseudoaneurysm of the renal artery.14–16 Crush injuries to the abdomen, such as by a lap seat belt or by a posterior blow to the spine, also may cause two different types of vascular injury. The first is an intimal tear or flap with secondary thrombosis of a vessel such as the superior mesenteric artery,17 infrarenal abdominal aorta,18,19 or iliac artery.20,21 The “seat belt aorta” is a classic example of an injury resulting from this mechanism.18,22 Direct blows can also completely disrupt exposed vessels, such as the left renal vein over the aorta23 or the superior mesenteric artery or vein at the base of the mesentery,24 leading to massive intraperitoneal hemorrhage, or even partly disrupt the infrarenal abdominal aorta, leading to a false aneurysm.25,26

■ Penetrating Trauma Penetrating injuries, in contrast, create the same kinds of abdominal vascular injuries as are seen in the vessels of the extremities, producing blast effects with intimal flaps and secondary thrombosis, lateral wall defects with hemorrhage or pulsatile hematomas (early false aneurysms), or complete transection with either free bleeding or thrombosis.27 On rare occasions, a penetrating injury may produce an arteriovenous fistula involving the portal vein and hepatic artery, renal vessels, or iliac vessels. Iatrogenic injuries to major abdominal vessels are an uncommon but persistent problem. Reported iatrogenic causes of abdominal vascular injury have included diagnostic procedures (angiography, cardiac catheterization, laparoscopy), abdominal operations (pelvic and retroperitoneal procedures), spinal operations (removal of a herniated disk), and adjuncts to cardiac surgery (cardiopulmonary bypass, intraaortic balloon assist).28–30

DIAGNOSIS ■ History and Physical Examination An abdominal vascular injury may present in one of three ways including free intraperitoneal hemorrhage, a contained intraperitoneal or retroperitoneal hematoma, and thrombosis of the vessel. As such, patients can be quickly divided into two major groups including those with ongoing hemorrhage and those without ongoing hemorrhage (contained hematoma or thrombosis). The presenting symptoms, thus, are variable based on both the event and the involved vessel. After blunt trauma, for example, free intraperitoneal hemorrhage may be seen with avulsion of mesenteric vessels and lead to secondary hypovolemic shock. Conversely, when thrombosis of the renal artery is present, the patient will be hemodynamically stable but may

CHAPTER 34

1 (supramesocolic)

Major Venous Branches Superior mesenteric vein

Major Arterial Branches Suprarenal aorta Celiac axis Superior mesenteric artery Proximal renal artery Infrarenal aorta

634

Management of Specific Injuries

SECTION 3

complain of upper abdominal and flank pain and will commonly have hematuria (70–80%).16 Thrombosis of the proximal superior mesenteric artery will cause severe abdominal pain, while thrombosis of the infrarenal abdominal aorta will cause pulseless lower extremities. Penetrating truncal wounds between the nipples and the upper thighs remain the most common cause of abdominal vascular injuries. The exact vessel injured is generally related to the track of the missile or stab wound. For example, gunshot wounds directly on the midline most commonly involve the inferior vena cava or abdominal aorta. Gunshot wounds traversing the pelvis will often injure branches of the iliac artery or vein, while gunshot wounds in the right upper quadrant may involve the renovascular structures, vascular structures within the porta hepatis, or the retrohepatic inferior vena cava. On physical examination, the findings in patients with abdominal vascular injury will obviously depend on whether a contained hematoma or active hemorrhage is present. Patients with contained hematomas in the retroperitoneum, base of the mesentery, or hepatoduodenal ligament, particularly those with injuries to abdominal veins, may be hypotensive in transit but often respond rapidly to the infusion of fluids. They may remain remarkably stable, with modest or even no peritoneal signs on examination, until the hematoma is opened at the time of laparotomy. These patients are candidates for the imaging studies mentioned below. Conversely, patients with active hemorrhage generally have a rigid abdomen and unrelenting hypotension. These patients should obviously undergo immediate laparotomy without further evaluation. In a review by Ingram et al. of 70 consecutive patients undergoing laparotomy for an abdominal vascular injury, patients could generally be divided into two groups based on an admission systolic blood pressure greater than or less than 100 mm Hg.31 In the former group, the mean base deficit on admission was 7.2, blood replacement in the operating room was 8.6 U, an isolated venous injury was present in 73.1% of patients, and survival was 96.2%. This was compared with a 43% survival and an average of 15.1 U of blood replacement in patients presenting with hypotension (Table 34-2). Indeed, admission base deficit was the only independent indicator of mortality in a recent series of

patients with abdominal vascular injuries from Lincoln Hospital in New York City.32 The other major physical finding that may be noted in patients with abdominal vascular injury is loss of the pulse in the femoral artery in one lower extremity when the ipsilateral common or external iliac artery has been transected or is thrombosed. In such patients, the presence of a transpelvic gunshot wound associated with a wavering or an absent pulse in the femoral artery is pathognomonic of injury to the ipsilateral iliac artery.

■ Imaging In both stable and unstable patients, a rapid surgeon-performed ultrasound (Focused Assessment for the Sonographic Evaluation of the Trauma Patient [“FAST”]) is useful in ruling out an associated cardiac injury with secondary tamponade or an associated hemothorax mandating the insertion of a thoracostomy tube.33–36 In a stable patient with an abdominal gunshot wound, a routine flat-plate x-ray of the abdomen is of diagnostic value, so that the track of the missile can be predicted from markers placed over the wounds or from the position of a retained missile. In former years, all patients who had suffered penetrating abdominal wounds and who were not in shock would undergo a one-shot intravenous pyelogram (IVP) in the emergency department. The major purposes of this study were as follows: to evaluate the function of both kidneys, with lack of flow to one kidney suggesting either absence of the kidney or thrombosis of the renal artery; the presence of active hemorrhage from the kidney itself; and the position and status of the ureters. This study is no longer performed routinely and is indicated only in stable patients with a flank wound and gross hematuria when the computed tomography (CT) scanner is not available. In patients with blunt abdominal trauma, hematuria, modest to moderate hypotension, and peritonitis in the emergency department, a preoperative one-shot IVP during resuscitation would still be useful for documenting the presence of an intact kidney. If the kidney is mostly intact without extravasation of the dye, the surgeon will not have to open a perirenal hematoma at the subsequent laparotomy. Nonvisualization of one

TABLE 34-2 Blood Pressure in the Emergency Department in Patients with Abdominal Vascular Injury

Lowest SBP in emergency room Admission base deficit Blood transfusion in operating room (U) Venous injury only Injury to one vessel only Survival

Systolic Blood Pressure 100 mm Hg (n ⴝ 26) 100 mm Hg (n ⴝ 44) 123 62 7.2 14.7 8.6 15.1 73.1% 40.9% 76.9% 52.3% 96.2% 43.2%

P-Value .001 .001 .003 .009 .04 .001

Reproduced from Ingram WL, Feliciano DV, Renz BL, et al. Blood pressure in the emergency department in patients with abdominal vascular injuries: effect on management and prognostic valve. Presented at: 55th Annual Meeting of the American Association for the Surgery of Trauma; September 27–30, 1995; Halifax, Nova Scotia, Canada.

Abdominal Vascular Injury

INITIAL MANAGEMENT AND RESUSCITATION ■ Prehospital Resuscitation Resuscitation in the field in patients with possible blunt or penetrating abdominal vascular injuries should be restricted to basic airway maneuvers such as intubation or cricothyroidotomy and decompression of a tension pneumothorax at the scene. Insertion of intravenous lines for infusing crystalloid solutions is best attempted during transport to the hospital. Restoration of blood pressure to normal levels is critical to neurologic recovery in the rare patients with associated blunt intracranial injuries and possible abdominal vascular injuries.43 In contrast, there is no consistent evidence to support either the aggressive administration of crystalloid solutions during the

short prehospital times in urban environments or the withholding of similar solutions (“delayed resuscitation”) in patients with penetrating abdominal vascular injuries.44,45 Indeed, a key component of “damage control resuscitation” as espoused by the US military and discussed below is minimization of early crystalloid resuscitation.46

■ Emergency Department Resuscitation In the emergency department, the extent of resuscitation clearly depends on the patient’s condition at the time of arrival. In the agonal patient with a rigid abdomen after a gunshot wound, emergency department thoracotomy with cross-clamping of the descending thoracic aorta may be necessary to maintain cerebral and coronary arterial flow, especially if the trauma operating room is geographically distant from the emergency department.47 Although all trauma surgeons agree that performing a thoracotomy in the emergency department will complicate the patient’s intraoperative course, the thoracotomy and cross-clamping are sometimes the only way to prevent irreversible ischemic changes in the patient’s brain and heart until a laparotomy with vascular control can be performed. It must be recognized, however, that the need for emergency department thoracotomy is essentially predictive of a 5% survival for the patient with blunt or penetrating abdominal trauma.48 In the large series by Feliciano et al.,47 only 1 of 59 patients with isolated penetrating wounds to the abdomen survived after undergoing a preliminary thoracotomy in the emergency department. In the patient arriving with blunt abdominal trauma, hypotension, and a positive surgeon-performed “FAST” or penetrating abdominal trauma and hypotension or peritonitis, a time limit of less than 5 minutes in the emergency department is mandatory. An identification bracelet is applied, an airway and thoracostomy tube are inserted if necessary, especially if the operating room is geographically distant, and blood samples for typing and cross-matching are obtained with the insertion of the first intravenous catheter. Whether more intravenous lines should be inserted in the emergency department or after arrival in the operating room is much debated. The authors have always believed that patients needing an emergency laparotomy should be in the operating room, as soon as the identification bracelet has been applied and a blood specimen has been sent to the blood bank. There are now multiple large-bore catheters, specialized administration sets, and heating elements commercially available for use in the emergency department or operating room. With short, large-bore (10-gauge or number 8.5 French) catheters in peripheral veins, flow rates of 1,400–1,600 mL/ min of crystalloid solutions can be obtained when an external pressure device is exerting 300 mm Hg pressure.49 Blood replacement during resuscitation is usually with type-specific blood, although universal donor type O negative blood may be used when there is no time for even a limited cross-match. Measures in the emergency department that will diminish the hypothermia of resuscitation include the following: a heated resuscitation room, the use of prewarmed (37–40°C [98.6–104.0°F]) crystalloid solutions, passage of all

CHAPTER 34

kidney on the IVP, suggesting thrombosis of the renal artery, was evaluated by renal arteriography in stable patients in the past. Experience with CT scanning of the abdomen in multiple patients with blunt trauma has documented that the absence of renal enhancement and excretion and the presence of a cortical rim sign are diagnostic of thrombosis of the renal artery, and arteriography is no longer indicated for this diagnosis.37 Similarly, any stable patient with blunt trauma who does not require an immediate laparotomy and who has significant hematuria should undergo an immediate abdominal CT scan without a preliminary one-shot IVP.38 Preoperative abdominal aortography should not be routinely performed to document intra-abdominal vascular injuries after penetrating wounds. This is because most patients with such wounds are not stable enough to undergo the manipulation required for appropriate studies of large vessels in an angiographic suite. In patients with blunt trauma, aortography is used to diagnose and treat deep pelvic arterial bleeding associated with fractures39 and to diagnose unusual injuries such as the previously mentioned intimal tears with thrombosis in the infrarenal aorta, the iliac artery, or the renal artery. The occasional patient is also a candidate for endovascular therapy and this will be discussed below. As the technology of CT scanning has advanced, many surgeons and radiologists are comfortable making therapeutic decisions based on data acquired from multiplanar scanning and formal CT angiography. Extensive literature exists on the diagnosis of traumatic thoracic aortic disruption with CT40 and at least one small prospective study has shown acceptable accuracy of CT angiography in extremity trauma.41 Conversely, data on the use of CT angiography as a method of diagnosis of abdominal vascular injury remain preliminary. Indeed, in one recent study, contrast-enhanced CT alone had a 94% sensitivity and 89% specificity for the diagnosis of active hemorrhage when compared with angiography.42 Most of the positive scans involved branches of the internal iliac artery with a concomitant pelvic fracture or injuries to solid organs and, thus, were not necessarily diagnostic of true abdominal vascular injury. Still, in the stable patient with blunt trauma, findings on CT that are suggestive of injury to the retroperitoneal great vessels warrant further evaluation with angiography or operative intervention.

635

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Management of Specific Injuries crystalloids and blood through high-flow warmers, and covering the patient’s trunk and extremities with prewarmed blankets or heating units.48–50

SECTION 3

■ Damage Control Resuscitation and Massive Transfusion In the last 5 years, based mostly on the military experience in Iraq, there has been a dramatic change in the resuscitation philosophy of critically injured patients in many centers. The military resuscitation philosophy of “damage control resuscitation” is seen as an extension of the concepts of “damage control surgery,” a term coined in the early 1990s by Rotondo et al.51 One cornerstone of damage control resuscitation is the early and aggressive use of either fresh whole blood or blood components (fresh frozen plasma and platelets) in high, defined ratios to packed red blood cells. In the civilian setting, this practice requires the support of the blood bank and a highly organized massive transfusion protocol (MTP). Multiple civilian centers have now published their results using institutionspecific MTPs, generally with significant improvements in patient outcome.52–55 As many patients with abdominal vascular injury will require massive transfusion, the treating surgeons should be familiar with the design and implementation of any MTP that exists in their institution. The concepts of damage control surgery, damage control resuscitation, and massive transfusion will be covered in much more detail elsewhere in this text.

OPERATIVE PREPERATIONS ■ Draping and Incisions In the operating room, the entire trunk from the chin to the knees is prepared and draped in the usual manner. Before making the incision for laparotomy, the trauma surgeon should confirm that the following items are available: blood components for transfusion, autotransfusion apparatus, a thoracotomy tray, an aortic compressor, a complete tray of vascular instruments, sponge sticks with gauze sponges in place for venous compression, as well as appropriate vascular sutures.

■ Maneuvers to Prevent or Decrease Hypothermia In addition to the maneuvers previously described for preventing hypothermia in the emergency department, operative maneuvers with the same purpose include warming the operating room to 85°F (29.4°C); covering the patient’s head; covering the upper and lower extremities with a heating unit (Bair Hugger, Augustine Medical, Inc, Eden Prairie, Minnesota); the irrigation of nasogastric tubes, thoracostomy tubes, and open body cavities with warm saline; and the use of a heating cascade on the anesthesia machine.56

■ General Principles A preliminary operating room thoracotomy with crossclamping of the descending thoracic aorta is used in some

centers when the patient’s blood pressure on arrival is less than 70 mm Hg.57–59 As previously mentioned, this maneuver will maintain cerebral and coronary arterial flow if the heart is still beating and may prevent sudden cardiac arrest when abdominal tamponade is released. Unfortunately, it has little effect on intra-abdominal vascular injuries because of persistent bleeding from backflow. Indeed, patients with unrelenting shock after cross-clamping of the descending thoracic aorta essentially never survive.59 A midline abdominal incision is made, and all clots and free blood are manually evacuated or removed with suction. A rapid inspection is performed to visualize contained hematomas or areas of hemorrhage. One intra-abdominal physical finding that may be of diagnostic benefit to the surgeon is “black bowel,” which has been seen in patients with total transection or thrombosis of the proximal superior mesenteric artery. In a patient with a penetrating upper abdominal wound, a large hematoma in the supramesocolic area, and black bowel, an injury to the superior mesenteric artery is likely to be present.60 Active hemorrhage from solid organs is controlled by packing, while standard techniques of vascular control are used to control the active hemorrhage from major intra-abdominal vessels. Finger pressure, compression with laparotomy pads, grabbing the perforated artery with a hand (common or external iliac artery), or formal proximal and distal control is needed to control any actively hemorrhaging major artery. Similarly, options for control of bleeding from major veins such as the inferior vena cava, superior mesenteric vein, renal veins, or iliac veins include finger pressure, compression with laparotomy pads or sponge sticks, grabbing the perforated vein with a hand, applying Judd-Allis clamps to the edges of the perforation,61 and the application of vascular clamps. Once hemorrhage from the vascular injuries is controlled in patients with penetrating wounds, it may be worthwhile to rapidly apply Babcock clamps, Allis clamps, or noncrushing intestinal clamps, or to rapidly use a surgical stapler to control as many gastrointestinal perforations as possible to avoid further contamination of the abdomen during the period of vascular repair. The abdomen is irrigated with an antibiotic–saline solution, the vascular repair is then performed, a soft tissue cover is applied over the repair, and the remainder of the operation is directed toward repair of injuries to the bowel and solid organs. Conversely, if the patient has a contained retroperitoneal hematoma at the time of laparotomy, the surgeon occasionally has time to first perform necessary gastrointestinal repairs in the free peritoneal cavity, change gloves, and irrigate with an antibiotic–saline solution. The surgeon can then open the retroperitoneum to expose the underlying abdominal vascular injury. Hematomas or hemorrhage associated with abdominal vascular injuries generally occur in zone 1, midline retroperitoneum; zone 2, upper lateral retroperitoneum; zone 3, pelvic retroperitoneum; or the portal–retrohepatic area of the right upper quadrant, as previously described (Table 34-1). The magnitude of injury is best described using the Organ Injury Scale of the American Association for the Surgery of Trauma (AAST).62

Abdominal Vascular Injury

Plane of dissection

MANAGEMENT OF INJURIES IN ZONE 1: SUPRAMESOCOLIC REGION ■ Exposure and Vascular Control The midline retroperitoneum of zone 1 is divided by the transverse mesocolon into a supramesocolic region and an inframesocolic region. If a hematoma or hemorrhage is present in the midline supramesocolic area, injury to the suprarenal aorta, celiac axis, proximal superior mesenteric artery, or proximal renal artery should be suspected. In such cases, there are several techniques for obtaining proximal vascular control of the aorta at the hiatus of the diaphragm. When a contained hematoma is present, as it frequently is with wounds to the aorta in the aortic hiatus, the surgeon usually has time to reflect all left-sided intra-abdominal viscera, including the colon, kidney, spleen, tail of the pancreas, and fundus of the stomach to the midline (left-sided medial visceral rotation) (Fig. 34-1).63–66 The advantage of this technique is that it provides extensive exposure for visualization of the entire abdominal aorta from the aortic hiatus of the diaphragm to the aortic bifurcation. Disadvantages include the time required to complete the maneuver (5–7 minutes), risk of damage to the spleen, left kidney, or posterior left renal artery during the maneuver, and a fold in the aorta that results when the left kidney is rotated anteriorly. One alternative is to leave the left kidney in its fossa, thereby eliminating potential damage to or distortion resulting from rotation of this structure. In either case, this maneuver provided the best exposure and allowed for the greatest survival in a series of 46 patients with suprarenal aortic injuries studied at Ben Taub General Hospital in Houston, Texas, in the 1970s.65 Because of the dense nature of the celiac plexus of nerves connecting the right and left celiac ganglia as well as the lymphatics that surround the supraceliac aorta, it is frequently helpful to transect the left crus of the aortic hiatus of the diaphragm at the 2 o’clock position to allow for exposure of the

A

Superior mesenteric a.

Left renal a.

Celiac axis

©Baylor College of Medicine 1986

Aorta B

FIGURE 34-2 (A) View of suprarenal aorta and major branches after left-sided medial mobilization maneuver. (B) Diagrammatic representation of structures with labels. (Reproduced with permission from Baylor College of Medicine.)

CHAPTER 34

FIGURE 34-1 Left medial visceral mobilization is performed in the retroperitoneal plane behind all left-sided intra-abdominal viscera in a patient with a supramesocolic hematoma in the midline. (Reproduced with permission from Feliciano DV. Truncal vascular trauma. In: Callow AD, Ernst CB, eds. Vascular Surgery. Theory and Practice. Stamford, CT: Appleton & Lange; 1995:1059–1085. © The McGraw-Hill Companies, Inc.)

distal descending thoracic aorta above the hiatus.67 With the distal descending thoracic aorta in the hiatus exposed, a supraceliac aortic clamp can be applied without difficulty. This allows for the extra few centimeters of exposure that is essential for complex repair of the vessels within this tightly confined anatomic area. Conversely, if active hemorrhage is coming from this area, the surgeon may attempt to control it manually or with one of the aortic compression devices.68,69 Failing this, an alternate approach is to divide the lesser omentum manually, retract the stomach and esophagus to the left, and digitally separate the muscle fibers of the aortic hiatus of the diaphragm from the supraceliac aorta to obtain similar, if not more, limited exposure as described for the left-sided medial visceral rotation, but more quickly.70 After either approach to the suprarenal abdominal aorta, cross-clamp time should be minimized to avoid the primary fibrinolytic state that occurs, presumably due to hepatic hypoperfusion.71 Distal control of the aorta in this location is awkward because of the presence of the celiac axis and superior mesenteric artery (Fig. 34-2).

637

638

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SECTION 3

In some patients with injury confined to the supraceliac aorta, the celiac axis may have to be divided and ligated to allow for more space for the distal aortic clamp and subsequent vascular repair. Necrosis of the gallbladder is a likely sequela, and cholecystectomy is generally warranted, although this may be done at repeat exploration when “damage control” techniques are required.72

■ Suprarenal Aorta With small perforating wounds to the aorta at this level, lateral aortorrhaphy with 3-0 or 4-0 polypropylene suture is preferred. If two small perforations are adjacent to one another, they should be connected and the defect closed in a transverse fashion with the polypropylene suture. When closure of the perforations results in significant narrowing, or if a portion of the aortic wall is missing, patch aortoplasty with polytetrafluoroethylene (PTFE) is indicated. The other option is to resect a short segment of the injured aorta and attempt to perform an end-to-end anastomosis. Unfortunately, this is often impossible because of the limited mobility of both ends of the aorta at this level. On rare occasions, patients with extensive injuries to the diaphragmatic or supraceliac aorta will require insertion of a synthetic vascular conduit or spiral graft after resection of the area of injury.73–75 Many of these patients have associated gastric, enteric, or colonic injuries, and much concern has been expressed about placing a synthetic conduit, such as a 12-, 14-, or 16-mm woven Dacron, albumin-coated Dacron, or PTFE prosthesis, in the abdominal aorta (Fig. 34-3). The data in the American literature describing young patients with injuries to nondiseased abdominal aortas do not support the concern about Dacron interposition grafts, and there are

FIGURE 34-3 A 22-year-old man with a gunshot wound to the right upper quadrant had injuries to the prepyloric area of the stomach and to the supraceliac abdominal aorta. The aortic injury was managed by segmental resection and replacement with a 16-mm polytetrafluoroethylene (PTFE) graft. The patient was discharged 46 days after injury. (Reproduced with permission from Feliciano DV. Injuries to the great vessels of the abdomen. In: Holcroft JW, ed. Scientific American Surgery. Trauma Section. New York: Scientific American; 1998:1–12.)

few reports describing the use of PTFE grafts in penetrating trauma to the abdominal aorta. Despite the available data, some clinicians continue to recommend an extra-anatomic bypass when injury to the abdominal aorta would require replacement with a conduit in the presence of gastrointestinal contamination.22 As previously noted, repairs of the intestine and the aorta should not be performed simultaneously. Once the perforated bowel has been packed away and the surgeon has changed gloves, the aortic prosthesis is sewn in place with 3-0 or 4-0 polypropylene suture. After appropriate flushing of both ends of the aorta and removal of the distal aortic clamp, the proximal aortic clamp should be removed very slowly as the anesthesiologist rapidly infuses fluids. If a long aortic clamp time has been necessary, the prophylactic administration of intravenous bicarbonate is indicated to reverse the “washout” acidosis from the previously ischemic lower extremities.76 The retroperitoneum is then copiously irrigated and closed in a watertight fashion with an absorbable suture. Cross-clamping of the supraceliac aorta in a patient with hemorrhagic shock results in severe ischemia of the lower extremities. Restoration of arterial inflow will then cause a reperfusion injury. In a patient who is hemodynamically stable after repair of the suprarenal (or infrarenal) abdominal aorta, measurement of compartmental pressures below the knees should be performed before the patient is moved from the operating room. Pressures in the range of 30–35 mm Hg should be treated with below-knee, two-incision, four-compartment fasciotomies.77 The survival rate of patients with penetrating injuries to the suprarenal abdominal aorta in eight series published from 1974 to 1992 was 34.8%65,75,78–83 (Table 34-3). Four more recent reviews have documented a significant decline in survival for injuries to the abdominal aorta (suprarenal and infrarenal), ranging from 21.1% to 50% (mean 30.2%) even when patients with exsanguination before repair or those treated with ligation only were excluded.8,9,84,85 In one series in which injuries to the suprarenal and infrarenal abdominal aorta were separated, the survival rate in the suprarenal group was only 8.3% (3/36).84 The reasons for this decrease in survival figures are not defined in the reviews described, although a likely cause is the shorter prehospital times for exsanguinated patients that have been realized with improvements in emergency medical services. Blunt injury to the suprarenal aorta is extraordinarily rare. While blunt injury to the descending thoracic aorta is well described throughout the trauma literature, only 62 cases of blunt trauma to the abdominal aorta were found by Roth et al. in a literature review in 1997.22 Of these, only one case was noted to be in the suprarenal aorta. The most common location is between the origin of the inferior mesenteric artery and the aortic bifurcation (see below). These injuries generally present with signs and symptoms of aortic thrombosis, rather than hemorrhage, with the most common signs being a lack of femoral pulses (81%), abdominal tenderness (55%), lower extremity weakness or paralysis (47%), and paresthesias (20%).22 Management of these injuries is discussed more extensively in Section “Infrarenal Aorta.”

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TABLE 34-3 Survival with Injuries to the Abdominal Aorta

39.1% (25/64)

Tyburski et al.84 21.1% (15/71)

Coimbra et al.85 50% (12/24)

Suprarenal aorta

8 series, 1974–199258,68,70–75 34.8% (54/155)

Tyburski et al.84 8.3% (3/36)

—

Infrarenal aorta

6 series, 1974–199270,72–75,101 46.2% (43/93)

Tyburski et al.84 34.2% (12/35)

—

a

Excludes patients with exsanguination before repair or ligation.

■ Celiac Axis Injury to the celiac axis is rare. One of the largest series in the literature, reported by Asensio et al., documented the treatment of 13 patients with this uncommon injury.86 Penetrating injuries were the cause in 12 patients, and overall mortality was 62%. Eleven patients were treated with ligation and one with primary repair, with the final patient exsanguinating prior to therapy. Of the five survivors, four had undergone ligation, and all deaths occurred in the operating room. This group also performed an extensive literature review and could only document 33 previously reported cases, all the result of penetrating trauma. Furthermore, they could find no survivor treated with any sort of complex repair.86 One case of injury to the celiac artery after blunt trauma was reported by Schreiber et al. and occurred in a patient with preexisting median arcuate ligament syndrome.87 Given these results, patients with injuries to the celiac axis that are not amenable to simple arteriorrhaphy should undergo ligation, which should not cause any shortterm morbidity other than the aforementioned risk of gallbladder necrosis. When branches of the celiac axis are injured, they are often difficult to repair because of the dense neural and lymphatic tissue in this area and the small size of the vessels in a patient in shock with secondary vasoconstriction. There is clearly no good reason to fix major injuries to either the left gastric or proximal splenic artery in the patient with trauma to this area. In both instances, these vessels should be ligated. The common hepatic artery may have a larger diameter than the other two vessels, and an injury to this vessel may occasionally be amenable to lateral arteriorrhaphy, end-to-end anastomosis, or the insertion of a saphenous vein or prosthetic graft. In general, however, one should not worry about ligating the hepatic artery proper proximal to the origin of the gastroduodenal artery, since the extensive collateral flow from the midgut through this vessel will maintain the viability of the liver.

■ Superior Mesenteric Artery Injuries to the superior mesenteric artery are managed based on the level of injury. In 1972, Fullen et al.88 described an anatomic classification of injuries to the superior mesenteric artery that has been used intermittently by subsequent authors in the trauma literature.60,89 If the injury to the

superior mesenteric artery is beneath the pancreas (Fullen zone 1), the pancreas may have to be transected between Glassman and Dennis intestinal clamps to control the bleeding point. Because the superior mesenteric artery has few branches at this level, proximal and distal vascular control is relatively easy to obtain once the overlying pancreas has been divided. Another option is to perform medial rotation of the left-sided intra-abdominal viscera, as previously described, and apply a clamp directly to the proximal superior mesenteric artery at its origin from the left side of the aorta. In this instance, the left kidney may be left in the retroperitoneum as the medial rotation is performed. Injuries to the superior mesenteric artery also occur beyond the pancreas at the base of the transverse mesocolon (Fullen zone 2, between the pancreaticoduodenal and middle colic branches of the artery). Although there is certainly more space in which to work in this area, the proximity of the pancreas and the potential for pancreatic leaks near the arterial repair make injuries in this location almost as difficult to handle as the more proximal injuries.60,88,89 If the superior mesenteric artery has to be ligated at its origin from the aorta or beyond the pancreas (Fullen zone 1 or 2), collateral flow from both the foregut and hindgut should maintain theoretically the viability of the midgut in the distribution of this vessel.90 In truth, however, exsanguinating hemorrhage from injuries in this area often leads to intense vasoconstriction of the more distal superior mesenteric artery. For this reason, collateral flow is often inadequate to maintain viability of the distal midgut, especially the cecum and ascending colon. In the hemodynamically unstable patient with hypothermia, acidosis, and a coagulopathy, the insertion of a temporary intraluminal shunt into the debrided ends of the superior mesenteric artery is most appropriate and fits the definition of damage control.91 If replacement of the proximal superior mesenteric artery is necessary in a more stable patient, it is safest to place the origin of the saphenous vein or prosthetic graft on the distal infrarenal aorta, away from the pancreas and other upper abdominal injuries (Fig. 34-4).60 A graft in this location should be tailored so that it will pass through the posterior aspect of the mesentery of the small bowel and then be sutured to the superior mesenteric artery in an end-to-side fashion without significant tension. It is mandatory to cover the aortic suture line with retroperitoneal fat or a viable omental pedicle

CHAPTER 34

Abdominal aorta overall

Davis et al.9a

Asensio et al.8 Isolated injury, With other arterial 21.7% (10/46) injury, 17.6% (3/17)

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factors for mortality in the multi-institutional study included injury to Fullen zone 1 or 2, transfusion of 10 U of packed red blood cells, intraoperative acidosis or dysrhythmias, and multisystem organ failure.89

■ Proximal Renal Arteries Injuries to the proximal renal arteries may also present with a zone 1, supramesocolic hematoma or with hemorrhage in this area. The left medial visceral rotation maneuver described earlier allows visualization of much of the posterior left renal artery from the aorta to the kidney. This maneuver does not, however, allow for visualization of the proximal right renal artery. The proximal vessel is best approached through the base of the mesocolon beneath the left renal vein and between the infrarenal abdominal aorta and inferior vena cava. Options for repair of either the proximal or distal renal arteries are described later in this chapter (Section “Management of Injuries in Zone 2”).

A

B

©Baylor Bay College of Medicine 1985

FIGURE 34-4 (A) When complex grafting procedures to the superior mesenteric artery are necessary, it may be dangerous to place the proximal suture line near an associated pancreatic injury. (B) The proximal suture line should be on the lower aorta, away from the upper abdominal injuries, and should be covered with retroperitoneal tissue. (Reproduced from Accola KD, Feliciano DV, Mattox KL, et al. Management of injuries to the superior mesenteric artery. J Trauma. 1986;26:313.)

to avoid an aortoduodenal or aortoenteric fistula at a later time. This is much easier to perform if the proximal origin of the graft is located on the distal aorta. Injuries to the more distal superior mesenteric artery (Fullen zone 3, beyond the middle colic branch, and zone 4, at the level of the enteric branches) should be repaired, since ligation in this area is distal to the connection to collateral vessels from the foregut and the hindgut.92 This may require microsurgical techniques.93 If this cannot be accomplished because of the small size of the vessel, ligation may mandate extensive resection of the ileum and right colon. The survival rate of patients with penetrating injuries to the superior mesenteric artery in six series published from 1972 to 1986 was 57.7% (Table 34-4).60,81,86,94–96 Four more recent reviews, including a large multi-institutional study,89 had a mean survival of 58.7%.8,9,84,89 In one of the older series, survival decreased to 22% when any form of repair more complex than lateral arteriorrhaphy was performed.60 Independent risk

■ Superior Mesenteric Vein One other major abdominal vessel, the proximal superior mesenteric vein, lying to the right of the superior mesenteric artery, may be injured at the base of the mesocolon. Injury to the most proximal aspect of this vessel near its junction with the splenic vein is difficult to manage. The overlying pancreas, proximity of the uncinate process, and close association with the superior mesenteric artery often preclude easy access to proximal and distal control of the vein. Therefore, as with injuries to the proximal superior mesenteric artery, the neck of the pancreas may have to be transected between noncrushing vascular and intestinal clamps to gain access to a perforation. More commonly, the surgeon will find a perforation inferior to the lower border of the pancreas. Often, the vein can be compressed manually or squeezed between the surgeon’s fingers as an assistant places a continuous row of 5-0 polypropylene sutures into the edges of the perforation. If a posterior perforation is present, multiple collaterals entering the vein at this point will have to be ligated to roll the perforation into view. Occasionally, the vein will be nearly transected and both ends will have to be controlled with vascular clamps. With an assistant pushing the small bowel and its mesentery back toward the pancreas, the surgeon can reapproximate the ends of the vein without tension. When multiple vascular and visceral injuries are present in the upper abdomen and the superior mesenteric vein has been severely injured, ligation can be performed in the young trauma

TABLE 34-4 Survival with Injuries to the Superior Mesentery Artery Reference 6 series60,81,88,94–96 Asensio et al.8 (Los Angeles County)

Year 1972–1986 2000

Asensio et al.89 (multi-institutional) Davis et al.9 Tyburski et al.84

2001 2001 2001

No. of Patients 116 27 (isolated injury) 7 (with other artery) 233 15 41

No. of Survivors 67 11 2 143 8 20

Survival (%) 57.7 40.7 28.6 61 53.3 48.8

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TABLE 34-5 Survival with Injuries to the Superior Mesenteric Vein Year 1978–1983 2000

Davis et al.9 Tyburski et al.84

2001 2001

No. of Patients 104 19 (isolated injury) 14 (with other vein) 21 32

patient. In three older reviews of injuries to the portal venous system, ligation of the superior mesenteric vein was performed in 27 patients, and 22 survived.81,97,98 In one review of injuries to the superior mesenteric vein, survival was 85% among 33 patients treated with ligation versus 64% in 77 patients who underwent repair.99 Stone et al. have emphasized the need for vigorous postoperative fluid resuscitation in these patients as splanchnic hypervolemia leads to peripheral hypovolemia for at least 3 days after ligation of the superior mesenteric vein.98 The survival rate of patients with injuries to the superior mesenteric vein in four series published from 1978 to 1983 was 72.1% (Table 34-5).81,96–98 Three more recent reviews had a mean survival of 58.3%.8,9,84

MANAGEMENT OF INJURIES IN ZONE 1: INFRAMESOCOLIC REGION ■ Exposure and Vascular Control The second major area of hematoma or hemorrhage in the midline is the inframesocolic area. In this location, abdominal vascular injuries include those to the infrarenal abdominal aorta or inferior vena cava. Exposure of an inframesocolic injury to the aorta is obtained by duplicating the maneuvers used to gain proximal aortic control during the elective resection of an abdominal aortic aneurysm. The transverse mesocolon is pulled up toward the patient’s head, the small bowel is eviscerated toward the right (surgeon’s) side of the table, and the midline retroperitoneum is opened until the left renal vein is exposed. A proximal aortic clamp should then be placed immediately inferior to the left renal vein. When a large retroperitoneal hematoma is present and proximal inframesocolic control is difficult to obtain, it should always be remembered that the hole in the aorta is under the highest point of the hematoma (“Mount Everest phenomenon”). Therefore, rapid finger splitting of the hematoma will generally bring the surgeon directly to the area of injury. Exposure to allow for application of the distal vascular clamp is obtained by dividing the midline retroperitoneum down to the aortic bifurcation, carefully avoiding the left-sided origin of the inferior mesenteric artery. This vessel, however, may be sacrificed whenever necessary for exposure. If the aorta is intact and an inframesocolic hematoma appears to be more extensive on the right side of the abdomen than on the left, or if there is active hemorrhage coming through the base of the mesentery of the ascending colon or hepatic flexure of the colon, injury to the inferior vena cava caudad to the liver should be suspected. Although it is possible

No. of Survivors 75 9 5 15 18

Survival (%) 72.1 47.4 35.7 71.4 56.3

to visualize the vena cava through the midline retroperitoneal incision previously described, most trauma surgeons are more comfortable in visualizing the vena cava by mobilizing the right half of the colon and C-loop of the duodenum and leaving the right kidney in situ (right medial visceral rotation) (Fig. 34-5). This permits the entire vena caval system from the confluence of the iliac veins to the suprarenal vena cava below the liver to be visualized. It is often difficult to define precisely where a hole is in a large vein of the abdomen, such as the inferior vena cava, until much of the loose retroperitoneal fatty tissue is stripped away from the wall of the vessel. Once this is done, the site of hemorrhage can be localized. If active hemorrhage appears to be coming from the anterior surface of the vena cava, a Satinsky-type vascular clamp should be applied directly to the perforation as it is elevated by a pair of vascular forceps or Allis clamps. When the vena cava has been extensively lacerated and partial occlusion cannot be performed, it is often helpful to compress the proximal and distal vena cava around the partial transection or extensive laceration using gauze sponges placed in straight sponge sticks. Because of back-bleeding from lumbar veins, it may be necessary to use

©Baylor College of Medicine 1981

FIGURE 34-5 Medial mobilization of right-sided intra-abdominal viscera except the kidney allows for visualization of the entire infrahepatic inferior vena cava. (Reproduced with permission from Baylor College of Medicine.)

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Reference 4 series81,96–98 Asensio et al.8

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Management of Specific Injuries

SECTION 3

large DeBakey aortic clamps and completely occlude the vena cava above and below some injuries. This maneuver carries a risk in the already hypotensive patient, since venous return to the right side of the heart is significantly impaired. For this reason, one should consider simultaneous clamping of the infrarenal abdominal aorta. The two areas in which proximal and distal control of the inferior vena cava below the liver is especially difficult to obtain are at the confluence of the common iliac veins and at the caval junction with the renal veins. Although sponge stick compression of the common iliac veins and the vena cava superiorly may control hemorrhage at the confluence, visualization of perforating wounds in this area is compromised by the overlying aortic bifurcation. In the case of difficult exposure, one technique is to divide and ligate the right internal iliac artery, which may allow for lateral and cephalad retraction of the right common iliac artery to expose the venous injury. An alternate and interesting approach, but one that is rarely necessary, is the temporary division of the overlying right common iliac artery itself, with mobilization of the aortic bifurcation to the left.100 This technique provides wide exposure of the confluence of the common iliac veins and the distal vena cava and the venous injury can then be repaired in the usual fashion. The right common iliac artery is reconstituted by an end-to-end anastomosis. When the perforation occurs at the junction of the renal veins and the inferior vena cava, it should be directly compressed with either sponge sticks or the fingers. An assistant then clamps or compresses the infrarenal vena cava and the suprarenal infrahepatic vena cava and loops both renal veins individually with vascular tapes to allow for the direct application of angled vascular clamps. When time does not allow for this dissection, medial mobilization of the right kidney may allow for the application of a partial occlusion clamp across the inferior vena cava at its junction with the right renal vein. This medial mobilization maneuver is also useful for exposing posterior perforations in the suprarenal infrahepatic vena cava.101 Should this latter maneuver be performed, care must be taken to divide and ligate but not avulse the first lumbar vein on the right as it frequently enters the junction of the right renal vein and inferior vena cava. One other useful technique for controlling hemorrhage from the inferior vena cava in all locations is to use a Foley balloon catheter for tamponade.102–105 Either a 5-mL or a 30-mL balloon catheter can be inserted into a caval laceration, the balloon inflated in the lumen, and traction applied to the catheter. Once the bleeding is controlled, either a purse-string suture is inserted or a transverse venorrhaphy is performed, taking care not to rupture the underlying balloon with the needle. The balloon catheter is then deflated and removed just before completion of the suture line.

■ Infrarenal Aorta As with injuries to the suprarenal aorta, penetrating or blunt injuries in the infrarenal abdominal aorta are repaired primarily with 3-0 or 4-0 polypropylene sutures or by patch aortoplasty, end-to-end anastomosis, or insertion of a woven Dacron graft, albumin-coated Dacron graft, or a PTFE graft—none of which require preclotting. Because of the small size of the aorta in

young trauma patients, it is unusual to be able to place a tube graft larger than 12, 14, or 16 mm in diameter if one is required, as previously noted. The principles of completing the suture lines and flushing are exactly the same as for aortic repairs in the suprarenal area. Since the retroperitoneal tissue is often thin in young patients, it may be worthwhile to cover an extensive aortic repair or the suture line of a prosthesis with mobilized omentum before closure of the retroperitoneum.106 After mobilization of the gastrocolic omentum off the transverse colon, it can be placed into the lesser sac superiorly and then brought down through a hole in the transverse mesocolon over the repair or graft in the infrarenal aorta. An alternate approach is to mobilize the gastrocolic omentum off the right side of the transverse colon and then bring the mobilized pedicle into the area just below the ligament of Treitz to once again cover the aortic repair or graft. This vascularized pedicle of omentum should prevent a postoperative aortoduodenal fistula. While the vast majority of injuries to the infrarenal aorta are penetrating in nature, a small number occur after blunt trauma. In the aforementioned review of 62 cases of blunt aortic trauma prior to 1997 reported by Roth et al., motor vehicle collisions accounted for 57% of the cases and 47% of the total were directly attributed to lap belts.22 The patients generally present with symptoms of acute arterial insufficiency as stated above, although a small number present in a delayed fashion with claudication, impotence, or, rarely, delayed rupture.22,107,19 The survival rate of patients with injuries to the infrarenal abdominal aorta in six series published from 1974 to 1992 was 46.2% (Table 34-3).78,80–83,108 As previously noted in the discussion of recent decreases in survival figures for injuries to the suprarenal abdominal aorta, the same has been true for injuries to the infrarenal abdominal aorta. In the one series, published in 2001, in which injuries to the suprarenal and infrarenal abdominal aorta were separated, the survival rate in the infrarenal group was only 34.2%.84 One peculiar and fortunately rare injury to the infrarenal abdominal aorta is rupture of a preexisting aortic aneurysm or distal embolization from an aneurysm secondary to blunt abdominal trauma.109,110

■ Infrahepatic Inferior Vena Cava Anterior perforations of the inferior vena cava are best repaired in a transverse fashion using a continuous suture of 4-0 or 5-0 polypropylene. If vascular control is satisfactory and a posterior perforation can be visualized adequately by extending the anterior perforation, the posterior perforation can be repaired from inside the vena cava, with the first suture knot outside the lumen. When a significant longitudinal perforation is present, especially when adjacent perforations have been joined, the repaired vena cava will often take on the appearance of an hourglass. This narrowing may lead to slow postoperative occlusion of the vena cava. In the unstable patient who has developed a coagulopathy, no further attempt should be made to modify the repair. In the stable patient, there may be some justification for applying a large venous patch taken from either the resected inferior mesenteric vein or an ovarian vein or applying a PTFE patch.

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TABLE 34-6 Survival with Injuries to the Inferior Vena Cavaa Tyburski et al.84 40.3% (31/77) 46.1% (30/65)

Sullivan et al.111 57.3% (43/75) 59.2% (32/54)

a

Excludes retrohepatic and supradiaphragmatic injuries.

In the case of a young patient who is exsanguinating and in whom extensive repair of the infrarenal inferior vena cava appears to be necessary, ligation of this vessel is usually well tolerated as long as certain precautions are taken. The first of these is to measure the pressures in the anterior compartments of the legs and to perform bilateral below-knee fourcompartment fasciotomies at the first operation if the pressure is 30–35 mm Hg, depending on the patient’s hemodynamic status. Bilateral thigh fasciotomies may be necessary, as well, within the first 48 hours after ligation. The second is to maintain circulating volume in the postoperative period through infusion of the appropriate fluids. The third is to apply elastic compression wraps to both lower extremities and keep them continuously elevated for approximately 5–7 days after operation. Patients should wear the wraps when they start to ambulate, as well. If there is some residual edema even with the wraps in place at the time of hospital discharge, the patient should be fitted with full-length, custom-made support hose. In a recent review of 100 injuries to the inferior vena cava, 25 underwent ligation, including 22 with injuries to the infrarenal vena cava. Survival to hospital discharge was 41%, and 1-year follow-up was available in seven of nine survivors and no patient had more than trace lower extremity edema.111 While the majority of patients, therefore, seem to have no or minimal long-term edema, there have been occasional reports of severe edema in the postoperative period that has required later interposition grafting.112 Ligation of the suprarenal inferior vena cava is performed only when the patient has an extensive injury at this location and appears to have terminal shock at operation. In the abovementioned series, three patients underwent ligation of the suprarenal inferior vena cava with only one long-term survivor. This patient required dialysis over his hospital course but gradually had a return of his renal function and was discharged without renal insufficiency. One-year follow-up in this patient revealed minimal lower extremity edema and normal renal function.111 Similarly, one other report described a patient treated with suprarenal ligation who did not develop acute renal failure and who continued to do well 2 years after injury.106 In order to avoid the risk of acute renal failure and massive edema of the lower half of the body that would ordinarily be associated with ligation at this level, several innovative approaches have been used. These include suprarenal insertion of a saphenous vein composite interposition graft, insertion of a Dacron or PTFE interposition graft, or insertion of a cavo-right atrial Dacron or PTFE bypass graft.112–114 While long-term data are lacking for both Dacron and PTFE interposition or bypass grafts in the major veins of the abdomen, the use of an externally supported

PTFE graft in combination with chronic anticoagulation would presumably offer the best long-term patency. Survival rates for patients with injuries to the inferior vena cava obviously depend on the location of injury. Survival after retrohepatic injury is rare, with only one survivor in the most recent series.111 If one eliminates injuries to the supradiaphragmatic and retrohepatic vena cava from seven series published from 1978 to 1994, the average survival for 515 patients with injuries to the infrahepatic vena cava was 72.2%.81,83,101,115–118 Further eliminating juxtarenal injuries, the average survival for 318 patients with true infrarenal caval injuries was 76.1% (Table 34-6).81,83,101,115–118 The two more recent series, in which injuries are stratified by location, again show lower overall survival rates (40–60%, Table 34-6).84,111 Finally, short-term patency of repair of the inferior vena cava has been studied by Porter et al.119 In 28 patients with prior lateral venorrhaphy of the inferior vena cava, patency of the cava was documented by sonography, CT scan, or both in 24 (86%).

MANAGEMENT OF INJURIES IN ZONE 2 ■ Exposure and Vascular Control If a hematoma or hemorrhage is present in the upper lateral retroperitoneum, injury to the renal artery, renal vein, or both, as well as injury to the kidney, should be suspected. Most patients with penetrating trauma to the abdomen are explored prior to extensive radiologic work-up; however, in selected patients who are hemodynamically stable after sustaining penetrating wounds to the flank, CT scan has been used to document an isolated minor renal injury and operation has been avoided.120 Conversely, patients found to have a perirenal hematoma at the time of exploration for a penetrating abdominal wound should have unroofing of the hematoma and exploration of the wound track. If the hematoma is not rapidly expanding and there is no free intraabdominal bleeding, some surgeons will loop the ipsilateral renal artery with a vascular tape in the midline at the base of the mesocolon.121 The left renal vein can be looped with a vascular tape in the same location; however, vascular control of the proximal right renal vein will have to wait for mobilization of the C-loop of the duodenum and unroofing of the vena cava at its junction with the renal veins. It should be noted that obtaining proximal vascular control prior to exploration of a perirenal hematoma is controversial. Indeed, in one study, preliminary vascular control of the renal hilum had no impact on nephrectomy rate, transfusion requirements, or blood loss.122

CHAPTER 34

Infrahepatic inferior vena cava Infrarenal inferior vena cava

7 Series, 1978–199481,83,101,115–118 72.2% (372/515) 76.1% (242/318)

644

Management of Specific Injuries

SECTION 3

Conversely, if there is active bleeding from the kidney through Gerota’s fascia or from the retroperitoneum overlying the renal vessels, central renovascular control is not obtained. The surgeon should simply open the retroperitoneum lateral to the injured kidney and manually elevate the kidney directly into the wound. A large vascular clamp can be applied proximal to the hilum either at the midline on the left or just lateral to the inferior vena cava on the right to control any further bleeding. Patients who present after blunt trauma may also have either a renovascular or renal parenchymal injury. Patients in the former group, however, generally present with renovascular occlusion, which will be discussed below. In patients who have suffered blunt abdominal trauma and have undergone a preoperative IVP, renal arteriogram, or CT of the kidneys that has demonstrated flow to the kidney and/or a low Organ Injury Scale grade of injury, there is no justification for exploring the perirenal hematoma should an emergency laparotomy be indicated for other reasons.

■ Renovascular Injuries: Renal Artery Renovascular injuries are difficult to manage, especially when the renal artery is involved. It is an extraordinarily small vessel that is deeply embedded in the retroperitoneum. Occasionally, small perforations of the artery from penetrating wounds can be repaired by lateral arteriorrhaphy or resection with an endto-end anastomosis. Interposition grafting using either a saphenous vein or PTFE graft for extensive injuries is indicated only when there appears to be a reasonable hope for salvage of the kidney. Borrowed arteries, such as the splenic artery to replace the left renal artery and the hepatic artery to replace the right renal artery, have been used rarely, but are not often indicated in hypotensive trauma patients with significant renovascular injuries from penetrating wounds.123 In these patients and those with multiple intra-abdominal injuries or a long preoperative period of ischemia, nephrectomy may be a better choice, as long as intraoperative palpation has confirmed a normal contralateral kidney. The survival rate of patients with injuries to the renal arteries from penetrating trauma in two older studies was approximately 87%, with renal salvage in only 30–40%.121,124 In three more recent series, the survival rate was 65.1%.8,9,84 Diagnosis of patients with blunt injury to the renal artery is more difficult. Intimal tears in the renal arteries may result from deceleration in motor vehicle crashes, automobile– pedestrian accidents, and falls from heights. These usually lead to secondary thrombosis of the vessel and complaints of upper abdominal and flank pain as previously noted. One older literature review noted that only 30% of patients with intimal tears in the renal arteries had gross hematuria, 43% had microscopic hematuria, and 27% had no blood in the urine.125 Hence, the diagnosis may be missed, because a CT scan may not be performed expeditiously in stable patients with normal abdominal examinations. If either an IVP or CT scan documents occlusion of a renal artery, the surgeon must decide on the need for either operation or endovascular intervention. The time interval from the

episode of trauma appears to be the most critical factor in saving the affected kidney.121 In one study, there was an 80% chance of restoring some renal function at 12 hours, but this dropped to 57% at 18 hours after the onset of occlusion.125 In a recent series, only two of five kidneys were salvaged after attempted revascularization, with one early salvage requiring a late nephrectomy at 6 months for severe hypertension, leading to a long-term salvage rate of only one kidney (20%). Of interest, only three of seven patients not undergoing revascularization required late nephrectomy.16 If surgery is performed, extensive mobilization of the injured renal artery will usually allow a limited resection of the area of the intimal tear 2–3 cm from the abdominal aorta, with an end-to-end anastomosis for reconstruction. Alternate approaches are nephrectomy, perfusion of the kidney with Euro-Collins solution, and autotransplantation.118 The latter approach is obviously only applicable to stable patients who, ideally, have isolated injuries. Documentation of a successful result is usually not possible until acute tubular necrosis resolves over several weeks.126 Endovascular techniques designed to revascularize the kidneys after renal artery injury are discussed below. It is of interest that case reports in the literature have documented either spontaneous recovery or the late successful revascularization of one or both kidneys after presumed blunt thrombosis of the renal artery.127 The authors of the report suggest that attempts at late revascularization may be occasionally rewarding and advise that early nephrectomy is unnecessary because of the low incidence of chronic hypertension in cases of renal artery thrombosis.127 In summary, because of the poor renal salvage rates after blunt occlusion of the renal artery discussed above, there is decreasing interest in operative renal revascularization especially after a delayed diagnosis or in a patient with a unilateral injury. Therefore, patients with injuries to only one renal artery should be considered for revascularization only if they are stable and have short warm ischemia times, ideally less than 5 hours. Other patients, assuming they have a normally functioning contralateral kidney, should be either observed or considered for endovascular procedures. Obviously, patients with bilateral renal artery injuries or those with injuries to a solitary kidney should be strongly considered for revascularization. In addition, prolonged follow-up should be arranged for all patients, as some of them will develop hypertension.16

■ Renovascular Injuries: Renal Vein Although blunt avulsion injuries of the renal vein may result in exsanguination, patients with penetrating wounds may be quite stable as a result of the previously described retroperitoneal tamponade. Either compression with a finger or the direct application of vascular clamps can be used to control bleeding from a perforation of the renal vein. Lateral venorrhaphy remains the preferred technique of repair. If ligation of the right renal vein is necessary to control hemorrhage, nephrectomy should be performed either at the initial operation or at the reoperation if damage control has been necessary. The

Abdominal Vascular Injury

MANAGEMENT OF INJURIES IN ZONE 3 ■ Exposure and Vascular Control The fourth major area of hematoma or hemorrhage is the pelvic retroperitoneum. In this location, the iliac artery, iliac vein, or both may be injured. The majority of injuries reported in major series are the result of penetrating trauma. It is of interest, however, that major blunt abdominal trauma or pelvic fractures, particularly of the open type, have, in the past 25 years, become a more frequent cause of occlusion or laceration of the iliac arteries than previously noted.20–22,130,131 In fact, a very recent study using the National Trauma Data Bank noted a 3.5% rate of blunt iliac artery injury in 6,377 patients with AIS 3 or 4 pelvic fracture.132 The presence of a blunt iliac arterial injury in combination with a pelvic fracture was associated with a significantly higher hospital mortality (40% vs. 15%) and was associated with a 7.7% amputation rate.132 If a hematoma or hemorrhage is present after penetrating trauma, compression with a laparotomy pad or finger or simply grabbing the bleeding vessels with a hand should be performed as proximal and distal vascular control is attained. The proximal common iliac arteries are exposed by eviscerating the small bowel to the right and dividing the midline retroperitoneum over the aortic bifurcation. In young trauma patients, there is usually no adherence between the common iliac artery and vein in this location, and vascular tapes can be passed rapidly around the proximal arteries. Distal vascular control is obtained at the point at which the external iliac artery comes out of the pelvis proximal to the inguinal ligament. The artery is readily palpable under the retroperitoneum and can be rapidly elevated into the field of view with a vascular tape. The major problem in this area is continued back-bleeding from the internal iliac artery. This artery can be exposed by further opening the retroperitoneum on the side of the pelvis, elevating the vascular tapes on the proximal common iliac and distal external iliac arteries, and looking for the large branch of the iliac artery that descends into the pelvis. When bilateral iliac vascular injuries are present, one of the former coauthors of this chapter (Jon M. Burch) has used the technique of total pelvic vascular isolation. This includes proximal cross-clamping of the abdominal aorta and inferior vena cava just above their bifurcations and distal cross-clamping of both the external iliac artery and vein with one clamp on each side of the pelvis. Back-bleeding from the internal iliac vessels is minimal with this approach.

Injuries to the iliac veins are exposed through a technique similar to that described for injuries to the iliac arteries. It is not usually necessary to pass vascular tapes around these vessels, however, because they are readily compressible with either sponge sticks or fingers. As previously noted, the somewhat inaccessible location of the right common iliac vein has led to the suggested temporary transection of the right common iliac artery in order to improve exposure at this location.100 Similarly, transection and ligation of the internal iliac artery on the side of the pelvis will allow improved exposure of an injured ipsilateral internal iliac vein.133

■ Common, External, and Internal Iliac Arteries Injuries to the common or external iliac artery should be repaired or temporarily shunted if at all possible. Ligation of either vessel in the hypotensive patient will lead to progressive ischemia of the lower extremity and the need for a high above-knee amputation or a hip disarticulation in the later postoperative course. In fact, in World War II, ligation of these vessels led to amputation rates of approximately 50%. Furthermore, in a large review by Burch et al. in the 1980s, mortality associated with ligation was 90%.134 In patients with severe shock, insertion of a temporary intraluminal shunt is a better choice for damage control.135 In contrast, an injured internal iliac artery can be ligated with impunity even with injuries that occur bilaterally. Options in the management of more stable patients with injuries to the common or external iliac artery include the following: lateral arteriorrhaphy, completion of a partial transection and end-to-end anastomosis, resection of the injured area and insertion of a saphenous vein or PTFE graft,136,137 mobilization of the ipsilateral internal iliac artery to serve as a replacement for the external iliac artery, or transposition of one iliac artery to the side of the contralateral iliac artery for wounds at the bifurcation.138 Extensive injuries to the common or external iliac artery in the presence of significant enteric or fecal contamination in the pelvis remain a serious problem for the trauma surgeon. Both end-to-end repairs and vascular conduits in this location have suffered postoperative pseudoaneurysm formation and even blowouts secondary to pelvic infection from the original intestinal contamination. Therefore, the authors have occasionally avoided an end-to-end anastomosis or the insertion of a saphenous vein or PTFE graft in either the common or external iliac artery in such a situation. Rather, the artery is divided just proximal to the injury, closed with a double-running row of 4-0 or 5-0 polypropylene sutures, and covered with noninjured retroperitoneum or a vascularized pedicle of omentum. If the patient’s lower extremity on the side of the ligation appears to be in jeopardy at the completion of the abdominal operation, an extra-anatomic femorofemoral crossover graft should be performed to return arterial inflow to the extremity.23,73 If the surgeon chooses not to perform a femorofemoral crossover graft until the patient’s condition has been stabilized in the surgical intensive care unit, an ipsilateral four-compartment below-knee fasciotomy should be performed, since ischemic edema below the knee will often lead to a compartment syndrome.

CHAPTER 34

medial left renal vein, however, can be ligated as long as the left adrenal and gonadal veins are intact.128 Repair is preferable if feasible, as a greater frequency of postoperative renal complications has been noted in older series when ligation was performed.129 The survival rate for patients with penetrating injuries to the renal veins has ranged from 42% to 88% in the older literature, with the difference presumably due to the magnitude and number of associated visceral and vascular injuries.116,120,121 In three recent reviews, survival ranged from 44.2% to 70% with a mean of 60.4%.8,9,84 Injuries to the renal parenchyma are covered elsewhere.

645

646

Management of Specific Injuries

TABLE 34-7 Survival with Injuries to the Iliac Artery and Vein

SECTION 3

Reference Millikan et al.139 Ryan et al.140 Sirinek et al.96 Burch et al.134 Wilson et al.144 Davis et al.9 Tyburski et al.84 Asensio et al.8 Overall

Year 1981 1982 1983 1990 1990 2001 2001 2001

No. of Patients 19 (6)a 66 (17)a 21 130 (34) — 55 70 — 361 (57)a

Iliac Artery No. of Survivors 9 (5)a 41 (15)a 15 80 (26)a — 35 37 — 217 (46)a

Survival (%) 47.4 (83.3) 62.1 (88.2)a 71.4 61.5 (76.5)a — 63.6 52.9 — 60.1 (80.7)a

No. of Patients 16 (8)b 97 (48)b 28 214 (81)b 49 76 73 37 (22)b 590 (159)b

Iliac Vein No. of Survivors 11 (8)b 71 (45)b 23 153 (70)b 24 58 40 23 (18)b 403 (141)b

Survival (%) 68.8 (100.0)b 73.2 (93.8)b 82.1 71.5 (86.4)b 48.9 76.3 54.8 62.2 (81.8)b 68.3 (88.7)b

a b

Isolated injury to iliac artery. Isolated injury to iliac vein.

The survival rate among patients with injuries to the iliac arteries will vary with the number of associated injuries to the iliac vein, aorta, and vena cava, but was approximately 61% in 189 patients reviewed in four large series published from 1981 to 1990 (Table 34-7).96,134,139,140 When patients with other vascular injuries, especially to the iliac vein, were eliminated, the survival rate among 57 patients in three series was 81% (Table 34-7).134,139,140 If the injury is large and free bleeding from the iliac artery into the peritoneal cavity has occurred during the preoperative period, the survival rate in one older series was only 45%.139 The survival rates in two recent series for patients with injuries to the common iliac artery (other vascular injuries not specified) ranged from 44.7% to 55.5% with a mean of 46.8% (Table 34-7).9,84 In the same series the survival rate with injuries to the external iliac artery was a mean of 64.1% (Table 34-7).9,84 Finally, in another recent series, survival was correlated most heavily with preoperative base deficit, pH, and temperature. It was also noted that, even in busy trauma centers, significant delays to operative intervention occur, most notably prolonged emergency department time and anesthesia preparation times, and these delays adversely affected patient outcome.141 As such, every effort should be made to expedite operative intervention in a patient with a suspected abdominal vascular injury. Blunt trauma to the iliac arteries is less common as they are protected by the bony pelvis and lie deep in the retroperitoneum. Partial transections, avulsions, and intimal injuries with secondary thrombosis have all been reported in association with pelvic fractures. Of the 10 patients with blunt thromboses reported in the literature until 1997, most had been treated with prosthetic interposition grafting, although several underwent primary repairs. Only one patient needed an amputation.131 As noted above, the recent study of patients in the National Trauma Data Bank documented a 7.7% amputation rate in patients with pelvic fractures and an associated injury to the iliac artery.132

■ Common, External, and Internal Iliac Veins Injuries to the common or external iliac vein are treated either with lateral repair using 4-0 or 5-0 polypropylene suture or with ligation. Ligation in the young patient has been well tolerated in the authors’ experience and that of others if the same precautions used after ligation of the inferior vena cava are applied142; however, some centers strongly recommend repair rather than ligation for injuries of the common or external iliac veins.143 When significant narrowing of the common or external iliac vein results from a lateral repair, postoperative anticoagulation is appropriate to lessen the risk of thrombosis and/or pulmonary embolism. The survival rate of patients with injuries to the iliac veins is variable, but was approximately 70% in 404 patients reviewed in five large series published from 1981 to 1990 (Table 34-7).96,134,139,140,144 When patients with other vascular injuries, especially to the iliac artery, were eliminated, the survival rate among 137 patients in three series was 95% (Table 34-7).134,139,140 The survival rate in three recent series in patients with injuries to the iliac vein (not otherwise specified or common/external/internal combined) was a mean of 65.1%.8,9,84

MANAGEMENT OF INJURIES IN THE PORTA HEPATIS ■ Exposure and Vascular Control If a hematoma or hemorrhage is present in the area of the portal triad in the right upper quadrant, there may be injury to the portal vein, hepatic artery, or both. Furthermore, this vascular injury may be in combination with an injury to the common bile duct. When a hematoma is present, the proximal hepatoduodenal ligament should be looped with a vascular tape or a noncrushing vascular clamp should be applied (the Pringle maneuver) before the hematoma is entered. If hemorrhage is occurring, finger compression of the bleeding vessels

Abdominal Vascular Injury

■ Hepatic Artery Due to its short course, injury to any portion of the hepatic artery is rare. Replacement of the injured common hepatic artery with a substitute vascular conduit is rarely indicated, since most patients with a portal hematoma or hemorrhage also have significant injuries to the liver, right kidney, or inferior vena cava. As previously noted, ligation of the proper or common hepatic artery appears to be well tolerated in the young trauma patient, even when performed beyond the origin of the gastroduodenal artery, owing to the extensive collateral arterial flow to the liver.146–151 Because of the small size of the right or left hepatic artery, lateral repairs are often difficult and will frequently be followed by occlusion of the vessel in the postoperative period. Because of its rarity, few large studies have been performed on injuries to the hepatic artery. A relatively large multicenter experience was published in 1995 by Jurkovich et al., which documented the course of 99 patients with injury to the portal

triad. Of this group, 28 patients had 29 injuries to a segment of the hepatic artery. Nineteen patients underwent ligation with eight survivors (mortality 42%). Only one patient developed hepatic necrosis requiring debridement, and this patient had an associated extensive injury to that lobe. Seven patients had attempts at repair with only one survivor, and two other patients exsanguinated prior to therapy.151 It should be noted, again, that selective ligation of the right hepatic artery warrants a cholecystectomy. Fortunately, injuries to the hepatic artery remain rare, and survival rates in cases of such injury are usually related to the number and magnitude of associated injuries.

■ Portal Vein As noted above, injuries to any portion of the portal vein are more difficult to manage than are injuries to the hepatic artery, owing to the posterior location of the vein, the friability of its wall, and the greater blood flow through it. Techniques for repair of the vein are varied, but lateral venorrhaphy with a 4-0 or 5-0 polypropylene suture is preferred. More extensive maneuvers that have occasionally been used with success include the following: resection with an end-to-end anastomosis, interposition grafting, transposition of the splenic vein down to the superior mesenteric vein to replace the proximal portal vein, an end-to-side portacaval shunt, and a venovenous shunt from the superior mesenteric vein to the distal portal vein or inferior vena cava.81,98,117,152–155 Such vigorous attempts at restoration of blood flow have resulted from the concern about viability of the midgut if the portal vein is ligated. Unfortunately, any type of portal–systemic shunt may have the undesirable effect of causing hepatic encephalopathy, since the direction of splanchnic venous flow with the shunt would mimic that in the patient with cirrhosis and hepatofugal flow in the obstructed portal vein. Ligation of the vein is compatible with survival, as both Pachter et al.153 and Stone et al.98 have emphasized. In the 1979 review of the literature on this subject by Pachter et al., one of six survivors of ligation of the portal vein developed portal hypertension.153 The 1982 series by Stone et al. included 9 survivors among 18 patients who underwent ligation of the portal vein.98 In essence, ligation of the portal vein should be performed if an extensive injury is present and the patient is hypothermic, acidotic, and/or coagulopathic (damage control indicated). The surgeon must then be prepared to infuse significant amounts of fluids to reverse the transient peripheral hypovolemia secondary to splanchnic hypervolemia.98 To apply some perspective to the somewhat controversial area of injuries to the portal vein, a review of techniques for their management is helpful. The comprehensive older review by Graham et al. of 37 patients with injuries to the portal vein reported that 26 underwent lateral venorrhaphy, 5 had packing or clamping only, 4 (none of whom survived) had ligation, 1 had an end-to-end anastomosis, and 1 had a portacaval shunt.97 In contrast, the aforementioned review by Stone et al. of 46 patients included 17 who had lateral venorrhaphy, 18 who had ligation (9 survived), 7 in whom no repair was done, 3 who underwent an end-to-end anastomosis, and 1 who had a portacaval shunt.98 Ivatury et al. have since reported on 14 patients

CHAPTER 34

will suffice until the vascular clamp is in place. The Pringle maneuver clamps the distal common bile duct as well as the bleeding vessels, but led to only one stricture of the common bile duct in one older series of hepatic injuries from the Ben Taub General Hospital in Houston, Texas.145 Because of the short length of the porta in many patients, it may be difficult to place a distal vascular clamp right at the edge of the liver. In such patients, manual compression with forceps may allow distal vascular control until the area of injury can be isolated. Because of the proximity of the common bile duct, no sutures should be placed into the porta until the vascular injury is precisely defined. Injuries to the portal vein in the hepatoduodenal ligament are isolated in much the same fashion as injuries to the hepatic artery. The posterior position of the vein, however, makes the exposure of these injuries more difficult. Mobilization of the common bile duct to the left and of the cystic duct superiorly, coupled with an extensive Kocher maneuver, will usually allow for excellent visualization of any suprapancreatic injury after proximal (and, if possible, distal) vascular control has been obtained. As with proximal wounds to the superior mesenteric artery or vein, division of the neck of the pancreas is necessary on rare occasions to visualize perforations in the retropancreatic portion of the portal vein. With the assistant compressing the superior mesenteric vein below and a vascular clamp applied to the hepatoduodenal ligament above, the surgeon should open both ends of the retropancreatic tunnel over the anterior wall of the portal vein by gently spreading a clamp or scissors. This maneuver may be prevented above by the position of the gastroduodenal artery, which should then be divided and ligated. When the tips of the surgeon’s index fingers touch under the neck of the pancreas, two straight noncrushing intestinal (Glassman or Dennis) or slightly angled vascular (Glover) clamps are placed across the entire neck of the pancreas. The pancreas is divided between the clamps and retracted away until the perforations in the portal vein or proximal superior mesenteric or splenic veins are visualized.

647

648

Management of Specific Injuries

TABLE 34-8 Survival with Injuries to the Portal Vein

SECTION 3

Reference Graham et al.97 Petersen et al.154 Stone et al.98 Kashuk et al.81 Sirinek et al.96 Ivatury et al.156 Overall

Year 1978 1979 1982 1982 1983 1987

No. of No. of Survival Patients Survivors (%) 37 18 48.6 28 17 60.7 41 22 53.7 9 3 33.3 5 0 0.0 14 7 50.0 134 67 50.0

with injuries to the portal vein, among whom exsanguination occurred in 3, venorrhaphy was performed in 10 (of whom 6 survived), and ligation was done in 1 (who survived).156 Finally, Jurkovich reported on 56 injuries to the portal vein with 33 patients undergoing primary repair (42% mortality), 1 undergoing complex repair (died), and 10 undergoing ligation (90% mortality). An additional 11 patients died before therapy. This led to an overall survival rate of 36% compared with the 50% survival rate among 134 patients with injuries to the portal vein in six series from 1978 to 1987 (Table 34-8).81,96–98,154,156 Wounds of the retrohepatic and supradiaphragmatic vena cava are discussed elsewhere in this text.

INDICATIONS AND TECHNIQUES OF ENDOVASCULAR INTERVENTION IN ABDOMINAL VASCULAR INJURY While patients with abdominal vascular injury who present with active hemorrhage generally require immediate open exploration, a smaller subset who present with contained hemorrhage or thrombosis may be candidates for endovascular techniques. While these techniques are now well accepted for contained disruptions of the thoracic aorta and have been very successful as an adjunct to nonoperative management of solid organ injuries, their role in true abdominal vascular injury is not as well established. Indeed, the literature describing endovascular techniques in these potentially devastating injuries is composed mostly of case reports and small case series, many of which are reviewed in the following sections.

■ Zone 1 Patients with injury to the intra-abdominal aorta, especially after penetrating trauma, often present with hemorrhagic shock from free intraperitoneal hemorrhage. Alternatively, they may present acutely or in a delayed fashion with thrombotic sequelae. First described by Campbell and Austin in 1969,157 “Seat belt aorta” describes acute aortic occlusion related to lap-belt injuries. While in the past, operative intervention has generally been the only option for definitive management, several endovascular techniques have recently been reported to address thrombotic complications of aortic injury in both the acute and chronic settings.

In 1997, Vernhet et al.158 described the management of three patients with acute infrarenal aortic dissection after trauma with percutaneous placement of a stent. These patients presented without obvious hemorrhagic shock and had varying degrees of arterial insufficiency. All were managed successfully in the early postinjury period with Wallstents (Schneider Wallstent, Schneider Stent Division, Pfizer, Minneapolis, Minnesota) used to cover their intimal injuries, obliterate the dissections, and restore perfusion. At 6-month to 2-year follow-up, no complications were noted.156 Other groups have presented similar case reports and case series, with successful use of stents to restore perfusion after blunt aortic injury.159,160 In recent years stent grafts have also been used to manage aortic trauma in both the acute setting and more chronic situations, especially in patients with missed injuries and “hostile” abdomens. Two groups have reported using stent grafts in a delayed fashion to manage abdominal aortic injury in patients with “hostile” abdomens from damage control laparotomy.161,162 In the first case report, a covered stent was placed in a patient with a contained zone 1 hematoma 6 days after a laparotomy after a motorcycle crash. At 24-month follow-up, no graft-related complications were noted.161 More recently, Yeh et al.162 reported the use of a Zenith stent graft (Cook Group, Inc, Bloomington, Indiana) in a patient 2 weeks after laparotomy for multiple gunshot wounds to the torso. This patient presented with abrupt onset of hemorrhage and hemodynamic instability in the face of matted viscera and a hostile abdomen. Attempts at open repair failed, and the patient was packed and brought to the interventional suite where the stent graft was placed with successful cessation of hemorrhage. This patient survived a prolonged hospital course and was noted to have no aortic complications at a 1-year follow-up. Similarly, two case reports report the successful use of stent grafts in the management of traumatic aortocaval fistulas.163,164 Injuries to the inferior vena cava are generally the result of penetrating trauma and have been managed with many techniques including ligation in the infrarenal inferior vena cava as described above. In the last few years, several reports have described the use of interventional techniques to assist in the management of these complex injuries. Castelli et al.165 reported on a patient who presented with hemorrhagic shock 4 hours after a motor vehicle collision. CT angiography revealed an injury to the vena cava at the confluence of the iliac veins. In the interventional suite, a Gore Excluder stent graft was used (W.L. Gore, Flagstaff, Arizona) to control hemorrhage from the injury. The duration of the procedure was 9 minutes. Unfortunately, the patient died of a severe traumatic brain injury on post-trauma day 2. Two other case reports describe a similar management technique.166,167 Clearly, in the right institution, the technology is available to perform these procedures expeditiously, and this technique may benefit a small group of patients. One concern over placing stent grafts in the venous system is a question of durability and the ability to administer postoperative anticoagulation. Stent grafts are felt to be highly thrombogenic in the first month, and it is unknown whether their insertion in major venous structures will require routine postoperative anticoagulation. This may limit the use of this technique in the multiply injured patient.

Abdominal Vascular Injury

■ Zone 2 As previously mentioned, renovascular injuries are difficult to manage operatively, especially when the renal artery is involved. As the diagnosis is often somewhat delayed and because of the relatively poor function of kidneys revascularized with open surgery, enthusiasm for attempts at open repair has waned. Therefore, multiple authors have described endovascular management of injuries to the renal vasculature. Renal arteries and major branches have been embolized in series back into the 1980s with good renal preservation. For example, Sclafani and Becker171 reported on eight patients with renal injuries who were treated with angiographic embolization. The injuries were the result of stab wounds in five patients, blunt trauma in two patients, and a gunshot wound in one patient. Angiographic findings included two pseudoaneurysms, two arteriovenous fistulas, two arteriocalyceal fistulas, and one renal artery–pleural fistula. Of interest, seven of eight patients had successful procedures, and all seven had preservation of the kidney, with one nephrectomy performed for persistent hematuria. A more recent study revealed renal vascular injury in eight patients, of whom seven were successfully treated with angiographic embolization, obviating the need for open surgery. At discharge, all survivors had normal renal function and all patients were normotensive.172 Thus, in the hemodynamically normal patient, transcatheter embolization has been used successfully to manage a variety of renovascular injuries and allow for organ preservation. In more recent years with improving technology, there has been an increased interest in preserving blood flow to the renal parenchyma with the use of expandable stents rather than transcatheter embolization. At least three case reports document the successful use of various stents to obliterate intimal

flaps in patients with renal artery injuries with preservation of renal function and no short-term complications.173–175

■ Zone 3 One of the earliest descriptions of endovascular management of traumatic aortoiliac disease was reported by Parodi et al. in 1993.176 Building on their experience with stent graft management of aortic aneurysmal disease, the management of arteriovenous fistulae in the iliac system was described in seven patients with up to 14-month follow-up and 100% technical success. In this study, PTFE grafts combined with Palmaz stents were used to repair the injured arterial wall under fluoroscopic guidance.176 In more recent years, several authors have reported on the use of stent grafts in traumatic iliac thrombosis. In 1997, Lyden et al.177 used a 10  60 mm Smart Stent (Cordis Endovascular, Miami, Florida) to manage a common iliac artery dissection and thrombosis after a motor vehicle collision. They were able to restore flow within 4 hours of injury, and while the patient had an excellent short-term result, he expired on hospital day 6 with a severe traumatic brain injury. Marin et al.178 also successfully managed several traumatic vascular injuries with stent grafts, including one injury to the common iliac artery, with patency documented at 2 months. One of the largest series of nonthoracic vascular injuries managed with covered stents in the literature was published in 2006.179 In this multicenter trial, 62 patients were managed with Wallgraft endoprosthesis grafts over 6 years. This included 33 patients with injuries to the iliac vessels, most of which were iatrogenic in nature, and included 27 perforations, 4 arteriovenous fistulae, 1 pseudoaneurysm, and 1 dissection. Technical success, as defined by total postprocedure exclusion, was achieved in all but one patient with an injury to the iliac artery and primary patency at 1 year was 76% for these patients. Early adverse events occurred in 14% of patients, mostly related to puncture site complications, and a late adverse event occurred in another 6.5% of patients with one systemic infection, one occlusion, and three stenoses of the repair. All-cause mortality was 6.5% in the early postprocedure period and 17.7% in later follow-up. None of the deaths was thought to be the result of the stent graft.179 Therefore, in reviewing the literature on interventional techniques as a mode of therapy in traumatic iliac vascular injuries, one comes to the conclusion that improving technology and techniques may have an expanding role in the management of such injuries in the future. Unfortunately, long-term follow-up data are nonexistent and, therefore, it is unknown whether or not an endovascular prosthesis will be subject to the same risk of contamination and failure that has been seen with prosthetic material placed surgically.

COMPLICATIONS The complications of vascular repairs in the abdomen are much the same as those seen in the extremities. They include such problems as thrombosis, dehiscence of a suture line, and

CHAPTER 34

As previously mentioned, injury to the main celiac axis is rare and, therefore, there have been no reports of the use of endovascular techniques for an injury to this vessel, although several authors have reported the use of endovascular techniques in the management of spontaneous celiac dissections and aneurysms.168 Whether this can be extrapolated to the trauma patient, most of whom are younger, healthier, and with longer life expectancy, is unknown. Branches of the celiac axis may be amenable to endovascular techniques. Splenic and hepatic artery injuries are covered elsewhere in this text. Successful embolization of a left gastric artery pseudoaneurysm after blunt abdominal trauma has been reported.169 Injury to the superior mesenteric artery is fortunately rare, with most cases being the result of penetrating trauma. Because most of these patients present with severe shock and there is a concomitant need to evaluate intestinal viability, endovascular management of traumatic injuries to the superior mesenteric artery has not been described and is likely unwise. This remains fundamentally different from patients with intestinal angina secondary to stenosis of their superior mesenteric artery or even atherosclerotic occlusion of the vessel, some of whom have been treated successfully with endovascular techniques.170

649

650

Management of Specific Injuries

Zone 1

SECTION 3

Supramesocolic

Inframesocolic

Proceed as for penetrating injury

Proceed as for penetrating injury

Zone 2

Zone 3

Portal area

Retrohepatic area

Do not open hematoma if kidney appears normal on preoperative CT or arteriography.

Do not open hematoma unless it is ruptured, pulsatile, or rapidly expanding or unless ipsilateral iliac pulse is absent.

Proceed as for penetrating injury

Proceed as for penetrating injury

If kidney does not appear normal, still do not open hematoma unless it is ruptured, pulsatile, or rapidly expanding.

Open hematoma.

FIGURE 34-6 Blunt abdominal vascular injury algorithm.

infection.180 Occlusion is not uncommon when small, vasoconstricted vessels, such as the renal artery or superior mesenteric artery, undergo lateral arteriorrhaphy. In such patients, it may be valuable to perform a second-look operation within 12–24 hours after the patient’s temperature, coagulation abnormalities, and blood pressure have returned to normal. When this is done, correction of a vascular thrombosis may be successful. Dehiscence of vascular suture lines in the abdomen occurred in two locations in the authors’ experience, and both have been previously discussed. First, a substitute vascular conduit inserted in the superior mesenteric artery near a pancreatic injury may be disrupted if a small pancreatic leak occurs in the postoperative period. For this reason, the proximal anastomosis of such a graft should be on the infrarenal abdominal aorta inferior to the transverse mesocolon and far away from the pancreas as previously noted. Second, the dehiscence of end-to-end anastomoses and conduit suture lines in the iliac arteries can be

Zone 1

Supramesocolic

Inframesocolic

Perform left medial visceral rotation.

Obtain exposure at base of transverse mesocolon. Obtain proximal control of infrarenal abdominal aorta.

Divide left crus of aortic hiatus. Obtain proximal control of distal descending thoracic aorta or diaphragmatic aorta.

avoided by limiting the extent of repair if there is significant enteric or fecal contamination in the pelvis and considering early extra-anatomic bypass if the patient’s limb is threatened. Finally, a vascular complication unique to the abdomen is the postoperative development of vascular–enteric fistulas. This will occur most commonly in patients who have anterior aortic repairs, aortic grafts, or grafts to the superior mesenteric artery from the aorta. Again, this problem can be avoided by proper coverage of suture lines on the aorta with retroperitoneal tissue or a viable omental pedicle106 and on the recipient vessel with mesentery.

SUMMARY Abdominal vascular injuries are commonly seen in patients with penetrating wounds to the abdomen (Figs. 34-6 and 34-7). They present either with a contained retroperitoneal,

Zone 2

Zone 3

Portal area

Retrohepatic area

Expose ipsilateral renal vessels at base of transverse mesocolon.

Expose bifurcation of infrarenal aorta and junction of inferior vena cava with iliac veins.

Perform Pringle maneuver for proximal control.

Do not open hematoma unless it is ruptured, pulsatile, or rapidly expanding.

Obtain proximal control of renal vessels.

Obtain proximal control of common iliac vessels and distal control of external iliac vessels.

Open hematoma.

FIGURE 34-7 Penetrating abdominal vascular injury algorithm.

Apply distal vascular clamp or forceps, if possible. Dissect common bile duct away from common hepatic artery and portal vein.

Abdominal Vascular Injury

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CHAPTER 34

mesenteric, or portal hematoma or with active hemorrhage. When tamponade is present, proximal and distal vascular control should be obtained before opening the hematoma causing the tamponade. If active hemorrhage is present, direct compression of the bleeding vessels with a finger, hand, laparotomy pad, or sponge stick at the site of injury is necessary until proximal and distal vascular control can be attained. Vascular repairs are generally performed with polypropylene sutures and can range from simple arteriorrhaphy or venorrhaphy to the insertion of substitute vascular conduits, much as in vascular injuries in the extremities. Also, in the occasional patient who presents with normal hemodynamics, thrombotic sequelae, or in a delayed fashion after abdominal vascular injury, endovascular techniques may have a role in management. Overall, if hemorrhage can be rapidly controlled and distal perfusion restored, many patients with major abdominal vascular injuries can be salvaged with the techniques described in this chapter.

651

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SECTION 3

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175. Villas PA, Cohen G, Putnam SG. Wallstent placement in a renal artery after blunt trauma. J Trauma. 1999;46:1137. 176. Parodi JC, Barone HD, Schonholz C. Transfemoral endovascular treatment of aortoiliac aneurysms and arteriovenous fistulas with stented Dacron grafts. In: Vejth FJ, ed. Current Critical Problems in Vascular Surgery. St. Louis, MO: Quality Medical Publishing; 1993:264. 177. Lyden SP, Srivastava SD, Wadlman DL, et al. Common iliac artery dissection after blunt trauma: case report of endovascular repair and literature review. J Trauma. 2001;50:339.

178. Marin ML, Veith FJ, Panetta TF, et al. Transluminally placed endovascular stented graft repair for arterial trauma. J Vasc Surg. 1994;20:466. 179. White R, Krajcer Z, Johnson M, et al. Results of a multicenter trial for the treatment of traumatic vascular injury with a covered stent. J Trauma. 2006;60:1189. 180. Feliciano DV. Management of infected grafts and graft blowout in vascular trauma patients. In: Flanigan DP, Schuler JJ, Meyer JP, eds. Civilian Vascular Trauma. Philadelphia, PA: Lea & Febiger; 1992:447.

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Pelvis George C. Velmahos

Pelvic injuries (PI) are frequent, particularly after blunt trauma (9% of all blunt trauma patients), and range from clinically insignificant minor pelvic fractures to life-threatening injuries that produce exsanguination (0.5% of all blunt trauma patients). The overall mortality rate of patients with pelvic ring fractures is approximately 6%. Uncontrolled pelvic hemorrhage accounts for 39% of related deaths, whereas associated head injury is responsible for 31% of the deaths. AP compression and vertical shear injuries are associated with a higher incidence of pelvic vascular injury and hemorrhage. There is little agreement about the preferred methods of management and, therefore, guidelines are vague or not followed. However, the recent evolution of rapid pelvic stabilization by external fixation or pelvic binding and of bleeding control by angiographic embolization or preperitoneal pelvic packing has significantly decreased the mortality rates of devastating PI. A multidisciplinary approach is crucial, as no single specialty has all the skills or controls all the resources that can be used to produce ultimately outcomes. Emergency medicine physicians, trauma and critical care surgeons, orthopedic surgeons, and interventional radiologists should play protagonist roles in a well-orchestrated trauma team that manages these complex patients.

PELVIC ANATOMY The pelvic ring comprises the sacrum and the two innominate bones, all attached with strong ligaments. The innominate bones join the sacrum at the sacroiliac joints and each other anteriorly at the pubic symphysis. The anterior and posterior sacroiliac ligaments include shorter and longer elements that extend over the sacrum and to the iliac crests, and provide vertical stability across the sacroiliac joints. The pelvic floor is bridged by the sacrospinous and sacrotuberous ligaments that

connect the sacrum to the ischial spine and the ischial tuberosity, respectively. The anterior elements, including the pubic rami and pubic symphysis, contribute to approximately 40% of the pelvic stability, but the posterior elements are more important, as shown by biomechanical studies. The internal iliac (hypogastric) arteries provide blood supply to the organs, bones, and soft tissues of the pelvis. The anterior division includes the inferior gluteal, obturator, inferior vesicular, middle rectal, and internal pudendal artery. The posterior division includes the iliolumbar, lateral sacral, and superior gluteal artery. The largest branch is the superior gluteal artery, which is the most commonly injured major arterial branch after pelvic fractures. Pelvic veins run parallel to the arteries and form an extensive plexus that drains into the internal iliac veins. The sacral venous plexus is adhered to the anterior surface of the sacrum and shredded after major pelvic fractures. Venous bleeding is more frequent than arterial bleeding after PI. The sciatic nerve is formed by the nerve roots of L4 to S3 and exits the pelvis under the piriformis muscle. The anterior roots of L4 and L5 cross the sacroiliac joints and can be injured in sacral ala fractures or sacroiliac joint dislocations. All pelvic organs are at risk of injury following severe PI with the bladder and urethra being the most frequently injured. The extraperitoneal rectum is also at risk in open pelvic fractures.

PELVIC FRACTURE CLASSIFICATION Despite multiple classification systems described, the two most commonly used are those described by Tile1,2 and Young– Burgess.3,4 The Tile classification categorizes pelvic fractures in three groups based on stability, as evaluated primarily by clinical examination and plain radiographs (Table 35-1):

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TABLE 35-1 Tile Classification of Pelvic Fractures

SECTION 3 X

Type Type A, posterior arch intact

A1, pelvic ring fracture (avulsion) A2, pelvic ring fracture (direct blow) A3, transverse sacral fracture

Type B, incomplete posterior arch disruption

B1, AP compression

A1.1 A1.2 A1.3 A2.1 A2.2 A2.3 A3.1 A3.2 A3.3 B1.1 B1.2

B2, lateral compression

B2.1 B2.2 B2.3

Type C, complete posterior arch disruption

Characteristics Anterior iliac spine avulsion Iliac crest avulsion Ischial tuberosity avulsion Iliac wing fracture Unilateral pubic rami fracture Bilateral pubic rami fracture Sacrococcygeal dislocation Nondisplaced sacral fracture Displaced sacral fracture Pubic diastasis, anterior SI joint disruption Pubic diastasis, sacral fracture Anterior sacral buckle fracture Partial SI joint fracture/ subluxation Incomplete posterior iliac fracture Bilateral pubic diastasis, bilateral posterior SI joint disruption

B3.1, AP compression

B3.1

B3.2, AP and lateral compression

B3.2

Ipsilateral B2 injury, contralateral B1 injury

B3.3, bilateral lateral compression

B3.3

Bilateral B2 injury

C1, vertical shear

C1.1 C1.2

Displaced iliac fracture SI joint dislocation or fracture/dislocation Displaced sacral fracture Ipsilateral C1 injury, contralateral B1 or B2 injury

C2, vertical shear and AP/lateral compression

C3, bilateral vertical shear

C1.3 C2

C3

Bilateral C1 injury

Hemipelvis Displacement None

Stability Stable

None

Stable

None

Stable

External rotation

Rotationally unstable, vertically stable Rotationally unstable, vertically stable

Internal rotation

External rotation

Ipsilateral internal rotation, contralateral external rotation Bilateral internal rotation

Vertical (cranial)

Ipsilateral vertical (cranial), contralateral internal or external rotation Bilateral vertical (cranial)

Rotationally unstable, vertically stable Rotationally unstable, vertically stable Rotationally unstable, vertically stable Rotationally unstable, vertically unstable Rotationally unstable, vertically unstable Rotationally unstable, vertically unstable

Pelvis

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FIGURE 35-1 Type B1 open-book injury. Diastasis of the pubic symphysis and fracture of the superior or inferior pubic rami may occur.

• Type A fractures are stable, as the posterior ligaments are intact. These fractures include transverse sacral, iliac wing, pubic rami, pure acetabular, and chip and avulsion fractures. • Type B fractures are caused by internal and external rotational forces and are “partially” stable (vertically stable but rotationally unstable). They include open-book and bucket-handle fractures (Figs. 35-1 to 35-3). • Type C fractures are vertically and rotationally unstable, as they involve a complete disruption of the sacroiliac complex (Fig. 35-4). The Young–Burgess classification divides pelvic fractures according to the vector of the force applied into anteroposterior

FIGURE 35-2 Type B2 lateral compression (ipsilateral) injury. Note overriding of the left hemipelvis and crush injury to ipsilateral sacrum and ipsilateral iliac fracture.

FIGURE 35-3 Type B3 lateral compression (contralateral) or bucket-handle injury. Note anterior rami fracture with contralateral posterior sacroiliac injury.

compression (APC), lateral compression (LC), and vertical shear fractures (Table 35-2): • APC injuries are produced by forces applied in the sagittal plane, as is usually the case with motor vehicle crashes. APC-I injuries may result in a small widening of the pubic symphysis (2.5 cm) but the posterior ligaments are intact. APC-II injuries include tearing of the anterior sacroiliac ligaments, as well as the sacrospinous and sacrotuberous ligaments, but the posterior sacroiliac ligaments are intact. The pubic symphysis diastasis may be more than 2.5 cm. Rotational instability is usually present and hemorrhage more likely. APC-III injuries are caused by high-energy transfer and the posterior sacroiliac ligaments are disrupted,

FIGURE 35-4 Type C1 unilateral injury with vertical instability. Involves symphysis disruption or rami fracture with ipsilateral sacroiliac joint or sacral injury.

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TABLE 35-2 The Young–Burgess Classification of Pelvic Fractures

SECTION 3 X

Mechanism and Type AP compression, type I AP compression, type II AP compression, type III Lateral compression, type I

Lateral compression, type II

Vertical shear

Characteristics Pubic diastasis 2.5 cm Pubic diastasis 2.5 cm, anterior SI joint disruption Type II plus posterior SI joint disruption Ipsilateral sacral buckle fractures, ipsilateral horizontal pubic rami fractures (or disruption of symphysis with overlapping pubic bones) Type I plus ipsilateral iliac wing fracture or posterior SI joint disruption Vertical pubic rami fractures, SI joint disruption  adjacent fractures

causing full instability of the hemipelvis with a high likelihood of bleeding, nerve damage, and organ injuries. • LC injuries are produced from lateral impacts across the horizontal plane, also common with motor vehicle crashes. LC-I injuries include transverse fractures of the anterior ring or impacted sacral fractures and are typically stable. LC-II injuries are caused by higher-energy forces that produce tearing of the posterior sacroiliac ligament and displacement of the sacroiliac joint or an oblique fracture of the ilium, the superior part of which remains attached to the sacrum, while the inferior is mobile (crescent fracture). Depending on the force applied, this fracture can be stable or unstable. LC-III injuries are severely unstable fractures, as the lateral force continues to compress and rotate the hemipelvis to the point of complete destruction of the sacroiliac joints, as well as the sacrospinous and sacrotuberous ligaments. Neurovascular and organ injuries are common. • Vertical shear injuries are typically produced by a fall from a height and involve anterior (pubic rami, pubic symphysis) and posterior (sacroiliac complex) fractures. Typically, they are unstable. • Combinations of the above types produce a variety of fracture patterns, most commonly involving LC and vertical shear injuries. Nearly one third of PI patients have combination injuries.

DIAGNOSIS Physical examination will establish the suspicion for a PI and assess for pelvic instability. With the examiner’s hands on the anterior iliac spines of the patient, a gentle compression toward the midline, as well as a mild anteroposterior movement of the

Hemipelvis Displacement External rotation External rotation External rotation Internal rotation

Stability Stable Rotationally unstable, vertically stable Rotationally unstable, vertically unstable Stable

Internal rotation

Rotationally unstable, vertically stable

Vertical (cranial)

Rotationally unstable, vertically unstable

hands, will provide evidence of pelvic instability. This must be done by an experienced physician who will interrupt the motion immediately if instability is produced. Aggressive handling of the pelvis, such as “rocking,” is discouraged because it produces pain, bleeding, and aggravation of the injury. Inspection of the perineum is critical to diagnose lacerations or hematomas, which are further indications of significant PI. In a study of 66 patients with Glasgow Coma Score over 12, a focused physical examination protocol, including posterior palpation of the sacrum and sacroiliac joint, anteroposterior and lateral iliac wing compression, active hip range of motion, and a digital rectal examination, resulted in 98% sensitivity and 94% specificity for the detection of posterior pelvic fractures.5 The plain anteroposterior pelvic film is part of the radiographic routine for blunt trauma. However, many studies indicate that in patients with a negative clinical exam for PI, the pelvic film is unnecessary. In a review of 743 blunt trauma patients with no pain or other clinical findings of PI, only 3 patients (0.4%) had a pelvic fracture.6 In all cases it was a single, nondisplaced pubic ramus fracture that required no treatment. In another study of 686 blunt trauma patients, 311 received a pelvic film, which carried a false-negative rate of 32%.7 Of the 375 patients who did not receive a pelvic film, 3% of the patients (13) were found to have small pelvic fractures, none of which required treatment. So, it seems that a routine pelvic film in asymptomatic patients is not useful. Similarly, a pelvic film in patients who have symptoms may be inadequately sensitive and, therefore, might be omitted in favor of a CT scan. In a study of 397 multiple injured patients who had a pelvic film and a CT scan, 43 patients had 109 pelvic fractures.8 The plain film did not diagnose 51 (47%) of the fractures in 9 (21%) patients. Iliac and sacral fractures were most frequently missed. The authors concluded that a screening pelvic film is unnecessary after blunt multitrauma.

Pelvis

Pelvic inlet and outlet films provide information about the anteroposterior displacement of the injury (inlet films) and vertical displacement (outlet films). CT scan with reconstructions (and recently three-dimensional reconstructions) has essentially replaced all other diagnostic modalities and is routinely performed to accurately characterize pelvic fractures, as well as identify associated pelvic organ injuries and hematomas (Fig. 35-5). Intravenous contrast is routinely administered, unless there is a contraindication. Oral and rectal contrast is not necessary for blunt trauma. Magnetic resonance imaging does not offer a distinct advantage over CT scan and is only considered if radiation exposure becomes an issue, as it is with pediatric patients, pregnant patients, or repeat imaging. On occasions, the ligaments need to be evaluated in more detail and this can be done with higher accuracy by magnetic resonance. The diagnostic peritoneal lavage has nearly completely disappeared from the algorithms of diagnosis of abdominal bleeding in modern trauma centers. On occasions, we use the aspiration portion of it only (diagnostic peritoneal aspiration) to detect any large volume of intraperitoneal bleeding.9 We perform it percutaneously and, when a PI is suspected, supraumbilically. The focused abdominal sonography for trauma (FAST) exam has become a routine part of the initial evaluation and screening for intra-abdominal fluid. In PI a number of findings can be useful: (1) the absence of intraperitoneal fluid in a hemodynamically unstable patient indicates the presence of a major retroperitoneal hemorrhage from PI; (2) a distorted bladder contour indicates the presence of a compressing pelvic hematoma; (3) the presence of intraperitoneal fluid indicates that intraperitoneal organ injury must be excluded by additional diagnostic methods or laparotomy.

■ Pelvic Binders Unstable pelvic fractures produce bleeding because of ongoing injury to small vessels, as the fractured elements continue to move, and because of the increased volume of the pelvis, as it happens in open-book fractures. Significant bleeding continues unchecked prehospitally and in the emergency department, as the therapeutic choices to counteract these two mechanisms are limited. Pelvic binders address temporarily these two issues by stabilizing the pelvis to stop the movement of the fractured elements and by decreasing the retroperitoneal volume (Fig. 35-6).

MANAGEMENT OF PELVIC BLEEDING As soon as significant pelvic bleeding is suspected, the patient should be resuscitated per routine and a decision should be made for additional diagnostic tests or immediate intervention.

FIGURE 35-6 Pelvic binder.

CHAPTER CHAPTER 35 X

FIGURE 35-5 Three-dimensional computed tomographic reconstructions provide a realistic assessment of the anterior and posterior elements in pelvic fractures.

The concept of hypotensive resuscitation (i.e., allowing a lower than normal blood pressure during the early phases of resuscitation in order to prevent ongoing hemodilution and bleeding) has been adequately established for penetrating trauma.10 However, it is not universally accepted for blunt trauma despite the encouraging reports.11 The coexistence of neurologic injuries, which have been shown to produce worse outcomes in the presence of hypotension, is the main deterrent to allow a low blood pressure in a hemodynamically unstable blunt trauma patient. We espouse the principles of hypotensive resuscitation even in blunt trauma and are very cautious with our early resuscitation efforts, rarely using massive crystalloid infusions. If we suspect correctable bleeding sites, we strive to control bleeding as early as possible and then assume full resuscitation. We pay particular attention to substitute lost blood with blood and blood product transfusion rather than acellular fluids, and we decrease the ratio of packed red blood cells to fresh frozen plasma to as close to 1:1 as possible.12 We are not convinced about the effectiveness of recombinant Factor VIIa, given that there is no Level 1 evidence, supporting the use of this very expensive medication.13 The only prospective randomized study was flawed by excluding early deaths.14 The benefit of patients who received recombinant Factor VIIa compared with placebo was modest at best, a reduction of blood transfusions by 2.6 U among blunt trauma patients. There was no benefit among penetrating trauma patients. Therefore, we use recombinant Factor VIIa only as rescue therapy in very selected cases, if at all.

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SECTION 3 X FIGURE 35-7 A fracture that would be inappropriate for a tight pelvic binder. Displacement with forceful lateral compression by the binder could be exacerbated and result in vascular injury.

The former effect can be produced by simply applying a binder with mild to moderate LC of the pelvis. The latter effect is possible only if the device applies significant compression in order to reduce an open pelvis and decrease the volume available for blood to spill. However, significant LC can create the opposite effect, if applied on the wrong type of fracture. For example, a moderately displaced LC fracture can become worse, if excessive compression is applied by a pelvic binder (Fig. 35-7). Under these principles, simple stabilization by a pelvic device is desirable in all unstable fractures but significant compression should only be used in certain fractures, most commonly those of the open-book variety. The military antishock trousers (MAST) garment became popular in the 1980s after initial reports of improved survival in patients with multiple injuries. However, in 1989 a definitive prospective randomized study found it to be associated with increased mortality.15 The MAST was for the most part abandoned, although some emergency medical systems still use it on patients with pelvic or lower-extremity fractures. Pelvic binders have been commercialized by different companies along the same principles with only a few differences among them. Typically, a binder consists of a wide belt with a velcro that attaches the two ends of the binder (which can be cut to customize its length according to the patient’s body habitus). On the belt there is a “buckle pulley” mechanism. By pulling the strings the binder tightens and compression increases. The device is radiolucent, which allows radiographic imaging with no artifacts. The evidence on the effectiveness of pelvic binders is poor.16,17 There are three major pitfalls related to its use. First, an inappropriately high placement of the binder can lead to excessive abdominal pressure and minimal pelvic stabilization. It is not uncommon to place the binder too high. Correctly, the binder must be centered around the greater trochanters and not over the iliac spines. Usually, it needs to be gently passed under the patient’s back and then pulled slightly lower and over the buttocks for proper placement. Second, indiscriminate pulling of the strings can lead to greater

compression than necessary. The binder is frequently placed before the pelvic fracture is fully characterized by a CT scan or even by plain radiographs. Therefore, the initial step should involve only moderate tightening until the exact type of fracture is diagnosed. The pulley mechanism attached on the binder makes tightening very easy, and with minimal force an enthusiastic operator can squeeze the binder tight, producing on occasions more harm than good. Third, the binder may compromise the viability of skin, subcutaneous tissue, or even muscle if left in place for too long. A general guideline of a maximum 24-hour placement exists but obviously even this may be too long after a tight application of the binder.18 The health care providers should understand that the binder is only an imperfect and temporary tool for bleeding control. Definitive pelvic reduction and cessation of hemorrhage should be planned immediately in order to minimize the need for a binder. A bed sheet is frequently used as an immediately available and inexpensive way to wrap the pelvis.19 The edges of the sheet are tied together and around a stick, which can be turned to tighten the sheet and apply the desired degree of compression (Fig. 35-8).

■ External Fixation External fixation has been popularized as a rapid means of controlling bleeding. In a few institutions this can be accomplished in the emergency room but in most centers the patients are transferred in the operating room. A number of clamps and devices have been used to provide external fixation. The C-clamp was designed for easy placement in the emergency room in the presence of posterior pelvic fracture.20 As opposed to other fixators, it is easy to assemble and apply. Its crossbar rotates around the fixation pins, which are anchored in the cancellous bone in both acetabula. The rotation of the clamp allows other procedures in the abdomen or pelvis to be offered without difficulty. The pins can be placed more anteriorly or posteriorly according to the location of the pelvic fracture and the need to reduce them. It is clearly a temporary method, which needs to be replaced later with either a proper pelvic frame or internal fixation. The C-clamp has been used more frequently in European than American trauma centers, which typically prefer a frame placed in the operating room. Early external fixation stabilizes the fractured elements, decreases the pelvic volume, and allows clot to form. There are a variety of external fixators. The early systems used small pins and heavy bars, whereas the newer systems are more compact, easy to adjust, and with larger pins. The standard placement of pins is in the superior iliac crest above the superior anterior iliac spine. Lower placement of the pins is also acceptable and can improve the access to the abdominal cavity. In certain designs more than one pin are placed on each side. Pins can be placed by an open or percutaneous technique. All single bar systems require two pins in each hemipelvis, whereas the frames require three pins on each side, except the Pittsburgh system which requires two clusters of two pins in each hemipelvis. In most cases of a true unstable pelvis, external fixators remain a temporary device, which bridges the period to definitive internal fixation. In the supine position, external fixation provides adequate

Pelvis

■ Angiographic Embolization

FIGURE 35-8 A simple sheet wrapped around the pelvis produces inexpensive and adequate reduction of a pelvic fracture. A significant pubic diastasis, as shown in the first image, is reduced by the sheet, as shown in the following image.

stability. In the standing position the vertical load is usually greater than the capacity of the external fixator to resist these forces. Dislocation of fractured elements can happen, particularly at the sacroiliac complex.21 After placement of the frame, reduction of the pelvic fracture is done by applying opposite forces to the ones that created the fracture. Open-book fractures are corrected by internal rotation of the pins, whereas LC fractures are reduced by external rotation. Vertical shear fractures required skeletal traction by placement of a femoral pin and are the ones least likely to be adequately reduced and stabilized by external fixation.22 If not converted to internal fixation, external fixators usually stay for 6–12 weeks. The most common complication is infection at the pin sites, ranging from mild to severe. Appropriate sterile technique during pin placement and proper care of the

Pelvic ring fracture producing hemodynamic instability is one of the most common indications for angiographic embolization. The ability to control the bleeding by minimally invasive techniques and without the need for an operation, which is routinely unsatisfactory, is very appealing. However, the appeal is hampered by the unavailability of interventional radiology teams around the clock, the poor monitoring available in an angiography suite, and the long times spent on the angiography table. All three reasons have ceased to exist in modern trauma centers. Interventional radiology teams are now immediately available with short notice in most Level 1 trauma centers. In our hospital the team is in house until late at night and expected to be assembled within 40 minutes after that. Monitoring and resuscitation in the angiography suite should be no different in a Level 1 trauma center than it is in the operating room. Highrate fluid infusion devices, noninvasive hemodynamic monitoring, mechanical ventilatory support, arterial blood gas assessments, blood transfusions, and aggressive resuscitation efforts should take place during angiography. The surgical team should be present throughout the procedure, exactly as it would be throughout an operation. An anesthesiologist and/or intensivist should be called according to the circumstances. Critical care nurses should participate in tasks with which radiology nurses are not familiar. Emergency angiography for bleeding control is not much different than an emergency laparotomy for the same reason. Shifting the care of the patient from the trauma team to the interventional radiologist during angiography is inappropriate. In our hospital the trauma team, including anesthesiology and critical care nursing when required, remains responsible for the monitoring and resuscitation of the trauma patient in the angiography suite during the emergency interventions for bleeding control. The concept of time spent for embolization is also important and will be discussed later. The first challenge for the clinician is to identify the correct indications for angiography. Approximately, one fourth of the angiographies performed find no direct or indirect evidence of bleeding24 and the risk of an unnecessary transfer to the

CHAPTER CHAPTER 35 X

pin sites is essential to avoid infection. If the pins become infected or loose, they must be removed and replaced. Other complications are typically associated with placement and include injury to the lateral femoral cutaneous nerve or other neurovascular structures. In general, it seems that external fixation should be considered in two stages, an early resuscitative and a later definitive stage. In the early stage the fixator is placed to stabilize the fracture and help control the bleeding. At a later stage a decision must be made about the long-term effectiveness of the external frame versus the need to convert to internal fixation. LC fractures are likely to respond to external fixation as the only method, if reduction is satisfactory. Vertical shear fractures are unlikely to be managed without definitive internal fixation.23 Each patient must be carefully assessed to balance the therapeutic choices of fixing the fracture while maintaining hemodynamic stability and inflicting the minimum physiologic insult during the initial critical hours after trauma.

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SECTION 3 X

radiology suite could have been avoided in favor of a direct transfer to the intensive care unit. However, there are no controlled studies in the present literature and the precise indications are unknown. In 97 patients with pelvic fractures retrospectively reviewed no factors predicted a positive angiogram with sufficient likelihood.24 Mechanism of trauma, injury severity, hemodynamic presentation, associated injuries, and hemodynamic presentation were similar between patients with and without radiographic evidence of pelvic bleeding. In a later prospective study by the same group, 65 patients with pelvic fractures were included in the study total of 100 consecutive patients evaluated by angiography for bleeding.25 Three independent predictors of bleeding were identified: age older than 55 years, absence of long-bone fractures (indicating that the pelvis was the main source for bleeding), and emergent angiography (indicating that semiacute interventions had a lower likelihood to identify bleeding). The predictive effect of age was confirmed by another prospective observational study.26 Ninetyfour percent of patients older than 60 years of age had a positive angiogram as opposed to 52% of younger patients. The authors recommended that angiographic embolization is offered liberally to pelvic fracture patients over 60 years old. Pelvic fracture pattern is considered a major predictor of bleeding. Traditionally, three types of PI are considered to be associated with hemorrhage: pubic symphysis diastasis of more than 2.5 cm, bilateral superior/inferior pubic rami fractures (butterfly), and posterior fractures (especially of the vertical shear variety).27 However, there is evidence that even anterior fractures can produce bleeding,24 particularly in older patients or those receiving anticoagulants. The presence of contrast extravasation on pelvic CT scan has also been widely used as a predictor of a positive angiogram.28,29 It is suggested that the sensitivity and specificity of a “contrast blush” on CT to identify bleeding that requires embolization is 84% and 85%, respectively, with an overall accuracy of 90%.29 However, our experience has been that the new-generation CT scanners are highly sensitive and—in combination with precise IV contrast infusion protocols—may pick up small bleeds that are potentially self-limited without further intervention. Therefore, the mere presence of contrast extravasation on CT is not an immediate indication for angiography in our institution. We consider contrast extravasation a crucial element of the constellation of symptoms, signs, and findings of PI and consider it in the context of the entire clinical picture. A patient who is hemodynamically labile and has a contrast blush is emergently transferred to the angiography suite. A patient with a contrast blush, who is hemodynamically stable, does not usually receive a preemptive angiogram but is rather placed under close observation. Similarly, the size of pelvic hematoma cannot be used as an isolated indication for angiography.30 Interventional radiologists typically seek to identify the precise site of bleeding and control it with coils. This requires subselective intubation of internal iliac artery branches, time, and larger doses of intravenous contrast. For true trauma emergencies the interventional radiologist should be in a different mindset. In alignment with surgical damage control principles, damage control angiography should be offered. The procedure should be rapid, effective, and temporary. Bilateral internal iliac artery

FIGURE 35-9 Truncation of all the branches of the internal iliac artery after injection of gelatin particles.

embolization embraces these principles. The interventional radiologist does not consume time maneuvering small catheters into small arterial branches. The bleeding is controlled by truncating all the branches of the internal iliac arteries by a temporary agent, such as gelatine sponge particles (Fig. 35-9). There are at least three reasons for performing bilateral internal iliac artery embolization: (1) at the time of embolization, the patient is often in shock and profoundly vasoconstricted. This prevents intravenous contrast extravasation during angiography and offers a misleading impression of bleeding control. Once the patient is resuscitated and vasoconstriction is reversed, bleeding may ensue. Blockage of all the branches of the internal iliac arteries prevents this problem. (2) The pelvic vascular network is so extensive that a bleeder may be fed reversely from the controlateral side. Embolizing only the unilateral internal iliac artery may not offer effective bleeding control (Fig. 35-10). (3) Some bleeders are right in the center and it is very difficult to discern if they are supplied by the right or the left arterial system. Embolizing both is the only way to control the bleeding (Fig. 35-11). The safety of bilateral internal iliac artery embolization has been shown in a study of 30 consecutive patients who received the procedure with no major complications.31 It seems that the extensive vascular supply of the pelvis ensures survival of pelvic tissues and organs during the few days of gelfoam embolization and until the arteries recanalize (Fig. 35-12). Gelfoam pledgets are usually cut to a size not smaller than 2 mm to prevent migration to smaller vessels and allow baseline collateral circulation. Despite isolated reports of serious complications with bilateral embolization for cancer,32,33 such as colon necrosis, perineal wound sepsis, or avascular necrosis of the femoral head, our experience over the last 15 years has been very encouraging and without any significant complications. In a case-matched study of similar male pelvic fracture patients with and without bilateral iliac artery embolization, the incidence of

Pelvis

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CHAPTER CHAPTER 35 X

FIGURE 35-10 A right pelvic bleed is fed via the extensive pelvic network through the left arterial circulation. In such cases bilateral embolization may be appropriate.

FIGURE 35-12 Heavy bilateral internal iliac artery embolization with near complete (but temporary) interruption of the pelvic circulation. The patient did well.

sexual dysfunction 1–2 years after the injury was high but not different between the two groups.34 Although major pelvic fractures affected sexual function, the addition of temporary embolization of both internal iliac arteries did not worsen the outcome. The authors assumed that, if this delicate function was not affected by embolization, it was unlikely that any other pelvic organ would suffer major long-term consequences. Failure of embolization occurs in approximately 15% of the patients and is typically associated with coagulopathy.35,36 In such patients the thrombogenic potential of the injected gelatin material may not be fully realized and vessels may not be effectively blocked, showing near-full recanalization within only hours of seemingly effective initial embolization. Superselective embolization is associated with a higher risk of rebleeding. Patients who continue to require blood transfusions within 72 hours after embolization should be taken back to the angiography suite, as repeat embolization is typically successful.

■ Preperitoneal Pelvic Packing

FIGURE 35-11 Midline bleeds can be hard to attribute to the left or the right circulation. Bilateral embolization may be appropriate.

Packing has been an important part of damage control operations for severe abdominal injuries. For the pelvis, packing has been an ineffective method of bleeding control because the incision of the peritoneum to place the packs releases the tamponade. Furthermore, the open funnel that the pelvis presents does not allow for the packs to remain in place and exercise a hemostatic effect by compression; they rather float free back toward the abdomen. Even if pelvic packing has not been popular in the United States, European trauma surgeons have used it more liberally. Ertel et al.37 from Switzerland showed excellent bleeding control

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SECTION 3 X

after major pelvic fractures using a combination of packing and external fixation by C-clamp. It is not clear which of the two techniques was primarily responsible for the outcomes. Recently, pelvic packing was reintroduced in the United States by the Denver trauma group.38 Their technique of preperitoneal pelvic packing addressed the previous problems of pack displacement and tamponade disturbance. By placing the packs behind the peritoneum through a separate low midline or suprapubic vertical incision, the peritoneal tamponade is not disturbed and the packs cannot float back toward the abdominal cavity. The authors have described the technique, which involves the opening of the fascia, retraction of the recti muscles laterally, and placement of approximately three packs on each side of the bladder deep into the pelvis. Attention is paid at all times to not open the peritoneum. For this reason, if a laparotomy is performed, the incision should be limited to the upper margin of the pelvic hematoma and not below that. Preperitoneal pelvic packing is then performed through a separate incision (Fig. 35-13). In our practice we have found the technique to be lifesaving in patients who are frankly unstable and cannot tolerate transport to the angiography suite. In these patients, the pelvic hematoma is typically very large and more than six packs may be needed to effectively compress all the bleeding sites. In a study of 28 patients receiving preperitoneal pelvic packing by the Denver trauma group, 21 (75%) survived. Only 14% of the patients had postoperative angiographic embolization.38

FIGURE 35-13 Note the Pfannenstiel incision, which is separate and distinct from the midline laparotomy, leading to the open abdomen. An external fixator is also placed to reduce the fracture. Very likely such a patient will also receive angiographic embolization, immediately following the operation.

In a similar study by a Norwegian group 13 of 18 patients (72%) with packing survived but postoperative angiographic embolization was used in 80% of the patients.39 One should consider these two procedures complementary rather than competing.40 Both of them can be offered on the same patient. We consider angiographic embolization as the preferred method of controlling pelvic bleeding for most patients. However, preperitoneal pelvic packing provides a useful alternative in the following circumstances if: (1) there is no angiographic support, as it may happen in non-Level 1 trauma centers; (2) there is angiographic support but the team cannot assemble expeditiously; (3) there is profound hemodynamic instability, which makes even mild delays unacceptable and calls for rapid packing in a ready operating room. Following packing, angiographic embolization should still be strongly considered.

DEFINITIVE FIXATION Unstable and bleeding pelvic ring fractures are usually managed by a staged repair, which includes a pelvic binder initially, external fixation shortly after that, and internal fixation as the final step to reconstruction. The details of the surgical approach for definitive internal fixation of the pelvis are beyond the scope of this chapter and will not be discussed. External fixation can serve as definitive therapy, particularly in anterior pelvic ring fractures. It does not offer adequate stability in posterior fractures, particularly in the vertical axis. External fixation is appealing as a long-term solution because it avoids the risks of open operation but the reduction needs to be precise. If a reduction to less than 1 cm of initial displacement is not maintained throughout the period of healing, then 80% of the patients require chronic analgesics compared with almost none with precise reduction.41 However, the complications rise as time progresses, and pin infection develops in 50% of definitive fixators, as opposed to 13% of temporary fixators.42 The most common cause for replacing an external fixator is aseptic pin loosening. Approximately 10% of patients require replacing external with internal fixation as definitive treatment. For APC-II injuries a plate across the pubic symphysis may be enough, as the posterior pelvic stability is maintained by the unaffected strong posterior sacroiliac ligaments. APC-III and most LC-II and vertical shear fractures typically required posterior stabilization by internal fixation. According to the specific type of fracture, sacroiliac screws (placed openly or percutaneously), special LC screws, or plates should be used. The complications of internal fixation are many and range from bleeding to injury of nerves, devascularization of muscle, infection, suboptimal reduction, and chronic pain. Equally important to the surgical technique is the timing of internal fixation. The term “damage control orthopedics” was introduced to denote that at the early stages fracture fixation should be minimized to the least necessary, followed by definitive repair when the patient’s physiologic status allows it.43,44 Early stabilization with later fixation is associated with lower levels of inflammatory cytokines and better outcomes compared with immediate fixation. The optimal time for definitive intervention is unclear and will probably vary from patient to patient.

Pelvis

ASSOCIATED INJURIES Major pelvic fractures are commonly associated with intra- and extra-abdominal injuries. Closed head injury occurs in 51%, long-bone fractures in 48%, and thoracic injury in 20% of the patients. Among the extra-abdominal injuries the association with thoracic aortic injury is of particular importance and ranges between 1.4% and 5.9% among all patients with pelvic fractures.46,47 The incidences of associated solid and hollow intraabdominal organs injuries have been reported as 11% and 4.5%, respectively, and diaphragmatic injuries occur in 2% of pelvic fractures.47 All these associations point out to the complexity of diagnosing all the injuries and choosing the correct therapy. A patient with a major pelvic fracture will usually have—at least lower—abdominal tenderness and hemodynamic fluctuations. The decision to explore or avoid the abdominal cavity is often hard as clinical examination, FAST, diagnostic peritoneal aspiration, or even CT scan may give equivocal information. The presence of a central neurologic injury will only confuse the picture further. The suggested algorithm in Fig. 35-15 can serve as a guideline for the management of major pelvic fractures, although each patient is unique and requires individualized decisions. Probably, the most notable association is between pelvic fracture and bladder or urethral injuries. The physical proximity of these injuries results in an injury rate of 6%, which increases by nearly 5-fold with male gender and severe fractures. The majority of bladder ruptures (80%) are extraperitoneal. They can be managed by simple Foley catheter drainage for 10–14 days. Intraperitoneal injuries require a laparotomy and direct repair. Urethral injuries are common and almost exclusively in males.48 Straddle injuries, typically producing bilateral pubic rami fractures, are associated with urethral injuries. The presence of a

perineal hematoma, blood at the urethral meatus, or a highriding prostate should alert the clinician about a urethral injury. A retrograde urethrogram should be performed before inserting a Foley catheter. On selected occasions, in which time is of the essence, advancing a Foley catheter without first performing a retrograde urethrogram is an acceptable alternative. It should be done by a senior person and with extreme care to stop and withdraw in the presence of any resistance. If a Foley catheter cannot be inserted because of a urethral injury, a suprapubic catheter is appropriate. Urethral injuries are usually repaired at a later stage after the inflammation has subsided but there are reports of successful aggressive early management. Obviously, these decisions will be made jointly by a urologist and the trauma surgeon.

OPEN PELVIC FRACTURES A combination of open wounds with pelvic ring injuries produces an extremely challenging situation, as bleeding and ongoing contamination are typically profound and death rates are usually in excess of 20% and up to 50%. Lacerations of the perineum are much more difficult to manage than anterior lacerations. These two types of open pelvic fractures should not be described as the same entity because the management should be different according to the location and extent of the skin laceration. The priorities in management of major open pelvic fractures are not much different than the management of any other devastating injury and include—in order of priority—the control of bleeding, control of contamination, and definitive fixation. Control of bleeding in open pelvic fractures involves packing through the laceration, application of a pelvic binder, angiographic embolization, and external fixation. Preperitoneal pelvic packing, as it was described above, may not be effective because the tamponade of the retroperitoneal pelvic space is already released to the external environment. There is a debate about the need for colostomy to control contamination. Many authors believe that a diverting colostomy should be routinely performed as an integral part of the surgical management of an open pelvic fracture (Fig. 35-14). In a study of 39 patients with open pelvic fractures the mortality was 26% and predicted by

FIGURE 35-14 Colostomy is advisable for lacerations that are in immediate proximity or involve the perineum and perianal region. This patient received debridement and packing of the perineal wound, external fixation of the pelvic fracture, and a diverting colostomy.

CHAPTER CHAPTER 35 X

It has been suggested that clinical markers (such as the Systemic Inflammatory Response Score) or laboratory values (such as interleukin-6) can be monitored to decide about timing.45 If the markers are on the rise, the inflammatory response is still rampant and a second hit may be detrimental. If the markers are decreasing or normal, definitive fixation is advisable.

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fracture instability and rectal injury. The authors suggested that early colostomy is important to survival.49 In another study of 44 patients, 23 were managed with a diverting colostomy and 21 without it. Even if the patients with colostomy were more severely injured, they had a lower 30-day mortality. Pelvic sepsis and anastomotic complications contributed to mortality in the no-colostomy group, and the authors recommended the liberal use of colostomy.50 However, a systematic analysis of the literature showed that there were no differences in outcome between patients with and those without a colostomy.51 Nevertheless, the authors recognized that the evidence was of poor quality and solid conclusions could not be made, and called for prospective randomized studies, a rather unlikely goal, given the low incidence of these injuries. A midway solution was described on 18 patients, of whom 5 had a colostomy because of perineal wounds, whereas 13 with anterior wounds were not subjected to this procedure.52 No patient without a colostomy developed pelvic sepsis, and the authors recommended a selective approach. This exactly is our approach too. Patients with rectal wounds or with wounds in immediate proximity to the anus usually receive a diverting colostomy. Patients with more distal wounds are usually managed without fecal diversion. Debridement of ischemic tissue is an important part of the management. Despite all strategies, the mortality of

open pelvic fractures remains very high, even in the modern era, even in expert hands. The Grady Memorial Hospital group described 44 such patients with a mortality of 45%.53 The presence of bleeding and need for angiographic embolization was associated with a grim prognosis. Late pelvic sepsis developed in five patients and three of them died. It, therefore, seems that primarily bleeding and secondarily sepsis continue to claim a heavy toll on the lives of patients with this devastating injury.

LONG-TERM OUTCOMES Neurologic injury is a characteristic disorder after pelvic trauma with serious long-term implications. In an electrodiagnostic study of 78 patients with pelvic trauma and lowerextremity neurologic symptoms, the incidence of gait instability and neuropathic pain was high.54 As already discussed, sexual dysfunction remains a major problem in approximately two thirds of male patients with major pelvic fractures.34 Sensory impairments were noted in 91% of the patients with unstable sacral fractures 1 year after the injury.55 Impaired gait was recorded in 63% and bladder, bowel, or sexual impairments in 59%. In a questionnaire study of 24 women with a Tile B or C pelvic fracture and a median age of 24 years,

Complex pelvic fracture APII-III, LC II-III, VS Hemodynamically unstable Hemodynamically stable

Small/moderate pelvic hematoma without blush (within pelvis)

FAST/DPA in trauma bay

Pelvic hematoma with blush or large hematoma without blush

Positive Negative OR for Ex-lap +/pelvic packing

ICU/TRACU observation/timely fixation

Consider angio/embolization and/or early fixation ICU admission

• The angiography room should be treated as an operating room with trauma/ortho teams present and resuscitation continues. • Temporary bilateral internal iliac artery embolization is preferred. • Technique of retroperitoneal pelvic packing is described by Cothren et al.38 • Large pelvic hematoma is defined as one that extends out of the pelvis.

Angio/embolization and/or early fixation/pelvic packing

Remains unstable

Consider repeat angio/embo

FIGURE 35-15 Algorithm for the management of major pelvic fractures.

Pelvis

CONCLUSION Major pelvic fractures are associated with significant bleeding, complications, and mortality. A multidisciplinary approach is important. The diagnosis of major pelvic bleed should be made in the trauma bay based on external clues of injury to the pelvis, physical examination indicating pelvic ring instability, and exclusion of other potential sources. The CT scan is currently the most useful test to characterize the fractures, detect hematomas and active contrast extravasation, and plan further treatment. In the presence of bleeding, angiographic embolization is indicated and should be done in most cases along the principles of damage control angiography. Pelvic binding in the emergency room and external fixation are important interventions to reduce bleeding, pain, and ongoing injury. Internal fixation is best left for a later stage. Preperitoneal pelvic packing can be a lifesaving maneuver for those patients who are too unstable to travel to the angiography suite or in these hospitals that do not have easy access to angiography. A general algorithm is provided (Fig. 35-15) but the exact sequence of interventions should be individualized to the particular complexities of these challenging patients.

REFERENCES 1. Tile M. Acute pelvic fractures: I. Causation and classification. J Am Acad Orthop Surg. 1996;4(3):143–151. 2. Tile M. Acute pelvic fractures: II. Principles of management. J Am Acad Orthop Surg. 1996;4(3):152–161. 3. Young MR, Burgess AR, Brumback RJ, Poka A. Pelvic fractures: value of plan radiography in early assessment and management. Radiology. 1988;160:445–459. 4. Burgess AR, Eastridge BJ, Young JW. Pelvic ring disruptions: effective classification system and treatment protocols. J Trauma. 1990;30(7): 848–856. 5. McCormick JP, Morgan SJ, Smith WR. Clinical effectiveness of the physical examination in diagnosis of posterior pelvic ring injuries. J Orthop Trauma. 2003;17:257–261. 6. Salvino CK, Esposito TJ, Smith LD, et al. Routine pelvic x-ray studies in awake blunt trauma patients: a sensible policy? J Trauma. 1992;33:413–418. 7. Guillamondegui OD, Pryor JP, Gracias VH, Gupta R, Reilly PM, Schwab CW. Pelvic radiography in blunt trauma resuscitation: a diminishing role. J Trauma. 2002;53:1043–1047. 8. Steward BG, Rhea JT, Sheridan RL, Novelline RA. Is the screening portable pelvis film clinically useful in multiple trauma patients who will be examined by abdominopelvic CT? Experience with 397 patients. Emerg Radiol. 2002;9:266–271. 9. Kuncir E, Velmahos GC. Diagnostic peritoneal aspiration: the foster child of DPL. Int J Surg. 2007;5:167–171. 10. Bickell WH, Wall MJ, Jr, Pepe PE, Martin RR, Ginger VF, Allen MK, Mattox KL. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994;331: 1105–1109. 11. Dutton RP, Mackenzie CF, Scalea TM. Hypotensive resuscitation during active hemorrhage: impace on in-hospital mortality. J Trauma. 2002;52: 1141–1146. 12. Tieu BH, Holcomb JB, Schreiber MA. Coagulopathy: its pathophysiology and treatment in the injured patient. World J Surg. 2007;31:1055–1064.

13. Levi M, Peters M, Bueller HR. Efficacy and safety of recombinant factor VIIa for the treatment of severe bleeding: a systematic review. Crit Care. 2005;33:883–890. 14. Boffard KD, Riou B, Warren B, et al. Recombinant factor VIIa as adjunctive therapy for bleeding control in severely injured trauma patients: two parallel randomized, placebo-controlled, double-blind clinical trials. J Trauma. 2005;59:8–15. 15. Mattox KL, Bickell W, Pepe PE, Burch J, Feliciano D. Prospective MAST study in 911 patients. J Trauma. 1989;29:1104–1112. 16. White CE, Hsu JR, Holcomb JB. Haemodynamically unstable pelvic fractures. Injury. 2009;40:1023–1030. 17. Krieg JC, Mohr M, Ellis TJ, et al. Emergent stabilization of pelvic ring injuries by controlled circumferential compression: a clinical trial. J Trauma. 2005;59:659–664. 18. Jowett AJ, Bowyer GW. Pressure characteristics of pelvic binders. Injury. 2007;38:118–121. 19. Nunn T, Cosker TD, Bose D, Pallister I. Immediate application of improvised pelvic binder as first step in extended resuscitation from lifethreatening hypovolaemic shock in conscious patients with unstable pelvic injuries. Injury. 2007;38:125–128. 20. Ganz R, Krushell RH, Jacob RP, Kuffer J. The antishock pelvic clamp. Clin Orthop. 1991;267:71–78. 21. Ponsen KJ, Hoek van Dijke GA, Joose P, Snijders CA. External fixators for pelvic fractures. Comparison of the stiffness of current systems. Acta Orthop Scand. 2003;74:165–171. 22. Yang AP, Iannacone WM. External fixation for pelvic ring disruptions. Orthop Clin North Am. 1997;28:331–344. 23. Tile M. The management of unstable injuries of the pelvic ring. J Bone Joint Surg Br. 1999;81:941–943. 24. Velmahos GC, Chahwan S, Falabella A, Hanks SE, Demetriades D. Angiographic embolization for intraperitoneal and retroperitoneal injuries. World J Surg. 2000;24:539–545. 25. Velmahos GC, Toutouzas KG, Vassiliu P, et al. A prospective study on the safety and efficacy of angiographic embolization for pelvic and visceral injuries. J Trauma. 2002;52:303–308. 26. Kimbrell BJ, Velmahos GC, Chan LS, Demetriades D. Angiographic embolization for pelvic fractures in older patients. Arch Surg. 2004;139:728–733. 27. Alonso JE, Lee J, Burgess AR, Browner BD. The management of complex orthopedic injuries. Surg Clin North Am. 1996;76:879–892. 28. Yoon W, Kim JK, Jeong YY, Seo JJ, Park JG, Kang HK. Pelvic arterial hemorrhage in patients with pelvic fractures: detection with contrastenhanced CT. Radiographics. 2004;24:1591–1605. 29. Cervas DS Jr, Mirvis SE, Shanmuganathan K, Kelly IM, Pais SO. Detection of bleeding in patients with major pelvic fractures: value of contrast-enhanced CT. AJR Am J Roentgenol. 1996;166:131–135. 30. Brown CV, Kasotakis G, Wilcox A, Rhee P, Salim A, Demetriades D. Does pelvic hematoma on admission computed tomography predict active bleeding at angiography for pelvic fracture? Am Surg. 2005;71: 759–762. 31. Velmahos GC, Chahwan S, Hanks SE, et al. Angiographic embolization of bilateral internal iliac arteries to control life-threatening hemorrhage after blunt trauma to the pelvis. Am Surg. 2000;66:858–862. 32. Perz JV, Huges MD, Bowers K. Angiographic embolization in pelvic fracture. Injury. 1998;29:187–191. 33. Obard RO, Sniderman KW. Avascular necrosis of the femoral head as a complication of complex embolization for severe pelvic hemorrhage. Br J Radiol. 1995;68:920–922. 34. Ramirez JI, Velmahos GC, Best CR, Chan LS, Demetriades D. Male sexual function after bilaterally internal iliac artery embolization for pelvic fracture. J Trauma. 2004;56:734–741. 35. Fang JF, Shig LY, Wong YC, Lin BC, Hsu YP. Repeat transcatheter arterial embolization for the management of pelvic arterial hemorrhage. J Trauma. 2009;66:429–435. 36. Gourlay D, Hoffer E, Routt M, Bulger E. Pelvic angiography for recurrent traumatic pelvic arterial hemorrhage. J Trauma. 2005;59:1168–1174. 37. Ertel W, Keel M, Eid K, Platz A, Trentz O. Control of severe hemorrhage using C-clamp and pelvic packing in multiply injured patients with pelvic ring disruption. J Orthop Trauma. 2001;15:468–474. 38. Cothren CC, Osborn PM, Moore EE, Morgan SJ, Johnson JL, Smith WR. Preperitoneal pelvic packing for hemodynamically unstable pelvic fractures: a paradigm shift. J Trauma. 2007;62:834–839. 39. Totterman A, Madsen JE, Skaga NO, Roise O. Extraperitoneal pelvic packing: a salvage procedure to control massive traumatic pelvic hemorrhage. J Trauma. 2007;62:843–852. 40. Suzuki T, Smith WR, Moore EE. Pelvic packing or angiography: competitive or complementary? Injury. 2009;40:343–353.

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16 reported de novo pelvic dysfunction.56 Bladder symptoms were present in 12, bowel problems in 11, and sexual dysfunction in 7. Malunion of fractures can produce leg-length discrepancies, creating gait instability and pain. It is, therefore, obvious that even with optimal management, severe pelvic fractures are associated with long-term sequelae. Pain and neurologic impairments are the most common problems that can compromise the quality of life.

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41. Guyton JL, Crockarell JR Jr. Fractures of acetabulum and pelvis. In: Canale ST, ed. Campbell’s Operative Orthopedics. 10th ed. St. Louis, MO: Mosby; 2003:2939–2984. 42. Mason W, Khan S, James C, Chesser T, Ward A. Complications of temporary and definitive external fixation of pelvic ring injuries. Injury. 2005;36:599–604. 43. Scalea TM, Boswell SA, Scott JD, Mitchell KA, Kramer ME, Pollak AN. External fixation as a bridge to intramedullary nailing for patients with multiple injuries and with femur fractures: damage control orthopedics. J Trauma. 2000;48:613–623. 44. Giannoudis PV, Pape HC. Damage control orthpaedics in unstable pelvic ring injuries. Injury. 2004;35:671–677. 45. Harwood PJ, Giannoudis PV, van Griensven M, Krettek C, Pape HC. Alterations in the systemic inflammatory response after early total care and damage control procedures for femoral shaft fracture in severely injured patients. J Trauma. 2005:58:448–454. 46. Ochsner MG, Hoffman AP, DiPasquale D, et al. Associated aortic rupture—pelvic fracture: an alert for orthopedic and general surgeons. J Trauma. 1992;33:429–434. 47. Demetriades D, Karaiskakis M, Toutouzas K, Alo K, Velmahos G, Chan L. Pelvic fractures: epidemiology and predictors of associated abdominal injuries and outcomes. J Am Coll Surg. 2002;195:1–10.

48. Kommu SS, Illahi I, Mumtaz F. Patterns of urethral injury and immediate management. Curr Opin Urol. 2007;17:383–389. 49. Jones AL, Powell JN, Kellam JF, McCormack RG, Dust W, Wimmer P. Open pelvic fractures. A multicenter retrospective analysis. Orthop Clin North Am. 1997;28:345–350. 50. Tsugawa K, Koyanagi N, Hashizume M, et al. New therapeutic strategy of open pelvic fracture associated with rectal injury in 43 patients over 60 years of age. Hepatogastroenterology. 2002;49:1275–1280. 51. Lunsjo K, Abu-Zidan FM. Does colostomy prevent infection in open blunt pelvic fractures? A systematic review. J Trauma. 2006;60:1145–1148. 52. Pell M, Flynn WJ Jr, Seibel RW. Is colostomy always necessary in the treatment of open pelvic fractures? J Trauma. 1998;45:371–373. 53. Dente CH, Feliciano DV, Rozycki GS, et al. The outcome of open pelvic fractures in the modern era. Am J Surg. 2005;190:830–835. 54. Chiodo A. Neurologic injury associated with pelvic trauma: radiology and electrodiagnosis evaluation and their relationship to pain and gait outcome. Arch Phys Med Rehabil. 2007;88:1171–1176. 55. Totterman A, Glott T, Madsen JE, Roise O. Unstable sacral fractures: associated injuries and morbidity at 1 year. Spine. 2006;31:E628–E635. 56. Baessler K, Bircher MD, Stanton SL. Pelvic floor dysfunction in women after pelvic trauma. BJOG. 2004;111:499–502.

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CHAPTER 36

Genitourinary Trauma Michael Coburn

Genitourinary injury occurs in 2–5% of all trauma patients and in at least 10% of patients with abdominal trauma, emphasizing the need for a close collaboration between the general and urologic trauma surgeon. This unique relationship that the urologist and general trauma surgeon share in the management of urologic injuries requires that common philosophies of management be applied. Controversies exist in the approach to urologic trauma, and recent efforts to achieve a broad consensus in the management of diverse urologic injuries have resulted in numerous publications. One such effort, sponsored by the World Health Organization and the Societe Internationale d’Urologie, involved a 25-year review of world literature focusing on levels of evidence and development of evidence-based management recommendations.1–5 Another similar effort through the European Association of Urology (EAU) had a similar focus.6 Both produced useful syntheses of a large body of literature. The current discussion will offer a broadly applicable approach to the management of urologic trauma based on current literature and local experience and perspective.

ANATOMY Beginning with surgical exposure for upper tract injuries, the contemporary approach to the injured kidney is through an anterior midline abdominal incision. Access to the kidneys and ureters is generally obtained by reflecting the colon on either side medially and exposing Gerota’s fascial envelope. While modern descriptions of exposing the injured kidney often involve a discussion of first obtaining vascular control of the renal vessels prior to entering the perirenal hematoma, the important element in this practice is achieving access to the pedicle such that atraumatic vascular clamping can be achieved if significant bleeding is encountered. This can be accomplished through individually dissecting and “looping” the renal vessels through an incision in the posterior perito-

neum over the aorta (which can allow access to either the left- or right-sided artery and the left-sided vein) or by first reflecting the colon on the side of injury and then obtaining vascular control or access to the pedicle. Obviously, the renal vessels should be approached first and dissected directly when there is suspicion of a renovascular injury (medial or perihilar hematoma, pulsatile hematoma). When suspicion of a renovascular injury is low, many urologic trauma surgeons successfully approach the kidney by first reflecting the colon and then achieving vascular control. This is achieved by individually dissecting the vessels, by using a vascular pedicle clamp, or through digital compression. The kidney is located high and posteriorly in the retroperitoneum. The midline incision may need to be extended to the xiphoid process and additional upper abdominal retraction inserted for proper exposure. The kidney overlies the diaphragm, transversus abdominis aponeurosis, and quadratus lumborum muscle laterally and psoas major muscle medially. Significant bleeding from these muscles and the deep muscles of the back can occur following penetrating trauma and may confuse the picture in which brisk bleeding is occurring in the renal fossa. The kidney is enclosed in a thin but strong fibrous capsule, which should be left intact during renal dissection and mobilization. As the capsule is usually lifted off the parenchyma by an underlying hematoma, the entire capsule may inadvertently be stripped off the kidney by the sweeping finger used to quickly elevate the kidney into the wound. Ideally, the kidney should be mobilized through sharp and blunt dissection working from a normal area toward the area of parenchymal injury to keep the capsule on the kidney. Stripping the capsule complicates the repair of the kidney and should be avoided. Recognizing patterns of injury is important, and the trauma surgeon should anticipate injuries to adjacent organs based on the relational anatomy of the kidney and ureter and the trajectory of a penetrating injury7 (Fig. 36-1). The left

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Management of Specific Injuries

SECTION 3

Apical Upper Middle Lower

Apical

Posterior

FIGURE 36-1 Renal anatomy: relational anatomy of the kidney. Note proximity of great vessels, duodenum, liver, spleen, pancreas, and colon, relevant to predicting patterns of injury and likely sites of concomitant organ injury in renal trauma.

kidney is crossed anteriorly in its upper portion by the tail of the pancreas and lies behind the lower portion of the spleen. On the right, the duodenum is immediately anterior to the hilar region. In the setting of a renal injury on the right side, the right colon, liver, and duodenum are commonly injured in penetrating trauma. With blunt trauma, an associated hepatic laceration is most common. On the left side, injuries to the left colon, stomach, spleen, and pancreas are common in penetrating trauma. And lacerations of the spleen are particularly common with blunt trauma to the left upper quadrant. Injuries to the diaphragm are also common with penetrating renal injury and less common with blunt injury. The left adrenal gland is located medial to the upper pole of the left kidney, while the right adrenal gland is located in a more cephalad position relative to the right upper renal pole and may be in a retrocaval position. At the level of the renal pedicle, there are most commonly single renal arteries and veins present bilaterally. The renal vein, artery, and renal pelvis are organized in an anterior-to-posterior orientation. On the right side, the gonadal vein arises from the vena cava at or slightly below the level of the renal pedicle. A lumbar vein, which may be quite large, often arises from the posterior aspect of the right renal vein, near the insertion with the inferior vena cava. The right adrenal vein enters directly into the vena cava, often on its posterolateral aspect. On the left, the main branches of the renal vein include the left gonadal, the adrenal, and one or more lumbar veins. This asymmetry of the collateral branches of the renal veins explains why the left renal vein can be safely ligated near the vena cava, with an 85% chance of renal preservation. In contrast, the right kidney will most likely develop venous thrombosis and become nonviable if the right renal vein is ligated.

Anterior

Lower Posterior

FIGURE 36-2 Intrarenal vascular anatomy: vascular branches supplying various arterial segments of the renal parenchyma. Knowledge of intrarenal anatomy is critical to successful reconstructive efforts.

For the urologic trauma surgeon who engages in intrarenal surgery and renal reconstruction, knowledge of the intrarenal anatomy is important (Fig. 36-2). The renal arterial supply consists of the following five segments: apical, superior (anterosuperior), middle (anteroinferior), lower (inferior), and posterior. The posterior branch crosses cephalad to the renal pelvis to reach its segment. About 25% of kidneys receive accessory arterial branches directly from the aorta. These may enter through the renal sinus or at the upper or lower poles. Certain anomalies of the upper urinary tract, such as horseshoe kidney and congenital obstructive and duplication types, must be familiar to the trauma surgeon, as they may impact management. The blood supply to the ureter is particularly important in surgery for urologic trauma (Figs. 36-3 and 36-4). The main sources are the renal artery from above, the aorta or common iliac arteries, and the vesical arteries from below. Branches approach the upper and midureter primarily from the medial side, while in the lower pelvis, the blood supply to the ureter enters primarily from a lateral direction. These branches form a long, predictable anastomotic chain usually with a single longitudinal vessel that runs the length of the ureter, in the plane between the ureteral adventia and muscularis. Anatomy of the urethra, perineum, and external genitalia may be less familiar to the general trauma surgeon. The gross anatomy and fascial layers of the genitalia and perineum are important in trauma, as they largely determine the manner in which blood and urine extravasate following urethral or genital trauma (Fig. 36-5).

Genitourinary Trauma

671

CHAPTER 36

Suprarenal Supra a. R Renal a.

I Interior vena cava Ureter Aorta Gonadal a.

A

IlIliac a.

Vaginal a. Va Middle hemorrh hemorrhoidal a.

Jtene a. Superior vessel a.

Bladder

FIGURE 36-3 The ureteral blood supply originates from branches of the adrenal and renal arteries in the upper third, branches of the aorta and gonadal arteries in the middle third, and the pelvic vessels as shown in the lower third. Knowledge of the ureteral blood supply and derangements due to preexisting pathology or prior surgery is important in maintaining ureteral viability during surgical mobilization and reconstruction.

B

FIGURE 36-5 Diagram of sites of extravasation, associated with urethral disruption. (A) With an intact Buck’s fascia, extravasation of blood and/or urine is isolated to the penile shaft. (B) With Buck’s facial defect, extravasation extends into the scrotal tissues and compartments.

Peritoneum

Arteriole Circular fibers Longitudinal fibers Capillary

Adventitial sheath

Transitional epithelium

Medial layer

Mucosa

FIGURE 36-4 Ureteral anatomy: the longitudinal blood vessels run deep to the adventitial sheath; it is important to achieve a dissection plane superficial to this layer to avoid devascularization of the ureter during surgical mobilization.

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Management of Specific Injuries

TABLE 36-1 Urologic Injury Scale of the American Association for the Surgery of Trauma

SECTION 3

Gradea Renal injury scale I Contusion Hematoma II Hematoma Laceration III Laceration IV

Laceration

V

Vascular Laceration Vascular

Ureter injury scale I Hematoma II Laceration III Laceration IV Laceration V Laceration Bladder injury scale I Hematoma Laceration II Laceration III Laceration IV Laceration V Laceration Urethral injury scale I Contusion II Stretch injury III Partial disruption IV

Complete disruption

V

Complete disruption

Injury Descriptionb Microscopic or gross hematuria; urologic studies normal Subcapsular, nonexpanding without parenchymal laceration Nonexpanding perirenal hematoma confined to the renal retroperitoneum 1 cm parenchymal depth of renal cortex without urinary extravasation 1 cm parenchymal depth of renal cortex without collecting system rupture or urinary extravasation Parenchymal laceration extending through the renal cortex, medulla, and collecting system Main renal artery or vein injury with contained hemorrhage Completely shattered kidney Avulsion of renal hilum that devascularizes kidney Contusion of hematoma without devascularization 50% transection 50% transection Complete transection with 2 cm devascularization Avulsion of renal hilum that devascularizes kidney Contusion, intramural hematoma Partial thickness Extraperitoneal bladder wall laceration 2 cm Extraperitoneal (2 cm) or intraperitoneal (2 cm) bladder wall lacerations Intraperitoneal bladder wall laceration 2 cm Intraperitoneal or extraperitoneal bladder wall laceration extending into the bladder neck or ureteral orifice (trigone) Blood at urethral meatus; urethrography normal Elongation of urethra without extravasation on urethrography Extravasation of urethrographic contrast medium at injury site, with contrast visualized in the bladder Extravasation of urethrographic contrast medium at injury site without visualization in the bladder; 2 cm of urethral separation Complete transection with 2 cm urethral separation, or extension into the prostate or vagina

a

Advance one grade for multiple injuries to the same organ. Based on most accurate assessment at autopsy, laparotomy, or radiologic study. Reproduced with permission from Moore EE, Shackford SR, Pachter HL, et al. Organ injury scaling: spleen, liver, and kidney. J Trauma. 1989;29:1664. b

INJURY GRADING AND SCORING SYSTEMS FOR GENITOURINARY INJURIES The American Association for the Surgery of Trauma (AAST) Injury Scaling Committee has devised a staging system for urologic injuries. The system, originally published in 1989 and since amended, addresses injuries to the kidney, ureter, bladder, urethra, testis, scrotum, and penis (Table 36-1).8 For some organs such as the kidney, the system has proven highly

applicable and has come into common use. For other organs, such as bladder and ureter, the AAST system has been less commonly utilized for a variety of reasons, largely relating to lack of specificity of available imaging approaches to provide the necessary data for assignment of a grade. The grading systems for urethra and external genitalia are coming into more common use and are of value in addressing outcomes following such injuries. Several aspects of the staging system have received attention regarding their clinical significance

Genitourinary Trauma

Grade I

Grade II

Grade III

CLINICAL PRESENTATION AND DIAGNOSIS OF RENAL TRAUMA ■ Incidence and Patterns of Injury Grade IV

Grade V

FIGURE 36-6 Organ injury scaling system for renal trauma.

and impact on decision making, complication rates, and patient outcomes.9–11 As noted, the renal Organ Injury Scale utilizes five grades of injury, ranging from contusion or subcapsular hematoma (I) to shattered kidney or avulsion of the hilum (V) (Fig. 36-6). It is valuable to specifically distinguish the parenchymal lacerations from renovascular trauma in the group IV and V injuries when reporting experience, as management and outcomes differ between these entities. The varying degrees of renal injury as described in the scaling system are depicted diagrammatically in Fig. 36-6. Recent data have shown support for the clinical utility and validity of the renal injury scale, indicating that this system is predictive of morbidity in blunt and penetrating renal injury, of mortality in blunt injury,10 and of the risk of nephrectomy with exploration for renal trauma. As the percentage of the circumference of the ureter that has been disrupted is difficult to determine from imaging studies, the ureteral scaling system is mainly amenable to the operative setting. For the bladder, the distinction of intraperitoneal from extraperitoneal rupture is important and is addressed in the scaling system, but whether the length of the laceration in the bladder wall truly has clinical significance has not been demonstrated. For urethral injuries, the scaling system addresses anatomic factors that can often be determined from retrograde urethrography (RUG) and provide advantages over the earlier system described by Calopinto and McCallum.12 The current AAST system addresses urethral disruption based on whether the injury is complete or incomplete (i.e., whether contrast enters the bladder) and on the length of the urethral defect and presence of extension into prostate or vagina. Endoscopic assessment indicates that in some cases where the retrograde urethrogram would suggest a complete disruption, partial circumference continuity does exist, at times allowing for insertion of a catheter into the bladder. Nevertheless, despite some lack

Renal injuries occur in approximately 1–3% of all trauma patients and up to 10% of patients with abdominal trauma. The percentage of blunt and penetrating trauma varies dramatically depending on the health care institution and the population served. In some urban trauma centers, penetrating injuries predominate,7,13–15 although overall, approximately 90% of significant renal injuries are due to blunt trauma in the United States.16 For penetrating trauma, nearly all renal gunshot wounds are associated with injuries to other intra-abdominal organs; for renal stab wounds, approximately 60% of cases occur in combination with another intra-abdominal injury. Kidneys with preexisting anatomic abnormalities appear to be more vulnerable to significant injury from seemingly minor blunt trauma.17,18 Such entities would include obstruction of the ureteropelvic junction, large cystic lesions, and renal neoplasms. Injuries to nonurologic structures in the abdomen are found in approximately 20–33% of patients with blunt renal injuries.

■ Clinical Presentation and Evaluation A history of a blow to the flank, deceleration trauma, fall from a height, or penetrating abdominal, pelvic, and lower chest injuries should raise the possibility of a renal injury. Hematuria is the most common sign of renal trauma, although the magnitude of the hematuria correlates poorly with the magnitude of injury. Physical examination in patients at risk for renal injury should include careful assessment of the abdomen, back, flank, and chest, along with a complete genitourinary examination. Findings suggestive of a renal injury include tenderness in the flank, costovertebral angle or abdomen, a palpable flank mass, or ecchymosis in the flank, back, or abdomen. Complete inspection of the trunk for a penetrating injury is critical. Stab wounds posterior to the anterior axillary line carry a risk of renal injury, with only about 12% of such injuries being associated with injury to another organ. Laboratory assessment should include urinalysis by dipstick, as well as microscopic examination for blood or infection. The first specimen in the emergency center should be analyzed for hematuria to optimize diagnostic accuracy. Determination of serum electrolytes, blood urea nitrogen (BUN) and serum creatinine, and hemoglobin is important. A blood sample for type

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of specificity, the AAST organ injury scaling system has substantial usefulness. The scaling system for organ-specific injuries as applied to genitourinary trauma (Tables 19-22 and 29-31 from AAST Web site) has introduced a needed advance in the field.8 The designations of the AAST system should be utilized whenever possible in clinical descriptions and published work on urologic trauma.

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SECTION 3

■ Radiographic Imaging for Renal Trauma Traditionally, all patients with abdominal trauma and any degree of hematuria were imaged in the emergency center on presentation. Using this approach, some series of renal trauma have shown that greater than 90% of imaged patients will have only minor injuries, primarily contusions or other minor injuries not requiring intensive monitoring or intervention. With an eye toward cost-effectiveness and minimizing the time and potential morbidity of unnecessary imaging, several groups have assessed the safety and feasibility of establishing more selective approaches toward renal imaging in the trauma setting.19 The disadvantages of imaging include expense, radiation exposure, possible allergic or nephrotoxic reactions to contrast, time expenditure, and the risk of moving the patient. These factors need to be balanced against the risk of missed injuries with a resultant delay in diagnosis. In 1985, the group from San Francisco General Hospital analyzed their renal trauma experience and found that the only findings that were predictive of significant renal injury were the presence of penetrating trauma, or blunt trauma with gross hematuria or with microhematuria and shock. Shock was defined as a systolic blood pressure 90 mm Hg at any time postinjury, including during transport by EMS. In a review of 812 patients with microhematuria but without shock, no significant renal injuries were detected. All 44 injuries in this original series were found among the 195 patients with gross hematuria or microhematuria and shock. This series has been extended over the years such that in the expanded patient group of 2,254 patients with renal trauma approximately one third were imaged and two thirds were not. Within this group, no major renal injuries were missed using the established criteria.20–22 Other investigators have modified these imaging criteria according to their own experience and judgment. Some have suggested including standard imaging for patients with injury to the brain, loss of consciousness, or altered mental status, with the belief that the loss of information on a physical examination and the magnitude of trauma in such patients may create a higher risk of a missed injury. Some have suggested extending imaging indications to patients with mechanisms of injury consistent with deceleration trauma. This approach avoids missing injuries to the renal pedicle (e.g., intimal disruption in the renal artery and renal devascularization), which may present with no hematuria in 20–33% of patients. The presence of fractures of long bones, fractures of the lower ribs, or fractures of transverse spinous processes has also been suggested as an indication to modify the previous imaging restrictions, possibly predicting a higher risk of occult renal injury. In the pediatric population (addressed in Section “Pediatric Renal Trauma”), imaging for patients with only microhematuria has been more liberally utilized. As noted, the criteria involving limiting imaging to patients with gross hematuria or microhematuria with shock have not been extended to those with penetrating trauma. Patients with penetrating trauma with any degree of hematuria, injury

proximity, or suspicion are appropriate candidates for imaging of the urinary tract, regardless of the presence or magnitude of hematuria. Significant penetrating injuries can present without hematuria, particularly if trauma to the major collecting system causes all urine from the injured kidney to exit into the retroperitoneum, preventing ureteral peristalsis. In penetrating trauma, imaging would generally be obtained in assessing a patient’s candidacy for nonoperative management in the appropriate clinical setting. The concept of obtaining preoperative renal imaging simply to demonstrate the presence of two functioning renal units prior to surgical intervention has become less popular in recent years. Instead, careful intraoperative palpation of the kidneys and, on occasion, intraoperative intravenous pyelogram (IVP) may be used selectively during a trauma laparotomy to demonstrate renal presence or function.23 The selection of imaging modalities has evolved greatly since the advent and availability of computed tomography (CT) scanning to emergency center evaluation.19 While the bolus IVP with nephrotomography had in the past been the standard imaging approach, the CT scan has, over the years, become the gold standard for precise staging of renal injuries (Fig. 36-7), and has largely replaced intravenous pyelography in most clinical settings. Although the IVP had in the past been described as being accurate for clinical staging purposes in 60–85% of patients, CT scanning offers a number of important advantages.24 Nevertheless, trauma surgeons and urologists should remain familiar with the findings suggestive of renal injury on IVP, as routine use of CT for trauma assessment is not consistently available, especially when considering variations in international practice and infrastructure, and intraoperative IVPs may still be necessary at times. These IVP findings include the presence of a fracture of a transverse process on the scout film, presence of a mass effect in soft tissue, loss of the psoas margin on the involved side, and alteration of the longitudinal axis or vertical displacement of the kidney. Loss of a clear renal cortical outline, gross extravasation of contrast, ipsilateral decrease in renal excretory function, and loss of opacification of portions of the collecting system should all be noted. The IVP allows confirmation of the presence of two renal units, gives general information of the extent of injury, and may show significant extravasation. Estimates of the accuracy of IVP in detection of renal injury vary. In general, the IVP should be viewed as a crude means of detection, rather than as a means to obtain precise staging. Some studies indicate that as many as 20% of patients with significant renal injuries may have a normal IVP. In addition, up to half of patients with reduced function or nonfunction of a kidney on IVP will have a reason for it other than arterial occlusion, including contusion, overhydration, and hypotension or hypoperfusion. Advantages of CT over IVP include identification of contusion and subcapsular hematoma, definition of the location and depth of parenchymal lacerations, more reliable demonstration of extravasation of contrast, and identification of injuries to the pedicle and artery (“rim sign,” “cutoff sign,” etc.). There is also enhanced imaging of the perinephric space, other solid viscera (liver, spleen, pancreas), as well as delineation of many cases of perforation of a hollow viscus and identification of free intraperitoneal fluid. For these and other reasons, the

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A B

FIGURE 36-7 Staging computed tomography scans for blunt renal injury. (A) Grade II injury: blunt trauma, small right posterior subcapsular and perirenal hematoma without obvious parenchymal laceration. (B) Grade II and III injury: blunt trauma, laceration posteromedially in left kidney without collecting system injury. (C) Grade IV parenchymal injury: blunt trauma, deeper laceration to right kidney, full-thickness parenchymal laceration with collecting system injury as indicated by contrast extravasation. Moderate-sized perinephric hematoma. No significant devitalized parenchyma noted. C

contrast-enhanced CT scan has largely replaced the IVP for trauma imaging. With the current spiral CT scanners, sequences are so rapid that it is important to be sure that delayed, excretory images are obtained to avoid missing extravasation from the collecting system or ureter, which may not be apparent from early images alone.25 Arteriography has had less of a role in the staging of a renal injury since CT has become popular, especially considering its cost, invasiveness, and the special expertise required. As the use of CT for diagnosis of a pedicle injury has become standard, far fewer arteriograms are being obtained. Still, precise delineation of arterial anatomy and interventions for control of hemorrhage mandate the continued use of renal arteriography on a selective basis (Fig. 36-8). In Europe and other parts of the world, abdominal ultrasound has been extensively utilized in diagnosing and assessing blunt renal injury. In the United States and elsewhere the Focused Assessment for the Sonographic Evaluation of the Trauma Patient (FAST) study is performed to assess for free intra-abdominal fluid rather than for the

delineation of an injury to parenchyma of solid organs. The ability to apply high-resolution Doppler techniques to assess renal perfusion and vascular anatomy may extend the use of ultrasound for renal imaging in the future. Retrograde pyelography plays a limited role in clearly defining anatomy of the ureter and collecting system when a pattern of medial extravasation or failure of ureteral opacification on CT or IVP is present.

PEDIATRIC RENAL TRAUMA Some studies suggest that the pediatric kidney is more vulnerable to trauma than is the adult kidney.26 Reasons for this include the relatively larger size of the kidneys compared with the adult, the relative deficiency of perinephric fat in the child, and, probably, the higher incidence of preexisting renal abnormalities. One recent review found that 8.3% of pediatric renal injuries occurred in the setting of preexisting renal abnormality,17 with other estimates of preexisting renal

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SECTION 3 A

B

FIGURE 36-8 (A and B) Renal artery occlusion due to intimal disruption following deceleration injury. Restrained driver in head-on motor vehicle collision. The left kidney is nonperfused and demonstrates minimal renal sinus vascular enhancement and cortical rim enhancement from capsular vessels. This finding is considered pathognomonic for this injury and does not require arteriographic confirmation unless the vascular surgeon believes further vascular imaging is necessary to plan therapy.

abnormality described in as many as 23% of major pediatric renal injuries due to blunt trauma. Some data suggest that the kidney is the most commonly injured intra-abdominal organ in children. It is nearly universally agreed that the presence of gross hematuria after trauma in the pediatric patient deserves further investigation with imaging of the urinary tract. As in the adult, the CT scan has the major role in staging such injuries for the same reasons as described earlier. Several studies suggest that only about 5% of pediatric patients with major renal

injuries will develop signs of shock, further emphasizing the importance of an aggressive diagnostic approach. Pediatric patients can maintain a normal blood pressure despite significant blood loss, and persistent tachycardia is a particularly important parameter to note in the pediatric patient as a potential sign of significant blood loss. The currently accepted approach in the adult is not applied liberally in the pediatric setting. Many authors suggest that all pediatric patients with any degree of hematuria after significant trauma should undergo renal imaging, while some have suggested modified criteria. One study has suggested that microscopic hematuria with greater than 50 red blood cells per high-power field in the pediatric setting should be considered an imaging criterion, regardless of hemodynamic parameters.27 Certain types of renal injuries are clearly more common in the pediatric patient. These include laceration of the renal pelvis, avulsion of the ureteropelvic junction, and forniceal avulsion. When extensive medial extravasation is noted and/ or the ureter does not opacify with contrast despite adequate excretion into the renal collecting system, a disruption of the major collecting system should be considered. In such cases, retrograde pyelography may be necessary to clarify the anatomy and achieve a diagnosis. As in the adult, the use of the rapid spiral CT scanner can lead to a pitfall in diagnosis if a delayed sequence is not requested. Limiting the study to a nephrographic or early excretory phase may fail to demonstrate extravasation or asymmetrical opacification of the ureters, which would be readily visible on later images. Overall, approximately 85% of pediatric renal injuries from blunt trauma are minor (contusions, superficial parenchymal lacerations) and are managed with bed rest and observation. Pedicle injuries comprise about 5% while major parenchymal injuries occur in 10–15% of patients. As in the adult, it is these latter groups for which management is somewhat controversial; however, it is largely agreed among pediatric urologists that operative decisions are based mainly on hemodynamic status rather than imaging criteria. The potential for successful management of kidneys that look very severely injured on imaging studies is remarkable in the pediatric population, and a nonoperative approach is the norm. Surgical treatment is generally reserved for patients with ongoing bleeding or hemodynamic instability, for those who have clearly failed an attempt at nonoperative management, and for penetrating injuries.28

CLINICAL PRESENTATION AND DIAGNOSIS OF TRAUMA TO THE URETER, BLADDER, URETHRA, AND EXTERNAL GENITALIA ■ Ureter Ureteral injuries are relatively uncommon, occurring in approximately 4% of patients with penetrating abdominal injuries and in less than 1% of those with blunt abdominal trauma. Concomitant visceral injury occurs in the majority of patients with ureteral injuries from penetrating trauma.

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While hematuria is an important sign of ureteral injury, it may be absent 15–45% of the time. As such, a high index of suspicion for ureteral injury is critical.29–32 In fact, ureteral injury is one of the most common sites of missed injury at laparotomy, with one recent report noting a missed injury rate of 11% (15). While direct visualization of the ureter is the mainstay of detection of ureteral injury at the time of laparotomy, imaging modalities useful for detection of ureteral trauma include an IVP and contrast-enhanced CT scanning.16 Modern spiral scanners move rapidly through the abdomen following administration of contrast, and, unless a delayed excretory phase is specifically requested, extravasation may be missed as previously described. Failure of the distal ureter to opacify on a CT scan should raise concern of an injury.33–35 When noninvasive imaging fails to provide sufficient detail regarding ureteral anatomy or the specific nature of an injury, cystoscopy with retrograde pyelography may be indicated.

■ Bladder Sudden compression of the full bladder, shear forces, or a pelvic fracture may result in a blunt rupture. Rupture may be accompanied by lower abdominal pain, by an inability to void, and by suprapubic or perineal ecchymoses. The cardinal sign of injury to the bladder is gross hematuria, present in greater than 95% of cases, while only about 5% of patients will have microscopic hematuria alone.36 Over 80% of patients with a bladder rupture have an associated pelvic fracture in centers with a high percentage of blunt trauma. An association of bladder rupture with disruption of the posterior urethra, also in the setting of pelvic fracture, may occur in 10–20% of patients.37,38 Overall, recent data indicate that genitourinary injury occurs in approximately 15% of pelvic fractures in the pediatric setting17 and that the incidence of injury to a pelvic organ is fairly comparable between adult and pediatric patients.39,40 Stress cystography is the standard study for diagnosis of injury to the bladder (Fig. 36-9).41 It is important that the bladder be adequately filled to avoid false-negative studies. For the adult bladder, the standard volume of filling is 300–400 mL of iodinated contrast (30% iodine commonly utilized), which is infused through the indwelling Foley catheter by gravity. Alternatively, the bladder can be filled by gravity to a point at which the patient describes a sense of bladder fullness. If the patient is obtunded or unable to indicate that there is a sense of fullness, using a standard filling volume is a useful methodology. A filling film is obtained that should be a vertically oriented abdominal image designed to show the entire abdomen. Patterns of contrast extravasation have been described for intraperitoneal, extraperitoneal, and combined ruptures (Fig. 36-10). Hematuria of bladder origin without contrast extravasation on a properly performed stress cystogram is consistent with a contusion or minimal mucosal injury, which is uniformly managed nonoperatively. Postdrainage washout films are generally recommended to avoid false-negative cystograms in which extravasated contrast may be missed if located only anterior or posterior to the distended bladder on an anteroposterior film.

677

A

B

FIGURE 36-9 (A and B) Stress cystogram: through Foley catheter, the bladder is filled by gravity to a standard volume (300–400 mL typically in adult), or to the point of perceived fullness by patient. Plain radiograph obtained to allow visualization of upper and lower abdomen, followed by washout film.

Currently, stress cystography is most commonly obtained using a CT technique (Fig. 36-11).42 The same general principles apply as for static cystograms (i.e., adequate bladder filling is essential to avoid missed injuries) (Fig. 36-11B and C). Studies comparing the accuracy of standard radiographic stress cystography with CT cystography suggest equivalent capability in defining and staging bladder injuries, while the CT cystogram provides enhanced information regarding the perivesical space and adjacent structures. Simply clamping a bladder catheter following intravenous contrast administration, with the expectation that passive filling with contrast-opacified urine will suffice, is not adequate and will result in an unacceptably high percentage of false-negative examinations, with either the standard radiographic or the CT technique.42 In selected cases, flexible cystoscopy may aid in the acute diagnosis of bladder injury.43

■ Urethra Trauma to the anterior urethra may result from straddle injuries with sudden compression at the level of the midurethra to deep bulbar urethra against the inferior pubic arch. Urethral distraction injuries, or posterior urethral disruption, may accompany pelvic fracture in 4% to 10% of patients. Bilateral fractures of the pubic rami, especially when accompanied by an open pelvic ring (abnormally distracted sacroiliac joint), may be present in patients who have suffered

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SECTION 3 A

B

C FIGURE 36-10 Bladder: stress cystograms for assessment of suspected bladder injury following blunt trauma to pelvis. (A) Stress cystogram in patient with gross hematuria and pelvic fracture, demonstrating adequate bladder filling and typical pattern of extraperitoneal extravasation—flame-shaped contrast density lateral to right lower bladder segment. Injury managed successfully with 10 days of catheter drainage. (B) Washout phase following stress cystogram. Extraperitoneal extravasation pattern noted in right hemipelvis. Washout films may reveal extravasated contrast anterior or posterior to the contrast-filled bladder, which can be missed on films obtained when the bladder is filled with contrast. (C) Lateral compression of bladder from pelvic hematoma, along with extraperitoneal extravasation pattern in right pelvis, on an incomplete washout film. (D) Intraperitoneal bladder rupture. Note extravasated contrast outlining colic gutters, surrounding loops of small bowel, and occupying cul-de-sac in pelvis, indicative of intraperitoneal contrast.

D

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F

E

G

FIGURE 36-10 (continued) (E) Intraperitoneal bladder rupture. Again, note contrast in pelvis and outlining of right colon and small bowel in pelvis. Cystograms following penetrating pelvic trauma with hematuria. (F) Gunshot wound to pelvis in patient with microscopic hematuria. Bladder is intact, but is displaced to right due to large, left-sided pelvic hematoma. Obturator vessel injury noted; vessels ligated following evacuation of hematoma at laparotomy and pelvic exploration. (G) Gunshot wound to bladder with intravesical clot creating filling defect in bladder. Bladder incompletely filled; extravasation noted on subsequent film, following optimal filling of bladder.

posterior urethral disruption as well. The classification system used to further describe urethral trauma is discussed in Section “Injury Grading and Scoring Systems for Genitourinary Injuries.” It is important to determine from the urethrogram if an injury is partial (contrast passes proximal to the point of extravasation filling the more proximal urethra or bladder) or complete (all contrast extravasates, and none enters the urethra proximal to injury or bladder), as this factor has an impact on selection of management.44 Blood appearing at the urethral meatus, inability to void, presence of a perineal hematoma, and inability to clearly

palpate the prostate on rectal examination should make one suspicious of urethral injury (Fig. 36-12). When urethral injury is suspected, a retrograde urethrogram should be performed (Fig. 36-13). Approximately 30 mL of iodinated contrast is instilled via a catheter inserted just within the urethral meatus, at which point a plain radiograph is obtained. A normal retrograde urethrogram should demonstrate contrast filling an intact urethra and entering the bladder without extravasation. No attempt at insertion of a bladder catheter should be pursued until a negative retrograde urethrogram is obtained to avoid further complicating a urethral rupture (Fig. 36-14).

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SECTION 3 A FIGURE 36-11 (A) Computed tomography (CT) cystogram demonstrating intraperitoneal bladder rupture. A standard stress cystographic technique has been employed, with instillation of 350 mL of contrast followed by scanning of upper, middle, and lower abdomen. Contrast is seen filling colic gutters and filling the true pelvis, in this case clearly outlining the ovaries. (B) False-negative CT cystogram. This image was obtained by clamping the indwelling Foley catheter and obtaining CT images of the pelvis with passive filling of the bladder following intravenous contrast administration. No extravasation is noted, but the bladder is not adequately filled to reliably exclude injury. A properly performed static cystogram following the CT revealed extensive intraperitoneal extravasation. Inadequate bladder filling is the most common reason for a false-negative cystogram. (C) Attempted CT cystogram following pelvic fracture in a 13-yearold male. Extravasation extends through the pelvic floor into the buttock, and no filling of the bladder is seen. The Foley balloon is actually positioned in the pelvic hematoma. The patient was found to have a bladder neck avulsion injury, which was initially managed with an open surgical cystostomy, and then surgically reconstructed 72 hours following injury.

Following placement of either a urethral catheter (if the urethra proved normal or by a urologist using direct vision techniques in selected incomplete injuries) or a suprapubic catheter (if urethral disruption was revealed), a stress cystogram should still be performed if hematuria is present. This is because 10–15% of patients with urethral disruptions from a pelvic fracture will have a concomitant injury to the bladder.

■ External Genitalia Genital injuries represent a diverse group of traumatic events.45 These include the classic blunt penile fracture (which occurs from forceful bending of the erect penis, often during intercourse), crush injuries with rupture of the testis, penetrating injuries, and industrial accidents. Amputation injuries of the penis or testicle can occur due to assaults, selfmutilation, or industrial trauma. After major blunt trauma to the scrotum, the risk of testicular rupture is approximately 50%. An ultrasound examination of the scrotum may be valuable to distinguish testicular rupture from a hematoma of the scrotal wall or hematocele (blood within the tunica vaginalis compartment).

B

C

NONOPERATIVE MANAGEMENT OF GENITOURINARY INJURIES While nonoperative management for many urologic injuries has become well established, the selection of operative versus nonoperative management for certain genitourinary injuries remains controversial. Recent reviews of urologic management based on careful assessment of levels of evidence reveal a notable paucity of level 1, prospective management studies.1–6 The relatively recent efforts to accurately and uniformly describe and stage the nature of injuries and the lack of long-term follow-up leave many questions as to the best way to manage many forms of genitourinary trauma.

■ Kidney It has long been accepted that low-grade renal injuries can be managed nonoperatively with a high success rate. Renal contusion and subcapsular hematomas are routinely managed expectantly and only rarely would surgical or other interventions be required in such cases. These injuries heal spontaneously with few exceptions as do low-grade parenchymal lacerations.

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FIGURE 36-12 Mechanism of anterior urethral disruption due to straddle injury; extravasation pattern and hematoma limited in this case by Colles’ fascia, due to rupture of Buck’s fascia along with full thickness of urethral wall. Hematoma and urinoma may extend along shaft of penis and into scrotum and perineum.

Depending on the institutional bias and experience, some urologic trauma surgeons may limit operative management of renal injuries to those in which the patient is hemodynamically unstable, almost regardless of imaging findings. Alternatively, others would include those injuries in which the grade of injury is high, presumably translating into a higher incidence of postinjury complications with nonoperative management. A number of indications for renal exploration following injury have been suggested by McAninch and Carroll.46 These include hemodynamic instability, ongoing hemorrhage requiring significant transfusion, pulsatile or expanding hematoma on exploration, and avulsion of the pedicle. These strong indications for surgical or other procedural intervention remain widely accepted. Relative indications for surgical intervention have included high-grade injuries, large perirenal hematoma, presence of urinary extravasation on contrast studies, significant devitalized fragments of parenchyma, and findings in the operating room during laparotomy with an incompletely staged injury. While there is lack of consensus regarding these relative surgical indications, there is a general trend toward nonoperative management in many of these situations, as long as hemodynamic stability is maintained.28 Proponents of the nonoperative management approach suggest that many high-grade injuries will heal without surgery,

complications can frequently be managed with nonsurgical techniques (percutaneous drainage, stenting, angiographic embolization), and renal salvage rates are better overall when renal exploration is avoided. This school of thought would maintain that, with few exceptions, it is only hemodynamic instability that should prompt surgical intervention for the injured kidney, not injury stage or other predetermined imaging criteria. In contrast, proponents of a more aggressive surgical approach would suggest that higher grades of renal injury carry an unacceptably high complication rate and that such complications, when they occur, have a high likelihood of resulting in otherwise avoidable morbidity or nephrectomy (Fig. 36-15). Proponents would suggest that early exploration and repair offer the advantage of early debridement of devitalized tissue, definitive hemostasis, repair of injuries to the collecting system, and early institution of appropriate drainage. As such, postinjury infection, urinoma, and hemorrhage risk are minimized. The descriptions of “absolute” and “relative” indications for renal exploration for trauma have been suggested to attempt to provide assistance in this decision-making process.46–48 For certain injuries, operative management is nearly universally accepted. These include blunt avulsion or penetrating lesions of the renovascular pedicle, AAST grade V parenchymal

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SECTION 3 FIGURE 36-13 Technique of retrograde urethrogram. Retrograde urethrogram: catheter is inserted into urethral meatus, with minimal balloon inflation to maintain position and allow hands to be out of x-ray field. Contrast is instilled to distend urethra.

injuries, and ureteropelvic avulsion or complete avulsion of the fornices. While occasional case reports have suggested that grade V renal injuries can be managed nonoperatively, most studies demonstrate that 90–100% of such injuries require urgent nephrectomy.49 In reviewing the literature on nonoperative management of grade V renal injuries, the accuracy of classification is questionable, and some reports of successful management of grade V injuries probably are actually describing grade IV parenchymal lacerations. In general, attempts at nonoperative management of true grade V renal injuries are not advised and may expose the patient to substantial risk, although there remains some controversy in this area.50 Patients with significant ongoing bleeding from an injured kidney where angiographic control is not likely to correct the problem, is not available, or has failed also require prompt operative attention. For penetrating renal injuries in cases where laparotomy will occur regardless, especially when preoperative radiologic staging has not been performed or is incomplete, operative management is widely recommended.

When moderate or high-grade renal injuries are selected for nonoperative management, certain general principles apply. Such patients are at risk for continued bleeding or significant delayed bleeding, and it is important that they be observed in the surgical intensive care unit. Serial abdominal examinations are essential, as are serial laboratory studies including hemoglobin level and electrolyte status. Typed and cross-matched blood should be available for the first 24–48 hours. The patient’s hemoglobin should be maintained in such a range that a sudden drop from renewed bleeding would not be catastrophic. Particular attention should be paid to the size of the perirenal hematoma on initial imaging. Large hematomas suggest bleeding from larger intrarenal vessels and, presumably, indicate cases in which the risk of continued bleeding is greater. Elderly patients or patients with cardiovascular disease should be transfused more liberally, with a low threshold for intervention, as any sudden substantial blood loss may not be tolerated. When managing high-risk renal injuries nonoperatively, it is advisable to reimage such injuries at 48–96 hours to allow early diagnosis of complications such as enlargement of the perirenal hematoma, formation of a urinoma, or evolution of ischemic parenchyma. Early knowledge of such untoward events allows for treatment before the patient demonstrates complications such as sepsis, azotemia, or severe anemia.51 It is routine to impose a period of strict bed rest with nonoperative management of a major renal injury, although specific data to support this policy are lacking. Nevertheless, it seems reasonable to have the patient remain at bed rest for the first 24–72 hours or until significant gross hematuria resolves, and then reinstitute ambulation cautiously and in a monitored environment. If nonoperative management has been successful, patients should be instructed to avoid significant physical exertion until follow-up imaging reveals adequate healing. Selecting between renal exploration and observation when the incompletely staged renal injury is encountered intraoperatively is difficult. Some authors recommend that the unstaged kidney be routinely explored, while others suggest a more selective approach. If no radiographic information is available, an intraoperative IVP may be selectively obtained to assist in this decision. A standard technique would involve the bolus injection of iodinated contrast (2 mL/kg body weight), and then obtaining a 10-minute excretion film. If significant anatomic distortion is observed, this is considered suggestive of major parenchymal disruption and/or injury to the collecting system, for which exploration may be of benefit. If the kidney appears grossly intact, observation would be selected, often with postoperative CT scanning for more precise imaging. Others would consider the size of the perirenal hematoma as an important parameter as well. In general, current trends in the urologic literature favor nonoperative management of most blunt renal injuries in the absence of staged grade V lesions, active bleeding noted intraoperatively, or hemodynamic instability. Injuries to branch renal arteries from blunt trauma, resulting in segmental devascularization without laceration, can be managed nonoperatively with a low complication rate. Penetrating injuries to the kidney are accompanied by injury to nonurologic organs in a large proportion of cases, and the majority of these patients will undergo laparotomy.

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B

A FIGURE 36-14 Urethra: posterior urethral disruption with pelvic fracture. (A) Retrograde urethrogram demonstrates extravasation of contrast both above and below urogenital diaphragm and no filling of prostatic urethra or bladder neck, consistent with complete disruption. Note pubic ramus fracture and marked cephalad elevation of bladder (bladder filling with contrast excreted following intravenous administration for computed tomography scan). Hemodynamically unstable patient required angiographic embolization for pelvic hemorrhage. Urethral disruption managed with open suprapubic cystostomy. (B) Combined antegrade and retrograde contrast studies 6 months postinjury, demonstrating obliterated posterior urethral distraction defect, in preparation for reconstructive surgery.

These patients may or may not be imaged preoperatively. The issue of whether to explore the (suspected) renal injury in such cases is addressed in Section “Operative Management of Specific Genitourinary Injuries.” When the general trauma surgeon sees no clear operative indication and penetrating renal injury is possibly present, the urologist will have to decide on operative versus nonoperative management based on the clinical status of the patient and, preferably, on the findings of a contrast-enhanced CT scan. In general, patients with penetrating injuries to the kidney that involve the lateral and peripheral parenchyma, with small perirenal hematomas, minimal if any extravasation of contrast, and in which the pedicle and renal sinus structures are not at risk, may be safely managed nonoperatively (Fig. 36-16). Conversely, penetrating renal lesions that result in large perirenal hematomas, traverse the deep, medial renal parenchyma, renal sinus, or hilar region, or cause major urinary or vascular extravasation carry higher risks for nonoperative management (Fig. 36-17). The risk of delayed bleeding from such injuries is significant, and some authors have suggested prophylactic arteriography with embolization of violated arterial branches prior to nonoperative management. In addition,

the risk of a missed associated visceral injury must be considered with nonoperative management of penetrating renal trauma. In one retrospective review of the nonoperative management of penetrating renal trauma, 55% of renal stab wounds and 24% of renal gunshot wounds were managed nonoperatively with a low complication rate.52 While an uncommon injury, blunt or penetrating trauma to the adrenal gland deserves brief mention. If an adrenal hematoma is not expansile, it is managed nonoperatively as with parenchymal injuries to other solid organs. If the adrenal is explored due to the path of a stab or bullet wound, suturing to achieve hemostasis is the standard approach, while extensive destruction of the gland is treated with adrenalectomy. As each adrenal gland has several sources of arterial blood supply, devascularization from trauma is rare.

■ Ureter Nonoperative management of ureteral trauma has limited applications. When a ureteral injury is recognized intraoperatively, surgical repair is favored (see later).32,53,54 Reviews of outcomes of ureteral injuries indicate that most types of

684

Management of Specific Injuries

SECTION 3 A

B

FIGURE 36-15 Grade V parenchymal injury. (A) This image through the upper abdomen demonstrates the upper pole of the left kidney to be elevated by a perinephric hematoma. The upper pole is well perfused and intact. (B) A lower section reveals a large, left retroperitoneal hematoma; the right kidney is perfused and appears normal. This is an early arterial and parenchymal phase, as indicated by the degree of enhancement of the aorta and right renal cortex. (C) A more caudal image demonstrates a large, devascularized fragment of the left kidney; this represents the lower third of the kidney that has been avulsed from the perfused portion of the kidney. This injury required operative repair, which involved removal of the avulsed parenchymal fragment, suturing of the large intrarenal vascular branches that were avulsed, and reconstruction of the collecting system and the level of the junction of the lower infundibulum with the renal pelvis. While some reports suggest that some grade V injuries may be manageable nonoperatively, most clinicians consider this anatomy of injury a surgical indication. Difficulties in classifying some parenchymal injuries as grade IV versus grade V may contribute to this apparent reported variability of opinion and outcome.

C

ureteral trauma fare better with early operative repair, as compared with delayed repair or attempts at nonoperative management, with the exception of limited iatrogenic injuries from endoscopy. This is the case for stab and gunshot wounds, as well as avulsion injuries from blunt trauma (Fig. 36-18). Nonoperative management is performed in selected patients with missed ureteral injuries or other settings of delayed diagnosis or in patients in whom damage control strategies are being adopted. Traditional urologic teaching dictates that if ureteral trauma is recognized in the early days after injury, operative repair is performed. More significantly delayed recognition is managed with utilization of endoscopic or interventional radiologic techniques (stenting or percutaneous nephrostomy diversion) followed by delayed operative reconstruction as indicated. This approach has developed due to the long-standing recognition of problems such as inflammation, edema, friability, presence of a urinoma, and increased risks and complications of reconstructive efforts encountered when operative intervention is pursued greater than 3–5 days postinjury. Ureteral contusions recognized intraoperatively, due to

either penetrating or blunt trauma, may be managed nonoperatively and simply observed; however, some reports suggest that the risk of late perforation and urinary extravasation may be reduced by intraoperative insertion of a ureteral stent.55 When nonoperative management is selected, retrograde ureteropyelography with attempted retrograde stent placement is often performed. Alternatively, percutaneous renal drainage may be the treatment of choice. The selection between these two approaches depends on the hemodynamic and metabolic stability of the patient, as well as specific anatomic and logistical factors. These include the appropriateness of performing a procedure under general anesthesia, the ability of the patient to undergo a procedure in a prone position (generally necessary for obtaining percutaneous renal access), the skill and availability of interventional radiology, and the expected ease of percutaneous access. The latter depends largely on the anatomy of and degree of distension of the collecting system and the presence of a perirenal hematoma. The finding of coagulopathy is often considered a relative contraindication to percutaneous renal drainage, as renal bleeding is always a risk

Genitourinary Trauma

■ Bladder A

B

FIGURE 36-16 Penetrating renal injury, successful nonoperative management. (A) Stab wound to left flank, just posterior to midaxillary line; patient is hemodynamically stable, with gross hematuria that rapidly clears. (B) Staging computed tomography scan demonstrating laceration to lateral left kidney. There is minimal perinephric hematoma, no urinary extravasation, and no devitalized parenchyma. Injury is lateral and laceration does not extend into hilar region or renal sinus structures. Posterior descending colon is in proximity to injury, but general surgeons are prepared to manage nonoperatively. Ideal candidate for nonoperative management of a penetrating renal injury.

of such procedures. Achievement of percutaneous access can be followed by antegrade ureteral stenting, if there is ureteral continuity and a guidewire can be placed across the injury into the bladder. Conversion of a nephrostomy tube to a percutaneous antegrade universal stent, which can be changed or manipulated and opened to external drainage or capped to allow internal drainage, may be attempted. Following an appropriate period, a pullback antegrade nephrostogram will determine if healing is complete and the patient is ready for stent removal with clamping of the nephrostomy tube. When this type of management is utilized, a rate of ureteral strictures of up to 50% may be expected. A stricture may

Nonoperative management of extraperitoneal injury to the bladder has been the standard approach for over 10 years, largely as a result of the studies of Corriere and coworkers and others in which catheter drainage alone was usually successful.56,57 An 18–20 French or larger bladder catheter should be utilized to allow free drainage in the adult. The catheter is left indwelling for 10–14 days followed by a cystogram to confirm cessation of extravasation prior to removal. After this period, 85% of bladder injuries will show absence of extravasation. If extravasation persists, another 7–10 days of catheter drainage followed by repeat cystography is appropriate. Rarely, persistent extravasation will occur after a prolonged period of catheter drainage. In such cases, CT scanning and/or cystoscopy is indicated to be sure a foreign body such as a bony spicule from a pelvic fracture or some other anatomic cause is not resulting in failure of the laceration to heal properly. Indications for initial selection of operative management instead of catheter drainage alone include concomitant injury to the vagina or rectum, injury to the bladder neck in the female, avulsion of the bladder neck in any patient,58 and the need for pelvic exploration for other surgical indications. If retropubic access is required for internal fixation of a pelvic fracture, surgical repair of the bladder is desirable to prevent continued extravasation adjacent to orthopedic hardware. Open pelvic fractures may also require operative repair of the bladder. The presence of combined extraperitoneal and intraperitoneal rupture or combined extraperitoneal bladder rupture and posterior urethral injury, for which catheter realignment is planned, would be considered an appropriate setting to proceed with operative repair of the bladder as well. Finally, clot formation with troublesome occlusion of the drainage catheter may mandate operative repair.59 Intraperitoneal ruptures of the bladder are uniformly managed with operative repair. Most such injuries result in large, stellate tears in the dome of the bladder due to the sudden rise in pressure within a full bladder as from a blow to the lower abdomen or compression by a seatbelt. Rare exceptions to the routine application of operative repair for intraperitoneal bladder rupture include minimal intraperitoneal perforations. These usually occur during cystoscopic procedures, mainly when a resectoscope is being utilized for resection of a bladder tumor or during biopsies of lesions of the

CHAPTER 36

undergo an attempt at endourologic management, although delayed surgical reconstruction of the ureter is often necessary. With blunt trauma, limited ureteral injuries with minimal extravasation may be treated nonoperatively with a retrograde stent. Retrograde pyelography is often necessary to document anatomy amenable to such management. For penetrating injuries, small-gauge shotgun pellet wounds may create minute ureteral perforations that can be managed nonoperatively as well. Such injuries may be noted at laparotomy or may be seen on a contrast-enhanced CT or intravenous or retrograde pyelography. Again, such cases represent the rare exception to the general principles favoring early operative exploration and repair when technically and medically feasible.

685

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Management of Specific Injuries

SECTION 3 A

B

FIGURE 36-17 Penetrating renal injury, complicated. (A) Staging CT scan of abdomen following single stab wound to right posterior flank, in patient presenting with gross hematuria. Deep laceration of right kidney with moderate-sized perinephric hematoma. Injury extends into renal sinus region, although no contrast extravasation is noted. After initial attempt at nonoperative management, patient develops major secondary hemorrhage manifested by profuse gross hematuria, resulting in hypotension, and requiring transfusion of 4 U packed red blood cells. (B) Arteriogram reveals two areas of arteriocalyceal fistula, successfully managed with subselective embolization. (C) Delayed arteriogram image demonstrates wedge-shaped infarct defect due to embolization. Remainder of hospital course uneventful. Embolization is ideal means of managing this problem, as the only indication for intervention is hemorrhage. C

dome and anterior wall, or other minimal iatrogenic injuries. Several reports have appeared in recent years describing laparoscopic techniques of repair for iatrogenic injuries,60,61 particularly when occurring during a primary laparoscopic procedure. The application of techniques of laparoscopic repair to the management of intraperitoneal rupture of the bladder from blunt trauma and other forms of bladder injury is being explored at several centers. For penetrating injury to the bladder, nonoperative management is occasionally applicable in carefully selected and fully evaluated patients with limited defects that are extraperitoneal.62 Such patients often require proctoscopy and/or sometimes arteriography. Selectively, peritoneal lavage or laparoscopy may play a role in such cases to ensure that the peritoneal surface of the pelvis is intact. In our experience, cystoscopy and upper tract imaging (IVP or retrograde

pyelography) has been helpful in assuring that the magnitude of the defect in the bladder is minimal and is likely to heal with catheter drainage alone. The considerations for conversion to operative management and postinjury monitoring and imaging and catheter management are comparable to those utilized with blunt extraperitoneal injuries.

■ Urethra The nature (blunt or penetrating), location of the injury (anterior vs. posterior urethra), completeness (partial vs. complete circumferential laceration), presence and seriousness of associated injuries, and the stability of the patient all impact the selection of management for urethral trauma.63–65 When urethral trauma is suspected, RUG should be performed. If the RUG reveals minimal extravasation and flow of contrast

Genitourinary Trauma

■ Genital Injuries

FIGURE 36-18 Ureter: gunshot wound to ureter with missed injury, in a patient who had no hematuria on initial presentation. Patient developed abdominal fluid collection postlaparotomy; intravenous pyelogram demonstrated missed ureteral injury 5 days postoperatively. Injury initially managed with percutaneous nephrostomy and antegrade placement of universal stent. Long, densely fibrotic stricture of midureter developed, as shown here, ultimately requiring nephrectomy. A high index of suspicion is necessary to detect penetrating ureteral injuries at the time of initial laparotomy; outcomes are significantly improved with early recognition and prompt operative repair in such cases.

past an anterior injury from blunt trauma into the proximal urethra and bladder, some authors have suggested that a single attempt at gentle passage of a bladder catheter should be performed. Other urologists believe that even minimal blind instrumentation of the injured urethra is ill-advised, preferring an endoscopically guided approach. In this author’s opinion, endoscopically guided instrumentation of the injured urethra is preferable to blind insertion of a catheter. The most conservative recommendation is to avoid any blind instrumentation of the injured urethra by the nonurologist. For incomplete anterior urethral injuries, urethral catheterization is reasonable therapy. Catheter-realignment techniques for posterior urethral trauma fall within the realm of the experienced urologist and constitute operative therapy and will be discussed later. Penetrating injuries to the anterior urethra are generally managed with operative exploration and repair.66

While penile fractures and testicular ruptures are best managed with early recognition and operative exploration and repair, certain genital injuries due to blunt trauma may be managed nonoperatively.67 This would be the case when the injury is limited to the subcutaneous tissues, the tunica albuginea and urethra of the penis are intact, and the tunica albuginea of the testes is intact as well. For penile injuries, nonoperative management is appropriate for rupture of subcutaneous vessels resulting in limited ecchymoses or a hematoma. Scrotal trauma may be managed nonoperatively when the testis is intact and there is a limited hematocele that is not particularly uncomfortable for the patient. In most situations, however, significant genital trauma is best managed by operative exploration and repair. If physical findings are suspicious for significant injury to deep tissue or such injury cannot be ruled out by imaging studies, operative exploration is prudent. This is because the outcomes of nonoperative management of such injuries as penile fracture or testicular rupture are poor, as compared with the very high success rates of early operative repair of such injuries.68 As the relative morbidity of surgical exploration of the external genitalia is minimal and the morbidity of missed injuries or delayed recognition is significant, one should err in the direction of operative management for such injuries.45,69 A scrotal ultrasound demonstrating heterogeneity of the testicular parenchyma is suggestive of testicular rupture, even if clear loss of continuity of the investing tunica albuginea cannot specifically be identified.70 Certainly, if a clear defect in the continuity of the testicular tunic is noted on ultrasound, the diagnosis of testicular rupture should be suspected and operative repair undertaken. Patients with a significant hematocele (blood and/or clot within the tunica vaginalis compartment) with an intact testis may be observed, although they may often have a quicker recovery of activity and more rapid resolution of scrotal pain and swelling if this lesion is evacuated surgically. An intratesticular hematoma without testicular rupture is generally managed nonoperatively. At times, testicular ultrasound may demonstrate an abnormality in which a preexisting testicular lesion such as a germ cell neoplasm is suspected. Such may be the case when relatively minor trauma causes a significant intratesticular bleed or testicular rupture. When preexisting testicular pathology is suspected and nonoperative management is selected for the traumatic lesion, it is critical that the testis be reevaluated until the suspicious abnormality resolves or its continuing presence mandates further imaging and intervention. For genital injuries involving significant loss of soft tissue or skin, nonoperative management may be appropriate as an initial approach, especially when more immediately life-threatening injuries demand priority. Wounds should be cleansed and a

CHAPTER 36

Penetrating injuries to the posterior urethra may present complex challenges in management, may be complicated by adjacent rectal injury or other intrapelvic or visceral injury, and are also considered later.

687

688

Management of Specific Injuries

SECTION 3

conservative approach should be adopted when determining whether to perform debridement of genital skin or soft tissues of marginal or questionable viability. Secondary operative management and delayed reconstruction with skin grafting or other tissue transfer techniques is often necessary when wounds are initially managed in this manner.71

OPERATIVE MANAGEMENT OF SPECIFIC GENITOURINARY INJURIES ■ Kidney Renal exploration for trauma begins with prioritization of the injuries and determining that the initial operation is in fact the appropriate time to embark on the renal exploration (see Section “Damage Control Principles in Genitourinary Trauma”). When contemplating exploration of an injured kidney in the absence of preoperative imaging, some assessment of the presence and normalcy of the contralateral kidney should be undertaken. Palpating the contralateral renal fossa for a grossly normal kidney is certainly appropriate and is often the only assessment necessary. In selected cases, an intraoperative IVP may provide more precise information. This can be performed by administering 1–2 mL/kg of iodinated contrast intravenously and then obtaining a 10-minute excretion film. This can occur while other general surgical tasks are being accomplished to avoid wasting time. While an intraoperative IVP provides some additional reassurance that a functional contralateral kidney is present when exploring an injured kidney, in our center we generally proceed with exploration of the injured kidney based on contralateral renal palpation alone. If it is jointly determined by the urologist and the general surgeon that renal exploration should occur, exploration is carried out through an anterior vertical incision in Gerota’s fascia. There has been some controversy regarding the importance of first obtaining vascular control of the renal pedicle prior to renal exploration as previously described.72,73 Some proponents claim a markedly reduced nephrectomy rate if the renal vessels are first dissected and controlled with vessel loops. Others claim that this maneuver is unnecessary to successful renal exploration and repair. This controversy is probably overstated, as even those who do not believe that individual dissection of the renal vessels is essential prior to renal mobilization generally use some other approach to control the pedicle or limit renal bleeding during examination and repair of the kidney. The bulk of the literature would suggest that the rate of otherwise unnecessary nephrectomies is minimized by having exposure and control of the renal pedicle prior to renal exploration. This can be achieved by the traditional maneuver of incising the posterior peritoneum lateral to the aorta and individually dissecting and looping the renal vessels on the side of injury (Fig. 36-19). This can also be achieved by reflecting the colon medially first, and then clamping the pedicle if significant bleeding is encountered on opening the Gerota’s fascial envelope (Fig. 36-20). Alternatively, the pedicle or the renal parenchyma can be compressed digitally (most applicable to polar injuries) without having individual control over the renal ves-

sels. Certainly if there is an injury to the pedicle, suggested by a large or expanding medial hematoma in the vicinity of the great vessels, there is broad agreement that central vascular control should be the initial maneuver. Following pedicle control or access, the colon and mesocolon on the side of injury are dissected medially following incision of the peritoneal reflection. When the anterior surface of Gerota’s fascia is fully exposed, a generous, vertical, anterior incision is made through the fascia, and the kidney is fully mobilized. As indicated earlier in Section “Anatomy,” it is important to dissect in an extracapsular plane and avoid inadvertently dissecting the renal capsule away from the underlying cortex. Accomplishing this is facilitated by beginning the dissection in an area of intact parenchyma rather than directly within the laceration. Completely mobilizing the kidney is very helpful, as it allows the kidney to be lifted anteriorly into the wound for complete inspection. If significant bleeding results during this maneuver, a noncrushing vascular clamp is applied to the renal artery, renal vein, or entire renal pedicle. An initial decision must be made regarding renal salvageability and the magnitude of the reconstructive effort that would be required to repair the injury. This is based largely on the amount of devitalized parenchyma, the degree of injury to the central vasculature and central collecting system, and the condition of the patient. If the kidney is felt to be reconstructible in an unstable patient, any significant intrarenal vascular injury can be rapidly sutured and the kidney can be packed off with laparotomy pads as other surgical injuries are treated (see Chapter 41). After repair of other injuries, or at the time of a secondary surgical procedure, formal exploration and reconstruction of the kidney is performed. If, based on the anatomy of the injury, the kidney is not considered reconstructible, a nephrectomy is performed. It is preferable to separately ligate the renal artery and vein to avoid the potential for arteriovenous fistula. A rapid search is made for accessory or polar vessels, which must be ligated also. While urologists frequently suture or simply ligate the renal artery and a long stump of vein, vascular surgeons and some urologists prefer to oversew the short right renal vein with a continuous 3-0 or 4-0 Prolene suture. For trauma nephrectomies, the ureter and adjoining vessels are ligated near the kidney, while the gonadal vein is ligated and divided when necessary, with no need for concern for adverse impact on the gonadal structures. If renal reconstruction is planned, several steps are generally followed (Fig. 36-21). Following evacuation of the hematoma, the kidney is carefully examined to identify lacerated vessels, the open collecting system, and devitalized parenchyma. Large areas of lacerated, devitalized parenchyma are excised sharply, with smaller vessels controlled with an absorbable 3-0 or 4-0 suture. In general, an absorbable suture is utilized for intrarenal suturing, as a permanent suture may create a nidus for stone formation if in contact with the collecting system. If adequate closure of the collecting system is achieved, there is no need for stenting or a nephrostomy. If repair of the collecting system is tenuous or incomplete, placement of an internal stent (complemented by a bladder catheter) or a nephrostomy tube may decrease the risk of postoperative urinary extravasation and the formation of a urinoma.

Genitourinary Trauma

689

Inferior mesenteric vein

CHAPTER 36

Inferior mesenteric vein

Left renal vein

Right renal vein

Left renal artery Gonadal vein

Right renal artery

Aorta

A

B

C

Partial nephrectomy for polar lesions is performed by a “guillotine” technique, with the transected vessels and collecting system closed as noted earlier (Figs. 36-22 and 36-23). Topical hemostatic agents may be placed within a parenchymal defect to aid in hemostasis, with the capsule closed over the defect and the hemostatic material. If the capsule can be closed with mattress sutures or absorbable bolsters following debridement or partial nephrectomy, parenchymal hemostasis is aided considerably. If capsular closure is not feasible either due to the shape and location of the parenchymal defect or due to loss of the capsule from the injury or dissection, utilizing absorbable materials or native tissue as a patch may be helpful if hemostasis is still problematic. The argon beam

FIGURE 36-19 Surgical management of renal trauma: vascular control. Diagram demonstrating early vascular control prior to renal exploration. (A) The posterior peritoneum is opened over the aorta medial to the inferior mesenteric vein. (B) The renal vessels are individually dissected and surrounded with vessel loops. (C) The colon is reflected medially exposing the perinephric hematoma. Some clinicians believe preliminary control of the renal vessels is not necessary when performing renal exploration for trauma, although best renal salvage rates are reported when vascular access or control is obtained.

coagulator has also been utilized successfully in the kidney to achieve hemostasis in the parenchyma, after suturing larger vessels and closing the collecting system. Topical hemostatic agents and tissue adhesives may be used on the kidney, collecting system, ureter, and other urologic repairs to aid in hemostasis and minimize the risk of postoperative urinary extravasation.74 Some data exist to suggest that the application of fibrin sealant over a urinary tract suture line may decrease the likelihood of postoperative urinary leakage.75 At times, wrapping the decapsulated kidney in absorbable mesh material has been utilized to provide mild temporary parenchymal compression for continued venous bleeding from lacerated parenchyma (Fig. 36-24).

690

Management of Specific Injuries

SECTION 3 B

FIGURE 36-20 (A) Alternate means of obtaining vascular pedicle access prior to renal exploration. Colon is reflected medially initially. Blunt dissection lateral to vena cava allows creation of space anterior to psoas muscle for placement of pedicle clamp if necessary on renal exposure. (B) Comparable technique on the left side, creating space for pedicle clamp lateral to aorta. This approach has been used successfully in the author’s center.

A

A

C

B

D

FIGURE 36-21 (A and B) Wedge resection of injured parenchyma. (C) Suturing of open collecting system and significant vessels with absorbable suture. (D) Capsule, if present, may be closed, or reconstructed using peritoneal patch, with absorbable gelatin sponge or local fat pedicle to aid in hemostasis.

Genitourinary Trauma

A

B C

FIGURE 36-22 (A and B) Partial nephrectomy for major injury to upper pole. (C) Repair of collecting system and suturing of bleeding vascular branches. (D) Mattress sutures of 2-0 chromic gut to reconstruct parenchyma and aid in hemostasis.

Injuries to adjacent organs such as the liver, pancreas, duodenum, and colon generally do not change the indications for renal salvage versus nephrectomy,76,77 as good results have been described for renal repairs in the setting of injuries to these adjacent organs. It is desirable, however, to separate the renal injury from the adjacent visceral injury using available viable tissue. This can be accomplished by replacing the kidney within Gerota’s fascia and closing the fascial layer over the kidney or by utilizing omentum in the form of a pedicle flap. Drains for renal injury are utilized when injury complex or incompletely repaired injuries to the collecting system are present, or there is concern for the need to evacuate blood postoperatively. Closedsuction drains are used as there is a lower risk of contributing to postoperative infection. In the setting of injury to an adjacent organ, the organ sites should be drained separately. Certain injuries are more common in the pediatric population and deserve specific mention. Avulsions of the fornices, ureteropelvic junction, and renal pedicle are more commonly seen in the pediatric population than they are in the adult.26 Complete forniceal avulsion injuries are managed with nephrectomy as repair is nearly impossible. Avulsions of the ureteropelvic junction are amenable to repair through a direct anastomosis. Lacerations of the renal pelvis should also alert the trauma surgeon to the possibility of a preexisting obstruction of the ureteropelvic junction. Repair of the obstructing lesion may need to be performed with closure of the pelvis, or nephrectomy may be preferable if the kidney appears to have minimal parenchyma due to long-standing obstruction. Renovascular injury from blunt or penetrating trauma presents certain challenges (see Chapter 37). As noted earlier, selected patients are taken to laparotomy for revascularization surgery based solely on a CT scan demonstrating the classic findings of renal nonperfusion following deceleration trauma. If exploration is undertaken based on the CT findings or if arteriographic imaging has been performed, the approach is

similar. The artery is dissected from its origin at the aorta toward the kidney and the arterial pulse is palpated or assessed with a Doppler instrument. The artery is clamped near the aorta and opened at the circular ring of hematoma, resected to the point of normal anatomy, and a direct end-to-end anastomosis performed. When necessary, an autogenous vein graft or prosthetic graft is interposed. As in the pediatric population (in which the injury is more common), avulsion injuries involving the renovascular pedicle require urgent surgical intervention. Most such patients are managed with nephrectomy, although isolated vascular repairs have been described depending on the level of the avulsion. Avulsion of multiple branches from within the renal sinus is virtually impossible to repair in the trauma setting and generally requires nephrectomy as well. While current data suggest that the likelihood of achieving a favorable outcome with renal revascularization following renal injury is low,78 patient selection is critical. In the appropriate clinical setting (brief warm ischemia time and a patient in suitable condition for surgery), the effort may be worthwhile in carefully selected patients. A collaborative approach involving the vascular surgeon and the urologist is highly applicable to cases in which renovascular reconstruction is planned. In selected cases in which an intimal disruption of the renal artery is documented arteriographically but perfusion is maintained, radiologic placement of a vascular stent may be applicable. Many limited penetrating injuries to the renal vein can be repaired, while arterial injuries have a high rate of nephrectomy. Injuries to branch vessels in a parenchymal laceration are ligated. When diagnosed on imaging studies in stable patients with intact parenchyma, nonoperative management is appropriate. Bilateral renal injuries are rare and present special problems.79 Assuming neither kidney is bleeding briskly, the kidney that seems to be less seriously injured (based on hematoma size and location, apparent orientation and location of

CHAPTER 36

D

691

692

Management of Specific Injuries

SECTION 3 A

B

C

D

E

F

FIGURE 36-23 Surgical management of renal trauma. (A) Partial nephrectomy for lower pole laceration due to gunshot wound. Excised fragment of devascularized, lower pole parenchyma, debrided. Bullet removed, found immediately posterior to kidney. (B) Appearance of lower pole following suture repair of vessels and repair of collecting system. Capsule has been reflected back for completion of partial nephrectomy and will be used for coverage of defect. (C) Defect covered with absorbable gelatin sponge soaked in thrombin. Note vessel loops surrounding renal vessels. (D) Defect covered with adjacent capsule and peritoneal patch, to aid in hemostasis. (E) Duodenal injury, repaired, immediately anterior to the renal injury. It is desirable to separate such injuries with viable tissue interposition, when possible, to minimize the risk of postoperative leak from either source affecting the other repair. (F) Gerota’s fascia closed over the kidney to separate the duodenal and renal injuries. Omental pedicle flaps are also very useful for this purpose. The renal repair was drained with an extraperitonealized closed-suction drain.

entrance and exit wounds, etc.) is assessed to be sure that renal salvage is feasible. One kidney can also be packed off temporarily after obtaining gross hemostasis while the opposite kidney is assessed in an effort to avoid nephrectomy in these cases whenever possible.

Although rarely indicated, ex vivo renal reconstructive surgery may be utilized in the trauma setting. This would be the case when a solitary (functionally or anatomically) kidney is injured, and a complex reconstruction is needed for salvage.

Genitourinary Trauma

693

CHAPTER 36

A

B

FIGURE 36-24 Surgical management of renal trauma: renal parenchymal injury due to blunt trauma. (A) Large, deep laceration through posterior parenchyma, left kidney. Bleeding sites are sutured, collecting system closed with absorbable suture. Venous bleeding continues from lacerated cortex. (B) Due to absence of renal capsule (dissected away from parenchyma by hematoma), absorbable surgical mesh is used to wrap renal parenchyma providing gentle compression to assist in achieving hemostasis.

■ Ureter The approach to ureteral repair depends largely on the level of the injury, the amount of ureteral loss, if any, and the condition of the local tissues. A ureteral laceration along with extensive destruction of the kidney from blunt or penetrating trauma is generally managed with nephrectomy. If the kidney is uninjured or the renal injury is limited and can be observed or repaired, ureteral repair is best performed at the time of recognition.80,81 Injuries to the ureter from blunt trauma require a high index of suspicion for diagnosis. Hematuria may be absent in such cases, and a delayed presentation is not uncommon. As noted earlier, the spiral CT scanners complete the initial renal imaging survey so rapidly that, unless a delayed excretory phase is requested, the study may be completed before the contrast has opacified the collecting system or injured ureter. Blunt avulsion of the proximal ureter or ureteropelvic junction is best managed with limited debridement to viable tissue and a spatulated end-to-end anastomosis using fine absorbable suture (3-0, 4-0, or 5-0). In general, ureteral repairs performed after trauma are most often stented. This can be performed with an internal double-J-type stent or an externalized single-J stent. The single-J stent is usually exteriorized through a small stab incision in the anterior bladder wall and secured with a purse-string suture. Some surgeons also secure the stent to the bladder mucosa just outside the ureteral orifice with a fine absorbable suture (4-0 or 5-0). For tenuous repairs of the proximal ureter, diversion using a nephrostomy tube may be considered, but it is generally unnecessary. A blunt injury to the midureter is uncommon, but when it is diagnosed, it is managed with a primary anastomosis. In the distal ureter (below the internal iliac artery), ureteral reimplantation into the bladder is preferred.

Injuries to the ureter from penetrating trauma also require a high index of suspicion for diagnosis. The presence of urine in the operative field may be difficult to appreciate, and the ureters, when at risk, must be thoroughly assessed by intraoperative inspection. The proximal and midureters down to the internal iliac arteries are easy to visualize and examine. For very distal injuries, a vertical cystotomy with observation of efflux from the ureteral orifices and intraoperative retrograde pyelography may be a less morbid means of assessing the area of concern, rather than embarking on a difficult dissection of the ureter all the way to the bladder in the setting of a pelvic hematoma. Alternatively, intraoperative flexible cystoscopy with retrograde pyelography may be performed, avoiding the cystotomy. For proximal and midureteral injuries, limited debridement of damaged tissue and a tensionfree, spatulated end-to-end anastomosis is the procedure of choice (Fig. 36-25). For very distal injuries (generally below the internal iliac artery), reimplantation into the bladder is preferred as noted earlier as the blood supply to the distal ureteral stump may be compromised. A direct anastomosis to the bladder avoids the potential ischemic complications of a very distal ureter-to-ureter anastomosis. Stenting of such repairs is routine as described previously. For injuries to the lower third of the ureter, it is not always possible to perform a direct anastomosis to the bladder without tension. In such cases, the bladder can be brought cephalad and lateral toward the injured side to achieve a tension-free anastomosis with the ureter by several techniques. The most commonly employed is the “psoas hitch” (Fig. 36-26). The bladder is opened anteriorly, lateral peritoneal attachments are divided as needed, and then the bladder body is displaced toward the side of the injury and sutured to the psoas muscle with 2-0 absorbable suture, taking care not to injure or entrap

694

Management of Specific Injuries

SECTION 3

A

B

C

D E

FIGURE 36-25 Techniques of ureteral reconstruction. Debridement and primary anastomosis for ureteral transection from gunshot wound. (A and B) Mobilization of ureter superficial to adventitial plane. (C) Limited debridement of lacerated ureter to viable tissue with spatulation for repair. (D and E) End-to-end anastomosis with fine absorbable suture, over stent (not shown).

any major nerves. The ureter can then be reimplanted into the bladder using a tunneled antirefluxing anastomosis, or the tunnel can be omitted if length is still a problem. It is important to ensure that no obstruction or acute angulation exists at the vesical hiatus where the ureter enters. If a psoas hitch cannot achieve a tension-free connection to the ureter, a bladder flap (Boari flap) can be created. This procedure has a higher complication rate than a psoas hitch and is performed only if the psoas hitch does not accomplish the required objective. The bladder flap may be performed in conjunction with the psoas

hitch to maintain the cephalad extension of the bladder wall posterior to the flap. Again, a nonrefluxing tunneled or a refluxing repair can then be performed. More complex techniques of ureteral reconstruction include transureteroureterostomy (TUU), ileal-ureteral replacement, and renal autotransplantation (Figs. 36-27 and 36-28). TUU is relevant when anastomosis to the bladder is not feasible due to inadequate length of the ureter or condition of the bladder, or when it is desirable to move the repair away from the ipsilateral hemipelvis due to local conditions of

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FIGURE 36-26 (A) Ureteral reimplantation with psoas hitch for lower ureteral injury: the bladder is opened either transversely or vertically and obliquely toward the side of injury, and then hitched to the ipsilateral psoas muscle with 2-0 or 3-0 Vicryl suture. A tunneled, antirefluxing anastomosis of the ureter to the posterior wall of the bladder is performed, being certain that an adequatewidth tunnel is created to prevent obstruction. If the available ureteral length is short, antirefluxing tunneling can be eliminated. Either an internal double-J-type stent or an externalized single-J stent can be used (not shown). (B) Psoas hitch ureteral reimplantation for penetrating injury to lower ureter, performed acutely during initial laparotomy in a hemodynamically stable patient. The bladder body can be seen sutured to the left psoas muscle, with the ureter entering cephalad. A single-J ureteral stent and suprapubic cystostomy exit from the bladder in the lower part of the photograph.

infection, prior pelvic radiation, etc. Ureteral replacement with the ileum is seldom performed in the acute trauma setting as it is preferable to have a fully prepped bowel when performing this procedure. Renal autotransplantation may be appropriate in the acute trauma setting if appropriate vascular surgical expertise is available and less complex options for ureteral replacement are not feasible. The proximal ureter can be anastomosed directly into the bladder, in the case of loss of the majority of the lower ureter, or an anastomosis can be performed to the lower ureter if it is clearly viable and not excessively distal. When ureteral repairs are performed in direct apposition to adjacent vascular or visceral repairs, separation of the repairs by an omental pedicle or other viable tissue is desirable to prevent a fistula or contact with urine at the site of the adjacent organ injury. External drainage of ureteral injuries, in addition to stenting or diversion, may be desirable, particularly if the repair is tenuous or the vascularity of the repaired tissues is questionable. Some urologists prefer Penrose drains for this purpose, to avoid having a closed-suction drain aspirating directly on a ureteral suture line. The author uses closed-suction drains, suturing them (with 4-0 chromic gut) to the psoas muscle or

other adjacent soft tissue to prevent the drain from migrating directly onto the ureteral repair. In the postoperative period, antibiotic administration may be desirable, especially if urinary extravasation persists. As noted later, ureteral injuries are also highly amenable to damage control strategies when the patient is not in suitable condition for repair at the time of the initial laparotomy. An external stent placed through the transected proximal ureteral stump allows maintenance of control of the urinary output while the patient is undergoing resuscitation in preparation for definitive delayed reconstruction.

■ Bladder Surgical repair of the bladder is performed for many iatrogenic injuries, for nearly all blunt intraperitoneal injuries, and for selected cases of blunt extraperitoneal rupture. Penetrating injuries to the bladder are also usually managed with operative repair. Intraperitoneal ruptures of the bladder are approached through a midline abdominal incision. The large laceration is nearly always in the dome of the bladder as previously

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SECTION 3 A

B C

FIGURE 36-27 (A–C) Transureteroureterostomy for reconstruction following extensive mid and lower ureteral injury. Prior bladder surgery or pelvic inflammatory or neoplastic disease, among other factors, may make psoas hitch or bladder flap repair undesirable. The injured ureter is mobilized and transposed to the contralateral side underneath the mesentery, and then anastomosed with an end-to-side technique to the recipient ureter.

described (Fig. 36-29). The interior of the bladder is palpated and inspected through the laceration to verify that no other injuries are present and that there is clear efflux from both ureteral orifices. The laceration may be extended into an anterior midline cystotomy if necessary for further assessment, but this is not usually necessary. The edges of the bladder laceration may require minimal debridement to remove devascularized tags of detrusor muscle or mucosa. The laceration is then closed using two layers of heavy absorbable suture. An adequate bore bladder catheter is used to allow free drainage of initially bloody efflux that clears in the first few days. The length of time of catheterization should consider the period needed for urinary efflux to clear and the ability of the patient to be ambulatory and void comfortably, but is usually 5–10 days. It is prudent to perform a cystogram prior to removal of the catheter following any operative repair, and it is mandatory with nonoperative management. As a well-sutured repair carries an extremely low postoperative risk of extravasation, some

FIGURE 36-28 Renal autotransplantation for reconstruction following extensive loss of midureter, making direct union of upper ureter to bladder impossible. Alternative to ileal-ureteral replacement of most of the ureter. Nephrectomy must be tailored to include as much of the renal vessels as possible to aid in anastomosis to iliac vessels (in general, vein generally transected flush with vena cava on right, with artery transected more proximally, behind vena cava, than shown here). Anastomosis of proximal ureter to viable lower ureter.

practitioners do remove the catheter without prior contrast imaging with excellent success. Suprapubic cystostomy catheters are not generally needed after repairs of intraperitoneal ruptures. They should be inserted only when there will be the need for long-term bladder drainage, as in the patient with a significant injury to the brain, trauma to the pelvis or a lower extremity, or other factors that would be expected to substantially delay a return to ambulation. For the selected cases in which extraperitoneal rupture of the bladder is managed with operative repair, there are several

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FIGURE 36-29 Operative appearance of intraperitoneal bladder injury from blunt trauma. (A) The anterior bladder wall is retracted at the top of the photograph, with the typical large, stellate defect noted in the bladder dome. (B) Appearance of the bladder dome after closure in two layers of 2-0 chromic gut.

important differences when compared with intraperitoneal repairs. When operating on the injured bladder during a laparotomy following a pelvic fracture, an effort should be made to avoid entering the retropubic hematoma. This avoids potentially serious hemorrhage from a site that is often tamponaded. If repair of the bladder is necessary in this setting (see Section “Nonoperative Management of Genitourinary Injuries”), one should enter the bladder through an anterior cystotomy incision cephalad to the pelvic hematoma. The laceration, which is usually located in the lower anterior or anterolateral bladder, can be sutured transvesically by introducing Deaver or malleable retractors into the bladder and retracting them laterally. Often, only a single-layer, full-thickness closure is possible in this setting. It is useful to communicate with the orthopedic surgeons when operating on extraperitoneal bladder ruptures in the setting of a pelvic fracture to allow for coordinated care. A penetrating injury to the bladder is most often managed operatively, although occasional patients as previously described may be candidates for nonoperative management.62 If a patient is undergoing laparotomy and has gross hematuria following penetrating pelvic trauma, the peritoneal surface of the bladder is examined first. The retropubic space is then entered and an anterior, midline cystotomy is created. This may be easier to accomplish if the bladder is partly filled with irrigant. For

laparotomies during which bladder surgery is likely, including the genitalia in the sterile field facilitates whatever manipulation may be necessary without abdominal contamination. Following cystotomy, the interior of the bladder is thoroughly examined, as are the ureteral orifices and the bladder neck. The urinary efflux from both orifices should be observed; if it is bloody or absent, further investigation for trauma to the ureters or upper tract is indicated. Penetrating injuries to the bladder are closed with two layers of absorbable suture as described earlier. In some patients, an iatrogenic or penetrating injury to the bladder may result in loss of a large portion of the detrusor of the bladder body. Closure over a bladder catheter is still recommended, as the bladder may expand to an acceptable volume with time. If minimal bladder capacity persists following a reasonable period of healing, augmentation cystoplasty can be performed electively. As for renal and ureteral injuries, injuries to the bladder in the unstable trauma patient are amenable to damage control strategies. These include externalized stenting of the ureters with pelvic packing and delayed repair of complex lacerations. Certain associated injuries impact on the management of bladder trauma. Contiguous injury to the vagina or rectum is such an example, requiring close collaboration between the

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SECTION 3 FIGURE 36-30 Bladder neck avulsion injury in an adult female with pelvic fracture. Operative appearance during surgical repair. An anterior midline cystotomy had been performed (to right in photo), with the tip of a Foley catheter protruding from the avulsed bladder neck for demonstration purposes. Anastomosis to urethral stump at level of pelvic floor performed over Foley catheter. The patient was initially managed with a percutaneous suprapubic cystostomy. This repair was performed 36 hours following injury, when the patient was hemodynamically stable and risk of excessive bleeding from the pelvic fracture would be lower.

clinical services involved in caring for these injuries. When such injuries are suspected, it is helpful to have the patient in a modified dorsal lithotomy position so simultaneous access to the perineum and abdomen can be obtained. During surgical repair, the bladder should be separated from the rectum or vagina by placing an interposition flap of viable tissue if the loss of tissue is significant and the injuries directly overlie each other. This effort at separation of the pelvic organs can be difficult in the trauma setting and, if the injuries do not directly overlie each other and tissue loss is minimal, simple transvesical closure is generally adequate. In this setting, longer indwelling catheter times, perioperative antibiotics, and radiographic imaging prior to removal of the catheter are recommended. Open pelvic fractures are among the most devastating injuries in orthopedic trauma, and injury to the lower urinary tract may complicate such injuries. A close interaction between the urologist, orthopedist, trauma surgeon, and interventional radiologist is necessary for management of such patients. Chronic disability is common following such injuries.82 Avulsion injuries of the bladder neck, more common in the pediatric population, require operative repair (Fig. 36-30).58 Repair for these complex injuries may be best delayed until 24–72 hours postinjury to support a damage control strategy and to minimize the risk of excessive hemorrhage from an associated pelvic fracture.

■ Urethra Operative management for urethral trauma includes the broad topic of elective urethral reconstruction following traumatic injuries and surgical repair of urethral strictures. There

are excellent reviews available on this latter topic.83,84 This discussion will focus on immediate and subacute surgical intervention for urethral trauma. Clinical guidelines have recently been reported for such injuries.85 Anterior urethral injuries that are incomplete may be managed with placement of a transurethral catheter or with suprapubic diversion. As noted above, the author favors using endoscopic guidance for any attempt to catheterize the traumatized urethra. If a blind attempt at catheterization is performed and any resistance is encountered, an endoscopically guided procedure should follow. Complete ruptures of the anterior urethra from blunt trauma are best managed with suprapubic diversion for 3 months, followed by elective end-to-end urethroplasty when the perineal hematoma and induration have fully resolved. Acute attempts at excision and repair are not recommended as it is unclear how much urethra to resect due to the crush injury and difficult to be sure that one is approximating viable, healthy tissue at the anastomosis. Penetrating injuries to the anterior urethra may be managed with local exploration and repair or with suprapubic diversion. With stab wounds or gunshot wounds from lowvelocity missiles, it is usually a simple matter to perform limited debridement and repair with a spatulated anastomotic technique. If the patient is not an appropriate candidate for immediate repair due to more pressing serious injuries, etc., suprapubic diversion or endoscopically guided insertion of a transurethral catheter placement is performed. Extensive loss of the urethra from penetrating trauma or industrial trauma may require a staged repair. The management of disruption or distraction injuries of the posterior urethra remains controversial. In recent years, there has been increasing interest in early catheter realignment for such injuries. Techniques utilized have included endoscopic guidance, open surgical approaches, and (historically) the use of interlocking magnetic sounds (Fig. 36-31).86–89 A potential advantage of endoscopic realignment is the possibility that the injury will heal free of intractable stricture. This would obviate the need for late urethroplasty, shorten the period of urinary intubation, and may improve the anatomic result as compared with the nonintubated state by reducing malalignment. The potential disadvantages of this approach are the risk of infecting the retropubic hematoma by the presence of the indwelling catheter with an adverse impact on late continence and sexual function and the high likelihood that a stricture will form anyway. When selected, catheter realignment should be performed by an experienced team in the operating room with endoscopic and fluoroscopic capability. Results are better for incomplete disruptions than they are for complete disruptions. Most patients managed in this manner do develop a stricture requiring endoscopic intervention, often involving multiple procedures. Overall, patients managed with catheter realignment may avoid a subsequent urethroplasty about 50% of the time. The traditional approach to a posterior urethral distraction injury is diversion with a suprapubic cystostomy, followed by a period of observation of 3–6 months while the pelvic hematoma resolves and the anatomy stabilizes. Repeat antegrade and retrograde urethrograms are then performed, and definitive

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B

A FIGURE 36-31 (A) Manipulating flexible cystoscope from above and rigid cystoscope sheath from below (beak placed at point of disruption at bulbomembranous junction), a guidewire is advanced across defect and continuity is achieved. A Foley catheter with end-hole punched is passed over the guidewire and positioned with balloon in bladder. Working sheath is removed after replacement of large-bore suprapubic catheter. This is one of a variety of techniques described for achieving catheter realignment using minimally invasive approaches. Primary urethral realignment for posterior urethral disruption. (A and B) Access to bladder, previously obtained via percutaneous cystostomy, is utilized for realignment. Retrograde flexible cystoscopy failed to demonstrate continuity; therefore, suprapubic tract was dilated and working sheath was placed into bladder using both direct vision and fluoroscopic guidance.

reconstructive surgery is planned. The ultimate success rate of this approach is over 90%; however, the need for a long-term indwelling suprapubic tube while awaiting surgery may be frustrating for the patient. Nevertheless, newer techniques such as catheter realignment must be compared with the excellent outcomes of patients managed in this traditional manner.90,91

■ Penis, Testis, and Scrotum Penile trauma is nearly always managed through operative exploration and repair.92 For blunt penile fractures, the penis is explored through either a ventral midline penoscrotal incision or a circumcising subcoronal incision. The defect in the tunica albuginea is exposed and closed with absorbable suture (Fig. 36-32). The outcomes following early operative repair of penile fractures are far superior to those resulting from nonoperative management. Deformity, painful erection, pseudoaneurysm, and loss of erectile function are common in nonoperative management of such injuries (Fig. 36-33).68 Penetrating penile injuries, similarly, should be managed with operative exploration and repair (Figs. 36-34 and 36-35).93 As combined cavernosal and urethral injury occurs in roughly 10% of penile fractures, a preoperative urethrogram or flexible cystoscopy is useful in planning the repair. In cases of penetrating penile injury, a similar surgical approach is utilized, with conservative debridement, repair of cavernosal and urethral injury, and microsurgical repair of dorsal neurovascular structures when possible. For limited

injuries, direct wound exploration may be preferable approach. The possibility of adjacent nonurologic injury (thigh, femoral vessels, pelvic organs) must always be considered in cases of penetrating genital injury. Penile strangulation injuries due to constricting bands or other devices are managed with removal of the constricting object in as atraumatic a manner as possible. Distal penile skin, glans, cavernosal, or urethral necrosis can occasionally occur in such cases. A conservative approach to debridement of tissues of questionable viability and diversion with a suprapubic cystostomy tube if the urethra is compromised are principles of management. Patients with traumatic amputation of the penis require specialized management (Fig. 36-36). Often, patients who suffer traumatic amputation through self-mutilation are psychotic and/or involved in substance abuse and require psychiatric as well as urologic intervention.94 The severed organ should be cleansed and kept in cold saline-soaked gauze in a sealed bag, which is then placed in ice. Replantation surgery is well described.95 In sequence, anastomosis of the corpora cavernosa, urethra, dorsal blood vessels, and nerves should be performed with appropriate microsurgical expertise. Functional outcomes are variable with such replantation efforts, largely reflecting the condition of the severed organ and the time that elapses prior to replantation. Scrotal trauma should be explored if there is a concern about testicular rupture. In blunt trauma, testicular ultrasound may be helpful in deciding if operation is indicated. In penetrating

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SECTION 3 A

FIGURE 36-32 Penile fracture. Appearance of penis during surgical exploration for penile fracture sustained during sexual intercourse. Patient reported classic findings of pain, swelling, and detumescence following sudden marked bending of erect penis. Note marked swelling of distal phallus with subcutaneous hematoma. Penis is explored through a ventral, midline, penoscrotal incision. Dissection to area of palpable irregularity along penile shaft reveals transverse laceration of tunical albuginea of corpus cavernosum. A penile tourniquet, utilizing a Penrose drain, is in place to reduce bleeding during repair. The hooks are part of a ring-retractor system commonly used in genital surgery. The tunica albuginea defect is closed with running 3-0 Vicryl suture. Early exploration and repair for penile fracture injuries produces the best results. Circumcising, subglanular incision is preferred by some surgeons for this type of exploration and repair.

trauma, we often utilize an oblique upper scrotal incision that provides access to the groin, spermatic cord, penile base, and scrotal contents. Most scrotal injuries should be explored with the goal of evacuation of the hematoma, debridement of devitalized tissue, and repair and salvage of the testicle (Figs. 36-37 and 36-38). Reproductive outcomes are favorable following such management.96 Cases of scrotal and other soft tissue loss in the genital region should be managed with a conservative approach to debridement of marginally vascularized skin and soft tissues as previously described. Delayed primary closure or reconstruction of significant scrotal loss using meshed split-thickness skin

B

FIGURE 36-33 Delayed presentation following penile fracture. (A) Note marked angulation to left with mass effect on right lateral side of penile shaft following untreated rupture. Patient presents 6 weeks postinjury; the subcutaneous hematoma has resolved, while the defect in the corpus cavernosum remains, resulting in angulation and pain with erection. (B) Appearance of penis at surgical exploration through circumcising incision. Note large encapsulated hematoma under Buck’s fascia, which, on incision, still communicates with cavernosal space. Defect repaired with correction of deformity.

grafting produces favorable results. Human bite wounds have a very high infection rate and should be left open if presenting in a delayed fashion (see Chapter 49).

COMPLICATIONS OF GENITOURINARY TRAUMA The management of complications of urologic injury is an important issue facing the trauma surgeon. Extensive reviews of this topic are available.97–99 Complications may be categorized as early and late occurrences and can occur in the setting of an early diagnosis of injury or a delayed diagnosis of injury. Early complications of injury to the upper urinary tract include bleeding, postinjury infections, problems related to urinary extravasation, and ischemic processes. Renal and ureteral injuries may also result in late complications including hyperten-

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B

C

FIGURE 36-34 Gunshot wound to penis with entrance at dorsal penile base. (A) Extensive injury to skin and subcutaneous tissues and laceration of tunica albuginea of corpus cavernosum. Penile tourniquet in place to allow injury assessment while minimizing bleeding. (B) Tunica albuginea has been conservatively debrided and closed with running Vicryl suture. (C) Appearance of penis following reconstruction of glans and skin tube. Subsequent scar revision was necessary for necrosis of skin edges (not shown). Preservation of soft tissues and conservative debridement demonstrated.

sion, hydronephrosis, and renal insufficiency. Functional abnormalities following trauma to the urinary tract may include a neurogenic bladder, urethral stricture, and sexual or reproductive dysfunction. Appropriate follow-up studies for high-risk injuries are critical in the early detection of complications of urologic trauma.

DAMAGE CONTROL PRINCIPLES IN GENITOURINARY TRAUMA Damage control surgery, or the process of intentionally delaying surgical interventions for lesions that are not immediately life-threatening, is an evolving strategy that is applicable to all surgical specialties.100–102 With the exception of major, active bleeding from the kidney or renal pedicle, virtually any urologic injury can be handled in a delayed fashion without exposing the patient to significant risk. If the patient becomes stable, interval imaging (generally with contrastenhanced CT or with arteriography if performed for another purpose) of a renal injury may allow selection of definitive nonoperative management. This avoids the time and potential morbidity of an unnecessary renal exploration at the second operative procedure. If, at the initial operation, bleeding from the kidney is not a major concern or hemostasis for significant bleeding has been obtained, the kidney can be packed. Renal reconstruction is then performed at a secondary laparotomy.

Ureteral injuries for which delayed management is necessary can be managed with externalized stenting (Fig. 36-39). A single-J urinary diversion stent can be passed up into the kidney through the lacerated or transected ureter, tied or sutured to the end of the proximal segment of ureter, and then externalized and attached to a drainage device. At secondary exploration, formal ureteral reconstruction can be completed. Alternatively, the injured ureter can be ligated or simply left to drain in situ, although these approaches have the disadvantages of either creating an obstruction or allowing urine to pool in the abdomen and increasing the risk of a postoperative infection. Certain bladder injuries may be difficult to repair at the initial operation as well. Visibility may be compromised by pelvic bleeding requiring packing, the complexity of the repair may require more time and blood loss than the patient can tolerate, or the degree of debridement needed may be unclear, as may be the case with a high-velocity gunshot wound. Delaying definitive repair may be accomplished by inserting bilateral externalized ureteral stents. The pelvis can then be packed for bleeding, compressing the open bladder against the pubis. Alternatively, placing an externalized suprapubic catheter (Malecot or Foley) within the injured bladder is also an option. If the catheter prevents tamponade of pelvic bleeding, it can be clamped temporarily and then reopened to drainage when the patient’s coagulopathy is corrected. The use of damage control principles for complex penetrating pelvic trauma in the battlefield setting has been

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SECTION 3 A

B

FIGURE 36-35 Gunshot wound to mons pubis region, cephalad and to left of penile base. (A) No palpable abnormality of penis is recognized. Small left scrotal hematoma present. (B) Surgical exploration of wound via oblique scrotal neck incision extends toward groin. Bleeding sites in left spermatic cord were controlled (not shown), followed by evacuation of hematoma resulting in significant bleeding. Dissection revealed complete transection of left corpus cavernosum at penile base, which was repaired. Case demonstrates importance of surgical exploration of penetrating injuries in proximity to male genitalia.

recently reported. In this series, 43% of patients had urologic injury while 50% had major vascular injury. A 21% mortality rate in the first week postinjury was reported, while 36% of patients with combined vascular and rectal injuries died.103 A staged, multidisciplinary approach to management and reconstruction was shown to be valuable in this experience. Injuries to the urethra and external genitalia can be temporarily managed with suprapubic catheterization or dressing applications pending the patient’s return to surgery for definitive management. The results of damage control management for urologic injuries in appropriately selected patients appear to be acceptable in terms of patient survival, renal salvage, and functional outcome.104,105

CONSULTATION AND INTERSERVICE INTERACTION A specialty service such as urology offers skills that are different from those of the general surgeon. These include endoscopic capability and familiarity with reconstruction of the urinary tract in the elective setting. The urology service should be informed of signs of urologic injury as early as possible, preferably from the emergency department. This allows the urologist to be involved in preoperative imaging and interpretation, later operative sequencing, and use of damage control strategies. The experience of large trauma centers in which an interested and capable urologic trauma team is involved often results in reduced rates of nephrectomy and improvements in other outcome measures.

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A B FIGURE 36-36 Subtotal penile amputation injury due to assault with knife. (A) Photograph demonstrates complete transection of body of penis with right-sided skin bridge attaching distal phallus to body. Left testis is exposed as well. (B) Preparing for surgical reconstruction—minimal debridement of corpora cavernosa and urethra, following extensive irrigation. (C) Corpora cavernosal anastomosis has been completed; urethral anastomosis about to be completed after spatulation and mobilization of distal ends to avoid tension on repair. Following completion of urethral repair over Foley catheter, microsurgical anastomosis of deep dorsal arteries, deep dorsal vein, and adjacent nerves was performed (not shown). C

A

B

C

FIGURE 36-37 Testis: testicular rupture due to blunt trauma. (A and B) Appearance of ruptured testis at surgical exploration following blunt trauma to scrotum. Note laceration of tunica albuginea with extruded seminiferous tubules. (C) Appearance of testis following minimal debridement of testicular parenchyma and repair of tunica albuginea with running 3-0 Vicryl suture.

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SECTION 3 B A

C

D

FIGURE 36-38 Scrotal exploration and testicular repair following gunshot wound to scrotum. (A) Entrance wound visible lateral to base of penis on left, exit just to the right of the median raphe; note marked left hemiscrotal swelling from hematoma. Surgical exploration is mandatory and preoperative scrotal imaging is unnecessary. (B) Scrotal exploration performed through high oblique scrotal incision for optimal exposure of scrotal contents and possible extension to groin if further spermatic cord exposure proves necessary. Entrance into tunica vaginalis visible. Testis introduced out of scrotum on spermatic cord pedicle. (C) Appearance of left testis demonstrating complex laceration of tunical albuginea with extruded testicular parenchyma. (D) Appearance of testis following limited parenchymal debridement and reconstruction of tunica albuginea. Testis is then returned to scrotum following evacuation of hematoma and extensive irrigation; Penrose drain placed through inferior stab incision in left hemiscrotum (not shown).

Genitourinary Trauma

Algorithm for Management of Penetrating Injury, Proximity to Lower Urinary Tract (bladder, lower ureters, urethra) Operative repair - options: - exploratory midline cystotomy - assess distal ureters, bladder, bladder neck - intraoperative imaging - cystography - bladder filling, observe for extravasation - intraoperative flexible cystoscopy

bladder injury

urethral injury

Anterior Midline Cystotomy

with urologic input, consider: - catheter alignment - surgical exploration/ repair - damage control approach (stage, divert, delayed reconstruction)

Proximity to trigone, ureters

bladder body injury, no proximity to trigone, ureters

Suture repair drainage - foley catheter - SP tube if - tenuous closure

Assess ureters - catherize - observe efflux - retrograde pyelograms

ureteral injury

ureters intact

Repair, consider damage control

FIGURE 36-40 Algorithm for management of penetrating injury, proximity to lower urinary tract (bladder, lower ureters, urethra).

CHAPTER 36

FIGURE 36-39 Patient managed with damage control laparotomy: gunshot wound to abdomen with injuries to small bowel, left iliac artery and vein, and left ureter. Patient was hemodynamically unstable following vascular repair, so ureteral injury was managed with damage control approach. Single-J stent was passed up proximal ureter at injury site and secured to end of ureter with silk tie; stent was externalized, exiting from left lower quadrant, as shown. Abdomen was closed with “Bogota bag” silo due to bowel and mesenteric edema. On return to operating room at 36 hours postinjury, formal ureteral repair with psoas hitch and ureteroneocystostomy was performed.

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MEDICOLEGAL CONSIDERATIONS SECTION 3

Urologists frequently become involved in the management of injuries that were not diagnosed at the initial operation. These are often recognized later in a patient’s clinical course, often after a complication (urinary extravasation, bleeding, azotemia, sepsis) initiates further testing and imaging studies. In this setting, it is important to communicate to the patient and family what is occurring and to document the events that have occurred in the medical record. It is important to educate patients and their families that traumatic injuries are complex and that certain complications are common and to be expected. Also, functional outcomes may be disappointing to patients. In urologic reconstruction, internal stents may be utilized, and patients may be discharged with indwelling catheters that may be invisible and/or require regular attention to avoid complications. As patients with internal stents placed in the trauma setting may be lost to follow-up, it is important that specific instructions be given to a patient regarding outpatient care and for a date of return to the clinic. If a nephrostomy tube must be changed after being in place for a month, it is best to arrange for this intervention prior to discharge. Also, it is important to explain and document the potential consequences of neglecting internal tubes, including calcification and obstruction. As it is important to monitor a patient for hypertension for 2 years following certain major renal injuries, this should be explained and documented as well.

CONCLUSION Much of the current consensus on approaches to genitourinary injury is based on retrospective studies. In fact, there are very few prospective studies in the urologic literature, leaving levels of evidence at a suboptimal state for evidence-based medical practice. Nevertheless, attempts at achieving a broad international consensus regarding the management of urologic injuries are ongoing.1–6 Important developments in body imaging, endoscopic approaches, endovascular stenting, and other radiologic and minimally invasive techniques have changed approaches to urologic trauma and selection of patients for operative versus nonoperative management. Further research will continue to impact the urologist’s role and approach in dealing with genitourinary injury (Fig. 36-40).

REFERENCES 1. Santucci RA, Wessels H, Bartsch G, et al. Consensus on genitourinary trauma. Evaluation and management of renal injuries: consensus statement of the renal trauma subcommittee. Br J Urol. 2004;93:937. 2. Chapple C, Barbagli G, Jordan G, et al. Consensus on genitourinary trauma. Consensus statement on urethral trauma. Br J Urol. 2004; 93:1195. 3. Gomez RG, Ceballos L, Coburn M, et al. Consensus on genitourinary trauma. Consensus statement on bladder injuries. Br J Urol. 2004;94:27. 4. Brandes S, Coburn M, Armenakas N, et al. Consensus on genitourinary trauma. Diagnosis and management of ureteric injury: an evidence-based analysis. Br J Urol. 2004;94:277. 5. Morey AF, Metro MJ, Carney KJ, et al. Consensus on genitourinary trauma. Consensus on genitourinary trauma: external genitalia. Br J Urol. 2004;94:507.

6. Lynch TH, Martinez-Pineiro L, Plas E, et al. European Association of Urology. EAU guidelines on urologic trauma. Eur Urol. 2005;47:1. 7. Hudak SJ, Hakim S. Operative management of wartime genitourinary injuries at Balad Air Force Theater Hospital, 2005 to 2008. J Urol. 2009;182:180. 8. Scaling System for Organ Specific Injuries., Trauma Resources, The AAST Injury Scale Tables (Tables 19-22, 29-31); 2007. Available at: http://www.aast.org. 9. Mohr AM, Pham AM, Lavery RF, et al. Management of trauma to the external genitalia: the usefulness of the American Association for the Surgery of Trauma organ injury scales. J Urol. 2003;170:2311. 10. Kuan JK, Wright JL, Nathens AB, et al. American Association for the Surgery of Trauma Organ Injury Scale for kidney injuries predicts nephrectom, dialysis, and death in patients with blunt injury and nephrectomy for penetrating injuries. J Trauma. 2006;50:351. 11. Tasian GE, Aaronson DS, McAninch JW. Evaluation of renal function after major renal injury: correlation with the American Association for the Surgery of Trauma Injury Scale. J Urol. 2010;183:196. 12. Calopinto V, McCallum RW. Injury to the male posterior urethra in fractured pelvis: a new classification. J Urol. 1977;118:575. 13. Kansas BT, Eddy MJ, Mydio JH, et al. Incidence and management of penetrating renal trauma in patients with multiorgan injury: extended experience at an inner city trauma center. J Urol. 2004;172:1355. 14. Voelzke BB, McAninch JW. Renal gunshot wounds: clinical management and outcome. J Trauma. 2009;67:677. 15. Shariat SF, Jenkins A, Roehrborn CG, et al. Features and outcomes of patients with grade IV renal injury. BJU Int. 2008;102:728. 16. Paparel P, N’Diaye A, Laumon B, et al. The epidemiology of trauma of the genitourinary system after traffic accidents: analysis of a register of over 43,000 victims. BJU Int. 2006;97:338. 17. McAleer IM, Kaplan GW, LoSasso BE. Congenital urinary tract anomalies in pediatric renal trauma patients. J Urol. 2002;168:1808. 18. Boone TB, Gilling PJ, Husmann DA. Ureteropelvic junction disruption following blunt abdominal trauma. J Urol. 1993;150:33. 19. Jankowski JT, Spirnak JP. Current recommendations for imaging in the management of urologic traumas. Urol Clin North Am. 2006;33:365. 20. Nicolaisen GS, McAninch JW, Marshall GA, et al. Renal trauma: reevaluation of the indications for radiographic assessment. J Urol. 1985;133:183. 21. Mee SL, McAninch JW, Robinson AL, et al. Radiographic assessment of renal trauma: a 10-year prospective study of patient selection. J Urol. 1989;141:1095. 22. Miller KS, McAninch JW. Radiographic assessment of renal trauma: our 15-year experience. J Urol. 1995;154:352. 23. Morey AL, McAninch JW, Tiller BK, et al. Single shot intraoperative excretory urography for the immediate evaluation of renal trauma. J Urol. 1999;161:1088. 24. Brown SL, Hoffman DM, Spirnack JP. Limitations of routine spiral computerized tomography in the evaluation of blunt renal trauma. J Urol. 1998;160:138. 25. Leslie CL, Zoha Z. Simultaneous upper and lower genitourinary injuries after blunt trauma highlight the need for delayed abdominal CT scans. Am J Emerg Med. 2004;22:509. 26. McAleer IM, Kaplan GW. Pediatric genitourinary trauma. Urol Clin North Am. 1995;22:177. 27. Morey AF, Bruce JE, McAninch JW. Efficacy of radiographic imaging in pediatric blunt renal trauma. J Urol. 1996;156:2014. 28. Umbreit EC, Routh JC, Husmann DA. Nonoperative management of nonvascular grade IV blunt renal trauma in children: meta-analysis and systematic review. Urology. 2009;74:579. 29. Perez-Brayfield MR, Keane TE, Krisnan A, et al. Gunshot wounds to the ureter: a 40-year experience at Grady Memorial Hospital. J Urol. 2001;166:119. 30. Azimuddin K, Milanesa D, Ivatory R, et al. Penetrating ureteric injuries. Injury. 1998;29:363. 31. Palmer LS, Rosenbaum RR, Gershbaum MD, et al. Penetrating ureteral trauma at an urban trauma center: 10-year experience. Urology. 1999;54:34. 32. Brandes SB, Chelsky MJ, Buckman RF, et al. Ureteral injuries from penetrating trauma. J Trauma. 1994;36:766. 33. Kunkle DA, Kansas BT, Pathak A, et al. Delayed diagnosis of traumatic ureteral injuries. J Urol. 2006;176:2503. 34. Medina D, Lavery R, Ross SE, et al. Ureteral trauma: preoperative studies neither predict injury nor prevent missed injuries. J Am Coll Surg. 1998;186:641. 35. Townsend M, DeFalco AJ. Absence of ureteral opacification below ureteral disruption: a sentinal CT finding. AJR Am J Roentgenol. 1995;164:253.

Genitourinary Trauma 67. Bandi, G, Santucci RA. Controversies in the management of male external genitourinary trauma. J Trauma. 2004;56:1362. 68. Kalash SS, Young JD Jr. Fracture of the penis: controversy of surgical versus conservative treatment. Urology. 1984;24:21–24. 69. Yapanoglu T, Aksoy Y, Adanur S, et al. Seventeen years’ experience of penile fracture: conservative vs. surgical treatment. J Sex Med. 2009;6:2058. 70. Fournier GR, Laing FC, Jeffrey RB, et al. High resolution scrotal ultrasonography: a highly sensitive but nonspecific diagnostic technique. J Urol. 1985;134:490. 71. Jordan GH. Scrotal trauma and reconstruction. In: Graham DS, ed. Glenn’s Urologic Surgery. 5th ed. Philadelphia, PA: Lippincott William & Wilkins; 1998:539. 72. Scott RF Jr, Selzman HM. Complications of nephrectomy: review of 450 patients and a description of a modification of the transperitoneal approach. J Urol. 1966;95:307. 73. Corriere JN, McAndrew JD, Benson GS. Intraoperative decision making in renal trauma surgery. J Trauma. 1991;31:1390. 74. Evans LA, Ferguson KH, Foley JP, et al. Fibrin sealant for the management of genitourinary injuries, fistulas and surgical complications. J Urol. 2003;169:1360. 75. Ramanathan R, Leveillee RJ. A review of methods for hemostasis and renorrhaphy after laparoscopic and robot-assisted laparoscopic partial nephrectomy. Curr Urol Rep. 2010;11:208. 76. Rosen MA, McAninch JW. Management of combined renal and pancreatic trauma. J Urol. 1994;152:22. 77. Wessels H, McAninch JW. Effect of colon injury on the management of simultaneous renal trauma. J Urol. 1996;155:1852. 78. Knudson MM, Harrison PB, Hoyt DB, et al. Outcome after major renovascular injuries: a Western trauma association multicenter report. J Trauma. 2000;49:1116. 79. Quesada ET, Coburn M. Bilateral penetrating renal injuries. In: South Central Section, American Urological Association 1993 Annual Meeting; 1993; Acapulco, Mexico. 80. Elliott S, McAninch JW. Ureteral injuries from external violence: the 25-year experience from San Francisco General Hospital. J Urol. 2003;170:1213. 81. Pereira BM, Ogilvie MP, Gomez-Rodriguez JC, et al. A review of ureteral injuries after external trauma. Scand J Trauma Resusc Emerg Med. 2010;2:18. 82. Brenneman FD, Katyal D, Boulander BR, et al. Long-term outcomes in open pelvic fractures. J Trauma. 1997;42:773. 83. Jordan GH, Schlossberg SM, Devine CJ. Surgery of the penis and urethra. In: Walsh PC, Retik AB, Vaughan ED, et al., eds. Campbell’s Urology. 7th ed. Philadelphia, PA: Saunders; 1998:3316. 84. Koraitim MM. Predictors of surgical approach to repair pelvic fracture urethral distraction defects. J Urol. 2009;182:1435. 85. Martinez-Pineiro L, Djakovic N, Plas N, et al. EAU guidelines on urethral trauma. Eur Urol. 2010;57:791–803 [Epub January 20, 2010]. 86. Follis HW, Koch MO, McDougal WS. Immediate management of prostatomembranous urethral disruptions. J Urol. 1992;147:1259. 87. Porter JR, Takayama TK, Defalco AJ. Traumatic posterior urethral injury and early realignment using magnetic urethral catheters. J Urol. 1997;158:425. 88. Jepson BR, Boullier JA, Moore RG, et al. Traumatic posterior urethral injury and early primary endoscopic realignment: evaluation of longterm follow-up. Urology. 1999;53:120–125. 89. Gheiler EL, Frontera JR. Immediate primary realignment of prostatomembranous urethral disruptions using endourologic techniques. Urology. 1997;49:596. 90. Corriere JN Jr, Rudy DC, Benson GS. Voiding and erectile function after delayed one-stage repair of posterior urethral disruptions in 50 men with a fractures pelvis. J Trauma. 1994;37:587. 91. Webster GD, Mathes GL, Selli C. Prostatomembranous urethral injuries: a review of the literature and a rational approach to their management. J Urol. 1983;130:898. 92. Phonsombat S, Master VA, McAninch JW. Penetrating external genital trauma: a 30-year single institution experience. J Urol. 2008;180:192. 93. Cerwinka WH, Block NL. Civilian gunshot injuries of the penis: the Miami experience. Urology. 2009;73:877. 94. Romilly CS, Isaac MT. Male genital self-mutilation. Br J Hosp Med. 1996;55:427. 95. Jordan GH, Gilbert DA. Management of amputation injuries of the male genitalia. Urol Clin North Am. 1989;16:359. 96. Lin WW, Kim ED, Quesada ET, et al. Unilateral testicular injury from external trauma: evaluation of semen quality and endocrine parameters. J Urol. 1998;159:841.

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36. Carroll PR, McAninch JW. Major bladder trauma: mechanisms of injury and a unified method of diagnosis and repair. J Urol. 1984;132:254. 37. Cass AS. The multiple injured patient with bladder trauma. J Trauma. 1984;24:731. 38. Cass AS, Luxenberg M. Features of 164 bladder ruptures. J Urol. 1987;138:743. 39. Spiguel L, Glynn L, Liu D, et al. Pediatric pelvic fractures: a marker for injury severity. Am Surg. 2006;72:481. 40. Demetriades D, Karaiskakis M, Velmahos GC, et al. Pelvic fracture in pediatric adult trauma patients: are they different injuries? J Trauma. 2003;54:1146. 41. Carroll PR, McAninch JW. Major bladder trauma: the accuracy of cystography. J Urol. 1983;130:887. 42. Peng MY, Parisky YR, Cornwell EE, et al. CT cystography versus conventional cystography in evaluation of bladder injury. AJR Am J Roentgenol. 1999;173:1269. 43. Patel H, Bhatia N. Universal cystoscopy for timely detection of urinary tract injuries during pelvic surgery. Curr Opin Obstet Gynecol. 2009;21:415. 44. Mundy AR, Andrich DE. Pelvic fracture-related injuries of the bladder neck and prostate: their nature, cause and management. BJU Int. 2010;105:1302. 45. Cass AS, Luxenberg M. Testicular injuries. Urology. 1991;27:528. 46. McAninch JW, Carroll PR. Renal exploration after trauma: indications and reconstructive techniques. Urol Clin North Am. 1989;16:203. 47. Husmann DA, Gilling PJ, Perry MO, et al. Major renal lacerations with devitalized fragments following blunt abdominal trauma: a comparison between non-operative (expectant) versus surgical management. J Urol. 1993;150:1774. 48. Alsikafi NF, McAninch JW, Elliott SP, et al. Nonooperative management outcomes of isolated urinary extravasation following renal lacerations due to external trauma. J Urol. 2006;176:2497. 49. Baverstock R, Simons R, McLoughlin M. Severe blunt renal trauma: a 7-year retrospective review from a provincial trauma center. Can J Urol. 2001;8:1372. 50. Eassa W, El-Ghar MA, Jednak R, et al. Nonoperative management of grade 5 renal injury in children: does it have a place? Eur Urol. 2010;57:154. 51. Shirazi M, Sefidbakht S, Jahanabadi Z, et al. Is early reimaging CT scan necessary in patients with grades III and IV renal trauma under conservative treatment? J Trauma. 2010;68:9. 52. McAninch JW, Carroll PR, Klosterman PW, et al. Renal reconstruction after injury. J Urol. 1991;145:932. 53. Steers WD, Corriere JN, Benson GS, et al. The use of indwelling ureteral stents in managing ureteral injuries due to external violence. J Trauma. 1985;25:1001. 54. Parpala-Sparman T, Paananen I, Santala M, et al. Increasing numbers of ureteric injuries after the introduction of laparoscopic surgery. Scand J Urol Nephrol. 2008;42:422. 55. Cass AS. Ureteral contusion with gunshot wounds. J Urol. 1984;24:59. 56. Hayes EE, Sandler CM, Corriere JN Jr. Management of the ruptured bladder secondary to blunt abdominal trauma. J Urol. 1983; 129:946. 57. Corriere JN Jr, Sandler CM. Management of the ruptured bladder: 7 years experience with 111 cases. J Trauma. 1986;26:830. 58. Merchant WC, Gibbons MD, Gonzales ET. Trauma to the bladder neck, trigone and vagina in children. J Urol. 1984;131:747. 59. Kotkin L, Koch MO. Morbidity associated with nonoperative management of extraperitoneal bladder injuries. J Trauma. 1995;38:895. 60. Appeltans BMG, Schapmans S, Willemsen PJ, Verbruggen PJ, Denis LJ. Urinary bladder rupture: laparoscopic repair. Br J Urol. 1998;81:764. 61. Helen MH, Bayne A, Cisek LJ, et al. Bladder injuries during laparoscopic orchiopexy: incidence and lessons learned. J Urol. 2009;182:280. 62. DeConcini DT, Coburn M. Penetrating bladder trauma: indications for non-operative management. In: South Central Section, American Urological Association 1997 Annual Meeting; 1997; Bermuda. 63. Pierce JM Jr. Disruptions of the anterior urethra. Urol Clin North Am. 1989;16:329. 64. Elgammal MA. Straddle injuries to the bulbar urethra: management and outcome in 53 patients. Int Braz J Urol. 2009;35:450. 65. Shlamovitz GZ, McCullough L. Blind urethral catheterization in trauma patients suffering from lower urinary tract injuries. J Trauma. 2007;62:330. 66. Husmann DA, Boone TB, Wilson WT. Management of low velocity gunshot wounds to the anterior urethra: the role of primary repair versus urinary diversion alone. J Urol. 1993;150:70.

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97. Coburn M, Guerriero WG. Complications of genitourinary trauma. In: Mattox KL, ed. Complications of Trauma. New York: Churchill Livingstone; 1994:533. 98. Brewer ME Jr, Stmad BT, Daley BJ, et al. Percutaneous embolization for the management of grade 5 renal trauma in hemodynamically unstable patients: initial experience. J Urol. 2009;181:1737. 99. Nuss GR, Morey AF, Jenkins AC, et al. Radiographic predictors of need for angiographic embolization after traumatic renal injury. J Trauma. 2009;67:578. 100. Rotondo MF, Zonies DH. The damage control sequence and logic. Surg Clin North Am. 1997;77:761. 101. Soderdahl DW. The current spectrum of battlefield urological injuries. J Trauma. 2007;62(6 suppl):S43.

102. Tezval H, Tezval M, von Klot C, et al. Urinary tract injuries in patients with multiple trauma. World J Urol. 2007;25:177. 103. Arthurs Z, Kjorstad R, Mullenix P, et al. The use of damage-control principles for penetrating pelvic battlefield trauma. Am Surg. 2006;191:604. 104. Coburn M. Damage control for urologic injuries. Surg Clin North Am. 1997;77:821. 105. Ball CG, Hameed SM, Navsaria P, et al. Successful damage control of complex vascular and urological gunshot injuries. Can J Surg. 2006;49:437.

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Trauma in Pregnancy M. Margaret Knudson and Daniel Dante Yeh

Penetrating injuries to the gravid uterus date back to antiquity, when wounding instruments included spears, sticks, and animal horns. Ambroise Paré, famous for his skills as a military surgeon, was also an obstetrician and was among the first to describe the treatment of gunshot wounds to the uterus. Paré wrote, “When the womb is wounded, the blood cometh out at the privites, and all other accidents appeared … ”1 Maternal deaths resulting directly from pregnancy or the complications of labor and delivery have declined sharply in recent years. In the United States, the absolute risk of pregnancyrelated death is estimated currently at 11.8 deaths per 100,000 live births, a reduction in death rate by 99% since 1900.2,3 In contrast, trauma has emerged as the leading cause of death during pregnancy, accounting for nearly 50% of maternal deaths in the United States and over 1 million deaths annually worldwide.3,4 An estimated 6–7% of pregnancies are complicated by trauma with 0.4% of all pregnant patients requiring hospitalization for the treatment of injuries.5 Interestingly, the incidence of trauma increases with each pregnancy trimester, with only 8% of injuries occurring during the first trimester and over 50% during the third trimester.6 The true number of injured gravid women is grossly underestimated by these figures, however, as many injuries are unreported, especially those resulting from domestic violence. Thus, it is essential that all trauma care professionals recognize the anatomic and physiologic changes unique to pregnancy and appreciate how these changes impact the evaluation and treatment of the injured gravid patient. Complete evaluation of these patients includes an assessment of the fetus, and the treating physician must not only be cognizant of the signs of fetal distress, but must also be able to make rapid interventions in the interest of saving both mother and baby.

EPIDEMIOLOGY OF TRAUMA IN PREGNANCY Weiss et al.7 examined data from the Pennsylvania state trauma registry and found that, among a total of 16,722 women of childbearing age who required hospitalization for injuries over a 1-year period, 761 were pregnant (4.6%). The leading causes of injury among pregnant women in this series were transportation-related (33.6%), falls, and assaults. Younger women (mean age 25) appeared to be at higher risk for injuries when compared to older gravid women. In a recent study from the state of Utah, pregnant women with an injury-related visit to an emergency department (ED) were more likely than noninjured women to experience preterm labor, placental abruption, and cesarean delivery, and infants born to women who were injured were more likely to be born preterm.8 In a related study that included data from 16 states, 240 trauma-related fetal deaths were identified (3.7 fetal deaths per 100,000 live births).9 Motor vehicle crashes were again the leading mechanism resulting in fetal death (82% of cases), followed by firearms (6%) and falls (3%). Placental injury was mentioned in 100 cases, and maternal death was the cause of fetal death in 11% of the cases. Again, pregnant mothers ages 15–19 years appeared to be at greatest risk for trauma-related fetal loss. Young pregnant women are at significant risk of sustaining injuries as the result of an assault also. Battering can begin or escalate during pregnancy, and it is estimated that between 10 and 30% of women are abused during pregnancy, with fetal death occurring in 5%.10 In a series of 41 injury-related deaths during pregnancy reported from North Carolina, half of the patients were known or suspected of having been abused.11 Physical abuse is suggested by proximal and midline injuries rather than distal injuries, trauma to the neck, breast

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and face, and injuries to the upper arms and lateral thighs. Cigarette burns and bites should raise the level of suspicion for the examiner also.12 A history of depression, substance abuse, or frequent visits to the ED are other factors that suggest domestic violence. Domestic violence is not dependent on age, race, or marital status and cuts across all socioeconomic classes. Thus, it is imperative that all health care providers recognize the signs and symptoms of physical abuse and the opportunity to intervene and protect both the mother and her fetus (see Chapter 46). Chang et al.13 recently summarized data from the Pregnancy Mortality Surveillance System at the Centers for Disease Control and Prevention (CDC), focusing on risk factors for pregnancy-associated homicide. According to this report, homicide was the third leading cause of injury-related death for all women of childbearing age, pregnant or not. The pregnancy-associated homicide ratio was 1.7 per 100,000 live births. Risk factors for homicide in this group included age younger than 20 years, black race, and either late or no prenatal care, and firearms were the leading mechanism (56.5%). It is hoped that the new surveillance system developed by the CDC, the National Violent Death Reporting System, which captures information about pregnancy status, victim–perpetrator relationships, and the presence of intimate partner violence, will provide more comprehensive data on this important mechanism of injury among women. Ikossi et al.14 utilized the American College of Surgeons’ National Trauma Data Bank (NTDB) to develop a profile of mothers

at risk for injury during pregnancy. Among the 77,321 women of childbearing age who were hospitalized after injury, 1,195 (1.5%) were pregnant. The major mechanism of injury among the pregnant patients was a motor vehicle crash (70%), followed by interpersonal violence (11.6%) and falls (9.3%). Young age, African American or Hispanic ethnicity, and insurance status (none or underinsured) identified women at highest risk for injury during pregnancy, and these groups are most likely to benefit from efforts at primary trauma prevention (see below).

ANATOMIC AND PHYSIOLOGIC CHANGES UNIQUE TO PREGNANCY Although the initial assessment and management priorities for resuscitation of the injured pregnant patient are the same as those for other traumatized patients (see Chapter 10), the specific anatomic and physiologic changes that occur during pregnancy may alter the response to injury and, hence, necessitate a modified approach to the resuscitation process. Most of these anatomic, physiologic, and biochemical adaptations occur in response to physiologic stimuli provided by the fetus. An understanding of these adaptations (summarized in Table 37-1) is necessary in order to provide appropriate and timely care to both mother and unborn child. Although nearly every system in the body is affected by pregnancy, the most important changes involve the cardiovascular, pulmonary, and reproductive systems.

TABLE 37-1 Summary of Normal Physiologic Changes During Pregnancy System Cardiovascular Blood volume Coagulation Respiratory

Gastrointestinal Hepatobiliary

Renal

Endocrine Musculoskeletal

Change ↓ Peripheral vascular resistance, ↓ venous return, ↓ blood pressure (10–15 mm Hg) ↑ Plasma volume, RBC volume, ↑ WBC (20,000 cells/mm3) Hypercoagulable; ↑ fibrinogen; ↑ factors VII, VIII, IX, X, XII; ↓ fibrinolysis ↑ Subcostal angle (68–103°), ↑ chest circumference (5–7 cm), ↑ diaphragmatic excursion (1–2 cm), elevated diaphragm, ↑ tidal volume, ↑ minute ventilation, ↓ FRC, ↓ PCO2, HCO3 ↓ Motility, ↓ intestinal secretion, ↓ nutrient absorption, ↓ sphincter competency (progesterone) Organ displacement ↑ Gallbladder volume, ↓ gallbladder emptying, ↓ albumin, ↑ AP, ↓ bilirubin (free), ↓ GGT ↑ Glomerular filtration rate, ↑ renal plasma flow, ↑ creatinine clearance, ↓ serum creatinine, ↓ BUN ↑ Parathormone, ↑ calcitonin Pelvic ligaments soften (relaxin, progesterone)

Potential Implication Supine hypotensive syndrome (10–15 mm Hg) Physiologic hypervolemia may mask hypotension secondary to blood loss ↑ Venous thromboembolism Alteration in FRC and lung volume, chronic compensated respiratory alkalosis

Aspiration Clinical examination unreliable Cholestasis, ↑ cholestasis saturation, ↑ chenodeoxycholic acid, ↑ gallstones Hydronephrosis, hydroureter Dilation of collecting system Bladder/urethral muscle tone ↑ Calcium absorption Pelvic widening, lordosis, shift in center of gravity

AP  alkaline phosphatase; BUN  blood urea nitrogen; FRC  functional residual capacity; GGT  γ-glutamyltransferase; RBC  red blood cell; WBC  white blood cell.

Trauma in Pregnancy

■ Cardiovascular System

■ Respiratory System Several changes in the maternal respiratory system occur during pregnancy to meet increased oxygen requirements. As the uterus enlarges, the diaphragm rises about 4 cm and the diameter of the

■ Reproductive System By the end of full-term gestation, the weight of the uterus has increased to 20 times its prepregnancy weight (i.e., from 60 to about 1,000 g). After the 12th week of pregnancy, the uterus extends out of the pelvis, rotates slightly to the right, and ascends into the abdominal cavity to displace the intestines laterally and superiorly. At 10 weeks’ gestation, uterine blood flow is estimated to be about 50 mL/min. With progressive uterine enlargement, uterine blood flow increases dramatically to approximately 500 mL/min at term, constituting up to 17% of the cardiac output.23 Uterine veins may dilate up to 60 times their size in the pre-pregnant state, allowing for adequate venous drainage to accommodate the uteroplacental blood flow. This increased vascularity carries an attendant risk of massive blood loss with a pelvic injury.

INITIAL ASSESSMENT AND MANAGEMENT ■ Prehospital Care Prehospital care is an extension of the trauma system (see Chapter 4) and must be appropriately adapted to the needs of the injured gravid patient. In particular, the importance of providing an adequate airway and supplemental oxygen to prevent fetal hypoxia must take priority during field transport. Also, it is important to recognize that the relative hypervolemia of pregnancy may mask the usual signs and symptoms of acute blood loss. Thus, intravenous fluids should be given liberally during transport in these patients. A wedge placed under the right hip may help avoid the vena cava compressive syndrome described above. Any information on the length of the gestation and prenatal care and complications that can be obtained should be relayed to the receiving trauma center.

■ Primary Survey As with any other injured patient, the primary survey of the injured pregnant patient addresses the airway, breathing, and circulation, with the mother receiving treatment priority (see Chapter 10). Ensuring an adequate maternal airway with supplemental oxygen is essential for preventing maternal and

CHAPTER CHAPTER 37 X

Plasma volume begins to expand at 10 weeks’ gestation and increases by 45% at full-term as compared to pregravid levels.15 This hypervolemic state is protective for the mother, as fewer red blood cells are lost during hemorrhage and, hence, the oxygen-carrying capacity of her blood is less affected.16 Furthermore, the hypervolemia prepares the patient for the blood loss that accompanies a vaginal delivery (500 mL) or cesarean section (1,000 mL). This pregnancy-induced hypervolemia, however, may create a false sense of security for the resuscitating physician because almost 35% of maternal blood volume may be lost before there are signs of hypovolemic shock. This increase in plasma volume is accompanied by an erythroid hyperplasia in the bone marrow, resulting in a 15% increase in red blood cell mass and a “physiologic anemia.” This anemia of pregnancy is greatest at 30–32 weeks’ gestation and will be most significant in patients who have not received iron supplements.16 In addition, factors VII, VIII, IX, X, and XII, and fibrinogen are increased, fibrinolytic activity is reduced, and the net result is a hypercoagulable state, putting the patient at increased risk for thromboembolic events. During the first trimester, maternal pulse rate increases by about 10–15 beats/min and remains elevated until delivery. As the diaphragm becomes progressively more elevated secondary to the enlarging uterus, the heart is displaced to the left and upward, resulting in a lateral displacement of the cardiac apex. Moreover, each pregnant woman has some degree of a benign pericardial effusion. Both of these changes result in an enlarged cardiac silhouette and increased pulmonary vasculature on the chest x-ray.17 Maternal blood pressure decreases during the first trimester, reaches its lowest level in the second trimester, and then rises toward pre-pregnancy levels during the final 2 months of gestation. The mean blood pressure values are 105/60 mm Hg for the first trimester, 102/55 mm Hg for the second trimester, and 108/67 mm Hg for the third. By the end of the first trimester, cardiac output increases to 25% above normal. In the healthy gravida, this increased workload on the heart is welltolerated. When the patient is in the supine position and the inferior vena cava is partially obstructed by the gravid uterus, there is a decrease in blood return to the heart resulting in a lower cardiac output and causing the “supine hypotensive syndrome.” This syndrome is marked by dizziness, pallor, tachycardia, sweating, nausea, and hypotension. Turning the mother onto her left side restores the circulation and increases cardiac output by about 30% after 20 weeks’ gestation. A point worth emphasizing is that in the supine position, the enlarged uterus also compresses the aorta, reducing the pressure in the uterine arteries and decreasing blood flow to the fetus.18 Importantly, the uterine arteries are maximally dilated during pregnancy so that autoregulation is absent and thus blood flow to the fetus is entirely dependent upon maternal mean arterial blood pressure.6

chest enlarges by 2 cm, increasing the substernal angle by 50%.19 Care should be taken to consider these anatomic changes when thoracic procedures such as tube thoracostomies and thoracenteses are being performed. Functional residual capacity (FRC) decreases because of a decline in expiratory reserve and residual volumes. The net result is an unchanged arterial partial pressure of oxygen (PaO2), a reduction in the partial pressure of carbon dioxide (PCO2) to 30 mm Hg, and a slight compensatory decrease in plasma bicarbonate levels.20 Therefore, pregnancy is a state of partially compensated respiratory alkalosis. Relative to these changes, the injured gravida tolerates apnea poorly because of the reduced FRC. Hence, supplemental oxygen is always indicated for these patients. Due to the weight gain associated with pregnancy, the Mallanpati score increases, making intubation more difficult and increasing the incidence of fatal failed intubation by 13 times.21,22

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fetal hypoxia (see Chapter 11). Because the oxyhemoglobin dissociation curve for fetal blood is different from that for maternal blood, small increments in maternal oxygen concentration improve the blood oxygen content and reserve for the fetus, even though the maternal arterial oxygen content does not change appreciably. Of note, because pseudocholinesterase levels decrease during pregnancy, lower doses of succinylcholine may be used during rapid sequence intubation.24 As mentioned above, due to the expansion of the intravascular volume, signs of shock in the mother may be delayed until over 35% of blood loss has occurred; however, the fetus will be in jeopardy before this point. Thus, fluid and blood resuscitation should be vigorous. In late pregnancy, it is wise to refrain from the use of femoral catheters for resuscitation. Although the role of ED thoracotomy in pregnancy remains to be defined, it is the opinion of the authors that it should be considered in conjunction with perimortem cesarean section (see below).25

■ Secondary Survey and Maternal Assessment Following the primary survey of the patient and performance of life-saving measures, the secondary survey is initiated. This consists of obtaining a thorough history, including an obstetric history. An accurate prenatal history is crucial because comorbid factors such as pregnancy-induced hypertension, diabetes mellitus, and congenital heart disease may alter management decisions. Furthermore, a history of preterm labor, placental abruption, or placenta previa puts the patient at increased risk for the recurrence of these conditions. The obstetric history includes the date of the last menstrual period, expected date of delivery, and date of the first perception of fetal movement, and any problems or complications of the current and previous pregnancies. Whenever possible, the obstetrical team should be immediately notified and respond to the trauma room for patients in their second or third trimester of pregnancy. During the secondary survey, appropriate x-rays should be ordered as during any trauma evaluation, shielding the uterus whenever possible (see below). The Focused Assessment with Sonography in Trauma (FAST) examination (see Chapter 16) is strongly recommended during the secondary survey to detect pericardial or peritoneal fluid in the mother. Although there is some debate on the sensitivity of ultrasound in this setting, most report an 80% sensitivity and a 100% specificity in detecting fluid using the FAST examination during pregnancy.26 A small amount of free fluid in the pelvis may be normal during pregnancy, but this trace amount (7–21 mL) is too small to be detected during a routine transabdominal ultrasound examanition.27 Therefore, any amount of fluid seen on the FAST examination should be considered pathologic even during pregnancy. As part of the abdominal examination, determination of the uterine size provides an approximation of gestational age and fetal maturity. Measurement of fundal height is a rapid method for estimating fetal age. If, for example, the most superior part of the fundus is palpated at the umbilicus, the fetal age is estimated to be 20 weeks. A discrepancy between dates and uterine size may result from a ruptured uterus or intrauterine

hemorrhage. Determination of fetal age and fetal maturity is an important factor in the decision matrix regarding early delivery. In general, a 25-week-old fetus is considered viable if given neonatal intensive care. Fig. 37-1 contains a helpful algorithm summarizing the initial evaluation of the injured pregnant patient.

■ Evaluation of the Fetal–Placental Unit Evaluation of the state of the pregnancy focuses on the following: (a) vaginal bleeding; (b) ruptured membranes (amniotic sac); (c) a bulging perineum; (d) the presence of contractions; and (e) an abnormal fetal heart rate (FHR) and rhythm. These five conditions indicate the acute status of the pregnancy. Vaginal bleeding prior to labor is abnormal and may indicate premature cervical dilation, early labor, placental abruption (separation of the placenta from the uterine wall), or placenta previa (location of the placenta over a portion of the cervical os). A ruptured amniotic sac should be suspected when cloudy white or green fluid is observed coming from the cervical os or perineum. The presence of amniotic fluid can be confirmed by the change in color of nitrazine paper from blue–green to deep blue when the fluid is tested. Rupture of the amniotic sac is significant because of the potential for infection and prolapse of the umbilical cord, the latter being an obstetric emergency requiring immediate cesarean section. Bloody amniotic fluid is an indication of premature separation of the placenta (placental abruption) or placenta previa. In the presence of known or continuous meconium staining (green amniotic fluid), continuous electronic fetal monitoring is necessary. A bulging perineum is caused by pressure from a presenting part of the fetus. If this occurs during the first trimester, spontaneous abortion may be imminent. Assessment of the pattern of uterine contraction is accomplished by resting the hand on the fundus and determining the frequency, duration, and intensity of contractions. Contractions are usually rated as mild, moderate, or strong. Strong contractions are associated with true labor, and assessment for their presence is important so that appropriate preparation can be made for delivery and resuscitation of the neonate if necessary. The Kleihauer–Betke (KB) test is used after maternal injury to identify fetal blood in the maternal circulation (i.e., fetomaternal transfusion). Adult hemoglobin (HbA) is eluted in the presence of an acidic buffer, whereas fetal hemoglobin (HbF) is resistant to elution. Fetal cells containing HbF are stained with erythrosine, whereas maternal cells containing HbA fail to stain and remain as “ghost cells” in the peripheral smear. Because the KB test can determine the risk of isosensitization in Rh-negative gravidas, it is recommended for detecting imminent fetal exsanguination in injured pregnant patients who are Rh-negative in the second or third trimester. If positive, the KB test should be repeated after 24 hours to identify ongoing fetomaternal hemorrhage. The initial dose of Rh-immune globulin is 300 μg, with an additional 300 μg given for every 30 mL of fetomaternal transfusion estimated by the KB test. Although the KB test is a very sensitive marker for even a small amount of fetomaternal transfusion, its clinical utility in Rh-positive mothers is uncertain.28 Indeed, the usefulness of the KB test after injury

Trauma in Pregnancy

713

ALGORITHM FOR MANAGEMENT OF THE PREGNANT TRAUMA PATIENT

Urine βhcg positive OR patient is known/observed (examined) to be pregnant.

Priority during resuscitations is always given to the mother, and the determination of gestational age, initiation of FHR monitoring, etc. must be prioritized in the context of the severity of maternal injuries.

NO Standard trauma management guidelines

Obtain urine βhcg on all women of childbearing age of unknown pregnancy status

YES Determine gestional age by history (EDD) and U/S for biparietal diameter (BPD) Pt with known pregnancy ≥ 24 weeks or BPD ≥ 58 mm

NO

Minimize fetal exposure to radiation. Send type & screen. For gestational age > 16 weeks & Rh (-); Send Kleinhauer-Betke & notify OB for advice on admin. of Rhogam.

YES Utilize left lateral tilt position for mother to the extent possible to minimize caval compression.

NO

Hemodynamicaily normal or “responder”?

OB should be notified immediately of all pregnant trauma patients whose gestational age is thought to be at least 20 weeks. An OB consult should be obtained for all other pregnant patients once patient stable re: appropriate OB f/u. Page OB using OB BATCH PAGER. Enter the OB trauma code: “911-8111” During pregnancy, other imaging procedures not associated with ionizing radiation should be considered.

• Continue resuscitation per ATLS, type & screen mother, O neg for fetus. • IF patient continues to have signs of shock, manage according to needs of the mother, including OR as needed. • If patient requires OR, activate neonate resuscitation team

• Consider delivery of fetus if mother requires OR • Establilsh continuous fetal monitoring if not proceeding to delivery. vs. delivery if mother requires OR • Consider delivery of previable fetus (20–24 weeks) with persistent/recurrent shock and confounding abdominal injuries (e.g. fractures w/packing, major abd. Vascular injuries, need for ‘damage control’, etc.)

TO O.R. IMMEDIATELY • Vertical incision should be performed to facilitate trauma ex lap • Neonatal resuscitation team should be present

During initial evaiuation, FHR will be continuously monitored by OB nurse or MD (for all gestional age ≥24 wks.). If discontinued for any reason, the OB attending must be notified immediately. Indications for immediate delivery include: • fetal bradycardia <70 for >8 mins • maternal cardiac arrest >4 mins • suspected large abruption • other ominous FHT patterns (persistent late decels with absent or decreased variability, sinusoidal)

YES Continuous fetal heart and uterine contraction monitoring per OB service (w/OB consult) indications present for immediate delivery??

YES

NO Possible use of BMZ, formal US with peak systolic velocity of MCA, r/o abruption, serial CBC w/PLTLS, fibrinogen

Further w/u & imaging studies TBD by trauma, EM, & OB teams

NO Other maternal injuries identified?

Admit mother to L&D w/ongoing monitoring/observation, f/u

Minimal observation of FHT/ uterine contraction: is 6 hrs after time of event. Prolonged monitoring (24 hrs) maybe warranted if there is concerned for placental abruption/PTL

YES

-Admit to trauma service -OB service to determine plan for FHR monitoring in ICU or elsewhere

ADDITIONAL NOTES • Exposure to less than 5 rad has not been associated with an increase in fetal anomalies or pregnancy loss and is herein deemed to be safe at any point during the entirety of gestation. • Perimortem Cesarean section should be considered in any moribund pregnant woman of ≥24 weeks gestation. Delivery in perimortem cesarean sections must occur within 20 minutes of maternal death but should ideally start within 4 minutes of the maternal arrest. Fetal neurological outcome is related to delivery time after maternal death. • Delivery of fetus at less than 24 weeks gestation is indicated to assist the resuscitation of a critically injured pregnant woman (i.e.: mother with HD instability proving difficult to manage (i.e., pelvic fracture, splenic laceration with pt's abd open; s/p splenectomy, packing pelvis with persistent hypotension), as delivery will lead to the extraction of a non-viable infant.

FIGURE 37-1 Algorithm for the initial evaluation and resuscitation of the injured mother and fetus.

has been challenged recently by several authors. Authors from the R Adams Cowley Shock Trauma Center in Baltimore reported that among 46 injured women who were KB-positive on admission, 44 had documented contractions.29 In that study, KB testing accurately predicted the risk of preterm labor after maternal trauma, whereas clinical assessment was insensitive in identifying women at risk for this complication. On the other hand, a recent study from Cincinnati documented that 5% of low-risk women had a positive KB test, compared to only 2.6% of injured patients.30 None of these positive results were associated with a clinical abruption or fetal distress. The authors concluded that the presence of a positive KB test alone does not necessarily indicate pathologic fetal–maternal hemorrhage in

patients with trauma, and that its routine use after injury should be abandoned.31 Unfortunately, direct assessment of the fetus following trauma is somewhat limited. Currently, the most valuable information regarding fetal viability can be obtained by a combination of monitoring of the FHR and ultrasound imaging. Fetal heart tones can be detected with a Doppler device around the 12th week of pregnancy. The normal FHR is between 120 and 160 beats/min. Because the fetal stroke volume is fixed, the initial response to the stress of hypoxia or hypotension is tachycardia. Severe hypoxia in the fetus, however, is associated with bradycardia (FHR 120 beats/min) and should be recognized as fetal distress, demanding immediate attention.

CHAPTER CHAPTER 37 X

WOMEN OF CHILDBEARING AGE: Prioritized management of airway, breathing, & fluid resuscitation (circulation)

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Management of Specific Injuries

SECTION 3 X

Initial FHR monitoring of all pregnant patients with potentially viable pregnancies (i.e., those that would survive if emergency delivery was required) is indicated, even following relatively minor abdominal trauma. This monitoring is best accomplished using cardiotocographic (CTM) devices, which record both uterine contractions and FHR. A lack of variability in heart rate may also indicate fetal distress, and if there is no response to conservative measures such as fluid administration, increasing inspired oxygen, or change in maternal position, an emergency delivery should be considered (Fig. 37-2). Blunt trauma to the abdomen can result in uterine rupture, but this event is uncommon, unlikely to be missed, and usually rapidly fatal for the fetus. A much more common event is placental separation from the uterus as the result of the shearing forces following blunt injury. This separation is termed placental abruption. Major cases of placental abruption (i.e., 50% separation) are uniformly fatal for the fetus, but more minor cases may initially go undetected. Vaginal bleeding is an unreliable sign of placental abruptions, occurring in only 35% of cases.25 On the other hand, in patients with placental abruption following trauma, CTM will detect early fetal distress, often manifested as a decelerated heart rate associated with uterine contractions. Most cases of placental abruption become evident within several hours of trauma, although late cases have been reported.25,32,33 A minimum of 24 hours of CTM is recommended for patients with frequent uterine activity (6 contractions per hour), abdominal or uterine tenderness, vaginal bleeding, or hypotension.34 A study of 271 pregnant patients who had sustained blunt trauma identified the following risk factors for fetal loss: ejections, motorcycle and pedestrian collisions, maternal tachycardia, abnormal FHR, lack of restraints, Injury Severity Score (ISS) 9, gestational age 35 weeks, and a history of assaults.35 Patients with any of these risk factors should be monitored for at least 24 hours. In the absence of these factors, asymptomatic trauma patients should undergo at least 6 hours of CTM prior to considering discharge. These patients should be counseled to observe for decreased fetal movement, vaginal bleeding, abdominal pain, or frequent uterine contractions, as partial placental lacerations have been reported to progress over time.36

■ Ultrasonography High-resolution real-time ultrasonography (US) has proven valuable for the assessment of fetal age and well-being, recognition and categorization of fetal abnormalities, and treatment of disease processes in the unborn patient. In the trauma setting, US is used primarily to identify acute problems that may be due to maternal events such as placental abruption, placenta previa, or cord prolapse. Although placental abruption is difficult to detect, US can accurately locate the lower margin of the placenta and its relation to the cervical os, hence demonstrating placenta previa.37 Additionally, it is routine to evaluate the fetus for gestational age, cardiac activity, and movement. In a study of 216 patients with high-risk pregnancies, fetal biophysical profile scores corresponded well with perinatal outcome.38 US findings consistent with uteroplacental injury may include

oligohydramnios secondary to uterine injury or ruptured membranes. Oligohydramnios should be suspected if less than a 1-cm layer of amniotic fluid surrounds the fetus.

■ Radiographic Examination Following the secondary survey and the initial assessment of the fetus, appropriate diagnostic studies should be utilized to fully evaluate the extent of maternal injuries. Although there is much concern about radiation exposure during pregnancy, a diagnostic modality deemed necessary for maternal evaluation should not be withheld on the basis of its potential hazard to the fetus. There are three phases of radiation damage related to the gestational age of the fetus.39 During preimplantation and early implantation (less than 3 weeks’ gestational age), exposure to radiation can result in death of the embryo. During organogenesis (from 316 weeks’ gestation), radiation can damage the developing fetal tube and results in the associated anomalies of exencephaly, dysraphism, single cerebral ventricle, hydrocephaly, and the hypoplastic brain syndrome. Skeletal and genital abnormalities, retinal pigmentation, and cataracts are associated with radiation received during the third and eleventh weeks of gestation. After 16 weeks, neurologic defects are the most common complications of radiation exposure, due to the sensitivity of neuroblasts, which persist in the human embryo from 16 days postconception to about 2 weeks after birth.39 Prenatal x-ray exposure may also be associated with the later development of childhood cancers.40 Most of the human data on exposure to radiation is based on the large doses received in an atomic bomb blast (which includes neutrons and gamma ray), rather than on doses applied during normal diagnostic (x-ray) studies. The rad is the unit of measurement for absorbed radiation and corresponds to an energy transfer of 100 erg/g of tissue. Absorbed radiation is expressed in Gray (Gy) units, with 1 Gy equal to 100 rad. The dose to the uterus/fetus from x-ray procedures depends on several factors, including the x-ray tube potential, the current, the exposure time, the size of the patient, the type of procedure, the source-to-film distance, and the type of x-ray generator (Table 37-2). It is estimated that the fetal radiation dose without shielding is 30% of that to the mother. The American College of Obstetricians and Gynecologists (ACOG) has produced a consensus statement on the use of diagnostic imaging during pregnancy.41 The authors emphasize the fact that most diagnostic radiologic procedures are associated with little, if any, known significant fetal risk. Specifically, exposure of the fetus to less than 5 rad has not been associated with an increase in fetal anomalies or pregnancy loss. A plain x-ray generally exposes the fetus to very little radiation, and the uterus is shielded for nonpelvic procedures during pregnancy. With the exception of a barium enema or small bowel series, most fluoroscopic examinations result in fetal exposure of just millirads. Radiation exposure from CT varies depending on the number and spacing of adjacent image sections (see Table 37-2). CT pelvimetry can result in fetal exposures as high as 1.5 rad but can be reduced by using a low-exposure technique as outlined by Moore and Shearer.42 Radiation exposure using helical CT is affected by slice

Trauma in Pregnancy

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CHAPTER CHAPTER 37 X

A

B

FIGURE 37-2 (A) Cardiotocographic strip demonstrating poor beat-to-beat variability in the fetus. (B) Return of beat-to-beat variability after resuscitation; variable decelerations with uterine contractions are within normal limits.

thickness, the number of cuts obtained, and the pitch (a ratio defined as the distance the couch travels during one 360° rotation divided by the section thickness). Thus, CT can be used, when indicated to diagnose both maternal and fetal injuries as well as evaluating the placenta.

In summary, the ACOG Committee recommends the following: • Women should be counseled that x-ray exposure from a single diagnostic procedure does not result in harmful fetal

716

Management of Specific Injuries

TABLE 37-2 Estimated Fetal Exposure From Some Common Radiologic Procedures

SECTION 3 X

Procedure Chest x-ray (anteroposterior/lateral) Abdominal plain x-ray Hip x-ray (single view) Head or chest CT Abdomen and lumbar spine CT Pelvis CT Anteroposterior pelvis Complete spine series

Fetal Exposure 0.02–0.07 mrad 100 mrad 200 mrad 1 rad 3.5 rad 0.25–1.5 rad 0.04 rad 0.37 rad

CT  computed tomography. Reprinted with permission from Desai P, Suk M. Orthopedic trauma in pregnancy. Am J Orthop. 2007;36:E162. Copyright © 2007 Quadrant HealthCom Inc. All rights reserved.

effects. Exposure to less than 5 rads is not harmful to the fetus or the pregnancy. • Concern about possible effects of high-dose ionizing radiation should not prevent medically indicated diagnostic x-ray procedures from being performed during pregnancy. • Other imaging procedures not associated with ionizing radiation, such as US or magnetic resonance imaging, which are not associated with known adverse fetal effects, should be utilized when appropriate. • Consultation with an expert in dosimetry calculation may be helpful when multiple diagnostic x-rays are required.41 For a more complete review of the effects of ionizing radiation in pregnancy, readers are referred to the recent publications by De Santis et al.43 and Mann et al.44 For the injured patient, the following guidelines are suggested: 1. The minimum number of x-rays should be ordered to obtain the maximum information. Careful planning prevents duplication. 2. The patient’s abdomen should be shielded with a lead apron. This reduces fetal exposure by a factor of 8. 3. When many x-rays are required over a long period, a thermoluminescent dosimeter or “radiation badge” may be attached to the patient to serve as a guide to the dosage of radiation delivered. This is particularly valuable for the critically ill patient, who may have a prolonged stay in the intensive care unit.

MANAGEMENT OF SPECIFIC INJURIES DURING PREGNANCY ■ Thoracic Trauma The management of thoracic trauma during pregnancy differs little from the nonpregnant state; however, strict attention to

oxygenation is essential in order to avoid fetal hypoxia (see above). Additionally, during placement of thoracostomy tubes in late pregnancy, the elevated location of the diaphragm must be considered. A few cases of traumatic aortic rupture during pregnancy have been reported, and there is evidence to suggest changes in the aortic wall during this period may make women particularly prone to these injuries.45

■ Blunt Abdominal Trauma Once diagnosed, the management of abdominal injuries during pregnancy differs little from the nonpregnant state. Nonoperative management of injuries to solid organs (liver, spleen, kidney) has been performed successfully in the gravid state and should be considered the treatment of choice in stable patients with these injuries (Fig. 37-3). In contrast, unstable patients or those in whom an intestinal injury is likely benefit from early operative treatment, as both hypotension and intraabdominal infection can be harmful and potentially lethal to the fetus. As with any other emergency laparotomy during pregnancy (i.e., for acute appendicitis, cholecystitis, etc.), the uterus should be left intact, unless it is directly injured or it presents a mechanical limitation for treatment of maternal injuries. The indications for cesarean section following trauma are discussed below. Although the experience with abdominal operative procedures in injured pregnant patients is generally limited, the data about the safety and timing of other nonobstetrical abdominal surgeries in pregnancy are available. A review of 77 patients requiring laparotomy demonstrated that preterm labor occurred in 26% of the second-trimester patients and 82% of the thirdtrimester patients.46 Preterm labor was most common in patients with appendicitis. Although preterm labor was significantly higher in the last trimester, fetal loss was not. The authors concluded that the severity of the underlying disease, not the operation, was the most important factor in determining fetal and maternal outcome. There are also important anesthetic considerations when performing surgery during pregnancy. The basic objectives in the anesthetic management of these patients include the following: (a) maternal safety; (b) avoidance of teratogenic drugs; (c) avoidance of intrauterine fetal asphyxia; and (d) prevention of preterm labor.47 Although a complete review of this subject is beyond the scope of this chapter, most studies to date indicate that surgery and anesthesia during pregnancy are unlikely to be associated with an increased incidence of congenital anomalies but may produce a slightly increased risk of miscarriage. When emergency surgery is required, the optimal anesthetic for the mother should be chosen and modified by considerations for maternal physiologic changes and fetal well-being.47 An obstetrician and/ or perinatologist should be consulted if there is time, and intraoperative fetal and uterine monitoring should be standard.

■ Pelvic Fractures The management of a pelvic fracture following blunt trauma may be particularly challenging during late pregnancy. Hemorrhage from massively dilated retroperitoneal vessels

Trauma in Pregnancy

717

CHAPTER CHAPTER 37 X

B

A

IUP: spine, femurs

Liver Laceration, Grade III, 6.2cm

C

D

FIGURE 37-3 (A) Left upper quadrant ultrasound examination of an injured gravid patient demonstrating fluid above the spleen. (B) Ultrasound of the fetus in the same patient showing ample amount of amniotic fluid and intact pregnancy. (C) Abdominal CT of the mother showing liver laceration as cause of the free fluid (blood) seen on ultrasound. (D) CT of fetus showing no injuries. Mother and fetus recovered completely with no surgical intervention. CT  computed tomography.

can obviously cause hemorrhagic shock.48 And, pelvic fracture is the most common injury to the mother that results in fetal death, with a fetal mortality rate as high as 35%.49 Fetal death may result indirectly from maternal shock or placental laceration or may be caused by direct injury to the head of the fetus. Although management of hemorrhage may include pelvic angiography and embolization of bleeding vessels, the dose of radiation associated with this approach usually exceeds the threshold that is considered safe during pregnancy, and these patients should be appropriately counseled. Operative fixation of unstable pelvic fractures, including acetabular fractures, has been reported during pregnancy, with good outcomes for both the mother and the fetus.50,51 The dose of radiation can be minimized and procedures chosen that do

not rely heavily on radiographic control. A recent review concluded that when operative therapy for pelvic fracture is indicated, both the timing of the operation in relationship to delivery and the operative approach may need to be altered.52 Some of these patients have gone on to have normal vaginal deliveries within weeks of their surgery to fixate a pelvic fracture (Fig. 37-4).

■ Fetal Injuries Following Blunt Trauma The fetus is generally well protected from blunt forces by the pelvic bones (until the third trimester) and by the cushion of amniotic fluid. Only 1% of blunt injuries to the abdomen are associated with direct fetal injuries.24 Occasionally, blunt

718

Management of Specific Injuries

SECTION 3 X FIGURE 37-4 X-ray of a patient in her third trimester sustaining a crush injury during the Haiti earthquake. Note the pelvic and femur fractures as well as the fetal head in the pelvis (arrow). A healthy baby was later delivered by cesarean section.

trauma to the fetus may result in fractures of the extremities or skull, although these usually occur in late pregnancy, especially when the head is engaged. Severe blunt trauma occasionally causes rupture of the uterus. Manifestations of uterine rupture include severe maternal shock, a uterus small for dates, and presence of fetal parts outside the uterus. Although the diagnosis of this catastrophic event is usually not difficult, ultrasound is very sensitive in detecting uterine rupture and the presence of intraperitoneal hemorrhage in less severe cases.53 More commonly, blunt abdominal trauma causes separation of the placenta from the relatively inelastic uterine wall, a condition termed placental abruption (or abruptio placenta). Although minor placenta abruptions may be tolerated by the fetus, major abruptions are the most common cause of fetal death if the mother survives. Separation of the placenta from the uterus reduces the area for fetomaternal exchange of respiratory gases and delivery of nutrients for the fetus. Perinatal death associated with placental abruption may be due to anoxia, prematurity, or exsanguination. The manifestations of placental abruption include vaginal bleeding (which may be relatively minor), abdominal pain, uterine tenderness, and contractions.54 Disseminated intravascular coagulation is one of the most serious complications associated with abruption, as thromboplastins from the injured placenta enter into the maternal circulation. In the absence of clinical symptoms, a pelvic ultrasound examination may be useful but will miss minor abruptions. As discussed earlier in the chapter, CTM is the most useful method of detecting clinically silent cases of placental separation that result in fetal distress.

■ Penetrating Trauma As the uterus expands out of the pelvis in the later stages of pregnancy, it frequently becomes the target for penetrating trauma. The maternal death rate from both gunshot wounds and stab wounds is lower than that of nonpregnant patients,

likely due to the fact that the uterus is frequently targeted rather than other abdominal organs.24 Low-velocity stab wounds rarely penetrate the thick uterine wall and usually present little risk to either the mother or her unborn child. Death of the mother after abdominal gunshot wounds is similarly uncommon, as only 20–30% have injuries outside of the uterus.55 In contrast, gunshot wounds to the upper abdomen can result in severe maternal damage, as the abdominal organs and vasculature are compressed into this small space. Up to 70% of fetuses will sustain injuries following abdominal gunshot wounds, and 40–65% will die, depending on the injury and the degree of prematurity.56 If the bullet has penetrated the uterus and the fetus is both viable and alive, cesarean section should be performed and the baby’s injuries addressed surgically, if indicated. Successful outcome with this approach has been reported. A nonoperative approach has been advocated when the entry site of a penetrating wound is anterior and below the uterine fundus, and when there is no evidence of fetal distress, but this approach should be restricted to high-volume trauma centers with close collaboration between experienced trauma surgeons and obstetricians.25 There have also been isolated reports of successful damage control laparotomy with open abdomens in pregnant patients.57

■ Neurologic Injury During Pregnancy The multi-institutional study by Kissinger et al.58 was the first to demonstrate the adverse effect of moderate and severe (Glasgow Coma Scale Score 12) trauma to the brain on fetal outcome. Severe injury to the brain was a significant risk factor for pregnancy loss in the investigation conducted by Ikossi et al.14 also. Certainly, maternal hypothalamic and pituitary dysfunction may accompany catastrophic brain injuries, and replacement of cortisone, thyroid, and vasopressin hormones may be required.59 Kelly et al.60 examined the function of both the anterior and posterior pituitary glands of 22 trauma patients of both sexes and demonstrated some degree of hypopituitarism in 40% of patients with moderate-to-severe traumatic brain injuries. Growth hormone and gonadotrophic deficiencies were the most commonly observed disorders. In addition, nutritional support, seizure control, and avoidance of infections and thrombotic complications are required in the care of the pregnant patient with a traumatic brain injury to ensure normal growth and development of the fetus. Because severe hyperventilation leads to a reduction in uterine blood flow through a mechanical reduction in venous return and subsequent decrease in cardiac output, the effective range of hyperventilation is reduced in pregnancy. Hypothermia and mannitol should both be avoided in pregnancy, whereas hypertonic saline has no known deleterious effects.61 The care of the pregnant patient with an acute injury to the spinal cord (see Chapter 23) is challenging, as well. For an extensive review of this subject, readers are referred to the excellent articles by Popov et al.62 and Gilson et al.63 In brief, inotropic agents such as dopamine and dobutamine may be required for blood pressure support in patients in spinal shock. These agents appear to be safe in pregnancy, as they do no reduce uterine perfusion and are not associated with a

Trauma in Pregnancy teratogenic effect on the fetus. Finally, patients with an injury to the spinal cord are at risk for unattended delivery secondary to unrecognized contractions.64

Burns occurring during pregnancy are not uncommon, particularly in major burn centers and in developing countries. A burn increases spontaneous uterine activity and it affects circulatory exchange in the uteroplacental unit due to volume changes, which can have an adverse effect on the fetus. The maternal outcome of burns during pregnancy is related to the total body surface area involved as in nonpregnant patients, but fetal survival depends upon the gestational age, the extent of maternal injury, and maternal outcome.65 Although the treatment of the burned patient during pregnancy does not differ significantly from the patient in the nongravid state (see Chap. 48), there are certain caveats to be considered. First, fluid resuscitation should be particularly vigorous, given the expanded intravascular volume during normal pregnancy. Second, hypoxia must be avoided, and this may be particularly challenging in patients with inhalational injury associated with the burn. Due to the Bohr effect on oxygen dissociation curves, the fetus preferentially takes up carbon monoxide (CO) into its circulation. It is estimated that the fetus takes up to five times longer than the mother to remove CO; therefore, oxygen therapy should be prolonged for up to five times that needed to normalize maternal CoHb levels.66 Additionally, the use of tocolytic drugs may worsen the pulmonary complications of inhalation injuries. For care of the burn wounds, silver sulfadiazine cream should be used sparingly because of the risk of kernicterus associated with sulfonamide absorption, whereas pain medications should be used liberally.

■ Cesarean Section Following Injury Guidelines for performing cesarean section following trauma as developed by the ACOG for the mother in extremis following a medical disaster (i.e., amniotic fluid embolism, major cardiac event) are summarized in Table 37-3. These guidelines apply to infants who are at least 25 weeks of gestation and would have a reasonable chance of surviving outside of the womb. The data suggest that, if a fetus is delivered within 5 minutes of maternal death, the anticipated fetal survival rate is 70%.67 In the trauma situation, if the mother presents in extremis, prompt cesarean section should be performed and combined with ED thoracotomy as described above.68 In a study representing nine major trauma centers, 441 pregnant trauma patients were described, including 32 patients who required cesarean section for either maternal or fetal distress.69 Fifteen (45%) of the fetuses and 23 (72%) of the mothers survived. Thirteen of the fetuses delivered had no fetal heart tones and none survived, whereas 20 infants with both fetal heart tones and an estimated gestational age of 26 weeks or more had a 75% survival rate. Five of the infants who died were potentially salvageable (i.e., had both fetal heart tones and an estimated gestational age of 26 weeks), but there was delayed recognition of fetal distress among mothers with moderate injuries (ISS 16). The use of CTM was not univer-

TABLE 37-3 Postmortem Cesarean Section Predictors of Successful Fetal Outcome Following Postmortem Cesarean Section 1. Duration of gestation Fetal viability generally is defined as 26–28 weeks’ gestation. This corresponds to a fundal height of approximately 26–28 cm above the pubis and/or uterus, halfway between the umbilicus and costal margin. At this age, the fetus, under optimal conditions, has a 40–70% estimated chance of survival without major handicap; therefore, cesarean section is indicated shortly after maternal death 2. Time between maternal death and delivery 5 min, excellent 5–10 min, good 10–15 min, fair 15–20 min, poor 20–25 min, unlikely Procedure 1. Establish viability 2. Complete the CPR sequence 3. Make a vertical midline incision through the abdominal layers into the uterus 4. Remove the fetus from the uterine cavity, clamp the cord, and hand the neonate to appropriate personnel for resuscitation 5. Remove the placenta 6. Continue CPR and assess for maternal signs of life; maternal survival is still possible after the uterus has been emptied and the supine hypotension syndrome has been resolved. CPR  cardiopulmonary resuscitation. Adapted with permission from Macmillan Publishers Ltd: Higgins SO: Perinatal protocol: trauma in pregnancy. J Perinatol. 1988;8:288; and adapted with permission from Seldin BS, Burkes TJ: Complete maternal and fetal recovery after prolonged cardiac arrest. Ann Emerg Med. 1988;17:346. © Elsevier.

sal among these patients even in these experienced trauma centers. The algorithm proposed from this study for emergency and perimortem cesarean section following maternal trauma is shown in Fig. 37-5. In most trauma centers, an obstetrician should be readily available to perform a cesarean section for fetal or maternal distress. Should the trauma surgeon be in the position to perform this operation, the key to success is the use of large incisions. A long, vertical abdominal incision is used to access the uterus, followed by a midline vertical incision through the upper uterine segment. The infant is removed immediately and suctioned, the cord is clamped and cut, and resuscitation initiated on the baby while the surgeon simultaneously tamponades bleeding from the placenta and uterine wall of the mother.

CHAPTER CHAPTER 37 X

■ Thermal Injuries in Pregnancy

719

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Management of Specific Injuries

Maternal trauma

SECTION 3 X

NO

FHT

ATLS resuscitation

YES Ultrasound

Fetus <26 weeks

EGA ≥26 weeks

No maternal distress

Fetal monitoring

Maternal distress

C-section

Fetal distress

CPR

Perimortem C-section

FIGURE 37-5 Algorithm for emergency cesarean section following trauma in pregnancy. CPR  cardiopulmonary resuscitation; EGA  estimated gestational age; FHT  fetal heart tones. (Reproduced with permission from Morris JA, Rosenbower TJ, Jurkovich GH, et al. Infant survival after cesarean section for trauma. Ann Surg. 1996;223:481.)

In the study using data from the NTDB cited above, Ikossi et al.14 reported that among the 1,195 pregnant women on whom data were available, 1,178 survived, 17 died, and 66 pregnancies were lost. Of those patients who delivered their infant during the admission after trauma, 75% underwent cesarean section. This is a 3-fold greater rate than the national average of 13–22%. Also, 75% of these cesarean sections were performed within 24 hours of admission, implying urgent operations. The indications for delivery (fetal or maternal distress etc.) are not currently available in the NTDB, nor are the outcomes of the fetuses. Only 3% of records included fetal monitoring in the data submitted, but this is likely under-reported, as there is no separate coding field for CTM data in the NTDB. The data capture fields on both the infant and the mother contained in the NTDB will need to be expanded in order to get a more complete picture of the impact of trauma on fetal outcome.

CRITICAL CARE OBSTETRICS Although a complete description of the care of the critically ill or injured obstetrical patient is beyond the scope of this chapter, a few conditions that might be encountered by the critical care surgeon in the postinjury state are worthy of mention. The first is pregnancy-induced hypertension, which in its most severe form includes preeclampsia and eclampsia. The risk factors for preeclampsia include first pregnancy, multiple gestations, and a positive family history. The criteria for preeclampsia include a sustained systolic blood pressure 160 mm Hg, a sustained diastolic pressure of 110 mm Hg, proteinuria 5 g/24 hours. Oliguria, pulmonary edema, and thrombocytopenia.70 Symptoms might also include headache and right upper quadrant pain in the abdomen. Although in its mild stages, preeclampsia can be managed expectantly, this syndrome

has been associated with intrauterine growth retardation. If near term, delivery should be considered. Conservative measures include treatment of the hypertension (i.e., hydralazine or beta-blockade) and administration of magnesium sulfate. In its most severe form, preeclampsia progresses to eclampsia with the onset of seizures. Eclampsia, in turn, may be associated with intracerebral hemorrhage, blindness, acute tubular necrosis, cardiac failure, and disseminated intravascular coagulation for which the only cure is evacuation of the uterus. Both amniotic fluid and pulmonary embolism remain major causes of morbidity and mortality during pregnancy. Amniotic fluid embolism is a catastrophic event that presents as severe hypoxia and cardiovascular collapse. Typically occurring during labor, the etiology was presumed to be the introduction of amniotic fluid into the maternal circulation inducing disseminated intravascular coagulation, pulmonary hypertension, and right heart failure. Recent data suggest that it may not be the components of the fluid itself that are detrimental, but rather an immunopathologic response to these components that leads to the listed complications.70 Treatment is largely supportive and includes cardiovascular support and correction of any coagulopathy. As previously mentioned, pregnancy is normally a hypercoagulable state due to increased production of clotting factors and fibrinogen directed at preventing hemorrhage during delivery. Additionally, the increased pressure on pelvic veins by the enlarged uterus increases the risk of both deep venous thrombosis and pulmonary embolism. The injured pregnant patient has the added thrombotic risk factors associated with trauma (pelvic and lower extremity fractures, immobility, neurologic injury, etc.). Prophylactic doses of enoxaparin should be utilized in all hospitalized pregnant patients. Enoxaparin is both safer and more effective than standard heparin, and it presents low risk to the fetus because it does not cross the placenta.

Trauma in Pregnancy

FETAL OUTCOME FOLLOWING TRAUMA AND PREGNANCY Although it is generally recognized that the most common cause of fetal death following trauma is maternal death, the actual ratio of fetal to maternal deaths ranges from 3:1 to 9:1.58,71 Several attempts have been made to identify factors that would predict a poor fetal outcome following trauma during pregnancy.14,58,71–81 Although not all studies are in agreement, it appears that maternal physiologic variables are poor predictors of fetal outcome. Factors generally associated with risk to the fetus include maternal hypotension, severe traumatic brain injury, high ISS, pelvic fracture, ejection from the vehicle, severe abdominal trauma, elevated serum lactate on admission, need for transfusion, low gestational age, and fetal tachycardia or bradycardia. A recent 10-year population-based study by Schiff et al. 77 examined the outcomes of both mother and infant after injury during pregnancy. Patients included 266 nonseverely injured gravid women (ISS of 1–8) and 28 severely injured women (ISS 9) who delivered during their hospitalization after injury. Even the nonseverely injured pregnant women were at increased risk of placental abruption, and their infants were at increased risk of suffering hypoxia and fetal death. Severely injured pregnant women were at a 17-fold increased risk of placental abruption and their infants were at increased risk of prematurity, low birth weight, and fetal distress, and had a 30-fold greater risk of fetal death. In a similar study from

TABLE 37-4 Risk Factors for Loss of Pregnancy After Trauma Risk Factor ISS 15 GCS 8 AIS 3 Head Thorax Abdomen Lower extremity

Odds Ratio 9.17 5.24 3.02 2.29 5.63 3.98

AIS  Abbreviated Injury Score; GCS  Glasgow Coma Score; ISS  Injury Severity Score. From Ikossi DG, Lazar AA, Morabito D, et al. Profile of mothers at risk: an analysis of injury and pregnancy loss in 1,195 trauma patients. J Am Coll Surg. 2005;200:49. © Elsevier.

California, women who delivered at the trauma hospital (Group 1) were compared with women who had a history of trauma during their pregnancy but delivered during a second hospitalization (Group 2), and with nontrauma controls.78 As would be anticipated, women in Group 1 had the worst outcomes, with an odds ratio (OR) of 60 for maternal death, 4.7 for fetal death, 43 for uterine rupture, and 9.2 for placental abruption. Women in Group 2 sustained a 2.7-fold increase in premature labor and a 4-fold increased risk of maternal death compared with uninjured women. In addition, they had higher rates of premature delivery and low birth weight at delivery compared with uninjured pregnant women, raising the suggestion that chronic abruptions secondary to trauma may lead to placental insufficiency and fetal compromise. In the large study compiled from data in the NTDB, the ORs for loss of a pregnancy after trauma were calculated based on the nature of the injury.14 As can be seen in Table 37-4, injuries to the head and abdomen carried the highest risk, as did an overall ISS of 15.

INJURY PREVENTION DURING PREGNANCY These poor outcomes for both the mother and her fetus associated with even relatively minor trauma highlight the need for attention to injury prevention during pregnancy, and three areas of injury prevention deserve specific attention. The first involves the use of drugs and alcohol (see Chapter 42). An alarming number of women test positive for illegal drugs and/ or alcohol when they are injured during pregnancy. Ikossi et al.14 reported that 13% of pregnant women tested positive for alcohol at the time of their trauma admission and 20% were using illicit drugs. In a more recent study of 84 injured pregnant women, an alarming 45 (50%) tested positive for alcohol.82 Patients who tested positive for alcohol were more likely to exhibit other risk-taking behaviors such as lack of restraints while driving also. Not only are these substances known to be harmful to the unborn child, but the association

CHAPTER CHAPTER 37 X

Another potential complication following severe trauma during pregnancy is premature labor. Premature labor is defined as uterine contractions combined with cervical change (effacement or dilation). In one study of relatively minor trauma, less than 1% of patients demonstrated preterm labor. In contrast, following severe trauma, most patients will exhibit some degree of uterine contractile activity.32,34 Although most of these contractions will resolve spontaneously over time, some patients may benefit from the pharmacologic inhibition of labor by the administration of tocolytic drugs. Drugs currently available for tocolysis include sympathomimetics such as terbutaline, indomethacin, and calcium channel blockers (nifedipine).5 All these drugs have side effects that may complicate their use in injured patients. Magnesium sulfate may cause hypotension and mental status changes, whereas indomethacin has been associated with oligohydramnios and promotes closure of the ductus arteriosus in the fetus.5 Additionally, indomethacin may produce bleeding in the trauma patient. Alpha-adrenergic drugs produce tachycardia, may mask blood loss, and may induce chest pain. The use of calcium channel blockers is associated with hypotension.5 Tocolytic drugs should not be used in patients with active vaginal bleeding or suspected placental abruption because blood may accumulate inside a relaxed uterus. Other contraindications to tocolysis include preeclampsia, eclampsia, uncontrolled diabetes mellitus, serious cardiac disease, and cervical dilatation greater than 4 cm. In patients in the last trimester of pregnancy who develop contractions or premature labor, betamethasone is administered in order to hasten lung maturation in the premature baby should delivery be necessary.

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between their use and both intentional and unintentional injuries has been well documented.83 Prenatal care must include education on the subject of substance abuse and provide opportunities for treatment for those women with a history of alcohol abuse. Intimate partner violence is the most common cause of trauma-related maternal death during pregnancy, and maternal deaths due to homicide exceed those due to any obstetric cause. It is estimated that between 6 and 22% of gravid women experience intimate partner violence during pregnancy.70 McLeer and Anwar reported that after staff in the ED were trained to recognize signs of battery, the number of women seeking emergency care who were identified as being physically abused rose from 6 to 30%.84 Similarly, McFarlane et al.12, using a threequestion Abuse Assessment Screen, detected a 17% prevalence of physical or sexual abuse during pregnancy, with 60% of women reporting two or more episodes of assault. Pregnant women reporting current violence were significantly more likely to report depressive symptoms, higher levels of psychosocial stress and substance abuse, as well.85 Other risk factors for pregnancy-related violence include low socioeconomic status, low levels of social support, first-time parenting, and carrying an unexpected or unwanted pregnancy.25 In another study of 203 injured pregnant patients, 32% were victims of intentional injury.84 In most cases, the husband or boyfriend was the offender. The incidence of fetal loss is surprisingly high in this group of battered women. In addition to fetal loss, abuse during pregnancy has been associated with low fetal birth weight, low maternal weight gain, maternal infections, anemia, and maternal alcohol and drug abuse. Interpersonal violence is not dependent on race, age, marital status, or socioeconomic status (see Chapter 46), thus making all pregnant women potential victims of abuse.86 A history of depression, substance abuse, or multiple visits to the ED should raise the level of suspicion for abuse, as should the presence of an overprotective partner.86 Abused women may initially delay seeking medical attention or give an implausible explanation for injuries. A history of “spontaneous” abortion, miscarriages, and premature labor may indicate violence occurring during pregnancy, also. Physical signs of abuse may include bruises on the breasts, abdomen, head, neck, genitals, or upper extremities, as well as the presence of injuries at multiple sites in various stages of healing. 24 Because pregnancy is often the only time that healthy women come into frequent contact with health care providers, it presents a unique opportunity to intervene in cases of intimate partner abuse and possibly prevents this tragic cause of homicides. Despite the recognition that fetal deaths are far more common in women who are ejected from moving vehicles, multiple studies have documented that pregnant women are frequently unrestrained, even if they have received specific information about seatbelt use in their prenatal visits. As mentioned above, those who are unrestrained are more likely to exhibit other risktaking behaviors such as alcohol and drug use and smoking during pregnancy, also. Sadly, fetal death is 3-fold more common in women who are unrestrained compared to their restrained gravid counterparts.87 Unrestrained pregnant women are also 1.9 times

more likely to have a low birth weight baby and 2.3 times more likely to give birth within 48 hours of a crash.88 Although the experience with air bags is limited, maternal and perinatal outcomes appear to be at least similar with or without air bag deployment. Also, there is no evidence that placental abruption is associated with air bag injuries.89,90 A comprehensive biomechanical program aimed at improving the safety of pregnant women and their fetuses in motor vehicle crashes is currently under way in several states.91,92 This type of research, combined with education and primary enforcement of seatbelt laws, could have a major impact on preventing maternal and fetal deaths following motor vehicle crashes during pregnancy.

REFERENCES 1. Keynes G. The Apology and Treatise of Ambroise Pare. London: Falcon Educational Books; 1951. 2. Lang CT, King JC. Maternal mortality in the United States. Best Pract Res Clin Obstet Gynaecol. 2008;22:517–531. 3. El Kady D. Perinatal outcomes of traumatic injuries during pregnancy. Clin Obstet Gynecol. 2007;50:582–591. 4. Fildes J, Reed L, Jones N, Martin M, Barrett J. Trauma: the leading cause of maternal death. J Trauma. 1992;32:643–645. 5. Lavery J, Staten-McCormick M. Management of moderate to severe trauma in pregnancy. Obstet Gynecol Clin North Am. 1995;22:69–90. 6. Kuczkowski KM. Trauma during pregnancy: a situation pregnant with danger Acta Anaesth Belg. 2005;56:13–18. 7. Weiss H. Pregnancy-associated injury hospitalizations in Pennsylvania, 1995. Ann Emerg Med. 1995;34:626–636. 8. Weiss HB, Sauber-Schatz EK, Cook LJ. The epidemiology of pregnancyassociated emergency department injury visits and their impact on birth outcomes Accid Anal Prev. 2008;40:1088–1095. 9. Weiss HB, Songer TJ, Fabio A. Fetal deaths related to maternal injury. JAMA. 2001;286:1863–1868. 10. Guth AA, Pachter HL. Domestic violence and the trauma surgeon. Am J Surg. 2000;179:134–140. 11. Parsons LH, Harper MA. Violent maternal deaths in North Carolina. Obstet Gynecol. 1999;94:990–993. 12. McFarlane J, Parker B, Soeken K, Bullock L. Assessing for abuse during pregnancy: severity and frequency of injuries and associated entry into prenatal care. JAMA. 1992;267:3176–3178. 13. Chang J, Berg CJ, Saltzman LE, Herndon J. Homicide: a leading cause of injury deaths among pregnant and postpartum women in the United States, 1991–1999. Am J Public Health. 2005;95:471–477. 14. Ikossi D, Lazar A, Morabito D, Fildes J, Knudson MM. Profile of mothers at risk: an analysis of injury and pregnancy loss in 1,195 trauma patients. J Am Coll Surg. 2005;200:49–56. 15. Harvey MG. Physiologic changes of pregnancy. In: Harvey CJ, ed. Critical Care Obstetrical Nursing. Gaithersburg, MD:Aspen; 1991:1. 16. Smith CV, Phalen JP. Trauma in pregnancy. In: Clark SL, Cotton DB, Hankins GDV, et al., eds. Critical Care Obstetrics. 2nd ed. Boston: Blackwell; 1991:498. 17. Lee W, Cotton DB. Cardiorespiratory changes during pregnancy. In: Clark SL, Cotton DB, Hankins GDV, et al., eds. Critical Care Obstetrics. 2nd ed. Boston: Blackwell; 1991:2. 18. Pirhonen JP, Erkkola RU. Uterine and umbilical flow velocity waveforms in the supine hypotensive syndrome. Obstet Gynecol. 1990;76:176–179. 19. Elkus R, Popovich J Jr. Respiratory physiology in pregnancy. Clin Chest Med. 1992;13:555–565. 20. Awe RJ, Nicotra MB, Newsom TD, Viles R. Arterial oxygenation and alveolar-arterial gradients in term pregnancy. Obstet Gynecol. 1979;53: 182–186. 21. Munnur U, Suresh MS. Airway problems in pregnancy. Crit Care Clin. 2004;20:617–642. 22. Lapinsky SE, Posadas-Calleja JG, McCullagh I. Clinical review: ventilatory strategies for obstetric, brain-injured and obese patients. Crit Care. 2009;13:206. 23. Grant NF, Worley RJ. Measures of uterine-placental blood flows in the human. In: Rosenfeld CR, ed. The Uterine Circulation. Ithaca, NY: Perinataology Press;1989:5.

Trauma in Pregnancy 52. Almog G, Liebergall M, Tsafrir A, et al. Management of pelvic fractures during pregnancy. Am J Orthop. 2007;36:E153–E159. 53. Harrison SD, Nghiem HV, Shy K. Uterine rupture with fetal death following blunt trauma. Am J Roentgenol. 1995;165:1452. 54. Green J. Placenta previa and abruptio placentae. In: Creasy R, ed. Maternal-Fetal Medicine: Principles and Practice. Philadelphia: Saunders; 1994:602. 55. Patterson RM. Trauma in pregnancy. Clin Obstet Gynecol. 1984;27: 32–38. 56. Sandy EA, Koerner M. Self-inflicted gunshot wound to the pregnant abdomen: report of a case and review of the literature. Am J Perinatol. 1989;6:30–31. 57. Staszewicz W, Christodoulou M, Marty F, Bettschart V. Damage control surgery by keeping the abdomen open during pregnancy: favorable outcome, a case report. World J Emerg Surg. 2009;4:33. 58. Kissinger DP, Rozycki GS, Morris JA, et al. Trauma in pregnancy: predicting pregnancy outcome. Arch Surg. 1991;126:1079–1086. 59. Countee, RT. Neurological injuries during pregnancy. In: Haycock C, ed. Trauma and Pregnancy. Littleton, MA: PSG Publishing; 1985:154. 60. Kelly DF, Gaw Gonzalo IT, Cohan P, Berman N, Swerdloff R, Wang C. Hypopituitarism following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a preliminary report. J Neurosurg. 2000;93: 743–752. 61. Oxford CM, Ludmir JB. Trauma in pregnancy. Clin Obstet Gynecol. 2009;52:611–629. 62. Popov I, Ngambu F, Mantel G, et al. Acute spinal cord injury in pregnancy: an illustrative case and literature review. J Obstet Gynaecol. 2003;23:596–598. 63. Gilson GJ, Miller AC, Clevenger FW, Curet LB. Acute spinal cord injury and neurogenic shock in pregnancy. Obstet Gynecol Surv. 1995;50: 556–560. 64. Pereira L. Obstetric management of the patient with spinal cord injury. Obstet Gynecol Surv. 2003;58:678–686. 65. Agarwal P. Thermal injury in pregnancy: predicting maternal and fetal outcome. Indian J Plastic Surg. 2005;38:95–99. 66. Gopu S, Wan Hussein HY, Ray S. Fire smoke inhalation in pregnancy J Obstet Gynaecol. 2007;27:525–526. 67. Katz VL, Dotters DJ, Droegemueller, W. Perimortem cesarean delivery. Obstet Gynecol. 1986;68:571–576. 68. Burke ME. The pregnant trauma patient in the intensive care unit: collaborative care to ensure safety and prevent injury. J Perinat Neonat Nurs. 2008;22:33–38. 69. Morris JA, Rosenbower TJ, Jurkovich GJ, et al. Infant survival after cesarean section for trauma. Ann Surg. 1996;223:481–491. 70. Williams J, Mozurkewich E, Chilimigras J, Van De Ven C. Critical care in obstetrics: pregnancy-specific conditions. Best Pract Res Clin Obstet Gynaceol. 2008;22:825–846. 71. Hoff WS, D’Amelio LF, Tinkoff GH, et al. Maternal predictors of fetal demise in trauma during pregnancy. Surg Gynecol Obstet. 1991;172: 673–674. 72. Esposito TJ, Gens DR, Smith LG, Scorpio R, Buchman T. Trauma during pregnancy: a review of 79 cases. Arch Surg. 1991;126:1073–1078. 73. Scorpio RJ, Esposito TJ, Smith LG. Blunt trauma during pregnancy: factors affecting fetal outcome. J Trauma. 1992;32:213–216. 74. Ali J, Yeo A, Gana TJ, McLellan BA. Predictors of fetal mortality in pregnant patients. J Trauma. 1997;42:782–785. 75. Shah KH, Simons RK, Holbrook T, et al. Trauma in pregnancy: maternal and fetal outcomes. J Trauma. 1998;45:83–86. 76. Rogers FB, Rozycki GS, Osler TM, et al. A multi-institutional study of factors associated with fetal death in injured pregnant patients. Arch Surg. 1999;134:1274–1277. 77. Schiff MA, Holt VL, Daling JR. maternal and infant outcomes after injury during pregnancy in Washington State from 1989 to 1997. J Trauma. 2002;53:939–945. 78. El Kady D, Gilbert WM, Anderson J, Danielsen B, Towner D, Smith LH. Trauma during pregnancy: an analysis of maternal and fetal outcomes in a large population. Am J Obstet Gynecol. 2004;190:1661–1668. 79. Baerga-Varela Y, Zietlow SP, Bannon MP, Harmsen WS, Ilstrup DM. Trauma in pregnancy. Mayo Clin Proc. 2000;75:1243–1248. 80. Aboutanos MB, Aboutanos SZ, Dompkowski D, Duane TM, Malhotra AK, Ivatury RR. Significance of motor vehicle crashes and pelvic injury on fetal mortality: a five-year institutional review. J Trauma. 2008;65: 616–620. 81. Cartin-Ceba R, Gajic O, Iyer VN, Vlahakis NE. Fetal outcomes of critically ill pregnant women admitted to the intensive care unit for nonobstetric. Crit Care Med. 2008;36:2746–2751.

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24. Muench MV, Canterino JC. Trauma in pregnancy. Obstet Gynecol Clin North Am. 2007;34:555–583. 25. Rudloff U. Trauma in pregnancy. Arch Gynecol Obstet. 2007;276: 101–117. 26. Brown MA, Sirlin CB, Farahmand N, Hoyt DB, Casola G. Screening sonography in pregnant patients with blunt abdominal trauma. J Ultrasound Med. 2005;24:175–181. 27. Ormsby EL, Geng GJ, McGahan JP. Pelvic free fluid: clinical importance for reproductive age women with blunt abdominal trauma. Ultrasound Obstet Gynecol 2005;26:271–278. 28. Mattox KL, Goetzl L. Trauma in pregnancy. Crit Care Med. 2005; 33:S385–S389. 29. Muench MV, Baschat AA, Reddy UM, et al. Kleihauer-Betke testing is important in all cases of maternal trauma. J Trauma. 2004;57: 1094–1098. 30. Dhanraj D, Lambers D. The incidences of positive Kleihauer-Betke test in low-risk pregnancies and maternal trauma patients. Am J Obstet Gynecol. 2004;190:1461–1463. 31. Cahill AG, Bastek JA, Stamilio DM, Odibo AO, Stevens E, Macones GA. Minor trauma in pregnancy—is the evaluation unwarranted? Am J Obstet Gynecol. 2008;198:E1–E5. 32. Pearlman MD, Tintinalli JE, Lorenz RP. A prospective controlled study of outcome after trauma during pregnancy. Am J Obstet Gynecol. 1990; 162:1502–1507. 33. Kaiser G. Do electronic fetal heart rate monitors improve delivery outcomes? J Fla Med Assoc. 1991;78:303–307. 34. Dahmus MA, Sibai BM. Are there any predictive factors for abruptio placentae or maternal-fetal distress? Am J Obstet Gynecol. 1993;169: 1054–1059. 35. Curet MJ, Schermer CR, Demarest GB, Bieneik EJ 3rd, Curet LB. Predictors of outcome in trauma during pregnancy: identification of patients who can be monitored for less than 6 hours. J Trauma. 2000; 49:18–25. 36. Fries MH, Hankins GV. Motor vehicle accident associated with minimal maternal trauma but subsequent fetal demise. Ann Emerg Med. 1989; 18:301. 37. Deutchman, M. Primary application of ultrasound. In: Heller MJ, ed. Pelvic Applications in Ultrasound in Emergency Medicine. Philadelphia: Saunders; 1995:106. 38. Manning FA, Platt LD, Sipos L. Antepartum fetal evaluation: development of a fetal biophysical profile score. Am J Obstet Gynecol. 1980;136:7 87–795. 39. Eliot G. Pregnancy and radiographic examination. In: Haycock C, ed. Trauma and Pregnancy. Littleton, MA: PSG Publishing; 1995:69. 40. Harvey EB, Boice JD Jr, Honeyman M, Flannery JT. Prenatal x-ray exposure and childhood cancer in twins. N Engl J Med. 1985;312:541. 41. ACOG Committee on Obstetric Practice. ACOG Committee Opinion #299. Guidelines for diagnostic imaging during pregnancy. Obstet Gynecol. 2004;104:647. 42. Moore MM, Shearer DR. Fetal dose estimates for CT pelvimetry. Radiology. 1989;171:265–267. 43. De Santis M, Di Gianantonio E, Straface G, et al. Ionizing radiations in pregnancy and teratogenesis: a review of literature. Reprod Toxicol. 2005; 20:323–329. 44. Mann FA, Nathens A, Langer SG, Goldman SM, Blackmore CC. Communicating with family: the risk of medical radiation to conceptuses in victims of major blunt force torso trauma. J Trauma. 2000;48:354–357. 45. Badmanaban B, Diver A, Ali N, Graham AN, McGuigan J, MacGowan S. Traumatic aortic rupture during pregnancy. J Card Surg. 2003;18: 557–561. 46. Visser BC, Glasgow RE, Mulvihil KK, et al. Safety and timing of nonobstetric abdominal surgery in pregnancy. Dig Surg. 2001;18: 409–417. 47. Levinson G. Anesthesia for surgery during pregnancy. In: Hughes SC, Levinson G, Rosen MA, eds. Anesthesia for Obstetrics. Philadelphia: Lippincott Williams and Wilkins; 2001:249. 48. Lavin JP Jr, Polsky SS. Abdominal trauma during pregnancy. Clin Perinatol. 1983;10:423–438. 49. Leggon RE, Wood CG, Indeck MC. Pelvic fractures in pregnancy: factors influencing maternal and fetal outcomes. J Trauma. 2002;53:796–804. 50. Loegters T, Briem D, Gatzka C, et al. Treatment of unstable fractures of the pelvic ring in pregnancy. Arch Orthop Trauma Surg. 2005;125: 204–208. 51. Kloen P, Flik K, Helfet DL. Operative treatment of acetabular fracture during pregnancy: a case report. Arch Orthop Trauma Surg. 2005;125: 209–212.

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82. Patteson SK, Snider CC, Meyer DS, et al. The consequences of high-risk behaviours: trauma during pregnancy. J Trauma. 2007;62:1015–1020. 83. ACOG Educational Bulletin. Teratology 236:1997. 84. McLeer SV, Anwar R. A study of battered women presenting in an emergency department. Am J Pub Health. 1989;79:65–66. 85. Datner EM, Wiebe DJ, Brensinger CM, Nelson DB. Identifying pregnant women experiencing domestic violence in an urban emergency department. J Interpers Violence. 2007;22:124–135. 86. Poole GV, Martin JN, Perry KG Jr, Griswold JA, Lambert CJ, Rhodes RS. Trauma in pregnancy: the role of interpersonal violence. Am J Obstet Gynecol. 1996;1996:1873–1878. 87. El Kady, D, Gilbert WM, Xing G, Smith LH. Maternal and neonatal outcomes of assaults during pregnancy. Obstet Gynecol. 2005;105:357–363. 88. Pearlman MD, Phillips ME. Seat belt use during pregnancy. Obstet Gynecol. 1996;88:1026–1029.

89. Schiff MA, Mack CD, Kaufman RP, Holt VL, Grossman DC. The effect of air bags on pregnancy outcomes in Washington State 2002–2005. Obstet Gynecol. 2010;115:85–92. 90. Metz T, Abbott JT. Uterine trauma in pregnancy after motor vehicle crashes with airbag deployment: a 30-case series. J Trauma. 2006;61: 658–661. 91. Moorcroft DM, Stitzel JD, Duma GG, et al. Computerized model of the pregnant occupant: predicting the risk of injury in automobile crashes. Am J Obstet Gynecol. 2003;189:540–544. 92. Pearlman MD, De Santis K, Schneider LW, et al. A comprehensive program to improve safety for pregnant women and fetuses in motor vehicle crashes: a preliminary report. Am J Obstet Gynecol. 2000;182: 1554–1564.

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CHAPTER 38

Trauma Damage Control Amy D. Wyrzykowski and David V. Feliciano

A number of new approaches to the management of patients with major truncal or extremity trauma have evolved over the past 20 years. These include the following: minimizing time at the scene of trauma and in the emergency department; the presence of in-house attending surgeons, particularly in centers with a significant percentage of penetrating trauma; minimizing admission laboratory testing; initiating resuscitation in the operating room for patients with severe hypotension, cardiac arrest, or external hemorrhage; and early operative control of hemorrhage. All of these are now accepted as major factors in decreasing morbidity and mortality.1–4 Another major change has been the recognition that conservative operative techniques and shortened operative times, even when all organ repairs have not been completed, will increase survival in civilian and military patients with cervical, truncal, or extremity injuries and intraoperative “metabolic failure.”5–22 Finally, it has been recognized that standard closure of a thoracotomy or the midline abdominal incision is impossible to achieve in many severely injured patients, is too time-consuming in others, and may cause an abdominal compartment syndrome in the postoperative period after a laparotomy.23–33 This chapter will describe the techniques used during “damage control” operations (as named by Rotondo et al.);7 prevention and sequelae of primary or secondary abdominal compartment syndrome; the alternate techniques for closure of a thoracic, abdominal, or extremity incision in patients with major trauma;34–43 care of the patient in the surgical intensive care unit (SICU) after a damage control operation; the approach to reoperation; and late repair of incisional hernias when the abdomen has been left open at a reoperation.41,44–47

DAMAGE CONTROL OPERATIONS ■ Definition Damage control operations are performed in injured patients with profound hemorrhagic shock and preoperative or intra-

operative metabolic sequelae that are known to adversely affect survival. The widely accepted three stages of damage control are: 1. Limited operation for control of hemorrhage and contamination. Includes control of hemorrhage from the heart or lung; conservative management of injuries to solid organs; resection of major injuries to the gastrointestinal tract without reanastomosis; control of hemorrhage from major arteries and veins in the neck, trunk, or extremities; packing of organs or spaces should a coagulopathy occur; and use of an alternate coverage or closure of a cervical incision, thoracotomy, laparotomy, or site of exploration of an extremity. 2. Resuscitation in the SICU. Includes vigorous rewarming of the hypothermic patient; restoration of a normal cardiovascular state by the infusion of blood, blood products, and fluids and the use of inotropic and related drugs; correction of residual coagulopathy after hypothermia is reversed; and supportive care to minimize the magnitude of acute lung injury (ALI) and acute kidney injury (AKI). 3. Reoperation. Includes completion of definitive repairs, search for missed injuries, and formal closure of the incision, if possible.

■ Clinical Recognition of Patients Likely to Need Damage Control Operations Reports to the hospital from prehospital providers or a rapid evaluation in the emergency department by experienced members of the trauma team are the mechanisms used to select patients for abbreviated resuscitation and immediate operation with damage control techniques in the operating room. Unless an emergency department thoracotomy is indicated, patients in this small subset (Table 38-1) should stop in the emergency department only long enough to obtain control of the airway, decompress an obvious pneumothorax, draw blood

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TABLE 38-1 Patients Likely to Need Damage Control Operations

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Thoracic trauma • Penetrating thoracic wound and systolic blood pressure 90 mm Hg • Pericardial fluid on surgeon-performed ultrasound after blunt or penetrating thoracic trauma • S/p emergency department thoracotomy for penetrating thoracic wound Abdominal or pelvic trauma • Penetrating abdominal wound and systolic blood pressure 90 mm Hg • Blunt abdominal trauma, systolic blood pressure 90 mm Hg, and peritoneal fluid on surgeonperformed ultrasound or gross blood on diagnostic peritoneal tap • Closed pelvic fracture, systolic blood pressure 90 mm Hg, and peritoneal fluid on surgeonperformed ultrasound or gross blood on diagnostic peritoneal tap • Open pelvic fracture Trauma to an extremity • Shotgun wound to femoral triangle of thigh • Mangled extremity from blunt trauma General • Emergency laparotomy to be followed by emergent craniotomy for compressive lesion, emergent thoracotomy for repair of ruptured descending thoracic aorta, or therapeutic embolization of pelvic bleeder related to fracture

for type and cross match, and apply an identification bracelet. These patients should then be transported immediately to the operating room. Patients arriving by air with hypotension or mangled extremities should bypass the emergency room entirely and be taken directly to the operating room from the helipad.

■ Intraoperative Indications to Perform Damage Control Operations The primary indication to modify the conduct of an operation for major trauma to the neck, chest, abdomen, or an extremity is unresolved metabolic failure despite control of hemorrhage by suture, resection, or packing. Metabolic failure is characterized by severe hypothermia despite warming maneuvers initiated in the emergency department and continuing in the operating room, persistent acidemia despite vigorous resuscitation and control of hemorrhage, and a coagulopathy (nonmechanical bleeding) not amenable to operative control.48–58Patients are more likely to die from their intraoperative metabolic failure than they are from the failure to complete organ repairs.5–9,12–14,51–58 Most have been massively transfused and have a mortality of 20–50%.7,12–14,52,59–63

Hypothermia Hypothermia continues to be a common problem in victims of major trauma. In one older series, 66% of severely injured patients with an Injury Severity Score (ISS) greater than or equal to 25 admitted to a level I trauma center were hypothermic (36°C [96.8°F] on an esophageal temperature probe), including 23% who were severely hypothermic (34°C [93.2°F]).64 Another older review documented that 57% of 74 trauma patients admitted directly to the operating room from the emergency department developed hypothermia (36°C [96.8°F]) between the time of injury and the time they were moved out of the operating room.65 There are many causes of hypothermia in victims of major trauma. Hypovolemic shock in the preoperative period adversely affects oxygen delivery and leads to decreases in oxygen consumption and, therefore, diminished production of heat.66–68 Should the patient be intoxicated at the time of injury, vasodilatation will further compromise the ability to retain heat. The trauma team itself may be responsible for accelerating the loss of heat from a victim in shock. Undressing the patient in a cool resuscitation room, failing to cover the patient’s head with a turban and the trunk and extremities with warm blankets or the Bair Hugger patient warming system (Augustine Medical, Inc, Eden Prairie, Minnesota) during resuscitation, and infusion of unheated crystalloids and packed red blood cells (PRBCs) are all sources of heat loss in the emergency department. Paralyzing the patient, which prevents shivering, and administering anesthetic agents, which prevent vasoconstriction; failing to cover areas of the body not undergoing operation; opening one or more body cavities in a cold operating room; and irrigating body cavities with unheated crystalloid solutions all further exacerbate heat loss during a thoracotomy or laparotomy. These multiple sources of heat loss cannot be adequately compensated for by increasing heat production in the patient in shock. The resuscitation and surgical teams are responsible for preventing or reversing hypothermia using the techniques listed in Table 38-2.48 The effect of hypothermia on mortality in severely injured patients is no longer controversial except for one study. In one large retrospective review, mortality among euthermic and hypothermic trauma patients was not significantly different when patients in both groups were stratified by physiologic and anatomic indicators of injury severity.69 This is in marked contrast to the review of iliac vascular injuries by Cushman et al. who noted that the risk of dying was nearly four times greater when the patient’s initial body temperature in the operating room was less than 34°C (93.2°F).70 If the patient’s last body temperature in the operating room was less than 35°C (95.0°F), the risk of death was nearly 41 times greater than it was for patients with a body temperature greater than 35°C. While hypothermia is helpful in certain elective operative procedures and has been used for cerebral protection in patients with injury to the brain, it has well-known adverse effects on the cardiovascular, respiratory, renal, gastrointestinal, endocrine, central nervous, and coagulation systems (see Chapter 49).48,71,72 Both terminal cardiac dysfunction and irreversible nonmechanical bleeding have been noted in many injured

Trauma Damage Control

Increase operating room temperature 85°F (29.4°C) Infuse crystalloid solution and blood through a warming device such as the Level 1 Fluid Warmera Cover patient’s head with a turban or warming device Cover body parts out of the operative field with a warming device such as the Bair Huggerb or Life-Airc system Irrigate nasogastric and thoracostomy tubes with warm saline during laparotomy Irrigate open pericardial cavity, pleural cavities, and peritoneal cavity during simultaneous stemotomy or thoracotomy and laparotomy a

Level 1 Technologies, Inc, Rockland, Massachusetts. Augustine Medical, Inc.

b c

Medical Products Group, Marshal, Minnesota.

hypothermic patients dying in the postoperative period after a trauma operative procedure. It would appear logical, therefore, to practice damage control and rapidly complete any trauma operation in which the patient’s initial body temperature is less than 34–35°C (93.2–95.0°F) or the temperature decreases below this level at any time during the operation.27,30,73 This is particularly true in patients undergoing thoracotomy or laparotomy because hypothermia will not be correctable until the chest or abdomen is closed.

Acidosis Prolonged hypovolemic shock produces a state of persistent metabolic acidosis in the patient with major trauma. This leads to a “circular” phenomenon in which secondary decreases in cardiac output, hypotension, and an increased susceptibility to ventricular arrhythmias may be irreversible, despite adequate volume replacement.8,49,50,55,58,74–76 Also, severe acidosis may cause the uncoupling of β-adrenergic receptors, with a secondary decrease in the patient’s response to endogenous and exogenous catecholamines.77 While acidosis by itself is an unusual reason to terminate a laparotomy being performed for trauma, it often accompanies hypothermia and a coagulopathy.49,50,51,53,55 A persistent metabolic acidosis is a manifestation of anaerobic metabolism occurring during hypoperfusion. Markers of this phenomenon in the injured patient that should initiate damage control operations are listed in Table 38-3.49,70,75,76,78

Coagulopathy Nonmechanical bleeding has been common during emergency trauma thoracotomies, laparotomies, or operative procedures in patients with exsanguination from an injury to an extremity in the past. With current massive transfusion protocols using a goal of 1 U PRBCs:1 U fresh frozen plasma:1 platelet pack,

TABLE 38-3 Intraoperative Indications to Perform Damage Control Operations49,69,74,75,77 Factor 1. Initial body temperature 2. Initial acid–base status • Arterial pH • Base deficit

• Serum lactate 3. Onset of coagulopathy

Level 35°C (95.0°F)69 7.269  15 mmol/L in patient 55 years of age74,75 or  6 mmol/L in patient 55 years of age75,77 5 mmol/L77 Prothrombin time and/or partial thromboplastin time 50% of normal8,55

Modified from Brasel KJ, Ku J, Baker CC, Rutherford EJ. Damage control in the critically ill and injured patient. New Horizons. 1999;7:73.

coagulopathies resulting in irreversible bleeding have become a less significant cause of mortality in the immediate postoperative period and have led to improved survival in massively transfused patients.63,79,80 It is now recognized that the historic replacement of volume losses with large amounts of crystalloid solutions and cold PRBCs leads to clotting abnormalities secondary to dilution, deficiency of clotting factors, and hypothermia.8,50,58,59,81–83 Hypothermia has a well-known adverse effect on enzymes associated with the coagulation cascade and on the function of platelets.7,12,13,59,81–83 In addition to a decrease in the incidence of coagulopathies, the implementation of improved transfusion ratios has been associated with reductions in multiorgan failure, fewer infectious complications, and a decreased incidence of the abdominal compartment syndrome.84 Improved transfusion ratios have been associated with decreased mortality in injured civilians, also.85–88 The role of recombinant activated factor VII (Novoseven, Novo Nordisk A/S, Bagsvaerd, Denmark) in the management of a life-threatening coagulopathy remains controversial. While the administration of rFVIIa appears to be safe in the trauma population and has not been associated with an increased risk of severe thrombotic events,89–91 it is extremely costly and the benefits remain unclear. Whereas early studies had promising results including decreased transfusion requirements and decreased 30-day mortality,91,92 more recent work has not found an improvement in outcome.93 When a coagulopathy does result, surgical attempts to control such nonmechanical bleeding, especially from the liver and retroperitoneum, are usually unsuccessful. In the major trauma patient who develops a coagulopathy characterized by an international normalized ratio (INR) or partial thromboplastin time 50% greater than normal during any major operative procedure after major sources of hemorrhage have been controlled,

CHAPTER CHAPTER 38 X

TABLE 38-2 Maneuvers to Prevent or Reverse Hypothermia During Damage Control Operations

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Management of Specific Injuries damage control would include the techniques to be described (see Table 38-3).

SECTION 3 X

■ Operative Techniques in Thoracic Trauma Lung Exsanguinating hemorrhage from the lung is most rapidly controlled by the application of a DeBakey aortic clamp to the hilum or by twisting the hilum to kink the major vessels in the emergency department or operating room (see Chapter 25).94 When the site of blood loss has been a stab wound deep into the pulmonary parenchyma or a gunshot wound completely through a lobe, the technique of pulmonotomy (sometimes called nonneurosurgical “tractotomy”) is used.95–97 Pulmonotomy refers to the division of pulmonary parenchyma between noncrushing vascular clamps or by using a linear stapling and cutting device to expose injured parenchymal vessels. After selective ligation of these, the pulmonary parenchyma is closed in the usual fashion using a continuous 0 or 2-0 absorbable suture, with reinforcement material added to the staple line, if possible. When the divided lung is edematous, it may not be possible to fully close the pulmonotomy.

Heart Other than compression with a finger, the quickest way to control hemorrhage from a small wound or rupture of a ventricle in the emergency department or operating room is to apply 6-mm-wide skin staples (Auto Suture 35 W, United States Surgical Corporation, Norwalk, Connecticut) (see Chapter 26).98,99 Formal cardiac repair with Teflon pledgets may then be accomplished over the staples or as they are sequentially removed in the operating room. Larger wounds or ruptures of a ventricle in patients surviving by virtue of tamponade may be controlled by the insertion of a Foley balloon catheter into the hole.100,101 With the balloon inflated and traction applied to the catheter, Teflon-pledgeted sutures can then be passed through the ventricle from side to side over the balloon. The thin wall of the right ventricle puts the inflated balloon at significant risk of puncture as each suture is placed. Pushing the catheter and balloon into the ventricle with each bite of the suture will avoid this complication, although blood loss may be significant. With a longitudinal perforation or significant rupture of a ventricle, the time-honored technique of inflow occlusion is useful in avoiding cardiopulmonary bypass.102 Curved aortic or angled vascular clamps are first applied to the superior and inferior vena cavae. As the heartbeat slows, horizontal mattress sutures are inserted rapidly on either side of the defect and then crossed to control hemorrhage. A continuous suture is placed to close the defect, and, before it is tied down, air is vented out of the elevated ventricle by releasing the clamps on the cavae.

■ Operative Techniques in Abdominal Trauma Liver The liver has a blood supply of 1,500 mL/min and is the major site of synthesis of all the coagulation factors except factor VIII

(see Chapter 29). Therefore, appropriate operative management of a major hepatic injury is a key component of a successful damage control laparotomy. There is ample historical evidence that an emergency hepatic resection performed by a general or trauma surgeon with little experience in a similar elective procedure will result in a mortality rate of 20–44%.103–108 This excessive mortality is certainly related to the magnitude of the hepatic injury, but also to the belated decision to resect at the same time that the aforementioned metabolic failure occurs in many patients. For this reason, more limited techniques of hemostasis should be applied when a hepatic injury is present and damage control is to be performed.109,110 Indirect control of hepatic hemorrhage may be accomplished by extensive compressive hepatorrhaphy, using a continuous suture or interrupted vertical mattress sutures of absorbable material. While this technique is used much less frequently than it was in the past, it is appropriate for a damage control operation. Damage control techniques in which the sources of hepatic hemorrhage are approached directly include hepatotomy with selective vascular ligation, resectional debridement with selective vascular ligation, and rapid resectional debridement.109 Both former techniques are performed with a vascular clamp on the porta hepatis (Pringle maneuver), and experience with the finger fracture technique should allow for early control of hemorrhage.109–111 When a coagulopathy is already present, hepatotomy or resectional debridement is not appropriate if the surgeon has only modest experience with hepatic trauma. After the Pringle maneuver is performed, rapid resectional debridement is initiated by applying a large Kelly clamp or vascular clamp just outside of a lateral area of partial avulsion (i.e., hepatic segments VI, VII on the right or II, III on the left) or by applying two clamps around the contused sides of a central laceration. The tissue within the clamps is then rapidly debrided, and an O-chromic tie can then be placed around the clamp and all the enclosed tissue ligated en bloc. An alternate technique is to use deep horizontal mattress sutures on either side of the debrided laceration and fill the space between with a viable omental pack (Fig. 38-1). Damage control techniques in which compression or tamponade rather than a suture or metal clip is used to control hepatic hemorrhage include balloon catheter tamponade, absorbable mesh tamponade, and perihepatic packing. Balloon catheter tamponade using a Foley or Fogarty balloon catheter or an inflated Penrose drain over a red rubber catheter is most useful to control hemorrhage from a deep lobar stab or missile track.101,112,113 Inflation of the balloon is performed at different levels of the track until hemorrhage is controlled. Removal of the balloon catheter is performed at a reoperation when the patient’s metabolic failure has been corrected. Alternatively, an absorbable mesh may be used to create a tamponade effect. Absorbable mesh can be used to reapproximate a disrupted lobe with viable fragments that are still attached to the hilum or to replace a disrupted Glisson’s capsule after rupture of a subcapsular hematoma and may be an excellent alternative to major hepatic resection.114,115 For the former, the technique involves mobilization of the injured lobe and circumferential wrapping

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FIGURE 38-1 Technique of rapid resectional debridement using large vascular clamps, horizontal mattress sutures, and omental pack. (Reproduced with permission from Feliciano DV, Pachter HL. Hepatic trauma revisited. Curr Probl Surg. 1989;26:453. © Elsevier.)

with a mesh sewn to itself at various locations. Although it may be time-consuming in the patient with a severe coagulopathy, it does avoid the need for reoperation. The insertion of dry laparotomy pads as perihepatic packs continues to be necessary in less than 10% of patients undergoing operative repair of hepatic injuries. Primary indications, in addition to the onset of metabolic failure, include the need to transfer the patient to a center with more experienced hepatic surgeons, a desire to avoid opening a large subcapsular hematoma, and the presence of bilobar injuries.57,116–118 The insertion of perihepatic packs mandates a reoperation and remains one of the classical indications for use of the alternate closures of the midline incision to be described. When placing perihepatic packs, one should be mindful of the possible need for hepatic angiography as an adjunct to laparotomy. If the radiopaque markers of the laparotomy pads are not strategically placed away from the hilum, they may obscure the visualization required for successful angiography. Operative venovenous bypass of the liver, postoperative venous stenting, and postoperative arterial embolization are all adjuncts to the standard damage control techniques described earlier. All have been applied successfully in selected patients in recent years.119–124

Spleen With American Association for the Surgery of Trauma (AAST) Organ Injury Scale (OIS) grade III, IV, or V injuries, splenectomy remains the safest choice when damage control is necessary (see Chapter 30).125,126 Should an AAST OIS grade I or II injury be present, rapid mobilization and direct suture may be faster than splenectomy and will avoid the creation of a denuded retroperitoneal area in the patient with a coagulopathy (Fig. 38-2). With rupture of the capsule, a topical agent such as microfibrillar collagen (Avitene, Bard, Murray Hill, New Jersey) or fibrin glue is applied to the parenchyma under an absorbable mesh. If the condition of the patient does not permit the time needed to suture absorbable mesh as a replacement capsule, a mesh sheet is compressed against the parenchyma with a laparotomy pad pack.

FIGURE 38-2 Rapid two-suture splenorrhaphy is faster than splenectomy for patients with AAST grade I or II injuries. (Reproduced with permission from Feliciano DV, Spjut-Patrinely V, Burch JM, et al. Splenorrhaphy: the alternative. Ann Surg. 1990;211:569.)

Gastrointestinal Tract Near transections of the duodenum are stapled shut, while an associated injury to the head of the pancreas is packed (see Chapters 31–33). At the reoperation after metabolic failure has been corrected, duodenal continuity can be restored with an end-to-end anastomosis. A pyloric exclusion with polypropylene suture (Fig. 38-3) and an antecolic gastrojejunostomy (Fig. 38-4) are added in selected patients with severe duodenal contusion, narrowing after a suture repair, or a combined complex pancreatoduodenal injury.127,128 In the patient with a limited number of enterotomies or colotomies from a penetrating wound, a rapid one-layer, fullthickness closure using a continuous suture of 3-0 or 4-0 polypropylene material is appropriate. Multiple large perforations within a short segment of the small bowel or colon are treated with segmental resection, using metallic clips for mesenteric hemostasis and staples to transect the bowel. In the unstable patient, neither an end-to-end anastomosis nor the maturation of a colostomy is performed until the reoperation in 12–72 hours.129 With shotgun wounds and multiple partial and fullthickness perforations of the jejunum, a jejunectomy may be appropriate as all of its absorptive capabilities are duplicated by the ileum.

Pancreas Parenchymal defects not involving the duct are either ignored at the damage control procedure or filled with omentum held in place by a tacking suture (see Chapter 32). The insertion of a closed-suction drain is delayed until the reoperation. Ductal transections to the left of the mesenteric vessels that do not

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Management of Specific Injuries

A

SECTION 3 X

B

©1978 Baylor College of Medicine

FIGURE 38-3 (A and B) Pyloric exclusion is performed through a dependent gastrotomy and completed with no. 1 polypropylene suture. (Reproduced with permission from Baylor College of Medicine.)

involve the splenic vessels are packed or drained, with the distal pancreatectomy and splenectomy once again delayed until the reoperation (Fig. 38-5). Major parenchymal or ductal injuries in the head or neck of the pancreas are also packed or drained, once hemorrhage from the gland or underlying mesenteric– portal vessels is controlled. Pancreatoduodenectomy or reconstruction after a pancreatoduodenectomy caused by the original injury is obviously delayed until the reoperation.129

Abdominal Arteries In any patient with multiple upper abdominal visceral and vascular injuries, a significant injury to the celiac axis or one of its branches is treated with ligation (see Chapter 34). An injury to the renal artery is also best treated with ligation and nephrectomy in the presence of a palpably normal contralateral kidney and multiple associated injuries, although the nephrectomy can be delayed until the reoperation. The use of a large intraluminal shunt (thoracostomy tube) is a theoretical consideration when there has been segmental loss of either the suprarenal or infrarenal aorta in a patient with profound shock; most experienced trauma surgeons, however, would choose to rapidly insert a 12-, 14-, or 16-mm woven Dacron, albumin-coated Dacron, or polytetrafluoroethylene (PTFE) interposition graft and accept an operative procedure that would be 20–25 minutes longer. The superior mesenteric artery or common or external iliac artery is smaller in young trauma patients, and an intraluminal Argyle, Javid, or Pruitt-Inahara shunt may be rapidly inserted under proximal and distal ties to avoid the need for ligation or

emergency interposition grafting.17,130 Should arterial ligation be chosen rather than repair or shunting for a significant injury to the common or external iliac artery, a rapid ipsilateral twoskin incision, four-compartment below-knee fasciotomy may prevent myonecrosis with its associated renal and septic problems should the patient survive to undergo an early (within 6 hours) extra-anatomic revascularization procedure.126 When life-threatening arterial hemorrhage from either a blunt pelvic fracture or a penetrating wound occurs in the deep pelvis and cannot be controlled by packing, several innovative approaches have been used in the past. The first is to insert a Fogarty balloon catheter into the internal iliac artery beyond a proximal tie on the side of the hemorrhage. Advancement of the balloon and sequential inflation is performed until the hemorrhage ceases.131 The catheter may then be folded on itself, the excess cut off, and a ligature applied to maintain inflation of the balloon.100,101,131 The other option is for the surgical team to inject a slurry of autologous clot, two cans of microfibrillar collagen (Avitene, MedChem Products, Inc, Woburn, Massachusetts), one packet of bovine topical thrombin (Armour Pharmaceutical Co, Kankakee, Illinois), and 1 g calcium chloride into the distal internal iliac artery beyond a proximal ligature.132

Abdominal Veins Ligation is the treatment of choice whenever there is a significant injury to the common or external iliac vein, infrarenal inferior vena cava, superior mesenteric vein, or portal vein in a patient with profound shock (see Chapter 34).133–137 After

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©1978 Baylor College of Medicine

FIGURE 38-4 An antecolic gastrojejunostomy is added to the pyloric exclusion to allow for oral intake before the pyloric exclusion opens. (Reproduced with permission from Baylor College of Medicine.)

ligation of the infrarenal inferior vena cava, bilateral fourcompartment below-knee fasciotomies should be performed immediately if the pressure in the anterior compartment of the leg is greater than 25–35 mm Hg, depending on the patient’s hemodynamic status. Bilateral thigh fasciotomies will likely be necessary, as well, within the first 48 hours after ligation. When there are large defects in the sacrum or pelvic sidewall involving numerous pelvic veins or in the paravertebral area, a number of innovative approaches are available to rapidly control hemorrhage. Included among these are packing the missile track with several vaginal packs (to allow for postoperative pelvic or paravertebral arteriography), inserting fibrin glue, or placing a Foley catheter with a 30-mL balloon inflated at the site of hemorrhage as previously described. Placing packs outside the blast cavity in the deep pelvis or paravertebral area often fails to control hemorrhage in the patient who develops a coagulopathy. Bleeding from presacral veins can be controlled by inserting sterile tacks directly into

the visible defect or by suturing a free piece of omentum into an obvious area of perforation.

Intra-Abdominal Packing When severe shock, hypothermia, acidosis, and massive transfusion have led to a coagulopathy and diffuse nonmechanical bleeding, the insertion of intra-abdominal packing for tamponade is appropriate.57,116–118,138–140 Diffuse intra-abdominal packing has been found to be particularly useful when a coagulopathy occurs and extensive retroperitoneal or pelvic dissection has been necessary during a laparotomy for a trauma. Dry, folded laparotomy pads much as described for perihepatic packing are preferred followed by an alternate form of incisional closure. In general, a relaparotomy is performed to remove the packs, irrigate out old blood and clot, and rule out injuries missed at the original damage control laparotomy. In the original series from Grady Memorial Hospital reported by Stone et al.,138 17 trauma patients with intraoperative

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Management of Specific Injuries

SECTION 3 X FIGURE 38-5 Distal pancreatectomy with splenectomy may be completed at the reoperation rather than at the damage control laparotomy. (Reprinted with permission from Cushman JG, Feliciano DV. Contemporary management of pancreatic trauma. In: Maull KI, Cleveland HC, Feliciano DV, et al., eds. Advances in Trauma and Critical Care. Vol. 10. St. Louis: Mosby; 1995:309–336. © Elsevier.)

coagulopathies underwent damage control laparotomy including the insertion of diffuse packing with laparotomy pads. Reexploration was performed at 15–69 hours in 12 surviving patients, and 11 survived removal of the packs and definitive laparotomy.138

■ Operative Techniques with Vascular Trauma in an Extremity Damage control operations on an extremity are appropriate when exsanguination has caused intraoperative metabolic failure (shotgun wound of femoral triangle); when multisystem injuries have occurred and an emergent craniotomy, thoracotomy, or laparotomy needs to be performed in addition to the vascular repair of the extremity (occlusion of superficial femoral artery from a femur fracture); or when the instability of an open fracture precludes formal repair of the associated vascular injury (mangled extremity) (see Chapter 41).141 After rapid control of hemorrhage, an intraluminal Argyle or Javid shunt is inserted into the debrided ends of the injured femoral or popliteal artery and tied in place to preserve distal flow as the patient is resuscitated in the intensive care unit.17 The Pruitt-Inahara shunt may be used also and has inflatable balloons on either end so that tying the shunt in place is not necessary. This shunt has a T-port, which allows for the infusion of heparin, a vasodilator such as papaverine, or for arteriography in the postoperative period. A recent 10-year review of the use of 101 intravascular shunts at a single center found that shunts have a thrombosis rate of 5% and a limb/patient survival rate of 73% supporting their use in damage control

procedures.17 In spite of their utility, the use of shunts nationwide is very limited.142 While ligation of major venous injuries in the extremities has been well tolerated in many stable patients,143,144 patients undergoing damage control operations often have severe sequelae.141 Among these are a compartment syndrome below the level of ligation in the lower extremity and excessive hemorrhage from soft tissue injuries and fasciotomy sites. Even if a compartment syndrome does not occur immediately, reperfusion injury as the patient undergoes resuscitation in the intensive care unit will often cause the syndrome to develop. For these reasons, venous outflow after segmental resection of an injured femoral or popliteal vein should be restored with a temporary intraluminal shunt as part of a damage control operation. Short segments of thoracostomy tubes (size 24–28 French) are used as shunts for the popliteal, superficial femoral, or common femoral veins. After removal of the shunt at a reoperation, an externally supported PTFE graft is used for segmental replacement.145 When vascular control has been difficult to obtain with combined femoral or popliteal arterial and venous injuries, there may be some delay before the intraluminal shunts are inserted. In such a situation or when ligation of the femoral or popliteal vein has been necessary to prevent exsanguination, additional time should be spent to complete an ipsilateral four-compartment below-knee fasciotomy as part of the damage control operation. With two attending surgeons or senior residents performing these procedures, they can be completed within 20 minutes. The additional time involved prevents myonecrosis in the early postoperative period and allows the critical care team to focus on respiratory, cardiac, and renal resuscitation.

Trauma Damage Control

INDICATIONS FOR ALTERNATE CLOSURES OF INCISIONS In the previously described patients with hypothermia (temperature 35°C [95.0°F]), persistent acidemia (pH 7.2), and/or the onset of an intraoperative coagulopathy, a damage control operation should be terminated with an alternate closure of the incision.

■ Planned Reoperation One of the fundamental principles of the damage control operation is that a reoperation will be necessary to complete repairs and resections, perform anastomoses, look for missed injuries, change thoracostomy tubes, insert drains, and attempt closure of the incision. There are also techniques utilized at first operations for trauma, whether damage control was necessary or not, that mandate an early reoperation. Patients in whom the following techniques are used will also benefit from alternate forms of closure of the thoracic or abdominal incision: • Insertion of perihepatic packing • Insertion of intra-abdominal packing • Planned second-look operation Examples of patients who may require an early secondlook procedure after laparotomy for abdominal trauma include those with primary repair of the renal or superior mesenteric artery and those with ligation of the superior mesenteric or portal vein. In the former group, repair of a small vasoconstricted artery in a hypotensive patient often leaves the surgeon with concern about an early postoperative thrombosis.137,146 Early reoperation allows for visual inspection of the end organ after the patient has become hemodynamically stable. With major venous injuries, the dusky and congested appearance of the bowel after major splanchnic venous ligation during the initial operation often prompts concerns about secondary infarction of the involved intestine.134–136 Planned reoperation is worthwhile in such patients, particularly if the base deficit does not correct in the first 8–12 hours after the ligation was performed.

■ Closure of the Incision Cannot Be Performed or Will Cause an Abdominal Compartment Syndrome Edema and distention of the midgut have been commonly noted in the past during prolonged laparotomies for trauma in which patients in shock have been treated with the old paradigm of massive crystalloid resuscitation in addition to blood. Presumably, these changes are related to cellular edema from metabolic failure of the sodium pump in the cell membrane, a “capillary leak” phenomenon with secondary interstitial edema related to the release of vasoactive substances, reperfusion injury, the development of an ileus, or some combination of

ABDOMINAL COMPARTMENT SYNDROME ■ Definition The abdominal compartment syndrome refers to new organ dysfunction/failure (especially decreased blood flow to the body wall and abdominal organs and secondary pressure effects on the respiratory, cardiovascular, and central nervous systems) when the intra-abdominal pressure (IAP) is sustained at greater than 20 mm Hg level.23,24,151 While occasionally discussed in the literature since the 1800s, it is only in the past 25 years that the diagnosis has been made on a regular basis in patients on a variety of surgical and medical services.25–33,151,152 The current subtypes of the abdominal compartment syndrome are defined as follows:151 1. Primary—acute or subacute intra-abdominal hypertension from an abdominal cause; 2. Secondary—subacute or chronic intra-abdominal hypertension from an extra-abdominal cause;153 and 3. Recurrent—redevelopment of the abdominal compartment syndrome following treatment of a primary or secondary type.

■ Measurement of Intra-Abdominal Pressure Direct measurement of IAP is accomplished by inserting an intraperitoneal catheter attached to a manometer or transducer.154 In the clinical setting, indirect measurement is possible through a catheter inserted into the urinary bladder,155,156 stomach,157 or inferior vena cava.158 The ease and accuracy of measuring IAP at the level of the symphysis pubis through a saline column (25 mL) previously injected into an empty bladder and connected to a pressure transducer or manometer is well known and remains the technique of choice.155,156 The validity of the bladder pressure as a measure of IAP has been well documented.159 A technique for the continuous measurement of IAP via the urinary bladder has also been described utilizing the irrigation port of a three-way Foley catheter; this technique may theoretically allow for a more timely identification of elevated IAP.160,161 The World Society of the Abdominal Compartment Syndrome (WSACS) defines IAP as being measured at end expiration in the relaxed patient in a supine position.151 This pressure is normally less than 10 mm Hg, while intra-abdominal hypertension is defined as a pressure greater than 12 mm Hg.

CHAPTER CHAPTER 38 X

■ Intraoperative Metabolic Failure

these.23,24,147–150 The volume of the midgut may increase significantly and, if perihepatic or intra-abdominal packs have been inserted as well, make formal fascial closure of the midline abdominal incision time-consuming and extraordinarily difficult. Should fascial closure be completed successfully, the increased volume and secondary increase in pressure (normal: 0 to subatmospheric) in the abdominal cavity may have severe adverse systemic effects, manifesting as the abdominal compartment syndrome.23–33

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Management of Specific Injuries

■ Clinical Manifestations of Intra-Abdominal Hypertension SECTION 3 X

A comprehensive discussion of all the effects of intra-abdominal hypertension causing an abdominal compartment syndrome is beyond the scope of this chapter, and the reader is referred to published clinical and laboratory reviews and studies (Table 38-4).24–33,151,152,162–189

■ Proposed Classification The group at Denver Health Medical Center first proposed a grading system for the abdominal compartment syndrome in 1996.24 This grading system was slightly modified in a subsequent publication and is presented along with recommendations for management based on an indirect measurement of IAP in Table 38-5.190 These recommendations were based on a study of 145 acutely injured patients (ISS 15) undergoing laparotomy, 21 of whom developed an abdominal compartment syndrome (Table 38-6). Of interest, this study validates an IAP of 25 mm Hg as an indicator to decompress the abdominal compartment syndrome.

TABLE 38-4 Clinical and Laboratory Manifestations of Increased Intra-Abdominal Pressure162–189 Abdominal Body wall162,163 Decreased blood flow Gastrointestinal tract164–168 Decreased mucosal blood flow and intramucosal pH Possible bacterial translocation Hepatic169,170 Decreased portal blood flow and hepatocyte mitochondrial function Renal171–177 Increased renal vein pressure Increased plasma renin and aldosterone Decreased renal blood flow, glomerular filtration rate, and urine output Thoracic Lung174,178–180 Increased intrathoracic pressure, peak airway pressure, peak inspiratory pressure, and intrapulmonary shunt Decreased dynamic compliance Heart/cardiovascular174,178,181–185 Decreased venous return and cardiac output “False” increase of central venous pressure and pulmonary artery wedge pressure Increased systemic and pulmonary vascular resistance Central nervous system186–189 Increased intracranial pressure secondary to decreased venous return Decreased cerebral perfusion pressure

TABLE 38-5 Grading of the Abdominal Compartment Syndrome Bladder Grade Pressure (mm Hg) I 10–15 II 16–25 III 26–35 IV 35

Recommendation Maintain normovolemia Hypervolemic resuscitation Decompression Decompression and reexploration

Reproduced with permission from Meldrum DR, Moore FA, Moore EE, et al. Prospective characterization and selective management of the abdominal compartment syndrome. Am J Surg. 1997;174:667. © Elsevier.

WSACS has subsequently defined the categories of intra-abdominal hypertension as follows:151 (1) grade I—IAP 12–15 mm Hg; (2) grade II—IAP 16–20 mm Hg; (3) grade III—IAP 21–25 mm Hg; (4) grade IV—IAP greater than 25 mm Hg. Using this classification system and the data in the older Denver paper, two thirds of patients now classified as grade IV would be expected to have the following: (1) a peak airway pressure greater than 45 cm H2O; (2) a systemic vascular resistance greater than 1,000 dynes . sec/cm5; and (3) a urine output less than 0.5 mL/(kg h).24,151

■ Abdominal Perfusion Pressure In one report, abdominal perfusion pressure defined as mean arterial pressure minus IAP was compared with IAP, arterial pH, base deficit, arterial lactate, and urinary output as an end point of resuscitation and as a predictor of survival.191 The authors found that an abdominal perfusion pressure of 50 mm Hg was a potential end point for resuscitation in the patient with

TABLE 38-6 Percentage of Patients with Respective Organ Dysfunction Per Grade of Abdominal Compartment Syndrome UO 0.5 Grade mL/(kg h) PAP 45 I 0% 0% II 0% 40% III 65% 78% IV 100% 100%

SVR 1,000 DO2I 60 0% 0% 20% 20% 65% 57% 100% 100%

DO2I  oxygen delivery index (mL O2/(min m2)); PAP  peak airway pressure (cm H2O); SVR  systemic vascular resistance (dynes • sec/cm5); UO  urine output (mL/min). Reproduced with permission from Meldrum DR, Moore FA, Moore EE, et al. Prospective characterization and selective management of the abdominal compartment syndrome. Am J Surg. 1997;174:667. © Elsevier.

Trauma Damage Control

■ Secondary Abdominal and Extremity Compartment Syndromes There is now widespread recognition that the abdominal compartment syndrome can occur in the absence of intra-abdominal injuries.28,30,31,33 This “secondary” abdominal compartment syndrome is thought to be due to an ischemia and reperfusion injury in the gastrointestinal tract as well as a capillary leak syndrome from abdominal viscera.28,30 All patients who have developed this syndrome present with severe injuries, sepsis, or burns 41% and usually 70% total body surface area. Massive resuscitation has been necessary in all patients reported to date (mean of 19  5 L of crystalloid and 29  10 U of PRBCs in one report).30 Of interest, the diagnosis of a secondary abdominal compartment syndrome has been made from 3 hours to 9 days after injury.28,30,31 The mortality in four reports has been 65.5% (19/29).28,30,31 Another related concern in the patient undergoing a massive resuscitation is the development of a secondary extremity compartment syndrome (SECS). Similar to secondary ACS, SECS is associated with extremely high morbidity and mortality (70%).192 Serial measurement of creatine phosphokinase (CPK) and urine myoglobin may be appropriate in high-risk patients as a screening tool. Any individual with persistently rising CPKs or the unexplained development of myoglobinuria may benefit from measurement of extremity compartment pressures and fasciotomies as appropriate.

■ Prevention and Management of the Abdominal Compartment Syndrome The abdominal compartment syndrome is prevented by leaving the midline celiotomy incision open in high-risk patients. Because the syndrome can have a delayed presentation after trauma and resuscitation or develop even though there are no abdominal injuries (secondary abdominal compartment syndrome), there are still critically injured or ill patients who will require treatment. Innovative approaches to avoiding a return to the operating room for abdominal decompression have included laparoscopic decompression or the insertion of either an angiocatheter or a peritoneal dialysis catheter to remove intraperitoneal fluid.193,194 Another interesting approach used successfully in a laboratory model has been the application of a continuous negative abdominal pressure (CNAP) device.189,195

OPERATIVE TECHNIQUES FOR THE OPEN ABDOMEN Management of the open abdomen can be divided into two phases. In the acute phase, the goal is to provide some variant of temporary coverage to allow the patient to be taken from the operating room to the intensive care unit for additional resuscitation and stabilization with the intent on returning to the operating room when normal physiology has been restored. In

the second phase, which follows reoperation, the issue is the management of the abdominal wound and techniques range from delayed fascial closure to planned ventral hernia.

■ Towel Clip or Suture Closure of the Skin The simplest and most rapidly performed technique for temporary closure of a thoracic, abdominal, or groin incision in the unstable trauma or septic patient is towel clip or suture closure of only the skin.23 Depending on the length of the incision, up to 25–30 standard towel clips may be necessary to complete closure of the wound during a 2-minute period. In order to prevent manipulation of the towel clips and minimize secondary contamination of the chest, abdomen, or groin through the spaces between the towel clips, a large adherent plastic drape is placed over the towel clips and Jackson-Pratt drains are placed lateral to the incision in the operating room prior to transfer to the intensive care unit. When suture closure of only the skin is chosen, 2-0 nylon or thicker suture material is used, depending on the tension of the closure. These skin-closure-only techniques are used much less frequently than they were in the past as increases in postoperative IAP have led to the abdominal compartment syndrome in a significant number of patients.

■ Temporary Silos When the extent of edema and distention of the thorax or the presence of multiple intra-abdominal packs prevents towel clip or suture closure of the skin of the abdominal incision, the insertion of a silo to cover the exposed viscera is performed (Fig. 38-6). Complete coverage of the open abdomen using a polyvinyl plastic silo was first performed by Oswaldo Borraez G. at the San Juan de Dios Hospital in Bogota, Colombia, in March 1984. As the technique of complete silo coverage has become more acceptable since that time, a variety of materials and techniques have been used. When only a small- or moderate-sized silo is needed, an adherent plastic wound drape (SteriDrape, 3M Healthcare, St. Paul, Minnesota) is applied to the skin edges around the open abdomen. In patients with significant distention of the midgut or peritoneal contents secondary to packs, the soft plastic drape will not be adequate to maintain the midgut within the confines of the abdominal incision. A readily available stronger silo is a 2.5-L plastic bag of irrigating solution used by the urology service (Fig. 38-7).196 A large silo of this material is constructed by cutting three seams of the bag open, and then gas autoclaving the large rectangular piece that results. This silo is sewn to the skin edges of the abdominal wound with 2-0 nylon or polypropylene suture. Another strong silo is Silastic sheeting (Dow Corning Corp, Midland, Michigan), but this is considerably more expensive than the bag of irrigating solution.197 Even the “fish” available in every operating room has been used as a temporary silo.198 Some groups have used gradual reduction in the size of the silo, much as has been described in the pediatric surgical literature for neonates with an omphalocele or gastroschisis.199 In patients with significant distension of the midgut after removal of the temporary silo at a first reoperation, application of a vacuum-assisted closure (VAC) device (Kinetic Concepts, Inc, San Antonio, Texas) is now commonly performed (see below).

CHAPTER CHAPTER 38 X

an elevated IAP. Also, the abdominal perfusion pressure was statistically superior to the other end points listed in predicting survival for patients with intra-abdominal hypertension and the abdominal compartment syndrome.

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Management of Specific Injuries

SECTION 3 X FIGURE 38-6 Esmarch bandage silo closure of bilateral anterolateral thoracotomy in patient with six missile perforations in the heart and inferior vena cava.

■ Combination Closure

■ Vacuum-Assisted Wound Closure

In patients with significant hepatic injuries requiring perihepatic packs, a combination of closures may be appropriate. In such a patient, it is sometimes desirable to have a “tight” closure of the upper abdomen to maintain tamponade of the injured liver. Partial fascial closure limited to the upper abdomen or partial towel clip closure of the same area may be used in conjunction with a silo placed over the lower abdomen. This arrangement maintains a tamponade effect on the injured liver while allowing ample room for expansion of the midgut to avert the development of an abdominal compartment syndrome.

A number of early reports described excellent results with “homegrown” vacuum pack coverage of the open abdomen.200,201 On a cellular level, studies have shown that the application of micromechanical forces created by the negative suction promotes cell division, angiogenesis, and the local elaboration of growth factors all without increasing apoptosis.202,203 Practically speaking, applying suction to the open wound over the midgut allows for the rapid removal of peritoneal fluid and collapses spaces between the viscera. As both of these results will make the contents of the abdominal

FIGURE 38-7 Plastic irrigating bag sewn to the skin edges of the abdominal wound makes an excellent silo.

Trauma Damage Control

■ Open Packing This older technique using nylon cloth material over the midgut has been used at Detroit Receiving Hospital for over 35 years.36,204 The cloth is covered with “generous” gauze packs, while several widely spaced retention sutures are placed through the abdominal wall above the packs. Every effort is made to keep the midgut below the aponeurotic edges. As midgut edema resolves, the patient is returned to the operating room for removal of the gauze and gradual tightening of the retention sutures until the linea alba can be closed. In the report by Bender et al., 15 of 17 patients surviving longer than 24 hours had successful closure of the midline incision using the technique described.204 There were no enterocutaneous fistulae or incisional hernias in the 14 long-term survivors. A number of related approaches have been described in the literature as well.41,42

described the use of a continuous arteriovenous rewarming (CAVR) device. In the patient with a systolic blood pressure greater than 80 mm Hg, femoral arterial and venous catheters are connected through the heating mechanism of a standard countercurrent fluid warmer. The patient’s own blood pressure drives the blood through heparin-bonded tubing; therefore, use of this system is limited in hypotensive patients. In a mixed group of 34 hypothermic patients (35°C [95.0°F]) with trauma, major operations, or near drowning, 16 patients treated with CAVR had resolution of their hypothermia in 39 minutes versus 3.23 hours in the group of 18 treated with the conventional methods described above. Inability to correct a patient’s hypothermia after a damage control operation is a marker of inadequate resuscitation or irreversible shock.70 The multifactorial coagulopathy still seen in some trauma patients must be aggressively managed, as well. Postoperatively, patients undergoing damage control procedures should have serial coagulation parameters monitored including routine measurement of fibrinogen levels to assess the need for cryoprecipitate in addition to fresh frozen plasma and PRBCs. Several parameters may be utilized to assess the adequacy of a resuscitation, with acidosis being one of the most common. It is generally accepted that resuscitation is not complete until the patient’s oxygen debt is repaid; simple restoration of normal vital signs is not adequate as a patient may simply be in “compensated” shock while continuing to have occult hypoperfusion and ongoing tissue damage.206 Extensive studies have been performed to determine the parameters that best define the end point of resuscitation. These end points can be divided into two broad categories, global and regional. In addition to acid–base status, parameters for monitoring global resuscitation include oxygen delivery, mixed venous saturation, right ventricular end-diastolic volume, left ventricular stroke work index, and others.206 From a regional perspective, gastric tonometry and intramucosal pH have been used to assess gastric perfusion. Additionally, both spectroscopy and electrodes have been applied to measure tissue pO2, pCO2, and pH in muscle and subcutaneous tissue to assess peripheral perfusion.206,207 While these techniques may all provide data that can be used to predict outcome, none has been proven to be a superior marker of the end point of resuscitation.208 Still, it is recommended that one of these end points be monitored in addition to the standard clinical parameters to assess the adequacy of resuscitation.209

INTENSIVE CARE BEFORE REOPERATION Following the control of surgical bleeding, patients are brought to the intensive care unit for ongoing resuscitation. The immediate goals are to both provide adequate oxygenation and reverse the effects of inadequate tissue perfusion and resultant metabolic failure. The lethal triad of hypothermia, coagulopathy, and acidosis must be aggressively rectified if the patient is to survive. All of the previously described warming maneuvers used in the emergency department and operating room—increased ambient temperature, external rewarming using a Bair Hugger or similar device, warming lights, and warmed fluid and blood products—are implemented in the intensive care unit, also. For refractory cases of hypothermia, Gentilello et al.205 have

REOPERATION ■ Emergency Reoperation Failure to attain the desired end points of resuscitation during the ICU phase of damage control may reflect continuing hemorrhage.57,210 An early return to the operating room is a difficult decision because the hypothermia-related coagulopathy is often not resolved. Therefore, the surgeon must decide whether mechanical or surgical hemorrhage is occurring versus diffuse oozing from a coagulopathy in which an early reoperation may not be indicated. Morris et al.211 have suggested several indicators for an emergent return to the operating room

CHAPTER CHAPTER 38 X

cavity smaller, there is a greater chance of formal aponeurotic closure of the midline incision. In the report by Barker et al.,38 216 vacuum packs were placed in 112 patients. While 22 patients (19.6%) died before abdominal closure was attempted, 62 (55.4%) went on to formal closure of the incision. The overall mortality rate in this large series was 25.9%. As previously mentioned, the Kinetic Concepts, Inc VAC system has been utilized in many centers.39 A nonadherent occlusive plastic barrier (Steri-Drape, 3M Healthcare) with small perforations placed in it is covered by an appropriately sized polyurethane foam sponge that is part of the VAC system. The suction tubing that is part of the system is attached, and the entire system is covered with an airtight occlusive drape. KCI has recently introduced an updated product, ABThera, which theoretically provides improved negative pressure distribution throughout the abdominal cavity. In the report by Garner et al.,39 13 of 14 injured patients in whom the original system was used underwent formal closure of the midline incision before discharge. Clinical studies on the ABThera are currently lacking. Also new to the market is the ABRA Abdominal Wall Closure System available from Canica (Ontario, Canada). This product integrates a silicone traction component with a skin fixation component. The combination is used to provide gentle elastic traction on the tissues theoretically preventing loss of abdominal domain and facilitating primary wound closure. As with the ABThera, clinical studies are still needed on this device.

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SECTION 3 X

TABLE 38-7 Indications for Emergent Return to the Operating Room After a Damage Control Laparotomy

TABLE 38-8 Guidelines for Elective Return to the Operating Room After a Damage Control Laparotomy

Blunt Trauma Normothermic but bleeding 2 U/h Abdominal compartment syndrome with ongoing blood loss

Temperature 30°C (96.8°F) Acid–base balance Base deficit corrected to  5 mmol/L if originally  15 mmol/L Serum lactate normal or correcting gradually Coagulation Prothrombin time 15 s Partial thromboplastin time 35 s Platelets 50,000/μL Cardiovascular Cardiac index 3 L/(min m2), with or without lowdose inotrope Pulmonary Fraction of inspired oxygen 0.50 O2 saturation 95%

Penetrating Trauma Bleeding 15 U and hypothermia Normothermic but bleeding 2 U/h Abdominal compartment syndrome with ongoing blood loss

Reproduced with permission from Morris JA Jr, Eddy VA, Rutherford EJ. The trauma celiotomy: the evolving concepts of damage control. Curr Probl Surg. 1996;33:611. © Elsevier.

based on continuing hemorrhage after a damage control laparotomy (Table 38-7).211 Another obvious indication for an early reoperation is the development of the previously described abdominal compartment syndrome. A progressive increase in inspiratory pressures on the ventilator coupled with oliguria and a “tight” abdomen mandates a rapid measurement of IAP through the bladder catheter.155,156 Reoperation is necessary when the clinical signs are accompanied by an IAP greater than 25 mm Hg, as previously described.24,190 Morris et al.57,211 and many others have noted that sudden release of the abdominal compartment syndrome at the time of reoperation may lead to a reperfusion phenomenon and a cardiac arrest. For this reason, Morris has recommended that volume loading with 2 L of a solution composed of 0.45% normal saline, 50 g mannitol/L, and 100 mEq sodium bicarbonate/L be performed before release of the abdominal wall.

■ Routine Reoperation When postoperative bleeding is not a concern, a return to the operating room is based on reversal of metabolic failure and normalizing of cardiovascular, pulmonary, and coagulation parameters as suggested by Morris et al. (Table 38-8).211 In a review of patients with perihepatic packs inserted to control hemorrhage, relaparotomy was performed at a mean time of 3.7 days from the original damage control operation.116 The timing of reoperation, however, may be more critical than has previously been thought, as it may act as a “trigger” for sensitized leukocytes circulating during post-traumatic inflammation (“second hit phenomenon”). As multiple-organ failure may result, the timing of reoperation may turn out to be one of the more critical factors in determining survival after a damage control operation.212–215 Another factor to consider is that the presence of intra-abdominal packs alone results in peritoneal endotoxin and accumulation of inflammatory mediators even when cultures are sterile.216

Modified with permission from Morris JA Jr, Eddy VA, Rutherford EJ. The trauma celiotomy: the evolving concepts of damage control. Curr Probl Surg. 1996;33:611. © Elsevier.

A patient who is normotensive, without a coagulopathy, and is in the diuretic phase of recovery after resuscitation from shock is an ideal candidate for reoperation. While this usually takes place within 48–72 hours of the damage control laparotomy, it may be delayed in patients with massive distention of the midgut so that a further diuresis may occur. If towel clips were used to close the abdominal wall at the damage control laparotomy, five of every six are removed at the first stage of reoperation. The remainder are then elevated off the abdominal wall by placing them on a sponge stick as scrubbing and painting of the abdominal wall are performed. After the surgical team has placed sterile towels around the wound, the final towel clips are removed. This technique prevents evisceration during the period of skin preparation. Once the towel clips, skin sutures, or silos have been removed, clots and packs are evacuated manually and with the suction device. A complete examination of all abdominal contents is performed to detect any injuries missed at the damage control laparotomy.23 Resections, anastomoses of the bowel, and maturation of colostomies are rapidly performed in the hemodynamically stable patient. Prior to closure, the abdominal cavity is vigorously irrigated with saline solution containing antibiotics. This solution is left in the abdominal cavity during the 3–5 minutes that it takes for the surgical team to change gloves and place towels around the wound. The irrigating solution is then aspirated from the abdominal cavity, and drains are inserted as indicated. The linea alba is closed with permanent suture, while the subcutaneous tissue and skin are packed open.

Trauma Damage Control

■ Techniques for the Management of the Open Abdomen at Reoperation When a VAC device is not available, a Steri-Drape or plastic silo may be reapplied at the reoperation in the distended patient as it protects the midgut, prevents evaporation, and allows for visual confirmation that the midgut is decreasing in size during the diuretic phase of recovery.43

Vacuum-Assisted Fascial Closure Any of the vacuum dressing techniques discussed in Section “Operative Techniques for the Open Abdomen” can also be initiated following resuscitation at the reoperation.39,217–219 Cothren et al.217 reported a 100% fascial closure rate using vacuum-assisted sequential fascial reapproximation. At the time of initial operation, a silo was applied. Following stabilization of the patient, they used a variant of the technique described by Miller et al.219—placing a nonadherent dressing over the viscera and under the fascia, using fascial sutures to provide moderate tension, placing a superficial sponge layer, and then placing the wound to suction. They returned patients to the operating room every 2 days for replacement of the sponges and gradual fascial closure. Other authors have reported excellent results with vacuum devices reporting closure rates ranging from 71.9% to 92% and few complications, also.39,218,219 At the present time, this appears to be the preferred technique for management of the open abdomen.

Zippers, Slide Fasteners, Velcro Analogue Originally described by Leguit in 1982,201 the zipper closure of the abdominal wall was popularized by Stone et al.220 in the United States in their open treatment of patients with pancreatic abscesses. Either a conventional zipper is sutured to the skin or fascia with a continuous suture of 0 or 2-0 nylon or polypropylene or a commercial zipper with adhesive side pieces is applied to the skin edges. The major advantage of using the skin is that it preserves the fascia for formal wound closure at an appropriate time. Another option for septic or trauma patients reported by Teichmann et al.,221 Wittmann et al.,222 and Aprahamian et al.223 is the Wittmann Patch (Starsurgical, Burlington, Wisconsin). In this system two sheets of Velcro-like biocompatible material are sewn to the aponeurotic edges of the midline incision. Closure is accomplished by the adherence between the overlapping Velcro-like sheets. As edema of the midgut resolves, excess patch material is trimmed, and the fascial edges can be pulled closer together. The major advantages of this system are in the ease of access for reoperations and the tension on the aponeurotic edges that prevents the usual lateral retraction. Tieu et al.224 reported an 82% closure rate using the Wittmann Patch in a mixed population of trauma and critically ill surgery patients. In a study by Weinberg et al.,225 delayed primary fascial closure was achieved in 78% of trauma patients treated with the Wittmann Patch. A “modified Wittmann” technique was described by Fantus et al.226 who placed a nonadherent

Permanent Meshes For the trauma patient with marked distention of the midgut, a PTFE body wall patch is strong and watertight and creates a smooth layer of granulation tissue that can be covered with a split-thickness skin graft when the prosthesis is removed. Unfortunately, this prosthesis is quite expensive, and similar results have been obtained with less expensive absorbable meshes as previously described. Numerous clinicians have described short-term success with closure of the abdominal wall with Marlex mesh in the presence of extensive fasciitis or intra-abdominal sepsis.227–230 Healing of the wound over the mesh has been reported in many patients, even in those in whom grossly purulent material surrounds the mesh.231 Numerous long-term complications, however, are common. In the report by Voyles et al.229 describing the use of Marlex (Bard) mesh in 31 acute abdominal wall defects, 9 wounds were closed by split-thickness grafts over granulated mesh. In each instance, extrusion of the mesh and/or enteric fistulae developed. Nine other wounds healed by secondary intention, and six of these developed extrusion of the mesh or enteric fistulae. Stone et al.228 reported on the use of Marlex mesh in 23 patients with acute full-thickness loss of the abdominal wall from trauma or sepsis and noted that the mesh eventually had to be removed in all but 2 patients. They also commented that “Marlex has twice the incidence of postoperative wound sepsis, almost six times as many associated bowel fistulas, and less than one third as many successful skin graft takes for cover” compared with Prolene mesh. These data strongly suggest that a permanent rigid prosthesis such as Marlex or Prolene mesh should not be inserted in abdominal wall defects in the presence of extensive contamination from a perforated gastrointestinal tract secondary to trauma, acute intra-abdominal sepsis, or necrotizing infection in the abdominal wall.232 The risk of secondary infection and damage to the underlying bowel as the prosthesis develops “wrinkles” from contraction of the wound has now been documented on numerous occasions.

Absorbable Meshes Synthetic meshes such as polyglactin (Vicryl) and polyglycolic acid (Dexon) have been available to the surgeon for the past 30 years. They have been used primarily for renorrhaphy, splenorrhaphy, and hepatorrhaphy in abdominal trauma and for closure of the pelvic floor after abdominoperineal resection of the rectum. In laboratory studies using absorbable meshes to repair defects in the abdominal wall, bursting strength has been comparable to that of permanent meshes for the first 8 weeks after insertion.233–235 Unfortunately, as the mesh is absorbed, hernias or decreased bursting strength at the site of the mesh develop by 10–12 weeks after insertion.233,235

CHAPTER CHAPTER 38 X

Repeat Application of a Silo

layer, such as the previously mentioned sterile x-ray cassette cover, under the abdominal wall and over the viscera to decrease the formation of adhesions that can form between the two hindering delayed fascial closure. They achieved good closure rates, also.

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Management of Specific Injuries

SECTION 3 X FIGURE 38-8 Remains of double-layer absorbable mesh coverage of open abdomen on the day a split-thickness skin graft is to be applied. Patient sustained quadriplegia, rupture of the descending thoracic aorta, and a secondary abdominal compartment syndrome after being struck by a motor vehicle.

The primary clinical use of absorbable meshes as an alternate form of coverage of the open abdomen on the trauma service has been in patients with marked distention of the midgut at the time of removal of a plastic silo or VAC device.236 It has been used in patients with open abdomens from septic processes in the abdominal wall or in the abdominal cavity, also.230,231 Fabian et al.45 have described four stages in the use of absorbable mesh to cover an open abdomen. These include the following: (a) coverage of the midgut; (b) removal of the mesh after granulation tissue has formed at 2–3 weeks (Fig. 38-8);

(c) split-thickness skin grafting of granulation tissue or abdominal skin and subcutaneous flap closure over the granulation tissue several days later (Fig. 38-9); and (d) definitive reconstruction in 6–12 months. One practical point in using absorbable mesh is that the Dexon variant has wider interstices that allow for drainage of intra-abdominal fluid.75 Another is to use fine mesh gauze packing above the absorbable mesh. The gauze packing will aid in keeping the small bowel below the level of the fascia of the abdominal wall, much as has been described by Bender et al.204

FIGURE 38-9 A meshed split-thickness skin graft has been applied to the granulated abdomen of the same patient as in Fig. 38-8.

Trauma Damage Control

WHAT HAPPENS TO PATIENTS WHEN A VACUUM-ASSISTED CLOSURE IS NOT USED? Tremblay et al.40 reported on a 4-year experience with 181 patients with an open abdomen who were managed with techniques other than VAC—silos, skin only or towel clip closure, open packing, and modified visceral packing. The morbidity in the series was high as 14% of patients developed enterocutaneous fistulas, 5% suffered wound dehiscence, and almost half of the patients in the series were left with large incisional hernias at the time of discharge. The results in this series do not compare favorably with the closure rates and complications associated with the use of the VACs (see above). It appears, then, that some method of vacuum-assisted technique should be applied in the majority of patients.

LATE CLOSURE OF THE INCISIONAL HERNIA Only 10–20% of patients undergoing use of a VAC device are left with an incisional hernia after damage control procedures. When a hernia does result, either following an attempted closure or as the planned result following the use of absorbable mesh, it is appropriate to delay closure for 6–12 months. Any stomas should also be taken down in the same delayed fashion. This interval allows the patient to improve his or her nutritional status, fully recover from the original injuries, and complete the formation of adhesions and scars in the abdominal cavity and body wall. When assessing the patient with a massive ventral hernia preoperatively, one must carefully examine the abdominal skin graft. If the physician can pull the graft up and off of the underlying small bowel, that is, if the patient passes the “pinch test,” the timing is supposedly right for repair.45 In truth, dense adhesions between the underside of the skin graft and the underlying small bowel are present in over half of the patients. Additionally, one must determine if adequate skin will be available to cover the viscera and prosthetic, if used, once the skin graft to the abdomen has been excised. If it appears that skin will be lacking, lateral tissue expanders should be placed

under the skin 2–3 months prior to undertaking reconstruction of the abdominal wall. Should scarring of the abdominal wall or the presence of a colostomy prevent the use of a tissue expander on one side of the abdominal wall, a tensor fascia lata myocutaneous flap may have to be elevated off the ipsilateral thigh, and then tacked back in place several weeks before reconstruction of the abdominal wall. Finally, there are patients in whom the extent of evisceration under the old skin graft brings the anterior and posterior abdominal walls into close proximity resulting in a loss of domain of the abdominal cavity. Such patients will usually require the insertion of large prosthetic patches to cover the hernia defect as well an extensive amount of skin to cover the patch. It is the policy of the senior author of this chapter to perform the takedown of end colostomies and restoration of gastrointestinal continuity before any reconstruction of the abdominal wall. As a first stage, the old skin graft is detached from the abdominal wall for 180° of its 360° attachment. For a left-sided colostomy, the best exposure for the takedown of the end colostomy and colon reanastomosis would result from detaching the skin graft from the 12- to 6-o’clock positions. The detached skin graft is folded back, adhesions are divided, the rectal or left colon pouch is mobilized, and the anastomosis is performed. The reflected skin graft is then returned to its original position and the abdominal viscera are covered by tacking the edge of the skin graft back down. The abdominal wall reconstruction is then performed at a later date. In selected patients, the narrow midline defect that remains after excision of the skin graft over the midgut can be readily closed with a continuous or interrupted suture technique using no. 1 polypropylene material.46 When it is not possible to close secondary to excessive tension on linea alba, the components separation technique of closure is used. The skin and fat are elevated off the underlying fascia through the midline incision or using a lateral laparoscopic approach until the flaps extend to several centimeters lateral to the rectus sheath. The external oblique aponeurosis is then divided lateral to the rectus muscle bilaterally from the lower thoracic wall to just above the inguinal ligament. Each relaxing incision usually creates an additional 4–5 cm of width to the abdominal wall and often allows for closure of the midline. This is, actually, the “second step” of the components separation technique first described by Ramirez et al.44 If this does not allow the linea alba to be reapproximated, the posterior rectus sheath is divided to complete the standard components separation. When there is extensive scarring of the remnant edge of the linea alba on either side of the midline, excision of the scar back to viable rectus muscle is necessary. When a greater release is needed, the modified technique described by Fabian et al.45 can be used. After the rectus abdominis muscle is separated from the posterior rectus sheath, the internal oblique component of the anterior rectus sheath is divided from the epigastrium to the arcuate line. The final stage involves suturing the anterior rectus sheaths in the midline, as well as approximating the medial border of the posterior rectus sheath to the lateral border of the previously divided anterior rectus sheath. Using the technique described in nine patients, one patient developed a wound infection and a recurrent incisional hernia. More recently,

CHAPTER CHAPTER 38 X

with their technique. This prevents the gradual dilation of the bowel and thinning of its wall as is commonly seen in patients in whom the abdomen has been left open and should significantly lower the incidence of enterocutaneous fistulas in such patients. In summary, absorbable meshes avoid the major problems associated with permanent meshes (see above). When placed loosely over the midgut, they allow for distention and prevent abdominal compartment syndrome. Also, erosion into the bowel or infection of the mesh secondary to contamination from trauma or a septic process in the abdomen or abdominal wall is less likely. They help prevent evisceration when gauze packing is placed above the mesh, are soft and pliable, allow for drainage of contaminated abdominal fluid through the mesh, and permit the ingrowth of granulation tissue.34,35,45,236 An incisional hernia occurs in all patients in whom the mesh is allowed to granulate, and repair is deferred until the patient has fully recovered from the original traumatic or septic event.

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Management of Specific Injuries

SECTION 3 X

bioprosthetics such as AlloDerm (Life Cell Corporation, Branchburg, New Jersey) are being utilized to enhance abdominal wall reconstruction and decrease the recurrence rate.237 The AlloDerm can be used as layered overlay patch or an underlay patch or both to help alleviate the tension on the midline fascial closure and reduce recurrence of the hernia. Buinewicz and Rosen238 achieved a recurrence rate of only 5% using the AlloDerm. Employing both an AlloDerm overlay and underlay, Kolker et al.239 had no recurrent hernias with a mean follow-up of 16 months. If the midline can still not be reapproximated, a prosthetic patch should be used. In the presence of complete omental coverage over the midgut, a polypropylene or Marlex mesh can be utilized. In the absence of omentum, a PTFE body wall patch is appropriate.23 If a colostomy is being taken down (as previously noted, this is not recommended by the authors) or there is other contamination during the procedure, a bioactive mesh may be preferable. Multiple options are currently available and the reader is referred to the available studies.237–239 The single greatest problem has been either persistent or recurrent incisional hernias when a bioprosthesis is used to bridge a significant gap in the abdominal wall.

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Management of Specific Injuries

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101. Ball CG, Wyrzykowski AD, Nicholas JM, et al. A decade’s experience with balloon catheter tamponade for the emergency control of hemorrhage. J Trauma. 2011;70:330–333. 102. Trinkle JK, Toon RS, Franz JL, et al. Affairs of the wounded heart: penetrating cardiac wounds. J Trauma. 1979;19:467. 103. McClelland R, Shires T, Poulos E. Hepatic resection for massive trauma. J Trauma. 1964;4:282. 104. Aronsen KF, Bengmark S, Dahlgren S, et al. Liver resection in the treatment of blunt injuries to the liver. Surgery. 1968;63:236. 105. Foster JH, Lawler MR Jr, Welborn MB Jr, et al. Recent experience with major hepatic resection. Ann Surg. 1968;167:651. 106. Payne WD, Terz JJ, Lawrence W Jr. Major hepatic resection for trauma. Ann Surg. 1969;170:929. 107. Donovan AJ, Michaelian MJ, Yellin AE. Anatomical hepatic lobectomy in trauma to the liver. Surgery. 1973;73:833. 108. Lim RD Jr, Giuliano AE, Trunkey DD. Postoperative treatment of patients after liver resection for trauma. Arch Surg. 1977;112:429. 109. Feliciano DV, Pachter HL. Hepatic trauma revisited. Curr Probl Surg. 1989;26:453. 110. Pachter HL, Spencer FC, Hofstetter SR, et al. Significant trends in the treatment of hepatic trauma. Experience with 411 injuries. Ann Surg. 1992;215:492. 111. Pachter HL, Feliciano DV. Complex hepatic injuries. Surg Clin North Am. 1996;76:763. 112. Poggetti RS, Moore EE, Moore FA, et al. Balloon tamponade for bilobar transfixing hepatic gunshot wounds. J Trauma. 1992;33:694. 113. Thomas SV, Dulchavsky SA, Diebel LN. Balloon tamponade for liver injuries: case report. J Trauma. 1993;34:448. 114. Stevens SL, Maull KI, Enderson BL, et al. Total mesh wrapping for parenchymal liver injuries—a combined experimental and clinical study. J Trauma. 1991;31:1103. 115. Jacobson LE, Kirton OC, Gomez GA. The use of an absorbable mesh wrap in the management of major liver injuries. Surgery. 1992;111:455. 116. Feliciano DV, Mattox KL, Burch JM, et al. Packing for control of hepatic hemorrhage. J Trauma. 1986;26:738. 117. Saifi J, Fortune JB, Graca L, et al. Benefits of intra-abdominal pack placement for the management of nonmechanical hemorrhage. Arch Surg. 1990;125:119. 118. Sharp KW, Locicero RJ. Abdominal packing for surgically uncontrollable hemorrhage. Ann Surg. 1992;215:467. 119. Horwitz JR, Black T, Lally KP, et al. Venovenous bypass as an adjunct for the management of a retrohepatic venous injury in a child. J Trauma. 1995;39:584. 120. Baumgartner F, Scudamore C, Nair C, et al. Venovenous bypass for major hepatic and caval trauma. J Trauma. 1995;39:671. 121. Rogers FB, Reese J, Shackford SR, et al. The use of venovenous bypass and total vascular isolation of the liver in the surgical management of juxtahepatic venous injuries in blunt hepatic trauma. J Trauma. 1997; 43:530. 122. Denton JR, Moore EE, Coldwell DM. Multimodality treatment for grade V hepatic injuries: perihepatic packing, arterial embolization, and venous stenting. J Trauma. 1997;42:964. 123. Biffl WL, Moore EE, Franciose RJ. Venovenous bypass and hepatic vascular isolation as adjuncts in the repair of destructive wounds to the retrohepatic inferior vena cava. J Trauma. 1998;45:410. 124. Asensio JA, Roldan G, Petrone P, et al. Operative management and outcomes in 103 complex hepatic injuries AAST-OIS grades IV and V trauma. Surgeons still need to operate, but angioembolization helps. J Trauma. 2003;54:647–653. 125. Moore EE, Cogbill TH, Jurkovich GJ, et al. Organ injury scaling: spleen and liver [1994 revision]. J Trauma. 1995;38:323. 126. Feliciano DV, Spjut-Patrinely V, Burch JM, et al. Splenorrhaphy. The alternative. Ann Surg. 1990;211:569. 127. Martin TD, Feliciano DV, Mattox KL, et al. Severe duodenal injuries. Treatment with pyloric exclusion and gastrojejunostomy. Arch Surg. 1983;118:631. 128. Feliciano DV, Martin TD, Cruse PA, et al. Management of combined pancreatoduodenal injuries. Ann Surg. 1987;205:673. 129. Carrillo C, Folger RJ, Shaftan GW. Delayed gastrointestinal reconstruction following massive abdominal trauma. J Trauma. 1993; 34:233. 130. Reilly PM, Rotondo MF, Carpenter JP, et al. Temporary vascular continuity during damage control: intraluminal shunting for proximal superior mesenteric artery injury. J Trauma. 1995;39:757. 131. Sheldon GF, Winestock DP. Hemorrhage from open pelvic fracture controlled intraoperatively with balloon catheter. J Trauma. 1978; 18:68.

132. Saueracker AJ, McCroskey BL, Moore EE, et al. Intraoperative hypogastric artery embolization for life-threatening pelvic hemorrhage: a preliminary report. J Trauma. 1987;27:1127. 133. Burch JM, Feliciano DV, Mattox KL, et al. Injuries of the inferior vena cava. Am J Surg. 1988;156:548. 134. Pachter HL, Drager S, Godfrey N, et al. Traumatic injuries of the portal vein. The role of acute ligation. Ann Surg. 1979;189:383. 135. Stone HH, Fabian TC, Turkleson ML. Wounds of the portal venous system. World J Surg. 1982;6:335. 136. Donahue TK, Strauch GO. Ligation as definitive management of injury to the superior mesenteric vein. J Trauma. 1988;28:541. 137. Feliciano DV, Burch JM, Graham JM. Abdominal vascular injury. In: Feliciano DV, Moore EE, Mattox KL, eds. Trauma. Stamford, CT: Appleton & Lange; 1996:615. 138. Stone HH, Strom PR, Mullins RJ. Management of the major coagulopathy with onset during laparotomy. Ann Surg. 1983;197:532. 139. Rumley TO. Improved packing technique in the control of diffuse hemorrhage of the abdomen. Surg Gynecol Obstet. 1983;156:82. 140. Talbert S, Trooskin SZ, Scalea T, et al. Packing and re-exploration for patients with nonhepatic injuries. J Trauma. 1992;33:121. 141. Feliciano DV. Evaluation and treatment of vascular injuries. In: Browner BD, Jupiter JB, Levine AM, Trafton PG, Krettek C, eds. Skeletal Trauma. Basic science, management, and reconstruction. Philadelphia: Saunders; 2009:323. 142. Ball CG, Kirkpatrick AW, Rajani RR, et al. Temporary intravascular shunts: when are we really using them according to the NTDB? Am Surg. 2009;75:605–607. 143. Mullins RJ, Lucas CE, Ledgerwood AM. The natural history following venous ligation for civilian injuries. J Trauma. 1980;20:737. 144. Timberlake GA, O’Connell RC, Kerstein MD. Venous injury: to repair or ligate, the dilemma. J Vasc Surg. 1986;4:553. 145. Feliciano DV, Herskowitz K, O’Gorman RB, et al. Management of vascular injuries in the lower extremities. J Trauma. 1988;28:319. 146. Accola KD, Feliciano DV, Mattox KL, et al. Management of injuries to the superior mesenteric artery. J Trauma. 1986;26:313. 147. Trunkey DD, Illner H, Wagner IY, et al. The effect of hemorrhagic shock on intracellular muscle action potentials in the primate. Surgery. 1973;74:241. 148. Bock JC, Barker BC, Clinton AG, et al. Post-traumatic changes in, and effect of colloid osmotic pressure on the distribution of body water. Ann Surg. 1989;210:395. 149. Doty DB, Hufnagel HV, Moseley RV. The distribution of body fluids following hemorrhage and resuscitation in combat casualties. Surg Gynecol Obstet. 1970;130:453. 150. McCord JM. Oxygen-derived free radicals in postischemic tissue injury. N Engl J Med. 1985;321:159. 151. Malbrain ML, Cheatham ML, Kirkpatrick A, et al. Results from the international conference of experts on intra-abdominal hypertension and abdominal compartment syndrome. I. Definitions. Intensive Care Med. 2006;32:1722. 152. Ball CG, Kirkpatrick AW. Intra-abdominal hypertension and the abdominal compartment syndrome. Scand J Surg. 2004;99:197. 153. Kirkpatrick AW, Balogh Z, Ball CG, et al. The secondary abdominal compartment syndrome: iatrogenic or unavoidable? J Am Coll Surg. 2006;202:668. 154. Emerson H. Intra-abdominal pressures. Arch Intern Med. 1911;7:754. 155. Kron IL, Harman PK, Nolan SP. The measurement of intra-abdominal pressure as a criterion for abdominal re-exploration. Ann Surg. 1984;199:28. 156. Iberti TJ, Kelly KM, Gentili DR, et al. A simple technique to accurately determine intra-abdominal pressure. Crit Care Med. 1987;15:1141. 157. Sugrue M, Buist MD, Lee A, et al. Intra-abdominal pressure measurement using a modified nasogastric tube: description and validation of a new technique. Intensive Care Med. 1994;20:588. 158. Lacey SR, Bruce J, Brooks SP, et al. The relative merits of various methods of indirect measurement of intra-abdominal pressure as a guide to closure of abdominal wall defects. J Pediatr Surg. 1987; 22:1207. 159. Fusco MA, Martin RS, Chang MC. Estimation of intra-abdominal pressure by bladder pressure measurement: validity and methodology. J Trauma. 2001;50:297–302. 160. Balogh Z, Jones F, D’Amours S, et al. Continuous intra-abdominal pressure measurement techniques. Am J Surg. 2004;188:679–684. 161. Zengerink I, McBeth PB, Zygun DA, et al. Validation and experience with a simple continuous intra-abdominal pressure measurement technique in a multidisciplinary medical/surgical critical care unit. J Trauma. 2008; 64:1159.

Trauma Damage Control 189. Saggi BH, Sugerman HJ, Bloomfield GL, et al. Nonsurgical abdominal decompression reverses intracranial hypertension in a model of acute abdominal compartment syndrome. Surg Forum. 1997;48:544. 190. Meldrum DR, Moore FA, Moore EE, et al. Prospective characterization and selective management of the abdominal compartment syndrome. Am J Surg. 1997;174:667. 191. Cheatham ML, White MW, Sagraves SG, et al. Abdominal perfusion pressure: a superior parameter in the assessment of intra-abdominal hypertension. J Trauma. 2000;49:621. 192. Tremblay LN, Feliciano DV, Rozycki GS. Secondary extremity compartment syndrome. J Trauma. 2001;53:833–837. 193. Corcos AC, Sherman HF. Percutaneous treatment of secondary abdominal compartment syndrome. J Trauma. 2001;51:1062. 194. Chen RJ, Fang JF, Lin BC, et al. Laparoscopic decompression of abdominal compartment syndrome after blunt hepatic trauma. Surg Endosc. 2000;14:966. 195. Bloomfield G, Saggi B, Blocher C, et al. Physiologic effects of externally applied continuous negative abdominal pressure for intra-abdominal hypertension. J Trauma. 1999;46:1009. 196. Fernandez L, Norwood S, Roettger R, Wilkins HE III. Temporary intravenous bag silo closure in severe abdominal trauma. J Trauma. 1996;41:258. 197. DiGiacomo JC, Kustrup JF Jr. Alternatives in temporary abdominal closures. Arch Surg. 1994;129:884. 198. Rowlands BJ, Flynn TC, Fischer RP. Temporary abdominal wound closure with a silastic “chimney.” Contemp Surg. 1984;24:17. 199. Schuster SR. A new method for the staged repair of large omphaloceles. Surg Gynecol Obstet. 1967;125:837. 200. Sherck J, Seiver A, Shatney C, et al. Covering the “open abdomen”: a better technique. Am Surg. 1998;64:854. 201. Leguit P Jr. Zip-closure of the abdomen. Neth J Surg. 1982;34:41. 202. Saxena V, Hwang CW, Huang S, et al. Vacuum-assisted closure: microdeformations of wounds and cell proliferation. Plast Reconstr Surg. 2004;114:1086–1096. 203. McNulty AK, Schmidt M, Feeley BS, Kieswetter K. Effects of negative pressure wound therapy on fibroblast viability, chemotactic signaling, and proliferation in a provisional wound (fibrin) matrix. Wound Repair Regen. 2007;15:838–846. 204. Bender JS, Bailey CE, Saxe JM, et al. The technique of visceral packing: recommended management of difficult fascial closure in trauma patients. J Trauma. 1994;36:182. 205. Gentilello LM, Cobean RA, Offner PJ, et al. Continuous arteriovenous rewarming: rapid reversal of hypothermia in critically ill patients. J Trauma. 1992;32:316. 206. Tisherman SA, Barie P, Bokhari F, et al. Clinical practice guideline: endpoints of resuscitation. J Trauma. 2004;57:898–912. 207. Crookes BA, Cohn SM, Bloch S, et al. Can near-infrared spectroscopy identify the severity of shock in trauma patients? J Trauma. 2005;58: 806–816. 208. Moore FA, Haenel JB, Moore EE, et al. Incommensurate oxygen consumption in response to maximal oxygen availability predicts postinjury multiple organ failure. J Trauma. 1992;33:58. 209. Durham RM, Neunaber K, Mazuski JE, et al. The use of oxygen consumption and delivery as endpoints for resuscitation in critically ill patients. J Trauma. 1996;41:32. 210. Hirshberg A, Wall MJ Jr, Mattox KL. Planned reoperation for trauma: a two year experience with 124 consecutive patients. J Trauma. 1994;37:365. 211. Morris JA Jr, Eddy VA, Rutherford EJ. The trauma celiotomy: the evolving concepts of damage control. Curr Probl Surg. 1996;33:611. 212. Botha AJ, Moore FA, Moore EE, et al. Postinjury neutrophil priming and activation: a vulnerable window. Surgery. 1995;118:358. 213. Botha AJ, Moore FA, Moore EE, et al. Early neutrophil sequestration after injury: a pathogenic mechanism for multiple organ failure. J Trauma. 1995;39:411. 214. Partrick DA, Moore FA, Moore EE. Neutrophil priming and activation in the pathogenesis of postinjury multiple organ failure. New Horizons. 1996;4:194. 215. Waydhas C, Nast-Kolb D, Trupka A, et al. Posttraumatic inflammatory response, secondary operations, and late multiple organ failure. J Trauma. 1996;41:624. 216. Adams JM, Hauser CJ, Livingston DH, et al. The immunomodulatory effects of damage control abdominal packing on local and systemic neutrophil activity. J Trauma. 2001;41:792. 217. Cothren CC, Moore EE, Johnson JL, et al. One hundred percent fascial approximation with sequential abdominal closure of the abdomen. Am J Surg. 2006;192:238–242.

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162. Mutoh T, Lamm WJ, Embree LJ. Volume infusion produces abdominal distension, lung compression, and chest wall stiffening in pigs. J Appl Physiol. 1992;72:575. 163. Diebel L, Saxe J, Dulchavsky S. Effect of intra-abdominal pressure on abdominal wall blood flow. Am Surg. 1992;58:573. 164. Diebel LN, Dulchavsky SA, Wilson RF. Effect of increased intraabdominal pressure on mesenteric arterial and intestinal mucosal blood flow. J Trauma. 1992;33:45. 165. Diebel LN, Dulchavsky SA, Brown WJ. Splanchnic ischemia and bacterial translocation in the abdominal compartment syndrome. J Trauma. 1997;43:852. 166. Chang MC, Miller PR, D’Agostino R, Meredith JW. Effects of abdominal decompression on cardiopulmonary function and visceral perfusion in patients with intra-abdominal hypertension. J Trauma. 1998;44:441. 167. Ivatury RR, Porter JM, Simon RJ, et al. Intra-abdominal hypertension after life-threatening penetrating abdominal trauma: prophylaxis, incidence, and clinical relevance to gastric mucosal pH and abdominal compartment syndrome. J Trauma. 1998;44:1016. 168. Friedlander MH, Simon RJ, Ivatury R, et al. Effect of hemorrhage on superior mesenteric artery flow during increased intra-abdominal pressures. J Trauma. 1998;45:433. 169. Diebel LN, Wilson RF, Dulchavsky SA, et al. Effect of increased intraabdominal pressure on hepatic arterial, portal venous, and hepatic microcirculatory blood flow. J Trauma. 1992;33:279. 170. Nakatani T, Sakamoto Y, Kaneko I, et al. Effects of intra-abdominal hypertension on hepatic energy metabolism in a rabbit model. J Trauma. 1998;44:446. 171. Shenasky JG, Gillenwater JY. The renal hemodynamic and functional effects of external counterpressure. Surg Gynecol Obstet. 1972; 134:253. 172. Harman PK, Kron IL, McLachlan HD, et al. Elevated intra-abdominal pressure and renal function. Ann Surg. 1982;196:594. 173. Richards WO, Scovill W, Shin B, et al. Acute renal failure associated with increased intra-abdominal pressure. Ann Surg. 1983;197:183. 174. Cullen DJ, Coyle JP, Teplich R, et al. Cardiovascular, pulmonary, and renal effects of massively increased intra-abdominal pressure in critically ill patients. Crit Care Med. 1989;17:118. 175. Sugrue M, Jones F, Janjua KJ, et al. Temporary abdominal closure: a prospective evaluation of its effects on renal and respiratory physiology. J Trauma. 1998;45:914. 176. Bloomfield GL, Blocher CR, Fakhry IF, et al. Elevated intra-abdominal pressure increases plasma renin activity and aldosterone levels. J Trauma. 1997;42:997. 177. Doty JM, Saggi BH, Blocher CR, et al. Effects of increased renal parenchymal pressure on renal function. J Trauma. 2000;48:874. 178. Ridings PC, Bloomfield GL, Blocher CR, Sugerman HJ. Cardiopulmonary effects of raised intra-abdominal pressure before and after intravascular volume expansion. J Trauma. 1995;39:1071. 179. Obeid F, Saba A, Fath J, et al. Increases in intra-abdominal pressure affect pulmonary compliance. Arch Surg. 1995;130:544. 180. Simon RJ, Friedlander MH, Ivatury RR, et al. Hemorrhage lowers the threshold for intra-abdominal hypertension-induced pulmonary dysfunction. J Trauma. 1997;42:398. 181. Richardson JD, Trinkle JK. Hemodynamic and respiratory alterations with increased intra-abdominal pressure. J Surg Res. 1976;20:411. 182. Diamant M, Benumof JL, Saidman LJ. Hemodynamics of increased intra-abdominal pressure: interaction with hypovolemia and halothane anesthesia. Anesthesiology. 1978;48:23. 183. Kashtan J, Green JF, Parsons EQ, et al. Hemodynamic effect of increased abdominal pressure. J Surg Res. 1981;30:249. 184. Barnes GE, Laine GA, Giam PY, et al. Cardiovascular responses to elevation of intra-abdominal hydrostatic pressure. Am J Physiol. 1985; 248:208. 185. Robotham JL, Wise RA, Bromberger-Barnea B. Effects of changes in abdominal pressure on left ventricular performance and regional blood flow. Crit Care Med. 1985;13:803. 186. Bloomfield GL, Dalton JM, Sugerman HJ, et al. Treatment of increasing intracranial pressure secondary to the acute abdominal compartment syndrome in a patient with combined abdominal and head trauma. J Trauma. 1995;39:1168. 187. Bloomfield GL, Ridings PC, Blocher CR, et al. Effects of increased intraabdominal pressure upon intracranial and cerebral perfusion pressure before and after volume expansion. J Trauma. 1996;41:936. 188. Bloomfield GL, Ridings PC, Blocher CR, et al. A proposed relationship between increased intra-abdominal, intrathoracic, and intracranial pressure. Crit Care Med. 1997;25:496.

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218. Stone PA, Hass SM, Flaherty SK, DeLuca JA, et al. Vacuum-assisted fascial closure for patients with abdominal trauma. J Trauma. 2004; 57:1082–1086. 219. Miller PR, Meredith JW, Johnson JC, et al. Prospective evaluation of vacuum-assisted fascial closure after open abdomen. Ann Surg. 2004;239:608–616. 220. Stone HH, Strom PR, Mullins RJ. Pancreatic abscess management by subtotal resection and packing. World J Surg. 1984;8:341. 221. Teichmann W, Wittmann DH, Andreone PA. Scheduled reoperations (etappenlavage) for diffuse peritonitis. Arch Surg. 1986;121:147. 222. Wittmann DH, Aprahamian C, Bergstein JM. Etappenlavage: advanced diffuse peritonitis managed by planned multiple laparotomies utilizing zippers, slide fastener, and Velcro analogue for temporary abdominal closure. World J Surg. 1990;14:218. 223. Aprahamian C, Wittmann DH, Bergstein JM, et al. Temporary abdominal closure (TAC) for planned relaparotomy (etappenlavage) in trauma. J Trauma. 1990;30:719. 224. Tieu BH, Cho SD, Leum N, et al. The use of the Wittmann patch facilitates a high rate of fascial closure in severely injured trauma patients and critically ill emergency surgery patients. J Trauma. 2008;65:865–879. 225. Weinberg JA, George RL, Griffin RL, et al. Closing the open abdomen: improved success with Wittmann patch staged abdominal closure. J Trauma. 2008;65:345–348. 226. Fantus RJ, Mellett MM, Kirby JP. Use of controlled fascial tension and an adhesion preventing barrier to achieve delayed primary fascial closure in patients managed with an open abdomen. Am J Surg. 2006;192:243–247. 227. Gilsdorf RB, Shea MM. Repair of massive septic abdominal wall defects with Marlex mesh. Am J Surg. 1975;130:634. 228. Stone HH, Fabian TC, Turkleson ML, et al. Management of acute full thickness losses of the abdominal wall. Ann Surg. 1981;193:612.

229. Voyles CR, Richardson JD, Bland KI, et al. Emergency abdominal wall reconstruction with polypropylene mesh: short-term benefits versus long-term complications. Ann Surg. 1981;194:219. 230. Wouters DB, Krom RA, Slooff MJ, et al. The use of Marlex mesh in patients with generalized peritonitis and multiple organ system failure. Surg Gynecol Obstet. 1983;156:609. 231. Usher FC, Ochsner J, Tuttle LLD. Use of Marlex mesh in the repair of incisional hernias. Am J Surg. 1958;24:969. 232. Jones JW, Jurkovich GJ. Polypropylene mesh closure of infected abdominal wounds. Am J Surg. 1989;55:73. 233. Lamb JP, Vitale T, Kaminski DL. Comparative evaluation of synthetic meshes used for abdominal wall replacement. Surgery. 1983;93:643. 234. Jenkins SD, Klamer TW, Parteka JJ. A comparison of prosthetic materials used to repair abdominal wall defects. Surgery. 1983;94:392. 235. Tyrell J, Silberman H, Chandrasoma P, et al. Absorbable versus permanent mesh in abdominal operations. Surg Gynecol Obstet. 1989;168:227. 236. Smith PC, Tweddell JS, Bessey PQ. Alternative approaches to abdominal wound closure in severely injured patients with massive visceral edema. J Trauma. 1992;32:16. 237. Gupta A, Zahriya K, Mullens PL, et al. Ventral herniorrhaphy: experience with two different biosynthetic mesh materials, Surgisis and Alloderm. Hernia. 2006;10:419–425. 238. Buinewicz B, Rosen B. Acellular cadaveric dermis (Alloderm): a new alternative for abdominal hernia repair. Ann Plast Surg. 2004;52: 188–194. 239. Kolker AR, Brown DJ, Redstone JS, et al. Multilayer reconstruction of abdominal wall defects with acellular dermal allograft (Alloderm) and component separation. Ann Plast Surg. 2005;55:36–42.

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CHAPTER 39

Upper Extremity Nata Parnes, Peleg Ben-Galim, and David Netscher

Treatment of the injured upper extremity and the appreciation of the severe disability that could result from poor management was the major driving force in the evolution of upper extremity and hand surgery as independent and distinct specialties.1 A primary theme was the recognition that many injuries to the upper extremity are combined injuries and that appropriate treatment could best be delivered by someone trained in management of both bone and soft tissue injuries. Today, the successful approach to the treatment of many upper extremity injuries requires microsurgical skills to deal with soft tissue coverage, nerve repair, and revascularization, in addition to fracture care.

HIGH-ENERGY VERSUS LOW-ENERGY TRAUMA One useful way to classify injuries to the upper extremity relates to the amount of energy involved in their generation. Lowenergy forces typically cause simple injuries, while high-energy forces lead to complex injuries involving soft tissue and bones that are often associated with joint, neurologic, or vascular involvement. A classic example is a distal radius fracture that typically occurs in two age groups with different mechanisms related to the transfer of energy. A low-energy distal radius fracture typically occurs in an elderly osteopenic woman where the mechanism was a simple fall on an outstretched hand. This usually results in a simple fracture pattern that may best be treated via closed reduction and splinting. A high-energy distal radius fracture, on the other hand, typically occurs in a young healthy and fit patient resulting from a high-speed motor vehicle crash or fall from a significant height. These injuries are associated with swelling of soft tissue, severely comminuted intra-articular shear-type fractures, and several associated potential complications. At first glimpse both scenarios share the diagnosis of “distal radius fracture” and may even seem similar, but it is extremely important to recognize that these are two very different entities. While the low-energy distal radius

fracture is simply treated as noted above, the high-energy counterpart should be closely monitored for swelling that may lead to an “acute carpal tunnel syndrome” with subsequent injury to the median nerve, breakdown of soft tissue, and vascular insufficiency. Furthermore, high-energy distal radius fractures will often require surgical treatment including open reduction and internal fixation to restore articular congruency. Similarly, soft tissue lacerations can be classified as high or low energy depending on the causative agent. A laceration from a sharp kitchen knife to the forearm is to be distinguished from a laceration to the same region caused by a high-speed electrical saw. While they may initially appear similar on presentation in the emergency department (ED), they are quite different. The former may be irrigated and sutured primarily, while the latter requires careful observation due to the late effects of thermal and kinetic energy causing burns of the skin and soft tissue. Skin breakdown with necrosis of the wound edges is typically seen with high-energy lacerations, and recurrent debridements in the operating room may be needed with more complex plastic reconstruction.

INJURY-SPECIFIC HISTORY AND PHYSICAL EXAMINATION It is useful to gather information regarding the mechanism of injury in the initial evaluation and to classify injuries based on whether they were caused by high or low energy. The exact type of mechanism such as blunt, penetrating, lacerating, shear, or degloving and crushing injuries should be elicited, as each of these will deserve specific attention related to the mechanism. Other important components of the history include time of injury, whether the environment was clean or contaminated, whether the injury was work related, the patient’s occupation, hand dominance, and important activities. Finally, a previous history of an injury to an upper extremity should be elicited and any prior functional limitations should be described.

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Once the airway, breathing, and circulation are stabilized, the physical examination of the upper extremity should focus primarily on the soft tissue components of artery, nerve, and tendon, before focusing on bony injuries. Circulation can be assessed by observation of the color of the skin and nail bed, skin temperature, and rate of capillary refill after blanching the skin with light pressure. One useful maneuver is to interpret findings by comparison with an uninjured extremity. This approach is useful in the evaluation of unclear x-ray findings, especially in the growing child, also. Arterial insufficiency produces a pale, cool limb with prolonged (2 seconds) or absent capillary refill and loss of turgor. Venous insufficiency will result in a purple, congested extremity with faster than normal capillary refill. Evaluation of arterial pulses begins proximally with palpation of the brachial artery followed by the radial and ulnar arteries. A manual Allen’s test should be performed when the injury allows. When clinically indicated, confirmation of a positive manual Allen’s test can be obtained using Doppler ultrasound, pulse oximetry, or angiography.2,3

Sensation and motor function should be tested if there is any question of injury to a peripheral nerve. There are three autonomous zones in the hand. The median nerve zone is the index fingertip, the ulnar nerve zone is the small fingertip, and the radial nerve zone is the dorsal side of the first web space over the first dorsal interosseous muscle. More proximally, standard dermatome maps can be utilized. For sensibility, the most useful screening test is light touch perception that can be elicited by gently scratching or tapping the area of interest with a broken applicator stick. A more precise evaluation of distal innervation density can be accomplished by determining static and moving two-point discrimination at the fingertip. At the pulp, normal static two-point discrimination should be 6 mm and moving two-point discrimination 3 mm. Occasionally, threshold testing with a Semmes-Weinstein monofilament or vibration sensibility evaluation may be indicated. Motor testing should begin distal to the level of suspected injury. A systematic evaluation of each muscle based on innervation is the ideal (Tables 39-1 and 39-2). In the trauma

TABLE 39-1 Nerves and Muscles of the Upper Extremity Nerve Spinal accessory

Muscles Innervated Stemocleidomastoid Trapezius

Dorsal scapular Suprascapular Long thoracic Subscapular Thoracodorsal Pectoral (medical and lateral) Musculocutaneous

Rhomboid Supraspinatus Infraspinatus Serratus anterior Subscapulans Latissimus dorsi Pectoralis major and minor Biceps

Axillary

Coracobrachialis Brachialis Deltoid

Radial

Teres minor Triceps Anconeus Brachioradialis Extensor carpi radialis longus and brevis Extensor carpi ulnaris Supinator Extensor digitorum communis Extensor indicis proprius Extensor digiti minimi Extensor pollicis brevis and longus Abductor pollicis longus

Test for Function Ipsilateral head tilt, contralateral head rotation. Scapular elevation rotation, adduction: head extension, rotation Scapular retraction; scapular stabilization Arm abduction Arm external rotation Scapular protraction: scapular stabilization Arm internal rotation, adduction Arm extension, internal rotation Arm internal rotation, flexion, adduction

Sensory Distribution

Arm and forearm flexion; forearm supination Arm flexion, adduction Forearm flexion Arm abduction; internal, external rotation Arm external rotation, adduction Arm and forearm extension

Lateral forearm (lateral antebrachial cutaneous) Lateral aspect of shoulder

Dorsoradial hand, thumb (superficial radial)

Forearm extension Forearm flexion Wrist extension

Forearm supination Finger, thumb extension

(continued )

Upper Extremity

749

TABLE 39-1 Nerves and Muscles of the Upper Extremity (continued ) Muscles Innervated Flexor carpi radialis

Test for Function Wrist flexion

Pronator teres and quadratus Flexor digitorum sublimis

Forearm pronation

Flexor digitorum profundus (index, long) Abductor pollicis brevis Opponens pollicis Flexor pollicis brevis (superficial head) Lumbricals (index, long) Ulnar

Flexor carpi ulnaris

Flexor digitorum profundus (ring, little) Abductor digiti minimi Flexor digiti minimi Abductor pollicis Flexor pollicis brevis (deep head) Interossei (volar, dorsal) Lumbricals (ring, little)

Sensory Distribution Volar thumb, index, long, radial half of ring finger; dorsum index, long, radial half of ring finger

Finger proximal interphalangeal joint flexion Finger distal interphalangeal joint flexion Thumb abduction Thumb opposition Thumb metacarpophalangeal joint flexion Metacarpophalangeal joint flexion Interphalangeal joint extension Wrist flexion

Volar and dorsum little. Ulnar half of ring finger; dorsal ulnar aspect of hand

Finger distal interphalangeal joint flexion Little finger abduction Little finger metacarpophalangeal joint flexion Thumb adduction Thumb metacarpophalangeal joint flexion Metacarpophalangeal joint flexion, interphalangeal extension Metacarpophalangeal joint flexion, interphalangeal extension

TABLE 39-2 Cervical and Thoracic Nerve Roots and Function Nerve Root C5 C6 C7

C8 T1

Test for Function (Muscle/Nerve) Shoulder abduction (deltoid/axillary) Elbow flexion (biceps/musculocutaneous) Wrist extension (extensor carpi radialis longus and brevis/radial) Elbow extension (triceps/radial) Wrist flexion (flexor carpi radialis/median: flexor carpi ulnaris/ ulnar) Finger extension (extensor digitorum communis, extensor indicis proprius, extensor digiti minimi/radial) Finger flexion (flexor digitorum superficialis, flexor digitorum profundus/median and ulnar) Finger abduction and adduction (dorsal and volar interossei/ulnar)

Sensory Distribution Lateral upper arm Lateral forearm, thumb, index finger Long finger

Reflex Biceps Brachioradialis

Medial forearm, ring, little fingers Medial forearm

None

Triceps

None

CHAPTER CHAPTER 39 X

Nerve Median

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Management of Specific Injuries

TABLE 39-3 Imaging Examinations for Shoulder Girdle Region

SECTION 3 X

Conditions Sternoclavicular dislocations Clavicle fracture Acromioclavicular dislocations Scapular fracture Acromion fracture Glenoid neck fracture Glenoid fracture Scapular body fracture Floating shoulder without associated clavicle fx Scapulothoracic dissociation Glenohumeral dislocation

X-Ray AP, serendipity view AP, apical/oblique views AP, apical/oblique views True AP, scapular Y, and axillary True AP, scapular Y, and axillary True AP, scapular Y, and axillary True AP, scapular Y, and axillary True AP, scapular Y, and axillary True AP, scapular Y, and axillary

Advanced Imaging CT

lateral lateral lateral lateral lateral lateral

views views views views views views

True AP, scapular Y, and axillary lateral views AP/Bloom–Obata modified Scapular Y view

setting, recreating the maneuvers of rock, paper, and scissors from the childhood game of “roshambo” demonstrates function of the median, radial, and ulnar nerves, respectively. Integrity of the musculocutaneous, axillary, and suprascapular nerves can be grossly evaluated by asking the patient to grasp a cup and simulate drinking. The examination must be interpreted in light of any other soft tissue or bony injuries that might bias the examination.

X-RAY EVALUATION The minimal x-ray examination includes the anterior–posterior (AP) or posterior–anterior (PA) and lateral views. When dealing with a long-bone fracture, an important rule is to image the entire bone from the joint above to the joint below the injury. Complete evaluation at any articular level, or within

CT

CT/MRI/angiography Axillary view CT/MRI

the hand itself, usually requires additional views designed to better visualize specific injuries. These may include fluoroscopic motion views and stress views to help diagnose ligamentous instability. More sophisticated x-ray studies such as arthrography, ultrasound, computed tomography (CT), and magnetic resonance imaging (MRI) may be important in future surgical planning, but are rarely indicated in the initial management of injury to an upper extremity. A practical guide to some commonly used x-ray views is suggested in Tables 39-3 to 39-6.

INJURIES NOT TO BE MISSED When assessing injuries in the upper extremity, it is important to avoid missing secondary problems as described in Table 39-7.

TABLE 39-4 Imaging Examinations for the Arm, Elbow, Forearm, and Wrist Conditions Proximal humerus fracture Humeral shaft fracture Elbow trauma Distal humeral fx Capitellum fracture Elbow dislocations/fracture–dislocations Fracture of proximal ulna Radial head fracture The floating elbow Monteggia fracture–dislocations Ulna shaft fracture Radial shaft fracture Distal radius injury/fracture Radius/ulna fractures Scaphoid fractures

X-Ray AP, transscapular lateral, Bloom–Obata modified axillary view AP, lateral AP, lateral AP, lateral AP, lateral AP, lateral AP, lateral AP, lateral AP, lateral AP, lateral of elbow and forearm AP, lateral AP, lateral AP, lateral AP, lateral PA, lateral, oblique, scaphoid

Advanced Imaging CT

CT CT CT

MRI

Upper Extremity

751

TABLE 39-5 Imaging Examinations for Wrist and Hand

Trapezoid fractures Capitate fractures Hamate fractures Hook fractures Lunate fractures Carpal dislocations Metacarpal fractures Phalangeal fractures Metacarpophalangeal dislocations Interphalangeal joint dislocations

X-Ray PA, lateral, oblique Carpal tunnel view and/or supinated oblique view Hyperpronated Roberts view, a Bett’s view, a carpal tunnel view PA, lateral, oblique PA, lateral, oblique, and scaphoid view Carpal tunnel view and/or supinated oblique view Carpal tunnel view and/or supinated oblique view PA, lateral, oblique PA, lateral, oblique PA, lateral, oblique PA, lateral, oblique PA, lateral, oblique PA, lateral, oblique

■ Compartment Syndrome Compartment syndrome is mentioned due to the importance of early recognition and the devastating consequences of a missed or delayed diagnosis (Fig. 39-1). While compartment syndrome has been described in the arm, it is much more common in the forearm and hand.4 The forearm is composed of three distinct compartments including the volar, dorsal, and the mobile wad, while the hand has four dorsal and three volar interosseous compartments. After trauma, if acute swelling of the forearm or hand occurs, then one should be suspicious that a compartment syndrome is present (Fig. 39-2). Clinically, pain out of proportion to the clinical findings and pain on passive tendon stretching are probably the most reliable indication to pursue further diagnostic testing or operative treatment. Prompt diagnosis and treatment must be initiated before irreversible ischemic necrosis and tissue damage ensues. Therefore, late findings such as pallor, pulselessness, paresthesia, or paralysis should not be awaited for since their appearance is associated with irreversible damage. If a compartment syndrome is suspected after application of a cast or splint, it should be immediately split to the underlying skin. At any time, measurement of a compartment pressure is a particularly valuable aid in diagnosis and may be the most useful tool in the unconscious or noncommunicative patient.

Advanced Imaging CT/MRI CT CT CT

CT CT CT/MRI

Controversy still exists over the compartment pressure at which fasciotomy is deemed necessary. Whitesides et al.5 recommended fasciotomy when the pressure was measured at 10–30 mm Hg below the diastolic blood pressure. Others in the general trauma and vascular community have recommended that the compartment pressure alone be used as a guide for fasciotomy, but this recommendation has varied from 30 to 50 mm Hg in normotensive individuals. Another practical and safe indication to help guide decision making is when the intracompartmental pressure of the affected limb is higher than in the contralateral normal limb and progressively rises above 30 mm Hg. Regardless of which of the above methods is used, once a clinical suspicion arises, it is better to err on the side of early release to avoid devastating sequelae. Muscle damage begins within 4 hours of ischemia and is irreversible by 6 hours. In addition, nerve damage can put distal intrinsic function at risk and further limit reconstructive options.

■ “Fight Bite” Injuries of the Head of the Metacarpal Bone It is important to recognize these injuries as they may lead to an intra-articular infection/septic arthritis of the metacarpophalangeal (MCP) joint. Clenched fist or “fight bite” injuries occur

TABLE 39-6 Imaging Examinations and Laboratory Tests of Common Upper Extremity Injuries—Fingers and Soft Tissues Condition Fingertip and nail bed injury Extensor tendon injury Thumb extensor injury Flexor tendon Vascular injury Peripheral nerve injury Compartment syndrome

X-Ray PA, lateral, PA, lateral, PA, lateral, PA, lateral,

Advanced Imaging oblique oblique oblique oblique

Ultrasound/MRI

MRA/angiography EMG-NCT Compartment pressure

Labs

CHAPTER CHAPTER 39 X

Conditions Triquetrum fractures Pisiform fractures Trapezium fractures

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Management of Specific Injuries

TABLE 39-7 Important Clinical Presentations and Their Associated Findings: What Not to Miss

SECTION 3 X

Condition Sternoclavicular dislocation

Do Not Miss!!! Posterior displacement into the mediastinum

Scapular fractures

High index of suspicion for other serious, possibly lifethreatening problems Nerve injuries are common, especially involving the axillary nerve

Proximal humeral fractures

Proximal humeral fractures

Open fractures into the armpit may be small and overlooked

Humeral shaft fractures

Elbow trauma

Elbow dislocations

Care should be taken to identify associated injuries, which may include trauma to the median, ulnar, and radial nerves, as well as the brachial artery Nerve and vascular injuries

Elbow dislocation, complex type

The “terrible triad of the elbow”

Supracondylar elbow fractures

Nerve injuries most commonly involve the median nerve or its anterior interosseous branch R/O brachial artery injuries Acute carpal tunnel syndrome

Distal radius fracture

Proximal radial head fractures

Distal radial shaft fractures

Associated injuries to the distal radioulnar joint with proximal migration of radius and injury to interosseous membrane Associated distal radioulnar joint dislocation

Radius and ulna shaft fractures

Associated risk of compartment syndrome has been reported

Comment Thoracic surgeon recommended for reduction Rule out injury to the chest, cervical spine, or neurovascular structures. A vascular injury may be present even if a radial pulse is palpable, due to the presence of multiple collateral vessels around the shoulder Small puncture lacerations are at high risk for severe infections of the chest wall (such as necrotizing fasciitis) The radial nerve is at highest risk, particularly in the distal third of the shaft Note this is a complex set of articulations including the ulnohumeral, radiocapitellar, and proximal radioulnar joints Always assess and note stability during range of motion after reduction Fracture–dislocation of the radial head, coronoid, and injury to the collateral ligaments Nerve injuries often recover with expectant management

Treatment Reduction (closed if possible)

This is a “compartment” syndrome involving the median nerve This is termed EssexLopresti fracture– dislocation

Urgent surgical decompression

Workup for other associated injuries

Early recognition of aggressive irrigation and debridement in OR and broad-spectrum IV antibiotic treatment Coaptation splint is effective for most humeral shaft fractures

Surgical treatment is required with reconstruction to restore stability to the elbow

Check for elbow and wrist stability and range of motion

This is termed “Galeazzi fracture–dislocation” and is more common in children

(continued )

Upper Extremity

753

TABLE 39-7 Important Clinical Presentations and Their Associated Findings: What Not to Miss (continued ) Do Not Miss!!! Scaphoid fractures

Comment These can be difficult to see radiographically on presentation

Hook of hamate fractures

Both ulnar and median nerve injuries may be associated with hook fractures

A thorough examination of motor and sensory function should be documented

Perilunate and carpal dislocations “Fight bite” or clenched fist injuries

Associated median nerve injury is common Septic arthritis of metacarpophalangeal joint

Felon

Direct extension of infection to periosteum

Compartment syndrome

Do not wait for paresthesia, pallor, or pulselessness

High-pressure injection injuries

Small puncture wound but these injuries travel proximally down the fascial planes

when the patient strikes the mouth of another person.6 This most commonly involves the metacarpal head of the long finger because of its prominence in the clenched position. The initial injury may appear quite innocuous; however, all injuries should be assumed to have penetrated deeper structures and to have entered the underlying joint. X-rays are mandatory for these

FIGURE 39-1 End stage of compartment syndrome. This patient had multiple secondary infections and finally required an aboveelbow amputation for this nonfunctional limb.

Always assume that the tooth entered deep into the joint Associated bone involvement of this deep infection Pain out of proportion should be enough to raise suspicion Verify the type of solution injected as oil-based paints create chemical burns

Treatment Conventional wisdom is to follow the clinical exam and picture more than initial radiographs

Systemic antibiotic and surgical arthrotomy and irrigation in the OR is the rule Deep incisions and drainage

Fasciotomies should be performed emergently Wide incision and drainage with debridement of all paint material

injuries, not only to look for a fracture but to rule out the presence of a retained tooth fragment also. Even when seen acutely, these injuries should be explored by a formal arthrotomy in the operating room where cultures are obtained and the joint irrigated. It is preferable to enter the joint by taking down the ulnar sagittal band to decrease the possibility of ulnar luxation or subluxation of the extensor hood. Operative intervention should be followed by intravenous antibiotics targeting Staphylococcus sp. for 24–48 hours (see Chapter 18).

FIGURE 39-2 Forearm compartment syndrome after formal volar fasciotomy. Pressures measured in this patient exceeded 100 mm. Note the extent of muscle expansion as it escapes the boundaries of the volar compartment following release via fasciotomy.

CHAPTER CHAPTER 39 X

Condition Wrist pain

754

Management of Specific Injuries

TREATMENT OF OPEN SOFT TISSUE INJURIES AND COMPLEX WOUNDS SECTION 3 X

Appropriate wound debridement must first be done before adequate soft tissue coverage can be safely provided.7 Irrigation with a pressure of at least 7 psi is mandatory. Earlier studies of complex wounds in the lower extremity have shown a clear advantage for wound closure after debridement within 5 days of the injury with regard to flap survival, most rapid time to bone healing, reduced infection, and lowest number of hospital days.8,9 So-called emergency free flaps have been shown to have a high degree of success for complex upper extremity wounds.10 While early wound closure is desirable, it depends on the energy of the initial injury, degree of contamination involved, vital structures exposed, and the general health of the patient, as well as the availability of a surgical team. Excessive delay of wound closure results in prolongation of the inflammatory response to wounding, increases the formation of edema, allows joints to become stiff, increases fibrosis around moving structures, and delays hand therapy. Early wound coverage with a flap aborts the extended inflammatory phase of healing that is encountered in chronic wounds and inhibits contraction of the wound. Well-vascularized axial pattern muscle flaps seem to help combat infection, also.11,12 If wound closure is done late, after granulation has developed, then the inhibitory effect on wound contraction is lost.13 Once the wound satisfies the requirements for closure, the reconstructive ladder is borne in mind, and the simplest option that is best suited to both the general condition of the patient and the local requirements of the wound is then selected. The reconstructive requirements for the upper extremity are listed as follows: 1. Replace missing tissue type with a similar type, for example, thin and pliable soft tissue coverage is required in the hand and fingers. 2. There may be a subsequent or simultaneous need for secondary reconstruction of bone, tendon, or nerve. 3. Flap reconstruction may need to be sensate. 4. The size of the defect must be considered threedimensionally to provide deep volume fill as well as coverage of surface area. 5. Flap reconstruction may be functional and provide motion. Skin grafts may be suitable for wounds of large surface area that do not expose important structures. In the hand, a more durable wound coverage such as a full-thickness skin graft or flap may be required to cover exposed important structures and to meet the frequent secondary need for later tenolysis and tendon transfers. Full-thickness skin grafts or flaps result in less wound contraction, probably by their effect on attenuating the life cycle of myofibroblasts.14 Axial and random pattern flaps may be helpful in covering large wounds, as well.15 The former is a single pedicled flap with an anatomically recognized arterial and venous system running along its axis. The groin flap was one of the first such axial pattern flaps that was used for resurfacing of the upper extremity, but suffers from the disadvantage of having to keep the arm dependent until it is cut free from the

groin pedicle at a later date. Microvascular free flap reconstruction may be more elegant than a groin flap since the upper extremity can remain elevated and therapy might be initiated sooner. Axial flaps, either free or pedicle flaps, may consist of skin only, fascia and fasciocutaneous tissue (such as radial forearm, lateral arm, temporoparietal), or muscle and musculocutaneous tissue (such as latissimus dorsi, rectus abdominis, and gracilis muscles). The radial forearm flap and posterior interosseous flap may be pedicled on the distal blood supply so that venous flow is actually retrograde. Flaps have many advantages over skin grafts15 in that they avoid wound contraction, fill dead space, cover important structures (such as exposed vessels, bone, tendons, and nerves), help “clean up” infection, enhance vascularity, and provide specific functions (such as a latissimus muscle transfer to restore biceps function).

TREATMENT OF INJURIES TO TENDONS IN THE DISTAL EXTREMITY ■ Extensor Tendons The extensor tendon is the end organ of a complex mechanism, which involves input from both the extrinsic and intrinsic muscles of the hand to maintain the balanced finger function that is expected by most individuals. Disruption of any component of this balance such as bone, skin, the musculotendinous system, or neurovascular structures can lead to stiffness and a poor functional outcome. In the evaluation of injury to an extensor tendon, the hand and distal forearm are divided into eight zones that aid in communication and, to a degree, guide treatment. Zone I injuries involve disruption of the extensor mechanism over the distal interphalangeal (DIP) joint resulting in the classic mallet finger deformity. Closed injury results from forced flexion while the finger is in rigid extension. Rupture of the terminal tendon itself or avulsion of its insertion with a variable sized bony fragment results in an inability to extend the distal phalanx. Lacerations or other open injuries, with combined skin and tendon loss, can result in a similar deformity. A closed acute mallet finger should be treated initially by continuous splinting in extension for 6 weeks.16 The splint should not incorporate the other joints of the finger or hand, and active motion of the proximal interphalangeal (PIP) joint should be encouraged. If resisted extension is present at the end of 6 weeks, the splint can be limited to nighttime use for an additional 6 weeks with close follow-up. Any relapse should be treated with 3 weeks of additional continuous splinting. Care must be taken during this prolonged period of splint use that skin maceration and necrosis do not occur. Occasionally, operative fixation by a variety of pinning methods is required for complete healing or to more appropriately manage subluxation of the DIP joint. Open mallet fingers can present a treatment challenge. Simple transverse lacerations are best treated by mass suturing with incorporation of the terminal tendon and skin with a series of interrupted, nonabsorbable sutures. Fingers with skin and tendon loss require soft tissue coverage and primary tendon grafting or late reconstruction. Emergency treatment consists of irrigation of the open wound/joint, dressing of the wound,

Upper Extremity rum communis (EDC) tendon into the ulnar gutter. Splinting may be with the wrist neutral, the MCP joints in extension and the PIP and DIP joints free,17 or a recently described fingerbased sagittal band bridge splint.18 If splinting for 6–8 weeks fails, or the injury is seen late, then operative recentralization should be performed. Zone VI injuries can occur distal or proximal to the juncturae tendini, the tendinous connections between the EDC tendons. Diagnosis and treatment of these injuries are difficult and beyond the spectrum of this chapter, since the finger will still extend at the MP joints via the transmission of the adjacent tendon action through the juncturae. In these situations, exploration may be the only means of diagnosis, short of imaging techniques such as ultrasound or MRI. Proximal retraction of the lacerated tendon will occur. In these instances, exploration in the operating room is probably preferable to exploration in the ED. Open injuries in Zone VI can be associated with extensive loss of soft tissue. Repair of such injuries often requires complex soft tissue coverage with immediate or delayed tendon reconstruction or transfer. Zone VII injuries to the extensor tendons occur at the level of the wrist retinaculum where the tendons are divided into six compartments. In this zone, retraction of the tendon ends always occurs, making formal operative exploration imperative. Repair needs to be meticulous to avoid adhesions to the overlying retinaculum that often needs to be expanded by z-plasty during closure. Failure to appropriately repair the retinaculum will result in bowstringing of the extensor tendons at the level of the wrist. An associated injury to the dorsal sensory branches of the radial and ulnar nerves can occur with these injuries and requires a high level of suspicion to prompt exploration and microneural repair. Ignoring these associated nerve injuries can lead to loss of sensation over a portion of the dorsum of the hand and chronic neuropathic pain. Zone VIII represents the musculotendinous junctions of the extensors. Injury at this level is always associated with penetrating trauma or massive injury to soft tissue, often with an associated open forearm fracture. Initial evaluation of penetrating trauma, usually by glass or knives, may show a relatively small wound that belies the damage that has been caused internally. Even with what appears to be normal extension on examination, significant damage can be found with surgical exploration.19 Repair of the musculotendinous junction itself is difficult because muscle does not hold sutures well. Large figure of eight sutures are required to restore continuity, and repair should be followed by 4–6 weeks of splinting with the wrist in 20° of extension and the MCP joints in 20° of flexion. If the injury is distal to the posterior interosseous nerve, good restoration of function is possible. Injury to the posterior interosseous nerve requires a thorough exploration and repair by an experienced microneural surgeon to maximize functional recovery. Even with meticulous repair of the nerve, a tendon transfer may be required at a later date. In order to salvage a functionally threatened extremity, a massive combined injury in Zone VIII requires application of the principles discussed in Section “Compound, Complex, and Mangled Upper Extremities.”

CHAPTER CHAPTER 39 X

antibiotic coverage, splinting in extension, and arranging urgent follow-up in the next 24 hours for surgical evaluation and treatment. Zone II injuries occur over the shaft of the middle phalanx and are usually associated with a laceration or open fracture. Lacerations involving less than 50% of the tendon width, and with no extensor lag, can be treated by wound care and splinting in extension for 7–10 days, followed by active range of motion. If more than 50% of the tendon is lacerated, or an extensor lag at the DIP joint exists, then the tendon should be repaired followed by splinting or pinning the DIP in extension for 6–8 weeks in a mallet finger protocol. Open fractures with tendon involvement require fracture and tendon repair and extensive therapy to regain range of motion. Zone III injuries involve the central slip of the extensor tendon over the PIP joint and initially result in loss of extensor power at this joint. Untreated, this injury results in palmar subluxation of the lateral bands and, within 1–2 weeks, development of the classic boutonniere (or buttonhole) deformity. With this deformity, the finger rests in a position of flexion at the PIP joint and hyperextension at the DIP joint. Physical examination will show weak or absent extension of the PIP joint with this injury. With a closed rupture of the central slip, initial evaluation may be difficult due to pain and swelling at the PIP joint. Extension splinting of the PIP joint with followup and reexamination at 7 days is a reasonable course of action in this situation. Splinting must not incorporate either the MCP joint or DIP joint. If, at 1 week, findings support the diagnosis of closed rupture of the central slip, then splinting should continue for 4–6 additional weeks with weekly followup. Formal therapy is usually required at the completion of splinting to successfully regain full range of motion. Open injury in Zone III requires wound management in the form of irrigation and debridement, formal arthrotomy if indicated, and soft tissue coverage if local tissue has been lost. Tendon repair may be primary or may be managed by transarticular pinning for 4–6 weeks to allow the tendon to heal on its own. Second intention healing of the tendon in this area is possible because of the design of the extensor apparatus that prevents retraction if the PIP joint is held in extension. Zone IV lies over the proximal phalanx, and injury at this level is often associated with a proximal phalangeal fracture. Many tendon injuries at this level are incomplete, due to the broad nature of the extensor hood. Like Zone III injuries, even a complete laceration will not result in proximal migration of the tendon due to the constraints of the sagittal bands that tether the severed end. Lacerations in Zone IV will need to be extended to allow complete exploration and primary repair. Early motion in this zone by an active flexion, passive extension protocol is recommended. When Zone IV injuries are associated with proximal phalangeal fractures, a stable repair of the fracture will greatly facilitate initiation of early tendon motion. Open Zone V injuries are commonly associated with the “fight bite” wound, and treatment is addressed in Section “Infections in the Hand.” Closed tendon injuries in this zone are less common and usually involve the radial sagittal band, which results in subluxation or luxation of the extensor digito-

755

756

Management of Specific Injuries

Thumb Extensor Injury

SECTION 3 X

The thumb represents a unique structure in many contexts including its extensor anatomy. Because the thumb has only two phalanges, the zones are slightly different and often referred to as T I–V. T I and T II are over the only interphalangeal joint of the thumb and the proximal phalanx, respectively. Injuries in these areas can result in a mallet deformity similar to Zone I injuries in the fingers. Treatment principles in these thumb zones remain the same as previously described for Zone I of the fingers. T III is over the MCP joint of the thumb and, unlike the fingers, two tendons are vulnerable to injury at this level. The extensor pollicis brevis (EPB) inserts here in the radial aspect of the base of the proximal phalanx, while the extensor pollicis longus (EPL) passes ulnarly and inserts on the distal phalanx. Injury to the EPB at this level can be isolated or associated with injury to the dorsal capsule and radial collateral ligament. Examination of patients with injury at this level should include a thorough evaluation of the stability of the MCP joint and, at surgical exploration, all potentially injured structures should be evaluated and repaired. After surgical repair, both the thumb and wrist should be immobilized. In T IV, the EPL and EPB tend to become more oval, making them amenable to both core and epitendinous sutures. These two tendons remain closely associated at this level, and, with isolated injury of one tendon, retraction may be prevented by the remaining intact tendon; however, one should be prepared for more proximal exploration, particularly with injury to the EPL. T V injuries may involve the EPL, EPB, and/or abductor pollicis longus. In addition, injury to branches of the superficial radial nerve is often present at this level. Failure to repair the superficial radial nerve branches can result in not only sensory loss in its distribution but also a syndrome of chronic neuropathic pain.

■ Flexor Tendons and “Spaghetti Wrist” Because of its complexity, the treatment of an injury to a flexor tendon is a major component of the history of the development of hand surgery.20 Today, despite many advances in the surgical treatment of an injury to a flexor tendon and rehabilitation, the care of these injuries remains a significant challenge. Because of the proximity of neurovascular structures at all levels along the course of the flexor tendons in the forearm, wrist, and hand, combined injury of these soft tissue structures is common and adds to the complexity of care. Examination of the flexor tendons of the fingers and thumb is based on the anatomical relationship of the flexors to specific joint function. In the fingers, both the DIP and PIP joints can be flexed by the flexor digitorum profundus (FDP), a muscle that has its radial component (index and long fingers) innervated by the anterior interosseous (median) nerve and its ulnar component (ring and small fingers) innervated by the ulnar nerve. In contrast, the flexor digitorum superficialis (FDS), which flexes the PIP joint alone, is innervated only by the anterior interosseous (median) nerve. Specific simple maneuvers, however, can be performed to separate FDP and FDS function during examination of the hand. The thumb is flexed predominantly by the flexor pollicis longus, which is innervated by

the anterior interosseous nerve and is solely responsible for flexion of the IP joint. Flexor tendon repair, in general, consists of both core and epitendinous sutures. A number of core stitches have been described, and while all have been shown to be effective when applied correctly, the recent addition of preformed loop sutures offers several advantages in repair and should be considered for use.21 These sutures allow easier placement of an increased number of strands, which proportionally increases the strength of the repair allowing earlier and more aggressive therapy.22 As with injuries to extensor tendons, various zones (I–V) have been defined for injuries to flexor tendons. This classification helps in communication when describing an injury and in determining appropriate treatment and rehabilitation. Zone I injuries involve the insertion of the FDP or FPL into the distal phalanx of the finger or thumb. If the distal stump is less than 1 cm, then suture repair will not be sufficient and the FDP should be advanced and reinserted into the bone. FDP avulsions at this level, often called “jersey fingers,” occur as three patterns of decreasing severity.23 Type I avulsions are the most severe and the most easily missed because of lack of x-ray evidence of injury. In this instance, the tendon pulls off the bone and ruptures the vincula within the finger. This allows complete retraction of the proximal tendon into the palm. Early recognition and treatment of this injury is necessary to avoid the need for two-stage tendon reconstruction. Repair can be accomplished early by a pullout button or suture anchor with equal outcome.24 In Type II avulsions, the tendon is held at the level of the vincula, which does not rupture. With a Type III avulsion, a large bony fragment is associated with the distal FDP, which causes the tendon to be retained at the level of the distal A-4 pulley. Repair in this instance is often possible by reinsertion using a pullout stitch or fixation of the bony fragment with a Kirschner wire or screw. Zone II has historically been referred to as “no-man’s land” because of the difficulty of rehabilitation with this level of injury.20 This zone is defined by the presence of the adjacent FDS and FDP within the flexor sheath. Skillful repair with preservation of the pulley system during this repair may require passage of the proximally retrieved end with a small catheter that has been passed from the distal site of the injury. Even when all principles are adhered to, secondary tenolysis may be required due to the development of peritendinous adhesions. Early motion protocols are needed for functional restoration. Zone III injuries are in the palm between the distal extent of the carpal tunnel and the proximal border of the A-1 pulley. Because this zone is not constrained by the fibro-osseous canal, the prognosis for recovery is markedly improved over an injury in Zone II. Zone IV (within the carpal tunnel) and Zone V injuries (distal to the musculotendinous junction) have a high probability of associated injuries to a major vessel and/or nerve. Preoperative examination should include a thorough evaluation of the motor and sensory status of the patient with appropriate documentation. Hemorrhage in these situations can be quite dramatic, but can usually be controlled by direct pressure. Blind clamping or use of a tourniquet is discouraged and is usually unnecessary. Only rarely, with laceration of both the

Upper Extremity

Spaghetti Wrist On the volar side of the wrist there are 16 structures, including 12 tendons, 2 nerves, and 2 arteries in close proximity to the skin. This leaves these structures vulnerable to trauma when the integument is violated. Because of the appearance when the wrist at this level is lacerated resulting in exposure of numerous white string appearing structures, the term “spaghetti wrist” has frequently been applied. Other colloquialisms include “full house wrist” and “suicide wrist.” Even when this injury is complete, with involvement of both the radial and ulnar arteries, only rarely is circulation to the hand compromised because of the abundant collateral circulation via the anterior and posterior interosseous arteries and dorsal branches from the ulnar and radial arteries. While blood loss may be dramatic, initial hemostasis can often be achieved by direct pressure or brief use of a tourniquet and closure of the skin. These maneuvers should be followed by application of a splint and compressive dressing. Once this is accomplished, if this was a self-inflicted injury, the patient’s inciting cause can be addressed and at least initial postoperative cooperation assured. Repair of the “spaghetti wrist” is performed in a sequential manner from deep to superficial. This is undertaken in the operating room with tourniquet control. Following a thorough exploration and cataloging of injured structures, tendon repair is usually followed by microscopic nerve repair, and, finally, repair of the ulnar and radial arteries. At this point the tourniquet is decompressed and final hemostasis is assured prior to closure of the skin. An initial dorsal blocking splint with the wrist neutral and the fingers in the intrinsic plus position is applied. A controlled tendon rehabilitation program is initiated as soon as the patient’s cooperation can be assured. As with most injuries of the upper extremity, the final determining factor in degree of disability in this injury is successful recovery of the injured nerve.25,26 Both sensory and motor recoveries are required for an optimal result. Factors that affect outcome even with application of modern microsurgical nerve repair are age (16 years with a better prognosis than 40 years), nerve repair before 3 months, and whether the ulnar nerve is involved. Sensory recovery is usually equal for both ulnar and median nerve injury and repair; however, the failure to recover critical intrinsic muscle function innervated by the ulnar nerve invariably leads to an unbalanced weak hand with significant long-term disability.

TREATMENT OF INJURIES TO THE FINGERTIP AND NAIL BED All patients who have injuries to the nail bed must have x-rays, and any underlying distal phalangeal fracture is appropriately reduced to improve alignment and splinted for protection. Internal fixation may occasionally be needed. This is generally performed by placing a longitudinal 0.028-in Kirschner wire.

These fractures are technically open, and appropriate antibiotics must be administered.

■ Dorsal Fingertip Injuries The least severe of these injuries is the nail bed hematoma. If it is seen early, the hematoma can be decompressed by perforating the nail plate after administration of a digital local anesthetic block.27 If the nail plate is split, then the nail should be gently removed to examine the underlying nail bed. Many injuries to a fingertip and/or nail bed can be evaluated and treated in the emergency room by simple placement of digital block anesthesia and use of a Penrose drain at the base of the finger to act as a tourniquet. Suture repair of the nail bed after irrigation and cleansing is performed by using loupe magnification and 6-0 catgut suture. Even in a crushing injury, a stellate injury of the nail bed can often be meticulously repaired. Once the nail bed has been repaired, the thoroughly cleaned nail can be placed back under the nail fold where it serves as a rigid splint for any underlying distal phalangeal fracture and prevents adhesions from forming between the germinal matrix and the nail fold. These synechiae would lead to a future unsightly “split” nail deformity and pterygium formation. If a portion of the nail bed is missing, the undersurface of the nail plate should be examined as the missing nail bed may often still be adherent to the nail. It can then be gently removed from the nail and replaced as a nail bed graft. If a substantial portion of the sterile nail bed matrix is missing, it cannot be replaced by a split-thickness skin graft since the outgrowing nail would not adhere to the surface provided. Such a missing piece of nail bed is best treated by obtaining a split nail bed graft from the adjacent nail or from a toenail bed. For more severe dorsal fingertip injuries, a reverse cross-finger subcutaneous fascial flap as described by Atasoy28 may provide an excellent bed on which to place either a split-thickness skin graft or a nail bed graft. When the dorsal fingertip injury is more extensive, and there is no hope of reconstructing the nail bed, preservation of digit length can still be achieved by use of the more recently described homodigital retrograde-flow intrinsic finger flap.29 This retrograde vascular flap is based on the extensive “stepladder”-type collateral arterial circulation between adjacent radial and ulnar digital vascular structures. Some fingertip injuries may be so severe that amputation revision is the most sensible functional solution.

■ Volar Fingertip Injures Smaller volar pulp injuries without exposure of bone and of a diameter less than 1 cm in an adult are best treated open with soaks and dressings and will heal with excellent cosmetic and functional results.27 Larger soft tissue wounds, but still without exposure of bone, may be more appropriately treated with a split-thickness skin graft. If bone is exposed, either flap coverage is required to maintain the length of the digit or the amputation is revised by trimming back exposed bone to accomplish coverage with soft tissue. Once again, a reverse-flow homodigital island vascular flap may provide good soft tissue coverage or a cross-finger flap should be considered.27 The cross-finger flap suffers from the disadvantage of a two-stage procedure and unnecessary flexion of the finger that may potentially lead to a

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ulnar and radial arteries is the hand truly threatened by ischemia. Collateral circulation through the interosseous arteries will maintain adequate distal perfusion if not obstructed by application of a proximal tourniquet.

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flexion contracture of the PIP joint.30,31 A large V-Y neurovascular homodigital island flap may be considered, especially when the distal amputation of soft tissue is angulated more dorsally.29 This technique requires capabilities.

■ Retained Amputated Fingertip If the amputated fingertip is retained and is not too severely crushed, reimplantation may be considered. Reimplantation of avulsed tissue containing a large proportion of thumb pulp should always be considered in view of the functional importance. If the amputated part from the thumb has been too severely crushed, then thumb pulp may be reconstructed with a neurovascular island sensate “kite flap” that is based on the vascular branches of the first dorsal metacarpal artery.29 Another consideration for reconstruction of the volar pulp of the thumb is a microvascular medial toe pulp transfer.32 For fingertip amputations, a simple revision of the amputation may be an option in spite of the patient bringing in the amputated tip or replantation may be considered. Replacement of the fingertip simply as a composite graft after removing distal bone may at least suffice as a biologic dressing for the healing fingertip even if it were to fail. As there is a high incidence of tissue necrosis with fingertip composite grafts, an alternate solution is to retain the perionychial tissues as a full-thickness graft and to reconstruct the volar pulp support with alternative measures such as one of the local flaps already described.33

TREATMENT OF HIGH-PRESSURE INJECTION INJURIES These injuries to the hand are relatively uncommon, but the consequences of a misdiagnosis are very serious.34,35 Highpressure injection guns are found in industrial settings and are used for painting, cleaning, and lubricating. Potential injected materials include paint, paint thinner, oil, grease, water, and plastics. The injection is most frequently at the level of the DIP joint of the nondominant index finger that is directly opposite to the nozzle of the injection gun. High-pressure injection guns generate pressures ranging between 3,000 and 12,000 psi. A pressure of 100 psi is sufficient to penetrate the skin. In addition to injection guns, these injuries may result from other sources such as pneumatic hoses and hydraulic lines. The type of material injected is the most important prognostic factor. Oil-based paints and paint thinners can generate significant inflammation and fibrosis. The injectate will generally enter the tendon sheath and flow down its path into the hand. X-rays are often helpful in determining the extent of dispersion of the injected material. Non-lead-based paints may appear as subcutaneous emphysema, grease may be lucent, and lead-based paints may be seen as radiopaque densities in soft tissue. Antibiotic prophylaxis is started, and incisions are made to decompress the affected part and to enable extensive exploration and debridement of injected material. Wounds are either closed loosely over Penrose drains or left open to be closed in a delayed manner. Despite recognition and treatment, many of these injuries can still ultimately result in surgical amputation of the affected digits.

TREATMENT OF FROSTBITE, CHEMICAL BURNS, ELECTRICAL INJURIES, AND THERMAL INJURIES ■ Frostbite The management of frostbite consists of restoring core body temperature by rapid rewarming of the frozen extremity in a 44°C water bath. Active hand therapy must be instituted, also. Ibuprofen may be helpful and has been recommended for potential prevention of frostbite injuries prior to cold exposure such as on mountaineering expeditions. Thrombolytic therapy using tissue plasminogen activator (tPA) early in treatment has recently emerged as a modality to save digits and limit the extent of subsequent amputation.36 It is important to avoid premature amputation, as demarcation and mummification of digits may take as long as 2–3 months. If a disabling vasospastic syndrome persists as a chronic problem following an occult cold injury, digital sympathectomy may be helpful.37 Many follow the therapy protocol described by McCauley et al.38 On completion of rewarming, the protocol is as follows: 1. White blisters are debrided, and topical aloe vera is applied every 6 hours in order to prevent the synthesis of thromboxane. 2. Hemorrhagic blisters are drained but left intact to prevent desiccation of the underlying dermis, and topical aloe vera is applied every 6 hours. 3. The injured part is splinted and elevated in order to minimize edema. 4. Tetanus prophylaxis is given as appropriate. 5. Intravenous narcotics may be utilized. 6. Oral ibuprofen is given in a dose of 400 mg every 12 hours to inhibit the eicosanoid cascade. 7. Penicillin G is administered intravenously in a dose of 500,000 U every 6 hours for 48 hours to potentially decrease streptococcal infection during the edema phase. 8. Daily hand therapy is instituted to provide both active and passive range of joint motion. (This protocol was suggested prior to recent research on tPA, and the surgeon may consider adding tPA to this regimen.) The long interval from initial injury to definitive debridement and reconstruction may subject patients to increased risk of local infection and may cause great psychological stress and inconvenience for the patient. The initial use of radioisotope scans has been helpful in predicting the need for future amputation.39 A triple-phase technetium (Tc-99) bone scan is performed within 48 hours of rewarming for all but the most superficial frostbite injuries. Patients with an absent early blood pool phase on scanning as well as no bone uptake are restudied 72 hours later. If the second scan does not demonstrate significant blood flow, then mummification and amputation are highly likely. Based on these findings the following protocol for deep frostbite injuries using technetium bone scans has been recommended. A triple-phase bone scan is performed at 48 hours and then at 5 days. If there are normal blood and bone pool images, then one proceeds with expectant observation. If there are diminished but visible blood pool images, then

Upper Extremity

■ Chemical Burns Chemical burns may affect hands and upper extremities in the industrial environment. The most important part of treatment is water lavage that must be started at the scene of the accident and is continued for 1–2 hours for acid burns and even longer for alkali burns. General principles of chemical burns follow those of thermal burns, but there are some specific therapeutic antidotes for chemicals.41 If massive water lavage is not immediately available, then reducing agents such as hydrochloric acid will only be diluted if small amounts of water are available. Under such circumstances the agent must be neutralized with soap or soda lime. Hydrofluoric acid is a common ingredient in rust removers and degreasers and causes hypocalcemia and hypomagnesemia with a burn greater than 5% of body surface area. Immediate water lavage is required followed by subdermal injection of 10% calcium and gluconate. This can be painful if it is not combined with local or regional anesthesia. More recently, calcium carbonate gel has been used for topical application instead of the injection therapy. In contrast, phenol is not water soluble and requires specific treatment with topical polyethylene glycol (PEG 400) followed by water lavage. Treatment of white phosphorous burns chiefly involves water lavage followed by identification and excision of any remaining phosphorus particles. A 1% copper sulfate irrigation solution helps identify these particles, and this is followed immediately by water lavage to avoid the toxic effects of the copper sulfate. Sterile debridement then follows.

■ Electrical Injuries When contact with high voltage occurs, it is usually established by an arc that is a hot, electrically conducting gas. Ten to 20 kV is required to establish an arc of a distance of 1 cm. Arcing also occurs across joint flexion creases such as the elbow. Current flow begins when a complete circuit is made. The hand and upper extremity are the most common body parts affected by electrical injuries since this is often the contact area for electrocution. The arc is intensely hot, usually in the range of 5,000– 20,000°C. In the body, current is carried by electrolyte ions in solution. Current density is highest at the contact points and rapid conversion to heat occurs, leading to the deepest burns at the entrance and exit wounds. As the current enters the deeper tissues, it spreads out in proportion with the conductance of the tissues. Injuries result both from the heating and from the direct electric forces acting on larger cells. The latter results in excessive charging of the cell membrane, high transmembrane potentials, and subsequent membrane electroporation.42 Tissue adjacent to bone appears to be damaged more severely since cortical bone is denser than soft tissue and may thus store the heat generated from the adjacent soft tissue. The heat is returned to the surrounding tissue later. Due to electroporation and deep tissue heating, the damage caused is

often nonuniform and difficult to interpret clinically. Electroporated muscle appears viable on gross inspection for hours and, coupled with subsequent damage from tissue reheating, initial diagnosis of the extent of the tissue undergoing necrosis remains problematic. High-tension electrical injuries are devastating, and a compartment syndrome may result. Not only is there a conversion of electrical energy into heat that causes coagulation necrosis of tissues, but also thrombosis of blood vessels may lead to further occlusion of major blood vessels and subsequent necrosis of tissue.43 Rhabdomyolysis may lead to myoglobinemia and myoglobinuria and possible renal failure. There may be coexistent problems such as cardiac arrhythmias, spinal fractures due to tetanic muscular contractions, other skeletal injuries, serum electrolyte derangements, and blast trauma. Because peripheral nerves are very sensitive to electrical injury, even minor electrical trauma may cause a temporary dysfunction. Once the patient has been stabilized, attention is directed toward debridement of clearly necrotic parts, preservation of residual function, and soft tissue coverage of open wounds (especially of exposed vital structures) to prevent infection. Also, forearm and hand fasciotomies may be required early in the treatment of electrical injuries to the upper extremity.44 One might use temporary soft tissue coverage with porcine or artificial skin substitutes, but, once the viability of the remaining tissue has been established, fasciocutaneous flaps or microvascular free flaps will close wounds and salvage the injured extremity.45,46 Occasionally, survival of the patient and the best functional outcome may mandate an early amputation of the proximal limb. Postoperative care will include physical therapy and, possibly, fitting of a prosthesis. Successful rehabilitation may require tendon transfers, transferring of innervated muscle, or even toe transfer for missing digits. The upper extremity is involved in about 80% of all electrical injuries, amputation rates range between 40% and 70%, and mortality ranges from 8% to 14%.47

■ Thermal Burns Treatment of major burns and resuscitation is outside of the scope of this chapter (see Chapter 48) that will focus only on the management of a burn in the upper extremity. Initial first aid for hand burns requires immediate cooling of the wound by rinsing in cold water for 5–10 minutes. This helps reduce subsequent edema formation, also.38 Capillary refill must be documented to decide upon the need for an escharotomy or fasciotomy. Full-thickness circumferential burns of an upper extremity frequently require an escharotomy.48 Fasciotomy of the hand for the interossei and the first web space should be performed in situations of severe edema of the hand.49 The hand often assumes the intrinsic minus posture because of swelling. The wrist is drawn into flexion with hyperextension at the MCP joints and flexion at the proximal and distal IP joints that results in a claw deformity. The thumb adducts toward the palm, and the interphalangeal joint is hyperextended.43 Appropriate early splinting is necessary to overcome this posture in the severely burned hand. Splinting in the

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continued observation is undertaken with delayed debridement if necessary. If there is little or no flow in either blood or bone pool images, early debridement or amputation is recommended with potential salvage with vascularized tissue.40

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intrinsic plus position places the ligaments of the digital joints in maximal stretch and minimizes their shortening. Customized thermoplastic splints are effective and can be adjusted easily. Local wound care depends on the depth of the burn. Partialthickness superficial second-degree burns are expected to heal within 7–14 days. Larger blisters may be aspirated or removed by incision and debridement. Moist wound healing is required for the wound to heal spontaneously. The burn wound is cleaned daily, followed by the application of an antibacterial cream. As epithelialization occurs, a bland ointment is helpful to prevent desiccation of the newly formed epithelium. Deep dermal and full-thickness burns of the hand are best treated by early excision and grafting. A burn wound is uninfected initially and suitable for primary surgical treatment during the first 5 days. Tangential excision is performed down to punctate bleeding. Blood loss can be minimized by use of an upper arm tourniquet. Exsanguination of the arm by simple elevation rather than by wrapping with a rubber bandage will still enable the surgeon to determine the appropriate depth of tangential excision and visualization of punctate bleeding. Residual devitalized tissue must not be left behind as this could be a cause of failure of a skin graft. Resurfacing the wound with a split-thickness skin graft is then immediately performed.50,51 Skin grafting is rarely necessary for palmar burns due to its capacity for spontaneous healing from the skin appendages at this site. A full-thickness burn, however, may occasionally lead to exposure of tendons, bones, and joints. In this situation primary coverage of soft tissue by regional flaps or even free flaps may be required. It has been found that fascial flaps are very useful to provide coverage of dorsal hand wounds since cutaneous flaps may be too thick. Suitable fascial flaps include temporoparietal, serratus anterior, or anterolateral thigh.52 After a skin graft is placed, the hand is immobilized for 5 days until healing of the graft has occurred. Passive and active hand therapy is then initiated to reduce stiffness and contractures. Once again, the importance of appropriate postoperative splinting should be emphasized. In the first few months following the burn injury, there is a period of scar hypertrophy. This scar tightness is overcome with range of motion exercises of the joints. An important adjunct to management of the scar is having the patient use a custom-fitted elastic pressure garment that should be initiated as early as 2–3 weeks after skin grafting. Pressure garments may be required for as long as 6 months, while secondary surgical procedures for release of contractures may be required at a later date.

VASCULAR INJURIES IN THE UPPER EXTREMITY A vascular injury can occur with either closed or open trauma (see Chapter 41). Closed injuries associated with arterial disruption include scapulothoracic dissociation, shoulder dislocation, and elbow fractures and dislocations. A scapulothoracic dissociation represents a complex injury with a high incidence of both vascular disruption and concurrent rupture or avulsion of the brachial plexus. Successful treatment requires prompt diagnosis, preoperative angiography, and reconstruction of the axillary or brachial artery with an interposition graft.

Despite the frequency of shoulder dislocations or fractures, an associated arterial injury remains a relatively rare complication. Anterior dislocation in the elderly patient is the most common scenario where vascular injury occurs with blunt shoulder trauma. Predisposing atherosclerotic disease with a more tortuous and noncompliant artery may play a role in this injury, and the injury is just as likely to occur during relocation for the same reasons. Because of this, the distal vascular status should be assessed prior to reduction of any anterior dislocation. Supracondylar fractures in children infrequently involve the brachial artery; however, the extension-type fracture with posterolateral displacement of the distal fragment and wide separation can result in injury to this vessel. The ischemia present after this injury can be caused by direct impingement from the medial spike, secondary to vascular spasm and progressive soft tissue swelling, or thrombosis of the distal brachial artery. When vascular trauma is suspected, a gentle closed manipulation of the fracture and percutaneous pin fixation should be followed by a repeat clinical examination. If distal pulses do not return with reduction, then angiography should be obtained. A surgical release of the artery from entrapment in the fracture or a formal vascular repair may be needed. An open injury with pulsatile hemorrhage in the upper extremity should be managed initially with pressure alone, whenever feasible. Blind clamping and ligation can lead to devastating injury of closely associated nerves that can result in a successfully revascularized, but worthless limb. With such injuries to nerves multiple procedures may be needed to restore less than satisfactory function. Similarly, use of the tourniquet should be limited to avoid contributing further to ischemic damage from occlusion of collateral flow. Once hemorrhage is controlled, few would argue that prompt surgical repair of a subclavian, axillary, or brachial artery injury is indicated. Less obvious is the treatment of a single-vessel injury in the forearm. Many have argued that, with documentation of adequate collateral flow from the remaining artery, it is more expeditious to ligate the injured vessel. With improvements in microvascular surgery, however, repair of arteries this size has become quite straightforward and the procedure itself adds little time to an exploration of the wrist or forearm where other associated injuries are being addressed.

NERVE INJURIES IN THE UPPER EXTREMITY Treatment of injury to a peripheral nerve represents a major component of upper extremity surgery, and the end result of the care of this injury is often the major determinant of the degree of functional recovery. A nerve injury should be looked for with a high level of suspicion based on the anatomical location of injury to the extremity. Furthermore, serial examinations over the course of the patient’s recovery are warranted. Also, if surgery is planned to deal with other injuries, the opportunity for direct exploration of known at-risk nerves in the zone of injury being addressed should not be missed. This is particularly indicated in the presence of sharp penetrating trauma. The terms neurapraxia, axonotmesis, and neurotmesis are commonly used to describe different degrees of the continuum

Upper Extremity injured nerve proximal and distal to the injury at the time of reexploration. Suture tagging the nerve to a stable adjacent structure, however, may serve to prevent the inevitable retraction and minimize the distance that requires grafting at the time of definitive repair. An exception to early exploration of penetrating injuries is the gunshot wound. In these injuries the mechanism of injury includes heat and shock wave effects, and expectant management is usually appropriate. A vascular injury where the vessel is enclosed with the nerve in a common sheath, however, may lead to similar injury to both the nerve and vessel. In these situations, it is imperative that continuity of the nerve is verified during repair of the vessel. Nerve transfer represents another option for dealing with both motor and sensory losses in what potentially would be a nonreconstructable injury.53,54 The theory behind nerve transfer is to convert a high-level nerve injury into a low-level injury. This is accomplished by utilizing redundant or unimportant nerves or fascicles of the donor nerve to innervate critical motor or sensory targets. Initial experience with this concept was in brachial plexus surgery with the now classic intercostal to musculocutaneous nerve transfer to restore elbow flexion. This technique has now been expanded in brachial plexus neurotization to a number of nerve transfers with specific functional targets and more recently to reconstruct a number of other injuries to nerves. An important example of a nerve transfer outside of the brachial plexus is the transfer of the distal anterior interosseous nerve to the motor branch of the ulnar nerve to restore intrinsic function. This gives a very simple functional alternative to complex tendon transfer and preserves muscle mass within the hand resulting in a more cosmetic outcome.

■ Brachial Plexus Injury Brachial plexus injuries most often occur in young active males participating in extreme sporting activities or involved in highspeed motor vehicle crashes. This is a devastating injury that frequently leads not only to physical disability but to psychological distress and socioeconomic hardship also. This injury is initially overlooked with some frequency when the surgical team is caring for the polytrauma patient with more obvious life-threatening injuries. Even when detected, treatment historically has been delayed in hopes of some type of spontaneous functional recovery. This delay is largely unjustified today and is now known to potentially compromise future reconstructive options. Common terms used to describe injuries to the brachial plexus are root rupture, root avulsion, preganglionic, postganglionic, supraclavicular, and infraclavicular.55 Supraclavicular injury refers to injury of the spinal nerves, trunks, or divisions, while infraclavicular injury refers to injury of the cords and their terminal branches. When an injury causes tearing of the rootlets from the spinal cord proximal to the dorsal root ganglion, the injury is classified as preganglionic or a root avulsion. If an injury is distal to the dorsal root ganglion, it is called a postganglionic injury. This type of injury is often associated with rupture of the root.

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of injury to a peripheral nerve, and each term correlates with the potential for recovery. Neurapraxia, the most minor form of injury, represents a conduction block with preservation of anatomical continuity. The neuropraxic injury may be complete or partial and, although recovery will be complete, it may take up to 3 months. Importantly, there is no nerve regeneration involved in this recovery and there is no advancing Tinel’s sign as there is no axonal involvement. It should be remembered that a neuropraxic injury can be associated with a concussive blow or a compressive injury such as a promptly released compartment syndrome or a tourniquet-type injury, as well. In axonotmesis there is structural damage to the axon while the endoneurium and perineurium remain intact. A Tinel’s sign is present in this form of injury, and it can be followed during recovery as it progresses distally with axonal regrowth. In this injury, there is classic histological Wallerian degeneration distal to the site of axonal disruption. Because the axon sheaths remain essentially undisturbed, complete restoration of the original pattern of innervation is possible. Neurotmesis represents complete severance of the nerve from traction, rupture, or penetrating trauma. Recovery in this situation is not possible without microsurgical repair. In large nerves it is possible to have all forms of injury present within the same nerve. This situation can complicate both initial diagnosis and interpretation of recovery as well as delay and complicate surgical intervention. Surgical interventions with injury to a peripheral nerve include decompression, neurolysis, direct repair, and nerve grafting.53 In complex injuries involving multiple nerves or nerve segments, all these techniques may be required. Direct nerve repair may be by epineural or fascicular suturing. While fascicular repair intuitively seems like it would give more precise anatomical alignment, this has never been substantiated and the principle of less is more seems to apply. Minimal foreign material in the form of suture, minimal or no tension, and minimal trauma are required for a successful repair. When a tension-free repair is not possible, a nerve conduit in the form of an autogenous nerve graft or a vein or artificial conduit for a short segment replacement must be utilized to fill the defect and serve as a guide for new axonal growth. A number of sensory nerves can be sacrificed with minimal deficit, but the most common is the sural nerve from the lower leg. Timing of nerve repairs can be defined as primary when repaired within 1 week of injury, while nerve repairs after this time are considered secondary. Direct end-to-end tensionless suture neurorrhaphy may not always be possible in the case of secondary repair, and one should be prepared for interposition grafting or employment of other techniques to achieve successful reinnervation. In general, nerve injuries associated with sharp penetrating trauma should be explored early. If the injury is a sharp laceration, immediate direct repair is usually the best option for optimal recovery. When the precise zone of injury to the nerve cannot be determined, as after a traction or crush injury, a delayed repair is indicated so that the zone of injury is more clearly defined. Simple tagging of injured nerves at the time of exploration in itself probably serves no useful purpose since the experienced peripheral nerve surgeon will readily locate the

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There are practical implications to determining a lesion to be preganglionic or postganglionic. At this time a preganglionic injury is not amenable to direct surgical repair and, therefore, alternate means of functional restoration must be explored. In contrast, postganglionic injuries can potentially be restored by insertion of an interposition nerve graft. Importantly, there are features in the history and clinical examination that can indicate a preganglionic versus a postganglionic injury. Horner’s syndrome is characterized by ptosis, miosis, anhydrosis of the cheek, and enophthalmos and suggests a preganglionic avulsion of C8 and T1. Winging of the scapula suggests a preganglionic avulsion of C6, as the serratus anterior muscle is supplied by the long thoracic nerve that arises predominantly from the anterior division of C6 close to the intervertebral foramen. Inability to move the scapula medially indicates rhomboid muscle dysfunction and is indicative of a C5 avulsion with compromise of the dorsal scapular nerve. This motion can be evaluated by asking the patient to attempt to bring the elbows together behind the back with the hands resting on the hips. Postganglionic injury occurs at points of tethering of the plexus to surrounding structures. Erb’s point where the suprascapular nerve comes off the upper trunk is a common and historic site of postganglionic injury. Rupture of C5 commonly occurs from the previously described fascial attachments from the transverse process. As they are particularly strong at this segment, this anatomical feature may help preserve C5 for grafting when other roots have been injured by avulsion. The suprascapular nerve is also confined at the suprascapular notch and can be injured with upward displacement of the scapula during trauma. Injury to a clavicle can result in injury to the brachial plexus at the level of the divisions where they are relatively immobile. The axillary nerve is tethered both at its point of takeoff from the posterior cord and as it passes through the quadrangular space and is vulnerable to injury at both these points. Advances in ancillary diagnostic tests have paved the way for early surgical intervention. When used appropriately, the combination of electrodiagnostic studies, CT myelography, and, occasionally, MRI can, when coupled with clinical findings, determine that significant recovery is not possible without surgical intervention. Nerve conduction studies (NCS) and electromyography (EMG) are the primary electrodiagnostic studies that can aid in the evaluation of a patient with a brachial plexus injury.56 With a nerve injury other than neuropraxia at 48–72 hours following injury, the axons distal to the lesion begin to undergo Wallerian degeneration and loose the ability to conduct. Unfortunately, it may take as long as 4–6 weeks after injury before fibrillation potentials that indicate muscle denervation are detected by EMG. NCS can be utilized to help differentiate between preganglionic and postganglionic injuries by evaluating the sensory nerve action potential (SNAP). This is possible because of the previously described location of the dorsal root ganglion outside the spinal cord proper. With a root avulsion the electrical circuit involved in SNAP recordings remains intact, whereas the ganglion circuit is disrupted with rupture distal to the dorsal root. This information can be extremely valuable both preoperatively and intraoperatively when trying to determine whether a root remains accessible for grafting. In practice,

electrodiagnostic studies should be initially performed at 4–6 weeks postinjury. Both CT and MRI have a place in the evaluation of brachial plexus pathology55,57; however, CT myelography remains the “gold standard” for demonstration of root avulsion in the setting of a traumatic brachial plexus injury. MRI, while being the preferred modality for compressive lesions or other nontraumatic brachial plexopathies, still suffers from too much motion artifact generated by pulsations of the cerebrospinal fluid. Therefore, it does not consistently demonstrate root avulsion and aid in surgical planning. Early CT myelography timed to coincide with the initial electrodiagnostic studies can allow for surgery within 2–3 months of injury, if not sooner. If these initial studies at 4–6 weeks are consistent with an in-continuity injury, then follow-up electrodiagnostic testing should be performed 6 weeks later to evaluate for evidence of reinnervation. This second study is still within the 3-month time frame for early aggressive intervention if indicated. While still a devastating injury, advances in the last 20 years have significantly improved the prognosis for some degree of functional recovery with trauma to the brachial plexus. Surgical options include neurolysis, nerve grafting, and neurotization. Neurolysis is the surgical technique of freeing intact nerves from scar tissue. With trauma to the brachial plexus, this technique is rarely a definitive treatment. More often neurolysis is an incidental technique that occurs during reconstruction of the plexus by nerve grafting or neurotization. Prior to undertaking nerve grafting or brachial plexus neurotization, prioritization is essential. It is generally agreed that elbow flexion is the most important function to restore followed by active shoulder control and scapular stabilization. Triceps control through restoration of radial nerve function may be achievable, also. Restoration of useful median and ulnar nerve function by nerve surgery alone, however, is probably not a realistic goal. Nerve grafting requires a suitable lead-in nerve source. C5 and C6 may serve this purpose even when a global brachial plexus injury is present. Grafting from these sources is targeted toward the above-listed priorities via the suprascapular nerve and posterior division of the upper trunk to allow for control of the shoulder. When only minimal suitable lead-in nerves are present, further supplementation via nerve transfer will be required for elbow flexion. The classic transfer for this additional function is the aforementioned intercostal nerve transfer directly to the musculocutaneous nerve. While the above approach has led to significant functional recoveries, it now needs to be weighed against more modern options. These include nerve grafting in conjunction with more aggressive nerve transfers utilizing the terminal branches of the spinal accessory and phrenic nerves. This can be performed in conjunction with functional free muscle transfers with one or two gracilis muscles revascularized and reinnervated via microsurgical techniques.58 These aggressive techniques have led to successful restoration of simple grasp, a previously unheard of functional restoration. While the focus of this review has been closed injuries, penetrating trauma accounts for 10–20% of injuries to the brachial plexus. These injuries are often infraclavicular and cause a more

Upper Extremity

INFECTIONS IN THE HAND Infection is a common occurrence in the hand with most organisms introduced by direct inoculation via puncture, laceration, open fractures, or bites (see Chapter 18). The apparent vulnerability of the hand to infection is probably related to the multiple anatomical closed spaces present. Untreated infection in these spaces can lead to severe damage and ultimately diminished or lost function. A careful history is important to determine not only possible accidental trauma but also other predisposing factors such as an immunocompromised state or intradermal or intravenous injection of illicit drugs. Despite a variety of initiating causes, the infection itself is usually caused by common gram-positive flora to the skin and mouth such as Staphylococcus sp. and Streptococcus sp. Exceptions to this occur in patients with diabetes mellitus or those who are intravenous drug users where gram-negative organisms are frequently encountered.60 Physical examination will often reveal erythema, warmth, tenderness, and swelling, as well as restricted function. Lymphangitic spread may be observed proximal to the site of infection. Careful palpation should detect areas of fluctuance that would require surgical drainage as opposed to monitored antibiotic treatment alone. The most common infections of the hand are paronychias and felons. Paronychias, or nail fold infections, occur when bacteria gain entrance through a break in the seal between the nail and fold. Nail biting and excessive manicuring may predispose to this infection. If cellulitis is present, soaks and antibiotic therapy targeting Staphylococcus species may lead to resolution of the infection. Once fluctuance is noted under the nail fold, surgical drainage is indicated. A simple approach to drainage is to sharply elevate the nail fold from the nail plate in the region of the fluctuance. If any dissection of purulence is noted under the nail at this time, then the involved portion of the nail plate or the entire nail plate should be avulsed to allow complete drainage. A felon is an abscess of the fingertip pulp that is confined by many fibrous vertical septa that secure the relationship between the bony tuft and overlying skin. When undrained, this

infection will ultimately liquefy the pulp fat and lead to malformation of the tip of the finger. Surgical drainage is always indicated once an abscess has developed, and a number of incisions have been advocated. A straight midaxial incision on the nonopposition side of the finger is preferred unless the abscess points volarly. In this instance, a straight longitudinal midline volar incision is acceptable. Suppurative flexor tenosynovitis represents an infection of the flexor tendon sheath, another confined space of the hand. This condition is usually diagnosed clinically and has the characteristic signs of partially flexed resting posture of the finger, pain with passive extension, fusiform swelling of the entire finger, and volar tenderness along the course of the flexor sheath. Delayed treatment of this condition can lead to scarring of the tendon or necrosis and, in the small finger and thumb, development of a horseshoe abscess because of the anatomical communication through the radial and ulnar bursa. Treatment with antibiotics alone is rarely successful for these infections unless initiated early after the onset of symptoms. Furthermore, it is difficult to advocate medical management because of the severe sequelae associated with a delay in definitive care. Early surgical intervention with open or closed irrigation of the sheath remains the “gold standard.” Interdigital infection of the web space (collar button abscess) and infections of the palmar space represent two additional infections of closed spaces that mandate prompt surgical intervention. The term “collar button abscess” refers to the hourglass shape of the abscess that occurs in a web space infection and its resemblance to the collar button used in dress shirts in the 1900s. Inspection of the hand in this instance will usually show an associated fissured callus at the involved web space and the two adjacent fingers in abduction. Physical examination will reveal tenderness and palpable swelling both dorsally and volarly. Because of this, dorsal and volar drainage is required through separate incisions that do not carry across the web space. The palm has three distinct anatomical spaces, all of which may become infected. These are the thenar space, midpalmar space, and hypothenar space. Of these, the thenar and midpalmar spaces are most frequently affected by a suppurative process. Patients with these infections almost always have a history of penetrating trauma with or without retention of a foreign body. On inspection, the hand will be swollen and erythematous volarly and will be exquisitely tender to palpation. If doubt exists as to the presence of an abscess versus cellulitis, aspiration or an ultrasound examination may be performed. As with suppurative flexor tenosynovitis, the severe sequelea of a delay in treatment means that a negative aspirate should not rule out the need for surgical exploration. As in all infections, routine x-rays should be obtained to rule out the presence of radiopaque material prior to exploration. Bite wounds from dogs and cats often serve as the source of bacteria responsible for the above-described closed space infection.61 Whether prophylactic antibiotics can prevent this infection when initiated early has been the subject of a great deal of research. It would appear that there are good prospective data to support the routine use of prophylactic antibiotics in human bite wounds. While retrospective data support antibiotic use in dog and cat bites, no similar prospective data exist.62

CHAPTER CHAPTER 39 X

selective loss of function. Sharp, penetrating injuries are often associated with a vascular injury that should be addressed with extreme care to avoid injury to the adjacent nerves. The plexus should then be explored by a surgeon with expertise in peripheral nerve injuries. Gunshot wounds present a more difficult dilemma.59 In the instance of a vascular injury requiring surgical exploration, the plexus must also be explored and any injuries identified. Acute repair is probably not indicated since the zone of injury to the nerve will be poorly defined, and this could cause an inadequate resection and failed grafting. Exploration at 6 weeks postinjury is recommended since nerve transection has been confirmed and there is no hope of spontaneous recovery. Gunshots without an associated vascular injury may be managed expectantly with serial examinations and sequential electrodiagnostic examinations at 6 and 12 weeks postinjury. If no recovery is detected at 12 weeks, then exploration is probably indicated.

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INJURIES TO JOINTS ■ Sternoclavicular Dislocation SECTION 3 X

Sternoclavicular dislocation is a rare, high-energy injury. The clavicle typically dislocates in an anterior direction, but posterior dislocations do occur and are more commonly associated with damage to surrounding structures in the neck and chest.63–65 Careful assessment of the patient is warranted, with particular attention paid to these structures. Plain x-rays are often difficult to interpret, but the injury and direction of displacement are generally identifiable on some views or on a CT. If performed early and with general anesthesia, closed reduction is usually successful, but residual subluxation may persist when an anterior displacement has occurred. Correction of posteriorly displaced injuries may require a towel clamp or similar instrument to obtain reduction. It is important that a thoracic surgeon is available at the time of reduction to assess and address any injury to the associated structures. Later referral to a peripheral nerve surgeon may also be required.

■ Scapulothoracic Dissociation Scapulothoracic dissociation is a rare but functionally devastating and potentially life-threatening injury that represents a closed amputation of the upper extremity. This should be suspected when the scapula appears laterally displaced on a nonrotated anterior–posterior (AP) chest x-ray (Fig. 39-3). CT or MRI findings may confirm the diagnosis and identify damage to the surrounding soft tissues, as well. An unusual intrathoracic variant can occur, in which the inferior angle of the scapula penetrates an intercostal space and becomes lodged within the chest. This musculoskeletal injury is often accompanied by injury to the subclavian artery and brachial plexus. Emergent surgical treatment may be required to revascularize the upper extremity. Simultaneous exploration of the plexus after the vascular repair is strongly recommended to accurately

TABLE 39-8 Classification of AC Joint Injuries Type Ligament Injury I Incomplete AC ligament injury II Complete AC, incomplete CC III

Complete AC, complete CC

IV

Complete AC, complete CC Complete AC, complete CC

V

VI

Complete AC, complete CC

Findings No displacement or instability No displacement,

anterior–posterior instability Inferior displacement of scapula, instability all planes Clavicle posteriorly dislocated through trapezius Deltoid and trapezius tear allow

instability and displacement Clavicle locked inferior to coracoid process

access the degree of neurologic injury. If a global injury to the brachial plexus is detected at this initial exploration, consideration should be given to primary amputation, as the chance of meaningful neurologic recovery is minimal.66–68

■ Acromioclavicular Dislocation A “shoulder separation” is a common diagnosis, especially among athletes. Injury to the acromioclavicular (AC) joint typically occurs due to a fall onto the acromion. Stability of the AC joint is dependent on both the AC and coracoclavicular (CC) ligaments. The severity and classification of the injury is based on which of these structures is injured and to what degree (Table 39-8). X-rays are often normal in mild injuries and, although they may confirm the diagnosis, stress x-rays are rarely indicated. Some still consider Type III injuries a relative indication for surgical treatment, but most orthopedic surgeons recommend initial nonoperative treatment for all Type I–III injuries.69,70 This typically consists of limited activity, analgesics, and sling support for a few days to a few weeks. Successful early rehabilitation is possible, especially in injuries of lesser severity. Types IV–VI are much less common, but generally require surgical reduction and ligamentous repair or reconstruction using a variety of surgical techniques. AC joint injuries may also contribute to the late development of an arthrosis and impingement necessitating excision of the distal clavicle.

■ Glenohumeral Dislocation FIGURE 39-3 An example of scapulothoracic dislocation. Note the lateral translation of the scapula relative to the chest wall. A fracture of the clavicle and a nondisplaced fracture of the glenoid neck are also present. The patient was noted to have a complete brachial plexus palsy.

The glenohumeral joint is among the most commonly dislocated joints with a reported incidence of 2% in the general population and as high as 7% in athletes. Dislocation can occur with highor low-energy injuries and may be anterior (95%), posterior (4%), or inferior (0.5%) in direction. In approximately 1% of these patients, there may be an associated fracture. In anterior

Upper Extremity

A

stability. If the duration of dislocation exceeds 6 months or if there is extensive damage to the joint, a glenohumeral arthroplasty may be indicated. Delayed treatment seldom results in the return of full function, highlighting the importance of accurate early diagnosis and treatment.76 X-ray evaluation of a suspected shoulder dislocation should include AP and Bloom–Obata modified axillary views. The Bloom–Obata modified axillary view, which includes the glenoid fossa and the humeral head, is of particular importance in evaluating the traumatized shoulder. AP x-rays of the shoulder may appear grossly normal despite dislocation of the glenohumeral joint, especially if the direction of the dislocation is posterior. Anterior or posterior displacement of the humeral head relative to the glenoid is readily apparent in the Bloom– Obata modified axillary view (Fig. 39-4).77 A CT or MRI is indicated if a more complicated injury is suspected. Urgent reduction of a glenohumeral dislocation is the preferred treatment. Many closed reduction techniques have been described, but most dislocations can be successfully reduced in the ED by manipulation with or without sedation. In general, maneuvers involve either traction on the humerus or manipulation of the scapula.78–80 Of the many named methods described for reduction, all have similar reported success rates of 70–90%. Failure to achieve reduction in the ED is an indication for general anesthesia and possible open reduction in the operating room. After successful closed reduction, most shoulder dislocations can be successfully managed by a period of immobilization and early rehabilitation. The ideal duration and position of immobilization continue to be debated, but adequate results are typically achieved with a simple sling and early, gentle pendulum exercises. Surgical indications include missed or recurrent dislocations, dislocations with associated injuries, and young, high-demand patients.

■ Trauma to the Elbow The elbow is frequently injured by falls from a standing height, especially in the elderly population. High-energy injuries are more common in younger patients and are typically sustained in

B

FIGURE 39-4 A posterior shoulder dislocation not ready apparent on a PA x-ray (A) becomes more obvious on an axillary lateral view (B).

CHAPTER CHAPTER 39 X

dislocations the extremity is typically adducted, and there is often a visible or palpable deformity of the anterior chest. Posterior dislocations present with a less obvious gross deformity and are often overlooked. Careful examination will show an inability to externally rotate the humerus and posterior prominence of the humeral head. It is important not to miss luxatio erecta, inferiorly dislocated shoulder locked in abduction with the forearm resting on the head.71 Inferior dislocations such as this are often associated with neurovascular injury, injury to the rotator cuff, labral tears, and/or greater tuberosity fractures.72 A common pattern of injury is a dislocation of the shoulder that occurs with an associated fracture of the greater tuberosity of the humerus. This should be reevaluated after closed reduction and, if there is persistent displacement of the fracture fragment (1 cm), surgical treatment may be indicated. Compression fractures, termed Hill–Sachs lesions, may occur in which the anterior glenoid impacts the posterior humeral head and can contribute to recurrent instability,73 as can displaced fractures of the glenoid rim.74 Patients aged 40 years and over are at increased risk for an associated rotator cuff tear that may require repair, also.75 Considering the range of injuries described above, it is impossible to detect all lesions simply using two-dimensional plain x-rays. When such associated injuries are suspected on x-rays or by physical examination, it is recommended that three-dimensional imaging (MRI or CT) be performed to better evaluate the nature of the injury. The patient with a shoulder dislocation is often in severe pain. A detailed physical examination should be performed before reduction as associated neurovascular injuries are relatively common. The neurovascular exam is repeated after the reduction of the dislocation, as well. An injury to the brachial artery should be explored and repaired. The most common neurologic injury is a traction neurapraxia of the axillary nerve, and these typically recover fully without surgical treatment if early reduction is performed. More serious neurologic injuries may occur, including complete disruption of the brachial plexus. A missed or unreduced shoulder dislocation can be functionally devastating. Late treatment often requires open reduction and additional bony and soft tissue procedures to attain

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SECTION 3 X

falls from a height, sport injuries, or vehicular trauma. It is important to remember that the elbow is not a single joint, but actually a complex set of articulations including the ulnohumeral, radiocapitellar, and proximal radioulnar joints. Preservation of an arc of motion from 30° short of terminal extension to 130° of flexion and at least 50° of pronation and 50° of supination is sufficient to allow patients to perform most routine tasks. In patients with a more severe post-traumatic contracture or limitation of motion due to heterotopic ossification that does not respond to nonoperative treatment, eventual closed manipulation or even open capsulectomy of the elbow may restore functional motion. Because of the relatively thin soft tissue envelope about the elbow, open fractures are common, and any open wound should be scrutinized with this in mind. Care should be taken to identify associated injuries, which may include trauma to the median, ulnar, and radial nerves, as well as to the brachial artery. X-rays of the severely traumatized elbow with displaced fragments or segments may be difficult to interpret due to nonanatomical overlap of the injured parts. Therefore, CT can be helpful in determining the size and location of small articular fragments and is valuable for preoperative planning. Once the extent of the injury is established, an effort should be made to provisionally reduce any dislocation or displacement as anatomically as possible. Distal neurovascular status should be carefully reassessed after any manipulation or reduction. Repeat x-rays should be carefully evaluated to assure that reduction is concentric and there are no fractures that were not identified in the original films. Definitive treatment should progress based on the pattern of injury. Elbow injuries present particular challenges to the surgeon charged with their repair and reconstruction due to the complex motion and stability that are normally present. Small articular or periarticular fractures can contribute to subtle, but significant, subluxation. If this is not recognized and corrected early, the resulting chronic instability may be functionally devastating. Further complicating treatment of elbow injuries is the tendency of this joint to become stiff and develop a posttraumatic contracture, especially if it is immobilized for any length of time. For these reasons, the goal of treatment in most cases is to achieve enough stability to allow early range of motion and prevent stiffness. The challenges of reaching this goal have led to an ongoing expansion of techniques and implants designed to address particular injuries. Despite this, most patients who sustain severe elbow trauma continue to have some permanent limitation of motion.

■ Dislocation and Fracture–Dislocation of the Elbow Of all dislocated joints, the elbow is second in frequency only to the shoulder. Dislocation of the elbow typically refers to dislocation of the humerus from both the radius and ulna (Fig. 39-5) and can be classified by the direction of displacement of the forearm segment. Posterior and lateral or posterior– lateral dislocations occur most frequently. Much less common are anterior, medial, and especially high-energy divergent dislocations in which the proximal radioulnar joint is also dislocated and the radius and ulna displaced laterally and medially,

FIGURE 39-5 Posterior elbow dislocation is noted on the lateral radiograph of the elbow.

respectively. Simple dislocations of the elbow result in injuries of the medial and lateral collateral ligament complexes without bony injury (Fig. 39-5). Complex dislocations are those associated with fractures about the elbow. Isolated dislocations of the radial head occur also, especially in children. If this injury is suspected in an adult, care should be taken to assure that it is not a part of a Monteggia fracture–dislocation. Prior to reduction, a careful examination is necessary to rule out an associated injury to the brachial artery, or the median, radial, and, most commonly, ulnar nerve. Urgent closed reduction is then recommended. Unless the joint has remained dislocated for some time, gentle traction on the distal segment and countertraction on the humerus under heavy sedation is usually successful. In thin individuals, it may be possible to pull distally on the subcutaneous olecranon that is palpable posteriorly. Any medial or lateral malalignment is corrected before flexion completes the reduction. Forced maneuvers against resistance and extreme hyperextension should be avoided, and general anesthesia and/or open reduction may be required. Difficulty obtaining a stable closed reduction should increase suspicion that a complex dislocation or other associated injuries are present. Once closed reduction is completed, the elbow should be passively flexed and extended to determine if there is a tendency to redislocate. The position at which this occurs should be noted, and a reevaluation of the neurovascular status should be performed. Simple dislocations are usually relatively

Upper Extremity

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CHAPTER CHAPTER 39 X

A

B

FIGURE 39-6 PA (A) and lateral (B) radiographs of transscaphoid perilunate dislocation with translocation of both the lunate and proximal pole of the scaphoid into the carpal tunnel.

stable following reduction and after immobilization in 90° of flexion for 7–10 days. Early range of motion activities may then be safely initiated to minimize long-term stiffness.81 X-rays should be repeated after reduction and carefully scrutinized to confirm a concentric reduction and identify any associated fractures that may not have been visible with the joint displaced. Simple dislocations rarely require surgical treatment. Any complex dislocation of the elbow should be definitively addressed within a few days or as soon as the patient’s overall condition allows. The longer the elbow remains in a dislocated or subluxated position, the more difficult it may be to achieve eventual stability. Complex dislocations are prone to redislocate if definitive treatment is delayed. In most patients, immobilization of the elbow in flexion and pronation imparts some stability. Patients immobilized in this way should be carefully monitored as this position may contribute to vascular compromise of the upper extremity as edema increases.82 A notoriously unstable injury is an elbow dislocation with associated fractures of the radial head and coronoid process of the ulna. This pattern has been termed the “terrible triad of the elbow.” Surgical treatment is required to restore stability to the elbow. Whenever possible this should include repair or reconstruction of the radial head, coronoid, and, if necessary, the collateral ligaments. In severe injuries dynamic external fixation or even transarticular pin fixation may be required.83 Restoration of full elbow function is rarely possible after severe injuries of this type.

■ Carpal Dislocations Compared with other types of injuries to the wrist, carpal dislocations are relatively infrequent in occurrence.84 Because these injuries are usually associated with high-energy trauma, they

may have devastating effects on future function of the wrist. Early diagnosis and aggressive treatment is indicated, but simple closed reduction rarely results in long-term stability of the wrist. Based on anatomical patterns of injury, these may be classified as perilunar, radiocarpal, midcarpal, axial, and isolated carpal dislocations. The most frequent traumatic carpal dislocations are perilunar dislocations and fracture–dislocations (Fig. 39-6). Radiocarpal and axial pattern dislocations are much less common, but still more frequent than isolated dislocations of the carpal bones. A pure midcarpal dislocation without an associated fracture is an extremely rare event. Perilunar dislocations represent part of a staged pattern of injury centered around the lunate.85 These can be purely ligamentous injuries, often referred to as lesser arc injuries, or they can be associated with fracture of a carpal bone and are known as greater arc injuries. These injuries are usually caused by motor vehicle crashes, a fall from a height, or sports. While these injuries often appear as a dramatic deformity of the wrist, the examiner should still perform a complete physical examination to rule out other more life-threatening injuries. Once this is accomplished, a focused examination of the upper extremity should include a documented neurologic examination because of the frequency of compromise of the median nerve with these dislocations. Posteroanterior and lateral x-ray views of the wrist should be obtained (Fig. 39-6). The lateral projection is particularly helpful to evaluate the relationship between the lunate, capitate, and distal radius. With a perilunate dislocation the lunate will retain its relationship with the radius, but the capitate will be displaced either palmarly or dorsally from the lunate. On a PA view the carpus will appear crowded due to overlap of the proximal and distal carpal rows.

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SECTION 3 X

Greater arc injuries will appear similar to lesser arc injuries on an x-ray of the wrist, but will include one or more fractures of the carpal bones and/or fractures of the radioulnar styloids. The most common type is the transscaphoid perilunate fracture–dislocation. It is important not to miss the much less frequent transscaphoid/transcapitate fracture–dislocation often referred to as the scaphocapitate fracture syndrome. Treatment should be initiated as soon as the patient is able to be safely sedated or anesthetized. Closed reduction in the ED with splinting or application of a bivalved cast may be an appropriate short-term solution to decompress the median nerve and restore a semblance of normal anatomical alignment. This cannot be considered definitive long-term treatment since residual instability and misalignment should always be considered to be present. Operative treatment consisting of open reduction through a palmar and dorsal approach for ligamentous repair and anatomical realignment followed by pin stabilization should be considered emergently or relatively urgently.86 When associated fractures are present, these should be stabilized with screw fixation. Even with ideal treatment, some loss of wrist motion should be anticipated.

■ Metacarpophalangeal Dislocations Dislocations of the finger MCP joints are relatively rare because of the stout ligamentous support and the associated flexor and extensor tendons. As would be expected, the index and small fingers are much more vulnerable to this type of injury than the central two fingers. Most dislocations occur dorsally, are associated with a hyperextension injury, and may be classified as simple or complex.87 Simple MCP joint dislocations are, in reality, subluxations. They differ anatomically from complex or complete dislocations, in that the volar plate is draped over and not entrapped above the metacarpal head. In a simple dislocation the proximal phalanx is locked in 60–80° of hyperextension. A key point in treatment of these injuries is to avoid hyperextension or traction during attempts at reduction, which could result in conversion of this injury to a complex dislocation. The correct reduction maneuver for incomplete dislocations is flexion of the wrist to relax the flexor tendons and application of simple distal- and volar-directed pressure to the dorsal base of the proximal phalanx. This maneuver slides the proximal phalanx and its attached volar plate over the metacarpal head into the reduced position. In contrast, patients with complex dislocations present with the finger held in only slight extension and an inability to flex.88 Palpation of the palm will demonstrate a bony prominence corresponding to the metacarpal head. X-rays will show a widened joint space, and a sesamoid bone will often be present within the joint confirming entrapment of the volar plate. Surgical reduction of a complex dislocation can be performed through a volar or a dorsal approach. Limitations of the dorsal approach are the assumption that the volar plate is the only blocking structure; however, this approach allows access for any associated fracture fixation and is applicable in most instances. In the event that reduction cannot be obtained by

longitudinally splitting the volar plate through a dorsal approach, a volar incision should be added. Most dislocations of the thumb MCP joint are dorsal and may be simple or complex. Like finger MCP dislocations, the mechanism is hyperextension with rupture of the volar plate proximally, distally, or through the sesamoids. Most dorsal dislocations are reducible, but entrapment of the flexor pollicis longus tendon, usually over the ulnar side of the metacarpal head, may create a noose in conjunction with the radially located intrinsic muscles. X-rays demonstrating entrapment of the sesamoid within the joint usually are consistent with a complex irreducible dislocation, whereas a fracture of the sesamoids usually predicts successful closed reduction. Closed management of these injuries should avoid longitudinal traction or hyperextension, which could convert a simple dislocation to a complex, irreducible dislocation. Instead, gentle pressure should be applied to the base of the proximal phalanx to push it over the head of the metacarpal. Failed attempts at reduction should be followed by operative intervention through a dorsal approach to split the volar plate longitudinally and remove other interposed tissue, thereby allowing reduction. Once any MCP dislocation is reduced, integrity of the collateral ligaments should be tested. If there is no injury to the collateral ligaments, the finger or thumb should be immobilized in flexion no longer than 14 days, at which point an active range of motion protocol should be initiated with a dorsal blocking splint.

■ Interphalangeal Joint Dislocations Dislocation of the PIP joint may occur in dorsal, volar, or lateral directions with reference to the position of the middle phalanx. Of these possibilities, dorsal dislocation is the most common and is usually associated with hyperextension of the PIP joint, often during ball sports.89 Dorsal dislocation may be a purely soft tissue injury or a fracture–dislocation. A greater axial force increases the likelihood that the volar lip of the middle phalanx will be sheared off. Reduction of a dorsal dislocation is by longitudinal traction under a local digital block. After reduction, x-rays should be obtained to ensure a concentric reduction, and the integrity of the collateral ligaments confirmed by a passive lateral stress test in both full extension and 30° of flexion. If the joint is stable, early motion should be encouraged by simple “buddy taping.” When instability exists, the point of dislocation is determined and the finger is flexed 10° further and an extension block splint is applied. Each week the block is decreased by 10° until full extension is achieved. Volar PIP dislocations exist in two forms and are much less common than dorsal dislocations. In the first type the central slip is disrupted by a straight volar dislocation of the PIP joint. These injuries can be treated by closed reduction with longitudinal traction and splinting of the PIP joint in extension for 6 weeks with the DIP joint free to flex and extend. The second type of dislocation is a volar rotary subluxation as a result of forces applied in a semiflexed position. This results in a split between the central tendon and the lateral band with buttonholing of the condyle through this split. Closed reduction of this type of

Upper Extremity

INJURIES TO BONES ■ Fracture of the Clavicle Fractures of the clavicle are among the most common injuries in the upper extremity. While they generally heal without major functional limitation, they can be associated with serious neurovascular injuries. Patients generally present after a fall or motor vehicle crash with pain and reluctance to move the shoulder. Inspection and palpation will usually identify the location of the fracture. Most fractures can be identified on standard AP radiographs of the shoulder, but additional apical oblique views may assist in characterizing the injury.90 Fractures of the clavicle are classified by the location of the fracture in the medial, middle, or distal third of the bone. Approximately 80% of clavicular fractures occur in the middle third and most of these are amenable to closed management. Fractures of the medial third are rare, but can usually be treated symptomatically if they are not associated with other injuries. Fractures of the distal third of the clavicle may be accompanied by injury to the CC ligament complex and are at particular risk for nonunion. Sling immobilization or a figure of eight bandage is adequate nonoperative treatment for most isolated fractures of the clavicle. Two to 3 weeks are sufficient for a patient’s symptoms to diminish so that he or she can tolerate pendulum exercises. After 6 weeks, the sling can be gradually discontinued and gentle activities resumed. Heavy activities are avoided for 8 weeks or until union is achieved. Because of the clavicle’s subcutaneous location, fracture callus is often palpable and may even be visible. Malunion of the clavicle can result in a functional deficit, particularly if there is angulation or shortening due to comminution.91 Malunited fragments or hypertrophic

callus may occasionally compress neurovascular structures requiring surgical treatment, also.92 In most patients, however, the concern is only cosmetic and slight misalignment does not interfere with daily activities. Surgical treatment of fractures of the clavicle has lately become more common with the appearance of specific clavicular plates. These are generally reserved for displaced fractures of the lateral clavicle, fractures of the middle third with 2 cm of shortening, open fractures, compromise of the skin by the edge of the fracture, symptomatic nonunions, or fractures with an associated neurovascular injury. Surgical stabilization of the clavicle may also be indicated in patients with a floating shoulder or other complex injuries to the shoulder girdle as this may improve overall stability of the upper extremity. Because fractures of the distal third of the clavicle are at particular risk for nonunion, some surgeons recommend consideration of surgical stabilization if there is significant displacement. Surgical treatment of a fracture of the clavicle can be performed with plate and screw fixation or with intramedullary implants.

■ Fractures of the Scapula As fractures of the scapula result from high-energy trauma,93 patients with these fractures should be closely evaluated with a high index of suspicion for other serious and life-threatening problems. These would include injury to the chest, cervical spine, or neurovascular structures. Initial evaluation of the patient should include a careful assessment of the neurologic and vascular status of the ipsilateral upper extremity. Scapular fractures can occur in the absence of an obvious shoulder deformity and may first be recognized on a routine chest x-ray. True AP, scapular Y, and axillary lateral views of the shoulder should always be obtained, and CT scans are often required to fully evaluate the injury.94

■ Floating Shoulder The term “floating shoulder” is used to describe a fracture of the neck of glenoid with an associated fracture of the clavicle. This combination of injuries leaves the glenohumeral joint with no intact bony contact to the rest of the skeleton. Surgery is often considered in these injuries, even if the fractures individually might not otherwise meet the criteria for surgical treatment, and particularly if the shoulder is displaced inferiorly.95,96 Stabilization of only one part of the injury, typically the clavicle, is necessary to impart some stability to the shoulder girdle.

■ Fractures of the Proximal Humerus These are relatively common fractures and occur most often as the result of falls or a motor vehicle crash. The incidence increases with age, and the cause is typically a low-energy injury in the elderly patient. Peripheral nerve injuries are common, especially involving the axillary nerve. Vascular injuries are also a concern, especially in an elderly patient who has calcification in vessel walls. It is important to note that a vascular injury may be present even if a radial pulse is palpable due to the presence of multiple collateral vessels around the shoulder. Shoulder dislocations and

CHAPTER CHAPTER 39 X

dislocation can be difficult, but can be attempted by flexion of the MCP and PIP joints with gentle manipulation of the middle phalanx. Failure to promptly achieve reduction should be followed by open reduction rather than repeated attempts at closed reduction. If the central slip is intact following reduction, early motion with buddy tape support should be utilized; however, if the central slip is disrupted, then 6 weeks of PIP extension splinting is required as in any rupture of the central slip. Lateral dislocations result from rupture of the volar plate and one collateral ligament. This results in asymmetric swelling of the joint with tenderness on the side of the ruptured collateral ligament. Closed reduction is usually easily accomplished by traction and manipulation. This is followed by 2 weeks of static splinting in extension followed by buddy tape protected motion. DIP dislocations are most often dorsal or lateral. In many patients these are open injuries because of the tightness of the soft tissue envelope at this level of the finger. Closed injuries can be reduced by longitudinal traction, while open dislocations require appropriate antibiotics and irrigation of the joint followed by reduction. Occasionally, an irreducible dislocation may result from interposition of the proximal volar plate or the flexor tendon. Splinting should be in slight flexion for 1 week followed by intermittent protected motion for an additional 1–2 weeks.

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Management of Specific Injuries rotator cuff tears commonly occur in association with proximal humeral fractures, as well.

SECTION 3 X

■ Fractures of the Shaft of the Humerus Fractures of the shaft of the humerus have an incidence and mechanism of injury similar to that of proximal humeral fractures. The unstable brachium is of significant discomfort to the patient who typically presents supporting the injured arm with the uninjured extremity. Instability and crepitus at the fracture site are often readily apparent clinically, while standard AP and lateral x-rays are diagnostic. Because of the risk of an associated neurovascular injury, a carefully performed and documented assessment of the patient’s status should be completed immediately on presentation and repeated after any treatment. The radial nerve is at highest risk of injury with a fracture in the distal third of the shaft, where it is closely associated with the bone in the spiral groove (Fig. 39-7). Nonoperative treatment is effective for most uncomplicated fractures of the shaft of the humerus. As true cast immobilization of the brachium is impractical due to the inherent difficulty of immobilizing the shoulder, a coaptation splint can provide a more practical alternative. Gentle traction usually

results in adequate reduction of even significantly displaced injuries. For this reason, some have advocated the use of a hanging arm cast for a brief period, especially early in the course of treatment. This consists of a long arm cast, which hangs from a loop around the patient’s neck. The weight of the cast maintains longitudinal traction on the fracture fragments and helps to assure adequate alignment. This does improve patient comfort, but requires an upright posture to be effective. The use of a fracture functional brace, either initially or after a short period of long arm casting, has many benefits. It is usually effective in maintaining an adequate reduction and allows active motion of the elbow. Many patients prefer to sleep in a reclining chair for the first few weeks because this allows the longitudinal traction provided by gravity to be effective in controlling the fracture even when they are somewhat recumbent. Union rates of over 95% have been reported with this device.97 Surgical treatment for fractures of the shaft of the humerus is indicated for open injuries, when multiple other fractures are present or when there is failure to maintain acceptable reduction that is less than 20° of anterior angulation, less than 30° of varus/valgus angulation, or less than 3 cm of shortening. In patients with multiple injuries, fixation of the humerus simplifies their care, improves pain control, and allows early mobilization. Surgical treatment is considered in patients who are intolerant of the extreme activity modifications closed treatment requires and in obese patients in whom it is a particular challenge to maintain an acceptable reduction. This is because the fracture tends to assume a position of varus angulation when the arm rests on the abdomen. Operative fixation of the humerus classically involves plate and screw fixation, but intramedullary nailing is becoming more common and results are comparable.98 When intramedullary nailing is performed, a limited approach to the fracture site will ensure that the radial nerve is not interposed between the fracture fragments and at risk for an iatrogenic injury. Injuries to the radial nerve occur in 12% of humeral fractures.99 Most nerve injuries associated with closed fractures of the humerus are neurapraxias, and at least 70% will resolve with expectant management. During recovery, patients benefit from splinting of the wrist and digits to improve function. Failure to improve over 3–4 months is an indication for surgical exploration of the nerve. Early surgical exploration is recommended in patients with open injuries where the risk of nerve transection is increased, as well.

■ Fractures of the Distal Humerus

FIGURE 39-7 An AP x-ray of a spiral fracture of the distal third of the humerus. This fracture is called a Holstein-Lewis fracture. It is frequently associated with radial nerve palsy.

The Orthopaedic Trauma Association system for classification of supracondylar and intracondylar humeral fractures includes the following: Type A, which are extra-articular; Type B, which are partial articular injuries of either the medial or lateral column; and Type C, complete articular injuries in which both columns of the distal humerus are fractured from the shaft and from each other. The elbow is usually grossly unstable, but x-rays may be required to distinguish this from other types of elbow trauma. Isolated fractures of the medial or lateral epicondyle occur, also. Although they are typically of lesser severity, they may require surgical treatment if significantly displaced.

Upper Extremity

■ Fractures of the Capitellum Isolated fractures of the capitellum are relatively rare, are due to low-energy trauma, and are more common in women. Unless there is displacement, this injury may be easily missed on AP and lateral x-rays of the elbow. CT may be helpful if plain x-rays do not fully demonstrate the injury. There are four types of fractures as follows: Type I fractures are a complete fracture of the entire capitellum from the remainder of the articular surface, Type II injuries involve only a thin wafer of cartilage and sub-

chondral bone, Type III injuries are comminuted fractures of the capitellum, and Type IV fractures are coronal shear injuries in which the capitellum as well as a significant portion of the anterior trochlea is fractured. Unless fragments are nondisplaced, open reduction and internal fixation is recommended when possible.106 In Types II and III, the fragments are often so small that stable internal fixation is not possible. In these patients, excision of the fragments may be a reasonable alternative.

■ Fractures of the Proximal Ulna Injuries through the articular surface of the proximal ulna are frequent. Fractures with less than 1–2 mm of articular displacement may be treated nonoperatively with a 1- to 2-week period of splinting, followed by gentle early range of motion activities. Frequent x-ray follow-up is important to assure that there is no increase in displacement. Most olecranon fractures have sufficient displacement to warrant operative treatment. The most common methods are tension band wiring and plate and screw fixation. Both may be effective in transverse or oblique injuries, but comminuted injuries require plate and screw constructs to prevent compression of the trochlear notch. Sufficient stability can usually be obtained to allow early motion, and a satisfactory outcome is likely. In extensively comminuted injuries, excision of up to half of the olecranon with advancement of the triceps muscle may be considered. Fractures of the coronoid process of the ulna represent the loss of the major anterior skeletal buttress preventing posterior subluxation of the elbow. Type I fractures are avulsions of the tip of the coronoid, Type II fractures involve 50% of the coronoid process, and Type III fractures involve 50% of the coronoid. These injuries are typically seen in association with a posterior dislocation of the elbow, and the elbow should be carefully examined for stability even if it appears well reduced. If not associated with significant instability, an avulsion fracture of the tip can be treated nonoperatively, similar to a simple elbow dislocation. Consideration should be given to fixation of some Type II and all Type III injuries and is required if there is instability of the elbow.107 Posteriorly placed screw, suture, or wire fixation into or around the coronoid is often sufficient, but a more medial approach with an anterior buttress plate may be required to prevent redisplacement. If small coronoid fragments are not amenable to rigid fixation, they may be excised with repair of the anterior capsule. Comminuted fractures of the olecranon that are accompanied by displacement of the coronoid process should be managed carefully. Even with anatomical fixation and union of the olecranon, the elbow may become unstable if the coronoid remains displaced. Stabilization of the coronoid process can be technically difficult, as access to the coronoid is extremely limited after fixation of the olecranon. Through a posterior approach, the proximal, fractured portion of the olecranon is retracted with the triceps muscle and the remainder of the ulna is subluxated dorsally, allowing access to the anterior portion of the joint. The coronoid process is reduced under direct visualization and stabilized as described above. Transolecranon fracture–dislocation of the elbow occurs when the distal humerus is driven distally through the proximal ulna. Displaced coronoid fragments are common in this injury pattern.108

CHAPTER CHAPTER 39 X

Rarely is nonoperative treatment indicated for a supracondylar fracture of the humerus. Occasionally, a brief period of immobilization followed by early rehabilitation may be sufficient for a patient with very limited functional expectations due to preexisting health problems. A preferred alternative to this technique in some elderly patients, particularly those with degenerative or rheumatoid arthrosis, is total elbow arthroplasty.100 In the vast majority of these patients, open reduction and internal fixation is indicated. Surgical treatment is technically demanding, especially if there is significant fragmentation of the joint surface.101 The surgical approach to intra-articular injuries often requires an osteotomy of the olecranon. The ideal biomechanical construct continues to be debated, but most agree that plating of both the medial and lateral columns is usually indicated.102 The goal of surgical treatment is to obtain sufficient stability to allow early motion of the elbow while the fracture proceeds to union. Even when this goal is achieved, a permanent loss of some elbow motion is common. Supracondylar humeral fractures in children aged 5–7 years are common injuries. Almost all supracondylar humeral fractures in this age group are extra-articular with posterior displacement of the distal fragment. Type 1 injuries are nondisplaced or minimally displaced, Type 2 injuries are displaced with an intact posterior cortex, and Type 3 injuries are completely displaced with disruption of the posterior cortex. Children may demonstrate only edema and pain in mild injuries or obvious hyperextension deformity in more severe cases. Most nondisplaced or minimally displaced injuries may be managed with casting for approximately 4 weeks, while surgical treatment is indicated in displaced injuries. Because late stiffness is much less common in children, management typically consists of closed reduction and pinning followed by a period of immobilization. If satisfactory closed reduction cannot be obtained, it may be due to interposed tissues such as the brachialis muscle or neurovascular structures. Open exploration and reduction are indicated in these patients and an effort should be made to operate during the first 12 hours.103,104 Associated injuries to the median nerve or its anterior interosseous branch often recover with expectant management. Injuries to the brachial artery are reported with some frequency, also. Because there is generally adequate collateral circulation, vascular reconstruction may not be required emergently if the extremity remains well perfused. The flexion of the elbow often required to maintain reduction of the fracture may further compromise blood flow, and patients should be carefully monitored for any signs of worsening vascular status or a compartment syndrome.105

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Management of Specific Injuries

■ Fractures of the Head of the Radius SECTION 3 X

Fractures of the head of the radius are common injuries and may occur in association with a dislocation of the elbow. The fractures are classified as follows: Type I fractures are nondisplaced, Type II fractures have single displaced fragments, Type III fractures have comminuted injuries, and Type IV are fractures of the head of the radius associated with a dislocation of the elbow. Patients may report relatively mild trauma, and physical findings may be subtle. Injuries to neurovascular structures are uncommon with this fracture. Standard x-rays are usually sufficient to make the diagnosis and, once a fracture is identified, the elbow should be carefully evaluated for stability and range of motion. It is important to examine the wrist and forearm to identify any associated injuries to the distal radioulnar joint or interosseous membrane. If pain prevents motion, the intraarticular hematoma should be evacuated and lidocaine injected into the joint. A mechanical block to motion in the anesthetized joint is an indication for surgical treatment. Type I and II injuries with 2 mm of displacement may be managed nonoperatively with early motion and follow-up to ensure that there is no interval displacement. Displaced Type II injuries of the head and neck are typically treated with open reduction and internal fixation. It is important that implants do not interfere with the proximal radioulnar joint. The safe zone for implants in the head of the radius is the area between lines extended proximally from the radial styloid and Lister’s tubercle, both of which are palpable at the wrist.109 Headless screws may also be of value when fixation is necessary outside this safe zone. Type III injuries are usually not amenable to open reduction and internal fixation, and excision of the head of the radius may be considered in some patients. This should not be performed if there is an associated dislocation of the elbow, coronoid fracture, valgus instability of the elbow, or longitudinal instability of the forearm, which would indicate an injury to the interosseous ligament. A fracture of the head of the radius with an associated injury to the interosseous membrane is termed an Essex-Lopresti fracture–dislocation.110 Clues to its presence include wrist pain, displacement at the distal radioulnar joint, and/or proximal migration of the radius evident on x-ray. If signs of instability in any plane are present, every attempt should be made to preserve the head of the radius or perform an arthroplasty with a metallic implant.

■ The Floating Elbow The floating elbow occurs when there are ipsilateral fractures of the humerus and bones in the forearm. This injury is the result of high-energy trauma and is often associated with injuries to neurovascular structures. The elbow segment is unsupported proximally and distally, and both injuries need to be stabilized. The prognosis for return of full function in these injuries is guarded, especially if the fractures are periarticular.111

■ Fractures of the Shaft of the Ulna Isolated fractures of the shaft of the ulna, commonly referred to as “nightstick fractures,” are usually amenable to a short period

of long arm casting. This is followed by functional bracing when there is less than 10–15° angulation and at least 50% contact area between fragments. Displaced fractures are usually treated with compression plating or, in the distal third, fixedangle locking plates. Intramedullary nailing in adults has limited application, but may be indicated with some segmental fractures, those associated with severe loss of soft tissue, or in patients with polytrauma. External fixation is really only indicated as a bridge to more definitive fixation. Special circumstances in the management of ulnar fractures involve those associated with distal radial fractures, isolated fractures of the head of the ulna, and Monteggia fractures. Fracture of the distal ulna associated with distal radial fracture may or may not require fixation; however, when the integrity of the distal radioulnar joint (DRUJ) is compromised, consideration should be given to fixation.112 Restoration can be by fixation of an ulnar styloid base or plating of the head of the ulna, usually with a small condylar blade plate or a small locking plate. Addressing the ulnar component of these fractures in this manner can often greatly facilitate initiation of early motion.

■ Fractures of the Shaft of the Radius Galeazzi fracture–dislocation is a complex traumatic disruption of the DRUJ that is associated with an unstable fracture of the radius.113 In these fractures, the injury to the DRUJ can be a pure ligamentous disruption or associated with a fracture of the ulnar styloid. Most commonly, the site of fracture is the junction of the middle and distal thirds of the radius. This injury can be associated with a low-energy fall from a standing height or associated with a high-energy mechanism, such as a fall from a height or a motor vehicle crash. This fracture has also been referred to as a “reverse Monteggia fracture” or “the fracture of necessity” since, in adults, operative intervention is almost always required for a good outcome. X-ray evaluation of these fractures demonstrates a short appearing radius relative to the ulna because of the pull of the pronator quadratus muscle (Fig. 39-8). On the PA view there will often appear to be an increase in space between the distal radius and ulna where they articulate. Definitive treatment is by operative fixation of the fracture of the shaft of the radius, usually through a volar approach. This is followed by an intraoperative examination of the DRUJ for instability, predominantly in supination. The intraoperative examination is the definitive test that determines a need to address the DRUJ, not the x-rays.114 Treatment of the unstable DRUJ is by fixation of the radius to the ulna in supination using a Kirschner wire, with or without direct repair of the ligamentous component or fracture of the styloid. This is followed by 6 weeks of above-elbow casting.

■ Fractures of the Distal Radius Fractures of the distal radius are the most common long-bone fracture of the upper extremity.115 Two primary age groups are involved with varying mechanisms. High-energy comminuted intra-articular fractures occur primarily in young patients, while low-energy extra-articular fractures occur predominantly in elderly patients.

Upper Extremity

■ Fractures of the Radius and Ulna Simultaneous fractures of the radius and ulna are relatively common injuries. Associated neurovascular injuries do occur, and a compartment syndrome may develop. AP and lateral x-rays that include both the elbow and wrist should be obtained. Fractures are classified based on their location as proximal, middle, or distal third, with or without comminution. While closed management is usually acceptable in children, open reduction with fixation using a compression plate has become the accepted standard of care for these fractures in adults.120

■ Fractures of the Scaphoid

FIGURE 39-8 Galeazzi fracture–dislocation. A true lateral radiograph of the forearm showing a fracture of the distal third of the radius. The ulnar head is dorsal to the radius indicating a dislocation of the radial head. Anatomical reduction of the radius and internal fixation should reduce the distal radioulnar joint.

During physical examination a careful assessment of median nerve function should be performed to rule out an acute carpal tunnel syndrome that is an indication for urgent surgical release. The goals of surgical repair are for anatomical restoration of radial length, radial inclination, and volar tilt and, ultimately, restoration of function of the hand. The three anatomical goals are based on the normal anatomy of the distal radius. This includes 21° of inclination, 12° of volar tilt, and length defined by baseline relationship to the ulna, which can be determined in most instances from the uninjured wrist. The ability to restore and maintain these relationships, as well as to restore articular congruity, is the prime determinant of the need for operative intervention.116 Because of the dorsal comminution that usually exists with the apex volar malformation that usually accompanies these fractures, maintenance of what appears to be a good reduction in the ED requires continued vigilance and early operative intervention if loss of reduction occurs. While no consensus exists for treatment of fractures of the distal radius, the recent addition of fixed-angle locking plates and fragment-specific fixation have led to more aggressive early

Fractures of the scaphoid account for over half of all isolated fracture of the carpal bones. The true incidence of injury to this bone, however, may be higher. This is because many fractures are not appreciated until later when they convert to a symptomatic nonunion, and many remain asymptomatic throughout life.121 Fractures of the scaphoid usually result from a fall onto an outstretched hand with the wrist extended and the forearm pronated. Fractures most commonly occur at the waist (75%), followed by the proximal pole (20%), and, least often, at the distal pole or tuberosity (5%). Location of the fracture is an important factor in prognosis for healing because of the blood supply of the scaphoid. As an intra-articular bone, the scaphoid receives its blood supply through ligamentous attachments, with the primary entry at the distal pole. This leaves the proximal pole with a consistently poor blood supply, which makes these fractures susceptible to nonunion or avascular necrosis. Other factors playing a role in the development of nonunion and malunion are stability of the fracture pattern and displacement. The diagnosis of a fracture of the scaphoid is first suggested by the mechanism of injury associated with the onset of wrist pain and/or swelling. Examination may show tenderness on palpation within the anatomical snuff box and over the scaphoid tubercle. Pain may also be elicited by pronation and ulnar deviation or by applying an axial load to the first metacarpal (scaphoid compression test); however, no maneuver is specific for injury to the scaphoid and appropriate x-rays are critical.122 Routine x-rays should include a posteroanterior, lateral, and oblique view in 45° of pronation and a posteroanterior view in slight ulnar deviation (“scaphoid view”). Even with a thorough examination and appropriate x-rays, a nondisplaced fracture may be missed. An appropriate course of action in the presence of negative x-rays, but positive clinical signs, would be an immediate MRI or application of a thumb spica cast with more definitive tests scheduled in 72 hours.123 The concept of an immediate MRI is based on its sensitivity to detection of early fracture-associated edema of the marrow.

CHAPTER CHAPTER 39 X

treatment of both intra- and extra-articular fractures.117,118 While there is still a role for closed reduction, percutaneous pinning, and/or external fixation, stable plate fixation is being applied on an increased basis to even very comminuted fractures with encouraging early results.119

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SECTION 3 X A

B

FIGURE 39-9 Right scaphoid fracture (A) repaired by volar approach and cannulated screw placement (B).

In addition, numerous studies have now demonstrated a cost benefit to this approach versus the classic approach of repeat x-rays, followed by more definitive studies if these remain negative.124,125 In centers that cannot perform the test expeditiously, a bone scan or a scheduled MRI in 72 hours is better than repeat x-rays over the course of several weeks. Surgical treatment is indicated for all displaced fractures of the scaphoid. An aggressive approach is supported by data reporting a 50–92% nonunion rate with displaced scaphoid fractures and development of degenerative joint disease with as little as 1 mm of displacement. An open approach through a dorsal or volar incision, followed by placement of a screw, is the most common means of treating these fractures. Percutaneous placement of a screw, with or without arthroscopically guided reduction, is becoming increasing popular as a minimally invasive option (Fig. 39-9).126–128

■ Other Fractures of Carpal Bones Of the remaining seven bones in the carpus, the triquetrum is the next most frequently injured bone.129 Dorsal avulsion fractures are the most common form, and, while painful, surgical intervention is rarely indicated except to excise a persistently painful fragment. Body fractures and volar avulsion fractures may occur and may be difficult to detect by plain x-rays, also. Both CT and MRI have been used to diagnose or more clearly delineate these fractures and, occasionally, fractures of the body will require fixation. In most instances, 6 weeks of immobilization in a short arm cast will resolve the pain associated with these fractures even though radiographic union may not occur. The pisiform is rarely fractured and, when this occurs, it is usually the result of a direct blow to the hypothenar eminence. Palpation of the pisiform elicits pain, and carpal tunnel and/or

supinated oblique x-rays are required to adequately image this bone. CT may be indicated in the presence of persistent pain and negative plain films. A thorough evaluation of the integrity of the ulnar nerve is required when dealing with injuries to the pisiform because of its close proximity.130 This is particularly important if surgical intervention is being considered. Initial treatment with immobilization is recommended. Of interest, a persistently painful fractured pisiform can be excised as definitive treatment, with no significant sequelae. Fractures of the trapezium are usually associated with a fracture of the first metacarpal or distal radius. These fractures may involve the body, margin of the metacarpal articular surface, or volar ridge. Volar ridge fractures may be associated with injury to the median nerve, and a thorough examination of both motor and sensory components of this nerve should be documented. X-ray diagnosis of any of these injuries requires a variety of special views including a hyperpronated “Roberts” view, a Bett’s view, and a carpal tunnel view, and CT may be required to further delineate a fracture of the ridge. Except for displaced body fractures, the initial treatment of trapezial fractures should consist of a 6-week period of immobilization. If, at the end of this time, persistent palmar pain is associated with a fracture of the volar ridge, then the fracture fragment should be excised. Displaced fractures of the body can usually be stabilized by lag screw fixation.131 Fractures of the trapezoid are exceedingly rare.132 Injury to this protected bone is often associated with a high-energy fracture–dislocation involving the index metacarpal bone. X-ray diagnosis of this injury is usually straightforward; however, an isolated injury or injury associated with a spontaneous reduction may require a CT scan to confirm diagnosis. Treatment of nondisplaced isolated fractures is by 6 weeks of immobilization. Displaced fractures or those associated with

Upper Extremity

■ Fractures of the Metacarpal Bones and Phalanges These are the most common fractures of the upper extremity. Metacarpal fractures may involve the base, shaft, neck, or head, and may be articular or nonarticular.142 In addition, when the fracture is at the base, it may be associated with a dislocation. The second and third CMC joints are relatively immobile and are injured less frequently than the more mobile fourth and fifth CMC joints. Thus, the most common metacarpal base fracture involves the small finger metacarpal and is almost always associated with a dislocation. This injury is inherently unstable because of the pull of the extensor carpi ulnaris, and closed reduction and cast immobilization as definitive treatment is usually doomed to failure. Therefore, initial splinting should be followed by scheduled outpatient closed reduction and pinning. When this is performed, care must be taken during the approach to avoid injuring the dorsal sensory branch of the ulnar nerve or entrapping it in the fixation. More complex injuries can result in the fourth metacarpal bone being dislocated with the fifth metacarpal bone or disruption of the entire finger ray. Both these injuries represent highenergy disruptions of the ligamentous support of these joints, and open reduction and internal fixation are usually necessary. In addition, concomitant injury to the ulnar nerve in these severe disruptions can lead to significant long-term morbidity. Many fractures of the metacarpal shaft present as stable, nondisplaced fractures. These can be managed by placement into a clam-digger cast or thermoplast splint until the fracture is clinically nontender. At this point, despite x-ray evidence of a fracture line, the hand can be mobilized. In particular, isolated fractures of the third and fourth metacarpal bones are amenable to this type of management because of continued support by the stout transverse metacarpal ligament. Fractures of the metacarpal bones proximal to the index and small fingers will more often develop some degree of malformation often expressed by crossing over of the fingers with flexion “scissoring.” Therefore, these fractures should be treated by operative intervention. Modalities available include open reduction and internal fixation, closed reduction and percutaneous pinning with Kirschner wires, or closed reduction and intramedullary nailing.143 Multiple metacarpal fractures lead to an inherently unstable hand, and operative intervention is always indicated. These injuries will require not only fracture fixation but repair of associated injuries to tendons and soft tissue also. Principles of treatment of this type of injury are covered in Section “Compound, Complex, and Mangled Upper Extremities.” A fracture of the neck is the most common fracture of a metacarpal and usually occurs in the fourth or fifth bone. Acceptable closed reduction of these fractures depends on the digit involved, with fracture angulation of 50–70° tolerable in the fifth finger and only 10–20° in the index finger.144,145 Fractures of the neck of the fifth metacarpal bone are referred to as “Boxer’s fractures” and are almost always associated with a clenched fist striking a solid object. The result is an apex dorsal angulated fracture with volar comminution. This comminution is the reason that most acute reductions fail, with rapid relapse in a splint or cast to the postinjury state. Because of this, it has

CHAPTER CHAPTER 39 X

carpometacarpal (CMC) dislocations require internal fixation or, occasionally, formal CMC arthrodesis with bone grafting to achieve stability and pain relief. Capitate fractures may be isolated, associated with a scaphoid fracture (“scaphocapitate syndrome”), or associated with another carpal injury. Isolated fractures are often nondisplaced and occur at the waist; however, similar to proximal pole fractures of the scaphoid, the proximal pole of the capitate is dependent on a distal blood supply and prone to avascular necrosis.133 Without treatment, symptomatic nonunion is a common occurrence and can lead to the need for midcarpal fusion if ignored. Both open reduction and percutaneous methods of primary fixation have been described. Scaphocapitate syndrome is caused by a direct blow to the dorsum of the hand while flexed or a fall onto an extended wrist and results in malrotation of the proximal capitate fragment.134 Following closed reduction of the associated dislocation of the wrist, careful evaluation of the capitate is necessary to detect persistent malrotation. Open reduction with fixation of both the capitate and scaphoid bones is required to restore the normal relationships within the wrist and, hopefully, prevent avascular necrosis of the capitate. Fractures of the hamate may involve the body, articular surfaces, and/or the hook/hamulus.135 Clinically, pain and tenderness on the ulnar aspect of the hand is present and is often associated with swelling. Injury to both the ulnar and median nerves may be associated with hook fractures, and a thorough examination of motor and sensory function should be documented. Standard x-rays may be inadequate to image the injury. A carpal tunnel view and an oblique view with the hand in 45° of supination and the wrist in radial deviation should be performed. CT may be required if symptoms persist in the presence of negative plain x-rays.136,137 Isolated fractures of the body are rarely displaced and are usually amenable to a period of immobilization. Those associated with high-energy injuries, such as CMC fracture– dislocations, require internal fixation.138 Fractures of the hamulus of the hamate (“hook fractures”) may be difficult to diagnose without CT, and this should be performed early when this fracture is clinically suspected. A delay in treatment of this fracture can result in rupture of the adjacent flexor tendon from attritional wear over the fracture site.139 Untreated, this fracture can cause chronic pain with many of the activities of daily living. Treatment is by excision of the hook, or open reduction and screw fixation. Neither method has been shown to have an advantage over the other.140 Fractures of the lunate are rare when one excludes those associated with idiopathic avascular necrosis or Kienbock’s disease. Accurate imaging to rule out predisposing avascular necrosis usually requires a CT and/or MRI in addition to plain x-rays. Acute fractures may involve the volar or dorsal lips or occur as transverse or sagittal fractures.141 Sagittal fractures and fractures of the dorsal lip are usually stable because of ligamentous support and require only a 6- to 8-week period of immobilization. Fractures of the volar lip and transverse fractures have a tendency to displace and require open reduction and internal fixation.

775

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Management of Specific Injuries

SECTION 3 X A

B

FIGURE 39-10 Bennett’s fracture (A) with a single fragment retained by the palmar oblique ligament and the metacarpal displaced proximally and radially by the pull of the abductor pollicis longus. Rolando fracture (B) demonstrating comminution of the first metacarpal base.

been recommended that the patient should initially be splinted in the intrinsic plus position. A reduction is then performed at 7–10 days when the fracture has begun to consolidate. Whether the hand is then splinted in extension to presumably enhance a “ligamentotaxis” effect and counteract the tendency to relapse into an apex dorsal deformity or splinted or casted in the classic “cobra” cast position makes little or no difference to long-term outcome. Four weeks should be the maximum period of immobilization after treatment of such a fracture. Fractures of the head of the metacarpal bone are usually intra-articular and are often associated with a clenched fist or “fight bite” injury. Closed fractures with significant intraarticular displacement should undergo open reduction and screw fixation. When significant comminution is present, fixation is probably not possible. Either acute replacement of the joint should be performed or the fracture should be allowed to heal. If significant morbidity develops, then replacement of the joint should occur at a later time. A fracture of the shaft of the first metacarpal bone requires less accurate reduction because of the mobility of the CMC joint; however, articular fractures of the base in the form of Bennett’s and Rolando fractures (Fig. 39-9) do not have this latitude. Bennett’s fracture is essentially a fracture–dislocation of the CMC joint. Axial loading results in the strong palmar oblique ligament retaining a fragment of bone while the metacarpal bone is dislocated radially and proximally by the pull of the abductor pollicis longus muscle. Post-traumatic arthritis frequently follows a Bennett’s-type fracture, and operative intervention is recommended. Either closed reduction and percutaneous pinning or open reduction and internal fixation is acceptable and both of them yield similar outcomes.146

The Rolando fracture is T- or Y-shaped fracture of the base of the first metacarpal bone and includes both the volar lip fracture seen in Bennett’s fracture and a large dorsal fragment (Fig. 39-10). These fractures are extremely difficult to manage and frequently lead to post-traumatic arthritis regardless of which technique is used for management. Surgical options include multiple K-wires, tension band wires, plates and screws, and external fixation. Phalangeal fractures are common in all age groups.115 The examination needs to differentiate between a fracture, rupture of the collateral ligament, rupture of the volar plate, and avulsion of a tendon, all of which may have similar signs on cursory inspection. At a minimum, PA, oblique, and lateral x-rays should be obtained. Nondisplaced, stable proximal and middle phalangeal fractures can be effectively managed by either buddy taping or immobilization in a splint. Many proximal and middle phalangeal fractures, however, have articular involvement or have significant malformation because of the effect of the flexor tendons and/or extensor apparatus. Closed reduction to align displaced fractures can be performed by a combination of axial traction and reversal of the deformity. Even what initially appears to be a nondisplaced articular fracture has the potential to displace. Therefore, if nonoperative management is selected as the primary treatment, then close follow-up and frequent x-rays are necessary to avoid missing displacement. Operative treatment of articular fractures entails closed reduction with placement of a percutaneous screw or Kirschner wire. More ridged fixation allows early initiation of range of motion. Pilon-type injuries require some type of traction fixation to allow motion with maintenance of articular

Upper Extremity

COMPOUND, COMPLEX, AND MANGLED UPPER EXTREMITIES As opposed to other extremity injuries, a mangled extremity typically involves a combination of severe injury to artery, bone, soft tissue, skin, and tendons. Such injuries require immediate multidisciplinary surgical treatment (Fig. 39-11). In general, prioritization is typically given to lifesaving efforts as well stated in the phrase “life before limb reconstruction.” Damage control surgery is used in order to save the patient’s life as well as to allow for limb salvage when possible. Therefore, temporary vascular shunting,149 temporary external fixation of the bones, and soft tissue flaps are the cornerstones of initial treatment. Damage control procedures (external fixation, fasciotomies) minimize time spent in the operating room. Furthermore, “damage control resuscitation” (see Chapters 12 and 13) has also been shown to provide a means to aid limb salvage. Fox et al.150 showed that the use of fresh warm blood, plasma, and recombinant factor VIIa before operation normalized physiologic parameters and allowed for more prolonged procedures, such as revascularization, without an increase in morbidity or graft failure. This is true for patients with a Mangled Extremity Scoring System (MESS) of 6–8 as their degree of shock is not as profound. Patients with a higher MESS should be considered for primary amputation. New technologies to aid in reconstruction include the use of negative pressure wound therapy, broader-spectrum antibiotics, bone morphogenetic proteins, dermal substitutes, bone grafting substitutes, nerve grafting substitutes, easier options for distraction osteogenesis, and shock wave therapy. While enabling better reconstructive options, none of those new technologies have changed the difficult initial decision making when treating these patients. An attempt at limb salvage, which

may involve multiple operations, is not without consequences, and there can be a risk of death.151 A valid and reliable scoring system that would help predict which extremity can be successfully reconstructed and which should be amputated would be useful. Orthopedic surgeons along with vascular, plastic, and general trauma surgeons have used several scoring systems to help guide the decision to amputate after severe lower limb trauma. The most commonly used scoring systems have been developed and designed to change a subjective clinical impression to an objective assessment.152–156 Unfortunately, the validation of these scoring systems is debatable at best. Due to the highenergy mechanism and the diversity of associated systemic injuries, most authors conclude that there are many exceptions to the rules of commonly used scoring systems. Efforts at validating these scores in subsequent studies in the civilian setting have shown low sensitivity.157,158 Furthermore, most scoring systems were developed for mangled lower extremities and their application to the upper extremity is limited. All would agree that the hypotensive patient with prolonged limb ischemia requiring reconstruction is an absolute indication for amputation, especially in an environment with limited recourses.156–158 Upper extremities differ from lower extremities when related to the approach to mangled extremity treatment for a number of reasons. Recent advances in the function and fitting of lower limb prostheses enable a relatively rapid return to good function. This is not true for the upper extremity whose function is more complex and critical and where such an injury is less likely to affect the survival of the patient. Therefore, most authors agree that reconstructive efforts are the rule when dealing with a complex injury in an upper extremity.

REPLANTATIONS OF THE UPPER EXTREMITY Replantation is the reattachment of a part that has been completely amputated. Revascularization requires reconstruction of vessels in a limb in which some soft tissue (skin, tendon, nerve) is intact.159 Minor replantation is reattachment at the wrist, hand, or digit level, whereas major replantation is that performed proximal to the wrist.159 In major replantations, ischemic time is crucial to muscle viability and functional outcome. The resulting myonecrosis and myoglobinemia and infection from ischemic muscle in major replantations may threaten the patient’s life as well as limb. Traumatic amputations may be classified into three types as follows: 1. Guillotine sharp amputation with minimal soft tissue damage. 2. Crush amputations where there is adjacent local crushing injury. 3. Avulsion amputations in which tendon, nerve, vessels, and soft tissue structures are all injured at different levels. This occurs with the so-called ring avulsion injury. Such amputations are the most unfavorable for replantation.

CHAPTER CHAPTER 39 X

congruity.147,148 Even with this type of approach, secondary arthroplasty procedures may be required. Transverse, spiral, oblique, and comminuted fractures of a phalangeal shaft may occur. The apex of a proximal phalangeal fracture angulates in a volar direction due to the strong pull of the interosseous muscles. Deformation of middle phalangeal fractures depends on the location of the fracture in the shaft with relation to the insertion of the superficialis tendon. An apex volar deformation results when the fracture is distal to the insertion of the superficialis tendon, while an apex dorsal deformation results from fractures proximal to the superficialis insertion. A variety of methods have been employed to overcome these distracting forces. These include static casting in the intrinsic plus position for a proximal phalangeal fracture, with early mobilization at 4 weeks with buddy tape support to the adjacent finger. Traction has also been utilized, with force exerted through the skin, pulp, nail plate, or skeleton. Difficulties with this technique include the awkwardness of the device, joint stiffness, and skin problems. Operative techniques include external fixation, percutaneous pinning, and open reduction and internal fixation with plates, screw, or interosseous wires. Of these techniques, percutaneous pin fixation seems to have the least long-term morbidity (Table 39-9).

777

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TABLE 39-9 Fractures and Dislocations of the Upper Extremity—Surgical Indications

SECTION 3 X

Injury Sternoclavicular dislocation Clavicle fractures

Acromioclavicular dislocation Scapula fractures

Glenoid fractures

Scapulothoracic dissociation Glenohumeral dislocations

Proximal humerus fractures/ fracture–dislocations Humeral shaft fractures

Distal humerus fractures Capitellum fractures Elbow dislocation Fractures of the proximal ulna Fractures of the coronoid process Radial head fractures Floating elbow Monteggia fracture–dislocations Isolated ulnar shaft fractures Radial shaft fractures

Distal radius fractures

Scaphoid fractures Triquetrum fractures Trapezium fractures Capitate fractures Hamate fractures Lunate fractures Perilunate dislocations/fracture– dislocations

Surgical Indications Acute posterior dislocation (thoracic surgeon on standby) Chronic symptomatic dislocation Middle third—neurovascular injury, skin compromise, open fractures, 2 cm shortening, ipsilateral displaced glenoid neck fracture Distal third—displaced fractures Grade IV, V, and VI (some grade III) Acromion large displaced fracture Coracoid large displaced fracture Scapula neck displaced fracture 2 mm displacement Involvement of 25% of surface Length of fracture glenoid radius Humeral head subluxation Always Failed closed reduction Vascular injury Recurrent dislocation Two-part displaced great tuberosity 5 mm Three-part fractures Four-part fractures 20° anterior angulation 30° varus/valgus angulation 3 cm shortening Open fractures Floating elbow Polytrauma patient Segmental fractures Bilateral humeral shaft fractures Adults—almost always Children—displaced fractures (Types 2 and 3) Displacement 2 mm Simple—failed closed reduction (interposed soft tissue or unstable postreduction) Complex (fracture–dislocations)—always Displacement 2 mm Unstable Type I–III Articular displaced 2 mm Comminuted fractures Always Always 10% angulation or 50% displacement Displaced fractures Galeazzi fracture–dislocation Radius and ulna shaft fractures Displaced intra- and extra-articular fractures (1–2 mm articular displacement, 15° dorsal tilt, 5 mm shortening) Volar and dorsal rim fractures (Barton) Displaced, unstable, proximal pole, nonunion Displaced body fractures Intra-articular displaced body fractures Displaced fractures Displaced or unstable fractures Displaced fractures Always (continued )

Upper Extremity

779

TABLE 39-9 Fractures and Dislocations of the Upper Extremity—Surgical Indications (Continued )

Metacarpophalangeal dislocation Phalangeal fractures

Interphalangeal joint dislocation

Surgical Indications Always Shaft—multiple metacarpal Isolated—shortening 3 mm, angulation 30°, scissoring of fingers Neck fractures—second/third finger 20° of angulation Fifth finger (Boxer’s fractures) 50° angulation, extension gap Head fractures—displaced, comminuted, or open (fight bite) Thumb base—unstable fractures (Bennett’s, Rolando) Dorsal complex dislocation Volar dislocations Proximal base fractures Collateral ligament avulsion—displaced Compression intra-articular base fractures Vertical shear fractures Diaphyseal unstable fractures Condylar displaced fractures Distal base with 50% of the articular surface involved or volar subluxation Failed close reduction, collateral ligament tear

While viability of the replantation is important, the most important measure of success is the useful function that can be achieved. Thus, replantation has both absolute and relative contraindications. Contraindications include a significant concomitant life-threatening injury, a severe chronic illness, or extensive injuries to the affected limb or amputated part. The following are important considerations:160 1. A warm ischemia time of 12 hours for an amputated digit is a relative contraindication. Prompt cooling of the amputated part to 4–10°C alters the ischemic factor. Ischemia time is even more crucial for replants above the proximal forearm, and these should not be considered after more than 6–10 hours of warm ischemia time. 2. Good candidates for replantation are patients with amputations of the thumb or multiple digits or through the palm, wrist, and individual fingers distal to the insertion of the tendon of the FDS. Single digit injuries in Zone II, other than the thumb, are generally not reattached because of unfavorable functional outcomes. Such a replantation may be considered in a young child, or, perhaps, driven by potential occupational demands. 3. Important considerations are not only sex, occupation, and age but the mental health of the patient also. Unfortunately, the mental stability of the patient is frequently difficult to assess in the limited time available for preoperative evaluation in the emergency room. FIGURE 39-11 Mangled upper extremity with complex loss of skin, soft tissues, and bone injuries is being evaluated in the emergency department shock room.

Amputation should not be considered an outmoded operation and is necessary when replantation is not indicated.160

CHAPTER CHAPTER 39 X

Injury Carpometacarpal dislocations Metacarpal fractures

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SECTION 3 X

Should replantation be a consideration, the amputated part is placed in a clean and dry plastic bag that is sealed and placed on top of ice in a Styrofoam container. This keeps the part sufficiently cool without freezing.159 In the operating room, one team can initiate exploration of the amputated parts for suitability of nerves and vessels even before the arrival of the patient. Shortening of the bones allows for skin to be debrided back to where it is free of contusion and where a direct tension-free closure can be achieved. This technique may reduce the need for vein and nerve grafting, also. A thumb bone, however, should not be shortened to less than 10 mm. The order of formal repairs is usually bone, tendons, arteries, nerves, and, finally, veins.159 For major replantations, reestablishing arterial circulation as rapidly as possible is crucial to limit ischemia time.159 An intraluminal vascular shunt may be placed between the arterial ends. Intermittent clamping of the shunt may, however, be necessary to restrict blood loss during the replantation. In the more proximal upper extremity, bone shortening can be aggressive to allow for primary neurovascular repairs and primary closure of the skin. Postoperative dressings consist of strips of nonadherent gauze mesh, loose fluff gauze, and a plaster splint, and elevation minimizes edema and venous congestion. The patient’s room must be kept warm, and smoking is absolutely forbidden. In addition to antibiotics and analgesics, one aspirin tablet a day is advised because of its effect on platelet aggregation. Close postoperative monitoring for color, pulp turgor, and digital temperature is mandatory.

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104. Loizou CL, Simillis C, Hutchinson JR. A systematic review of early versus delayed treatment for type III supracondylar humeral fractures in children. Injury. 2009;40:245. 105. Blakey CM, Biant LC, Birch R. Ischaemia and the pink, pulseless hand complicating supracondylar fractures of the humerus in childhood: longterm follow-up. J Bone Joint Surg Br. 2009;91:1487. 106. Sano S, Rokkaku T, Saito S, et al. Herbert screw fixation of capitellar fractures. J Shoulder Elbow Surg. 2005;14:307. 107. Regan W, Morrey B. Fractures of the coronoid process of the ulna. J Bone Joint Surg Am. 1989;71:1348. 108. Ring D, Jupiter JB, Sanders RW, et al. Transolecranon fracture– dislocation of the elbow. J Orthop Trauma. 1997;11:545. 109. Caputo AE, Mazzocca AD, Santoro VM. The nonarticulating portion of the radial head: anatomic and clinical correlations for internal fixation. J Hand Surg [Am]. 1998;23:1082. 110. van Riet RP, Morrey BF, O’Driscoll SW, et al. Associated injuries complicating radial head fractures: a demographic study. Clin Orthop. 2005;441:351. 111. Solomon HB, Zadnik M, Eglseder WA. A review of outcomes in 18 patients with floating elbow. J Orthop Trauma. 2003;17:563. 112. May MM, Lawton JN, Blazar PE. Ulnar styloid fractures associated with distal radius fractures: incidence and implications for distal radioulnar joint instability. J Hand Surg [Am]. 2002;27:965. 113. Eberl R, Singer G, Hoellwarth ME, et al. Galeazzi lesions in children and adolescents: treatment and outcome. Clin Orthop Relat Res. 2008; 466:1705. 114. Ring D, Rhim R, Carpenter C, et al. Isolated radial shaft fractures are more common than Galeazzi fractures. J Hand Surg [Am]. 2006;31:17. 115. Chung KC, Spilson SV. The frequency and epidemiology of hand and forearm fractures in the United States. J Hand Surg [Am]. 2001; 26:908. 116. Ilyas AM, Jupiter JB. Distal radius fractures—classification of treatment and indications for surgery. Hand Clin. 2010;26:37. 117. Orbay JL, Fernandez DL. Volar fixation for dorsally displaced fractures of the distal radius: a preliminary report. J Hand Surg [Am]. 2002; 27:205. 118. Orbay JL, Fernandez DL. Volar fixed-angle plate fixation for unstable distal radius fractures in the elderly patient. J Hand Surg [Am]. 2004;29:96. 119. Margaliot Z, Haase SC, Kotsis SV, et al. A meta-analysis of outcomes of external fixation versus plate osteosynthesis for unstable distal radius fractures. J Hand Surg [Am]. 2005;30:1185. 120. Goldfarb CA, Ricci WM, Tull F, et al. Functional outcome after fracture of both bones of the forearm. J Bone Joint Surg Br. 2005;87:374. 121. Kozin SH. Incidence, mechanism, and natural history of scaphoid fractures. Hand Clin. 2001;17:515. 122. Esberger DA. What value the scaphoid compression test? J Hand Surg Br. 1994;19:748. 123. Low G, Raby N. Can follow-up radiography for acute scaphoid fracture still be considered a valid investigation? Clin Radiol. 2005;60:1106. 124. Brooks S, Cicuttini FM, Lim S, et al. Cost effectiveness of adding magnetic resonance imaging to the usual management of suspected scaphoid fractures. Br J Sports Med. 2005;39:75. 125. Yin ZG, Zhang JB, Wang XG, et al. Diagnosing suspected scaphoid fractures: a systematic review and meta-analysis. Clin Orthop Relat Res. 2010;468:723. 126. Slade JF III, Jaswhich D. Percutaneous fixation of scaphoid fractures. Hand Clin. 2001;17:553. 127. Slade JF III, Geissler WB, Gutow AP, et al. Percutaneous internal fixation of selected scaphoid nonunions with an arthroscopically assisted dorsal approach. J Bone Joint Surg Am. 2003;85-A:20. 128. Shih JT, Lee HM, Hou YT, et al. Results of arthroscopic reduction and percutaneous fixation for acute displaced scaphoid fractures. Arthroscopy. 2005;21:620. 129. Hocker K, Menschik A. Chip fractures of the triquetrium. Mechanism, classifications and results. J Hand Surg [Br]. 1994;19:584. 130. Matsunaga D, Uchiyama S, Nakagawa H, et al. Lower ulnar nerve palsy related to fracture of the pisiform bone in patients with multiple injuries. J Trauma. 2002;53:364. 131. McGuigan FX, Culp RW. Surgical treatment of intraarticular fractures of the trapezium. J Hand Surgery [Am]. 2002;27:697. 132. Miyawaki T, Kobayashi M, Matsuura S, et al. Trapezoid bone fracture. Ann Plast Surg. 2000;44:444. 133. Vander Grend R, Dell PC, Glowczewskie F, et al. Intraosseus blood supply of the capitate and its correlation with aseptic necrosis. J Hand Surg [Am]. 1984;9:677.

134. Aspergis E, Darmanis S, Kastanis G, et al. Does the term scaphocapitate syndrome need to be revised? A report of 6 cases. J Hand Surg [Br]. 2001;26:441. 135. Kapickis M, Looi KP, Khin-Sze Chong A. Combined fractures of the body and hook of hamate: a form of ulnar axial injury of the wrist. Scand J Plast Reconstr Surg Hand Surg. 2005;39:116. 136. Andresen R, Radmer S, Sparmann M, et al. Imaging of hamate bone fractures in conventional x-rays and high-resolution computed tomography: an in vitro study. Invest Radiol. 1999;34:46. 137. Kato H, Nakamura R, Horii E, et al. Diagnostic imaging for fracture of the hook of the hamate. Hand Surg. 2000;5:19. 138. Wharton DM, Casaletto JA, Brown DJ. Outcome following coronal fractures of the hamate. J Hand Surg Eur. 2010;35:146. 139. Grant I, Berger AC, Ireland DC. Rupture of the flexor digitorum profundus tendon to the small finger within the carpal tunnel. Hand Surg. 2005;10:109. 140. Scheufler O, Andresen R, Radmer S, et al. Hook of hamate fractures: critical evaluation of different therapeutic procedures. Plast Reconstr Surg. 2005;115:488. 141. Teisen H, Hjarbaek J. Classification of fresh fractures of the lunate. J Hand Surg [Br]. 1988;13:458. 142. Henry MH. Fractures of the proximal phalanx and metacarpals in the hand: preferred methods of stabilization. J Am Acad Orthop Surg. 2008;16:586. 143. Freeland AE, Orbay JL. Extraarticular hand fractures in adults: a review of new developments. Clin Orthop Relat Res. 206;445:133. 144. Ali A, Hamman J, Mass DP. The biomechanical effects of angulated boxer’s fractures. J Hand Surg [Am]. 1999;24:835. 145. Leung YL, Beredjiklian PK, Monaghan BA, et al. Radiographic assessment of small finger metacarpal neck fractures. J Hand Surg [Am]. 2002;27:443. 146. Lutz M, Sailer R, Zimmermann R, et al. Closed reduction transarticular wire fixation versus open reduction internal fixation in the treatment of Bennett’s fracture dislocation. J Hand Surg [Br]. 2003;28:142. 147. Ruland RT, Hogan CJ, Slade JF, et al. Use of dynamic distraction external fixation for unstable fracture–dislocations of the proximal interphalangeal joint. J Hand Surg Am. 2008;33:19. 148. Badia A, Riano F, Ravikoff J, et al. Dynamic intradigital external fixation for proximal interphalangeal joint fracture dislocations. J Hand Surg [Am]. 2005;30:154. 149. Rasmussen TE, Clouse WD, Jenkins DH, Peck MA, Eliason JL, Smith DL. The use of temporary vascular shunts as a damage control adjunct in the management of wartime vascular injury. J Trauma. 2006;61:8–12. 150. Fox CJ, Gillespie DL, Cox ED, et al. The effectiveness of a damage control resuscitation strategy for vascular injury in a combat support hospital: results of a case control study. J Trauma. 2008;64:S99–S106 [discussion S106–S107]. 151. Bondurant FJ, Cotler HB, Buckle R, Miller-Crotchett P, Browner BD. The medical and economic impact of severely injured lower extremities. J Trauma. 1988;28:1270–1273. 152. Johansen K, Daines M, Howey T, Helfet D, Hansen ST Jr. Objective criteria accurately predict amputation following lower extremity trauma. J Trauma. 1990;30:568–572 [discussion 572–573]. 153. Howe HR, Poole GV, Hansen KJ, et al. Salvage of lower extremities following combined orthopedic and vascular trauma. A predictive salvage index. Am Surg. 1987;53:205–208. 154. McNamara MG, Heckman JD, Corley FG. Severe open fractures of the lower extremity: a retrospective evaluation of the mangled extremity severity score (MESS). J Orthop Trauma. 1994;8:81–87. 155. Krettek C, Seekamp A, Köntopp H, Tscherne H. Hannover fracture scale ’98—re-evaluation and new perspectives of an established extremity salvage score. Injury. 2001;32:317–328. 156. Russell WL, Sailors DM, Whittle TB, Fisher DF Jr, Burns RP. Limb salvage versus traumatic amputation. A decision based on a seven-part predictive index. Ann Surg. 1991;213:473–480 [discussion 480–481]. 157. Bosse MJ, MacKenzie EJ, Kellam JF, et al. A prospective evaluation of the clinical utility of the lower-extremity injury-severity scores. J Bone Joint Surg Am. 2001;83:3–14. 158. Bonanni F, Rhodes M, Lucke JF. The futility of predictive scoring of mangled lower extremities. J Trauma. 1993;34:99–104. 159. Scheker LR, Netscher DT. Replantations and amputations of the upper extremity. In: Kasdan ML, ed. Occupational and Upper Extremity Injuries and Diseases. Philadelphia: Hanley and Belfus; 1991:215–231. 160. Zhong-Wei C, Meyer DE, Kleinert HE, et al. Present indications and contraindications for replantation as reflected by long-term functional results. Orthop Clin North Am. 1981;12:849–870.

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Lower Extremity Philip F. Stahel, Wade R. Smith, and David J. Hak

INTRODUCTION Lower extremity injuries represent the primary cause of more than half of all hospitalizations for trauma. Their frequency, severity, and costs emphasize the impact of those injuries on society.1,2 Lower extremity fractures may be caused by either low- or high-energy forces and occur both in isolation and as multiple injuries. The mechanism of injury defines the specific individual fracture pattern. Typical trauma mechanisms include blunt versus penetrating trauma, low-energy versus high-energy forces, twisting, bending, or crushing forces. Significant lower extremity injuries compromise functional outcome and can lead to long-term pain, abnormal gait, degenerative joint disease, chronic infection, and limb loss. Dislocations of the hip, knee, or more distal joints, as well as displaced fractures, may cause pressure on nerves, vessels, or skin, resulting in permanent deficits. Delay of more than a few hours in reducing a dislocated hip significantly increases the risk of avascular necrosis of the femoral head. Displaced intracapsular femoral neck fractures also have a high risk of avascular necrosis, which can be lowered by urgent reduction and fixation. In young patients, this injury may appropriately be considered as an “ischemic surgical emergency.” Failure to recognize an undisplaced fracture of the femoral neck may result in its displacement, with a much greater likelihood of poor outcome. Open fractures of the lower extremities are true emergencies, requiring a timely surgical treatment to minimize the risk of infection and limb loss. The wide prevalence of safety belt usage and mandatory airbags in vehicles leads to an increased number of survivors of high-energy crashes, who consequently suffer from a higher severity of lower extremity injuries. Any trauma victim involved in a high-energy trauma mechanism may have associated potentially life-threatening injuries to the head and torso. Thus, the initial evaluation of lower extremity fractures must focus on the patient as a whole, and not focus exclusively on the injured

limb.3–5 The concept of “damage control orthopedics” (DCO) was established based on the principle that prolonged early definitive treatment of long bone fractures can be detrimental for severely injured patients who are in unstable physiological conditions.6,7 In these patients, the early mitigation of the “lethal triad” of persistent metabolic acidosis, hypothermia, and coagulopathy represents the prime goal for survival.4 The controversial concept of “limb for life” entails the early amputation of a mangled lower extremity in critically injured patients with the aim of increasing the likelihood of survival. The ideal timing and modality of long bone fracture fixation in multiply injured patients, particularly in presence of severe head or chest trauma, represents another controversial topic of debate related to the care of lower extremity injuries.3,8 A relatively recent concept in lower extremity fracture care is that the majority of fractures can be treated entirely or in part with minimally invasive fixation. The evolution of techniques for percutaneous reduction and fixation of fractures, coupled with technological adaptation of fracture implants, has completely revolutionized fracture fixation.9 While intra-articular fractures usually require some form of open reduction to restore articular congruity, most diaphyseal and metaphyseal lower extremity fractures can be treated with minimally invasive surgery. The decreased blood loss, lowered risk of infection, and increased rate of healing likely have positive implications for the injured patient with lower extremity fractures.

HISTORICAL PERSPECTIVE Orthopedic surgery has developed through the need to alleviate pain, correct deformity, and restore function following fractures. Evidence of splinted fractures and the first successful amputations dates as far back as the fifth Egyptian Dynasty, about 4,500 years ago. The Corpus Hippocrates described the principles of traction, countertraction, and external fixation. Surgeons have built on these past foundations with the

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advancement of technology. In England, Thomas described the traction splint that still bears his name. In France, Malgaigne described the external fixator, and Delbet reported use of a weight-bearing cast for tibial fractures. In the United States, Buck described skin traction, while Steinmann in Switzerland and Kirschner in Germany introduced skeletal traction. Another German, Küntscher, made many contributions to modern intramedullary nailing. In Austria, Böhler established hospitals devoted to the care of injuries and published a comprehensive text on fracture surgery. Lambotte, a Belgian, is the father of modern internal fixation, which was advanced further by his countryman, Danis, who demonstrated that rigid fixation could result in direct bone healing without callus formation. The Swiss-based “Arbeitsgemeinschaft für Osteosynthesefragen” or “Association for the Study of Internal Fixation” (AO/ASIF) was founded in 1958 by a group of Swiss surgeons to produce and disseminate a system of fracture care based on stable fixation with preservation of soft tissue, active motion, and functional rehabilitation.10 This association has earned itself a worldwide reputation as an international authority in the treatment of trauma through its continuing research and development of instrumentation. Further advances continue, with emphasis on indirect reduction techniques, closed or minimally invasive fracture fixation, and stable but less rigid fixation that promotes rather than suppresses indirect, callus-dependent healing of bone.9 At about the same time in the Soviet Union, Professor Ilizarov, working in the Siberian town of Kurgan, developed and refined the concept of distraction osteogenesis, permitting healthy de novo bone to be created in vivo through distraction with a ring external fixator system with Kirschner-type wires. His work led to significant advances in the use of external fixators as definitive treatment for a variety of traumatic injuries and post-traumatic complications. The increasing ability of orthopedic surgeons to obtain early fracture stability with relatively low complication rates has led to improvements in postinjury rehabilitation. Rehabilitation concepts have changed from the prolonged rest suggested by Thomas to the present emphasis on rapid restoration of skeletal stability that allows for prompt mobilization of injured extremities and patients. Early weight bearing is encouraged, whenever possible to promote bone healing and overall physiological restoration. Detailed knowledge of a patient’s musculoskeletal injuries, his or her treatment, and his or her response is crucial for appropriate decision making in both the acute and late phases of care. Therefore, the orthopedic surgeon should ideally be directly involved from the trauma bay to the entire recovery process.

PATHOPHYSIOLOGY AND BIOMECHANICS Fractures occur when the applied load to the bone exceed its load-bearing capacity. Fracture patterns relate to bone strength and the forces that cause the injury. Young, active individuals have strong bone. Children’s bones can undergo plastic deformation and may bend without breaking. Elderly, osteoporotic individuals have diffusely weak bone. Focal bone defects may weaken a bone so significantly that it fails under a load that

would normally pose no problem, resulting in a pathologic fracture. Such pathologic fractures may be due to tumor, infection, or dysplasia, as well as more generalized conditions that severely weaken bone, such as osteoporosis. The amount of energy that produced a given fracture is suggested by the patient’s history and the fracture pattern. Comminution (the presence of more than two fracture fragments) implies a higherenergy injury that will produce multiple fracture lines. Displacement and the extent of local damage to soft tissue also reflect the amount of absorbed energy. Spiral fractures are produced by indirect, torsional forces. Less local soft tissue damage is generally present, but a very comminuted spiral fracture may have required such force that each fracture fragment acted as a high-velocity “internal missile,” producing significant damage in the surrounding tissues. Transverse fractures are caused by directly applied forces. A wedge or “butterfly” fragment is often seen on the side of the bone where the fracturing force was applied as a result of local compression, while the opposite cortex fails transversely in tension.

MECHANISM OF INJURY Obtaining a thorough patient history provides the physician with useful information to begin forming a list of differential diagnoses in his or her mind prior to radiographic examination of the patient. The history should specify the mechanism of injury, provide information regarding the severity of the applied forces, and alert the physician to associated injuries, illness, or medically relevant problems. While an accurate history may be difficult or impossible to obtain initially in a seriously injured patient, more details should always be sought and reconfirmed as the patient improves or more information becomes available. The history may be particularly helpful in managing open fractures by providing information on the following: the identification of the source and extent of contamination, the time elapsed from the moment of injury, and whether bone was initially protruding from an extremity wound. A history inconsistent with the extent of injury suggests either a pathologic fracture or the possibility of abuse. A normal child, particularly under 2 years, should not fracture his or her femur while playing, even roughly, with a friend or parent. An elderly patient will not normally sustain a hip fracture from turning over in bed. Although pathologic fractures should be suspected in a patient with known malignant or metabolic disease and can be preceded by local pain, fractures may occur in completely asymptomatic patients as the initial presentation of an underlying disorder. In a young child, multiple fractures at various stages of healing are pathognomonic of child abuse, the diagnosis and appropriate management of which may be lifesaving. The report of pain or impaired function of an extremity requires careful evaluation to exclude a fracture or injury to a joint, nerves, muscles, or vascular structures.

CLINICAL ASSESSMENT Examination according to the Advanced Trauma Life Support (ATLS®) protocol provides a systematic method of thoroughly examining the trauma patient and minimizing missed

Lower Extremity

RADIOGRAPHIC DIAGNOSTICS As per ATLS® protocol, an anteroposterior (AP) chest and pelvis, and adequate lateral cervical spine radiographs are indicated early in the evaluation and resuscitation of the injured patient during the primary survey.4,11 X-rays of injured extremities are of much lower priority and fall into the secondary survey. The obviously injured extremity should be dressed and stabilized with a splint. Resuscitation of the patient should never be delayed or interrupted for x-rays of the extremities. X-rays can be taken after urgent surgical treatment for other life-threatening problems. In the unstable patient, care should be concurrent and not contiguous, implying that x-rays and fracture stabilization can occur concomitantly in the operating theater or resuscitation bay with lifesaving maneuvers such as laparotomy or thoractomy. If adequate extremity radiographs can be obtained without delaying other essential aspects of the evaluation and treatment of the trauma patient, they can be valuable in making the initial care plan. Extremity x-rays should show both AP and lateral views of the entire bone in question. If the need for surgical treatment has been determined, further views may be better obtained in the operating room under anesthesia or after traction has realigned and separated the fracture fragments sufficiently to improve visualization. There is an ongoing debate related to the importance of obtaining prereduction radiographs for joint dislocations. In general, any joint dislocation should be reduced as soon as possible, in order to avoid strain on associated structures, including vessels and nerves. For this reason, some physicians argue that x-rays of dislocated joints should never be obtained under any circumstance. The opposite point of view is based on the notion that some injury patterns are not amenable to closed reduction, and that such in vain manipulations

and reduction maneuvers may increase the risk of inducing or exacerbating the severity of associated injuries. A reasonable guideline for the acute management of joint dislocations is to reduce dislocated joints in anatomic locations that are not frequently associated with neurovascular injuries without prereduction x-rays (e.g., ankle fracture–dislocations), and to obtain x-rays in all cases of more “at-risk” anatomic locations, such as the knee or hip joint. Postreduction x-rays must be obtained in all cases, to ensure anatomic joint reduction and to design a final treatment plan for the individual injury patterns. Certain complex articular fractures are best visualized with computerized tomography (CT) scans. If a patient is hemodynamically stable and requires other CT studies, extremity CTs may be obtained at the same time. Early involvement of the orthopedic surgeon ensures proper x-rays and avoidance of unnecessary diagnostic studies.

ASSOCIATED INJURIES ■ Vascular Injuries A high “level of suspicion” for a significant associated vascular injury, in conjunction with a thorough clinical exam (Table 40-1), should help in the guidance of the acute management of joint dislocations. Any pulse deficit or measurable reduction in arterial pressure index (API), before or after manipulation, must be considered evidence of a vascular injury. The accuracy of pulse examination alone for the detection of an arterial injury is very low. The five clinical “hard

TABLE 40-1 Clinical Signs for Determining the Likelihood of a Significant Vascular Injury Associated with Lower-Extremity Fractures and Dislocations “Hard Signs” Active or pulsatile hemorrhage Pulsatile or expanding hematoma Clinical signs of limb ischemia Diminished or absent pulses Bruit or thrill, suggesting AV fistula

“Soft Signs” Asymmetric extremity blood pressures Stable and nonpulsatile hematoma Proximity of wound to a major vessel Peripheral neurological deficit Presence of shock/ hypotension

The presence of a “hard sign” of an arterial injury warrants an immediate surgical exploration with the option of an on-table angiography. In contrast, the “soft signs” are less specific in predicting a significant arterial extremity injury. In exclusive presence of a “soft sign,” such as an asymmetric ankle–brachial index, the recommended further diagnostic workup includes an angiography or CT angiography.

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injuries.4,11 In addition, the importance of continuous detailed documentation of the physical findings cannot be overemphasized. Assessment of patient progress may suffer due to a lack of reexamination and thorough documentation. Local tenderness at a fracture site may be masked or completely absent in a severely injured patient. Deformity, swelling, or both almost inevitably occur with fractures or dislocations of the lower extremity, although swelling may be delayed, especially if the patient arrives in a hypovolemic state. Truly occult fractures are rare indeed. Displaced long bone fractures result in shortening, malrotation, or angulation. Immediate reduction and splint placement reduces pain and blood loss, and often restores circulation to a pulseless extremity. The diagnosis of a joint dislocation is established by a thorough clinical exam in conjunction with conventional x-rays. Dislocations typically assume characteristic positions, and may be masked by associated fractures. Intra-articular injuries usually cause a hemarthrosis unless the joint capsule is disrupted, in which case more diffuse soft tissue swelling occurs about the joint. Instability or abnormal motion when stressing the joint may be difficult to elicit if the region is tender, but is particularly important and useful in the anesthetized patient. Immediate relocation of a dislocated joint is warranted especially when circulatory compromise is apparent.

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signs” of an arterial injury (Table 40-1)12 are present in more than two thirds of all dislocations with an associated significant vascular injury and are of paramount importance in the clinical guidance for decision making related to the acute management concept (i.e., the operative exploration vs. further diagnostics/angiography vs. clinical observation).12–14 In presence of a “hard sign” of arterial injury, operative exploration with or without intraoperative (“on-table”) arteriogram is indicated. The majority (95%) of arterial injuries occur in proximity to the site of the fracture or joint dislocation. Delay in diagnosis or worse, observation alone, can result in limb loss. The use of “soft signs” to detect occult vascular injury is less clear (Table 40-1). The yield of arteriography in the setting of clinical “soft signs” is very low and the lesions that are typically identified are nonocclusive lesions: intimal flap, contusion, spasm, and pseudoaneurysm. The natural history of these lesions is benign and self-limiting, and they rarely require surgical repair. The neurovascular status may be difficult to assess clinically in a severely injured patient. Therefore, a high level of suspicion is required for identifying and treating potentially catastrophic vascular injuries. Capillary filling is not, by itself, adequate clinical evidence of an intact proximal vascular flow. Distal pulses may be present after a significant arterial injury. Perhaps the most familiar arterial injury in the lower extremity involves the popliteal artery in association with knee dislocations or periarticular fracture. Late thrombosis of an initially nonocclusive injury may result in limb loss. Frequent assessment of pedal pulses is required for such patients. Any alteration of pedal pulses requires assessment, at least with Doppler pressure measurement. Assessment of ankle systolic blood pressure is an important adjunct to the physical exam. Pressure below 90% of that in the arms or the opposite leg requires prompt evaluation by a vascular surgeon. Doppler sonography or contrast arteriography may be considered if pulses decrease, but should not delay consultation with a trauma surgeon. Risk factors for limb loss include delayed surgery, arterial contusion with consecutive thrombosis, and, most importantly, failed revascularization. An arterial injury in combination with an orthopedic injury, such as a traumatic joint dislocation or fracture– dislocation, requires a coordinated approach by the acute care surgery and orthopedic teams. The use of a temporary arterial shunt to restore limb perfusion and minimize tissue ischemia in the management of complex extremity injury is an emerging concept in DCO surgery (Fig. 40-1). Both civilian and military experiences demonstrate temporary vascular shunting as a useful adjunct in successful limb salvage. Tanner and colleagues reported 100% early limb preservation following temporary vascular shunts placed in forward combat surgical centers with 96% of shunts remaining patent until arrival to a facility where definitive arterial reconstruction could be performed. Arterial repair is completed by autologous repair of the vessel when indicated. Time to revascularization is of utmost concern since delays in excess of 8 hours after injury carry a risk of amputation in excess of 80%. In contrast, successful operative vascular repair within 8 hours of injury yields excellent rates of limb salvage.

■ Nerve Injuries The neurological status of the extremity should be documented before any definitive treatment, whenever possible. The neurological examination, like the vascular examination, may be unreliable in the severely injured patient or extremity. Stocking hypoesthesia may be due to acute ischemia, direct nerve injury, or psychogenic mechanisms. Absent sensation restricted to the isolated sensory area of a peripheral nerve suggests injury to that nerve. Impaired motor function may be caused by pain and instability, a peripheral nerve injury, or a spinal cord injury. Peripheral nerve damage is associated with certain lower extremity injuries. Posterior dislocations of the hip may injure the sciatic nerve, most often its peroneal component. Knee dislocations or equivalent injuries may injure the common peroneal and/or tibial nerves in the popliteal fossa, a possible clue to an associated arterial injury. Pressure from a splint or cast may also injure the peroneal nerve as it encircles the neck of the fibula at the knee. Most peripheral nerve injuries associated with traumatic joint dislocations are due to shearing mechanisms (“neurapraxia”) and most commonly resolve without the need for surgical exploration and/or repair. Typical locations include the axillary nerve for shoulder dislocations, the ulnar nerve for elbow dislocations, and the sciatic nerve for posterior hip dislocations. A peripheral nerve injury is assessed by clinical examination. The incidence of peripheral nerve injury in extremity trauma is very low, around 1–2%. Early nerve conduction studies within 6 weeks after trauma can aid in defining the extent and prognosis of injury. A delayed nerve repair should be performed at that time, if complete nerve injury is confirmed. However, successful repair, for example, by grafting with autologous peripheral nerve tissue, is rarely successful in elderly or comorbid patients, and the indication is therefore restricted to the pediatric population and to young and healthy adults. The sural nerve is the most common donor site for autologous nerve grafting.

■ Injury Combinations Awareness of typical combinations of lower extremity injuries aids diagnosis and may decrease the risk of missing important injuries. One mechanism can produce several injuries. An unrestrained passenger in a head-on motor vehicle collision may strike his or her knee against the dashboard, sustaining a patellar fracture or injury to knee ligaments, depending on the point of impact. The force indirectly applied along the femur then dislocates the flexed hip, concurrently producing a posterior wall acetabular fracture and/or fracture of the femoral head. The association between femur fractures and pelvic or acetabular fractures is so strong that careful review of a pelvic x-ray is mandatory for all patients with femoral shaft fractures. Patients who fall from a height and land on their feet may have both calcaneal fractures and injuries to the thoracolumbar spine— another “classic” combination. Patients with fractures of the femoral shaft may have associated fractures of the femoral neck, either obvious or undisplaced and occult. The trauma surgeon should be aware of the association of ruptures of the thoracic aorta with pelvic fractures and of the frequently observed multiple injuries seen with “floating knees” (simultaneous ipsilateral

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FIGURE 40-1 Limb salvage procedure in a 35-year-old male patient who was involved in a high-speed motorcycle collision. The patient sustained right-side traumatic lower leg amputation (A and B) and a contralateral type IIIC open traumatic “floating knee” injury, with a combination of a displaced intra-articular distal femur fracture and a comminuted proximal tibia fracture. On presentation to the emergency department, the left lower extremity was dysvascular, pulseless, with a pathologic ankle–brachial index (ABI) of 0.5. The patient was immediately taken to the operating room for spanning external fixation of the left knee and vascular repair. Intraoperative shunting was performed to reconstitute temporary blood flow distal to the SFA (C). Successful vascular repair was performed with a saphenous vein graft from the contralateral side. The amputated residual limb on the contralateral side was debrided and successfully closed by a split-thickness skin graft within 2 weeks (D). The patient recovered well from his injuries and was able to ambulate without support within 3 months using a custom-made above-knee prosthesis for the right residual limb, and functional rehabilitation on the left lower extremity.

femoral and tibial fractures), which also have a high incidence of associated injuries to soft tissue at the knee joint. Isolated fibular fractures may be associated with traction injuries of the peroneal nerve or with ligamentous disruptions of the knee or ankle. While fractures are often distractingly obvious on x-rays, injuries to joints such as subluxations and even dislocations may easily be overlooked unless one is suspicious.

■ Joint Dislocations A “joint dislocation” describes the complete separation of at least two articular surfaces of adjacent bones, by which the functional contact between those articular surfaces is lost. In contrast, the term “joint subluxation” defines the partial

disruption of articular surfaces, in which some functional contact within the joint remains. The direction of displacement of the distal bone involved in the joint determines the type of displacement. For example, a “posterior knee dislocation” describes a state in which the tibial head is displaced posteriorly to the femoral condyles. Traumatic joint dislocations represent frequent orthopedic injuries, which can be successfully treated by simple closed reduction maneuvers and early functional aftercare in most cases. Most traumatic joint dislocations do not require surgical fixation, except in the case of associated fractures (“fracture–dislocation”) or multiligamentous joint instability. Care must be taken in the case of complex fracture– dislocations, which may require a primary open reduction and fixation. Extensive closed reduction maneuvers may lead to

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complications related to associated neurovascular injuries. A high level of suspicion must be raised for associated vascular injuries that may lead to a detrimental outcome with delayed limb loss, if missed during the first few hours after trauma. Patients “at risk” are mainly young individuals with high-energy trauma mechanisms, particularly in case of traumatic hip or knee dislocations. However, minor trauma mechanisms, such as simple mechanical falls, do not preclude from a significant vascular injury. The clinical assessment by “hard” and “soft” signs of vascular injury (Table 40-1), including the determination of blood pressure gradients on the extremity, will help in the guidance for decision making on timing and modality of treatment. The presence of clinical “hard signs” mandates immediate surgical exploration and repair, with optional “ontable” angiography, if needed. Urgent assessment and treatment, generally without exceeding 6–8 hours of ischemic time, is of crucial importance for successful limb salvage. Associated nerve injuries are managed nonoperatively and will resolve in most cases.

SOFT TISSUE INJURIES AND COMPARTMENT SYNDROME Soft tissue injuries to the lower extremity are critical in the decision making for the timing and modality of fracture fixation, particularly in high-energy tibial fractures (Fig. 40-2). Tense swelling and increasing pain is typical of compartment syndrome, which must be suspected in every injured lower extremity.15,16 Impaired sensory or motor function in the setting of

FIGURE 40-2 Critical soft tissue injury in a 43-year-old patient who sustained a high-energy proximal tibia fracture after a motorcycle crash. Fracture blisters developed within 24 hours of injury. The critical soft tissue conditions mandated a staged treatment concept by initial spanning external fixation and delayed conversion to internal fixation once the tissue swelling had subsided and the fracture blisters had healed. Despite the high-energy injury pattern and critical soft tissues, this patient did not develop a compartment syndrome and had an uneventful long-term recovery.

TABLE 40-2 Hannover Classification System for Soft Tissue Injuries, According to Tscherne and Oestern Score 0

I

II

III

Description No soft tissue injury, indirect trauma mechanism, simple fracture pattern Superficial skin abrasion, skin contusion by internal pressure of fracture fragments Deep soft tissue contamination, skin contusion by direct force, impending compartment syndrome, complex fracture pattern Severe soft tissue contusion with skin necrosis, myonecrosis, degloving injury, acute compartment syndrome, comminuted fracture pattern

Example Indirect torsion fracture of the tibia Unreduced fracture– dislocation of the ankle Bumper injury to the lower leg

High-energy rollover trauma

compartment syndrome is a late presentation and correlates compartment necrosis. Compartment syndromes typically develop several hours or more after injury, before or after treatment has begun, and may be related to a cast or dressing that has become tight as the enclosed limb swells. Immediate release of such a constricting dressing aids diagnosis and may be therapeutic. Compartment syndrome is most effectively diagnosed by an experienced examiner and remains primarily a clinical diagnosis. Intracompartmental monitoring with arterial lines or specialized “compartment monitors” can be helpful in the obtunded patient. In the awake patient, unremitting pain and a tense or swollen limb should be assumed to be compartment syndrome. Patients with suspected compartment syndrome should be taken to the operating room immediately and undergo fasciotomy of all compartments (three in the thigh, four in the tibia, nine in the foot). Partial fasciotomies, or the use of limited incisions, in general are not appropriate in the trauma patient. Quantification of soft tissue injury severity has been attempted by many investigators. Tscherne emphasized that the severity of injury depends largely on the extent of damage to soft tissue in both closed and open fractures. The Oestern/Tscherne classification focuses on categorization of the soft tissue injury17 (Table 40-2). Open fractures require urgent surgical treatment for debridement and fracture stabilization. Closed fractures with high-energy soft tissue damage also require urgent stabilization as well as close monitoring for compartment syndrome.

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OPEN FRACTURES AND THE “MANGLED LIMB”

TABLE 40-3 Classification of Open Fracture Types, According to Gustilo et al. Type I

II

III

IIIA IIIB IIIC

Description Clean wound 1 cm, inside-out perforation, little or no contamination, simple fracture pattern Skin laceration 1 cm, surrounding soft tissue without signs of contusion, vital musculature, moderate to severe fracture instability Extensive soft tissue damage, wound contamination, exposed bone, marked fracture instability due to comminution or segmental defects Adequate soft tissue coverage of the fractured bone Exposed bone with periosteal stripping Any open fracture with associated arterial injury requiring vascular repair

All open fractures require urgent surgical treatment to reduce the risks of infection, soft tissue damage, and ongoing bleeding. In the emergency department, the wound is kept covered with a sterile dressing, pressure is applied as necessary to control bleeding, and the limb is splinted. Tetanus prophylaxis and systemic antibiotics are given. Generally, a first-generation cephalosporin is used for 24–48 hours following wound closure. For more severe wounds or contamination, additional coverage is added (e.g., an aminoglycoside or thirdgeneration cephalosporin for grade III open fractures, or highdose penicillin for “barnyard” injuries with risk of clostridial contamination). As soon as the patient’s condition permits, radiographs of the injured limb are obtained. Operative care of the open fracture must fit appropriately into the care of the patient’s other problems. This should be done in an operating room with general or regional anesthesia. Debridement should preferably be performed within 6 hours of injury, unless more time is required for resuscitation of the patient or for treatment of injuries that pose a greater threat to life or limb. Longer delays likely increase the risk of infection. After thorough debridement of devascularized muscle, fascia, subcutaneous tissue, skin, and bone, removal of all foreign material, and copious irrigation, wound care is enhanced by appropriately chosen fracture fixation. Generally, this involves screw and/or plate fixation for joint fractures, intramedullary nails, or external fixators for diphyseal fracture. Intramedullary nails in the tibia and femur can safely be placed in reamed fashion, even in open fractures. However, in multiply injured, concern for marrow extravasation and subsequent development of systemic inflammatory response syndrome (SIRS) has led to the use of unreamed, small-diameter nails, temporary external fixators, or reamer–irrigator–aspirator (RIA) systems to decrease marrow embolization.22,23

CHAPTER CHAPTER 40 X

Open fractures should be quickly assessed on arrival of the patient in the emergency room. The wound should be covered with a sterile saline dressing and only examined in the operating room in order to avoid further contamination and soft tissue damage. Extensive exploration or manipulation of exposed bone should not be attempted in the emergency department. Bleeding, even from amputation wounds, can almost always be managed with a pressure dressing. A tourniquet should be reserved for uncontrollable hemorrhage from penetrating lower extremity injuries.18 A “mangled extremity” defines a severely injured limb secondary to trauma in which there is a significant risk of amputation as a potential outcome. More specifically, a functional limb is composed of the following critical elements: skin and subcutaneous tissue, blood vessels, muscles and tendons, bones, joints including cartilage and ligaments, and peripheral nerves. Irreparable injury to one or more elements may significantly impair the function of a limb and lead to disability. A mangled extremity, the most severe form of injury, encompasses significant injury to multiple elements critical to limb function. In the event of multiple injuries, hemorrhagic shock, prolonged delay to definitive care, and/or risk of death, amputation may be the preferred option: “limb for life concept.” Once the patient responds to resuscitative efforts, the extremity is carefully examined during the secondary survey. Evaluation focuses on signs of arterial injury, extent of soft tissue and bone injury, and degree of contamination. A search for “hard signs” and “soft signs” (Table 40-1) of arterial injury is essential since both civilian and combat experiences demonstrate that the risk of limb loss correlates with a delay in revascularization beyond 6 hours. The risk of limb loss is further increased in the setting of ischemia with associated major venous, soft tissue, and muscle injury.19 Since a significant percentage of injuries, particularly those involving the distal extremity and the major joints, are missed during the initial trauma evaluation, repeated exams are essential, especially as the patient’s recovery permits more cooperation. At least one “tertiary” survey is an important part of each significantly injured patient’s diagnostic evaluation. Grading systems for open fractures have been proposed by Gustilo et al., among others20 (Table 40-3). Despite a significant interobserver variability and limitations related to the wide spectrum of open fracture types covered in three categories, the Gustilo classification is very practicable and therefore well accepted among orthopedic surgeons. Newer classification systems, such as the Ganga Hospital Score from India,21 attempt to overcome the shortcomings from the Gustilo classification by increasing the number of categories and correlating the total score with a guideline for treatment. As such, the Ganga Hospital Score for open fractures will mandate treatment protocols including the “Fix and close” protocol, “Fix, Bone Graft and Close” protocol, “Fix and Flap” protocol, or the “Stabilise, Watch, Assess and Reconstruct” protocol.21

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SECTION 3 X FIGURE 40-3 Free microvascular fibula transfer (arrows) for early bone grafting of a comminuted distal femur fracture with significant bone loss.

After fracture fixation, the open fracture wound, extended as required for debridement and fixation, is left open initially, under a sterile moisture-retaining dressing. Recent randomized studies indicate that there may be a role for primary closure in well-debrided open injuries. Antibiotic-impregnated methylmethacrylate beads placed in large or contaminated wounds may significantly reduce the risk of infection. Severe open fracture wounds mandate a return to the operating room within 24–48 hours to assess the adequacy of debridement and to further debulk potential bacterial contamination. Delayed primary closure, generally after 3 or 4 days, reduces the risk of wound infection. Unless the local tissues are intact enough to permit delayed suture closure, or split-thickness skin grafting, open wounds often require muscle flaps, either swung locally or brought in from a distance with microvascular anastomoses.24,25 Severe open fractures often require bone grafting to gain union. While bone grafting may be essential, it should be postponed until the wound is securely healed, as the risk of infection is increased if bone grafting is performed at the time of initial open fracture surgery or at delayed closure of the wound (Fig. 40-3).

CURRENT CHALLENGES AND CONTROVERSIES ■ Long Bone Fractures The large volume of musculoskeletal tissue in the lower extremities, including the pelvis, increases the potential systemic effects of lower extremity injuries. Bleeding and accumulation of extracellular fluid may cause hypovolemia and contribute to systemic hypotension.26 Several units of blood can be lost into severely injured thighs, and preoperative blood loss associated with a single femur fracture is up to 1,500–2,000 mL. A crushing wound of the lower extremity releases intravasated debris (e.g., bone marrow), myoglobin, related muscle breakdown products, and various inflammatory mediators. The release of these substances may cause fat embolism and adult respiratory distress syndrome (ARDS), acute renal failure, and multiple organ failure (MOF).23,27,28 Life-threatening infections such as clostridial myonecrosis or necrotizing fasciitis can rapidly develop in the tissues of the lower extremities. While proper early operation may prevent these, immediate recognition and treatment are vital to the salvage of any patient who develops such an infection.29

Lower Extremity

■ Limb Salvage versus Amputation One of the most challenging decisions involved in the care of an injured patient is whether or not to attempt salvage of a severely injured limb.37 Although every appropriate effort

should be made to preserve functional and anatomic integrity, for some severe lower extremity injuries, an amputation and prosthesis may be more effective for the patient than a limb that is still attached but is of limited use. In the acute phase, the decision to amputate will depend primarily on the immediate condition of the patient and the feasibility of stabilizing/revascularizing the injured limb (Fig. 40-1). If the limb is initially salvaged, then further decisions must be made regarding the desirability of maintaining the salvage effort, which usually involves multiple further operations. Key factors in this decision process include the patient status, the level of potential amputation, as well as the wishes of the patient in those cases in which he or she is cognizant. In all situations involving a decision between limb salvage and amputation, the two primary concerns are (a) the systemic consequences of either alternative for the patient and (b) the likelihood of achieving a functional limb versus the problems associated with limb salvage (time involved, duration of disability, medical risks, socioeconomic costs, number of operations and hospitalizations, etc.).2,38,39 If a limb is severely injured, it is rare that either amputation or salvage will completely restore function. In those cases in which the patient is hemodynamically unstable and revascularization cannot be accomplished without increasing the chance of death, amputation is the only choice. In these cases a guillotine-type amputation is appropriate, but every effort should be made to preserve length and coverage options. In particular, efforts to preserve the potential for a below-knee amputation (BKA) by preserving any viable distal muscle and/or skin will improve the patient’s outcome.40 Free tissue transfers, rotational flaps, and skin grafts can all be used effectively to improve length and provide a durable, useful stump. Many surgeons are unaware that skin grafting of wellpadded stumps is feasible and highly successful. Similarly, latissimus dorsi free flaps, combined with skin grafts, preservation of vascularized heel pads, and turndown procedures, using vascularized portions of bone from the zone of injury, can effectively preserve a BKA despite severe soft tissue loss. Unfortunately, in many cases, the decision to amputate is made in the middle of the night, without opportunity for consultation with experienced salvage surgeons. Multidisciplinary decision making in these severe cases may provide increased reconstructive options whether the limb is salvaged in entirety or amputated. The level of amputation greatly impacts future function. Proximal amputations have greater functional impairment and are often less satisfactory then prosthetic alternatives. Prosthetic replacement of the foot and ankle is highly functional. A through- or above-knee amputation, however, requires a prosthesis that requires more energy for ambulation and is less functional than one used after a BKA. Thus, every reasonable effort is appropriate to preserve the patient’s own knee joint and enough proximal tibia (at least 10 cm below the joint) to provide for good prosthetic fitting. Prostheses for very proximal femoral amputation levels, hip disarticulation, or hemipelvectomies are rarely functional for ambulation; therefore, efforts are also appropriate to preserve an adequate above-knee amputation level.

CHAPTER CHAPTER 40 X

As demonstrated by Tscherne, Bone et al., Trentz and coworkers, and others, prompt surgical treatment for severe extremity injuries benefits the whole patient.5,30,31 Early fracture stabilization reduces the systemic effects of fractures, including SIRS, sepsis, MOF, and ARDS. Early stabilization reduces pain and the need for analgesic medication, and promotes mobilization of the patient with attendant benefits to the respiratory and gastrointestinal systems. While fracture fixation is particularly beneficial for the patient with injuries to the lower extremity and pelvis, “damage control” procedures should be undertaken if the patient is in shock, coagulopathic, hypothermic, or has an actively developing traumatic brain injury.3,4,32–34 The concept of DCO emphasizes rapid provisional skeletal stabilization with simple external fixators, followed by delayed definitive fixation when the patient is stable and the inflammatory system is less primed, usually at 5–10 days postinjury.4,6,7,32,35 While controversy exists concerning the utility of orthopedic damage control in specific patient subsets, the concept of rapid, minimally invasive fracture fixation has been found safe and cost-effective. A significant body of research has shown that the timing and type of fracture fixation may be critical in specific patient subsets. Intramedullary instrumentation of the femoral shaft can affect circulating neutrophil cell membranes causing surface receptor changes known as “priming” or “activation.” The “primed” neutrophil when “activated” releases mediator and cytokine substances that alter endothelial membrane permeability throughout the body, resulting in systemic inflammatory syndrome and fluid entering the alveoli.36 All of these changes are part of the “second hit” phenomena in which the damage of the initial trauma (first hit) is augmented by further damage from a second “hit.”4 The second “hit” may be caused by secondary procedures such as prolonged surgery with blood loss or instrumentation of the femoral canal. The initial approach to fracture care in the polytraumatized patient must take into account these physiological realities. However, the clinical implications of neutrophil changes and mediator release have not been directly correlated with clinical outcome, in part because of the large cohort numbers required to achieve statistical significance for such a study. Fractures, whether isolated or in polytrauma, have farreaching implications for the patient. The results of a “fracture” often depend more on damage to the soft tissues of the limb than on the isolated bony injury. Thus, accurate evaluation of an extremity injury requires assessment of the following: (a) skin and subcutaneous tissue; (b) muscles and tendons; (c) bones; (d) joints, including ligaments and articular cartilage; (e) arteries and veins; and (f ) peripheral nerves. Acute as well as final functional outcome will depend on treatment of the entire spectrum of injury.

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SECTION 3 X

The classic injury requiring a decision of amputation versus salvage is an open tibial fracture, with arterial injury (Gustilo type IIIC). Gregory et al. have defined a mangled extremity as one with significant injuries to three of the following four components: integument, bone, nerve, and vessel.41 Some element of subjective assessment of severity is inevitably involved in the evaluation of severe limb injuries. Several predictive scoring systems have been proposed to aid decisions about limb salvage. These necessarily require consideration of multiple factors. Unfortunately, none of these scoring systems reliably predict the need for amputation and, while they suggest which limbs may be salvaged, they do not correlate with functional outcome. Variables that must be considered in the decision for limb salvage are both systemic and local. The severity and duration of shock, the severity of other injuries (Injury Severity Score [ISS]), the patient’s age, and preexisting medical conditions are crucial. Important features of the extremity injury include duration of ischemia, causative mechanism, fracture pattern, location of vascular injury, neurological status, condition of the foot, and muscle viability following revascularization. The patient’s occupation and subjective desires merit consideration. One limb injury scoring scale is the “mangled extremity severity score” (MESS) developed by Johansen et al.42 Such scales were originally described for open type IIIC injuries, but their use has been extended by other investigators to complex lower extremity trauma. A total MESS of 7 or more suggests the need for primary amputation, since limbs with such scores rarely are salvaged successfully. The sensitivity and specificity of the MESS, however, have not gone unquestioned. Bonanni et al. have critically reviewed the MESS score, comparing it with three similar indices.43 Applying these scores to 58 lower extremities with salvage attempts, they found that none of the scores had a predictive value significantly better than chance in determining which limbs would be successfully salvaged. Bosse et al., in a large prospective multicenter study of patients with severe injuries to the lower extremity, demonstrated that current severity scores of limb injury cannot be used to effectively predict the need for amputation and functional outcome of the patient.44,45 They also found that patients with tibial nerve injury did not necessarily have a dismal outcome with salvage and that the 2-year outcome differences between amputation and salvage patients was minimal.46

■ Replantation Technically, replantation is possible for complete and subtotal lower extremity amputations. However, given the current near impossibility of lower extremity nerve regeneration in adults, the functional outcome is questionable. In general, only cleanly separated traumatic amputations in young individuals without significant systemic risk factors, including smoking, deserve consideration for replantation. Revascularization in the face of severe neuromuscular injury may result in a viable but painful, dysfunctional limb. Consultation with an experienced replantation team is essential. Preservation of the amputated part is

according to the same principles for upper extremity replantation. Care must be taken to not jeopardize the patients’ life in lower extremity replantation and revascularization. Reestablishment of blood flow after a period of prolonged hypoxia can have a toxic effect, causing systemic inflammation and MOF. Consideration should be given to rapid external fixator and arterial shunt placement to “buy time” and permit an overall reassessment of the patient and of the desirability of reattachment of the limb.

MANAGEMENT OF COMMON FRACTURES AND DISLOCATIONS ■ Acetabular Fractures Fractures of the acetabulum are articular injuries with profound implications for the long-term function of the hip joint. Successful open reduction and internal fixation (ORIF) of displaced acetabular fractures significantly improves the prognosis of these potentially devastating injuries and permits early mobilization of a patient who might previously have been managed with many weeks of skeletal traction and bed rest (Fig. 40-4). Judet and Letournel’s seminal work has led to our current classification, understanding, and management of acetabular fractures. Oblique x-rays and CT scans are used to classify the acetabular fracture, to assess displacement and need for surgical treatment, and to determine the best surgical approach. There are multiple surgical approaches to the acetabulum including the Kocher-Langenbeck, the ilioinguinal, the extended iliofemoral, the modified iliofemoral, the Stoppa, the triradiate, and combined anterior/posterior and percutaneous. The surgical approach is dictated by the fracture pattern and the overall condition of the patient. A complete three-dimensional understanding of the fracture is essential for formulating a preoperative surgical plan. Preservation of soft tissue attachments is needed to promote healing and avoid osteonecrosis. Vital neurovascular structures must be protected. A precise anatomic reduction must be achieved and fixed stably, generally with screws and plates, which must not encroach upon the articular surface. Intraoperative fluoroscopy has become a valuable tool for ensuring appropriate placement of orthopedic hardware around the acetabulum. Minimally invasive percutaneous screw fixation represents a challenging but valid alternative to open reduction with internal fixation in minimally displaced fractures or in patients with significant risk for wound complications or a “second hit” insult related to extensive surgical procedures (Fig. 40-5). Complications and poor results become less frequent with increasing experience of the acetabular surgeon. Acetabular fracture surgery remains among the most challenging procedures in orthopedics. These difficult and dangerous reconstructive surgeries should generally be done in specialized centers to ensure that each patient receives optimal treatment. Acetabular fractures in osteoporotic individuals pose special problems. Comminution is often so severe and bone quality so poor that conventional fixation techniques are doomed to

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FIGURE 40-4 A 74-year-old lady with severe osteoporosis who sustained a displaced right acetabular fracture after a fall (A). The fracture was treated by angular-stable bridge plating with two anterior locking plates (B). Conventional, nonlocking screws and plates have a high risk of failure in osteoporotic cancellous bone. The patient is fully weight bearing on the right side, 3 months after surgery (C).

failure. In these instances, total hip arthroplasty with specialized acetabular reconstruction devices allows improved fixation and early weight bearing of the elderly patient. Because the femoral head is removed in total hip arthroplasty, extensile or combined exposures may not be required, and operative morbidity may be reduced. Acetabular fractures are usually closed injuries, without need for immediate operation. If surgery is delayed for 3–5 days, operative bleeding is reduced, and preoperative planning may be improved. Patients with pelvic and acetabular fractures have a significant risk of thromboembolic complications. Intermittent venous compression devices, anticoagulation with fractionated or low-molecular-weight heparin, and insertion of retrievable inferior vena cava filters for high-risk patients are all appropriate strategies for these injuries.

FIGURE 40-5 Polytrauma patient with combined pelvic ring and acetabular fracture. Due to the high-risk constellation in this patient, all fractures were treated by closed reduction and percutaneous cannulated screw fixation.

■ Hip Dislocation Posterior dislocations of the hip result from direct blows to the front of the knee or upper tibia of a sitting patient, most typically an unrestrained passenger in a motor vehicle (Fig. 40-6).

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SECTION 3 X

C FIGURE 40-6 Traumatic posterior hip dislocation in a 25-year-old woman who sustained a high-velocity motorcycle accident (A). After closed reduction, a traumatic defect of the femoral head is seen on the AP x-ray, classified as a Pipkin type II fracture (B, arrow). A trochanteric Ganz osteotomy was performed with a surgical hip dislocation to assess and repair the defect (C). Postoperative x-ray shows the partially filled defect by an osteochondral autologous graft (D, arrow).

A fracture of the posterior wall of the acetabulum occurs if the leg is more abducted and pure dislocations occur if the leg is adducted at the time of impact. The typical appearance of a patient with a posterior hip dislocation is with a hip that is flexed, adducted, internally rotated, and resistant to motion. This appearance may be lacking if a significant fracture of the posterior wall exists. An associated sciatic (often peroneal component alone) nerve palsy must be checked for. Anterior dislocations are rarer (5%) and are due to forced abduction and external rotation, which are also the characteristic deformity. An AP pelvis x-ray usually shows obvious signs of a hip dislocation or fracture–dislocation. Additional views may be needed, however, to assess adequately the proximal femur where an associated fracture of the head or neck may be present. A CT scan is required after reduction of a dislocated hip to assess its adequacy and the integrity of the acetabulum, as well as to exclude intra-articular bone fragments. Fractures of the femoral head occasionally occur with hip dislocations. They must be recognized and treated appropriately.

Dislocations of the hip are painful dramatic injuries that demand immediate reduction. Improvised splinting in situ with pillows or folded linen is unsatisfactory when compared with prompt reduction for pain relief. After initial x-rays, reduction can be done with intravenous analgesia, but may be gentler and easier for both patient and surgeon with general anesthesia and muscle relaxation. A rapid reduction (under 6–8 hours if at all possible) is crucial to minimize the risk of avascular necrosis of the femoral head. This disastrous complication results in destruction of the hip joint, with arthroplasty or arthrodesis almost always needed. Stability of the hip joint is usually restored by adequate reduction of pure dislocations, but the reduced joint must be checked for stability. Acetabular wall fractures of any significant size can result in instability, which, if present, is an indication for surgical repair within a few days after injury. A stable, concentrically reduced dislocation of the hip usually becomes comfortable within a very few days. While applying weight to the hip in an unstable position (e.g., getting up

Lower Extremity

■ Fractures of the Proximal Femur (“Hip Fractures”) Hip fractures represent the most common major injury in the elderly and are associated with a high rate of morbidity and mortality. The peer-reviewed literature reports a 1-year mortality of patients with hip fractures in the range of 14–47%. The currently largest prospective study assessing the outcome of surgery for hip fractures in more than 16,000 elderly patients reported a 30-day mortality of 8–17% and 120-day mortality of 21–38% in different age groups.47 A time delay of 4 days from injury to surgery was shown to increase the 30-day mortality significantly. Patients with hip fractures who had a comorbidity requiring preoperative medical workup had 2.5 times the risk of death within 30 days, compared with patients without comorbidities that delayed surgery.48 The prevention of hip fractures includes the dietary and medical management of osteoporosis, the prevention of falls by physical exercises, and the use of hip protectors in selected patients. While there is a consensus that the treatment of hip fractures consists of a surgical management almost exclusively, the timing and modality of fracture fixation depending on fracture pattern and patient age remains an ongoing topic of debate.49 Hip fractures represent an important socioeconomic factor due to the increasing life expectancy. The worldwide prevalence of hip fractures is estimated to be around 4.5 million and is associated with unacceptably high morbidity and mortality rates.47,49 Of note, these numbers are estimated to double by the year 2040, thus placing an enormous burden on global health care systems. While young patients sustain hip fractures due to high-energy trauma, the predominant mechanism in elderly patients is a same-level fall in conjunction with poor bone quality. Postoperative geriatric care is required in about 75% of all cases and 6-month mortality in this cohort has been shown to be around 20–30%.47,48,50 Measures to prevent falls, to reduce their consequences, and to prevent and treat osteoporosis are essential if we are to reduce the tremendous socioeconomic consequences of these injuries in the older population. In contrast, proximal femur fractures represent a rare entity in young patients and are usually the consequence of high-energy trauma.49 These patients are often severely injured and associated injuries to pelvis, abdomen, and chest are common. Early surgical fixation of proximal femur fractures is important in order to reduce the incidence of posttraumatic complications.51 Patients with displaced proximal

femur fractures usually have significant pain and obvious physical abnormalities, typically shortening and external rotation of the injured limb, with an inability to move the leg significantly because of hip pain, usually felt in the groin. Occasionally, hip fractures are undisplaced. These may be occult with pain and tenderness but no radiographic findings. The distinct anatomic regions of hip fractures that are typically distinguished radiographically include femoral neck fractures (intracapsular/extracapsular), trochanteric (pertrochanteric/ intertrochanteric), and subtrochanteric fractures. The location of a hip fracture has important implications for treatment and outcome. In all cases, the goal of surgical treatment is to stabilize the bone sufficiently to allow mobilization of the patient, to minimize the risk of destruction of the hip joint, and also to restore normal anatomic shape of the proximal femur. This is important for normal hip function, which is crucial for most activities of work and daily living. Preoperatively, light skin traction, as with a padded Buck’s traction boot, or skeletal traction for more unstable injuries is appropriate for immobilizing hip fractures until surgery. Traction is not essential for elderly patients with low-energy hip fractures. Nonambulatory patients with osteoporotic bone quality are occasionally best treated nonoperatively.52

■ Femoral Neck Fractures Femoral neck fractures are classified into (1) displaced versus nondisplaced, (2) stable versus unstable, and (3) intracapsular versus extracapsular (basicervical) fractures.49 The extent of displacement is classically described by the Garden classification. However, more recent validation studies have revealed that the interobserver accuracy of the Garden classification is very poor, particularly for differentiation between types 1 and 2, and between types 3 and 4.53 The Pauwels classification was originally described to determine fracture patterns that may warrant a primary valgus (Pauwels) osteostomy, based on the fracture angle/obliquity. Similarly to the Garden system, the Pauwels classification has a poor clinical applicability due to the lack of adequate fracture angle determination on preoperative x-rays, related to the external malrotation of the distal fragment.54 The comprehensive AO/OTA classification was recently revised and expanded.55 This system classifies trochanteric fractures as 31-A, and femoral neck fractures as 31-B types. The AO/OTA subtypes correlate with the extent of instability. While a 31-B1 type corresponds to a nondisplaced, valgusimpacted femoral neck fracture, the 31-B2 type reflects a transcervical or basicervical type, while the 31-B3 type classifies displaced subcapital fractures (Garden type 4). While nondisplaced, valgus-impacted femoral neck fractures (Garden and Pauwels type 1) are widely managed nonoperatively in Europe, the general practice in the United States tends toward operative fixation of all femoral neck fractures, independent of the aspects of stability and displacement. This fairly aggressive modality is possibly coguided by medicolegal aspects, aside from biomechanical considerations. The choice of implant for fixation of hip fractures is mandated by the fracture pattern (classification) and by associated

CHAPTER CHAPTER 40 X

from a low chair or toilet or getting into or out of a car) must be avoided until soft tissue healing has occurred, most patients can get out of bed and ambulate as soon as they can move and control their leg. Skeletal traction is required only for unstable hips, which will usually require surgery. Long-term outcome of hip dislocations includes an acknowledged significant risk of osteoarthritis, as well as some stiffness and limping that may never resolve. Avascular necrosis, the risk of which increases dramatically (from about 2% to 15%) if initial reduction is delayed more than a few hours, usually appears during the first year, with essentially all cases evident within 3 years after injury.

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SECTION 3 X FIGURE 40-7 Displaced vertical femoral neck fracture (Pauwels type 3) in a 65-year-old male patient who fell 6 ft from a tree (A). Anatomic reduction was achieved on a fracture table, with lag screw fixation using three 7.3 mm cannulated screws in an inverted triangle pattern (B and C). Despite anatomic reduction and adequate fixation (D), the fracture collapsed into varus and the patient developed a nonunion at 6 months (E). The arrows point out the nonunion and the lateral protrusion of the screws. This complication emphasizes the inherent instability of Pauwels type 3 fractures and the rationale for a primary joint arthroplasty in elderly patients with displaced femoral neck fractures.

parameters, such as bone quality and individual patient characteristics. For displaced femoral neck fractures, the widely accepted consensus is that patients under 60–65 years of age should be treated by anatomic reduction and internal fixation.49,51,56 The ideal treatment for patients over 75–80 years of age is a prosthetic replacement.57,58 In the group of patients between 65 and 75 years, the treatment modality must be guided by individual patient characteristics, including medical comorbidities, ambulatory status, and the apparent biological/physiological age.49 The “classic” fixation modality of intracapsular femoral neck fractures consists of three cannulated large-fragment screws (6.5 or 7.3 mm) that are placed percutaneously, in a triangular fashion, with the base of the triangle cephalad. Only one screw is placed at the calcar in order to avoid a potential stress raiser by two screws at the lateral cortex, which may lead to a delayed subtrochanteric fracture. The screws must be placed in a parallel and

well-spread fashion, in order to achieve fracture compression and adequate buttress of the posteromedial and posterolateral cortices. It is of crucial importance to place the screws orthogonal to the fracture line and to ensure that the threads of the screw heads are completely engaged across the fracture line. For this reason, short-threaded screws with 16 mm threads are usually preferred over screws with 32 mm threads. While adequate fracture healing can usually be achieved in AO 31-B1 and -B2 fractures treated by cancellous screw fixation, the vertical obliquity of 31-B2.3 and -B3 patterns (Pauwels type 3) has been associated with a high rate of malunion and nonunion, despite an excellent primary reduction and adequate fixation59 (Fig. 40-7). Extracapsular (basicervical) neck fractures may alternatively be fixated by a gliding hip screw/ plate device, preferentially with an additional antirotation screw proximal to the hip screw (6.5 or 7.3 mm cannulated lag screws).

Lower Extremity

■ Trochanteric Fractures Trochanteric fractures are located distal to the femoral neck and are generally categorized into displaced versus nondisplaced and stable versus unstable fracture patterns.65 These basic classification modalities are helpful in clinical decision making. The AO/OTA classification defines trochanteric fractures as the 31-A type.55 The stability of trochanteric femur fractures is determined by the integrity of the medial cortex. As such, 31-A1 types are considered stable fractures with an intact lesser trochanter/medial buttress, while the A2 and A3 types are considered unstable fractures. The 31-A2 type corresponds to the classic “three-part fracture,” with a fracture of the medial cortex and a variant multifragmentary component.65 The 31-A3 type classifies the most unstable trochanteric fractures, such as the “reverse obliquity” pattern (31-A3.1) and the classic

“intertrochanteric” transverse fracture pattern (31-A3.2). The A3 types are defined by a breach in the lateral femoral cortex that is associated with a higher risk of failure after surgical fixation.66 The AO/OTA classification for trochanteric fractures appears very reliable in clinical practice for guiding the optimal treatment and implant choice. Trochanteric fractures are an unequivocal entity of surgical management. A topic of ongoing debate is the question of whether to use a sliding hip screw/plate device as opposed to an intramedullary nail with cephalic interlock for trochanteric fracture fixation. While the implant choice may be guided by individual surgeons’ preference, some biomechanical aspects must be taken into consideration. The stable 31-A1 pattern with intact medial buttress is considered the classic indication for a sliding hip screw/plate fixation (Fig. 40-8). In contrast, the highly unstable 31-A3 types, particularly the “reverse obliquity” pattern, represent a contraindication for a sliding screw device and an indication for a cephalomedullary nail, respectively66 (Fig. 40-9). A similar biomechanical aspect accounts for any trochanteric fracture with an associated fracture of the lateral femoral wall. In this regard, the integrity of the lateral femoral wall has been shown to represent a key predictor of reoperation secondary to failure of fixation.66 Thus, fractures with a compromised lateral femoral wall are considered a contraindication for a sliding hip screw/plate construct. The most frequent trochanteric fracture pattern, the 31-A2 type (e.g., the classic three-part fracture), may be stabilized by either a cephalomedullary nail or a gliding hip screw/plate device, leading to similar outcomes reported in the peer-reviewed literature.67 Fixation is, naturally, more tenuous in osteoporotic bone. The fracture is initially reduced with the aid of a fracture table and image intensifier fluoroscope. Occasionally, actual open reduction is required in order to correct a varus malreduction. Overall, the “cutout” rate of the femoral neck screw with requirement for revision surgery lies below a 10% margin in the literature. A key aspect for maintaining implant fixation and fracture reduction is defined by a “tip–apex distance” of 2.5 cm, which is calculated as the cumulative distance from the tip of the hip screw to the apex of the femoral head in AP and lateral x-ray views.68 Above the cumulative distance of 2.5 cm, the risk of failure due to femoral neck screw cutout was shown to be significantly increased. Thus, aside from a perfect anatomic reduction, the adequate femoral neck screw placement in both planes (AP and lateral) represents a crucial parameter for a successful outcome after fixation of trochanteric hip fractures. With modern internal fixation devices properly applied, union is typically achieved within 3 months, with acceptable alignment and a low incidence of fixation failure, for all categories of trochanteric fractures. Newer-generation implants aimed at reducing the incidence of failure due to cutoff of the femoral neck screw by replacing the screw with a twisted blade, or by the use of modern angular-stable plates.69 While biomechanical testing has suggested an improved cutout resistance of these new implants, prospective clinical trials that provide a scientific evidence for the superiority of new-generation plates and nails, compared with conventional implants, are still lacking.

CHAPTER CHAPTER 40 X

Regarding the issue of anatomic versus valgus reduction, recent clinical studies have suggested that in younger patients (age 60 years) an anatomic reduction leads to better longterm results in Pauwels type 1 and Garden type 2 fractures, whereas a valgus reduction is recommended for Pauwels II/III and Garden III/IV type fractures due to the increased risk of a secondary loss of reduction59,60 (Fig. 40-7). Displaced femoral neck fractures are associated with a high risk of nonunion and avascular necrosis of the femoral head, where the blood supply runs along the neck in extraosseous retinacular vessels that are torn or kinked by displaced fractures. The expanding intracapsular hematoma may contribute to further hypoperfusion through compression of the nutrient vessels. These complications are so serious for younger patients that most orthopedic traumatologists consider fracture of the femoral neck in a young person to be a surgical emergency. Urgent anatomic reduction, decompressive capsulotomy, and secure fixation of a displaced femoral neck fracture provide the best opportunity for salvage of the patient’s own hip joint.51 Extra-articular femoral neck fractures are less cumbersome to treat than intracapsular fractures and are not generally associated with the above-mentioned complications, such as post-traumatic avascular necrosis. The method of choice for stabilization of these fractures is a sliding hip screw/plate device and early functional rehabilitation with full weight bearing. The treatment of choice for elderly patients (80 years) or for patients with an according biological/physiological age consists of a primary arthroplasty.58,61–63 This modality has been shown to be more efficient clinically, with regard to the incidence of complications and long-term outcomes, and more cost-effective from an economic point of view.57,58,64 Although hip fracture fixation is more cost-efficient in the early phase, this initial advantage is eroded by significantly increased costs related to subsequent rehospitalizations for failure of fixation and associated complications.49,57 The question of whether to choose a total hip arthroplasty over a hemiarthroplasty for elderly patients with displaced femoral neck fractures remains a topic of debate. The pertinent literature suggests a trend toward a more favorable outcome in patients with a total hip replacement, compared with those with a hemiarthroplasty.49,57,58

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SECTION 3 X A

B

C

D

FIGURE 40-8 Trochanteric femur fracture (AO/OTA type 31-A2.1) in a 51-year-old construction worker who sustained a fall from a ladder (A and B). The fracture was treated by closed reduction and fixation with a gliding hip screw/plate device. X-rays taken at follow-up after 4 months show a healed fracture in anatomic position (C and D).

■ Subtrochanteric Fractures Subtrochanteric fractures are classified as a 32-X.1 region by the AO/OTA classification,55 as opposed to the 31-X type of classification for the trochanteric and femoral neck fractures. In young patients, subtrochanteric fractures result from high-energy forces, typically motor vehicle crashes and falls from heights, and usually extend into the femoral shaft. In accordance with the high-energy trauma mechanism these young patients are usually severely injured and the traumatic impact is associated with severe soft tissue injuries and bleeding. In contrast, the subtrochanteric fracture pattern in older patients is different due to the usual low-energy mechanism of injury, similar to osteoporotic trochanteric fractures. Subtrochanteric fractures, a less frequent variety of hip fracture, still represent

challenging injuries because of frequent failures of surgical fixation. Significant advances in understanding of fracture healing and of fixation techniques have improved the management of these fractures. Each of the typical modalities for osteosynthesis of subtrochanteric fractures has its pitfall. When treated by closed reduction and intramedullary nailing, the proximal fragment is difficult to reduce adequately and tends to malreduce in varus position and anteflexion. Often, this problem is overcome intraoperatively by additional cerclage wires, which however may contribute to impaired periosteal blood supply to the fracture. On the other hand, the exact anatomic reduction by ORIF technique uses a 95° angular blade plate remains challenging. Such operative techniques that fully expose the fracture and devascularize bone fragments may

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A

B

C

FIGURE 40-9 Highly unstable trochanteric femur fracture in a 20-year-old female medical student who was involved in a motor scooter crash. The unstable fracture pattern (A3 type) with a breach to the lateral wall (arrow in A) mandates fixation with a cephalomedullary nail (B). The fracture healed uneventfully with full weight bearing within 6 weeks (C). The nail was removed after 1 year due to symptomatic hardware.

produce a “nicer x-ray,” but interfere significantly with fracture healing and thus lead to delayed union with loosening or fatigue failure of fixation. The location of a subtrochanteric fracture is important for choosing fixation. If there is a large enough proximal femoral segment to insert a long intramedullary nail, this type of fixation is preferred. If the lesser trochanter is intact, a standard proximal interlocking configuration can be used. If the lesser trochanter is involved, the usual proximal locking screw has insufficient anchorage, and a cephalomedullary (“reconstruction-type”) nail is used instead, with locking screws inserted proximally into the femoral head. If the fracture involves the nail entry site, special care is required for intramedullary fixation. A blade-plate or screwplate device, with indirect reduction technique, may be easier and more reliable. Although technically demanding, indirect reduction techniques with blade-plate or screw-plate devices can leave the fracture site undisturbed and yield predictable healing without bone grafting or high risk of fixation failure. The key to such procedures is that they maintain the soft tissue envelope around the fracture site, thus providing an improved biological environment for healing. This concept was recently advanced by the introduction of angular-stable locking plates for the proximal femur, which can be applied in a less invasive technique and do not compress the bone, thus leaving periosteal vascularization intact.

■ Rehabilitation of Patients with Hip Fractures For all patients with hip fractures, the goals of surgery include maximal restoration of function, maintaining low morbidity and mortality, while rapidly mobilizing the patient

out of bed. Modern surgical techniques usually achieve these ends. Elderly patients may not be able to limit their weight bearing. Therefore, hemiarthroplasty, which offers greater mechanical stability than fracture fixation of osteopenic femoral neck fracture, may be the more appropriate treatment for these intracapsular fractures. Although today’s hip screw devices generally permit weight bearing for patients with intertrochanteric fractures, significant osteoporosis or comminution may require protection until fracture consolidation has occurred. In young patients, limited weight bearing is generally easy with crutches and is routinely advocated initially. Early rehabilitation thus typically involves teaching the patient to do transfers and gait to the point of documenting safe ambulation with crutches or walker. Range-ofmotion and strengthening exercises are routine. Depending on the injury and operative treatment, the patient may need to avoid certain activities such as loading the significantly flexed hip or crossing the legs in a way that might lead to prosthetic dislocation. Nutritional supplementation, prophylaxis against deep vein thrombosis, monitoring and managing intercurrent medical and psychiatric problems, and, in some cases, formal geriatric rehabilitation programs are also beneficial for patients with hip fractures. Early stability of a repaired fracture depends on the quality of reduction, and of fixation, as well as bone density. These factors cannot be assessed by radiographic appearance alone and are not constant from patient to patient. No one is in a better position to judge them than is the surgeon who did the original fixation. Unless union occurs within a reasonable period, any fracture fixation implant will inevitably fail. For subtrochanteric fractures, this may take 6–9 months or more. For these reasons, the operating surgeon remains an essential part of the patient’s rehabilitation team and should direct

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Management of Specific Injuries graded progression of weight bearing and resumption of activities while maintaining personal follow-up.

SECTION 3 X

■ The Future of Hip Fracture Care: Geriatric Fracture Centers Geriatric fracture centers have recently emerged as a new modality for a standardized comanagement of elderly patient with hip fractures, between orthopedic surgeons, hospitalists, and geriatricians. The model is based on the principle that shorter times to surgery will result in less time to develop iatrogenic complications related to prolonged bed rest and unfixated fractures.70 Standardized order sets and protocols are used at each stage of patient care, and discharge planning is already initiated at the time of admission. Frequent communication between the comanaging attending physicians will improve patient care and reduce the incidence of perioperative complications. A recently published retrospective analysis from this program showed that the comanagement of elderly patients with hip fractures and associated comorbid conditions by geriatricians and orthopedic surgeons, based on a standardized protocol of care, leads to shorter times to surgery, fewer postoperative infections and overall complications, and a shorter length of hospital stay, compared with a center with standard level of care in absence of a geriatric fracture management service.70 Based on these promising early findings, the implementation of geriatric fracture centers should likely be promoted as a new cornerstone for the acute management and rehabilitation of elderly patients with hip fractures.

■ Fractures of the Femur Shaft Femoral shaft fractures invariably represent severe injuries due to high-energy trauma and are associated with a significant blood loss of up to 1,500–2,000 mL. Thus, an isolated femur shaft fracture alone can be the cause of a traumatic hemorrhagic shock. Most patients, however, suffer severe associated injuries to the torso, pelvis, and soft tissues. Thus, every femoral shaft fracture must be appraised as a highly critical, potentially lethal injury pattern. Early fixation of femur fractures is essential, in order to avoid or reduce the incidence of complications such as fat embolism syndrome, and ARDS.71 Furthermore, early fracture fixation pays tribute to the intrinsic load to the patient by reducing stress and pain, which represents an important cardiovascular risk factor and may contribute to secondary deterioration of traumatic brain injuries due to increases in intracranial pressure.3,4,32,35,72,73 Intramedullary nailing of a femoral shaft fracture was performed for the first time by the German surgeon Gerhard Küntscher in November 1939. Despite the revolutionary innovation introduced by this new “biological” osteosynthesis, intramedullary nailing of long bone fractures has fallen into oblivion for several decades and had its “renaissance” only in the late 1980s by the introduction of solid and cannulated nails. Currently, the concept of closed reduction and fixation with a reamed interlocked intramedullary nail represents the

“gold standard” for the treatment of femoral shaft fractures (Fig. 40-10). This procedure is associated with about 99% union rates in the literature, a low complication rate, and the possibility of early functional aftercare with weight bearing. Intramedullary nailing provides generally reliable fixation for any femoral fracture with sufficient intact bone proximally and distally. Interlocking screws were adopted to improve control of comminuted fractures. Intramedullary reaming permits use of a larger-diameter nail with larger-diameter locking bolts. Small femoral medullary canals may not permit insertion of an implant with sufficient strength and durability to avoid the risk of fixation failure. As a result, reaming has generally been recommended as a routine. Awareness of intravasation of reaming debris (fat, bone marrow fragments, inflammatory mediators, etc.) has led to concerns that their embolization to the lung might increase the risk of pulmonary complications and induce ARDS.74 Clinical trials and experimental animal studies in recent years have ended the decadelong debate on the clinical relevance of reaming the intramedullary canal as opposed to using unreamed femoral nails.75,76 The current consensus implies that the reaming procedure does in fact not increase the risk of intraoperative and postoperative pulmonary complications.22,23 Thus, the reamed interlocking nail represents the current standard of care for femoral shaft fractures. Further controversy exists on the optimal entry point of intramedullary nails (piriformis vs. trochanter). While the piriformis entry poses a theoretical risk of avascular necrosis due to iatrogenic injury to the nutrient artery, and for an iatrogenic femoral neck fracture due to an incorrect entry point (too anterior and too medial), clinical trials have failed to prove a benefit in outcome for the femoral nails with a trochanteric entry point.77 A newer generation of trochanteric femoral nails has improved the design with regard to a more anatomic bending radius of 150 cm (as opposed to 120 cm in conventional nails) and a 6° angle of the proximal nail segment that allows insertion through the major trochanter. Future clinical studies will have to determine the potential benefits of these new implants, compared with the conventional piriformis nails, with regard to outcome. Severely injured polytrauma patients (ISS 17) as well as patients with a concomitant chest trauma (AIS for chest wall or lung injury 2 pt) or significant head injury (GCS 13) should be treated by the DCO procedure, as described in a previous paragraph. This implies an early fracture fixation by closed reduction and external fixation, followed by conversion to an intramedullary nail during the “time window of opportunity” between days 5 and 10 after trauma. A few highly critical patients with head or chest injuries and persisting morbidity due to increased intracranial pressure or ventilatory problems may be candidates for a minimally invasive “biological” plating of femur shaft fractures.78 This modality strictly avoids any potential second hits to the injured brain or the pulmonary endothelium due to the intramedullary insertion of femoral nails. Intramedullary nailing has been demonstrated to be a safe treatment modality also for open femur fractures (types I, II, and IIIA).

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CHAPTER CHAPTER 40 X

FIGURE 40-10 “True” percutaneous femoral nailing technique by the use of a cannulated femoral nail that is reamed through a small 1 cm proximal skin incision (A). This 51-year-old polytraumatized patient sustained a transverse femur shaft fracture (AO/OTA 32-A3) that was treated by closed reduction and stabilization with an interlocked cannulated femur nail (B–D) and an ipsilateral, comminuted metadiaphyseal proximal tibia fracture (AO/OTA 41-A3.3) that was stabilized by a minimally invasive locking plate (E and F). Both measures are considered “biological” techniques since they spare the soft tissue envelope by the use of minimally invasive skin incisions.

Patients with severe open femoral shaft fractures (types IIIB and IIIC) need individualized decisions about fixation techniques. Preferably, external fixation represents a safe modality for early stabilization of these severe open injuries, followed by conversion to an internal fixation (nail or plate) at the time of definitive soft tissue coverage.

■ Fractures of the Distal Femur The osteosynthesis of supracondylar (AO/OTA type 33-A) and transcondylar distal femur fractures (type 33-C) has represented a significant challenge for a long time, due to high complication rates. A problem unique to these fractures is the loss of fixation of the distal femoral fragment, particularly in osteoporotic bone, by the use of conventional implants, such as the condylar buttress plate. Both the conventional plate osteosynthesis and intramedullary nailing procedures were associated with high rates of primary or secondary loss of

reduction, malunions, nonunions, and infections. The recent emphasis on more “biological” approaches with minimally invasive techniques in conjunction with the development of angular-stable implants that allow the percutaneous placement of locking head screws has resulted in improved outcomes.79 These include increased union rates without the need for additional bone grafting and decreased rates of infection and loss of reduction by the use of minimally invasive or less invasive locked plating techniques or retrograde intramedullary nails (Fig. 40-11). Generally accepted principles of management for articular fractures include anatomic reduction and fixation of the articular surface, with sufficiently stable fixation to permit immediate active and/or passive motion of the joint, and delayed weight bearing until the articular surface has recovered and the fracture has healed sufficiently. A classical implant developed in the 1960s by Maurice Müller in Switzerland is the 95° condylar blade plate that provides sufficient stability

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Management of Specific Injuries

SECTION 3 X B B

A A

E E FIGURE 40-11 A 40-year-old dentist who sustained bilateral femur fractures (A–D) after a high-energy motorcycle crash, with a nondisplaced left extracapsular femoral neck fracture (AO/OTA type 31-B2.1), an ipsilateral femur shaft fracture (32-B1.2), and a proximal pole transverse patella fracture (45-C1.2). The injury on the right side consisted of a distal femur fracture with a comminuted metaphysis and an intra-articular split (33-C2.3). The femoral neck fracture was closed reduced and fixed with a dynamic hip screw (DHS) and an anti-rotation screw on day 1 (D), whereas both femur fractures were stabilized by external fixation for “damage control.” Five days later, the patient was taken back to surgery for conversion to a minimally invasive locking plate on the right side (E and F) and a retrograde femur nail on the left side (G). This latter procedure was chosen due to the impossibility of using an antegrade nail related to the proximal DHS. The bilateral femur fractures showed progressive callus formation within 5 months after injury (H and I) and the left femoral neck fracture was healed at this time (J). The patient was ambulating with full weight bearing bilaterally and a free range of motion of both knee joints.

G G

F F

H H

D D

C C

II

J J

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CHAPTER CHAPTER 40 X

FIGURE 40-12 “Classic” use of a 95° angular blade plate and lag screw fixation of a simple intra-articular and comminuted metaphyseal distal femur fracture (AO/OTA type 33-C2), with primary bone grafting of the metaphyseal bone loss (arrow).

for treatment of distal femur fractures80–82 (Fig. 40-12). However, the technique of blade plating requires a high level of skill and experience and may result in failure if not applied properly (Fig. 40-13). Partial intra-articular fractures of the femoral condyles (AO/ OTA type 33-B) are usually treated by open reduction and internal screw fixation, in order to ensure anatomic reduction of fractures of the articular surface. A typical example is the “Hoffa fracture” that corresponds to a coronal split of the femur condyle (B3 type). Extra-articular components in C-type fractures can often be managed by indirect reduction techniques to restore proper alignment of the articular segment to the limb, relying on proper use of specialized, minimally invasive or less invasive implants, such as the new-generation locking plates.83 However, these new-generation locking plates have been associated with an increased rate of complications related to difficulty of hardware removal, particularly in the case of cold-welded locking head screws.84 Much interest has developed in retrograde intramedullary nail fixation for distal femoral fractures.85 These nails are inserted in a minimally invasive fashion via the knee joint, into the intercondylar notch of the distal femur, and across the fracture site (Fig. 40-11). Fractures of the articular surface must be reduced and fixed first, with precautions to avoid displacement or interference with hardware as the nail is inserted and its

distal and proximal locking screws are placed. Retrograde femoral nail techniques and implants are still evolving. Operations to fix distal femoral fractures can pose formidable technical challenges, especially for the surgeon who does not frequently treat such injuries, with one of the major pitfalls being a malreduction of the distal fragment in varus/valgus or retrocurvatum. However, with appropriate application, this technique is suitable for all fractures of the distal third of the femoral shaft including highly unstable bicondylar fractures without damage to the soft tissues and the knee joint. The primary aim of all surgical techniques applied for fixation of distal femur fractures consists of an early functional rehabilitation, preservation of knee joint range of motion, and an uneventful fracture healing.

■ Patella Fractures Patellar fractures usually result from a direct blow to the flexed knee. Displaced transverse fractures lead to a loss of continuity of the extensor mechanism, which produces extension of the knee both by pulling through the patella (via quadriceps tendon proximally and patellar ligament distally) and through the medial and lateral patellar retinacula. Nonoperative treatment is recommended for undisplaced fractures with a clinically intact extensor mechanism, that is,

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Management of Specific Injuries

SECTION 3 X FIGURE 40-13 Wrong technique of plating for an open (Gustilo–Anderson grade IIIB) distal femur shaft fracture in a 55-year-old patient with an ipsilateral proximal tibia fracture and a “floating knee.” The 95° condylar blade plate—which is designed for lateral insertion for fixation of distal femur fractures—was applied medially through the open wound, leading to a nonreduced fracture and an acute vascular compromise of the femoral artery, as revealed by the postoperative angiography (A and B). Inadequate intraoperative decision making in conjunction with an inappropriate surgical technique led to chain of complicating events that ultimately resulted in an above-knee amputation of the injured extremity (C).

in those cases where the patient can raise the fully extended leg against gravity. In contrast, a surgical treatment by ORIF is generally indicated in cases with a compromised extensor mechanism as well as in displaced fractures with an incongruity of the articular surface. Depending on the exact fracture type, location, and the amount of comminution, repair may involve ORIF by lag screws and tension banding, and rarely by primary partial or total patellectomy. In all cases, the patellar retinacula must be repaired. Treatment of a patellar fracture should allow early range of motion of the knee, but weight bearing on the flexed knee must be prevented until healing is sufficient to tolerate the powerful tensile stresses produced by the quadriceps muscle. The usual postoperative concept consists of mobilization with touchdown bearing for 4–6 weeks and early limitation of knee flexion to about 60°, with progressive increase in the range of motion to about 90° until the fracture is consolidated.

■ Knee Dislocations and Ligamentous Injuries Knee dislocations may involve either the patellofemoral or the tibiofemoral joints. Lateral patellar dislocations typically occur in adolescent females with a genu valgus alignment. True tibiofemoral dislocations are much less common and generally require significant injury forces, although occasionally they are caused by a simple slip and fall. They are important to recognize because of extensive ligamentous disruption and risk of associated neurovascular injuries. A high level of suspicion for these associated vascular injuries is mandatory when evaluating a patient with a tibiofemoral dislocation and the potential for limb loss due to a missed blunt injury to the popliteal artery must be kept in mind (Table 40-1). Patellar dislocations are usually lateral and involve indirect stresses applied by the patient pivoting on or forcefully extending

Lower Extremity injury, which are present in about two thirds of all cases, are outlined in Table 40-1. In cases of a suspected arterial injury, either an (on-table) arteriography or a surgical exploration is mandatory, since observation alone will have detrimental consequences for the patient. Injuries to the peroneal or tibial nerve, with motor and/or sensory impairment, may be associated with an arterial occlusion. Such neurological lesions also interfere with recognition of ischemic pain due to arterial occlusion or an acute compartment syndrome. A popliteal artery injury associated with dislocation of the knee is repaired in the operating room with both vascular and orthopedic surgeons present. Adequate reduction and stabilization of the knee dislocation is required, and external fixation is well suited for provisional stabilization. A simple external fixator, connecting two self-drilling pins in the femur to two similar pins in the tibia with a bridging bar anterior to the knee, can be applied so rapidly that it will not delay arterial repair. It can readily be adjusted to allow intraoperative motion of the knee, should that help with vascular repair, and furthermore provides a nonconstricting splint for postoperative immobilization and protection of the vascular graft. With regard to ligamentous injuries, the currently favored concept of treatment consists of an early, but not immediate, surgical repair. While the incision for arterial repair must be chosen by the vascular surgeon, consideration should be given to the exposure required for secondary ligamentous repair and whether or not this might safely and appropriately be combined with the emergency vascular repair. Trauma teams that treat these relatively rare injuries may manage them more effectively by developing collaborative protocols for knee dislocations with concomitant injuries to the popliteal artery. Below-knee four-compartment fasciotomy is routinely advisable after popliteal artery repair in order to avoid a secondary compartment syndrome due to ischemia–reperfusion injuries. Ligamentous and meniscal injuries without dislocation of the knee may occur in multiple trauma patients or as isolated injuries. Hemarthrosis, swelling, pain, tenderness, and impaired motion of the joint are typical findings. If a knee cannot be examined initially because of adjacent fractures, ligamentous stability must be assessed as soon as those fractures are stabilized. Associated knee injuries are not uncommon with femoral or tibial fractures and particularly when both are present in a so-called floating knee. Inability to passively extend the knee suggests a mechanical block, usually a meniscal tear, whereas instability indicates a ligamentous injury. Both knees should be examined for comparison, because individuals have different amounts of intrinsic laxity. Initial examination of the knee requires x-rays to rule out associated fractures. Aspiration of a tense hemarthrosis under sterile conditions can relieve pain. Complete evaluation may also require arthroscopy or magnetic resonance imaging (MRI) to identify ligamentous or meniscal injuries, but such studies are rarely needed emergently. Although many acute ligamentous injuries of the knee can be treated nonoperatively, major reconstructions may be required to restore function. Accurate diagnosis of ligamentous injuries is crucial for planning appropriate treatment. Relatively infrequent disruptions of the posterolateral ligamentous complex

CHAPTER CHAPTER 40 X

a flexed knee in valgus. A hemarthrosis or effusion soon develops. Recurrent patellar dislocations are not infrequent, because anatomic abnormalities are often predisposing factors. The dislocated patella is palpable laterally, although it may have been reduced by straightening the knee for immobilization or x-ray. Closed reduction, if necessary, is obtained by passively extending the knee, flexing the hip to relax the rectus femoris, and applying medially directed pressure to the patella. Immobilization for 4–6 weeks allows healing of the medial retinacular tear that typically accompanies an initial dislocation, although acute repair of the medial patellofemoral ligament may be considered. Recurrent dislocations should be evaluated for elective surgical reconstruction. Complete knee dislocations usually produce obvious deformity and difficulty moving the involved joint, as well as a radiographically evident dislocation, usually anteriorly or posteriorly, but sometimes medially or with rotation to any quadrant. Multiligamentous injuries in the knee with similar neurovascular concerns may be present without obvious deformity on exam or x-rays. It is often stated that these injuries are dislocations that have spontaneously reduced. Knee instability may be due to a purely ligamentous injury or may involve both ligament disruption and a fracture of the proximal tibia, typically a marginal avulsion (so-called Segond fracture or Moore type III fracture–dislocation) or a fracture of the medial tibial condyle (Moore type I fracture–dislocation).86 Gross instability of the knee in more than one direction is the key diagnostic finding. With a torn articular capsule, hemarthrosis may be absent. With time, however, periarticular swelling is usually evident. Instability of the knee should always be considered when a patient presents with evidence of acute distal neurovascular compromise. A knee dislocation should be reduced as soon as possible after recognition. This can usually be done by traction and gentle manipulation in the emergency department. The early recognition of an associated popliteal artery injury is crucial, which has been described in 14–34% of all cases with traumatic knee dislocations. While a complete arterial disruption may be obvious early after trauma due to clinical signs of peripheral ischemia, an incomplete dissection or intimal injury by stretching forces may be missed. Intimal tears can lead to delayed thrombosis and secondary limb ischemia in spite of the absence of apparent early clinical evidence for a vascular injury. Due to the often asymptomatic nature of blunt popliteal injuries, the amputation rate for blunt vascular trauma is about three times higher than that after penetrating injuries and lies in the range of 15–20%. Thus, a high index of suspicion is required for blunt popliteal injuries in all cases of knee dislocation and defined diagnostic algorithms should help establish an accurate diagnosis early on. Any pulse deficit or measurable reduction in ankle–brachial Doppler-assisted API, before or after manipulation, should be considered evidence of a vascular injury. This includes the reported absence of pulses at the accident site even when pulses return to normal after reduction of the knee dislocation. Based on large meta-analyses in the literature, the accuracy of pulse examination alone is very low, yielding a sensitivity of only about 79% for the detection of an arterial injury.12,87 The five clinical “hard signs” for an arterial

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Management of Specific Injuries

SECTION 3 X

should be repaired within the first 2 weeks. Isolated ruptures of the medial collateral ligament do well with nonoperative management in a hinged knee brace. Delayed reconstruction is often advisable for disruptions of the cruciate ligaments, unless avulsed with a bone fragment, for example, in combination with Moore-type fracture–dislocations of the tibial head.

valgus stress mechanisms of injury, the more severe bicondylar fractures (Schatzker types V and VI) and fracture–dislocations (Moore types I–V) are mainly due to direct high-energy forces with significant soft tissue compromise and a risk for acute compartment syndrome.86 Those fractures are inherently unstable, difficult to reduce and stabilize, and associated with a high rate of complications, such as malreduction, secondary loss of reduction, infections, and nonunions. Isolated fractures of the medial condyle (Schatzker type IV and Moore type I) are more rare and often require special approaches for adequate reduction and stabilization, for example, by a direct posterior approach86 (Fig. 40-14). For the accurate diagnosis of a tibial plateau fracture, routine x-rays of the knee should be complemented by a CT scan with 2D reconstruction, in order to allow an adequate planning of surgical approaches and fixation strategies. Undisplaced

■ Fractures of the Tibia Proximal Tibia Proximal tibia fractures are differentiated as extra-articular metaphyseal fractures (AO/OTA 41-A type), intra-articular tibial plateau fractures (41-B/41-C types and Schatzker classification), and fracture–dislocations (Moore classification). While the typical split-depression-type fractures (Schatzker types I–III) of the lateral condyle are usually due to low-energy, indirect

A

E

C

B

F

G

D

H

I

FIGURE 40-14 Bilateral complex tibia fractures in a 52-year-old lady who sustained a collision as a car driver against a truck. She sustained a severely comminuted tibial pilon fracture on the right side (AO/OTA 43-C3; A and B) as well as a contralateral, unstable bicondylar tibial head fracture (Schatzker type V; E and F). Both injuries were initially immobilized in an external fixator due to the critical soft tissue conditions. Once the soft tissue swelling subsided within 10 days, the fractures were converted to internal fixation. The bicondylar tibial head fracture was stabilized through a direct posterior approach with a posterior antiglide plate and completed by a lateral buttress plating with a locking plate (C and D). The pilon fracture was stabilized by initially fixing the fibula for correct length and rotation and by open reduction of the articular part of the pilon fracture with two lag screws and minimally invasive osteosynthesis with a locking plate (G–I). The patient recovered well without postoperative complications and was non-weight bearing bilateral for 10 weeks.

Lower Extremity

Tibial Shaft Fractures of the tibial shaft range from low-energy, indirect torsional injuries that do well with nonoperative treatment to severe high-energy fractures with severe soft tissue damage and a high incidence of acute compartment syndrome.88 The amount of energy absorbed by the leg is suggested by the radiographic appearance of a fractured tibia. The severity of the soft tissue injury, whether open or closed, is most important for the overall outcome of tibial shaft fractures. For example, the presence of severely crushed soleus and gastrocnemius muscles makes a plastic coverage of an open tibia fracture by a local rotational flap impossible. The soft tissue envelope on the medial border of the tibia is very thin; thus, minor open fractures may have major therapeutic implications for covering the exposed bone, ranging from skin grafts to local or free microvascular flaps, to a lower limb amputation. Compartment syndromes develop frequently in tibial shaft fractures due to direct compression forces. They are especially common if the soft tissues have been crushed or if a period of ischemia has occurred. The initial symptom is leg or ankle pain out of proportion to the physical signs and exacerbated by passive motion of the ankle and toes. Indurated swelling of the calf and, occasionally, the foot is noted. Hypesthesia of the foot and reduced motor strength are due to ischemia of the muscles and nerves within the calf compartments and represent late signs of a (missed) compartment syndrome. Skin perfusion and distal pulses remain intact until late in the evolution of compartmental syndromes, since the obstruction, within the involved spaces, is to capillary rather than arterial flow. The diagnosis is made clinically. Measurements of intracompartmental pressures are required in obtunded or comatose patients and to rule out compartment syndrome in unclear or borderline cases. The treatment for an acute calf compartment syndrome is immediate decompression by a four-compartment fasciotomy, which is performed with medial and lateral incisions. Timing and treatment modalities for tibial shaft fractures are dependent on the severity of injury and associated problems. Limb-threatening complications such as open fractures, vascular injuries, and compartment syndromes require

immediate surgery. In absence of such complications, a provisional closed reduction and application of a long leg cast provide initial immobilization. In tibial shaft fractures of minor severity and dislocation, closed treatment is the method of choice.89 Weight bearing begins as tolerated in the long leg cast, proceeding to a patella tendon bearing short leg cast or brace, as soon as patient comfort and stability of the fracture permit. Although this approach can succeed with more severe tibial shaft fractures, it is often associated with delayed union, deformity, and prolonged disability. Surgical fixation, which provides better control of alignment and allows motion of the foot and ankle, as well as the possibility of earlier weight bearing, is more appropriate for these injuries. Intramedullary reamed nailing is the fixation of choice.88 The indications for intramedullary nailing are increasingly expanding to more proximal and distal metaphyseal fractures due to the availability of new-generation interlocking nails that allow threedimensional interlocking in very proximal and distal areas of the tibia (Fig. 40-15). One of the important risks of extending the indication for tibia nails to the proximal and distal metaphysis is a malalignment in valgus or varus, unless fractures are reduced adequately, for example, by the use of blocking screws. Reaming of the tibial medullary canal permits use of nails with large enough diameters to provide adequate fixation for most tibial shaft fractures. Such nails have large enough diameters to permit the use of locking screws of adequate strength to ensure definitive control of alignment. The strength and fatigue life of smaller-diameter unreamed nails, and especially of their small-diameter locking screws, is not sufficient for keeping the reduction of tibial fractures throughout their healing period.90 Thus, the unreamed tibia nail has been associated with a high risk of complications, such as breaking locking bolts, malunion, and nonunion (Fig. 40-16). Multiple large clinical trials have demonstrated that both the nonoperative treatment and unreamed nailing strategies have the highest incidence of nonunion and malunion, as opposed to fracture fixation by reamed cannulated nails. The use of blocking (“Poller”) screws represents an important intraoperative trick for achieving and maintaining reduction and axial alignment.88,91,92 External fixation is still a valuable technique for selected tibial fractures. These include high-energy trauma with significant soft tissue injury, vascular injuries requiring repair, and in the setting of polytrauma patients, as a “damage control” procedure.4 External ring fixators may furthermore be applied for segment transport in situations with significant bone loss, and for correction of malunions and nonunions. Long-term use of an external fixator (14 days) is associated with bacterial colonization of the pin tracts and a risk of infection from subsequent intramedullary nailing. Use of an external fixator for only a few days, however, can safely precede intramedullary nailing for definitive management of tibial shaft fractures. A variety of fixator designs are available, with no clearly established proof that one is better than another. Generally, transfixion pins or wires are used only in the very proximal or distal zones of the tibia, and “half-pins”—screws with long shafts inserted through the subcutaneous anteromedial surface of the tibia—are used to anchor the external fixator frame

CHAPTER CHAPTER 40 X

proximal tibial fractures can usually be treated with early motion and touchdown weight bearing in a hinged knee brace for 6–12 weeks. The need to stabilize a severely injured limb, especially in a multiply injured patient, can be met initially with a spanning external fixator. Significant deformity of the articular surface, instability, and/or displacement are frequent indications for surgical treatment. To be successful, this must achieve stable fixation and early motion of an anatomically reduced articular surface. Unless these goals can be met, the results of surgery are typically worse than those of nonoperative care. The recent availability of angular-stable locking plates has enabled less invasive approaches and diminished the requirement for primary bone grafting of metaphyseal defects. For example, intra-articular fractures of the lateral plateau (Schatzker types I–III) are nowadays frequently treated by less invasive procedures, whereby the adequacy of articular reduction is intraoperatively assessed by arthroscopic or fluoroscopic control.

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B

FIGURE 40-15 (A and B) A 19-year-old girl who was accidentally shot in the right leg as a victim of a drive-by shooting. She was immediately taken to the OR and treated by local wound debridement and intramedullary fixation of her tibial shaft fracture. She did not have any neurovascular injuries. Her postoperative course was uneventful and she was allowed to ambulate with weight bearing as tolerated on the right side. No postoperative infection occurred.

(Fig. 40-17). Leaving the external fixator in place until the fracture is healed helps prevent the typical complication of late loss of alignment, commonly seen with premature removal of the fixator. Early posterolateral bone grafting may be advisable to accelerate union of tibial shaft fractures with primary bone loss. Plate fixation of acute fractures of the tibial shaft is generally reserved for periarticular injuries too proximal or distal for intramedullary nailing.93 If severe injuries to soft tissue are present, such plating involves a significant risk of sloughing of the incision and/or infection. Techniques of plating that emphasize gentle handling of soft tissues, the avoidance of devascularizing flaps, and use of indirect reduction methods can further reduce the risk of surgical complications of plate fixation.93 Locking plates that allow less invasive or minimally invasive plating techniques are ideal for bridging comminuted metaphyseal fractures that may be too proximal or too distal for intramedullary nailing techniques.

Pilon Fractures Tibial pilon (plafond) fractures are highly challenging intraarticular injuries of the distal tibia that are typically caused by axial loading forces with concurrent distortion and of the ankle, leading to a disruption of the tibial articular surface by

the twisted and rotated body of the talus. Pilon fractures are classified as AO/OTA types 43-B (partial intra-articular) and 43-C (complete intra-articular) (Fig. 40-14). These fractures typically involve a significant damage to soft tissue, whether or not an open wound is present. Traditional ORIF techniques have a high risk of wound dehiscence and infection, particularly if surgery is performed during the phase of post-traumatic inflammation and soft tissue swelling within the first days after trauma. Clinical studies have clearly revealed an improved outcome of tibial pilon fractures when staged procedures are applied, such as early external fixation and later conversion to ORIF once the soft tissue swelling has subsided.94 The concept of definitive surgery for pilon fractures involves a standard technique in four “classical” steps, according to Sommer and Rüedi: (1) plating of the fibula for anatomic length of the lower leg; (2) anatomic reconstruction of the tibial articular surface; (3) bone grafting of the metaphyseal gap; (4) buttress plating of the distal tibia. Depending on the degree of comminution, the individual bone quality, and the extent of soft tissue compromise, the postoperative rehabilitation of pilon fractures is either by early functional after treatment or by immobilization in a lower leg cast for about 6 weeks. As for all metaphyseal fractures, weight-bearing status must be restricted to touchdown weight bearing until the fracture is healed, usually for 10–12 weeks.

Lower Extremity

Ankle Injuries Ankle injuries represent overall the most frequent musculoskeletal injuries. The mechanism and severity of injury has been historically classified by the Lauge-Hansen classification system.95 The ankle is a hinge joint, in which the body of the talus dorsiflexes and plantarflexes within a mortise-like socket formed by the distal tibia (medial malleolus and plafond) and distal fibula (lateral malleolus). Integrity of the mortise is maintained by the ligamentous connections between tibia and fibula, just above the ankle joint (anterior and posterior syndesmosis). Widening of this mortise results in talar instability, which predisposes to post-traumatic arthritis. The lateral malleolus is the prime determinant of talar alignment. Restoration of its proper relation with the distal tibia is “key” to treating malleolar injuries. This may require anatomic ORIF of a displaced lateral

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FIGURE 40-16 Varus malunion of a tibia shaft fracture after failure of fixation with an unreamed interlocking tibia nail. This is a typical complication of the first-generation unreamed solid tibia nails due to the thin diameter of the implant and interlocking bolts.

malleolar fracture and/or restoration of the disrupted syndesmosis by returning the fibula precisely to its location adjacent to the tibia. Stable, minimally displaced lateral malleolar fractures can be managed nonoperatively with closed treatment, typically with about 6 weeks of immobilization, followed by rehabilitative exercises to restore the range of motion. If the ankle is unstable, it will need to be temporarily fixed with a syndesmotic screw until ligamentous healing is secure, usually for 6 weeks. Patients who require syndesmotic fixation have a significantly worse long-term outcome than patients with ankle fractures and a stable syndesmosis.96 Medial ankle disruptions may involve the medial malleolus, which should be reduced and fixed, or the deltoid ligament, which need not be repaired if the remainder of the joint is reduced and repaired properly. Several authors have determined that a widened “medial clear space”—under stress exam or gravity stress test—of more than 4-5 mm represents an indication for surgical ankle fracture fixation.97 The posterior lip of the tibial plafond, the so-called posterior malleolus or Volkmann’s triangle, is frequently fractured in malleolar injuries. The designation of a “trimalleolar” fracture implies those injuries that involve the posterior tibial plafond in addition to the medial and lateral malleoli. Large posterior tibial plafond fractures of more than one fifth of the articular surface should be reduced and fixed to avoid posterior subluxation of the talus and/or incongruency of the joint. Malleolar fractures are produced by indirect forces, generally caused by the body’s momentum when the foot is planted on the ground in one of several typical positions. Depending on the position of the foot and direction of motion, typical combinations of fractures and ligamentous injuries result, with progressively greater damage and displacement, up to and including talar dislocation. Knowledge of these patterns improves the surgeon’s understanding and treatment of such injuries. The basic principle of treatment remains open reduction of displaced injuries, with anatomic reduction and rigid fixation. If significant displacement is present, prompt closed reduction is urgent, while definitive fixation can be delayed, depending on the quality of the individual soft tissue situation. As with pilon fractures, significant swelling is an indication for a delay in surgery to decrease complications with wound healing.98 Some authors have suggested a staged protocol for complex ankle fractures with significant soft tissue compromise, with initial closed reduction and transarticular pin fixation, followed by delayed ORIF once the soft tissue swelling has subsided.99 The soft tissue envelope about the ankle and foot is thin, with little muscle coverage. This renders simple lateral malleolar fractures susceptible to significant soft tissue complications, including skin necrosis, wound dehiscence, and infections. Open fractures of the malleoli may require a microvascular free flap transfer due to the bad quality soft tissue coverage and the impossibility of local rotational flap in this distal area of the leg. Recognition and appropriate management of open ankle injuries is essential to minimize complications and avoid adverse outcomes, which may require a BKA. This notion emphasizes again, as mentioned above for the pilon and tibial shaft fractures, the “key” aspect of the soft tissues for uneventful fracture healing. Ligamentous injuries of the ankle most commonly involve the lateral collateral ligament complex, which provides inversion

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B

C

D

E

F

FIGURE 40-17 Segment transport using an external Ilizarov frame in case of a severely comminuted and contaminated tibial shaft fracture (A and B). After a proximal corticotomy (C and D), the bone loss was replaced by means of a distraction osteogenesis, and the distal docking site healed uneventfully (E and F).

stability of the talus within the mortise. Inversion of the foot normally occurs at the subtalar joint, between the talus and calcaneus. If forced to the limit, however, the lateral collateral ligament stretches or ruptures, producing the typical “sprained ankle” with lateral pain, swelling, and ecchymosis and tenderness over the injured ligament distal and anterior to the lateral malleolus. Minor ankle sprains can be treated symptomatically, with restricted activities, elevation, ice, and support as needed for comfort. More severe sprains require immobilization and/or crutches for comfort and to decrease the risk of late instability, which is manifested by recurring episodes of “giving way” of the ankle. After a brief period of rest, most injuries to the lateral collateral ligament of the ankle are effectively treated with a functional brace. Since it is difficult to differentiate a simple distortion from a fracture in the acute phase, due to nonspecific symptoms such as pain, tenderness, and swelling, a precise diagnosis usually requires adequate radiographs. A “true” AP view of the ankle (so-called mortise view) requires internal rotation of about 15–20° to position the joint axis, which runs between the tips of the two malleoli, in a plane parallel to the x-ray film. The mortise view and a lateral view are usually sufficient to adequately diagnose most ankle fractures. Oblique views and foot

x-rays may be required to identify more occult or associated injuries, such as a base of the fifth metatarsal avulsion fracture, lateral process of talus (“snowboarder’s injury”), or anterior process of calcaneus fractures.

■ Fractures and Dislocations of the Foot Injuries of the foot typically result from a direct blow or crushing force. Extreme dorsiflexion or plantarflexion and rotation outward (pronation) or inward (supination) can also produce significant bony and joint injuries of the foot. These injuries may be unrecognized or underestimated, especially in a multiply injured patient, and a delay in definitive treatment may compromise outcome (Fig. 40-18). Disability due to a significant foot injury is often far greater than that resulting from more dramatic injuries to long bones. Open fractures may result from crushing injuries, which can severely damage the surrounding skin envelope, as well as from lacerations and gunshot wounds.100 Neurovascular structures and tendons may be involved, and their function must be carefully assessed with any injury. Compartment syndromes occasionally develop due to severe crush mechanisms; however, they are much rarer in the foot than in the lower leg.

Lower Extremity

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A

C

B

FIGURE 40-18 Combined navicular fracture–dislocation and metatarsal I Lisfranc dislocation of the left foot (A and B) in a severely injured polytrauma patient. The foot injury was treated by open reduction and internal fixation of the navicular fracture with two 2.0 mm mini-AO screws and a 3.5 mm joint-transfixing screw as temporary arthrodesis (C). This screw was removed after 3 months and the patient could walk with full weight bearing without pain.

A swollen, tender, or painful foot following trauma should be assumed to be a fracture or dislocation until proven otherwise. Radiographs must be obtained to demonstrate suspected or obvious fractures and to locate possible foreign bodies. Major injuries such as tarsometatarsal dislocations often have subtle x-ray findings, while less severe fractures may be quite obvious. Fractures of the talus and calcaneus result from a direct blow to the plantar surface, usually transmitted through the heel. Undisplaced and extra-articular fractures of the calcaneus can be managed nonoperatively. Improved surgical approaches and fixation techniques, coupled with detailed demonstration of the pathologic anatomy of calcaneal fractures provided by CT scanning, have focused surgical treatment on restoration of the typical post-traumatic varus deformity as well as reconstruction of the frequently involved subtalar articular surface (so-called posterior facette) and the calcaneocuboideal joint. Interestingly, large prospective trials have impressively shown that the nonoperative treatment of displaced intra-articular calcaneus fractures

yields similar long-term results as in operative cases where the articular surfaces have been anatomically restored. Furthermore, operative interventions bear a high risk for severe soft tissue complications, since the surgical approach typically dissects through the thin skin envelope over the lateral calcaneus. For this reason, ORIF should be delayed until soft tissue swelling is completely resolved. This may take up to 2–3 weeks for severely displaced and comminuted calcaneus fractures. Displaced fractures and fracture–dislocations of the talus require precise reduction and rigid fixation with an interfragmentary screw. Displaced talar neck fractures represent a surgical emergency due to the high risk of post-traumatic avascular necrosis. This risk gradually increases with the severity of injury, as graded by the Hawkins classification (I–IV). Posttraumatic arthritis and osteonecrosis may require an ankle fusion in the end stage. Isolated, minimally displaced or undisplaced metatarsal fractures are treated nonoperatively. Treatment options include

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a hard-soled stiff shoe and a brace or cast for comfort, with weight bearing allowed as tolerated. Displaced midfoot fractures and dislocations require anatomic reduction, which is best achieved by an open technique. Typical fracture–dislocations at the Lisfranc or Chopart joints require ORIF by temporary arthrodesis, usually with small- or mini-fragment screws for about 3 months. While dislocations of a toe should be reduced promptly, phalangeal fractures generally require little specific treatment. Open fractures of the foot are treated with debridement, repair of critical structures, and fixation of fractures as needed to preserve stability and alignment. Loss of skin at the foot represents a serious problem, which can be addressed in part with skin grafting but may require free tissue transfer or even amputation. Mangling injuries of the toes are usually treated with primary amputation.100

LATE COMPLICATIONS ■ Nonunion A diagnosis of nonunion is made when there is failure of complete healing within a 6- to 9-month time period following definitive fracture care. Fractures have different expected time periods of healing depending on the type of fracture and the location. Tibia fractures are relatively slow healing, particularly open fractures. Femur fractures heal more rapidly. Nonunions complicated by bone loss, significant malalignment, or infection are extremely difficult challenges for the patient and surgeon (Fig. 40-19). Treatment to gain union may require 2–5 years and numerous revision surgeries. Nonunions are categorized as hypertrophic, normotrophic, and atrophic. These distinctions are critical in that they describe the underlying cause of the nonunion and therefore point toward correct treatment options. Hypertrophic nonunions are fractures that have failed to heal in spite of a good local blood supply and obvious formation of callus. Mechanical stabilization alone usually produces union in this situation. Normotrophic nonunions show minimal callous formation but no bony resorption. These need mechanical stabilization and some improvement of the local biology, usually by local autogenous bone grafting. Atrophic nonunions show little to no callus formation and have local bone resorption. The atrophic nonunion has poor local blood supply and will require rigid mechanical stabilization, local bone grafting, and in many cases resection of dead bone and flap coverage. If the bone resection is significant, distraction osteogenesis with a ring or monolateral transport external fixator will be necessary. If deformity coexists with a nonunited fracture, both problems should be addressed simultaneously if possible.

■ Malunion Malunion involves shortening, angulation, and/or malrotation following fracture. While some amount of shortening is well tolerated, shortening greater than 2 cm in the lower extremity requires a built-up shoe to equalize leg length for stance and gait. Elective limb lengthening, contralateral extremity shortening, and even amputation are surgical alternatives to a significant leg length discrepancy. A variety of techniques are available

using external fixators or specialized lengthening intramedullary nails to regain limb length. Rotational and angular deformities may be better tolerated in the femur than in the tibia. Varus or valgus deformity may be cosmetically unacceptable and can produce knee and ankle symptoms that warrant corrective osteotomy. Significant deformity may also predispose to progressive osteoarthritis from asymmetric loading of joints. Malunion of hindfoot or metatarsal fractures may result in painful weight bearing, requiring osteotomy for realignment, with or without arthrodesis of adjacent joints.

■ Sequelae of Joint Trauma Stiffness, ankylosis, and contracture may follow an injury to a joint or to the proximal muscles that control it. Direct injury to articular cartilage, joint malalignment, or incongruity increases the risk of post-traumatic arthritis. Significant arthritis leads to pain with weight bearing and eventually loss of normal functional activities, necessitating joint replacement or fusion. Anatomic reduction and early motion of injured joints provides the best chance of preventing post-traumatic arthrosis. Unfortunately, perfect postoperative reductions do not guarantee perfect functional outcomes. Factors out of the control of the surgeon such as cartilage damage occurring at the time of injury, soft tissue injuries, and postinjury psychological distress have significant impact on the overall outcome. Flexion contractures of the hip, knee, and ankle may occur in patients who do not perform frequent prophylactic extension stretching exercises of these joints. This is particularly true for intensive care patients who remain intubated for extended periods of time. Equinus ankle contractures predictably develop if appropriate splinting and stretching exercises are not provided for the posterior calf muscles. Flexion contractures of the toes may follow injuries to the leg and foot. Passive toe stretching is required to ensure adequate dorsiflexion for normal gait. Toe clawing is the result of contractures of the leg and/or foot muscles following injury, scarring, traumatic neuropathy, or ischemic contractures from a compartment syndrome. Surgical correction may be required. Prevention of contracture with appropriate splinting and early exercises is more effective than late correction. Traumatic arthritis may develop in any injured joint. While ankle and subtalar joint arthrosis is usually evident within a year, the hip and knee may require several years before symptoms are significant. Rapid deterioration of the hip joint may be caused by avascular necrosis, typically after delayed reduction of a hip dislocation or a displaced femoral neck fracture. Avascular necrosis eventually results in segmental joint collapse, typically seen in 1 or 2 years after injury. Pain and disability do not always correlate with x-ray findings. Pain with activity is the typical major symptom of post-traumatic arthritis. If symptoms are not too disabling, then conservative measures such as a cane or brace or intermittent use of anti-inflammatory drugs are indicated. Although arthroplasty of the hip or knee is a satisfactory reconstructive procedure for elderly adults with severe symptoms of traumatic arthritis, there is still no uniformly satisfactory procedure for alleviating the condition in the young, vigorous patient.

Lower Extremity

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FIGURE 40-19 Salvage procedure of an infected subtrochanteric femoral nonunion after osteosynthesis with a 95° condylar blade plate in a 62-year-old male patient who had been previously treated in an outside hospital 7 years prior to admission. Initial x-rays of the right hip reveal a lack of stability due to placement of the condylar blade outside of the femoral neck, with evidence of failure of fixation and osteolytic changes around the screw holes in the femoral shaft (A and B). A staged surgical revision was performed, by hardware removal, radical surgical debridement, and external fixation (C). Intraoperative tissue cultures revealed growth of Enterococcus spp., thus confirming the presence of an infected nonunion. After a 6-week course of i.v. antibiotics, revision blade plating was performed, in conjunction with autologous bone grafting through an RIA harvest from the contralateral femur (D and E). The fracture was clinically and radiologically healed within 4 months after the last revision procedure (F), and the patient was able to ambulate with full weight bearing and minimal residual hip pain.

CONCLUSION Lower extremity injuries have an enormous impact on the acute and long-term functional outcome of the traumatically injured patients. Advances in orthopedic trauma care center on multidisciplinary cooperation and management, with an emphasis on prudently aggressive stabilization of the multiply injured patient. The plethora of effective techniques and approaches to early stabilization mandates an ongoing conversation between the orthopedic surgeon, general/trauma surgeon, and neurosurgeon regarding the management of individual patients. Clearly, in this day and age, the placement of multisystem trauma patients in splints and traction is suboptimal for most major lower extremity injuries. Whether “damage control” external fixation or definitive minimally invasive fixation is chosen, early aggressive care is part of an optimal management paradigm.

Isolated lower extremity injuries can be devastating with potential loss of life and limb or appear to be relatively benign. Unfortunately, nondramatic injuries such as foot fractures can have lifetime consequences and prevent a patient from returning to his or her work and life activities. Therefore, each injury should be carefully evaluated, thoughtfully treated, and followed long term to insure the best possible physical and psychological result.

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4. Stahel PF, Smith WR, Moore EE. Current trends in resuscitation strategy for the multiply injured patient. Injury. 2009;40(suppl 4):S27–S35. 5. Pape HC, Giannoudis PV, Krettek C, Trentz O. Timing of fixation of major fractures in blunt polytrauma: role of conventional indicators in clinical decision making. J Orthop Trauma. 2005;19:551–562. 6. Scalea TM, Boswell SA, Scott JD, Mitchell KA, Kramer ME, Pollak AN. External fixation as a bridge to intramedullary nailing for patients with multiple injuries and with femur fractures: damage control orthopedics. J Trauma. 2000;48:613–621 [discussion 21–23]. 7. Pape HC. Effects of changing strategies of fracture fixation on immunologic changes and systemic complications after multiple trauma: damage control orthopedic surgery. J Orthop Res. 2008;26:1478–1484. 8. Pape HC, Tornetta P 3rd, Tarkin I, Tzioupis C, Sabeson V, Olson SA. Timing of fracture fixation in multitrauma patients: the role of early total care and damage control surgery. J Am Acad Orthop Surg. 2009;17:541– 549. 9. Perren SM. Evolution of the internal fixation of long bone fractures. The scientific basis of biological internal fixation: choosing a new balance between stability and biology. J Bone Joint Surg Br. 2002;84:1093–1110. 10. Helfet DL, Haas NP, Schatzker J, Matter P, Moser R, Hanson B. AO philosophy and principles of fracture management—its evolution and evaluation. J Bone Joint Surg Am. 2003;85-A:1156–1160. 11. Soreide K. Three decades (1978–2008) of Advanced Trauma Life Support (ATLS) practice revised and evidence revisited. Scand J Trauma Resusc Emerg Med. 2008;16:19. 12. Bravman JT, Ipaktchi K, Biffl WL, Stahel PF. Vascular injuries after minor blunt upper extremity trauma: pitfalls in the recognition and diagnosis of potential “near miss” injuries. Scand J Trauma Resusc Emerg Med. 2008;16:16. 13. Miranda FE, Dennis JW, Veldenz HC, Dovgan PS, Frykberg ER. Confirmation of the safety and accuracy of physical examination in the evaluation of knee dislocation for injury of the popliteal artery: a prospective study. J Trauma. 2002;52:247–251 [discussion 51–52]. 14. Stannard JP, Sheils TM, Lopez-Ben RR, McGwin G Jr, Robinson JT, Volgas DA. Vascular injuries in knee dislocations: the role of physical examination in determining the need for arteriography. J Bone Joint Surg Am. 2004;86-A:910–915. 15. Kashuk JL, Moore EE, Pinski S, et al. Lower extremity compartment syndrome in the acute care surgery paradigm: safety lessons learned. Patient Saf Surg. 2009;3:11. 16. Olson SA, Glasgow RR. Acute compartment syndrome in lower extremity musculoskeletal trauma. J Am Acad Orthop Surg. 2005;13:436– 444. 17. Oestern HJ, Tscherne H. Pathophysiology and classification of soft tissue damage in fractures. Orthopade. 1983;12:2–8. 18. Swan KG Jr, Wright DS, Barbagiovanni SS, Swan BC, Swan KG. Tourniquets revisited. J Trauma. 2009;66:672–675. 19. Glass GE, Pearse MF, Nanchahal J. Improving lower limb salvage following fractures with vascular injury: a systematic review and new management algorithm. J Plast Reconstr Aesthet Surg. 2009;62:571–579. 20. Gustilo RB, Mendoza RM, Williams DN. Problems in the management of type III (severe) open fractures: a new classification of type III open fractures. J Trauma. 1984;24:742–746. 21. Rajasekaran S, Naresh Babu J, Dheenadhayalan J, et al. A score for predicting salvage and outcome in Gustilo type-IIIA and type-IIIB open tibial fractures. J Bone Joint Surg Br. 2006;88:1351–1360. 22. Pape HC, Zelle BA, Hildebrand F, Giannoudis PV, Krettek C, van Griensven M. Reamed femoral nailing in sheep: does irrigation and aspiration of intramedullary contents alter the systemic response? J Bone Joint Surg Am. 2005;87:2515–2522. 23. Giannoudis PV, Tzioupis C, Pape HC. Fat embolism: the reaming controversy. Injury. 2006;37(suppl 4):S50–S58. 24. Parrett BM, Matros E, Pribaz JJ, Orgill DP. Lower extremity trauma: trends in the management of soft-tissue reconstruction of open tibia– fibula fractures. Plast Reconstr Surg. 2006;117:1315–1322 [discussion 23–24]. 25. Hallock GG. Utility of both muscle and fascia flaps in severe lower extremity trauma. J Trauma. 2000;48:913–917. 26. Rossaint R, Cerny V, Coats TJ, et al. Key issues in advanced bleeding care in trauma. Shock. 2006;26:322–331. 27. Dewar D, Moore FA, Moore EE, Balogh Z. Postinjury multiple organ failure. Injury. 2009;40:912–918. 28. Ciesla DJ, Moore EE, Johnson JL, Burch JM, Cothren CC, Sauaia A. The role of the lung in postinjury multiple organ failure. Surgery. 2005;138:749–757 [discussion 57–58]. 29. Shimizu T, Tokuda Y. Necrotizing fasciitis. Intern Med. 2010;49: 1051–1057.

30. Bone LB, Johnson KD, Weigelt J, Scheinberg R. Early versus delayed stabilization of femoral fractures. A prospective randomized study. J Bone Joint Surg Am. 1989;71:336–340. 31. Tscherne H. John Border Memorial Lecture. Trauma care in Europe before and after John Border: the evolution in trauma management at the University of Hannover. J Orthop Trauma. 1998;12:301–306. 32. Keel M, Trentz O. Pathophysiology of polytrauma. Injury. 2005;36:691– 709. 33. Giannoudis PV, Veysi VT, Pape HC, Krettek C, Smith MR. When should we operate on major fractures in patients with severe head injuries? Am J Surg. 2002;183:261–267. 34. Stahel PF, Flierl MA, Moore EE, Smith WR, Beauchamp KM, Dwyer A. Advocating “spine damage control” as a safe and effective treatment modality for unstable thoracolumbar fractures in polytrauma patients: a hypothesis. J Trauma Manag Outcomes. 2009;3:6. 35. Gebhard F, Huber-Lang M. Polytrauma—pathophysiology and management principles. Langenbecks Arch Surg. 2008;393:825–831. 36. Ciesla DJ, Moore EE, Zallen G, Biffl WL, Silliman CC. Hypertonic saline attenuation of polymorphonuclear neutrophil cytotoxicity: timing is everything. J Trauma. 2000;48:388–395. 37. Higgins TF, Klatt JB, Beals TC. Lower Extremity Assessment Project (LEAP)—the best available evidence on limb-threatening lower extremity trauma. Orthop Clin North Am. 2010;41:233–239. 38. MacKenzie EJ, Bosse MJ. Factors influencing outcome following limbthreatening lower limb trauma: lessons learned from the Lower Extremity Assessment Project (LEAP). J Am Acad Orthop Surg. 2006;14:S205–S210. 39. Bosse MJ, MacKenzie EJ, Kellam JF, et al. An analysis of outcomes of reconstruction or amputation after leg-threatening injuries. N Engl J Med. 2002;347:1924–1931. 40. Stahel PF, Oberholzer A, Morgan SJ, Heyde CE. Concepts of transtibial amputation: Burgess technique versus modified Bruckner procedure. ANZ J Surg. 2006;76:942–946. 41. Gregory RT, Gould RJ, Peclet M, et al. The mangled extremity syndrome (M.E.S.): a severity grading system for multisystem injury of the extremity. J Trauma. 1985;25:1147–1150. 42. Johansen K, Daines M, Howey T, Helfet D, Hansen ST Jr. Objective criteria accurately predict amputation following lower extremity trauma. J Trauma. 1990;30:568–572 [discussion 72–73]. 43. Bonanni F, Rhodes M, Lucke JF. The futility of predictive scoring of mangled lower extremities. J Trauma. 1993;34:99–104. 44. Bosse MJ, MacKenzie EJ, Kellam JF, et al. A prospective evaluation of the clinical utility of the lower-extremity injury-severity scores. J Bone Joint Surg Am. 2001;83-A:3–14. 45. Ly TV, Travison TG, Castillo RC, Bosse MJ, MacKenzie EJ. Ability of lower-extremity injury severity scores to predict functional outcome after limb salvage. J Bone Joint Surg Am. 2008;90:1738–1743. 46. Bosse MJ, McCarthy ML, Jones AL, et al. The insensate foot following severe lower extremity trauma: an indication for amputation? J Bone Joint Surg Am. 2005;87:2601–2608. 47. Holt G, Smith R, Duncan K, Hutchison JD, Gregori A. Outcome after surgery for the treatment of hip fracture in the extremely elderly. J Bone Joint Surg Am. 2008;90:1899–1905. 48. Moran CG, Wenn RT, Sikand M, Taylor AM. Early mortality after hip fracture: is delay before surgery important? J Bone Joint Surg Am. 2005;87:483–489. 49. Flierl MA, Gerhardt DC, Hak DJ, Morgan SJ, Stahel PF. Key issues and controversies in the acute management of hip fractures. Orthopedics. 2010;33:102–110. 50. Vidal EI, Moreira-Filho DC, Coeli CM, Camargo KR Jr, Fukushima FB, Blais R. Hip fracture in the elderly: does counting time from fracture to surgery or from hospital admission to surgery matter when studying in-hospital mortality? Osteoporos Int. 2009;20:723–729. 51. Ly TV, Swiontkowski MF. Treatment of femoral neck fractures in young adults. J Bone Joint Surg Am. 2008;90:2254–2266. 52. Raaymakers EL. The non-operative treatment of impacted femoral neck fractures. Injury. 2002;33(suppl 3):C8–C14. 53. Zlowodzki M, Bhandari M, Keel M, Hanson BP, Schemitsch E. Perception of Garden’s classification for femoral neck fractures: an international survey of 298 orthopaedic trauma surgeons. Arch Orthop Trauma Surg. 2005;125:503–505. 54. Raaymakers EL. Fractures of the femoral neck: a review and personal statement. Acta Chir Orthop Traumatol Cech. 2006;73:45–59. 55. Marsh JL, Slongo TF, Agel J, et al. Fracture and dislocation classification compendium—2007: Orthopaedic Trauma Association classification, database and outcomes committee. J Orthop Trauma. 2007;21: S1–S133.

Lower Extremity 78. Angelini AJ, Livani B, Flierl MA, Morgan SJ, Belangero WD. Less invasive percutaneous wave plating of simple femur shaft fractures: a prospective series. Injury. 2010;41:624–628. 79. Kao FC, Tu YK, Su JY, Hsu KY, Wu CH, Chou MC. Treatment of distal femoral fracture by minimally invasive percutaneous plate osteosynthesis: comparison between the dynamic condylar screw and the less invasive stabilization system. J Trauma. 2009;67:719–726. 80. Jaakkola JI, Lundy DW, Moore T, Jones B, Ganey TM, Hutton WC. Supracondylar femur fracture fixation: mechanical comparison of the 95 degrees condylar side plate and screw versus 95 degrees angled blade plate. Acta Orthop Scand. 2002;73:72–76. 81. Petsatodis G, Chatzisymeon A, Antonarakos P, Givissis P, Papadopoulos P, Christodoulou A. Condylar buttress plate versus fixed angle condylar blade plate versus dynamic condylar screw for supracondylar intraarticular distal femoral fractures. J Orthop Surg (Hong Kong). 2010;18: 35–38. 82. Higgins TF, Pittman G, Hines J, Bachus KN. Biomechanical analysis of distal femur fracture fixation: fixed-angle screw-plate construct versus condylar blade plate. J Orthop Trauma. 2007;21:43–46. 83. Smith WR, Ziran BH, Anglen JO, Stahel PF. Locking plates: tips and tricks. J Bone Joint Surg Am. 2007;89:2298–2307. 84. Suzuki T, Smith WR, Stahel PF, Morgan SJ, Baron AJ, Hak DJ. Technical problems and complications in the removal of the less invasive stabilization system. J Orthop Trauma. 2010;24:369–373. 85. Ostrum RF, Maurer JP. Distal third femur fractures treated with retrograde femoral nailing and blocking screws. J Orthop Trauma. 2009;23:681–684. 86. Fakler JK, Ryzewicz M, Hartshorn C, Morgan SJ, Stahel PF, Smith WR. Optimizing the management of Moore type I postero-medial split fracture dislocations of the tibial head: description of the Lobenhoffer approach. J Orthop Trauma. 2007;21:330–336. 87. Barnes CJ, Pietrobon R, Higgins LD. Does the pulse examination in patients with traumatic knee dislocation predict a surgical arterial injury? A meta-analysis. J Trauma. 2002;53:1109–1114. 88. Flierl MA, Stahel PF, Morgan SJ. Surgical fixation of extraarticular tibia fractures: tips and tricks. Minerva Orthop Traumatol. 2009;60: 527–540. 89. Sarmiento A, Latta LL. Functional fracture bracing. J Am Acad Orthop Surg. 1999;7:66–75. 90. Finkemeier CG, Schmidt AH, Kyle RF, Templeman DC, Varecka TF. A prospective, randomized study of intramedullary nails inserted with and without reaming for the treatment of open and closed fractures of the tibial shaft. J Orthop Trauma. 2000;14:187–193. 91. Krettek C, Miclau T, Schandelmaier P, Stephan C, Mohlmann U, Tscherne H. The mechanical effect of blocking screws (“Poller screws”) in stabilizing tibia fractures with short proximal or distal fragments after insertion of small-diameter intramedullary nails. J Orthop Trauma. 1999;13:550–553. 92. Shahulhameed A, Roberts CS, Ojike NI. Technique for precise placement of Poller screws with intramedullary nailing of metaphyseal fractures of the femur and the tibia. Injury. 2011;42:136–139. 93. Guo JJ, Tang N, Yang HL, Tang TS. A prospective, randomised trial comparing closed intramedullary nailing with percutaneous plating in the treatment of distal metaphyseal fractures of the tibia. J Bone Joint Surg Br. 2010;92:984–988. 94. Sirkin M, Sanders RW, DiPasquale T, Herscovici D Jr. A staged protocol for soft tissue management in the treatment of complex pilon fractures. J Orthop Trauma. 2004;18(suppl 8):S32–S38. 95. Shariff SS, Nathwani DK. Lauge-Hansen classification—a literature review. Injury. 2006;37:888–890. 96. Egol KA, Pahk B, Walsh M, Tejwani NC, Davidovitch RI, Koval KJ. Outcome after unstable ankle fracture: effect of syndesmotic stabilization. J Orthop Trauma. 2010;24:7–11. 97. Park SS, Kubiak EN, Egol KA, Kummer F, Koval KJ. Stress radiographs after ankle fracture: the effect of ankle position and deltoid ligament status on medial clear space measurements. J Orthop Trauma. 2006;20: 11–18. 98. Ng A, Barnes ES. Management of complications of open reduction and internal fixation of ankle fractures. Clin Podiatr Med Surg. 2009;26: 105–125. 99. Przkora R, Kayser R, Ertel W, Heyde CE. Temporary vertical transarticular-pin fixation of unstable ankle fractures with critical soft tissue conditions. Injury. 2006;37:905–908. 100. Tintle SM, Keeling JJ, Shawen SB. Combat foot and ankle trauma. J Surg Orthop Adv. 2010;19:70–76.

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56. Molnar RB, Routt ML Jr. Open reduction of intracapsular hip fractures using a modified Smith-Petersen surgical exposure. J Orthop Trauma. 2007;21:490–494. 57. Keating JF, Grant A, Masson M, Scott NW, Forbes JF. Randomized comparison of reduction and fixation, bipolar hemiarthroplasty, and total hip arthroplasty: treatment of displaced intracapsular hip fractures in healthy older patients. J Bone Joint Surg Am. 2006;88:249–260. 58. Baker RP, Squires B, Gargan MF, Bannister GC. Total hip arthroplasty and hemiarthroplasty in mobile, independent patients with a displaced intracapsular fracture of the femoral neck: a randomized controlled trial. J Bone Joint Surg Am. 2006;88:2583–2589. 59. Liporace F, Gaines R, Collinge C, Haidukewych GJ. Results of internal fixation of Pauwels type 3 vertical femoral neck fractures. J Bone Joint Surg Am. 2008;90:1654–1659. 60. Fuchtmeier B, Hente R, Maghsudi M, Nerlich M. Reduction of femoral neck fractures in adults: valgus or anatomical position? Unfallchirurg. 2001;104:1055–1060. 61. Bjorgul K, Reikeras O. Hemiarthroplasty in worst cases is better than internal fixation in best cases of displaced femoral neck fractures: a prospective study of 683 patients treated with hemiarthroplasty or internal fixation. Acta Orthop. 2006;77:368–374. 62. Macaulay W, Pagnotto MR, Iorio R, Mont MA, Saleh KJ. Displaced femoral neck fractures in the elderly: hemiarthroplasty versus total hip arthroplasty. J Am Acad Orthop Surg. 2006;14:287–293. 63. Macaulay W, Nellans KW, Garvin KL, Iorio R, Healy WL, Rosenwasser MP. Prospective randomized clinical trial comparing hemiarthroplasty to total hip arthroplasty in the treatment of displaced femoral neck fractures: winner of the Dorr Award. J Arthroplasty. 2008;23:2–8. 64. Blomfeldt R, Tornkvist H, Ponzer S, Soderqvist A, Tidermark J. Comparison of internal fixation with total hip replacement for displaced femoral neck fractures: randomized, controlled trial performed at four years. J Bone Joint Surg Am. 2005;87:1680–1688. 65. Lichtblau S. The unstable intertrochanteric hip fracture. Orthopedics. 2008;31:792–797. 66. Palm H, Jacobsen S, Sonne-Holm S, Gebuhr P. Integrity of the lateral femoral wall in intertrochanteric hip fractures: an important predictor of a reoperation. J Bone Joint Surg Am. 2007;89:470–475. 67. Parker MJ, Pryor GA. Gamma versus DHS nailing for extracapsular femoral fractures. Meta-analysis of ten randomised trials. Int Orthop. 1996;20:163–168. 68. Baumgaertner MR, Curtin SL, Lindskog DM, Keggi JM. The value of the tip–apex distance in predicting failure of fixation of peritrochanteric fractures of the hip. J Bone Joint Surg Am. 1995;77:1058–1064. 69. Hasenboehler EA, Agudelo JF, Morgan SJ, Smith WR, Hak DJ, Stahel PF. Treatment of complex proximal femoral fractures with the proximal femur locking compression plate. Orthopedics. 2007;30:618–623. 70. Friedman SM, Mendelson DA, Bingham KW, Kates SL. Impact of a comanaged Geriatric Fracture Center on short-term hip fracture outcomes. Arch Intern Med. 2009;169:1712–1717. 71. Ciesla DJ, Moore EE, Johnson JL, et al. Decreased progression of postinjury lung dysfunction to the acute respiratory distress syndrome and multiple organ failure. Surgery. 2006;140:640–647 [discussion 7–8]. 72. Pape HC, Grimme K, Van Griensven M, et al. Impact of intramedullary instrumentation versus damage control for femoral fractures on immunoinflammatory parameters: prospective randomized analysis by the EPOFF Study Group. J Trauma. 2003;55:7–13. 73. Harwood PJ, Giannoudis PV, van Griensven M, Krettek C, Pape HC. Alterations in the systemic inflammatory response after early total care and damage control procedures for femoral shaft fracture in severely injured patients. J Trauma. 2005;58:446–452. 74. Hildebrand F, Giannoudis P, van Griensven M, et al. Secondary effects of femoral instrumentation on pulmonary physiology in a standardised sheep model: what is the effect of lung contusion and reaming? Injury. 2005;36:544–555. 75. Hupel TM, Aksenov SA, Schemitsch EH. Effect of limited and standard reaming on cortical bone blood flow and early strength of union following segmental fracture. J Orthop Trauma. 1998;12:400–406. 76. Morley JR, Smith RM, Pape HC, MacDonald DA, Trejdosiewitz LK, Giannoudis PV. Stimulation of the local femoral inflammatory response to fracture and intramedullary reaming: a preliminary study of the source of the second hit phenomenon. J Bone Joint Surg Br. 2008;90:393–399. 77. Starr AJ, Hay MT, Reinert CM, Borer DS, Christensen KC. Cephalomedullary nails in the treatment of high-energy proximal femur fractures in young patients: a prospective, randomized comparison of trochanteric versus piriformis fossa entry portal. J Orthop Trauma. 2006;20:240–246.

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CHAPTER 41

Peripheral Vascular Injury Michael J. Sise and Steven R. Shackford

INTRODUCTION Vascular trauma in the extremities is challenging to manage. The risk to life and limb is high and the margin for error is very thin. The presentation varies from obvious life-threatening external hemorrhage to limb ischemia in the unconscious patient with multisystem injury. An organized approach with well-planned and implemented practice guidelines converts an error-prone process into one of opportunity for effective treatment (Table 41-1). Planning and preparation are essential to the success of this approach in view of the numerous causes of delayed recognition and lack of timely treatment. The need for an organized approach is made even more compelling by the advent of trauma systems and improved prehospital care with the resulting increase in the number of patients with what were previously fatal vascular injuries arriving at trauma centers still alive, but in immediate danger of death.1,2 This chapter reviews the pathophysiology, clinical presentation, diagnostic workup, management, and outcome of extremity vascular injuries. The educational objectives of this review include the following: 1. To identify the mechanisms of extremity vessel injury and the resulting clinical manifestations; 2. To describe an organized approach to rapidly assess injured patients for the presence of extremity vascular injuries; 3. To present management guidelines and examples of checklists to assist in the decision of which treatment options best apply and how to effectively implement them; 4. To articulate management guidelines that result in improved clinical outcomes following extremity vascular injuries; and 5. To present illustrative cases that demonstrate the principles of evaluation and management of peripheral injuries.

THE LESSONS OF WAR The history of the surgical management of extremity vascular injury is laced with the lessons of war. In the beginning of the 20th century, the evolving science and practice of surgery included initial attempts at repairing injured blood vessels. Armed conflicts in the first two decades including the war in the Balkans and the Great War saw large numbers of limbs lost to the ligation of injured vessels with the resulting ischemic tissue loss.3,4 There were reports of successful lateral suture repair and anastomosis of injured vessels, but these techniques were not widely adopted.3 During World War II ligation continued to predominate the management of injured vessels.4,5 It was not until the Korean War that vessel repair by combat surgeons was employed on a widespread basis.6 The timing of arrival of casualties to combat hospital was, in part, a determinant of this successful change in management. Korea was the first conflict in which aeromedical evacuation was widely used. Casualty arrival times decreased significantly and injuries that were previously fatal were managed successfully by surgeons in mobile hospital units.6 In the Vietnam War, the practice of vascular repair coupled with an even more efficient evacuation system led to the development of many of the current techniques and management guidelines in the care of extremity vascular injuries. The Vietnam Vascular Registry maintained by Rich et al. proved a valuable clinical research tool in this process.7 The civilian experience in the subsequent three decades following the Vietnam War further improved the care of extremity vascular injury. The epidemic of urban violence in the 1990s provided urban trauma centers with extensive experience in the management of these injuries.8 The management guidelines and recommendations that resulted steadily advanced the practice of trauma vascular surgery. Surgeons trained in civilian trauma centers went to war in Operations Enduring Freedom and Iraqi Freedom prepared to manage extremity vascular injuries. These combat surgeons took the clinical management one

Peripheral Vascular Injury

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TABLE 41-1 Potential Errors in the Recognition, Preoperative Preparation, and Operative Management of Extremity Vascular Trauma Error Lack of recognition of life-threatening extremity vascular injury when torso workup negative Undetected extremity ischemia Missed compartment syndrome

Preoperative preparation

Operative management

Inadequate resuscitation Lack of documented extremity neurologic examination Fail to give preoperative antibiotics, systemic heparin, when indicated Fail to adequate widely prep and drape and to include uninjured leg Lack of appropriate instruments, sutures, graft material, etc. Absence of orthopedic surgeon, plastic surgeon consultants to plan for operative approach in complex mangled extremity or severe degloving injury extremity injuries Failure to recognize need for damage control techniques Inadequate exposure and control Failure to perform fasciotomy Failure to recognize failure of the vascular repair

Risk Management Reassess all extremity wounds

Use checklist to include extremity pulse exam and Doppler pressures Include extremity exam and pressure measurements for compartment syndrome on checklista Create and follow guideline with appropriate checklist Use checklist with standard documentation form Create and use checklist Create and use checklist Organize, list, and periodically inventory equipment, supplies Include early notification in guideline and checklist

Guideline and checklist to include decisionmaking criteria Guideline and checklist criteria Guideline and checklist criteria Guideline to include intraoperative assessment and postoperative monitoring

a

See examples of checklists in Figs. 41-4 and 41-8.

step further with the widespread use of vascular damage control techniques including intraluminal shunt placement and delayed primary repair.9 The experience gained was brought home to civilian centers with valuable applications in the management of patients with extremity vascular injuries. The lessons of war coupled with the organized approach to trauma management in civilian trauma centers resulted in the guidelines and recommendations included in this chapter.

EPIDEMIOLOGY Vascular injuries of the extremities are infrequent but not uncommon in both civilian and military trauma patients.1,9 They are predominantly a problem in young men in their third and fourth decades.1,2 Whether blunt or penetrating mechanisms, they occur in association with high-risk behavior.1,10 Substance abuse, violence, and late night hours are commonly associated factors in civilian extremity vascular injuries. The trauma center’s rates of blunt versus penetrating injury will

largely determine the most common local causes of these injuries. Civilian centers have a distinctly different pattern of extremity vascular injuries compared with combat medical facilities. Blunt trauma with extremity fractures, small-caliber handguns, and knives cause the vast majority of civilian extremity vascular injuries. In military series, high-caliber rounds and explosive ordinance with shrapnel are the predominant wounding agents. The force, trajectory, and tissue damage associated with military injuries are much more devastating than those seen in civilian series.1,7,9 Survivable vascular injuries are most common in the extremities because of the lethality of torso vascular wounds. Both combat wounds and interpersonal civilian violence yield a significant rate of extremity vascular injuries. Vascular trauma occurs in less than 2% of combatants in military series and in less than 4% of patients in civilian series.1,8,10,11 Overall, vascular injuries occur most commonly in the extremities. This is due partly to selection bias because great vessel injuries of the torso, head, and neck are highly lethal and the patients succumb before arrival at the trauma center.

CHAPTER CHAPTER 41 X

Phase of Care Diagnosis

818

Management of Specific Injuries

SECTION 3 X

The great majority of vascular injuries are due to penetrating trauma. In the recent military experience in the Middle East, 89% of vascular injuries were due to a penetrating mechanism, either fragment wounds from explosive devices (64%) or gunshot wounds (25%).8 Penetrating trauma also predominates in the civilian setting, particularly in some urban environments where the incidence can be as high as 90%, most of which are due to gunshot wounds.1 Rural settings have a higher proportion of blunt injuries, but they still make up less than 45% of the total.10 Vascular injuries do not occur in isolation. Because the vascular structures often lie in close proximity to nerves and bones, associated skeletal and nerve injury occurs in approximately 25% of patients.1,6,7,9 Mattox et al. documented a 400% increase in civilian cardiovascular injuries in Houston between 1958 and 1988, with 50% of all vascular injuries over this 30-year period occurring in the last 10 years of this study.1 The recent decline observed in urban violence has mitigated this trend somewhat, but random shootings with multiple casualties still occur. Iatrogenic arterial injuries continue to increase. This increase parallels the rapid rise in endoluminal procedures, which increased 40% between 1996 and 2003.12 The postprocedure iatrogenic arterial injury rate is now 0.6% and appears to be specialty related.13 Cardiologists have a significantly higher rate (1.3%) than either the interventional radiologists (0.9%) or the vascular surgeons (0.5%).13

PATHOPHYSIOLOGY Arteries and veins are composed of three tissue layers including the outer adventitia of connective tissue, the central media of smooth muscle and elastic fibers, and the inner intima or endothelial cell layer. Trauma to a blood vessel (artery or vein) can produce hemorrhage, thrombosis, or spasm, either alone or in combination, depending on the magnitude of the force applied to the vessel. Hemorrhage occurs when there is a transmural defect—all of the layers (intima, media, and adventitia) are disrupted or lacerated. If the bleeding is controlled by the surrounding tissue (i.e., muscle or fascia), a hematoma is produced, which may or may not be pulsatile. If bleeding is not controlled or tamponaded, exsanguination can occur. Thrombus or thrombosis is produced if there is damage to the intima and the subendothelial tissues are exposed to the bloodstream. Local thrombus may embolize or propagate and eventually occlude the lumen. The injured intima may form a flap that can prolapse into the lumen (as a result of blood flow dissecting under it) producing partial or complete obstruction. Trauma to surrounding bony structures may cause external compression of the vessel, interrupting flow and producing thrombosis. Spasm or segmental narrowing is the result of mechanical trauma, such as occurs if the vessel is stretched or contused (Fig. 41-1). Severe spasm can also be produced by bleeding adjacent to a vessel due to the vasoconstrictive effects of hemoglobin. Spasm, by reducing the cross-sectional area of the vessel, reduces flow. Penetrating injury has a much different pathophysiology than blunt injury. These injuries tend to be more discrete or focal, while blunt injury is more diffuse with injury not only to

Compressed JPEG

FIGURE 41-1 Severe spasm of tibial vessels following blunt force tibia and fibula fracture and internal fixation. After catheter-based nitroglycerin drip for 24 hours, normal ankle pulses and normal CT angiogram with normal caliber and no occlusion of all three calf vessels. Patient made a full recovery.

the vascular structures but also to the adjacent bone, muscle, and nerves. The diffuse nature of the blunt injury not only affects the major arteries and veins but also disrupts smaller vessels that would normally provide collateral flow around an occluded or narrowed vessel. As a result, ischemia is worsened or exaggerated. Penetrating injury is generally classified as low velocity (2,500 ft/s). This includes stab wounds, fragment injuries, and low-velocity gunshot wounds. High-velocity (2,500 ft/s) wounds, such as those caused by a military assault rifle wound, produce significantly more tissue damage than low-velocity weapons due to the energy imparted. The kinetic energy of a wounding missile equals the mass of the projectile multiplied by the velocity squared. The missile creates a rapidly expanding and rapidly contracting cavity that can reach a size equal to 30 times the diameter of the projectile. This occurs at right angles to the missile tract and stretches and tears the adjacent tissue. Fragments of the deteriorating projectile become missiles themselves and cause additional injuries.14 In addition to the acute pathophysiology produced by hemorrhage and thrombosis, trauma can produce subacute or chronic injuries, which may not become apparent for years. The most common of these chronic injuries are arteriovenous fistula and pseudoaneurysm. An arteriovenous fistula typically occurs after penetrating trauma that causes injury to both an artery and a vein in close proximity. The high-pressure flow from the artery will follow the path of least vascular resistance

Peripheral Vascular Injury

into the vein producing local, regional, and systemic signs and symptoms (Fig. 41-2). These include local tenderness and edema, regional ischemia from “steal,” and congestive heart failure if the fistula enlarges.15 A pseudoaneurysm is a result of a puncture or laceration of an artery that bleeds into and is controlled by the surrounding tissue (see Section “Case 6,” Fig. 41-21). The artery remains patent; blood flows into and out of the pseudoaneurysm—much like the ebb and flow of ocean water into and out of a tide pool. They can enlarge and produce local compressive symptoms, erode adjacent structures, or, rarely, be a source of distal emboli.15 Initially, they can be clinically occult, but with time become symptomatic. Not all arterial injuries require an intervention. During the past two decades, it has been convincingly demonstrated that many asymptomatic traumatic vascular injuries have a benign natural history and either completely resolve or remain stable.8,16 At the present time it is impossible to predict which lesions will heal, which will progress and remain asymptomatic, and which will eventually develop either acute or chronic symptoms. Acute interruption of blood flow to an extremity results in a number of systemic pathophysiologic disturbances that may threaten life as well as the affected limb. Ischemia results from a failure of oxygen delivery to meet tissue metabolic needs. The vulnerability of a tissue to ischemia depends on its basal energy requirement, substrate stores, and duration and severity of the ischemic insult. Peripheral nerves are most vulnerable to ischemia because they have a high basal energy requirement and virtually no glycogen stores. Therefore, motor and sensory deficits are often the first manifestations of arterial occlusion. Skeletal muscle is more tolerant of decreased blood flow; histologic changes are not evident unless ischemia has been present for 4 hours. Reversible changes occur in 4–6 hours following onset of ischemia if reperfusion is established by the end of that interval. The more complete the interruption of arterial inflow,

■ Compartment Syndrome One of the most devastating early complications of extremity vascular injury is compartment syndrome. All muscle compartments in the extremities are vulnerable to intracompartmental hypertension that can lead to muscle necrosis. This may occur primarily from decreased perfusion and ischemia, secondary to intracompartmental hemorrhage from direct trauma, or after successful revascularization with reperfusion edema. Compartment syndrome results from swelling of muscle in a confined space (i.e., bound by inflexible structures such as fascia and bone) due to either reperfusion or crush injury. This swelling increases the tissue pressure within the confined space or “compartment” compressing both venous and lymphatic outflow as well as arteriolar inflow, further increasing tissue pressure and reducing perfusion, ultimately resulting in ischemic neurolysis and myonecrosis if unrecognized and not treated promptly. Compartment syndrome occurs most commonly in the muscle compartments of the lower leg. It may be life threatening because of the systemic effect of rhabdomyolysis, myoglobin-induced renal failure, and hyperkalemia.8,19 Proximal extremity venous obstruction accentuates the rise in compartmental pressure and is often a major contributing factor to compartment syndrome The anterior compartment of the calf is the least compliant area of muscle surrounded by fascia in the extremities and is the most vulnerable to compartment syndrome. Acute complete traumatic occlusion or ligation of the popliteal vein may cause enough increase in compartment pressure to cause compartment syndrome, particularly in the anterior compartment. The upper extremity has more extensive venous drainage and is less prone to develop compartment syndrome than the lower extremity following venous occlusion or ligation. Compartment syndrome follows less than 10% of brachial

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FIGURE 41-2 Acute axillary artery pseuodoaneurysm and arteriovenous fistula following stab wound in right axilla. Vessels repaired by simple closure.

such as occurs with occlusion of a major arterial conduit and disruption of collateral vessels, and the longer the duration of interrupted flow, the greater the potential for irreversible ischemic damage. After prolonged complete ischemia, damage may be extended rather than reversed by reperfusion. Reperfusion injury is initiated with the reintroduction of oxygen and the conversion of hypoxanthine, a metabolite of ATP in ischemic tissue, to xanthine with the generation of the highly reactive superoxide and hydroxyl radicals. Leukocytes are thought to be the major source of free radicals in reperfused muscle. Such radicals and reactive oxygen species attack cell membrane lipids, proteins, and glycosaminoglycans, disrupting the integrity of the capillary, resulting in microvascular occlusion and elevated interstitial fluid pressure. This leads to a “no-reflow” phenomenon, and, ultimately, to irreversible ischemia and necrosis of both nerve and muscle.17 With muscle necrosis or rhabdomyolysis, myoglobin and potassium are released into the circulation, which may lead to fatal arrhythmias and renal failure. Thus, in addition to potential local and regional effects on limb dysfunction and limb loss, acute interruption of extremity blood flow can have systemic consequences of organ failure and death if not recognized promptly and treated aggressively.18,19

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artery injuries and is not a complication of upper extremity venous ligation unless there is extensive soft tissue injury.20,21 Although the anterior compartment and forearm are the most susceptible areas, compartment syndrome may occur in any area of extremity muscle including the foot, hand, thigh, upper arm, and buttocks.

■ Missile Emboli Intravascular migration of bullets, shotgun pellets, and other foreign bodies is uncommon and occurs in less than 1% of extremity vascular injuries.22,23 The most common occurrence is the migration of small-caliber shotgun pellets from the proximal extremity veins through the right side of the heart and into the pulmonary circulation. Larger bullets may enter arteries and embolize to distal vessels causing ischemia. Bullets that enter the great veins may embolize proximally to the heart or, by the force of gravity, travel in a retrograde fashion into the lower extremity veins. Diagnosis requires a high index of suspicion and a thorough peripheral vascular examination. Entrance wounds without associated bullets on radiographs should raise the alert that bullet embolism may have occurred. Extremity radiographs or fluoroscopy should be performed to rule out bullet embolism when they are unaccounted for in proximity to entrance wounds or along suspected trajectories within the patient. Acute limb ischemia requires prompt operation for bullet retrieval. In the absence of limb threat, angiography and snare deployment under fluoroscopy can be successful in bullet retrieval. A cutdown under local anesthesia at the snare introduction site is usually required to remove the retrieved bullet. Asymptomatic small-caliber shotgun pellets in the extremities are best left alone.

PROGNOSTIC FACTORS There are a number of factors that are significant in determining the outcome of extremity vascular injury. These include the location of the injury and mechanism, amount of hemorrhage, severity of associated musculoskeletal injury, time interval between injury and control of hemorrhage and restoration of flow, and the preexisting health status of the patient. All of these factors influence outcome and need to be considered in the management of extremity vascular injury. However, the most critical factor remains the time between injury and control of hemorrhage and restoration of flow. This generates a time urgency in the diagnostic workup and treatment of these injuries that must always be part of the management strategy. Both recent military and civilian series demonstrate the importance of timely treatment in successful limb salvage following vascular injury in the extremities.1,7,9,24 Delays beyond 6–12 hours were associated with a rise in limb loss from 22% to 93% in a recent combat series. The association with musculoskeletal and soft tissue trauma also impacts this salvage rate because of the loss of collateral circulation. These recent reports reaffirm the tradition concept of a “golden period” of 6–8 hours following extremity vascular injury in which adequate flow must be established to avoid limb loss.

Not only do blunt mechanisms of injury cause greater damage to extremity vessels and surrounding structures than penetrating trauma, but their effects are also more widely distributed up along the course of the extremity and often involve associated significant torso injuries. These injuries are more likely to be difficult to diagnose than more clinically obvious and often localized penetrating injuries. Major torso injuries divert attention away from the extremities and the overall trend is for a delay in the recognition of blunt vascular injuries. This delay compounds the already worsened outcome because of the commonly associated soft tissue and musculoskeletal blunt force injuries. In penetrating injuries, the wound force of gunshot wounds varies according to the type of projectile and, more importantly, its velocity. High-velocity, assault weapon–style injuries are extremely destructive in the extremities and have a high associated limb loss rate. Civilian handgun wounds with their low velocity have a much better prognosis. Knife wounds remain the least destructive mechanism of vascular injury and are often the easiest to manage. However, in the upper extremity, the association of median nerve injury with brachial artery lacerations negatively impacts overall functional outcome. The muscle mass and collateral flow is significantly different in the upper versus lower extremities. The arm tolerates arterial occlusion much better than the lower extremity with its large muscle groups, greater length, and relatively poor collateral flow. Amputation rates in the lower extremity are approximately double those in the lower extremity following traumatic arterial occlusion in both military and civilian series.1,7,9 Both brachial artery and popliteal artery occlusions, however, have a very high risk of eventual limb loss and require the same expeditious workup and treatment. The disparity in size and collateral blood flow between the extremities also makes complications including compartment syndrome and the venous insufficiency more likely and more morbid in the lower extremity. However, because of the importance of hand function, the long-term effects of nerve damage are much more consequential in the upper extremity.

CLINICAL PRESENTATION The presentation of extremity vascular injury varies from obvious life-threatening external hemorrhage from penetrating injury to occult extremity ischemia from blunt force arterial disruption and occlusion. A history of active bleeding, hematoma, or the findings of arterial occlusion and ischemia are present in most extremity vascular injuries.1,7,9,25–27 Less commonly, extremity vascular occlusion is masked by the presence of multisystem torso and extremity injuries. Failure to systematically evaluate the extremities with a clinical vascular exam augmented by Doppler studies is one of the most common causes of preventable limb loss. Blunt force injury resulting in extremity fracture must always be assumed to place the regional vascular structures at risk for injury. Fracture and dislocation patterns are also key indicators of the risk of extremity vascular injury. In the upper extremity, supracondylar humerus fracture is associated with a risk of brachial artery laceration. In the

Peripheral Vascular Injury

DIAGNOSTIC EVALUATION ■ Physical Examination A thorough physical examination with careful palpation of extremity pulses remains the basis for accurate and timely diagnosis of extremity vascular injury. This includes a vascular and neurologic examination of each extremity with careful palpation of peripheral pulses, assessment of color, warmth, and capillary refill. There is an unfortunate tendency to “overcall” the presence of pedal pulses. Once any examiner calls a pulse present when it is, in fact, absent, a cascade of errors may be initiated that result in limb-threatening ischemia. When in doubt, declare the pulse absent and add adjunctive assessment measures to make certain adequate perfusion is present. There are very distinct physical findings that clearly indicate the presence of extremity vascular injury. In addition to these “hard signs,” there are less obvious but equally important “soft signs” that should bring attention to the possibility of extremity vascular injury (Table 41-2). The hard signs indicate a high probability of major vascular injury requiring immediate surgical

TABLE 41-2 “Hard” and “Soft” Signs of Vascular Injury Hard

Indicate need for operative intervention • Pulsatile bleeding • Expanding hematoma • Palpable thrill • Audible bruit • Evidence of regional ischemia – Pallor – Paresthesia – Paralysis – Pain – Pulselessness – Poikilothermia

Soft

Suggest need for further evaluation • History of moderate hemorrhage • Injury (fracture, dislocation, or penetrating wound) • Diminished but palpable pulse • Peripheral nerve deficit

repair.25–27 Lack of recognition of these hard signs of vascular trauma on the initial evaluation of injured extremities is the most common reason for the development of limb-threatening complications.1,19,24 The presence of soft signs of vascular injury mandates further workup with vascular imaging techniques and, less frequently, surgical exploration.25,26 Doppler assessment of pulsatile flow in the extremity is the primary adjunctive measure to physical examination. The experienced examiner can assess flow based on the character of the audible Doppler signals. However, the best way to use the Doppler device is in conjunction with a systolic blood pressure determination. The manual blood pressure cuff is placed at the wrist or ankle in the injured extremity and the probe placed over the distal vessel. The cuff is slowly inflated and the cessation of signal indicates the systolic blood pressure at the level of the cuff. The uninjured contralateral extremity and an uninjured arm pressure are determined. The normal ankle–brachial index is 1.1. Unless the patient has preexisting peripheral vascular occlusive disease, the ankle– brachial index should be at least 0.9 and there should be less than a 20 mm Hg difference between extremities.28 An absolute pressure below 50–60 mm Hg at the wrist or ankle indicates immediate limb-threatening ischemia in the patient with a normal systemic blood pressure. Beware the patient with advanced peripheral vascular disease, particularly if it is related to diabetes. Calcified extremity vessels are noncompressible and cannot be occluded by inflation of the blood pressure cuff (even with inflation pressures of 200–300 mm Hg), resulting in a falsely elevated systolic pressure. Physical examination may be unreliable in the detection of compartment syndrome. This is particularly true in patients with altered mental status from injury, intoxication, or medication and who have a lower extremity neurologic deficit. When present, pain on passive stretch or pain out of proportion to

CHAPTER CHAPTER 41 X

lower extremity, posterior knee dislocation carries a high risk of popliteal artery injury. The presence of unexplained hemorrhagic shock in patients without evidence of head, neck, or torso injury should redirect attention to apparently trivial extremity lacerations. This is particularly important in wounds in the antecubital fossa, groin, and popliteal fossa. Initial external hemorrhage from laceration of the regional vessels may have led to hypotension with subsequent thrombosis and cessation of bleeding. There is the potential for large extremity dressings to mask recurrent hemorrhage after restoration of circulating blood volume and these should be promptly removed to assess the underlying wounds. Delayed presentation of major complications of extremity vascular injury, although uncommon, should be considered in all blunt and penetrating extremity wounds. The tertiary survey later on the day of admission or the next morning should include a reassessment of extremity blood flow. This includes palpation of the distal pulses, assessment of the extremity for hematoma or muscle tenderness, and, if appropriate, Doppler interrogation of flow. No cast or dressing placed by an orthopedic surgery colleague should be left in place if there is any question about the adequacy of blood flow or the possibility of a missed vascular injury. Compartment syndrome may develop insidiously. Irreversible tissue damage can occur in the absence of clinical signs and symptoms. When present, pain on passive stretch or pain out of proportion to findings should alert the examining physician to the possibility of compartment syndrome. Palpable distal pulses remain intact long after muscle blood flow has ceased in the compartment with tissue pressures above 25 mm Hg. Muscle and nerve necrosis can occur well before major arterial inflow is occluded. Therefore, the pulse examination is not sufficient to detect the development of a compartment syndrome. Measurement of compartment pressure is the only reliable means of detecting the presence of compartment syndrome.

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Management of Specific Injuries findings should alert the clinician to the possibility of compartment syndrome. In such cases it is best to directly measure the compartment pressures.

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■ Arteriography The traditional debate over the role of preoperative arteriography for patients with extremity vascular injury was based on two key facts. First, there are many injuries easily and accurately diagnosed by physical examination and, second, time can be lost in obtaining formal catheter angiography leading to prolonged ischemia and poor outcome. There remain a significant number of extremity vascular injuries that are best managed by immediate operation and in which arteriography may be a needless waste of time and resources. There is an arteriogram time equation that should be considered in the workup of these injuries. Is the information obtained worth the time delay in restoring flow in the ischemic limb? Even if there is an angiogram suite on standby, ready to go, it requires a minimum of 90 minutes to obtain formal arteriography. The second part of this calculation answers the question: will the arteriogram direct the choice of operative versus nonoperative therapy or focus the operative approach to improve outcome? Multilevel blunt extremity injuries associated with ischemia and multiple penetrating injuries to an extremity (such as occurs with wide pattern shotgun blast injury) fall into this category and, thus, necessitate contrast imaging. The advent of widely available high-resolution multidetector CT angiography has radically changed the approach to contrast imaging for extremity vascular trauma and made the old debate largely irrelevant. Catheter arteriography for the evaluation of injured extremities has become relatively uncommon at most trauma centers. High-resolution CT scanning with the appropriate imaging protocols produces rapidly available visualization of extremity vessels that rivals that of catheter arteriography (see Section “Case 6”). This results in images available in minutes rather than hours. The reluctance to perform catheter angiography in the past because of this delay has been replaced with a liberal use of CT angiography. The indications remain the same for both methods of vascular imaging (Table 41-3). However, in diffuse extremity injury from shotgun wounds, catheter-based angiogram may be

TABLE 41-3 Indications for Arteriography in Patients with Extremity Injuries Blunt force injury Multilevel extremity fractures with distal ischemia Crush injury with diminished blood flow Extensive hematoma with intact distal flow Presence of a thrill or bruit over an area of injury Penetrating injury Significant hematoma in proximity to wound with intact distal flow Multilevel penetration from a shotgun blast Presence of a thrill or bruit over an area of injury

TABLE 41-4 Technique for “Single-Shot” Extremity Arteriography 1. Place a radiograph cassette beneath the area of concern in the extremity 2. Insert and hold steady an 18 gauge needle or short 16 gauge catheter in the femoral or axially artery 3. Aspirate blood to the level of the syringe containing contrast to avoid air bubbles 4. Rapidly inject 20 mL of full-strength intravenous contrast agent for the leg, and 10 mL for the arm 5. Delay x-ray exposure for 2 seconds for the proximal upper extremity and proximal thigh, 3 seconds for the forearm and distal thigh, 4 seconds for the popliteal level, and 5 seconds for the tibial vessels 6. Fluoroscopy with the digital subtraction angiography mode may also be used

more accurate than CT angiography because of the scatter effect of the numerous metal projectiles that obscure the arterial lumen. Also, catheter angiography remains essential in those patients who may require an endoluminal therapy, such as infusion of a vasodilator or placement of a covered stent, at the time of the diagnostic angiogram. Patients with spasm without significant arterial wall injury may benefit from this added capability. Single-injection arteriogram in the trauma room or operating room is a quick and accurate method of definitive imaging in unstable patients with associated torso injuries or multilevel extremity injuries who require immediate operation. This simple and direct technique is quickly performed and effective in the unstable patient with multiple injuries who needs prioritization of management by evaluating extremity blood flow (see Section “Case 7,” Figure 41-27). The technique of trauma resuscitation room arteriogram is described in Table 41-4.

■ Noninvasive Evaluation The widespread availability of duplex scanning led to its application in the workup of vascular imaging.28 However, it has not proven useful in the diagnosis of acute arterial injury because it requires the presence of a skilled vascular technologist to perform the test and an experienced provider to interpret the study—neither of which is usually available on an expedient basis. Duplex color flow imaging has great usefulness in the diagnosis of chronic injuries, such as pseudoaneurysms and arteriovenous fistulae, and in the postoperative follow-up of vascular repairs.

■ Practice Recommendation for Extremity Vascular Diagnostic Evaluation An outline of the recommended approach to the prompt diagnosis of extremity vascular injury is detailed in Fig. 41-3. Physical examination remains the most important element of this process. Common sense dictates that those with obvious

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FIGURE 41-3 Diagnostic evaluation of extremity vascular injury.

injury go directly to the operating room to delineate and repair the injury. Imaging with either high-resolution CT angiogram or catheter arteriography must make sense in terms of the expense of time and the value of the results in deciding and directing the operative approach.

MANAGEMENT ■ Minimal Vascular Injury and Nonoperative Management The widespread application of arteriography in the evaluation of injured extremities results in the detection of clinically insignificant lesions. There is now an extensive body of experience with lesions that are not clinically significant. These minimal vascular injuries include intimal irregularity, focal spasm with minimal narrowing, and small pseudoaneurysms. They are often asymptomatic and usually do not progress. A small, nonocclusive intimal flap is the most common clinically insignificant minimal vascular injury. The likelihood that it will progress to cause either occlusion or distal embolization is approximately 10–15%.16,29 This progression, if it occurs, will be early in the postinjury course. Spasm is another common minimal vascular injury. This finding should resolve promptly after initial discovery. Failure of the return of normal extremity perfusion pressure indicates that a more serious vascular injury is

present and intervention is needed. Small pseudoaneurysms are more likely to progress to the point of needing repair and must be actively followed with duplex color flow imaging. Arteriovenous fistulae always enlarge over time and should be promptly repaired. Considerable evidence suggests that nonoperative therapy of many asymptomatic lesions is safe and effective. However, successful nonoperative therapy requires continuous surveillance for subsequent progression, occlusion, or hemorrhage. Operative therapy is required for thrombosis, symptoms of chronic ischemia, and failure of small pseudoaneurysms to resolve.

■ Endovascular Management The use of endovascular therapy for the treatment of atherosclerotic arterial disease has become widespread. What began as a simple balloon dilation in the common iliac arteries over 30 years ago has grown to include a wide variety of techniques. Whether it is endoluminal stent deployment for occlusive lesions or aortic aneurysms, there is a strong tendency to generalize from the elective use in nontrauma patients to the treatment of acute vascular injuries. Almost every major trauma center has its share of cases successfully treated with the use of elective techniques for acute vascular lesions. However, the evidence to support these approaches is not well developed and there have been problems. A review of available evidence combined with common sense should help define the current role of endovascular management of traumatic injuries.8,30,31

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Extremity vascular injury resulting in hemorrhage is best treated by promptly performed open surgical techniques. The use of stent grafts in the extremity vascular injuries is becoming more common.30,31 However, the results are not yet well documented. Caution may well be the best approach. Covered stents are easily placed in partially occluded vessels and although they have initially favorable early patency rates, they are prone to occlusion. In comparison, autologous vein interposition grafts have excellent long-term patency rates and remain the gold standard for vascular repairs in the extremities. Catheter-directed therapies for hemorrhage from branch vessels in the extremities can be effective in successfully managing these injuries. These measures, in addition to ultrasoundguided thrombin injection, are effective in iatrogenic acute pseudoaneurysms following invasive procedures; this approach is not effective in most extremity vascular injuries. The small hole in the artery following removal of an arterial sheath is very different than the larger defects seen with vascular trauma. The risk of complete arterial thrombosis or distal emboli is high with this approach.8,19

Who Should Perform Endovascular Repairs Have the right person do the right thing in the right place at the right time. This simple rule needs to apply at all times. Endovascular surgery, like all operations, should be performed by readily available trained clinicians. In most centers this includes the interventional radiologist. Other centers have catheter-trained vascular surgeons and a few others have trauma surgeons who are capable of performing catheter-based vascular interventions. It does not require a fully capable endovascular operating room suite to perform endovascular techniques. A modern digital C-arm with digital subtraction angiography capability for fluoroscopy, lead aprons for the OR team, and the appropriate guidewires and catheters turns any OR into an endovascular capable room. However, this cannot be improvised the first time it is needed. Planning and preparation are essential for success. A team approach is essential to be ready for the opportunity to perform endovascular techniques when indicated. This approach is most successful in centers with an active elective endovascular program.

Operative Management The successful operative management of extremity vascular injuries requires both prompt control of hemorrhage and timely restoration of adequate perfusion. These priorities must be orchestrated with the overall care of the patient. Both adequate resuscitation and the role of damage control are important factors in the management of extremity vascular injuries. Secondary considerations include adequate tissue coverage of repair sites, orthopedic surgical procedures, the prevention of compartment syndrome, early recognition of thrombosis of repaired vessels, and wound management. Minimal vascular injuries may be successfully managed nonoperatively with careful observation. There is also a limited, but emerging, role for endovascular therapy.

Who Should Perform Vascular Trauma Surgery In an era of fewer open vascular procedures and falling numbers of major vascular cases performed during surgical training, the repair of extremity vascular injury may not be within the reasonable practice capabilities of many trauma surgeons. Operative procedures to manage vascular injuries should be limited to those surgeons who are capable, experienced, and qualified. This is not a trivial matter. Board certification in vascular surgery is not enough to qualify a surgeon as capable to handle these injuries just as the lack of certification does not necessarily disqualify a surgeon. Many surgeons who perform elective vascular surgery are not sufficiently experienced in the management of vascular trauma. Conversely, there are many trauma surgeons who are very skilled in vascular technique by virtue of their interest and experience. Surgeons with experience in vascular techniques and management of vascular injuries need to be available at all trauma centers to deal with these challenging injuries. This may be provided by members of the primary trauma on-call panel or vascular surgery specialists available on a backup call panel.

■ Preoperative Preparation Successful operative management of extremity vascular injuries requires a systematic approach with careful preparation. This process is very amenable to a checklist to assure thorough preparation and to avoid errors (Fig. 41-4). There is considerable risk involved if the care of the extremity vascular injury is not properly orchestrated with the overall care of the patient. This begins with airway control, adequate intravenous access, and availability of blood products. The administration of these blood products, however, should not begin before obtaining control of hemorrhage unless the patient is profoundly hypotensive.32–34 Damage control resuscitation with permissive hypotension, avoiding unnecessary fluid infusion, prompt hemorrhage control, and restoration of blood volume with blood products is the best approach in patients with hemorrhagic shock. If the blood pressure remains below 80–90 mm Hg, the goal should be to provide adequate volume restoration with type O-negative packed cells and type AB fresh frozen plasma infusion to support prompt transport to the operating room for definitive hemorrhage control. Volume infusion that raises the blood pressure above a systolic of 90–100 mm Hg may increase bleeding and negatively impact outcome particularly if the infusion delays transport to the operating room.33,34 Crystalloid infusion risks causing both recurrent hemorrhage and dilutional coagulopathy and should be avoided. There is evidence that, once hemorrhage is controlled, restoring blood volume by transfusion with equal ratios of units of packed cell, fresh frozen plasma, and platelets improves outcomes.35 Extremity hemorrhage from vascular injuries requires prompt control. There are a variety of commercially available disposable tourniquets that are very effective in providing temporary control. The favorable results from the widespread use of tourniquets in Operations Enduring Freedom and Iraqi Freedom are compelling.9 There should be no hesitation to use them when indicated in the care of civilian injuries. However,

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FIGURE 41-4 Preparation checklist for extremity vascular repair.

proper use requires appropriate placement on the extremity proximal to the area of injury with sufficient pressure to occlude flow without crushing tissue. The time of placement should also be carefully recorded to keep track of occlusion time and avoid permanent damage from ischemia and delayed restoration of adequate flow. There is no role and no need for blind clamp placement in the injured extremity with active hemorrhage. Properly placed tourniquets or a gloved hand compressing the bleeding site during transfer to the operating room is the only appropriate measure. There is also no role and clear danger involved in local wound exploration in the trauma resuscitation bay for vascular control. The operating room with all its capabilities is the proper place for exposure and control. Preoperative preparation should include the administration of broad-spectrum preoperative antibiotics and, if there is a penetrating wound or open fracture, tetanus toxoid. If there is an isolated extremity injury without significant hemorrhage, a bolus of 5,000 U of heparin should also be given intravenously. However, avoid systemic heparinization in patients with head, torso, or multiple extremity injuries. The most commonly omitted step in preparation to repair extremity vascular injury is a failure to document preoperative extremity neurologic examination findings. The presence of a neurologic deficit after operative

vascular repair without knowing the preoperative status presents a very difficult management challenge. This may prompt unnecessary reexploration. A new neurologic deficit after vascular repair merits investigation and, possibly, reoperation. Therefore, a thorough preoperative neurologic examination and careful documentation are needed to compare with postoperative status and effectively manage potential complications. Early involvement of orthopedic surgery and plastic and reconstructive surgery colleagues is essential in the presence of fractures or extensive soft tissue injuries associated with extremity vascular injuries. Consultation should be undertaken immediately on recognition of these injuries to involve these specialists in preoperative planning and intraoperative decision making. The sequencing and conduct of the operation should also be discussed with these colleagues.36 For example, the initial use of temporary vascular shunts to reperfuse an injured extremity followed by orthopedic stabilization can remove the sense of urgency to definitively restore blood flow. Extensive soft tissue injuries may compromise the proper coverage of vascular repairs and fracture fixation. The choice of definitive internal fixation versus external fixation of fractures requires consideration of both the vascular repair and the extent of soft tissue injury and plans for coverage and reconstruction. The

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discussion and subsequent decision making is a preoperative step that cannot be deferred without risking the ultimate successful outcome. Once operative priorities have been established in patients with extremity vascular injuries, it is important to communicate with the operating room. Proper preparation includes the availability of the appropriate instrument sets, appropriate positioning of the patient, availability of sutures and graft material, and other ancillary equipment, such as loupe magnification and coaxial lighting. Communication with the anesthesiologist involved in the planned operation should also occur and include an assessment of the patient’s resuscitation needs, estimated duration of operative intervention, plans for multispecialty approach, need for blood products and a cell saver device, and estimated duration of operation. Vascular repairs in the extremities require general anesthesia, an arterial line for blood pressure monitoring, and adequate venous access. Warming devices are also essential to prevent hypothermia. Even the most experienced vascular surgeon plans on a considerably long operative time to complete these repairs. Specific equipment, suture, and graft material requests should be communicated as soon as possible to the operating room team. Most operating rooms have major vascular instrument sets for the extremities. Ask to have them opened and ready. Prepare heparinized saline (5,000 U of heparin per 500 mL of saline for injection for a 10 U/mL solution) for locally flushing vessels. Low-molecular-weight Dextran (40,000) and papaverine hydrochloride (30 mg/mL) for treatment of vascular spasm should also be available in the operating room. Also request the appropriate vascular sutures. For suture repair, 5-0 Prolene on a C-1 needle is very useful. A variety of sutures should be available for vascular anastomosis. Request 5-0 Prolene on a BV-1 and C-1 needle or 6-0 Prolene on a BV-1 needle. For tibial and forearm vessels, either a 6-0 Prolene on a BV-1 needle or a 7-0 Prolene on a BV-175 needle should be available. All sutures should be of appropriate length and be on double-armed needles. PTFE graft material of various sizes (6 and 8 mm diameter) with external rings should also be readily available if saphenous vein is not of sufficient size or an extra-anatomic bypass is needed in injuries associated with extensive soft tissue loss. Preparation also includes personal supervision of positioning, prepping, and draping. Proximal areas of the torso including the chest and shoulder for upper extremity injuries and the abdomen for lower extremity injuries should be prepped and draped with the injured extremity. Always prep and drape an uninjured leg for saphenous vein harvest if needed. Review the instrument trays, sutures, graft material, and presence of heparinized saline to make certain that the operative procedure can proceed smoothly without unnecessary interruption. Plan ahead and have a standard set of equipment, sutures, and graft material routinely prepared and frequently checked by experienced operating room staff. The middle of the night is not the time to pull together this equipment from various parts of the operating room to manage a patient who is actively bleeding from an extremity vascular injury. Vascular injury in the extremities associated with major torso injuries must be managed in an orchestrated fashion to

achieve operative goals in a timely fashion. It may require two teams operating simultaneously, particularly if damage control measures, including temporary shunt placement, are used in the ischemic extremity form vascular injury associated with lifethreatening torso injuries. The planning before beginning the operation must be carefully done to achieve a successful outcome. This requires both effective teamwork and communication. The use of checklists is essential to properly complete this phase of the care of these challenging injuries.

■ Principles of Operative Management The key factors in successful operative management of extremity vascular injuries are exposure and vascular control, debridement of injured vessel wall, proximal and distal balloon catheter thrombectomy, and a tension-free repair or interposition graft of appropriate size. Soft tissue coverage, fracture fixation, and timely fasciotomy are also essential to complete management. Each of these steps is prone to error and must be thoughtfully and effectively completed.

Exposure and Control The incisions for exposure of extremity vascular injuries should be both appropriately placed and generous in length to expose noninjured adjacent proximal and distal segments of the injured vessels for vascular control. There is a tendency of some surgeons to use the small incisions for elective extremity vascular surgery. This leads to the risk of inadequate exposure and incomplete hemorrhage control. In proximal extremity injuries with active hemorrhage, the first incision site is chosen to give the fastest exposure of inflow vessels for clamping. For proximal upper extremity injuries in the axilla, this should include incisions over the infraclavicular region of the chest for access to the proximal axillary vessels. For injuries in the groin, prepare to enter the lower quadrant of the abdomen for access to the external iliac vessels. In mid and distal extremity vascular injuries where tourniquets have been applied to obtain control in the trauma resuscitation room, a sterile tourniquet can be placed. In the operating room, have one team member precisely compress the bleeding site with a gloved hand and a sponge, remove the tourniquet, and prep the extremity. A 5,000 U heparin bolus is then given if this is an isolated injury. The extremity is prepped and draped and a sterile tourniquet is placed proximal to the wound and inflated. The injury site can then be explored in a controlled fashion and clamps or vessel loops placed above and below the vascular injury. The tourniquet can then be deflated. Incisions for vascular exposure in the extremities are discussed in Section “Vascular Injuries by Anatomic Region.” It is worth reemphasizing that the use of small incisions may lead to error in identifying the extent of vascular injury, adequately controlling branch vessel hemorrhage, and identifying associated venous lacerations. There are important considerations at other extremity joints for both adequate control and a good functional outcome. In general, dividing the inguinal ligament in the groin, dividing the pectoralis major muscle in the axilla, and removing the midportion of the clavicle are not often required. However, in

Peripheral Vascular Injury

Arterial Repair Once adequate exposure and vascular control has been obtained, a systematic approach in choosing the technique of arterial repair needs be quickly used (Fig. 41-5). The injured ends of the vessel should be sharply debrided to a level of normal arterial wall. Fogarty balloon catheters must be carefully passed proximally and distally to clear thrombus and insure adequate flow. Heparinized saline in a syringe with a vessel irrigator should then be gently flushed proximally and distally after first aspirating blood to insure that the tip is in the lumen. Care should be used flushing the proximal brachial artery. As little as 10 mL flushed vigorously may force thrombus or air back up the proximal vessels to the origin of the vertebral arteries and cause a posterior circulation stroke. The debrided and appropriately flushed artery should then be assessed to select the method of repair that should be tension free and of adequate diameter. Normal arteries in the extremities of young patients are highly elastic and retract a remarkable distance. There is a significant risk of stenosis and thrombosis when undue tension is placed in an attempt to perform a primary repair. Transverse or short oblique lacerations without vessel wall disruption from knife wounds may be repaired with simple sutures. The laceration should be extended transversely to inspect the intima and debride as needed. The arteriotomy is then closed with a transverse running suture or interrupted

sutures. Longitudinal and long oblique lacerations cannot be closed without compromising luminal diameter. The injured site should be opened longitudinally a sufficient length to inspect and debride vessel wall. An oval vein patch can then be used to close the arterial defect without compromising the diameter of the lumen. A PTFE patch is an acceptable alternative in the common superficial femoral arteries if vein is not available. When there is complete vessel transaction, there is a commonly quoted “2 cm” rule that implies that up to 2 cm of brachial and superficial femoral artery length may be resected followed by primary anastomosis. This is very misleading. Even if there is minimal debridement, the vessel ends should be spatulated to assure a nonstenotic anastomosis. The 2 cm vessel length is quickly lost. Additional vessel length may be obtained for a tension-free anastomosis by mobilizing proximal and distal segments of normal artery. Care should be taken however to limit this dissection to a reasonable length. When in doubt about length and the amount of tension, perform an interposition graft. Vessel injuries that cannot be repaired by primary end-toend technique require an interposition graft. The optimal interposition graft material is autologous greater saphenous vein harvested from an uninjured leg.8 Native vein graft is preferable because it has elastic properties that make it very compliant with the normal pulsatile flow of an artery. It also has a diameter that approximates that of an extremity artery and produces an adequate size match for grafting in the arm and leg. Venous intima is less likely to be thrombogenic and it has superior long-term patency when compared with prosthetic material when used with smaller vessels (popliteal and tibial). Cephalic vein and lesser saphenous vein have been suggested as suitable second choices, but cephalic vein is less muscular than the greater saphenous. Both the cephalic vein and the lesser saphenous vein are difficult to harvest in trauma patients.19 Saphenous vein is not always suitable because of inadequate size or extensive bilateral lower extremity injuries, or because it has been harvested previously for elective cardiac or peripheral vascular bypass.37 A synthetic graft is an acceptable second choice. Initial experiences with the use of prosthetic material (Dacron) in traumatic vascular injuries were disappointing. Reports from the Vietnam War revealed a complication rate of over 75% and infection and thrombosis were the most common.38 However, more recent experience with PTFE has shown improved patency of 70–90% in short term and infections are rare even in contaminated wounds.37,39,40 It is clear that patency with PTFE is equivalent to vein for injuries proximal to the popliteal artery, but inferior to vein for popliteal and more distal vessels and that PTFE grafts of at least 6 mm diameter should not be used.39,40 Both PTFE and vein grafts must be covered or there is a significant risk of hemorrhage from desiccation of the vein with subsequent autolysis or breakdown of the anastomosis.41 Single-vessel arterial injuries in the distal forearm and distal calf may be ligated if there is sufficient collateral flow through the remaining vessels. This is best assessed by observing backflow through the distal cut end of the vessel. Doppler signals in the hand or forefoot vessels are a reassuring sign of adequate peripheral perfusion. When in doubt, perform an intraoperative arteriogram.

CHAPTER CHAPTER 41 X

life-threatening hemorrhage that cannot be controlled by any other approach, they should not stand in the way of adequate exposure and control. In the upper extremity, incisions across the antecubital fossa should be crafted in an “S” shape across the joint to prevent wound contracture and limitation of elbow joint movement. There are a variety of adjunctive measures that can obtain temporary control in the operating room. Insertion of an appropriately sized Fogarty balloon-tip catheter on a threeway stopcock under direct vision in the artery above or below the level of injury with balloon inflation at the site of injury may gain control in difficult to reach anatomic areas. Insertion of balloon catheters in the operating room under fluoroscopy for control in centers with immediately available equipment and trained personnel by the surgeon with endovascular skills also has a role. However, this capability is uncommon and limited to a few centers. However, this minimally invasive adjunct to vascular control will probably become a routine part of managing extremity and torso vascular injuries in the future. Control of proximal and distal flow is best achieved by double passing silastic vessel loops around the vessel above and below the area of injury and gently retracting until flow ceases. Place the vessel loops a sufficient distance away from the injury to allow them to not slide to the area of injury. Bleeding side branches should be occluded with removable metal clips. If clamps are needed, choose the appropriately sized noncrushing vascular clamp and apply closing the ratcheted handle only as much as needed to occlude the vessel. Carefully support the clamps to avoid twisting and inadvertent stretching of the vessels. Clamp trauma can cause intimal disruption and early thrombosis or the late development of stenosis.

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SECTION 3 X FIGURE 41-5 Decision making in extremity arterial and venous repairs in stable patients.

Venous Repairs The decision to repair major venous injuries in the extremities is based on the physiologic status of the patient and whether or not the operating surgeon is capable of performing venous reconstruction. The decision to ligate major venous injuries is discussed in Section “Vascular Damage Control.” The skill and experience of the operating surgeon must also be considered. Lateral venorrhaphy without creating significant stenosis is possible in very few venous injuries. Vein patch closure or panel graft interposition is frequently required (Fig. 41-5). These procedures, while not beyond the technical ability of all trauma surgeons, require previous experience if they are to be performed in a timely and effective fashion. Consequently, many vein injuries, if not most, are ligated. In the lower extremity, major venous ligation leads to venous hypertension in the calf

and places the patient at a higher risk for compartment syndrome. As discussed in Section “Vascular Damage Control,” calf fasciotomy should be performed in this setting. Lateral venous repair, when possible, is best performed with a 6-0 or 7-0 Prolene running suture, taking care to avoid undue tension and purse-stringing. Autologous vein patch angioplasty should be considered in more extensive injuries with sufficient remaining uninjured vein wall. The vein patch needs to be of a generous size to maintain adequate luminal diameter. Uncommonly, stab wounds result in a transversely oriented transaction that may be primarily repaired by simple anastomosis of the cut ends without causing significant stenosis. More extensive circumferential injuries require a saphenous vein panel graft interposition. This is performed by harvesting a long segment of saphenous vein, opening it longitudinally,

Peripheral Vascular Injury

Intraoperative Assessment of Vascular Repairs On completion of a vascular repair, local and distal pulse examination should be performed. Handheld Doppler interrogation of the repair site and distal flow should also be performed. Constant high-pitched signals indicate the presence of stenosis and should prompt inspection for technical problems at the sutures line. Ankle or wrist Doppler pressure measurements may be misleading because of regional vasospasm in the proximal injured extremity resulting in a reduced distal pressure compared with the uninjured leg. Intraoperative duplex scanning is useful but requires significant training and experience to perform it adequately. Unexpected problems at the suture line occur in as many as 10% of vascular repairs.19 The presence of early platelet thrombus, kinking, or an intimal flap may cause early failure. In distal repairs or those of questionable patency, an intraoperative arteriogram is essential.19 Either single-injection radiography or fluoroscopy is effective in providing images in the operating room (see Section “Case 7,” Fig. 41-27). Intraoperative radiographic imaging remains the most accurate and useful method to detect technical problems with a vascular repair or to determine the presence of thrombus in the runoff vessels distal to a repair.

■ Role of Tissue Coverage No vascular repair will be successful if it is not covered with healthy tissue, preferably muscle. Desiccation or superficial infection in the inadequately covered repair leads to suture disruption and hemorrhage or thrombosis of the vascular repair site. In crushed or badly mangled extremities, this can be a difficult challenge. Tissue avulsion from automobile or motorcycle crashes with extremities dragged along the pavement or closerange shotgun blasts are the most common causes of these injuries in civilian centers (see Section “Case 4,” Fig. 41-17). Rotation of regional muscle or skin flaps may be required for coverage of vessel repair sites. The early involvement of a plastic and reconstructive surgeon is essential to obtain tissue coverage when there is extensive soft tissue injury or loss. Local muscle should be advanced into the wound at the initial operation. For extensive tissue loss, a pedicled transposed muscle flap, free tissue transfer, myocutaneous flap, or fasciocutaneous flaps may be indicated.43 However, complex myocutaneous flaps or free tissue transfer are rarely indicated or appropriate at the initial operation

because they are very time consuming and put the patient at risk for hypothermia and metabolic derangements. These are more safely performed in a delayed fashion when the patient has recovered from the initial physiologic effects of injury. In wounds with significant contamination and questionable local muscle viability (such as may occur following a shotgun wound or blast injury) temporary coverage can be obtained using cadaver skin homograft or porcine xenograft.44 The homograft or xenograft will be temporarily adherent, provide coverage, and often can stay in place for 5–7 days or longer. This biologic dressing allows time for local tissue inflammation to decrease. Subsequent split-thickness skin graft application, tissue rotation, or, in limbs with extensive tissue loss, pedicle flaps or free tissue transfer can then be performed. In extreme cases of tissue loss or subsequent disruption of an inadequately covered vascular repair, extra-anatomic bypass may be required. Preferably, an autologous vein bypass can be routed through adjacent healthy tissue in the extremity. Less commonly, externally supported PTFE grafts are tunneled around the vascular injury site to supply distal perfusion. The synthetic bypass may be definitive revascularization or a temporizing step to allow healing and later placement of a vein graft through the site of injury.45

■ Role of Fasciotomy Failure to perform an adequate fasciotomy after revascularization of an acutely ischemic limb is the most common cause of preventable limb loss.8,19 Calf compartment syndrome is the most common indication for fasciotomy. The primary major goal of management is prompt detection and treatment before tissue damage has occurred. There are a variety of settings in which preemptive fasciotomy should be performed. In patients with prolonged ischemia, crush injury, or combined arterial and venous injury, especially if major veins have been ligated, fasciotomy should be performed in conjunction with the initial vascular repair. Compartment pressure should be measured early and often in patients at risk. The handheld solid state transducer device (Stryker Surgical, Kalamazoo, Michigan) should be used. If not available, pressure tubing on a three-way stopcock with a blood pressure cuff monometer may be used to create an improvised device that accurately measures pressure (Fig. 41-6). Normal tissue pressures are below 15 mm Hg and any pressure above 25 mm Hg mandates immediate intervention.46,47 Fasciotomy should be performed by someone with knowledge and experience with performing the procedure. Most trauma surgeons have experience with fasciotomies in the calf. However, forearm fascitomies are usually performed by orthopedic surgeons and, unless experienced in this technique, trauma surgeons should call for help in this area. The same applies to fasciotomy in the upper arm, thigh, hand, foot, and buttocks.

Calf Fasciotomy There are four compartments in the calf that need to be released (Fig. 41-7). These include the anterior and lateral compartments on the anterior lateral aspect of the calf and the deep and

CHAPTER CHAPTER 41 X

wrapping it around a large chest tube or other appropriate large cylindrical structure, and sewing it in a spiral fashion to create a panel graft. This large-diameter graft is a suitable conduit for venous reconstruction. This technique is tedious and requires significant vascular technical ability and experience. It should not be tried without the help of an experienced colleague. The continuous passive motion device used in major joint surgery is an excellent adjunct in improving venous draining in bed-bound patients after major venous injury and either repair or ligation. This device has proven effective in reducing the risk of deep venous thrombosis following major orthopedic trauma in the lower extremity.42 It markedly improves venous drainage and should be considered in any patient with significant lower extremity venous trauma.

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SECTION 3 X A

B

FIGURE 41-6 (A) Stryker pressure measurement device (Stryker Surgical). (B) Pressure measurement device constructed of connection tubing, syringe, stopcock, and manometer from blood pressure cuff.

superficial posterior compartments. The best approach for release is two long incisions, one each on the lateral and medial aspects of the calf. Although isolated anterior compartment syndrome occurs in some settings, four-compartment release is usually required (see Section “Case 5,” Fig. 41-19). The lateral incision needs to be generous. It should start 2 cm anterior to the fibula and no higher proximally than 4 cm below the fibular head in order to avoid the peroneal nerve. The incision should be taken distally to within 2–3 cm of the lateral malleolus. The fascia of both the anterior and the lateral compartments should be incised in the same region. Take care not to carry the incision beyond the limits of the skin incision proximally to avoid the peroneal nerve. Make certain that the anterior compartment is fully released by visualizing and pal-

pating the tibia anteriorly beneath the incised fascia. Misplacing the incision posterior to the interosseous membrane can lead to mistaking the lateral compartment for the anterior compartment. This results in failing to release the anterior compartment with devastating consequences. The use of a checklist is helpful in preventing the many errors that can occur in performing this procedure (Fig. 41-8). The medial calf incision should be made 2–3 cm behind the posterior margin of the tibia to avoid lacerating the greater saphenous vein. The fascia over the gastrocnemius should be fully incised proximally and distally. The gastrocnemius and soleus muscles are retracted posteriorly in the distal calf to expose the deep posterior fascia. This layer needs to be incised under direct vision to avoid lacerating the posterior tibial artery.

FIGURE 41-7 Cross-section of mid-calf showing the four fascial compartments and their contents. Open arrows show sites of doubleincision fasciotomy; closed arrow shows site of single-incision fasciotomy. (Reproduced with permission from Frykberg ER. Compartment syndrome. In: Cameron JL, ed. Current Surgical Therapy. 5th ed. St. Louis, MO: Mosby-Yearbook; 1995:850, © Elsevier.)

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1. Mark landmarks and incision lines – note head of fibula and mark 2 finger breadths below for exclusion zone for peroneal nerve safety

3. Anterior compartment release –generous longitudinal antero-lateral incision—stay below peroneal nerve exclusion zone proximally 4. Incise anterior compartment fascia proximally and distally, avoiding peroneal nerve exclusion zone proximally 5. Probe under anterior compartment fascia to the tibia to assure in the anterior compartment 6. Release lateral compartment fascia in similar fashion probing under fascia to confirm in proper space posterior to the intermuscular septum 7. Posterior compartment release—generous longitudinal medial incision 2 cm behind tibia and avoid the saphenous vein 8. Superficial posterior fascia release under direct vision 9. Go distal and deep to gastocnemius and soleus muscles to visalize deep posterior compartment—release fascia under direct vision to locate and avoid posterior tibial artery—do entire length of release under direct vision 10. Hemostasis on skin, check muscle contraction with electrocautery in all compartments 11. Place loose moist sponge in wounds—wrap leg very loosely 12. Recheck perfusion at DP, PT, 13. Reassess wounds for hemorrhage and dressing tension frequently over next 24 hours— avoid recurrent compression from dressings FIGURE 41-8 Four-compartment calf fasciotomy checklist.

Once all four compartments are adequately released and adequate hemostasis is obtained, a loose dressing is applied. Care should be taken to avoid tight dressings that will recreate the syndrome when muscle swelling occurs. Postoperatively, the extremity should remain elevated above the level of the patient’s heart to reduce edema formation and facilitate wound closure, which can occur in 48–72 hours. Split-thickness skin graft may be required.

Thigh Fasciotomy Thigh fasciotomy is uncommonly required. There are three compartments to release: lateral, medial, and posterior. Two incisions, one lateral for the lateral compartment and one medial for the other two compartments, are sufficient. These need to be generous in their length. If one is unfamiliar with

thigh muscle anatomy, consult an orthopedic surgery colleague. Loose dressings should be applied to avoid recreating the compartment syndrome.

Forearm and Upper Arm Fasciotomy The forearm and upper arm are areas of multiple motor and sensory nerves important to hand function and a lack of familiarity with the anatomy when performing a fasciotomy can lead to significant nerve damage. Call an orthopedic surgery colleague for help if you do not have experience performing this procedure. Generous dorsal and volar incisions are required to release the dorsal and volar compartments and the mobile wad. Each major muscle group fascia must be incised. There are numerous superficial cutaneous nerves that must be carefully avoided. Upper arm fasciotomy is best performed

CHAPTER CHAPTER 41 X

2. Skin incisions—full length of calf to create dermotomy

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SECTION 3 X

through medial and lateral incisions. There are medial and lateral muscle compartments to release and the deltoid compartment at the proximal extent of the lateral incision must also be addressed.

■ Vascular Damage Control Damage control principles and techniques have gained widespread acceptance in trauma surgery. In torso trauma, they are directed at rapid control of hemorrhage and closure of enteric wounds so that the patient can be warmed and resuscitated. In the extremity, damage control involves temporary restoration of blood flow with intraluminal shunts and selective ligation of major vessels.8,9,19 Fasciotomy also has a role in damage control in the extremities. The choice between definitive time-consuming vascular repairs and temporary measures that achieve hemorrhage control and restoration of perfusion must be made early in the care of patients with vascular injury and hypovolemic shock. This is particularly important when an extremity vascular injury is associated with major torso injuries. Ligation should be reserved for vessels with adequate distal collateral flow. In the upper extremity, proximal injuries of the axillary artery and distal injuries to either the radial or ulnar arteries may be ligated provided there is evidence of adequate distal collateral flow assessed by either physical exam or continuous-wave Doppler interrogation. Similarly, in the lower extremity, ligation of a single tibial vessel or the peroneal can be performed following a similar assessment. If distal perfusion is compromised, an intraluminal shunt should be inserted, rather than ligating the vessel. Ligation of the brachial, external iliac, and superficial femoral or popliteal arteries has a high likelihood of producing limb-threatening ischemia resulting in amputation and should be avoided. There are a variety of commercially available shunts that can be used for damage control. The 10 or 12 French straight carotid shunts are the most commonly used for this purpose. If these are not available, sterile intravenous tubing or endotracheal suction tubing of adequate size is used as a shunt material for both the artery and the vein of the extremities. Venous shunt placement instead of ligation may improve extremity perfusion and lower the risk of compartment syndrome. The common femoral vein may be shunted with a larger plastic catheter to achieve adequate luminal diameter. Damage control shunt placement begins with obtaining adequate proximal and distal control. Thrombus should be cleared with a Fogarty embolectomy catheter followed by the instillation of regional heparinized saline (10 U/mL). The shunt should be placed in a straight line and long enough to remain safely held in place in the proximal and distal vessels with a tied umbilical tape or 2-0 silk tie at each end. Long, looped shunts run the risk of becoming dislodged during subsequent dressing changes and should be avoided. For patients who will be transported to another facility, ties around the center of the shunt with each tied to the proximal and distal shunt holding ties will insure that they do not become dislodged or migrate. The ties securing the shunt cause arterial wall and intimal damage and those portions of the artery will need to be debrided at the time of definitive vascular repair.

Avoid unnecessarily damaging proximal and distal artery wall remote to the site of injury and place ties to secure the shunt as close to the injury site as is safely possible. Ligation of proximal lower extremity vein should be performed for damage control only when subsequent venous obstruction is not anticipated. Shunts should be placed in the common femoral and superficial femoral veins whenever possible. This allows the option of repair versus ligation at a later time when the patient is stable. Ligation results in local thrombosis and subsequent venous repair will not be possible. However, in dire situations with a profoundly unstable patient, venous ligation may be the best option. Add calf fasciotomy in this damage control setting to forestall the development of compartment syndrome. The early postinjury course and condition of the patient determines the timing of definitive vascular repair following damage control procedures. Hemorrhage must be controlled and hypothermia, coagulopathy, and acidosis corrected prior to performing definitive repair. The treatment of torso injuries should also be factored in during planning for a return to the operating room. However, there is a significant risk of shunt thrombosis and limb ischemia if repair is unnecessarily delayed.

■ Combined Arterial and Skeletal Extremity Trauma Complex extremity trauma with both vascular injury and fractures or dislocations is infrequent.1,48,49 However, this combination presents one of the most significant management challenges. There is a difference in perspective between orthopedic surgeons and trauma surgeons with regard to this complicated type of injury. Vascular injury complicated less than 2% of extremity fractures and dislocations, but skeletal trauma is present in over 10–70% of series of extremity vascular injuries.49 The majority of these injuries in civilian trauma centers are due to blunt force trauma.1,10 In military series, high-velocity penetrating injuries are the most common cause.7,9 In both civilian and military series, combined arterial and skeletal extremity trauma carries a substantially higher risk of limb loss and limb morbidity than do isolated skeletal and arterial injuries. A 10-fold increase has been noted in most studies, including those recently reported.9,26,48–55 Successful management requires both prompt diagnosis and effective early management with coordination of surgical consultants from orthopedics, neurosurgery, and plastic surgery. This requires that a high index of suspicion of arterial trauma be applied to every injured extremity by performing a careful physical examination augmented by Doppler pressure measurements at the ankle or wrist. When indicated, CT angiography is extremely helpful in detecting the presence of arterial injuries in these mangled extremities. In certain injuries that require extensive exposure for orthopedic surgery techniques, operative exploration of potential injured vessels may be appropriate. An intraoperative plain film single shot angiography, or fluoroscopy is helpful in delineating anatomy and identifying injury in this setting. Combined injuries require team work and coordination of the efforts of both the orthopedic and vascular surgeons.

Peripheral Vascular Injury the artery should repaired and the limb followed for return of neurologic function. Many patients ultimately request amputation because of the burden of an insensate and paralyzed arm that sustains repeated injury.

■ Role of Immediate Amputation Immediate amputation is limited to devastating extremity injuries with extensive soft tissue avulsion or crush wounds. With the application of damage control techniques and plastic and reconstruction surgery options, primary, early, or immediate amputation has become less common in the management of complex extremity injuries. Patients with extensive soft tissue loss, neurologic deficit, comminuted fractures, and vascular injuries should be evaluated collaboratively with orthopedic, neurosurgical, and plastic and reconstructive surgery colleagues to determine if primary amputation is the best initial management. The use of scoring systems to predict the need for amputation has not been consistently useful.48,56–58 There are objective data showing a higher limb salvage rate than would be predicted by many scoring systems.56–58 It may be best to proceed with initial intraoperative evaluation and documentation with pictures, radiographs, and consultation and then perform damage control using intravascular shunts for the vascular injuries. Plan a second look in 24 hours. The key decision-making factors in early amputation are the extent of skeletal and soft tissue injury, absence of plantar or palmar sensation, and the need for vascular repair.58 This second look allows for a reconsideration of limb salvage. Marginally viable tissue often takes hours to demarcate or declare and tissue loss will be more apparent at the second operation. The interval of time allows communication with the patient and the family with support for the emotional impact of losing a limb. Allowing the patient to see the devastating wounds prior to amputation often allows better acceptance of the loss and prompts healthy grieving. If immediate amputation is required at the first operation, extensive documentation of the extremity injury with photographs placed in the chart will be helpful in later explaining the decision to the patient and family and will help with their acceptance of this drastic surgical procedure.59,60 The decision to perform immediate or early amputation is one of the most compelling clinical decision-making processes that any surgeon can face. It requires a collaborative approach and honest discussion between vascular, orthopedic, plastic and reconstructive, and trauma surgery colleagues. It is not easily made and is based on the collective experience and wisdom of surgeons dedicated to the care of the injured.

■ Early Postoperative Management

FIGURE 41-9 Arteriogram in patient with blunt left should injury with transaction and thrombosis of brachial artery and brachial plexus stretch injury with insensate and paralyzed arm.

The successful management of extremity vascular injury includes an organized approach to the postoperative phase of care, particularly during the first 24 hours when technical problems are most likely to present. Close clinical surveillance of the injured limb is critical. This includes not only distal pulse examination and, if indicated, Doppler pressure determinations but also frequent assessment of the extremity for compartment syndrome. Physical examination alone may not detect the presence of a compartment syndrome. Frequent

CHAPTER CHAPTER 41 X

Timing of their fracture fixation and the vascular repairs should be discussed. Clinical series have shown a substantially higher rate of limb salvage in combined injuries when the vascular repair is performed first compared with those in which it follows skeletal fixation.53 It may be appropriate to place temporary intraluminal shunts prior to the orthopedic fracture fixation and soft tissue debridement. Once the extremity is stabilized, the definitive vascular repair can be performed. In most complex injuries, external fixation is commonly used because of the commonly associated soft tissue injuries and open fractures.48–54 However, internal fixation has been increasingly used successfully in this setting if the patient’s condition permits.48,54 Damage control in complex combined injuries in unstable patients requires rapid placement of intravascular shunts, fasciotomy, and rapid external fixation. There are two particularly devastating combined skeletal and vascular extremity injuries that have a high risk for poor functional outcome. They are posterior knee dislocation with popliteal artery and vein disruption and the scapulothoracic dissociation injury with axillary artery injury. The combination of severe ligament disruption with complex vascular injury in the knee leads to significant permanent impairment even if the vascular repair is performed in a timely and appropriate fashion with an associated calf fasciotomy. Management of these injuries often involves delay in revascularization or early thrombosis of the repair with worsened outcome including a significant risk of limb loss.24 Scapulothoracic dissociation is a devastating injury of the upper extremity and shoulder girdle caused by blunt force stretch injury. It is rarely complete, which involves separation of the musculoskeletal attachments of the shoulder girdle in addition to avulsion of the cervical nerve roots and transaction of the brachial artery and vein. More commonly, it is a partial avulsion or stretching of the nerve roots and axillary artery disruption (Fig. 41-9). The outcome is uniformly poor because of the neurologic injury and less likely due to the arterial injury.8,55 Poor prognosis in brachial plexus stretch injuries is associated with proximal location of neurologic injury, injury of multiple roots, and complete brachial plexus palsy.8,55 Acutely,

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compartment pressure measurement is the only way to accurately assess the injured extremity in patients who are not conscious and cooperative. New-onset neurologic deficits are an important indicator of ongoing ischemia and should prompt assessment of both the patency of the vascular repair and the pressure within muscle compartments. The most important element of this clinical surveillance is the willingness to return to the operating room for reexploration as soon as there are any indications of problems with the repair or the presence of early postinjury complications. The use of anticoagulation or antiplatelet agents in the early postoperative period may be of value in preventing early thrombus formation in the area of vascular repair. Full anticoagulation with heparin is reserved for isolated extremity injuries with tenuous repair of small vessels. Low-molecular-weight Dextran (40,000) infused at 40 mL/h over the first 24 hours has a beneficial rheologic and mild antiplatelet effect in small vessel repairs. Long-term antiplatelet agents and anticoagulants are not of proven benefit. Any suggestion of thrombosis, hemorrhage, or compartment syndrome should prompt an immediate return to the operating room. A second operation should never be seen as a sign of failure. Reoperation is inevitably required in 5–10% of vascular repairs to achieve an overall successful outcome. Most experienced vascular surgeons will accept a certain rate, although low, of reexploration without needing to revise anything in order to remain vigilant enough to avoid a missed opportunity to salvage the repair. The failure of vascular repairs from thrombosis usually occurs within the first 24–48 hours. Infection is usually delayed beyond the first 72 hours and is usually manifested by either hemorrhage or, less commonly, thrombosis. Dessication and erosion of the exposed vessel from inadequate soft tissue coverage presents in a fashion similar to infection. Both require an immediate return to the operating room and a complete resection of the repair, a new repair, and adequate coverage of the repair with viable muscle. Extra-anatomic bypass may also be required.

■ Common Management Errors and Pitfalls The most common errors in the operative management of extremity vascular injury are inadequate exposure and control, failure to recognize the need for damage control techniques, failure to perform fasciotomy, and failure to recognize an early postoperative thrombosis (Table 41-1). Each of these errors can be mitigated with the use of guidelines and checklists. These organizational tools are of little use unless they are actively used and regularly revised with the lessons learned in their application. They became a repository of not only the intended plan of action but also lessons learned from experience. They help insure the best possible outcome following extremity vascular repair.

VASCULAR INJURIES BY ANATOMIC REGION ■ Upper Extremity Vascular Injuries Penetrating injury is the most common etiology of upper extremity vascular injuries and usually presents with a history

of significant bleeding or active, ongoing bleeding. Blunt injury is often associated with fractures or dislocations and is usually evident with signs of acute arterial occlusion and ischemia. Significant neurologic injury is present in 60% of patients with upper extremity arterial injury.1,9,10,55 The median nerve is most commonly involved due to its course in close proximity to the brachial artery throughout the upper arm. Concomitant venous injury is also commonly associated with arterial injury in the arm. Upper extremity arterial occlusion is easily missed in the setting of multisystem injury. However, all significant vascular injuries of the upper extremity result in clinical findings that are apparent on thorough physical examination.61 Distraction by focusing on associated severe torso or lower extremity injuries can lead to a failure to recognize the upper extremity injury. Delays in diagnosis and treatment are common in collected series of patients with upper extremity arterial injury following blunt force trauma.24,55 The diagnosis of upper extremity arterial injury is usually made on physical exam alone. Patients with obvious arterial or venous laceration from penetrating trauma or those with blunt trauma and “hard findings” (Table 41-2) should be taken directly to the operating room. The upper extremity arteries are very sensitive to the effects of agents that produce vasoconstriction. Thus, intense vasoconstriction to the point of diminished or absent peripheral pulses can occur following hypovolemic shock, severe pain, or the ingestion of illicit drugs, such as cocaine and methamphetamine. Complex fractures or crush injuries of the upper extremity associated with absent pulses are an indication for CT angiogram or catheter angiogram to assess patency. Bleeding from a partially transected arm or forearm vessel can be significant. The senior surgeon should make certain that adequate control is obtained and maintained during resuscitation, transportation to the operating room, and surgical prep and drape. Pneumatic tourniquets should be used appropriately and placed and carefully monitored for adequacy of compression and duration of application by the senior surgeon.

■ Subclavian and Axillary Vascular Injuries Penetrating trauma is more common than blunt trauma as the cause of these proximal upper extremity vascular injuries. Injuries to the most proximal portion of the subclavian are discussed in the thoracic trauma chapter 24 of this book. Supraclavicular subclavian and proximal axillary artery injuries with active hemorrhage are very challenging. They require immediate operative management for control of hemorrhage and repair. Occlusion of the subclavian and axillary vessels is well tolerated because of the extensive collateral vessels. If there is evidence of satisfactory distal perfusion, management of a thrombosed axillary or subclavian artery may be delayed to complete management of other life- or limb-threatening injuries. Surgical exposure requires a wide prep and drape of the shoulder, chest, and ipsilateral arm. Supraclavicular injuries of the left subclavian vessels may require an anterolateral thoracotomy through the third intercostal space for proximal control. On the right, a sternotomy may be required for proximal control. Distal control may require an infraclavicular incision to

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CHAPTER CHAPTER 41 X

C A

B

clamp the axillary vessels. The site of injury is then approached directly through a supraclavicular incision. An effect adjunct to proximal control in partial arterial wall laceration is the introduction of an occluding balloon-tip catheter retrograde through the axillary artery to the site of injury. The subclavian may then be directly approached. The portion of the subclavian vessels directly behind the clavicle may be exposed by dividing the clavicle medially and retracting it inferiorly to be reattached later. A portion of the middle of the clavicle may also be resected if needed. Exposure of the axillary vessels is obtained through a transverse infraclavicular incision carried down to the pectoralis minor muscle by muscle-splitting incision carried through the pectoralis major muscle. The pectoralis minor tendon is divided at its insertion on the coracoid process. The axillary artery and

FIGURE 41-10 Approach to the axillary artery for proximal arterial control. (A) Location of infraclavicular incision. (B) Division of pectoralis minor muscle at coracoid process. (C) Exposure and control of axillary artery. (Reproduced, with permission, from Rutherford RB, ed. Atlas of Vascular Surgery: Basic Techniques and Exposures. Philadelphia: WB Saunders; 1993. © Elsevier.)

vein are located immediately below the muscle (Fig. 41-10). Care must be taken to avoid the cords of the brachial plexus, which are in close proximity to the axillary vessels. More distal exposure may require completely dividing the pectoralis muscle; however, this is uncommonly needed. Injuries of the subclavian and axillary vessels are rarely amenable to simple suture repair. Subclavian arterial injuries may be repaired with an interposition of PTFE. The axillary artery is best repaired with a vein conduit. Venous injuries may be ligated unless there is extensive soft tissue injury with disruption of collaterals. Occasionally, vein or PTFE patch repair is possible. The risk of venous hypertension is low and ligation should be used unless the vein repair can be done expeditiously. Forearm or upper arm fasciotomy is rarely required with vascular injuries at the subclavian and axillary level. However, close

836

Management of Specific Injuries follow-up in the postoperative period for the development of compartment syndrome is mandatory.

SECTION 3 X

■ Brachial Artery Injuries Penetrating injuries from interpersonal violence or punching a hand through a window with laceration from glass shards are the most common causes of brachial artery injuries. Blunt trauma with fracture and arterial laceration or contusion leading to thrombosis is much less common. Supracondylar humerus fracture is the most commonly associated orthopedic injury with brachial artery occlusion. Both blunt and penetrating injuries are easily diagnosed on physical examination. Angiography is rarely indicated unless there are multilevel musculoskeletal or crush injuries. Active bleeding should be controlled by tourniquet application or direct pressure while the patient is transported to the operating room. Exposure is obtained though a longitudinal incision over the course of the artery on the medial aspect of the upper arm. Proximal control for high brachial artery injuries may require proximal control at the level of the axillary artery in the infraclavicular region. Distally, the incision can be extended with an “S”-shaped extension across the antecubital fossa from ulnar to radial aspect and onto the forearm to expose the origins of the forearm vessels. Proximal control for injuries of the distal brachial artery and the forearm vessels may be temporarily obtained with a sterile pneumatic tourniquet. This adjunct, however, should be removed as soon as vessel loops or vascular clamps can be applied in close proximity to the injury in order to restore collateral flow. Vascular repair requires attention to detail. Simple laceration may be repaired by direct suture repair if the repair can be performed without tension. Saphenous vein interposition should be chosen whenever vessel injury is extensive or if primary tension-free repair is not possible. PTFE has no role in the upper extremity below the shoulder and should be a reluctant second choice when autologous vein is not available. There is no role for brachial vein repair unless there is extensive soft tissue injury. Repair of associated median nerve injuries is an important part of over 50% of operations for brachial artery laceration. This should be accomplished by an experienced surgeon with loupe magnification and fine sutures. Postoperative splinting in a forearm flexed position is important in combined brachial artery and median nerve injuries. Forearm fasciotomy, particularly in the setting of prolonged ischemia, must always be considered prior to completion of the operation for brachial artery repair. Intraoperative compartment pressure measurements may help in the decision making. However, if normal pressures are obtained, eventual reperfusion edema and subsequent swelling may produce a delayed compartment syndrome. Postoperative follow-up is essential to prevent and identify this late development.

■ Forearm Arterial Injuries The brachial artery gives rise to the ulnar and radial arteries after crossing the antecubital fossa. The ulnar artery is larger than the radial artery in the upper arm and gives rise to the

interosseus artery. Although the radial artery is more superficial and easily palpated at the wrist, the ulnar artery is the dominant blood supply to the hand in 60% of patients. Both vessels contribute to the superficial and deep palmar arches. The ulnar artery is the dominant supply to the palmar aspect of the hand and the radial artery is the dominant supply to the dorsum. The palmar arches are incomplete in up to 30% of patients. Surgical exposure is obtained through a longitudinal incision on the volar aspect of the forearm, taking care to avoid the many cutaneous nerves in this area. Combined ulnar and radial artery injuries in the forearm require repair of at least one vessel (Fig. 41-11). The ulnar artery is usually larger in the proximal forearm and is a better target for direct repair or saphenous vein bypass. Distally, the vessel repair should be performed in whichever vessel is largest or amenable to simple repair. Collateral flow should be evaluated by either completion arteriogram or Doppler flow examination. Isolated ulnar or radial artery injuries can be managed with simple ligation only if there is absolute certainty that flow through the remaining vessel is adequate. Close inspection of the forearm and hand with palpation of pulses augmented by Doppler examination is essential. Isolated forearm arterial injury may be repaired if the patient is stable and there are no other pressing management priorities (Fig. 41-11).

■ Lower Extremity Vascular Injuries Vascular injuries in the legs are less common in civilian practice than they are in military series (20% vs. 30–40%).1,7,9,26 All lower extremity vascular injuries are highly morbid. Penetrating injuries are more common than blunt force trauma. Hemorrhage may be life threatening from penetrating wounds and blunt force injuries with occlusion have a high risk of ultimate limb loss. Venous injuries with major vein occlusion have a significant risk of causing calf compartment syndrome and there is also a significant risk of deep venous thrombosis and pulmonary embolism. Physical examination is usually sufficient to make the diagnosis of lower extremity arterial injury.61 Venous injuries are less obvious unless associated with external bleeding. There is a high rate of associated fractures in blunt force vascular injuries in the leg. The calf muscle compartments are always at risk for compartment syndrome in lower extremity vascular injury and should be carefully monitored. There is a role for liberal use of prophylactic compartment release in combined femoral or popliteal arterial and venous injuries or when there has been prolonged ischemia. Amputation remains relatively common after lower extremity vascular injury. Limb loss rates vary from 15% to 35%.1,7,9,26 Rapid diagnosis and prompt restoration of blood flow is the best way to reduce the threat of limb loss. Failure to perform fasciotomy in patients who develop compartment syndrome is the most common reason for preventable limb loss.1,7–9,26,47 Associated musculoskeletal and soft tissue injuries are also an important determining factor in limb loss. Decision-making needs to be well organized in treating lower extremity vascular injury to maximize the chances for a good outcome (Fig. 41-5).

Peripheral Vascular Injury

837

Active hemorrhage

Ischemia, obvious site of occlusion

Direct to OR

Unstable patient

Arteriography positive

To OR ASAP

Crush injury, unclear vascular status

Orthopedic repairs: Follow closely for compartment syndrome

Arteriography negative

Primary tension-free repair when possible or vein interposition, forearm fasciotomy for prolonged ischemia, crush injury

Brachial artery injury

One vessel injury

Repair if collateral flow poor or if stable patient and simple repair

Both vessels or complex injury

Simplest repair of largest vessel, check for adequate collaterals, consider forearm fasciotomy

Ulnar or radial artery injury

FIGURE 41-11 Guideline for management of upper extremity arterial injury.

■ Common Femoral Vascular Injuries Common femoral vascular injuries are frequently encountered in both civilian and military series. Penetrating injuries are more common than blunt. Hemorrhage is often severe with these injuries. Less commonly, hemorrhage is contained with thrombosis within the femoral sheath. Combined arterial and venous injuries are common. Diagnosis is made almost exclusively by physical examination. Active hemorrhage is common and many patients require direct pressure for hemorrhage control and immediate transfer to the operating room. Proximal vascular control may require an incision above the inguinal ligament for exposure of the external iliac artery in the retroperitoneum (Fig. 41-12). A longitudinal incision over the common femoral vessels should be generous enough to expose the superficial femoral artery and vein to gain control below the injured common femoral vessels. The proximal common femoral, profunda femoral, and superficial femoral arteries are best controlled with encircling double-passed silastic vessel loops. Primary arterial repair is occasionally possible, but most injuries are complex and require either a saphenous vein or PTFE interposition graft. Venous injuries are also more often

complex. They usually require careful clamp placement for vascular control. There are numerous side branches that must be controlled. Vein clamping results in venous hypertension if the artery is not also occluded. Vein patch repair or saphenous vein panel interposition graft may be required. In unstable patients, venous ligation may be the best course of action. Calf fasciotomy should always be considered when the major veins of the lower extremity are ligated. The profunda femoral artery is well collateralized by branches of the hypogastric artery to the gluteal and upper thigh region. Although simple lacerations should be repaired, more extensive injuries should be ligated unless there is extensive soft tissue injury and loss of collaterals in the buttock and upper thigh. Patients with preexisting stenosis or occlusion of the superficial femoral artery should undergo repair of the profunda femoral artery because of its important role in providing collateral flow to the lower extremity.

■ Superficial Femoral Vascular Injuries Penetrating injuries are much more common than blunt trauma vascular injuries in the thigh. The superficial femoral is located

CHAPTER CHAPTER 41 X

Classical signs of vascular injury

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Management of Specific Injuries

SECTION 3 X A

C

B

FIGURE 41-12 Approach to the external iliac artery in the retroperitoneum for proximal arterial control. (A) Location of right lower quadrant incision. (B) Retroperitoneal approach by retracting away peritoneum and contents. (C) Exposure of external iliac artery. (Reproduced, with permission, from Rutherford RB, ed. Atlas of Vascular Surgery: Basic Techniques and Exposures. Philadelphia: WB Saunders; 1993. © Elsevier.)

just behind sartorius muscle as it spirals from superior lateral to inferior medial in the thigh. Distally, it passes through the adductor canal to become the popliteal artery. It remains relatively superficial and significant hemorrhage is common with penetrating arterial injuries. Consequently, diagnosis is usually made in the operating room while gaining control of the bleeding. Exposure is obtained through an incision over the artery in its course down the anterior–medial aspect of the thigh. The sartorius muscle is retracted either anteriorly or posteriorly to expose the superficial femoral artery and vein. The incision should be long enough to obtain both proximal and distal

control. Although simple repair may be possible in some wounds, most require an interposition graft. Reversed autologous saphenous vein from the uninjured leg should be used if at all possible. The superficial femoral vein should be repaired if possible. However, it is usually ligated. Consideration should always be given to calf fasciotomy in any patient with superficial femoral arterial injury with prolonged occlusion and those with ligation of the superficial femoral vein. If fasciotomy is not performed, compartment pressures should be measured both before leaving the operating room and frequently in the early postoperative period.

Peripheral Vascular Injury

■ Popliteal and Tibial Artery Injuries

COMPLICATIONS AND OUTCOME The most immediate and dangerous early complication of extremity vascular repair is thrombosis with distal ischemia.1,7,8,9,19 Postoperative vascular checks need to be performed frequently and effectively. There is a tendency of inexperienced examiners to imagine that a pulse is present when it is not. Doppler devices should be used and ankle or wrist pressure should be determined often to make certain that repaired vessels remain patent. If there is any evidence of occlusion or any doubt about patency, the patient should be returned to the operating room for direct inspection of the repair. Early return to the operating room for revision or replacement of the vascular repair is essential to restore flow and preserve limb viability. The most common causes of early repair failure are technical errors.1,8,10,19,26 These include intimal flaps, kinking, undue tension, and stenosis at the repair site. Less commonly, platelet thrombus accumulates on a technically adequate repair site. This may occur from the generalized platelet activation of injury. It is often associated with extensive muscle injury or crush injury. Less commonly it is a manifestation of a heparin allergic reaction and activation in the process of heparin-induced thrombocytopenia. This is a crisis to be managed aggressively. Low-molecular-weight Dextran (40,000) should be given as a 40 mL bolus and then infused at 40 mL/h for 24 hours. Once the repair has been reopened by thrombectomy, it needs to be followed very closely for recurrent occlusion. A laboratory study to rule out heparin-induced thrombocytopenia should also be obtained. Postoperative anticoagulation is not usually helpful in arterial repairs for vascular trauma. However, it may have a role in venous repairs and should be considered in otherwise stable patients.62 Antiplatelet agents are of little use unless there is platelet-induced thrombosis. Long-term antiplatelet therapy may be helpful in preventing saphenous vein interposition graft failure. However, there is no compelling evidence to support these drugs in vascular trauma repairs. Infection at the site of an arterial repair is a devastating complication. Early wound problems in the area of vascular repairs should be explored in the operating room for infection, debrided aggressively, and reclosed with health tissue. In complicated wounds, a muscle flap to cover the vascular repair site is the best way to avoid infection and vessel erosion with hemorrhage. Once a repair has eroded and bled, it should be ligated and replaced with an extra-anatomic bypass. Prevention is the key to avoiding this unfortunate complication with its high rate of ultimate limb loss. The ultimate outcome from extremity vascular injury is largely determined by the associated musculoskeletal and neurologic injuries.48,50,53,56–58 Long after vessel repairs have healed, the insensate foot or hand will severely limit the patient with associated severe neurologic injury. Modern physical therapy techniques have resulted in excellent functional outcomes for many patients with devastating injuries. Delayed soft tissue and bone reconstruction also serve to optimize recovery. Late sequelae from venous injuries are more troublesome than those of arterial injuries.1,8,10,26 Venous insufficiency can be disabling if not adequately treated. Support stockings are

CHAPTER CHAPTER 41 X

The relationship of the popliteal artery with the adductor magnus muscle in the lower thigh and the gastrocnemius muscle in the upper calf as it transits the knee joint places it at risk for severe injury in dislocation of the knee joint. In full knee extension, the popliteal artery is under considerable tension. The back of the tibial plateau, as it moves posteriorly in a dislocation, impacts and stretches the popliteal artery, often completely disrupting it. The popliteal vein may suffer the same fate. There is a 20–30% rate of popliteal artery occlusion with posterior dislocation of the knee.1,8,9,19,26 This injury merits a CT angiogram of the leg even if distal pulses are present. Penetrating injury from gunshot wounds and shotgun wounds is also an important cause of popliteal disruption. Hemorrhage is not as common as thrombosis in popliteal and tibial artery injuries. A pair of popliteal veins accompanies the artery and complete venous disruption is uncommon. Blunt trauma from a bumper strike in pedestrian trauma is also an important cause of injury. This is particularly true when a pedestrian is pinned between the bumpers of two automobiles. Distal popliteal or proximal tibial vessel injury is common in this setting. Adequate exposure of the popliteal artery for injuries associated with posterior knee dislocations requires a medial incision from the proximal popliteal space to the distal popliteal space with division of the medial head of the gastrocnemius muscle and the semimembranosis and semitendonosis muscles with full view of the popliteal artery and vein and the tibial nerve. This insures adequate vascular control and the opportunity for successful repair. When closing the wound, approximation of the divided muscle yields with absorbable sutures will insure an excellent functional result. Distal popliteal and proximal tibial vessel injuries are approached through a medial incision below the knee along the posterior margin of the tibia. This may be extended distally by dividing the soleus muscle over the course of the tibial-peroneal trunk and the posterior tibial vessels. Popliteal and tibial artery injuries are usually complex and primary repair is rarely possible. Saphenous vein interposition grafts are the best method of reconstruction. PTFE is to be avoided in all but the most dire circumstances when no lower extremity or upper extremity vein conduit is available. It has a high late failure rate. These injuries are often associated with orthopedic injuries. The vascular repair should be performed first or, if absolutely necessary, shunts should be placed while the orthopedic procedure is performed. Four-compartment calf fasciotomy should be added in most popliteal artery injuries in view of the common finding of thrombosis and an interval of ischemia. It should always be performed in the setting of combined popliteal arterial and venous injuries. Tibial vessel injuries may be ligated if there is adequate flow through the remaining vessels. When in doubt, an intraoperative arteriogram should be obtained. In multiple tibial vessel injuries, a saphenous vein interposition should be performed to the distal tibial vessel that best supplies the foot and that can be most easily covered with healthy soft tissue.

839

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Management of Specific Injuries

SECTION 3 X

essential in patients with the postplebitic syndrome. Patient education is an important part of gaining their cooperation in pursuing measures to limit venous hypertension and its complications. Late neurologic sequelae are also uncommon.63,64 Causalgia, burning pain within 24 hours of injury in a specific nerve distribution, is rare.63,64 Few patients progress to the point of requiring sympathetic nerve blocks. Complex regional pain syndromes are also very uncommon and rarely require intervention. Modern pain management and physical therapy help mitigate the effects of posttraumatic peripheral neuropathy.63,64 Late development of either a pseudoaneurysm or an arteriovenous fistula is very uncommon.1,8,10,26 This is most likely due to early recognition and effective management of most extremity vascular injuries. Aggressive CT imaging has also limited the number of missed injuries that present later in their course. Vein interposition grafts are at risk for late development of stenosis or aneurysmal dilatation. Patients who have undergone complex vascular repairs should be followed yearly for the rest of their lives in order to detect complications early in their course. All of these complications are amenable to effective surgical and endovascular treatment.

EXTREMITY VASCULAR TRAUMA CASE PRESENTATIONS ■ Upper Extremity Case 1 History. An 18-year-old male was stabbed in the right axilla with pulsatile bleeding. Paramedics arrive at the trauma resuscitation bay with direct pressure on the axilla. Exam. BP 70/40, HR 120, Resp 28, temperature 37°C, GCS 12. Absent pulses, paralysis, and paresthesias in right arm with active arterial bleeding when direct pressure released from wound in right axilla. This is an isolated injury.

FIGURE 41-13 Incisions for proximal control axillary artery in the infraclavicular region and exposure of brachial artery injury in the upper arm and axilla.

Systemic heparin given in view of isolated injury and temporary control and gently occluded. Attention turned to axilla where longitudinal incision made while direct pressure held on upper arm to occlude venous inflow and arterial backflow. Lacerated axillary artery identified; take care to avoid median and ulnar nerves. Vein found to be intact. Small vascular clamp placed proximally and distally to injured artery and vessel loops in proximal vessels and pressure on upper arm released. No other injuries present (Fig. 41-13). One centimeter segment of proximal brachial artery lacerated longitudinally. Local Fogarty catheter thrombectomy performed and heparinized saline (10 U heparin/mL) flushed, taking care to limit infusion volume and avoid air and debris flush into level of vertebral origin. Debridement and spatulation of proximal and distal artery leads to over 2 cm defect with undue tension when approximation assessed with tension on clams. Saphenous vein segment harvest from left ankle region and interposition graft placed (Fig. 41-14).

Decision Making. Obvious axillary artery injury with hard signs present. Significant volume loss has occurred. Patient needs protection of the airway, direct control of hemorrhage, and immediate operation. Permissive hypotensive is indicated with immediate infusion of type O-negative packed red blood cells to raise systolic BP to no higher than 80–90 mm Hg. This may begin on the way to the operating room, but should not cause any delay. Proximal vascular control will require access to the axillary artery in the infraclavicular region. Saphenous vein interpostition graft may be required. Operative Management. Sterile prep and drape right arm with senior team member keeping direct pressure on injury site to control bleeding. Prep right shoulder and chest wall, and entire right leg to give access to saphenous vein if needed. First incision in the infraclavicular region carried down by musclesplitting pectoralis major muscle. Pectoralis minor tendon divided at coracoid process to expose axillary artery and vein that are encircled with double-passed silastic vessel loops.

FIGURE 41-14 Saphenous vein interposition graft for repair of brachial artery laceration.

Peripheral Vascular Injury

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CHAPTER CHAPTER 41 X

FIGURE 41-15 Right upper arm puncture wounds from pet pit bull bite.

FIGURE 41-16 Thrombosis of brachial artery deep to the largest puncture wound from the dog bite.

Distal pulses and Doppler flow assessed and found to be normal. Wound closed primarily. Thin sponge and tape dressing applied.

Saphenous vein interposition graft performed. Distal pulses and Doppler flow assessed and found to be normal. Wound closed primarily. Thin sponge and tape dressing applied.

Postoperative Plan. Serial right arm pulse examinations, neurologic examinations, and assessment muscle compartments in addition to inspection of right axillary wound site for presence of hematoma. Outcome. Fully recovered without neurologic deficit and with normal upper extremity blood flow.

Postoperative Plan. Serial right pulse examinations, neurologic examinations, and assessment of muscle compartments in addition to inspection of upper arm wound axillary wound site for presence of hematoma. Outcome. Fully recovered without neurologic deficit and normal upper extremity blood flow.

Case 2 History. A male in his 70s presents to the emergency department with a dog bite in the left arm. This occurred 2 hours ago and he reports rapid onset of severe pain and inability to move his arm. His pit bull has bitten him on two other extremities within the last 2 weeks. The patient has a history of hypertension, hyperlipidemia, cigarette smoking, and coronary artery disease. Exam. BP 180/90, HR 80, Resp 20, temperature 37°C. Nonbleeding puncture wounds in left medial aspect upper arm. Absent pulses below the level of the puncture wounds, paralysis, and paresthesias in right arm. Superficial wounds in left arm and left leg with normal neurovascular examination (Fig. 41-15).

Case 3 History. A 42-year-old male, restrained driver of sport utility vehicle crashes head-on into tree. Aspirated in the field and arrives 40 minutes after injury. He has been intubated in the field. Exam. BP 120/80, HR 110, Resp 18, temperature 37°C, GCS 8T, no wrist pulses in right arm, wrist Doppler pressure 70 mm Hg, FAST, x-rays, and CT imaging reveal severe head injury, chest injuries, Grade II splenic laceration, complex pelvis fractures with hematoma, and right humerus fracture. To angiogram for embolization hypogastric arteries, right arm arteriogram obtained (Fig. 41-17).

Decision Making. Obvious brachial artery injury with thrombosis and occlusion occurred. Now 2 hours of ischemia with limb threat to right arm. Patient needs expeditious restoration of blood flow. Physical examination indicates extent of injury and further imaging unnecessary and time consuming, increasing risk of prolonged ischemia and risk of limb loss. Patient needs to go directly to the operating room. Comorbidities place him at increased risk and the anesthesiologist needs to be alerted regarding patient’s medical history. Operative Management. Sterile prep and drape right arm, shoulder, and right leg for possible saphenous vein harvest. Incision made along medial aspect of arm from above to below; puncture wounds made avoiding including wounds to reduce wound infection risk. Vessel injury site and sufficient uninjured proximal and distal brachial artery exposed. Thrombosis of brachial artery segment deep to the largest puncture wound found (Fig. 41-16).

FIGURE 41-17 Thrombosis of brachial artery at fracture site with profunda brachial artery collateral flow to distal brachial artery. Wrist pressure 70 mm Hg.

842

Management of Specific Injuries

SECTION 3 X

Decision Making. Brachial artery injury with collateral flow generated wrist pressure of 70 mm Hg is not immediate limb threat. There are multiple potentially life-threatening injuries that preclude immediate extremity vascular repair. Management. Stabilized with critical care management of his multiple injuries including placement of intracranial pressure monitor. Right arm splinted and followed closely for adequacy of collateral flow. Compartment pressures in forearm measured daily and remained normal. Temporized for 72 hours, overall status improved. To operating room for saphenous vein interposition brachial artery and fixation humerus. Outcome. Slow recovery with mild central neurologic deficit. Normal motor and sensory exam in right arm, full function and normal upper extremity blood flow.

Case 4 History. A 20-year-old man suffers close-range shotgun wound to the left arm while bird hunting with his father and brother. He presents 1 hour after injury with severe pain and a pressure dressing and splint on this left arm. Exam. BP 130/80, HR 120, Resp 20, temperature 37°C. Isolated shotgun wound in left arm with extensive tissue loss. The arm is insensate, paralyzed, and pulseless below the level of the elbow. He has extensive bone and tissue loss (Fig. 41-18). Decision Making. Obvious severe loss of major vascular and neurologic structures and extensive musculoskeletal tissue in left forearm. This patient needs to go directly to the operating room with orthopedic surgery, vascular surgery, and plastic and reconstructive surgery colleagues to perform an assessment and determine whether limb salvage or amputation needs to be performed. Operative Management. Examination under anesthesia in the operating room by the trauma surgeon and specialty colleagues confirms extensive tissue loss including loss of long segments of the median, ulnar, and radial nerves. The prognosis for limb salvage is extremely grave and there is no chance for functional recovery even if extensive vascular artery and vein grafting and free tissue transfer are performed. This is not a salvageable limb and immediate amputation just above the elbow is performed. The trauma surgeon talks with family to

explain the situation. A complete series of pictures of the extremity injury is taken and copies placed in the chart. Outcome. Patient recovers rapidly and is fitted with robotic arm prosthesis. He returns to college the next semester.

■ Lower Extremity Case 5 History. A 23-year-old male struck in left groin by shrapnel from exploding gas canister aboard a Navy ship; transected femoral artery and vein were ligated aboard ship. Now, 13 hours later he arrives by helicopter transport. Exam. BP 120/80, HR 100, Resp 20, temperature 37°C. Isolated left groin injury packed with moist gauze. Left leg is cool, anesthetic, paralyzed, and pulseless. Calf compartments are tense. Decision Making. The patient is not well beyond the “golden period” of 6–8 hours and already has signs of compartment syndrome. The risk of limb loss is very high. The only hope for limb salvage is the prompt restoration of blood flow and calf compartment fasciotomy. Operative Management. Patient is given 5,000 U heparin bolus. A four-compartment fasciotomy of the calf is performed first. Generous incisions are made and the muscle appears ischemic (Fig. 41-19). Exploration of the femoral region reveals that the superficial femoral artery and the common femoral vein have been ligated. Clamps placed above and below ligation sites, ligatures removed,

A

B FIGURE 41-18 Shotgun wound to left arm. No sensation or motor function and wrist pulses and Doppler signals absent.

FIGURE 41-19 Fasciotomy incisions: (A) lateral incision releasing anterior and lateral compartments and (B) medial incision for release of posterior compartments.

Peripheral Vascular Injury

843

pain and swelling. Small tear in jeans and puncture wound on midleft anterior–medial thigh.

FIGURE 41-20 Left groin repair site. Common femoral artery, profunda femoral artery, vein interposition in superficial femoral artery, and spiral vein graft in the common femoral vein.

Fogarty catheter thrombectomy performed, heparin saline flushed, and 12 French shunt inserted in superficial femoral artery. Copious amounts of thrombus flushed out of distal veins by tightly wrapping the leg with an Esmark bandage from the foot to the upper thigh. Proximal femoral vein back flushed copiously to clear small amount of thrombus. Small chest tube cut to fashion suitable size shunt and placed in the common femoral vein. Long segment of vein harvested from uninjured right leg. Interposition graft performed in the superficial femoral artery. Panel graft fashioned by opening long segment of saphenous vein longitudinally and sewing it in a spiral around a 36 French chest tube. This graft is interposed in the common femoral vein (Fig. 41-20). Femoral wound closed and fasciotomy wounds loosely wrapped. Central line placed to follow volume status and maintain high urine output because of risk of acute renal failure from myoglobinuria. Leg placed in continuous passive motion device. Full anticoagulation with heparin begun 12 hours following operation. Outcome. Early to mild myoglobinuria without significant increase in creatinine. Rapid swelling muscles of calf but all remained viable. Rapid return of motor and sensory function in first week. However, postischemic neuropathic pain continued for 4 weeks. Fasciotomy wounds covered with split-thickness skin grafts at 7 days. Muscles remained viable and, by 6 weeks, neurologic function returned to 90% of normal with mild residual sensory deficit. Postoperative screening using duplex scan of veins of lower extremity weekly—no thrombus formation. Patient remained on warfarin for 3 months.

Case 6 History. A 27-year-old male construction worker grinding steel fitting felt stinging sensation in left mid thigh and rapid onset of

A

B FIGURE 41-21 CT angiogram. (A) Cross-section and (B) VTR views revealing lacerated left superficial femoral artery with acute pseudoaneurysm within the sartorius muscle.

CHAPTER CHAPTER 41 X

Exam. BP 130/80, HR 90, Resp 20, temperature 37°C. Firm swelling in area of puncture wound and obliquely from mid upper thigh to lower anterior–medial thigh. Normal pulses throughout left leg and ankle–brachial index normal and equal to right leg. CT angiogram of left leg obtained (Fig. 41-21).

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Management of Specific Injuries

SECTION 3 X FIGURE 41-22 Left leg preparation and draping. Landmarks marked on leg to outline site injury, course of artery, sartorius muscle, and margin femur leg. Incision made over course of sartorius muscle.

Decision Making. Partial injury of superficial femoral artery with acute pseudoaneurysm requires immediate exploration and repair. Depending on status of the vessel wall, local repair, vein patch angioplasty, or interposition graft will be required. Operative Management. Left and right legs prepped and draped. Incision made along course of artery of sufficient length for proximal and distal control. Longitudinal 15 mm laceration with remainder of artery wall normal and no vein injury found. Vein patch angioplasty performed. Hematoma evacuated and wound closed with closed suction drain (Figs. 41-22 to 41-24).

FIGURE 41-24 Saphenous vein patch repair with preservation of normal luminal diameter of superficial femoral artery.

Exam. BP 110/60, HR 100, Resp 16, temperature 37°C. Isolated through and through right calf wound. Extensive tissue damage (see below). Pulses and Doppler signals absent at ankle. Plantar sensation intact but diminished. Dorsiflexion of foot intact, plantar flexion present but diminished. Catheter arteriogram obtained (Fig. 41-25). Decision Making. Although severe vascular and musculoskeletal injury, nerve damage is limited with partial motor and

Outcome. Discharged home on day 4 following operation. Returned to work at 1 month.

Case 7 History. A 30-year-old male police officer shot close range with shotgun at scene of domestic violence call. Through-and-through wound in upper right calf. Minimal blood loss at scene and pressure dressing in place with bleeding controlled.

FIGURE 41-23 Longitudinal 15 mm laceration from shrapnel wound to left superficial femoral artery.

FIGURE 41-25 Arteriogram revealing occlusion of proximal posterior tibial and peroneal arteries and at mid-anterior tibial artery. Associated fracture of tibia and extensive loss in midportion of fibula.

Peripheral Vascular Injury

845

CHAPTER CHAPTER 41 X

A

FIGURE 41-27 Intraoperative completion angiogram at distal anastomosis of reverse saphenous vein popliteal to posterior tibial bypass. B FIGURE 41-26 (A) Medial calf entrance wound and (B) lateral exit wound in shotgun injury.

proximal tibial fracture with active bleeding. Tourniquet and pressure dressing applied.

sensory deficit. Saphenous vein bypass to distal tibial vessel and orthopedic stabilization with external fixation has favorable prognosis for limb salvage and recovery of function.

Exam. BP 100/50, HR 120, Resp 25, temperature 37°C, GCS 15. Complain of severe right leg pain. Tourniquet in place. Dressing taken down. No sensation or movement of foot and calf and no pedal pulses or Doppler tones present at ankle. Lines placed, intubated, and taken directly to the operating room. X-rays reveal extensive disruption of femoral condyles, patella, tibial plateau, and proximal tibia (Fig. 41-28).

Operative Management. Patient is given 5,000 U heparin bolus in trauma bay. Both legs prepped and draped. Injury has decompressed the anterior and lateral compartments. Medical compartments decompressed through same long medial incision on calf to expose distal posterior tibial artery. Saphenous vein bypass to distal posterior tibial artery performed. Extensive debridement wounds and external fixation performed by orthopedic surgery colleague. Partial closure of wounds with application of Wound Vac™ dressings. Split-thickness skin graft applied at 5 days after initial operation. Compartment fasciotomy of the calf is performed first (Figs. 41-26 and 41-27). Outcome. At 3 weeks, discharged home with external fixation tibia, continued physical therapy. Ultimately recovered with mild weakness in plantar flexion of foot and mild sensory deficit in heel and plantar aspect of foot. Promoted to sergeant and given desk job.

Case 8 History. A 35-year-old male bag handler at the airport distracted, drives tractor into a flatbed baggage trailer. Open right knee and

FIGURE 41-28 Open fractures with bone fragments missing distal femur, tibial plateau, proximal tibia, and severe soft tissue injuries.

846

Management of Specific Injuries

SECTION 3 X FIGURE 41-29 Exploration reveals complete transaction and maceration popliteal vessels and tibial and peroneal nerves and extensive open fractures. Patient required an above knee amputation.

Decision Making. Extensive soft tissue and skeletal trauma and associated vascular injury with need for tourniquet need immediate operative management. Portable x-rays and intraoperative angiogram can be performed as needed. Orthopedic surgery colleague needs to be involved as soon as possible to manage injuries, assess chances of limb salvage, and decide if immediate amputation needed. Trauma surgeon needs to discuss preoperatively with patient and family, if at all possible, the threat of limb loss and the possible need for immediate amputation. The status of the peroneal and tibial nerves will be one of the most important determinants of the possibility of limb salvage. Operative Management. Prep and drape of both legs, proximal control of popliteal vessels above the knee obtained, and tourniquet removed. Exploration of knee and upper calf reveals transaction and maceration of popliteal artery, vein, tibial nerve, and peroneal nerve. Extensive open fractures with bone fragments completely avulsed femoral condyles, tibial plateau, and proximal tibia. The decision is made to perform guillotine amputation above the knee and delay closure for 48 hours to assess extent of further muscle necrosis (Fig. 41-29). Outcome. Recovered and was fitted with dynamic above-knee prosthesis. Returned to work with some limitations 4 months later.

REFERENCES 1. Mattox KL, Feliciano DV, Burch J, et al. Five thousand seven hundred sixty vascular injuries in 4459 patients. Epidemiologic evolution 1958 to 1987: Ann Surg. 1989;209:698–707. 2. Davis TP, Feliciano DV, Rozycki GS, et al. Results with abdominal vascular trauma in the modern era. Am Surg. 2001;67:565–571. 3. Soubbotitch V. Military experiences of traumatic aneurysms. Lancet. 1913;2:720. 4. Makins GH. Injuries to the blood vessels. In: Official History of the Great War Medical Services: Surgery of the War. London, England: His Majesty’s Stationery Office; 1922:170.

5. De Bakey ME, Simeone FA. Battle injuries of the arteries in World War II: an analysis of 2,471 cases. Ann Surg. 1946;123:534. 6. Hughes CW. Arterial repair during the Korean War. Ann Surg. 1958; 147:555. 7. Rich NM, Baugh JH, Hughes CW. Acute arterial injuries in Vietnam: 1,000 cases. J Trauma. 1970;10:359–369. 8. Sise MJ, Shackford SR. Extremity vascular trauma. In: Rich NM, Mattox KL, Hischberg A, eds. Vascular Trauma. 2nd ed. Philadelphia: ElsevierSaunders; 2004:353–389. 9. Fox CJ, Gillespie DL, O’Donnell SD, et al. Contemporary management of wartime vascular trauma. J Vasc Surg. 2005;41:638–644. 10. Oller DW, Rutledge R, Clancy T, et al. Vascular injuries in a rural state: a review of 978 patients from a state trauma registry. J Trauma. 1992;32:740–746. 11. Rich NM, Manion WC, Hughes CW. Surgical and pathological evaluation of vascular injuries in Vietnam. J Trauma. 1969;9:279–291. 12. Giswold ME, Landry GJ, Taylor LM. Iatrogenic arterial injury is an increasingly important cause of arterial trauma. Am J Surg. 2004;187: 590–593. 13. Eslami MH, Csikesz N, Schanzer A, Messina LM. Peripheral arterial interventions: trends in market share and outcomes by specialty, 1998–2005. J Vasc Surg. 2009;50:1071–1078. 14. Amato JJ, Rich NM, Billy LJ, et al. High-velocity arterial injury: a study of the mechanism of injury. J Trauma. 1971;11:412–416. 15. Rich NM. Historic review of arteriovenous fistulas and traumatic false aneurysms. In: Rich NM, Mattox KL, Hirshberg A, eds. Vascular Trauma. Philadelphia: Elsevier Saunders; 2004:457–524. 16. Dennis JW, Frykberg ER, Veldenz HC, et al. Validation of nonoperative management of occult vascular injuries and accuracy of physical examination alone in penetrating extremity trauma: 5- to 10-year follow-up. J Trauma. 1998;44:243–253. 17. Menger MD, Pelikan S, Steiner D, et al. Microvascular ischemia– reperfusion injury in striated muscle: significance of “reflow paradox.” Am J Physiol. 1992;263:H-1901–H-1906. 18. Cambria RA, Anderson RJ, Dikdan G, et al. Leukocyte activation in ischemia–reperfusion injury of skeletal muscle. J Surg Res. 1991;51:13–17. 19. Frykberg ER, Schinco MA. Peripheral vascular injury. In: Feliciano DV, Mattox KL, Moore EE, eds. Trauma. 6th ed. New York: McGraw-Hill; 2004:941–971. 20. Mubarak SJ, Hargens AR. Acute compartment syndromes. Surg Clin North Am. 1983;63:539–565. 21. Williams AB, Luchette FA, Papconstantinou HT, et al. The effect of early versus late fasciotomy in the management of extremity trauma. Surgery. 1997;122:861–866. 22. Patel KR, Cortes LE, Semel L, et al. Bullet embolism. J Cardiovasc Surg. 1989;30:584–590. 23. Rich NM, Collins GJ, Anderson CA, et al. Missile emboli. J Trauma. 1978;18:236–239. 24. Perry MO. Complications of missed arterial injuries. J Vasc Surg. 1993; 17:399–407. 25. Frykberg ER, Dennis JW, Bishop K, et al. The reliability of physical examination in the evaluation of penetrating extremity trauma for vascular injury: results at one year. J Trauma. 1991;31:502–511. 26. Feliciano DV, Herskowitz K, O’Gorman RB, et al. Management of vascular injuries in the lower extremities. J Trauma. 1988;28:319–328. 27. Gonzalez RP, Falimirski ME. The utility of physical examination in proximity penetrating extremity trauma. Am Surg. 1999;65:784–789. 28. Johansen K. Vascular diagnostic options in extremity and cervical trauma. In: Rich NM, Mattox KL, Hischberg A, eds. Vascular Trauma. 2nd ed. Philadelphia: Elsevier-Saunders; 2004:125–136. 29. Dennis JW. Minimal vascular injury. In: Rich NM, Mattox KL, Hischberg A, eds. Vascular Trauma. 2nd ed. Philadelphia: Elsevier-Saunders; 2004: 85–96. 30. Cothren CC, Moore EE, Ray CE Jr, et al. Carotid artery stents for blunt cerebrovascular injury: risks exceed benefits. Arch Surg. 2005;140: 480–486. 31. Xenos ES, Freeman M, Stevens S, et al. Covered stents for injuries of the subclavian and axillary arteries. J Vasc Surg. 2003;38:451–454. 32. Harbrecht BG, Forsythe RM, Peitzman AB. Management of shock. In: Feliciano DV, Mattox KL, Moore EE, eds. Trauma. 6th ed. New York: McGraw Hill; 2008:213–233. 33. Jansen JO, Thomas R, Loudon MA, Brooks A. Damage control for resuscitation for patients with major trauma. BMJ. 2009;338: 1436–1440. 34. Bickell WH, Wall MJ, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994;331:1105–1109.

Peripheral Vascular Injury 51. Palazzo JC, Ristow AB, Cury JM, et al. Traumatic vascular lesions associated with fractures and dislocations. J Cardiovasc Surg. 1986;27: 688–696. 52. Rozycki GS, Tremblay LN, Feliciano DV, et al. Blunt vascular trauma in the extremity: diagnosis, management, and outcome. J Trauma. 2003; 55:814–824. 53. Romanoff H, Goldberger S. Combined severe vascular and skeletal trauma: management and results. J Cardiovasc Surg. 1979;20: 493–498. 54. Zalarvares CG, Marcus RE, Levin LS, Patzakis MJ. Management of open fractures and subsequent complications. J Bone Joint Surg Am. 2007; 89:884–895. 55. McCready RA. Upper-extremity vascular injuries. Surg Clin North Am. 1988;68:725–740. 56. Bosse MJ, MacKenzie EJ, Kellam JF, et al. A prospective evaluation of the clinical utility of the lower-extremity injury-severity scores. J Bone Joint Surg Am. 2001;83:3–14. 57. Durham RM, Mistry BM, Mazuski JE, et al. Outcome and utility of scoring systems in the management of the mangled extremity. Am J Surg. 1996;172:569–574. 58. Swiontkowski MF, MacKenzie EJ, Bosse MJ, et al. Factors influencing the decision to amputate or reconstruct after high-energy lower extremity trauma. J Trauma. 2002;52:641–649. 59. Singh R. The rapid resolution of depression and anxiety symptoms after lower limb amputation. Clin Rehabil. 2007;21:754–759. 60. Singh R, Ripley D, Pentland B, et al. Depression and anxiety symptoms after lower limb amputation: the rise and fall. Clin Rehabil. 2009;23: 281–286. 61. Rutherford RB. Diagnostic evaluation of extremity vascular injuries. Surg Clinic North Am. 1988;68:683–691. 62. Parry NG, Feliciano DV, Burke RM, et al. Management and short-term patency of lower extremity venous injuries with various repairs. Am J Surg. 2003;186:631–635. 63. Pollawski ZJ, Wiley AM, Murray JF. Post-traumatic dystrophy of the extremities. J Bone Joint Surg. 1983;65:642–655. 64. Wasner G, Backonja MM, Baron R. Traumatic neuralgias—complex regional pain syndromes (reflex sympathetic dystrophy and causalgia): clinical characteristics, pathophysiologic mechanisms and therapy. Neurol Clin. 1998;16:851–868.

CHAPTER CHAPTER 41 X

35. Duchesne JC, Islam TM, Stuke L, et al. Hemostatic resuscitation during surgery improves survival in patients with traumatic-induced coagulopathy. J Trauma. 2009;67:33–39. 36. Hirschberg A, Scott BG. Vascular damage control. In: Rich NM, Mattox KL, Hischberg A, eds. Vascular Trauma. 2nd ed. Philadelphia: ElsevierSaunders; 2004:165–179. 37. Vertrees A, Fox CJ, Quan RW, et al. The use of prosthetic grafts in complex military vascular trauma: a limb salvage strategy for patients with severely limited autologous conduit. J Trauma. 2009;66:980–983. 38. Rich NM, Hughes CW. The fate of prosthetic material used to repair vascular injuries in contaminated wounds. J Trauma. 1972;12:459–467. 39. Martin LC, McKenney MG, Sosa JL, et al. Management of lower extremity arterial trauma. J Trauma. 1994;37:591–599. 40. Feliciano DV, Mattox KL, Graham JM, et al. Five-year experience with PTFE grafts in vascular wounds. J Trauma. 1985;25:71–82. 41. Lau JM, Mattox KL, Beall AC, et al. Use of substitute conduits in traumatic vascular injury. J Trauma. 1977;17:541–546. 42. Fuchs S, Heyse T, Rudofsky G, et al. Continuous passive motion in the prevention of deep-vein thrombosis: a randomized comparison in trauma patients. J Bone Joint Surg Br. 2005;87:1117–1122. 43. Mellisinos EG, Parks DH. Post-trauma reconstruction with free tissuetransfer—analysis of 442 consecutive cases. J Trauma. 1989;29:1095–1102. 44. Ledgerwood AM, Lucas CE. Biologic dressings for exposed vascular grafts: a reasonable alternative. J Trauma. 1975;15:567–574. 45. Feliciano DV, Accola KD, Burch JM, et al. Extraanatomic bypass for peripheral arterial injuries. Am J Surg. 1989;158:506–510. 46. McDermott AGP, Marble AE, Yabsley RH, et al. Monitoring acute compartment pressures with the STIC catheter. Clin Orthop. 1984;190: 192–198. 47. Feliciano DV, Cruse PA, Spjut-Patrinely V, et al. Fasciotomy after trauma to the extremities. Am J Surg. 1988;156:533–536. 48. Howe HR, Poole GV, Hansen KJ, et al. Salvage of lower extremities following combined orthopaedic and vascular trauma: a predictive salvage index. Am Surg. 1987;53:205–208. 49. Bishara RA, Pasch AR, Lim LT, et al. Improved results in the treatment of civilian vascular injuries associated with fractures and dislocations. J Vasc Surg. 1986;3:189–195. 50. Johansen K, Daines M, Howey T, et al. Objective criteria accurately predict amputation following lower extremity trauma. J Trauma. 1990; 30:568–573.

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SECTION 4

SPECIFIC CHALLENGES IN TRAUMA

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CHAPTER 42

Alcohol and Drugs Larry M. Gentilello

There are over 1,675 trauma centers in the United States. Although there are still gaps in coverage, particularly in rural areas, 82% of the U.S. population has rapid access to a trauma center. And, there is a 25% reduction in mortality after injury with trauma center care compared to treatment at a nontrauma center. The rapid development of trauma centers and systems across the United States is one of the most important developments in the history of surgery.1 Despite this success, injuries are still the fifth leading cause of death. This figure actually understates their impact. Years of Potential Life Lost (YPLL), which subtracts the age a person dies from their life expectancy, is a better measure of burden of disease. When a man in the United States dies from an injury at the age of 20, the YPLL is 58 because the average life expectancy for a man in the United States is 78. If he dies of heart disease at the age of 77, there is only one YPLL. Heart disease causes five times the number of deaths as injuries, but injuries account for one and one half times as many years of life lost, and more than the amount attributable to all malignant neoplasms.2 Thus, the task of reducing injury-related mortality is far from complete. In a 12-year longitudinal study that tested the impact of a rigorous emphasis on continuous quality improvements, the center involved was unable to reduce major complications or mortality during the entire study period, despite implementation of numerous protocols.3 The authors concluded that mature trauma centers have already reached the limits of their effectiveness at reducing injury-related deaths. Further reductions in trauma mortality will require new strategies. The reasons for this were demonstrated in a study that looked at 753 consecutive deaths in a trauma center.4 Over 40% of those who died received cardiopulmonary resuscitation in the field and had nonsurvivable injuries. The leading cause of death was severe traumatic brain injuries. Roughly 90% of patients who died had such severe organ damage and destruction

that no current or conceivable future treatments would ever be able to prevent their death. Late deaths due to multiple organ failure, secondary brain injury, sepsis, and pulmonary emboli accounted for only 6% of deaths. The preventable death rate was 2.6%. Thus, a research breakthrough that prevents all deaths due to complications and eliminates all medical errors would have only a marginal effect on survival rates in trauma centers. The actual reductions would be much less than that. Up to 75% of injury-related deaths occur in the field. Autopsy reports suggest that most field deaths probably occur within minutes of injury before help has a chance to arrive. These patients will not benefit from improvements in care. The most promising way to reduce trauma mortality is to implement evidence-based injury prevention programs. Numerous studies have documented that misuse of alcohol and other drugs is the leading risk factor for injury, and there are highly effective methods to reduce these problems. In 1990, a report by the Institute of Medicine declared that the scientific basis for implementing routine screening for alcohol problems in medical settings and for providing brief interventions to those who screen positive was well-established and should now be adopted into routine practice.5 There have been over 100 clinical trials, most of them prospective controlled trials enrolling more than one-half million patients, demonstrating the positive effects of interventions. Given the relationship between alcohol and injury, trauma centers are ideal sites for establishing such programs.6 Studies conducted specifically in trauma centers have demonstrated their ability to reduce alcohol intake, injury recidivism, and drunk driving arrests. Such programs are not only cost-effective, but result in cost-savings to the hospital also.7–9 In 2006, the American College of Surgeons Committee on Trauma (COT) added two new requirements for trauma center verification. Level I and Level II centers must have a mechanism in place to identify injured patients who have

Alcohol and Drugs

MAGNITUDE OF THE PROBLEM Between 35 and 50% of patients admitted to a trauma center are under the influence of alcohol. The number of drivers using illicit drugs has recently been revealed to be as large, if not larger, than the problem of drunk drivers. In the 2007 roadside survey conducted by the National Highway Traffic Safety Administration, the percentage of weekend nighttime drivers testing positive for alcohol dropped from 36.1% in 1973 to 12.4% in 2007. Drivers with a blood alcohol concentration (BAC) over the legal limit of 0.08 g/dL dropped from 7.5% in 1974 to 2.2% in 2007; however, 16.3% of drivers tested positive for drugs. Of these, 11.3% were positive for illegal drugs, and 1.1% tested positive for a combination of illegal drugs and prescription narcotics or psychoactive medications.10 In 2001, alcohol misuse resulted in 34,833 deaths by causing or exacerbating 70 associated medical disorders such as cirrhosis, hepatitis, oropharyngeal cancers, gastrointestinal disorders, and other chronic diseases. In contrast, there were 40,933 alcohol-related injury deaths, which was more than all deaths due to alcohol-related chronic medical problems. Also, alcohol misuse also caused 788,005 YPPL as a result of all of its associated medical diseases, whereas the YPLL due to alcoholrelated injuries alone was nearly four times as high at 3,279,322. The only medical settings with as high a proportion of patients with substance use problems as trauma centers are inpatient psychiatry units. It is far more common for these patients to receive treatment for an injury than for any other medical or psychiatric problem. Thus, addressing substance misuse, which particularly overburdens trauma centers, is a natural part of a trauma center’s mission.

NATURE OF THE PROBLEM Since the beginning of the 20th century, the prevailing belief was that people who use alcohol could be divided into two types. One type was considered social drinkers, even if they

drank heavily. The others passed a certain irreversible threshold and became known as “alcoholics.” In the early 1980s, the Diagnostic and Statistics Manual III (DSM III) replaced the word alcoholism with the terms alcohol abuse and alcohol dependence syndrome. Alcohol abuse referred to patients who experienced repeated adverse consequences of their drinking, but displayed no signs of addiction or dependence. Such patients can quit ingesting alcohol on their own if they are sufficiently motivated. Patients with dependence syndrome demonstrate tolerance, withdrawal symptoms, and such loss of control that they are usually, but not always, unable to stop drinking without treatment. This is true despite experiencing repeated, often catastrophic, social, legal, and medical consequences. Alcohol abuse and alcohol dependence are mutually exclusive terms. This classification system will be replaced in DSM-V, scheduled for publication in 2013, to reflect more recent research about the nature of unhealthy substance use. Alcohol and drug problems are similar to hypertension; that is, their severity can be measured along a continuous scale of problem severity. The severity in any single individual varies over time from no problem, to a mild, moderate, or severe problem, based on a variety of environmental and social stresses that interact with genetic and other factors. The term “alcohol abuse” will be dropped because it is stigmatizing and clinically detrimental.

■ The Spectrum of Severity In the United States, approximately 30% of people do not use alcohol. Another 45% use it in a way that poses no risk to their health (Fig. 42-1). The remaining 25% use alcohol in ways that can damage their health in one of the two following ways: (1) acute intoxication that causes an injury (often referred to as binge drinking); or (2) long-term excessive use that results in chronic medical diseases. These two types of problems can together be called “unhealthy alcohol use,” a nonstigmatizing, nonjudgmental term that reflects a physician’s appropriate concern about his or her patient’s health.

Types of drinkers Alcohol dependent

Risky or harmful

Low- risk or abstinent

Prevalence in U.S. ~ 4%

Trauma center goa Brief intervention and referral

~25%

~70%

Brief intervention

No intervention

FIGURE 42-1 Matching interventions to problem severity for trauma patients who use alcohol or drugs. (Reproduced with permission from Daniel Hungerford, PhD, National Center for Injury Prevention and Control, Centers for Disease Control and Prevention).

CHAPTER 42

a drinking problem, and Level I centers must have a mechanism in place to offer an intervention to those who screen positive, as well. This pioneering COT mandate was the first time in the history of health care in the United States that any regulatory organization required that patients with a substance use problem, or any type of mental health problem, receive necessary counseling. The purposes of this chapter are as follows: (1) to review the scientific basis for the recommendation for routine provision of Screening, Brief Intervention, and Referral to Treatment (SBIRT) in a trauma center; (2) to provide guidance on optimal screening methods for alcohol and drug use disorders; (3) to review the key elements of a brief intervention; (4) to provide step-by-step guidance on how to establish an evidence-based SBI program in a trauma center, and (5) to review relevant legal, billing, and confidentiality concerns.

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SECTION 4

The threshold for unhealthy alcohol use is defined as more than four drinks for a male or three drinks for a female on any single drinking occasion. Such intake in average sized individuals would result in a BAC above the legal limit for driving and is associated with a greater than 2-fold risk of being injured due to intoxication. An additional definition is more than 14 drinks per week in a male or more than seven in a female. Even if the drinking episodes are spread out over a week and the person never reaches intoxication, alcohol is toxic to virtually every organ system. Therefore, exceeding these amounts over time will significantly increase the likelihood of developing a chronic alcohol-related medical disease. In recent years, there has been an unprecedented increase in drug overdoses. Deaths due to drug overdose are included as a form of unintentional injury in the International Classification of Disease Version 9 (ICD-9) codes. For decades, motor vehicle crashes were the leading cause of unintentional injury death, followed by falls. The problem has become so severe that deaths from drug overdoses have surpassed falls and are now the second leading cause of unintentional injury-related death. In 15 states, deaths due to drug overdoses have surpassed motor vehicle crashes and are the leading cause of death due to unintentional injury. The death rate from drug overdose is now seven times higher than it was at the height of the heroin epidemic in the early 1970s, and three and one half times as high as it was at the height of the crack cocaine epidemic in the 1980s. Illicit “street drugs” are not the primary cause of these fatal drug

overdoses. More than half are due to misuse of legal prescription drugs, most often obtained from a physician. The exploding overdose rate closely corresponds to a 6-fold increase in the amount of opiates and benzodiazepines prescribed since 1997 (Fig. 42-2). The appropriate goal of an intervention at the trauma center is to capitalize on the effects of the injury to increase a patient’s motivation to change their pattern of usage of intoxicants and to refer the smaller proportion with chronic dependence to available community treatment resources or support systems. Most patients with unhealthy alcohol use will respond to appropriately and skillfully delivered “brief interventions.” Research has demonstrated that even in dependent patients brief interventions more than double the likelihood that they will follow through on a treatment referral. Brief interventions, which will be further described below, are time-limited (10–30 minute), focused, nonconfrontational discussions between the patient and doctor or other health care professional. They are designed to raise the patient’s level of awareness of their need for behavioral change and their commitment to pursue it. They have specific elements and can be provided by anyone who is able to speak to patients with unhealthful alcohol use in a nonjudgmental, nonconfrontational manner. They are not, however, adequate as a stand-alone treatment for most patients with dependence. The largest study to date of Screening, Brief Intervention, and for patients who need it, Referral to Treatment (SBIRT),

Unintentional drug poisoning death rates, U.S., 1970–2004 Crude rate per 100,000

852

FIGURE 42-2 Unintentional drug poisoning death rates, United States, 1970–2004. (Courtesy of Leon J. Paulozzi, MD, MPH, National Center for Injury Prevention and Control, Centers for Disease Control and Prevention.)

Alcohol and Drugs

ALCOHOL DEPENDENCE SYNDROMES The relatively small percentage of patients with dependence require more than a brief intervention. Although alcohol use begins as a choice, for some patients it has become a disease that they have little control over, and they require medical treatment. Trauma centers are not able to act as treatment centers; however, they should have a list of treatment resources available in the community to provide to patients. Brief interventions have been shown to cause a greater than 2-fold increase in the probability that patients will follow through with a referral. Whether or not these patients require prophylaxis or treatment for withdrawal syndromes is an important consideration. The goals of prophylaxis and treatment are to minimize the risk of serious complications such as seizures, delirium tremens, and the cardiovascular morbidity that occurs as a result of sympathetic overload. Clinicians should consider treating withdrawal as the first step in a comprehensive plan aimed at referring these patients to treatment. Withdrawal is characterized by signs and symptoms that are the opposite of the pharmacologic effects of the drug that is the cause of the addiction. The four primary categories of addicting agents are alcohol, sedative-hypnotics (benzodiazepines, barbiturates), opiates, and stimulants. All drugs in each category are associated with similar withdrawal syndromes, but they differ in their intensity, timing of onset, and duration. Symptoms from cessation of short-acting drugs such as alcohol may emerge within 6–24 hours, whereas withdrawal from long-acting benzodiazepines may not emerge for several days. Alcohol and sedative-hypnotic drugs have similar pharmacologic effects and similar withdrawal symptoms. Cessation of stimulant use is characterized by depression and a risk of suicidal behavior.

SCREENING, BRIEF INTERVENTION, AND REFERRAL TO TREATMENT ■ Evidence of Effect in Trauma Settings One study of brief interventions analyzed their efficacy at reducing the recurrence of injury in injured adolescents by randomly assigning patients age 18 or 19 years to receive either a 30-minute brief intervention or standard care. At 6-month follow-up, the intervention group had a significant reduction in drinking and driving, moving violations, alcohol-related problems, and less than half as many alcohol-related injuries as patients in the control group.12 Another randomized, prospective, controlled trial was performed on 762 patients admitted to a Level 1 Trauma Center.7 Patients who screened positive were randomized to a single 15–30 minute brief intervention or to a no-intervention control group. At 1-year follow-up, the intervention group decreased their alcohol intake by 22 drinks per week compared to a 2, drink reduction in the conventional care group. A statewide registry was used to detect readmission to any hospital for treatment of an injury over a 3-year follow-up period. There was a 47% reduction in trauma readmissions in the intervention group compared to controls. There was also a 48% reduction in returns to the emergency department for treatment of another injury (Fig. 42-3). Another randomized, prospective trial of brief interventions showed that one driving under the influence (DUI) was prevented for every nine brief interventions performed at 3-year follow-up.13 Through their effect on reducing trauma recurrence, brief interventions have also been shown to result in cost-savings to trauma centers.8 The savings in health care costs over 3 years were $320 per intervention performed and $3.81 for every dollar invested in the screening and brief intervention program.

Intervention Control 0.10

Injury 0.05 recurrence

0.00

0

90

180

270 Days

360

FIGURE 42-3 Risk of repeat injury requiring treatment in the Harborview Medical Center, Emergency Department, Seattle Washington (hazard ratio 0.53, 95% CI 0.26–1.07). (Reproduced with permission from Gentilello LM, Rivara FP, Donovan DM, et al. Alcohol interventions in a trauma center as a means of reducing the risk of injury recurrence. Ann Surg. 1999;230(4):473–483.)

CHAPTER 42

was a multistate program delivered across six states and several tribal nations.11 It was conducted in trauma centers, primary care clinics, emergency departments, general medical and surgery wards, and college health clinics, and enrolled a diverse population. Screening was administered to all adult patients who presented to the study sites for care, unless they were too severely ill or injured. There were 459,599 patients screened using standardized questionnaires, making it the largest study of its kind. Nearly one out of four patients who presented for medical care (22.7%) screened positive for unhealthy alcohol or drug use; however, screening results indicated that 15.9% of patients were considered nondependent, and in need of a brief intervention only. An additional 3.2% would benefit from having two to three additional sessions that could be administered during return visits. Only 3.7% of patients, or one out of six patients who screened positive, were considered dependent and in need of formal treatment. Studies show that the majority of patients with unhealthy alcohol use that results in encounters with the medical system, including studies conducted in trauma centers, are appropriate candidates for a brief intervention.

853

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Specific Challenges in Trauma

TABLE 42-1 The Alcohol Use Disorders Identification Test (AUDIT) Was Designed to Detect Alcohol Problems Across a Range of Severity, Including Harmful or Nondependent Drinking.

SECTION 4

AUDIT Questionnaire Hazardous Use 1. How often do you have a drink containing alcohol? Never Monthly or less 2–4 times/month 2–3 times/week 2. How many drinks of alcohol do you have on a typical day when you are drinking? 1–2 3–4 5–6 7–9 3. How often do you have six or more drinks on one occasion? Symptoms of Dependence 4. How often during the last 5. How often during the last 6. How often during the last drinking session? 7. How often during the last 8. How often during the last had been drinking?

4 times/week 10 or more

year have you found that you were not able to stop drinking once you had started? year have you failed to do what was normally expected from you because of drinking? year have you needed a first drink in the morning to get yourself going after a heavy year have you had a feeling of guilt or remorse after drinking? year have you been unable to remember what happened the night before because you

Responses to Questions 3–8 Never Less than monthly

Monthly

Weekly

Daily or almost daily

Consequences of Drinking 9. Have you or has someone else been injured as a result of your drinking? 10. Has a relative, friend, or a doctor or other health worker been concerned about your drinking or suggested you cut down? Responses to Questions 9–10 No Yes, but not in the last year

Yes, during the last year

Questions 1–8 are scored 0, 1, 2, 3, or 4 points. Questions 9 and 10 are scored 0, 2, or 4 points only. A total score of 8 or more points indicates a strong likelihood of hazardous or harmful alcohol consumption. Reproduced with permission from The Alcohol Use Disorders Identification Test, Version 2. Geneva: World Health Organization; 2001.

■ Screening Methods A best-practice screening model combines both a standardized questionnaire with a laboratory test (urine toxicology screen or blood alcohol test). Patients with a very high BAC or positive toxicology screen should be considered as screening positive. Many physicians are mistrustful of patient self-report, but patients with an alcohol problem do not typically underreport their drinking when asked in a respectful, concerned, and confidential manner.14 Toxicology testing may be a better means of detecting drug use, as patients may be less willing to disclose use of an illegal substance. A screening questionnaire must be sensitive enough to detect the full spectrum of alcohol problems from mild unhealthy drinking to severe dependence. The Cut down on drinking, Angry when criticized about drinking, Guilty feelings about drinking, Eye-opening morning drinking (CAGE) and Michigan Alcohol Screening Test (MAST) questionnaires have been used for decades, but were primarily designed to detect dependence and are less sensitive to more moderate drinking problems.

The Alcohol Use Disorders Identification Test (AUDIT) is a 10-question, self-report screening tool developed by the World Health Organization, and it has been validated in trauma patients and in numerous languages and cultures15 (Table 42-1). It was designed to be sensitive to a broad spectrum of harmful drinking levels. It assesses drinking quantity and frequency (three questions), problems caused by drinking (two questions), and symptoms of dependence (five questions). It takes less than 2–4 minutes to administer and seconds to score the results. A score of 8 or more is considered to be a positive screen. Because the safe recommended level of alcohol intake is different between males and females, the three quantity and frequency questions decrease the sensitivity of the AUDIT in females, and a lower cutoff score of five points has been recommended.16 Patients who score over 20 points should be considered as being likely to have alcohol dependence and require further assessment and, most likely, a referral to treatment. The AUDIT can often be abbreviated because many patients drink infrequently or not at all. If the answer to question one is zero concerning frequency

Alcohol and Drugs

■ Guidelines for Brief Interventions for Trauma Patients Most studies of successful brief interventions have used a patient-centered style of motivational counseling derived from Motivational Interviewing. Healthy change occurs when people perceive a large enough discrepancy between the status quo and how they would prefer things to be. It is the clinician’s behavior during the intervention that strongly influences how the patient talks about his or her drinking. An interviewing style of polite and genuine curiosity facilitates change. On the other hand, an interviewing style that the patient experiences as attacking or confrontational provokes resistance and slows down the process. Research has failed to support the concept that patients with alcohol problems have personality traits such as poor motivation and rigid defense mechanisms such as denial. Rather, these factors are an outcome of the style of interaction between the clinician and patient. When patients “in denial” are heard to argue in favor of the status quo (more drinking), it is usually because he or she has encountered a confrontational or authoritarian counselor. Confrontational tactics are particularly counterproductive in a trauma center because the “denial” they provoke requires too much time and skill to undo.

■ Application of Brief Intervention FRAMES. The basic elements of a brief intervention can be summarized by the acronym FRAMES. They consist of providing nonpersonal, concerned Feedback of the patient’s personal risk or impairment related to alcohol consumption; emphasizing their personal Responsibility to change; giving clear Advice that change is needed; and presenting a Menu of alternative strategies that may be appropriate and helpful. This material is presented in an Empathetic manner intended to increase the patient’s sense of Self-efficacy, optimism, and confidence that change is possible.

SUM. Another acronym that has been used to summarize the key components of a brief intervention is SUM or Screening feedback, Understanding the patient’s views, and providing a Menu of change options. The two main sources of feedback for trauma patients are their BAC upon admission and how their score on a questionnaire compares to established standards. This information can be presented on personalized feedback forms or verbally. For giving feedback about their BAC a simple five-step acronym is “RANGE.” Tell patients the Range of possible BAC results, from 0 (sober) to 0.6 (fatal). State that All drivers know that 0.08 is the beginning of drunk driving. Normal drinkers stay under 0.05, even when not driving. Then, Give the patient his or her BAC result in relation to 0.08; for example, “Your BAC was 0.16, which is twice the 0.08 figure for drunk driving.” Elicit the patient’s reaction and do not argue. If the patient challenges the validity of the BAC test, the clinician might state, “The best way to explain this is to show you an illustration that indicates that at your blood alcohol concentration of 0.14, you are 48 times more likely to have a serious crash than if you had not been drinking.” It is important for clinicians to tell patients that they are not concerned with labels (alcoholism), “but I am concerned if alcohol is hurting you.” The goal of an intervention is to establish empathy, not to administer blame. Empathy is the clinician’s primary tool in avoiding resistance or denial. Studies demonstrate that drinking is more likely to be reduced when the counseling style is empathetic, rather than confrontational. Understanding (from SUM) the patient’s views can be done by asking them about the “pros and cons” of their drinking. After the clinician has listened to and summarized what the patient believes are benefits such as “It helps me to relax,” “It makes it easier to interact with others,” or “It helps me to have a good time,” he or she may ask the patient to explore the “cons” by asking, “What are some of the things you don’t like about drinking?” For example, if the patient indicates that one of the negative aspects of drinking has been frequent arguments with family members, the clinician might ask, “How does your alcohol use affect your ability to have a stable family life?” The goal is to raise doubt by having the patient, rather than the clinician, articulate how alcohol use is having an adverse effect on their family, health, work, finances, driving record, or legal status. Asking for and then summarizing the pros and cons is a central brief intervention technique. It allows the patient to state the ways that their use of alcohol is adversely affecting them so that recommendations for change are based upon the goals and values that are important to them. Menus of strategies are offered when the SUMS technique is used. When given a choice the patient is more likely to find an approach that is acceptable to his or her own particular situation. For example, a patient may refuse a referral to formal treatment or to a self-help group, but may be willing to accept an incremental change. Examples would be setting specific limits on their alcohol intake and agreeing to seek further help if they are unable to stay within the negotiated limit. Or, the patient may only be willing to agree to avoid drinking and driving and agree to become involved with a self-help group if they are unable to do so.

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of use, no further questioning is necessary. The AUDIT is quickly becoming the standard of care in most clinical settings and is widely available in downloadable form.17 At a minimum, reasonably effective screening for drinking above safe guidelines can be performed by asking only one question. In a study of 1,537 patients who presented to the emergency department with an injury, researchers asked the question, “when was the last time you had five or more drinks in one day (more than four drinks for women)?” Formal interviews by trained staff were then conducted to determine if an alcohol problem was present. This single question had sensitivities and specificities of 85 and 70% in males and 82 and 77% in females. This indicates that asking only one straightforward question can be used as a brief screening method. If the patient answers “within the past three months,” then the full AUDIT should be administered.18 Although more timeconsuming, the Alcohol, Smoking, and Substance Involvement Screening Test (ASSIST) is another instrument that was designed to detect and score problems with alcohol, drugs, and tobacco.19

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The “menu of options” list is most often presented in ascending order of commitment as follows: no change whatsoever, merely think about it and notice more about your drinking in the future, cut down, or quit. If the patient is able to select one of these options, then a plan for obtaining this goal can be discussed. Giving advice is also an important part of the menu. It is appropriate for the clinician to weigh in with an opinion. This usually means offering clear advice to the patient regarding the need to change his or her drinking pattern. Most studies of brief interventions with positive outcomes have used non–substance abuse specialists. This means that to successfully use these techniques a clinician does not have to have special training and expertise in managing unhealthy substance use. Brief interventions can be performed by anyone who is willing to learn the methods and who is capable of showing respect and concern for injured patients who sometimes drink too much and take dangerous risks. There are multiple individuals in every trauma center who meet these criteria. The list includes but is not limited to nurses, social workers, physician assistants, psychologists, chaplains, peer-counselors, health educators, and physicians. Although trauma surgeons may obtain the training necessary to perform brief interventions and should have the skills needed to screen and counsel patients with a problem, time demands and staffing constraints will usually prevent them from being the primary providers of this service. The role of the trauma surgeon, however, is critical in providing administrative support through education and advocacy for these services.

■ Ask, Advise, Assist, Arrange This acronym is recommended by the National Institute of Alcohol Abuse and Alcoholism and the National Institute on Drug Abuse. If the patient is ready to change, the clinician assists in setting goals and agreeing on plans to arrange mechanisms to support these efforts. There is a wealth of information online, including scripts, manuals, and videos.20,21

HOW TO ESTABLISH AN EVIDENCE-BASED SBIRT PROGRAM When considering starting an SBIRT program many feel that their first and only concern is to assign willing individuals to obtain the required training. In reality, training is the last step in the process. If there is little administrative support for the SBIRT program within the hospital and among those in positions of leadership and decision making, it is unlikely that the program will succeed, even if there are several enthusiastic supporters. The first step is to make a case for establishing the SBIRT program. Hundreds of studies have established effectiveness, and some concisely summarize these results and will help to make the case.22,23 The message should be concise and simple. In appealing to potentially interested colleagues, research, and evidence of patient benefits should be provided and an attempt made to recruit additional stakeholders into the process. Once buy-in is achieved, the next step is to organize implementation. A team approach works best, and this involves

recruiting people from multiple departments such as the following: psychiatry, addiction medicine, social work, nursing, trauma leadership, surgery and emergency medicine colleagues and chairs, clergy, pain medicine staff, hospital executives, billing personnel, and anyone else who might contribute. It is important to gain their respect and trust and the authority to carry out the project. At meetings of interested parties key decisions can be made such as whether the program will require recruiting additional staff or changes in the responsibilities of the existing staff. The key to establishing the need for an SBIRT program is to convey concern, to provide everyone involved with information about what it is and how it works, to establish goals and plans to work together, and to develop timelines and responsibilities. The fourth step is to determine who will provide the intervention. Someone on staff may be able provide the entire service. Alternatively, screening may be performed by one individual and the intervention provided by another. Time, availability, background knowledge and experience, interpersonal skills, and willingness to participate will help determine the appropriate candidates. Other factors need to be considered such as typical length of stay, how to handle early discharges, how many patients will need to be screened, and how many interventions are likely to be needed. The type of intervention should then be chosen based upon a variety of available models. These range from 5 minutes of brief advice to more extensive motivational interviews that consist of 15–20 minute sessions. Ideally, all patients should be screened, but this may not be practical. Policies and procedures to determine who should be screened should be established in order to train staff and for subsequent evaluation of the program. Next, screening procedures should be established. A single question followed by a full AUDIT if indicated is only one of many evidence-based screening procedures. Screening for drugs can be accomplished when using the single question initial screen. The patient is asked whether they have exceeded safe alcohol intake limits in the past three months “or used street drugs or prescription drugs to get high.” As with screening, step seven is a determination of how to establish the intervention procedures that follow. This will include when the intervention will be delivered, how the person who is to deliver the intervention is to be notified of a positive screening result, and the development of forms, handouts, and other materials that will be used during the intervention. Step eight is to establish procedures to manage patients who are dependent and who will require a referral to treatment. This will involve developing a list of resources in the community that can be provided to patients. Included would be contact numbers for self-help groups, formal treatment, and for determining insurance coverage and health plans. The next step before initiation of the process is to seek long-term buy-in for the plan by reviewing it with all levels of employees. Finally, it is time to train staff who will provide the screening and the intervention service. It is useful to try to include others such as supervisors and administrators, who will not provide the service, but who need a better understanding of what SBIRT is and why it is important. There are a variety

Alcohol and Drugs

ADDITIONAL CONSIDERATIONS ■ Billing for SBIRT In 2008, the American Medical Association, the group responsible for maintaining the Common Procedural Terminology (CPT) codes used for billing, passed and established new CPT codes for SBIRT. There are two codes, 99408 and 99409, for SBIRT lasting greater than 15 or 30 minutes. Most insurers have agreed to pay for these codes, and a requirement that insurers cover SBIRT in their plans is written into the health care reform bill that will be implemented throughout the United States over the next 5 years. Nonphysician providers such as nurse practitioners, physician’s assistants, and others who provide services “incident” to a physician may use these codes also. The Center for Medicare and Medicaid Services (CMS) passed similar codes (G0396 and G0397) in 2008 to cover SBIRT services in Medicare patients. Medicaid also passed billing codes (H0049 and H0050); however, Medicaid is a joint federal and state program that requires cost sharing. As of 2010, approximately 15 states have adopted the Medicaid codes. A complete primer and web-based source on how to use these codes is available in an on-line form that includes webinars and recordings.25

■ Uniform Policy and Provision Laws In 1948, the National Association of Insurance Commissioners (NAIC) adopted a model law that stated that if a patient is injured while under the influence of any intoxicant, the insurance company is not liable for any resulting hospital or medical charges. This law was adopted in some form in 42 states and provided a strong disincentive to determine a patient’s BAC, which can be an important tool when provided as a part of feedback during a brief intervention.26 Since 2001, nearly half of the states that had these laws have repealed them. In states that still have these laws, none of the screening questionnaires such as the AUDIT can be used as a basis to deny a claim. This is because they discuss alcohol use over a period of months and do not determine if the patient was intoxicated at the time of injury. Trauma centers in states that still have these laws may wish to avoid BAC measurements and rely solely on questionnaires.

■ Confidentiality Concerns The Code of Federal Regulations known as 42 CFR Part 2 “Confidentiality of Alcohol and Drug Abuse Patients Records” governs the management and disclosure of any information related to screening, treatment, or referral of patients with unhealthy alcohol use for treatment. Patients with substance use are still subject to stigma, with potential loss of employment, insurance, loss of child custody, housing, and other requirements of life. The purpose of the law was to ensure that patients who were willing to receive help do not suffer losses that other patients with a problem can avoid by denying their need for help. The “Part 2” statute is much more restrictive than the Health Insurance Portability and Accountability Act, which allows for disclosure of health information to other health care workers within the same facility without written authorization from the patient. CFR 42, Part 2, allows disclosures concerning substance use only to other staff within the same facility who have a need for the information to perform their duties. With only several exceptions trauma centers that screen and provide interventions or referrals or who employ staff whose primary responsibility is to perform such procedures must abide by this law. They have an ethical and legal duty to ensure that information on alcohol and drug use is not disseminated to those who do not have a right to know.27

CONCLUSION The United States Preventive Services Task Force provides guidelines to Congress and payers concerning evidence-based preventive services. In a cost–benefit ranking based on the magnitude of the disease burden and the evidence of benefit that highlighted which preventive services should be prioritized, alcohol screening and brief intervention were tied at second place with colorectal cancer and screening for hypertension. Also, it was ranked ahead of cervical Pap smears, cholesterol measurements, mammograms to detect breast cancer, screening for diabetes mellitus, education for injury prevention, and other services.28 The brief intervention procedures discussed in this chapter have been tested and applied in a variety of health care settings, and a large number of research studies have established their effectiveness. When receiving medical care, patients have the right to expect that the underlying causes of their disease will be sought and addressed. The field of trauma surgery has taken the lead in ensuring that this is being done.

REFERENCES 1. MacKenzie EJ, Rivara P, Jurkovich G, et al. A national evaluation of the effect of trauma-center care on mortality. N Engl J Med. 2006;354:366–378. 2. WISQARS (Web-based Injury Statistics Query and Reporting System), National Center for Injury Prevention and Control, Centers for Disease Control. Available at: http://www.cdc.gov/injury/wisqars/index.html. 3. Hoyt DB, Coimbra R, Potenza B, et al. A twelve-year analysis of disease and provider complications on an organized level I trauma service: as good as it gets? J Trauma. 2003;54:26–36. 4. Stewart RM, Myers JG, Dent DL, et al. Seven hundred fifty-three consecutive deaths in a level I trauma center: the argument for injury prevention. J Trauma. 2003;54:66–70.

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of training programs available at conferences, on websites, and videos, and at a variety of ongoing training seminars. Once ongoing means of support and a mechanism of troubleshooting are available, the program is initiated. It is also important to develop a monitoring system and quality improvement process. This monitoring would include the percentage of patients screened, number of interventions performed per positive screen, patients referred, and other possible measures. A complete program with information on how to navigate the above steps has been specifically designed for trauma centers and is available in a format that can be downloaded from the Centers for Disease Control and Prevention, National Center for Injury Prevention and Control.24

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5. Broadening the Base of Treatment for Alcohol Problems. Institute of Medicine. Washington, DC: National Academy Press; 1990. 6. Developing Best Practices of Emergency Care of the Alcohol-impaired Patient. Recommendations from the National Conference. National Highway Traffic Safety Administration. Washington, DC: S Department of Transportation; 2000. 7. Gentilello LM, Rivara FP, Donovan, DM, et al. Alcohol interventions in a trauma center as a means of reducing the risk of injury recurrence. Ann Surg. 1999;230:473–483. 8. Gentilello LM, Ebel BE, Wickizer TM, Salkever DS, Rivara FP. Alcohol Interventions for trauma patients treated in emergency departments and hospitals: a cost benefit analysis. Ann Surg. 2005;241:541–550. 9. Schermer CR, Moyers TB, Miller WR, Bloomfield LA. Trauma center brief interventions for alcohol disorders decrease subsequent driving under the influence arrests. J Trauma. 2006;60:29–34. 10. National Institute of Drug Abuse. Drugged Driving. Future Research Directions. http://druggeddriving.org/pdfs/NIDAMarch192010Drugged DrivingMeetingSummary.pdf. 11. Madras BK, Compton WM, Avula D, et al. Screening, brief interventions, referral to treatment (SBIRT) for illicit drug and alcohol use at multiple healthcare sites: comparison at intake and 6 months later. Drug Alcohol Depend. 2009;99:280–295. 12. Monti PM, Colby SM, Barnett NP, et al. Brief intervention for harm reduction with alcohol-positive older adolescents in a hospital emergency department. J Consult Clin Psychol. 1999;67:989. 13. Schermer CR, Moyers TB, Miller WR, Bloomfield LA. Trauma center brief interventions for alcohol disorders decrease subsequent driving under the influence arrests. J Trauma. 2006;60:29–34. 14. Donovan DM, Dunn CW, Rivara FP, et al. Comparison of trauma center patient self-reports and proxy reports on the Alcohol Use Identification Test (AUDIT). J Trauma. 2004;56:873–882. 15. Management of Substance Abuse: Screening and Intervention for Alcohol Problems in Primary Health Care. World Health Organization (WHO). http://www.who.int/substance_abuse/activities/sbi/en/ (accessed 3/29/2011). 16. Neumann T, Neuner B, Gentilello LM, et al. Gender differences in the performance of a computerized version of the Alcohol Use Disorders Identification Test in subcritically injured patients who are admitted to the emergency department. Alcohol Clin Exp Res. 2004;28: 1693–1701.

17. AUDIT. The Alcohol Use Disorders Identification Test, Version 2. Geneva Switzerland: World Health Organization; 2001. http://whqlibdoc.who. int/hq/2001/who_msd_msb_01.6a.pdf. 18. Canagasaby A, Vinson DC. Screening for hazardous or harmful drinking using one or two quantity-frequency questions. Alcohol. 2005;40:208–213. 19. Screening for Drug Use in General Medical Settings. Bethesda, MD: NIDA; 2008. http://www.nida.nih.gov/nidamed/resguide/resourceguide.pdf. 20. Helping Patients Who Drink too Much. Bethesda, MD: National Institute on Alcohol Abuse and Alcoholism. Accessible at http://pubs.niaaa. nih.gov/publications/Practitioner/CliniciansGuide2005/clinicians_guide. htm. 21. NIDAMED. Resources for Medical and Health Professionals. Bethesda, MD: National Institute on Drug Abuse. Available at http://www. drugabuse.gov/nidamed/. 22. Babor TF, McRee BG, Kassebaum PA, et al. Screening, brief intervention, and referral to treatment (SBIRT): toward a public health approach to the management of sub-stance abuse. Subst Abus. 2007;28:7–30. 23. Alcohol Alert. Brief Interventions. National Institute on Alcohol Abuse and Alcoholism Number 66, July 2005. Accessible at: http://pubs.niaaa.nih. gov/publications/AA66/AA66.htm. 24. Screening and Brief Interventions (SBI) for Unhealthy Alcohol Use. A Step-by-Step Implementation Guide for Trauma Centers. John HigginsBiddle, PhD Dan Hungerford, DrPH Kathryn Cates-Wessel. Available at: http://www.cdc.gov/InjuryResponse/alcohol-screening/pdf/SBIImplementation-Guide-a.pdf. 25. Osman P, Brown RL. Billing and Reimbursement. Wisconsin Initiative to Promote Healthy Lifestyles (WIPHL). Available at: http://www.wiphl.com/ bills/index.php?category_id4648. 26. Gentilello LM, Donato A, Nolan S, et al. Effect of the Uniform Accident and Sickness Policy Provision Law on Alcohol Screening and Intervention in Trauma Centers. J Trauma. 2005;59:629–636. 27. Gentilello LM, Samuels PN, Henningfield JE, et al. Alcohol screening and intervention in trauma centers: confidentiality concerns and legal considerations. J Trauma. 2005;59:1250–1254. 28. Maciosek MV, Coffield AB, Edwards NM, et al. Priorities among effective clinical preventive services. Results of a systematic review and analysis. Am J Prev Med. 2006;31:52–61.

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The Pediatric Patient David W. Tuggle and Nathaniel S. Kreykes

Pediatric trauma is the leading cause of death of children, as well as the leading cause of permanent disability in this population. It has often been said that children are not merely small adults, and this is never more accurate than in pediatric trauma.1 Although the principles of trauma care are the same for children as with adults, the differences in care required to optimally treat the injured child require special knowledge, careful management, and attention to the unique physiology and psychology of the growing child or adolescent. With this in mind, it is important to view pediatric trauma as a similar but separate entity from adult trauma. It was Haller of Johns Hopkins University who stressed the importance of regional trauma systems for pediatric patients. His system for safe care included two-way communication, dependable transportation, emergency medical technicians trained in the care of newborns, infants, and children, a designated pediatric intensive care unit (ICU), and rehabilitation.2 His work has helped shape and improve our pediatric trauma care significantly.

EPIDEMIOLOGY OF THE INJURED CHILD Although medical science has made vast strides in the surgical care of the neonate and child, injury remains the leading cause of childhood death in patients under 14 years of age.3 As developing countries become more sophisticated, injury becomes the leading cause of death in children.4 Of interest, there was a 45.3% reduction in the mortality rates from unintentional injury in children in the United States from 1979 to 1996.5 This reduction is crucial if one accepts that the treatment of injuries sustained in the year 2000 will ultimately cost $406 billion—$80.2 billion in medical costs and $326 billion in productivity losses.6 Of that total, injuries among children aged 0–14 account for $51 billion.6 Using the Centers for Disease Control and Prevention Web-Based Injury Statistics Query and Reporting System (WISQARS), a death and injury report for any age group and any type of injury can be obtained.

Children have different patterns and causes of injury depending on age, further emphasizing the need for regional pediatric trauma centers. The defined age range constituting a pediatric age group, however, varies between institutions. The mechanisms of injury and mortality in children have remained remarkably consistent. In children over 1 year and under 14 years of age, motor vehicle crashes cause 44.2% of all pediatric trauma deaths (2000–2005). A detailed review of mortality statistics reveals the home as an area of continuing concern.7 Other areas of concern include falls, bicycle-related injuries, and injuries associated with crashes of all-terrain vehicles.8 Childhood injuries most commonly occur as energy is transferred abruptly by rapid acceleration, deceleration, or a combination of both. The body of a child is very elastic and energy can be transferred creating internal injuries without significant external signs. Due to the relative close proximity of vital organs when compared with adults, children can have multiple injuries from a single exchange of energy. Penetrating trauma is a much less common form of injury in small children, accounting for 1–10% of admissions to pediatric trauma centers. No matter the type of injury, the health care professional evaluating the injured child should keep in mind these significant differences during evaluation and management.

INITIAL ASSESSMENT AND RESUSCITATION OF THE INJURED CHILD Primary survey with simultaneous resuscitation and secondary survey with definitive care, as promoted by the Advanced Trauma Life Support (ATLS) course of the American College of Surgeons Committee on Trauma (ACSCOT), apply to a child as well as the adult. Multiple organ injuries are much more common in the child than in the adult and, as a result, it is best to manage children as if every organ is injured until proven otherwise.

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The care of the injured child often starts with a brief evaluation in the prehospital setting. The ASCOT has published a minimum set of criteria for the definition of a “major resuscitation” once the patient arrives at the hospital.9 A patient who needs major resuscitation is typically a child who would benefit from the trauma surgeon being present at the bedside at this point. This condition is ideally determined in the field as noted above or from a referring hospital. Although these criteria are the same for injured patients of all ages, hypotension is age specific.

■ Airway Management Assessment of the child’s airway is the first step. Most children do not have preexisting pulmonary disease, so a room air saturation of greater than 90% indicates effective gas exchange. Children also tolerate lower oxygen saturations than adults, up to a point. If oxygenation is difficult, then an injury to the lung, a pneumothorax, or aspiration should be considered. In children, hypoventilation is common in the presence of a traumatic brain injury or shock. If any of these conditions exist, intubation is appropriate. Respiratory compromise requiring intubation commonly indicates a very severe injury. Although none of the previously mentioned criteria to determine a major resuscitation has been validated in children, compromise of the airway and intubation suggest a population that has a higher mortality when compared with those injured children who do not have airway issues.10 A child who is comatose or unresponsive is fairly easy to intubate with an appropriately sized orotracheal tube. Typically, this tube is not cuffed in children less than 8 years of age since the narrowest part of the airway, the cricoid ring, will stabilize the tube without the need for a cuff. Care must be taken to stabilize the cervical spine with appropriately sized pediatric cervical collars during critical maneuvers such as intubation and transportation. Children who are combative from hypoxia or from emotional distress may need to be intubated to facilitate evaluation, including computed tomography (CT) scanning. For intubation, the injured child is best managed with a protocol for rapid sequence intubation (RSI). Table 43-1 describes an RSI protocol that is both safe and effective. If there is time, preoxygenating the child is useful. The tube size can be roughly approximated by either the width of the nail or the size of the child’s fifth finger. These rough calculations may not be accurate in children of Chinese descent.11 The use of the Broselow Pediatric Resuscitation Measuring Tape has become the standard for determining height, weight, and the appropriate size for resuscitative equipment in a child. The Broselow cart has been found to be more useful than older “standard” carts for children.12 In addition, this tape has been useful in determining drug doses and drip concentrations throughout the hospitalization.13 Intubating the injured child can be a very stressful event for those who are less familiar with the technique. The head should be held in line with cervical traction. After selecting the appropriately sized noncuffed tube and employing pharmacological adjuncts as needed for RSI, the airway is approached with a properly sized laryngoscope. The smaller the child, the more

TABLE 43-1 Pediatric Rapid Sequence Intubation (RSI) Preoxygenate Atropine Sulfate IV 0.1–0.5 mg Sedation

Hypotensive Etomidatea 0.3 mg/kg Or Midazolam 0.1 mg/kg (maximum 5 mg)

Normotensive Etomidate 0.3 mg/kg Or Midazolam 0.1 mg/kg (maximum 5 mg)

Cricoid Pressure Paralysis Succinylcholineb 10 kg give 2 mg/kg 10 kg give 1.5 to 2 mg/kg Intubate Check tube position Release Cricoid pressure a b

Avoid etomidate if there is concern for seizures. Vecuronium 0.2 mg/kg is another option.

likely successful intubation can be achieved with a straight blade. Gentle cricoid pressure is useful to guide the larynx into view and to help close the esophagus during manipulation of the oropharynx. The endotracheal tube should be advanced about 3 cm beyond the vocal cords. Bilateral breath sounds along with symmetric chest excursion are assessed, followed by confirmation with a device that measures exhaled carbon dioxide. Due to the thin tissues of the chest wall, gastric insufflation may be confused with normal breath sounds. A chest x-ray should be obtained to confirm the correct position of the tube since a right mainstem intubation is the most common complication of pediatric intubation after missed intubation. Nasotracheal intubation is generally not used in small children in the emergency setting. The need for invasive emergency airway access for acute obstruction of the pediatric airway is a very uncommon event. If needed, a 14 or 16 gauge angiocatheter may be placed through the cricothyroid membrane or even the tracheal wall. Care should be taken to not penetrate the posterior tracheal membrane. Oxygen can then be administered through the catheter, allowing time for attempts at orotracheal intubation. The needle cricothyroidotomy is preferred in patients under

The Pediatric Patient

■ Vascular Access As in injured adult patients it is important to obtain reliable, quick, and safe intravenous access. Simpler measures should be attempted first and, if not successful, proceeding to more invasive measures may be necessary (Table 43-2). The ideal initial sites for vascular access for children are the peripheral veins in the upper extremities, especially the antecubital fossa. Ultrasonography may be used to aid in finding peripheral veins, as well.14 A percutaneous femoral venous catheter below the inguinal ligament is the next best choice and the most commonly used route for emergency venous access in the child.13 This should be done with the Seldinger technique to avoid a cutdown procedure. If the trauma team is unable to establish intravenous access using these techniques, a cutdown on the saphenofemoral junction or saphenous vein at the ankle will work in the emergency setting, as well.15 Surgeons who are familiar with subclavian or internal jugular vein catheterization in the child may utilize this route as the next choice as

TABLE 43-2 Pediatric Vascular Access Peripheral Veins ⴛ 2 Preferably antecubital fossa If unable

Intraosseous access If unable

Percutaneous Central Venous Access Femoral vein If unable

Venous cutdown (Distal saphenous preferred) If unable

Percutaneous External Jugular/Subclavian/Internal Jugular

there are very few complications. This is especially true if a chest tube is already in place on the selected side of the subclavian venipuncture. Intraosseous access is a very useful technique for pediatric trauma victims without intravenous access. Contraindications include proximal fractures and sites of infection. The anteromedial surface of the proximal tibia is used, 2–4 cm distal to the tibial tuberosity. For insertion in the proximal tibia, the needle is directed inferiorly at a 45° angle from the perpendicular. If the insertion site is the distal tibia, the needle should be angled 45° superiorly. In both instances the goal is to angle away from the region of the growth plate and/or joint. There are specialized needles readily available to use with this technique. If these are not available, a spinal needle with a trocar may be employed. Multiple entries into the medullary cavity should be avoided as the leakage that occurs with multiple attempts may cause an iatrogenic compartment syndrome.

■ Restoration of Circulation Age-specific hypotension is an indication for major resuscitation of an injured child. In an analysis of the National Pediatric Trauma Registry, 38% of recorded deaths occurred in children whose systolic blood pressure was less than 90 mm Hg.16 This group represented 2.4% of the study population. To determine which child has “age-specific hypotension” requires knowledge of normal blood pressures in children. National guidelines for the ranges of normal childhood blood pressures based on age were published in 2004.17 Health care professionals caring for injured children should be familiar with normal age-dependent blood pressures (Table 43-3). A child with an injury that produces significant blood loss may present with a normal blood pressure. The otherwise healthy child can readily compensate for blood loss by mounting a significant tachycardia coupled with peripheral vasoconstriction. Therefore, a normal blood pressure in a child does not mean that circulating blood volume is at normal levels. An accurate assessment is made by monitoring blood pressure and heart rate combined with a clinical assessment of peripheral perfusion. Clinical signs of poor perfusion in conjunction with altered mentation are the classic findings in pediatric hypovolemic shock. If these are present, an immediate bolus of 20 mL/kg of an isotonic crystalloid solution is indicated. If a second bolus is needed and there is little improvement, typespecific packed red blood cells or O-negative blood should be administered immediately followed by the standard infusions of fresh frozen plasma and platelets. As noted above, this scenario occurs in less than 3% of injured children. Caution must be employed, as overresuscitation may be as problematic as underresuscitation, especially in the presence of a traumatic brain injury. Overtreatment with crystalloid solutions may exacerbate cerebral edema in certain circumstances. In adults, excess infusions of crystalloid solutions may result in poor formation of clot and worsening of a compromised hemorrhagic state, and may have no impact on survival.18 One study in injured adults showed that supranormal trauma resuscitation increased the likelihood of an abdominal compartment syndrome, as well. Anecdotal reports of abdominal compartment

CHAPTER 43

10 years of age as the cricoid cartilage is very delicate and could be injured easily with a surgical incision. The needle cricothyroidotomy may then be followed by tracheostomy in a more organized fashion. Postintubation issues include gastric decompression and surveillance for a pneumothorax. Gastric decompression with a nasogastric or orogastric tube should be employed in every patient since gastric distention will impair diaphragmatic excursion and cause respiratory compromise in the small child. A pneumothorax is especially treacherous in the child due to mediastinal mobility. A tension pneumothorax in a patient with a mobile mediastinum causes compression of the ipsilateral and contralateral lungs, as well as vascular compromise. If a pneumothorax is present, needle decompression can be employed, but this should be followed by immediate insertion of a thoracostomy tube.

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TABLE 43-3 Vital Functions for Children

SECTION 4

Age Group (Years) Infant (0–1) Toddler (1–3) Preschool (3–5) School age (6–12) Adolescent (12)

Weight Range (kg) 0–10 10–14 14–18 18–36 36–70

Heart Rate (Beats/min) 160 150 140 120 100

Blood Pressure (mm Hg) 60 70 75 80 90

Respiratory Rate (Breaths/min) 60 40 35 30 30

Urinary Output (mL/(kg h)) 2.0 1.5 1.0 1.0 0.5

Modified from American College of Surgeons. ATLS Student Manual. 8th ed. Chicago, IL: American College of Surgeons; 2008:235.

syndrome following massive crystalloid resuscitation in children have been reported.19 Hypothermia is an extremely common occurrence in injured children and may occur at any time of the year, even in the heat of summer. The response to hypothermia includes catecholamine release and shivering, with an increase in oxygen consumption and metabolic acidosis. Hypothermia as well as acidosis then contributes to a posttraumatic coagulopathy.20 A warm room, warmed fluids, heated air-warming blankets, or externally warmed blankets should be utilized during the initial resuscitation of an injured child. This aggressive approach to rewarming should be extended to the radiology suite during evaluation. If at all possible, the room should be warmed to 37°C or warmer, even if the trauma team feels some discomfort. Fluids and blood should be warmed to 39°C if the child is cool (36°C). Conversely, care should be taken to avoid hyperthermia in the child with a traumatic brain injury21; therefore, maintenance of a normal core temperature is the goal for management. There is some evidence, however, to suggest that early, carefully controlled hypothermia in the child with a severe injury to the brain and no other injuries may be beneficial, but this treatment option is still experimental.22

DIAGNOSTIC ASSESSMENT The physical examination is a crucial first step in diagnosis as it will direct all other forms of assessment. It is the baseline for serial physical examinations by the trauma team performed later in the hospitalization. After the physical examination, other diagnostic adjuncts may be employed. During the initial assessment diagnostic testing with standard x-rays is performed with a portable machine or one dedicated to the trauma room, thus avoiding transport of the patient. Frequently ordered imaging studies in the emergency department include the following: plain x-rays of the chest, abdomen, pelvis, cervical spine, and extremities. Thoracic and lumbar spinal x-rays are commonly ordered when neurological injuries are suspected or when the physical examination reveals point tenderness over the spine. The role of cervical, thoracic, or abdominal computed tomography (CT) with reconstruction to evaluate the vertebral column can be helpful. Detecting a pneumothorax, pneumoperitoneum, pelvic fracture, or fracture of a

long bone is an important component of the initial care of an injured child. Plain x-rays of the skull may document fractures, but they have little value in directing management of the child with an injury to the brain, except for a penetrating injury or suspected child abuse.23,24 The inability of x-rays to predict intracranial bleeding in the injured child has been documented, also.25 In the past decade, surgeon-performed ultrasonography has been popularized in the United States. Several recent studies by adult and pediatric trauma surgeons have attempted to determine the role of the focused assessment for the sonographic examination of the trauma patient (FAST) in the evaluation of the injured child. The FAST evaluation examines the pericardium, right and left upper quadrants, and the pelvis for fluid. Some surgeons include a thoracic evaluation to detect a hemothorax or pneumothorax. The technique of B-mode ultrasound in the hands of experienced ultrasonographers should be as accurate in detecting blood in the abdomen as CT scanning or diagnostic peritoneal lavage (DPL).26–28 In a collected series of over 4,900 patients, surgeons who performed ultrasound to detect hemoperitoneum and visceral injury demonstrated a sensitivity of 93.4%, a specificity of 98.7%, and an accuracy of 97.5%.26–29 A second study reviewed 1,043 patients in whom the ultrasonographic study was performed by radiologists. This collected series showed a sensitivity of 90.8%, a specificity of 99.2%, and an accuracy of 97.8%.30–33 Both of these series included adults as well as children. Surgeon-performed ultrasound evaluation in children should be coupled with the physical examination.34 The typical FAST examination takes less than 2 minutes when performed by a physician experienced in its use. A 3.5 MHz probe is used for children over 10 kg, while either a 3.5 or a 5 MHz probe can be used for children under 10 kg. Obvious benefits of the FAST evaluation include its portability, repeatability, elimination of the need to transport the child to the radiology suite, and the decreased radiation exposure to the child. CT scans of the head, chest, and abdomen are the accepted diagnostic radiologic studies of choice in the vast majority of hemodynamically stable injured children suspected of having a potentially life-threatening injury. Despite liberal use of CT scans of the head, a normal initial scan of a child may not detect

The Pediatric Patient much greater sensitivity to radiation in the pediatric population when compared with adults. The lifetime risk of cancer is significantly increased when children are exposed to diagnostic radiation. The current scientific evidence suggests that the risk of cancer from low-level radiation such as from CT may be as high as one fatal cancer death for every 1,000 CT performed in children.42 The amount of radiation a CT scan imparts depends on many factors, and protocols can be adjusted to provide adequate image quality while reducing exposure. Minimizing the risk of radiation exposure in diagnostic imaging is a complex task and a multidisciplinary approach is needed. Trauma clinicians should be aware of the potential risks and benefits of CT and consider these issues when selecting imaging studies.

■ Laboratory Studies The routine use of laboratory studies in the ED, in general, has not been shown to be of significant value in the pediatric trauma population.43–45 Some specific clinical laboratory tests such as urinalysis and arterial blood gases with base deficit may be of limited benefit in selected circumstances.46 More often, laboratory testing delays the clinical decision-making process occurring in the ED during evaluation and resuscitation, and point-of-care testing has not altered this concept.47 In the presence of a possible injury to the brain, testing for a coagulopathy, thrombocytopenia, or hyperglycemia may be of benefit to establish a baseline for later determinations or to assist in assessing the risk of morbidity or mortality.48–50 During hospitalization, routine laboratory testing is appropriate as long as specific indications exist for monitoring, such as nonoperative management of an injury to the spleen or pancreas.

MANAGEMENT OF SPECIFIC INJURIES ■ Injury to the Head and Central Nervous System Acute traumatic brain injury is the most common cause of death and disability in the pediatric population.51 In those who survive, minor injuries can be associated with reversible defects while major injuries can result in severe disabilities. The mechanisms of injury to the brain in children are related to age. Infants typically suffer more from falls such as from a table or the arms of a caregiver. Intentional injury is a common cause of death in children under 2 years of age. Injury with intention, independent of severity, raises the mortality in children with traumatic brain injuries.52 In older children the usual cause of injuries to the brain is from vehicle-related accidents or recreational activities. Although children have a better survival rate with injury to the brain when compared with adults, this does not mean they have a lesser morbidity with similar injuries. Children have a plasticity of the neuron related to myelination and the establishment of neuronal interconnections. This allows a given focal injury to produce a less severe deficit when compared with a mature brain. This same lack of maturity may also make the child more susceptible to a diffuse injury with greater cognitive impairment.53

CHAPTER 43

late manifestations of a neurological injury or cerebral edema.35 Unless an absolute indication for surgery is present, the majority of stable children with suspected intra-abdominal injuries should have a CT scan performed prior to instituting operative or nonoperative management. Although CT scanning is the imaging modality of choice in the evaluation of a stable injured child, it is generally accepted that a high percentage of those scans will reveal no injuries. CT scans of 1,500 consecutive children were performed after blunt abdominal trauma, and abnormal CT scans were seen in only 26% of patients.35 A normal study was found to strongly predict a lack of deterioration as only one delayed laparotomy was required in the 1,112 children in this group. In addition, a CT scan affected the decision to operate on children with a solid organ injury in a very small subset of patients (5 of 1,500). The technique for performing an emergency CT scan on an injured child, with regard to the use of contrast material, remains unclear. Most institutions will perform an initial CT of the head without using intravenous contrast. The use of intravenous contrast during a CT scan to evaluate intrathoracic or intra-abdominal trauma improves its diagnostic accuracy, but is not required and can be omitted during the initial scan depending on the experience and protocols of the particular trauma center. The benefit of using oral contrast for an abdominal CT in injured children is also a matter of debate. In a randomized prospective clinical trial in adults, the addition of oral contrast to an acute abdominal CT scan for trauma was found to be unnecessary and caused a delay in the time to CT scanning.36 In a review of 2,162 patients with blunt trauma and an abdominal CT, Tsang et al.37 found that all 7 patients with an intestinal perforation had studies that showed neither extraluminal air nor extraluminal oral contrast. In some centers, due to the length of time needed to fill the bowel with contrast and the resultant full stomach that increases the risk of vomiting and aspiration, gastrointestinal (GI) contrast is avoided in the initial CT scan of the abdomen in the injured child. Other centers suggest that it improves the accuracy of abdominal CT scans when intestinal or retroperitoneal injury is suspected and that oral contrast in adults and children is safe and has a minimal incidence of aspiration.38,39 In summary, at the present time the use of GI contrast in emergency CT scans of the abdomen for trauma is a matter of institutional preference. Evidence of intra-abdominal injuries requiring operative correction on the CT scan may be subtle. Findings of free intraperitoneal or retroperitoneal air, extravasation of GI contrast, defects in the bowel wall, and active hemorrhage are often obvious and have a high correlation with an injury to the intestine that will require operative intervention.40 There are, however, potentially life-threatening intestinal injuries that may present with only focal thickening of the bowel wall or the presence of peritoneal fluid without injury to a solid organ.41 Other less specific findings associated with intestinal injuries include mesenteric stranding, fluid at the mesenteric root, focal hematomas, mesenteric pseudoaneurysm, and the hypoperfusion complex. Repeated CT scanning during an acute hospitalization may expose children to very high doses of radiation and an increased risk of cancer. Epidemiologic studies have demonstrated a

863

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Specific Challenges in Trauma

SECTION 4

The head of an infant constitutes 15% of the total body mass, while the head of an adult makes up only 3%. Acceleration and deceleration injury in pediatric trauma, therefore, yields a greater amount of force applied to the brain. The neck muscles do not support this relatively larger head as well as they do in teenagers and adults. Also, the skull of the infant is thin and soft, and the closure of fontanelles and sutures is not completed until age 3. In addition, the volume of cerebrospinal fluid is smaller than that of the adult and the child’s brain has greater water content. Finally, myelination occurs between 6 and 24 months, making the brain very soft and prone to disruption prior to completion of this process. Injuries to the brain are classified as primary and secondary. Primary injuries are those inflicted immediately by the trauma, while secondary injuries are those resulting from ischemia, hypoxia, hypotension, infection, hydrocephalus, seizures, or increased intracranial pressure (ICP). Children are more likely to have low-pressure venous bleeding from an overlying skull fracture than from arterial injuries resulting in a lower incidence of epidural hematoma. The very young infant can actually have a critical reduction in blood volume from intracranial bleeding due to the relatively large size of the brain compared with the body mass. Much as in adults, diffuse axonal injury is a shear stress to the brain caused by acceleration/deceleration mechanisms, often with angular or rotational motion. Even minor shearing can cause severe neurological deficits. Secondary injury is most often the result of an elevated ICP. An elevated ICP may be caused by increased cerebral blood volume, increased brain volume, or hematomas. An elevated ICP can cause direct injury due to compression resulting in herniation under the falx cerebri or through the tentorium cerebelli. Increased ICP causes a reduction in cerebral perfusion pressure (CPP). The CPP should be 60–80 mm Hg in older children and at least 50 mm Hg in children under the age of 8. Injury to the brain can impair autoregulation, and inappropriate vasodilation may occur resulting in significant increases in tissue volume and ICP. With this deranged physiology, even minor injuries to the brain in children can lead to global hyperemia and death.54 The Brain Trauma Foundation has published guidelines for the management of trauma to the brain in children.55 These recommendations are based on the available literature, at times drawing from adult data. Few definitive guidelines exist, and the majority of recommendations are based on treatment options commonly used in the clinical setting. The Glasgow Coma Scale (GCS) can be used for children over the age of 5, while some modification is often used for children under 5 (Table 43-4). If a score of less than 9 is determined, that patient typically requires airway management and measurement of the ICP. During the initial evaluation and resuscitation of the child with an injury to the brain, care should be taken to avoid a secondary injury due to the causes noted above. Also, clinical and radiologic evaluation of the cervical spine is important to rule out injury. The presence of cervical tenderness mandates the application of a rigid collar and imaging aimed at identifying the possible injury. Three-view x-rays of the cervical spine are a necessary start followed by a CT scan or MRI as needed depending on the age of the child.

TABLE 43-4 Pediatric Glasgow Coma Scale Score 6 5 4 3

Eyes Open — — Spontaneous To voice

Verbal — Age appropriate Cries/consolable Irritable

2

To pain

Restless

1

None

None

Motor Spontaneous Localizes Withdraws Flexion posture Extension posture None

Once the patient has undergone an initial evaluation, causes of secondary brain injury have been managed, and the cervical spine has been stabilized, a CT of the head and brain should be obtained, ideally 30–60 minutes after arrival depending on the hemodynamic stability of the patient. If there is evidence of swelling of the brain, monitoring of ICP is indicated. This is best done with a ventriculostomy that allows for drainage of cerebrospinal fluid. The ICP should be maintained under 20 mm Hg, while cerebral perfusion pressure (CPP  MAP ICP) should ideally be in the range of 40–65 mm Hg as noted previously. Avoiding hyperthermia is important as this may cause a secondary injury to the brain. Another management technique is hyperosmolar therapy with hypertonic saline or mannitol. Hypertonic saline is delivered in a continuous 3% solution at 0.1–1.0 mL/(kg h) on a sliding scale to keep ICP 20 mm Hg, while mannitol is used as a bolus at 0.25–1 g/kg of body weight. Euvolemia should be maintained with appropriate administration of intravenous fluids. The serum osmolarity should be maintained at 320 mOsm for mannitol, and below 360 mOsm with hypertonic saline. Other methods to decrease ICP and protect the injured brain include sedation, the rare use of hyperventilation, the administration of barbiturates, and decompressive craniectomy. The latter approach should only be considered in children with cerebral edema and medically uncontrolled intracranial hypertension. It is not likely to be useful in children who have suffered an extensive secondary injury to the brain or in those who have an admission GCS of 3 and no improvement with therapy. Nutritional support, avoiding the use of steroids, and treating postinjury seizures are also important aspects of the care of the child with an injury to the brain.

■ Injury to the Cervical Spine Injuries to the cervical spine represent less than 1% of all pediatric fractures.56 Trauma to the upper cervical spine tends to occur in younger children (less than 8 years), while midcervical injuries occur in older children. Motor vehicle crashes are the primary cause of associated injuries to the spinal cord in younger children while sporting activities are more common in older children.57 Children have more flexible interspinous ligaments and joint capsules, flatter facet joints, and vertebral bodies that are wedged anteriorly and tend to slide forward

The Pediatric Patient

A

B

FIGURE 43-1 (A) Normal pediatric C spine x-ray. (B) Mild pediatric pseudosubluxation at C2–C3. (C) Moderate pediatric pseudosubluxation at C2–C3. C

CHAPTER 43

be easily confused for fractures. A careful physical exam is always warranted, as spinal cord injury without radiographic abnormalities (SCIWORA) has been shown to occur in as many as 66% of children.58 The pediatric trauma population can be divided into two populations with respect to injuries to the cervical spine, including those 8 years of age and less and those 9 years and older. Each

with flexion. Their head to neck ratio is also different, placing them at risk for different injuries than in adults. The diagnosis of injuries may be challenging, as radiologic differences exist in the maturing cervical spine. There may be anterior displacement of C2 on C3 appearing as a subluxation. This is a normal pediatric variant described as a pseudosubluxation (Fig. 43-1A–C). In addition, skeletal growth centers may

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Specific Challenges in Trauma

SECTION 4 FIGURE 43-2 MRI of C spine showing cord compression.

group has different patterns of injury to the cervical spine as a result of differing anatomic and biomechanical properties, and a tailored evaluation and management of these injuries is required. The anatomy/biomechanical profile of children 9 years and older mirrors that of adults, and evaluation of cervical spine can be accomplished with adult protocols. A modified approach to the child 8 years of age or less should be employed. If history or examination suggests a child at risk for injury, then a two-view cervical spine series would be indicated to identify any obvious injury. If plain films are negative in this age group and there is still concern for injury, the available data would suggest that flexion extension films or an MRI should be obtained since most injuries are ligamentous in nature. Given the high frequency of SCIWORA in this age group, one should proceed to MRI if there is a neurological deficit (Fig. 43-2). In the interim the child’s head and neck should remain immobilized at all times.

■ Injury to the Thorax Thoracic trauma is an important cause of morbidity and mortality in children. It accounts for 4–25% of pediatric injuries and is associated with a greater mortality rate when compared with injuries in other systems.59,60 Isolated thoracic trauma in a child is associated with a mortality rate of approximately 5%59 and is largely due to penetrating trauma. About 80% of thoracic injuries in children are from a blunt mechanism. Children with associated neurosurgical trauma, thoracic trauma, and abdominal trauma may have a mortality rate that approaches 40%. Thoracic trauma is likely to be present in children who present with a low systolic blood pressure, an elevated respiratory rate, abnormalities on physical examination of the thorax, and the presence of a fracture of the femur.61 The child’s thorax has unique anatomic and physiologic properties that are important to the diagnosis and treatment of

thoracic trauma. The trachea is shorter relative to body size, more anterior, narrower, and more easily compressed as compared with the adult. Also, the subglottic region is the narrowest part of the airway. Therefore, the pediatric airway is more susceptible to mucus plugging and edema. The chest wall is more compliant in children with less muscle mass, and this allows a greater transmission of energy to underlying organs when injury occurs. Finally, the mediastinum is more mobile than in older patients, especially in young children. Unilateral changes in thoracic pressure such as with a tension pneumothorax can lead to a shift of the mediastinum to the extent that venous return is markedly reduced. This response is more pronounced than typically seen in an adult. Young children have a compliant thorax that becomes more adult-like at 8–10 years of age. As a consequence, rib fractures are relatively uncommon in young children and occur more frequently in adolescents. Although rib fractures are uncommon, injuries to the lung, liver, and spleen lying underneath the ribs are quite common. One of the most common thoracic injuries in children is a pulmonary contusion, which can occur with blunt or penetrating trauma. The presence of a pulmonary contusion contributes to decreased pulmonary compliance, hypoxia, hypoventilation, and a ventilation perfusion mismatch. A chest x-ray taken during the initial assessment may demonstrate a pulmonary contusion, while a thoracic CT scan may show areas of pulmonary contusion not appreciated on the x-ray. Treatment of a pulmonary contusion includes appropriate fluid resuscitation, supplemental oxygen, pain management, and strategies to prevent atelectasis and pneumonia. Unfortunately, some patients may develop pneumonia or respiratory distress syndrome (RDS) after sustaining a pulmonary contusion.62 In an occasional patient, a large pulmonary contusion may cause life-threatening hypoxia that cannot be supported with conventional or advanced techniques of ventilation including high-frequency oscillation. Extracorporeal life support has been used in extreme circumstances to support patients with severe pulmonary contusions and secondary RDS. A pneumothorax is typically treated with a thoracostomy tube appropriately sized for the patient, while a hemothorax is treated with the largest tube that can be inserted. Intrathoracic blood loss of 15 mL/kg immediately or ongoing losses of 2–3 mL/(kg h) for 3 hours mandate thoracic exploration to control bleeding in children.63,64 Cardiac injuries are extremely rare, as are tracheobronchial or esophageal injuries. They do occur, however, and should be ruled out in any child with cervicothoracic injuries. Similarly, injuries to the great vessels occur in children with rapid deceleration injuries, and these types of injuries should be considered in any child with the appropriate mechanism.65 Injuries to the thoracic aorta are rare in the pediatric population and are often lethal. Aortic injury is the second leading cause of death in the pediatric population and accounts for 14% of trauma deaths.66 The age of victims of aortic injury has been shown to range from 6 to 17 years, and most are victims of motor vehicle crashes. Several identifiable risk factors have been associated with blunt injury to the thoracic aorta. Clinical predictors that have been noted include a low systolic blood

The Pediatric Patient

■ Injury to the Abdomen Due to the relatively thin pediatric abdominal wall, a modest amount of force may cause a significant injury to one or more organs in the abdomen. Multiple organs may be injured from a single blow due to proximity. The assessment for abdominal injury begins with the physical examination, and inspection may reveal bruising, a mark from a lap seat belt, or abdominal distention. Tenderness on physical examination should prompt a higher level of evaluation with CT scanning. A nasogastric or orogastric tube should be placed to decompress the stomach. With the emphasis on nonoperative management of abdominal injuries in children, injuries requiring operative management have been missed for hours to days. It has been noted that a delay in diagnosis is not usually associated with an increased mortality; however, an increase in septic complications has been seen when operative intervention is delayed more than 24 hours postinjury. This phenomenon is peculiar to children and, as a result, inhospital observation with serial examinations should be employed in all children with abnormal abdominal examinations. Repeat ultrasound is particularly useful in this subset of patients. When abdominal injuries occur under suspicious circumstances, the diagnosis of child abuse should be entertained. Blunt diaphragmatic rupture is an uncommon injury in children. The left hemidiaphragm is more likely to be injured, but bilateral ruptures have occurred. The frequency of associated injuries, especially the liver and spleen, is very high.68 An abnormal contour of the diaphragm, a high-riding diaphragm, or a questionable overlap of abdominal visceral shadows may indicate injury on a chest x-ray. Visceral herniation, the abnormal position of a nasogastric tube overlaying the hemithorax, or early intestinal obstruction after trauma makes the diagnosis likely. CT has been used to establish this diagnosis, but may appear normal in some patients. Therefore, ultrasound or a high-resolution CT scan through the diaphragm may be needed to establish a diagnosis. Many diaphragmatic ruptures are not identified in the first few days after injury and may not be detected for a considerable period of time.69 Repair of an acute diaphragmatic rupture is best accomplished with an abdominal approach. If a late diagnosis of a diaphragmatic injury is made, a thoracic approach to repair is often considered secondary to the scarring and adhesions that may have formed.

Blunt injuries to the stomach are the third most common perforation of the GI tract in the injured child and occur relatively more frequently in children than in adults.70 The site of perforation is most often the greater curve of the stomach. The diagnosis is usually made quickly, due to the common occurrence of peritonitis and free air seen on an initial x-ray in the emergency department or a bloody nasogastric aspirate. At operation, the stomach is closed in two layers when possible, with the use of a decompressive gastrostomy considered when a massive injury is present. Every effort should be made to salvage the spleen during repair of the gastric injury. Duodenal injuries are uncommon in children. The child with a duodenal injury that requires surgery most often presents with abdominal distention, bilious vomiting, peritonitis, and pneumoperitoneum on an abdominal x-ray. In a recent review from 2 busy pediatric trauma centers, 42 patients with a duodenal injury were identified in 10 years.71 There were 33 blunt and 9 penetrating injuries. Operative management was necessary in 24 patients and included primary repair, duodenal resection, and gastrojejunostomy with pyloric exclusion. In contrast, a duodenal hematoma is usually treated nonoperatively with nasogastric decompression and total parenteral nutrition. This management has a high rate of success, but may take as long as 3 weeks for the obstruction to resolve. A late diagnosis of duodenal perforation can occur with this injury and is usually associated with an increase in complications, but not mortality. The jejunum and ileum are the most common parts of the GI tract to sustain injury in the child. The mechanism of injury to the small bowel is a crush injury between the delivered force and the vertebral column. Adult-sized seat belts are often employed by conscientious parents and, as a result, the risk of injury to the small bowel increases. This increase in risk is remarkable in children under 100 lb in weight. If a hematoma from a seat belt is present on the abdominal wall, the risk of an intra-abdominal injury is 232 times more likely. Therefore, a higher index of suspicion should be employed.72 Children with rupture of the small bowel due to blunt trauma invariably have an abnormal physical examination. A recent multi-institutional review suggested that delay in operative intervention does not have a significant effect on prognosis after pediatric blunt intestinal injury.73 Free fluid seen on ultrasound (FAST) or CT scan, coupled with a tender abdomen and no injury to a solid organ on the CT, mandates an abdominal exploration for a suspected injury to the small bowel. Even if no perforation is identified at surgery, care should be taken to repair mesenteric rents, evacuate large hematomas, and rule out retroperitoneal injuries. In this same setting, an associated compression injury of the lumbar vertebrae (Chance fracture) is often present. Injuries to the colon and rectum are not common in children. Accidental causes of colon and rectal injuries include motor vehicle crashes with pelvic fractures and penetration of the rectum by bone shards, occasional serosal injuries from seat belts, and straddle injuries. Nonaccidental injuries are invariably related to abuse, typically from instrumentation. If the mucosa is injured or the injury is superficial, observation is appropriate. Full-thickness injuries of the distal rectum can be managed with primary repair in many cases. Similar to adults,

CHAPTER 43

pressure on admission, increased respiratory rate, abnormal thoracic exam, especially chest auscultation, an associated fracture of the femur, and a GCS of less than 15.60 If there is a high index of suspicion based on history, physical examination, or an x-ray of the chest, further testing is required. Helical chest CT and transesophageal ECHO (TEE) have been found to be equally sensitive when compared with aortography in the detection of an aortic injury. Once the injury is found, the treatment of thoracic aortic injuries is similar to that in adults. Betablockers should be started early, while treatment options include nonoperative management, operative management, and the use of an endovascular stent graft if a correctly sized graft is available. The long-term outcome of endovascular stenting in children is unknown.67

867

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Specific Challenges in Trauma

SECTION 4 A

B FIGURE 43-3 (A) Note the grade IV spleen injury. (B) The admission chest x-ray of the child injured in Fig. 43-1A , and the chest x-ray 4 days later showing a pleural effusion.

devastating colon injuries above the peritoneal reflection occasionally need temporary fecal diversion.74 As the injured spleen in a child will usually stop bleeding without intervention, nonoperative management is widely accepted.75 Occasionally, a child with a severely injured spleen may develop a left pleural effusion (Fig. 43-3A and B). After an occult diaphragmatic injury has been ruled out, the effusion can typically be treated with a thoracostomy tube. Children who have received or are likely to receive half their blood volume in transfusions within 24 hours of injury (40 mL/kg) have progression of the rupture during nonoperative management or have hemodynamic instability and should be treated operatively. The physiologic response to splenic injury correlates with the grade of splenic injury.76 If splenectomy must be performed,

postsplenectomy immunization and antibiotic therapy is appropriate and necessary based on available guidelines.77 It is recommended that all persons aged 2–64 years receive pneumococcal vaccine and meningococcal vaccine, with Haemophilus influenzae type B vaccine administered to high-risk patients, as well. Vaccination should be given 2 weeks after emergency splenectomy. A booster dose of pneumococcal vaccine is recommended after 5 years, while no revaccination recommendation is made for meningococcal or H. influenzae type B vaccine. In addition, many children are given penicillin on a daily basis if the splenectomy is performed before the age of 5 years. Nonoperative management of hepatic injuries is now widely accepted. Injuries to the liver parenchyma, without involvement of a major intrahepatic vessel or bile duct, can nearly

The Pediatric Patient

CHAPTER 43

always be successfully treated with observation. This is especially true in patients with isolated hepatic injuries, although these are associated with a slightly higher mortality rate when compared with splenic injuries. The combination of hepatic and splenic injuries is clearly associated with a higher mortality rate, which increases as the severity of injury rises.78 As with splenic injuries, operative intervention is indicated when half of the blood volume has been transfused. If a blush is seen on CT, angioembolization may replace operation in the stable patient. Others have advocated early operative packing in more unstable patients coupled with embolization and early reoperation as a means to improve survival.79 The physiologic and hematologic effects of massive transfusion in the child often make the operative management of a major hepatic injury very difficult unless the new paradigm of a 1:1:1 red blood cell unit:fresh frozen plasma unit:platelet transfusion is followed. When perihepatic packing has been necessary or the midgut is edematous after a major hepatic repair, a commercially available vacuum system or off-the-shelf supplies such as soft bowel bags, laparotomy packs, adhesive dressings, and silastic drains placed on suction can provide a very effective damage control dressing. Eventual fascial closure should be able to be accomplished with most survivors (see Chapter 38).80 Pediatric pancreatic injuries are uncommon and are most often due to blunt trauma81 (Fig. 43-4). A common mechanism is contact with the handlebar of a bicycle. The majority of pancreatic injuries in children may be treated successfully with nonoperative management including gut rest, intravenous nutrition, and, occasionally, pancreatic antisecretory medication. Conservative management of children with a pancreatic transection is much more controversial. A small group of patients with a prolonged median hospitalization and incomplete follow-up has been reported, and nonoperative management was

FIGURE 43-5 Left renal injury.

advocated.82 Late pancreatic pseudocysts were common and required intervention. Others have reported the beneficial effects of a spleen-sparing distal pancreatectomy even in the face of a delayed diagnosis.83 Operative intervention allowed an earlier return to normal activities and avoided the stress of prolonged hospitalization. When capabilities for pediatric ERCP are available, ductal stenting may be of significant benefit.84 Some surgeons have been able to employ laparoscopic distal pancreatectomy with splenic salvage for pancreatic transection when stenting could not be accomplished.85 Blunt trauma is the most common mechanism of renal injury in children (Fig. 43-5). Contusion is the most common injury seen, and renal injury can occur in the absence of hematuria. Nonoperative management of most pediatric renal injuries (grades I–IV) can be accomplished safely, and operative renal salvage for grade V injuries appears to be uncommon.86,87 Some investigators have noted a good salvage rate with nonoperative management of grade V injuries, but scarring and loss of parenchymal volume did occur.88 Ureteral stenting for urine leaks may be needed in patients with injuries of the collecting system. Rarely, nephrectomy for exsanguinating injury may be needed. The majority of patients will not require an emergency intervention, but angioembolism may be considered in selected cases of intraparenchymal bleeding. Since most injured children now undergo abdominal CT scanning, CT cystography may be considered on every child to evaluate for the presence of an injury to the bladder.89 The majority of retroperitoneal bladder ruptures can be treated successfully with urethral catheters, without the need for additional suprapubic drainage.90

■ Injury to Blood Vessels

FIGURE 43-4 Transection of the pancreas; arrow denotes the transection point.

869

Injuries to vessels in the extremities are equally divided between blunt and penetrating mechanisms.91 Such injuries in children are uncommon, and children can tolerate complete vascular occlusion to the extremities to a greater extent than adults. Due to the elastic nature of the child’s body, injuries to

870

Specific Challenges in Trauma

SECTION 4

large vessels do not occur as often as adults. Limb salvage is typically greater than 95% using a team approach to care for associated orthopedic and soft tissue injuries. Pediatric peripheral vascular injuries requiring resection are repaired with autologous tissue whenever possible.92 Injuries to the abdominal aorta have been caused by seat belts, bicycle crashes, and ATV crashes.93 These are repaired immediately, and missed abdominal aortic injuries have resulted in late deaths.94 The rare injuries to the thoracic aorta in children have been treated like those in adults with good results.67 The use of endovascular stents in children, while successful in the short term, has not been evaluated for long-term use.

■ Injury to the Skeletal System Orthopedic injuries are the most common injuries requiring operative intervention in the injured child. These injuries are often painful and may distract the child from complaining of other more serious injuries. As orthopedic injuries can be missed in the injured child, a tertiary examination should be considered for all children admitted to the hospital to evaluate for possible missed injuries.95 As previously discussed, injuries to the cervical spine are often misdiagnosed, and most of the missed injuries are due to normal variants.96 Orthopedic injuries in children may involve the growth plate. The physis, also known as the growth plate, exists in the immature skeleton and can cause potential confusion on diagnostic studies and with treatment. New bone is laid down by the physis near the articular surfaces and causes lengthening of the bone. When an injury occurs before the physis has closed, retardation of normal growth and development of the bone may occur. As children grow and bones mature, changes in porosity, composition of collagen fibers, and mineral content occur. Due to the immature, elastic nature of immature bones, specific fractures can be seen in children. Greenstick fractures are incomplete fractures with angulation supported by cortical splinters on the concave surface. Buckle fractures can be seen in growing bones and are angulations due to cortical impaction. Other fractures that may cause injury to the growth plate include supracondylar fractures of the humerus or femur. These fractures may be associated with vascular injuries. Blood loss is associated with fractures of long bones and the pelvis. The blood loss is proportionately less than in adults and usually not enough to cause shock. If hemodynamic instability exists with an isolated fracture of the femur or pelvis, an evaluation for other sources of blood loss should be undertaken starting with the abdomen. The key principle of the treatment of fractures is immobilization and splinting of fractured extremities until more definitive treatment is undertaken. Also, it is important to obtain a good vascular exam in every patient with fracture of a long bone. Compromise of arterial inflow requires an early diagnosis, realignment of the fracture, and an occasional revascularization procedure to prevent permanent dysfunction or loss of tissue. Finally, it is important to be aware that a compartment syndrome secondary to hemorrhage from the fracture may occur and should be addressed within 6 hours of injury to prevent permanent damage.

PEDIATRIC CRITICAL CARE In general, hemodynamic instability, traumatic brain injury, altered mental status, significant injuries of the spleen, liver, or pancreas, multiple orthopedic injuries, severe pulmonary contusion, and polytrauma require more care than can be provided in a general hospital setting. Patient management in the ICU allows for continuous monitoring of vital signs, oxygen saturation levels, urine output, and neurological exams. There are data that suggest that the care of injured children in a pediatric ICU improves survival.97 Monitoring in the ICU may be noninvasive or invasive. Arterial lines, which allow for closer observation of blood pressure and for drawing of blood gases, should be placed in the ICU. A line to measure central venous pressure should be inserted, as well. Acute respiratory distress syndrome (ARDS) may occur within 3–4 days after major trauma, and ventilation modes are somewhat similar to adults in concept. The two common modes of ventilation are based on pressure and volume. Pressure control is rapid variable flow that provides a peak inspiratory pressure throughout inspiration. Volume control provides a constant tidal volume and minute ventilation regardless of pulmonary compliance. Pressure-regulated volume control is a combination that has a set tidal volume and inspiratory time, but allows the ventilator to adjust the flow rate. If the patient’s respiratory status is refractory to conventional modes of ventilation, the oscillator or high-frequency ventilation may be necessary. This allows for continuous high airway pressures, low tidal volumes, and a very fast rate. If all modes of ventilation have failed and the patient is a candidate, extracorporeal membrane oxygenation (ECMO) may be necessary as previously mentioned. It is important to note that ECMO does not reverse any disease process, but allows the heart and lungs to rest in order to heal the primary process.

PEDIATRIC REHABILITATION Rehabilitation is an important part of the recovery from injury for both children and adults. A rehabilitation facility assists patients with new-onset disabilities and impairments due to trauma to regain function and autonomy. The rehabilitation team focuses on medical issues as well as teaching compensatory techniques, lifestyle modifications, use of adaptive equipment depending on injury, how to deal with posttraumatic psychological impairment, and prevention of deterioration. The major difference between adult and pediatric rehabilitation is that growth and development must be taken into account with children. The age of the child must be considered at every stage of the process to ensure that appropriate developmental goals are set and being met if possible. Rehabilitation begins by carefully outlining all the injuries, disabilities, and impairments. Based on age, a multidisciplinary team formulates a plan with the family and patient (if possible). It is important to acknowledge and treat any grief, sadness, anger, or depression that is present and may impede the process of rehabilitation. Prior to discharge a plan with the family and patient should be in place. Follow-up with the surgical team should continue throughout rehabilitation and after as needed.

The Pediatric Patient

CHILD ABUSE

EMERGENCY DEPARTMENT MANAGEMENT AND FAMILY RELATIONS The majority of injured children are not cared for at pediatric trauma centers.99 Every emergency department should have the equipment, supplies, and the mindset to care for an injured child. Many nontrauma centers see children with injuries that are beyond their capabilities. With this in mind, establishing good communication and plans for transfer to referral centers that care for large volumes of children is mandatory. Also, many pediatric trauma centers are allowing families at the bedside of children with severe injuries, after or during the initial resuscitation. Some centers even have the family at the bedside while cardiopulmonary resuscitation is

in progress. This takes a serious commitment to professionalism and sensitivity during a time when stress in the emergency room is at its highest.

■ Acknowledgment This work is supported in part by the Paula Milburn Miller/ CMRI Chair in Pediatric Surgery.

REFERENCES 1. Kissoon N, Dreyer J, Walia M. Pediatric trauma: differences in pathophysiology, injury patterns and treatment compared with adult trauma. CMAJ. 1990;142(1):27–34. 2. Haller JA Jr. Toward a comprehensive emergency medical system for children. Pediatrics. 1990;86(1):120–122. 3. Vyrostek SB, Annest JL, Ryan GW. Surveillance for fatal and nonfatal injuries—United States, 2001. MMWR Surveill Summ. 2004;53(7):1–57. 4. Inon AE, Haller JA Jr. Caring for the injured children of our world: a global perspective. Surg Clin North Am. 2002;82(2):435–445, ix. 5. Rivara FP. Pediatric injury control in 1999: where do we go from here? Pediatrics. 1999;103(4 pt 2):883–888. 6. Bergen G, Chen LH, Warner M, Fingerhut LA. Injury in the United States: 2007 Chartbook. Hyattsville, MD: National Center for Health Statistics; 2008. www.cdc.gov/nchs/data/misc/injury2007.pdf 7. Bernard SJ, Paulozzi LJ, Wallace DL. Fatal injuries among children by race and ethnicity—United States, 1999–2002. MMWR Surveill Summ. 2007; 56(5):1–16. 8. Killingsworth JB, Tilford JM, Parker JG, Graham JJ, Dick RM, Aitken ME. National hospitalization impact of pediatric all-terrain vehicle injuries. Pediatrics. 2005;115(3):e316–e321. 9. American College of Surgeons. Committee on Trauma. Resources for optimal care of injured patients. Chicago, IL: American College of Surgeons; 2006:59. 10. Edil BH, Tuggle DW, Jones S, et al. Pediatric major resuscitation— respiratory compromise as a criterion for mandatory surgeon presence. J Pediatr Surg. 2005;40(6):926–928 [discussion 928]. 11. Wang TK, Wu RS, Chen C, Chang TC, Hseih FS, Tan PP. Endotracheal tube size selection guidelines for Chinese children: prospective study of 533 cases. J Formos Med Assoc. 1997;96(5):325–329. 12. Agarwal S, Swanson S, Murphy A, Yaeger K, Sharek P, Halamek LP. Comparing the utility of a standard pediatric resuscitation cart with a pediatric resuscitation cart based on the Broselow tape: a randomized, controlled, crossover trial involving simulated resuscitation scenarios. Pediatrics. 2005;116(3):e326–e333. 13. Chiang VW, Baskin MN. Uses and complications of central venous catheters inserted in a pediatric emergency department. Pediatr Emerg Care. 2000;16(4):230–232. 14. Bair AE, Rose JS, Vance CW, Andrada-Brown E, Kuppermann N. Ultrasound-assisted peripheral venous access in young children: a randomized controlled trial and pilot feasibility study. West J Emerg Med. 2008;9(4):219–224. 15. Rogers FB. Technical note: a quick and simple method of obtaining venous access in traumatic exsanguination. J Trauma. 1993;34(1):142–143. 16. Tepas JJ, Schinco MA. Pediatric trauma. In: Moore EE, Feliciano DV, and Mattox KL, eds. Trauma. 5th ed. New York: McGraw-Hill Companies, Inc; 2004:1021–1040. 17. National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents. The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. Pediatrics. 2004;114(2 suppl 4th report):555–576. 18. Dula DJ, Wood GC, Rejmer AR, Starr M, Leicht M. Use of prehospital fluids in hypotensive blunt trauma patients. Prehosp Emerg Care. 2002;6(4):417–420. 19. Balogh Z, McKinley BA, Cocanour CS, et al. Supranormal trauma resuscitation causes more cases of abdominal compartment syndrome. Arch Surg. 2003;138(6):637–642 [discussion 642–643]. 20. Martini WZ, Pusateri AE, Uscilowicz JM, Delgado AV, Holcomb JB. Independent contributions of hypothermia and acidosis to coagulopathy in swine. J Trauma. 2005;58(5):1002–1009 [discussion 1009–1010]. 21. Adelson PD, Bratton SL, Carney NA, et al. Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents. Chapter 14. The role of temperature control following severe pediatric traumatic brain injury. Pediatr Crit Care Med. 2003;4 (3 suppl):S53–S55.

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Child abuse is a serious problem and represents 3–4% of all traumatic injuries seen in pediatric trauma centers.98 It is important for clinicians to know the signs of child abuse in order to protect and care for those who cannot protect themselves. A thorough history and physical examination are paramount. Suspicion should be raised if there is a discrepancy between the history and the extent of injury, there are explanations that do not fit, and a long period of time has passed from the incident to when medical advice was sought. Unexplained events such as loss of consciousness should be questioned. A history of repeated trauma treated at different emergency rooms with “doctor shopping” is also ominous. Fractures from different time periods as well as long bone fractures in children under 3 years of age should alert the clinician to the possibility of child abuse. In addition, if the history changes between caregivers and there is inappropriate behavior displayed from parents or caregivers in regard to the medical advice given, a suspicion should be raised. It is important to observe the relationship between the child and the parents and decipher whether the relationship appears strained or abnormal. On examination, it is very important to observe multicolored bruises signifying different stages of healing and evidence of frequent injuries demonstrated by old scars or healed fractures on x-ray. Long bone fractures in children younger than 3 years old, multiple subdural hematomas, especially without a new skull fracture, and retinal hemorrhage are suspect injuries. Other concerning injuries are those in odd places such as the perioral, genital, or perianal areas. Ruptured internal viscera without a history of major blunt trauma have also been associated with abuse. Finally, it is important to recognize and thoroughly investigate abnormal injuries such as bites, cigarette burns, or rope marks as well as sharply demarcated second- and third-degree burns in odd locations. The workup should include a skeletal survey to look for other or old fractures. CT scans and MRIs should be obtained accordingly. It is important to emphasize that it is a requirement for the examining physician in all 50 states to report any questionable circumstance to Child Protective Services (CPS). Once reported, it is up to CPS to investigate and proceed with the appropriate measures.

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22. Adelson PD, Ragheb J, Kanev P, et al. Phase II clinical trial of moderate hypothermia after severe traumatic brain injury in children. Neurosurgery. 2005;56(4):740–754 [discussion 740–754]. 23. Merten DF, Carpenter BL. Radiologic imaging of inflicted injury in the child abuse syndrome. Pediatr Clin North Am. 1990;37(4): 815–837. 24. Lloyd DA, Carty H, Patterson M, Butcher CK, Roe D. Predictive value of skull radiography for intracranial injury in children with blunt head injury. Lancet. 1997;349(9055):821–824. 25. Wang MY, Griffith P, Sterling J, McComb JG, Levy ML. A prospective population-based study of pediatric trauma patients with mild alterations in consciousness (Glasgow Coma Scale score of 13–14). Neurosurgery. 2000;46(5):1093–1099. 26. Kimura A, Otsuka T. Emergency center ultrasonography in the evaluation of hemoperitoneum: a prospective study. J Trauma. 1991;31(1):20–23. 27. Tso P, Rodriguez A, Cooper C, et al. Sonography in blunt abdominal trauma: a preliminary progress report. J Trauma. 1992;33(1):39–43 [discussion 43–44]. 28. Hoffmann R, Nerlich M, Muggia-Sullam M, et al. Blunt abdominal trauma in cases of multiple trauma evaluated by ultrasonography: a prospective analysis of 291 patients. J Trauma. 1992;32(4):452–458. 29. Rozycki GS, Ochsner MG, Jaffin JH, Champion HR. Prospective evaluation of surgeons’ use of ultrasound in the evaluation of trauma patients. J Trauma. 1993;34(4):516–526 [discussion 526–527]. 30. Mutabagani KH, Coley BD, Zumberge N, et al. Preliminary experience with focused abdominal sonography for trauma (FAST) in children: is it useful? J Pediatr Surg. 1999;34(1):48–52 [discussion 52–54]. 31. Luks FI, Lemire A, St-Vil D, Di Lorenzo M, Filiatrault D, Ouimet A. Blunt abdominal trauma in children: the practical value of ultrasonography. J Trauma. 1993;34(5):607–610 [discussion 610–611]. 32. Sarkisian AE, Khondkarian RA, Amirbekian NM, Bagdasarian NB, Khojayan RL, Oganesian YT. Sonographic screening of mass casualties for abdominal and renal injuries following the 1988 Armenian earthquake. J Trauma. 1991;31(2):247–250. 33. Bode PJ, Niezen RA, van Vugt AB, Schipper J. Abdominal ultrasound as a reliable indicator for conclusive laparotomy in blunt abdominal trauma. J Trauma. 1993;34(1):27–31. 34. Suthers SE, Albrecht R, Foley D, et al. Surgeon-directed ultrasound for trauma is a predictor of intra-abdominal injury in children. Am Surg. 2004;70(2):164–167 [discussion 167–168]. 35. O’Sullivan MG, Statham PF, Jones PA, et al. Role of intracranial pressure monitoring in severely head-injured patients without signs of intracranial hypertension on initial computerized tomography. J Neurosurg. 1994; 80(1):46–50. 36. Stafford RE, McGonigal MD, Weigelt JA, Johnson TJ. Oral contrast solution and computed tomography for blunt abdominal trauma: a randomized study. Arch Surg. 1999;134(6):622–626 [discussion 626–627]. 37. Tsang BD, Panacek EA, Brant WE, Wisner DH. Effect of oral contrast administration for abdominal computed tomography in the evaluation of acute blunt trauma. Ann Emerg Med. 1997;30(1):7–13. 38. Federle MP, Yagan N, Peitzman AB, Krugh J. Abdominal trauma: use of oral contrast material for CT is safe. Radiology. 1997;205(1):91–93. 39. Lim-Dunham JE, Narra J, Benya EC, Donaldson JS. Aspiration after administration of oral contrast material in children undergoing abdominal CT for trauma. AJR Am J Roentgenol. 1997;169(4):1015–1018. 40. Strouse PJ, Close BJ, Marshall KW, Cywes R. CT of bowel and mesenteric trauma in children. Radiographics. 1999;19(5):1237–1250. 41. Cox TD, Kuhn JP. CT scan of bowel trauma in the pediatric patient. Radiol Clin North Am. 1996;34(4):807–818. 42. Rice HE, Frush DP, Farmer D, Waldhausen JH. Review of radiation risks from computed tomography: essentials for the pediatric surgeon. J Pediatr Surg. 2007;42(4):603–607. 43. Keller MS, Coln CE, Trimble JA, Green MC, Weber TR. The utility of routine trauma laboratories in pediatric trauma resuscitations. Am J Surg. 2004;188(6):671–678. 44. Ford EG, Karamanoukian HL, McGrath N, Mahour GH. Emergency center laboratory evaluation of pediatric trauma victims. Am Surg. 1990; 56(12):752–757. 45. Bryant MS, Tepas JJ 3rd, Talbert JL, Mollitt DL. Impact of emergency room laboratory studies on the ultimate triage and disposition of the injured child. Am Surg. 1988;54(4):209–211. 46. Peterson DL, Schinco MA, Kerwin AJ, Griffen MM, Pieper P, Tepas JJ. Evaluation of initial base deficit as a prognosticator of outcome in the pediatric trauma population. Am Surg. 2004;70(4):326–328. 47. Asimos AW, Gibbs MA, Marx JA, et al. Value of point-of-care blood testing in emergent trauma management. J Trauma. 2000;48(6):1101–1108.

48. Carrick MM, Tyroch AH, Youens CA, Handley T. Subsequent development of thrombocytopenia and coagulopathy in moderate and severe head injury: support for serial laboratory examination. J Trauma. 2005;58(4):725–729 [discussion 729–730]. 49. Cochran A, Scaife ER, Hansen KW, Downey EC. Hyperglycemia and outcomes from pediatric traumatic brain injury. J Trauma. 2003; 55(6):1035–1038. 50. Tepas JJ 3rd, DiScala C, Ramenofsky ML, Barlow B. Mortality and head injury: the pediatric perspective. J Pediatr Surg. 1990;25(1):92–95 [discussion 96]. 51. Sills MR, Libby AM, Orton HD. Prehospital and in-hospital mortality: a comparison of intentional and unintentional traumatic brain injuries in Colorado children. Arch Pediatr Adolesc Med. 2005;159(7):665–670. 52. Kriel RL, Krach LE, Panser LA. Closed head injury: comparison of children younger and older than 6 years of age. Pediatr Neurol. 1989; 5(5):296–300. 53. Bauer R, Fritz H. Pathophysiology of traumatic injury in the developing brain: an introduction and short update. Exp Toxicol Pathol. 2004;56 (1–2):65–73. 54. American Association for the Surgery of Trauma, Child Neurology Society, International Society for Pediatric Neurosurgery, et al. Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents. J Trauma. 2003;54(6 suppl):S235–S310. 55. Peclet MH, Newman KD, Eichelberger MR, Gotschall CS, Garcia VF, Bowman LM. Thoracic trauma in children: an indicator of increased mortality. J Pediatr Surg. 1990;25(9):961–965 [discussion 965–966]. 56. Gray A. Pediatric orthopedic trauma. In: Cooper A, Sherer LR III, Stylianos S, Tuggle D, eds. Pediatric Trauma. New York: Taylor & Francis; 2006:325–356. 57. Platzer P, Jaindl M, Thalhammer G, et al. Cervical spine injuries in pediatric patients. J Trauma. 2007;62(2):389–396 [discussion 394–396]. 58. Dickman CA, Zabramski JM, Hadley MN, Rekate HL, Sonntag VK. Pediatric spinal cord injury without radiographic abnormalities: report of 26 cases and review of the literature. J Spinal Disord. 1991;4(3):296–305. 59. Peterson RJ, Tepas JJ 3rd, Edwards FH, Kissoon N, Pieper P, Ceithaml EL. Pediatric and adult thoracic trauma: age-related impact on presentation and outcome. Ann Thorac Surg. 1994;58(1):14–18. 60. Holmes JF, Sokolove PE, Brant WE, Kuppermann N. A clinical decision rule for identifying children with thoracic injuries after blunt torso trauma. Ann Emerg Med. 2002;39(5):492–499. 61. Allen GS, Cox CS Jr. Pulmonary contusion in children: diagnosis and management. South Med J. 1998;91(12):1099–1106. 62. Rielly JP, Brandt ML, Mattox KL, Pokorny WJ. Thoracic trauma in children. J Trauma. 1993;34(3):329–331. 63. Peterson RJ, Tiwary AD, Kissoon N, Tepas JJ 3rd, Ceithaml EL, Pieper P. Pediatric penetrating thoracic trauma: a five-year experience. Pediatr Emerg Care. 1994;10(3):129–131. 64. Tiao GM, Griffith PM, Szmuszkovicz JR, Mahour GH. Cardiac and great vessel injuries in children after blunt trauma: an institutional review. J Pediatr Surg. 2000;35(11):1656–1660. 65. Canty TG Sr, Canty TG Jr, Brown C. Injuries of the gastrointestinal tract from blunt trauma in children: a 12-year experience at a designated pediatric trauma center. J Trauma. 1999;46(2):234–240. 66. Cooper A. Thoracic injuries. Semin Pediatr Surg. 1995;4(2):109–115. 67. Karmy-Jones R, Hoffer E, Meissner M, Bloch RD. Management of traumatic rupture of the thoracic aorta in pediatric patients. Ann Thorac Surg. 2003;75(5):1513–1517. 68. Koplewitz BZ, Ramos C, Manson DE, Babyn PS, Ein SH. Traumatic diaphragmatic injuries in infants and children: imaging findings. Pediatr Radiol. 2000;30(7):471–479. 69. Guth AA, Pachter HL, Kim U. Pitfalls in the diagnosis of blunt diaphragmatic injury. Am J Surg. 1995;170(1):5–9. 70. Ciftci AO, Tanyel FC, Salman AB, Buyukpamukcu N, Hicsonmez A. Gastrointestinal tract perforation due to blunt abdominal trauma. Pediatr Surg Int. 1998;13(4):259–264. 71. Clendenon JN, Meyers RL, Nance ML, Scaife ER. Management of duodenal injuries in children. J Pediatr Surg. 2004;39(6):964–968. 72. Lutz N, Nance ML, Kallan MJ, Arbogast KB, Durbin DR, Winston FK. Incidence and clinical significance of abdominal wall bruising in restrained children involved in motor vehicle crashes. J Pediatr Surg. 2004;39(6): 972–975. 73. Letton RW, Worrell V. Delay in diagnosis and treatment of blunt intestinal injury does not adversely affect prognosis in the pediatric trauma patient. J Pediatr Surg. 2010;45(1):161–165 [discussion 166]. 74. Haut ER, Nance ML, Keller MS, et al. Management of penetrating colon and rectal injuries in the pediatric patient. Dis Colon Rectum. 2004;47(9):1526–1532.

The Pediatric Patient 88. Keller MS, Eric Coln C, Garza JJ, Sartorelli KH, Christine Green M, Weber TR. Functional outcome of nonoperatively managed renal injuries in children. J Trauma. 2004;57(1):108–110 [discussion 110]. 89. Deck AJ, Shaves S, Talner L, Porter JR. Computerized tomography cystography for the diagnosis of traumatic bladder rupture. J Urol. 2000; 164(1):43–46. 90. Parry NG, Rozycki GS, Feliciano DV, et al. Traumatic rupture of the urinary bladder: is the suprapubic tube necessary? J Trauma. 2003; 54(3):431–436. 91. Harris LM, Hordines J. Major vascular injuries in the pediatric population. Ann Vasc Surg. 2003;17(3):266–269. 92. Milas ZL, Dodson TF, Ricketts RR. Pediatric blunt trauma resulting in major arterial injuries. Am Surg. 2004;70(5):443–447. 93. Lin PH, Barr V, Bush RL, Velez DA, Lumsden AB, Ricketts J. Isolated abdominal aortic rupture in a child due to all-terrain vehicle accident—a case report. Vasc Endovascular Surg. 2003;37(4):289–292. 94. Tracy TF Jr, Silen ML, Graham MA. Delayed rupture of the abdominal aorta in a child after a suspected handlebar injury. J Trauma. 1996; 40(1):119–120. 95. Soundappan SV, Holland AJ, Cass DT. Role of an extended tertiary survey in detecting missed injuries in children. J Trauma. 2004;57(1): 114–118 [discussion 118]. 96. Avellino AM, Mann FA, Grady MS, et al. The misdiagnosis of acute cervical spine injuries and fractures in infants and children: the 12-year experience of a level I pediatric and adult trauma center. Childs Nerv Syst. 2005;21(2):122–127. 97. Odetola FO, Miller WC, Davis MM, Bratton SL. The relationship between the location of pediatric intensive care unit facilities and child death from trauma: a county-level ecologic study. J Pediatr. 2005;147(1): 74–77. 98. Cox C. Trauma from child abuse. In: Cooper A, Sherer LR III, Stylianos S, Tuggle D, eds. Pediatric Trauma. New York: Taylor & Francis; 2006: 325–356. 99. Segui-Gomez M, Chang DC, Paidas CN, Jurkovich GJ, Mackenzie EJ, Rivara FP. Pediatric trauma care: an overview of pediatric trauma systems and their practices in 18 US states. J Pediatr Surg. 2003;38(8): 1162–1169.

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75. Stylianos S. Compliance with evidence-based guidelines in children with isolated spleen or liver injury: a prospective study. J Pediatr Surg. 2002; 37(3):453–456. 76. Mooney DP, Downard C, Johnson S, Atkinson CC, Forbes PW, Taylor GT. Physiology after pediatric splenic injury. J Trauma. 2005;58(1): 108–111. 77. Howdieshell TR, Heffernan D, Dipiro JT. Surgical infection society guidelines for vaccination after traumatic injury. Surg Infect (Larchmt). 2006;7(3):275–303. 78. Paddock HN, Tepas JJ 3rd, Ramenofsky ML, Vane DW, Discala C. Management of blunt pediatric hepatic and splenic injury: similar process, different outcome. Am Surg. 2004;70(12):1068–1072. 79. MacKenzie S, Kortbeek JB, Mulloy R, Hameed SM. Recent experiences with a multidisciplinary approach to complex hepatic trauma. Injury. 2004;35(9):869–877. 80. Markley MA, Mantor PC, Letton RW, Tuggle DW. Pediatric vacuum packing wound closure for damage-control laparotomy. J Pediatr Surg. 2002;37(3):512–514. 81. Gross JA, Vaughan MM, Johnston BD, Jurkovich G. Handlebar injury causing pancreatic contusion in a pediatric patient. AJR Am J Roentgenol. 2002;179(1):222. 82. Wales PW, Shuckett B, Kim PC. Long-term outcome after nonoperative management of complete traumatic pancreatic transection in children. J Pediatr Surg. 2001;36(5):823–827. 83. Meier DE, Coln CD, Hicks BA, Guzzetta PC. Early operation in children with pancreas transection. J Pediatr Surg. 2001;36(2):341–344. 84. Canty TG Sr, Weinman D. Management of major pancreatic duct injuries in children. J Trauma. 2001;50(6):1001–1007. 85. Sayad P, Cacchione R, Ferzli G. Laparoscopic distal pancreatectomy for blunt injury to the pancreas. A case report. Surg Endosc. 2001;15(7):759. 86. Nance ML, Lutz N, Carr MC, Canning DA, Stafford PW. Blunt renal injuries in children can be managed nonoperatively: outcome in a consecutive series of patients. J Trauma. 2004;57(3):474–478 [discussion 478]. 87. Rogers CG, Knight V, MacUra KJ, Ziegfeld S, Paidas CN, Mathews RI. High-grade renal injuries in children—is conservative management possible? Urology. 2004;64(3):574–579.

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The Geriatric Patient Jay A. Yelon

INTRODUCTION According to U.S. census projections the elderly population, defined as age 65 years, is experiencing the largest growth in history. The post–World War II “baby boom” (75 million people born from 1946 to 1964) was 46–64 years old in 2010. By the year 2030, the elderly population will number 38 million and will usher in the gerentological explosion by 2050 in which 1 in 5 Americans will be elderly.1 The overwhelming evidence of this demographic imperative will result in an elderly population that is active and vital. The everincreasing mobility and active lifestyles of today’s elderly place them at increased risk for serious injury. In fact, data from the National Trauma Data Bank (NTDB) for the year 2008 revealed that 30% of all patients in the registry were 55 years old or older.2 Injury is now the fifth leading cause of death in the elderly population.3 Older individuals sustaining injury respond differently than younger patients. The elderly have a higher morbidity and mortality, have more preexisting medical problems, and demonstrate a senescent physiologic response to injury when compared with younger individuals. Many of the reasons for the differing response are unknown. The literature, albeit plentiful, can be contradictory in places and there are few prospective randomized trials that focus specifically on the elderly. This is best demonstrated by a lack of consensus on the definition of what age constitutes elderly. Historically geriatric patients were considered to be patients over the age of 65 years. There are a variety of organ-specific injuries that demonstrate rising morbidity and mortality at chronological ages less than 65 years. As such, elderly should be viewed from the vantage of the physiologic response to an injury or injury complex rather than a specific age. Despite these limitations, this chapter will focus on an overview of care for the injured geriatric patient.

AGING Declining cellular function is part of the aging process. Eventually, this will lead to organ failure. The aging process is characterized by impaired adaptive and homeostatic mechanisms, resulting in increased susceptibility to the stress of injury. This is commonly perceived as decreased physiologic reserve. Insults commonly tolerated by younger patients can lead to devastating results in the elderly patient. Differences in the metabolic response to injury were studied by Frankenfield and colleagues. In their study, they compared injured patients by dividing them into those older than 60 years and those who were younger. These investigators concluded that the metabolic response to injury is significantly attenuated in the elderly population. This was demonstrated by the older group having less fever, less oxygen consumption, more hyperglycemia, and more azotemia.4 This may be driven by the fact that there is evidence that immune function is significantly attenuated during the aging process and that cytokine response is impaired. This immune senescence is, in part, a function of reduced neutrophil function. Butcher et al. investigated a group of patients older than 65 years sustaining mild trauma (hip fracture). Neutrophil phagocytic function was assessed immediately after injury and patients were followed for 5 weeks for clinical infection. When compared with a younger cohort, the older patients had a significant reduction in neutrophil phagocytic function as measured by significantly depressed superoxide production.5 Additionally, nearly half of the elderly population suffered bacterial or fungal infection within the study period, compared with no infection in the younger patients. These authors suggest that the aging immune system may be a result of falling dehydroepiandrosterone (DHEA). In the presence of the physiologic stress of injury, patients have an obligatory rise in corticosterone levels, which is immune suppressive. The elderly patient, with a depressed

The Geriatric Patient DHEA level, produces a milieu of corticosterone excess contributing to neutrophil dysfunction.

■ Cardiac Cardiovascular comorbidities are most frequently seen in the elderly patient. Cardiac function declines by 50% between the ages of 20 and 80 years. The declining function is combined with a decreased sensitivity to catecholamines.6 The expected cardiovascular response to hypovolemia may not be apparent. This may be further complicated by a variety of medications, which includes β-blocker therapy.7 The cellular elements of the conductive system and the myocytes themselves are gradually replaced by fat and fibrous tissue. The resultant stiffer heart is more prone to dysfunction and to dysrythmias. Atherosclerotic changes to the arteries are common and valvular anatomy is changed by tissue thickening. The increased afterload causes an increase in systolic blood pressure and enlargement of the heart. The system is generally well compensated while at rest. However, in the event of hypovolemia, elderly patients generally are unable to compensate with tachycardia and an increase in cardiac output. The response is generally characterized by an increase in systemic vascular resistance. Traditional vital signs can be misleading. Despite “normal” blood pressure, many of these patients have evidence of tissue hypoperfusion.8

■ Pulmonary There are significant anatomic and physiologic changes that occur in the respiratory system that are associated with aging. Grossly, with age-related loss in bone density, there is development of thoracic kyphosis. Rib calcification is associated with a decrease in transverse thoracic diameter. Muscle mass is reduced and the elastic recoil of the lung decreases with age. These anatomic changes result in a decreased compliance of the chest. Reduction in functional residual capacity and gas exchange is obligatory.9 The elderly commonly experience decreased cough reflex, decreased function of the mucociliary epithelium, decreased response to foreign antigen, and increased oropharyngeal colonization with microorganisms. These changes place the elderly patient at risk for hospital-acquired pneumonia.10 There is a decrease in alveolar surface area after the age of 30 years. This results in decreased alveolar surface tension that ultimately interferes with alveolar gas exchange. The alveoli are also noted to flatten and become shallow, thereby decreasing effective surface area for gas exchange. Diffusion capacity is decreased because of the decrease in effective surface area and an increase in alveolar–capillary membrane thickness.11

■ Renal System Above the age of 50 years, renal mass is lost. Progressive sclerosis of the glomeruli occurs with normal aging. Between the ages of 50 and 80 years, there is a decrease in glomerular filtration rate (GFR) by about 45%.6 Generally, this is not detected by routine renal function testing, as it is accompanied by a decrease in total muscle mass and production of creatinine. The

■ Skin/Soft Tissue and Musculoskeletal System Older people undergo an obligatory loss of lean body mass. This loss is estimated to be about 4% every 10 years after the age of 25. This loss then increases to approximately 10% after the age of 50. The loss of muscle is accompanied by a proportional increase in adipose tissue. From a skeletal aspect, osteoporosis is a common feature of aging. Over time, this loss can amount to 60% of trabecular bone and 35% of cortical bone.14 This makes the elderly individual at risk for fractures, especially those involving the vertebrae, hip, and distal forearm. There are age-associated changes of the joints and cartilages resulting in osteoarthritis and other degenerative features affecting nearly all joints. Degenerative changes to the cervical spine are particularly worrisome in the older population. Mobility is greatly affected putting this area at risk for injury. Additionally, oral intubation can be affected by this loss of mobility.15 Changes of the skin and soft tissue with loss of elastin and subcutaneous fat not only place the patient at risk for direct skin injury but may also complicate underlying fractures, such as pelvic fractures or open fractures.

■ Endocrine There are age-related changes that affect endocrine function. The tissue responsiveness to thyroxin and its production is reduced.6 Secretion of cortisol does not seem to change with aging, but given decreases in DHEA production, this may predispose the physiologically stressed elderly patient to a hypercortisone state.

■ Functional Reserve Maintaining homeostasis in the face of physiologic stress is a demonstration of good functional reserve. Declining functional reserve in the elderly may precipitate a decline in performance when the patient is exposed to chronic or acute illness. When faced with a physical insult, homeostasis may be poorly maintained (Table 44-1; Fig. 44-1). The decline in functional reserve is heterogeneous. A variety of factors will impact on the magnitude of the loss of functional reserve. These include age-related disease and their treatments, genetics, lifestyle choices, and environmental factors. It is clear

CHAPTER 44

ORGAN FUNCTION AND AGING

Cockroft–Gault formula can be used to estimate the degree of dysfunction. Furthermore, the endocrine response of the kidney to ADH and aldosterone is abnormal. This results in a decrease in the ability of the kidney to concentrate urine. Elderly patients may be able to maintain a deceptively adequate urine flow despite hypovolemia. As such, urine output should be used cautiously as a surrogate for renal perfusion.12,13 These age-related changes in renal function put the older patient at significant risk for acute kidney injury following trauma. Likewise, the elderly are at risk for developing untoward effects of aggressive volume resuscitation—such as hyperchloremic metabolic acidosis and volume overload. Care must be maintained when dosing renally excreted drugs to these patients.

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TABLE 44-1 Organ System Changes with Aging Functional Changes Declining function Decreased sensitivity to catecholamines Decreased myocyte mass Atherosclerosis of coronary vessels Increased afterload Fixed cardiac output Fixed heart rate (β-blockers) Thoracic kyphoscoliosis Decreased transverse thoracic diameter Decreased elastic recoil Reduced FRC Decreased gas exchange Decreased cough reflex Decreased mucociliary function Increased oropharyngeal colonization Loss of renal mass Decreased GFR Decreased sensitivity to ADH and aldosterone

Pulmonary

Renal

Skin/soft tissue/ musculoskeletal

Loss of lean body mass Osteoporosis Changes in joints and cartilages Degenerative changes (including c-spine) Loss of skin elastin and subcutaneous fat

Endocrine

Decreased production and response to thyroxin Decreased DHEA

% Maximal organ function

SECTION 4

Organ System Cardiac

80 Maximal

Increased risk for respiratory failure Increased risk for pneumonia Poor tolerance to rib fractures

Routine renal labs will be normal (not reflective of dysfunction) Drug dosing for renal insufficiency Decreased ability to concentrate urine Urine flow maybe normal with hypovolemia Increased risk for acute kidney injury Increase in body fat Increased risk for fractures Decreased mobility Difficulty for oral intubation Risk of skin injury due to immobility Increased risk for hypothermia Challenges in rehabilitation Occult hypothyroidism Relative hypercortisone state Increased risk of infection

that older patients do not tolerate injury as well as younger patients. What is not clear is the reason for this discrepancy. The impact of preexisting medical problems,16–18 in combination with a declining functional reserve, results in poor outcome. This impact on outcome can be reduced by an aggressive management approach to the patient.

100

60

Implications for Care Lack of “classic” response to hypovolemia Risk for cardiac ischemia Increased risk of dysrythmias Elevated baseline blood pressure

Functional reserve

MANAGEMENT

40

■ Triage

Basal 20 20

30

40

50 60 Age (years)

70

80

90

FIGURE 44-1 The functional reserve is the difference between basal function (red line) and maximal function (blue line). Even in healthy individuals, this functional reserve is reduced. (From Muravchick S. Geroanesthesia: Principles for Management of the Elderly Patient. St. Louis, MO: Mosby; 1997, with permission. Copyright © Elsevier).

Improper triage seems to contribute to the poor outcomes experienced by some elderly trauma patients. The effectiveness of triage can be evaluated by looking at the interaction between injury severity and complication rate, mortality, or requirement for intervention.19 Elderly patients with severe injury who are not treated with full trauma team activation (TTA) would be considered to be undertriaged. Multiple studies have shown a large incidence of undertriage as compared with younger patients.19–22 Undertriage can be viewed as a modifiable risk factor for poor outcome in the older patient. Lehmann et al.

The Geriatric Patient

■ Initial Assessment Airway The elderly airway poses specific challenges for providers. Given the fact that the elderly have significant loss of protective airway reflexes, timely decision making for establishing a definitive airway can be lifesaving. Patients may have dentures or be edentulous, the former making bag–mask ventilation easier. Arthritic changes may make mouth opening difficult. Choice of appropriately sized direct laryngoscopy equipment is mandatory. When performing rapid sequence intubation the doses of barbiturates, benzodiazepines, and etomidate should be reduced between 20% and 40% to minimize the risk of cardiovascular depression.25

Breathing The anatomic and physiologic changes in the respiratory system associated with aging are reviewed above. Changes in the compliance of both the lungs and the chest wall result in an increased work of breathing with aging. These changes associated with the possibility of nutritional deficits and the supine position place the elderly trauma patient at high risk for respiratory failure. Given a suppressed heart rate response, as a result of aging, to hypoxia, respiratory failure may present in a more insidious fashion. Diagnosis can sometimes be difficult in interpreting clinical and laboratory information in the face of preexisting respiratory disease or nonpathologic changes in ventilation

associated with age. Frequently, decisions to secure a patient’s airway and provide mechanical ventilation may be made prior to fully appreciating underlying premorbid respiratory conditions. This action may be lifesaving. However, intubation and mechanical ventilation in the elderly patient should not be taken lightly. The risk of ventilator-associated pneumonia and the possibility of prolonged ventilation are significant.25 The role for noninvasive mechanical ventilation in the acute resuscitative phases of trauma care seems to be very limited and is likely associated with significant risk to the patient.

Circulation Age-related changes in the cardiovascular system place the elderly trauma patient at significant risk for mislabeling the patient as being “hemodynamically normal.” Since the elderly patient may have a fixed heart rate and cardiac output, response to hypovolemia will occur by increasing systemic vascular resistance. To further demonstrate the lack of classic symptoms as they relate to cardiovascular pathology, Chong and colleagues evaluated troponin I levels following emergency orthopedic surgery. One hundred and two patients over the age of 60 were evaluated, of which 52.9% of patients had elevated levels. The majority of patients with elevated troponin levels had no cardiac symptoms and had an increased mortality within 1 year of the event. Furthermore, since many elderly patients have preexisting hypertension, the seemingly “acceptable” blood pressure may truly reflect a relative hypotensive state. As such, identifying the patient who has significant tissue hypoperfusion is mandatory. Several methodologies have made, and continue to be used to make, this diagnosis. These include base deficit, serum lactate, age-adjusted Shock Index, and tissue-specific end points.8,26–28 Resuscitation of the geriatric hypoperfused patient is the same as all other patients and based on appropriate fluid and blood administration. The elderly trauma patient with evidence of circulatory failure should be assumed to be bleeding. However, given the incidence of elderly people with preexisting disease states, one should keep in mind that some physiologic event may have triggered the incident leading to injury. Ultimately an aggressive approach to resuscitation of the elderly patient with overt shock or a tissue-hypoperfused state will result in acceptable outcomes. Less aggressive measures based on the patient’s age are not acceptable.

Disability Traumatic brain injury (TBI) is a problem of epidemic proportion in the elderly population.29 Older age is a known variable for poor outcome following brain injury. Aging will cause the dura to become more adherent to the skull. Additionally, older patients are more commonly prescribed anticoagulant and antiplatelet medications for preexisting medical conditions. These two factors place the elderly individual at high risk for intracranial hemorrhage. Atherosclerotic disease is common with aging and may contribute to primary or secondary brain injury. Moderate cerebral atrophy will permit intracranial pathology to initially present with a normal neurologic examination. Early identification and timely appropriate support including correction of therapeutic anticoagulation can improve outcomes.30

CHAPTER 44

demonstrated that the classic physiologic criteria for TTA, that is, blood pressure and heart rate, failed to independently predict hospital mortality or the need for urgent interventions.20 These authors attribute the older patient’s “pseudostability” to declining functional reserve and the interaction of premorbid medications. Use of initial vital signs in the elderly population can be misleadingly normal. In a study from Los Angeles patients 70 years of age and older admitted to the trauma center were reviewed. Sixty-three percent of patients with an Injury Severity Score (ISS) 15 and 25% of patients with an ISS 30 did not meet the hypotension or tachycardia criteria for TTA. In this study, the overall mortality in “stable” patients not meeting any of the standard TTA criteria was 16%.19 The impact of apparently “minor” injury can have major impact on the older patient. Rib fractures and pulmonary contusions can lead to an abrupt decompensation and injuries such as intracranial hemorrhage are commonly underappreciated. It has been suggested that patient age of 70 or older be used as a criterion for TTA.19 The age at which triage and management issues become problematic is also controversial. The current recommendation of the ATLS program is 55 years of age.23 This is based on data from the Major Trauma Outcomes study that noted a significant increase in mortality between the 45- and 54-year-olds.24 TRISS uses a similar age cutoff, although a recent work examining TRISS methodology seems to indicate an older age is more accurate. Caterino et al., using the Ohio trauma registry, examined mortality trends. Regression analysis identified 70 years of age to be the most promising cutoff for predicting increased odds of mortality.21

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Exposure

SECTION 4

Musculoskeletal changes associated with the aging process pose special concerns during this aspect of the initial assessment of the elderly trauma patient. Loss of subcutaneous fat, nutritional deficiencies, chronic medical conditions, and the associated medical therapies will place the elderly patient at risk for hypothermia and the risks associated with immobility (pressure ulcers, delirium). Rapid evaluation and, when possible, early mobilizations will prove to minimize the morbidities.

SPECIFIC INJURIES ■ Traumatic Brain Injury In the elderly age group, TBI accounts for more than 80,000 emergency department visits each year of which a majority result in hospitalization. Falls are the leading cause of TBI for people over the age of 65 years (51%), followed by motor vehicle collisions (9%).29 Health care costs associated with the treatment of TBI in the elderly exceeded $2.2 billion in 2003.31 TBI is clearly a major health care problem in the elderly population. The current evidence-based approach to treating severe TBI in the adult is a “one size fits all” approach, neglecting specific issues of the older adult. Old age remains an independent predictor of worse outcome in TBI. An investigation using the New York State Trauma Registry compared mortality and functional outcome in elderly versus younger patients.32 In this study, Susman et al. demonstrated increased mortality in patients older than 65 years, but also showed that mortality increases as patients continue to age. These investigators also showed that a majority of elderly patients sustain TBI from falls and appear to have only mild TBI at admission and still had a much higher mortality as compared with younger patients. This same group then looked at the total effect of age on mortality after TBI.33 They concluded that mortality from TBI increases after 30 years, but has a sharp rise after 70 years. Given the anatomic changes associated with aging on the brain and the fact that a majority of elderly patients present with a GCS consistent with mild brain injury, a high index of suspicion must be maintained with the elderly patient presenting with any mechanism of head trauma. To address this, Mack et al. investigated the use of head computed tomography (CT) in elderly patients.34 This study specifically looked at mild head injury (GCS 13–15). In their study of 133 elderly patients, 14.3% had radiographic evidence of acute intracranial pathology. The authors also noted that there were no useful clinical predictors of intracranial injury and liberal use of head CT is recommended. Despite a higher mortality in general, patients surviving hospitalization will required aggressive rehabilitation. In a multi-institutional trial a group of elderly patients surviving their initial moderate to severe brain injury (head AIS  3) were evaluated following discharge from acute care. In this cohort, there were few patients with low GCS who survived, and left patients with GCS of 13–15 to be evaluated. Functional outcome for these patients, as measured by the Glasgow Outcome Scale (GOS) and modified FIM, is good to excellent. Older patients required more inpatient rehabilitation and took longer to recover when compared with a younger patient

cohort.35 Aggressive initial management and long-term rehabilitation in the elderly patient with TBI is required for acceptable outcomes.

■ Rib Fractures Rib fractures in the elderly population pose a significant risk for morbidity and mortality when compared with younger patients, who, in general, suffer little morbidity. The morbidities include inadequate pain management, need for intubation, prolonged ventilatory support, and the development of pneumonia. Bulger et al. investigated the impact of rib fractures after blunt chest trauma in the elderly.36 This study showed a linear relationship between age, number of rib fractures, complications, and mortality. In a similar study, Holcomb et al. retrospectively evaluated 171 patients. These authors demonstrated an increase in negative outcomes based on increasing age and number of rib fractures. By grouping ages and number of rib fractures their data revealed that patients with more than four rib fractures who are older than 45 years exhibit increased morbidity (ICU length of stay [LOS], total LOS, ventilator days, and pulmonary complications). Given the impact of type of analgesia at reducing ventilator days and pulmonary complications, the authors attempted to determine the impact of epidural analgesia. Their data were unable to demonstrate a decreased incidence of morbidity and mortality. Given that this was only a portion of their entire population, it is possible that their results suffer from a type II statistical error. Analgesia is an important aspect of the care of the elderly trauma patient with rib fractures. The Eastern Association for the Surgery of Trauma has a Practice Management Guideline on chest trauma analgesia management.37 Readers are encouraged to refer to this document on evidence-based guidelines for analgesia. In an evaluation of data from the NTDB of the American College of Surgeons Committee on Trauma, Flagel et al. reviewed a large patient population.38 These investigators showed that the overall mortality rate for patients with rib fractures was 10%. This rate increased for each additional rib fracture independent of age. There was a similar trend of increasing pulmonary complication with additional rib fractures. The incidence of pneumonia in patients with up to five rib fractures was between 3% and 5.2%. This increased to 6.8–8.4% for patients with six or more rib fractures. These authors were unable to demonstrate that age is a risk factor for mortality in patients with rib fractures. Most recent data from a multicenter study of 1,621 patients were published by the Research Consortium of New England Centers for Trauma.39 These investigators evaluated patients over the age of 50 years with nearly isolated rib fractures. Thirty-five percent of the patients were admitted to the ICU with an average ICU LOS of 16.5 days and a total hospital LOS of 27.5 days. Intubation was required in 12% of patients and 4.3% went on to require tracheostomy. Univariate analysis of the data revealed risk factors for mortality were preexisting coronary artery disease or CHF, increasing age, ISS, number of ribs fractured, and increasing AIS for associated body regions. On multivariate analysis the strongest predictors of mortality were admission to a high-volume trauma center, preexisting CHF, intubation, and increasing age. Patient-controlled

The Geriatric Patient

■ Abdominal Injury The nonoperative management of solid organ injury has generally become the preferred method of treatment for the hemodynamically normal patient. However, in the elderly trauma patient this approach must be used with caution. The classical physiologic response to hemorrhage that may be used as a criterion to attempt nonoperative care or as a marker for “failure” of nonoperative management may not be present. In a 6-year retrospective analysis of patients sustaining blunt splenic injury, Albrecht et al. evaluated the utility of nonoperative management of spleen injury in patients older than 55 years.40 In this small study of 37 patients meeting inclusion criteria, 13 patients went directly to the operating room; of the remaining 23 patients, nonoperative management was successful in 15 (62.5%) and failed in 8 (33.3%). Characteristics of the group that failed nonoperative management included higher AAST splenic injury grades and a greater likelihood of a large hemoperitoneum. In a larger retrospective study of 1,482 patients, 15% (n  224) of who were 55 years or older, the mortality of the older population was significantly higher (43% vs. 23%) than the younger group. In this study 80% of patients over the age of 55 years were successfully managed nonoperatively, with 24 patients of the original 132 patients subsequently requiring exploration. Although not statistically significant, there was a trend toward increased failure rate with increasing grade of injury. When evaluated by grade of injury, grade I injuries had success rate for nonoperative management that was similar for younger and older patients. Success rates for older patients were lower for grade II (73% vs. 54%) and grade III (52% vs. 28%). All elderly patients with grade IV–V injuries required operation, either immediately or for failed nonoperative management.41 The data suggest that nonoperative management of splenic injury in the elderly patient should be undertaken with caution. Clear understanding of the grade of injury and assuring hemodynamic stability are absolute requirements. Elderly patients who fail nonoperative management may have a higher mortality as compared with younger patients.

■ Pelvic Fractures Bone fractures are extremely common in the elderly population. Women are at particular risk because of osteoporosis. Relatively minor trauma can lead to significant bone injury. Pelvic fractures pose a significant risk for elderly patients, including the acute phase of fracture management, timing of operation, and functional outcome. The group from the R Adams Cowley Shock Trauma Center compared outcomes of patients sustaining pelvic fractures over a 2-year period.42 These investigators compared patients using age 55 years as a cutoff.

Blood transfusion was required in 62% of older patients compared with 36% in the younger population (P  .0035). Further analysis revealed that patients who received transfusion were 2.8 times more likely to be over the age of 55. Mortality for the younger group was 6.2% compared with 20.5% for the older group (P  .0034), meaning the older group was four times more likely to die than the younger patients. Even after adjusting for ISS, death was four times more likely in the elderly patients. The authors suggest that every elderly patient with a pelvic fracture should be considered hemodynamically unstable until proven otherwise. Another consideration in the management of the elderly patient with orthopedic trauma is the timing of operation. The decision to proceed with orthopedic operation is made with the consideration of multiple variables that include extra-orthopedic injuries, physiologic status, and the magnitude of the operation planned. In a series of 367 elderly patients with hip fracture, a delay in operation for more than 2 days was associated with more than double the risk of death within the first postoperative year.43 Most believe that orthopedic operation to allow for mobilization from bed should occur as soon as possible when physiologic conditions have been optimized. Functional outcome is an additional consideration in caring for fractures in the elderly. Careful consideration by the orthopedic traumatologist is required when deciding between operative and nonoperative management as it relates to function. Osteopenic bones also need to be taken into consideration when dealing with periarticular fractures. Aggressive physical and occupational rehabilitation have been shown to improve outcomes as determined by patient satisfaction.

■ Burns Burn injury in the elderly population is particularly devastating. The elderly burn patient has a higher mortality for a given size burn than younger patients. In fact, predictors of survival from burn injury continue to rely on age as a significantly weighted variable. Despite significant advances in the science and management of burn injury, the LD50 for burns in the 65 years or older population remains approximately 20% total body surface area (TBSA). Older individuals are at a significant risk for burn injury due to impaired mobility, diminished senses, and slower reaction time, all characteristics making it difficult to escape harm, ultimately leading to deeper and more extensive burns. Predicting survival in older burn patients is important. It provides a framework for discussing realistic clinical expectations with patients and their families, and may allow for appropriate utilization of resources associated with the intensive care of burn patients. Wibbenmeyer et al. attempted to address this predictive model in relation to modern burn care.44 They reviewed 308 burn patients over the age of 60 years. A majority of these patients sustained flame burns of which 41.4% were sustained in household incidents. Sixty-four percent of the patients had at least one preexisting medical problem. The median TBSA size was 13%. The mortality for the cohort was 30.2%, with an LD50 of 30%. When this was further evaluated, the LD50 was age dependent. Specifically, for patients aged 60–69.9 it was 43.1%, for ages 70–79.9 it was 25.9%, and for

CHAPTER 44

analgesia showed a trend toward improving survival but was not statistically significant. The only therapeutic maneuver that proved to be protective of survival was tracheostomy. Identification of the elderly patient with rib fractures and early recognition of respiratory failure with aggressive supportive maneuvers will potentially reduce morbidity and mortality of this lethal injury in the older patient.

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SECTION 4

those 80 years and older the LD50 was 13.1%. As expected, the presence of an inhalation injury significantly impacted survival negatively. These authors concluded that death was significantly related to age, TBSA burn, and presence of inhalation injury. Comorbidities did not impact on mortality. The Baux score is calculated as the sum of the age of the patient and the TBSA burn is an estimate of the percent mortality and is supported by data from this study. The abbreviated burn injury severity (ABSI) score, calculated as the weighted sum of age, gender, TBSA, percentage of full-thickness injury, and presence of inhalation injury, was also predictive of survival, but less so than the Baux score. The authors were unable to demonstrate an improvement in survival over the 20-year period of data collection. Another study from the Burnett Burn Center at Kansas University Medical Center retrospectively reviewed three decades of care for the elderly burn patient.45 Two hundred and one patients over the age of 75 years were evaluated. This group showed a 77% mortality rate in the 1970s, compared with a combined overall mortality of 41% during the 1980s and 1990s, suggesting a decrease in mortality with improved overall care of this population; however, the LD50 remained 20% TBSA. Ho et al. reported outcome data from their regional burn center.46 They evaluated 94 patients over the age of 60 years. When compared with a younger population of burn patients, the older patients had a longer LOS, a mortality of 7.4%, and no differences in outcome based on early versus late excision. Timing of excision has yielded conflicting data. Deitch prospectively showed that early wound closure decreased LOS and number of septic complications and improved mortality.47 The studies by Ho and Wibbenmeyer did not show the benefits of early excision. Finally, gender seems to impact outcomes in elderly burn patients. Chang et al., from the University of Utah, demonstrated a higher mortality, longer LOS, and less likelihood of being discharged home in older female patient when compared with older men.48 Maintaining an aggressive approach to the older burn patient is warranted in the context of survivable injuries. Advanced age, larger burns, and the presence of inhalation injury are all negative predictors of survival in this population. Realistic therapeutic expectations are important for patients, their families, and the burn team when taking care of these very challenging patients.

■ Penetrating Trauma With the growth in the proportion of elderly people there will be an obligatory rise in the number of elderly trauma patients. By far, blunt trauma is the predominant mechanism for injury; however, there are still a significant number of people over the age of 65 years who are victims of penetrating injury. It should be remembered that many of these patients may be victims of suicide attempt, a major cause of death in the geriatric population. In the original Major Trauma Outcome Study (MTOS), when examining patients over the age of 55 between the years 1982 and 1987, elderly patients had a higher mortality when compared with a younger cohort.49 Also, Finelli et al. reported a significantly higher mortality in the elderly (52%) compared

with younger patients (20%) sustaining gunshot wounds.50 In contrast, Roth et al. from Los Angeles County and the University of Southern California retrospectively reviewed 79 patients over the age of 55 years suffering penetrating injuries. Their data showed no difference in mortality between elderly and younger patients (23% vs. 18%). Interestingly, 50% of the elderly patients who died presented with “normal” vital signs.51

■ Critical Care In a large retrospective statewide trauma registry review of 22,571 blunt trauma patients of which 7,117 were elderly, ICU utilization was evaluated.52 The entire population had an ICU admission rate of 42.7% with a mean ICU LOS of 5.77  8.86 days. The elderly patients, in contrast, had a lower ICU admission rate of 36.7% when compared with the younger population (45.5%). Interestingly, those elderly patients admitted to the ICU had a significantly longer ICU LOS. The lower utilization of ICU resources in the elderly may be explained by a higher early mortality and/or end-of-life (EOL) decisions that may have precluded admission to an ICU setting. Preventable complications in the elderly trauma patient significantly impact outcome. DeMaria et al. demonstrated an association of complications with death (32%) and an association of deaths from multisystem organ failure (62%).53 The relationship between senescence and infection deserves mention. Bochicchio et al. showed an increase risk of infection in elderly patients (39%) when compared with a younger population (17%) (P  .05).54 Once infected, the elderly patients are at much higher risk for death (28%) than their younger counterparts (5%) (P  .005). An aggressive approach to the older patient with infection is essential for improved outcomes. The aggressive management may include hemodynamic monitoring. Scalea et al. suggested that early invasive monitoring of the geriatric trauma patient can improve outcome.55 Noninvasive monitoring of elderly patients has been investigated in the critical care setting, but little has been concluded regarding the critically ill trauma patient.56 Because the elderly will fail to demonstrate the classic physiologic responses to shock, it is important to maintain an aggressive approach toward monitoring and resuscitation. The utility of invasive monitoring and aggressive critical care is demonstrated in a study on outcomes of elderly patients with acute respiratory distress syndrome (ARDS). In this study, Eachempati et al. evaluated a protocol approach to ARDS utilizing lung protective ventilator strategy and invasive hemodynamic monitoring. The investigators were able to demonstrate, in a group of 210 elderly patients with ARDS, a lower mortality when compared with historical controls despite higher illness severity.57 Delirium in the elderly trauma population is now being recognized as a significant risk factor for morbidity and mortality in the ICU. Delirium is characterized as a disturbance of consciousness associated with fluctuating mental status and disorganized thought. It complicates at least 20% of hospitalized patients over the age of 65 years, and increases hospitals costs by $2,500 per patient resulting in $6.9 billion of Medicare hospital expenditures.58 There is also a 3-fold higher mortality over 6 months following a single episode of delirium in the

The Geriatric Patient

OUTCOMES Injured elderly patients admitted to the hospital consume significant health care resources. Average hospital lengths of stay are generally around 10 days and these patients usually stay in the ICU longer than younger patients (except for early deaths). Hospital-acquired complications are independent predictors of mortality in this age group. Richmond et al., in 2002, reported their 10-year retrospective statewide trauma registry review of geriatric trauma.64 They evaluated all patients 65 years or older who were included in the registry. Nearly 62% of the patients were injured as a result of a fall. This was followed by motor vehicle collisions in 22.6%. Operation was required in 28% of cases, and 37% of the cohort had a preexisting medical condition. Average LOS was 11.5 days and one third of the group required ICU admission. Ten percent of all patients died. These investigators found that as age increased the patients had higher mortality and more complications, and in those who survived, more patients required discharge to a facility other than home.

The patients who died had a greater number of injuries with more body regions involved with a resultant higher ISS. Admission physiologic markers may predict those at risk for mortality. In a statewide trauma registry review from Pennsylvania, elderly patients who were hypotensive, had a GCS of 3, or had a respiratory rate of less than 10 had a significantly increased risk of death.52

■ Preexisting Conditions (PECs) The interaction between injury and patient factors has been studied extensively. Data are conflicting regarding the impact of these factors on mortality. Despite this, there is a large body of evidence that PECs will impact morbidity and likely mortality. Morris et al. identified five PECs that appeared to influence outcomes.18 In that study of over 3,000 patients, one fourth of patients over the age of 65 years had one of the five PECs. These investigators identified cirrhosis, congenital coagulopathy, COPD, ischemic heart disease, and diabetes as PECs that influenced outcomes in trauma patients. Patients with one or more of these PECs were nearly two times more likely to die than those without PECs. These same authors then reported the interaction between injury and host factors, which included age, gender, and PECs.17 Although injury severity was the primary determinant of mortality, host factors also played a significant role. These studies were later corroborated by a study by Grossman et al., in which an ISS 30 was considered the LD50, each additional year of age greater than 65 years carried a mortality increase of 6.8%, and PECs with the greatest impact on mortality were hepatic disease, renal disease, cancer, and congestive heart failure.16

■ Complications There seems to be a relationship between PECs and the development of postinjury complications. The additional morbidity of a complication increases mortality. In a study by Taylor et al., reviewing a large statewide trauma registry, 6.2% of elderly patients developed pneumonia. Both preexisting pulmonary disease and increased ISS were risk factors for the development of pneumonia. Pneumonia predicted both an increased ICU and an increased hospital LOS. In this study, 5.9% of patients developed acute kidney injury that incurred a greater than 10-fold increase in mortality. Finally, the development of sepsis, which occurred in only 1.2% of patients, significantly increased mortality, ICU LOS, and hospital LOS. The only risk factor identified with the development of sepsis was increased ISS.65

■ Resource Utilization The association between age as an independent predictor and outcome as documented by increased mortality and hospital LOS is well supported in the literature. Although hospital LOS is increased, ICU utilization is less than that by a younger population.52,65 This is due to an increased early mortality that is seen in the elderly, as well as decreased ICU admission resulting from advanced directives. Data from the Healthcare Financing Administration demonstrate that ICU use decreased with age and was least likely for age over 85 years.31 Young et al.

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ICU.59 Understanding of the impact of delirium in the trauma patient has only recently been investigated. Pandharipande et al. undertook a prevalence study of delirium in their trauma and surgical ICUs. Using a validated screening tool, the CAMICU, these investigators found an overall prevalence of delirium of 70% (73% in surgical patients and 67% in trauma patients).60 The group from the trauma center at Denver General Health Science Center performed a 4-month study of 69 patients admitted to their trauma ICU following injury. They found a 59% incidence of delirium overall, and higher if the patient was mechanically ventilated. On univariate analysis, age proved to be a predictor for the development of delirium. However, on multivariate analysis the strongest predictors for transitioning into delirium were lower arrival GCS, higher packed red blood cell transfusion, and higher multiple organ failure (MOF) score.61 Most recently, a two-center study examining the impact of delirium on outcomes was performed. A total of 134 patients were evaluated, of which 63% progressed to delirium during their ICU stay. The patients with delirium had more ventilator days and longer ICU and hospital LOS. These investigators were unable to show a relationship between increasing age and the development of delirium.62 The association of advanced age and delirium is strong; in fact, delirium and dementia are highly interrelated; however, the nature of this interrelationship remains poorly examined.58 The association of delirium with opiod narcotics and benzodiazepines is well established and care must be taken in prescribing these medications to all patients, but especially the elderly. The issue of appropriate and goal-directed analgesia and sedation is commonly faced by the ICU staff. Finally, delirium represents one of the most common preventable adverse events among older persons during hospitalization.63 As such, the development of delirium in a patient may reflect processes of care in the hospital and therefore a reflection of the quality of care of that individual. Those caring for elderly injured patients must be aware of the development, diagnosis, prevention, and, if needed, appropriate treatment of delirium in order to provide the highest quality of care to this population.

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looked at outcome in a cohort of elderly trauma patients.66 In this study, although the older group had a higher mortality rate, there were no differences in hospital or ICU LOS, or in ICU admission rate. In a study by Taylor et al., the elderly group had a lower ICU admission rate (36.7%) compared with younger trauma patients (45.5%). However, elderly patients, once admitted to the ICU, had a longer ICU LOS.52 The impact of withholding or withdrawal of care may influence ICU LOS. Plaisier et al. examined the practices of EOL care in a group of trauma patients. They divided their patients into elderly and younger groups that they cared for in their single institution. These investigators found there was no age bias in the elderly trauma patients admitted to the ICU.67

STRATEGIES FOR IMPROVING OUTCOMES ■ Triage There are numerous studies suggesting that elderly trauma patients are undertriaged to trauma centers despite the proven mortality benefit of trauma center care. Statewide data from Maryland demonstrated that fewer elderly trauma patients were transported to trauma centers despite meeting physiologic criteria for trauma triage.68 In a similar study evaluating the Washington State trauma registry, Lehmann et al. demonstrated that patients over the age of 65 years despite having ISS 15 were less likely to have the prehospital trauma system activated, the trauma team activated, and a full trauma team response.20 The group of undertriaged elderly patients had a significantly higher mortality, discharge disability rate, and complication rate when compared with a group of younger patients. Meldon et al. demonstrated a significant survival benefit for severely injured elderly patients when treated in a trauma center (56%) versus a nontrauma center (8%).69 It is not clear why older patients are undertriaged; however, this group is less likely to demonstrate hypotension and tachycardia that are commonly seen in younger patients.

■ Medications The increased awareness in medication reconciliation and its impact on patient safety is prominent in health care regulation. Medication-related problems are a significant health care problem. This is an important consideration in caring for the injured elderly patient. The acuteness of the hospital admission, and, at times, the initial underappreciation of significant anatomic injury, results in a potentially modifiable situation highlighting the importance of knowledge of a patient’s premorbid medications and the potential interaction of any newly prescribed medications. The Beers criteria are consensus criteria for safe medication use in elderly patients.70 Use of this system, along with expert input from geriatricians and pharmacists, may prove to reduce adverse drug reactions in older patients. There are a number of medications that deserve mention specifically relating to the trauma patient. β-Blockers are used in approximately 20% of elderly patients with coronary artery disease and 10% of patients with hypertension. The inherent physiologic blockade of the expectant response to hypovolemia may provide triage

and treatment obstacles. Additionally, the impact of prolonged β-blockade on the progression and outcome of trauma and burn injury is not fully understood. Anticoagulation, in the form of both warfarin and antiplatelet therapy, poses significant problems for the bleeding patient. Warfarin therapy is used in a variety of commonly seen medical conditions in the older individual. The therapy itself carries a 1% per year risk of spontaneous intracranial hemorrhage. Assessment of the therapeutic level is important as many patients will be subtherapeutic or supratherapeutic. Many studies assessing the impact of warfarin on trauma, and specifically head injury, are limited in that they do not address the clinical level of anticoagulation. To address this limitation, a study of 3,242 trauma patients over the age of 50 years was performed. In this retrospective analysis international normalization ratio (INR) data were used as a surrogate for warfarin anticoagulation. These investigators demonstrated a mortality rate of 22.6% in the group with an INR 1.5 compared with 8.2% for those with an INR 1.5. After adjusting for age and ISS the odds of death for each 1 U increase in INR were 30%.30 Patients with supratherapeutic anticoagulation fare even worse. In a study of 49 patients with severe TBI and an average INR of 6.5, the mortality rate was 87.8%.71 A more recent study comparing head and nonhead injury patients on anticoagulation with a matched control group showed no difference in mortality.72 A limitation in this study was that INR data were not included. Antiplatelet therapy is less well studied. This class of drugs includes aspirin (ASA) and clopidogrel, among others, is increasingly used for a wide variety of cardiovascular problems. In a registry review of patients over the age of 50 years sustaining TBI, patients taking ASA or clopidogrel were compared with those not receiving antiplatelet therapy. A statistically different mortality rate was observed for the two groups. The group receiving antiplatelet therapy had a mortality of 23% compared with 8.9% (P  .016) in the control group. Risk factors for death in this study included age 76 years and GCS 12.73 Rapid reversal of anticoagulation with FFP transfusion is beneficial. Reversal of an elevated INR to normal within 2 hours reduced mortality from 48% to 10%.74 The role for factor VIIa is not completely clear; however, it seems to be effective in reversing anticoagulation in patients receiving warfarin.75

■ Specialists The role for the geriatrician in the management of elderly trauma patients is logical. There are age-specific nuances in the care of these patients that make the geriatric specialist an invaluable member of the extended trauma team. Landefeld has shown that geriatric medical patients cared for in a special geriatric unit were less likely to require long-term care facilities than those cared for in standard medical wards.76 Fallon et al. had developed the idea of a “geriatric trauma team.”77 This involves the mandatory consultation from a group of interested and dedicated geriatricians. The consultants were able to address a variety of medical conditions in the study sites elderly trauma patients. These included pain management, rehabilitation, delirium, and advanced care planning, to name a few. Most notably, the group of patients seen in consultation had a lower mortality than a group of elderly trauma patients not

The Geriatric Patient

END OF LIFE The ICU is an environment in which EOL decisions are made on a regular basis. In fact, in the United States, 38% of all hospitalized patients who died spent at least 10 days in the ICU.79 Older patients, having an understanding of their own wishes regarding health care, frequently utilize advanced directives and health care proxies. Many times, patients are educated regarding these legal entities through interaction with an astute family physician or by way of a previous elective hospital admission. Understanding the logistics of these documents is mandatory when caring for trauma patients. Given the acute onset of trauma, patients’ inability to predict future injury requires trauma practitioners to rely on a written document that may have been written years prior or by interactions with a health care proxy. The health care proxy is an individual who is appointed by a competent adult, who in the event that the individual is no longer able to make health care decisions would “speak” on behalf of the patient. There is evidence that physicians frequently have differing opinions regarding clinical outcome compared with the health care proxy, as well as personal beliefs that can influence EOL decisions.79 Withholding and withdrawing life support is commonly practiced in ICUs. Common reasons for this are futility, patient suffering, and the anticipation of a poor quality of life. In order to investigate the potential bias of age in withholding or withdrawing support, Plaisier et al. studied practice in their ICU. Despite a small patient population, this single-institution study was unable to show a difference between young and old regarding these EOL decisions.67 Futility is a concept with distinct ethical definition. Unfortunately, the term is applied frequently in situations that are strongly influenced by local environment and culture. What may be viewed as futile by one physician may not be seen in the same way by another. As such, utilization of ethics consultation will be important. The perception of suffering of elderly trauma patients is a cause of emotional distress for the ICU staff.80 The ubiquitous use of analgesics and sedatives in the ICU is necessary, but the science is imprecise. Most surgical ICU patients who survive indicate that they would repeat the experience again if necessary.81 EOL decisions based on this argument are not indicated. Using the argument of a poor quality of life is commonly based on the perceptions, beliefs, and personal interpretation of quality of life of the health care providers. Care must be taken to not interject one’s own beliefs when

counseling families. When elderly ICU survivors were studied, most agreed that they have an acceptable quality of life and would undergo treatment again.82 Quality of life following ICU treatment in trauma is not widely available. Limiting care in the elderly trauma patient in whom likely survival is nil is a necessary and ethical aspect of care provided by trauma practitioners. Utilizing standard ethical concepts and precise diagnoses will help facilitate discussions with families. Palliative care consultations have been used successfully with trauma patients, which can improve family and staff satisfaction with EOL care.83

CONCLUSION The elderly population continues to grow at an exponential rate. Coupled with improved medical care and quality of life, the older individual is able to participate in a fulfilling and active lifestyle. As such, the elderly individual is at risk for injury. It is mandatory that trauma practitioners become familiar with the anatomic, physiologic, and philosophical needs of older people. Understanding these changes will allow appropriate delivery of high-quality trauma care to this population. Falls and motor vehicle collision remain the primary mechanisms for injury. Preexisting medical problems, including depression, place these individuals at high risk for poor outcomes. Similarly, depression and chronic medical problems make suicide a true health care problem in this vulnerable population. Early identification of the older patient with shock using nontraditional end points, coupled with an aggressive approach at resuscitation, monitoring, and treatment, will improve outcomes, ultimately returning the elderly patient to an acceptable quality of life.

REFERENCES 1. United States Census. Available at: http://www.census.gov/apsd/wepeople. 2. American College of Surgeons Committee on Trauma. National Trauma Data Bank. Available at: http://www.facs.org/trauma/ntdb. 3. CDC. Available at: http://www.cdc.gov/mmwr/preview/mmwrhtml/ 00001819.htm. 4. Frankenfeld D, Cooney RN, Smith JS, et al. Age-related differences in the metabolic response to injury. J Trauma. 2000;48:49–57. 5. Butcher SK, Killampalli V, Chahal H, et al. Effect of age on susceptibility to post-traumatic infection in the elderly. Biochem Soc Trans. 2003;31: 449–451. 6. Lewis MC, Abouelenin K, Paniagua M. Geriatric trauma: special considerations in the anesthetic management of the injured elderly patient. Anesth Clin. 2007;25:75–90. 7. Neideen T, Lam M, Brasel KJ. Preinjury beta blockers are associated with increased mortality in geriatric trauma patients. J Trauma. 2008;65: 1016–1020. 8. Martin JT, Alkhoury F, O’Connor JA, et al. “Normal” vital signs belie occult hypoperfusion in geriatric trauma patients. Am Surg. 2010;76:65–69. 9. Williams JM, Evans TC. Acute pulmonary disease in the aged. Clin Geriatr Med. 1993;9:527–545. 10. Janssens JP. Aging of the respiratory system: impact on pulmonary function tests and adaptation to exertion. Clin Chest Med. 2005;26:469–484. 11. Cardus J, Burgos F, Diaz O, et al. Increase in pulmonary ventilation– perfusion inequality with age in healthy individuals. Am J Respir Crit Care Med. 1997;156:648–653. 12. Muhlberg W, Platt D. Age dependent changes of the kidneys: pharmacological implication. Gerontology. 1999;45:243–253. 13. Buemi M, Nostro L, Aloisi C, et al. Kidney aging: from phenotype to genetics. Rejuvenation Res. 2005;8:101–109.

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seen by a geriatrician. There seem to be age-specific interventions that may improve outcome in this population. One of the first attempts to address this was work from Kings County trauma service. In this study, the authors were able to demonstrate an outcome benefit from early invasive monitoring and intervention.55 Recently, a study by Nathens et al. investigated the impact of an intensivist-model ICU on trauma-related mortality.78 In this large multicenter study, the authors concluded that an intensivist-model ICU when compared with an open-model ICU significantly reduced mortality. Furthermore, the greatest risk reduction was seen in the elderly population (RR, 0.55 [0.39–0.77]).

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14. Mandavia D, Newton K. Geriatric trauma. Emerg Med Clin North Am. 1998;16:257–263. 15. Lowery DW, Wald MM, Browne BJ, et al. Epidemiology of cervical spine injury victims. Ann Emerg Med. 2001;38:12–16. 16. Grossman MD, Miller D, Scaff DW, et al. When is an elder old? Effect of preexisting conditions on mortality in geriatric trauma. J Trauma. 2002;52:242–246. 17. Morris JA, MacKenzie EJ, Damiano AM, et al. Mortality in trauma patients: the interaction between host factors and severity. J Trauma. 1990;30:1476–1482. 18. Morris JA, MacKenzie EJ, Edelstein SL. The effect of preexisting conditions on mortality in trauma patients. JAMA. 1990;263:1942–1946. 19. Demetriades A, Sava J, Alo K, et al. Old age as a criterion for trauma team activation. J Trauma. 2001;51:754–757. 20. Lehmann R, Beekley A, Casey L, et al. The impact of advanced age on trauma triage decisions and outcomes: a statewide analysis. Am J Surg 2009;197:571–575. 21. Caterino JM, Valasek T, Werman HA. Identification of an age cutoff for increased mortality in patients with elderly trauma. Acad Emerg Med. 2010;28:151–158. 22. Jacobs DG. Special considerations in geriatric injury. Curr Opin Crit Care. 2003;9:535–539. 23. American College of Surgeons Committee on Trauma. Advanced Trauma Life Support Student Manual. Chicago, IL: American College of Surgeons Committee on Trauma. 2009. 24. Bergeron E, Rossignol M, Osler T, et al. Improving the TRISS methodology by restructuring age categories and adding comorbidities. J Trauma. 2004;56:760–767. 25. Milzman DP, Rothenhaus TC. Resuscitation of the geriatric patient. Emerg Med Clin North Am. 1996;14:233–244. 26. Callaway DW, Shapiro NI, Donnino MW, et al. Serum lactate and base deficit as predictors of mortality in normotensive elderly blunt trauma patients. J Trauma. 2009;66:1040–1044. 27. Zehtabchi S, Baron BJ. Utility of base deficit for identifying major injury in elder trauma patients. Acad Emerg Med. 2007;14:829–831. 28. Schulman AM, Claridge JA, Young JS. Young versus old: factors affecting mortality after blunt traumatic injury. Am Surg. 2002;68: 942–948. 29. Thompson H, McCormick WC, Kagan SH. Traumatic brain injury in older adults: epidemiology, outcomes, and future implications. J Am Geriatr Soc. 2006;54:1590–1595. 30. Williams TM, Sadjadi J, Harken AH, et al. The necessity to assess anticoagulation status in elderly injured patients. J Trauma. 2008;65: 772–777. 31. Healthcare Cost and Utilization Project. Available at: http://hcupnet. ahrq.gov. 32. Susman M, DiRusso SM, Sullivan T, et al. Traumatic brain injury in the elderly: increased mortality and worse functional outcome at discharge despite lower injury severity. J Trauma. 2002;53:219–224. 33. Harris C, DiRusso S, Sullivan, et al. Mortality risk after head injury increases at 30 years. J Am Coll Surg. 2003;197:711–716. 34. Mack LR, Chan SB, Silva JC, et al. The use of head computed tomography in elderly patients sustaining minor head trauma. J Emerg Med. 2003;24:157–162. 35. Mosenthal AC, Livingston DH, Lavery RF, et al. The effect of age on functional outcome in mild traumatic brain injury: 6-month report of a prospective multicenter study. J Trauma. 2004;56:1042–1048. 36. Bulger EM, Arneson MA, Mock CN, et al. Rib fractures in the elderly. J Trauma. 2000;48:1040–1047. 37. Simon BJ, Cushman J, Barraco R, et al. Pain management in blunt thoracic trauma. J Trauma. 2005;59:1256–1267. Available at: http:// www.east.org/tpg. 38. Flagel BT, Luchette FA, Reed L, et al. Half-a-dozen ribs: the breakpoint for mortality. Surgery. 2005;138:717–725. 39. Harrington DT, Phillips B, Machan J, et al. Factors associated with survival following blunt chest trauma in older patients. Arch Surg. 2010;145:432–437. 40. Albrecht RM, Schermer CR, Morris A. Nonoperative management of blunt splenic injuries: factors influencing success in age 55 years. Am Surg. 2002;68:227–231. 41. Harbrecht BG, Peitzman AB, Rivera L, et al. Contribution of age and gender to outcome of blunt splenic injury in adults: multicenter study of the Eastern Association for the Surgery of Trauma. J Trauma. 2001;51: 887–895. 42. Henry SM, Pollack AN, Jones AL, et al. Pelvic fracture in geriatric patients: a distinct clinical entity. J Trauma. 2002;53:15–20.

43. Zuckerman JD, Sakales SR, Fabian DR, et al. Hip fractures in geriatric patients. Results of an interdisciplinary hospital care program. Clin Orthop Relat Res. 1992;27:213–225. 44. Wibbenmeyer LA, Amelon MJ, Morgan LJ, et al. Predicting survival in an elderly burn patient population. Burns. 2001;27:583–590. 45. Lionelli GT, Pickus EJ, Beckum OK, et al. A three decade analysis of factors affecting burn mortality in the elderly. Burns. 2005;31: 958–963. 46. Ho WS, Ying SY, Chan HH. A study of burn injuries in the elderly in a regional burn centre. Burns. 2001;27:382–385. 47. Deitch E. A policy of early wound excision and grafting in elderly burn patients shortens hospital stay and improves survival. Burns. 1985;12: 109–114. 48. Chang EJ, Edelman LS, Morris SE, et al. Gender influences on burn outcome in the elderly. Burns. 2005;31:31–35. 49. Champion HR, Copes WS, Sacco WJ, et al. The major trauma outcomes study: establishing national norms for trauma care. J Trauma. 1990;30:1356–1365. 50. Finelli FC, Jonsson J, Champion HR, et al. A case control study for major trauma in geriatric patients. J Trauma. 1989;29:541–548. 51. Roth BJ, Velmahos GC, Oder DB, et al. Penetrating trauma in patients older than 55 years: a case–control study. Injury. 2001;32:551–554. 52. Taylor MD, Tracy JK, Meyer W, et al. Trauma in the elderly: intensive care unit resource use and outcome. J Trauma. 2002;53:407–414. 53. DeMaria EJ, Kenney PR, Merriam MA, et al. Aggressive trauma care benefits the elderly. J Trauma. 1987;27:1200–1206. 54. Bochicchio GV, Joshi M, Knorr KM, et al. Impact of nosocomial infections in trauma: does age make a difference? J Trauma. 2001;50:612–617. 55. Scalea TM, Simon HM, Duncan AO, et al. Geriatric blunt multiple trauma: improved survival with early invasive monitoring. J Trauma. 1990;30:129–134. 56. Brown CVR, Shoemaker WC, Wo CCJ, et al. Is noninvasive hemodynamic monitoring appropriate for the elderly critically injured patient? J Trauma. 2005;58:102–107. 57. Eachempati SR, Hydo LJ, Shou J, et al. Outcomes of acute respiratory distress syndrome (ARDS) in elderly patients. J Trauma. 2007;63: 344–350. 58. Inouye SK. Delirium in older persons. N Engl J Med. 2006;354: 1157–1165. 59. Ely EW, Shintani A, Truman B, et al. Delirium as a predictor of mortality in mechanically ventilated patients in the intensive care unit. JAMA. 2004;291:1753–1762. 60. Pandharipande P, Cotton BA, Shintani A, et al. Prevalence and risk factors for development of delirium in surgical and trauma intensive care unit patients. J Trauma. 2008;65:34–41. 61. Angles EM, Robinson TN, Biffl WL, et al. Risk factors for delirium after major trauma. Am J Surg. 2008;196:864–870. 62. Lat I, McMillian W, Taylor S, et al. The impact of delirium on clinical outcomes in mechanically ventilated surgical and trauma patients. Crit Care Med. 2009;37:1898–1905. 63. Rothschild JM, Bates DW, Leape LL. Preventable medical injuries in older patients. Arch Int Med. 2000;160:2717–2728. 64. Richmond TS, Kauder D, Strumpf N, et al. Characteristics and outcomes of serious traumatic injury in older adults. J Am Geriatr Soc. 2002;50: 215–222. 65. Aitken LM, Burmeister E, Lang J, et al. Characteristics and outcomes of injured older adults after hospital admission. J Am Geriatr Soc. 2010; 60:1–8. 66. Young JS, Cephas GA, Blow O. Outcome and cost of trauma among the elderly: a real-life model of a single-payer reimbursement system. J Trauma. 1998;45:800–804. 67. Plaisier BR, Blostein PA, Hurt KJ, et al. Withholding/withdrawal of life support in trauma patients: is there an age bias? Am Surg. 2002;68: 159–162. 68. Ma MH, MacKenzie EJ, Alcorta R, et al. Compliance with prehospital triage protocols for major trauma patients. J Trauma. 1999;46:168–175. 69. Meldon SW, Reilly M, Drew BL, et al. Trauma in the very elderly: a community based study of outcomes at trauma and non-trauma centers. J Trauma. 2002;52:79–84. 70. Fick DM, Cooper JW, Wade WE, et al. Updating the Beers criteria for potentially inappropriate medication use in older adults. Arch Int Med. 2003;163:2716–2724. 71. Cohen DB, Rinker C, Wilberger JE. Traumatic brain injury in anticoagulated patients. J Trauma. 2006;60:533–537. 72. Wojcik R, Cipolle MD, Seislove E, et al. Preinjury warfarin does not impact outcome in trauma patients. J Trauma. 2001;51:1147–1151.

The Geriatric Patient 79. The SUPPORT Principal Investigators. A controlled trial to improve care for seriously ill hospitalized patients. The study to understand prognoses and preferences for outcomes and risk of treatments (SUPPORT). JAMA. 1995;274:1591–1598. 80. Levy MM. Caring for the caregiver. Crit Care Clin. 2004;20:541–547. 81. Fakhry SM, Kercher KW, Rutledge R. Survival, quality of life, and charges in critically ill surgical patients requiring prolonged ICU stays. J Trauma. 1996;41:999–1007. 82. Stricker KH, Cavegn R, Takala J, et al. Does ICU length of stay influence quality of life? Acta Anaesthesiol Scand. 2005;49:975–983. 83. Mosenthal AC, Murphy PA, Barker LK, et al. Changing the culture around end-of-life care in the trauma intensive care unit. J Trauma. 2008;64:1587–1593.

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73. Ohm C, Mina A, Howells G, et al. Effects of antiplatelet agents on outcomes for elderly patents with traumatic intracranial hemorrhage. J Trauma. 2005;58:518–522. 74. Ivascu FA, Howells GA, Junn FS, et al. Rapid warfarin reversal in anticoagulated patients with traumatic intracranial hemorrhage reduces hemorrhage progression and mortality. J Trauma. 2005;59:1131–1137. 75. Dutton RP, McCunn M, Hyder M, et al. Factor VIIa for correction of traumatic coagulopathy. J Trauma. 2004;57:709–718. 76. Landefeld CS. Improving health care for older persons. Ann Int Med. 2003;139:421–424. 77. Fallon WF, Rader E, Zyzanski S, et al. Geriatric outcomes are improved by a geriatric trauma consultation service. J Trauma. 2006;61:1040–1046. 78. Nathens AB, Rivara FP, MacKenzie EJ, et al. The impact of an intensivist-model ICU on trauma-related mortality. Ann Surg. 2006;244: 545–554.

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CHAPTER 45

Ethics of Acute Care Surgery Laurence B. McCullough

INTRODUCTION Trauma care is undertaken in order to save the lives and protect the health of patients who have experienced injuries. The ethical obligation to provide trauma care, however, is not unlimited. Sometimes it becomes ethically justified to set limits on the medical or surgical management of trauma, especially on the basis of clinical judgments of futility. In general terms, futility means that a clinical intervention is reliably expected not to have its usually intended outcome. The clinical applicability of this general notion of futility requires that the outcome be clearly specified. Otherwise, clinical discourse among physicians or with patients and their families is at high risk of gridlock from unnecessary confusion about what is meant by saying that an intervention is “futile.” Ethical challenges involved in setting limits on clinical management of patients’ diagnoses have been recognized in medical ethics since ancient times. In The Art, for example, the Hippocratic writers define medicine to include refusing to “treat those who are overmastered by their diseases, realizing that in such cases medicine is powerless.”1 More recently, the issue of setting limits has arisen in the context of critical care and how physicians should respond to requests for inappropriate continuation of life-sustaining interventions such as mechanical ventilation, provision of fluids and nutrition, and pharmacologic support of cardiac function. Issues concerning setting limits now arise routinely in the postoperative setting, and futility is sometimes invoked as a justification for setting limits.2 The purpose of this chapter is to identify four major concepts of futility that have been developed in the bioethical and medical literature and to incorporate these concepts with definitions of terminal and irreversible conditions into an algorithm that can be used to set ethically justified limits on the medical and surgical management of trauma patients.

FOUR CONCEPTS OF FUTILITY The first three concepts of futility appeal to the ethical principle of beneficence as the basis for the requisite specification. This ethical principle obligates the physician and other healthcare professional to seek the greater balance of clinical goods over clinical harms to the patient. The key component of beneficence for clinical judgments of futility is that for an intervention to be reasonable to offer and perform in patient care, it must hold out the prospect of at least a modicum of potential clinical benefit.3 Tomlinson and Brody introduced the first beneficencebased concept of futility, physiologic or strict futility.4 An intervention is judged to be futile in this first sense when it is reliably expected not to produce its usually intended physiologic outcome. For example, cardiopulmonary resuscitation that continues for such a prolonged period of time that restoration of spontaneous circulation is no longer reasonably expected is properly judged physiologically futile, because there is at this point no reliable expectation, based on outcomes data, to support a clinical judgment that the outcome of resuscitation can be achieved. Brody and Halevy introduced the second beneficence-based concept of futility, imminent demise futility.5 An intervention is judged to be futile in this third sense when it is reliably expected that the patient will die before discharge and not recover consciousness beforehand. For example, two large case series have shown that for patients who arrested in the field but were not successfully resuscitated upon arrival in the emergency department (ED) all were dead at discharge and with rare exceptions never recovered consciousness.6,7 Schneiderman et al. introduced the third beneficence-based concept of futility clinical or overall futility.8 An intervention is judged to be futile in this second sense when it is reliably expected not to result in maintenance of any ability by the patient to interact with the environment and continue to develop as a human

Ethics of Acute Care Surgery

AN ALGORITHM FOR MAKING CLINICAL JUDGMENTS OF FUTILITY TO SET LIMITS ON TRAUMA CARE It is well understood in the ethics of the informed consent process that the physician is obligated to offer information to the patient (or the patient’s surrogate) information about the medically reasonable alternatives for managing the patient’s condition. “Medically reasonable” means that the intervention meets the “modicum of benefit” test of beneficence-based clinical judgment: there is a reasonable expectation of net clinical benefit.3 Not all intervention that is technically possible in the trauma care setting is medically reasonable. Clinical judgments of futility mean that the intervention in question, including life-sustaining interventions in medical and surgical intensive care units, do not meet this test. Futile interventions are not medically reasonable. The physician should therefore recommend against their use and be prepared to meet requests for them with sensitive, but firm resistance. The proposed algorithm for clinical judgments of futility links the above four concepts of futility to the informed consent process, so that the physician stays in control of this process, which is among his or her fundamental ethical and professional responsibilities.12,13 The proposed algorithm emphasizes a preventive ethics approach to setting limits. Preventive ethics develops and uses

policies and decision-making tools to anticipate and prevent ethical conflicts. A preventive ethics approach to setting limits is better than a reactive approach to ethical conflict, because a preventive ethics approach should reduce the biopsychosocial toll of decision making at the end of life on patients, their family members, healthcare professionals, and the culture of healthcare organizations. Futile interventions are not expected to result in acceptable outcomes. “Acceptable outcome” can be defined from a clinical perspective or from the patient’s perspective. From the clinical perspective an acceptable outcome is one that prevents imminent death, accomplishes its usually expected physiologic outcome, preserves at least some functional status and therefore interactive capacity, and prevents unnecessary pain, distress, and suffering, both disease-related and iatrogenic. Pain, distress, and suffering are unnecessary when they are not required as disease/injury-related or iatrogenic cost of achieving above goals and when they cannot be managed to an acceptable level. From the patient’s perspective an acceptable outcome is one that preserves an acceptable quality of life. As explained above, quality of life mean engaging in life tasks and deriving satisfaction from doing so. The clinical component of the patient’s quality-of-life assessment is whether the resulting functional status from an intervention is expected to support the patient engaging in valued life tasks and deriving sufficient satisfaction from doing so. This is a judgment that only the patient can make for herself or, by a surrogate decision maker, or on basis of reliable account of patient’s valued life tasks and whether predicted functional status supports those life tasks. Physicians should be very wary indeed about making quality-of-life judgments about their patients. This is because of the risk of erroneous external evaluation of patient’s quality of life by health care professionals, whose quality-of-life assessment tends to be lower than patients’ self-assessments.11 It is crucial to recognize that resuscitation is often the initial step of the subsequent critical care management of the trauma patient. Critical care intervention is now understood to be trial of management. There is an ethical obligation, as a matter of professional integrity, to initiate or continue a trial of intervention ends when there is no reasonable expectation of achieving the intervention’s goals. Critical care intervention has two goals. The short-term goal is the prevention of imminent death and the long-term goal is survival with an acceptable outcome, defined from either a clinical or the patient’s perspective as appropriate. The first step of the algorithm (Fig. 45-1) invokes applicable advance directives/end-of-life legislation. The alternative of discontinuing life-sustaining treatment becomes medically reasonable and should be offered, with an explanation that the use of critical care interventions is not the standard of care for such patients. The second step of the algorithm invokes physiologic futility. In addressing this question the physician should specify the outcome precisely. For example, the outcome of resuscitation is the restoration of spontaneous circulation. The outcome of mechanical ventilation is maintenance of adequate levels of oxygenation. It is important to distinguish clearly specified physiologic outcome from physiologic effect (e.g., transient heart beat during resuscitation).

CHAPTER 45

being. For example, a patient diagnosed to be a permanent vegetative state according to accepted criteria or who has suffered severe and extensive head trauma resulting in neurologic devastation has irreversibly lost the capacity to interact with the environment and continue to develop.9 Although interventions such as provision of nutrition and fluids continue to be physiologically effective, these interventions do not alter the outcome: irreversible loss of the capacity to interact with the environment. The fourth concept of futility appeals to the ethical principle of respect for autonomy. This ethical principle obligates the physician to seek the greater balance of goods over harms to the patient as those goods and harms are defined from the patient’s perspective, which can range far beyond the relatively narrow scope of clinical goods and harms. Tomlinson and Brody introduced the fourth concept of futility, quality-of-life futility.10 An intervention is judged to be futile in this fourth sense when it is reliably expected that the patient’s quality of life (engaging in life tasks and gaining satisfaction from doing so) will be unacceptable to the patient. This can occur when it is reliably expected that the patient will not be able to either engage in valued life tasks or derive sufficient satisfaction from doing so. The patient retains the ability to interact with the environment and develop, but judges the outcomes of doing so to be unacceptable. This concept does not appeal to an observer’s rating of the patient’s quality of life, because such external evaluation of quality of life is unreliable.11 Using this concept of futility requires the reliable identification of the patient’s preferred life activities and expectations of satisfaction from them. Obviously, the person in the best position to make such a judgment for the patient is the patient himself or herself, with surrogates who know the patient well making such judgments for patients no longer able to do so for themselves.

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SECTION 4 FIGURE 45-1 Decision-making algorithm.

Ethics of Acute Care Surgery outcomes with the patient’s preferred quality of life is not the standard of care for such patients. If the answer to this question is no, the physician should prospectively manage uncertainty of by being alert to a developing prognosis or trend toward of one or more of these three concepts of futility. There should be open and complete discussion between ED physician and his or her critical care colleagues in the hospital concerning admission plans for patients for whom the ED physicians reliably thinks that there are such trends toward futility. The ED physician and hospital colleagues should work together to prepare surrogate decision makers for subsequent decisions about setting limits on critical care intervention should any one of the above questions in the proposed algorithm be answered affirmatively.

CONCLUSION Ethics is an essential component of the surgical and medical management of the trauma patient. The physician’s and team’s obligation is to undertake clinical intervention that is reliably expected to prevent the trauma patient’s imminent death and achieve an acceptable outcome of subsequent critical care intervention. This is obligation comes with ethically justified limits, based on advance directive legislation and four concepts of futility. These limits can be addressed in a systematic fashion by using a decision-making algorithm to make responsible decisions and recommendations in the care of the trauma patient.

REFERENCES 1. Hippocrates. The art. In: Reiser SJ, Dyck AJ, Curran WJ, eds. Ethics in Medicine: Historical Perspectives and Contemporary Concerns. Cambridge, MA: MIT Press; 1977:6. 2. Halevy A, Baldwin JC. Poor surgical risk patients. In: McCullough LB, Jones JW, Brody BA, eds. Surgical Ethics. New York: Oxford University Press; 1998:152–170. 3. Brett A, McCullough LB. When patients request specific interventions: defining the limits of the physician’s obligations. N Engl J Med. 1986;315:1347–1351. 4. Tomlinson T, Brody H. Ethics and communication in do-not-resuscitate orders. N Engl J Med. 1988;318:43–46. 5. Brody BA, Halevy A. Is futility a futile concept. J Med Philos. 1995; 25:28–36. 6. Gray WA, Capone RJ, Most AS. Unsuccessful emergency medical resuscitation: are continued efforts in the emergency department justified? N Engl J Med. 1991;325:1393–1398. 7. Sirbaugh PE, Pepe PE, Shook JE, et al. A prospective, population-based study of the demographics, epidemiology, management, and outcome of out-of-hospital pediatric cardiopulmonary arrest. Ann Emerg Med. 1991;33:174–184. 8. Schneiderman LJ, Jecker NS, Jonsen AR. Medical futility: its meaning and ethical implications. Ann Intern Med. 1990;112:949–954. 9. American Academy of Neurology, Quality Standards Subcommittee. Practice parameter: assessment and management of patients in the persistent vegetative state. In: Brody BA, Rothstein MA, McCullough LB, Bobinski MA, eds. Medical Ethics: Codes, Opinions, and Statements. Washington, DC: Bureau of National Affairs; 2000:393–397. 10. Tomlinson T, Brody H. Futility and the ethics of resuscitation. JAMA. 1990;264:1276–1280. 11. Leplège A, Hunt S. The problem of quality of life in medicine. JAMA. 1997;278:47–50. 12. Rabeneck L, McCullough LB, Wray NP. Ethically justified, clinically comprehensive guidelines for percutaneous endoscopic gastrostomy tube placement. The Lancet. 1997;349:496–498. 13. McCullough LB, Jones JW. Postoperative futility: a clinical algorithm for setting limits. Br J Surg. 2001;88:1153–1154.

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If the answer to this second question is yes, then the ethical obligation to continue intervention has ended because of physiologic futility. An evidence-based judgment of physiologic futility of a critical care intervention means that imminent death cannot be prevented. There is therefore no reasonable expectation that the short-term goal and, therefore, the longterm goal of continued critical care intervention can be achieved. The alternative of discontinuing life-sustaining treatment becomes medically reasonable and should be offered, with an explanation that the use of critical care interventions that are not expected to produce their intended functional outcome is not the standard of care for such patients. If the answer to this second question is no, then the critical care intervention should be continued while the third question is addressed, which invokes imminent demise futility. If the evidence-based answer is yes, the ethical obligation to continue intervention has ended, because of imminent demise futility. There is no reasonable expectation that the short-term goal and, therefore, the long-term goal of continued critical care intervention can be achieved. The alternative of discontinuing life-sustaining treatment becomes medically reasonable and should be offered, with an explanation that the use of critical care interventions that are not expected to prevent death for patients who are not expected to recover consciousness before they die is not the standard of care for such patients. If the answer to the third question is no, then critical care intervention should be continued while the fourth question is addressed, which invokes clinical or overall futility. If the answer to this question is yes, the ethical obligation to continue intervention has ended, because of clinical or overall futility. The justification is more complex than in the first two questions. There is a reasonable expectation that the short-term goal can be achieved but there is no reasonable expectation that the long-term goal of critical care intervention can be achieved because of unacceptable outcome from a clinical perspective. The alternative of discontinuing life-sustaining treatment becomes medically reasonable and should be offered, with an explanation that the use of critical care interventions for patients who are not expected ever to recover consciousness and interactive capacity is not the standard of care for such patients. If necessary, the distinction between the short-term goal of critical care, which can be achieved, and the long-term goal of critical care, which is not expected to be achieved, should be explained. If the answer to this fourth question is no, critical care intervention should be continued and the fifth question addressed. If the answer is yes, the ethical obligation to continue intervention has ended, because of quality-of-life futility. The justification becomes slight more complex. There is a reasonable expectation that the short-term goal can be achieved. However, there is no reasonable expectation that the long-term goal of critical care intervention can be achieved because of unacceptable outcome from patient’s perspective (even though outcome is acceptable from a clinical perspective). The alternative of discontinuing life-sustaining treatment becomes medically reasonable and should be offered, with an explanation that the use of critical care interventions that are not consistent in their

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Social Violence James W. Davis

Trauma care is, by definition, tertiary prevention or treatment. Understanding the root causes of the injury may aid in better comprehension and treatment of the trauma victim. Improvements in trauma care should incorporate consideration of the psychosocial aspects of such injuries as well as the needs of an impact on the larger health care system. Patients who are victims of family and community violence may have relatively simple traumatic injuries but often have complex psychosocial issues that affect their response to injury. Simply treating the injuries and not intervening with the underlying causes makes recidivism of these patients the likely end result. Early detection and efforts at prevention of interpersonal violence must be part of the trauma center’s prevention program. Violence may be defined as “the intentional use of physical force against another person or against oneself, which results in or has a high likelihood of resulting in injury or death.”1 Its frequency is documented in the following facts. Homicides and suicides are the second and third leading causes of death among children and youth under the age of 21.2 Domestic violence is the most common cause of injury to women in the United States.3 One person dies every 4 minutes as a result of intentional injury.4 The literature is replete with studies identifying the scientifically proven risk factors for interpersonal violence.2,5–7 Despite this potential knowledge base, physicians are often hesitant to utilize this information.8–10 Early recognition and intervention may prevent future incidents and decrease rates of complications such as posttraumatic stress disorder.2,10–12 The statistics on death and injury from intentional violence are only the tip of the iceberg. The cost to society of violent behavior also includes the price of legal battles, incarceration, and the economic effects on the health care system as a whole, as well as the psychological stress to victims and the families of victims.3,4 The purpose of this chapter is to provide the practicing surgeon with some basic information on intentional violence with a focus on intimate partner and community violence, so

that he or she may be a better provider of care for these patients with special needs.

DOMESTIC VIOLENCE Domestic violence refers to those acts of interpersonal violence resulting in physical or psychological injury to members of the same family or household or to intimate acquaintances in heterosexual or homosexual. Another definition of domestic violence goes further, including “a pattern of coercive control consisting of physical, sexual, and/or psychological assault against former or current intimate partners.”13 Other reports have acknowledged that child14,15 and elder abuse may also be included in the spectrum of “domestic violence.”16 Intimate partner violence (IPV) and elder abuse will be covered here, child abuse will be addressed in the chapter on pediatric trauma. Domestic violence is not new, it has long plagued mankind. A 15th-century scholar argued that a man should beat his wife, “not in rage but out of charity and concern for her soul.”17 English Common Law established “the Rule of Thumb” in 1895, stating that a husband could not beat his wife with a switch greater in diameter than the width of his thumb.18 The legal right of men to beat their wives was not abolished until 1871 in the United States.19 Until the 1970s, assaults on wives were considered misdemeanors, when an equal assault against a stranger would have been considered a felony.20 In 1992, it became a requirement of the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) that all accredited hospitals have policies and procedures in their emergency departments and ambulatory care facilities for identifying, treating, and referring victims of abuse.20

■ Incidence and Prevalence The actual incidence of intimate partner and/or domestic violence is not known. In 1985, C. Everett Koop, as U.S. Surgeon

Social Violence

• The cumulative lifetime prevalence to domestic violence of women seen in the emergency department was 54–60%24,27 • 1 out of 3 women around the world has been beaten, coerced into sex, or otherwise abused during her lifetime28 • 12–25% of visits by women to the emergency department were from domestic violence27 • Physical abuse occurs in 7–20% of pregnancies29 • Women are 3.6 times more likely to be shot by a spouse or ex – significant other than by a stranger30 • 4 women are murdered everyday by husbands or boyfriends. Additionally, marital violence is a significant predictor of physical child abuse. In one study, the probability of child battering increased from 5% with one act of marital violence to near certainty with 50 or more acts of wife battering.31 Child battering occurs in 59% of the homes with spousal abuse and may be as high as 77% with severe wife abuse.32,33 The victim is frequently demoralized, and is so lacking in self-esteem that it is difficult to leave the situation.34 Additionally, the threats of retaliation, injury to children or pets and death increase the victim’s fears and helplessness. Indeed, the risk of physical violence actually increases after moving out.35

■ Diagnosing Domestic Violence A three-phase cycle has been described for battering, the first with a gradual build up of tension, then escalation with name calling, intimidation, and mild physical abuse. The second phase has an uncontrollable discharge, with verbal and physical attack and frequently injury. In the third phase, the abuser apologizes and asks for forgiveness and promises that it will not recur. With repeated cycles, the first phase increases in length,

the violence may become more acute and the third phase decreases. The victim is frequently demoralized, and is so lacking in self-esteem that it is difficult to leave the situation.34 The second cycle for victims of domestic violence involves the failure to make the diagnosis even after the patient arrives in the emergency department. In a study of battered women presenting to the emergency department, 23% had presented 6 to 10 times previously and 20% had 11 prior emergency department visits.36 In 40% of cases with known domestic violence, physicians made no response at all and in 92% of cases, physicians made no referral for the abuse.37 Victims of domestic violence view physicians as least effective in helping them compared to women’s shelters, social services, clergy, police, and lawyers.37 There are some characteristics of injury type and location in domestic violence. Injuries tend to be central; face, head, neck, breast, and abdomen versus more peripheral injuries in accidents. In one study of injury locations, the head, face, neck, thorax, and abdomen significantly more injured than accident victims (P  0.001).38 Because victims of IPV may be fearful or ashamed, nontrauma complaints predominate as reasons for physician visit. Even after violent episode, only 23% had injury related complaints. Domestic violence victims rarely volunteer information; only 13% after battering either told staff or were asked about the possibility of abuse.39 However, domestic violence victims were not offended when asked about abuse in a nonjudgmental manner.40 Further, the failure of health care providers to ask about domestic violence may be perceived as evidence of a lack of concern and add to feelings of entrapment and helplessness.41 The use of a specific screening tool for domestic violence has been shown to be more effective than routine social services evaluation.40 One such tool, the Partner Violence Screen,42 consists of three questions, takes about 20 seconds to perform and can identify up to 65–70% of the victims of domestic violence (Fig. 46-1). Although some data suggest battered women prefer nonface-to-face screening,36,43 directly asking about

Domestic violence:

Partner violence screen 1. Have you ever been kicked, hit, punched or other-wise been hurt by someone within the last year? If so, by whom? 2. Do you feel safe in your current relationship? 3. Is there a partner from a previous relationship that is making you feel unsafe now?

FIGURE 46-1 Partner violence screen. (Reprinted with permission from Feldhaus KM, Koziol-McLain J, Amsbury HL, et al. Accuracy of three brief screening questions for detecting partner violence in the emergency department. JAMA. 1997;277:1357–1361. Copyrighted 1997, American Medical Association. All rights reserved.)

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General, estimated that over 6 million women a year are beaten or physically abused by boyfriends or husbands in the United States, with an act of domestic violence occurring every 18 seconds. He also noted that battery and assault against women occurred more frequently than rape, mugging, and motor vehicle accidents combined.21 Both men and women can be victims of IPV, studies suggest that 30–85% of victims are women.22,23 Estimates of the incidence vary widely; the U.S. Department of Justice crime data brief on IPV reported almost 700,000 “nonfatal, violent victimizations” in 2001, and highlighted a nearly 50% decline in IPV against females since 1993.23 However, at the same time a report from the National Institute of Justice and the Centers for Disease Control and Prevention (CDC) estimated that 1.5 million women are physically assaulted or raped by an intimate partner in the United States annually.24 The American Psychological Association Presidential Task Force on Violence and the Family put the number still higher, stating that 4 million women experience a serious assault by a partner during an average 12-month period.25 The National Violence Against Women Survey, done by the National Institute of Justice and the CDC in 2003, estimated 5.3 million IPV incidents against women annually, with more than 550,000 requiring medical attention, loss of 8 million days of paid work, and 5.6 million days of household productivity as a result of the violence.26

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abuse has been shown to yield more positive results than written questionnaires.44 Screening for IPV should be approached in a quiet environment, separate from the partner, with a nonjudgmental opening such as “because we see a lot of patients coping with abusive relationships, we now ask about domestic violence routinely.” Although there is not good data about the effectiveness of screening or even intervention for domestic violence, numerous organizations (American College of Physicians, American College of Obstetrics and Gynecology, American Medical Association, Eastern Association for Trauma and the Western Trauma Association) recommend screening for domestic violence.

■ Treatment and Referral, Documentation, and Reporting Once the diagnosis of domestic violence has been made, the responsibilities are to treat the patient, reassure them about safety, and make the appropriate referral to social services. It is important to carefully document the injuries in the medical record. Regardless of the legal requirement to report domestic violence, failure to do so may have lethal consequences. In several studies of women murdered by their spouses or boyfriends, the majority had accessed the health care system within a year or two of their deaths, most for injury and even when the diagnosis was made, there was no referral for the abuse.45,46

■ Summary on Domestic Violence Domestic violence is common and commonly undiagnosed. As recommended in the landmark position paper by the Eastern Association for the Surgery of Trauma (1999),16 all female trauma patients be screened for domestic violence. The use of a specific screening tool is strongly recommended. Trauma centers and trauma surgeons should have ongoing education about domestic violence to improve the recognition and management of this epidemic problem.

■ Diagnosis Some of the findings are similar to other forms of abuse: skin injury and tears, and bruising. Fractures in the elderly are unfortunately common, but fractures in places besides the hip, vertebrae or wrists, or spiral fractures may be suspicious of abuse. Malnutrition and dehydration may be a sign of neglect in a dependent elder.52 As with IPV, there are a number of screening tools that may be used for assessment of elder neglect and/or abuse. A simple three-question screen has been advocated53: Do you feel safe where you live? Who prepares your meals? Who handles your checkbook? The responses might lead to further questions and additional information may need to be obtained both from others who are not under suspicion and from physical findings.

■ Treatment and Referral When elder abuse is suspected, as in IPV, medical treatment comes first. If there is reason to believe that an elder is suffering from abuse, neglect, or exploitation referral for possible elder abuse should occur. Reporting elder abuse is required in most states. Documentation of injuries on the medical record should be meticulous.

Summary Elder abuse is less common than IPV (2–10%) but is associated with significant morbidity and mortality. Seniors with risk factors should undergo brief screening questions as listed above. If elder abuse or mistreatment is suspected based on answers to the screening questions or physical findings, further assessment is indicated. If there is reason to believe that there is abuse or neglect, reporting and careful documentation are essential.

ELDER ABUSE Elder abuse includes physical, sexual, and psychological or emotional abuse as well as neglect or abandonment. Self-neglect is most common and the prevalence of elder abuse in the community is estimated to range from 2 to 10%.47 A World Health Organization review of studies from the United States, Canada, Great Britain, and Finland found combined rates of elder abuse of 4–6%.48 The estimates on institutional mistreatment are limited, but from 1999 to 2001, fully one third of nursing homes in the United States were cited for abuse violations.49 There is a significant association between elder abuse and risk of morbidity and mortality. One prospective cohort study found a 3-fold increase in mortality for persons ages 65 and older that were referred to Adult Protective Services for mistreatment and a 1.7-fold increase for those with self-neglect.50 Elder abuse is most common in women and persons older than 80 years of age with a family member being the abuser in 90%.51

COMMUNITY VIOLENCE ■ History of the Problem The issue of interpersonal violence as a public health problem has gained significant national attention. The United States exceeds all other high-income nations in violent death (graph from up to date?).54 The United States also has the highest youth homicide rate of the 26 industrialized nations.55 Gunshot suicide deaths account for 49% of the violent deaths and occur 30 times more frequently in the USA than in Great Britain.56 Over 1.5 million emergency department visits are due to violent injury annually in the United States.57 In 2000, the total cost associated with fatal and nonfatal injuries due to violence was estimated to be at least $70 billion.58 Most violence occurs not with strangers but with intimate partners, friends, and acquaintances.59–61

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■ Risk Factors

SURGEON’S ROLE Physicians are poised in key positions from which to impact the lives of victims of interpersonal violence.73 The timing and proximity of our contact with the patient are crucial components of the formula for successful intervention. There are barriers to intervening but despite these barriers, physicians can and should address the issue of intentional violence. Many professional organizations have published position statements and/or guidelines. Most guidelines advocate for the routine incorporation of questions regarding

SUMMARY Violence in our society represents a complex, multifaceted problem. In many ways, violence is like a chronic disease. This “disease” is related to both lifestyle and environment. Sims and coworkers at Henry Ford Hospital found that trauma is a recurrent disease, with 44% having recurrent injury and an overall 5-year mortality rate of 20% clearly demonstrates that this “disease” should not be ignored.76 The enormity of this problem requires an ordered, disciplined approach such as that developed by the public health community to address infectious diseases.1 This approach should include event surveillance, epidemiologic analysis, intervention design and evaluation, and a focus on prevention. Our educational efforts should be based on clear competencies77 and interventions should be evidence-based.

REFERENCES 1. Rosenberg ML, O’Carroll PW, Powell KE. Let’s be clear, violence is a public health problem. JAMA. 1992;267:3071–3072. 2. Centers for Disease Control and Prevention. Web-based Injury Statistics Query and Reporting System (WISQARS) [Online]. National Center for Injury Prevention and Control, Centers for Disease Control and Prevention (producer). 2006. Available from: http://www.cdc.gov/ncipc/wisqars/. 3. Chambliss LR, Bay RC, Jones RF. Domestic violence: an educational imperative? Am J Obstet Gynecol. 1995;172:1035–1038. 4. Fleming AW, Sterling-Scott RP, Carabello G, et al. Injury and violence in Los Angeles: impact on access to health care and surgical education. Arch Surg. 1992;127:671–676. 5. Burke LK, Follingstad DR. Violence in lesbian and gay relationships: theory, prevalence, and correlational factors. Clin Psychol Rev. 1999;19: 487–512. 6. Durant RH, Altman D, Wolfson M, et al. Exposure to violence and victimization, depression, substance use, and the use of violence by young adolescents. J Pediatr. 2000;137:707–713. 7. Kyriacou DN, Hutson HR, Anglin D, et al. The relationship between socioeconomic factors and gang violence in the City of Los Angeles. J Trauma. 1999;46:334–339. 8. Knudson MM, Vassar MJ, Straus EM, et al. Surgeons and injury prevention: what you don’t know can hurt you! J Am Coll Surg. 2001;193:119–124. 9. Guth AA, Pachter HL. Domestic violence and the trauma surgeon. Am J Surg. 2000;179:134–140. 10. Rusch MD, Gould LJ, Dzwierzynski WW, et al. Psychological impact of traumatic injuries: what the surgeon can do. Plast Reconstr Surg. 2002;109:18–24. 11. Nelson BV, Patience TH, MacDonald DC. Adolescent risk behavior and the influence of parents and education. J Am Board Fam Pract. 1999;12:436–443. 12. Fein JA, Ginsburg KR, McGrath ME, et al. Violence prevention in the emergency department: clinician attitudes and limitations. Arch Pediatr Adolesc Med. 2000;154:495–498.

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Injuries resulting from violence occur when people have learned to use force to “solve” problems. Most age and population groups in the United States are actually at relatively low risk. A number of risk factors have been identified for community violence and related injury: age, socioeconomic status, race, access to firearms, alcohol and other drug use, gang involvement, exposure to domestic violence and child abuse and media violence. The most significant risks are male gender, being adolescent or young adult, and low socioeconomic status.56,62 Men younger than 65 years were 4-fold more likely to be murdered than women or people over 65 years of age. Homicide is the second leading cause of death for men between 15 and 24 years and the leading cause in African American men between 15 and 24 in the United States.63 Increased concerns about violence have led to more Americans obtaining and carrying firearms for protection,64 but this actually leads to increased risk of firearm injury or death. It is estimated that 40–50% of American households have guns.80,65 A gun in the home is associated with a 40-fold greater chance of killing a family member or acquaintance (homicide, suicide, or accidental) deaths than an intruder in self-protection.66 Alcohol and drug use are also associated with an increased risk of violence. In one study, individuals who began drinking before age 14 were significantly more likely to have been in an alcohol-related fight than those who began drinking after age 21.67 Alcohol is involved in one half to two thirds of homicides, half of serious assaults and more than 25% of rapes.68 A national survey of youth gangs reported more than 20,000 gangs with 650,000 members in 1995.69 More than 94% of cities with a population greater than 100,000 have street gangs.70 Individuals that participate in gangs are more likely to be involved in fights, take weapons to school, and use drugs or alcohol at school.71 The media’s glamorized version of violence is seen by millions daily. The use of violence is an acceptable, if not the preferred method of dealing with conflict and used by heroes as well as villains. A longitudinal study of young adults demonstrated that those with childhood high-violence television viewing were significantly more likely to have grabbed, pushed, or shoved their spouses and that the men in this group were three times more likely to be convicted of crimes.72

safety and exposure to interpersonal violence into the history. Alpert and colleagues have made a list of age-specific screening questions that can be easily covered.74 The value of this routine asking is partly about identifying individual victims but also represents an opportunity to improve overall health care. Routine screening provides physicians with opportunities to express concern for the patient and to express the antiviolence message.75 Indeed, when patients were given an opportunity to tell physicians how to intervene in family conflict, the overwhelming majority thought physicians should ask.10

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13. Flitcraft AH, Hadley SM, Hendricks-Matthews MK, et al. American Medical Association Diagnostic and treatment guidelines on domestic violence. Arch Fam Med. 1992;1:39–47. 14. Anderson RJ, Taliaferro EH. Violence: recognition, management and prevention. Injury prevention and control. J Emerg Med. 1998;16: 489–498. 15. Barrier PA. Domestic violence. Mayo Clin Proc. 1998;73:271–274. 16. Sisley A, Jacobs LM, Poole G, et al. Violence in America: a public health crisis: domestic violence. The violence prevention task force of the Eastern Association for the Surgery of Trauma. J Trauma. 1999;46:1105–1113. 17. Harvard Law Review. Developments—Domestic Violence. 1993;106: 1501–1574. 18. Delahunt EA. Hidden trauma: the mostly missed diagnosis of domestic violence. Am J Emerg Med. 1995;13:74–76. 19. US Commission on Civil Rights. Under the Rule of Thumb: Battered Women and the Administration of Justice. Washington DC: US Commission on Civil Rights; 1982. 20. American Medical Association. Diagnostic and treatment guidelines on domestic violence. Arch Fam Med. 1992;1:39–47. 21. Koop CE, Rosenberg ML, Mercy JA, et al. Violence as a public health problem. Background papers prepared for the Surgeon General’s Workshop on Violence and Public Health, October 27–29, 1985, Leesburg, VA. Atlanta, GA: The Violence Epidemiology Branch, Center for Health Promotion and Education, Centers for Disease Control, U.S. Public Health Service; 1985. 22. Grisso JA, Schwarz DF, Hirschinger N, et al. Violent injuries among women in an urban area. N Engl J Med. 1999;341:1899–1905. 23. Rennison CM. US Department of Justice, Bureau of Justice Statistics Crime Data Brief, Intimate partner violence, 1993–2001, February 2003, NCJ 197838. 24. Tjaden P, Thoennes N. Prevalence, Incidence and Consequences of Violence Against Women: Findings From the National Violence Against Women Survey. Research in Brief. Washington, DC and Atlanta, GA: National Institute of Justice and the Centers for Disease Control and Prevention; 1998. 25. American Psychological Association. Issues and Dilemmas in Family Violence: Report of the American Psychological Association Presidential Task Force on Violence and the Family. Washington, DC: American Psychological Association; 1996. 26. National Center for Injury Prevention and Control. Costs of Intimate Partner Violence Against Women in the United States. Atlanta, GA: Centers for Disease Control and Prevention; 2003. 27. Abbot J, Johnson R, Koziol-McLain J, et al. Domestic violence against women: incidence and prevalence in an emergency department population. JAMA. 1995;273:1763–1767. 28. Silverman JG, Raj A, Clements K. Dating violence and associated sexual risk and pregnancy among adolescent girls in the United States. Pediatrics. 2004;114:e220–e225. 29. Gazmararian JA, Lazorick S, Spitz AM, Ballard TJ, et al. Prevalence of violence against pregnant women. JAMA. 1996;275:1915–1920. 30. Wiebe DJ. Sex differences in the perpetrator-victim relationship among emergency department patients presenting with nonfatal firearm-related injuries. Ann Emerg Med. 2003;42:405–412. 31. Ross SM. Risk of spousal abuse to children of spouse abusing parents. Child Abuse Neglect. 1996;20:589–598. 32. McKibben L, DeVoss E, Newberger E. Victimization of mothers of abused children; a controlled study. Pediatrics. 1989;4:531–535. 33. Strauss MA, Gelles RJ. How violent are American families? Estimates from the National Family Violence Resurvey and other studies. In: Strauss MA, Gelles RJ, eds. Physical Violence in American Families: Risk Factors and Adaptations to Violence in 8145 Families. New Brunswick, NJ: Transaction; 1990. 34. Walker LE. The Battered Woman Syndrome. New York: Springer; 1984. 35. Sev’er A. Recent or imminent separation and intimate violence against women. A conceptual overview and some Canadian examples. Violence Against Women. 1997;3:566–589. 36. Stark E, Flitcraft A, Zuckerman D, et al. Wife Abuse in the Medical Setting: An Introduction for Health Personnel. Washington, DC: Office of Domestic Violence; 1981: Monograph 7. 37. Bowker LH, Maurer L. The medical treatment of battered wives. Women Health. 1987;12:25–45. 38. Muelleman RL, Lenaghan PA, Pakieser RA. Battered women: injury locations and types. Ann Emer Med. 1996;28:486–492. 39. Stark E, Flitcraft A, Frazier W. Medicine and patriarchal violence: the social construction of a private event. Int J Health Serv. 1979;9:461–493. 40. Norton LB, Peipert JF, Zierler S, et al. Battering in pregnancy an assessment of two screening methods. Obstet Gynecol. 1995;85: 321–325.

41. Council on Scientific Affairs, American Medical Association. Violence against women, relevance for medical practitioners. JAMA. 1992;267: 3184–3189. 42. Feldhaus KM, Koziol-McLain J, Amsbury HL, et al. Accuracy of three brief screening questions for detecting partner violence in the emergency department. JAMA. 1997;277:1357–1361. 43. MacMillan HL, Wathen CN, Jamieson E, et al. Approaches to screening for intimate partner violence in health care settings: a randomized trial. JAMA. 2006;296:530. 44. McFarlane J, Christoffel K, Bateman L, et al. Assessing for abuse: selfreport versus nurse interview. Public Health Nurs. 1991;8:245–250. 45. Wadman MC, Muelleman RL. Domestic violence-related homicide: emergency department use before victimization. Am J Emerg Med. 1999;17:698–691. 46. Sharps PW, Koziol-McLain J, Campbell J, et al. Health care providers missed opportunities for preventing femicide. Prev Med. 2001;33: 373–380. 47. Lachs MS, Pillemer K. Elder abuse. Lancet. 2004;364:1263–1272. 48. Wolf R, Daichman L. Abuse of the elderly. In: Krug E, et al., eds. World Report on Violence and Health. Geneva: World Health Organization; 2002:123. Available at: http://whqlibdoc.who.int/publications/2002/ 9241545615_eng.pdf 49. Wei GS, Herbers JE Jr. Reporting elder abuse: a medical, legal and ethical overview. J Am Med Womens Assoc. 2004;59:248–254. 50. Lachs MS, Williams SC, O’Brien S, et al. The mortality of elder mistreatment. JAMA. 1998;280:428–432. 51. Tatara T. The National Elder Abuse Incidence Study. The National Center on Elder Abuse; 1998. Available at: www.ncea.aoa.gov/ncearoot/Main_ Site/Library/Statistic_Research/Natioanl_Incident.as px 52. Dyer CB, Connolly MT, McFeeley P. The clinical and medical forensics of elder abuse and neglect. In: National Research Council. Panel to review Risk and Prevalence of Elder Abuse and Neglect. Bonnie RJ, Wallace RB, eds. Elder Mistreatment: Abuse, Neglect and Exploitation in an Aging America. Washington, DC: Committee on National Statistics and Committee on Law and Justice, Division of Behavioral and Social Sciences and Education, The National Academies Press; 2003:339. 53. Lachs MS, Pillemer K. Abuse and neglect in elderly persons. N Engl J Med. 1995;332:437–443. 54. Krug EG, Dahlberg LL, Mercy JA, et al. World Report on Violence and Health. Geneva: World Health Organization; 2002. 55. Rates of homicide, suicide and fire-arm related death among children: 26 industrialized countries. MMWR Morb Mortal Wkly Rep. 1997;46: 101–105. 56. Karch DL, Lubell KM, Friday J, et al. Surveillance for violent deaths: National Violent Death Reporting System 16 states, 2005. MMWR Surveill Summ. 2008;57:1–45. 57. National Center for Health Statistics. National Hospital Ambulatory Medical Care Survey, 2002. Washington, DC: Emergency Department Survey, US Dept of Health and Human Services; 2004. 58. Corso PS, Mercy JA, Simon TR, et al. Medical costs and productivity losses due to interpersonal and self-directed violence in the United States. Am J Prev Med. 2007;32:474–482. 59. Federal Bureau of Investigation. Crime in the United States 1996: Uniform Crime Reports. Washington, DC: Government Printing Office; 1997. 60. Sege R, Stigol LC, Perry C, et al. Intentional injury surveillance in a primary care pediatric setting. Arch Pediatr Adolesc Med. 1996;150:277–283. 61. Slaby RG, Stringham P. Prevention of peer and community violence: the pediatrician’s role. Pediatrics. 1994;94:608–616. 62. Cubbin C, LeClere FB, Smith GS. Socioeconomic status and the occurrence of fatal and nonfatal injury in the United States. Am J Public Health. 2000;90:70–77. 63. Centers for Disease Control and Prevention. National Center for Injury Prevention and Control. WISQARS (web-based injury statistic query and reporting system). Available at www.cdc.gov. 64. Reiss AJ, Roth JA, eds. Understanding and Preventing Violence. Washington, DC: National Academy Press; 1993. 65. Zuckerman DM. Media violence, gun control, and public policy. Am J Orthopsych. 1996;66:378–389. 66. Kellerman AL, Reay DT. Protection or peril? An analysis of firearmrelated deaths in the home. N Engl J Med. 1986;314:1557–1560. 67. Hingson R, Hereen T, Zakocs R. Age of drinking onset and involvement in physical fights after drinking. Pediatrics. 2001;108:872–877. 68. Martin SE. The epidemiology of alcohol-related interpersonal violence. Alcohol Health Res World. 1992;16:230–240. 69. US Department of Justice. 1995 National Youth Gang Survey: Program Summary. US Department of Justice, Office of Juvenile Justice and Delinquency Prevention, NCJ 164728, Washington, DC; 1997.

Social Violence 74. Alpert EJ, Sege RD, Bradshaw YS. Interpersonal violence and the education of physicians. Acad Med. 1997;72:S41–S50. 75. Gerbert B, Caspers N, Bronstone A, et al. A qualitative analysis of how physicians with expertise in domestic violence approach the identification of victims. Ann Intern Med. 1999;131:578–584. 76. Sims DW, Bivins BA, Obeid FN, et al. Urban trauma: a chronic recurrent disease. J Trauma. 1989;29:940–946. 77. Knox LM, Spivak H. What health professionals should know: core competencies for effective practice in youth violence prevention. Am J Prev Med. 2005;29:191–199.

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70. Liscum KR, Cornwell EE III, Bjerke S, Chang DC. Youth and family violence. In: Feliciano DV, Mattox KL, Moore EE, eds. Trauma. 6th ed. New York, NY; 2008. 71. Pratt HD, Greydanus DE. Adolescent violence: concepts for a new millennium. Adolesc Med. 2000;11:103–125. 72. Huesman LR, Moise-Titus J, Podolski C, Eron LD. Longitudinal relations between children’s exposure to TV violence and their aggressive and violent behavior in young adulthood: 1977-1992. Dev Psychol. 2003;39:201–221. 73. McAfee RE. Physicians and domestic violence: can we make a difference? JAMA. 1995;273:1790–1791.

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Wounds, Bites, and Stings Charles A. Adams, Jr., Daithi S. Heffernan, and William G. Cioffi

INTRODUCTION Wound healing and patients with altered or delayed healing cover the entire spectrum of surgical care. This chapter will review wounds, wound healing and closures, coverage options, and abnormalities in wound healing. It will focus on general principles and concepts rather than specific topics since the majority of these are dealt with in greater detail in other chapters. First, the biology and pathophysiology of wound healing will be explored in depth. Next, bites and stings, including emerging threats in the United States, will be detailed as our knowledge in these areas continues to advance. Each year in the United States, millions of individuals sustain traumatic injuries but the overwhelming majority of these are simple and readily treated with minor interventions. In practical terms, satisfactory healing of wounds such as these would take place regardless of the treatments that they received. This chapter will focus on more severe wounds or those wounds that would not have a satisfactory outcome without special attention. The main principles in treating these wounds are preventing infection, retaining maximal function, and achieving acceptable cosmesis. The spectrum of health care providers who care for these wounds is extensive, including emergency medicine physicians, advanced practice nurses, family physicians, surgeons, and surgical subspecialists, but the treatment philosophy is the same. The nature and mechanism of the wound, its anatomic location, preexisting comorbidities, and the current clinical situation all dictate the approach to the wound but in general the simplest technique that fulfills the previously stated objections should be embraced. Fig. 47-1 provides a treatment algorithm for acute wounds that is applicable to a wide array of clinical scenarios and wounds. Wound healing has always held an important status in medical care throughout recorded history. The Egyptians practiced advanced wound care as evidenced by the Edwin Smith and Ebers papyruses as did the ancient Greeks

whose doctrine on the care of acute and chronic wounds in gladiators was described by Galen of Pergamum.1 The ancients observed that dead tissue and foreign bodies had to be removed in order for normal wound healing to progress and that cleanliness prevented infection. They recognized that organized collections of pus required drainage and that honey (a hypertonic, hygroscopic, and bactericidal fluid) could prevent infections while dirt and dung promoted them. However, the biology of this effect was a mystery to them.2 Later in the 1500s, the scholarly treatise on wounds by French surgeon Ambroise Pare established a truism that is still applicable today: “Do not put anything in a wound that you would not put in your own eye.” Despite the seminal contributions of Lister, Semmelweis, Ehrlich, Fleming, and Florey, it was not until the very end of the 20th century that our understanding of the biology of wound healing grew to the point that physicians are now able to manipulate wounds utilizing translational techniques taken from cellular and molecular biology. Wounds are generally classified into one of the following two categories: acute and chronic. Acute wounds follow a systematic, organized series of stages that ultimately result in restoration of skin integrity. In contrast, chronic wounds follow many of the same steps but do not result in reestablishment of skin integrity. Generally, a wound that fails to fully heal by 3 months is said to be a chronic wound. However, such an arbitrary definition fails to consider the size or anatomic location of the wound or other impediments to healing. We will focus on the healing of acute, cutaneous wounds since they represent the vast majority of traumatic wounds.

NORMAL WOUND HEALING Unlike humans, many lower life forms have the ability to regenerate after wounding. In humans only the liver and bone retain the ability to heal by regeneration. Excluding these two tissues,

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FIGURE 47-1 Algorithm for the treatment of an acute wound. aAppropriate tetanus, rabies, and antibiotic prophylaxis. bIntermediaterisk wounds require more judgment. cSee Table 47-9.

all other mammalian tissues heal through scar formation. The steps of scar formation or wound healing are classically divided into three distinct phases: inflammatory, proliferative, and remodeling (Table 47-1). These phases usually take place in a stepwise fashion, although, as we will discuss later, there are varying degrees of overlap and in certain wounds all phases may coexist simultaneously.

■ Inflammatory Phase The inflammatory, or reactive, phase constitutes the first phase of wound healing and commences as soon as the injury occurs. All traumatic wounds lead to bleeding, disturbances in hemostasis, and an inflammatory reaction due to cellular destruction. The main goals of this stage are to stop bleeding, prevent

TABLE 47-1 Phases of Wound Healing Inflammatory Proliferative Remodeling

infection, and remove devitalized tissue. Wounding invariably leads to disruption of blood vessels with ensuing bleeding that ranges from a slow ooze from capillaries to an exsanguinating hemorrhage if large arteries or veins are involved. In order to stop the bleeding, coagulation of blood must occur in a tightly regulated fashion so that clotting is confined to the site of injury but not at remote vascular locations. Blood vessel injury leads to the exposure of subendothelial, collagen, thrombin, and other procoagulant elements that bind and activate platelets. An important early response to vascular injury is contraction of the smooth muscle within the endothelium. Endothelin, a powerful vasoconstrictor, is released directly from the endothelium of the damaged vessel, an event occurring prior to the activation of platelets.3 Prostaglandins from injured cells, as well as circulating catecholamines following the trauma, also contribute to this early vasoconstrictive response. Additional stimuli for vasoconstriction occur via platelet activation with the resultant release of bradykinin, fibrinopeptides, serotonin, and thromboxane A2. Platelet activation leads to a chain reaction culminating in the formation of an aggregate of platelets known as the “platelet plug.” Subendothelial matrix collagen interacts with circulating platelets leading to subsequent platelet adhesion. This is achieved via a complex of the platelet glycoproteins VI,

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Ib–V–IX, and collagen-bound von Willebrand factor on exposed collagen, as is mediated by platelet integrins. Since platelets are the first major cell to respond to wounded tissue, activated platelets serve as the platform on which clotting factors interact to form an insoluble fibrin meshwork that is generated from soluble, circulating fibrinogen. This fibrin mesh is cross-linked and traps circulating erythrocytes and activates additional platelets resulting in a tight, hemostatic plug.4 Shortly after coagulation is initiated, the complement cascade is set also in motion that leads to the release of potent neutrophil chemotactic factors, such as C5a.5 Large wounds or massive trauma may lead to an overly robust activation of this complement cascade and is thought to contribute to the subsequent development of the systemic inflammatory response syndrome (SIRS).6 C5a is believed to play a key role in the apoptotic response that occurs in immune cells shortly following a traumatic event.7 Complement is also involved in the destruction of bacteria through formation of the membrane attack complex, as well as opsonizing bacteria that facilitates their phagocytosis. Effective hemostasis leads to a relative lack of blood flow to the wound microenvironment. This, coupled with anaerobic metabolism by leukocytes, leads to a locally hypoxic, acidotic wound environment. Such settings are known to be a stimulus for leukocyte activation so that coagulation is quickly followed by inflammation, but there is some overlap in these processes.8 Activated platelets and endothelial cells release cytokines that attract neutrophils and macrophages to the area. If thrombin is present, endothelial cells exposed to leukotrienes C4 and D4 will release the potent proinflammatory phospholipid plateletactivating factor (PAF) that enables neutrophil adhesion.9 Excessive PAF activation and involvement may lead to chronic and poorly healing wounds.10 Accordingly, by the end of the first hour and for the first 2–3 days after wounding, the dominant cell type in the wound is the neutrophil. The main purpose of the neutrophil is destruction of bacteria through phagocytosis and the generation of reactive oxygen species through a process called “respiratory burst.” Respiratory burst results in the formation of many reactive oxygen species such as superoxide anion (SO2−), hydrogen peroxide, hydroxyl radicals, and hypochlorous acid. Neutrophils also debride the wound by elaborating activated proteases and elastases that break down devitalized tissues and cells. Unfortunately, the release of activated lysosomal enzymes along with reactive oxygen species leads to the indiscriminant collateral damage of otherwise healthy host cells as well.11 Ultimately, the action of neutrophils leads to the generation of pus that is simply a collection of dead neutrophils and bacteria along with tissue breakdown products. Once neutrophils have completed their job, they undergo apoptosis, or programmed cell death, and are eliminated by macrophages in a process that is remarkably free of inflammation. Of all the cells involved in wound healing, none is as critical as the macrophage.12 Activation of platelets, endothelial, and other cells in the wound leads to the generation of inflammatory substances such as histamine, serotonin, prostaglandins, kinins, platelet-derived growth factor (PDGF), transforming growth factor beta (TGF-β), insulin-like growth factor-1

(IGF-1), fibronectin, fibrinogen, von Willebrand factor, thrombospondin, and thromboxanes. These substances have many varied effects including increasing capillary permeability by disrupting the integrity of the endothelium, both vasoconstriction and vasodilatation, and the recruitment of several other inflammatory cell types. Monocytes respond to chemotactic signals such as fibrin and fibrinopeptides and leave the blood vessels via diapedesis. This migration is facilitated by capillary leak and interstitial edema that results from the action of inflammatory substances such that by the end of 1.5 days postinjury the numbers of monocytes in the wound reaches its peak. The inflammatory milieu of the wound then stimulates the monocyte to become a macrophage and it is these macrophages in conjunction with resident tissue macrophages that orchestrate the entire wound healing process. Macrophages release over 20 different growth factors and cytokines and can perform a wide range of functions so that they are truly the central cell in wound healing.13 Just like the neutrophil, macrophages contribute to clearing the wound of bacteria, although neutrophils remain the prime antibacterial cell in the wound. The phagocytic function of macrophages is not limited to bacteria alone since they also clear away apoptotic neutrophils and other cells via phagocytosis. Recent evidence is emerging pointing to a key role of invariant natural killer T cells in the proper functioning of macrophages for acute processes such as wound healing and bacterial clearance.14 Unlike neutrophils, phagocytosis is not the main function of the macrophage and this activity is typically manifested only in the very early stages of wound healing. As the wound is cleared of bacteria, the macrophages release growth factors that reinforce endothelial cell activation and are chemotactic signals for various cells. Activated endothelial cells display adhesion molecules so that additional inflammatory cells can bind to the activated endothelium and be recruited into the wound.15 Initially, leukocytes tether and roll on the exposed vascular endothelial cells, before they are activated to adhere firmly with the ultimate goal of migration into the extravascular space. Leukocyte tethering and rolling is primarily mediated via selectins. The later firm adhesion is mediated via the immunoglobulin (Ig) superfamily members, including intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), and their integrin ligands, including lymphocyte function-associated antigen-1 (LFA-1, CD11a/CD18) and very late antigen-4 (VLA-4, CD49d/ CD29). The three cell-surface molecules expressed by leukocytes (L-selectin), vascular endothelium (E- and P-selectins), and platelets (P-selectin) comprise the selectin family. Each selectin exhibits a characteristic time frame. L-selectin is constitutively expressed on most leukocytes, whereas ICAM-1 is constitutively expressed at low levels by endothelial cells. ICAM-1 can be rapidly upregulated during inflammation. P-selectin is rapidly mobilized to the surface of activated endothelium or platelets. E-selectin expression is induced within several hours after activation with inflammatory cytokines. The combination of endothelial cell activation and the release of chemotactic and growth factors leads to the next stage of wound healing, the migratory phase.

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■ Migratory Phase

CHAPTER 47

The next phase of wound healing is the migratory phase. The initial “platelet plug and clot” need to be replaced with cells capable of achieving proper closure of the gap that was created from trauma, as well as to replenish the lost tissue. While the migratory phase is initiated early on in the wound healing process, its duration is highly variable and dependent on the size and nature of the wound that needs to be healed. The interaction of activated endothelial cells with circulating inflammatory cells leads to the margination of leukocytes. At this point, there is significant alteration in the cell–cell and cell– matrix adhesions to enable the progression from a lamininV- and collagen-IV-rich basement membrane to provisional matrix substances.16 Migrating cells also assemble actin-rich lamellar protrusions that will enable crawling,17 and upregulate the expression of the proteolytic enzymes such as matrix metalloproteinases (MMPs). The migrating cells traverse the blood vessel wall through diapedesis and migrate along chemotactic gradients to the site of injury. Meanwhile, macrophages are progressing from bacterial phagocytosis to the coordination of the complex cell–cell interactions and are now the dominant cell type in the wound supplanting neutrophils and monocytes. The relatively hypoxic wound environment causes macrophages to release angiogenic growth factors, key among which is hypoxia-induced factor (HIF).18 HIFs are transcriptional complexes that are regulated by protein degradation, thereby allowing a swift response. Using an HIF-knockout mouse, investigators have shown that HIF-alpha deficiency leads to a pattern of multiorgan dysfunction with significant anaerobic metabolism.19 A further key player in angiogenesis is PDGF that is released by activated platelets.20,21 Vascular endothelial growth factor (VEGF) stimulates angiogenesis in a strict dosedependent fashion.22 Many other factors, such as angiopoietin-2/ angiopoietin-1,23 PDGF, basic fibroblast growth factor (bFGF), and monocyte chemoattractant protein-1 (MCP-1),24 have been shown to be indispensable in increasing vascular permeability, endothelial growth, remodeling, cell proliferation, and vascular lumen formation. PDGF also stimulates fibroplasia by stimulating the normally present but quiescent fibroblasts to begin replicating by releasing them from their G0 arrest. Cytokines such as IGF-1 and epidermal growth factor (EGF) released from activated macrophages and platelets cause the fibroblasts to begin replicating. Additional fibroblasts from outside the wound environment arrive by traveling over the scaffold of the fibrin clot by binding to fibronectin within it. While angiogenesis and fibroblast proliferation occur simultaneously, it is obvious that like all cellular synthetic functions, fibroblast synthetic function is dependent on oxygen. Thus, in the healing wound, angiogenesis and fibroplasia are interconnected processes.25 Angiogenesis is dependent on the action of endothelial cells derived from the nearby uninjured portion of blood vessels.26 These endothelial cells first generate plasminogen activator to degrade the clot at the site of vessel injury so that they can migrate out into the extracellular matrix.25 This action is reliant on the activity of zinc-dependent MMPs that are required to dissolve the basement membrane and collagenases.26 Specifically,

MMP-2 and MMP-9 have been shown to be prominent in the angiogenic response to hypoxia. Neutrophil granules are potent sources of MMP-9. Further neutrophils can release tissue inhibitors of matrix metalloproteinases (TIMP-1) pro-MMP-9 that can activate latent pro-MMP-9 in the wound environment.27 The newly “liberated” endothelial cells then migrate through the surrounding extracellular matrix by extending pseudopodia, just like leukocytes do, in response to chemotactic signals released by platelets and macrophages. The relatively hypoxic local wound environment leads to the formation of lactic acid through anaerobic metabolism, which has been shown to be a potent stimulus for macrophages to release endothelial cell growth factors.13 When tissue oxygen tension improves and the macrophages are no longer hypoxic, they stop elaborating endothelial cell growth factors in an elegant feedback loop controlling angiogenesis. Further, with restoration of oxygen to the wound, HIF-1alpha proteins are downregulated by the oxygen-dependent inhibitor, factor inhibiting HIF-1 (FIH-1).28 Thus, wound revascularization removes the stimulus for endothelial cell growth and migration and similarly to the preceding neutrophils, the endothelial cells also undergo apoptosis. The typical beefy red color of granulation tissue is a result of dense collections of capillaries formed through the process of angiogenesis. While angiogenesis is occurring within the wound, reepithelialization is occurring at the margin of the wound. This process begins approximately 24 hours postinjury and is driven primarily by transforming growth factor alpha (TGF-α) that is released by platelets and macrophages. If a wound is sufficiently deep enough to destroy the stratum basale of the skin, keratinocytes from the wound edges or from deep skin appendages such as hair follicles, sweat glands, or sebaceous glands spared by the wounding insult serve as the source for reepithelialization. Interestingly, reepithelialization of the wound is almost entirely dependent on migration of keratinocytes, which occurs as sheets of cells move in from the wound periphery, rather than mitosis of keratinocytes within the wound. In order for keratinocytes to migrate they must detach themselves from their basement membrane by dissolving their anchoring desmosomes. Following this, they display integrins and migrate across the early wound matrix using fibronectin cross-linked with fibrin as adhesion sites exactly like the fibroblasts before them. As the keratinocytes migrate they elaborate MMPs, collagenases, plasminogen activator, and other proteases to dissolve debris as well as phagocytosize dead cells blocking their path. As the sheet of migrating epithelial cells advances, new cells are formed at the wound margin by greatly upregulated mitosis to replenish the advancing cells. The rate of mitosis at the wound margin may be 17 times higher than that seen in normal tissue and remains the only focus of epithelial cell mitosis in the wound.29 The migration continues until keratinocytes encounter other cells that stop their advancement through contact inhibition, and downregulation of their fibronectin receptors that are necessary for their movement.25 Reepithelialization proceeds more rapidly if the basement membrane is intact, otherwise new basement membrane substances must be secreted.30 Keratinocytes will then reanchor themselves to the basement membrane and each other using desmosomes and hemidesmosomes and normal skin stratification is established

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by cell division of the basal layer of cells. Critical to this stability is the interaction between the hemidesmosomes, integrinalpha6-beta4, and plectin.31 Thus, by the conclusion of the migratory phase, new blood vessels are being formed and fibroblasts are appearing in the wound and begin replicating so that fibroplasia may take place, while at the wound margin an advancing sheet of epithelial cells moves inward. Table 47-2 reviews some of the more important cytokines and growth factors involved in the regulation of wound healing.

■ Proliferative Phase The next phase of wound healing, the proliferative phase, is marked by the migration of multiple cell types including monocytes, lymphocytes, and endothelial cells into the wound along with the emergence of active fibroblasts. This phase usually commences around day 5 and is characterized by the dramatic increase in the number of cells and the production of collagen. The production of collagen may be detected as early as 10 hours after injury. However, collagen production reaches maximum velocity by day 7. Collagen synthesis continues at a vigorous pace until approximately day 21 when the wound approaches its peak of collagen content and collagen production plateaus. This is the physiologic basis for the practice of

leaving retention sutures, used to reinforce tenuous laparotomy closures, in place until day 21. Eventually, granulation tissue is formed as the fibrin– fibronectin network that comprises the blood clot along with the makeshift wound matrix of proteoglycans, glycosaminoglycans, and hyaluronic acid is replaced by a combination of collagen, new capillaries, and numerous inflammatory cells and fibroblasts. This process is largely accomplished by fibroblasts that interact with several adhesive ligands in the wound matrix such as laminin, tenascin, and fibronectin while they release hyaluronidases that degrade the provisional wound medium. This early wound continues to evolve as collagen is haphazardly laid down on the fibronectin and glycosaminoglycan scaffold. The amount of granulation tissue in the wound is dependent on the size and depth of wounds that are allowed to heal by secondary intention. Large wounds need to “fill in” with granulation tissue so that epithelial cells from the wound margin can migrate across and reepithelialize the wound. Alternatively, the development of a healthy bed of granulation tissue is the sign that a wound is ready to accept an autologous skin graft. It is the rich network of capillaries along with the relatively aqueous environment that supports the transplanted epithelium by bathing it in a flow of nutrient-containing fluid and oxygen. Full-thickness skin grafts are an important modality to mitigate the next step of wound healing that is contraction.

TABLE 47-2 Cytokines and Growth Factors Peptide G-CSF

Site of Synthesis Fibroblasts, monocytes

Regulation Induced by IL-1, LPS, IFN-$aL

GM-CSF

IL-3 has almost identical effects

Endothelial cells, fibroblasts, macrophages, T lymphocytes in bone marrow

IFN-$aL, -$bT, -$gM

Epithelial cells, fibroblasts, lymphocytes, macrophages, neutrophils

IL-1

Endothelial cells, keratinocytes, lymphocytes, macrophages

Induced by viruses (foreign nucleic acids), microbes, microbial foreign antigens, cancer cells Induced by TNF-$aL, IL-1, IL-2, C5a. Suppressed by 1 L-4, TGF-$bT

Target Cells Committed neutrophil progenitors (CFU-G, Gran) Induced by IL-1, TNF

Lymphocytes, macrophages, infected cells, cancer cells

Monocytes, macrophages, T cells, B cells, NK cells, LAK cells

Effects Supports the proliferation of neutrophilforming colonies. Stimulates respiratory burst Granulocyte–erythrocyte–monocyte– megakaryocyte progenitor cells (CFUGEMM, CFU-MEG, CFU-Eo, CFU-GM) Supports the proliferation of macrophage-, eosinophil-, neutrophil-, and monocytecontaining colonies Inhibits viral multiplication. Activates defective phagocytes, direct inhibition of cancer cell multiplication, activation of killer leukocytes, inhibition of collagen synthesis Stimulates T cells, B cells, NK cells, LAK cells. Induces tumoricidal activity and production to other cytokines, endogenous pyrogen (via PGE2 release) Induces steroidogenesis, acute-phase proteins, hypotension; chemotactic neutrophils. Stimulates respiratory burst (continued )

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TABLE 47-2 Cytokines and Growth Factors (Continued ) Site of Synthesis Monocytes

Regulation Induced by GM-CSF, LPS, IgG

IL-2

Lymphocytes

Induced by IL-1, IL-6

IL-4

T cells, NK cells, mast cells

Induced by cell activation, IL-1

IL-6

Endothelial cells, fibroblasts, lymphocytes, some tumors

Induced by IL-1, TNF-$aL

IL-B

Endothelial cells, fibroblasts, lymphocytes, monocytes Endothelial cells, fibroblasts, monocytes Committed monocyte progenitors (CFU-M, Mono)

Induced by TNF, IL-1, LPS, cell adherence (monocytes) Induced by IL-1, LPS, 1

M-CSF

FN-$aL

MCP-1, MCAF

TNF-$aL (LT has almost identical effects)

Monocytes. Some tumors secrete a similar peptide Macrophages, NK cells, T cells, transformed cell lines, B cells (LT)

Supports the proliferation of monocyteforming colonies. Activates macrophages Induced by IL1, LPS, PHA

Suppressed by PGE2, TGF-$bT, IL-4. Induced by LPS

Target Cells Blocks type 1 IL-1 receptors on T cells, fibroblasts, chondrocytes, endothelial cells T cells, NK cells, B cells, activated monocytes All hematopoietic cells and many others express receptors T cells, B cells, plasma cells, keratinocytes, hepatocytes stem cells Basophils, neutrophils, T cells

Effects Blocks type 1 IL-1 receptors on T cells, chondrocytes, endothelial cells. Ameliorates animal models of arthritis, septic shock, and inflammatory bowel disease

Unstimulated monocytes

Chemoattractant specific for monocytes

Endothelial cells, monocytes, neutrophils

Stimulates T cell growth. Direct cytotoxin to some tumor cells. Profound proinflammatory effect via induction of IL-1 and PGE2. Systemic administration produces many symptoms of sepsis. Stimulates respiratory burst and phagocytosis

Stimulates growth of T cells, NK cells, and B cells Stimulates B cell and T cell growth. Induces HLA class II molecules

B cell differentiation. Induction of acute-phase proteins, growth of keratinocytes. Stimulates growth of T cells and hematopoietic stem cells Induces expression of endothelial cell LECAM-1 receptors, $bT2 integrins, and neutrophil transmigration. Stimulates respiratory burst

Key: CFU, colony-forming unit; G-CSF, granulocyte colony-stimulating factor; GM-CSF, granulocyte-macrophage colonystimulating factor; IFN, interferon; IL interleukin; IL-1ra, interleukin-1 receptor antagonist; LPS, lipopolysaccharide; LT, lymphotoxin; MCAF, monocyte chemotactic and activating factor; M-CSF, macrophage colony-stimulating factor; MCP-1, monocyte chemotactic peptide-1; NK, natural killer (cell); PHA, phytohemagglutinin; TGF-$bT, transforming growth factor beta; TNF-$aL, tumor necrosis factor alpha.

CHAPTER 47

Peptide IL-1ra

902

Specific Challenges in Trauma

SECTION 4

Wounds that are allowed to heal by secondary intention, and to a much lesser degree wounds closed primarily, undergo the phenomenon of wound contraction, which is a process whereby the wound edges and surrounding skin are pulled in toward the center of the wound. Contraction usually starts around 1 week after wounding, peaks in intensity around day 10, and may persist for weeks with a reported speed of nearly 0.75 mm per day. This process is a highly efficient way of reducing the surface size of the wound and decreases the amount of reepithelialization that needs to occur. Unfortunately, this process can be particularly debilitating if the wound overlies a joint, flexible part of the body or crucial orifice such as the eye or mouth. Significant loss of function due to the presence of a contracting wound is clinically called a “contracture.” Differences in the thickness of skin in various anatomic locations along with the laxity of the surrounding skin lead to variable degrees of contraction. Typically, the perineum and trunk experience the greatest degree of contraction while the extremities exhibit the least, while the head and neck exhibit an in-between amount of wound contraction. The exact mechanism of wound contraction is not well elucidated but appears to be dependent on modified fibroblasts that contain microfilaments and alpha smooth muscle actin and phenotypically resemble smooth muscle cells.32 The true phenotypic characteristics and capabilities of myofibroblasts are still poorly understood, but knowledge is growing as the role of the myofibroblast in pathological processes such as tumor dissemination is being better appreciated.33 Myofibroblasts are richly endowed with adhesion molecules in order to complex with a vast array of components making up the early wound environment. It is these attachments that allow them to bind and draw the wound edges together. As the wound contracts, other fibroblasts continue to synthesize collagen that effectively holds the wound together. Nearly 20 different types of collagen have been identified and all share a common structural similarity known as the right-handed triple helix. Each type of collagen has unique structural properties that are attributed to specific breaks in the triple helix pattern. In general, collagen triple helices are composed of three alpha peptide chains that undergo extensive modification both in and outside the fibroblast. Collagen is the major component of all human tissues and is distinctive in that it contains large quantities of the unique amino acids hydroxyproline and hydroxylysine. The hydroxylation of specific prolines in the early peptide chain is extremely important because error at this stage of collagen synthesis leads to the creation of an unstable collagen that is quickly degraded in the extracellular environment. The hydroxylation of proline and lysine requires ascorbic acid (vitamin C), which is the mechanism whereby vitamin C deficiency leads to impaired wound healing, and even opening of previous healed wounds, as seen in the disease scurvy. Regulation of collagen synthesis occurs at many levels, beginning with the transcription. Collagen transcription takes place on several different chromosomes from discontinuous genes resulting in a large precursor molecule that must be modified within the nucleus; thus, only limited amounts of messenger ribonucleic acid (RNA) are created. This highly modified mRNA then undergoes translation on ribosomes of the endoplasmic

reticulum so that by the time the collagen molecule is ready to leave the Golgi apparatus, it has undergone significant glycosylation with glucose and galactose and has had “extension” peptides placed on its amino and carbon terminals to facilitate its orientation and handling. These procollagen monomers leave the cell where additional modification takes place extracellularly, resulting in highly cross-linked collagen fibers. The extracellular modification process is fairly unique to collagen, and it is during this juncture that the extension peptides are cleaved from the end of procollagen, which are then taken back into the cell and downregulate collagen expression. At the end of this stage of wound healing, sufficient collagen fibers have been synthesized and the wound is more appropriately called a scar.

■ Remodeling Phase Although it seems contradictory, it is true that collagen must be degraded at the same time it is created in order for normal wound healing to occur. When the rate of collagen synthesis is balanced by an equal rate of collagen degradation, the wound is said to have reached the remodeling or maturational phase. This phase of wound healing may last for several months or even years for large wounds that heal by second intention. The tensile strength of the wound increases over time as the disorganized type III collagen that was laid down initially is degraded by MMPs and slowly replaced by type I collagen. The activity of the MMPs is itself regulated by TIMPs so that a balance between synthesis, deposition, and degradation of extracellular matrix is maintained.34 Progression from laying down collagen haphazardly to the organized structure seen at the end of the remodeling phase requires a careful balance within the wound environment. This balance may be quite delicate as evidenced by the role of arginine. Therapeutic supplementation with arginine has been proposed as a safe method of providing the necessary proline and polyamines to improve wound healing; however, excess arginine has been associated with poor collagen matrix formation, impaired collagen remodeling and cross-linking, and altered wound tensile strength. It is believed that this occurs via excess nitric oxide production rather than ornithine and an imbalance in the pace of collagen remodeling.35 As type I collagen is laid down and oriented parallel to lines of stress, the tensile strength of the wound increases. This increase is most rapid during the first 6 weeks, and then slows down but may persist for over a year or more. The tensile strength of the wound approaches 50% of normal skin by 3 months after injury and plateaus out about 80% by the end of remodeling, although this process continues on at an extremely slow rate for several more years. The increase in tensile strength is attributed to collagen cross-linking since the collagen content of the wound does not change beyond the third week. The scar that was originally red or purple in color due to the tremendous amount of capillaries it contains gradually turns white as these are readsorbed and replaced with type I collagen. The final result of the repair is an inelastic, avascular, brittle scar that is devoid of skin appendages such as hair follicles and sweat glands and never recovers more than 80% of the tensile strength of unwounded skin.

Wounds, Bites, and Stings

CLINICAL MANAGEMENT OF WOUNDS

Wound closure falls into one of the following four general categories: primary, secondary, delayed primary, and tissue transfer. In primary closure, the cutaneous defect is approximated through the use of sutures, staples, adhesive dressings, or topical sealants and the previously described phases of wound healing occur albeit on a limited scale. These wounds are typically closed in layers along tissue planes and derive their strength from collagen-rich layers such as dermis or fascia. The duration of healing and the final cosmetic result are closely linked to the amount of devitalized tissue, bacteria, and blood left in the wound at the time of closure. Meticulous debridement of the wound along with scrupulous hemostasis minimizes the inflammatory phase of wound healing and allows the wound to progress rapidly to the migratory and proliferative phases of the healing process and promotes earlier wound closure with improved cosmesis as well. The decision to close a wound primarily is based on the judgment by the clinician that the wound is at minimal risk for wound infection or that subsequent wound infection after primary closure is less detrimental than open management of the wound. Wounds that are felt to be at excessive risk for infection are best left open to heal by secondary intention. Spontaneous or secondary intention closure occurs when the wound edges are not reapproximated and the wound must undergo contracture, granulation, and reepithelialization in order to close. Open wounds are much less likely to become infected, but they are not immune to wound infection. The presence of increased bacteria and tissue debris leads to a longer, more intense inflammatory phase that results in more scarring and decreased cosmesis. Failure of healing by secondary intention leads to a chronic wound and in large part is due to a fundamental shift in the type and quality of wound inflammation. Chronic wounds, which are practically defined as a wound that has failed to close within 3 months, exhibit much higher levels of collagenases and MMPs, yet have reached a point of stasis and do not ultimately heal. In delayed primary closure, a wound is left open for a few days and is treated much the same as a wound that is healing by second intention. The difference is that after a certain time the wound is then closed primarily. The main reason that a wound is handled in this fashion is that there is too much bacterial contamination, tissue trauma, or foreign bodies to allow a primary closure and the wound is left open so that wound care and dressing changes can remove these impediments to infection-free healing.36 There tends to be more inflammation in wounds that are managed by delayed primary closure than in those managed by primary closure, but eventually these wounds exhibit the same tensile strength and cosmesis as wounds that were initially closed primarily and with lower infection rates.36 Some authors have advocated delayed primary closure, rather than closure by secondary intention, for gunshot wounds. However, this needs to be applied on a case-by-case basis.37 Open wounds and those with extensive soft tissue loss that are technically difficult to close are best treated by application

■ Wound Management Decision Making The way a wound is treated is dependent on several decisions and sound clinical judgment. The first determination in whether to close a wound or leave it open is related to the time since injury. In general, wounds that have been open for more than 6–8 hours should be left open, otherwise primary closure is advantageous. Obviously, there are many exceptions to this “rule” since open wounds on the face or scalp tend to do well even when closed more than 8 hours after wounding. This observation is due to the relatively low levels of commensal bacterial colonization coupled with an outstanding blood supply in these locations. On the other end of the spectrum, a 4-hour-old wound in an ischemic extremity in a diabetic is best left open since neither bacterial flora nor blood supply favors infection-free healing. The next consideration in establishing a treatment plan for the wound is based on the mechanism of wounding. Highvelocity gunshot wounds, crush injuries, close-range shotgun wounds, and high-energy open fractures are all characterized by extensive soft tissue destruction and are frequently complicated by wound infection.39 Heavily contaminated wounds such as human bites, farming-related accidents, and wounds with gross contamination, especially soil, are at exceedingly high risk for subsequent wound infection and are best managed open. These contaminated wounds are at risk for tetanus and the patient should receive tetanus prophylaxis. Tetanus prophylaxis is detailed in Table 47-3, while Table 47-4 reviews the characteristics of a wound that is tetanus prone. Guidelines have been published detailing the indications and considerations for tetanus and other vaccines following traumatic injuries.40 In addition to local wound factors, systemic conditions can also increase the incidence of wound infection. Hemorrhagic shock has been identified as a strong risk factor for wound infection.41,42 This phenomenon is likely multifactorial since trauma and hemorrhage affects blood flow on both the global and tissue levels and causes immune,43 hemtapoeitic,44 and myelopoeitic45 bone marrow dysfunction. Diabetes,46 connective tissue disorders,47 advanced cancers,48 immunosuppressed states, atherosclerosis, hypothermia, malnutrition,49 COPD, corticosteroid therapy, and a multitude of other systemic disease processes all negatively impact

CHAPTER 47

■ Types of Wound Closure

of a skin graft or tissue transfer. In general, the simplest technique that will result in a closed wound should be employed so that a flap should not be done when a skin graft would suffice, and a free flap should be avoided if a rotational flap will be satisfactory. The timing of grafting or flapping is somewhat controversial and is best determined by the overall physiologic condition of the patient. Vascular anastomoses and exposed blood vessels are special cases and need to be covered as soon as possible to prevent catastrophic “blowouts.” In patients with an open abdomen it is highly desirable to get coverage of intestinal anastomoses with omentum, absorbable mesh, or the abdominal wall since uncovered they have a tendency to break down leading to devastating “enteroatmospheric fistulas.”38 Splitthickness skin grafts are usually applied 5 days after injury but this is based more on tradition than physiology.

903

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TABLE 47-3 Tetanus Prophylaxis

SECTION 4

Nontetanus-Prone Wounds History of adsorbed tetanus toxoid (doses) Unknown or less than three doses Three or more dosesb

TABLE 47-5 Threats to Infection-Free Wound Healing

Tetanus-Prone Wounds TIG Td Tda TIG Yes

No

Yes

Yes

Noc

No

Nod

No

Td, tetanus and diphtheria toxoids adsorbed (for adult use); TIG, tetanus immune globulin (human). Tetanus toxoid and TIG should be administered with different syringes at different sites. a

For children younger than 7 years old: diphtheria– tetanus–pertussis (DPT) vaccination (DT, if pertussis vaccine is contraindicated) is preferred to tetanus toxoid alone. For persons 7 years old or more, Td is preferred to tetanus toxoid alone. b

If only three doses of fluid toxoid have been given, a fourth dose of toxoid, preferably an adsorbed toxoid, should be given. c

Yes, if more than 10 years since last dose.

d

Yes, if more than 5 years since last dose.

wound healing and need to be considered in the wound treatment plan. Thus, the decision to close a wound is based on a series of assessments of the mechanism of injury, anatomic location, degree of contamination, and physiologic and medical condition of the patient.

TABLE 47-4 Wound Characteristics Relating to Likelihood of Tetanus

Depth Mechanism of injury

1 cm Sharp surface

Signs of infection Devitalized tissue Contaminants (dirt, feces, soil, etc.) Ischemic or denervated tissue

Absent

Tetanus-Prone Wounds 6 h Stellate wound, avulsion, abrasion 1 cm Crush, bum, missile wound, other Present

Absent

Present

Absent

Present

Clinical Features Age of wound Configuration

Nontetanus-Prone Wounds 6 h Linear

Necrotic tissue Inadequate hemostasis Foreign body Heavy contamination Local ischemia Local conditions Shock Systemic conditions Malnutrition Immunosuppression Shock Diabetes Renal insufficiency Steroids Cytotoxic drugs Vitamin and trace metal deficiency Collagen vascular disease

In addition to the factors predisposing to wound infection discussed above, additional variables leading to wound infections have been identified. These threats to infection-free healing are listed in Table 47-5. Devitalized tissue is a common finding in high-velocity gunshot and high-energy wounds and represents a major risk factor for wound infection. Such tissue acts as a culture medium for bacteria, is poorly penetrated by immune cells and antibiotics, and incites an increased inflammatory response. Debridement is an effective way of removing this source of infection and inflammation and is an integral part of wound care.50 Meticulous hemostasis is often cited as a key component to normal wound healing; however, the rationale behind this statement is frequently omitted. Iron is an essential component for bacterial replication,51 so it is tightly regulated in vivo by sequestration in macrophages as well as by hepcidin, an ironbinding protein released by the liver in response to inflammation.52 Wound hematomas lead to increased infections by overwhelming the body’s ability to restrict iron and inhibit bacterial growth, and thus render a wound susceptible to infection by smaller bacterial numbers. In a similar fashion, foreign body contamination also leaves a wound more susceptible to smaller bacterial burdens by reducing granulocyte phagocytosis. If adequate hemostasis cannot be obtained due to coagulopathy or extensive injury or if debridement is inadequate, it is best to postpone primary closure until these conditions are corrected. Such wounds can be managed as open wounds and then treated by delayed primary closure at the bedside or taken to the operating room for further debridement and eventual closure.

■ Operative Versus Nonoperative Absent

Present

Wound Management

Similar to the decision process regarding closure of a wound, the setting of wound care is equally important. In general, large complex contaminated wounds containing foreign bodies or

Wounds, Bites, and Stings

TABLE 47-6 Conditions Requiring Management in Operating Room

devitalized tissue are best managed in the operating room. The anatomic location of the wound can be critical as well since perineal, facial, and severe hand injuries can have serious consequences if initially mismanaged. Noncompliant patients and those with hazardous communicable diseases are best treated in the operating room for safety reasons for the patient and clinician alike. Although a wound may be impressive, it is frequently the associated injury that is most threatening to the patient. A 2-cm neck wound is not impressive; however, it may lead to a disastrous sequence of events if it overlies the carotid artery. In general, attempting to manage a major wound without adequate light, exposure, anesthesia, equipment, or patient cooperation leads to missed injuries, retained foreign bodies, inadequate debridement, wound hematomas, and soft tissue infections or worse. Table 47-6 summarizes some conditions mandating operative management of a wound.

■ Operative Issues Once the decision is made to proceed to the operating room, the next step is to consider patient positioning and skin preparation. In general, the patient should be positioned in such a way so that access to other body cavities and surfaces is maintained. The lateral decubitus position offers excellent access to a hemithorax but does so at the expense of access to the contralateral chest and abdomen. Extremities are best fully prepped and free draped to maximize exposure and operative options. After positioning, the patient’s skin is prepared with an antiseptic. As part of this preparation, body hair may need to be removed to facilitate wound exploration and exposure and to prevent hair from becoming trapped in the wound and functioning as a foreign body leading to increased wound infections. Shaving hair should be avoided since it has been shown to lead to higher wound infection rates when compared with depilatories or clippers.53 While depilatories may be useful in elective surgery, they have little role in the management of urgent traumatic wounds; thus, surgical clippers with disposable heads should be readily available in the emergency department and operating room. Hair should be removed in an atraumatic fashion so as not to cause additional injury. Loose foreign bodies and debris should be removed as well. Eyebrows should not be removed since in a minority of patients their regrowth can be inadequate.54

■ Local Anesthetics Operative treatment of a wound gains the added benefit of effective analgesia and anesthesia administered by an additional clinician, the anesthesiologist. For wounds cared for in other venues, local anesthesia plays a crucial role, and is typically administered by the clinician caring for the wound. Local anesthesia facilitates excision of devitalized tissue and removal of foreign bodies, and enhances patient comfort and cooperation during closure of the wound. Most local anesthetics work by binding neural cell membrane sodium channels to block depolarization and conduction of noxious stimuli. These drugs are weak polar bases that are structurally composed of an aromatic, hydrophobic ring, a hydrophilic tertiary amino group, and an intermediary chain. It is the presence of an ester or amide linkage in the intermediary chain that is used to broadly classify the

CHAPTER 47

Large or complicated soft tissue injury Extensive amount of necrotic or ischemic tissue Heavy contamination Associated injury Visceral Vascular Fracture Perineal wounds Compartment syndrome High-pressure injection injuries

The most common skin antiseptics are povidone–iodine solution (Betadine®) and chlorhexidine gluconate solution (Hibiclens®). Both agents are rapidly bactericidal; however, emerging evidence shows that chlorhexidine is a superior prep agent since it has more residual activity and is associated with lower rates of infection.55–57 A 2% chlorhexidine in 70% alcohol solution has been shown to be the most efficacious form of chlorhexidine and is now available commercially (ChloraPrep®).58 Both povidone–iodine and chlorhexidine are toxic to normal tissue, so they should only be used as preparatory agents rather than topical wound treatments.59 Ambroise Pare admonished against putting anything into a wound that would not be tolerated in one’s eye, but this is especially true for chlorhexidine since it causes direct corneal injury.60,61 Povidone–iodine or hexachlorophene solution (PHisoHex®) should be used for prepping the face to avoid corneal damage and possible blindness.62 One of the hallmarks of operative management of heavily contaminated wounds centers on the use of high-pressure pulse lavage systems. In the past, it was felt irrigation had to be performed at high pressure in order to effectively remove microparticulate contaminants and bacteria.63 Lavage of contaminated wounds with a bulb syringe or low-pressure systems was thought to be ineffective. While commercially available high-pressure irrigating systems are undoubtedly effective, their destructive effects on already injured tissues are frequently overlooked. In addition to the increased devitalization of the wound, high-pressure irrigation can also have detrimental effects on immune function and wound healing.64 Emerging evidence suggests that in addition to local trauma, highpressure irrigation may not be as effective in removing contamination as gentler methods and may in fact drive bacteria deeper into tissues.65 Sharp debridement, curettage, suction, and irrigation of all nonvariable and grossly infected tissues should be undertaken until the wound is left with only clean, healthy, and well-perfused tissues. Outside of the operating room, one of the simplest irrigation systems can be made by punching several holes in the top of a 0.5-L bottle of saline utilizing an 18-gauge needle. Alternatively, a syringe and angiocatheter can be fashioned into an effective irrigator as demonstrated in Fig. 47-2.

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SECTION 4 FIGURE 47-2 Technique for high-pressure syringe irrigation of a wound.

local anesthetics.66 Ester local anesthetics are rapidly metabolized by plasma pseudocholinesterases and the resultant hydrophilic metabolites are renally excreted. In contrast, amide anesthetics are metabolized by the liver, so their clearance is a much slower process and the potential for adverse effects is greater due to accumulation of the drug or impaired clearance secondary to hepatic dysfunction.67 The lipid solubility of a local anesthetic is proportional to the drug’s potency while its protein binding helps regulate its duration of action. The duration of action of local anesthetics may be enhanced by the addition of dilute concentrations of epinephrine in order to cause vasoconstriction and impair the clearance of the drug from the tissues. The addition of epinephrine to the local anesthetic increases the maximum dose since vasoconstriction reduces systemic absorption. Obviously, local anesthetics containing epinephrine should not be injected into tissues perfused by end arterioles such as the fingers, toes, nose, penis, or ear since vasoconstriction may result in tissue necrosis. Although some recent literature has challenged this dogma, it is still prudent to avoid this complication altogether.68,69 Inadvertent intravascular injection is another potential pitfall when using these agents; thus, the syringe should be aspirated slightly to exclude this possibility prior to injecting the drug. Lastly, there is some concern that the injection of

epinephrine into a contaminated wound may result in an increased incidence of wound infection.70 Injections of local anesthetics are inherently painful; however, several simple techniques can be utilized in order to minimize patient discomfort. Small-gauge needles, as fine as 30 gauge, should be utilized and the drug administered by a technique of slow infiltration. Beginning the process through the existing break in the dermis rather than injecting into intact skin can also lessen pain. Intradermal injections should only be administered when needed and only after attempts of subdermal administration fail. Perhaps the most effective method for reducing the pain associated with local anesthetics can be achieved through the addition of sodium bicarbonate to buffer the pH of the anesthetic (49–52).71–74 What remains puzzling is why this well-described and efficacious technique is so underutilized in medicine today.75 Shortly after Carl Koller popularized the local anesthetic properties of cocaine in 1884, clinicians began noting serious unintended side effects.76 While cardiac toxicity is most pronounced with cocaine, it is seen with all local anesthetics and is related to their effect on sodium channels in excitable membranes. Like the cardiovascular system, the central nervous system (CNS) also contains excitable cell membranes and is the other major site of local anesthesia toxicity. Increasing concentrations of local anesthetics lead to blockade of the inhibitory pathways in the amygdala and result in excess neural stimulation.77 Local anesthetic CNS toxicity is initially manifested as muscle twitching, tinnitus, and agitation that can progress to seizures, coma, and death as levels continue to rise. The cardiovascular system is relatively more resistant than the CNS to local anesthetic toxicity but arrhythmias and cardiovascular collapse are the most feared complications of local anesthetic use. Unfortunately, as the potency of a local anesthetic increases, so does its potential for cardiac depression and arrhythmias.78 This observation is borne out by the fact that the potent anesthetic bupivacaine exerts a greater degree of cardiac toxicity than the weaker related amide anesthetic lidocaine (see Table 47-7 for a review of the symptoms of local anesthesia toxicity). Lidocaine and bupivacaine are the two most commonly used local anesthetics in the United States. Both are amide-type anesthetics and are available in combination with dilute concentrations of epinephrine (1:100,000 to 1:400,000) that

TABLE 47-7 Symptoms of Local Anesthetic Overdose Central nervous system Excitability Dizziness Tinnitus Nystagmus Seizures Cardiopulmonary Hypotension Myocardial collapse Respiratory arrest

Wounds, Bites, and Stings

907

TABLE 47-8 Local Anesthesia Class Amide

Onset 1–5 min

Duration 30–120 min

Amide

2–10 min

3–7 h

Maximum Dose 4.5 mg/kg, 7–8 mg/kg with epinephrine 175 mg, 0.3 mg/kg (not for use in children)

Metabolism Liver Liver

lessens systemic absorption of the anesthetic due to vasoconstriction. As a result, the maximum dosage for lidocaine for infiltrative anesthesia goes from 4.5 mg/kg for plain lidocaine to 7 mg/kg when it is combined with epinephrine. The best way to avoid local anesthetic toxicity is to be cognizant of the total dose being administered. Bupivacaine is far more potent, as well as toxic, than lidocaine due to its lipophilicity. It also has a much longer onset of action than lidocaine; thus, lidocaine is the most commonly used local anesthetic in clinical medicine. Lidocaine is occasionally administered in combination with bupivacaine in order to capitalize on lidocaine’s short onset of action coupled with the high potency and long half-life of bupivacaine (please refer to Table 47-8 for a summary of both agents). For large areas where the dose of anesthetic required to achieve anesthesia would be prohibitive or areas that are technically difficult to infiltrate, a regional block may be an excellent way to achieve anesthesia.79 Local blocks can be more efficacious than infiltrative anesthesia with less pain and a smaller volume of anesthetic used. Knowledge of the neural anatomy relevant to the sensory innervation of the region to be blocked is critical and allows complete anesthesia of the region of interest. Two of the most commonly employed peripheral blocks are the median and ulnar nerve blocks that are reviewed in Figs. 47-3 and 47-4, respectively. Fig. 47-5 illustrates the ubiquitous digital block that is an extremely helpful technique utilized in the management of trauma to the fingers.

■ Antibiotic Usage for Acute Wounds

FIGURE 47-3 Technique of median nerve block anesthesia.

FIGURE 47-4 Technique of ulnar nerve block anesthesia.

For over 50 years, it has been known that administering an antibiotic well in advance of bacterial inoculation is a highly effective method of reducing wound infection; however, when dealing with traumatic wounds, this is simply not possible. Since traumatic wounds are always contaminated with bacteria prior to their clinical presentation, the use of antibiotics for acute wounds is considered empiric rather than prophylactic. Accordingly, there is little role for empiric antibiotics in the management of open wounds except for a few special circumstances. Although controversial, most clinicians would agree to the use of antibiotics in the following situations: 1. Open fractures or open joints. An open fracture, defined as communication of a fracture site with the outside environment through an associated wound in the skin, can have devastating long-term consequences if nonunion or osteomyelitis sets in. Similarly, bacterial destruction of the articular surfaces of a joint can also lead to significant morbidity. Accordingly, these wounds are best treated with antibiotics; however, in this capacity the antibiotics are an adjunct to basic wound and fracture care consisting of

CHAPTER 47

Name Lidocaine HCI (xylocaine, dilocaine, nervocaine) Bupivacaine (marcaine, sensorcaine)

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Specific Challenges in Trauma

SECTION 4 FIGURE 47-5 (A) Method of executing a digital block. (B) Position of skin wheals and level of cross-section.

surgical debridement, joint irrigation, and fracture fixation.80–83 2. Heavily contaminated extensive soft tissue wounds. Similar to traumatic orthopedic injuries, antibiotics serve an adjunctive role in the management of heavily contaminated soft tissue injuries. However, the mechanism of injury and degree of contamination remain far more predictive of subsequent wound infection than the choice of antibiotic.84 Data are lacking about the duration of antibiotic usage in such wounds, but in general the shorter the course, the better. 3. Delayed presentation. Traumatic wounds that present in a significantly delayed fashion are well along on the continuum from contaminated to infected and likely would benefit from antimicrobial therapy. 4. Host factors. Patients with profound immunosuppression, indwelling foreign bodies such as mechanical heart valves, and those unable to tolerate transient bacteremias are all likely to derive benefit from antibiotic therapy in the management of an acute wound. This decision is not based on evidence-based recommendations but rather on clinical judgment since trials of efficacy in these populations will never be undertaken for ethical reasons.

■ Wound Dressings Rather than delve into the seemingly infinite number of wound gels, foams, and dressings individually, we will approach the topic of wound dressing in a similar fashion to the chapter as a whole: focusing on general ideas and concepts rather than specifics. This decision is in fact a necessity since despite the tremendous number of wound products available, there is a paucity of large, randomized prospective controlled trials comparing various dressings with each other.85 For over

100 years, the benefits of keeping a wound moist have been known86; however, it was not until the seminal article by Winter in 1962 showing that an occlusive dressing led to 40% faster healing than wounds left open to air did the concept of “wet” wound healing take hold.87 Unfortunately, for many clinicians the choice of wound dressings is based on tradition and experience rather than data88 and one of the most painful, labor-intensive dressing remains the most commonly used: the wet to dry gauze dressing. This dressing is composed of salinemoistened gauze in close contact with the wound covered by several layers of dry gauze. By the time this dressing is changed, it typically dries out and sticks to the wound so that when it is removed it debrides the wound of necrotic tissue, secretions, and bacteria while causing significant pain and occasional bleeding. One particularly useful type of dressing is a modification of the technique used on split-thickness skin graft donor sites to treat asphalt abrasions or “road rash.” Road rash is a common finding after motorcycle or bicycle collisions, ejection from automobiles, or in pedestrians struck by automobiles. These wounds are typically contaminated with small stones, dirt, and other road substances and can present a serious challenge to the treating physician. For patients with small wounds, a combination of a topical viscous lidocaine solution with systemic analgesics can facilitate scrubbing and debridement; however, extensive wounds are best managed in the operating room. After adequate anesthesia, the wound can be scrubbed clean of all foreign bodies using a presurgical scrub brush. Failure to fully debride the wound will lead to “tattooing” or retention of foreign bodies in the healing wound causing discoloration. Following debridement, the wound can be treated like a donor site; hemostasis is achieved through the application of epinephrine-soaked lap sponges followed by a petrolatum-impregnated dressing that will adhere to the wound. This dressing can then

Wounds, Bites, and Stings

1. Encourage a moist but not macerated wound environment. As discussed earlier, moist wound healing is far superior to dry wound healing; however, a major concern surrounds avoiding skin maceration. Macerated skin can serve as a portal of entry for skin bacteria and may lead to infection. 2. Avoid the presence of toxic substances. Previously we have learned that povidone–iodine, chlorhexidine, acetic acid solutions, and dilute sodium hypochlorite solutions (Dakin’s) all exhibit some degree of fibroblast or keratinocytes toxicity and should be avoided. 3. Avoid leaving foreign bodies in the wound. Foreign bodies are undesirable because they retard phagocytosis and delay wound healing.89 4. Prevent bacterial contamination. The dressing must not be penetrable to the outside environment and bacteria. 5. Maintain optimal temperature and pH. Wound healing proceeds faster at physiologic temperature and pH.90 6. Require less frequent dressing changes. Many of the newer hydrocolloid, alginate, and foam dressings are very expensive. It is surmised that they may be cost-effective if the need for them to be changed is infrequent since skilled labor cost is one of the most expensive aspects of modern medical care. Regrettably, studies are still lacking. 7. Cause less patient discomfort. 8. Serve as a vehicle to deliver wound care adjuncts. Topical silver,91 anti-infectives,92 and growth factors93 have all been delivered by some of the newer surgical dressings.

■ Subatmospheric Sponge Dressings One of the biggest advances in wound management of the last decade has centered on the use of the “vac sponge.” Vacuumassisted closure of difficult wounds as initially described by Argenta and Morykwas94 consists of an open-cell foam sponge, connected to a controlled vacuum device. The sponge is covered by a thin, adhesive occlusive dressing so that the wound environment remains subatmospheric. Kinetic Concepts, Inc (KCI, San Antonio, Texas) has patented Argenta’s system (V.A.C.® system) and offers a vast array of vacuum dressing products and wound therapies such as ionic silver-impregnated sponges, irrigating vacuum systems, and polyvinyl alcohol sponges for use in tunnels and on top of skin grafts. The applications of this technology continue to grow and now several versions are commercially available. Subatmospheric dressings have to a large part simplified wound care, wound closures and reconstructions, and skin grafting as well. These dressings have been shown to speed up the development of granulation tissue95 and often allow a simple skin graft to be placed instead of a complex plastic surgery flap procedure. The reason why these dressings speed

up the healing process is poorly understood and may be related to reducing wound edema, increasing blood flow,95 increasing cellular proliferation,96 or removing inhibitor substances from the wound milieu. Additional benefits of these types of dressings include keeping the wound environment moist and drawing the edges of the wound closer together that presumably combined with the natural process of wound contraction leads to faster closure times and reduced wound size. In a recent systematic review of the use of negative pressure dressings, there was no clinically significant advantage when used in chronic wounds, but was associated with more wound healing, and in a faster time.97 Early reports reported that an infected wound was a contraindication to the use of a V.A.C. system; however, a significant body of literature is building on the role of such a device with infected wounds.98 Overall, while authors do not report any major complications, in general the V.A.C. system should be changed, and the wound reviewed by the clinician, more frequently than if the wound was not infected. Some centers advocate changing the V.A.C. as often as every 8 hours. Further, the system may be impregnated with silver in an effort to reduce the bioburden and to minimize the development of a biolayer. The use of silver has been demonstrated to have broad-spectrum antibacterial and antifungal properties. Silver has many mechanisms of action including inhibition of cellular respirations, denaturing nucleic acids, and altering cellular membrane permeability.99 However, the optimal dose of silver in any dressing is yet to be elucidated, with some authors expressing concern for the effect of silver on surrounding normal tissue viability.100 While negative pressure wound therapy represents a major advance in the wound care armamentarium for both acute and chronic wounds, it is not a panacea for all wounds. Failure to fully debride a necrotic wound before placing the sponge can lead to ongoing necrosis, infection, and clinical deterioration. The currently recognized contraindications to negative pressure wound therapy include wounds with necrotic tissue, malignancy within the wound, exposed arteries, veins, or vascular grafts, untreated osteomyelitis, and fistulas between epithelial surfaces. Wound ischemia and severe malnutrition are relative contraindications. Some physicians have reported success treating fistulas, and while this is an off-label use, it is rapidly becoming standard therapy.101

BITES AND STINGS ■ Human Bites Human bites may be the most common bites seen in many urban emergency rooms. The main clinical problem in human bites relates to soft tissue infection since human saliva contains up to 1011 bacteria/mL, and plaque on teeth has even greater numbers of bacteria. Common infecting organisms include Streptococcus viridans, Staphylococcus spp., Eikenella corrodens, Bacteroides spp., and microaerophilic streptococci. The most common serious infections develop when there has been penetration of the joint capsule, which typically occurs when a clenched fist strikes the tooth of the person being assaulted

CHAPTER 47

be trimmed as reepithelialization takes place underneath it, much like the donor site of a split-thickness skin graft. Wound dressings can be roughly broken down into several groups, including gauzes, semipermeable occlusive film dressings, foam dressings, alginates, and hydrocolloids, all of which are reviewed in Table 47-9. In general, the perfect dressing does not exist, but if it did, it would have the following properties:

909

SECTION 4 Material Cotton gauze

Functions Absorbs fluid, removes exudate with changes

Use Open or infected wounds

Examples Kerlix fluffs 4  4s

Disadvantage Frequent changes, foreign body in wound, desiccation if not kept moist Some seepage with heavily exudative wounds, difficult to seal wounds of complex shape, probably not indicated for infected wounds

Hydrocolloid

Hydrophilic colloidal particles with adhesive matrix (usually as a film or foam covered by a piece of release paper)

Full- or partialthickness wounds, decubitus ulcers, primary dressing for closed wounds

DuoDERM, Granuflex, Restore, Comfeel, IntraSite, Ultec, J & J ulcer dressing, Tegasorb, Dermiflex, IntraSite, Biofilm

Absorptive powders and pastes

Colloidal hydrophilic particles

Maintains moist wound environment with optimum temperature and pH, adherence without adhesion, promotes granulation and epithelialization, seals and protects wound, wound debridement by autolysis See above (“Hydrocolloid”)

DuoDERM granules, Hydrogran, Hollister exudate absorber, Geliperm, Spand-Gel

Probably not for use in infected wounds

Alginates

Calcium alginate fibers (brown seaweed species)

Absorbs fluid and exudate, maintains moist wound environment

Full-thickness wounds, deep angles, wound with heavy exudate Open or infected wounds

Sorbsan, Kaltostat, Tegagel, Ultraplast, Stop Memo

Not for use in wounds with little or no exudate as it does not form a gel

Films

Semipermeable membranes (polyurethane or copolyester)

Occlusive dressing

IV site dressings, partial-thickness, minimally exuding wounds

Opsite, Opsite 3000, Tegaderm, Bioclusive, Blisterfilm, Visulin

Highly variable water vapor permeability among different products; not for use alone in heavily exuding wounds; skin maceration with bacterial overgrowth in products with low H2O permeability

Advantages Readily available

Optimal wound environment, improved healing of some wounds, infrequently needs changing, decreased pain, no foreign body residual High absorbancy, debridement with autolysis (see “Hydrocolloid” above) May be used in infected or contaminated wounds, infrequent dressing changes Mimics skin performance, seals wound, may be used in combination with other dressings (i.e., alginates)

Specific Challenges in Trauma

Classification Gauze

910

TABLE 47-9 Wound Dressing Materials

Wounds, Bites, and Stings

■ Cat Bites Cat bites, like human bites, tend to be heavily contaminated. Cats tend to leave deep, small punctures that may penetrate all the way to bone. Commonly isolated organisms include Pasteurella multocida and Staphylococcus spp. Ampicillin plus a beta-lactamase inhibitor provides reasonable empiric coverage and tetanus and rabies prophylaxis should be given if indicated (Tables 47-3, 47-4, 47-10, and 47-12).

■ Dog Bites Dog bite wounds are another common clinical problem. Wound concerns center around injury to soft tissue since large dogs can generate tremendous force with their muscles of mastication. Soft tissue infections following dog bites are not as common as after cat and human bites, but they do occur. The bite wound should be copiously irrigated, and empiric preventive antibiotics are generally recommended. Facial dog bite wounds are usually closed, while wounds in other locations are managed with delayed primary closure or healing by secondary intention. Common infecting organisms include P. multocida, S. viridans, Bacteroides spp., Fusobacterium, and Capnocytophaga. As in the case of human and cat bite wounds, ampicillin plus a beta-lactamase inhibitor provides reasonable empiric coverage

for dog bite wounds. Tetanus and rabies prophylaxis should be administered if indicated (see Tables 47-3, 47-4, 47-10, and 47-12).40

■ Rabies Prophylaxis A number of different strains of highly neurotropic viruses cause clinical rabies infection. Most of these viruses belong to a single serotype in the genus Lyssavirus, family Rhabdoviridae. The virion contains a single-stranded, nonsegmented, negativesense RNA genome, which encodes for five structural proteins.102 Guidelines for the administration of rabies vaccine as well as for tetanus among others vaccines following traumatic injuries have been published by the Surgical Infection Society of North America.40 Susceptibility to rabies infection varies according to species, although most wild mammals can become infected with the virus. Foxes, coyotes, wolves, and jackals are most susceptible; skunks, raccoons, bats, bobcats, mongooses, and monkeys are intermediate; and opossums are surprisingly resistant.102 In the United States, rabies is found in terrestrial animals in 10 distinct geographic areas. In each of these areas, one species is the predominant reservoir, with one of the distinct antigenic variants predominating. Bats account for an additional eight variants, accounting for sporadic outbreaks throughout the United States. The majority of the cases of rabies encephalitis acquired in the United States probably originate from exposure to bats. The epidemiology of human rabies reflects the geographic distribution of animals, emphasizing the fact that rabies is primarily a disease of nonhuman mammals. Vaccination programs for domestic animals in the United States have been responsible for a dramatic decline in rabies acquired from domestic dog and cat bites (Tables 47-10 and 47-11). Internationally, the majority of human rabies is still acquired from dog bites, where canine rabies is still endemic.102 In humans, the established disease is almost always fatal. The diagnosis is relatively straightforward when a history of an animal bite is obtained; however, the history of a probable bite is inconsistently reported. Clinical symptoms of human rabies include pain at the bite site, dysphagia, pharyngeal spasms, paralysis, hydrophobia, and seizures. Distinguishing rabies from other causes of viral encephalitis or tetanus can be difficult. An effective vaccine is available for preventing the onset of clinical rabies. The dismal prognosis of rabies encephalitis emphasizes the importance of appropriate use of the vaccine and Ig preparations to prevent infection. The risk of acquiring rabies depends on the probability of rabies infection in the animal and the amount of inoculum delivered into the wound, with the greatest risk from a bite. All animal wounds should be irrigated and cleansed with soap or a detergent. This has been shown to protect 90% of experimental animals from infection following inoculation of rabies virus into a wound. Because public health officials monitor the incidence of rabies in populations of domestic and wild animals, a treating physician should be familiar with the local incidence of rabies in his or her region. Several historical clues may be of benefit in determining the likelihood that the animal was rabid. If the bite

CHAPTER 47

(“fight bite”). These wounds usually involve the metacarpophalangeal (MCP) or the proximal interphalangeal (PIP) joints. These are usually benign-appearing wounds and are frequently missed unless the examiner is aware of the potential problems of joint penetration. Such wounds may not be directly over the MCP joint unless the hand is examined with the fist clenched. These wounds should be seen in consultation with a hand surgeon and are usually best treated with intraoperative irrigation, intravenous antibiotics, and elevation of the hand and arm but should not be treated on an outpatient basis. In general, human bites should not be closed, with the exception of wounds on the face. Antibiotic prophylaxis for human bites consists of ampicillin plus a beta-lactamase inhibitor (intravenous ampicillin/ sulbactam or amoxicillin/clavulanate). Alternative agents include cefoxitin or ampicillin alone or in combination with clindamycin. Although the incidence is unknown, hepatitis and infection with human immunodeficiency virus (HIV) are potentially transmissible by human bites. As with other exposures, the risk of infection depends on the size of the inoculums and the virulence of the viral agent. HIV exists in relatively low concentrations in human saliva and is relatively fastidious, presumably making its transmission difficult. Hepatitis B and C require a much smaller inoculum, and their transmission in a human bite is theoretically a greater risk. If the individual responsible for the bite is known or available for evaluation, serologic testing for HIV and hepatitis B and C is recommended. If the individual responsible for the bite is unavailable for testing, the administration of gamma globulin and hepatitis B vaccination should be considered in nonimmunized patients. Tetanus immunization should be given if indicated40 (see Table 47-4).

911

912

Specific Challenges in Trauma

TABLE 47-10 Treatment Recommendations and Estimates of the Risk of Rabies, According to Type of Exposure and Geographic Area

SECTION 4

Geographic Area Group 1: rabies endemic or suspected in species involved in the exposure

Group 2: rabies not endemic in species involved in the exposure, but endemic in other terrestrial animals in area

Animalsa Bats anywhere in the United States; raccoons, skunks, foxes; mongooses in Puerto Rico; dogs in most developing countries and in the United States along Mexican border (3–80% rabid) Most wild carnivores (wolves, bobcats, bears) and groundhogs (2–20% rabid)

Dogs and cats (0.1–2% rabid) Rodents and lagomorphs except groundhogs (about 0.01% rabid) Group 3: rabies not endemic in species involved in the exposure or in other terrestrial animals in the area

Dogs, cats, many wild terrestrial animals in Washington, Idaho, Utah, Nevada, Colorado (0.1–0.01% rabid)

Treatment Recommendationsb,c Bite No Bite Treat Treat

Cases of Rabies/10,000 Untreated Exposuresc Bite No Bite 0.3–160 150–5,000

Treat

Treat or consult

10–1,200

0.2–40

Observe or consult Consult or do not treat Consult or do not treat

Observe or consult Do not treat

0.5–120

0.01–4

0.05–0.6

0.001–0.02

Consult or do not treat

0.05–6

0.001–0.2

a

Percentages are the approximate proportions of indicated species found rabid when submitted and tested in state health department laboratories. b

“Consult” denotes consultation with a state or local health department. If the risk of rabies in the species involved in the exposure is low and the animal’s brain is available, treatment is sometimes delayed up to 48 hours pending the results of laboratory testing. A healthy domestic dog or cat that bites a person should be confined and observed for 10 days. Any illness in the animals should be evaluated by a veterinarian and reported immediately to the local health department. If signs suggestive of rabies develop, treatment is begun immediately. If the animal is a stray or unwanted dog or cat, it should be killed immediately and the head removed and shipped, under refrigeration, for examination by a qualified laboratory. c

Rabies develops in 50–60% of untreated humans bitten by a rabid animal, and in 0.1–2% of those exposed to a rabid animal but not bitten (scratched or licked on an open wound or mucous membrane). The number of cases per 10,000 untreated patients was derived by multiplying the prevalence of rabies in a geographic area by the proportion of untreated humans in whom rabies would be expected to develop after exposure to a rabid animal. Reproduced with permission from Fishbein D, Robinson L. Rabies. N Engl J Med. 1993;329:1635. Copyright © 1993 Massachusetts Medical Society. All rights reserved.

was unprovoked or the animal was behaving erratically prior to the bite, the chance of rabies inoculation is increased. Bites from most wild carnivores, skunks, raccoons, and bats should be considered as rabid, while bites from immunized animals should be considered low risk. Healthy dogs and cats in nonendemic areas are low risk. Tables 47-10 and 47-12 summarize recommendations regarding the risk of transmission of rabies and treatment. If there is any question concerning prophylaxis, public health officials should be promptly consulted.

■ Snakebites Snakebite is a challenging but rare problem that is more common in the Southern United States and Mexico than elsewhere in North America. Like most other traumatic illnesses, it is more common in men than it is in women. Approximately 50% of patients are bitten during recreational activity or while working outdoors, while the remaining half are bitten by pet snakes or snakes being handled for some other reason.

Wounds, Bites, and Stings

913

TABLE 47-11 Human Rabies Cases in the United States by Exposure Category, 1946–1995a Domestic 86 21 6 6 2

Unknown (%) 26 (22) 10 (26) 2 (13) 11 (55) 14 (78)

Case Total 120 38 16 20 18

a

Through October 1995. Reproduced from Rupprecht CE, Smith JS, Fekadu M, Childs JE. The ascension of wildlife rabies: a cause for public concern or intervention? Emerg Infect Dis.. 1995;1:107–114. Available at: http://wwwnc.cdc.gov/eid/article/ 1/4/95-0401_article.htm.

Snakebites are responsible for an average of only 12 deaths per year in the United States with rattlesnakes causing the majority of severe envenomations. Venomous snakes indigenous to the continental United States are either crotalids, which include rattlesnakes, copperheads, and cottonmouths, or elapids, of which coral snakes are the only indigenous species in the United States (Table 47-13 reviews the common Crotalidae of North America). Since no evidence-based recommendations can be made for the treatment of snakebite, treatment recommendations are based on clinical series, animal studies, and common sense. While the clinical data are conflicting, the experimental animal data are clear. In this chapter, a treatment regimen for snakebite

is proposed, pertinent controversies are discussed, and a rationale for the treatment scheme is presented (Fig. 47-6).

Identification of the Snake Because the majority of snakebites in the United States are nonvenomous, an attempt should be made to identify the snake. This is possible by history as well as direct observation, particularly if the victim brings the snake to the emergency department for this to occur. If at all possible, the snake should be identified by someone knowledgeable in herpetology and no identification should be attempted by hospital personnel unless the snake is dead or completely contained. For patients who are snake handlers or those bitten by pet snakes, the patients

TABLE 47-12 Schedule of Prophylaxis Recommended in the United States After Possible Exposure to Rabies Vaccination Status Not previously vaccinated Local wound cleansing Rabies immune globulin

Regimena

Vaccine

Immediate cleansing with soap and water 20 IU/kg of body weight (if anatomically feasible, up to half the dose be infiltrated around the wound or wounds and the rest should be administered intramuscularly in the gluteal area. Never give more than the recommended dose. Do not use the syringe used for vaccine or inject into the same anatomic site) 1.0 mL of HDCV or RVA intramuscularly in the deltoid areab on days 0, 3, 7, 14, and 28

Previously vaccinatedc Local wound cleansing Rabies immune globulin Vaccine

Immediate cleansing with soap and water Should not be given 1.0 mL of HDCV or RVA intramuscularly in the deltoid areab on days 0 and 3

a

The regimens are applicable to all age groups, including children.

b

The deltoid area is the preferred site of vaccination for adults and older children. For younger children, the outer aspect of the thigh may be used. Vaccine should never be administered in the gluteal area. c

“Previously vaccinated” indicates previous vaccination with HDCV or RVA, or any other type of rabies vaccine and a documented history of antibody response. HDCV, human diploid cell vaccine; RVA, rabies vaccine adsorbed. Reproduced, with permission, from Fishbein D, Robinson L. Rabies. N Engl J Med. 1993;329:1636. Copyright © 1993 Massachusetts Medical Society. All rights reserved.

CHAPTER 47

Years 1946–1955 1956–1965 1966–1975 1976–1985 1986–1995a

Exposure Source Wildlife Other 8 0 7 0 7 1 1 2 2 0

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Specific Challenges in Trauma

TABLE 47-13 Crotalidae of North America

SECTION 4

Genus Agkistrodon

Common Name Moccasins, copperheads

Characteristics No rattles, large plates on crown

Crotalus Sistrurus

Rattlesnakes Massasaugas and pygmy rattlesnakes

Rattles, small scales on crown Rattles, large plates on crown

themselves will be the best resource to identify the type of snake. Fig. 47-7 summarizes the physical characteristics of crotalid snakes. The three important genera of Crotalidae in the United States are Crotalus and Sistrurus (rattlesnakes) and Agkistrodon (copperheads and water moccasins; Table 47-13). These snakes are characterized by a broad triangular head, relatively thick body, elliptical pupils, and facial pits. All but one species of rattlesnakes have rattles, which distinguishes them from copperheads and water moccasins. The only other snakes of clinical importance in the continental United States are the coral snakes. The two species of these that are common to the United States are Micrurus fulvius fulvius (Eastern coral snake) and the Micrurus fulvius tenere (the Texas coral snake). The Sonoran coral snake (Micrurus euryxanthus) is present in a small area of Southern Arizona, but is mostly indigenous to Mexico. These snakes are brightly colored, with red, yellow, white, and black rings. They are relatively small bodied and have small nontriangular heads without facial pits. Their rings encircle the

Range North America, Southeastern Europe, Asia North, Central, and South America North America

body and the mouth area is black. Their characteristic coloring pattern of a red band adjacent to a yellow one distinguishes coral snakes from other snakes that are brightly colored but nonvenomous, which is the justification for the idiom, “Red on yellow, kill a fellow, red on black, venom lack.” Coral snakes belong to the family Elapidae, or elapid, which includes cobras, kraits, mambas, and the poisonous snakes of Australia. Coral snakes tend to be secretive, burrowing, and nonaggressive, accounting for the low incidence of bites by these animals. They do not have large fangs, and when they do bite, they tend to chew on the offending animal or part.

Crotalid Envenomation An assessment for envenomation must be made in cases of bites by poisonous snakes. If there are no fang marks, envenomation is not possible and even with the presence of fang marks, approximately 20–25% of patients will not have been envenomated. It is estimated that another 50% have minimal to mild

FIGURE 47-6 Algorithm for the treatment of snakebite, only in a setting in which anaphylaxis can be treated.

Wounds, Bites, and Stings

First Aid

FIGURE 47-7 Characteristics of poisonous and nonpoisonous snakes.

envenomation, which would not be a threat to life or limb. Agkistrodon (moccasin and copperhead) bites tend to be less severe than rattlesnake bites and rarely require antivenin or invasive treatment. With rattlesnake bites, it is usually easy to assess whether envenomation has occurred. Crotalid venoms are a mixture of enzymes, polypeptides, and glycosylated peptides that have broad biologic actions; however, one of the common features of these venoms is local tissue destruction. This locally destructive action is an accurate marker of the degree of envenomation. A great deal of pain, edema, and frequently discoloration or formation of bullae is associated with envenomation. Recent data appear to point to the presence of metalloproteinases in crotalid venom as a major source of local and systemic adverse effects.103 Given the relatively rare nature of severe envenomation, there is little in the literature pertaining to scoring the severity of the injury. One group has proposed and validated a Snakebite Severity Score (SSS).104 This takes into account not only the potential for the dose of the envenomation but also the variability in response between patients. The scoring system reviews both the local wound of the bite and any possible systemic (pulmonary, GI, cardiovascular) symptoms, and was useful in determining the level and type of care needed. Since the signs and symptoms of envenomation have a rapid onset, it is probable that if by the time the patient arrives there

First aid is defined as the care delivered to the patient prior to arrival in the hospital. “First do no harm” should be loudly emphasized for first aid in the treatment of snakebites. A large number of first aid measures have been proposed for the treatment of venomous snakebites, and many, if not most, have carried a high risk of harm to the patient. The atmosphere at the scene of a snakebite is usually characterized as chaotic at best, punctuated by poorly trained first aid providers. This combination sets the stage for a therapeutic disaster if overly aggressive therapy is initiated at the scene of the bite. The most common potentially harmful treatments include incision and suction, electrical shock therapy, use of tourniquets, and limb immersion in ice. Incision and suction have been shown experimentally to remove subcutaneously injected venom from animals; however, unless this is done very soon after envenomation, the yield of extracted venom is low.105 The risk of incision and suction is significant when one considers that the person making the incision is probably doing it for the first time, the patient is in pain and unanesthetized, and there is probably no knowledge of anatomy by either person involved in the procedure. It should also be remembered that 25% of the victims of snakebite will have no envenomation or a trivial one. For these reasons, incision and suction has fallen into disfavor as a first aid measure. In a series of letters to the editor of the Lancet, a group of physicians practicing medicine in Ecuador advocated the use of electrical shock therapy for snakebite. They presented a series of 34 patients who were treated with electrical current using a modification of a stun gun.106 A stun gun is a personal protective device that delivers an extremely high voltage with very little current, which when used on attackers, temporarily disables them. The Ecuadorean investigators used this device on a group of patients with snakebite, probably from Bothrops atrox. All of the patients were said to have fared well, with immediate improvement. Follow-up in this series was not described, and there were no controls. This report led to the widespread use and indeed to the marketing of the stun gun for use in human snakebite. This treatment is typical of snakebite therapy throughout history. A theoretical treatment plan, usually with the potential for great pain or harm, is proposed, implemented,

CHAPTER 47

is no edema or pain, a significant envenomation has not occurred, or the patient was bitten by a moccasin or copperhead. These points are emphasized because no treatment advocated for a rattlesnake bite is free of risk (most actually have a relatively high risk) and because, in the absence of envenomation or with mild exposure only, supportive care alone will suffice. This point is one that makes evaluation of the snakebite literature difficult. If the clinical series in question includes a large number of Agkistrodon bites or patients with mild envenomations, the outcome will almost always be favorable, regardless of the treatment applied. The real concern in the treatment of snakebite relates to the patient with a severe envenomation associated with extensive destruction of local tissue or systemic signs of toxicity. The outcome for this type of patient is harder to assess from clinical series involving humans.

915

916

Specific Challenges in Trauma

SECTION 4

and adopted without any degree of scrutiny. Several controlled animal studies have now shown electrical shock therapy to be ineffective in the treatment of snakebite. Ice therapy for snakebite has been advocated on the basis of decreasing the optimal temperature range for the enzyme component of the venom, and thus decreasing local tissue damage.107 This topic has been hotly debated without any clear resolution; however, the weight of the evidence would suggest that ice therapy is not efficacious. It has the potential for harm in cases of snakebite, and its use is discouraged. While putting a topical ice pack on the wound carries no risk, it is immersion of the extremity containing a bite or adding salt to the ice that has been associated with problems. The use of a tourniquet has also been a debated issue in first aid for snakebite. A loosely applied venous tourniquet may decrease systemic absorption of the venom and delay the onset of symptoms; however, it certainly does not help the affected extremity and, if applied too tightly or if excessively tightened by the formation of edema, it carries the potential for causing great harm. Data from Australia suggest a treatment that would seem to be logical and safer that involves the application of a compression bandage and immobilization of the bitten extremity, instead of a tourniquet. With a compression bandage alone there is a great delay in the systemic absorption of venom.108 A splint and elastic bandage wrap or an inflatable air splint could also be used for this purpose. These measures have much less associated risk than placing a tourniquet on the involved extremity. In summary, immobilization, neutral positioning, and a compression dressing of some sort are recommended as first aid in cases of snakebite, followed by rapid transport of the patient to a hospital. If a skilled surgeon is present and there is a significant and obvious envenomation, immediate incision and suction or local excision of the bite wound may be considered.109

Definitive Care The care of the patient in the hospital is no less controversial than is first aid for snakebite.110 The principal debates center around: (a) the use of antivenin therapy, (b) aggressive debridement and fasciotomy, and, more recently, (c) observation with supportive care alone. For severe bites, antivenin use is favored along with the aggressive use of supportive care. Fasciotomy is reserved only in the treatment of compartment syndrome. The use of antivenin for mild or even moderate envenomations is not appropriate since the patient will almost certainly do well without any therapy. Immediate surgical debridement for the purpose of removal of venom and nonviable muscle is also not recommended. Experimentally, this approach does not remove the venom, and it is impossible to determine if muscle tissue is viable on the basis of the usual clinical criteria.111 Supportive care alone is not recommended for severe envenomations, although patients with all but the most massive envenomations could probably survive with aggressive modern intensive care and replacement of blood factors.112 In the case of rattlesnake bites there is a relatively effective treatment that limits the amount of tissue damage and systemic action of the venom if administered early. The problem is not efficacy but safety. Antivenin therapy carries a definite risk of anaphylaxis

and serum sickness; however, the risk of its use is outweighed by the potential benefits in victims with life- or limbthreatening bites.

Antivenin Therapy A polyvalent equine antivenin (Wyeth-Ayerst Laboratories, Marietta, Pennsylvania) and an ovine Crotalidae polyvalent immune Fab antivenin, consisting of cleaved Fab antibody fragments (CroFab; Protherics, Inc, Nashville, Tennessee), are currently commercially available for the treatment of crotalid envenomations. These products are manufactured by immunizing animals to crotalid venoms and then pooling the globulin fraction containing the antibodies. The ovine Fab product, CroFab, undergoes further modification by cleavage of the Fab antibody fragments and purification with affinity chromatography. Experimentally, antivenin has been shown to be effective in preventing death following the injection of rattlesnake venom. In an animal model, it also preserves muscle function and minimizes the systemic side effects of the venom. Like all antibody therapies, the equine antivenin is most effective if given immediately before envenomation; however, it is also effective when given after envenomation.111 It has also been shown to be effective if given up to 4 hours after envenomation, although there is little evidence to support its use beyond 4 hours. There have been anecdotal reports of clinical responses when it is given later than this, however, and it is recommended for use in life-threatening envenomations for up to 24 hours following a crotalid bite. Nevertheless, it must be emphasized that if antivenin therapy is going to be used, it should be used as soon as possible after envenomation. Although widely used clinically, there are significant problems with the unmodified polyvalent equine antivenin. It is a foreign, impure horse serum protein fraction and has been associated with severe and even life-threatening anaphylactic reactions. The exact incidence of such reactions is unclear, ranging from 1% to as high as 39%. The antivenin infusion should be started at a very slow rate and stopped with any signs of an allergic reaction. The antivenin may also cause a dosedependent, delayed-type serum sickness, which is much less severe than an anaphylactic response, although probably more common with massive infusions of antivenin. These side effects have fueled a debate over use of the antivenin. CroFab is an attempt to make the immunotherapy safer by purification of Ig and cleavage of the Fc fragment to produce Fab fragments.113 An increasing body of evidence supports the safety and efficacy of the Fab product, although additional postmarketing clinical data will ultimately be required.114 The Fab fragment has not been directly compared with other antivenin products. CroFab appears to be different than the older equine antivenin in that it probably requires repeat dosing in the immediate period after administration.113,114 In addition to being given as early as possible and in doses large enough to effect a difference, antivenin should not be administered in any setting in which anaphylaxis cannot be treated (i.e., in the field) and should initially be infused very slowly, with the infusion stopped with signs of hypersensitivity as noted earlier. The dose of antivenin to be given is empiric and based on the physician’s assessment of the amount of

Wounds, Bites, and Stings

TABLE 47-14 Treatment for Anaphylaxis

IM, intramuscularly; IV, intravenously; SQ, subcutaneously.

venom injected. The dose is the same in children as in adults, again being based on the amount of venom to be neutralized rather than on the weight of the patient. A minimum of 6–10 vials of CroFab is used for severe bites, although this amount is increased as needed. Various schemes have been devised for assessing the dose of antivenin based on the severity of envenomation. As the antivenin should not be used for mild or uncomplicated, moderate envenomations, these classification schemes are not clinically useful. Skin testing prior to antivenin administration should probably be eliminated and replaced by a very small, very slow intravenous injection of the antivenin, with constant monitoring for signs of anaphylaxis. The manufacturer recommends skin testing, but there have been anaphylactic reactions to the skin test, and the presence or absence of a wheal does not always predict anaphylaxis. The treatment of anaphylaxis is reviewed in Table 47-14.

Fasciotomy An ongoing debate during the past several decades has concerned the role of surgery in treating a rattlesnake bite. The theoretical rationale for surgical intervention is based on several observations. Crotalid venoms have very powerful, locally destructive effects. Part of the venom can be removed by incision and suction when this follows immediately after injection of the venom but intramuscular injection of the venom produces extensive edema that can lead to a compartment syndrome. These three observations lead to the conclusion that a rattlesnake bite is a local problem that should be amenable to local therapy (i.e., excision of the venom, dead muscle, and relief of a compartment syndrome). Excellent results have been claimed in clinical series in which this approach has been used.115 Unfortunately, no controlled trials have been conducted, and there are large series in which excellent results have been reported without operative intervention.116,117 An animal study performed in rabbits using an intracompartmental injection of western diamondback rattlesnake (Crotalus atrox) venom has yielded interesting results.111 In this study, animals were randomized to undergo fasciotomy with debridement alone, fasciotomy with antivenin alone,

Coral Snake Envenomation The symptoms of coral snake envenomation include local pain at the bite site, but the venom has primarily systemic effects consisting of respiratory depression and changes in CNS function.123 Antivenin and supportive care are the mainstays of treatment for coral snake envenomations. A commercially available antivenin exists for subspecies of Micrurus fulvius (the Eastern and Texas coral snake). This product probably has little cross-reactivity with the venom of M. euryxanthus (the Sonoran coral snake). Patients with fang marks or fang scratches should be admitted for observation. Any signs or symptoms should be treated with between three and five vials of antivenin. It is probably not wise to wait for full-blown systemic symptoms to develop before initiating treatment. If signs of respiratory distress develop, the patient should be treated supportively with intubation and mechanical ventilation as needed.

BITES AND STINGS BY MARINE ANIMALS ■ Marine Invertebrates Marine invertebrates, Cnidaria, are a heterogeneous group of phylogenetically primitive animals that are responsible for a

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1. Airway control 2. Epinephrine, 0.5 mg SQ (may be given IV with major anaphylactic reaction). May be repeated every 20 min 3. Volume expansion 4. H1 antagonists (diphenhydramine, 25–50 mg IV or IM) 5. H2 antagonists (ranitidine, 50 mg IV) 6. Glucocorticoids (hydrocortisone, 125 mg IV). No effect for several hours, but may prevent recurrence of symptoms 7. Inhaled β2 agonist for recurrent bronchospasm (albuterol, 0.5 mg) 8. Removal of bee stinger

fasciotomy with debridement plus antivenin, or to have no treatment. Antivenin therapy prevented loss of muscle and improved survival, while surgery alone did not. It was also clear that muscle that would have survived was removed in the group that had the combination of antivenin plus surgery, since late muscle function was significantly worse in this group than it was in that treated with antivenin alone. The authors concluded, therefore, that although the theory of local treatment of rattlesnake bite was attractive, it was not supported by the data. The issue of fasciotomy alone was not addressed in this study. Based on these unanswered questions, fasciotomy should be done infrequently, and should be reserved for the usual indication of compartment syndrome, which would only occur if there is an intramuscular or intracompartmental envenomation.112 Although rare, this does occur, being more common over the anterior leg, fingers, and the hand. If there is a tight compartment with evidence of compartment syndrome, a fasciotomy should be performed.112 No debridement should be done acutely, as injured muscle may be salvaged with immunotherapy. Supportive care should consist of fluid resuscitation, tetanus prophylaxis, appropriate monitoring, and the correction of coagulopathy. The bacteriology of rattlesnake mouths has been studied. Commonly present organisms include Pseudomonas spp., Enterobacteriaceae, Staphylococcus spp., and Clostridia.118,119 An extended-spectrum penicillin with a beta-lactamase inhibitor would provide reasonable empiric coverage; however, the weight of evidence supports not using empiric antibiotics.120,121 Coagulopathy due to fibrinolysis is a common complication of envenomation and should be corrected with fresh frozen plasma and cryoprecipitate. The patient’s prothrombin time/ international normalized ratio, partial thromboplastin time, fibrinogen concentration, and platelet count should all be monitored, with replacement therapy based on these values and evidence of clinical bleeding.122

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large number of sea-water envenomations.124 The phylum is divided into four major groups including Scyphozoa (true jellyfish), Hydrozoa (Portuguese Man o’ War and hydras), Anthozoa (corals and anemones), and Cubozoa (box jellyfish and sea wasps). All of these animals have specialized organelles known as nematocysts for poisoning and capturing prey. Most nematocysts cannot penetrate human skin and cause only a painful superficial skin reaction; however, full-thickness penetration can lead to serious illness and even death. Common manifestations of jellyfish stings include local pain and eruption, edema, urticaria, anaphylaxis, and, rarely, cardiorespiratory arrest. The principles in the management of such stings are to minimize the number of nematocysts being discharged and minimize the harmful effects of discharged nematocysts. Any adherent tentacles should be carefully removed. Unexploded nematocysts should be deactivated with a sodium bicarbonate slurry, papain (meat tenderizer), or a vinegar soak. The management of systemic side effects is largely supportive. Hypotension is treated with fluids and inotropic agents if necessary, while pain should be controlled with systemic narcotics. Calcium gluconate may improve the muscle spasms sometimes seen in cases of stings by marine invertebrates.

these fish have lived in the warm waters of South and Central America, with most reports of attacks emerging from Brazil. Reports have recently emerged of piranha located in lakes within the United States, with evidence of such fish as far north as Lake Winnebago in Wisconsin. It is speculated that this fish may have been dumped into the cold lake by illegal exotic fish traders to avoid getting caught. Rather than dying in the cold lake waters, it is theorized that they found an area of water that was just warm enough year-round to sustain the fish. The red-bellied piranhas (Pygocentrus nattereri) have established a fearsome reputation in the Amazon forests for attacking their victims in large groups. However, the reported medical literature differs from lay press anecdotal descriptions, in that the medical literature often relates victims sustaining only one or two bites. It is believed that these bites relate to the fish defending its brood.127 Further, many of the victims relate prior open wounds that may have attracted the fish to the swimmer in the first place. There are no reports of envenomation associated with these piranha bites, and if encountered, these wounds should be treated akin to any other dirty laceration, with good local wound care and antibiotics reserved for infected or heavily contaminated wounds.

■ Venomous Fish

■ Shark Bites

Most venomous fish are slow swimmers that are relatively nonmigratory and are not typically found in North American waters. Stingrays are the most clinically significant with regard to causing stings and envenomation. Typically this occurs when the stingray is stepped on by a swimmer. The wounds are a combination of laceration and puncture. Treatment consists of irrigation and soaking of the wound in warm water. Much of the venom may be removed by simple mechanical irrigation. Tetanus prophylaxis should be given; however, no antivenin exists for stingray envenomation.125 Travelers to tropical waters and aquarium workers may encounter other venomous creatures such as the blue-ringed octopus (Haplochlaena spp.), stonefish (Synanceia spp.), lionfish (Pterois volitans), and cone shells that posses potent venoms, some of which can be fatal to humans. Only an antivenin to stonefish toxin has been created, which is helpful in ameliorating the excruciating, narcotic-resistant pain associated with this venom.125 This antivenin may have some usefulness in the treatment of lionfish stings, which may be of particular interest to aquarium workers.126

The chance of being bitten by a shark is exceedingly rare but these wounds do occur in all coastal areas of the world.128 The principles described in Section “Clinical Management of Wounds” should be employed for the management of complex shark bite wounds. These wounds should be considered tetanus prone and preventive antibiotics are generally recommended, especially againstVibrio spp. and Aeromonas spp., in the management of these wounds.128

Piranha Attacks There has been a recent alarming increase in the number of reported piranha attacks within the United States. Piranhas belong to the subfamily Serrasalminae, and only four genera (Pristobrycon, Pygocentrus, Pygopristis, and Serrasalmus) are considered true piranhas. The characteristic feature that is most harmful to humans and other animals is the extremely sharp nature of their teeth. President Roosevelt, on a visit to Brazil, was afforded an opportunity to see their destructive nature up close. In his 1914 book Through the Brazilian Wilderness, he described these fish as “the most ferocious fish in the world … more formidable than sharks or barracudas.” Traditionally,

■ Insect and Bug Bites Insect bites are usually more of a nuisance than a serious medical problem, and most are not seen by a physician. Allergic reactions are the most common serious problem following insect bites. Because of their widespread distribution and proximity to humans, bees and wasps kill more people per year through fatal anaphylactic reactions to their venoms than do all other venomous animals combined. Fire ants were imported to Mobile, Alabama, in the early part of the 20th century. The black fire ant (Solenopsis richteri) was the first species to be imported from Uruguay and Argentina and has a limited range along the Mississippi– Alabama border. The red fire ant (Solenopsis invicta), which originates from Brazil and Northern Argentina, has had tremendous success in colonization and now has a range extending over most of the Southeastern United States.129 Its adaptability and aggressiveness have been remarkable. S. invicta tends to give multiple bites that are usually limited, but nearfatal cases of multiple bites have been reported. The bites of the imported fire ant have a typical appearance consisting of an initial vesicle, followed by the development of a sterile pustule. The venom of the fire ant is unique among that of venomous animals. It consists of 95% nonprotein alkaloid, in contrast to most other venoms, of which protein is a major component.

Wounds, Bites, and Stings

■ Spider Bites All spiders have a venom apparatus for killing other insects or spiders, although most pose no danger to humans. Of the two common species dangerous to humans in the continental United States, bites by the brown recluse spider (Loxosceles reclusa) are the most clinically significant. This is a brown spider with three pairs of eyes (dyads), one anterior and two lateral, with a violin-shaped carapace on its body, although this may be absent or difficult to discern.130 Usually, there is minimal pain following a brown recluse bite, which often makes exact identification of the location of the bite difficult. In serious bites, a hemorrhagic blister develops with progression to a dark black necrotic area that may extend over several centimeters. Systemic symptoms may be present, but these are usually mild, and respond well to supportive care. Initial reports131 that early treatment with dapsone prevented ulceration or hastened healing have been largely superseded by evidence showing that adverse effects of dapsone are common and its efficacy is doubtful.130,132 Bites by the black widow (Lactrodectus macrotans) spider are characterized by a systemic toxic reaction. Only the female black widow spider, identified by her large size and shiny black body with a red hourglass on the underside of her abdomen, contains sufficient venom to envenomate a human.133 Symptoms of envenomation are usually rapid, beginning within 1 hour of biting, and include pain, muscle rigidity, altered mental status, and seizures. Death rates from severe bites have been reported to be as high as 5%. Treatment is supportive, although an equine antivenin is available for use in severe cases. Muscle rigidity has been effectively treated with dantrolene,134 as well as calcium and methocarbamol.135

■ Bee and Wasp Stings Bee and wasp stings are very common throughout the world but most victims never seek medical attention and recover uneventfully. The most serious problem in cases of bee and wasp stings relates to the development of an immediate hypersensitivity reaction. As noted earlier, due to the large number of bees in the United States and their close proximity to humans, anaphylactic reactions from bee stings are responsible for more deaths than all other venomous animal bites and stings, including rattlesnake bites. Honeybees were not indigenous to the Americas, but were imported to the continent in the 1600s (the European honeybee). While exceedingly popular in the media, the Africanized honeybee (“killer bees”) is still a member of the same species as the European honeybee (Apis mellifera). Africanized honeybees are a population that has evolved under different environmental conditions, and has significantly different behavior than the common honeybee. African honeybees were imported to Brazil in 1956 with the hope of creating bees that would be more suited to a tropical

environment. Unfortunately, they escaped and bred with the local European honeybees and have been slowly migrating northward ever since. The first Africanized honeybee colony in the United States was discovered in South Texas in 1990. Africanized honeybees tend to be aggressive, and persons stung by them are more likely to sustain multiple stings, although the stings themselves are no different than those of other honeybees. Bees sting with double-barbed lancets, which tend to anchor the bee to the victim’s skin. When the bee dislodges itself, it usually leaves its stinging apparatus behind, thus killing the bee. The exuded venom sac of the bee should be scraped with a knife, instead of squeezing the skin to get the poison sac out, in order to avoid injecting the venom remaining in the sac. Application of an ice pack to the local area tends to alleviate the associated pain. The treatment of anaphylaxis from bee stings and other bites and stings is outlined in Table 47-14. Patients who have a known sensitivity to bee or wasp stings should carry an emergency kit for the injection of epinephrine (EpiPen®, Dey, Inc, Napa, California) and should wear a medical identification bracelet identifying their hypersensitivity.

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50. Fowler E, van Rijswijk L. Using wound debridement to help achieve the goals of care. Ostomy Wound Manag. 1995;41(7A suppl):23S–36S. 51. Schaible U, Kaufmann S. Iron and microbial infection. Nat Rev Microbiol. 2004;2:946–953. 52. Ganz T. Hepcidin, a key regulator of iron metabolism and mediator of anemia of inflammation. Blood. 2003;102:783–788. 53. Alexander J, Fischer J, Boyajian M, et al. The influence of hair removal methods on wound infections. Arch Surg. 1983;118:347–352. 54. Fezza J, Klippenstein K, Wesley R. Cilia regrowth of shaven eyebrows. Arch Facial Plast Surg. 1999;1:223–224. 55. Chaiyakunapruk N, Veenstra D, Lipsky B, et al. Chlorhexidine compared with povidone–iodine solution for vascular catheter-site care: a meta-analysis. Ann Intern Med. 2002;136:792–811. 56. Bibbo C, Patel D, Gehrmann R, et al. Chlorhexidine provides superior skin decontamination in foot and ankle surgery: a prospective randomized study. Clin Orthop Relat Res. 2005;438:204–208. 57. Kinirons B, Mimoz O, Lafendi L, et al. Chlorhexidine versus povidone iodine in preventing colonization of continuous epidural catheters in children: a randomized, controlled trial. Anesthesiology. 2001;94:239–244. 58. Adams D, Quayum M, Worthington T, et al. Evaluation of a 2% chlorhexidine gluconate in 70% isopropyl alcohol skin disinfectant. J Hosp Infect. 2005;61:287–290. 59. Wilson J, Mills J, Prather I, et al. A toxicity index of skin and wound cleansers used on in vitro fibroblasts and keratinocytes. Adv Skin Wound Care. 2005;18:373–378. 60. Varley G, Meisler D, Benes S, et al. Hibiclens keratinopathy: a clinicopathologic case report. Cornea. 1990;9:341–346. 61. Murthy S, Hawksworth N, Cree I. Progressive ulcerative keratitis related to the use of topical chlorhexidine gluconate (0.02%). Cornea. 2002; 21:237–239. 62. McRae S, Brown B, Edelhauser H. The corneal toxicity of presurgical skin antiseptics. Am J Ophthalmol. 1984;97:221–232. 63. Gross A, Cutright D, Bhaskar S. Effectiveness of pulsating water lavage in the treatment of contaminated crushed wounds. Am J Surg. 1972;124: 373–377. 64. Wheeler C, Rhodenheaver G, Thacker J, et al. Side effects of high pressure irrigation. Surg Gynecol Obstet. 1976;143:775–778. 65. Draeger R, Dahners L. Traumatic wound debridement: a comparison of irrigation methods. J Orthop Trauma. 2006;20:83–88. 66. Tetzlaff J. The pharmacology of local anesthetics. Anesthesiol Clin North America. 2000;18:217–233. 67. McLure H, Rubin A. Review of local anesthetic agents. Minerva Anestesiol. 2005;71:59–74. 68. Krunic A, Wang L, Soltani K, et al. Digital anesthesia with epinephrine: an old myth revisited. J Am Acad Dermatol. 2004;51:755–759. 69. Wilhelmi B, Blackwell S, Miller J, et al. Epinephrine in digital blocks: revisited. Ann Plast Surg. 1998;41:410–414. 70. Stratford A, Zoutman D, Davidson J. Effect of lidocaine and epinephrine on Staphylococcus aureus in a guinea pig model of surgical wound infection. Plast Reconstr Surg. 2002;110:1275–1279. 71. Bartfield J, Crisafulli K, Raccio-Robak N, et al. The effects of warming and buffering on pain of infiltration of local. Acad Emerg Med. 1995; 2:254–258. 72. Masters J. Randomized control trial of pH buffered lignocaine with adrenalin in outpatient operations. Br J Plast Surg. 1998;51:385–387. 73. Colaric K, Overton D, Moore K. Pain reduction in lidocaine administration through buffering and warming. Am J Emerg Med. 1998; 16:353–356. 74. Fitton A, Ragbir M, Milling M. The use of pH adjusted lignocaine in controlling operative pain in the day surgery unit: a prospective randomized trial. Br J Plast Surg. 1996;49:404–408. 75. Mader T, Playe S. Reducing the pain of local anesthetic infiltration: results of a national clinical practice survey. Am J Emerg Med. 1998; 16:617. 76. Calatayud J, Gonzalez A. History of the development and evolution of local anesthesia since the coca leaf. Anesthesiology. 2003;98:1503–1508. 77. Buckenmaier C, Bleckner L. Anesthetic agents for advanced regional anesthesia: a North American perspective. Drugs. 2005;65:745–759. 78. Mather L, Copeland S, Ladd L. Acute toxicity of local anesthetics: underlying pharmacokinetic and pharmacodynamic concepts. Reg Anesth Pain Med. 2005;30:553–566. 79. Crystal C, Blakenship R. Local anesthetics and peripheral nerve blocks in the emergency department. Emerg Med Clin North Am. 2005;23: 477–502. 80. Hauser C, Adams CJ, Eachempati S. Surgical Infection Society: prophylactic antibiotic use in open fractures: an evidence-based guideline. Surg Infect. 2006;7(4):379–405.

Wounds, Bites, and Stings 108. Sutherland S, Coulter A, Harris R. Rationalisation of first-aid measures for elapid snakebite. Lancet 1979;1:183. 109. Gold B, Barish R, Dart R. North American snake envenomation: diagnosis, treatment and management. Emerg Med Clin North Am. 2004; 22:423–443. 110. Lindsey D. Controversy in snakebite—time for a controlled appraisal. J Trauma. 1985;25:462. 111. Stewart R, Page C, Schwesinger W, et al. Antivenin and fasciotomy/ debridement in the treatment of the severe rattlesnake bite. Am J Surg. 1989;158:543. 112. Hall E. Role of surgical intervention in the management of crotaline snake envenomation. Ann Emerg Med. 2001;37:175–180. 113. Burch J, Agarwal R, Mattox K, et al. The treatment of crotalid envenomation with antivenin. J Trauma. 1988;28(1):35–43. 114. Schmidt J. Antivenom therapy for snakebites in children: is there any evidence? Curr Opin Pediatr. 2005;17:234–238. 115. Dart R, Seifert S, Boyer L, et al. A randomized multicenter trial of crotalinae polyvalent immune Fab (ovine) antivenom for the treatment for crotaline snakebite in the United States. Arch Intern Med. 2001;161: 2030–2036. 116. Glass T. Early debridement in pit viper bites. JAMA. 1976;235:2513. 117. Russell F, Carlson R, Wainschel J, et al. Snake venom poisoning in the United States: experiences with 550 cases. JAMA. 1975;233:341. 118. Ledbetter E, Kutscher A. Aerobic and anaerobic flora of rattlesnake fangs and venom. Arch Environ Health. 1969;19(6):770–778. 119. Clark R, Selden BS, Furbee B. The incidence of wound infection following crotalid envenomation. J Emerg Med. 1993;11:583–586. 120. Kerrigan K, Mertz B, Nelson S, et al. Antibiotic prophylaxis for pit viper envenomation: prospective, controlled trial. World J Surg. 1997;21: 369–373. 121. Blaylock R. Antibiotic use and infection in snakebite victims. S Afr Med J. 1999;89:874–876. 122. White J. Snake venoms and coagulopathy. Toxicon. 2005;45(8): 951–967. 123. McCollough N, Gennaro J. Coral snake bites in the United States. JFMA. 1963;49:968. 124. Nimorakiotakis B, Winkel K. Marine envenomations. Part 1—jellyfish. Aust Fam Physician. 2003;32:969–974. 125. Nimorakiotakis B, Winkel K. Marine envenomations—part 2—other marine envenomations. Aust Fam Physician. 2003;32:975–979. 126. Church J, Hodgson W. Adrenergic and cholinergic activity contributes to the cardiovascular effects of lionfish (Pterois volitans) venom. Toxicon. 2002;40:787–796. 127. Haddad V, Sazima I. Piranha attacks on humans in southwest Brazil: epidemiology, natural history, and clinical treatment, with description of a bite outbreak. Wilderness Environ Med. 2003;14(4):249–254. 128. Caldicott D, Mahajani R, Kuhn M. The anatomy of a shark attack: a case report and review of the literature. Injury. 2001;32:445–453. 129. Burke W. The red imported fire ant (Solenopsis invicta). A problem in North Carolina. N C Med J. 1991;52:153–158. 130. Swanson D, Vetter R. Bites of brown recluse spiders and suspected necrotic arachnidism. N Engl J Med. 2005;352(7):700–707. 131. King L, Rees R. Dapsone treatment of a brown recluse bite. JAMA. 1983;250:648. 132. Mold J, Thompson D. Management of brown recluse spider bites in primary care. J Am Board Fam Pract. 2004;17:347–352. 133. Saucier J. Arachnid envenomation. Emerg Med Clin North Am. 2004;22:405–422. 134. Ryan P. Preliminary report: experience with the use of dantrolene sodium in the treatment of bites by the black widow spider Latrodectus hesperus. J Toxicol Clin Toxicol. 1983;21(4–5):487–489. 135. Key G. A comparison of calcium gluconate and methocarbamol (robaxin) in the treatment of latrodectism (black widow spider envenomation). Am J Trop Med Hyg. 1981;30(1):273–277.

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81. Bergman B. Antibiotic prophylaxis in open and closed fractures. A controlled clinical trial. Acta Orthop Scand. 1982;55:57–62. 82. Patzakis M, Harvey J, Ivler D. The role of antibiotics in the management of open fractures. J Bone Joint Surg Am. 1974;56:57–62. 83. Benson D, Riggins R, Lawrence R, et al. Treatment of open fractures: a prospective study. J Trauma. 1983;23:25–30. 84. Weigelt J. Risk of wound infection in trauma patients. J Trauma. 1985; 150:782–784. 85. Vermeulen H, Ubbink D, Goossens A, et al. Systematic review of dressings and topical agents for surgical wounds healing by secondary intention. Br J Surg. 2005;92:665–672. 86. Rose A. Continuous water baths for burns. JAMA. 1906;47:1042–1046. 87. Winter G. Formation of the scab and the rate of epithelialization of superficial wound in the skin of the young domestic pig. Nature. 1962; 193:293–294. 88. Lewis R, Whiting P, ter Riet G, et al. A rapid and systematic review of the clinical effectiveness and cost-effectiveness of debriding agents in treating surgical wound healing by secondary intention. Health Technol Assess. 2001;5:1–131. 89. Truscott W. Impact of microscopic foreign debris on post-surgical complications. Surg Technol Int. 2004;12:34–46. 90. McGuiness W, Vella E, Harrison D. Influence of dressing changes on wound temperature. J Wound Care. 2004;13:383–385. 91. Ip M, Lui S, Poon V, et al. Antimicrobial activities of silver dressings: an in vitro comparison. J Med Microbiol. 2006;55:59–63. 92. Phaneuf M, Bide M, Hannel S, et al. Development of an infectionresistant, bioactive wound dressing surface. J Biomed Mater Res A. 2005; 74:666–676. 93. Lee A. Enhancing dermal matrix regeneration and biochemical properties of 2nd degree burn wounds by EGF-impregnated collagen sponge dressing. Arch Pharm Res. 2005;28:1311–1316. 94. Argenta L, Morykwas M. Vacuum-assisted closure: a new method for wound control and treatment: clinical experience. Ann Plast Surg. 1997; 38:563–677. 95. Morykwas M, Argenta L, Shelton-Brown E, et al. Vacuum-assisted closure: a new method for wound control and treatment: animal studies and basic foundation. Ann Plast Surg. 1997;38:553–562. 96. Olenius M, Dalsgaard C, Wickman M. Mitotic activity in the expanded human skin. Plast Reconstr Surg. 1993;91:213–216. 97. Ubbink D, Westerbos S, Nelson E, et al. A systematic review of topical negative pressure therapy for acute and chronic wounds. Br J Surg. 2008; 95(6):685–692. 98. Gabriel A, Shores J, Bernstein B, et al. A clinical review of infected wound treatment with vacuum assisted closure (V.A.C.) therapy. Experience and case series. Int Wound J. 2009;6(2):1–25. 99. Driver V. Silver dressings in clinical practice. Ostomy Wound Manag. 2004;50(9A suppl):11S–15S. 100. Cochrane C, Walker M, Bowler P, et al. The effect of several silver containing wound dressings on fibroblast function in vitro using the collagen lattice contraction model. Wounds. 2006;18(2):29–34. 101. Erdmann D, Drye C, Heller C, et al. Abdominal wall defect and enterocutaneous fistula treatment with the vacuum-assisted closure (V.A.C.) system. Plast Reconstr Surg. 2001;108:2066–2068. 102. Fishbein D, Robinson L. Rabies. N Engl J Med. 1993;329(22): 1632–1638. 103. Teixeira CF, Fernandes C, Zuliani J, et al. Inflammatory effects of snake venom. Mem Inst Oswaldo Cruz. 2005;100(suppl 1):181–184. 104. Dart R, Hurlbut K, Garcia R, et al. Validation of a severity score for the assessment of crotalid snakebite. Ann Emerg Med. 1996;27(3):321–326. 105. Snyder C, Pickins J, Knowles R, et al. A definitive study of snake bite. JFMA. 1968;55:330. 106. Gudarian R, MacKenzie C, Williams J. High voltage shock treatment for snakebite. Lancet. 1986;2:229. 107. Stewart M, Greenland S, Hoffman J. First-aid treatment of poisonous snakebite: are current recommended procedures justified? Ann Emerg Med. 1981;10(6):331–335.

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CHAPTER 48

Burns and Radiation Jong O. Lee and David N. Herndon

BURNS ■ Epidemiology While the number of burn injuries is decreasing in the United States, nearly 1.25 million people are burned every year.1 Of these, 60,000–80,000 patients per year require hospitalization due to burn injuries, and about 5,500 of these patients die.1,2 Burns requiring hospitalization typically include burns greater than 10% of the total body surface area (TBSA) or significant burns of the face, hands, feet, or perineum. The highest incidence of burn injury occurs during the first few years of life and between 20 and 29 years of age. The major causes of severe burn injury are flame burns, which cause most of the burn deaths, and liquid scalds. From 1971 to 1991, burn deaths decreased by 40%, with a concomitant 12% decrease in deaths associated with inhalation injury.2 Since 1991, burn deaths per capita have decreased another 25% according to statistics from the Centers for Disease Control and Prevention (www.cdc.gov/ncipc/wisqars). These improvements are due to prevention strategies resulting in fewer burns of lesser severity, as well as significant improvements in the care of severely burned patients, especially children. In 1949, Bull and Fisher first reported the expected 50% mortality rate for burn sizes in several age groups based on data from their unit.3 They reported that approximately one half of children aged 0–14 years with burns of 49% TBSA would die.3 This dismal statistic has dramatically improved, with the latest reports indicating 50% mortality for 98% TBSA burns in children 14 years and under.4,5 A healthy young patient with any size burn might be expected to survive.6 The same cannot be said, however, for those aged 45 years or older. Improvements in this group have been much more modest, especially in patients over 65 years of age where a 35% burn still kills half of the patients.7 The improved survival figures after massive burns are due to advances in understanding of resuscitation, improvements in wound coverage by early excision and grafting, better support

of the hypermetabolic response to injury, early nutritional support, more appropriate control of infection, and improved treatment of inhalation injuries. Aggressive treatment of patients with severe burns has improved outcomes to the point that survival in massive injuries is common. Future breakthroughs in the field are likely to be in the area of faster and better return of function and improved cosmetic outcomes.

■ Criteria for Referral to Burn Centers Some burn patients benefit from treatment in specialized burn centers. These centers have dedicated resources and the expertise of all the required disciplines to maximize outcomes from such devastating injuries.8 The American Burn Association and the American College of Surgeons Committee on Trauma have established guidelines about which patients should be transferred to a specialized burn center. Patients meeting the following criteria should be treated at a designated burn center: 1. Second- and third-degree burns of greater than 10% TBSA 2. Full-thickness burns in any age group 3. Any burn involving the face, hands, feet, eyes, ears, or perineum that may result in cosmetic or functional disability 4. Electrical injury 5. Inhalation injury or associated trauma 6. Chemical burns 7. Burns in patients with significant comorbid conditions (e.g., diabetes mellitus, chronic obstructive pulmonary disease, cardiac disease) Patients meeting the following criteria can be treated in a general hospital setting: 1. Second-degree burns of less than 10% TBSA 2. No burns to areas of special function or risk and no significant associated or premorbid conditions

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TABLE 48-1 Definition of Burn Types, Zones, and Depth of Injury

Scald

Categories Flash Flame Liquid —Spill —Immersion Grease Steam

Zones of Injury Zone of coagulation

Burn Depth First degree (superficial)

Zone of stasis

Superficial second degree (superficial partial thickness)

Zone of hyperemia

Deep second degree (deep partial thickness) Third degree (full thickness) Fourth degree (deep organ tissue or organ involvement)

Contact Chemical Electrical Radiation

■ Pathophysiology Burns are classified into six causal categories, three zones of injury, and five depths of injury (Table 48-1). The causes include injury due to fire, scald, contact, chemicals, electrical current, and radiation. Fire burns are divided into flash and flame burns; scald burns into those caused by liquids, grease, or steam; and liquid scald burns can be further divided into spill and immersion scalds. Flame, scald, and contact induce cellular damage primarily by the transfer of energy that induces coagulative necrosis, while direct injury to cellular membranes is the cause of injury in chemical and electrical burns. The skin generally provides a barrier to limit transfer of energy to deeper tissues. After the source of burn is removed, however, the response of local tissues can lead to further injury. The necrotic area of a burn is termed the zone of coagulation in the center. The area immediately surrounding the necrotic zone has a moderate degree of injury that initially causes a decrease in tissue perfusion. This area is termed the zone of stasis and depending on the environment of the wound, can progress to coagulative necrosis if local blood flow is not maintained. Thromboxane A2, a potent vasoconstrictor, is present in high concentrations in burn wounds, and local application of thromboxane inhibitors has been shown to improve blood flow and may decrease this zone of stasis.9 Antioxidants10 and inhibition of neutrophil-mediated processes11 may also improve blood flow, preserve this tissue, and affect the depth of injury. Endogenous vasodilators such as calcitonin gene-related peptide and substance P, whose levels are increased in the plasma of burned patients,12 may also play a role. The last area is the zone of hyperemia related to vasodilation from inflammation surrounding the burn wound. This zone contains the clearly viable tissue from which the healing process begins (Fig. 48-1).

permeability after burns, including prostaglandins, catecholamines, histamine, bradykinin, vasoactive amines, leukotrienes, and activated complement.13 Mast cells in the burned skin release histamine in large quantities immediately after injury,14 which will cause a characteristic response in venules by increasing the space in intercellular junctions.15 The use of antihistamines in the treatment of burn edema, however, has had limited success with the possible exception of H2-receptor antagonists.16 In addition, aggregated platelets release serotonin, which plays a major role in the formation of edema. This agent acts directly to increase pulmonary vascular resistance and indirectly aggravates the vasoconstrictive effects of various vasoactive amines. Serotonin blockade has been shown to improve cardiac index, decrease pulmonary artery pressure, and decrease oxygen consumption after burns.17 Another mediator likely to play a major role in changes in vascular permeability and tone is thromboxane A2. It has been shown that levels of thromboxane increase dramatically in the plasma and wounds of burned patients.18,19 This potent vasoconstrictor leads to platelet aggregation in the wound, contributing to expansion of the zone of stasis. Also, it causes prominent mesenteric vasoconstriction and decreased blood flow to the gut in animal models that compromise gut mucosal integrity and immune function.20

Epidermis

Dermis

■ Inflammatory Response Massive release of inflammatory mediators is seen with a significant burn, both in the wound and in other tissues. These mediators produce vasoconstriction and vasodilation, increased capillary permeability, and edema locally and in distant organs. Many mediators have been proposed to explain the changes in

Zone of coagulation

Zone of stasis Zone of hyperemia

FIGURE 48-1 Illustration of the zones of injury after burn. Factors likely to affect the zone of stasis determine the extension of injury from the original zone of coagulation.

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Burn Fire

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Specific Challenges in Trauma

■ Changes in Organ Function SECTION 4

Cardiac effects include marked loss of plasma volume, increased peripheral vascular resistance, and decreased cardiac output,21 and pulmonary effects include a decrease in pulmonary static compliance.22 These changes are associated with mild direct cardiac damage.23 Renal blood flow decreases with a fall in glomerular filtration rate, which may result in renal dysfunction. Metabolic changes are highlighted by an early depression followed by a marked, sustained increase in resting energy expenditure, increased lipolysis and proteolysis, and an increase in oxygen consumption. This is driven in part by an increase in production of catecholamines, cortisol, and glucagon.24 Increased peripheral lipolysis results in hepatic steatosis. There is a generalized impairment in host defenses with depressed production of immunoglobulin, decreased opsonic activity, and depressed bactericidal activity,25 and these cause the burned patient to become especially prone to infection.

■ Initial Care The burning process is stopped by removing the patient from the source of burn, and clothing and jewelry are removed immediately (see Chapter 10). The patient is kept warm by being wrapped in a clean sheet or blanket. The immediate treatment of a burn patient should proceed as with any trauma patient, and any potential life-threatening injuries should be identified and treated. Assessment of the patient starts with the airway. One hundred percent oxygen is administered, and oxygen saturation is monitored using pulse oximetry. Stridor, wheezing, tachypnea, and hoarseness indicate impending airway obstruction due to an inhalation injury or edema, and immediate treatment is required. If the patient has labored breathing or signs of obstruction, immediate orotracheal intubation should be performed with in-line stabilization of the neck if an injury to the cervical spine is suspected. Arterial blood gas and carboxyhemoglobin levels are obtained when appropriate. The presence of carbon monoxide (CO) in the blood, which has an affinity 210–280 times that of oxygen for hemoglobin (Hb), can falsely elevate oxygen saturation levels that are determined colorimetrically. Use of a pulse oximeter may not be effective, as patients with CO poisoning may have a normal oxygen saturation level on the device. Use of a pulse CO-oximeter measures absorption at several wavelengths to distinguish oxyhemoglobin from carboxyhemoglobin saturation and determines the blood oxygen saturation more reliably using the total amount of Hb, including carboxyhemoglobin, met-Hb, and reduced Hb. The treatment for CO inhalation is 100% O2 by endotracheal tube or face mask. This will decrease the half-life of CO from 4 to 6 hours at room air to 40–80 minutes with 100% O2. In 3 atm absolute 100% oxygen in a hyperbaric chamber, the half-life decreases further to 15–30 minutes. Full-thickness circumferential burns of the chest can interfere with ventilation, so bilateral expansion of the chest should be observed to document equal air movement. If the patient is on a ventilator, airway pressure and pCO2 should be monitored. If ventilation is compromised with a rising airway pressure and pCO2, an escharotomy on the chest should be performed to allow better movement of the chest and

improve ventilation. Measurement of a noninvasive blood pressure may be difficult in patients with burned extremities, and such patients may need an arterial line to monitor their blood pressure during transfer or resuscitation. A radial arterial line may not be reliable in patients with upper extremity burns and is difficult to secure. Therefore, the insertion of a temporary femoral arterial line may be more appropriate.

■ Fluid Resuscitation After a serious burn, there is a systemic capillary leak that increases with burn size. Capillaries usually regain competence after 18–24 hours if resuscitation has been successful. Increased times to beginning resuscitation of burned patients result in poorer outcomes, and delays should be minimized.26 The best intravenous (IV) access is with short peripheral catheters through unburned skin; however, veins beneath burned skin can be used to avoid a delay in obtaining IV access. Central venous lines are required when peripheral IV access is difficult. In children, intraosseous access can be utilized in the proximal tibia until IV access is accomplished. Lactated Ringer’s solution without dextrose is the fluid of choice except in children under 2 years of age, who should receive some 5% dextrose in the lactated Ringer’s solution. This can be accomplished by giving 5% dextrose as maintenance fluid and lactated Ringer’s solution as resuscitation fluid. The initial rate can be rapidly estimated, using a modified formula developed at Parkland Memorial Hospital in Dallas, Texas, by multiplying the estimated TBSA burned by the weight in kilograms, which is divided by 4 for the first 8 hours. Thus, the rate of infusion for an 80-kg man with a 40% TBSA burn would be 80 kg  40% TBSA/4  800 mL/h for the first 8 hours. Different formulas, all originating from experimental studies on the pathophysiology of burn shock, have been devised to assist the clinician in determining the proper amount of resuscitation fluid. Early work by Baxter and later by G. T. Shires established the basis for modern protocols for fluid resuscitation.27 They showed that edema fluid in burn wounds is isotonic and contains the same amount of protein as plasma and that the greatest loss of fluid is into the interstitial fluid compartment. They used varying volumes of intravascular fluid to determine the optimal delivered amount in terms of cardiac output and extracellular volume in a canine burn model. These findings led to a successful clinical trial of the “Parkland formula” in resuscitating burned patients (Table 48-2). Also, it was shown that changes in plasma volume were not related to the type of resuscitation fluid used in the first 24 hours but colloid solutions could increase plasma volume after this time. From these findings, it was concluded that colloid solutions should not be used in the first 24 hours until capillary permeability returned closer to normal. Others have argued that normal capillary permeability is restored somewhat earlier after a burn (6–8 hours) and therefore, suggest that colloids can be used at this point.28 Moncrief and coworkers also studied the hemodynamic effects of fluid resuscitation in burns, which resulted in the Brooke formula21 (Table 48-2). They showed that fluid loss in

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TABLE 48-2 Resuscitation Formulas Crystalloid Volume 4 mL/(kg  % TBSA burn) 1.5 mL/(kg  % TBSA burn) 5,000 mL/m2 TBSA burned

1,500 mL/m2 TBSA

Colloid Volume None 0.5 mL/(kg  % TBSA burn) None

Free Water None 2.0 L None

TBSA  total body surface area. moderate burns resulted in an obligatory 20% decrease in both extracellular fluid and plasma volume during the first 24 hours after injury. In the second 24 hours, plasma volume returned to normal with the administration of colloid. Cardiac output was low the first day in spite of resuscitation but subsequently increased to supernormal levels as the flow phase of hypermetabolism was established.21 Since these studies, it has been found that much of the fluid needs are due to capillary leak that permits passage of large molecules and water into the interstitial space. Intravascular volume follows the gradient into the burn wound and nonburned tissues. Approximately 50% of fluid resuscitation needs are sequestered in nonburned tissues in 50% TBSA burns.29 Hypertonic saline solutions have theoretic advantages in the resuscitation of burned patients. These solutions have been shown to decrease net fluid intake,30 decrease edema,31 and increase lymph flow probably by the transfer of volume from the intracellular space to the interstitium. When using these solutions, one must take care to avoid serum sodium concentrations greater than 160 mEq/dL.13 Of note, it has been shown that patients with over 20% TBSA burns who were randomized to resuscitation with either hypertonic saline or lactated Ringer’s solution did not have significant differences in total volume requirements or in changes in percent weight gain over the days after the burn.32 Other investigators have found an increase in renal failure with hypertonic solutions that has tempered further enthusiasm for their use in resuscitation.33 Some burn units have successfully used a modified hypertonic solution by adding one ampule of sodium bicarbonate to each liter of lactated Ringer’s solution.34 Further research will need to be done to determine the optimal formula to reduce formation of edema as well as maintain adequate cellular function. Of interest, it has been shown that resuscitation volumes required in the severely burned patient decreased when highdose IV ascorbic acid was administered during resuscitation. This was associated with decreased weight gain and improved oxygenation.35 Most burn centers around the country use something similar to the Parkland or Brooke formula in which varying amounts of crystalloid and colloid solutions are administered for the first 24 hours postburn (Table 48-2). IV fluids are generally changed in the second 24 hours to more hypotonic solutions. These formulas are guidelines to the amount of fluid necessary to maintain adequate perfusion. This is monitored in burned patients by following the volume of urine output, which should be maintained at 0.5 mL/kg per hour in adults and 1.0 mL/kg per hour in children. Other parameters

such as heart rate, blood pressure, mental status, and peripheral perfusion are monitored, also. Changes in the rates of infusion of IV fluids should be made on an hourly basis as determined by the response of the patient to the particular fluid volume administered. In pediatric burns, the commonly used formulas are modified to account for changes in surface area to mass ratios. Children have a larger body surface area relative to their weight than do adults and generally have somewhat greater fluid needs during resuscitation. The Galveston formula is based on body surface area and uses 5,000 mL/m2 TBSA burned for resuscitation 1,500 mL/m2 TBSA for maintenance in the first 24 hours (Table 48-2). This formula accounts for both the resuscitation fluid requirements and maintenance needs of a child with burn. All of these formulas calculate the amount of volume given in the first 24 hours, one half of which is given in the first 8 hours and next one half of which is given over next 16 hours. Some dextrose is added to the resuscitation fluid in children under 2 to prevent hypoglycemia because they have limited glycogen stores. It is best to use two IV fluids in infants, lactated Ringer’s solution for resuscitation and 5% dextrose in lactated Ringer’s solution for maintenance.

■ Other Injuries Other traumatic injuries may be present in patients who have been burned. Each patient should be fully evaluated for associated injuries that may be more immediately life threatening, and the burn wounds can be addressed after standard evaluation and resuscitation. Burned patients should initially be placed on sterile or clean sheets. Cold water and ice may, in large burns, harm patients by inducing hypothermia and should be avoided. The patient should be kept warm and the wounds clean until assessment by the physicians responsible for the definitive care of the burn. Nasogastric tubes and bladder drainage catheters are placed in patients requiring transfer to a burn center to decompress the stomach and to monitor the progress of resuscitation.

■ Determination of Burn Depth The depth of burn determines outcome in terms of survival and scarring. Although technologies such as the laser Doppler flow meter with multiple sensors hold promise for quantitatively determining burn depth, it is most accurately assessed by the judgment of experienced physicians. Determination of depth is critical in the treatment plan as there are wounds that will heal with local treatment versus those that will require operative

CHAPTER 48

Formula Parkland Brooke Galveston (pediatric)

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Specific Challenges in Trauma

SECTION 4

intervention for timely healing. Being able to determine who will need operative intervention will facilitate care. Superficial (first-degree) burns are confined to the epidermis. These burns are painful, erythematous, and blanch to the touch with an intact epidermis without blister. Examples include sunburn, a minor scald, or flash burn. These burns will heal in 3–6 days and will not result in scarring. Treatment is aimed at comfort with the use of topical soothing salves with or without aloe and nonsteroidal anti-inflammatory drugs or acetaminophen. Partial-thickness (second-degree) burns are divided into two types, superficial and deep. All partial-thickness burns have some degree of dermal damage, and the division is based on the depth of injury into this layer. Superficial partial-thickness burns are erythematous, painful, wet, blanch to touch, and often form blisters, although blistering may not occur for some hours following injury. Burns thought to be first degree may subsequently be diagnosed as partial-thickness burns by the second day. These wounds will spontaneously reepithelialize from retained epidermal structures in the rete ridges, hair follicles, and sweat glands in 7–14 days. The injury may cause skin discoloration over the long term. Deep partial-thickness burns into the reticular dermis will appear dry, more pale than pink, or mottled. They may not blanch to touch but will remain painful to pinprick. In deeper partial-thickness burns, the sensation becomes blunted (less sensitive to pinprick than surrounding normal skin). Capillaries may refill slowly after compression or not at all. These burns will heal in 21–28 days or longer, depending on the depth of burn, by reepithelialization from hair follicles and keratinocytes in sweat glands, often with hypertrophic scars. The longer the wound takes to heal, the worse the scarring will be. Full-thickness (third-degree) burns are burns through the dermis down to the subcutaneous tissue and are characterized by a firm leathery eschar that is painless and black, white, or cherry red in color. An eschar is insensitive to pinprick but may feel pressure on palpation. No epidermal or dermal appendages remain, and these wounds must heal by reepithelialization from the wound edges by contraction, which takes a protracted time. Full-thickness burns require excision and grafting with autograft skin to heal the wounds in a timely fashion and to decrease scarring. Deep partial-thickness burns often require grafting to facilitate healing, as well. Fourth-degree burns involve other tissues or organs beneath the skin, such as muscle, tendon, and bone. They have a charred appearance that usually results from prolonged duration of contact with fire or an object such as a hot muffler or from high-voltage electrical injury.

■ Determination of Burn Size The most commonly used method of determining the burn size in adults is the “rule of nines” (Fig. 48-2). Each upper extremity and the head and neck are 9% of the TBSA; each lower extremity, the anterior trunk, and posterior trunk are 18%; and the perineum and genitalia are assumed to be 1% of the TBSA. For smaller burns, burn size can also be estimated by examining the area of the patient’s open hand, which is approximately 1%

FIGURE 48-2 Determining burn size by the “rule of nines.”

TBSA, and visually transposing this onto the wound to determine burn size. Children have a relatively larger portion of the body surface area in the head and neck and smaller surface area in the lower extremities. Infants have 21% of the TBSA in the head and neck and 13% in each leg, with these proportions incrementally approaching adult proportions as age increases. The Berkow formula or Lund Browder chart can be helpful in determining burn size in children (Table 48-3).

■ Escharotomies With circumferential constricting deep partial- and full-thickness burns to an extremity, peripheral circulation to the limb can be compromised by edema. Development of generalized edema beneath a nonyielding eschar impedes venous outflow

TABLE 48-3 Berkow Chart for Estimation of Burn Size in Children Area Head Neck Anterior trunk Posterior trunk Buttock Genitalia Arm Forearm Hand Thigh Leg Foot

1 Year 19 2 13 13 2.5 1 4 3 2.5 5.5 5 3.5

1–4 Years 17 2 13 13 2.5 1 4 3 2.5 6.5 5 3.5

5–9 Years 13 2 13 13 2.5 1 4 3 2.5 8 5.5 3.5

10–14 Years 11 2 13 13 2.5 1 4 3 2.5 8.5 6 3.5

15 Years 9 2 13 13 2.5 1 4 3 2.5 9 6.5 3.5

Burns and Radiation

■ Inhalation Injury An associated inhalation injury is one of the factors that contributes to mortality in burns. Inhalation injury adds another inflammatory focus to the burn and impedes the normal gas exchange that is vital for critically injured patients. The presence of such an injury can be used as a significant predictor of outcome in massive burns. In one study, the amount of time spent on a ventilator in the first 28 days was the strongest predictor of mortality in a group of children with over 80% TBSA burns. As expected, inhalation injury was present in the majority of these children.26 In most inhalation injuries, damage is caused primarily by inhaled toxins. Heat is generally dispersed in the upper airways, whereas the cooled particles of smoke and toxins are carried distally into the bronchi and alveoli. The injury is principally chemical in nature. The response is an immediate increase in blood flow in the bronchial arteries to the bronchi with formation of edema and increases in lung lymph flow. The lung lymph in this situation is similar to serum, indicating that permeability at the capillary level is markedly increased. The edema that results is associated with an increase in neutrophils in the lung, and it is postulated that these cells may be the primary mediators of pulmonary damage with this

injury. Neutrophils release proteases and oxygen-free radicals that can produce conjugated dienes by lipid peroxidation. High concentrations of these conjugated dienes are present in the lung lymph and pulmonary tissues after inhalation injury, suggesting that increased neutrophils are active in producing cytotoxic materials.36 Separation of the ciliated epithelial cells from the basement membrane followed by formation of exudate within the airways is another hallmark of inhalation injury. The exudate consists of proteins found in the lung lymph that eventually coalesce to form fibrin casts. Clinically, these fibrin casts can be difficult to clear with standard techniques of airway suction, and bronchoscopy is often required. These casts can also add barotrauma to localized areas of lung by forming a “ball valve.” During inspiration, the airway diameter increases, and air flows past the cast into the distal airways. During expiration, the airway diameter decreases, and the cast effectively occludes the airway, preventing the inhaled air from escaping. Increasing volume leads to localized increases in pressure that are associated with numerous complications, including pneumothorax and decreased lung compliance. Therapy aimed at clearing the airway and minimizing complications would likely improve outcomes after this injury. Patients with smoke inhalation often present with a history of exposure to smoke in a closed space, stridor, hoarseness, wheezing, carbonaceous sputum, facial burns, and singed nasal vibrissae. Each of these findings has poor sensitivity and specificity; therefore, the diagnosis is often established by the use of bronchoscopy. Bronchoscopy can reveal early inflammatory changes such as erythema, edema, ulceration, sloughing of mucosa, and prominent vasculature in addition to infraglottic soot. Mechanical ventilation may be needed to maintain gas exchange, and repeated bronchoscopies may reveal continued ulceration of the airways with the formation of granulation tissue and exudate, inspissation of secretions, and edema. Management of inhalation injury is directed at maintaining open airways, clearing secretions, and maximizing gas exchange while the lung heals. A coughing patient with a patent airway can clear secretions very effectively, and efforts should be made to treat patients without mechanical ventilation, if possible. If respiratory failure is imminent, intubation should be instituted early, with frequent chest physiotherapy and suctioning performed to maintain pulmonary hygiene. Frequent bronchoscopies may be needed to clear inspissated secretions. Mechanical ventilation should be used to provide gas exchange with as little barotrauma as possible. Inhalation treatments have been effective in improving the clearance of tracheobronchial secretions and decreasing bronchospasm. IV heparin has been shown to reduce the formation of tracheobronchial casts, minute ventilation, and peak inspiratory pressures after smoke inhalation. When heparin was administered directly to the lungs in a nebulized form to reduce bleeding complications, it was shown to have similar effects on casts without causing a systemic coagulopathy. When N-acetylcysteine treatments are added to nebulized heparin in burned children with inhalation injury, reintubation rates and mortality are decreased.37 In addition to the preceding measures, adequate humidification and treatment of bronchospasm with β-agonists is indicated.

CHAPTER 48

and will eventually affect arterial inflow to the distal beds. This can be recognized by numbness and tingling in the limb and increased pain in the digits. Arterial flow can be assessed by pulse oximetry and determination of Doppler signals in the digital arteries and the palmar and plantar arches in affected extremities. Capillary refill is assessed, also. Extremities at risk are identified on clinical examination, which mandate an escharotomy performed at the bedside. The release of a burn eschar is performed by lateral and medial incisions on the extremity with an electrocautery. The entire constricting eschar must be incised to relieve the obstruction to blood flow. If the hand is involved, two incisions are made on the dorsal surface and along the medial or lateral sides of the digits with care not to damage the neurovascular bundles. These bundles are located slightly to the palmar side of the digit. If it is clear that the wound will require excision and grafting because of its depth of injury, escharotomies are the safest route to restore perfusion to the underlying nonburned tissues. If vascular compromise has been prolonged, reperfusion after an escharotomy may cause a reactive hyperemia and further formation of edema in the muscle, making continued surveillance of the distal extremities necessary. Increased pressures in the underlying musculofascial compartments are treated with standard fasciotomies. A circumferential burn of the chest with a constricting eschar can cause a similar phenomenon, except the effect is to decrease ventilation by limiting excursion of the chest wall. Any decrease in ventilation documented by an increase in peak airway pressure and pCO2 of a burned patient should be followed by inspection of the burn on the chest wall. When necessary, escharotomies are performed in the lateral chest bilaterally with a connecting incision across the chest to relieve the constriction and allow for adequate ventilation.

927

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Specific Challenges in Trauma

SECTION 4

In addition to conventional ventilator methods, novel ventilator therapies such as high-frequency percussive ventilation have been devised to minimize barotrauma. This method combines standard tidal volumes and respirations (ventilator rates 6–20 breaths/min) with smaller high-frequency respirations (200–500 breaths/min) and has been shown to permit adequate ventilation and oxygenation in patients who had failed conventional ventilation. An explanation for the greater utility of this method is the ability to recruit alveoli at lower airway pressures.38 This ventilator method may also have a percussive effect to loosen inspissated secretions and improve pulmonary hygiene.

■ Chemical Burns Prompt treatment is imperative in minimizing tissue damage in chemical burns. A chemical burn should be copiously irrigated with water, and care must be taken to direct the drainage of the irrigating solution away from unburned areas to limit the area of skin exposed to chemicals. If the chemical composition is known, monitoring of the irrigated solution pH will give an indication of the effectiveness of the irrigation. Attempts at neutralization of either acidic or basic solutions can result in heat production and extend the injury. Generally, acids cause coagulative necrosis and are confined to the skin, while basic solutions cause liquefactive necrosis and extend further into the tissues until removal. Emergent operative debridement with pH testing of each tangential slice may be necessary to ensure no further injury after exposure to solutions with a high pH. After the chemical injury has been controlled, the remaining burn is treated in the same way as thermal injuries. Assessment of burn depth is often difficult, but is typically deeper than it appears. Hydrofluoric acid is a highly dangerous substance that causes severe burns and systemic effects, yet it is used widely in industrial and domestic settings.39 When exposed to biological tissues, the fluoride ion precipitates calcium and may cause systemic hypocalcemia. This may occur even with a very small burn. Management of burns caused by this substance differs from burns caused by other acids. In addition to copious irrigation of the burned area, the exposed skin should be treated with 2.5% calcium gluconate gel to provide pain relief and limit the spread of the fluoride ion. For hand burns, even intra-arterial calcium gluconate has been advocated. Patients should be monitored closely for prolongation of the QT interval, torsade de pointes, or ventricular fibrillation. Changes in the QT interval should be treated with 20 mL of 10% calcium gluconate repeated as needed to maintain normal levels of serum calcium. Other serum electrolytes such as magnesium must also be closely monitored.

■ Electrical Burns Electrical burns are unique in that the location of the injury may be mostly internal. Electrical current proceeds down the path of least resistance, which is via nerves, blood vessels, and muscle, thus sparing the skin except at the contact points of the electrical current. If the resistance of contact sites of highvoltage current is high, the local injury may be extensive, with loss of digits or even entire extremities. Electrical injury may be associated with blunt trauma from tetanic contractions of muscles or a fall.

With any significant electrical injury, vigorous IV resuscitation should be given with attention to myoglobinuria from muscle damage. Urine output should be maintained at greater than 1 mL/kg per hour with administration of fluids and an osmotic diuresis using mannitol to increase renal tubular flow if needed. The administration of IV bicarbonate to alkalinize the urine should be considered to decrease precipitation of hemochromogens in the renal tubules, but it has not been proven in prospective studies. Patients should be monitored for cardiac arrhythmias for 24 hours after admission. Serial examinations of the extremities are necessary to detect any vascular compromise, and fasciotomies of the involved limbs are often necessary. Debridement of nonviable tissue is appropriate. If operative exploration is necessary, complete fasciotomies with inspection of deep tissues should be undertaken. Acute and chronic neuropathies are common and may be permanent. Development of cataracts is also common after severe electrical injury and may be delayed for months, so close ophthalmologic follow-up is necessary.

■ Care of Burn Wound Improvements in the treatment of burn wounds and utilization of antimicrobial dressings have dramatically decreased the incidence of fatal sepsis in burned patients.40 The previous technique of allowing separation of eschar with lysis by bacterial enzymes has given way to wound closure using early excision and grafting. In those wounds that will heal spontaneously without skin grafts, topical antimicrobial agents limit wound contamination and provide a moist environment for healing. Current therapy for burn wounds can be divided into the following three stages: assessment, management, and rehabilitation. Once the extent and depth of the wounds have been assessed and the wounds thoroughly cleaned and debrided, the management phase begins. Each wound should be dressed with an appropriate covering that serves three functions. First, it protects the damaged epithelium and dermis. Second, the dressing should be occlusive to reduce evaporative heat loss. Third, the dressing should provide comfort over the painful wound. The choice of dressing should be individualized based on the characteristics of the burn. First-degree burns are minor with minimal loss of barrier function. These wounds require no dressing and are treated with topical salves to decrease pain and keep the skin moist. Second-degree wounds can be treated by daily dressing changes with an antibiotic ointment such as silver sulfadiazine covered with several layers of gauze under elastic wraps. Alternatively, the wounds can be covered with a temporary biological or synthetic covering to close the wound. These coverings eventually slough as the wound reepithelializes underneath. These types of dressings provide stable coverage with decreased pain and a barrier to evaporative losses. They may also have the added benefit of not inhibiting epithelialization, a feature of most topical antimicrobial agents. These coverings include allograft (cadaver skin), porcine xenograft (pigskin), and Biobrane (Bertek, Morgantown, West Virginia).41,42 The advantages and disadvantages of the various coverings are listed in Table 48-4. These should generally be applied within 24 hours

Burns and Radiation

929

TABLE 48-4 Advantages and Disadvantages of Alternative Wound Coverings Material Cadaver skin (fresh or frozen)

Xenograft Biobrane

Pigskin Synthetic nylon and silicon

Advantages Reduces bacterial colonization, vascularizes Readily available Readily available

Disadvantages Expensive, limited availability, exposure to hepatitis and CMV Does not resist infection Must be placed early, no antimicrobial property

CMV  cytomegalovirus.

of the burn before bacterial colonization of the wound occurs. As synthetic coverings such as Biobrane have no antimicrobial property, close observation is required.

■ Surgical Management of Burn Wound Full-thickness burns will not heal in a timely fashion without autografting, and the same is true for some deep partial-thickness burns. These burned tissues serve as a nidus for inflammation and infection that can lead to death of the patient. Early excision and grafting of these wounds is now practiced by most burn surgeons in response to reports showing benefits over serial debridement in terms of survival, blood loss, and length of hospitalization.43–45 These excisions can be performed with tourniquet control or with application of topical epinephrine and thrombin to minimize blood loss. After a burn wound has been excised, the wound must be covered with either autograft skin or some other covering. This covering is ideally the patient’s own skin. Wounds less than 20–30% TBSA can usually be closed in one operation with autograft skin taken from the patient’s available normal nonburned skin (donor site). In these operations, the skin grafts are either not meshed or meshed with a narrow ratio (2:1 or less). In major burns, donor site may be limited to the extent that the entire wound cannot be covered with autograft skin in one operation. The availability of allograft skin to cover these wounds has changed the course of modern treatment for massive burns. A typical method of treatment is to use widely expanded autografts (4:1 or greater ratio) covered with allograft skin to completely close the wounds. The 4:1 expended autograft skin heals underneath the allograft skin by reepithelialization in approximately 21 days, and the allograft skin will slough as autograft skin heals. Massively burned patients are profoundly immunosuppressed, and rejection of allograft skin is rarely a problem. Portions of the wound that cannot be covered with widely meshed autograft are covered with allograft skin temporarily in preparation for autografting when donor sites are healed and ready. Ideally, areas with less cosmetic importance are covered with the widely meshed skin to close most of the wound prior to using nonmeshed grafts for the cosmetically important areas, such as the hands and face. Most surgeons excise the full-thickness burn wound within the first week, sometimes in serial operations, removing 20% of

the burn wound at a time per operation on subsequent days. Others remove the total burn wound in one operative procedure; however, this can be difficult in patients with large burns and complicated by the development of hypothermia or massive blood loss. It is the authors’ practice to perform the excision immediately after stabilization of the patient, because blood loss diminishes if the operation can be performed the first day after injury. This may be due to the relative predominance of vasoconstrictive substances such as thromboxane and catecholamines in the circulation and the natural edema planes that develop immediately after the injury. When the wound becomes hyperemic after 2 days, blood loss during excision can be a considerable problem. Early excision should be reserved for full-thickness burn typically caused by flame. This is highlighted because scald burns are very common. These injuries are often partialthickness or a mixture of partial- and full-thickness and should be covered with substances such as allograft, porcine xenograft, or Biobrane, allowing the wound, which will heal, to be protected. A deep partial-thickness burn can appear clinically to be a full-thickness burn at 24–48 hours after injury, particularly if it has been treated with topical antimicrobials that combine with wound drainage to form a pseudoeschar. A randomized prospective study comparing early excision with conservative therapy with late skin grafting with scald burns showed that patients undergoing early excision had more wound excised, more blood loss, and more time in the operating room. No difference in hospital length of stay or rate of infection was seen.46 Loss of a skin graft after an operation is due to one or more of the following reasons: presence of infection, fluid collection under the graft, shearing forces that disrupt the adhered graft, or an inadequate excision of the wound bed leaving residual necrotic or nonviable tissue. Infection is controlled by the appropriate use of perioperative antibiotics and covering the grafts with topical antimicrobial agents at the time of surgery. Meticulous hemostasis, appropriate meshing of grafts, or “rolling” of nonmeshed grafts postoperatively and/or use of a bolster dressing over the graft minimizes fluid collections. Shearing is decreased by immobilization of the grafted area. Inadequately excised wound beds are uncommon in the practice of experienced surgeons. Punctate bleeding or color of the dermis or fat in areas excised under a tourniquet denotes the proper level of excision.

CHAPTER 48

Covering Allograft

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Specific Challenges in Trauma

■ Control of Infection SECTION 4

Decreased invasive infections in burn wounds are due to early excision and closure and the timely and effective use of antimicrobials. The antimicrobials that are used can be divided into those given topically and those given systemically. Available topical antibiotics can be divided into salves and soaks. Salves are generally applied directly to the wound with dressings placed over them, and soaks with antimicrobial solutions are generally poured into dressings on the wound. Each of these classes of antimicrobials has its advantages and disadvantages. Salves may be applied once or twice a day but may lose their effectiveness in between dressing changes. Soaks will remain effective because antimicrobial solution can be added without removing the dressing; however, the underlying skin can become macerated. Topical antibiotic salves include 8.5% mafenide acetate (Sulfamylon), 1% silver sulfadiazine (Silvadene), polymyxin B, neomycin, bacitracin, and mupirocin. No single agent is completely effective, and each has advantages and disadvantages. Mafenide acetate has a broad spectrum of activity through its sulfa moiety, particularly for Pseudomonas and Enterococcus species. It also has the advantage of penetration of eschar. Disadvantages include pain on application, an allergic skin rash, and inhibition of carbonic anhydrase activity that can result in a metabolic acidosis when applied over large surfaces. For these reasons, mafenide sulfate is typically reserved for small full-thickness injuries and ear burns to prevent chondritis. Silver sulfadiazine, the most frequently used topical agent, has a broad spectrum of activity from its silver and sulfa moieties that covers gram-positive organisms, most gram-negative organisms, and some fungi. Some Pseudomonas species, however, possess plasmid-mediated resistance. It is painless on application and is easy to use. Occasionally, patients will complain of some burning sensation after it is applied, and some patients will develop a transient leukopenia 2–4 days following its continued use. This leukopenia is generally harmless and resolves with cessation of treatment in 2–3 days. When the leukopenia resolves, silver sulfadiazine may be reapplied without recurrence of this problem. Petroleum-based antimicrobial ointments with polymyxin B, neomycin, and bacitracin are clear on application, painless, allow for observation of the wound, and provide a moist environment. These agents are commonly used for the treatment of facial burns, graft sites, healing donor sites, and small partial-thickness burns. Mupirocin is an ointment that has improved activity against gram-positive bacteria, particularly methicillin-resistant Staphylococcus aureus. Nystatin in powder form can be applied to wounds to control fungal growth, and it can be combined with topical agents such as polymyxin B to decrease colonization of both bacteria and fungi. Available agents for application as a soak include 0.5% silver nitrate solution, 0.5% sodium hypochlorite, 5% acetic acid, and 5% mafenide acetate solution. 0.5% silver nitrate has the advantage of painless application and almost complete antimicrobial coverage. The disadvantages include its staining of surfaces to a dull gray or black when the solution is exposed to light. The solution is hypotonic and continuous use can cause

leaching of electrolytes, with rare methemoglobinemia as another complication. 0.5% hypochlorite is a basic solution with effectiveness against most microbes, but it has a cytotoxic effect on wounds, thus inhibiting healing. Low concentrations of sodium hypochlorite (0.025%) have less cytotoxic effects while maintaining the antimicrobial effects. In addition, hypochlorite ion is inactivated by contact with protein, so the solution must be continually changed. The same is true for acetic acid solutions, although this solution may be more effective against Pseudomonas. Mafenide acetate solution has the same characteristics as the mafenide acetate cream. The use of perioperative systemic antimicrobials has a role in decreasing sepsis in the burn wound until it is healed, also. Common organisms that must be considered when choosing a perioperative regimen include S. aureus and Pseudomonas sp., which are prevalent in wounds. Acinetobacter sp. has emerged as a significant organism in burn wounds, as well.

■ Management of Organ Systems Major burns result in a number of effects to organ systems in addition to injury to the skin. The immense inflammatory focus incited by the burn causes the release of numerous cytokines and inflammatory mediators that have many systemic effects and ultimately, may result in multiorgan dysfunction and death. The systemic inflammatory response syndrome is present in every major burn, but with differing severity, and the kidneys, liver, heart, lungs, hematopoietic system, and coagulation system may be affected. Each of these systems must be supported through the course of the burn injury. After resuscitation and stabilization, evaporative losses through wounds including the area of burn and any donor sites remain high. Many of these patients are placed in air-fluidized beds to decrease shearing of grafts, which also increases evaporative losses. Approximately 3,750 mL/m2 per day of free water is lost through open wounds, and an additional 1 L/m2 per day is lost through continuous airflow past open wounds if treated in an air-fluidized bed. These insensible losses must be added to urine output, stool volume, and respiratory losses in determining fluid balances. Daily weights are useful in determining the response to fluid management. Sodium, potassium, calcium, magnesium, and phosphate are also lost into burn wounds and will require constant monitoring and replacement. Renal failure after a burn occurs in a bimodal fashion, with an early peak that is due to acute tubular necrosis from inadequate early resuscitation and a later peak at 2–4 weeks that is likely due to sepsis and nephrotoxic medications.47,48 Treatment is as with any cause for renal failure. Indications for dialysis include life-threatening congestive heart failure, pulmonary edema, hyperkalemia, and metabolic acidosis refractory to medical management. Continuous venovenous hemodialysis (CVVHD) may have some advantages over routine hemodialysis because of slower fluid fluxes. Peritoneal dialysis is an option in these patients as well, with the same advantages as CVVHD. Catheters for any of these approaches can be placed through burned tissue, although intact skin is preferable.

Burns and Radiation

■ Hypermetabolism in Burns Patients with major burn injury have the highest metabolic rate of all critically ill or injured patients.50 The metabolic response to a severe burn injury is characterized by a hyperdynamic cardiovascular response, increased energy expenditure, loss of lean body mass and body weight, accelerated breakdown of glycogen and protein, lipolysis, immune depression, and delayed wound healing.51,52 This response is mediated by increases in circulating levels of the catabolic hormones including catecholamines, cortisol, and glucagon.52,53 Marked wasting of lean body mass occurs within a few weeks of injury. Modern techniques using immediate total burn excision, rapid wound closure, adequate early enteral feeding, critical care, and control of infection have resulted in a significant reduction in mortality. Hypermetabolism and catabolism of muscle protein continue up to 6–9 months after a severe burn.54 Therefore, nutritional support of burn patients becomes an essential part of treatment during their hospitalization. Pharmacological agents have been used to attenuate catabolism and to stimulate growth after burn injury. Erosion of lean body mass can be further minimized through the use of anabolic hormones such as growth hormone, insulin, insulin-like growth factor (IGF)/IGF-binding protein-3, oxandrolone, and fenofibrate as well as catecholamine antagonists such as propranolol. These agents contribute to maintenance of lean body mass and promote wound healing.55–61

■ Nutritional Management of Burn Patients Nutritional support of severely burned patients is best accomplished by early enteral nutrition that can abate the hypermetabolic response to a burn.62,63 Early enteral feeding preserves gut mucosal integrity, improves intestinal blood flow and motility, and decreases translocation of intestinal bacteria.62 Therefore, nasoduodenal or nasojejunal tube feeding should be commenced as early as within the first 6 hours postburn as long as the patient is not in hypovolemic shock.

TABLE 48-5 Curreri Formula for Estimating Caloric Requirements for Adult Burn Patients64 16–60 years 60 years

25 kcal/kg per day, 40 kcal/% burn per day 25 kcal/kg per day, 65 kcal/% burn per day

The caloric requirements needed to reach weight and nitrogen balance have been calculated from linear regression analysis of weight change versus predicted dietary intakes in adults at 25 kcal/kg plus 40 kcal/% TBSA burn for 24 hours (Table 48-5).64 Nutritional requirements for pediatric patients are based on body surface area (Table 48-6).65–70

RADIATION INJURIES ■ Introduction Our society has used radioactivity to its benefit as an energy source, defensive weapon, and diagnostic and therapeutic medical tool since the discovery of radiation by Becquerel over 100 years ago. With these benefits come hazards in the form of accidents in nuclear power plants, threat of nuclear war, terrorist acts, and potential for radiation injuries from improper use of radioactive isotopes and ionizing radiation. The threat of nuclear or radiation accidents resulting in mass casualties is real and has never been greater as radiation sources are ubiquitous and are available from industrial, military, and medical sources. Major industrial accidents at Three Mile Island, Chernobyl, Goiania, Brazil, and the Tukushima Oaichi Nuclear Power Plant on the eastern shore of Japan after the tsunami on March 11, 2011 have highlighted the need for knowledge of radiation effects and treatment. Exposure to radiation can be classified into the following three types:71 1. Small, contained events affecting one or more persons, either localized or affecting the whole body, for example, laboratory accident or damage from x-ray machines

TABLE 48-6 Formulas for Estimating Caloric Requirements for Pediatric Burn Patients65–70 (Shriners Hospitals for Children at Galveston, Texas) 0–1 year 1–11 years 12–18 years

2,100 kcal/m2 TBSA per day

1,000 kcal/m2 TBSA burn per day 1,800 kcal/m2 TBSA per day

1,300 kcal/m2 TBSA burn per day 1,500 kcal/m2 TBSA per day

1,500 kcal/m2 TBSA burn per day

TBSA  total body surface area.

CHAPTER 48

Hepatic dysfunction can occur because of toxins associated with chemical injury or flame burns in which the patient was doused with chemicals, particularly gasoline. The direct hepatotoxicity that results is manifested by early increases in hepatocellular enzymes. Support through the recovery period is indicated. Later evidence of hepatic dysfunction from sepsis is also common. A striking finding associated with larger burns is the development of a fatty liver, which can increase hepatic size 2- to 3-fold.49 The primary determinant seems to be a relative decrease in efficiency of the very-low-density lipoprotein system to handle the massive increase in delivery of free fatty acids from peripheral lipolysis induced by sustained elevations in serum catecholamines. Fat that cannot be exported is deposited in the liver. Coagulopathies from decreased hepatic synthetic production of coagulation factors, thrombocytopenia, or dilutional effects of massive blood transfusions can occur after a major burn. Treatment is directed toward prevention of massive blood loss through the use of tourniquets, epinephrine application, and thrombin topical sprays.

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2. Industrial accidents affecting large numbers of people with varying degrees of severity, for example, meltdown of a nuclear power plant 3. Detonation of a nuclear device with injuries to hundreds or thousands of people with associated trauma Specific changes noted in association with radiation make these injuries unique and require consideration as a separate form of trauma.72 In explosions, however, the release of kinetic energy can cause other more standard injuries commonly associated with blunt mechanisms. The patients may present with trauma and burns in addition to radiation exposure and explosions. The intent of this part of the chapter is to provide information regarding the terminology associated with radiation, pathophysiology of injury, and diagnosis and treatment of these injuries, including triage and decontamination.

■ Radiation Incidents Radiation incidents within the United States must be reported to the Radiation Emergency Assistance Center/Training Site (REAC/TS) at the Oak Ridge Institute for Science and Education, Oak Ridge Associated Universities in Oak Ridge, Tennessee (http://www.orau.gov/reacts). This agency is funded by the U.S. Department of Energy and provides assistance in the response to all types of radiation accidents or incidents on a 24 hour per day basis. The agency has the capability of providing medical attention and should be contacted to both inform and receive advice about specific incidents. They can assist with calculations of absorbed dose. The telephone number for REAC/TS is (865) 576-1005. The majority of incidents are associated with sealed highly radioactive sources often used in industrial radiography followed by those associated with x-ray machines or the use of unsealed radioisotopes in medicine and uranium products. When fissionable material, usually enriched uranium, has enough neutron flux to undergo a spontaneous nuclear reaction, the material has reached “critical mass,” with the release of uncontrolled radiation. The majority of deaths from radiation incidents occurred after 1975, with most (40) being associated with the Chernobyl incident in 1986. The most devastating loss of life associated with radiation was with the detonation of atomic bombs in Nagasaki and Hiroshima in World War II. Fifty percent of the deaths were related to burn injuries, 30% of which were flash burns from the explosion. Physicians caring for the patients noticed that the burns began to heal, and then, at 1–2 weeks after the injury, began to deteriorate with infection and disordered formation of granulation tissue. A gray, greasy coating of the wounds was described. Associated thrombocytopenia caused bleeding into the wounds and gastrointestinal tract with the ultimate demise of most of these patients. These observations have led to studies into the pathophysiology of these injuries.

■ Measuring Exposure to Radiation Radiation consists of both particles (α, β, and neutrons) and photons (γ and x-rays), which have specific energies and tissue penetrance (Table 48-7). Ionizing radiation can strip electrons

TABLE 48-7 Types of Radiation, Relative Energies, Penetrance, and Relative Hazard

α β γ

Relative Energy (MeV) 1–5 0.2–1.0 0.1–10

Penetrance into Tissue (cm) 0.0007–0.004 0.017–0.34 20–150

Relative Hazard Low Moderate High

from atoms to cause chemical change, resulting in biological damage. The potential for biological injury for each of these depends on the amount of energy transmitted by the particle or photon when it interacts with the target. Each type of radiation has different qualities, and each will be absorbed in differing amounts in tissue. Distance, time, and shielding can reduce exposure from a radiation source. The delivered dose of radiation diminishes over distance from its source by the inverse law.73 If the distance between an object and the source of exposure is doubled, exposure is reduced to one fourth its original value. Dosimetry is the measurement of radiation exposure by detectors that indicate the type, quality, flux, and rate of exposure dependent on the distance of the detector from the source. Geiger–Müller instruments detect β and γ radiation and are useful in the assessment of the effectiveness of decontamination procedures.74 These instruments read counts per minute or milliroentgens per hour of β and γ irradiation. Individual exposure to radiation can be determined using radiation badges that contain a thermoluminescent dosimeter to record the cumulative dose of ionizing radiation on a photographic emulsion.

■ Pathophysiology Cell damage from radiation is caused by the transfer of kinetic energy from particles or photons to existing molecules, causing ionization of mostly oxygen and formation of free radicals such as the hydroxyl radical. These highly toxic compounds react with normal biological molecules to cause cellular damage, mostly to the phospholipid membranes and deoxyribonucleic acid.75 Cell types have different sensitivities to radiation based on individual characteristics. Cells with high proliferation rates are the most sensitive, while those with low proliferation rates are relatively resistant (Table 48-8). For organs made up of resistant cells, most of the effects are on the microvasculature. The overall effect depends on the extent of cellular mass exposed, the duration of exposure, and the homogeneity of the radiation field. Radiation injuries are either localized or whole body, depending on the circumstances of the exposure. The term localized radiation injury refers to an injury involving a relatively small portion of the body that does not lead to systemic effects.73 This is mostly associated with local exposure to low-energy radiation, such as handling of sealed radiation sources of 60Cobalt or 192Iridium for industrial purposes or inadvertent exposure to x-ray beams.74

Burns and Radiation

TABLE 48-9 Four Phases of Acute Radiation Syndrome

Radiosensitivity Cell Types Very high Lymphocytes Hematopoietic cells Intestinal epithelium Spermatogonia, ovarian follicular cells High Urinary bladder epithelium Esophageal epithelium Intermediate Endothelium Fibroblasts Pulmonary epithelium Renal epithelium Hepatocytes Low Hematopoietic stem cells Myocytes Chondrocytes Neural cells

Prodromal phase Latent phase

Dose of exposure determines injury severity. Erythema of the skin is often the first sign, and the sooner its appearance, the higher the dose of exposure. It often appears as a superficial burn at the following intervals of time: (a) early, which will be transitory and short-lived; (b) secondarily, often 2–3 weeks after exposure and immediately preceding moist desquamation; and (c) late, 6–18 weeks after exposure, heralded by vasculitis, swelling, and pain. Depilation is also used to determine the extent of localized injury and may occur as early as 7 days after exposure. It is usually associated with doses of 7–10 Gy, and the hair loss is permanent. Alternatively, with lower doses of 3–5 Gy, depilation occurs at 18–30 days and the hair loss is temporary. Moist desquamation is equivalent to a partial-thickness burn. This develops over a period of 3 weeks and occurs with doses of 12–20 Gy. The latency period is shorter with higher doses. Fullthickness ulceration and necrosis are caused by doses in excess of 25 Gy, and the onset varies from weeks to months after exposure. The microvasculature changes in a characteristic pattern, with surviving superficial vessels becoming telangiectatic and deeper vessels developing obliterative endarteritis. Occlusion of deeper vessels results in full-thickness necrosis.

■ Acute Radiation Syndrome Detonation of a nuclear device can result in enough radiation exposure to cause immediate death for exposed individuals within the lethal area of the blast. The severity of injury from the acute radiation exposure is directly related to the effective dose of radiation to the whole body. Radiation exposure to less than 1 Gy is associated with minimal symptoms and no mortality, but exposure to greater than 8 Gy has 100% mortality.76 LD50/60 is a lethal dose required to kill 50% of the population within 60 days. LD50/60 for human beings is 250–450 rad. The hematopoietic and gastrointestinal systems are affected by radiation because they have rapidly dividing cells. Loss of

Manifest phase

Recovery phase

Nausea, vomiting, fever Symptom-free interval following acute nausea/vomiting Symptoms of hematopoietic, gastrointestinal, and neurologic injury Variable

stem cells and rapidly dividing cells from hematopoietic and gastrointestinal tissues can lead to bleeding, infection, and diarrhea. Acute radiation syndrome has four phases of severity of signs and symptoms (Table 48-9). In the prodromal phase, onset is related to total dose of radiation received. It can be minutes, if a lethal dose (8 Gy) is received, to hours if 2 Gy is received. Fever, nausea, vomiting, and anorexia may last for 2–4 days or longer if a higher dose is received. Gastrointestinal symptoms appearing within 2 hours of radiation usually indicate a fatal outcome. When signs and symptoms regress, the latent phase starts. This may last a few hours to 2–3 weeks or longer depending on the dose of radiation. As the dose of radiation increases, the latent phase becomes shorter. Symptoms of hematopoietic, gastrointestinal, and neurologic syndromes are expressed in a manifest phase following the latent phase. Nausea, vomiting, diarrhea, and bleeding characterize this phase. A recovery phase follows the manifest phase. This phase is variable and may last weeks to months, and if the dose is high enough, death ensues.

■ Whole-Body Exposure Effects of whole-body exposure depend on the dose of radiation absorbed by all tissues of the body. As opposed to local exposure to just the skin, whole-body exposure will lead to much more absorption of energy. For instance, a 5 Gy exposure to the skin of a finger (10 g of tissue) will be a total amount of absorbed energy equaling 500,000 erg. For an absorbed dose of 5 Gy over the whole body (100 kg  100,000 g), the absorbed energy will total 5,000,000,000 erg. Thus, a lower absorbed dose may actually mean a much higher amount of absorbed energy when considered over the whole body. The effects are primarily on the cardiovascular, hematopoietic, gastrointestinal, and central nervous systems. With relatively lower doses, bleeding, infection, and loss of electrolytes can occur from damage to the intestinal mucosa and blood cell components. Higher doses will cause cardiovascular collapse and circulatory failure. The dose absorbed will determine one of the following three courses: 1. Hematopoietic syndrome—Exposure to 1–4 Gy causes pancytopenia with an onset of 48 hours and a nadir at 30 days. Spontaneous bleeding can occur from thrombocytopenia, and opportunistic infections can occur from granulocytopenia. 2. Gastrointestinal syndrome—Exposure to 8–12 Gy will cause gastrointestinal symptoms in addition to pancytopenia.

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TABLE 48-8 Radiosensitivity of Human Cell Types

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Severe nausea, vomiting, abdominal pain, and watery diarrhea occur within hours of the exposure. This resolves, and then the mucosa of the intestine sloughs in 4–7 days, which causes bloody diarrhea and loss of the intestinal barrier and translocation of bacteria. Sepsis and massive fluid losses ensue and cause hypovolemia, acute renal failure, and death. 3. Neurovascular syndrome—An exposure to 15 Gy causes immediate total collapse of vascular tone that is superimposed on the preceding syndromes. This may be caused by the massive release of vasodilatory mediators or destruction of the endothelium.77 This progresses rapidly to shock and death. Regardless of the dose, the first symptom encountered is usually nausea and vomiting, which may resolve before the onset of the other symptoms.

■ Assessment Need for effective field triage and evacuation of casualties is important. In addition, an effective decontamination plan is essential. During stabilization of the patient, information about the incident including the type of radiation, the duration of the exposure, and the distance from and direct contact with the source should be obtained. This information will be necessary to calculate the dose of radiation. Other important information is the background radiation level of the involved area at the time of a radiation incident. Average radiation background in the United States is 360 mrem per year. Any radiation above background level is considered contamination. The history should also include any previous exposures to ionizing radiation. The individual radiation dose is assessed by determining the time to onset and severity of nausea and vomiting, decline in absolute lymphocyte count over several hours or days after exposure, and appearance of chromosomal aberrations including dicentric and ring forms in lymphocytes in peripheral blood. Documentation of clinical signs and symptoms affecting the hematopoietic, gastrointestinal, neurovascular, and cutaneous systems over time is essential for triage of victims, selection of therapy, and assignment of prognosis. A complete blood count with differential should be performed as soon as possible and every 4 hours, with particular attention to the total lymphocyte count (TLC) as the most accurate indication of radiation injury. The rate of decrease in TLC varies inversely with the dose of radiation and therefore, portends the prognosis. A decrease in the TLC by 50% or an absolute TLC of 1,200/mm3 within 48 hours of exposure indicates that at least a moderate dose of radiation has been encountered (Table 48-10).78 Increases in serum amylase and diamine oxidase (specific to enterocytes) may be helpful in determining injury to the intestinal mucosa.79 In patients who have received a large dose of radiation, chromosome dicentric counting should be obtained. Chromosomal analysis of lymphocytes allows for accurate prediction of the received dose of radiation at 48 hours; however, this is impractical in determining the dose acutely.80 Doses under 1 Gy usually will cause no symptoms and do not require admission to the hospital. In similar fashion, patients who are asymptomatic for 24 hours have no major injury.

TABLE 48-10 Significance of Absolute Lymphocyte Count on Prognosis Lymphocyte Count 2,000/mm3 1,200–2,000/mm3 500–1,200/mm3 100–500/mm3 100/mm3

Significance and Prognosis Normal; no injury suspected; prognosis good Mild exposure; significant but probably not lethal Moderate exposure; prognosis guarded Severe exposure; prognosis poor Lethal

■ Triage Like other disaster situations, major radiation accidents and exposures can quickly overwhelm any response system. Treatment facilities may be destroyed, supply distribution may be hampered, and health care workers can be among the injured. For these reasons, triage with resources directed toward those likely to survive is paramount to limit casualties. Unfortunately, the extent of radiation injury may not be initially apparent. Victims should be evacuated as quickly as possible to limit exposure. The patient’s injuries including burns or traumatic injury should be treated, and then symptomatic treatment for the radiation illness should commence. Thermal burns are likely to occur in combination with radiation injury, which makes for a deadly combination. Over 50% of the deaths in Hiroshima and Nagasaki were from thermal burns.81 A thermal burn and radiation injury are synergistic, as animals that receive both injuries have a higher mortality beyond that expected for these injuries either alone or added together.82,83 In case of a nuclear explosion, it has been proposed that patients with burns alone between 20% and 70% should receive the most attention, as they can be expected to survive with adequate treatment. With the addition of a significant radiation injury, only those with less than 30% could be expected to survive.84 Therefore, available resources should be directed at this group if the system is overwhelmed. Under most circumstances, the immediate resuscitation and treatment of life-threatening injuries supersedes treatment for radiation exposure, as the effects of radiation are relatively delayed.

■ Decontamination The first priority in treatment of radiation injury is the stabilization of the patient. Once the resuscitation has begun and the initial assessment is complete, decontamination should be started. Decontamination should occur before access to hospital or treating facility to reduce continued radiation exposure to the patient and eliminate radiation risk to others. Removal of clothing and jewelry and irrigation or washing of the body is an effective way of removing any radioactive contamination. Simply removing the clothes eliminates 90% of the contamination. Decontamination begins with the areas of highest levels of

Burns and Radiation

■ Management of Local Injuries Most radiation injuries are local injuries, frequently involving the hands. These local injuries seldom cause the classical signs and symptoms of the acute radiation syndrome. Local injuries to the skin evolve very slowly over time, and symptoms may not occur for days to weeks after the exposure. Mild erythema should be treated conservatively with dressings, if needed. The lesion may progress to ulceration or chronic radiodermatitis. If no signs or symptoms develop in the first 48 hours, a less severe course can be expected. Dry desquamation can be treated with lotions to moisturize the skin. Moist desquamation should be treated as a second-degree wound with daily dressing changes and topical antimicrobials. Wounds with high radiation exposure may ultimately convert to full-thickness necrosis from obliterative endarteritis and may require skin grafting, flap coverage, or amputation. Early skin grafts may be successfully used on injuries from β radiation, as these particles do not penetrate as deeply. For other types of radiation, vascularized tissue is preferable to skin grafts laid on a wound bed with a questionable long-term blood supply. The decision regarding operative treatment of these wounds is difficult due to the slow progression of the injury. If intervention is performed too early, failure may occur due to progression of the injury. If intervention is performed too late, a chronic wound that may be associated with an increased risk of infection will result.

■ Management of Whole-Body Injuries The management of whole-body irradiation is aimed primarily at symptoms of cellular loss until these systems can regenerate themselves. Except for removal of internal radiation, no

treatment can interrupt the process. Antiemetics to provide symptomatic relief from nausea and vomiting are indicated. Resuscitation may be needed to maintain euvolemia because of volume losses. Patients with exposure to less than 1 Gy can be treated in the outpatient setting if there are no other injuries. For patients with more than 1 Gy exposure, admission to the hospital is indicated until symptoms have subsided. Gastrointestinal bleeding, diarrhea, infections, anemia, and diffuse bleeding from pancytopenia may occur with varying degrees of severity. If the exposure is more than 2 Gy, a bone marrow transplant as a salvage maneuver should be considered. This treatment is performed within 5 days of exposure (transplant will not function for 10–14 days) in a designated center. The blood analysis and cell typing should be completed promptly. A unique and important feature of radiation injury is that a severe exposure may so rapidly deplete the peripheral lymphocytes that none remain to serve as a basis for identification of a donor after the process has begun.85 Infections become problematic in these patients who are profoundly immunosuppressed. Opportunistic organisms are often the cause, and a thorough search for these should ensue when an infection develops. Treatment by physicians experienced in the management of profoundly immunosuppressed patients, particularly those with transplants, is important for success in these situations. All blood products should be irradiated to prevent graft versus host disease. Transplants should be performed at the peak of immunosuppression, which is between 3 and 5 days after a high-dose exposure. The use of hematopoietic growth factors such as granulocyte colonystimulating factor (G-CSF) and granulocyte–macrophage colony-stimulating factor (GM-CSF) has been shown to decrease recovery time, return levels of granulocytes to normal after irradiation, and increase survival in animals and primates.86 Because G-CSF approved for clinical use is readily available, it could be used for radiation victims. GM-CSF is approved for clinical use to increase recovery after bone marrow transplantation.87

SUMMARY The treatment of burns and radiation injuries is complex. Knowledgeable physicians can treat minor injuries in the community. Moderate and severe injuries, however, require treatment in dedicated facilities with resources to maximize the outcomes from these often devastating injuries. The care of patients has markedly improved over the last 40 years, and most patients with massive injuries now survive. Challenges for the future will be in modulation of scar formation and in shortening the time to a functional and visually appealing outcome.

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contamination. Contaminated wounds should be decontaminated prior to decontaminating intact skin. Nasal swabs from each nostril and a throat swab are performed to detect inhalation or radioactive contaminants. If patient has ingested or inhaled radioactive material, urine and stool samples are obtained to measure insoluble radioactive isotopes. Open wounds should be covered with a clean dressing. These wounds are assumed to be contaminated with radioactive material and should be gently irrigated with copious amounts of water, saline, or 3% sodium hydroxide solution. The irrigant should be rinsed to a safe drain with the goal of diluting any radioactive particles without spreading them to adjacent uncontaminated areas. Irrigation is continued until the area indicates a steady state or absence of radiation with a Geiger counter or reaches the background radiation level. Attention should then be turned to the intact skin, where decontamination involves gentle scrubbing of the contaminated sites with a soft brush under a steady stream of water. A 3- to 4-minute scrub with a mild soap or detergent is adequate, also. Following this, an application of povidone iodine or hexachlorophene solution and a 2-minute scrub is recommended. This should be repeated until the skin has a steady state of radiation. After two rounds of the preceding treatment, a diluted mixture of 1 part commercial bleach to 10 parts water can be used to remove further radioactive particles.

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Burns and Radiation 75. Neel JV. Update on the genetic effects of ionizing radiation. JAMA. 1991;32:698. 76. Guskova AK, Baranov AE, Gusev IA. Acute radiation sickness: underlying principles and assessment. In: Guskova AK, Mettler FA Jr, eds. Medical Management of Radiation Accidents. 2nd ed. Boca Raton, FL: CRC Press; 2001:33. 77. Dainiak N, Waselenko JK, Armitage JO, et al. The hematologist and radiation casualties. Hematology. 2003:473. 78. Waselenko JK, MacVittie TJ, Blakely WF, et al. Medical management of the acute radiation syndrome: recommendations of the Strategic National Stockpile Radiation Working Group. Ann Intern Med. 2004; 140:1037. 79. Walden TL, Farzaneh MS. Biological assessment of radiation damage. In: Walker RI, Cerveny TJ, eds. Textbook of Military Medicine. Vol. 2. Virginia: TMM Publications; 1989. 80. Hirsch EF, Bowers GJ. Irradiated trauma victims: the impact on ionizing radiation on surgical considerations following a nuclear mishap. World J Surg. 1992;16:918. 81. Glasstone S, Dolan PJ, eds. The Effects of Nuclear Weapons. Washington, DC: US Atomic Energy Commission; 1977:541. 82. Brooks JW, Evans EI, Han WT. The influence of external body radiation on mortality from thermal burns. Ann Surg. 1953;136:533. 83. Alpen EL, Sheline GE. Combined effects of thermal burns and whole body X irradiation on survival time and mortality. Ann Surg. 1954;140:113. 84. Becker WK, Buesher TM, Cioffi WG. Combined irradiation and thermal injury after nuclear attack. In: Browne D, Weiss JF, MacVittie TJ, et al., eds. Treatment of Radiation Injuries. New York: Plenum; 1990:245. 85. Gale RP. The role of bone marrow transplantation following nuclear accidents. Bone Marrow Transplant. 1987;2:1. 86. Dubos M, Neveux Y, Monpeyssin M, et al. Impact of ionizing radiation on response to thermal and surgical trauma. In: Walker RI, Gruber DF, Mac Vittie TJ, et al., eds. The Pathophysiology of Combined Injury and Trauma. Baltimore: University Press; 1985. 87. Weisdorf D, Chao N, Waselenko JK, et al. Acute radiation injury: contingency planning for triage, supportive care, and transplantation. Biol Blood Marrow Transplant. 2006;12:672.

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60. Cree MG, Zwetsloot JJ, Herndon DN, et al. Insulin sensitivity and mitochondrial function are improved in children with burn injury during a randomized controlled trial of fenofibrate. Ann Surg. 2007;245:214. 61. Herndon DN, Hart DW, Wolf SE, et al. Reversal of catabolism by betablockade after severe burns. N Engl J Med. 2001;345:1223. 62. Mochizuki H, Trocki O, Dominioni L, et al. Mechanism of prevention of postburn hypermetabolism and catabolism by early enteral feeding. Ann Surg. 1984;200:297. 63. Dominioini L, Trocki O, Fang CH, et al. Enteral feeding in burn hypermetabolism: nutritional and metabolic effects at different levels of calorie and protein intake. JPEN J Parenter Enteral Nutr. 1985;9:269. 64. Curreri PW, Richmond D, Marvin J, et al. Dietary requirements of patients with major burns. J Am Diet Assoc. 1974;65:415. 65. Hildreth M, Carvajal HF. Calorie requirements in burned children: a simple formula to estimate daily caloric requirements. J Burn Care Rehabil. 1982;3:78. 66. Hildreth MA, Herndon DN, Parks D, et al. Evaluation of a caloric requirement formula in burned children treated with early excision. J Trauma. 1987;27:188. 67. Hildreth MA, Herndon DN, Desai MH, et al. Caloric needs of adolescent patients with burns. J Burn Care Rehabil. 1989;10:523. 68. Hildreth MA, Herndon DN, Desai MH, et al. Reassessing caloric requirements in pediatric burn patients. J Burn Care Rehabil. 1988;9:616. 69. Hildreth MA, Herndon DN, Desai MH, et al. Current treatment reduces calories required to maintain weight in pediatric patients with burns. J Burn Care Rehabil. 1990;11:405. 70. Hildreth MA, Herndon DN, Desai MH, et al. Caloric requirement of burn patients under 1 year of age. J Burn Care Rehabil. 1993;14:108. 71. Eckerman KF. Annual limits on intakes of radionuclides. In: Lide OR, ed. CRC Handbook of Chemistry and Physics. New York: CRC Press; 2002:16. 72. Conklin JJ, Walker RI, Hirsch EF. Current concepts in the management of radiation injuries and associated trauma. Surg Gyn Obstet. 1983; 156:809. 73. Nenot JC. Medical and surgical management for localized radiation injuries. Int J Radiat Biol. 1990;57:784. 74. Kelsey CA, Mettler FE. Instrumentation and physical dose assessment of radiation accidents. In: Mettler FA, Kelsey CA, Ricks RC, eds. Medical Management of Radiation Accidents. Boca Raton, FL: CRC Press; 1990:294.

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CHAPTER 49

Temperature-Related Syndromes: Hyperthermia, Hypothermia, and Frostbite David H. Ahrenholz

As humans, we are homeothermic mammals who maintain our core temperature within a very narrow range, with a normal diurnal variation of about 1.5°C.1 Temperate climates present a range of temperatures that cause rapid loss of body heat to the environment, and three specific behaviors—fabrication of clothing, shelter-building, and control of fire—have allowed us to populate the earth. But hypothermia occurs when external heat loss exceeds the rate of endogenous thermogenesis. In the initial stages there are no irreversible changes as the metabolic rate slows about 50% for each 10°C drop in core temperature (Arrhenius’ law).2 Under rigidly controlled anesthesia, asystolic arrest occurs between 15–20°C, and a brief state of “suspended animation” can facilitate the completion of otherwise impossible surgical procedures in a relatively bloodless field.3

SYSTEMIC HYPOTHERMIA ■ Primary Accidental Hypothermia Accidental nontraumatic hypothermia, with a core temperature below 35°C, occurs if a normal person is exposed to cool temperatures with inadequate clothing or shelter, and is most common during winter months.4 Initially there is an intense cutaneous vasoconstriction to reduce heat loss, and the exposed skin can rapidly cool to the ambient temperature. The patient experiences thermogenic shivering, which markedly increases oxygen consumption and depletes glycogen stores.5 As the temperature drops, metabolism progressively slows and shivering ceases. The patient becomes confused, lethargic, and cold to the touch. Urine production is profuse as the kidneys lose the ability to transport sodium and other ions. The patient exhibits bradycardia, hypotension, hypovolemia, and metabolic acidosis with elevated blood lactate. Agitation, irrational behavior, and combativeness are replaced by obtundation and finally coma. When cardiac arrest occurs, death is not immediate, but is inevitable without medical intervention.

Cooling is accelerated in windy conditions, but immersion in cold water will remove heat up to 25 times faster than air at the same temperature. Although exceptional athletes can swim for hours in cold water, an unconditioned person may become unconscious within 30 minutes of immersion in 4°C water. Children immersed in cold water quickly become hypothermic and comatose, but if the glottis closes and excludes water from the lungs, they may be resuscitated even if vital signs are undetectable. If a rescued child is given cardiopulmonary resuscitation (CPR) and rapidly rewarmed, survival without neurologic impairment is possible.6 For the responsive hypothermic patient with a core temperature above 34°C, passive rewarming measures with convective warming blankets and warm fluids are adequate.5 Severely hypothermic patients require warmed parenteral fluids to correct the cold-induced diuresis. Urine output will remain brisk during rewarming and is NOT an indicator of adequate intravascular volume. Subclavian or internal jugular catheter placement is avoided because the guide wire can easily trigger ventricular fibrillation of the cold myocardium. A Foley catheter with an integral temperature probe is optimal to monitor the core temperature. Comatose patients require endotracheal and nasogastric tubes to protect the airway and prevent aspiration. If any perfusing rhythm can be detected, administer pressor agents, but avoid chest compressions that may trigger intractable ventricular fibrillation. If no perfusing cardiac activity is noted, begin CPR, and continue until the patient is rewarmed to a temperature that permits successful defibrillation (30°C) (Figure 49-1). During rewarming monitor the patient for electrolyte imbalances, respiratory and renal complications, which may have delayed onset. Mortality of 17–27% is reported.7,8 Patients with hypothermia routinely present with a skin temperature more than 15°C lower than the core temperature,5 so that even in a warmed environment, the core temperature can continue to fall, a phenomenon referred to as “afterdrop.”

Temperature-Related Syndromes: Hyperthermia, Hypothermia, and Frostbite

939

Hypothermia? (T < 35ºC)

Coagulopathic, bleeding in shock?

Intact circulation? Yes

T < 30ºC or highrisk?

CHAPTER 49

Secondary

Primary

No

No

Yes

T < 34.5ºC or decreasing?

CPR Yes

Yes No

Invasive core rewarming and external rewarming

No

Noninvasive core rewarming and/or external rewarming

FIGURE 49-1 Management algorithm for treatment of hypothermia. All patients should also be closely monitored for physiologic complications associated with hypothermia. (Reproduced with permission from Reed RL III, Gentilello LM. Temperature associated injuries and syndromes. In: Mattox KL, Moore EE, Feliciano DV, eds. Trauma. 6th ed. New York: McGraw-Hill; 2008:1071.)

Once shivering stops the patient has little capacity for thermogenesis.5 Immersion of the patient in 40°C water is the most rapid rewarming technique,9 but is contraindicated if the patient requires CPR, emergency surgery, or treatment of open wounds or unstable fractures. Extremely cold or even frozen extremities are not rewarmed until the core temperature reaches 33°C. Then each affected extremity is sequentially immersed as the patient is monitored for any temperature decrease.10 If immersion is not possible, the patient can be rewarmed by extracorporeal bypass11 or with a multiport central venous catheter designed to induce therapeutic hypothermia, usually placed via the femoral vein into the inferior vena cava. Balloons integral to the catheter are irrigated with warm saline via a closed circuit.

1.40–1.71).14 Wang et al. reported similar data from analysis of 38,520 patients in Pennsylvania Trauma Outcome Study (odds ratio 3.03, 95% CI 2.62–3.51).15 Inaba et al. reviewed the mortality of trauma patients undergoing cavitary surgery. Postoperative hypothermia was an independent predictor of mortality (odds ratio 3.2 CI 1.9-5.3).16 Mortality was increased 7-fold for patients with a temperature 33°C versus 35°C. Gentilello et al. showed that hypothermic trauma patients who were aggressively rewarmed had a markedly improved survival compared to those treated with less aggressive methods (Figure 49-2).17 100 90

■ Secondary Metabolic Hypothermia A number of pathophysiologic states can interfere with mechanisms to maintain normothermia. These occur in debilitated or elderly patients secondary to hypothyroidism, adrenal insufficiency, sepsis, or stroke.12 Trauma profoundly disrupts temperature homeostasis and is the most common cause of secondary hypothermia.

% of patients

80 70 60 50 40

Rapid rewarming Slow rewarming

30 20 10 0

■ Hypothermia in Trauma Hypothermia increases the mortality across all trauma age groups. Jurkovich et al.13 reported a 40% mortality in trauma patients with a core temperature 34°C, which increased to 100% in those patients with a core temperature 32°C. A larger retrospective study from the National Trauma Databank using stepwise logistic analysis found that hypothermia independently predicted mortality after trauma (odds ratio 1.54, 95% CI

0

12

24

36

48

72

Survival duration (hours)

FIGURE 49-2 Adjusted cumulative survival (Kaplan–Meier) trauma of patients randomized to rapid or slow rewarming, demonstrating an increase in mortality during resuscitation with slow rewarming (P  0.047). (Reproduced with permission from Gentilello LM, Jurkovich GJ, Stark MS, et al. Is hypothermia in the victim of major trauma protective or harmful? A randomized, prospective study. Ann Surg. 1997;226:439.)

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Hypothermia and Metabolic Reserves

SECTION 4

It is unclear if hypothermia causes increased mortality or if a falling core temperature is a preterminal event as the energy stores are exhausted. Blood adenosine triphosphate (ATP) levels are lower and remain depressed longer in hypothermic trauma patients compared to persons with hypothermia following elective surgery18 or patients with therapeutic hypothermia induced under anesthesia.19 This depletion may be hormonally mediated. Trauma and hypothermia induce profound stress by activating the adrenomedullary hormonal system, hypothalamic–pituitary–adrenocortical axis, and sympathetic nervous system.20

Hypothermia and Immunity Hypothermia impairs immune function by a direct effect on leukocyte-mediated microbial killing. Intraoperative hypothermia is associated with an increase in superficial wound infections following elective surgery.21

Hypothermia and Cardiac Function Hypothermia causes bradycardia, and cardiac output decreases about 7% for each 1°C drop in temperature. The cold myocardium is irritable and ventricular fibrillation is common if chest compressions are used in the presence of bradycardia. Defibrillation is difficult until the heart is rewarmed.22

Hypothermia and Coagulation Cold exerts its most profound adverse effect on the coagulation system, with a marked increase in clinical bleeding even before a change in coagulation test values, which are routinely performed on blood samples warmed to 37°C.23 A host of mechanisms have been implicated including depressed platelet function,24 impaired platelet delivery,25 slowed coagulation enzyme activation,26 activation of protein C,27 and activation of fibrinolysis.28 All of these can contribute to traumatic bleeding, depending upon the temperature and degree of acidosis. The “trauma triad of death” has been defined as hypothermia, acidosis, and massive bleeding following trauma.29 The resulting exsanguination depletes calcium, platelets, and clotting factors and requires early replacement with whole blood. Trauma control laparotomy is optimal in these patients.30 Immediate control of surgical bleeding, packing of the body cavity and temporary closure, followed by intensive efforts to correct acidosis, hypothermia, and replace lost blood are lifesaving.31

THERAPEUTIC HYPOTHERMIA Paradoxically, there is mounting evidence that the effects of cellular hypoxia caused by exsanguinating bleeding are attenuated by subsequent systemic hypothermia.32,33 Reperfusion normally is associated with the elaboration of oxidative metabolites, which increase the ischemic injury. If surgical control of hemorrhage is adequate, induced hypothermia may reduce the hypoxic neurologic sequelae, although the risk of rebleeding is presumably increased.34 Whole body hypothermia has now been advocated to limit the neurologic deficits following treated cardiac arrest, traumatic head injuries35 and even

TABLE 49-1 Clinical Differences Between Potentially Reversible Frostbite and Irreversible Rapid Freeze Injuries

Mechanism of heat transfer Ice location

Cold Contact Injury Flash Freeze Injury Very rapid Any exposed surface Conduction, evaporation Intracellular

Cellular injury

Cellular rupture

Treatment

Topical antimicrobials

Outcome

Delayed skin grafting

Rate of cooling Area affected

Frostbite Relatively slow Digits, nose, ears Convection, radiation Mostly extracellular Dehydration, ischemia, progressive vascular thrombosis Rapid thawing, possible thrombolytics Delayed amputation

hemorrhagic and ischemic stroke.36 Induced hypothermia is used only in the absence of persistent bleeding, with precise monitoring of vital signs and the core temperature. The combination of meperidine and buspirone is most effective to suppress the shivering response.37 The core temperature is maintained at 32–33°C for several days before gradually returning to normothermia. Large randomized clinical trials are planned to study induced hypothermia in carefully selected patients.38

LOCALIZED HYPOTHERMIA Although surgeons describe every local cold injury as frostbite, ice formation in tissue can produce two distinct clinical injuries, frostbite or rapid freeze injury, and both can occur in the same patient (Table 49-1). For human tissue cryopreservation, split thickness skin grafts are slowly frozen, stored at 70°C and will remain viable for a decade or more. Similar slow cooling conditions cause a frostbite injury. But rapid freezing of the same tissue produces immediately nonviable skin, as large intracellular ice crystals rupture the cells (flash freeze injury).39

FROSTBITE Frostbite occurs during moderate rates of tissue cooling, and at about 4°C, ice crystals form in the extracellular fluid. The ice removes water and increases the solute concentration around the cells, which begin to dehydrate and collapse. Cellular metabolism slows and oxygen delivery is reduced. Proximal vasoconstriction preserves core body heat as the distal body parts cool, so the injury is always circumferential, extending from distal to proximal in the digits, ears, and nose.10

Temperature-Related Syndromes: Hyperthermia, Hypothermia, and Frostbite

■ Cold Contact or Flash Freeze Injuries Exposure to cold or pressurized gases (like carbon dioxide, oxygen, nitrogen, or propane), or contact with a cold object, can produce an irreversible freeze injury.44 Plantar injury occurs when walking on ice or snow with unprotected feet. Huge ice crystals form both extracellularly and intracellularly, immediately rupturing the affected cells. The injury may have the appearance of a thermal burn and can affect any body part because escaping gas can pass through layers of clothing. The wounds are treated with topical antimicrobials and skin grafts are applied if the wounds granulate. Lytic agents have no benefit and are contraindicated in these patients.

■ Nonfreezing Cold Injuries Rapid cooling of the exposed skin causes severe pain and pale skin color called frostnip, and have little clinical significance.

Immediate rewarming prevents tissue freezing, but the tissue remains sensitive to changes in temperature. Repeated episodes of near freezing cause chilblains, with intense vasospasm and damage to local nerves. Subsequent cold exposure triggers marked pain with features of Raynaud’s syndrome, which increases the risk of a secondary freezing injury. Treatment is symptomatic.45

SYSTEMIC HYPERTHERMIA Hyperthermia causes more deaths in the United States each year than accidental hypothermia, with epidemics reported in large cities following prolonged hot and humid weather.46 The “heat index” used by the National Weather Service combines environmental temperature and relative humidity to estimate the risk of overheating.

■ Exercise-induced Hyperthermia Exercise increases heat production, which can exceed the cooling capacity of the body. Hyperthermia is common in military training or combat, and in strenuous contact sports or distance running. Certain drugs, especially antipsychotic and anticholinergic agents, block systemic thermoregulation mechanisms and increase the risk of hyperthermia. Systemic hyperthermia begins as heat stress and progresses to heat exhaustion as fluid losses mount and core temperature increases. The hallmarks are intense thirst, weakness, confusion, slurred speech, and incoordination, progressing to weakness, muscle cramps, nausea, and vomiting. The patient is flushed, is sweating profusely, and feels acutely ill. Symptoms persist until the core temperature is lowered and lost fluids and electrolytes are replaced.47 Heat stroke results from a sudden failure of the normal cooling mechanisms as the cutaneous blood vessels paradoxically vasoconstrict and sweating stops.48 The core temperature rises catastrophically and the obtunded patient is unable to seek help. The clinical picture is easily mistaken for a cerebrovascular accident because the patient is pale, cool to the touch and disoriented, paretic, or comatose. Prolonged elevation of core temperature produces irreversible central nervous system injury. Heat stroke accounts for 2% of sudden deaths among competitive athletes,49 and rapid cooling by every means is indicated. Immersion is an ice bath is optimal,50 but removal of clothing, and exposure to any cold object, followed by fluid and salt replacement, can be lifesaving. Heat stroke has been treated with activated protein C.51 Complications of heat stroke include disseminated intravascular coagulation and multiple organ failure, mediated by massive cytokine activation. An extremely high core temperature causes rhabdomyolysis and myoglobinuria, associated with compartment syndrome in affected muscles. Survival in such cases is rare.

■ Iatrogenic Hyperthermia Syndromes Malignant hyperthermia is caused by exposure of susceptible individuals with a unique genetic composition to halogenated anesthetic agents. The prevalence is estimated as high as 1 in 3,000. There is an uncoupling of oxidative phosphorylation,

CHAPTER 49

The tissue is cold, stiff, pale, and insensate. Passive rewarming causes an ischemic injury as metabolism increases before the return of local blood flow. The optimal treatment for frozen digits is rapid rewarming in 40°C water to quickly restore blood flow to tissues as the metabolic rate increases. This is painful and requires parenteral narcotics.40 Immediately after thawing, the frozen tissue becomes bright pink. But the injured endothelial cells predispose to progressive vascular infarction.41 Damaged skin quickly blisters and hemorrhagic bullae indicate a deep injury. The digits turn purplish and mummify over a period of weeks. Traditional treatment includes deflation of blisters, gentle daily cleansing, elevation of the affected parts, and oral ibuprofen.42 Physical therapy is begun as the affected parts heal or demarcate. At Regions Hospital Burn Center since 1994 we have used catheter directed thrombolytic agents in highly selected patients to treat angiographically documented intra-arterial thrombi caused by severe frostbite.43 The angiograms must be performed within 24 hours of rewarming, before a prolonged warm ischemia injury occurs. Arterial catheters are used to infuse thrombolytics to the affected digits and angiograms are repeated daily for a maximum of 72 hours. The infusion is terminated if there is complete return of blood flow to the affected digits or if there is no improvement in flow over 24 hours. In our review of 63 treated patients, 482 digits showed impaired blood flow following frostbite injury. Of the 201 digits with complete resumption of blood flow, only 4 (2%) required an amputation. With partial return of flow, 64% (133/206) of digits were salvaged, but if no distal digit perfusion was obtained, only 5.3% of digits survived. Evaluation and treatment in a burn center is recommended, because lytic therapy is contraindicated if the patient cannot consent, is combative, has a delayed presentation, or has experienced a hemorrhagic stroke, major solid organ injury, recent surgical procedures, or other trauma, freeze– thaw–refreeze injuries, or delay of greater than 24 hours after thawing. Severe arthritis and joint pain secondary to loss of articular cartilage are the most common sequelae of salvaged digits, associated with prolonged severe cold sensitivity or even Raynaud’s phenomenon.

941

942

Specific Challenges in Trauma

SECTION 4

and glucose is rapidly converted to lactate. The heat released causes a precipitous spike in the core temperature that can be rapidly lethal. The treatment follows several steps. First, stop the anesthetic agent and ventilate with pure oxygen to drive off the anesthetic, treat acidosis and reverse anaerobic metabolism. Immediately remove occlusive drapes and begin active cooling— an ice bath is ideal. Then infuse dantrolene to reverse the effects of the anesthetic, and administer glucose to replace the depleted glycogen reserves. Patients with the genetic abnormality can safely receive general anesthesia with alternative anesthetic agents, nitrous oxide and nondepolarizing muscle relaxants.52 The malignant neuroleptic syndrome (MNS) is a rare event in patients receiving antidepressant medications that block dopamine. It has been reported in trauma patients treated with haloperidol for agitation.53 It is also caused by atypical antipsychotic agents, or sudden withdrawal of dopamine agonists such as levodopa. The risk is increased with lithium administration, dehydration, or low serum iron levels. The patient presents with high fever and intense muscle rigidity; lesser features include depressed mentation or coma, tremors, autonomic dysfunction, or dysphagia. The illness is easily mistaken for meningitis, malignant hyperthermia, or drug-induced delirium. Laboratory tests are not diagnostic, although creatinine kinase levels are elevated. The treatment is rapid cooling and rehydration, discontinuation of dopamine blocking agents or restoring dopamine agonists, and supportive measures in the ICU. The reported mortality is 10%.54 Serotonin syndrome is caused by serotonin uptake inhibitors, tricyclic and atypical antidepressants, and monoamine oxidase (MAO) inhibitors. The trauma surgeon encounters the syndrome in association with the use of cocaine, ecstasy, amphetamines, tramadol, fentanyl, or even linazolid. Nausea and diarrhea indicate a mild illness, but delirium, hyperthermia, and autonomic instability can be life threatening. These patients exhibit agitation rather than the stupor of MNS, and require benzodiazepines for sedation, combined with cessation of the causative agent and supportive measures.

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11. Gregory JS, Bergstein JM, Aprahamian C, et al. Comparison of three methods of rewarming from hypothermia: advantages of extracorporeal blood warming. J Trauma. 1991;31:1247–1251. 12. Cooper KE, Ferguson AV, Pozos RS, et al. Thermoregulation and Hypothermia in the Elderly. Minneapolis, MN: University of Minnesota Press; 1983:35. 13. Jurkovich GJ, Greiser WB, Luterman A, et al. Hypothermia in trauma victims: an ominous predictor of survival. J Trauma. 1987;27:1019–1024. 14. Martin RS, Kilgo PD, Miller PR, et al. Injury-associated hypothermia: an analysis of the 2004 National Trauma Data Bank. Shock. 2005;24: 114–118. 15. Wang HE, Callaway CW, Peitzman AB, et al. Admission hypothermia and outcome after major trauma. Crit Care Med. 2005;33:1296–1301. 16. Inaba K, Teixeira PGR, Rhee P, et al. Mortality impact of hypothermia after cavitary explorations in trauma. World J Surg. 2009;33:864–869. 17. Gentilello LM, Jurkovich GJ, Stark MS, et al. Is hypothermia in the victim of major trauma protective or harmful? A randomized, prospective study. Ann Surg. 1997;226:439–447 (discussion 447–449). 18. Seekamp A, van Griensven M, Hildebrandt F, et al. Adenosine-triphosphate in trauma-related and elective hypothermia. J Trauma. 1999;47:673–683. 19. Pape HC. Pathophysiologic changes and effects of hypothermia on outcome in elective surgery and trauma patients. Am J Surg. 2004; 187(3):363–371. 20. Goldstein DS, Kopin IJ. Adrenomedullary, adrenocortical, and sympathoneural responses to stressors: a meta-analysis. Endocr Regul. 2008;42(4):111–119. 21. Kurz A, Sessler DI, Lenhardt R. Perioperative normothermia to reduce the incidence of surgical-wound infection and shorten hospitalization. Study of Wound Infection and Temperature Group. N Engl J Med. 1996; 334:1209–1215. 22. Paton BC, Pozos RE, Wittmer LE. Cardiac Function During Accidental Hypothermia. Minneapolis, MN: University of Minnesota Press; 1983:133–142. 23. Reed R, Johnson T, Hudson J, et al. The disparity between hypothermic coagulopathy and clotting studies. J Trauma. 1992;33:465–470. 24. Valeri C, Feingold H, Cassidy G, et al. Hypothermia-induced reversible platelet dysfunction. Ann Surg. 1987;205:175–181. 25. Cosgriff N, Moore EE, Sauaia A, et al. Predicting life-threatening coagulopathy in the massively transfused trauma patient: hypothermia and acidoses revisited. J Trauma. 1997;42(5):857–862. 26. Brohi K, Cohen MJ, Davenport RA. Acute coagulopathy of trauma: mechanism, identification and effect. Curr Opin Crit Care. 2007;13(6): 680–685. 27. Fries D, Innerhofer P, Schobersberger W. Time for changing coagulation management in trauma-related massive bleeding. Curr Opin Anaesthesiol. 2009;22(2):267–274. 28. Watts DD, Trask A, Soeken K, et al. Hypothermic coagulopathy in trauma: effect of varying levels of hypothermia on enzyme speed, platelet function, and fibrinolytic activity. J Trauma. 1998;44(5):846–854. 29. Mikhail J. The trauma triad of death: hypothermia, acidosis, and coagulopathy. AACN Clin Issues. 1999;10(1):85–94. 30. Stone HH, Strom PR, Mullins RJ. Management of the major coagulopathy with onset during laparotomy. Ann Surg. 1983;197:532. 31. Blackbourne LH. Combat damage control surgery. Crit Care Med. 2008;36(7 suppl):S304–S310. 32. Fukudome EY, Alam HB. Hypothermia in multisystem trauma. Crit Care Med. 2009;37(7 suppl):S265–S272. 33. Varon J. Therapeutic hypothermia: implications for acute care practitioners. Postgrad Med. 2010;122(1):19–27. 34. Kheirbek T, Kochanek AR, Alam HB. Hypothermia in bleeding trauma: a friend or a foe? Scand J Trauma Resusc Emerg Med. 2009;17(1):65. 35. Sinclair HL, Andrews PJD. Bench-to-bedside review: hypothermia in traumatic brain injury. Critical Care. 2010;14:204–214. 36. Linares G, Mayer SA. Hypothermia for the treatment of ischemic and hemorrhagic stroke. Crit Care Med. 2009;37(7 suppl):S243–S249. 37. Sessler DI. Defeating normal thermoregulatory defenses: induction of therapeutic hypothermia. Stroke. 2009;40(11):e614–e621. 38. van der Worp HB, Macleod MR, Kollmar R; European Stroke Research Network for Hypothermia (EuroHYP). Therapeutic hypothermia for acute ischemic stroke: ready to start large randomized trials? J Cereb Blood Flow Metab. 2010;30(6):1079–1093. 39. Ahrenholz DH. Frostbite injuries. Probl Gen Surg. 2003;20:129–137. 40. Purdue GF, Hunt JL. Cold injury: a collective review. J Burn Care Rehabil. 1986;7(4):331–342. 41. Britt LD, Dascombe WH, Rodriguez A. New horizons in management of hypothermia and frostbite injury. Surg Clin North Am. 1991;71(2): 345–370.

Temperature-Related Syndromes: Hyperthermia, Hypothermia, and Frostbite 49. Maron BJ, Doerer JJ, Haas TS, et al. Sudden deaths in young competitive athletes: analysis of 1866 deaths in the United States, 1980–2006. Circulation. 2009;119(8):1085–1092. 50. McDermott BP, Casa DJ, Ganio MS, et al. Acute whole-body cooling for exercise-induced hyperthermia: a systematic review. J Athl Train. 2009;44(1):84–93. 51. Chen CC, Chen ZC, Lin MT, et al. Activated protein C improves heatstroke outcomes through restoration of normal hypothalamic and thermoregulatory function. Am J Med Sci. 2009;338(5):382–387. 52. Wappler F. Anesthesia for patients with a history of malignant hyperthermia. Curr Opin Anaesthesiol. 2010;23(3):417–422. 53. Bellamy CJ, Kane-Gill SL, Falcione BA, et al. Neuroleptic malignant syndrome in traumatic brain injury patients treated with haloperidol. J Trauma. 2009;66(3):954–958. 54. Nisijima K, Shioda K, Iwamura T. Neuroleptic malignant syndrome and serotonin syndrome. Prog Brain Res. 2007;162:81–104.

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42. McCauley RL, Hing DN, Robson MC, et al. Frostbite injuries: a rational approach based on the pathophysiology. J Trauma. 1983;23(2):143–147. 43. Jenabzadeh K, Ahrenholz DH, Mohr Wm III. Frostbite: a single institution’s twenty year experience with intra-arterial thrombolytic therapy. J Burn Care Res. 2009;30(2 suppl):S103. 44. Camp DF, Ateaque A, Dickson WA. Cryogenic burns from aerosol sprays: a report of two cases and review of the literature. Br J Plast Surg. 2003;56(8):815–817. 45. Prakash S, Weisman MH. Idiopathic chilblains. Am J Med. 2009;122 (12):1152–1155. 46. Semenza JC, Rubin CH, Falter KH, et al. Heat-related deaths during the July 1995 heat wave in Chicago. N Engl J Med. 1996;335:84–90. 47. Noakes TD. Hydration in the marathon: using thirst to gauge safe fluid replacement. Sports Med. 2007;37(4–5):463–466. 48. Bouchama A, Dehbi M, Chaves-Carballo E. Cooling and hemodynamic management in heatstroke: practical recommendations. Crit Care. 2007; 11(3):R54

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Organ Procurement for Transplantation Aditya K. Kaza and Max B. Mitchell

This chapter is relevant to all surgeons caring for victims of trauma because traumatic injury is a leading cause of brain death and subsequent organ donation. Because of the severe shortage of organ donors, it is critical that traumatologists recognize potential organ donors as early as possible and care for these patients assuming that organ donation may occur. It is important for physicians to understand the criteria for brain death and the local requirements for the pronunciation of brain death. This chapter provides an overview of the procurement organization and how organs are allocated. The responsibilities of the local organ procurement organizations (OPOs) are underscored in this chapter (i.e., community education, evaluation and screening of potential donors, local hospital coordination, and family counseling). The trauma team’s role is to resuscitate the patient and maintain perfusion of the organs. Once a potential donor is identified the trauma team must coordinate its efforts with the OPO. Once a patient is declared brain dead the trauma team’s role does not end. Cooperation between the trauma team and representatives of the OPO will help to maximize donation of organs and is important for preserving the function of donated organs.

INTRODUCTION The combined developments of effective immunosuppressant therapy and sophisticated surgical techniques have made organ transplantation very successful in treating the end-stage failure of most solid organs. Transplantation is now the treatment of choice for end-stage heart, lung, liver, and renal disease for patients who have no contraindications to transplantation. Pancreas transplantation has also proven successful in the treatment of diabetes mellitus. In addition, there is increasing demand for bone, skin, and other tissues used in the treatment of other disease processes. Despite advances in living-related solid organ transplantation,1 the majority of transplant recipients remain dependent on cadaveric organ donors.2 Improved

supportive care for patients with advanced organ failure and expanded indications for transplantation have increased the numbers of patients waiting for organs. In contrast, efforts at increasing the pool of suitable organ donors have had comparatively little success in increasing the supply of organ donors; however, there is a slow increase in living donors as noted from 1988 to 2005 (Fig. 50-1). Consequently, the number of patients on the various transplant waiting lists continues to outpace the available donor pool. In the year 2000, an average of 114 patients were placed on waiting lists each day while an average of 63 patients per day received organ transplants.3 During the same year, an average of 16 patients per day died awaiting transplantation.3 Traumatic brain injury is the most common cause of death leading to cadaveric solid organ donation.4 Clinicians caring for severely injured patients necessarily play a key role in the initiation and implementation of the transplantation process. Early recognition of potential organ donors is critical to maximizing the available pool of donor organs and the number of transplantable organs per donor. It is essential for those caring for potential organ donors to be knowledgeable about the criteria and process for declaring brain death and the physiologic effects of brain death. Familiarity with local OPOs is important because of the vital role they play in counseling the families of potential organ donors and coordinating the transplant process. Lastly, following the declaration of brain death, treatment priorities aimed at minimizing brain injury require adjustment. Physiologic support directed at maintaining perfusion of potentially transplantable organs assumes priority, and timely initiation of this support is crucial to increasing the probability of successful transplantation.

ORGAN DONATION AND ALLOCATION Under the National Organ Transplant Act (Pub. L. No. 98-507, Title I, 1984), the U.S. Congress established The Organ Procurement and Transplantation Network (OPTN).

Organ Procurement for Transplantation

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Donor type Deceased donor Living donor

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20,047

Transplants

16,038

12,028

8,019

4,009

0 2005

2004

2003

2002

2001

2000

1999

1998

1997

1996

1995

1994

1993

1992

1991

1990

1989

1988

Transplant year

FIGURE 50-1 Total patients in the United States who underwent organ transplantation from deceased and living donors from 1988 to 2005. (Reproduced with permission from United Network for Organ Sharing website. Accessed February 2005. http://www.unos.org/Data.)

The OPTN is a unique public–private partnership linking professionals involved in the organ donation and transplantation system. Subsequent federal legislation mandated that all U.S. transplant centers and OPOs must be members of the OPTN to receive any funds through Medicare or Medicaid (H. Rep. No. 100-383, 1987, and Pub. L. No. 100-607, Title IV, 1988). Other members of the OPTN include independent histocompatibility laboratories involved in organ transplantation; relevant medical, scientific, and professional organizations; voluntary health and patient advocacy organizations; and members of the general public with a particular interest in organ transplantation. The OPTN is administered by the United Network for Organ Sharing (UNOS). UNOS is a private nonprofit charitable organization contracted by the Health Resources and Services Administration of the U.S. Department of Health and Human Services (DHHSS) to develop organ transplantation policy.5 Policy recommendations are then adopted and enforced by the DHHSS. UNOS facilitates organ transplantation by organizing the medical, scientific, public policy, and technologic resources required to maintain an efficient national transplantation system. UNOS is responsible for developing recipient priority policies and for managing the national transplant waiting lists. UNOS also sets professional standards for efficiency and patient care for transplant centers. UNOS maintains the national transplant database, plays a very important role in raising public awareness of the importance of organ donation, and helps to keep patients informed about transplant issues and policy.6 Organ donation, allocation, and procurement require a closely coordinated and complex series of efforts. In the United States, this process is coordinated by independent local OPOs. OPOs employ specially trained professionals who assist with the evaluation of potential organ donors, the declaration of

brain death, counseling of donor family members, management of the donor, organ allocation, and the procurement process. When an organ donor is identified, the local OPO serves to ensure that brain death has been established and assists in obtaining consent for organ donation. Thereafter, coordination of organ placement and the procurement of the organs are facilitated by the OPO. There are currently 51 cooperating OPOs in the United States, distributed among 11 geographic regions. The regional system plays a pivotal role in the current process of allocating organs for transplantation. It was established to help reduce organ preservation time and improve organ quality and survival outcomes. In addition, it was intended to reduce the costs of organ transplantation and provide equal access to transplantation for patients regardless of where they live. Donor organs are matched to individual patients according to waiting lists developed and coordinated by UNOS. Each organ waiting list incorporates specific criteria to establish individual patient ranking on the list. All lists incorporate patient waiting time and patient ABO blood grouping. For lung transplantation, these are the primary factors. The kidney waiting list also incorporates the degree of human lymphocyte antigen matching so that top priority is given to patients with a perfect human leukocyte antigens (HLA) match. This is not done for other organs. The heart and liver waiting lists differ by including organ-specific criteria to establish severity of illness prioritizing the sickest patients. All lists are patient specific so that organs are offered to an individual patient on a center’s list as opposed to the center. Organs are first offered locally within the boundaries of the involved OPO. If the organ is declined by all local centers, it is then offered regionally followed by national offers. There has been significant recent debate regarding the current allocation system with some parties advocating a nationally based system.7 Such a system would be predicated

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primarily on the severity of illness followed by waiting time while eliminating consideration of the region from which the organ originates. At this time, no changes in this system have been adopted.

DONOR SCREENING The screening process for organ donors begins when a potential organ donor is identified. All patients who have suffered severe brain injuries and are either brain dead or likely to progress to brain death should be considered for organ donation regardless of their age, underlying cause of illness, and overall social history. Although perceived contraindications to donation may exist, they should be discussed with a representative of the local OPO before concluding that a given patient is not a candidate for organ donation (Table 50-1). The physician caring for the patient is responsible for notifying the local OPO of such patients. In many states physicians are legally required to notify the local OPO of each in-hospital death. All OPOs employ personnel who are responsible for advising health care providers on the suitability of an individual patient for organ donation. Communication with local forensic authorities is extremely important. The OPO will contact the medical examiner or coroner in order to obtain permission to proceed with organ donation. Once a donor is identified, the OPO is responsible for obtaining family consent for organ donation. Organ procurement specialists are trained in counseling families about the importance and process of organ donation, and it is advisable to refer families to these specialists when potential organ donation is discussed. These individuals also perform a careful review of the potential donor’s social and past medical history. The circumstances leading to brain death are very important, as is any history of the occurrence and duration of cardiopulmonary arrest. Screening also includes an extensive laboratory and serologic evaluation to exclude chronic disease and transmissible infections. A donor profile is then generated and includes current hemodynamics as well as an assessment of current organ function. The assessment of organ function is individualized to the donor based on the donor profile, the specific organs under consideration, and the level of medical support required to maintain the donor. The overall profile that is generated is crucial for transplant physicians who must evaluate the suitability of a given organ donor for the individual recipient.

TABLE 50-1 Contraindications to Organ Donationa Absolute Uncontrolled sepsis Extracranial malignancy Chronic transmissible infections: Tuberculosis HIV Coroner exclusion a

Relative Bacteremia Fungemia High-risk social history

Organ-specific exclusions also exist.

DECLARATION OF BRAIN DEATH Ethical standards in the United States mandate that all organ donors must be declared dead before organ donation can proceed. Brain death must therefore constitute a sufficient basis on which to declare a person legally dead. Despite continued interest in non-heart beating donors, the vast majority of cadaveric organs are procured from donors whose deaths are declared on the basis of brain death. Consequently, cadaveric solid organ donation is dependent on the ability to reliably determine that a patient is brain dead.8 Unfortunately, many clinicians remain poorly informed about brain death and how it is defined. The current concept of brain death used in the United States is based on guidelines published in 1981 by the President’s Commission for the Study of Ethical Problems and adopted under the Uniform Determination of Death Act (Table 50-2).9,10 This act states that death has occurred when there is irreversible cessation of all functions of the brain including the brain stem. Each state government has adopted these guidelines in legislating local criteria for the determination of brain death. The qualifications and number of physicians who must agree on the diagnosis of brain death in order to legally declare a patient brain dead vary considerably among the 50 states. Some states require two separate declaration procedures with a defined time interval between the two examinations. Some states require that the declaration be made by two separate physicians. In other states a single physician may declare a patient brain dead on the basis of one examination. In no case can the declaring physician take part in the recovery or transplantation of organs from the donor. Most hospitals have established policies within state guidelines for physician qualifications required to make the diagnosis of brain death. Physicians caring for these patients should be aware of local requirements and hospital guidelines in order to facilitate the declaration process and allow termination of care for brain dead patients who will not be organ donors.

TABLE 50-2 Defining Brain Death: Guidelines of the President’s Commission for the Study of Ethical Problems in Medicine (1981) Preconditions Coma with known cause Documentation of irreversible structural brain injury Exclusions (preclude diagnosis of coma) Hypotension Hypothermia Hypoxemia Drug intoxication Metabolic derangements Tests Absence of brain stem function pupillary, corneal, oculovestibular, gag, cough reflexes absent Apnea (strict definition) EEG not indicated

Organ Procurement for Transplantation used for this purpose with the exception of brain death determination in young infants. BAER testing involves measuring electrical waveforms generated in the brain stem in response to an auditory stimulus transmitted by headphones. In the brain dead patient no waveform will be detectable. BAER testing is rarely used at this time. Demonstration of the absence of cerebral blood flow is the most common confirmatory test currently in use. Methods used to make this determination include cerebral angiography, cerebral blood flow Doppler ultrasound scanning, and radionucleide cerebral blood flow scanning. The latter two methods are noninvasive, low risk, relatively inexpensive, and are more readily available than cerebral angiography. These tests are highly accurate in verifying the absence of cerebral blood flow and are useful in reducing the time required to establish the diagnosis of brain death. Conversely, an examination that indicates continued cerebral blood flow does not necessarily exclude the diagnosis of brain death. Uncommonly, cerebral blood flow may persist despite brain death due to testing before increasing intracranial pressure completely shuts down flow, skull pliability in infancy or in the presence of decompressing fractures, ventricular shunts, ineffective deep brain flow, reperfusion, brain herniation, jugular reflux, the presence of emissary veins, and pressure injection artifacts.14 Appropriate documentation of brain death is very important in facilitating organ donation for a brain dead patient. The diagnosis of brain death must be documented in writing and it must be unequivocal. The circumstances leading to brain injury, the specific findings of the neurologic examination, and the results of any confirmatory tests should be clearly recorded. Lastly, the date and time of the declaration of brain death must be noted before OPO personnel may obtain the permission of local authorities and the consent of the potential donor’s family. Despite the presence of evidence indicating a person’s desire to be an organ donor, family consent for donation must be obtained. Family refusal is the most common reason that otherwise suitable donors do not become organ donors. If consent for donation is declined, appropriate testing and documentation of brain death is necessary in order to initiate the withdrawal of care.

PHYSIOLOGIC CONSEQUENCES OF BRAIN DEATH Brain death has profound effects on virtually all organ systems either directly or secondarily as a consequence of the accompanying effects on the cardiovascular and respiratory systems.15 Disruption of normal autonomic innervation may lead to profound vasodilation and hypotension. In turn decreased organ perfusion is injurious to potentially transplantable organs. Direct myocardial depression may occur and is largely due to increased sympathetic outflow as a response to sudden increases in intracranial pressure.15 This may lead to arrhythmias, myocardial ischemia, and in some cases myocardial infarction. Circulatory instability impairs distal organ perfusion leading to significant injury that may preclude organ donation. Respiratory dysfunction associated with brain death will have profound effects on all other organ systems. Impaired gas exchange is common in brain dead patients who have required mechanical ventilation for any length of time. Pulmonary infection and or aspiration injury frequently occur in potential organ donors

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Symptoms that support the diagnosis of brain death are the absence of brain stem reflexes, absence of cortical activity, and the demonstration of the irreversibility of this state.8 Therefore, in order to declare brain death there must be proof of the cause of brain injury; otherwise, the irreversibility requirement cannot be met.11 A patient found unresponsive with no clear cause of brain death generally cannot be an organ donor. Secondly, all reversible causes of coma must be excluded. Causes of reversible coma include hypothermia, hypoxia, hypoglycemia, hyperglycemia, uremia, hepatic failure, Reye’s syndrome, hyponatremia, hypercalcemia, myxedema, adrenal failure, and central nervous system (CNS) depressants. The presence of CNS depressing agents such as narcotics, sedatives, anticonvulsants, anesthetics, and alcohol must be assessed. If any of these agents are present, confirmatory testing is usually required to declare brain death.12 In the brain dead patient, all cranial nerve function will be absent. The absence of brain stem reflexes must be confirmed by careful neurologic examination. Neuromuscular conduction must be intact in order to allow adequate examination; consequently, the presence of neuromuscular blocking agents must be excluded. The most definitive finding supporting the diagnosis of brain death is the presence of apnea. The apnea test remains one of the most important parts of the neurologic evaluation of potential organ donors.13 To perform a reliable apnea test the PaCO2 is normalized to 40 mm Hg. The patient is preoxygenated with 100% O2 for at least 5 minutes. The patient is then disconnected from the ventilator and placed on 100% O2 delivered passively to the endotracheal tube via a T-piece at 8–12 L/min. The PaCO2 is allowed to rise to 60 mm Hg, confirmed by a blood gas drawn after approximately 10 minutes. If hemodynamic instability occurs, the patient should be immediately returned to mechanical ventilation and a blood gas should be drawn to assess the PaCO2. If there is any evidence of respiratory activity, the patient is not brain dead and should be immediately returned to the ventilator. If there is no evidence of spontaneous respiratory activity, the PaCO2 has reached 60 mm Hg, and the pH is acidotic, apnea is established and is strongly supportive of brain death. In many cases confirmatory testing must be performed in addition to a careful neurologic examination in order to firmly establish the diagnosis of brain death. Patients with cervical fractures above the level of C4 may not have intact diaphragmatic function precluding a reliable apnea test. Apnea testing is also unreliable in cases involving overdoses of substances that depress respiratory drive such as alcohol, antiseizure medications, and sedatives. Hemodynamic instability during apnea testing will also preclude the establishment of the diagnosis of brain death on the basis of apnea. In other cases local requirements and or hospital policy may dictate the use of additional confirmatory testing. Confirmatory tests may also be useful in demonstrating a clear etiology for brain death or severe anatomic damage and can decrease the observation period required to establish the diagnosis of brain death.12 Confirmatory tests of brain death include electroencephalogram (EEG), testing of brain stem auditory-evoked response (BAER), and methods of demonstrating the absence of cerebral blood flow. EEGs are not entirely reliable and are now rarely

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either prior to or early after the time of endotracheal intubation. Neurogenic pulmonary edema is another cause of impaired gas exchange that may accompany brain death.16 Myocardial dysfunction may also contribute to lung dysfunction due to increases in left atrial pressure thereby potentiating pulmonary edema. Similarly, hypoxemia will further impair myocardial function leading to a precarious hemodynamic state. Endocrine dysfunction is also common. The absence of hypothalamic function leads to the loss of thermoregulation and is manifested by the development of hypothermia. Impaired thyroid regulation contributes to hypothermia, and circulatory instability. Diabetes insipidus is common because antidiuretic hormone is no longer released from the posterior pituitary. If not managed appropriately diabetes insipidus will have a profound effect on fluid and electrolyte balance. The systemic release of substances from necrotic brain tissue may lead to disseminated intravascular coagulation producing a consumptive coagulopathy that is often exacerbated by hypothermia. Without appropriate intervention brain death is followed by severe injury to all other organs, and circulatory collapse will usually occur within 48 hours.

DONOR MANAGEMENT Prior to the declaration of brain death, the treatment of patients with severe brain injury is directed at controlling intracranial pressure and preserving cerebral perfusion pressure in order to limit secondary brain injury. Once the diagnosis of brain death is established and a patient is recognized as a potential organ donor, treatment priorities must shift in favor of preserving the function of potentially transplantable organs. Preservation of organ function requires maintenance of adequate organ perfusion. Therefore, the goal of donor management should be to normalize hemodynamics and maintain biochemical parameters of organ function in as normal a condition as possible. Because of the profound effects on the cardiovascular system, invasive hemodynamic monitoring is essential to guide the appropriate resuscitation of brain dead patients. Central venous access should be obtained to allow measurement of volume status and to provide a reliable means of administering vasoactive drugs. Arterial access is required to facilitate continuous monitoring of blood pressure and frequent measurements of acid–base status, gas exchange, and serum biochemical parameters. Hypovolemia is common in brain dead patients due to vasodilation and in some cases blood loss as a result of trauma or fluid loss due to diabetes insipidus. In general, patients should be resuscitated with crystalloid and appropriate blood products based on measurements of hematocrit and coagulation status. Resuscitation should be guided by frequent monitoring of central venous pressure or pulmonary capillary wedge pressure. Body temperature must be monitored and should be maintained above 36°C using passive warming as needed. Urine output should be maintained at 2 mL/kg/h. Renal dose dopamine (3–5 μg/kg/min) is recommended for nearly all donors unless higher doses are required to maintain perfusion. Vasopressin should be infused to treat diabetes insipidus when present, and fluids should be adjusted on the basis of electrolyte measurements.17 This will usually require the administration of 5% dextrose solution.

Serum sodium and osmolarity should be kept as normal as possible. Replacement fluids should be based on measurements of serum electrolytes and urine output. Frequent serum glucose measurements are required to facilitate treatment of hyperglycemia. Excess fluid administration may lead to pulmonary edema causing the lungs to become unsuitable for transplantation. Therefore, judicious fluid resuscitation is important in order to maximize the number of transplantable organs. Inotropic support should be introduced to support blood pressure if initial volume resuscitation fails to restore adequate perfusion pressure.18 Dopamine is usually the first agent of choice. Pure vasoconstrictors such as norepinephrine should be avoided whenever possible due to deleterious effects on myocardial, and splancnic perfusion. Dobutamine is frequently added to increase cardiac output. If these agents are not effective at restoring hemodynamic stability, an epinephrine infusion should be initiated and titrated to the lowest dose required to achieve adequate support. Thyroxine (T4) or triiodothyronine (T3) infusions are commonly used due to their inotropic effects and potentiation of myocardial catecholamine sensitivity.19 However, there is continuing controversy regarding whether or not the use of thyroid hormone infusions have a beneficial effect on organ function following transplantation. Consequently, thyroid infusions should be used primarily at the discretion of OPO representatives in consultation with their medical directors and the involved transplant physicians. Ventilator management in potential organ donors is dependent on the respiratory function of the donor. Pulmonary injury is common in brain dead patients, and all attempts should be made to preserve the possibility of lung donation. As mentioned previously, fluids must be managed carefully and should be guided by measurements of central venous pressure. Chest radiographs should be obtained to assess pulmonary expansion, guide appropriate intervention to counteract atalectasis, and assess the suitability for transplantation. A nasogastric tube should be placed and kept on suction in order to minimize gastric distension and the risk of aspiration. An endotracheal tube with an internal diameter of 7.5 mm or larger should be inserted whenever possible in order to accommodate a therapeutic size fiberoptic bronchoscope. This will assist in the evaluation of potential lung donation and will facilitate clearing secretions to optimize lung expansion. Excessive mean airway pressures should be avoided. Tidal volumes and physiologic levels of positive end-expiratory pressures (PEEP) should be maintained to provide adequate lung expansion and minimize atalectasis. High concentrations of inspired oxygen are injurious to the lungs and should be avoided. The inspired oxygen concentration should be titrated to maintain an oxygen saturation of 95%. In patients with significant pulmonary injury, lung donation is unlikely; therefore, increased levels of PEEP and higher inspired oxygen concentrations may be required.

ORGAN PROCUREMENT The actual process of multiorgan procurement occurs in the operating room environment under the usual sterile conditions.20 Representatives of the local OPO will coordinate the use of the operating room with the arrival of the various transplant

Organ Procurement for Transplantation

CONCLUSION Organ transplantation benefits thousands of people every year in the United States alone. However, donor organs remain a precious resource as evidenced by increasing recipient waiting

times and the increasing number of patients who die waiting for donor organs. Efforts at expanding the available donor pool have not kept up with the need for organs. More recent efforts include the use of non-heart beating donation strategies,21 the relaxation of donor organ criteria for recipients who would otherwise not be candidates for transplantation,22 and other strategies. In general, these measures have not been widely adopted and the donor to recipient disparity will undoubtedly continue. Advances in the development of artificial organs and xenotransplantation hold great promise in relieving this situation. Nevertheless, health care providers who care for traumatically injured patients will continue to play an important role in the identification and critical care management of potential organ donors for the foreseeable future.

REFERENCES 1. Bak T, Wachs M, Trotter J, et al. Adult-to-adult living donor liver transplantation using right-lobe grafts: results and lessons learned from a single-center experience. Liver Transpl. 2001;7:680. 2. UNOS Website. 2000 Annual report of the U.S. Scientific Registry for transplant recipients and the Organ Procurement and Transplant Network transplant data: 1990–1999. http://www.unos.org/Data/ anrpt00/ar00_data_fig_01.htm. Accessed January 6, 2002. 3. UNOS Website. http://www.unos.org/Newsroon/archive_newsrelease_ 20011220_statquote.htm. Accessed January 12, 2002. 4. UNOS Website. 2000 Annual report of the U.S. Scientific Registry for transplant recipients and the Organ Procurement and Transplant Network transplant data: 1990–1999. http://www.unos.org/Data/ anrpt00/ar00_table12_05_alld.htm. Accessed January 6, 2002. 5. UNOS Website. http://www.unos.org/About/who_main.htm. Accessed January 12, 2002. 6. UNOS Website. http://www.unos.org/About/what_main.htm. Accessed January 12, 2002. 7. Fung J. Survival of the sickest. Organ allocation should be based on patients’ medical need, not location. Mod Healthc. 1998;28:29. 8. Beresford HR. Brain death. Neurol Clin. 1999;17:295. 9. President’s Commission for the Study of Ethical Problems in Medicine and Biomedical Behavioral Research: Defining Death. A Report on the Medical, Legal, and Ethical Issues in Determination of Death. Washington, DC: U.S. Government Printing Office; 1981:1. 10. Beecher HK, Adams RD, Banger AC. A definition of irreversible coma. Report of the Ad Hoc Committee of the Harvard Medical School to Examine the Definition of Brain Death. JAMA. 1968;205:337. 11. Lazar NM, Shemie S, Webster GC, et al. Bioethics for clinicians: 24. Brain death. CMAJ. 2001;164:833. 12. Lopez-Navidad A, Caballero F, Domingo P, et al. Early diagnosis of brain death in patients treated with central nervous system depressant drugs. Transplantation. 2000;70:131. 13. Lessard M, Mallais R, Turmel A. Apnea test in the diagnosis of brain death. Can J Neurol Sci. 2000;27:353. 14. Flowers WM Jr, Patel BR. Persistence of cerebral blood flow after brain death. South Med J. 2000;93:364. 15. Power BM, Van Heerden PV. The physiological changes associated with brain death–current concepts and implications for treatment of the brain dead organ donor. Anaesth Intensive Care. 1995;23:26. 16. Rogers FB, Shackford SR, Trevisani GT, et al. Neurogenic pulmonary edema in fatal and nonfatal head injuries. J Trauma. 1995;39:860. 17. Powner DJ, Kellum JA, Darby JM. Abnormalities in fluids, electrolytes, and metabolism of organ donors. Prog Transplant. 2000;10:88. 18. Powner DJ, Darby JM. Management of variations in blood pressure during care of organ donors. Prog Transplant. 2000;10:25. 19. Roels L, Pirenne J, Delooz H, et al. Effect of triiodothyronine replacement therapy on maintenance characteristics and organ availability in hemodynamically unstable donors. Transplant Proc. 2000;32:1564. 20. Van Buren CT, Barakat O. Organ donation and retrieval. Surg Clin North Am. 1994;74:1055. 21. Fung JJ. Use of non-heart-beating donors. Transplant Proc. 2000; 32:1510. 22. Laks H, Marelli D. The alternate recipient list for heart transplantation: a model for expansion of the donor pool. Adv Card Surg. 1999;11:233.

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procurement teams involved with a particular donor. Frequently, this procedure may involve several teams whose members are operating together for the first time. In addition, the initial phases of the transplant operations for heart and lung recipients are commonly carried out simultaneously with the donor procurement procedure in order to minimize graft ischemia time. An anesthesiologist is required to provide physiologic support of the donor during the procurement procedure. The donor patient is prepped and draped to allow an incision from the sternal notch to the pubis. In this manner, the thoracic and abdominal organs can be evaluated and procured simultaneously. In all cases, the final determination of organ suitability for transplantation is made after visual inspection and manual palpation of the organ. Biopsy of any suspicious lesions should be performed, and pathologic evaluation of frozen sections must be confirmed before the recipient transplant operation is initiated. Similarly, a liver biopsy may be required to evaluate the degree of fatty infiltration present in some donors. Following inspection the thoracic and abdominal organs are dissected to allow rapid removal after flushing with the appropriate preservation solution. There are numerous preservation solutions in use and vary according to the organ being procured and the preference of the procuring institution. All preservation solutions are kept at approximately 4°C because hypothermia is a key element of organ preservation. After all intended organs are dissected, the patient is systemically anticoagulated with heparin. Appropriate vascular cannulas are inserted in the abdominal and thoracic vessels to allow rapid flushing of the organs being procured. When all members of the procuring teams are prepared the superior vena cava, ascending aorta, and the supraceliac aorta are clamped. The inferior vena cava is transected at the cavoatrial junction and blood is suctioned from the open inferior vena cava exsanguinating the patient. The left atrium is vented in order to prevent left ventricular distension and back pressure on the pulmonary vascular bed. Preservation fluids are infused through the previously placed cannulas flushing the procured organs of blood and rapidly lowering their temperature. Topical ice is applied augmenting rapid cooling. Thereafter, the heart and lungs are usually removed first. Donor hepatectomy is then carried out followed by removal of the kidneys. Variations in this sequence are required when the pancreas and or small bowel are also procured. The iliac vessels and occasionally segments of the descending thoracic aorta are then removed to provide additional vascular conduits that are sometimes necessary for complex vascular reconstructions at the time of organ implantation. All organs are inspected on the back table to ensure that no surgical damage has occurred. Finally, the organs are placed in sterile containers containing cold preservation solution or saline. The containers are then packed in ice in preparation for transport to the location where transplantation will occur. Once all solid organs are removed any additional tissues approved for donation are removed.

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Rehabilitation Paul F. Pasquina, Caitlin L. McAuliffe, and Kevin F. Fitzpatrick

INTRODUCTION The goal of rehabilitation is to maximize an individual’s physical, cognitive, and psychological recovery from a disease, injury, or traumatic event. An interdisciplinary team of professionals applies fundamental rehabilitation principles with the objective of preventing secondary injury, achieving optimal pain control, employing therapeutic exercise to meet established goals, utilizing appropriate assistive technology (AT), and providing education and counseling to the patient and family. While the first priority in treating a trauma patient is to preserve life and limb, early initiation of rehabilitation can have a significant impact on recovery, length of stay, reintegration into the community, and, ultimately, quality of life. Trauma patients, especially those with spinal cord injury (SCI), traumatic brain injury (TBI), burns, and amputations, are particularly vulnerable to secondary complications and multisystem problems that are best treated if recognized early. In order to most appropriately address these unique needs, transfer to a specialized rehabilitation facility should be considered as soon as possible after the acute medical and surgical issues are addressed. The optimal timing for transfer is largely dependent on the condition of the patient and comfort level of the providers at both the discharging and receiving institutions, but generally occurs when the emphasis of care transitions from the acute medical and surgical issues to recovery. It is not uncommon for patients who require additional medical or surgical procedures to transfer back to the acute care hospital from the rehabilitation facility in order to facilitate optimal recovery. As in other areas of medicine, subspecialty designation within the rehabilitation field is common. Many physicians, therapists, nurses, and counselors receive subspecialized training and board certification in areas such as spinal cord medicine, neurological impairments, limb loss, and cognitive rehabilitation. Rehabilitation facilities themselves receive

special accreditation by the Commission on Accreditation of Rehabilitation Facilities (CARF), which helps to ensure quality.1 The National Institute on Disabilities and Rehabilitation Research (NIDRR) also recognizes excellence in rehabilitation institutions with their Models Systems Programs for Burns, SCI, and TBI.2 Trauma providers should not wait until the resolution of all medical and surgical issues before engaging in rehabilitation; rather, it should be an integral part of every trauma patient’s care starting from initial hospitalization. Trauma professionals should also recognize that the medical and surgical care they provide during the acute phase of treatment may have longlasting implications for a trauma patient’s overall health, recovery, and quality of life.

EFFECTS OF IMMOBILITY The fundamental principles of rehabilitation are founded on mitigating and preventing (when possible) the effects of immobility. The physiological and psychological effects of immobility lead to adverse organ system changes that may complicate healing and recovery. Therefore, a thorough understanding of these potential consequences will help optimize any treatment plan.

■ Musculoskeletal Effects Muscle Atrophy and Weakness Muscle responds to alterations in loading conditions. While increased activity leads to muscle fiber hypertrophy, less may result in disuse atrophy. The muscles most affected by such disuse atrophy during bed rest or immobilization are the antigravity muscles of the lower limbs and trunk. Thus, muscles with different functional roles atrophy at different rates during unloading.3 During immobilization, the rate of protein

Rehabilitation activities as soon as determined to be safe by the medical and surgical team. Resistance exercise has been shown to both maintain muscle protein synthesis and increase bone mass, reducing the incidence of muscle atrophy and disuse osteoporosis during immobilization.4 Electrical stimulation may also be helpful by passively contracting skeletal muscle and maintaining muscle oxidative capacity.14 Daily stretching has been shown to prevent serial sarcomere loss and reorganization of tissue components,12 leading to a reduced risk of muscle atrophy and contracture formation. Daily range of motion, flexibility, and muscle strengthening exercises help maintain the appropriate balance of muscles across joints and can be used to both prevent and treat muscle atrophy, disuse osteoporosis, and contracture formation.

Disuse Osteoporosis Bone, like muscle, is sensitive to loading stresses. Bone mass increases under mechanical stress and decreases in the absence of muscle activity or gravitational force. An unloaded skeleton during bed rest results in a decrease in bone formation with little to no impact on rates of bone reabsorption. Thus, disuse osteoporosis occurs because of a mismatch between bone growth and bone loss, resulting in a 1–2% reduction in bone mineral density each month.9 Bed rest also leads to an increased excretion of compounds released during bone degradation such as hydroxyproline, pyridinoline, and deoxypyridinoline complexes.10 Greater calcium excretion in the urine, combined with decreased intestinal absorption, results in the negative calcium balance characteristic of loss of bone minerals.11 Patients with preexisting osteopenia, osteoporosis, or SCI are especially susceptible to an increase in bone turnover during immobilization and have a higher risk of osteoporotic-related fractures.

Contractures A contracture is defined as a shortening of muscle, characterized by flexion that prevents movement through the normal range of motion. Joint contractures are classified according to etiology as either myogenic or arthrogenic. Myogenic contractures are caused by changes in muscle, tendon, or fascia. While reduction in muscle length clearly contributes to the formation of a myogenic contracture, remodeling of intramuscular connective tissue during immobilization also plays a significant role. Such changes have only been observed, however, when the muscle is immobilized in a shortened position, suggesting that limb position plays a direct role in connective tissue properties.5,12 Arthrogenic contractures are caused by changes in bone, cartilage, synovium/subsynovium, capsule, or ligaments. Proliferation of intra-articular connective tissue, adaptive shortening of the capsule, and increases in cross-linking of collagen fibrils promote this type of contracture formation.13

Prevention and Treatment The best way to prevent the deleterious effects of immobility on the musculoskeletal system is to keep bed rest or immobilization to a minimum. Strength, endurance, and flexibility programs are integral to both the prevention and treatment of musculoskeletal damage. Physical therapists (PTs), occupational therapists (OTs), and the nursing staff should promote

■ Cardiovascular Effects Shift of Body Fluids Lying in a supine position eliminates the gravitational gradient normally present with standing, causing a fluid shift of approximately 1 L from the legs to the thorax. The resultant increase in pressure within the heart’s ventricles leads to an increase in diastolic filling and stroke volume. Volume regulatory mechanisms within the heart react to the increase in volume of intrathoracic fluid and trigger urinary excretion and reduced thirst, resulting in a resetting of the cardiopulmonary baroreflex and a reduction in plasma volume.15,16

Cardiac Effects Skeletal muscles generally compress major veins, forcing blood upwards and ensuring its return to the heart. The loss of skeletal muscle during bed rest impairs this venous return, compounding the reduction in blood volume and leading to decreases in diastolic pressure and stroke volume. To counteract this decrease in stroke volume and maintain sufficient cardiac output, heart rate increases. After 4 weeks of bed rest, the resting heart rate is typically increased by approximately 10 beats/min. The heart rate after exercise is increased by almost 40 beats/min, and this places greater demand on the heart. Similar to skeletal muscle, cardiac muscle is also plastic in response to stress. Therefore, as stroke volume decreases, the heart is required to do less work and begins to atrophy. The resulting decrease of cardiac mass and myocardial thinning reduce the effectiveness of the cardiac pump.17,18

Orthostatic Hypotension Immobilized patients have a reduction in blood volume, venous return, and stroke volume. These factors in conjunction with cardiac deconditioning and myocardial thinning lead to the development of orthostatic hypotension.17 Orthostatic hypotension is characterized by an excessive fall in stroke volume on assuming an upright position and has been reported after as little as 20 hours of bed rest.19,20 Orthostasis is magnified for patients with SCI as a loss of sympathetically mediated vasoconstriction compounds venous pooling in the abdomen and lower limbs and leads to a decrease in arterial blood pressure. This results in dizziness, lightheadedness, or loss of consciousness

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synthesis declines while proteolysis increases. The resulting loss in total body protein is accompanied by a significant remodeling of muscle architecture, including a loss of sarcomeres both in series and in parallel; this leads to reduced muscle thickness and length.4 Muscle atrophy occurring from immobilization results in diminished force production and a loss of strength of 10–15% per week.5,6 Interestingly, muscle strength decreases at a faster rate than muscle size, indicating that, in addition to atrophy, other factors contribute to muscle weakness.7 Immobilization also leads to a decrease in density of mitochondrial volume, reducing muscle oxidative capacity and leading to a loss of endurance—an early trigger of anaerobic metabolism.8

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when assuming an upright position. Symptoms of orthostatic hypotension may significantly interfere with a patient’s ability to perform activities of daily living (ADLs) or participate in therapy.

Aerobic Capacity Maximal oxygen consumption (VO2max) is a measure of cardiovascular fitness and has been shown to decrease during bed rest in proportion to the duration of immobilization.21 Both peripheral (muscular) and central (cardiovascular) factors play a role in the decrease in VO2max resulting from immobility.8 Individuals with preexisting cardiovascular disease, therefore, present a higher risk for cardiac complications when recovering from a traumatic event and will require clear cardiovascular guidelines for participation in therapy. Typical guidelines include not exceeding a greater than 10–15 mm Hg rise in systolic blood pressure or greater than 60–65% maximal heart rate. Perceived exertion scales such as the Borg scale are often used to help monitor effort, and, when needed, supplemental oxygen and monitoring with pulse oximetry should be used during therapy.

Venous Thrombosis and Pulmonary Embolus The incidence of deep venous thrombosis (DVT) after major trauma has been reported to be as high as 58%.22,23 Without prophylaxis, its incidence after a motor complete SCI may be as high as 72%.24 Typical features of DVT include swelling, erythema, and pain in the affected extremity. A pulmonary embolism (PE) is a potentially fatal consequence of a DVT, caused by part of the clot breaking away from the vein wall and lodging in a pulmonary artery. Typical symptoms include tachycardia, dyspnea, and chest pain. Unfortunately, both DVT and PE may manifest silently without producing any traditional symptoms, especially in patients with paralysis, sensory loss, or impaired consciousness.25 Computed tomographic pulmonary angiography (CTPA) has emerged as the preferential test in diagnosing a PE, due to its high accuracy, ease of use, and ability to provide alternate diagnoses.26 Other common tests for DVT and PE include ultrasound, lung ventilation perfusion scans, and blood tests including D-dimer.

Prevention and Treatment Minimizing the effects of cardiovascular deconditioning is achieved by reintroducing activities as soon as possible during the initial care of an injured patient. Management of orthostatic hypotension begins with preventing venous pooling in the abdomen and lower limbs by using abdominal binders and lower limb compression stockings. If necessary, the use of medications such as midodrine or florinef may also be helpful in treating or preventing episodes of orthostatic hypotension.27 The incidence of DVT can be reduced to 7–10% with appropriate prophylaxis.24 The current recommendation for the prevention of DVT and PE following trauma is to initiate pharmacological anticoagulation within 72 hours of the injury, provided no contraindications exist (e.g., bleeding, ongoing surgical procedures, or progressive changes in the brain on

computed tomography [CT]). Anticoagulation may be accomplished with low-molecular-weight heparin or adjusted dose unfractionated heparin. In addition to pharmacological prophylaxis, use of mechanical prophylaxis such as compression hose or intermittent compression boots should be initiated as soon as possible and continued for at least 2 weeks. If contraindications to pharmacological prophylaxis exist, strong consideration should be given to insertion of a vena cava filter to prevent PE. Duration of pharmacological prophylaxis is dependent on the extent of trauma and continued risk as follows: (1) until hospital discharge for those with uncomplicated motor incomplete SCI; (2) 8 weeks for those with uncomplicated motor complete SCI; and (3) 12 weeks for those with complicated SCI (e.g., lower limb fracture, age 70, or history of thrombosis, cancer, heart failure, or obesity).28 Lifestyle modifications including avoiding immobility and dehydration, stopping smoking, and maintaining normal blood pressure can also help prevent DVT/PE.

■ Pulmonary Effects Lung Volume and Structural Changes Patients take fewer deep breaths when lying down due to decreased respiratory muscle strength during immobilization. This decreased tidal volume (amount of air inhaled or exhaled during normal respiration) contributes to a 25–50% decrease in total respiratory capacity. A similar reduction in the diameter of the airways leads to a decrease in functional residual capacity (the amount of air left in lungs after expiration), which can restrict airways and decrease gas exchange.29 Further complicating respiratory function, bed-ridden patients have difficulty clearing secretions leading to accumulation of mucous in the air passages and secondary atelectasis and pneumonia.30,31

Prevention and Treatment Promoting deep inspiration with an incentive spirometer is important for all trauma patients. Chest physiotherapy, vibration, and postural drainage techniques can be administered by a respiratory therapist and should be considered for any patient with acquired pneumonia while on bed rest. Clearing secretions is especially challenging for patients with paralysis from an SCI. Special coughing techniques, such as the “quad cough,” should be utilized and taught to the patient and family members by a trained therapist.31,32

■ Urinary System Effects Urinary Retention/Stones/Urinary Tract Infection The urge to urinate is often lessened when supine, even when the bladder is full, and this contributes to urinary retention. An overdistended bladder may cause the stretch receptors to lose sensitivity, further reducing the urge to urinate. The aforementioned bone loss due to immobilization results in hypercalciuria, increasing the risk of forming bladder and renal stones. Urinary retention also encourages the growth of bacteria that

Rehabilitation raise the pH of urine and increase the risk of infection as well as precipitation of calcium that exacerbates stone formation.33,34

■ Integumentary System Effects

Prevention and Treatment

Immobilization is strongly associated with the formation of decubitus ulcers. Bony prominences such as the occiput, shoulder blades, sacrum, and heels are of greatest risk for supine patients.39 Ulcerations that occur over the ischial tuberosities are generally attributable to increased seating pressure. As immobilized patients are unable to make natural postural changes that alleviate pressure on susceptible body parts, blood flow to tissues can become obstructed, leading to necrosis of soft tissue and skin.40 Patients with impaired cognition or sensation are particularly susceptible to the formation of pressure ulcers and between 25% and 80% of patients with an SCI eventually develop them, with up to 8% developing fatal complications.31 In addition, urinary and fecal incontinence may lead to excessive skin maceration and subsequent breakdown.41 When present, pressure ulcers can have a significant negative impact on successful rehabilitation, recovery, and quality of life.42

■ Gastrointestinal Effects Appetite and Gastric Transit Time Bed rest negatively impacts taste acuity, leading to a reduction in food intake.36 In addition, immobilization results in structural and functional changes of the gastrointestinal tract, including atrophy of the mucosal lining and reduced glandular capacity.37 Gastric transit time is prolonged during bed rest, also. A decreased rate of evacuation from the stomach may cause symptoms of gastroesophageal reflux, regurgitation, and heartburn. The rate of peristalsis and of food absorption is slowed during bed rest, as well.38 Longer transit time increases water reabsorption through the gut, which can lead to constipation and fecal impaction.34

Prevention/Treatment Minimizing immobility, promoting activity, and ensuring adequate hydration are essential components of proper bowel management. The use of a bedside commode or bathroom toilet rather than a bedpan is encouraged. Bowel management should be targeted to the specific dysfunction that is present. Effective bowel programs include techniques such as timed stooling, dietary modifications, timing evacuation about 30 minutes after a meal to take advantage of the gastrocolic reflex, and manual disimpaction, especially for individuals with neurogenic bowel dysfunction from an SCI. If further treatment is required, medications such as bulk-forming agents (e.g., Colace), enemas, colonic irritants (e.g., Dulcolax), and intestinal motility agents (e.g., senna) may be used. The ability of the patient to independently perform manual disimpaction or self-administer enemas or suppositories will depend on his or her level of impairment. A surgical colostomy may be necessary to provide continence in certain patients, and appropriate colostomy care should be taught to the patient or caregiver.

Decubitus Ulcers (Pressure Sores)

Prevention/Treatment Frequent skin inspection, appropriate hygiene, achieving urinary and fecal continence, proper fitting of orthotics, and avoiding excessive pressure through a regular turning schedule are all critical aspects of caring for the skin of a trauma patient. Providers should remain particularly attentive to the pressuresensitive areas of the body and the placement of devices such as cervical collars and multipodus boots. The utilization of specialty beds and seating cushions is encouraged but should not replace vigilant medical and nursing care. Many trauma centers have a dedicated skin and wound care team. These professionals should be consulted at the earliest signs of skin breakdown and should be involved in continuous education of the medical, nursing, and therapy staff. The primary treatment of pressure ulcers should focus on prevention through frequent position changes by a caregiver or the patient. This may require education of caregivers and patient as well as specialized equipment such as wheelchairs with appropriate cushioning and adjustable tilting features.

UNIQUE COMPLICATIONS OF TRAUMA PATIENTS Heterotopic ossification (HO) is the formation of mature lamellar bone in tissue that is not normally ossified. It commonly develops in patients with TBI, SCI, burn injury, or blastrelated amputations. The most common site of HO following SCI is the hip, but it may also occur in the elbow, shoulder, and knee.43 For patients with burns, 92% of cases occur in the elbow,44,45 and up to 80% of patients who sustain an amputation from a blast injury may develop HO.46 The clinical presentation of HO may include a decrease in range of motion and erythema and swelling about the involved joint. It is important to distinguish HO from a DVT, which may involve a similar clinical presentation. Studies such as x-rays, bone scans, and monitoring of serum alkaline phosphatase levels can aid in the diagnosis. Prophylaxis with etidronate, nonsteroidal anti-inflammatory

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For most trauma patients, an indwelling catheter is placed to ensure adequate emptying of the bladder, prevent fluid stasis and subsequent infection, and prevent a high-pressure system that may lead to hydronephrosis and renal damage. An indwelling catheter also allows the trauma team to monitor fluid output and assess fluid status. Indwelling catheters should be removed as soon as medically possible to prevent urethral or bladder damage and to avoid reducing bladder compliance and storage capacity. After removing an indwelling catheter, it is important to monitor initial postvoid residual bladder volumes (PVR) to ensure adequate emptying. A PVR greater than 50–100 cm3 usually mandates replacement of the indwelling catheter and urological consultation.35 Patients with neurogenic bladders from an injury to the central or peripheral nervous system should be on a bladder program as soon as the indwelling catheter is removed (see Section “Spinal Cord Injury”).

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drugs (NSAIDs), and local irradiation may prevent HO.47 Treatment of HO involves active and passive range of motion to prevent worsening; in severe cases, surgical excision may be required to improve functional outcomes.43,48 Even when treated aggressively, HO may still result in significant restrictions in range of motion and subsequent disability. Spasticity is defined as a velocity-dependent increase in muscle tone that occurs following injury to upper motor neurons. Typically, it is associated with increased deep tendon reflexes and other signs of upper motor neuron disease. Spasticity occurs frequently in patients with TBI and SCI and may significantly impede successful rehabilitation if not treated appropriately. During the acute stage, however, a patient with SCI may have diffusely diminished reflexes below the level of injury. This period of hypotonicity and hyporeflexia is referred to as spinal shock. In the weeks following SCI, reflexes return and gradually increase while spasticity develops. The incidence of spasticity following SCI at 1 year is estimated to be 65–78%.49 Spasticity can result in significant pain, difficulty with transfers, and increased risk of skin breakdown. In certain circumstances, spasticity may be of benefit to the patient, particularly when lower limb tone is used to aid in transfers. Therefore, the decision to treat spasticity should be based on improving patient function, hygiene, or care. Conservative treatment of spasticity begins with positioning, stretching, splinting, and range of motion exercises. Medications used for spasticity include GABA agonists (e.g., baclofen), centrally acting alpha-2 agonists (e.g., tizanidine), and medications that inhibit skeletal muscle contraction (e.g., dantrolene). The appropriate choice of medication should be based on the patient’s response as well as the presence of adverse side effects. Botulinum toxin or phenol injections may also be helpful in spasticity management. Implanted pumps may be used to deliver highly concentrated doses of medications directly to the spinal cord through an intrathecal catheter, which minimizes systemic side effects, and surgical treatment of spasticity may be required to correct fixed deformities.49

PAIN MANAGEMENT ■ Background Inadequate pain control is associated with delayed healing, increased complications, prolonged hospitalization, poor sleep, and diminished quality of life.50 It has also been shown to be a significant cause for hospital readmission.51 Therefore, aggressive pain management should be a priority for any trauma team. Unfortunately, many patients who present to the emergency department (ED) with acute pain are undertreated for their pain.52 Multiple professional organizations, including the American Pain Society (APS) and the Agency for Healthcare Research and Quality (AHRQ), have developed and disseminated clinical practice guidelines to address the insufficient treatment of pain in America’s health care delivery system.53 In addition, the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) introduced new standards for pain assessment and management, advocating pain management as a patient right and requiring health care organizations to

employ effective pain management policies.54 Despite these initiatives, significant challenges still remain in changing clinical practice.55 Postoperative pain is a significant problem for most hospitals and demands special attention from the trauma team.56 While a multitude of pain interventions currently exist, numerous barriers prevent patients from receiving optimal care.57 Expecting it as part of the surgical process, patients often underreport their level of pain or are reluctant to ask for pain medication. Pain medications prescribed on an “as-needed” basis can cause a lag in treatment and a “peak and trough” pain pattern of analgesia. Such poor pain management may lead to significant anxiety, poor sleep, and loss of appetite. Given the difficulty in treating established pain, preventative measures such as around-the-clock analgesia represent the best way to ultimately prevent severe pain. In addition, uncontrolled or protracted acute pain may lead to chronic pain states, which may have long-term negative implications on function, return to work, and quality of life.58,59 Providers traditionally underestimate a patient’s level of discomfort. Therefore, it is important to establish a standardized method of communication between the patient and provider. To determine pain levels, most health care organizations utilize a visual analog scale (VAS) typically ranging from 0 (no pain) to 10 (worst imaginable pain). In addition to communicating pain levels, this tool may also be used to assess the effectiveness of pain interventions, and establish therapeutic goals for each patient. Determining pain levels for children or individuals with cognitive impairment may be challenging. In such cases, providers may use the FACES scale, in which images of faces ranging from smiling to grimacing reflect pain scores.60 A speech language pathologist (SLP) may be of great assistance to the patient and treatment team by developing an effective communication system for more challenging communication barriers. Family members should also be engaged with the treatment team to help provide feedback on the patient’s nonverbal expression of pain and response to therapeutic interventions.

■ Terminology and Pathophysiology While a detailed discussion is beyond the scope of this chapter, the proper treatment of pain requires a basic understanding of common pain terminology and a familiarity with nervous system physiology (Table 51-1).

■ Treatment Pain management strategies should target the suspected source of nociception (Fig. 51-1). Issues such as positioning, poor sleep, anxiety, and depression may augment the perception of pain. In addition, chronic underlying conditions such as migraine headaches, diabetic neuropathy, osteoarthritis, or other musculoskeletal injuries may be exacerbated by trauma, adding to a patient’s discomfort. Therefore, a thorough history and physical examination is critical in evaluating every trauma patient. It is also possible that other injuries may have been overlooked during the initial trauma screen; therefore, a tertiary survey is necessary in injured patients. Pain management strategies should be readily discussed among the trauma team

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TABLE 51-1 Common Pain Terminology

Protopathic sensations Visceral pain Somatic pain Acute pain Chronic pain

Definition The neural process of encoding and processing noxious stimuli An increased sensitivity or response to a painful stimulus A painful response to a normally nonpainful stimulus An unpleasant or painful sensation that occurs spontaneously A sensation of a tingling or numbness of the skin or region of the body that occurs spontaneously Nonpainful sensations such as light touch, vibration, and position sense, transmitted through low-threshold, large-diameter myelinated nerve fibers Painful sensations transmitted through high-threshold, small-diameter unmyelinated nerve fibers Pain generated through internal nocioceptors as a result of internal organ damage Pain generated from peripheral nocioceptors within the skin, muscle, soft tissue, and bone Pain associated with an acute event, generally lasting less than 30 days A pain syndrome lasting beyond 3–6 months or pain that extends beyond the expected period of healing

and a pain specialist should be consulted for patients with complex pain problems. Treatment strategies generally include both pharmacological and nonpharmacological approaches.

Pharmacological • Opioids are the most common analgesic drug used during acute care of the trauma patient and may be administered orally, intramuscularly, or intravenously. Meperidine’s active metabolite, normeperidine, has a prolonged half-life and may cause seizures, limiting its use especially in the

elderly or those with renal impairment. Morphine is the opioid of choice because of its clear analgesic, amnestic, and sedative effects, and it is also readily available and costeffective. Fentanyl may also be used, but has a shorter halflife, produces weaker sedation, and costs more.61 Patients on chronic opioids may be safely treated with intravenous opioid bolus dosages up to 20% of their total daily use.62 • NSAIDs can be very helpful in relieving peripherally generated pain by blocking cyclooxygenase and the subsequent formation of prostaglandins, which promote

Perception

Cortex

Modulation Thalamocortical projections

Thalamus

Excitatory Substance P Substance K Glutamate Aspartate Calcitonin gene related peptide Cholecystokinin Vasoactive intestinal peptide Spinothalamic tract

Inhibitory Serotonin Norepinephrine Opioids GABA Somatostatin Galanin Transmission Opioid receptors

Transduction C A-delta

Primary afferent nociceptor

PG E2 Sub P Bradykinin Interleukins

Noxious stimulus

FIGURE 51-1 Afferent nociception pathway: demonstrates pain signals originating from a peripheral noxious stimulus, traveling along sensory afferents through the dorsal root ganglion and into the spinal cord, where both excitatory (red) and inhibitory (green) neurotransmitters modulate impulses before the signal is perceived within the brain.

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Term Nociception Hyperalgesia Allodynia Dysesthesia Paresthesia Epicritic sensations

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•

•

•

pain and inflammation. There are two isomers of cyclooxygenase (COX-1 and COX-2), each involved in a range of physiological functions. For example, the prostaglandins produced by COX-1 also protect the stomach and support platelet aggregation. Therefore, nonselective COX inhibitors should be used with caution in the injured patient to avoid the possible side effects of peptic ulceration and dyspepsia. Ketorolac is the only NSAID in the United States available in an injectable form. Its administration, either intravenously or intramuscularly, has analgesic effects similar to morphine. Unlike morphine, however, it has a maximum dose of 60 mg and cannot be dose adjusted. Antiseizure medications such as gabapentin, pregabaline, carbamazepine, valproic acid, or oxcarbazepine are often used to help treat neuropathic pain and may be effective in treating phantom limb pain for those with amputations, also. These medications act as membrane stabilizers to the axons in the central and peripheral nervous systems. Antidepressant medications have long been used to help augment pain management, particularly for neuropathic pain. Tricyclic antidepressants (TCAs) are effective, but have sedative effects. They also have anticholinergic properties, which may lead to secondary problems such as confusion and urinary retention, especially in the elderly. Therefore, side effects should be monitored and the dose of medication adjusted accordingly. Duloxetine is an antidepressant medication with fewer side effects than TCAs and is approved for the treatment of diabetic nerve pain. Although the effect of selective serotonin reuptake inhibitors (SSRIs) on acute or chronic pain is unclear, these medications should be considered to treat depression or anxiety, which may be a contributing factor to the patient’s pain. Continuous infusion analgesia and anesthesia may be achieved with intravenous patient-controlled anesthesia (PCA) or with regional anesthesia through a peripherally placed catheter. Intravenous opioid administration through a PCA helps to avoid the “peak and trough” phenomenon of inadequate pain management. Continuous infusion of an anesthetic agent through a catheter in the region of a peripheral nerve or plexus offers outstanding pain control for limb injuries and avoids the secondary cognitive effects of systemic opioids. Regional anesthesia catheters should be monitored for effectiveness as well as signs of infection and have been reported to be safe for up to 34 days in combat-related injuries.63 Sympathetic blockade may be helpful in patients with sympathetically mediated complex regional pain syndrome (CRPS). CRPS should be suspected if the pain in an extremity persists long after what would be normally expected in patients with similar injuries. Symptoms typically include regional pain, allodynia, hyperalgesia, swelling, and local dysautonomia (sweating, discoloration, or temperature changes). As prolonged immobility may be a precursor to CRPS, early rehabilitation may prevent its occurrence. When CRPS is suspected, a pain specialist consultation is recommended.

Nonpharmacological • Modalities such as heat or ice may provide effective pain relief for injured patients and should be made available as needed. Caution should be observed when using these modalities for patients with injuries to the central or peripheral nervous system or those with cognitive impairment. Lack of protective sensation or awareness my lead to a significant skin injury or burn. • Interventions such as acupuncture, desensitization techniques, self-hypnosis, biofeedback, and music therapy may also provide some pain relief for injured patients. Such therapies are generally well received and can be administered without fear of side effects or adverse interaction with other medications.

FUNCTIONAL IMPROVEMENT THROUGH INTERDISCIPLINARY TEAM CARE As already stated, the early application of rehabilitation principles helps prevent secondary injury and facilitates patient recovery. Consultation with rehabilitation specialists should be considered for every injured patient. An interdisciplinary rehabilitation team employs a variety of specialists from physiatry, physical therapy, occupational therapy, mental health, and speech language pathology. For patients with cognitive impairment, a neuropsychologist may offer invaluable assistance in identifying cognitive deficits and formulating management decisions. In addition to providing holistic care, these providers will spend additional time with the patient and his or her family to determine premorbid and current functional levels as well as to help develop short- and long-term goals for functional improvement. • Physical medicine and rehabilitation (PM&R) specialists (physiatrists) are board-certified physicians who specialize in neuromusculoskeletal disorders and rehabilitation. They are skilled at integrating medical and surgical treatment plans with the rehabilitation team. Physiatrists are also helpful in establishing safety precautions for the patient, managing pain and bowel/ bladder issues, and aiding in appropriate discharge planning and disposition. Subspecialty certifications currently exist in spinal cord medicine, TBI, and pain management. • PTs help assess motor function and mobility. This includes assessing range of motion of joints and motor strength as well as a patient’s balance and ability to sit, stand, transfer, or walk independently or with an assistive device. Treatment should begin early during the acute care hospitalization and continue until goals are met. PT assessments are very helpful in guiding appropriate discharge planning. It is important for the trauma physician to provide the therapist with guidance on appropriate weight bearing, range of motion, or activity precautions. • OTs help assess a patient’s ADLs and instrumental ADLs (IADLs). ADLs include feeding, toileting, dressing, and hygiene. IADLs refer to activities beyond basic personal

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•

•

•

provides credentialing to suppliers, health care providers, and engineers to ensure quality in products and service delivery. • Peer support visitors are trauma survivors who receive training to provide support to patients and their families. Peer visitors generally have suffered a similar life-changing injury as the patient and are able to exemplify successful recovery by adapting and returning to community participation. Peer support visitors are especially beneficial for individuals with paralysis, vision loss, disfiguring scars, or limb loss. The Amputee Coalition of America (ACA) offers a peer support training program, which may be helpful for individuals or institutions interested in initiating such a program. • Vocational rehabilitation specialists interview patients and match career goals with functional capacity, AT, and professional talents. Community reintegration and return to vocation should be in the long-term goals of all trauma patients. Although controversy exists as to the optimal timing of intervention, discussing vocation during early hospitalization may facilitate engagement in rehabilitation and hasten recovery. • Case managers and social work services are essential to adequately address discharge planning, transfer to the next level of care, coordinate equipment needs, and provide patient and family education. Therefore, these professionals should be an integral part of the trauma treatment team.

SPECIAL CONSIDERATIONS FOR SPECIFIC TRAUMATIC INJURIES ■ Spinal Cord Injury Introduction Injury to the spinal cord results in impaired motor strength and sensation below the level of injury, and bowel and bladder function, sexual function, and autonomic control are frequently impaired, also. Approximately 12,000 SCIs occur nationally each year, and approximately 259,000 SCI survivors are living in the United States. Males account for approximately 80% of all injuries, and motor vehicle accidents account for the largest proportion of injuries, followed by falls, violence, and sports injuries. The societal impact of SCI is staggering, resulting in total lifetime costs of up to $3 million per patient.67

Classification SCIs are classified by their severity and level of injury, using the American Spinal Injury Association (ASIA) Standard Neurological Classification Worksheet.68 This worksheet provides guidelines for measuring key motor levels and sensory examination points that represent function at a given spinal level. According to this method of classification, patients are given two scores, with one based on level and the other on the degree of impairment. The neurological level of injury is defined as the lowest level of normal functioning. The impairment is rated as A, B, C, D, or E. An A is assigned to a patient

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•

care, typically requiring devices such as a telephone, kitchen utensils, or appliances. Examples of IADLs include managing finances, preparing meals, and doing laundry. A patient’s independence in ADLs and IADLs will help determine appropriate discharge planning. OTs are also skilled at helping those with extremity trauma or nervous system injury regain both gross and fine motor hand function. SLPs help assess, diagnose, and treat patients with difficulties related to speech, language, swallowing, or cognitive–communication deficits. Since adequate nutrition is necessary for tissue healing and recovery, assessing a patient’s ability to swallow safely may help guide appropriate interventions to ensure adequate caloric intake. Additionally, the SLP may help develop ways to improve the necessary communication between the treatment team and the patient. Orthotists and prosthetists (O&P) are certified in evaluating, fabricating, and custom fitting orthopedic braces (orthotics) and artificial limbs (prostheses). Orthotics are devices used to align, support, protect, or improve the function of a body part. Examples of orthotics used in trauma casualties include halo cervical traction splints, ankle foot orthotics (AFO), and thoracolumbosacral orthotics (TLSO). Orthotics may be either static (rigid) or dynamic (assist with desired motion). Prostheses may be utilized for upper or lower limb amputations, and are composed of a socket, suspension, joint(s), shank, and terminal device (hook, hand, or foot). Early prosthetic fitting may enhance acceptance and functional recovery. Mental health professionals should be a part of any interdisciplinary team. Traumatic events have a significant psychological impact on the patient, family members, and caregivers. Nearly all survivors of a major traumatic event will exhibit stress-related symptoms and up to 40% may have a psychiatric disorder at 1 year following trauma.64 For combat casualties, rates of comorbid post-traumatic stress disorder (PTSD) have been reported to be 16.7%.65 Fear of isolation, lack of wholeness, and concerns about the future are common, but can be eased by supportive family members and caregivers. A preventative medicine approach to psychiatry helps to decrease stigmatization, foster acceptance of mental health care, and prevent the development of a disabling psychiatric disorder after trauma.66 Special consideration should also be made when introducing children to a parent who suffered limb loss or other disfiguring injury. Rehabilitation engineers/AT specialists specialize in the development, fitting, and training of AT devices. AT devices provide essential support for individuals with disabilities, allowing them to perform ADLs and return to work, sports, and recreational activities. They include manual and powered wheelchairs, seating systems, standing systems, adaptive vehicles, augmentative communication systems, electronic aids, and assistive robotics. As technology becomes more sophisticated, expertise is needed in these areas. The Rehabilitation Engineering and Assistive Technology Society of North America (RESNA) currently

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with a complete injury, with no motor or sensory function in the S4 or S5 levels. B represents an incomplete injury with sensory sparing, but no motor activity below the level of injury. A patient with some motor (nonfunctional) strength below the level of injury is assigned a C, whereas a D classifies a patient with more motor sparing below the level of the lesion, as indicated by antigravity strength in greater than 50% of those muscles spared. A classification of E represents normal strength and sensation.

Functional Outcomes after Spinal Cord Injury The expected level of independence and functional capacity after SCI depends largely on the level of injury and the impairment rating. While lifelong mechanical ventilation is typically required for patients with complete injuries at the level of C3 or above, it is often not necessary for those with injuries at C4 or below. An injury at the C5 level is expected to result in independent mobility in an electrically powered wheelchair and driving in a van with appropriate modifications. C7 level injuries allow independence with transfers, weight-shifting maneuvers, and bowel and bladder management. While individuals with thoracic level injuries have full function of the upper limbs, they typically require the use of a manual wheelchair with varying degrees of truncal support. Patients with an L1 or L2 injury also generally require a manual wheelchair but have independent truncal control; patients with L3 or L4 injuries may be able to ambulate with assistive devices and those with injuries at L5 or below should be able to independently ambulate.69

Acute Management of Spinal Cord Injury Treatment of acute SCI in a trauma center has a significant positive impact on survival and long-term functional recovery.70 Immediate spinal stabilization is essential to prevent further neurological compromise. While not all patients require surgery after SCI, animal models have shown that surgical treatment relieving spinal cord compression can prevent further neurological deterioration. The National Acute Spinal Cord Injury Study recommended that high-dose methylprednisolone be administered for 24–48 hours following acute SCI. These guidelines had been widely followed by the international community.71 Because of concerns over infection, gastrointestinal bleeding, and steroid myopathy, trauma centers came to question the efficacy and safety of this protocol. Therefore, the use of steroids following SCI is currently considered a treatment option rather than the standard of care.

Complications after SCI The management of patients with SCI is focused on the prevention of complications that may interfere with successful rehabilitation. The recognition of and attention to these complications is a critical component of a successful rehabilitation program. • Autonomic dysreflexia (AD) is a severe and life-threatening complication of SCI that occurs in patients with lesions at or above T6. AD typically occurs as a result of a noxious

stimulus below the level of the injury, which triggers a sympathetic reflex that goes “unchecked” or uncorrected because of injury to the descending inhibitory tracts within the spinal cord. This results in elevated blood pressure, bradycardia or tachycardia, headache, and sweating or piloerection above the level of the injury. If not recognized and treated properly, stroke or death may occur. Once AD is recognized, the patient’s head should be elevated and the noxious stimulus should be identified. Noxious stimuli often result from tight or constricted clothing, pressure on the skin, bladder distension, or bowel impaction. If an indwelling catheter is in place, it should be thoroughly examined for constriction or kinks that may cause distension. If replacement is needed, it should be inserted with the use of lidocaine jelly to prevent a further noxious stimulus. If symptoms persist, manual fecal disimpaction should be performed using lidocaine jelly. If blood pressure remains elevated, pharmacological management may include the use of nitroglycerin paste (which can be easily removed to prevent rebound hypotension) and chewable calcium channel blockers. During the management of AD, blood pressure should be continually monitored, and the patient should be continually reexamined for sources of noxious stimulation.27,72 • Hypercalcemia as a result of upregulation in osteoclast activity may occur in individuals with SCI, especially adolescent and young adult males. This may result in lethargy, abdominal pain, nausea, vomiting, psychological changes, polydipsia, and polyuria. If hypercalcemia is suspected, serum calcium levels should be monitored and treated appropriately.73 • Bladder dysfunction following SCI may lead to incontinence and urinary retention. In a typical upper motor neuron lesion, the bladder will become spastic and inadequately store urine, resulting in frequent episodes of small-volume incontinence. In lower motor neuron lesions, the bladder may become flaccid, resulting in failure to empty and overflow incontinence. Many patients with SCI may also develop detrusor–sphincter dyssynergia, characterized by a detrusor contraction against an unrelaxed sphincter, leading to failure to empty and a high-pressure urinary system. Management of bladder dysfunction aims to prevent incontinence and urinary reflux and infection, while ensuring adequate voiding at socially acceptable times. Options for bladder voiding include indwelling catheters (e.g., Foley catheter or suprapubic catheter) or clean intermittent catheterization (Crede maneuver) in which the patient or a caregiver provides manual pressure to the suprapubic region to facilitate bladder emptying. Pharmacological management of a hyperactive bladder consists primarily of anticholinergic medications to relax the detrusor muscle. Intravesical administration of botulinum toxin may also be considered to treat detrusor spasticity. Surgical options include augmentation cystoplasty, cutaneous conduits, and urinary diversions.74 • Bowel dysfunction is common after SCI due to a loss of bowel control from the central nervous system, resulting in constipation, delayed gastric emptying, and poor colonic

Rehabilitation

TABLE 51-2 Traumatic Brain Injury Classification Injury Severity Mild Moderate Severe

Glasgow Coma Scale 14–15 9–13 3–8

Post-Traumatic Amnesia 24 h 1–7 days 7 days

■ Traumatic Brain Injury Introduction TBI is the leading cause of death and disability in young adults in the United States. Over 1.4 million individuals sustain a TBI annually, with approximately 90,000 injuries resulting in a permanent disability.76 In addition, it is estimated that up to 20% of service members who are deployed sustain a concussion or mild TBI.77 TBI can occur from multiple mechanisms of injury including blunt trauma, penetrating trauma, or blast. Additionally, hypovolemia, anoxia, and metabolic changes after trauma may result in significant brain damage. Injury to the brain may occur in discrete lesions or more diffusely such as in diffuse axonal injury (DAI). Neuroimaging, including CT, magnetic resonance imaging (MRI), functional MRI (fMRI), and diffusion tensor imaging (DTI), is a helpful diagnostic tool and should complement a thorough evaluation of mental status and physical examination.78

Classification Much debate surrounds the optimal way to classify TBI. Most trauma centers rely on the Glasgow Coma Scale (GCS) or length of post-traumatic amnesia (PTA) to determine severity of the TBI (Table 51-2). PTA is the time between injury and the development of new memories, demonstrated by the

patient’s ability to recall daily events. It may be more formally assessed using tools such as the Galveston Orientation and Amnesia Test (GOAT).79 The Ranchos Los Amigos Scale is also often used to describe a patient’s level of awareness, cognition, behavior, and interaction with the environment after a TBI (Table 51-3).80 Patients who are mobile, but confused or agitated, will likely require a secured inpatient setting. Predicting outcomes after TBI is extremely challenging because of imprecise classification systems. In addition, issues such as heterogeneity of injury patterns, premorbid cognitive and physical functioning, family support, and psychosocial factors all play differential roles in recovery.81 Reports indicate that 38–80% of patients experiencing mild TBI will develop postconcussive syndrome (PCS), characterized by headache, fatigue, anxiety, and impaired memory, attention, and concentration.82 The best predictor of outcome after TBI is the patient’s speed of recovery and response to treatment; therefore, monitoring patient performance in multiple functional domains is important. Numerous outcome instruments are currently in practice including the Glasgow Outcome Scale (GOS), Functional Independence Measure (FIM), Community Integration Questionnaire (CIQ), Craig Handicap Assessment and Reporting Technique (CHART), and Disability Rating Scale (DRS). For a more comprehensive reference on TBI

TABLE 51-3 Ranchos Los Amigos Scale Cognitive Level I II

Outcome No response Generalized response

III

Localized response

IV

Confused and agitated

V

Confused and inappropriate

VI

Confused and appropriate

VII

Automatic and appropriate

VIII

Purposeful and appropriate

Patient Response No response to sounds, sights, touch, or movement Limited response, which is inconsistent and nonpurposeful; responses to sounds, sights, touch, or movement Inconsistent but purposeful response in a more specific manner to stimuli; may follow simple commands Confused and often frightened; overreactions to stimuli by hitting or screaming; highly focused on basic needs (e.g., eating, toileting); difficulty following directions Appears alert and responds to commands; easily distracted by the environment; frustrated and verbally inappropriate; focused on basic needs Follows simple directions consistently; may have some memory but lacks details, attention span of about 30 min Follows a set schedule; does routine self-care without help; attention difficulty in distracting or stressful situations; problems in planning and following through Realizes difficulties with thinking and memory; less rigid and more flexible thinking; able to learn new things; demonstrates poor judgment; may need guidance for decisions

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motility.75 Both incontinence and failure to empty may result (see Section “Effects of Immobility”). • Spasticity, orthostatic hypotension, skin breakdown, and HO are also significant problems for patients with SCI. The reader should refer to the previous discussion of these topics.

959

960

Specific Challenges in Trauma outcome tools the reader is referred to the National Institute of Neurological Disorders and Stroke’s Traumatic Brain Injury Common Data Element Standards.83

SECTION 4

Treatment A comprehensive discussion of treatment strategies for individuals with TBI is beyond the scope of this chapter. Trauma teams should consider the effects of immobility as described above and apply the appropriate rehabilitation principles. Patients with severe TBI should be transferred to a specialized rehabilitation facility as soon a possible. For those with impairments that prohibit participation in an acute care rehabilitation facility, transfer to a skilled nursing facility (SNF) may be necessary. Patients who sustain significant extremity trauma, but deny TBI or cognitive difficulties, may still have significant cognitive deficits during formal neuropsychological testing. Common symptoms of TBI include headache, visual and hearing disturbances, balance difficulties, poor sleep, irritability, and impaired cognition.84 Pharmacological interventions for neuroprotection and management of neurobehavioral disorders following TBI continue to lack significant scientific evidence in the medical literature. Neuroprotective agents seek to prevent death of neurons after injury. While some agents have shown promise in animal studies, large clinical trials in humans have not revealed strong evidence in support of a single agent. In addition, numerous medications have been advocated to help facilitate recovery of functional deficits after TBI. Clinicians should consider the following pharmacological management: (1) for arousal, methylphenidate, amantadine, modafinil, and zolpidem; (2) for attention and memory, methylphenidate, dextroamphetamine, amantadine, physostigmine, and donepezil; and (3) for agitation, irritability, and aggression, propranolol, quetiapine, clozapine, valproate, and antidepressants.85 Post-traumatic seizures (PTS)/epilepsy occur in 2–47% of patients with TBI. PTS are typically characterized as immediate (within the first 24 hours), early (within the first week), or late (occurring after the first week). Risk factors for early PTS include intracerebral hematoma, subdural hematoma in children, younger age, severity of injury, and alcoholism, while risk factors for late PTS include early PTS, intracranial bleed, severity of injury, and age 65.86 Management of seizures is usually achieved with antiepileptic medications such as carbamazepine and valproate. The use of phenytoin is limited because of the risk of cognitive side effects. Patients with TBI are also at significant risk for developing HO, DVT/PE, spasticity, bowel and bladder incontinence, and skin breakdown. The reader should refer to discussion of these topics earlier in the chapter.

■ Burn Injuries Introduction Burns often occur simultaneously with other traumatic injuries including orthopedic injuries, TBI, SCI, or amputations. Severe disability, altered body image, and numerous physical and medical complications often lead to a diminished quality

of life among survivors of burns.87 Burn injuries account for 40,000 hospital admissions annually in the United States and are the fifth most common cause of unintentional death. Advances in early resuscitation techniques, topical chemotherapy, early wound excision, isolation practices, infection control, antibiotics, and grafting techniques have contributed to the improved survival rates from severe burns.88,89

Classification Burns are classified by size and thickness. The size of a burn is measured as a percentage of total body surface area, with the rule of nines providing a rough estimation of the area that has been burned. Using this rule, the head and neck and both upper extremities account for 9% each of the total body surface area, the lower extremities and the anterior and posterior trunk are 18% each, and the perineum and genitalia are 1%. Thus, an estimate of the total body surface area involved in a burn can be quickly calculated. The thickness of a burn is classified as superficial, partial thickness, or full thickness. A superficial burn affects only the epidermis, while a partial-thickness burn extends through the epidermis to part of the dermis. A fullthickness burn affects the epidermis and entire dermis and may also involve underlying muscle, tendon, fascia, or bone.

Complications After acute treatment, the focus of burn care shifts to rehabilitation and restoration of function. Attention to the prevention and treatment of the following complications is an important aspect of burn rehabilitation: • Hypertrophic scarring : Excessive scarring following burns may result in significant joint contractures and disfigurement, negatively impacting functional capabilities and quality of life. Despite little evidence of its efficacy, the most widespread method of preventing excessive scarring is the application of pressure garments. Other preventative measures include splinting, stretching, and range of motion exercises.88,90 • Weakness and protein catabolism: Following severe burns, a dramatic increase in protein catabolism results in weakness, decreased exercise tolerance, and functional deficits. Treatment and prevention consists of strength training and endurance exercises, which may be effective in increasing strength and function.91 In addition to exercise programs, treatment with anabolic agents such as oxandrolone has been observed to reduce or prevent weakness in a burn population.92 • Heat intolerance : The ability to regulate and tolerate heat is often decreased following burn injury.93 The mechanism for heat intolerance may be rooted in changes in central and peripheral thermoregulation; however, studies have suggested still yet unknown factors.94 Despite the uncertainty surrounding the etiology of heat intolerance in burn patients, it must be recognized and incorporated into the rehabilitation program of this population. • Pain after burn injuries : Pain after a burn depends on the depth of the injury. In a partial-thickness burn, nerve endings in the dermis may remain intact, resulting in

Rehabilitation

■ Amputation Introduction The incidence of traumatic amputation continues to decline in the United States because of improved safety standards, along with advances in surgical techniques to salvage severely injured limbs. Despite these improvements, however, trauma still remains a significant contributor to pediatric and upper limb amputations. In fact, 68.6% of all traumatic amputations occur in the upper limb. Major limb loss presents numerous physical, psychological, and functional challenges, which may be even further magnified by the presence of other comorbid injuries, paralysis, or cognitive deficits. The decision to amputate or salvage a limb depends on the extent of injury and tissue viability. Evidence suggests that at 2 and 7 years postinjury, there are no significant functional outcome differences between those who undergo limb salvage surgery and those who undergo amputation, although limb salvage patients are more likely to have longer hospital stays, more operative procedures, and a higher complication rate in the short term. Long-term follow-up of both groups demonstrates a lower quality of life compared with age-matched controls. Patients who need an amputation are also at a higher risk for pain syndromes (phantom and residual limb pain), skin problems in the residual limb, overuse injuries of intact limbs,

as well as cardiovascular disease and glucose intolerance. For children, psychological acceptance, altered self-image, and the common development of bony overgrowth of the amputated limb are of particular concern.97,98

Treatment For a comprehensive review of amputee care, the reader is referred to the Textbook of Military Medicine: Care of the Combat Amputee.99 While there have been great advances in the rehabilitation methods and prosthetic devices that are currently available for individuals with major limb amputation, the acute medical and surgical care of these patients has longlasting implications for community reintegration and quality of life. Decisions such as optimizing limb length, balancing muscles, appropriately managing transected nerves, and achieving adequate soft tissue coverage are fundamental surgical principles that will greatly affect prosthetic fitting and training. Aggressive acute pain management, physical and occupational therapy, and balance and gait training, along with reduction of cardiovascular risk and nutritional counseling, will likely reduce long-term complications. Introduction of a prosthesis early during the course of treatment is essential, especially for individuals with upper limb loss, in order to promote lifelong bimanual activity and help ovoid overuse injuries of the intact limb. Prosthetic fitting and training for children with amputation(s) is especially challenging and should be guided by the child’s developmental milestones (e.g., reaching, standing, walking). It is also important to introduce play, sport, and recreational activities with appropriate adaptive equipment to help facilitate socialization and reintegration into the community.

■ Peripheral Nerve Injuries and Complications Introduction Traumatic injuries to the peripheral nervous system may contribute to a significant loss of function and independence, which may not be readily evident during the initial trauma screen. Peripheral nerve injuries may also occur as a complication of medical care. Improper bed positioning, compressive casts, poor fitting orthotics, excessive pressure during surgery, or inadvertent needle sticks may lead to injury to a peripheral nerve. Common sites of nerve injury include the brachial plexus, ulnar nerve at the elbow, and peroneal nerve at the fibular head. Cognitive impairment or injury to the spinal cord may limit the ability to fully assess the peripheral nervous system. In addition, confounding conditions such as critical illness neuropathy or critical illness myopathy may also contribute to sensory or motor dysfunction especially for patients requiring extended intensive care. Electrodiagnostic testing may be helpful in assessing the presence and extent of peripheral nerve damage as well as establishing the prognosis for recovery. Typically nerve injuries are classified as either complete or incomplete. Neuropraxia refers to an incomplete injury, characterized by demyelination, and typically has an excellent prognosis for recovery; on the other hand, damage to

CHAPTER 51

significant pain. In contrast, pain may be less or absent in areas of full-thickness burns because of loss of nerve endings. Approximately 35% of burn survivors continue to report significant pain more than a year following the injury88 (see Section “Pain Management”). • Amputation(s): Despite aggressive limb preservation procedures after a burn, the extent of tissue damage or secondary complications such as infection or ischemia may mandate amputation.88 The combination of comorbid burns and amputation presents unique rehabilitation challenges, especially with regard to the prosthetic socket interface and skin breakdown. • Psychological complications: Following burn injuries, emotional complications including depression, body image dissatisfaction, and PTSD may complicate recovery and rehabilitation. Depression occurs with an incidence of 17% during the 12 months following burns.95 While no studies specifically investigate the treatment of depression following burns, standard cognitive and pharmacological treatments are often implemented. Hypertrophic scarring often causes facial and limb disfigurement, which can lead to significant body image dissatisfaction and difficulty with community reintegration. PTSD has been reported to occur in 13–25% of patients with burn injuries.88 While there is little evidence for specific treatment recommendations, it has been established that “debriefing” sessions may actually be harmful or increase the rate of PTSD following traumatic events.96 The recognition and treatment of psychological complications of burn injuries is crucial to the design and implementation of a successful rehabilitation program.

961

962

Specific Challenges in Trauma the axon (axonotmesis) signifies a more severe injury with a poorer prognosis. Axon regeneration can be estimated to occur at a rate of 1–5 mm per day or 1 in per month.

SECTION 4

Prevention/Treatment A discussion of repair or grafting for peripheral nerve injuries is beyond the scope of this chapter; however, if repair is undertaken, proper postoperative positioning, splinting, and activity precautions should be clarified to the patient and treatment team to help support healing and prevent damage. Peripheral nerve care and injury prevention requires serial neurological examinations, attention to patient positioning, and frequent monitoring of pressure-sensitive areas. Positioning is particularly important during surgical procedures. Frequent turning by nursing staff may be necessary if the patient’s injuries do not allow independent position changes. Special attention is also required when placing casts or external fixation devices. The use of ultrasound to guide interventional procedures may also help to avoid inadvertent iatrogenic injuries.

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49. Adams MM, Hicks AL. Spasticity after spinal cord injury. Spinal Cord. 2005;43(10):577–586. 50. Ferrell BR. The impact of pain on quality of life. A decade of research. Nurs Clin North Am. 1995;30(4):609–624. 51. Grant M, Ferrell BR, Rivera LM, et al. Unscheduled readmissions for uncontrolled symptoms. A health care challenge for nurses. Nurs Clin North Am. 1995;30(4):673–682. 52. Wilson JE, Pendleton JM. Oligoanalgesia in the emergency department. Am J Emerg Med. 1989;7(6):620–623. 53. Agency for Healthcare Research and Quality. Acute Pain Management: Operative or Medical Procedures and Trauma, Clinical Practice Guideline. Rockville, MD: Agency for Healthcare Research and Quality; 1992. Available at: www.ahrq.gov/clinic/medtep/acute.htm#acutefind. Accessed January 15, 2010. 54. Berry PH, Dahl JL. The new JCAHO pain standards: implications for pain management nurses. Pain Manag Nurs. 2000;1(1):3–12. 55. Todd KH, Ducharme J, Choiniere M, et al. Pain in the emergency department: results of the pain and emergency medicine initiative (PEMI) multicenter study. J Pain. 2007;8(6):460–466. 56. Sherwood GD, McNeill JA, Starck PL, et al. Changing acute pain management outcomes in surgical patients. AORN J. 2003;77(2): 377–380, 384–390. 57. Neighbor ML, Honner S, Kohn MA. Factors affecting emergency department opioid administration to severely injured patients. Acad Emerg Med. 2004;11(12):1290–1296. 58. Coderre TJ, Katz J, Vaccarino AL, et al. Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence. Pain. 1993;52(3):259–285. 59. Howard RF. Current status of pain management in children. JAMA. 2003;290(18):2464–2469. 60. Belville RG, Seupaul RA. Pain measurement in pediatric emergency care: a review of the faces pain scale—revised. Pediatr Emerg Care. 2005; 21(2):90–99. 61. Zohar Z, Eitan A, Halperin P, et al. Pain relief in major trauma patients: an Israeli perspective. J Trauma. 2001;51(4):767–772. 62. O’Connor AB, Zwemer FL, Hays DP, et al. Outcomes after intravenous opioids in emergency patients: a prospective cohort analysis. Acad Emerg Med. 2009;16(6):477–487. 63. Clark ME, Bair MJ, Buckenmaier CC, et al. Pain and combat injuries in soldiers returning from Operations Enduring Freedom and Iraqi Freedom: implications for research and practice. J Rehabil Res Dev. 2007;44(2): 179–194. 64. O’Donnell ML, Creamer M, Pattison P, et al. Psychiatric morbidity following injury. Am J Psychiatry. 2004;161(3):507–514. 65. Koren D, Norman D, Cohen A, et al. Increased PTSD risk with combatrelated injury: a matched comparison study of injured and uninjured soldiers experiencing the same combat events. Am J Psychiatry. 2005; 162(2):276–282. 66. Wain HJ, Grammer GG, Stasinos JJ. Psychiatric intervention for medical and surgical patients following traumatic injuries. In: Ritchie EC, Watson PJ, Friedman MJ, eds. Interventions Following Mass Violence and Natural Disasters: Strategies for Mental Health Practice. New York, NY: The Guilford Press; 2007:278–298. 67. National Spinal Cord Injury Statistical Center. Facts and Figures at a Glance 2009. Available at: https://www.nscisc.uab.edu/public_content/ facts_figures_2009.aspx. Accessed January 20, 2010. 68. American Spinal Injury Association. Available at: http://www. asia-spinalinjury.org/. Accessed February 23, 2010. 69. Kirshblum SC, Priebe MM, Ho CH, et al. Spinal cord injury medicine. 3. Rehabilitation phase after acute spinal cord injury. Arch Phys Med Rehabil. 2007;88(3 suppl 1):S62–S70. 70. Bracken MB, Shepard MJ, Collins WF Jr, et al. A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinalcord injury. Results of the Second National Acute Spinal Cord Injury Study. New Engl J Med. 1990;322(20):1405–1411. 71. Krassioukov A, Warburton DE, Teasell R, et al. A systematic review of the management of autonomic dysreflexia after spinal cord injury. Arch Phys Med Rehabil. 2009;90(4):682–695. 72. Paralyzed Veterans of America/Consortium for Spinal Cord Medicine. Acute Management of Autonomic Dysreflexia: Individuals with Spinal Cord Injury Presenting to Health-Care Facilities. 2nd ed. Washington, DC: Paralyzed Veterans of America (PVA); 2001.

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Modern Combat Casualty Care Jay Johannigman, Peter Rhee, Donald Jenkins, and John B. Holcomb

INTRODUCTION With malice toward none, with charity for all, with firmness in the right as God gives us to see the right, let us strive on to finish the work we are in; to bind up the nation’s wounds; to care for him who shall have borne the battle, and for his widow and his orphan—to do all which may achieve and cherish a just and lasting peace, among ourselves, and with all nations. Lincoln’s Second Inaugural Address, March 4, 1865 This memorable quote hangs over the door of many US operating rooms in the combat theater. It provides an appropriate focus regarding the privilege and responsibility of those engaged in military medicine. Caring for those who have been injured on the battlefield has been an integral part of the fabric of medicine since the days of the ancient Greeks. Working in an austere, and often hostile, environment with limited resources is a humbling and intensely emotional experience. It is an unfortunate but equally accurate truism that war advances our understanding of care of the injured patient unlike any other worldly event.1 The scope of this chapter will attempt to characterize the most recent recognitions and advances that have emerged as lessons learned over the past years of armed conflict. Many of the lessons of modern military medicine are, in fact, not new but simply principles recognized by many previous generations of combat medics. Hypotensive resuscitation (Walter Cannon, MD, World War I), the value of whole blood transfusion (Edward Churchill, MD, World War II), and the utility of vascular shunts (the Korean War) are just a few examples of the pivotal lessons “rediscovered” during the current conflicts. Military medicine by its very nature is challenged by the task of preserving its own history and the lessons learned. The majority of providers of combat medicine return home and to civilian and academic practices without fully cataloging and preserving lessons learned. The military medical corps’

challenge is to maintain and promote ongoing combat medical support and research in periods between conflicts. Generations of medical officers may come and go without seeing an armed conflict, and lessons learned are all too often lessons forgotten. Modern warfare has changed in scope and condition. The classic large battlefield campaigns witnessed in World War I, World War II, and Korea (and feared during the Cold War with Russia) are less relevant in today’s global security scenario. Over recent decades, armed conflict in the Global War on Terror has emphasized the necessity of fluidity, precision, and speed of engagement. The current battlefield is shaped by the reality of the asymmetrical or nonlinear battlefield. Lines of engagement may be spread out over a wide geographical continuum and the forward edge of the combat zone may shift hundreds of miles in a single day as rapidly mobile armored and cavalry units mobilize with dramatic speed and capability. One of the key elements in lessons learned during the reshaping of military medicine has been the recognition (learned long ago) that the military medic must remain close to the forward deployed soldier in order to make a difference. The “reengineering” of modern military medicine has emphasized the necessity of mobility and proximity for forward medical units. This has resulted in the (re)creation of small, robust surgical teams that can deploy rapidly (hours) and conduct lifesaving/life-stabilizing procedures. This far-forward presence is combined with the development of a logistics and evacuation process providing rapid, high-intensity, and ongoing care from these far-forward locations to more rearward facilities. Fig. 52-1 is illustrative of one of these small austere forward units. The reader is urged to note that despite the changes of modern medicine, many of the aspects of these units look very similar to the iconic Mobile Army Surgical Hospital (MASH) units of Korea. The reader is also encouraged to consider the context of this austere setting over the course of this chapter. This chapter will attempt to detail the current state of the art from prehospital care to far-forward surgery, and the en route care process.

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FIGURE 52-1 The outside structure (top right and top left), the operating room (bottom left), and the medical personnel of the 909th Forward Surgical Team; FOB Shank/Afghanistan.

Key medical lessons learned will be highlighted, as well as a discussion of the systemwide changes implemented across the medical corps of all services.

■ Definitions As a first order of business, it is appropriate to establish definitions used by the military (and in this chapter) with respect to the military patient. Holcomb et al.2 clarified our understanding and attempted to provide a uniform framework for discussion of combat casualties. The following definitions taken from the article of Holcomb and Bellamy standardize the numbers and allow a reasonable retrospective comparison between various military conflicts.

■ Wounded in Action (WIA) This is a term used to define combat-injured casualties and is the sum of three subgroups as demonstrated in Fig. 52-2. Conventionally, the subgroup of surviving WIAs who return to duty (RTD) within 72 hours is excluded from the denominator when proportional statistics are presented. This is significant because this group traditionally represents almost 50% of all

WIAs. The number and classification of wounded and deaths from combat is classically used to provide insights into the lethality of battle and the effectiveness of the systems of care and evacuation, and to focus attention on required areas of research.

■ Case Fatality Rate (CFR) This term refers to the fraction of the injured, all those WIAs including all those who die, expressed as a percentage (Fig. 52-3). Summary statistics provides a measure of the overall lethality of the battlefield in those who are wounded. It includes those who are returned to duty that are excluded in the denominator of died-of-wounds (DOW) and killed-in-action (KIA) rates defined below. A point of confusion in the past has been use of this statistic with and without the RTD population, thereby creating a major source of confusion when comparing data sets from different conflicts using a differing definition. Insufficient detail is provided by a CFR for detailed medical planning for reasons that will be discussed subsequently. The CFR is not a total mortality rate that would describe all deaths relative to the entire deployed population at risk.

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CFR = KIA + DOW  100 KIA + WIA

SECTION 4

BATTLEFIELD

MILITARY TREATMENT FACILITY (MTF) LEVELS I – IV

%KIA = DEATHS BEFORE MTF  100 KIA + (WIA-RTD)

%DOW = DEATHS AFTER REACHING MTF  100 (WIA–RTD)

Wounded In Action (WIA)

DOW

Admitted to MTF for treatment

Minor injuries Returned to Duty (RTD) 72 hours

FIGURE 52-2 Explanation of terminology for combat casualty calculation(s).

■ Killed in Action This term refers to the number of combat deaths that occur prior to reaching a medical treatment facility (MTF such as battalion aid station [BAS], forward surgical unit, combat support unit, or higher levels of hospital care where a medical officer is present) (Fig. 52-4). This term is expressed as a percent of the WIA minus the RTD. This statistic provides a measure of (1) the lethality of the weapons employed in the conflict; (2) the effectiveness of the point of wounding and medical care far forward; and (3) the availability of evacuation from the tactical setting. Factors that impact on KIA rate include body and vehicle armor, effectiveness of the trauma systems in the forward area, timing from wounding to first treatment, and care in the field by the casualty, buddy care, or the medic/corpsman.

■ Died of Wounds This term refers to the number of all deaths that occur after reaching an MTF. This term is expressed as a percentage of the total wounded minus the RTD (Fig. 52-5). This statistic provides a measure of the effectiveness of the MTF care and perhaps also the appropriateness of field triage, initial care, optimal evacuation routes, and application of a coordinated trauma systems approach to a combat setting. Deaths that occur anytime after admission to an MTF are included in this category. It is important to note that the calculation of KIA and DOW utilizes different mathematical terms. The statistical figure of DOW focuses on the survival of the cadre who are alive long enough to undergo treatment at an MTF. Thus, the DOW rate is a surrogate of the effectiveness of MTF care. It must also be recognized that the final value(s) of KIA and DOW are in part reciprocal in nature and influenced by tactical considerations of the theater. Extremely rapid evacuation from the point of wounding to an MTF will increase the relative number of dramatically injured casualties who arrive alive in order to receive care. This may shift the relative death rate from

those killed in action in the field to those who died of wounds at medical treatment facilities. In previous conflicts (World War II, Korea) or in instances of increased evacuation times (remote regions of Afghanistan), the number of casualties who succumb prior to entering an MTF (i.e., KIA) will increase. With this perspective and background in mind, a more meaningful comparison may be obtained when comparing the current conflict with previous wars, as displayed in Table 52-1. Thoughtful reviews of KIA, DOW, and CFR rates for combat trauma are important for optimal medical planning, training, research, and resource allocation. The need to bring combat casualty epidemiology to a civilian standard requires utilization of both technology and organization that are routinely utilized in the US civilian trauma community. Thanks to efforts by the Deputy Assistant Secretary of Defense for Health Affairs and the Surgeons General of each of the armed services, raw data appropriate for this effort are currently being collected. Standard operational definitions are in use for the cataloging and analysis of this complex information. Currently

CFR =

KIA + DOW × 100 KIA + WIA

FIGURE 52-3 Mathematical calculation of case fatality rate.

% KIA =

Deaths before MTF × 100 KIA + (WIA – RTD)

FIGURE 52-4 Mathematical definition of killed in action.

% DOW =

Died after reaching MTF × 100 (WIA – RTD)

FIGURE 52-5 Mathematical definition of died of wounds.

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TABLE 52-1 US Military Deaths in Historic Context Deaths Per Year 493 565 4,428 124,605 2,446 58,258 81,080 9,144 5,291 382 51 580

US Population During the War 3,929,884 7,036,509 17,019,678 30,383,684 61,116,815 91,641,186 130,962,661 149,895,183 178,554,916 248,709,873 290,809,777 293,655,404

Deaths/Year/ 100,000 12.6 8.0 26.0 410.1 4.0 63.7 62.6 6.2 3.0 0.05 0.02 0.2

Afghanistan and Iraq Wars were ongoing at the time of this table generation. The Iraq War excludes the 485 nonbattle injury deaths.

the Joint Theater Trauma Registry (JTTR) employs approximately 75 civilian personnel in the United States and 10 military personnel deployed in a far-forward setting. Injury severity data are recorded, scored, and analyzed by methods that both meet trauma-community standards and are appropriate to meet the unique aspects of battle injuries. The current conflict will be the first in history from which detailed, concurrent analyses of the epidemiology, nature and severity of injuries, care provided, and patient outcomes can be used to guide research, training, and resource allocation for improved combat casualty care.

COMBAT TRAUMA EPIDEMIOLOGY A recurrent theme throughout this chapter is the significant synergy or shared information between the civilian trauma community and military medicine. In the decades following the Vietnam War, the American College of Surgeons and its Committee on Trauma developed and matured a robust trauma system and care model. A generation of trauma providers trained and came to understand the benefits of working within a mature trauma system (including verified trauma centers) as well as the utility of trauma registries and performance improvement processes. These same providers were trained in the civilian trauma sector and subsequently brought this model forward as a desired standard of care when entering military service. One of the most important elements of this “translational” process was the recognition of the need for a capable and effective trauma registry tool for the military and its combat casualties. In all previous conflicts (including the first Gulf War), collection of wounding data was, at best, haphazard and retrospective. In response to the lack of a Department of Defense registry, a JTTR was developed prior to the initiation of the Global War on Terrorism. The registry process was heavily modeled after civilian counterparts such as the National

Trauma Data Bank (NTDB). Through the efforts of the three Surgeons General and the Department of Health Affairs, a policy paper and minimum essential data element set was created.3 The repository for these data is at the US Army Institute of Surgical Research at Fort Sam Houston, Texas. The JTTR has provided the basis for a significant number of peerreviewed papers over the past 8 years and continues as an invaluable tool to the continued understanding of military wounding data and epidemiology. Accurate understanding of the epidemiology and outcome of battle injury is essential to improving combat casualty care. The process of accurate data collection during combat medical operations remains notoriously difficult due to the austere and fluid nature of combat medicine. The ability to account for mechanism of injury, time to evacuation, the use of body armor, and the prehospital care rendered are just a few of the critically important, yet very difficult parameters that require tracking. The Department of Defense is actively investigating electronic and automated data acquisition systems for forward field use (electronic dog tag, PDAs, etc.). At this time, the majority of data retrieval and transmission continues to rely on pencil and paper. In its current form, the JTTR employs a cadre of approximately 75 civilian personnel within the continental United States (CONUS) and 10 forward deployed trauma registry personnel in the theater of combat.

DISTRIBUTION OF INJURIES The sources of injuries during the Iraq/Afghanistan war are not entirely different than previous conflicts. The increasingly widespread use of the improvised explosive device (IED) has led to the recognition of a particularly devastating wounding pattern combining high blast energy with multiple penetrating fragmentary wounds and thermal injury. The continued evolution and maturation of the JTTR has provided the basis for

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Revolution (1775–1783) War of 1812 (1812–1815) Mexican War (1846–1848) Civil War (1861–1865) Spanish–American War (1898) World War I (1917–1918) World War II (1941–1945) Korean War (1950–1953) Vietnam War (1964–1975) Persian Gulf War (1990–1991) Afghanistan War (October 7, 2001–2005) Iraq War (March 19, 2003–2005)

Total Deaths 4,435 2,260 13,283 623,026 2,446 116,516 405,399 36,574 58,200 382 255 1,739

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TABLE 52-2 Mechanism and Distribution of Injury Encountered During Operation Iraqi Freedom and Operation Enduring Freedom

SECTION 4

Number Percent Mechanism of injury of all wounded combatants GSW 270 19 MVC 36 2 1,146 79 Explosion 38 IED 558 2 Landmine 41 Mortar 281 19 33 2 Bomb 16 Grenade 233 GSW Explosion Mechanism of injury within regions (%) Head and neck 8 88 Thorax 19 78 17 81 Abdomen 17 81 Extremity

MVC 4 3 2 2

MVC, motor vehicle collision; GSW, gunshot wound. (Reproduced with permission from Owens BD, Kragh JF Jr, Wenke JC, Macaitis J, Wade CE, Holcomb JB. Combat wounds in Operation Iraqi Freedom and Operation Enduring Freedom. J Trauma. 2008;64:295–299.)

relatively frequent analysis of wounding patterns and wounding outcomes. The most recent analysis (2008) is presented in Table 52-2. Whether from small arms fire or from IED injuries, combat wounds are generally distinct from those encountered in an urban trauma center setting. High-velocity military weapons create much greater patterns of tissue injury and destruction than seen with handguns. Fragmentary projectiles created by IEDs (secondary blast effect) prove to be unpredictable in depth of penetration and injury potential. The universal employment of effective body armor by US and coalition forces has pushed the relative distribution of the injuries away from the core structures (head, chest, and abdomen) and toward the extremities and unprotected regions (arms, legs, neck, and groin) (Fig. 52-6). The protective effect of body armor is obvious during the recent conflicts and is best exemplified by comparing the distribution of injuries between US combat forces and civilian casualties (Fig. 52-7). Due to the evolution of the IEDs, the military has adopted increasing emphasis on protective strategies for both individual personnel and vehicles. In previous conflicts, antipersonnel devices were limited in explosive power in order to create a maiming injury that incapacitated the individual and diverted resources to care of the injured soldier (medic/litter bearers). The continued evolution of the IED (and its more devastating relative, the explosive fused projectile [EFP]) has created an increasingly powerful and destructive weapon. The scope of energy and injury of these devices is unlike that encountered in

FIGURE 52-6 Typical distribution of protective body armor for US forces.

any other setting. Examples of the force of these devices and wounding patterns are depicted in Figs. 52-8 to 52-12. The IEDs are ingenious and available at relatively small cost. Military artillery rounds are commonly used in series or clusters combined with simple but effective triggering mechanisms including cell phones, garage door openers, and timing clocks. Recent tactics employed by the enemy insurgents include incapacitation of a primary vehicle through the use of an initially triggered IED. As the vehicle survivors dismount or on the arrival of reinforcements, a second or third IED is detonated in the same region. In addition, snipers are at the ready to target the dismounted soldiers and have learned to target gaps in body armor that include the sides of the torso, the neck, the lower back, and the groin. High-velocity sniper rounds are capable of penetrating the standard Kevlar helmet, and the subsequent cranial injury proves devastating. Explosive devices may also be loaded into vehicles (vehicleborne improvised explosive device [VBIED]) and are capable of transmitting enormous, lethal, and widespread damage. Suicide improvised explosive devices (SIEDs) prove to be particularly hard to detect and defeat among large urban populations as freedom of access and movement increases during the postconflict phase. Continued experience with IEDs and the newer EFPs has driven a continued evolution of larger vehicles collectively referred to as mine-resistant/ambush-protected vehicles (MRAPs). Increasing efforts are being directed to improve the interior cabin design of these vehicles to mitigate indirect injuries such as lumbar spine injuries from seat or blast impact. Interior design is also meant to limit secondary strike injuries as soldiers are thrown about the interior of the vehicle following a blast. General design features of these vehicles include elevated, V-shaped hulls to deflect blast injuries and devices to defeat the IED (Figs. 52-13 and 52-14). Specifics of wounding and wound care management will be discussed in greater detail later in this chapter. The importance

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40.0%

U.S.

35.0%

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FIGURE 52-7 Comparative distribution of injuries between US soldiers (protected body armor) and civilians.

FIGURE 52-8 IED explosion near Humvee.

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SECTION 4 FIGURE 52-9 IED explosion underneath mine-resistant/ ambush-protected vehicle (MRAP).

FIGURE 52-11 Typical high-energy thermal and penetrating injury secondary to IED.

of recognition of the energy and highly variable pattern of distribution of these wounds cannot be overemphasized.

such individuals as Captain Frank Butler (US Navy, Retired), the standards of military field care were examined and completely restructured and revised.4 The Committee on Tactical Combat Casualty Care (CoTCCC) was formed in 2002 and serves today as the military’s premier source of information and leadership for the prehospital care arena. The CoTCCC consists of civilian and military medical providers (officers, enlisted personnel, Special Forces, and civilian medical experts) (Fig. 52-15). The Committee continually reviews the current evidence-based material regarding casualty care in the field and makes recommendations that are applicable to the military medic. The most current set of recommendations is published as a portion of the Pre-Hospital Trauma Life Support Manual as well as a freestanding version known as the military edition (Elsevier Publishers, 7th ed.) (Fig. 52-16). The unique product of the CoTCCC is the division of prehospital field care during combat situations into three distinct phases referred to as:

FIELD CARE Ensuring the survival of the wounded soldier begins at the point of wounding. In the decades following the Vietnam War, the military field medic was schooled in the basics of prehospital care, as though the principles of civilian and urban trauma care were equally applicable to the tactical combat situation. The sobering encounters during Mogadishu (“Black Hawk Down”) as well as other Special Forces encounters highlighted the flawed logic and often lethal consequences of this assumption. The Special Forces medical community recognized that good medicine could lead to bad military tactics, and, in turn, bad military tactics resulted in casualties and mission failure. As a result of this recognition and through the leadership of

1. Care under fire 2. Tactical field care 3. Tactical evacuation care (TACEVAC)

FIGURE 52-10 Heavily damaged MRAP after IED explosion (note passenger hull largely intact).

FIGURE 52-12 Typical multiple penetrating fragmentary injuries from IED (note relative sparing of trunk secondary to body armor).

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FIGURE 52-13 Exterior appearance of Mine Resistant Ambush Protected (MRAP) personnel carrier.

The interested reader is referred to the military edition of the Pre-Hospital Trauma Life Support Manual for a detailed description of these recommendations (summarized in Table 52-3). While many recommendations are similar to civilian care, there are also significant distinctions. The principles of care under fire emphasize the tactical necessity of defeating enemy fire while minimizing further casualties (soldier as well as medic). Tactical field care has embraced the use of tourniquets, hemostatic agents, and limited fluid resuscitation strategies based on recent evidence-based reviews. The section of TACEVAC incorporates principles of far-forward en route care while recognizing the limitations imposed by an austere environment.

FIGURE 52-15 The logo of the Committee on Tactical Combat Casualty Care. (Reproduced with permission of the Committee on Tactical Combat Casualty Care (coTCCC). Copyright © coTCCC. All rights reserved.)

MILITARY MEDICAL CARE STRUCTURE There are five basic levels of care in the military medical evacuation and care system (previously referred to as echelons). These levels are not to be confused with American College of Surgeons’ designation of US trauma centers (Table 52-4). Different levels of field care are intended to denote differences in resource capability, but not the quality of care. Each level has the capability of the level forward of it, and expands further upon that capability. Soldiers with injury or illness effectively treated at any level should be returned to duty at that level whenever possible. All other casualties are prepared for safe evacuation and subsequent transport to a higher echelon of care. Level I. First aid and immediate lifesaving measures are delivered at the scene of wounding. Care is administered by the injured soldier himself (“self-aid and buddy aid”), a combat lifesaver, or a combat medic or corpsman. A combat lifesaver is trained in basic first aid, while a combat medic or corpsman is trained as an emergency medical technician-basic. The most forward medical facility available is a BAS. These facilities may be located in a tent or in any other opportune structure. These facilities are capable of performing treatment and triage. Typically, the highest level of medical provider at a BAS is a physician assistant or a nonsurgical physician. The function of the BAS will be to treat and evacuate or to return the casualty to duty as appropriate to the level of injury. The BAS has extremely limited holding capability of 6 hours or less.

FIGURE 52-14 Demonstration of energy-displacing effects of typical MRAP hull.

Level IIA. Medical Company. Generally, these are somewhat larger facilities ranging from 20 to 50 personnel. They have limited inpatient bed space and can hold or treat casualties

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SECTION 4 FIGURE 52-16 The military edition of Pre-Hospital Trauma Life Support (PHTLS), which contains the current guidelines of the Committee on Tactical Combat Casualty Care. (Reproduced with permission from Committee on Tactical Combat Casualty Care. Pre-Hospital Trauma Life Support—Military Edition. St. Louis: Mosby-Elsevier; 2007, © Elsevier.)

for up to 72 hours. The services that are available at this level include primary care (sick call), as well as dental care. Usual ancillary services include laboratory and x-ray capability. Some of these facilities have optometry and psychiatry services on an intermittent basis. Each military service has a slightly different unit designation at this level. This level does not offer routine surgical capability but may be able to offer lifesaving interventions such as endotracheal intubation and placement of chest thoracostomy tubes. Level IIB. The medical company or BAS may be augmented with surgical capability. If this is the case, the designation of

this facility becomes Level IIB. The Army provides this supplementation in the form of a forward surgical team (FST— 20-member team) (Fig. 52-1). The Navy provides surgical capability via a forward resuscitative and surgical system (FRSS—eight-member team). The Air Force’s concept utilizes a five-member team referred to as a Mobile Field Surgical Team (MFST). Each of these military medical units is designed to provide basic capabilities of resuscitative surgery. Using these building blocks, these highly mobile teams can typically provide one to two operating room tables within 30–60 minutes of advancement. They can be set up in a mobile environment, climate-controlled tents, or shelters of opportunity. These

TABLE 52-3 Summary Statement of Current Recommendations of the Committee on Tactical Combat Casualty Care

2. Direct/expect casualty to remain engaged as a combatant, if appropriate

3. Direct casualty to move to cover/apply self-aid if able

Tactical Field Care Casualties with an altered mental status should be disarmed immediately Airway management (a) Unconscious casualty without airway obstruction: • Chin-lift or jaw-thrust maneuver • Nasopharyngeal airway • Place casualty in recovery position (b) Casualty with airway obstruction or impending airway obstruction: • Chin-lift or jaw-thrust maneuver • Nasopharyngeal airway: – Allow conscious casualty to assume any position that best protects the airway, to include sitting up – Place unconscious casualty in recovery position if measures above unsuccessful • Surgical cricothyroidotomy (with lidocaine if conscious)

Airway management (a) Unconscious casualty without airway obstruction: • Chin-lift or jaw-thrust maneuver • Nasopharyngeal airway • Place casualty in recovery position (b) Casualty with airway obstruction or impending airway obstruction: • Chin-lift or jaw-thrust maneuver • Nasopharyngeal airway: – Allow conscious casualty to assume any position that best protects the airway, to include sitting up – Place unconscious casualty in recovery position if measures above unsuccessful • Surgical cricothyroidotomy (with lidocaine if conscious) or • Laryngeal mask airway/ILMA or • Combitube or • Endotracheal intubation or • Surgical cricothyroidotomy (with lidocaine if conscious) (c) Spinal immobilization is not necessary for casualties with penetrating trauma Breathing (a) Consider tension pneumothorax and decompress with needle thoracostomy if casualty has torso trauma and respiratory distress (b) Consider chest tube insertion if no improvement and/or long transport anticipated (c) Most combat casualties do not require oxygen, but administration of oxygen may be of benefit for the following types of casualties: • Low oxygen saturation by pulse oximetry • Injuries associated with impaired oxygenation • Unconscious patient • TBI patients (maintain oxygen saturation 90) • Casualties in shock • Casualties at altitude (d) Sucking chest wounds should be treated by applying a Vaseline gauze during expiration, covering it with tape or a field dressing, and monitoring for development of a tension pneumothorax (continued )

Modern Combat Casualty Care

Breathing (a) Consider tension pneumothorax and decompress with needle thoracostomy if casualty has torso trauma and respiratory distress (b) Sucking chest wounds should be treated by applying a Vaseline gauze during expiration, covering it with tape or a field dressing, and monitoring for development of a tension pneumothorax

CASEVAC Care

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Care Under Fire 1. Return fire, take cover

SECTION 4 5. Airway management is generally best deferred until the tactical field care phase

6. Stop life-threatening external hemorrhage if tactically feasible: • Direct casualty to control hemorrhage by self-aid if able • Use a tourniquet for hemorrhage that is anatomically amenable to tourniquet application • For hemorrhage that cannot be controlled with a tourniquet, apply HemCon dressing with pressure

Tactical Field Care Bleeding (a) Assess for unrecognized hemorrhage and control all sources of bleeding (b) Assess for discontinuation of tourniquets once bleeding is controlled by other means. Before releasing any tourniquet on a patient who has been resuscitated for hemorrhagic shock, assure a positive response to resuscitation efforts (i.e., a peripheral pulse normal in character and normal mentation if there is no TBI) IV (a) Start an 18-gauge IV or saline lock, if indicated: • If resuscitation is required and IV access is not obtainable, use the intraosseous route Fluid resuscitation Assess for hemorrhagic shock; altered mental status in the absence of head injury and weak or absent peripheral pulses are the best field indicators of shock (a) If not in shock: • No IV fluids necessary • PO fluids permissible if conscious (b) If in shock: • Hextend® 500 mL IV bolus • Repeat once after 30 min if still in shock • No more than 1,000 mL of Hextend® (c) Continued efforts to resuscitate must be weighed against logistical and tactical considerations and the risk of incurring further casualties (d) If a casualty with TBI is unconscious and has no peripheral pulse, resuscitate to restore the radial pulse

CASEVAC Care Bleeding (a) Assess for unrecognized hemorrhage and control all sources of bleeding (b) Assess for discontinuation of tourniquets once bleeding is controlled by other means. Before releasing any tourniquet on a patient who has been resuscitated for hemorrhagic shock, assure a positive response to resuscitation efforts (i.e., a peripheral pulse normal in character and normal mentation if there is no TBI)

IV (a) Reassess need for IV access: • If indicated, start an 18-gauge IV or saline lock • If resuscitation is required and IV access is not obtainable, use intraosseous route Fluid resuscitation (a) Reassess for hemorrhagic shock; altered mental status (in the absence of brain injury) and/or abnormal vital signs (b) If not in shock: • No IV fluids necessary • PO fluids permissible if conscious (c) If in shock: • Hextend 500 mL IV bolus • Repeat once after 30 min if still in shock • No more than 1,000 mL of Hextend (d) Continue resuscitation with PRBC, Hextend, or LR as indicated (e) If a casualty with TBI is unconscious and has a weak or absent peripheral pulse, resuscitate as necessary to maintain a systolic blood pressure of 90 mm Hg or above

Specific Challenges in Trauma

Care Under Fire 4. Try to keep the casualty from sustaining additional wounds

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TABLE 52-3 Summary Statement of Current Recommendations of the Committee on Tactical Combat Casualty Care (continued )

8. Communicate with the patient if possible: (a) Offer reassurance and encouragement (b) Explain first aid actions 9. 10. 11.

Prevention of hypothermia (a) Minimize casualty’s exposure to the elements. Keep protective gear on or with the casualty if feasible (b) Replace wet clothing with dry if possible (c) Apply Ready-Heat™ blanket to torso (d) Wrap in Blizzard™ Rescue Blanket (e) Put Thermo-Lite® Hypothermia Prevention System Cap on the casualty’s head, under his or her helmet (f) Apply additional interventions as needed/ available (g) If mentioned gear is not available, use dry blankets, poncho liners, sleeping bags, body bags, or anything that will retain heat and keep the casualty dry Monitoring—pulse oximetry should be available as an adjunct to clinical monitoring. Readings may be misleading in the settings of shock or marked hypothermia

Prevention of hypothermia (a) Minimize casualty’s exposure to the elements. Keep protective gear on or with the casualty if feasible (b) Continue Ready-Heat™ blanket, Blizzard™ Rescue Blanket, and Thermo-Lite® cap (c) Apply additional interventions as needed (see Table 3-1) (d) Utilize the Thermal Angel™ or other portable fluid warmer on all IV sites, if possible (e) Protect the casualty from wind if doors must be kept open

Inspect and dress known wounds Check for additional wounds Analgesia as necessary (a) Able to fight (these medications should be carried by the combatant, and selfadministered as soon as possible after the wound is sustained): • Mobic® 15 mg PO qd • Tylenol®, 650 mg bilayer caplet, 2 PO q 8 h (b) Unable to fight (Note: Have naloxone readily available whenever administering opiates): • Does not otherwise require IV/IO access: (i) Oral transmucosal fentanyl citrate 400 μg transbuccally: – Recommend taping lozenge on a stick to casualty’s finger as an added safety measure – Reassess in 15 min

Inspect and dress known wounds if not already done Check for additional wounds Analgesia as necessary (a) Able to fight (these medications should be carried by the combatant, and self-administered as soon as possible after the wound is sustained): • Mobic® 15 mg PO qd • Tylenol®, 650 mg bilayer caplet, 2 PO q 8 h (b) Unable to fight (Note: Have naloxone readily available whenever administering opiates): • Does not otherwise require IV/IO access: (i) Oral transmucosal fentanyl citrate 400 μg transbuccally: – Recommend taping lozenge on a stick to casualty’s finger as an added safety measure – Reassess in 15 min – Add second lozenge, in other cheek, as necessary to control severe pain – Monitor for respiratory depression

Monitoring—institute electronic monitoring of pulse oximetry and vital signs if indicated

Modern Combat Casualty Care

(continued )

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7. Prevent hypothermia: Wrap casualty in Blizzard Rescue Blanket Cover scalp with Thermo-Lite cap

SECTION 4 12. 13.

14.

15.

16.

Tactical Field Care – Add second lozenge, in other cheek, as necessary to control severe pain – Monitor for respiratory depression • IV or IO access obtained: (i) Morphine sulfate 5 mg IV/IO: – Reassess in 10 min – Repeat dose q 10 min as necessary to control severe pain – Monitor for respiratory depression (ii) Promethazine 25 mg IV/IO/IM q 4 h, for synergistic analgesic effect, and as a counter to potential nausea Reassess splint fractures and recheck pulse Antibiotics: recommended for all open combat wounds (a) If able to take PO: • Gatifloxacin 400 mg PO qd (b) If unable to take PO (shock, unconsciousness): • Cefotetan 2 g IV (slow push over 3–5 min) or IM q 12 h or • Ertapenem 1 g IV or IM q 24 h Communicate with the patient if possible (a) Encourage, reassure (b) Explain care Cardiopulmonary resuscitation Resuscitation on the battlefield for victims of blast or penetrating trauma who have no pulse, no ventilations, and no other signs of life will not be successful and should not be attempted Document clinical assessments, treatments rendered, and changes in casualty’s status. Forward this information with the casualty to the next level of care

CASEVAC Care • IV or IO access obtained: (i) Morphine sulfate 5 mg IV/IO: – Reassess in 10 min – Repeat dose q 10 min as necessary to control severe pain – Monitor for respiratory depression (ii) Promethazine 25 mg IV/IO/IM q 4 h, for synergistic analgesic effect, and as a counter to potential nausea

Reassess fractures and recheck pulses Antibiotics: recommended for all open combat wounds (a) If able to take PO: • Gatifloxacin 400 mg PO qd (b) If unable to take PO (shock, unconsciousness): • Cefotetan 2 g IV (slow push over 3–5 min) or IM q 12 h or • Ertapenem 1 g IV or IM q 24 h Pneumatic antishock garments (PASG) may be useful for stabilizing pelvic fractures and controlling pelvic and abdominal bleeding. Their application and extended use must be carefully monitored. They are contraindicated for casualties with thoracic and brain injuries Document clinical assessments, treatments rendered, and changes in casualty’s status. Forward this information with the casualty to the next level of care

Specific Challenges in Trauma

Care Under Fire

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TABLE 52-3 Summary Statement of Current Recommendations of the Committee on Tactical Combat Casualty Care (continued )

Modern Combat Casualty Care

TABLE 52-4 Echelons of Care

Description Major trauma center with teaching and research Major trauma center Regional trauma center, limited capability, 30-day ICU holding capability Community hospital with limited emergency surgery capability Outpatient clinic EMS/corpsman/ medic

US Civilian Trauma Designation I

II III

IV

— —

BAMC/ISR, Brooke Army Medical Center/Institute of Surgical Research; WHMC, Wilford Hall Medical Center (both BAMC/ISR and WHMC at San Antonio, Texas; level V also provides rehabilitation centers); NNMC, National Naval Medical Center in Bethesda, Maryland; WRAMC, Walter Reed Medical Center in Washington, DC; FRSS, forward resuscitative and surgical system; FST, forward surgical team; EMEDS, expeditionary medical support.

teams carry enough equipment and supplies to perform somewhere between 10 and 40 life-stabilizing operations. While designed for 24–72 hours of continuous operations without resupply, these teams may be employed in a nonconventional configuration and provide ongoing support to small maneuvering elements if they have the opportunity for adequate resupply. A comparative summary of capabilities and requirements for these surgical augmentation teams is provided (Table 52-5). These facilities do not usually have significant holding capability, and rely on a capable and robust en route evacuation and care system in order to maintain their surgical volume. Level III. This level represents the highest level of medical care available within the combat theater of operations. Usually the largest bulk of inpatient beds within a combat theater are located at Level III facilities. Most deployable hospitals are modular in nature, allowing the commander to tailor the medical response to the expected or actual demand. These hospitals may be set up in a mobile fashion, but may also use buildings such as churches or abandoned hospitals if such opportunities are available. The Army’s nomenclature for these units is the combat support hospital (CSH), which has replaced the historic MASH unit. The Navy has the fleet hospital, which

TABLE 52-5 Definition of Level IIB Surgical Augmentation Teams Army 24-Member team

Navy 8-Member team

40 operations 3 general surgeons 1 orthopedic surgeon 2 anesthetists Critical care nursing and operative technical support

18 operations 2 general surgeons

1 anesthesiologist Critical care nursing and operative technical support

Air Force 5-Member team 10 operations 1 general surgeon 1 orthopedic surgeon 1 anesthetists Critical care nursing and operative technical support

is now termed Expeditionary Medical Unit (EMU), and the Air Force the Expeditionary Medical Support (EMEDS) system. The difference in capability between the Level II and III facilities is that they have subspecialty care available and other services to typically include computerized tomography and increased blood bank and laboratory capability (Figs. 52-17 and 52-18). Current doctrine maintains full holding and recovery capability at Level III facilities. The length of time that US casualties are held at a Level III facility has dramatically changed during this current conflict as the result of the introduction of a capable and robust en route care system. In previous conflicts, casualties recovered at the Level III facilities until they were very stable and essentially ambulatory. The fluidity of medical support for an asymmetrical battle space, as well as the deployment of far-FSTs, has driven the development of an equally capable evacuation system. In response to the need, and in recognition of other shortcomings, the US Air Force developed and subsequently deployed Critical Care Air Transport Teams (CCATT) to fulfill this need. A CCATT consists of an intensivist physician, a critical care nurse, and a respiratory therapist (Table 52-6). The role of a CCATT is to provide continuous

FIGURE 52-17 The Level III medical facility at Craig Joint Theater Hospital, Bagram, Afghanistan.

CHAPTER 52

Military Designation Echelon of Care V (e.g., BAMC/ISR and WHMC) IV (NNMC, WRAMC) III (e.g., Landstuhl, Germany, and theater hospitals in Iraq) IIB (e.g., surgical company, FRSS, FST, EMEDS) IIA I

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SECTION 4

being transported from the southwest Asia theaters of Iraq and Afghanistan. This facility is jointly manned by members of the US Army, Navy, and Air Force medical corps. The LRMC has been verified as meeting the criterion of a Level II trauma facility by the American College of Surgeons Committee on Trauma. It is the first facility outside of the CONUS to receive this designation.5 Level V. These facilities represent the zone of the interior, CONUS-based hospitals outside the combat zone. These facilities include military medical centers, other federal hospitals (Veterans Affairs hospitals), and civilian contracted hospitals. These facilities represent the most definitive care possible and include burn care, long-term convalescence, and specialized rehabilitation.

OVERVIEW OF MOVEMENT OF PATIENTS FIGURE 52-18 An aerial depiction of the Level III medical facility at the 332nd Air Force Theater Hospital Balad, Iraq.

en route, high-intensity care from far-forward austere locations to more rearward (more capable and resource abundant) facilities. As a result of the deployment of CCATT, the average duration that a current casualty is in theater is less than 48 hours (including one to two stabilizing surgery procedures). The role of the CCATT and the en route care system will be discussed later in this chapter. Level IV. Level IV facilities represent the larger, more capable military hospitals outside of the theater of combat. These hospitals may be located in Europe or the United States. Although the three services have many hospitals worldwide, only a few select hospitals receive casualties from the war. The Landstuhl Regional Medical Center (LRMC) is the hub for all casualties

The distribution and triage destination of casualties from the forward edge of the battle zone can be a complex and varying discussion. As with civilian trauma systems, the ideal situation is to provide an integrated spoke-and-hub trauma system that matches the patient’s needs to the facility’s resources. The complexity of this process is multiplied by considerations of lines of battle, maturity of the theater and medical facilities, and the evacuation capability within the theater. Continual evaluation of appropriate patient movement, triage, and flow is an absolute imperative. The current conflict is the first opportunity for the military medical corps to evaluate the effectiveness of this process utilizing a trauma systems approach. The military has looked to the American College of Surgeons Committee on Trauma and the greater than 30 years of trauma systems experience as a model to evaluate its own efficacy. A discussion of trauma system development as it applies to the current military medical system will be considered later in this chapter (see Section “Military Trauma Systems”).

COMBAT CASUALTY CARE TABLE 52-6 Composition of Three-Member CCAT Team Description 1. Intensivist physician Capable of providing short-term life support, including advanced airway management, ventilator management, and limited invasive (nonoperative) procedures Trained in critical care medicine, anesthesiology, or emergency medicine 2. Critical care or emergency medicine nurse Experienced in managing patients requiring mechanical ventilation, invasive monitoring, hemodynamic support 3. Cardiopulmonary technician Experienced in management of patients requiring mechanical ventilation, invasive monitoring Experienced in troubleshooting ventilatory support and monitoring systems

It is an appropriate (but sad) truism that the conduct of war advances the science of trauma care. The conflicts of Operation Enduring Freedom and Operation Iraqi Freedom have resulted in a wide spectrum of changes to our thought processes as well as to the clinical practice in care of the injured patient. In some instances innovations have occurred by remembering lessons from the past. Other advances have resulted from new insights derived from the experience of managing a significant volume of severely injured casualties. The following section will describe some of the innovations brought from the battlefield to advance the care of the injured patient.

■ Prehospital Care Advances As described previously, the CoTCCC has taken the lead in defining and shaping the practice guidelines for combat casualty care in the field. In the process of defining care during the three time frames of field care (care under fire, tactical field care, and TACEVAC), the CoTCCC has reshaped many principles.

Modern Combat Casualty Care Tourniquets. The use of tourniquets is depicted in ancient Greek literature and their presence on the battlefield has been a constant in military medicine since that time. Hemorrhage from extremity injuries has been recognized in wars throughout history as the leading cause of potentially preventable deaths. Autopsy findings from the earliest portion of this conflict have confirmed this finding.15 Widespread endorsement of the use of tourniquets has been tempered by anecdotal literature reports and current dogma that suggests that the risk of tourniquet use (limb ischemia, pressure necrosis, etc.) outweighs the potential benefits of their use. Historically, in the US Civil War, the Spanish Civil War, and World War I, tourniquets were employed but lost favor due to their mechanical and perceived clinical ineffectiveness. The ineffectual strap-and-buckle tourniquet that was a standard issue in the US military for the last five decades may have accounted for this perception. With recent insights, a coherent move to a better designed tourniquet on the battlefield has occurred. The pertinent issues include the use of tourniquets in patients at risk of lethal exsanguination, improved tourniquet science and design, appropriate training and doctrine, and documentation of clinical research and experience (Fig. 52-19). Kragh et al. recently published what proved to be the most extensive review of tourniquet use in a combat setting.16,17 This study examined a cadre of 232 patients who had 428 tourniquets applied to 309 injured limbs. The study demonstrated an acceptably low major complication rate (less than 3%) as well a positive risk/benefit ratio in terms of survival. In a subsequent follow-on study, the same group demonstrated a statistically significant survival benefit when tourniquets were applied in the field and prior to the onset of shock (loss of peripheral pulses). The results forwarded from the current combat operations as well as the institution of appropriate practice guidelines have resulted in tourniquets being advocated as a fundamental care process by the CoTCCC and by all military

FIGURE 52-19 The combat application tourniquet.

CHAPTER 52

Fluid Resuscitation. The CoTCCC currently recommends a strategy of “permissive hypotension” for the management of combat casualties with penetrating injuries. This conclusion is based on a growing wealth of evidence that suggests that restoration of blood pressure prior to surgical hemorrhage control leads to adverse outcomes as well as increased mortality.6–8 There is no evidence to support the notion that prehospital fluids offer a survival advantage—despite years of dogma insisting on their use.9 The strategy of permissive hypotension stresses external hemorrhage control (as possible) with judicious monitoring of the patient to include intact mentation or the presence of a palpable peripheral pulse. Resuscitation of blood pressure is deferred until the casualty is in an environment where definitive hemorrhage control may be obtained. This strategy relieves the burden of additional or accelerated blood loss and ongoing hemorrhage control in the field where IV fluids are difficult to carry and, in fact, may negatively influence outcomes. Clinical practice in Vietnam advocated the early and aggressive use of crystalloid resuscitation. This practice may have been in part a consequence of the misinterpretation of early resuscitation literature that discussed the use of crystalloid fluids (until whole blood was available).10 The clinical practice of aggressive crystalloid resuscitation was translated back to the civilian sector and became integrated as a fundamental tenet of the Advanced Trauma Life Support (ATLS) course over the next 30 years.11 Recent basic scientific research has challenged the wisdom of the use of crystalloid solutions by demonstrating adverse immunological consequences following their use.12 Lactated Ringer’s solution was initially developed with both racemic forms of lactate (D and L isomers of lactate). Research has suggested that the elimination of the D isomer may be beneficial.13 An additional detriment of crystalloid resuscitation (normal saline or Ringer’s lactated solution) is that it adversely contributes to systemic acidosis via the intrinsically low pH of these solutions (5.0 and 6.5, respectively). The choice of fluid to be used in the military field setting has also changed. The CoTCCC recommends the use of smallvolume colloid solutions. These solutions can achieve similar clinical volume expansion benefits while reducing the clinical weight and volume of material that must be carried forward in the medic’s backpack.14 The current recommendation of the CoTCCC has been to obtain IV access (heparin lock) on all casualties. Fluid administration is withheld unless the casualty demonstrates loss of consciousness or loss of palpable peripheral pulses. Fluid resuscitation consists of a 500 cm3 bolus of a colloid solution (Hextend), and this may be repeated one time. Oral hydration of the casualty is permissible. Traditional civilian care tenets have maintained the patient in an NPO status for fear of aspiration at the time of future surgical intervention. The military system accepts this minimal risk and acknowledges that all urgent operations must assume a full stomach (from previous meals) at the time of induction of anesthesia. The use of oral hydration of casualties accommodates for care in the situations where evacuation may be delayed hours or even days secondary to tactical considerations.

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medical commands. The addition of tourniquets to standard equipment sets for civilian ambulance services in the United States will become recommended practice as of 2012. The most common form of tourniquet adopted by the US military is depicted in Fig. 52-19.

taining pressure is not adequate. After 3 minutes of direct manual pressure, a pressure dressing may be applied over the wound to cover the wound and the agent as well as to maintain a degree of pressure.

Damage Control Resuscitation Topical Hemostatics The subject of topical hemostatics is an exciting and progressively evolving area of interest that is rapidly being translated from combat care to the civilian arena. The high incidence of extremity injury in a combat setting is a result of the increased use and effectiveness of body armor. This reality is combined with the sobering fact that perhaps one third of all preventable combat deaths are the result of potentially compressible hemorrhage of the extremities. This had led to renewed interest in hemorrhage control techniques. The use of tourniquets was previously described. The incorporation of topical hemostatics (combined with the appropriate use of tourniquets) is seen as a key component of this innovative process. A plethora of agents have been forwarded by multiple manufacturers in response to the significant interest and focus placed on this topic by the military medical corps. The lead agency for review process has been the CoTCCC. The CoTCCC reviews the available peerreviewed literature as well as evidence forwarded from the US Army Institute of Surgical Research and its standardized hemorrhage control model. As a result of the most recent recommendation, the CoTCCC guidelines were changed to recommend Combat Gauze© as the first-line treatment for lifethreatening hemorrhage that is not amenable to tourniquet placement (Fig. 52-20).18 Combat Gauze© offers the medic the advantage of being a gauze-type (malleable) agent rather than a granular agent. Strong preference was voiced by combat medics for a gauze-type agent rather than a powder or granule. This was based on the experience in combat that powder or granular agents do not work well in wounds where the bleeding vessel is at the bottom of a deep and narrow wound tract. A gauze-type hemostatic agent has been found to be more easily applied in this setting. Combat Gauze© should be applied with 3 minutes of sustained direct pressure over the bleeding site in order to be effective. Simply applying the agents without main-

Perhaps the most significant contribution of the current conflict to our understanding of care of the injured patient is the restructuring of the approach to the patient with major hemorrhage. The significant military experience gained over the past decade of armed conflict has created a paradigm shift in the management of the patient requiring massive transfusion (defined as transfusion of greater than 10 U of packed red blood cells [RBCs] in a 24-hour period). Collectively, this approach has been coalesced under the term damage control resuscitation (DCR). DCR is appropriately considered a comprehensive approach to the patient with major traumatic injury and life-threatening hemorrhage. It consists of multiple, ongoing, horizontally based resuscitation principles including: 1. 2. 3. 4.

Recognition of the patient at risk Permissive hypotension Immediate institution of hemostatic resuscitation Damage control surgical principles

RECOGNITION OF THE PATIENT AT RISK Traditional trauma principles have emphasized recognition of trauma patients at risk of adverse outcomes by a definition of shock based on parameters of pulse, blood pressure, and urinary output (ATLS). Extensive experience with significant numbers of young combat casualties has led to the conclusion that awaiting the onset of abnormalities of blood pressure, pulse, and urinary output creates significant and often life-threatening delay in recognition of patients who are in distress. The current emphasis has been realigned to early detection and avoidance of the components of the so-called lethal triangle or triad of death. The presence of acidosis, hypothermia, and coagulopathy (Fig. 52-21) following traumatic injury significantly alters outcome and increases the risk of mortality.19 Review of combat wounding data at the time of the presentation of a casualty to

The Lethal Triad

Acidosis

Hypothermia

Death

Coagulopathy FIGURE 52-20 QuikClot Combat Gauze©.

FIGURE 52-21 The lethal triad.

Modern Combat Casualty Care

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50% 45%

CHAPTER 52

Prob. of death Low Upper

40% 35%

Mortality

30% 25% 20% 15% 10% 5% 0% 1

1.5

2 2.5 International normalized ratio

3

3.5

FIGURE 52-22 The relationship between initial INR in the ED and subsequent mortality. (Reproduced with permission from Niles SE, McLaughlin DF, Perkins JG, et al. Increased mortality associated with the early coagulopathy of trauma in combat casualties. J Trauma. 2008;64(6):1459.)

the surgical field hospital has led to the description of key “trigger points.” Each of these trigger points is associated with statistically significant outcome differences in the trauma patient. These trigger points may be readily identified within the first 5 minutes of care. Additionally, these trigger points may be reliably identified in combat casualties long before the so-called traditional shock parameters appear. These five trigger points consist of the following parameters and will be discussed sequentially: 1. 2. 3. 4.

Acidosis as manifested by a base deficit greater than 6 Coagulopathy (INR greater than 1.5) Hypothermia (temperature less than 96°) Systolic hypotension at presentation (blood pressure less than 90 mm Hg) 5. Hemoglobin value of less than 11 g

■ Acidosis The presence of systemic acidosis, defined as a base deficit of greater than 6, can be rapidly identified in the first minutes following the arrival of the combat casualty (or civilian trauma victim). A base deficit of greater than 6 in trauma patients is associated with a demonstrated increased transfusion requirement,20 a longer ICU stay,21 and increased occurrence of massive transfusion as well as an increased patient mortality rate.22 The presence of a base deficit is detectable long before blood pressure drops and is indicative of systemic cellular hypoxia. Acidosis contributes to coagulopathy more than any other factor due to the negative impact on the function of the clotting cascade.23

■ Coagulopathy The presence of coagulopathy in the trauma bay identifies a cohort of patients at increased risk of death. This association was originally described in a civilian population.19 Through evaluation of data in the JTTR, this same association has also been demonstrated to have an exponential impact on mortality (Fig. 52-22).24 The presence of coagulopathy is a part of the lethal triad, and its rapid correction following identification will be discussed below.

■ Hypothermia The presence of hypothermia, defined as a core temperature of less than 96°, is the third arm of the lethal triad. Hypothermia can be detected at the time of arrival of the trauma patient. A temperature less than 96° is associated with increased mortality as well as increasing the intrinsic dysfunction of the clotting cascade.25 Coagulation disorders are associated with temperature-related deficits in clotting factor enzyme function, platelet aggregation function, and fibrinolytic activity.26 These series of enzymatic reactions of the coagulation cascade are strongly inhibited by hypothermia.

■ Systolic Hypotension It is difficult to ascertain how the so-called critical threshold of hypotension was initially established as 90 mm Hg. Previous experience has demonstrated that blood pressure measurements early in the course of shock are not well correlated with blood flow or cardiac output. Significant tissue hypoperfusion

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Specific Challenges in Trauma 35

Age < 43 Age >= 43

30

20 15 10 5 0 60

65

70

75

80

85

90

95

100 105 110 115 120 125 130 135 140 145 150 155 160

Systolic blood pressure in the ED

35

Male Female

30 % Mortality

SECTION 4

% Mortality

25

25 20 15 10 5 0 60

65

70

75

80

85

90

95

100 105 110 115 120 125 130 135 140 145

150 155 160

Systolic blood pressure in the ED

FIGURE 52-23 Relationship between initial systolic blood pressure and mortality based on age (upper) and gender (lower). (Reproduced with permission from Eastridge BJ, Salinas J, McManus JG, et al. Hypotension begins at 110 mm Hg: redefining ‘hypotension’ with data. J Trauma. 2007;63:291.)

is demonstrated in hypovolemic laboratory models as well as in blunt and penetrating trauma patients. This observation is valid despite normal vital signs. The demonstration of a “normal blood pressure” following trauma may be particularly deceptive in young, previously healthy patients. Eastridge et al. examined the records of over 850,000 trauma patients entered into the National Trauma Database with respect to the initial presenting blood pressure.27 This study revealed that at 110 mm Hg, the slope of the mortality curve increased such that mortality was 5% greater for every 10 mm Hg detriment in systolic blood pressure (Fig. 52-23). The conclusion of this group was that a systolic blood pressure less than 110 mm Hg is a more clinically relevant definition of hypotension and hypoperfusion than the current standard of 90 mm Hg.

■ Hemoglobin Less Than 11 Early hemoglobin measurements obtained within minutes of patient arrival in the emergency room are a reliable indicator of ongoing hemorrhage. Early hemoglobin levels are significantly lower in patients who require emergent intervention(s) to control hemorrhage.28 Studies from the JTTR and other sources are continuing to define the predictive value of these “trigger points” with respect to the need for massive transfusion. Through analysis of 680 massively transfused combat patients, the relationship appears

to be progressive and linear (Fig. 52-24).29 The absolute precision, specificity, and sensitivity remain to be determined.

■ Diagnosis Done—Damage Control Resuscitation Once a patient at increased risk for blood loss, blood transfusion, or massive transfusion is identified, it is of value to develop a strategy recently coined as “DCR.” DCR consists of a 3-fold approach adopted by military medics as a result of significant experience with gravely injured, penetrating trauma patients. The first step is early recognition by use of clinical judgment, injury pattern recognition, and the trigger points discussed above. The second arm of DCR is to employ permissive hypotension until definitive surgery and hemorrhage intervention is established. The third arm is to employ a modified field resuscitation guideline that eliminates the use of excessive crystalloid fluids while infusing blood, plasma, and platelets in a balanced ratio of 1 U packed RBCs to 1 U of plasma to 1 U of platelets. The intent of this third arm is to initiate early and immediate restoration of a competent coagulation cascade as soon as the high-risk patient is identified in the trauma bay. To coin a famous phrase: “it is better to stay out of trouble than to get out of trouble.” Hypotensive resuscitation has been a respected portion of military medicine since at least the First World War. Walter

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90 n = 62 80

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70

% Massive transfusion

n = 115 60 50 n = 151 40 30 n = 202 20 n = 168 10 0 0

1

4

3

2 Score

FIGURE 52-24 Risk of undergoing massive transfusion based on number of positive “trigger points” in the emergency room. (Reproduced with permission from McLaughlin DF, Niles SE, Salinas J, et al. A predictive model for massive transfusion in combat casualty patients. J Trauma. 2008;64:S57.)

Perhaps one of the most important papers to be published from the conflict is the work of Borgman et al.33 This study analyzed the survival outcomes of combat casualties who required a massive transfusion at the two large CSHs located in Iraq. This is a group of interest since previous military and civilian work has demonstrated that patients requiring a massive transfusion have a mortality rate as high as 40%. This study group analyzed survival based on the relative ratio of plasma infused with respect to units of packed RBCs transfused (Fig. 52-25). The analysis demonstrated a dramatic and

70

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60 50 Mortality

Cannon, MD, described the utility of this strategy as early as 1916. Permissive or hypotensive resuscitation was again highlighted by Edward Churchill, MD, during the Second World War. Since that time, there have been numerous basic science publications as well as clinical series that have demonstrated the utility and survival advantage of judicious resuscitation prior to definitive hemorrhage control.30–32 The benefit of prehospital or presurgical crystalloid infusion has never been demonstrated. Further studies will be required to fully elucidate the degree and duration to which permissive hypotension may be productively carried out. It is also important to note that permissive hypotension in the combat setting takes full advantage of the young and robust physiologic reserve of the injured soldier. It remains to be determined whether this principle may be equally applied to the more diverse (older) civilian population with varying mechanisms of injury. The third, and final, arm of DCR is the employment of a fluid resuscitation strategy that immediately focuses attention on correcting the lethal triad (acidosis, coagulopathy, and hypothermia). During the early phase of OIF/OEF, the majority of field hospitals developed a resuscitation strategy that paired aggressive use of plasma with implementation of whole blood transfusions. This was at first a practical necessity since platelet components could not be forwarded to the far-forward field locations. Early transfusion of whole blood from volunteer (military) donors proved to be a pragmatic and dramatically effective solution to restoration of both blood volume and a competent clotting cascade. Plasma was used liberally during resuscitation as a result of its favorable pH balance as compared with the relative acidity of normal saline or Ringer’s lactate.

40

34%

30 19%

20 10 0 (Low) 1:8

(Medium) 1:2.5

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Plasma: RBC ratio groups

FIGURE 52-25 Mortality ratio(s) based on relative ratio of plasma to units of PRBCs administered. (Reproduced with permission from Borgman MA, Spinella PC, Perkins JG, et al. The ratio of blood products transfused affects mortality in patients receiving massive transfusions at a combat support hospital. J Trauma. 2007;63:805.)

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statistically significant reduction of mortality the closer the transfusion ratio approximated 1:1. This observation is dramatically different than the traditional resuscitation strategy advocated by ATLS, which includes initial crystalloid resuscitation of 2 L followed by the sequential administration of 6 U of packed RBCs and then fresh frozen plasma followed by more crystalloid solution. Since Borgman’s original work, there have been numerous additional publications from both civilian and military data sources that appear to confirm this same observation.34–37 In a large retrospective civilian sector publication,38 the outcome of massively transfused trauma patients across 25 trauma centers was measured and was consistent with this same finding. At the time of this writing, the results of a definitive, prospective observational trial are currently being collated as the prospective outcome measurement(s) for massively transfused trauma patients (PROMTTT) trial. This effort will prospectively catalog the time course, sequence, and resultant outcome of blood and blood product administration across 450 patients at 10 major US trauma facilities. Recent publications have also examined the impact of a 1:1 ratio of PRBCs to platelets. In a fashion similar to the data presented above, there is growing evidence of a survival benefit for patients requiring massive transfusion secondary to hemorrhagic shock if the platelet to PRBC ratio is equalized.39,40 Thus, the current clinical practice guideline (CPG) for DCR in the theater for patients requiring massive transfusion is to establish a 1:1:1 (PRBCs:plasma:platelets) ratio of fresh products wherever possible.

■ Whole Blood The approach to transfusion of the combat-injured patient has evolved continually since it was first introduced during World War I. The evolutionary process has included whole blood, modified whole blood, and, finally, the current use of component therapy.41,42 Component therapy was developed following the Korean War in the attempt to more effectively transport and store RBCs harvested in the United States that were destined for use in combat zone(s) overseas (Vietnam). During this era (1950s to 1960s) modified whole blood was stored up to 3 weeks. Logistical and transport considerations created enormous difficulties in the timely delivery and maintenance of whole blood products to the theater of operations. During the Korean conflict it was estimated that as much as 70% of all blood products shipped to this conflict were subsequently discarded secondary to aging expiration. This change to component therapy took place without evidence comparing the benefits, risk, or efficacy of these products (components) with the predecessor agent (whole blood). Current “classic” transfusion guidelines regarding indications for blood component therapy are based on expert opinion, experiments in euvolemic patients undergoing elective surgery, and modified whole blood that is no longer commonly available.43,44 In addition, the storage of RBCs has progressively increased over time to the current limit of 42 days without the appropriate prospective evaluation of the impact of increased storage time on the critically ill patient.

Recently there has been a shift in opinion by a portion of the trauma community regarding the transfusion approach to hemorrhagic shock. The concept of DCR as the optimal approach for the treatment of patients with life-threatening hemorrhagic injuries is gaining increasing acceptance as a result of the published experience from the battlefield. The use of warm fresh whole blood (WFWB) has also been utilized in US military combat support facilities. This practice pattern was adopted as a pragmatic solution to maintaining the principles of DCR in the austere setting where banked blood and component therapy principles were not applicable due to logistical and transport considerations.45 A recent review describes the transfusion of over 6,000 U of WFWB during combat operations.46 The recent large scale use of WFWB by the US military has rekindled interest in its use for patients at high risk of death from hemorrhage.47 Theoretically, WFWB may be advantageous as compared with component therapy in patients with hemorrhagic shock. This may reflect the improved function of RBCs, plasma, and platelets in WFWB as well as the avoidance of the adverse effects of the storage lesions when older RBCs or plasma are transfused.48–50 The assessment of the risks and benefits of the transfusion of either WFWB or component therapy (especially when RBCs of advanced storage age are transfused) must be balanced in perspective to the high mortality rate for patients with traumatic hemorrhagic shock and massive transfusion. This balance is impacted by the severity of illness and injury as well as the age of the patient. In patients who do not have life-threatening bleeding the risks of WFWB may outweigh the potential benefit. Conversely, for patients with traumatic hemorrhagic shock it may be the case that the survival advantage provided by WFWB outweighs the risk, especially if the alternative approach includes significantly aged RBCs. A growing body of literature has demonstrated that aged RBCs may pose a significant liability with respect to the inflammatory and vascular modulation cascade(s).48 An additional concern with the utilization of component therapy in the setting of hemorrhagic shock and massive transfusion is the increased volume of anticoagulants and additives that are delivered by component therapy. The process of distributing and separating the components from a single unit of whole blood results in the addition of approximately 280 cm3 of anticoagulant solutions to every initial 500 mL of whole blood. This represents a dilution of approximately 40% (compared with WFWB) in addition to providing factors that directly impede the coagulation process (citrate).47 This observation may explain the observed increased risk of dilutional coagulopathy and significant anticoagulation observed in patients with hemorrhagic shock who receive significant volumes of component therapy. As future studies are designed, it will be imperative to account and assay for the anticoagulants and volume contributed by the component separation process. A third potential mechanism to explain the striking difference seen with the use of WFWB in combat casualties is the use of fresh blood product versus old blood product. Logistical constraints and transport issues in a combat zone impede the

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delivery of blood products to the far-forward theater facilities. The median storage age of RBCs transfused in Iraq (during the first 5 years of the conflict) was 33 days. This is not entirely dissimilar to the average storage age of 21 days reported in the United States. A recently published series of coronary artery bypass graft patients examined the effect of transfused blood on outcome.51 Patients who were given older units had a higher rate of in-hospital mortality, intubation beyond 72 hours, renal failure, and sepsis. A composite complication was more common in patients given older blood and at 1 year mortality was significantly less in patients given newer blood. As a result of a concerted quality improvement effort, the current average age of blood components transfused during Operation Enduring Freedom is now 23 days. In summary, the modern-day battlefield concepts of resuscitation of the severely injured patient include early recognition, avoidance of the lethal triad, permissive hypotension, and aggressive resuscitation of the hemostatic properties of blood through a 1:1:1 approach. This strategy emphasizes staying out of trouble rather than getting out of trouble. There is a significant wealth of interest from both the civilian and military trauma care communities actively pursuing further information in this area.

FIGURE 52-26 A Critical Care Aeromedical Transport Team (CCATT) preparing a casualty for evacuation onboard a C-17 cargo aircraft.

EN ROUTE CARE This chapter has highlighted the changes implemented by military medicine to provide far-forward surgical capability and simultaneously employ an operative strategy of damage control—rapidly stabilize and then evacuate. The success of this strategy relies on the concomitant evolution of a timely and rapid evacuation system capable of transporting stabilized (but not necessarily stable) patients. This transport must occur without interruption in the intensity or quality of life-sustaining support. By doctrine, the US Air Force is responsible for the transport (evacuation) of all casualties from forward surgical facilities. The solution to this care need was the creation of CCATT by the USAF. A CCATT consists of an internist physician (surgeon, anesthesiologist, pulmonologist, or emergency medicine), an ICU nurse, and a respiratory therapist. Each team is self-contained and capable of supporting up to six critically ill patients (three of whom may be intubated) for a period of 12–24 hours. A CCATT is capable of moving forward to an austere setting and assuming the task of ongoing critical care and resuscitation while escorting the patients to a more secured, robust facility. The transport may take place from a remote forward surgical company to a Level III theater hospital, from a theater hospital (Iraq or Afghanistan) to Germany, or from Germany to the United States. A CCATT equipment set consists of small, lightweight transport ventilators, vital signs monitors, handheld blood analyzers, and a myriad of other hardware and medical supplies to support this mission (Figs. 52-26 and 52-27). A current focus of USAF research is to improve equipment capabilities as well as algorithms of care. During the current conflict, it is estimated that over 4,000 CCATT missions have been accomplished with a mortality rate of less than 1%.52

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DAMAGE CONTROL SURGERY PRINCIPLES The principles of DCR are complemented by a surgical operative technique collectively termed damage control surgery. This concept (first forwarded by Rotondo et al.53) has been taken to an entirely new level during this conflict. The military experience has demonstrated that this technique is amazingly effective even when integrated across an entire theater trauma system. Far-FSTs (Army FST, Navy FRSS, or Air Force MFST) leverage the opportunity to stop exsanguinating hemorrhage, secure the airway, restore peripheral perfusion via shunts, and pack cavity wounds with hemostatic agents. Resuscitation employs early use of whole blood (as necessary) to initiate restoration of the coagulation cascade. The far-forward team completes only that which is necessary to stabilize and then rapidly moves the patient to the next (higher) echelon of care. In turn, the next level facility may conduct further resuscitation surgery or “washouts” prior to preparing the patient for transport to the Level IV facility at LRMC. Each team along the way adapts an approach of “trust no one, check everything” and in turn understand that these patients (and their work) will be rechecked by the next team further up the chain. With continued experience and maturation, this process has proven dramatically capable. It is an appropriate testimony to the effectiveness of this system that the average duration that a casualty is in theater (including one to two damage control operations) is less than 48 hours. Celiotomy in the combat setting requires speed and experience. Tactical damage control surgery is not a specific procedure, but refers to a state of mind. As opposed to civilian damage control surgery, tactical damage control surgery is somewhat

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SECTION 4 FIGURE 52-27 A CCATT patient with portable transport equipment configured for movement.

different. In civilian terminology, it refers to an abbreviated operation due to physiologic exhaustion. In the military setting, damage control takes into account the tactical scenario, the resources available, the likelihood of further casualties, and best treatment options while leveraging the understanding that the casualty (in most instances) will be rapidly evacuated to a higher level of care. Speed and efficiency during the operative procedure is vital. There will be circumstances where simple reconstruction should be deferred to the next echelon of care (i.e., bowel anastomosis) in order to prepare for other casualties or to take advantage of evacuation flights of opportunity. There will be other scenarios where more definitive intervention is indicated, even in a far-forward setting. Vascular shunting is such an example. In the presence of arterial injury and distal limb ischemia, the placement of a temporary shunt is an effective, timely, and straightforward surgical procedure that converts a cold/ischemic limb into a perfused extremity that will remain viable during the process of evacuation to a higher level of care (Fig. 52-28). Significant experience has been gained with the use of temporary intravascular shunts and they have proven to be particularly effective at saving lives and limbs.54 With transected vessels, shunting the artery and/or vein should be the initial approach. This can, and should be, completed rapidly with a minimum of surrounding dissection. The shunt is maintained in place with simple ligatures around the shunt and vessel at both the proximal and distal limbs. Once shunted, a decision

may be made (based on tactical considerations and professional qualifications) regarding definitive repair. If appropriate resources and personnel are available, the vessel may be repaired at this same setting. If concomitant injuries and/or tactical considerations dictate that repair is deferred to a later time, the casualty may be managed or evacuated with the shunt remaining in situ. In either case (shunted or definitive repair) a com-

FIGURE 52-28 Example of temporary vascular shunt in the superficial femoral artery.

Modern Combat Casualty Care

DAMAGE CONTROL PACKING In austere settings, the casualty will be most appropriately managed by an operative strategy of damage control surgery, packing, and rapid evacuation to a higher echelon of care. The primary operative goal is to detect and control sources of exsanguinating hemorrhage. Identification of vascular injuries and/or significant organ hemorrhage is the first priority. Definitive vascular injury control or shunting is achieved along with control of contamination. Rapid control of intestinal injuries is achieved by stapling, with proximal NG drainage. Definitive restoration of intestinal continuity is deferred to a later procedure. Solid organ hemorrhage is managed by resection (if possible) or by packing as appropriate with use of topical hemostatic agents. Damage control operative techniques are employed in close concert with DCR principles including aggressive resuscitation of the coagulation cascade. Rapid temporary abdominal closure may be achieved in any of a number of ways (Fig. 52-29) in anticipation of evacuation and reexploration at a higher level of care. During the evacuation and transport process, judicious monitoring of resuscitation parameters includes full restoration of the clotting cascade while maintaining a degree of permissive hypotension. Resuscitation end points include serum lactate and central venous oxygen saturation. Significant attention is directed to restoration and/or maintenance of core body temperature to avoid hypothermic coagulopathy.

MILITARY TRAUMA SYSTEMS The development of trauma care has always been a synergistic relationship between the military and the civilian sector. Dr Michael Debakey famously noted that wars have always promoted advances in trauma care because of the concentrated (and focused) exposure of military providers to large numbers of injured people over a relatively short span of time.

CHAPTER 52

plete four-compartment lower extremity fasciotomy is strongly encouraged for all casualties who have had any period of distal ischemia. The necessity of complete (full skin incisions) fasciotomy is another primary lesson learned during this conflict. Most deployed military surgeons predicate the need for fasciotomy on prior experience from the civilian experience with older patients with preexisting vasculopathies. The resultant reperfusion edema that may occur in the civilian setting (older patient, long-standing ischemia with atrophic distal musculature) is vastly different than that encountered in the combat zone. In the military setting the management of young, muscular soldiers who have experienced vascular ischemia requires recognition of the significant swelling and edema that occurs as a result of the primary injury (blast effect, cavitation injury, etc.) or the massive reperfusion edema that follows in these young patients with (previously) healthy muscle. Military experience with this strategy of vascular shunting has demonstrated that definitive repair may be deferred to a later time. The distal extremity remains perfused with a greater than 85% patency rate if a shunt is used in a proximal position of the arm or leg.55

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FIGURE 52-29 Damage control temporary closure.

Furthermore, wartime medical experience fosters an intense and fundamental desire to improve outcomes and standards of care on behalf of the soldier on the front lines. In Vietnam, lessons learned regarding aeromedical evacuation, field medical care, and resuscitation were rapidly incorporated into civilian paradigms and practice. At this same time (1966), the National Academy of Sciences published Accidental Death and Disability: The Neglected Disease of Modern Society. This publication cited civilian trauma in the United States as one of the most significant public health problems faced by the nation. The combination of battlefield medicine and the call to action by the National Academy prompted a concerted evaluation of trauma care. In 1976, the American College of Surgeons produced the first iteration of injury care guidelines entitled Optimal Resources for Care of the Injured Patient.56 This concept rapidly evolved into the development of formal, integrated networks of care known as trauma systems. Trauma centers and trauma systems in the United States have had a remarkable impact on improving outcomes of injured patients and reduction of mortality. As the military medical corps prepared itself for the first Gulf War and subsequently the Global War on Terror, it was able to look to the American College of Surgeons and its Committee on Trauma for a template of trauma systems. The evolution of trauma systems would be a transformational step for military medicine as it faced the enormous challenge of coordinating care of the injured soldier across a diverse and asymmetrical landscape that featured combatants capable of moving in advance with lightning speed. These recent conflicts would also be the first where the majority of military medical providers had been afforded the opportunity to train in or work at US trauma systems participating in an organized system of care. The lessons and examples provided by civilian trauma systems in the United States from 1970 to 2000 served as an initial blueprint template on which the current generation of military medical providers could build.

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Operation Desert Shield and Desert Storm (1991–1992) highlighted a number of issues in which the US military had fallen behind the successful construct fostered by civilian systems of injury care. Inadequacies were formally noted in both preparation and delivery of trauma care in the combat environment. In 1996, the Government Accountability Office (GAO) issued a report addressing shortfalls from Operation Desert Storm including shortcoming in the Department of Defense’s ability to provide adequate, timely medical support during contingencies and problems with the planning and execution of these efforts. The Joint Staff also identified problems with the design of the wartime medical system. As a result, the Department of Defense and the military medical corps (Army, Navy, and Air Force) embarked on a series of initiatives intended to correct shortfalls in wartime medical capabilities and to improve medical readiness. This initiative was rapidly accelerated by the events and circumstances following the terrorist attacks of 9/11 and the subsequent Global War on Terror. The goal was to develop and implement a true trauma system, modeled after the successes of civilian systems, but modified to account for the realities of combat. The result was the development of the Joint Theater Trauma System (JTTS). The stated vision of the JTTS is to ensure that every soldier, marine, sailor, or airman injured on the battlefield has the optimal chance for survival and maximal potential for functional recovery. The purview of the JTTS includes injury prevention, prehospital care, acute hospital care, education, leadership and communication, quality improvement/performance improvement, research, and associated information systems. Some of the preeminent functions of the JTTS are discussed below.57

Data gathered regarding wartime injury patterns have driven force protection changes in combatant training and equipment. The impact of personal protective equipment (body armor) fielded during this conflict has been substantial. As the conflict transitioned from a maneuver war to an insurgency characterized by ambushes and IEDs, wounding patterns changed from small arms injuries to multiple fragment injuries. Rapid fielding initiatives led to changes in vehicular armoring as well as vehicle interior design. The MRAP evolution is an example of a data-driven (injury pattern/severity/ number) analysis combined with a prevention initiative forwarded by the JTTS and executed through the line of the military.

■ Prevention

■ Coordination of Care/Leadership

The implementation of the military trauma system (JTTS) has been accompanied by a marked reduction in the number of soldiers killed from combat wounds. The current care fatality rate from Operation Iraqi Freedom and Operation Enduring Freedom of 8.8% compares with the rate of 16.5% during Vietnam. The two primary modes of prevention influenced by the JTTS include realistic/relevant predeployment training and personnel protective equipment. As a result of the GAO report(s) of the mid-1990s, the Department of Defense partnered with a number of premier Level I civilian trauma centers throughout the United States. This initiative was undertaken to ensure that the military medic would be able to train in a consistent trauma system setting with access to high-volume, high-intensity trauma care. There are currently five major military/civilian collaborative training centers that have evolved to train providers to treat combat injuries and prepare them for the realities of care on the battlefield. These centers include the Navy Trauma Training Center (NTTC) at the University of Southern California (LAC-USC), the Army Trauma Training Center at Ryder Trauma Center (Jackson Memorial Hospital in Miami), and the three Air Force Centers for Sustainment of Trauma and Readiness Skills (C-STARS) located at Baltimore’s Shock Trauma Institute, the University Hospital in Cincinnati, and St. Louis University Hospital.

The necessity of establishing a position of trauma system director for the theater of operation (Area of Responsibility [AOR]) was identified early during this conflict. With the support of the Central Command (CENTCOM) Surgeon and the three Surgeons General, the position of trauma system director (JTTS Forward) was rapidly incorporated as a general staff position within the theater medical command. This leadership position (JTTS-F) is responsible for oversight and coordination of the military trauma system within the theater. Responsibilities of the JTTS-F include coordination of patient care/flow across all echelons of care, the implementation of CPGs, capture and analysis of trauma registry data, performance improvement initiatives, and liaison with the medical services of coalition partners. The intrinsic leadership qualities incorporated into the JTTS-F are intended to drive advances within the theater by the process of assured oversight of medical processes combined with advocacy and education. At the individual combat hospital facility, the development of the JTTS has led to a parallel maturation of trauma leadership positions at a local level. The current theater policy advocates the appointment of a senior trauma clinician at all Level III facilities within the theater. In addition, one trauma coordinator is required for oversight at each CSH to help ensure compliance with guidelines, improve information management, and enable trauma registry data collection.

■ Battlefield Care— Clinical Practice Guidelines The JTTS is responsible for providing clinical oversight of the standard of care across all levels and all services of care both within the theater of care and worldwide. The intent of the JTTS CPG process is to provide continually updated, evidence-based, best practice guidelines for a wide variety of medical circumstances encountered in the battlefield setting. The CPGs are the backbone of the JTTS performance improvement systemwide program. These guidelines are developed and implemented by clinical subject matter experts in response to needs identified in the theater. Currently there are over 30 published CPGs ranging from the management of amputation to vascular injuries. The CPGs are subjected to regular review and are (as possible) based on current evidencebased literature.

Modern Combat Casualty Care

■ Research Before the current conflict, much of the data on combat injury were derived from the Vietnam conflict and the Wound Data and Munitions Effectiveness Trauma database. The data obtained were often fragmentary, always retrospective, and consisted primarily of small series or case reports. Prior to this conflict, there was recognition (from the US civilian trauma system example) that outcome analysis must be data driven and based on an accurately robust and prospectively collected data registry. The development of the JTTR was proposed as a solution to this need. The JTTR was originally fielded prior to this conflict and is in a process of continued maturation and evaluation. It is a registry tool collected on every injured combatant to capture demographics, mechanistic, physiologic, diagnostic, therapeutic, and outcome data. As of January 2010, the JTTR has collected data on over 14,000 casualties. The JTTR is administered by the JTTS. Currently there are over 75 personnel stationed within the CONUS and 10 deployed personnel responsible for the collection, collation, and reporting of the JTTR data. A typical summary of the JTTS-reported data from the conflict is depicted in Fig. 52-30. The commitment of the Department of Defense, the military medical services, and the JTTS to the continued

OIF cumulative monthly avg CFR%, DOW%, KIA% and ISS Jan 2004 – Feb 2008 12

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Month and Year FIGURE 52-30 Representative cumulative data from the Joint Theater Trauma Registry.

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development of the JTTR has resulted in a powerful analysis tool of the current state of military combat medical care. In a yet to be published report, Jenkins and colleagues collected data from combat casualties arriving to LRMC and compared them with the NTDB from the same time frame. This study resulted in the analysis of 1,600 military casualties from this time period. The data demonstrated that the military population was on average younger, more severely injured (ISS score), and more likely to be injured by a penetrating injury or explosive device. The observed care fatality rate for severely injured patients (ISS  24) was 29/100 in the NTDB and 8.6/100 for the JTTR. Analysis of the Z score revealed a statistically significant number of unexpected survivors in the military population compared with the NTDB. The calculated Z score (actual vs. predicted survivor) was 5.07 with a resultant W score (unexpected additional survivors/100 casualties) of 2.75. This paper and its data serve as a telling and important tribute not only to the JTTR and JTTS but also to the selfless dedication of those deployed in support of the military medical system. The privilege of serving those who serve our nation is indeed very special. The authors of this chapter wish to acknowledge the men and women of the US military and the dedicated corps of medics deployed throughout the world.

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REFERENCES SECTION 4

1. DeBakey ME. History, the torch that illuminates: lessons from military medicine. Mil Med. 1996;161:711. 2. Holcomb JB, Stansbury LG, Champion HR, et al. Understanding combat casualty care statistics. J Trauma. 2006;60(2):397. 3. Winkenwerder WJ. Coordination of Policy to Establish a Joint Theater Trauma Registry. Memorandum, Department of Defense Health Affairs; December 22, 2004. 4. Butler F. Tactical combat casualty care: combining good medicine with good tactics. J Trauma. 2003;54(5):S2. 5. Knudson MM, Mitchell FL, Johannigman JA. First trauma verification review committee site visit outside the U.S.: Landstuhl Regional Medical Center, Germany. Bull Am Coll Surg. 2007;92:16. 6. Kowalenko T, Stern S, Dronen S, et al. Improved outcome with hypotensive resuscitation of uncontrolled hemorrhagic shock in a swine model. J Trauma. 1992;33:349. 7. Stern SA, Dronen SC, Birrer P, et al. The effect of blood pressure on hemorrhage volume and survival in near-fatal hemorrhage model incorporating a vascular injury. Ann Emerg Med. 1993;22:155. 8. Burris D, Rhee P, Kaufmann C, et al. Controlled resuscitation for uncontrolled hemorrhagic shock. J Trauma. 1998;46:216. 9. Kaweski SM, Sise MJ, Virgilio RW. The effect of prehospital fluids on survival in trauma patients. J Trauma. 1990;30:1215. 10. Carrico CJ, Canizaro PC, Shires GT. Fluid resuscitation following injury: rationale for the use of balanced salt solutions. Crit Care Med. 1976; 4(2):46. 11. American College of Surgeons Committee on Trauma. Advanced Trauma Life Support. 7th ed. Chicago: American College of Surgeons; 2006. 12. Rhee P, Wang D, Ruff P, et al. Human neutrophil activation and increased adhesion by various resuscitation fluids. Crit Care Med. 2000;28:74. 13. Jaskille A, Alam HB, Rhee P, et al. D-Lactate increases pulmonary apoptosis by restricting phosphorylation of Bad and eNOS in a rat model of hemorrhagic shock. J Trauma. 2004;57:262. 14. Wade CE, Grady JJ, Kramer GC, et al. Individual patient cohort analysis of the efficacy of hypertonic saline/dextran in patients with traumatic brain injury and hypotension. J Trauma. 1997;42:61S. 15. Holcomb JB, McMullen NR, Pierce L, et al. Causes of death in US Special Operation Forces in the global war on terrorism: 2001–2004. Ann Surg. 2007;245:986. 16. Kragh JF, Walters TJ, Baer GC, et al. Practical use of emergency tourniquets to stop bleeding in major limb trauma. J Trauma. 2008; 64:S38. 17. Kragh JF Jr, Littrel ML, Jones JA, et al. Battle casualty survival with emergency tourniquet use to stop limb bleeding. J Emerg Med. 2011;41(6): 590–597. 18. Committee on Tactical Combat Casualty Care. Pre-Hospital Trauma Life Support—Military Edition. St. Louis: Mosby-Elsevier; 2007. 19. Brohi K, Singh J, Heron M, et al. Acute traumatic coagulopathy. J Trauma. 2003;54:1127. 20. Hess JR, Lawson JH. The coagulopathy of trauma versus disseminated intravascular coagulation. J Trauma. 2006;60(6):S12. 21. Martin M, Murray J, Berne T, et al. Diagnosis of acid–base derangements and mortality prediction in the trauma intensive care unit: the physiochemical approach. J Trauma. 2005;58(2):238. 22. Holcomb JB, Jenkins D, Rhee P, et al. Damage control resuscitation: directly addressing the early coagulopathy of trauma. J Trauma. 2007;62:307. 23. Martini WZ, Pusateri AE, Uscilowicz JM, et al. Independent contributions of hypothermia and acidosis to coagulopathy in swine. J Trauma. 2005; 58(5):1002. 24. Niles SE, McLaughlin DF, Perkins JG, et al. Increased mortality associated with the early coagulopathy of trauma in combat casualties. J Trauma. 2008;64(6):1459. 25. Greiser B, Jurkovich G, Luterman A. Severe hypothermia: an ominous predictor of mortality in trauma victims. J Trauma. 1986;26(7):675. 26. Hess JR, Brohi K, Dutton RP, et al. The coagulopathy of trauma: a review of mechanisms. J Trauma. 2008;65:748. 27. Eastridge BJ, Salinas J, McManus JG, et al. Hypotension begins at 110 mm Hg: redefining ‘hypotension’ with data. J Trauma. 2007;63:291. 28. Bruns B, Lindsey M, Rowe K, et al. Hemoglobin drops within minutes of injuries and predicts need for an intervention to stop hemorrhage. J Trauma. 2007;63:312. 29. McLaughlin DF, Niles SE, Salinas J, et al. A predictive model for massive transfusion in combat casualty patients. J Trauma. 2008;64:S57.

30. Bickell WH, Wall MJ Jr, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994;33:1105. 31. Roberts K, Revell M, Youssef H, et al. Hypotensive resuscitation in patients with ruptured abdominal aortic aneurysm. Eur J Vasc Endovasc Surg. 2006;31:339. 32. Lu YQ, Cai XJ, Gu LH, et al. Experimental study of controlled fluid resuscitation in the treatment of severe and uncontrolled hemorrhagic shock. J Trauma. 2007;63:798. 33. Borgman MA, Spinella PC, Perkins JG, et al. The ratio of blood products transfused affects mortality in patients receiving massive transfusions at a combat support hospital. J Trauma. 2007;63:805. 34. Spinella PC, Holcomb JB. Resuscitation and transfusion principles for traumatic hemorrhagic shock. Blood Rev. 2009;23:231. 35. Beekley AC. Damage control resuscitation: a sensible approach to the exsanguinating surgical patient. Crit Care Med. 2008;36:S267. 36. Blackbourne LH. Combat damage control surgery. Crit Care Med. 2008; 36:S304. 37. Gunter OL Jr, Au BK, Isbell JM, et al. Optimizing outcomes in damage control resuscitation: identifying blood product ratios associated with improved survival. J Trauma. 2008;65:527. 38. Holcomb JB, Wade CE, Michalek JE, et al. Increased plasma and platelet to red blood cell ratios improves outcome in 466 massively transfused civilian trauma patients. Ann Surg. 2008;248(3):447. 39. Perkins JG, Cap AP, Spinella PC, et al. An evaluation of the impact of apheresis platelets used in the setting of massively transfused trauma patient. J Trauma. 2009;66:S77. 40. Cotton BA, Au BK, Nunez TC, et al. Predefined massive transfusion protocols are associated with a reduction in organ failure and postinjury complications. J Trauma. 2009;66:41. 41. Hess JR, Thomas MJ. Blood use in war and disaster: lessons from the past century. Transfusion. 2003;43:1622. 42. Starr D. Blood: An Epic History of Medicine and Commerce. New York: Harper-Collins; 1998. 43. Ho AM, Karmakar MK, Dion PW. Are we giving enough coagulation factors during major trauma resuscitation? Am J Surg. 2005;190:479. 44. McMullin NR, Holcomb JB, Sondeen J. Hemostatic resuscitation. In: Vincent JL, ed. Yearbook of Intensive Care and Emergency Medicine. New York: Springer; 2006:265. 45. Spinella PC, Moore FA, Holcomb JB, et al. Fresh whole blood transfusions in coalition military, foreign national, and enemy combatants during Operation Iraqi Freedom at a US combat support hospital. World J Surg. 2008;32:255. 46. Spinella PC. Warm fresh whole blood transfusion for severe hemorrhage: U.S. military and potential civilian applications. Crit Care Med. 2008; 36:S340. 47. Spinella PC, Perkins JG, Gratwohl KW, et al. Fresh whole blood is independently associated with improved survival for patients with combat-related traumatic injuries. J Trauma. 2009;66:S69. 48. Makley AT, Goodman MD, Friend L, et al. Resuscitation with fresh whole blood ameliorates the inflammatory response after hemorrhagic shock. J Trauma. 2010;68:305. 49. Spoerke N, Zink K, Cho SD, et al. Lyophilized plasma for resuscitation in a swine model of severe injury. Arch Surg. 2009;144:829. 50. Alam HB, Bice LM, Butt MU, et al. Testing of blood products in a polytrauma model: results of a multi-institutional randomized preclinical trial. J Trauma. 2009;67:856. 51. Koch CG, Li L, Sessler DI, et al. Duration of red-cell storage and complications after cardiac surgery. N Engl J Med. 2008;358(12):1229. 52. Johannigman JA. Maintaining the continuum of en route care. Crit Care Med. 2008;36:377. 53. Rotondo MF, Schwab CW, McGonigal MD, et al. Damage control: an approach for improved survival in exsanguinating penetrating abdominal injury. J Trauma. 1993;35:375. 54. Rasmussen TE, Clouse WD, Jenkins DH, et al. The use of temporary vascular shunts as a damage control adjunct in the management of wartime vascular injury. J Trauma. 2006;61:8. 55. Clouse WD, Rasmussen TE, Peck MA, et al. In-theater management of vascular injury: 2 years of the Balad Vascular Registry. J Am Coll Surg. 2007;204:625. 56. American College of Surgeons Committee on Trauma. Resources for Optimal Care of the Injured Patient: 2006. Chicago: American College of Surgeons; 2007. 57. Eastrdige BJ, Jenkins D, Flaherty S, et al. Trauma system development in a theater of war: experiences from Operation Iraqi Freedom and Operation Enduring Freedom. J Trauma. 2006;61:1366.

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CHAPTER 53

Genomics and Acute Care Surgery Grant E. O’Keefe and J. Perren Cobb

INTRODUCTION Variability is a hallmark of clinical medicine. Why do patients with seemingly similar injuries or severity of acute illness, receiving comparable and appropriate treatment, often follow different trajectories? For example, one patient recovers uneventfully from massive transfusion for hemorrhagic shock while another follows a prolonged course complicated by nosocomial pneumonia and organ failure. Consider also, the seemingly more straightforward task of preventing or treating deep venous thromboembolic disease. Despite our understanding of the biology of coagulation and pharmacotherapeutic strategies, therapy sometimes fails with fatal consequences. Numerous clinical (environmental) and genetic factors contribute to this variability. The completion of the Human Genome Project provided the foundation on which to build knowledge of genetic variation in both humans and animal models.1 This in turn has been used to establish genotype–phenotype associations for common polygenic diseases, such as diabetes mellitus (metabolic syndrome), cancer, and hypertension. Using this genetic variability to understand disease biology and to better direct therapy (such as drug selection and dosing) are the goals of the field of “Genomic Medicine.”2 At the cellular level, differences in DNA sequence can alter RNA transcription and protein translation, which alters clinical phenotypes. For instance, drug absorption, metabolism, and excretion are all affected by genetic variation (pharmacogenomics). Recent progress in these fields and the application of this knowledge to critically injured patients is the focus of this chapter.

STRUCTURE OF THE GENOME Since the discovery and publication of the molecular structure of nucleic acids by Watson and Crick in 1954, the genetic basis for many conditions has been determined.3,4 Misconceptions remain,

however, regarding the role of genetics and genomics in clinical medicine. Despite the commonly held notion that genetics had little influence on clinical medicine in the past, genetics has, in fact, played an important role in understanding disease for a minority of conditions and patients. As a result of the advances described above, we have entered a period of tremendous growth in our knowledge of genomics that will influence care for all patients.5 In order for clinicians to understand and participate in these advances, we must become “literate” in the language of genetics and genomic medicine. Box 53-1 includes some important definitions of genetic concepts for clinicians, some of which will be more completely developed below. Much is known about the human genome. We know that the minority of the 3 gigabases of DNA sequence codes for proteins. It is estimated that only 2% of our DNA sequences code for approximately 20,000 protein coding genes. The function of the remaining 98% of DNA is perhaps the most fascinating aspect of genomics. Figure 53-1 illustrates the general structure of a typical gene. The 5′ control region, often termed the “promoter,” includes DNA sequences that recognize and bind to proteins called transcription factors, whose function is to modify gene expression by controlling transcription. The “start codon” is a series of nucleotides that are recognized by this transcriptional machinery, which initiates generation of messenger RNA (mRNA) from DNA. Not all of this mRNA sequence encodes for protein. Exons are the regions of DNA that are transcribed into RNA to make amino acids. In most genes, multiple exons are separated by introns, which are removed from mRNA prior to translation into protein. The end of transcription is signaled by a series of nucleotides at the end of the coding sequence, referred to as a “stop codon.” The DNA sequence after this end codon, termed the 3′ control region, can also influence the rate of gene transcription and may affect the stability of the mRNA sequence and its translation into protein.

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Box 53-1: Definitions

SECTION 4

Allele: One of two or more versions of a genetic sequence at a particular location in the genome. Base pair (bp): Two nitrogenous bases paired together in double-stranded DNA by weak bonds; specific pairing of these bases (adenine with thymine and guanine with cytosine) facilitates accurate DNA replication; when quantified (e.g., 8 bp), bp refers to the physical length of a sequence of nucleotides. Complex condition: A condition caused by the interaction of multiple genes and environmental factors. Examples of complex conditions, which are also called multifactorial diseases, are sepsis, cancer, and heart disease. DNA: Deoxyribonucleic acid, the molecules inside cells that carry genetic information and pass it from one generation to the next. Exon: The portion of a gene that encodes amino acids. Gene: The fundamental physical and functional unit of heredity. A gene is an ordered sequence of nucleotides located in a particular position on a particular chromosome that encodes a specific functional product (i.e., a protein or an RNA molecule). Gene chip: A solid substrate, usually silicon, onto which a microscopic matrix of nucleotides is attached. Gene chips, which can take a wide variety of forms, are frequently used to measure variations in the amount or sequence of nucleic acids in a sample. Genome: The entire set of genetic instructions found in a cell. In humans, the genome consists of 23 pairs of chromosomes, found in the nucleus, as well as a small chromosome found in the cells’ mitochondria. Genome-wide association study (GWAS): An approach used in genetics research to look for associations between many (typically hundreds of thousands) specific genetic variations (most commonly SNPs) and particular diseases. Genotype: A person’s complete collection of genes. The term can also refer to the two alleles inherited for a particular gene. Haplotype: A set of DNA variations, or polymorphisms, that tend to be inherited together. A haplotype can refer to a combination of alleles or to a set of SNP found on the same chromosome. HapMap: The nickname of the International HapMap (short for “haplotype map”) Project, an international venture that seeks to map variations in human DNA sequences to facilitate the discovery of genetic variants associated with health. The HapMap describes common patterns of genetic variation among people. Human Genome Project: An international project completed in 2003 that mapped and sequenced the entire human genome. Microarray: A technology used to study many genes at once. Thousands of gene sequences are placed in known locations on a glass slide. A sample containing DNA or RNA is deposited on the slide, now referred to as a gene chip. The binding of complementary base pairs from the sample and the gene sequences on the chip can be measured with the use of fluorescence to detect the presence and determine the amount of specific sequences in the sample. Mutation: A change in a DNA sequence. Germ-line mutations occur in the eggs and sperm and can be passed on to offspring, whereas somatic mutations occur in body cells and are not passed on. Pharmacogenomics: The branch of pharmacology that deals with the influence of genetic variation on drug response in patients by correlating gene expression or SNPs with a drug’s efficacy or toxicity. By doing so, pharmacogenomics aims to develop rational means to optimize drug therapy, with respect to the patients’ genotype, to ensure maximum efficacy with minimal adverse effects. Phenotype: The observable traits of an individual person, such as height, eye color, and blood type. Some traits are largely determined by genotype, whereas others are largely determined by environmental factors. Point mutation: An alteration in DNA sequence caused by a single-nucleotide base change, insertion, or deletion. Ribonucleic acid (RNA): The molecule synthesized from the DNA template; contains the sugar ribose instead of deoxyribose, which is present in DNA; three types of RNA exist including messenger RNA (mRNA), transfer RNA (tRNA), and ribosomal RNA (rRNA). Single-nucleotide polymorphism (SNP): A single-nucleotide variation in a genetic sequence; a common form of variation in the human genome. Systems biology: Research that takes a holistic rather than reductionist approach to understanding organism functions. Transcription: The synthesis of an RNA copy from a sequence of DNA (a gene); a first step in gene expression. Translation: During protein synthesis, the process through which the sequence of bases in a molecule of messenger RNA is read in order to create a sequence of amino acids.

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Sections within a typical gene

Start code

End code

3′ Control region

Coding region: Codes for mRNA and ultimately for protein. This region includes exons and introns..

FIGURE 53-1 The general structure of a typical gene.

THE GENETIC BASIS FOR DISEASE Despite our limited knowledge of the function of much of the genome, our knowledge of the genetic basis for disease is, in fact, extensive. Basic research and clinical observation have elucidated the inheritance of single-gene, Mendelian disorders (transmitted according to Mendel’s laws of inheritance). Most of these are uncommon, and taken together, the most prevalent such as cystic fibrosis or hemochromatosis affect no more than one in several hundred people; however, when the genetic variant is present, its effect on individual patients is substantial. Furthermore, understanding the mechanisms underlying many monogenic disorders has provided pathophysiological information about related and more common disorders. For instance, we have learned a great deal about the pathophysiology of cardiovascular disease from discoveries related to familial hypercholesterolemia, a rare genetic disorder leading to premature atherosclerosis. The most common type of DNA sequence variation is single base substitutions termed single nucleotide polymorphisms or single-nucleotide polymorphisms (SNPs). SNPs have emerged as powerful genetic markers for studying multifactorial diseases.6 Polymorphisms occur in all individuals and, by strict definition, SNPs exist with a frequency of ⬎1%.7 Therefore, the term SNP does not include numerous other single base substitutions in which the least common allele is present at a frequency of ⱕ1% (such as “personal mutations” that may be limited to one family), nor does the term encompass other variations such as insertion/deletion polymorphisms. Importantly, SNPs should be distinguished from disease “causing” mutations, which are generally much less common, but have higher penetrance (e.g., sickle cell anemia). Therefore, SNPs typically do not cause disease but in aggregate may influence the risk for developing a disease (e.g., diabetes mellitus, asthma) or the outcome from a disease or condition (e.g., death from sepsis, rate of atherosclerosis in recipients of cardiac transplants).8,9 SNPs that exist in mRNA-coding regions (exons) of DNA can lead to amino acid substitutions, and therefore, may change the structure of the resultant protein. This type of variant potentially has the most profound impact on protein function; however, this type of SNP is the least common.5 SNPs in the regulatory (promoter) region of a gene may influence (increase or, more often,

decrease) transcription of that gene, and therefore, may influence the amount of protein available.10 Yet, other SNPs may not directly alter protein abundance or function, but may be important markers for other (unidentified) functional variants— a concept known as linkage.11 The analysis of SNPs has been facilitated by two recent and related developments as follows: (1) the establishment of large data repositories of SNPs; and (2) the availability of relatively affordable “high-throughput” methods for genotyping. Recent techniques have identified at least 10 million SNPs interspersed throughout the human genome, at a frequency of one SNP per ∼300 base-pairs.12 Their role in critical illness, both as risk factors and in determining treatment response, has been investigated for several candidate genes.13 It is hoped that these studies will contribute to the understanding of the biology of critical illness and toward characterizing patient risk, treatment response, and outcome.14 Microsatellite and insertion/deletion polymorphisms represent other genetic variation that may be used to characterize an individual’s risk for disease and response to therapy. Microsatellite or simple sequence repeat (SSR) polymorphisms are created by the presence of short sequences (generally 2–4 base pairs) repeated multiple times in tandem. Insertion/deletion polymorphisms are characterized by the presence or absence of a single base in some cases or a longer fragment in others. Microsatellite and insertion/deletion polymorphisms are generally considered to be markers for other functional variants and are not themselves functional, but in some cases may directly alter gene activity.15,16 Typically, they occur in nonfunctional regions or in gene regulatory regions and not in coding regions as they would likely lead to a truncated, completely nonfunctional protein.

GENE EXPRESSION PROFILING AFTER TRAUMA AND BURNS As described above, transcription of DNA into mRNA, commonly called “gene expression,” is the first step in the path to new protein production. The specificity of Watson–Crick base pairing allows for the measurement of mRNA abundance using technology similar to that enabling DNA sequencing. Only a short sequence (⬍100 nucleotides) is required to uniquely identify each gene and its associated mRNA. Small wafers arrayed with minute

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5′ Control region – “promoter”

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quantities of short, gene-specific nucleotides (called “microarrays”) are now used routinely to monitor gene expression for all human genes in any tissue of interest. The field of measuring the dynamics of mRNA abundance across the genome is called “gene expression profiling,” an approach used to estimate changes in global gene transcription based upon the good correlation between alterations in relative RNA abundance as measured by microarrays and changes in gene transcription. Of note, the correlation between changes in gene expression (mRNA production) and gene translation (protein production) is not as strong.17 Over the last decade, a team of investigators have been supported by the NIH to study the systemic response to blunt trauma and burn injury—the Inflammation and Host Response to Injury Program (also referred to as the “Glue Grant”). This team has applied these techniques of gene expression profiling to blood and tissue samples from subjects enrolled across the United States.18,19 The application of new computational approaches to gene expression data revealed novel insight into the biology of the response to injury. For example, network-based analysis of circulating white blood cells revealed that acute systemic inflammation induces transient dysregulation of bioenergetic pathways and modulation of leukocyte translational machinery.20 In addition to improving our understanding of pathophysiology, gene expression profiling also holds promise as a novel tool to improve the classification of disease and clinical phenotyping.21 The potential application to diagnostics and therapeutics in critically ill and injured patients is significant.22 If one assigns baseline or “reference” status to the averaged leukocyte gene expression profiles of healthy human volunteers, gene expression profiles from patients 12 hours after injury can be used to compute a difference-from-reference (DFR) score for each patient. In effect, these scores describe an overall response at the mRNA level, which can be compared with standard clinical scores based upon acute physiology, chronic health, and metrics of injury severity.23 These DFR scores early after injury have been associated significantly with adverse outcomes that developed later in the patient’s hospital course, including multiple organ dysfunction, length of mechanical ventilation and hospital stay, and infection rates. These associations remained statistically significant after adjustment for injury severity, indicating that the DFR score provides novel, important clinical information. Similarly, profiling of circulating leukocyte gene expression show promise as a novel tool to measure immune health and to diagnose infection.24 For instance, riboleukograms or graphs of circulating leukocyte changes in relative RNA abundance (gene expression) can be used to track the dynamics of the host response to systemic inflammation and the DFR.25 The diagnostic potential of riboleukograms was reported recently for adult trauma patients who developed ventilator-associated pneumonia and for pediatric patients with acute appendicitis.24,26

GENETIC RISK FACTORS AND PHARMACOGENOMICS Genomic medicine holds the promise of personalized medicine or individualized treatment based upon a patient’s gene-associated disease risks. Venous thromboembolic disease is one example where understanding genetic risk factors may be important for optimizing care for critically ill patients. Clot formation is deter-

TABLE 53-1 Genetic “Causes” of Venous Thrombosis Antithrombin deficiency Protein C deficiency Protein S deficiency Activated Protein C resistance Increased prothrombin

Prevalence, % 4.3 5.7 5.7 45

Mutations ⬎79 ⬎160 ⬎69 1

18

1

Adapted with permission of American Association of Clinical Chemistry, from Bertina RM. Factor V Leiden and other coagulation factor mutations affecting thrombotic risk. Clin Chem. 1997;43(9):1678; permission conveyed through Copyright Clearance Center, Inc.

mined by a delicate balance of procoagulant and anticoagulant processes interacting via a complex system of cofactors and inhibitor regulated by an elaborate feedback mechanism.27 When this balance is disrupted, abnormal bleeding or clotting may ensue, a common occurrence in the intensive care unit. There are five established genetic defects considered as risk factors for venous thrombosis (Table 53-1).6 Deficiencies in protein C, protein S, and antithrombin III lead to defects in the anticoagulant pathways of blood coagulation and together are found in ∼15% of people with familial thrombophilia.28 The factor V Leiden mutation and increased prothrombin associated with the prothrombin 20210 A allele are much more prevalent and together may account for ⬎60% of familial thrombophilia. Protein C, protein S, and antithrombin deficiencies all involve defects in anticoagulant pathways, whereas the factor V Leiden mutation and the prothrombin gene mutation involve procoagulant factors. Multiple genetic defects are responsible for protein C, protein S, and antithrombin deficiencies whereas both the factor V Leiden and prothrombin defects are caused by single mutations. These mutations are particularly relevant in patients with deep venous thrombosis occurring in the absence of a clear risk factor such as traumatic injury. Up to 50% of such individuals have an underlying defect including these genetic causes, which may contribute to the development of venous thromboembolism even when patients receive appropriate pharmacologic prophylaxis.28 Although it is likely that trauma such as fractures in an extremity or injury to the spinal cord is sufficient to lead to deep venous thrombosis in the absence of prophylaxis, it is possible that failure of prophylaxis may be, in part, due to the aforementioned genetic variants. Nevertheless, it is presently not recommended that patients with so-called provoked deep venous thrombosis undergo screening for these genetic variants. In part, the rationale is due to the notion that treatment will not be affected by the presence of these mutations.29 If the risk of failure of conventional prevention strategies is related to mutations causing thrombophilia, however, it may be possible to provide more aggressive prophylaxis to those at greatest risk for failure. For most patients, treatment for established deep venous thrombosis transitions from heparin-based therapy to warfarinbased therapy. The marked interindividual variability in response and a narrow therapeutic window make safe and

Genomics and Acute Care Surgery

GENETIC RISK FACTORS FOR SEPSIS AND ORGAN DYSFUNCTION Genetic variation influences the risk for and outcome from acute surgical illness and its complications, such as infection and acute lung injury.13,35 The earliest evidence favoring a role for genetic differences in risk of infection and outcome came from an epidemiological study of adoptees and their biologic and adoptive parents. A strong association between early death from infection in adoptees and their biologic, but not adoptive, parents suggested a genetic influence on the risk for and outcome from infection.36 Subsequent studies determined that inflammatory responses in blood were heritable and were associated with outcomes from meningococcal sepsis.37 Following these initial observations, reports have identified associations between specific SNPs and sepsis (reviewed in reference38). Unfortunately, many of the initially striking associations between SNPs and sepsis risk and outcome have not been independently replicated.39,40

Despite the challenges discussed above, genomic variation likely will help us gain a better understanding of the biology of infection and organ failure, help us refine and target our therapies in critically ill patients and help us more accurately estimate prognosis. Along these lines, genetic differences may help explain why “anti-mediator” therapies, often observed to be beneficial in preclinical models and small clinical trials, have not improved outcomes in Phase III clinical trials.41–43 Much of our understanding of the biology of inflammation comes from highly controlled models systems. Examples include the discovery of the roles of tumor necrosis factor-α and toll-like receptor-4 in the inflammatory response.44,45 In genetically diverse populations (like humans), however, genetic variability creates sufficient background “noise” above which it may be difficult to discern true treatment effects (in other words, a low signal to noise ratio). In addition, new discoveries continue to refine our understanding of the pathways involved in the response to infection and inflammation and this improves our understanding of human inflammation and sepsis.46 Also, these pathways are likely influenced by genetic variation that, in turn, will influence clinical outcomes. Coupled with better biomarker-directed classification as described above, identifying important genetic risk factors will likely add to predictive accuracy. Finally, better risk stratification (by clinical and genetic factors) will better inform therapeutic decisions, directing therapy to patients most likely to benefit.18,20,47 Many challenges remain to be addressed before SNPs can be used in the clinical setting. Most importantly, the usefulness of individual SNPs to predict predisposition and response has met with little success, as most SNP–disease associations are not reproduced in subsequent studies.43 Moreover, the largest, most robust genome-wide association study studies published to date on polygenic diseases such as diabetes mellitus, inflammatory bowel disease, heart disease, and cancer indicate that the additional informational value for predicting a given phenotype is small.5 Once the predictive SNPs have been identified, it will be necessary to determine whether directing interventions to particular (“high-risk”) patients improves outcomes. In sepsis and shock, multiple genetic and environmental factors influence an individual’s risk and clinical course as in more common heart disease, diabetes mellitus, hypertension, and cancer. Within infectious and inflammatory disorders, patient factors, such as age and comorbidity, and disease factors, such as infectious strain, exposure, and concomitant injury, contribute to disease risk and severity making the study of genetic risk factors particularly challenging.

SUMMARY AND IMPLICATIONS FOR CLINICAL PRACTICE A growing body of information indicates that genomic data will enhance our understanding of common diseases including sepsis and organ failure.18,20 Similarly, genetic influences on many biological responses, such as drug metabolism, contribute to clinically important differences in responses to treatment. The role of genomic medicine in critical illness and injury is potentially great, but remains unanswered. Gene expression studies have provided new genomics tools such as the riboleukogram

CHAPTER 53

effective dosing of warfarin a challenge. Variability in the response to warfarin can be due to genetic differences at a number of steps in its metabolism. The metabolism of warfarin and many other drugs used in critically ill patients is dependent on the cytochrome P450 (CYP) enzyme system. Not only is this system sensitive to influences of diet and medications, genetic differences exist in many of the cytochrome subfamilies, leading to varied pharmacological responses. For instance, cytochrome P450 2C is the subfamily responsible for the metabolism of many drugs and the CYP2C9 isoform is responsible for the catabolism of warfarin.30 Warfarin acts through the interference with vitamin K epoxide reductase, leading to secretion of inactive vitamin K–dependent clotting factors.31 Vitamin K epoxide reductase is encoded by the VKORC1 gene. It is now well recognized that the CYP2C9 genotype, when combined with the VKORC1 genotype, is predictive of dose requirement for oral anticoagulants, a fact that is likely to have clinical utility. In addition to variation in these two genes (which are estimated to contribute to ∼60% of the variation in effective warfarin dose), variation in eight additional genes has been reported to influence warfarin dose, even though to a lesser degree.32 In the near future, pharmacogenomic approaches will likely serve to reduce complications associated with important but risky therapies.33 The arrival of large-scale, individualized, whole-genome sequencing will provide rich opportunities for advancing our knowledge of pharmacogenomics in the intensive care unit beyond treatment for deep venous thrombosis. In the broadest sense, adverse drug events (ADEs) span a wide spectrum that includes errors related to administration to undesired responses occurring at normal drug dosages. There are few situations where the risk for ADEs is higher than in critically ill patients. Drug-induced toxicity in the context of cancer chemotherapy has been investigated using genome-wide approaches.34 These same techniques that identify genetic variation (SNPs) across the entire genome could be used to predict responses to anticoagulants, antibiotics, vasopressors, drugs active in the central nervous system, and the like, in critically ill patients.

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and significant novel insight that may facilitate more accurate diagnosis and therapy. The successful integration of genomics into caring for critically ill and injured patients, in particular, demands that clinicians become genomically literate.1,28 This chapter provides a framework in which to begin that process.

REFERENCES 1. Guttmacher AE, Collins FS. Realizing the promise of genomics in biomedical research. JAMA. 2005;294(11):1399. 2. Collins FS, Green ED, Guttmacher AE, et al. A vision for the future of genomics research. Nature. 2003;422(6934):835. 3. Watson JD, Crick FH. Molecular structure of nucleic acids; a structure for deoxyribose nucleic acid. Nature. 1953;171(4356):737. 4. Watson JD, Crick FH. A structure for deoxyribose nucleic acid. 1953. Nature. 2003;421(6921):397. 5. Guttmacher AE, Collins FS. Genomic medicine—a primer. N Engl J Med. 2002;347(19):1512. 6. Cardon LR, Bell JI. Association study designs for complex diseases. Nat Rev Genet. 2001;2:91. 7. Brookes AJ. 4th International Meeting on Single Nucleotide Polymorphism and Complex Genome Analysis. Various uses for DNA variations. Eur J Hum Genet. 2002;10(2):53. 8. Mira JP, Cariou A, Grall F, et al. Association of TNF2, a TNF-alpha promoter polymorphism, with septic shock susceptibility and mortality: a multicenter study. JAMA. 1999;282(6):561. 9. Tambur AR, Pamboukian S, Costanzo MR, et al. Genetic polymorphism in platelet-derived growth factor and vascular endothelial growth factor are significantly associated with cardiac allograft vasculopathy. J Heart Lung Transplant. 2006;25(6):690. 10. Wilson AG, Symons JA, McDowell TL, et al. Effects of a polymorphism in the human tumor necrosis factor alpha promoter on transcriptional activation. Proc Natl Acad Sci U S A. 1997;94(7):3195. 11. Feero WG, Guttmacher AE, Collins FS. Genomic medicine—an updated primer. N Engl J Med. 2010;362(21):2001. 12. Palmer LJ, Cardon LR. Shaking the tree: mapping complex disease genes with linkage disequilibrium. Lancet. 2005;366(9492):1223. 13. Wurfel MM, Gordon AC, Holden TD, et al. Toll-like receptor 1 polymorphisms affect innate immune responses and outcomes in sepsis. Am J Respir Crit Care Med. 178(7);710. 14. Wurfel MM. Genetic insights into sepsis: what have we learned and how will it help? Curr Pharm Des. 2008:14(19):1900. 15. Marshall RP, Webb S, Bellingan GJ, et al. Angiotensin converting enzyme insertion/deletion polymorphism is associated with susceptibility and outcome in acute respiratory distress syndrome. Am J Respir Crit Care Med. 2002;166(5):646. 16. Menges T, Hermans PW, Little SG, et al. Plasminogen-activator-inhibitor-1 4G/5G promoter polymorphism and prognosis of severely injured patients. Lancet. 2001;357(9262):1096. 17. Pene F, Courtine E, Cariou A, et al. Toward theragnostics. Crit Care Med. 2009;37(1 suppl):S50–S58. 18. Cobb JP, Mindrinos MN, Miller-Graziano C, et al. Application of genome-wide expression analysis to human health and disease. Proc Natl Acad Sci U S A. 2005;102(13):4801. 19. Feezor RJ, Baker HV, Mindrinos M, et al. Whole blood and leukocyte RNA isolation for gene expression analyses. Physiol Genom. 2004; 19(3):247. 20. Calvano SE, Xiao W, Richards DR, et al. A network-based analysis of systemic inflammation in humans. Nature. 2005;437(7061):1032. 21. Quackenbush J. Microarray analysis and tumor classification. N Engl J Med. 2006;354(23):2463. 22. Cobb JP, O’Keefe GE. Injury research in the genomic era. Lancet. 2004; 363(9426):2076.

23. Warren HS, Elson CM, Hayden DL, et al. A genomic score prognostic of outcome in trauma patients. Mol Med. 2009;15(7–8):220. 24. Cobb JP, Moore EE, Hayden DL, et al. Validation of the Riboleukogram to detect ventilator-associated pneumonia after severe injury. Ann Surg. 2009 Oct;250(4):531–539. 25. Polpitiya AD, McDunn JE, Burykin A, et al. Using systems biology to simplify complex disease: immune cartography. Crit Care Med. 2009; 37(1 suppl):S16–S21. 26. Muenzer JT, Jaffe DM, Schwulst SJ, et al. Evidence for a novel blood RNA diagnostic for pediatric appendicitis: the riboleukogram. Pediatr Emerg Care. 2010;26(5):333. 27. Majerus PW. Human genetics. Bad blood by mutation. Nature. 1994; 369(6475):14. 28. Bertina RM. Factor V Leiden and other coagulation factor mutations affecting thrombotic risk. Clin Chem. 1997;43(9):1678. 29. Weitz JI, Middeldorp S, Geerts W, et al. Thrombophilia and new anticoagulant drugs. Hematol Am Soc Hematol Educ Program. 2004;424. 30. Kumar V, Wahlstrom JL, Rock DA, et al. CYP2C9 inhibition: impact of probe selection and pharmacogenetics on in vitro inhibition profiles. Drug Metab Dispos. 2006;34(12):1966. 31. Wadelius M, Pirmohamed M. Pharmacogenetics of warfarin: current status and future challenges. Pharmacogenomics J. 2007 Apr;7(2):99–111. 32. Wadelius M, Chen LY, Eriksson N, et al. Association of warfarin dose with genes involved in its action and metabolism. Hum Genet. 2007 Mar; 121(1):23–34. 33. Tan GM, Wu E, Lam YY, et al. Role of warfarin pharmacogenetic testing in clinical practice. Pharmacogenomics. 2010;11(3):439. 34. Gamazon ER, Huang RS, Cox NJ, et al. Chemotherapeutic drug susceptibility associated SNPs are enriched in expression quantitative trait loci. Proc Natl Acad Sci U S A. 2010;107(20):9287. 35. Reddy AJ, Christie JD, Aplenc R, et al. Association of human NAD(P)H: quinone oxidoreductase 1 (NQO1) polymorphism with development of acute lung injury. J Cell Mol Med. 2009;13(8B):1784. 36. Sorensen TI, Nielsen GG, Andersen PK, et al. Genetic and environmental influences on premature death in adult adoptees. N Engl J Med. 1988; 318(12):727. 37. Westendorp RG, Langermans JA, Huizinga TW, et al. Genetic influence on cytokine production and fatal meningococcal disease. Lancet. 1997: 349(9046):170. 38. Lin MT, Albertson TE. Genomic polymorphisms in sepsis. Crit Care Med. 2004;32(2):569. 39. Imahara SD, Jelacic S, Junker CE, et al. The TLR4 +896 polymorphism is not associated with lipopolysaccharide hypo-responsiveness in leukocytes. Genes Immun. 2005;6(1):37. 40. O’Keefe GE, Hybki DL, Munford RS. The G→A single nucleotide polymorphism at the –308 position in the tumor necrosis factor-alpha promoter increases the risk for severe sepsis after trauma. J Trauma. 2002; 52(5):817. 41. Opal SM, Cross AS. Clinical trials for severe sepsis. Past failures, and future hopes. Infect Dis Clin North Am. 1999;13(2):285, vii. 42. Vincent JL, Sun Q, Dubois MJ. Clinical trials of immunomodulatory therapies in severe sepsis and septic shock. Clin Infect Dis. 2002;34(8): 1084. 43. Zeni F, Freeman B, Natanson C. Anti-inflammatory therapies to treat sepsis and septic shock: a reassessment. Crit Care Med. 1997;25(7):1095. 44. Beutler B, Poltorak A. Positional cloning of Lps, and the general role of toll-like receptors in the innate immune response. Eur Cytokine Netw. 2000;11(2):143. 45. Tracey KJ, Fong Y, Hesse DG, et al. Anti-cachectin/TNF monoclonal antibodies prevent septic shock during lethal bacteraemia. Nature. 1987; 330(6149):662. 46. Riewald M, Petrovan RJ, Donner A, et al. Activated protein C signals through the thrombin receptor PAR1 in endothelial cells. J Endotoxin Res. 2003;9(5):317. 47. Bernard GR, Wheeler AP, Russell JA, et al. The effects of ibuprofen on the physiology and survival of patients with sepsis. The Ibuprofen in Sepsis Study Group. N Engl J Med. 1997;336(13):912–918.

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Trauma, Medicine, and the Law Kenneth L. Mattox and Stacey A. Mitchell

Trauma team and law enforcement activities repeatedly intersect in various locations for a variety of reasons in the course of mutual and integrated responsibilities: • • • • • • • • • • • • • • •

System and organizational regulation and review Preventive strategies Prehospital care and patient protection Disaster planning and response Emergency center Operating room Intensive care units and hospital nursing units and clinics Office practice Patients complaints and undesirable results Formulation of patient care policy and laws Licensure Quality review and reporting obligations Disaster medical response Professional liability Testifying in court/depositions.

This chapter addresses intersection/interaction among trauma, forensic medicine, and the law. Forensic and legal issues surface daily in trauma care but may be overlooked or unidentified due to the urgency of the situation. Health care providers are able to and, indeed, need to provide lifesaving measures and “think forensically” at the same time. By considering the forensic and legal implications, evidence that may be vital to the outcome of a legal case is preserved without impeding appropriate medical care.

CLASSIC KEY POINTS (Adapted from Weigel, Charles in Trauma, Moore, Feliciano, Mattox, 2nd edition).18 1. When in doubt and time and life are running out, TREAT

2. Have specific instructions for judicial intervention and emergency psychiatric detention readily available in the trauma center. 3. Be mindful of Hippocrates admonition, “which ought not be spoken of abroad, I will not divulge, as reckoning that all should be kept secret.” 4. Compliance with local reporting laws is essential to the avoidance of potential criminal penalty and civil liability. 5. The police department’s duty is containment and control; the trauma team’s is care and cure. To each his own. 6. Avoidance of malpractice claims depends on the exercise of skill based on knowledge of reasonable, ordinary, prudent physicians under similar circumstances. 7. An unfavorable outcome does not, of necessity, imply or result in a legal lawsuit; if such were the case, 50% of all attorneys in court cases would be so guilty. 8. Standing orders, best practices, protocols, guidelines, and electronic recommended practices all have value, but the ultimate hallmark of the professional is the exercise of sound judgment in any particular case. 9. Records must be made for the patient’s benefit, not the attending physician, hospital, attorneys, or quality surveillance. Records must be complete, accurate, timely, legible, and honest. Corrections to records can be made, dated, and timed, but the original entry must not be removed. 10. Difficulty and recurring problems can be more efficiently resolved through judicious preconsideration and planning. 11. The physician is an integral and essential part of the judicial system, and knowledgeable participation will benefit the physician, his or her patient, and health care in general. 12. Commonsense and human care and communication can be as important insulation factors from legal liability as good technique and clinical care.

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13. Freely use consultation and escalation of concerns when indicated. There are always persons, processes, and resources to provided unknown, unfamiliar, or clarified information. Over 1.6 million people lose their lives throughout the world each year as the result of violence.1 Countless others sustain injury. Violence and the social disruption that follows are addressed by everyone involved in trauma care. By understanding the law and the health care forensic implications of the law, identifying and preserving evidence during the course of evaluation and treatment, and accurate documentation of all aspects of wounds/care, the surgeon not only is an indirect advocate for the patient, but also provides much-needed information that will be used by law enforcement and the justice system.

CONCEPTS, PRINCIPLES, AND DEFINITIONS Although not standard in every political jurisdiction, some general principles and commonly used definitions are cited in this section. Often, a legal and a medical definition or concept might differ. Such variances in perception are important to medical personnel interacting with forensic and legal personnel, especially in a courtroom, deposition, or adversarial situation. • Abandonment—Terminating care of a patient without assuring that a continuum of the same or higher level of care exists • Assault and/or battery—Unlawful touching of a person or patient without appropriate consent for that contact • Confidentiality—Protecting medical information on any patient under the care of a hospital, nurse, doctor, or other ancillary personnel • Competence—The ability of a patient to understand questions asked them by health care personnel, as well as understand the various aspects of treatment recommendations and decisions • Negligence—Deviation from an accepted standard of care rendered by a similar practitioner in similar situation

■ Duty to Treat In the “modern” version of the Hippocratic Oath, the phrase, “ … there is the obligation to all my fellow human beings to treat those of sound mind and body as well as the infirm, … ” establishes the tone of the regulations for a duty to treat any patient who presents with an immediate life-threatening condition.2 Wide interpretation discrepancies exist regarding “duty to treat,” depending on urgency of clinical condition, availability of appropriately skilled clinician, availability and infrastructure of treating facility, and availability of higher level of care within the geographic area. Once a patient enters a treatment facility and on initial evaluation is found to have an immediate life-threatening condition, the obligation to continue the treatment is understood, as is the now established physician/patient and hospital/patient relationship. That relationship continues until one or the other terminates, by mutual consent, services

are no longer needed, or the physician properly withdraws from the relationship.3 The Emergency Medical Treatment and Active Labor Act (EMTALA), passed by Congress in response to hospitals refusing to treat patients based upon ability to pay, requires hospitals and physicians to provide a medical screening examination and stabilizing treatment for patients who present with an emergency medical condition.3,4 The physician’s duty to treat and/or stabilize the patient for transfer for a higher level of care is clear. Should a physician misrepresent a patient’s condition to facilitate a transfer for any other than higher level of care, civil penalties exist (Legal Information Institute), including fines and exclusion from participating in Medicare and Medicaid programs.3,4 The Americans with Disabilities Act of 1990 prohibits the denial of individual access to health care based on a disability, unless providing said care poses a direct threat to the health and safety of others.3,5 Implicit in these laws is that inability to pay is not an acceptable (or legal) reason for nontreatment of any patient presenting with a life-threatening condition. The duty to treat a patient does not change, even if the patient is the perpetrator of a violent crime. The fact that the patient was injured or injured others while driving intoxicated or while wielding a gun is irrelevant. The physician has a duty and ethical obligation to treat the patient, regardless of the situation surrounding the injury.

■ Consent Numerous terms and concepts apply to the many consent issues involved in patient care. • Express consent—The patient gives permission for recording his or her history, physical examination, and appropriate tests, with appropriate treatment. The doctor (preferably) or other health care worker describes the reason for examination and treatment, the treatment to be rendered, the risks of such treatment, and possible side effects and complications. If in writing, the expressed consent should include the doctor’s name, the location of the treatment and with the appropriate date and time of the treatment. • Implied consent—Under emergency conditions, when the patient’s clinical condition prevents him or her from speaking for themselves or when a surrogate consent cannot be obtained, it is assumed that if a patient or surrogate could speak, they would desire lifesaving evaluation and intervention. • Waived consent—Under some investigational review board (IRB)-approved research, where a form of treatment does not have scientific universal standards and a new treatment is being evaluated for emergency conditions when there is no time to obtain informed consent, the United States Food and Drug Administration (FDA) has outlined the conditions for wavier of consent. In such circumstances, it is appropriate to inform the patient and the family as soon as possible after the emergency and then obtain, in writing, the fact that the patient and/or family understands and gives consent, after treatment.

Trauma, Medicine, and the Law

Except in urgent, life-threatening situations, at its simplest, consent is required anytime a health care provider intends to render care to a patient.6 The physician’s (and hospital’s) duty extends beyond obtaining a patient’s signature.7 Informed consent includes providing sufficient information to the patient about the procedure, the risks and benefits, and any alternative treatments for an “informed” decision to be made.6,7 As outlined by the Joint Commission for Hospital Accreditation, the consent process has several components, including the nature of care, medications, procedures, possible risks and benefits, and any limitations on confidentiality of information learned from or about the patient.8 As a patient enters an emergency center or is admitted to the hospital, consent to be evaluated and treated is usually routinely obtained. Many patients do not completely read the “fine print” above the signature block, often being eager to get on with an emergency evaluation. Beyond this initial consent and signature, additional informed consent is required for more detailed treatment (such as an operation), once that more specific treatment is deemed necessary. There are two types of consent for competent patients— express and implied. Express consent may be either oral or written,6 although written and signed documentation is preferable, including date, time, physician name, location, and procedure. Oral (without any written or electronic documentation) consent is difficult to prove/defend in a court of law, whereas a written and thoroughly documented, informed consent is difficult to dispute in that same setting. In emergency situations, consent is presumed or “implied,”6 that is, when a patient presents with traumatic injuries or severe medical condition such that he or she cannot understand or communicate, it is presumed the patient would want treatment unless there is a living will or an advanced directive specifically requesting no heroic lifesaving measures be undertaken.8 Rarely does the trauma patient present with such documents, but it may occur, and the trauma team should be made aware immediately. Often, only after a blood transfusion has been initiated is the team made aware that the patient or his or her family is opposed to such intervention. The members of the treating team should, if time permits, attempt to ascertain the presence of any advanced directive or official treatment requests prior to initiating treatment. If an objection to treatment has been

established, that treatment must not be started, and if already begun, must be stopped. The only recourse the treating team has in these circumstances is to seek legal intervention, which time does not often allow. In obtaining consent, there are several considerations for the surgeon. In certain circumstances (emergency care, emancipated minor), minors, for example, may provide consent without parental involvement.9 Individual state regulations also outline other situations in which minors may give consent, such as treatment for sexually transmitted infections, abortions, contraception, and prenatal care.9 In the event a patient lacks the capacity to consent, health care decisions may be made by the patient’s legal representative, a parent, family member, guardian, surrogate, or medical power of attorney.6 Hospital policies list the priority of surrogate consent, and these policies usually reflect local or state laws. Competency in medicine is different from the legal connotation. Competency or capacity refers to the patient’s ability to understand what is best and right for him or her, and the decision is autonomous.8 Capacity is generally not an issue unless the patient suffers from a cognitive deficit, such as Alzheimer’s disease. Substance abuse or withdrawal from a substance that has caused altered mental status affects capacity as well.9 All attempts should be made to obtain consent. Hospital administrators may assist when there is an issue with capacity and no patient representative present. Under such circumstances, an ad litem (court appointed) representative of the patient might be considered. Local, state, and federal regulations define the process and payment for ad litem representation. Where there is consent, there is also the refusal of consent. Competent patients may refuse care, which includes procedures, admission, or a laboratory test.8 Although this may be troubling and frustrating for the physician, the right to refuse treatment must be recognized and respected. Refusal to consent is usually reserved for a patient who has reached majority. In the case of a parent issuing a “refusal to consent or treat” a minor child, family court judges often get involved with hospital administrations and physicians to determine what is permissible. The physician must consider competency a subjective assessment, and judgment of such falls to medical professionals.10 The physician must ensure all information is provided and any questions answered so the patient has the data to make an informed decision. This may take time, but time that is well spent if the patient’s immediate clinical condition allows such a delay. For some approved, randomized research studies under critical and emergency conditions, the FDA allows for waiver of consent, but such must be under strict review and protocol by the FDA and local IRBs. For these protocols, the patient must not be able to give meaningful consent because of his or her clinical condition, and time to treatment is critical. Prepatory to initiating research that is conducted with waivers of consent, researchers educate the community about the protocol and publicize an “opt-out” method for the potential patient population. The patient or the family should be informed of the study at the first available time. At any time after enrollment, if the patient or the family determines he or she wishes to be removed from the study, that option should be available. With consultation among the study coordinators, the

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• Surrogate consent—Both state and hospital policies define who may give informed consent for a patient whose clinical condition does not allow him or her to speak for themselves or who, for a variety of reasons, cannot understand the implications of information given to. • Refusal of consent—Adult patients who fully understand the implications of proposed treatment have the right to refuse to be examined or treated. Under some circumstances, local law or hospital policy requires that the local ethics committee or a court-appointed ad litem become involved, especially if the adult refusing treatment has minor children or is mentally incompetent. If treatment is refused, it is important to adequately document the conditions of the refusal and names of all involved in advising and interacting with the patient.

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Specific Challenges in Trauma local approving IRB, and the FDA, waiver of consent can provide new and valuable evidenced information that benefits patients and society.

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FORENSIC AND MEDICAL IMPLICATIONS The very nature of traumatic injuries leads one to consider forensic implications. The legal impact may be great in certain cases. For example, preserving the clothing in gunshot cases may be critical to the outcome of courtroom proceedings. Obtaining blood samples from a potentially intoxicated driver is considered essential by some political jurisdictions. The local laws concerning a hospital or physician’s rights and responsibilities in ordering laboratory data for the sole purpose of obtaining forensic evidence are inconsistent, and clinicians must be cognizant of hospital, local, and state regulations concerning this issue. Traditionally, forensic issues have not received much, if any, priority, since lifesaving measures are the primary objective. However, given a firm grasp of the basics and a desire, physicians and other providers are quite able to render necessary care while also taking care to preserve evidence in the appropriate ways.

FORENSIC NURSING AND TRAUMA SYSTEMS Proper evidence collection and preservation may be accomplished with the assistance of forensically trained personnel. Forensic nursing has emerged during the past two decades to become a recognized function of emergency medicine, public health, hospital nursing practice, and trauma care. Trauma care extends across many venues, including EMS, the shock rooms, imaging locations, operating rooms, intensive care units, nursing hospital units, follow-up clinics, and the morgue. The forensic nurse is specially educated and trained in both the health care and legal arenas,11 and provides direct services to patients, physicians, the trauma management and evaluation teams, regional trauma review processes, general nursing, medical- and law-related agencies, and expert court testimony.11 Affected patient populations include victims of sexual assault, interpersonal violence (domestic violence, physical assault, dating violence), elder maltreatment, and child abuse, among others. The forensic nurse is trained in injury identification and documentation, forensic photography, evidence collection, death investigation, and addressing the psychosocial needs of the patient and family. These nurses may be present in the trauma room to collect and preserve evidence and document injuries through photographic means or using body diagrams. Clothing, for example, as it is removed, is handed to the forensic nurse, who places and appropriately labels each piece in separate containers to prevent contamination. The forensic nurse interfaces with law enforcement agencies to release evidence. In addition, bullet fragments removed during surgery may be given to the forensic nurse, who will ensure chain of custody and release to the investigating agency. Patients presenting with traumatic injuries may not be able to provide a history of the precipitating event. The forensic nurse anticipates the types of evidence that may need to be preserved, and his or her presence in the trauma room allows

the surgeon to concentrate on lifesaving measures, while confident that evidence is appropriately preserved. Information, including photographs obtained for forensic purposes, is logically available during the trauma quality review process, and, once identification markers have been removed (HIPPA requirements), might also be very helpful in clinical scientific preparations for publication.

INJURY IDENTIFICATION, CLASSIFICATION, AND GRADING The trauma center, along with the trauma system, has many responsibilities, not the least of which is evaluation of injuries, underlying nontrauma conditions, assessment of risks, classification of injuries, and some sort of grading as injuries are entered into appropriate registries for quality and epidemiologic review. A broad injury documentation of “laceration” or “stab wound” may be insufficient. Use of an established injury classification schema is essential, such as those developed by professional organizations (American Association for the Surgery of Trauma, American College of Surgeons, and others). Such classification and grading systems are consistent with ICD-9 operation codes, CPT codes, and regionalized trauma registries. However, it is not always immediately clear that a wound is caused from a blunt or penetrating force or even the identity of a specific wounding agent. Therefore, the final coding by the trauma service is determined at the end of the hospital admission. Especially at the initial evaluation, clinicians are often confused as to the exact wounding agent or effects of the agent. Forensic determinations should therefore not be arrived at until all the data are collected. For example, “blunt force trauma” can cause lacerations, abrasions, contusions, and fractures, and refers to wounds caused by an impact with a blunt object. Blast force is similar to blunt force and can create similar injury. The severity of the injury depends on the amount of force, the area of the body involvement, when the injury occurred, and the object used.12 External cutaneous characteristics used to identify blunt force trauma include tears in the skin that are not easily approximated, jagged edges and abrasions on the wound edges, bruising, and discoloration. Tissue bridging, where pieces of tissue that are attached inside, to the sides of the wound is often noted within the wound.12 The tissue forms “bridges” that may be identified upon further inspection. Abrasions are the superficial scraping away of the outer layers of skin that occur as the wounding object is rubbed or scraped over the skin.13 Contusions or bruises result from a blow or squeezing motion of the tissue. The blood vessels are crushed, causing bleeding under the skin surface.13 Contusions vary in color based upon the time interval from the time of the wounding and the amount of healing process. Skin tone and turgor affect the appearance of bruises.12 Therefore, from a forensic standpoint, it is recommended that contusions NOT be dated or aged, but, rather, careful, detailed documentation of the color(s) is suggested. Sharp force injuries are caused by an object that has sharp edges, the most common “culprit” being a knife. Sharp force injuries consist of stab wounds and cuts. A stab wound is a wound that is deeper than it is wide, while a cut is longer than it is deep.12 Smooth edges and the lack of

Trauma, Medicine, and the Law

WOUNDS FROM FIREARMS Firearm injuries may be identified as gunshot, shotgun, or rifle wounds, and vary in nature based on the type of weapon used. For the purposes of this chapter, gunshot wounds will be the focus, as these are often encountered by physicians managing trauma patients. Physical findings in and around the wound are naturally clinically important to the trauma team, but they also provide evidence that is often equally useful in the police investigation, so accurate and complete documentation of findings is essential. From a practical, clinical standpoint, whether the wound site is entrance or exit is immaterial. The decision for an operation is not based on direction of the trajectory, but rather on disruption of vital tissues or organs, obstruction, ischemia, or contamination. Evaluation is accomplished to gather information to determine the need for an operation or other intervention. Initially, it is difficult to discern an entrance wound from an exit wound, so careful inspection is required if the clinician or forensic nurse is seeking such information. Entrance wounds are divided into four categories (distant, intermediate, close, and contact), based on the range of fire or distance from the muzzle to the victim.14 Normally, when a gun discharges, more than just the bullet exits at the end of the gun barrel. Hot gases and burning gunpowder are expelled. Depending on the range of fire, evidence of these may be present in and around the wound. In distance wounds, the only evidence is the presence of the bullet and/or fragments, and entrance site is characterized by an abrasion surrounding the wound.14 Powder burns or “powder tattooing” are characteristic of intermediate gunshot wounds, appearing as red-brown or orange-red punctate wounds around the entrance wound.4 Soot or gunpowder is deposited around the wound in the close-range gunshot wound, with soot concentration varying with the distance of the muzzle to the victim. The muzzle of a handgun is typically 6 inches or less from the victim.14 Finally, often confused with exit wounds, the contact wound is usually a large wound, with the muzzle of the gun having been pressed against the skin. These wounds, generally head wounds, may have searing or burning of the wound edges due to hot gases expelled from the gun.14 The stellate wounds contain soot around and often inside the wound.4 Exit wounds are typically larger and slit-like in appearance.4 The amount of energy on the bullet as it exits the skin determines the size of the wound.14 The “yaw” or spinning and the shape of the bullet may contribute to wound irregularity.14 It is better for the clinician to merely document the characteristics of a wound, rather than speculate about kinematics. Inconsistent findings between the surgeon and a medical examiner may prove detrimental to a court case, so be precise and accurate in your documentation. Although this chapter is not intended to address kinesiology or wound ballistics, a basic working knowledge is helpful from both clinical

and forensic standpoints. For cases involving gunshot wounds where it is known or suspected the patient may have been the shooter, bagging the hands for later examination by forensic investigators is advocated, when possible. Bullets and fragments removed during emergency treatment are evidence and should be treated as such. In preserving the evidence and assuring appropriate “chain of evidence,” there are several cautions and principles. In removing a metallic foreign body, the following considerations are important: • Avoid using a metal instrument to extract the metal foreign body. Metal on metal creates “scoring” on the missile that might distort the forensic evidence. • Avoid dropping a metallic missile into a metal container— again, may score the missile. Gently place the foreign body into the routine plastic specimen and tissue cups available in hospitals, assuring that a label of the patient is on the side and the cap of the specimen cup. • Do not scratch your initials and the date on the foreign body. Use appropriate/approved methods of documentation, in accordance with the established hospital policy of managing forensic evidence and the chain of custody. Assure that the container is properly labeled and contains a date and time, with tape positioned over the top and on the container. • The physician removing the foreign body should record in the written or electronic medical record and the operative dictation the details of the foreign body removal and to whom the missile was given as well as the instructions given to this individual. • The person receiving the foreign body and placing it into the plastic cup should also document the same in the record, as well as to whom the container was given (hand-off ). • The exact process and the offices where forensic evidence is maintained in each hospital are determined by each hospital and clearly stated in that hospital’s “Chain of Evidence” policy.

CLOTHING Clothing that may contain valuable evidence for the police investigation is often cut and discarded on the floor or thrown into the garbage. When possible, avoid cutting through defects or holes, which can destroy evidence, and cut around the defect or along the seam, placing individual items of clothing in separate paper bags. The top of the bag is folded over, sealed with tape, and labeled with the examiner’s initials.15 The presence of a forensic nurse in these instances expedites and assures good procedure in handling, photographing, packaging, and labeling clothing. Once bagged, the clothing will be released to law enforcement or stored in an appropriately locked area of the hospital.

LABORATORY SPECIMEN COLLECTION FOR LAW ENFORCEMENT PURPOSES Trauma patients present under many circumstances, and in some instances, the patient is the alleged perpetrator of a crime. Occasionally, there is a need to identify illegal substances or high

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tissue bridging are characteristic, and wound edges may easily be approximated.12 During the time of blunt force injury, a detached or sharp piece of the environment, such as a portion of a disintegrating automobile, may produce penetrating wounds in addition to the blunt force injury.

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levels of alcohol in a presenting patient, primarily for legal rather than clinical reasons. Although trauma centers often perform blood alcohol and urine drug screens, forensic toxicology studies are performed in crime laboratories where assays identify and quantify submitted specimens. Laboratory studies conducted in hospital laboratories are used primarily for determining medical treatment, and the routine consent to treat covers the process of obtaining these specimens/studies. However, obtaining specimens specifically for legal reasons is a different matter, and local and state laws differ with regard to the need for patient (or surrogate) permission for blood, urine, tissue, or exhaled air specimens. All members of the treating team should know the dictates of local/state law, as well as related individual hospital policies. When laws and/or policies mandate patient/surrogate consent, the physician must assure that the patient’s cognitive condition allows for informed consent. Some states have mandatory requirements, whereas others require a search warrant or court order for specimen collection.16 Blood samples should be obtained within 3–4 hours of a trauma incident to provide accurate blood alcohol content, and it is critical to assure that specimen collection time(s) are accurately recorded.16 Commercial kits are available to aid in the specimen collection and chain of custody.

CHAIN OF CUSTODY Chain of custody is the “paper trail” that documents each person who has custody and control of a particular piece of evidence or a specimen.15 The chain begins with the person who collects the evidence and continues with each subsequent person who handles the evidence until it reaches the crime laboratory. The following information should be documented in the medical record17: • Each person who handled the specimen(s) • Name and badge number of the officer receiving the specimen/evidence • Other law enforcement agency personnel who might be present • Date and time the specimen/evidence is released Failure to maintain the chain of custody opens the door for attorneys to dispute the validity of the evidence.17

LEGAL CONSIDERATIONS DURING MASS CASUALTY AND DISASTER SITUATIONS The principles of interaction between medicine and the law should not change in the face of a disaster situation, although accomplishing mutual goals may be more challenging. The principles relating to licensure, credentialing, and consent continue to apply, even in extreme or special circumstances. The fact that a physician (or other health worker) may be from an outside geographical or political jurisdiction does not remove the organizational and personal responsibility to comply with local credentialing and licensing laws. During disasters, supplies, equipment, and personnel may be limited. This does not remove the responsibility for the physician and the clinical

team to comply with professionalism and standard best practices within their capability and resources. Although ethical standards and practice are not altered because of a declared or undeclared disaster, The Institute of Medicine has developed guidance for establishing standards of care for use in disaster situation. Record keeping may be a challenge, but detailed and accurate records must be one of the undisputed goals during these times. During a disaster, any personnel working in the hospital is subject to the bylaws and policies of the hospital, as well as state and local law. All questions relating to medical authority, supervision, coordination, and action during the time of a declared disaster in regional shelters are subject the Regional Incident Command structure and its Medical Branch. Any outside agency must function under the authority of the regional authority, unless subject to federal law.

INTERACTING WITH ATTORNEYS ■ Hospital Bylaws, Committees, Credentialing, Policies As part of any hospital, clinic, or health department function, and especially in any trauma care facility, it is axiomatic that surgeons and other trauma team members will interact with attorneys on a relatively frequent basis. Most hospitals, medical schools, and medical facilities have in-house legal counsel to assist in development and review of bylaws, policies, and procedures, as well as credentialing, outside regulatory review, and the interpretation of local, state, and federal law.

■ Professional Liability, Depositions, and Testifying in Court Despite best intention to practice the highest quality of medicine possible, dissatisfaction, complications, and misadventures will occur. At the hospital level, such events are reviewed by the hospital quality review process, including mortality and morbidity meetings, performance improvement committees, peerreview committees, and sentinel event committees. Except for criminal cases, the minutes and proceedings of these reviewing entities are protected from discovery. Physicians should participate in these hospital activities, including reviews of their own cases. In the course of caring for trauma patients, receiving a subpoenas notifying one he or she is being sued, being asked to review records of another physician, or asked to testify in court about an injury is not uncommon. On receipt of a subpoena, the first step is to contact your attorney or in-house council and insurance carrier. From that moment on, talk to no one else about the involved case without the advice and/or presence of your attorney. Prepatory to a deposition, review all related records to the depth and detail you would in preparing for a board exam. At the time of a deposition or court testimony, listen carefully to every question asked, and answer that question; do not volunteer any additional information (even when sorely tempted)! If you do not understand the question, so indicate. If you are interrupted by the judge or an attorney, stop talking (in mid sentence, if necessary) and listen carefully to the

Trauma, Medicine, and the Law

REFERENCES 1. World Health Organization (WHO). Violence and injury prevention and disability. 2009. http://www.who.int/violence_injury_prevention/ violence/en/. 2. MedicineNet.com. Definition of Hippocratic Oath. 2002. http://www. medterms.com/script/main/art.asp?articlekey=20909. 3. Katz LL, Paul MB. When a physician may refuse to treat a patient. Physician News Digest. 2002. http://www.physicansnews.com/law/202.html. 4. Legal Information Institute. Examination and treatment for emergency medical conditions and women in labor. n.d. http://www.emtala.com/law/ index.html. DiMaio VJ. Gunshot Wounds: Practical Aspects of Firearms, Ballistics and Forensic Techniques. 2nd ed. Boca Raton: CRC Press; 1999.

5. Department of Justice. American with disabilities act of 1990, as amended. 2009. http://www.ada.gov/pubs/adastatute08.htm. 6. Aiken TD. Legal, Ethical and Political Issues in Nursing. 2nd ed. Philadelphia: F.A. Davis Company; 2004. 7. Thiess DE, Sattin JA, Larriviere DG. Hot topics in risk management in neurologic practice. Neurol Clin. 2010;28(2):429–439. 8. Magauran BG. Risk management for the emergency physician: competency and decision making capacity, informed consent, and refusal of care against medical advice. Emerg Med Clin North Am. 2009;27:605–614. 9. Tillett J. Adolescents and informed consent: ethical and legal issues. J Perinat Neonat Nurs. 2005;19(2):112–121. 10. Carey B. Consent and refusal for adolescents: the law. Br J Nurs. 2009; 18(22):1366–1368. 11. IAFN. What is forensic nursing? 2006. http://www.iafn.org/displaycommon. cfm?an=1&subarticlenbr=137. 12. DiMaio VJ, DiMaio D. Forensic Pathology. 2nd ed. Boca Raton, FL: CRC Press; 2001. 13. Spitz WU. Spitz and Fisher’s Medical Legal Investigation of Death. 3rd ed. Springfield, IL: Charles C. Thomas; 1993. 14. The McGraw-Hill Companies. Emergence medicine atlas: gunshot wounds. 2006. http://atlas-emergency-medicine.irg.ua/ch.17.htm. 15. Savino JO, Turvey BE. Rape Investigation Handbook. New York: Elsevier; 2005. 16. Hedlund JH, Ulmer RG, Northrup VS. State laws and practices for BAC testing and reporting drivers involved in fatal crashes. For the US Department of Transportation. 2004. http://www.nhtsa.dot.gov/people/ injury/alcohol/BAC-Testing/images/state%20laws_low.pdf. 17. American College of Emergency Physicians. Evaluation and Management of the Sexually Assaulted or Sexually Abused Patient. Dallas, TX: US Dept of Health & Human Services; 1999. 18. Weigel CJ. Medicolegal aspects of trauma. In: Mattox KL, Moore EE, Feliciano DV, eds. Trauma. Norwalk, Connecticut: Appleton & Lange; 1988;53–61.

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nature of any objection or interruption. Do not continue until your attorney or the judge advises you to do so. You may ask that a previous response or question be read back to you by the court recorder. The two categories of witnesses are fact and expert. A fact witness is called to enter into the record the facts of the case, as he or she remembers them, discovered them in the medical record, or otherwise knew the information. An expert witness is certified by the court as having special knowledge and is called upon to elaborate on information pertinent to the case from the vantage of his or her special knowledge, background, and experience. An expert witness might also be a fact witness, but not usually vice versa.

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Principles of Critical Care Raul Coimbra, Jay Doucet, and Vishal Bansal

INTRODUCTION The last two decades have seen great advances in the care of the injured patient, both in prehospital triage and transport and in the intensive care unit (ICU). More than ever, the outcome of these patients, in terms of both morbidity and mortality, is very dependent on a solid understanding of the pathophysiology and also of the evolution of certain injuries. Attention to detail is critical and an awareness of the pitfalls is essential, if one has to be successful in avoiding preventable morbidity and mortality. Excluding early deaths in the operating room, most complications and subsequent deaths following injury will occur in the ICU. Care in the ICU is designed to reestablish normal homeostasis and minimize complications of primary, secondary, and iatrogenic injury. Surgical critical care is inherently different from medical intensive care insofar as surgical patients, and particularly trauma patients, require intensive care as the result of an acute surgical intervention or injury and not as part of the (often inexorable) progression or exacerbation of chronic disease. This fundamental difference affects a multitude of patient management practices and decisions. In the last several years, increasing emphasis has been placed on quality of care indicators and physician staffing models for ICUs. Therefore, a modern surgical ICU in the 21st century has to provide evidence-based care using algorithms, clinical management guidelines (CMGs), and checklists, use cuttingedge technology for physiologic monitoring, and has to have a robust continuous quality improvement process to constantly evaluate its outcomes and to identify opportunities for improvement. This chapter focuses on elements of critical care essential to the management of the acutely injured patient, reviews some recent advancements in the monitoring of the critically ill patient, and lists some of the common complications and pitfalls observed in the ICU.

ORGANIZATION OF THE ICU Given the wide variety of clinical expertise and patient populations, several patterns of ICU physician organization have developed. The first is the “closed” unit that relies almost exclusively on a critical care team (or attending intensivist) for primary patient management. Under this scheme, comprehensive management is assumed by the ICU team along with responsibility for all orders and procedures, with other services providing care as consultants on an as-needed basis. Most medical ICUs are staffed in this manner along with some surgical ICUs where the ICU team is directed by another surgeon. In an alternative model, the “open” unit, there may or may not be a designated ICU director, a separate ICU team, or even an intensivist immediately available to the ICU. Under this system, individual physicians manage and direct intensive care for their respective patients, depending on their institutional privileges, with or without house staff. Consultative involvement of a board-certified intensivist is at the discretion of each primary attending physician, and is neither required nor necessarily expected. Many larger surgical ICUs have a “semi-open” or transitional unit plan of practice whereby the ICU is staffed, 24 hours a day, 7 days a week, with dedicated on-site ICU physicians. On-call physicians are often attending-supervised house staff in larger teaching centers, and responsibility for care is shared between the ICU team and the primary specialty service. With the 24/7 in-unit staffing in the semi-open model, critical care team involvement in each patient is typically either mandatory or expected. There are often specific areas of designated critical care autonomy, such as the management of mechanical ventilators, invasive hemodynamic monitoring, pain management, and conscious sedation. In these units, the ultimate responsibility for the patient remains with the primary team, but patient care is a collaborative effort. This semi-open model combines the advantages of maintaining a separate in-house critical care

Principles of Critical Care

CONTINUOUS QUALITY IMPROVEMENT IN THE SURGICAL ICU Quality assurance and performance improvement in a surgical CCU are complex processes requiring the ongoing identification of outcome measures or performance indicators, data collection and analysis, and the development of action plans to correct deficiencies and subsequent monitoring of the

performance (outcome) measures. The underlying goal of delivering high-quality care also depends, to a significant degree, on specialization (critical care specialists), provider education and training, and good communication and collaborative interaction between specialty and ancillary services. Existing critical care quality assurance programs have used a variety of clinical indicators or “filters” as a measure of the quality of care. These indicators may reflect process measures (e.g., percentage of eligible patients receiving deep venous thrombosis prophylaxis in a timely manner), and outcome measures (complicaton rate [%] for central venous line sepsis). Illness severity indices have been developed for the purpose of predicting outcome of critically ill patients and are being increasingly used as benchmarking tools, allowing participating units, through the use of statistical comparisons, to compare their outcomes with those predicted by the various indices. These performance measurement systems will become increasingly important in allowing managed care organizations to assess program performance. In addition to improved instruments for assessing critical care outcome, the development and implementation of clinical protocols and CMGs9,10 directed at reducing undesirable treatment variability will be linked to CCU performance improvement. Protocols and guidelines, once developed and implemented, can later be analyzed in terms of their clinical efficacy and cost-effectiveness and can be subsequently modified and further developed as part of the overall programs in performance improvement and cost control. The effectiveness of protocols and CMGs has been demonstrated for a variety of problems and conditions including ventilator weaning, pneumonia, nutrition, and sedation.11–17 The difficulties that most institutions experience, however, relate more to the implementation of CMGs rather than to their development. Current methods of improving implementation of and compliance with CMGs include ongoing education, standing (preprinted) order forms, the assignment of some management responsibilities to specialized teams (e.g., nutrition, respiratory therapy), and the use of advance practice staff (nurse practitioners, physician’s assistants). More recently, several fields in medicine, motivated by an increased awareness about errors in medical care delivery and mandatory reporting of quality measures, have incorporated lessons learned from the aviation industry to clinical practice in an attempt to improve quality and patient safety. A checklist is just one of the tools used in the aviation industry that have been tested in many ICUs to potentially improve safety, quality, and consistency as part of a continuous quality process.18,19 A detailed description of how to develop and implement a quality improvement program in the ICU is beyond the scope of this chapter but important information can be found in the excellent reviews by Curtis et al.,15 and McMillan and Hyzy.20 Inspired by an article by Vincent21 where he described a checklist using the mnemonic FASTHUG (feeding, analgesia, sedation, thromboembolic prevention, head of the bed elevation, stress ulcer prophylaxis, and glucose control), we implemented a modified checklist (mFASTrHUGS) by adding mouth care (m), restraints (r), and skin care (s) (Table 55-1). We use the checklist as a template for daily multidisciplinary

CHAPTER 55

team 24 hours per day while maintaining primary surgical service responsibility for overall patient management. This arrangement is consistent with Accreditation Council for Graduate Medical Education (ACGME) program requirements for general surgery training programs as well as guidelines for the optimal care of the injured patient suggested by the American College of Surgeons Committee on Trauma for Level 1 Trauma Centers.1 There is now a growing body of work examining the relationship between ICU staffing models and patient outcome. For these purposes, rather than trying to compare various models of care, a distinction has been made between “high-intensity” and “low-intensity” physician staffing models. Loosely translated, a “high-intensity” model involves 24/7 dedicated ICU physician staffing and mandatory ICU team involvement with patient management. This includes all closed units and most semi-open units (as previously defined). The remaining “open” units typically involve “low-intensity” ICU physician staffing. The principal hypothesis is that dedicated, higher-intensity intensivist staffing for ICU patients will ultimately improve outcome from a variety of conditions and illnesses. In a meta-analysis of 26 pooled studies, Pronovost et al. found a relative risk of 0.71 (95% CI  0.62–0.82) for hospital mortality and 0.61 (95% CI  0.5–0.75) for ICU mortality associated with high-intensity ICU staffing for adults and children.2 This validated previous work done by the same author.3,4 Similar results were found by Nathens et al. who specifically examined the effect of high-intensity staffing on outcome from major trauma.5 Utilizing prospective cohort data from 68 trauma centers, the authors reported a relative risk reduction of 0.78 (95% CI  0.58–1.04) for ICUs whose patients were either managed (closed unit) or comanaged (semi-open) by board-certified intensivists. The effect of dedicated intensivist involvement seems to extend also to neurology and neurosurgical patients, with reports demonstrating improved overall mortality and length of stay.6,7 These and other observations have led to attempts to improve patient safety in the ICU. In 2000, a group of Fortune 500 companies and large public and private health care purchasers formed the Leapfrog Group for the purpose of identifying and creating incentives for sustained patient safety measures in acute care hospitals. This group has identified standards for physician staffing the ICU that involves the presence of experienced intensivists providing daytime care and response requirements for off-hours care.8 The intent of the Leapfrog initiative is to provide market incentives designed to stimulate preferential use of institutions adhering to these types of guidelines. However, the current shortage of critical care specialists makes it impossible to maintain care in “closed” units.

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TABLE 55-1 “mFASTrHUGS” for SICU TEAM Rounding Tool

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Mouth care Feeding Analgesia

Sedation

Thromboprophylaxis Restraints Head of bed 30° Ulcer Glucose Gut Skin care

Teeth cleaning and oral moistening q 4 h Commence by day 1 in ICU, follow protocol Review medication record. Give pain score using visual or nonverbal scale Review ventilation, GCS, and reason for sedation. Assess and specify target RASS score. Daily awakening qAM Prescribe SCDs and/or heparin type or alternative Assess, reorder, or discontinue restraints. Universal consent obtained Head of bed up 30° or more. Get C-spine cleared! Review GI ulcer prophylaxis Maintain tight glucose control per protocol Last BM is specified, appropriate bowel protocol Note potential areas of pressure breakdown; progress to healing. Does patient need special bed?

rounds and the nursing staff use it at the end of their shift for turnover. Each item on the checklist is reviewed during rounds assessing its implementation and need. If any item has not been implemented for a particular patient, then the team has to identify a contraindication (e.g., pharmacologic DVT prophylaxis during the first day following a significant traumatic brain injury), otherwise the measure has to be implemented. mFASTrHUGS is a package implemented to all patients in our surgical ICU. Other variations of the original mnemonic have been reported recently.22

PHYSIOLOGIC MONITORING IN THE CRITICAL CARE UNIT One of the characteristics of the ICU is the utilization of intensive physiologic monitoring. In past years there were a limited number of types of ICU monitoring available. There has been a dramatic increase in recent years in the ability to monitor a wider variety of physiologic parameters. Today significant issues for trauma surgeons deciding which monitoring to use include lack of familiarity and required training, maintenance, acquisition costs, safety, and efficacy. Patients admitted to the ICU will have an anticipated and possibly optimal clinical “trajectory” that will be the expectation of the experienced clinician. A considerable effort is expended by the critical care physician in determining if the

patient is following the anticipated trajectory, and in anticipating and detecting complications. Monitoring is used to determine that the patient has stable organ function, and detect anomalies that may indicate organ dysfunction and incipient or actual complications. Monitors can be useful in determining if a patient trajectory is deviating from the anticipated or optimal course; however, any monitor’s output requires interpretation and integration with the clinical picture and clinical experience. Monitoring itself is associated with serious and lethal complications, including complications associated with invasive monitoring, and errors in interpretation of results that can lead to error in clinical decision making. The questions that must be addressed with any form of monitoring include “when?” (indication and timing), “what?” or “how much?” (which specific monitoring tools or techniques), and “why?” (an analysis of the associated risks and benefits).

HEMODYNAMIC MONITORING Hemodynamic monitoring is directed at assessing the results of resuscitation and as a guide to reestablishing and maintaining tissue and organ perfusion (see Chapter 56). The restoration of normal arterial blood pressure, central venous pressure, pulmonary arterial (PA) pressure, and cardiac output provides some reassurance that there is adequate organ perfusion. This reduces the likelihood of death and serious morbidity due to complications of hemorrhagic shock, including postinjury inflammatory response syndrome and multiple organ failure (see Chapter 61). However, the phenomenon of regional circulation and inadequate perfusion of some organs, particularly the gut, in the presence of normal arterial pressures remains a concern. Direct monitoring of tissue perfusion, particularly in potentially comprised capillary beds such as the intestine, is more difficult and not commonly performed. New types of monitors are becoming available that have some promise to determine perfusion at the tissue level in organs of interest.

■ Arterial Pressure Monitoring Noninvasive blood pressure monitoring is available throughout the Medical Center by the use of the automated blood pressure cuff. These devices can be set to do repetitive blood pressure measurements as frequently as every minute. However, these are usually considered insufficient in patients who are having significant hypotension due to the lack of sensitivity of the cuff at low blood pressures as well as the intermittent nature of the readings. Insertion of an arterial intraluminal catheter or “arterial line” allows instantaneous measurement and display of arterial blood pressure, even at very low blood pressures. Arterial lines are the preferred method of arterial blood pressure management in patients receiving continuous drips of vasoactive drugs as they allow better drug titration and have a wide variety of indications (Table 55-2). They also allow for the ready sampling of arterial blood for laboratory testing including arterial blood gas and lactate. Arterial lines are typically placed in the radial artery, although they can also be placed in the femoral artery or brachial artery. Infection of arterial lines is less common than that of central venous lines; however, sterile technique should still be utilized to avoid the risk of infectious

Principles of Critical Care

TABLE 55-2 Indications (Suggested) for Hemodynamic Monitoring

Central venous pressure monitoring Volume status in acute head injury Complex trauma/pelvic fracture Shock dates Hypokalemia Acute renal failure Vasoactive drug infusions Monitoring during acute ICU hemodialysis Cardiac pacing Elderly trauma patient Massive transfusion Pulmonary contusions PA catheter monitoring Refractory septic and cardiogenic shock states Severe hypoxemia, pulmonary edema/embolism/ARDS High-risk intraoperative monitoring Barbiturate coma (iatrogenic myocardial depression) Moderate or mixed venous O2 (SVO2) Diagnoses: explained shock, hypoxemia, renal failure

complications. Thrombotic complications can occur at any arterial line site; these may be as common as 30–40% and may lead to tissue loss, including loss of digits. This is particularly common in patients who had prolonged hypotension or sepsis or who have been treated with pressors. Although Allen tests are frequently performed before the insertion of a radial arterial line, these do not exclude the possibility of this complication. Minimally invasive continuous arterial pulse waveform analysis devices are available that look at variation in area under the arterial pressure waveform as a surrogate for stroke volume variation with respiration. These devices can provide an estimate of cardiac output without need of a PA catheter, although they are subject to error.

■ Central Venous Pressure Monitoring Monitoring central venous pressure is most useful in patients at high risk of overresuscitation or underresuscitation (see Chapter 56). These include patients with limited cardiac reserve,

■ Pulmonary Artery Catheters The introduction of the Swan Ganz PA catheter in 1970 was followed by wide adoption in critical care units. However, in the mid-1990s there were a number of reports questioning their efficacy and safety. A study by Connors et al. concluded that use of PA catheters increased mortality and led to increased utilization of resources.26 A more recent meta-analysis has not demonstrated increased major adverse sequelae associated with the PA catheter27; however, its utilization in ICUs has decreased significantly. ICUs typically restrict use of the PA catheter to patients who have known or possible myocardial dysfunction, or in those patients who are thought to be sensitive to changes in preload, contractility, or afterload.28 In 2000 an NHLBI workshop report on PA catheters and clinical outcomes produced a consensus statement that indicated that a clinician’s ability to obtain and interpret PA catheter data and intervene appropriately is an important determinant of outcome.29 An assumption is that if the PA catheter use changes therapy and is used to correct physiologic deficits, mortality and morbidity can be reduced. In surgical patients it appears that monitoring data obtained through the PA catheter results in therapy changes in 30–60% of cases. Of these, estimated at

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Arterial line monitoring Shock states (any) Cardiac Septic Neurogenic Hypovolemia/hemorrhage Monitoring intraoperatively/postoperatively Head injury Serial monitoring of ABG Labile hemodynamic status Respiratory failure Hypertensive crisis Vasoactive drug infusions High-risk or elderly trauma patient

including elderly patients and patients with cardiac disease. Patients with traumatic brain injury are another group in whom central venous pressure monitoring is frequently performed to avoid hypotension associated with underresuscitation or overresuscitation resulting in increased cerebral edema. Patients with pulmonary contusions can suffer from overresuscitation, which can lead to increased lung water and worsening respiratory status. Interpretation of the central venous pressure in a ventilated patient should optimally be done while the patient has been removed from positive end-expiratory pressure (PEEP). Central venous pressure can also be approximated by subtracting the level of PEEP in excess of 5 mm Hg from the CVP measurement. The central venous catheter can also be used to obtain a central venous blood sample; this can be used to obtain a mixed venous blood gas measurement. Since the mixed venous oxygen saturation (MVO2) is usually slightly lower in the SVC as compared with that in the IVC due to the relatively low oxygen consumption (VO2) of the kidneys, the blood oxygen saturation obtained from a central venous catheter is usually slightly higher than that obtained from a PA catheter. MVO2 is sometimes used as a surrogate for global perfusion; falling MVO2 is frequently associated with hypovolemic shock and worsening tissue perfusion.23 A rise in MVO2 above baseline may represent decreased VO2 such as in sepsis or poisoning. Central venous catheters that have an oximetric tip can measure the saturation of blood at the tip of the central venous catheter or ScvO2. This allows another surrogate measure of global perfusion on a continuous basis. Combination of the oximetric CVP catheter data and the stroke volume variation from arterial line catheter waveform analysis data in a commercially available monitor can allow continuous estimates of cardiac output, SVR, and stroke volume without the use of a PA catheter.24 Initial validation studies of one system (FloTrac/ Vigileo) were disappointing, but better results may be obtained with improved software.25

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25–30%, are major therapeutic changes. Since there is less experience available in interpretation of PA catheter data for trainees in critical care, courses and online training are available that allow interpretation of simulated data to improve understanding of PA catheter data. A useful tool that can help validate the data obtained with the PA catheter at insertion and at intervals thereafter is the use of echocardiography.

■ Echocardiography Echocardiography has been available in the ICU for years, usually as a service performed by the hospital’s cardiology service. The formal transthoracic echocardiogram (TTE) can be invaluable in determining the function and structure of the heart as well as the health of its components including valves and chambers. Patients in the operating room undergoing major procedures such as coronary artery bypass grafting or liver transplantation and patients with major trauma procedures are frequently monitored using transesophageal echocardiography (TEE). TEE has been used in the ICU to provide excellent visualization of the heart and its functions as well as detection of such injuries as blunt aortic rupture (see Chapter 26).30,31 However, frequent use of TEE in the ICU is usually limited due to the availability of the devices, cleaning requirements, and the skill required by the operator. Repeated measurements with the TEE are usually impractical for these reasons. However, there are now FDA-approved TEE devices using a disposable probe that can be left in the esophagus and stomach for up to 72 hours that allow for repeated measurements. This can permit observation of ventricular function and ejection fraction over time, and may have a safety advantage over PA catheters. The increasing utilization of ultrasonography by critical care clinicians now means many North American ICUs have clinician-performed ultrasound available. This has led to a number of studies and protocols utilizing a limited TTE by noncardiologists in trauma and critical care patients who may be too hemodynamically unstable to wait for formal TTE. In a patient who is hypotensive with an unclear etiology, visualization of ventricular size and function can be very useful in determining whether shock has a hypovolemic or cardiogenic origin. Limited TTE can also detect such conditions as pneumothorax and pleural effusions. However, in about 50% of trauma patients it is difficult or impossible to perform a complete TTE exam due to issues such as chest trauma, subcutaneous air, obesity, and dressings. Despite this, clinicians often attempt limited TTE in patients with hypotension or during cardiac arrest, due the utility of visualizing cardiac motion in successful examinations. Simplified protocols such as the “focus assessed transthoracic echo” (FATE) or the “bedside echocardiographic assessment in trauma/critical care (BEAT)” can be utilized by trauma and critical care physician to rapidly determine the cause of hemodynamic instability.

■ Other Monitoring Modalities Gastric Tonometry Gastric tonometry is one of the few modalities utilizing a direct measurement of gut perfusion as end point in resuscitation.

The rationale for measuring the intramucosal pH (pHi) is based on the observation that splanchnic perfusion can be impaired in the setting of adequate blood pressure and cardiac output, leading to impaired GI mucosal barrier function that may induce multiple organ dysfunction (see Chapter 61). The catheter used resembles an NG tube with a saline-filled silicone balloon at the tip. When the balloon is in contact with the stomach wall, oxygen and carbon dioxide in the saline-filled balloon will equilibrate with oxygen and carbon dioxide in the stomach mucosa. Measurement of the pCO2 of the saline in the balloon allows determination of pHi via the Henderson– Hasselbalch equation. Gastric tonometry has not demonstrated a clear advantage compared with conventional resuscitation end points and its use has not been widely adopted.32,33

Bioimpedance Transthoracic impedance, also known as bioimpedance cardiography, as a method to continuously measure cardiac output has been evaluated for decades. A high-frequency, low-alternating electrical current is applied to the thorax, and changes in bioimpedance to this current are related to cardiac events and blood flow in the thorax. The technique has been refined by looking at differing algorithms and different parts of the signal such as electrical velocimetry, phase, or frequency. However, results of studies have led to conflicting and inconclusive results, which may lead to inappropriate clinical interventions. As a result, transthoracic impedance has not yet been widely adopted as a method to measure cardiac output in noninvestigational settings. A new device is available that utilizes impedance electrodes on the outside surface of an endotracheal tube.34 This allows impedance measurements in the trachea immediately adjacent to the aorta. This has had promising results in initial studies in cardiac surgery patients.

NIRS Near-infrared spectroscopy (NIRS) is a noninvasive technique in which a probe utilizing near-infrared light is applied to the thenar eminence. This allows detection of the tissue oxygen saturation (StO2) of the muscle of the thenar eminence. Decreased StO2 correlates with increased mortality and organ failure in patients with hemorrhagic shock or sepsis.35

■ Hemoglobin Therapies Transfusions Blood transfusions independent of shock or injury/disease severity are associated with worse outcomes. Increased infection, multiple organ dysfunction, and mortality are correlated with the amount of blood transfused and pH of transfused blood. Blood transfusions are common in the ICU with 40–45% of critically ill patients receiving an average of 5 U of packed red blood cells. Lowering target hemoglobin from 10–12 to 7–9 g/L was associated with improved outcomes in ICU patients in the Transfusion Requirements in Critical Care (TRiCC) study.36 In a medical population, the trial by Rivers et al. found a 30% relative survival advantage for a bundle of interventions, including inotropes and transfusion to maintain

Principles of Critical Care

Erythropoiesis-Stimulating Agents (ESAs) The anemia of critical illness resembles that of chronic inflammatory disease; low circulating erythropoietin levels are found in critical illness and are thought to be one of the causative factors. Although epoetin alfa and darbepoetin alfa, ESAs, have been widely accepted for the indication of anemia due to chronic kidney disease, these agents are also attractive for anemia of acute critical illness as they may allow more rapid restoration of hemoglobin levels without transfusion. However, the optimal hemoglobin targets and dosing have not been established and clinical trials have used target hemoglobins higher than those suggested by TRiCC. The Normal Hematocrit Study used larger doses of epoetin alfa to increase hematocrit to 42  3% or to continue epoetin alfa therapy to maintain a hematocrit value of 30  3%; the trial was stopped early due to 1.3 times increased mortality and nonfatal myocardial infarction in the 42  3% hematocrit group.40 Increased adverse outcomes have been seen in subsequent ESA trials, the Correction of Hemoglobin and Outcomes in Renal Insufficiency (CHOIR) trial, using a target of 13.5 g/dL, and the Trial to Reduce Cardiovascular Events with Aranesp Therapy (TREAT) at a 13.0 g/dL target.41,42 CHOIR was halted at an interim analysis when mortality reached 17.5% of patients in the high-hemoglobin group and in 13.5% of patients in the low-hemoglobin group (hazard ratio, 1.34; 95% CI, 1.03–1.74; P  .03). TREAT showed no increase in mortality but there were significant increased risks of fatal and nonfatal stroke and thromboembolic complications. Studies of ESAs in critical illness have sometimes shown a reduction in need for transfusions. The EPO-1 pilot study (n  160) demonstrated a reduction in red blood cell transfusion and a rise in hemoglobin with epoetin alfa treatment using a dose of 300 U/kg per day for 5 days and then every other day.43 The follow-up study (EPO-2, 1,302 patients), using a significantly lower dose of epoetin alfa (40,000 U per week), confirmed the transfusion findings.44 A third randomized study (EPO-3, 1,460 patients) was performed using a weekly epoetin alfa dose of 40,000 U in

which the primary outcome was again transfusion reduction.45 No transfusion reduction was identified with epoetin alfa treatment in this third trial, although hemoglobin concentration did rise. A subsequent subset analysis of the trauma patients in the EPO-2 and EPO-3 studies suggested there was approximately a 50% reduction in 29-day mortality.46 There is no clear consensus on ESA dosing in trauma patients. A multicenter study in anemic (Hb 12 g/dL) ICU patients (n  60) examined six different dosing regimens, intravenous or subcutaneous for epoetin alfa administered for a duration of 15 days.47 Only 30 patients were evaluable. Erythropoietin serum concentrations were 10–45 times greater for intravenous compared with subcutaneous dosing. Mean absolute reticulocyte count peaked on day 11 or 15, and absolute reticulocyte count was greater for subcutaneous dosing, but the pharmacokinetics did not predict pharmacodynamic response in these anemic critically ill patients. More frequent administration of lower doses of epoetin alfa was not superior to less frequent administration of larger doses, but the total cumulative doses of epoetin alfa were similar in all groups (120,000–170,000 IU). This would suggest that subcutaneous, weekly dosing is as effective as other regimens, although the optimal dosing regimen and route of administration of ESAs in critically ill patients for the treatment of anemia are yet to be determined. Optimal response to ESAs may not be achieved in the presence of relative iron deficiency, which is common in ICU patients. Concomitant iron administration has been recommended with ESAs. Overall the benefits of ESAs appear to be related to a reduced need for transfusion rather than an improvement in other outcomes. A retrospective study of a revised trauma practice guideline for anemia after deletion of ESAs showed a significant cost reduction and no increase in blood product utilization.48

NEUROLOGIC MONITORING One of the principal indications for admission to the ICU for trauma patients is in need for frequent neurologic assessments in those with known or suspected traumatic brain injury (see Chapter 19). There are two goals for monitoring traumatic brain injury: one, the avoidance of secondary brain injury by avoidance of hypoxia and hypotension and maintenance of cerebral perfusion; and second, the detection of increased intracranial pressure (ICP) due to posttraumatic phenomenon such as cerebral edema or expanding intracranial hematomas. The neurologic assessments are composed of the Glasgow Coma Scale for assessment of the verbal, motor, and ocular responses in association with pupillary exam. Patients with coma and patients requiring sedation and ventilation require frequent assessment of brainstem reflexes. Reassessment is done frequently as even subtle changes may herald increases in ICP or cerebral ischemia.

■ Intracranial Pressure Monitoring ICP monitoring with a ventriculostomy catheter or through a subdural bolt is a common practice in most major centers for patients who have neurologic exam that is unavailable or unreliable following traumatic brain injury. The Brain Trauma

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a central venous oxygenation of 70%.37 Based on this, the “Surviving Sepsis” guidelines currently recommend to “transfuse packed red cells if necessary to hematocrit of 30%.”38 However, the TRiCC guidelines have been more recently reaffirmed by a guideline from the Eastern Association for the Surgery of Trauma and Society of Critical Care Medicine (EAST-SCCM), referring to multiple studies that failed to find physiologic benefit from red cell transfusion in septic patients.39 The EAST-SCCM guidelines do support aggressive, empirical transfusion in trauma and other surgical patients with uncontrolled hemorrhage. A general approach to transfusion is that patients with hemorrhage need transfusion, while those who are not bleeding infrequently require immediate transfusion. In the trauma bay, operating room, and ICU, red blood cells are often the most available and effective initial resuscitation fluid, and prudence suggests a liberal transfusion strategy until anatomic hemorrhage control is achieved and laboratory values stabilize. Coagulopathy associated with trauma and massive transfusion may require the early ministration of plasma at a 1:1 ratio with packed red cells (see Chapter 13).

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Foundation Guidelines recommend early and aggressive monitoring of ICP and the calculated cerebral perfusion pressure (CPP), which is the difference between the mean arterial pressure (MAP) and ICP.49 Monitoring of the ICP and CPP can be used to guide therapy such as vasopressors or opening the ventriculostomy catheter to drainage and to provide surveillance for increasing cerebral edema or intracranial hemorrhage. ICP monitoring in a large population of traumatic brain injury patients was found to improve survival versus those who did not receive ICP monitoring despite a higher severity of injury in the ICP-monitored group, 51% versus 35%.50 Investigational noninvasive monitoring systems for ICP include transocular ultrasound monitoring of optic nerve sheath diameter (ONSD).51,52 The optic nerve sheath is an extension of the intracranial dura matter and has been shown to become distended with elevated ICP. Continuous transcranial Doppler ultrasound monitoring of cerebral vessels is another investigational approach for ICU monitoring of traumatic brain injury.

NUTRITIONAL MONITORING Current guidelines indicate the need for nutritional assessment and monitoring for patients admitted to the ICU (see Chapter 60). Enteral nutrition, which may help preserve gut mucosal barrier function, is the preferred approach. Nutritional monitoring should begin with an assessment of the degree of preinjury malnutrition as well as current requirements. Weekly assessments in the ICU should include a calculation of nitrogen balance; this calculation takes a difference between excreted nitrogen from a 24-hour urine urea nitrogen and the ingested nitrogen. An overall goal is to have the patient had a 2–4 g positive nitrogen balance if possible. Indirect calorimetry (metabolic cart) provides an assessment of caloric requirements and metabolic rate. It may be significantly more accurate than predictions based on formulae such as the Harris–Benedict equation.53 This technique uses the rate at which gases are produced in the intubated patient to estimate caloric expenditure. The device calculates VO2 and carbon dioxide production (VCO2). Standard metabolic carts requiring an integral mechanical ventilator were intended for intermittent use; however, newer devices can be used with standard ventilators with an adapter that can then continuously sample end-tidal oxygen and carbon dioxide. CO2 and pCO2 can be used to then determine the respiratory quotient (RQ) and caloric needs can be estimated. The RQ can also be used to determine the prominent nutritional substrate being used, excess carbohydrates leading to RQs of 1.0 or more, with RQs below 0.8 indicating possible excess lipid utilization.

TIGHT GLYCEMIC CONTROL IN THE ICU Hyperglycemia with or without insulin resistance appears to be a common phenomenon in the critically ill patients. Based on literature that indicated outcomes were improved if blood sugars were maintained below 215 mg/dL, van den Berghe et al. hypothesized that hyperglycemia leads to worse outcomes in a critically ill population.54 In their prospective randomized

controlled trial, their group demonstrated that tightly controlled blood glucose levels (at or below 110 mg/dL) with intensive insulin therapy improved mortality and reduced complications such as infection rate, multiorgan failure rate, ventilator days, and morbidity. The adverse consequences of hyperglycemia may be associated with even worse mortality in trauma patients. A retrospective analysis of 12 years of data on trauma and on trauma patients showed that hyperglycemia in trauma patients correlated with higher mortality rates than in other surgical patients.55 The intensive insulin regimen initially proposed by van den Berghe et al. has been associated with increased hypoglycemic complications and lack of benefit in subsequent multi-institutional studies such as VISEP, GLUCONTROL, and Normoglycemia in Intensive Care Evaluation Survival Using Glucose Algorithm Regulation (NICE-SUGAR).56–58 The NICE-SUGAR trial showed the primary outcome variable of 90-day mortality was actually increased in patients randomly assigned to intensive insulin therapy, as compared with an intermediate target range for blood glucose. Improved glucose control is still a guideline used in most major centers; however, a less intensive insulin protocol than that suggested by van den Berghe et al. may be prudent in avoiding the likelihood of severe hypoglycemia.

ADRENAL INSUFFICIENCY The normal response to physiologic stress leads to increased levels of tissue corticosteroids; this is also seen in the patient’s response to critical illness. Failure to recognize and treat adrenal insufficiency has been associated with increased mortality. Normal corticosteroid response can be impaired in a variety of conditions including sepsis, systemic inflammatory response syndrome (SIRS), and traumatic brain injury. The use of steroid therapy in sepsis and critical illness has been a topic of an extensive literature and pendulum has swung between apparent benefit and apparent risk. Identification of patients with acute adrenal insufficiency can be difficult; random cortisol sampling (15 μg/dL) and corticotropin stimulation tests (15–34 mg/dL) were often used to identify patients suitable for low-dose steroids (100–300 mg per day hydrocortisone). Patients with abnormal stimulation tests (increases 9 mg/dL) were felt to require corticosteroid supplementation. While a 2002 study by Annane et al. suggested benefit to low-dose steroids in sepsis, the 2008 multi-institutional CORTICUS trial did not show any 28-day mortality benefit with 300 mg per day of hydrocortisone in patients with septic shock, either overall or in patients who did not have a response to corticotropin.59,60 However, hydrocortisone did hasten reversal of shock in CORTICUS study patients. Lacking adequately powered positive studies, low-dose steroid therapy should probably be limited to patients with septic shock whose blood pressure is poorly responsive to fluid resuscitation and vasopressor therapy. Corticotropin stimulation probably has no role in determining steroid use in patients with septic shock. Steroids should be discontinued if the patient does not respond to treatment given the potential risks of infection, hyperglycemia, and critical illness polyneuropathy (CIP).

Principles of Critical Care

INFECTIOUS MONITORING AND SURVEILLANCE

MECHANICAL VENTILATION: GENERAL PRINCIPLES The need for mechanical ventilation is the most common indication for admission to the ICU. Familiarity and advanced understanding of mechanical ventilation principles is the lynchpin to managing severely injured patients in the ICU. Ventilator management can change rapidly; therefore, a nucleus of critical care expertise is needed not only to optimize respiratory support but also to interpret acute changes in pulmonary mechanics that can often be a harbinger of systemic physiologic pathology.

TABLE 55-3 Noninfectious Sources of Fever in Critical Illness Rhabdomyolysis SIRS/sepsis syndrome Adrenal cortical insufficiency Pheochromocytoma (rare) Drug fevers Transfusion reaction Malignant hyperthermia Malignant neuroleptic syndrome Pancreatitis Burn injury Pulmonary embolism/DVT Alcohol and drug withdrawal CNS hemorrhage

Providing a secure airway via endotracheal intubation generally happens early during the initial resuscitation. Even though intubation for airway security can be secondary to ventilatory insufficiency, the two can be mutually exclusive. The general principles for intubation and mechanical ventilation are the following: 1. 2. 3. 4.

Secure and establish an airway Decrease the work of breathing (WOB) Improve oxygenation Improve ventilation (CO2 gas exchange) and maintain control of PaCO2 especially in acute brain injury 5. Anticipate worsening respiratory status or airway patency such as the need for large-volume resuscitation, severe neck/thoracic trauma, upper torso/facial burns, and inhalation injury Since the development of modern ventilatory support in the 1960s, significant technological advancements have been made to improve the ventilators themselves. Using contemporary ventilator technologies, new modes of mechanical ventilation are often introduced, each with an acronym and specific terminology. Despite these advancements, the essential physical principle of mechanical ventilation remains constant, which, simply put, is pushing oxygen-rich air into the lungs by positive pressure and removal of waste CO2 by negative pressure. Understanding this fundamental principle simplifies even the most “advanced” modes of ventilation and therefore allows the surgeon a streamlined method to manage complex ICU patients with clarity and an evidence-based approach.

MONITORING OF GAS EXCHANGE Rapid assessment of arterial oxygen tension (PaO2) is essential for both evaluating and managing the adequacy of alveolar– arterial oxygen gas exchange. Oxygen is driven from the alveolar airspace into the pulmonary capillaries primarily due to the difference in the O2 diffusion gradient between the respective tissue beds. Measuring PaO2 quickly and reliably from arterial

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Mortality after trauma in the ICU is often attributed to infection. Infections are thought to contribute to more than 88,000 ICU deaths annually in the United States.61 Infectious complications of major injury (see Chapter 18) may be due to the results of the injury itself (e.g., open fractures), as a result of complications of treatment (e.g., anastomotic leak), or as iatrogenic complications of critical care management (e.g., ventilator-associated pneumonia [VAP], central line infection). Specific monitoring for infections will depend on injury type and severity, types of interventions performed, and the duration of postinjury critical illness. Regulatory authorities have recently mandated surveillance cultures on admission to the ICU for certain health care–associated infections (HAIs) such as nasal swabs for methicillin-resistant Staphylococcus aureus (MRSA), which is required in some states. In a study using multiple regression analysis, the most common variables for infection were found to be central venous catheters, mechanical ventilation, chest tubes, and trauma with open fractures.62 Patients at risk for infectious sequelae should be routinely tested by culture and examined for clinical indications such as fever, leukocytosis, change in physical examination, pyuria, and development of purulent sputum or new infiltrate on chest x-ray. HAIs such as central line–associated bloodstream infection (CLABSI) may have standardized definitions in some jurisdictions and regulatory requirements for surveillance. Other HAIs such as VAP may require adoption of a local or institutional standard definition and therapy in the lack of a national consensus. The decision to start presumptive (empirical) antibiotics should be based on risk factors, the expected sequelae of injury, and prior infections. Presumptive treatment should be started, if indicated, at defined end point for culture-negative patients and applied and reviewed with sensitivity- and spectrum-based adjustment when final culture information is available. Importantly, all critically injured trauma patients with unexplained fevers do not require antibiotics. Persistently febrile, culture-negative patients often present a difficult diagnostic and therapeutic challenge. Fever in these patients may have a noninfectious origin (Table 55-3) or be due to occult infection that has not been considered, successfully cultured, or has no identifiable signs or symptoms. Fungal sepsis should be considered in patients with prolonged ICU stays, multiple prior antibiotic therapies, and immunosuppression.

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blood gas samples may be taken for granted in modern ICU care. The physical basis for measuring PaO2 is a result from the development of the oxygen electrode and measuring resultant electrical current that is directly proportional to oxygen concentration.63 Calculating the efficiency of pulmonary oxygen exchange can be cumbersome since the equation for the A–a gradient requires alveolar and arterial CO2 concentrations, shunt fraction, water vapor pressure, and body temperature. A more convenient and simple bedside index of oxygen exchange is the PaO2/FiO2 (P/F) ratio that adjusts for a fluctuating FiO2 and helps in defining lung injury (see below). The use of pulse oximetry to determine arterial oxygen saturation (SaO2) has replaced continuous arterial blood gas measurements as a realtime, noninvasive method to assess arterial oxygenation.64 There are limitations to SaO2 and its nuances are important in interpreting the significance of an absolute SaO2 percentage. First, because of the kinetics of oxygen–hemoglobin binding, SaO2 and the oxygen dissociation curve is sigmoidal and not linear. Therefore, small changes in SaO2 may reflect a much larger drop in PaO2. Second, under instances of carbon monoxide poisoning or severe circulatory shock, oxygen delivery will be abnormally low despite a near-normal SaO2. Finally, SaO2 is not indicative of ventilation. A rising PaCO2 and subsequent acidosis may not initially affect SaO2 especially if a patient is on high FiO2 settings. For these reasons, it is important to interpret SaO2 in combination with appropriate PaO2 measurements to individually determine a patient’s ability for oxygen exchange.

MONITORING VENTILATION Adequate pulmonary exchange, exhalation of CO2, and resultant arterial CO2 tension (PCO2) have important physiologic and clinical implications. The immediate detection of CO2 through disposable endotracheal capnography relies on the lower pH of EtCO2-rich air changing the color of pH-sensitive filter paper in the capnograph. As a rule, a disposable capnograph remains purple if EtCO2 is 0.5%, whereas a yellow color change is equivalent to EtCO2 of 2.0%.65 Normal EtCO2 is 4%; therefore, capnography turns yellow when the endotracheal tube is positioned correctly. The accuracy of this device is very sensitive unless the patient is in circulatory arrest and adequate pulmonary perfusion is compromised. The presence of a large volume of acidic gastric contents may also give a false impression of successful endotracheal intubation even though it is the esophagus that has been intubated. In these circumstances, initial detection of EtCO2 decreases rapidly with subsequent tidal volumes. Clogging of the capnograph with mucous and enteric contents can also give false readings. The measurement of PCO2, through blood gas analysis, remains the most accurate measure of assessing ventilation. Continuous capnography analyzes EtCO2 and, depending on the alveolar–arterial gradient, can give an indication of the arterial PCO2. After anatomic dead space has been cleared, EtCO2 rises until the end of exhalation. This rise is generally steep but plateaus during the alveolar phase of ventilation. In patients without preexisting pulmonary disease, the normal alveolar– arterial gradient is between 1 and 3 mm Hg. Therefore, using

continuous capnography in a ventilated patient estimates the patient’s PCO2 especially during the initial resuscitation phase. Utilizing capnography can be helpful particularly in brain injury where hyperventilation may curtail rising ICP. However, EtCO2 measurements are affected by pulmonary dead space fraction and pulmonary perfusion that can be greatly altered in cases of hemorrhagic shock, thoracic trauma, and increased airway resistance. Warner et al. performed a prospective study of 180 freshly intubated trauma patients and correlated EtCO2 measurements with PCO2 from blood gas analysis.66 Using regression analysis, the authors found a direct correlation between EtCO2 and PCO2; however, patients ventilated with an EtCO2 of 35–40 mm Hg were likely to have a PCO2 40 mm Hg 80% of the time, and a PCO2 50 mm Hg 30% of the time. In severely injured patients, where an increase in pulmonary shunt may exist, appropriate confirmation of EtCO2 by blood gas sampling is important. Causes of hypoventilation can be multifactorial. Severe thoracic injury resulting in pulmonary contusion or flail chest can be a factor warranting expedient intubation. Increased dead space from pulmonary contusion, ALI, acute pulmonary embolism, and oversedation can be contributing factors causing hypercapnia especially during the weaning phase of mechanical ventilation.

ASSESSMENT OF LUNG MECHANICS AND INSPIRATORY/EXPIRATORY PRESSURE The mechanically ventilated lung is an active continuum that reflects real-time physiologic complexities of an ICU patient. Assessing specific pulmonary mechanics can significantly aid in diagnosing and treating a patient’s sudden or progressive pulmonary insufficiency. One of the most important parameters to measure is compliance as is the ability to distinguish between static and dynamic compliance. Compliance, the change in volume produced by a change in pressure, is calculated based on measurements taken from the ventilatory circuit itself. In general, a sudden decrease in compliance will mean a concomitant rise in both plateau pressure and peak inspiratory pressures (PIPs) for a given tidal volume as seen in pneumothorax or in abdominal compartment syndrome. However, measuring the individual changes of either static or dynamic compliance may indicate specific pulmonary pathology.

Static Compliance If the respiratory system is reduced to a simple model of a straw and a balloon, the straw would represent the airway, and its resistance, and the balloon would represent the elastic recoil of the lung and the chest wall. In static compliance, the change of volume produced is measured from the inspiratory hold pressures or plateau pressure using the following formula: Compliancestatic  Volumetidal/Pressureplateau  PEEP. Thereby static compliance measures the pressure resistance of the alveoli and chest wall, not of the airways. Cases of decreased static compliance (normal  50–100 mL/cm H2O) with normal or elevated PIP generally indicate intra-alveolar pathology such as acute respiratory distress syndrome (ARDS), ALI, and pulmonary edema.

Principles of Critical Care

Dynamic Compliance

VENTILATORY CAPACITY

Pressure–Volume Curves A well-accepted principle in mechanical ventilation is the importance of increasing alveolar recruitment to improve oxygenation. Assessment of the pressure–volume curve in mechanical ventilation has been utilized to determine the mean pressure needed for the inflection point, or Pflex (Fig. 55-1). This point, corresponding to the transition between the curve’s flat portion and linear portion during inhalation, represents the critical pressure needed to open collapsed alveoli and corresponds to the zone of optimal alveolar recruitment and gas exchange. Initial driving pressure therefore precedes alveolar filling and corresponds to gas flow within the airways. The pressure reading at the inflection point may reflect an optimal PEEP setting. In healthy lungs with normal compliance, oxygenation and ventilation is achieved with modest PEEP (5 cm H2O) and plateau pressures (Pmax) less than 30 cm H2O. In ARDS, ALI, and pulmonary edema the normal pressure–volume curve is shifted (Fig. 55-1) leading to derecruitment of alveolar units and increasing pulmonary shunt. During these instances, increasing driving pressure and increasing PEEP are often employed to maximize gas exchange in the zone of optimal ventilation. However, using pressure–volume curves alone in clinical decision making has been neither shown to be efficacious nor shown to improve outcomes. There are significant inconsistencies in curve interpretation, which leads to significant operator variability. A standardized method of pressure curve interpretation may aid in predicting the development of ALI and ARDS.

Assessing ventilatory capacity in the mechanically ventilated patient can be an important physiologic indicator to monitor clinical improvement and predict successful extubation. Its use is particularly applicable in patients who have been intubated for prolonged periods of time, have spinal cord injury or injury to the thorax such as flail chest or rib fractures, or patients with neuropathic disease (i.e., Guillain–Barré syndrome, myasthenia gravis). A forced vital capacity (FVC) and a negative inspiratory force (NIF) are the most frequent measured indices of ventilator capacity. A normal vital capacity, which consists of both inspiratory capacity and expiratory reserve, is between 65 and 75 cm3/kg depending on ideal body weight and sex. An FVC of 10–15 cm3/kg is an acceptable value to predict successful extubation.67 The NIF, in conjunction with FVC and the rapid shallow breathing index (RSBI; see below), is also an important variable during weaning. Despite the need for a cooperative and awake patient, the NIF estimates inspiratory muscle strength using a one-way valve manometer attached to the airway. The inspiratory force is then calculated based on the negative force generated by the patient during occlusion of the valve. A value of 25 to 30 cm H2O is indicative of adequate inspiratory force to maintain airflow after extubation.67 Despite estimating ventilatory capacity and other respiratory parameters, there exists great variability in practice in when and how parameters are determined. In a survey of nine Los Angeles area ICUs, Soo Hoo and Park found significant variability in the method and frequency of both NIF and FVC measurements. This study only further underscores the notion that current weaning practice is just as much art as science.68

VENTILATOR-INDUCED LUNG INJURY It is well established that high airway pressures during positive pressure ventilation can cause lung injury secondary to overdistension and alveoli rupture (see Chapter 57).69 Ventilatorinduced lung injury can be delineated into mechanical and

Pmax B

Pflex

A

Pressure FIGURE 55-1 Pressure–volume curves.

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Dynamic compliance measures compliance by equating the pressure, PIP, needed to overcome the resistance of the airways or the straw using the balloon analogy (Compliancedynamic  Volumetidal/PIP  PEEP). Cases of a sudden decrease in dynamic compliance or a measured difference between static and dynamic compliance are a reflection of increased airway resistance during bronchospasm, mucous plugging, kinked endotracheal tube, or foreign body aspiration.

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inflammatory categories since these processes differ in their pathophysiology and treatment. Repetitive distention and collapse of lung tissue from mechanical ventilation is the basic mechanical pathophysiology that is thought to cause ventilator-induced lung injury from inflammatory changes. Pathologic features of ventilator-induced lung injury include edema and an upregulation of inflammatory cytokines and cells, the combination of which can further damage pulmonary tissue and progressively lead to pneumonia and sepsis. Webb and Tierney conducted the first comprehensive study in rats demonstrating that 1 hour of positive pressure ventilation, with peak pressure at 30 cm H2O or higher, caused pulmonary edema.70 Several other experiments also show pulmonary edema with a progressive increase in inflammatory cytokines, such as IL-1, TNF-α, and IL-8, following mechanical ventilation, although larger animals and humans require longer periods of intubation for these inflammatory changes to occur.71 Given these initial experimental observations, several human studies were initiated with the intent to demonstrate that decreasing alveolar stretch by lower tidal volumes will prevent ongoing lung injury and improve ICU outcomes. A detailed description of current ventilating modalities used in the management of ARDS is beyond the scope of this chapter (see Chapter 57).

VENTILATORY MODES Spontaneous breathing utilizes negative intrathoracic pressure to fill alveoli (Fig. 55-2). In contrast, mechanical ventilation utilizes the principles of external insufflation generating positive pressure to fill alveoli and negative pressure for exhalation. Positive pressure mechanical ventilation can improve gas exchange by recruiting atelectatic alveoli, increasing functional residual capacity, and improving areas of ventilation/perfusion mismatch, and thereby decreases pulmonary shunt fraction. Negative effects of mechanical ventilation vary according to ventilatory mode; however, adverse effects common to all

positive pressure modes include barotrauma, ventilator-induced lung injury, and impairment of cardiac output from decreased venous return. As previously mentioned, the physical simplicity of mechanical ventilation is often lost within the technical jargon of individual ventilator modes. It is important to assess the physical mechanics behind each mode of ventilation since correct management of ventilated patients will decrease total ventilation days and improve patient outcome. In choosing which mode of ventilation is best suited for a particular patient, it is helpful to evaluate the patient’s current oxygenation, ventilation, pulmonary compliance, muscular strength, and mental status.

CONTINUOUS MANDATORY VENTILATION AND ASSIST-CONTROL MODE VENTILATION Both continuous mandatory ventilation (CMV) and assistcontrol (AC) mode ventilation are preset volume-cycle modes that deliver a fixed tidal volume at a specific respiratory frequency. The individual names of these modes are commonly referenced interchangeably; however, CMV delivers a set tidal volume exclusive of a patient’s ventilatory effort, whereas AC, in addition to a set frequency, synchronizes a set tidal volume with each patient-initiated breath. During a patient-initiated breath in CMV mode, the ventilator will not provide support or, conversely, a full tidal volume may be delivered if the patient is spontaneously exhaling. Consequently, an awake and breathing patient will have episodes of respiratory dyssynchrony causing significant discomfort, breath stacking, and barotrauma.72,73 Given these reasons, CMV mode should rarely be used. In AC, the ventilator recognizes a patient-triggered breath (either flow or pressure mediated) and immediately delivers a synchronous, identical preset tidal volume accordingly (Fig. 55-3). To assure appropriate synchrony, the ventilator must sense the patient’s spontaneous effort to trigger tidal volume delivery. In older ventilators, a “pressure trigger” mechanism relied on pressure sensors that were activated by negative inspiratory

Spontaneous

Inspiration

Expiration

Pressure

1016

Time FIGURE 55-2 Spontaneous breathing mode of ventilation.

Principles of Critical Care

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A/C

Pressure

Time FIGURE 55-3 Assist-control mode ventilation.

pressure generated by a patient breath. Most modern ventilators are now “flow triggered” where a continuous flow of gas passes around the breathing system. Patient inspiration deflects this flow, and triggers the ventilator to deliver a full tidal volume. AC modes have a background set rate to assure ventilation in an apneic, paralyzed, or heavily sedated patient. If under these circumstances patients do not initiate breathing, AC becomes indistinguishable from CMV since there is complete absence of patient-triggered breathing. In an awake or lightly sedated patient, full synchronous respiratory support will be achieved with each initiated breath, thereby decreasing WOB and assuring adequate ventilation. It is important that there is consistent evaluation of patients on AC. Awake or agitated patients may trigger several full tidal volume breaths causing high minute ventilation and respiratory alkalosis. In a prospective analysis of intubated patients, Sternberg and Sahebjami showed AC to have significantly higher peak airway pressures compared with the same patient on a pressure support mode, although during AC there was a decreased incidence of hypoxia and tachypnea.74 It is important to frequently assess a patient’s ability to transition from AC to a pressure support mode with the goal of eventually weaning from mechanical ventilation.

PRESSURE-REGULATED VOLUME CONTROL VENTILATION Excessive airway pressures (50 cm H2O) can increase the incidence of barotrauma and lung injury especially in states of decreased pulmonary compliance. Pressure-regulated volume control (PRVC) ventilation is a relatively new ventilatory mode that modulates the inspiratory flow pattern during a volume-controlled breath, thus attenuating and limiting PIP. This flow pattern, coined “decelerating inspiratory flow,” is in contrast to pure AC/CMV modes where there is constant inspiratory flow resulting in a continuous rise in airway pressure. Despite the theoretical advantage, few studies have

shown any clinical benefit with PRVC in the adult population. In a small study of ARDS patients, Guldager et al. showed that PRVC mode had mean PIPs of 20 cm H2O compared with 24 cm H2O under volume control; however, there was no difference in mortality or days of ventilation between each group.75

SYNCHRONOUS INTERMITTENT MANDATORY VENTILATION (SIMV) SIMV allows for spontaneous ventilation with the addition of intermittent volume-controlled breaths determined by a preset rate and tidal volume (Fig. 55-4). The “synchronous” component allows the ventilator to detect patient-initiated negative inspiratory flow and accordingly times delivery of a preset tidal volume, thus preventing breath stacking and patient discomfort. In contrast to AC ventilation, where each patient-initiated breath receives a full tidal volume, SIMV mode allows for respiratory work between the preset tidal volumes. The degree of ventilatory support can be increased or decreased by adjusting the set rate. This mode was originally developed to wean patients from mechanical ventilation and continues to be a widely used method of stepwise weaning despite evidence that this method has decreased efficacy in comparison to pressure support trials (see Section “Weaning from Mechanical Ventilation”). However, SIMV can be useful to reduce minute ventilation in patients who cannot be transitioned to full pressure support mode yet are significantly overbreathing during AC ventilation causing respiratory alkalosis.

PRESSURE SUPPORT VENTILATION (PSV) PSV, originally termed pressure assist, provides a baseline level of inspiratory airway pressure and decreases the WOB by augmenting spontaneous respiration (Fig. 55-5).76 The patient,

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Patient triggered ventilator breath

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Management of Complications after Trauma

SIMV

Pressure

Spontaneous breathing

Time FIGURE 55-4 Synchronous intermittent mandatory ventilation.

therefore, is aided in overcoming the resistance of the ventilatory circuit and has complete control over the rate, and tidal volume. Each PSV breath is supported by a specific flow limited by a preset pressure that is triggered by patient inspiration. Termination of pressure support occurs when the patient’s inspiratory tidal volume nears the preset pressure limit (usually 25% of preset peak) allowing spontaneous expiration. Thus, each tidal volume varies according to the patient-derived inspiratory effort. Because this mode requires spontaneous breathing, PSV can only be utilized in lightly sedated or awake patients without paralytic therapy or neuromuscular disease. Although PSV can be used as a sole ventilation mode, perhaps the single most important use of PSV is in the process of weaning (see Section “Weaning from Mechanical Ventilation”). Several trials, including the Esteban Spanish Collaborative

study, have shown weaning protocols incorporating lowerpressure PSV mode are advantageous to IMV or high-pressure PSV weaning.77 Intermittent use of PSV with higher set pressures may improve muscle conditioning in chronically ventilated patients. However, data supporting this approach to hasten mechanical ventilation weaning have not been conclusive.

TIME-CYCLED PRESSURE-CONTROLLED VENTILATION (TCPV) As the correlation between higher plateau pressures, excessive peak airway pressures, and ALI/ARDS is increasingly recognized, the limitations of volume-cycled ventilation become apparent in the setting of poor pulmonary compliance. To achieve a specific preset tidal volume, progressively higher airway

PS

Pressure

SECTION 5

Ventilator breath synchronized with patient effort

Time FIGURE 55-5 Pressure support ventilation.

Principles of Critical Care

AIRWAY PRESSURE RELEASE VENTILATION (APRV) APRV, sometimes referred to as bilevel ventilation, is essentially continuous positive airway pressure ventilation with the exception that the pressure setting is generally higher (Phigh) for a longer duration (Thigh) than typical CPAP and there is a short “release” of high pressure (Tlow and Plow) allowing for ventilation and CO2 exhalation. The long duration of Phigh (as long as 6 seconds) is thought to improve alveoli recruitment and gas exchange, similar in concept to TCPV, and decrease overall minute ventilation.78 Perhaps APRV’s greatest benefit is due to the presence of a floating release valve that allows for patients to breathe spontaneously during the prolonged Phigh phase. This, in principle, provides greater patient comfort and decreases the need for sedatives. Few studies have been able to show sufficient evidence supporting this theory. Initially, APRV was heralded as a rescue ventilation mode for severe ARDS/ ALI; however, subsequent studies have not shown APRV to be superior to standard mechanical ventilation protocols. However, if the Phigh setting is appropriate (30 cm H2O in ARDS) and oxygenation/ventilation goals are met, an APRV mode can still relatively adhere to guidelines established by ARDSNet and may benefit individual patients.

HIGH-FREQUENCY OSCILLATORY VENTILATION (HFOV) The largest experience with HFOV has been in neonatal patients who present with severe hypoplastic lung disease and a variety of other congenital or acquired pulmonary pathology.

The principle behind HFOV is to optimally utilize open airways and literally “oscillate” air within open alveoli to provide gas exchange. This process is theorized to prevent lung injury by reducing the repetitive opening and closing of airways and alveoli. The mechanics of the HFOV ventilator utilizes a piston assembly structure and an electronic control magnetic motor that provides the rapid frequency for oscillation. The frequency of oscillation (1 Hz  1 breath/s  60 breaths/min) can be adjusted to achieve a patient’s pulmonary requirement. Adjusting oscillation varies inspiratory time, mean airway pressure, and ultimately gas exchange. It is recommended that the lung be optimally recruited before beginning HFOV to maximize open alveoli. Beyond the neonatal population, several studies have shown moderate efficacy of HFOV improving oxygenation in severe cases of ARDS. Fort et al. initially demonstrated an efficacy and safety profile in 17 patients with severe ARDS.79 In a recent comparison of HFOV to conventional ventilation modes, Bollen et al. failed to show any difference in mortality between the two strategies, although there was slight improvement in initial oxygenation on first receiving HFOV.80 Future investigations will be needed to determine the utility and practicality of HFOV in ALI and ARDS.

ADJUVANT THERAPIES IN RESPIRATORY THERAPY Severe respiratory failure can be a daunting task to the ICU team and difficulty maintaining adequate oxygenation, despite attempting various ventilation modes, can at times seem futile. In the past several years adjunct therapies, both mechanical and pharmaceutical, have been evolving, although with variable efficacy.

■ Prone Positioning The concept of prone positioning to improve oxygenation was demonstrated by Douglas et al. in a prospective study of six patients with severe ARDS.81 Poorly or nonaerated lung units localize in the dependent lung zones while in the supine position. Prone positioning may improve gas exchange and ventilation/perfusion mismatch by expanding atelectatic portions of the lung akin to the zones of West. One of the largest prospective trials evaluating the efficacy of prone positioning to date randomized 342 patients with moderate and severe ARDS.82 The authors reported that prone positioning did not improve 28-day or 6-month mortality compared with nonprone patients. The prone cohort also had a significantly higher incidence of complications such as hypoxia, need for neuromuscular blockade, loss of vascular access, and endotracheal tube dislodgment. However, some reports suggest that the maximal benefits of prone positioning are only realized when implemented in early ARDS and should be utilized before refractory hypoxia ensues.

■ Pharmacologic Agents Based on promising animal data, inhaled nitric oxide (NO) was quickly introduced to improve hypoxia in severe ARDS. The mechanism is likely related to the relaxation of vascular

CHAPTER 55

pressure must be delivered as lung compliance worsens increasing the likelihood of barotrauma and alveolar damage. In contrast to volume control, TCPV delivers a breath at a fixed flow rate dictated by a preset pressure (driving pressure). Regardless of pulmonary or chest wall elasticity, the PIP is fixed and will not exceed the set driving pressure; however, the delivered tidal volume will vary as a function of changing pulmonary compliance. TCPV is useful in patients with progressive pulmonary insufficiency or ARDS, while also meeting acute respiratory distress syndrome network (ARDSNet) criteria so long as the set driving pressure and PIPs are below 30 cm H2O. Importantly, TCPV is not well tolerated by awake patients and normally requires deep sedation. Under deep sedation, inverse ratio ventilation (IRV) can also be used with the goal of increasing oxygenation. In conventional AC/CMV mode the inspiratory to expiratory ratio is approximately 1:2, thereby minimizing airway pressures and allowing adequate ventilation. Typically IRV allows I:E ratios 1.5:1 to 2:1 achieved by inspiratory flow rates and decelerating flow patterns dictated by the set diving pressure. In principle, IRV allows maximal recruitment of alveoli by expanding marginal airspaces. Beyond the theoretical short-term advantage, few existing studies show any benefit in mortality or long-term ventilatory improvement versus conventional ventilation. When using IRV, it also is important to be cognizant of rising intrinsic PEEP that can lead to barotrauma or a progressive decrease in cardiovascular return effecting cardiac output.

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SECTION 5

smooth muscle in the lung, thereby improving shunt fraction and optimizing the ventilation/perfusion ratio.83 Clinical trials, however, have shown NO therapy to have limited improvement in oxygenation and no significant difference in mortality except possibly in the pediatric population. Other early promising pharmacologic therapies for ARDS, including sildenafil, corticosteroids, and exogenous surfactant, have not been shown to be consistently efficacious.

TABLE 55-4 Factors Contributing to Respiratory Failure Physiologic Factors Thoracic injury

Abdominal injury

WEANING FROM MECHANICAL VENTILATION Managing and weaning a patient from mechanical ventilation is highly variable where the duration and success of weaning is completely dependent on each specific clinical scenario. Some patients are weaned and extubated within hours; others may take weeks to months. It is additionally important to separate the principles of weaning from extubation despite the fact that the terminology is used interchangeably. Weaning is best described as the physical transition and liberation from mechanically assisted ventilation to patient physical autonomy responsible for moving air into and out of the lungs. The process of weaning is not standardized, and various ICUs approach weaning through a variety of methods that often times lack empirical support. As a set of general principles: (1) weaning should be considered early in the course of a ventilated patient, (2) pressure support weaning or AC mode transitional weaning seems to be the most tolerated, and (3) spontaneous breathing trial is the best diagnostic test to assess progress of weaning. Several factors influence successful weaning including the type of injury sustained, preexisting medical problems, patient toxicology, comorbid or preinjury conditions, and the general state of health. When ventilatory reserve and requirements are exceeded by WOB requirements, patients are considered to be in ventilatory failure and thus mechanical ventilation becomes necessary. It is important to delineate contributing factors leading to respiratory failure since efforts at weaning should be targeted to these conditions to decrease WOB and improve ventilatory capacity (Table 55-4).

Spinal cord injury

Excessive agitation/ anxiety

Decreased pulmonary compliance Increased airway resistance

Refractory hypoxia

Hypercapnia

Malnutrition/ metabolic considerations Cardiac insufficiency

Causes Pain, disruption of chest wall stability (flail chest), large hematomas, persistent pneumothorax/hemothorax Pain, disruption of abdominal accessory muscles, abdominal hypertension or compartment syndrome, ascites Loss of diaphragm and accessory motor strength, loss of airway protection capacity Inappropriate sedation or analgesia, post-TBI effects, acute alcohol or drug withdrawal, sepsis ARDS/ALI, edema, pulmonary fibrosis, empyema, severe pneumonia Bronchospasm, endotracheal obstruction or narrowing, mucus plugging of airway or bronchioles Pneumonia, pulmonary emboli, ARDS/ALI, sepsis, barotrauma, pneumothorax/hemothorax, decreased cardiac output Sepsis, overfeeding syndrome, inadequate weaning parameters or settings Persistent catabolic state, respiratory muscle atrophy, electrolyte abnormalities, pulmonary edema Decreased cardiac output (MI, blunt contusion, preexisting disease) causing hypoxia or pulmonary edema

WORK OF BREATHING The concept of WOB is a function of the force required to expand the airways, lungs, and chest wall to an appropriate volume in order to meet oxygen and physiologic demands (pressure  volume/time). Excess WOB may be secondary to inappropriate ventilator settings (i.e., ineffective triggering, inappropriate pressure support, decelerating flow rates), increased airway resistance (mucous plugging, bronchospasm), and decreased pulmonary or thoracic wall compliance (pulmonary edema, ARDS, or hematoma). Additionally, increased WOB may also reflect higher CO2 production from sepsis, fever, or overfeeding. These factors increase respiratory rate since a higher minute ventilation is needed to compensate for acidosis. In concept, overfeeding can be monitored and prevented by a metabolic cart that can assess the RQ calculated from CO2 generated divided by O2 consumed. However,

studies supporting the fact that frequent metabolic monitoring improves weaning have been lacking.

VENTILATORY CAPACITY Ventilator capacity encompasses the ability of a patient to generate muscular forces needed to meet the ventilatory work required for physiologic demand. To that end, muscle strength (diaphragm, intercostals, and abdominal musculature) combined with other conditions (spinal injury, CIP, nutritional state, metabolic and endocrine disorders) plays a role in defining a patient’s ventilatory capacity. Significant thoracic trauma, such as severe rib fractures or flail chest, can also limit a patient’s ventilatory capacity. It is also

Principles of Critical Care important to consider the effects of pain, improper analgesia, and recent abdominal surgery when beginning the weaning process as overall ventilatory capacity may transiently be decreased.

■ The Weaning Process The process of weaning can be long and variable and in some instances may account for over 40% of total ventilator time.84 The fact that after several decades of mechanical ventilation therapy, a uniform weaning protocol has not been adopted is testimony to great variability in practice and highlights the paucity of empirical data available to standardize weaning management. Nevertheless, weaning should utilize the concept of conditioning and target strengthening the muscles of breathing (diaphragm, intercostals, and abdominal) that respond similarly to other skeletal muscle conditioning. However, testing strength of conditioning is often difficult and varies greatly depending on injury patterns and overall respiratory health including underlying pneumonia, ALI, and previous medical comorbidities such as COPD. The methodology of weaning has evolved in the last three decades from a physician-driven approach to a modern protocol-based approach. Under a “stepwise” methodology, patients’ ventilatory requirements are decreased in a stepwise manner, often using a progressive lower set frequency through IMV mode. This method is safe and is highly successful in patients with low WOB and high ventilatory capacity and, during the 1980s, replaced spontaneous breathing trials. However, in the stepwise approach there is no set period of unassisted respiratory exercise. Thus, in a subset of patients with high WOB requirements, a stepwise weaning methodology will prolong mechanical ventilation and may lead to chronic fatigue and deconditioning.84 This method is in contrast to the “sprint” approach (spontaneous breathing trials) where intermittent trials of spontaneous breathing are used once or twice daily and an assessment of WOB and ventilatory capacity is determined accordingly. In an effort to empirically evaluate optimal weaning techniques, the Spanish Lung Failure Collaborative Group analyzed four weaning methods in an important, large (n  546), multicenter, prospective trial.77 In this study, Esteban et al. randomized patients deemed ready to wean into a stepwise progressive mode: (1) IMV where patients had a set mean frequency of 10 breaths/min and decreased, (2) PS where support was initially a mean of 18 cm H2O and decreased, or into an intermittent spontaneous breathing method, (3) two or times a day with PS 5 cm H2O, or (4) once daily T-piece for 2 hours only. This study reported that both spontaneous breathing methods had the highest rate of successful weaning. Spontaneous breathing led to extubation three times more quickly than IMV and about twice as quickly as high PS ventilation. There was no statistical difference in the rate of success between a once-daily trial and multiple daily trials of spontaneous breathing. Among the three most popular weaning modes, T-piece wean, PS wean, and IMV wean, current data suggest a trend that IMV weaning

PROTOCOLS FOR WEANING Despite the controversy that exists in method of weaning, the benefit of a formal ICU-wide weaning protocol to hasten weaning is clear.85 Implementing an aggressive weaning protocol should incorporate the Screen, Trial, Exercise, Evaluate, and Report (STEER) Principle. Using this protocol, a team of highly trained respiratory therapists, in conjunction with the ICU team, implement the following daily regimen on each mechanically ventilated patient: Screen for weaning contraindications (hypoxia, fevers, hemodynamic instability, high WOB, uncontrollable ICP, sedation). Trial of minimum support breathing (i.e., PS 5 cm H2O). Exercise according to set protocol (i.e., a 2-hour PS trial, or T-piece trial). Evaluate progress. Report the results to the ICU team. These protocols are designed to reduce physician practice variability and have been shown, in several studies, to reduce ventilator days, ICU days, and weaning duration.

■ Extubation The weaning process, in principle, begins shortly after mechanical ventilation is initiated. However, extubation, the final removal of the artificial airway, should not be equated or confused with weaning. In a collective national task force consensus paper, discontinuation of mechanical ventilation should be considered if the following physiologic parameters were met86: 1. Reversal of underlying cause of respiratory failure 2. Adequate oxygenation (P/F ratio 150–200 with PEEP 5–8, FiO2 0.4–0.5, and pH 7.25) 3. Hemodynamic stability 4. The capability to initiate a respiratory effort As in weaning, prediction of successful extubation varies greatly and traditional parameters such as tidal volume, NIF, and minute ventilation are not well standardized. In a prospective study of 100 weaning patients, Yang and Tobin studied the predictive value of the RSBI calculated by frequency/tidal volume (f /Vt) during spontaneous respiration and the CROP index—a more complicated equation including compliance, rate, oxygenation, and maximal inspiratory pressure.84 Success was defined as patients who remained extubated greater than 24 hours from initial extubation and subsequent isopleths and ROC curves were generated accordingly to predict likelihood of success. The authors concluded that an RSBI 100 breaths/(min L) was 95% likely to fail; conversely, an RSBI 100 breaths/(min L) was 80% likely to succeed. Although these authors have

CHAPTER 55

WEANING AND EXTUBATION

leads to a longer duration of mechanical ventilation process than spontaneous trials; however, it is important to note that little data have shown any link between weaning method and mortality.

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TABLE 55-5 Criteria for Extubation

SECTION 5

Criteria Ability to maintain oxygenation Ability to maintain ventilation

Ability to maintain airway

Ability to clear secretions Physiologic considerations

Physical Findings O2 saturation above 95% with FiO2 0.4 on minimal CPAP or T-piece RSBI 100 f/Vt, NIF  30 cm H2O, forced TV 10 mL/kg, PaCO2 45 mm Hg on minimal CPAP or T-piece Appropriate mental status, adequate strength, intact gag and cough, positive endotracheal leak with deflated cuff Paucity of secretions, adequate gag and cough reflex, adequate strength No indication of sepsis, adequate sedation and analgesia, no anticipated decrease in mental status

initiating mechanical ventilation. In one of the few prospective trials addressing this question, Rumbak et al. randomized 120 medical ICU patients into an early percutaneous tracheostomy group (within 48 hours of ICU admission) and a delayed tracheostomy group (14–16 days).87 Patients in the early tracheostomy cohort had 50% decreased mortality and an 80% decrease in pneumonia compared with the delayed group. Conversely, in another study, Sugerman et al. found no difference in ICU days, ventilation days, pneumonia, or mortality between patients randomized to either early (3–5 days) or late (10–14 days) tracheostomies, although the earlier cohort did have a decrease in vocal cord ulceration and subglottic inflammation.88 Perhaps the greatest benefit of early tracheostomy may be seen in the traumatic brain injury population. One prospective study and several retrospective analyses have shown early tracheostomy in severe head injury decreases ventilation days and decreases the incidence of pneumonia, although no benefit in mortality was conferred.89 Ultimately, timing of tracheostomy will be guided by the individual patient, although the need for tracheostomy seems to be directly proportional to the severity of injury.

■ Unplanned Extubations demonstrated the importance of an RSBI, other criteria should be utilized when deciding extubation, including ability for airway protection, secretion control, and sustainability (Table 55-5). Head injury patients can be particularly difficult to manage, since neurologic symptoms can change making criteria for airway and secretion control difficult to evaluate. A GCS of 8 is generally associated with the greatest extubation success. In these patients, early tracheostomy may be a consideration to establish definitive airway control (see Section “Tracheostomy”).

TRACHEOSTOMY Tracheostomy in a chronically ventilated patient can offer several advantages including improved oral care, improved pulmonary toilet, decreased oral and vocal cord ulcerations, decreased airway resistance, and improved ability to aggressively wean ventilation while maintaining a secure airway. However, tracheostomy is also associated with such complications as stomal infection, subcutaneous emphysema, hemorrhage, tracheal stenosis, innominate artery fistula, tracheomalacia, and excessive granulation tissue. In a 10-year retrospective analysis, Goettler et al. found that higher injury severity, low admission GCS, higher age (50 years), and refractory intracranial hypertension all predicted the need for tracheostomy.86 Nevertheless, significant controversy still exists regarding optimal timing for tracheostomy and has broadly resulted in an “early” or “delayed” tracheostomy management approach. Despite several prospective and retrospective studies, definitive and consistent evidence supporting improved outcomes from early tracheostomy has been lacking. Defining what constitutes early tracheostomy further complicates interpreting existing literature since an “early tracheostomy” can vary from 48 hours to 8 days from

Despite rigorous patient observation and appropriate sedation, unplanned extubations remain a serious complication with a reported incidence of 3–8% in both the medical and surgical ICU.90 The mortality for these events is near 2% and is mostly a result of sudden hypoxia and ensuing cardiopulmonary arrest. It has also been reported that unplanned extubations requiring reintubation increase the risk of VAP.90 In a prospective study analyzing the risk for unplanned extubations, Chevron et al. found that agitation is the highest risk factor followed by oral intubation.91 The authors also measured nursing workload and noted that higher nursing workloads were not predictive of higher unplanned extubations. Interestingly, unplanned extubations were relatively well tolerated in this group and only 37% required reintubation. Predictors of reintubation include a GCS 11, accidental versus patient-initiated extubations, hypoxia, and PaO2/FiO2 ratio of 200. Preventing unplanned extubations requires attention to endotracheal tube security with particular attentiveness during patient transfers, bedside procedures, or prone positioning. Adequate sedation and analgesia are paramount and, although their use should be limited, physical restraints, especially in patients with high sedative tolerance, may be temporarily necessary. An emergency protocol should be readied in the event of an unplanned extubation. Reintubation may be difficult and a team of experts with appropriate experience that can provide a surgical airway should be immediately present.

ANALGESIA AND CONSCIOUS SEDATION Patients suffering traumatic injury may be suffering severe pain and may require directed and effective analgesic therapy. Trauma of significant severity may lead to prolonged critical illness, mechanical ventilation, and long-term conscious sedation. Many trauma patients have a history of substance abuse

Principles of Critical Care

No

• Rule out/correct reversible causes • Use nonpharmacologic treatment • Optimize the environment

Is patient comfortable and at goal for Sedation and Analgesics?

management of pain, sedation, and delirium. An example of an ICU patient assessment algorithm is shown in Fig. 55-6.

CHOICE OF PARENTERAL OPIOID FOR ANALGESIA Pain is almost universal in trauma patients; it has been described as an unpleasant sensory or emotional experience that is associated with tissue damage or described in terms of tissue damage. Many patients later recall unrelieved pain when interviewed about their ICU stays. It is a standard of practice to regularly and frequently assess pain; this is readily accomplished by the use of validated pain scores. The Joint Commission has labeled the pain score “the fifth vital sign.” The patient’s sedation should be assessed together with pain as the patient’s comfort is affected by both variables. Parenteral opioids have a long history of efficacy and safety for pain and ICU patient. Since bioavailability and efficacy is variable in this patient population, the intravenous route is to be used whenever possible. Intramuscular and subcutaneous roots should be avoided due

Yes

• Reassess goal daily • Titrate and taper therapy to maintain goal • Perform awakening trial, if appropriate

Hemodynamically Stable - FentaNYL - HYDROmorphone Primary approach for - Morphine Is patient in pain? pain: bolus for pain Consider Hemodynamically Unstable • Use pain scale to assess patient control and then infusion potential causes - FentaNYL • Set goal for analgesia to sustain control. Renal Impairment - FentaNYL TARGET: Non-Verbal Pain Scale: 0–2 - HYDROmorphone Critical Care Pain Observation Tool: 0–1 - FentaNYL infusion at 25–50 mcg/hr - HYDROmorphone infusion at 0.4–0.8 mg/hr - Morphine infusion at 2–4 mg/hr Pain

See Daily Awakening Protocol

Signs & Symptoms of Opiate Withdrawal Pupil dilation Sweating Lacrimation Rhinorrhoea Piloerection Tachycardia

Vomiting Diarrhea Hypertension Fever Tachypnea Agitation

TITRATING OFF INFUSIONS: The potential for opioids withdrawal should be considered for patients receiving high doses or seven (7) days of continuous therapy. Doses should be tapered systematically (i.e. 10–30% per day) to prevent withdrawal symptoms.

Sedation DRUG SELECTION: Anticipate sedation (≤ 72 hours) - Midazolam Is patient agitated/anxious? Consider - Propofol • Use scale to assess patient potential causes - Dexmedetomidine • Set goal for sedation Anticipate sedation (>72 hours) - LORazepam TARGET: Richmond Agitation Sedation Scale (RASS): 0 to –3 Patient has renal impairment Riker Sedation-Agitation Scale (SAS): 3 to 4 - LORazepam - Propofol

SEDATION: Use for RASS greater or equal to 2 levels below what is ordered (e.g., RASS of –2 with an ordered goal of 0) 1.) LORazepam/midazolam continuous infusion: Hold infusion until patient reaches RASS goal, then resume at one-half previous rate. Titrate per written orders. 2.) Propofol continuous infusion: Decrease rate 5–10 mcg/kg/min every 10 minutes until patient reaches RASS goal. Titrate per written orders. 3.) Morphine/HYDROmorphone/fentaNYL continuous infusion: Hold until patient reaches RASS goal, then resume at one-half previous rate. Titrate per written orders.

Pharmacologic Treatment for Delirium: NPO: Dexmedetomidine 0.2–1.5 mcg/kg/hr (Consider in patients failing spontaneous breathing trials secondary to agitation) Is patient delirious? Consider potential Haloperidol 2.5–5 mg IV q15 min prn + delirium (suggested max 35 mg/ causes • Use scale to assess patient day) (Consider decreased dose in hypoactive delirium) PO: Aripiprazole 10–15 mg po daily (Consider when baseline QTc > 440 msec) Confusion Assessment Method for the ICU (CAM-ICU) Haloperidol 2.5–5 mg po q6 hr (Caution if baseline QTc > 440 msec) Intensive Care Delirium Screening Checklist (ICDSC) QUEtiapine 50–200 mg po q12 hr (Consider if sedative properties desired) NOTE: Provided dosing ranges are general guidelines Risperidone 0.5–1 mg po q12 hr (Caution baseline QTc > 440 msec) and are not intended to supersede clinical judgment of prescriber. Delirium

FIGURE 55-6 San Diego Patient Safety Council ICU Sedation Guidelines of Care.

Non-Pharmacologic Treatments for Delirium: - Ensure Daily Awakening Trials conducted - Continually reorient patient - Perform early mobilization - Promote effective sleep/awake cycles - Perform timely removal of catheters/physical restraints - Ensure the use of eyeglasses, magnifying lenses, and hearing aids - Minimize noise/stimulation at night - Minimize Benzodiazepines for sedation

CHAPTER 55

and are at risk for acute withdrawal symptoms and opiate and benzodiazepine tolerance. Inadequate control of pain, agitation, anxiety, and delirium can lead to patient suffering, additional complications, and unnecessarily prolonged intubation, mechanical ventilation, and ICU stay. The need for adequate analgesia and sedation must be balanced against the risks of oversedation. Oversedation may result in hemodynamic instability, increased length of stay and costs, increased respiratory complications including VAP, and possibly long-term decreases in cognitive function. Oversedation may also increase the risks of delirium and possibly posttraumatic stress disorder (PTSD). Delirium is related to increased length of hospital stay, increased health care costs, and higher mortality. ICU care may lead to pain and discomfort due to catheters, drains, endotracheal tubes, and performance of routine nursing care such as airway suctioning, physical therapy dressing changes, and an enforced mobilization. There is practice variation between caregivers and institutions; therefore, several organizations have proposed guidelines for ICU analgesia, sedation, and delirium.92,93 Most academic ICUs employ algorithms for assessment and

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TABLE 55-6 Suggested Intravenous Opioid Doses for Adult ICU Patientsa (San Diego Patient Safety Council)

SECTION 5

Agent Fentanyl

Approximate Equivalent Single IV Dose (mg) 100–200 mcg

Typical Infusion Rate 50–200 mcg/h

Onset Peak Effect (min) 2–5 min

Duration 0.5–2 h

Hydromorphone

1.5–2 mg

0.2–3 mg/h

20–30 min

3–4 h

Morphine

10 mg

2–10 mg/h

20–30 min

3–4 h

Average Price Per Daya $26 per day at a rate of 100 mcg/h $23 per day at a rate of 1.6 mg/h $20 per day at a rate of 10 mg/h

Comments Fastest onset and shortest duration 5–10  more potent by weight than morphine Avoid in hypotension. Active metabolite accumulates in renal dysfunction. May cause itching due to histamine release (not a true allergy). Decreases preload that may be beneficial in pulmonary edema

a

UCSD Medical Center 2/2010, will vary depending on institution.

to irregular absorption and highly variable serum levels. Patient-controlled analgesia (PCA) may be of great utility in patients able to use it due to the self-control and immediate administration of agent given to the patient. Recent guidelines have recommended preferred parenteral likely agents in the treatment of pain and adult ICU patient. Table 55-6 lists characteristics of the preferred agents in the guidelines: morphine, fentanyl, and hydromorphone (Dilaudid®).92

■ Morphine Morphine remains the most commonly used opioid analgesic in the ICU setting due to clinicians’ familiarity in dosing and pharmacokinetics and low cost. It penetrates the blood brain barrier slowly to its poor lipid solubility. This results in a delayed peak effect and a long-acting effect as compared with more lipid-soluble agents such as fentanyl. Morphine does not have a direct negative inotropic effect; however, it has predictable effects of arterial and venous dilation. Morphine also can increase venous capacitance to a greater extent than arteriolar capacitance and also decreases heart rate through a central sympatholytic effect and also direct effect on the spinal atrial node. These effects suggest morphine may be advantageous in the hemodynamically stable or hypertensive patient with myocardial ischemia or cardiogenic pulmonary edema; morphine is recommended as the first-line open agent for parenteral use in the ICU. Disadvantages of morphine and other opioid agonists are the opioid receptor–associated side effects, the most serious of which is centrally mediated respiratory

depression. Other effects include sedation, nausea, and sphincter of Oddi spasm. Adverse effects can be reversed if necessary with careful titration of the opioid receptor antagonist naloxone. Careful titration of naloxone may allow reversal of side effects without complete reversal of analgesia. Naloxone must be administered with care as access effect is associated with undesirable hemodynamic effects such as hypertension, tachycardia, and myocardial ischemia as well as acute pulmonary edema. Morphine is also associated with a non-receptor-associated effect of histamine release, and this can result in undesired hypotension, tachycardia, and possibly exacerbating bronchospasm in patients with reactive airway disease. Prolonged use of morphine, especially in renal impairment, can result in the accumulation of a metabolite, morphine-6 glucuronide, and may result in a prolonged sedative effect.

■ Fentanyl Fentanyl is a lipid-soluble synthetic opioid having a more rapid onset of action than morphine. It is also inexpensive with costs similar to morphine. With small doses the duration of action is short due to redistribution. When large doses are administered, especially by continuous infusion, termination of effect requires elimination, probably due to the saturation of poorly perfused adipose tissue. The pharmacokinetics of fentanyl is not much altered by the presence of cirrhosis, and clearance appears to remain normal in renal failure. Hemodynamically fentanyl maintains cardiovascular stability and does not have significant negative inotropic effect. In the presence of high sympathetic

Principles of Critical Care

■ Hydromorphone (Dilaudid®) Hydromorphone is a semisynthetic opioid agent that is lipophilic and 5–10 times more potent than morphine. Time to onset of action and duration of action are similar to those of morphine, and hydromorphone’s terminal half-life is 184 minutes. Hydromorphone appears to have minimal hemodynamic effect and does not result in release of histamine. Like morphine and fentanyl, hydromorphone is inexpensive, and is recommended as a third-line agent after morphine and fentanyl.92

PARENTERAL AGENTS FOR ANXIETY Critical care practice guidelines for pain, sedation, and delirium, such as those developed by the SCCM, recommend regular assessment and response to therapy.92 The appropriate target level of sedation is a calm patient who can be easily aroused with maintenance of the normal sleep–wake cycle. Some patients require deeper levels of sedation to facilitate mechanical ventilation or reduce ICP. Use of a sedation scale such as the Richmond Agitation Sedation Scale (RASS) or Riker Sedation Agitation Scale (SAS) is common in most ICUs.94 The choice of intermittent or continuous sedation is important; intermittent sedation relies on recognition of anxiety or agitation and subsequent preparation and administration of the sedative. Continuous sedation reduces the likelihood of delay in administration of sedatives; however, continuous sedative infusions for ICU patients have been shown to increase the duration of mechanical ventilation and length of ICU stay. Weaning of patients from mechanical ventilation is often hampered by oversedation. The benzodiazepines (midazolam and lorazepam) are the most commonly used agents in the ICU for sedation. Propofol and dexmedetomidine have expanded the number of agents available for ICU sedation. The provision of anxiolysis and amnesia are of major importance for critical care patients undergoing intermittently painful procedures or mechanical ventilation. It has been demonstrated that the majority of patients surviving prolonged mechanical ventilation found memory of the experience to be unpleasant. Recent recommendations suggest the use of propofol or midazolam for shortterm ICU sedation and lorazepam for long-term sedation.92 Due to its potential to form active metabolites with prolonged duration of action, diazepam is not recommended for a routine

use in critical care patients. Characteristics of commonly used benzodiazepines, dexmedetomidine, and propofol are found in Table 55-7.

■ Midazolam Midazolam has a rapid onset of action and relatively short elimination half-life (2–2.5 hours). In ICU patients, particularly those with impaired hepatic metabolism, its elimination half-life may be prolonged (4–12 hours). Additionally, midazolam can cause hypotension, particularly in the presence of hypovolemia. Respiratory depression is an expected side effect, but infusions of midazolam need not be completely withdrawn to the patient successfully from mechanical ventilation. Midazolam is metabolized to compounds known as hydroxymidazolam, which have minimal intrinsic benzodiazepine activity. A critical care task force has recommended midazolam as a firstline benzodiazepine for short-term (less than 24-hour) sedation and anxiolysis than in the critical care setting.92

■ Lorazepam Lorazepam is a potent benzodiazepine having a lower lipid solubility than either diazepam or midazolam, but higher receptor specificity. The lower lipid solubility delays penetration of the blood brain barrier, resulting in longer time to take effect despite a short distribution half-life. The duration of clinical effect from a single bolus dose is also longer than that obtained with a single bolus of midazolam or diazepam. Lorazepam has an intermediate terminal half-life of 10–20 hours and is metabolized into compounds with no intrinsic benzodiazepine activity. Theoretically, lorazepam’s lower lipid solubility and lack of active metabolites decrease the likelihood of prolonged sedation after large doses, relative to midazolam and diazepam. There is no randomized controlled trial comparing the benefits of the benzodiazepines as long-term sedatives in the ICU; however, lorazepam has been recommended as the first-line benzodiazepine for sedation and anxiolysis in the ICU patients requiring sedation for the medium term (24 hours). Due to its low water solubility, lorazepam is provided in a polyethylene glycol–containing solution that may cause phlebitis or intravascular catheter infiltration on injection. This carrier may cause myocardial depression in large doses. Lorazepam is inexpensive in comparison to midazolam.

■ Propofol Propofol is a lipid-soluble alkyl phenol intravenous anesthetic that is insoluble in water and formulated in a lipid emulsion. It has hypnotic, amnestic, and antiemetic properties but is devoid of analgesic effect. When used at low doses, it produces sedation. Propofol has minimal active metabolites, even with repeated administration. In critically ill patients sedated with continuous infusions of propofol for a mean of 86 hours, serum levels declined by 50%, 10 minutes after termination of the infusion. Controlled trials of propofol for sedation have shown that doses of 17–52 g/(kg min) of propofol effectively sedate most critically ill patients.95 The effect is rapid and predictable and recovery occurs quickly when the drug is terminated. In a

CHAPTER 55

tone, fentanyl may decrease blood pressure indirectly by decreasing central sympathetic output. Fentanyl also predictably causes a decrease in heart rate by a central vagotonic effect. The receptor-associated side effects of fentanyl and their management are the same as described for morphine. Fentanyl is 80–100 times more potent than morphine and has a more rapid onset of action, requiring vigilance with its use. Unlike morphine, fentanyl does not release histamine and therefore may be a better choice in patients who are hemodynamically unstable or who have reactive airway disease. For ICU patients, fentanyl has been recommended as an alternative to morphine in situations of hemodynamic instability, known allergy to morphine, or previous histamine release with morphine.92

1025

SECTION 5 Typical Infusion Rate 5–80 mcg/(kg min)

Onset Peak Effect 1–2 min

Duration 20 min

Midazolam

1–6 mg

1–10 mg/h

5–10 min

1.5–2 h

$70 per day at a rate of 8 mg/h

Lorazepam

1–3 mg

2–10 mg/h

15–20 min

2–4 h

$38 per day at a rate of 4 mg/h

Dexmedetomidine

Bolus not recommended: 1 mcg/kg over 20 min

0.2–1.5 mcg/(kg h)

30 min

2–4 h

$408 per day at a rate of 0.8 mcg/ (kg h)

a

UCSD Medical Center 2/2010, will vary depending on institution.

Average Price Per Daya $36 per day at a rate of 50 mcg/ (kg min)

Comments Fastest onset and shortest duration. Avoid in hypotension. Dose/rate-related hypotension/ bradycardia. Avoid IV push bolus due to increased risk of hypotension (if bolus required and low risk of hypotension, limit dose to 10–20 mg). Monitor triglycerides. Provide 1.1 kcal/mL. Monitor for propofolrelated infusion syndrome Fast onset—good for acute agitation/ anxiety. Active metabolite accumulates in renal dysfunction. Midazolam 2–3 mg is approximately equivalent to 1 mg lorazepam. Midazolam is associated with increased incidents of delirium Slower onset but longer duration. Risk of propylene glycol toxicity with high doses (anion gap acidosis, ↑ serum creatinine, ↑ lactate). Monitor serum osmolality if rate 6 mg/h and consider possible PG toxicity if osmol gap 10–15. Lorazepam is associated with increased incidents of delirium Limited data for use as a first-line agent; Drug is expensive. FDA approved for use 24 h (studied up to 7 days in literature). FDA-approved maximum dose  0.7 mcg/ (kg h) (studied up to 1.5 mcg/(kg h)). No respiratory depression—consider for patient failing spontaneous breathing trial due to agitation/anxiety. Dose/rate-related hypotension and bradycardia—bolus not recommended. May cause hypertension/ hypotension. Consider higher starting dose if used as monotherapy.

Management of Complications after Trauma

Typical IV Bolus Dose 0.03–0.15 mg/kg (maximum 20 mg)

Agent Propofol

1026

TABLE 55-7 Suggested Intravenous Sedation Agents for Adult ICU Patientsa (San Diego Patient Safety Council)

Principles of Critical Care

■ Dexmedetomidine Dexmedetomidine is an imidazole compound that is a highly selective agonist of the alpha-2 adrenergic receptor with eight times greater affinity than clonidine. It is also shorter acting than clonidine that allows use as an intravenous infusion. Initially evaluated as an anesthetic, it was found to be associated with excess bradycardia and hypotension. Lower doses produce reliable sedation and dexmedetomidine is approved in the adult ICU as a sedative infusion. Initially it was approved for 24 hours or less but has been used in clinical trials for up to 5 days and longer. Patient selection and proper drug infusion are needed to avoid significant hemodynamic effects. Avoiding the initial bolus dose can reduce the incidence of significant bradycardia and hypotension on administration. Dexmedetomidine produces sedation but easy arousal, analgesic-sparing effect, and minimal depression of the respiratory drive. These characteristics are unique in that patients appear to be sedated but are readily roused and interactive and can follow commands. This makes the drug highly suited for patients who are being weaned from the ventilator, especially those who become agitated when other sedation is reduced. Dexmedetomidine is more expensive than benzodiazepines or propofol; however, studies suggest it is cost-effective as it reduces patient ventilator days, delirium, and ICU length of stay as compared with midazolam.97

MONITORING AND DAILY AWAKENING Monitoring of sedation within the ICU can be performed by the Ramsey, RASS, or Riker (SAS) scales (Table 55-8). The scales have midrange scores that indicate a calm, cooperative

TABLE 55-8 Richmond Agitation Sedation Scale (RASS)2 Target RASS Value 4 combative 3 very agitated 2 agitated 1 restless 0 alert and calm 1 drowsy 2 light sedation 3 moderate sedation 4 deep sedation 5 Unarousable

RASS Description Combative, violent, immediate danger to staff Pulls or removes tubes or catheter; aggressive Frequent nonpurposeful movement; fights ventilator Anxious, apprehensive but movements not aggressive or vigorous Not fully alert, sustained awakening to voice (eyes open and contact 10 s) Briefly awakens to voice (eye opening and contact 10 s) Movements or eye opening to voice (but no eye contact) No response to voice; moves or eyes open to physical stimulation No response to voice or physical stimulation

patient with high and low scores indicating excess anxiety or agitation or oversedation. A common sedation scale should be used throughout the institution for consistent and effective use. Daily interruption of continuous IV sedation until awakening of mechanically ventilated patients decreases duration of mechanical ventilation and ICU length of stay. The daily awakenings allow for titration of sedation, making the dosing of sedation intermittent. Combination of daily awakening with spontaneous breathing trials results in patients spending less time on mechanical ventilation, less time in a sedative coma, and less time in the ICU and in the hospital. Daily awakening trials are most effective when following a standardized nursedriven consistent protocol. Patients who should be excluded from a daily awakening trial include those with increased ICP or neuromuscular blockade, those requiring high levels of ventilatory support, and those who are postcoronary artery bypass grafting. The daily awakening period should be synchronized with spontaneous breathing trial; in a study of 336 mechanically ventilated ICU patients, doing so achieved significant reduction in ventilator-free days and ICU and hospital length of stay.98 The daily awakening also provides an opportunity for early exercise and mobilization (physical and occupational therapy) (Table 55-9). A recent study of early mobilization during daily awakening in 104 mechanically ventilated patients demonstrated increased independent functional status at hospital discharge, shorter duration of delirium, and fewer ventilator-free days during the 28-day follow-up period than those observed in controls.99 An example of the recent trends toward less use of continuous sedation includes a recent trial of

CHAPTER 55

study comparing propofol with midazolam for sedation of ICU patients, time to wake up and tracheal extubation were significantly shorter in the group sedated with propofol.96 Propofol has predictable hemodynamic effects, including arterial and venous dilation, decreased inotropic effect, and decrease of systolic blood pressure of 20–30%. Propofol given as a loading dose will cause profound ventilatory depression. For this reason it is typically limited to mechanically ventilated patients only. Propofol has been recommended as an agent for short-term (less than 24 hours) sedation in the ICU. A study of ventilated patients receiving long-term infusions of propofol as compared with midazolam showed a shorter time to awakening (1 hour vs. 37 hours) and a shorter time to extubation (2 hours vs. 55 hours), suggesting that propofol may be useful for sedation of critically ill patients for longer than 24 hours. SCCM guidelines recommend the use of propofol for up to 48 hours, except in traumatic brain injury patients in whom it may be considered for use up to 5 days.92 Patients on propofol for longer than 24 hours need to be monitored carefully for propofol infusion syndrome. Hypertriglyceridemia and lipid-induced pancreatitis have been reported during prolonged infusion of propofol in the ICU, suggesting that serum triglyceride levels should be monitored in these patients. A lipid solution of propofol also supports rapid bacterial growth at room temperature, and a number of postoperative bacteremias had been linked to poor administration technique.

1027

1028

Management of Complications after Trauma

TABLE 55-9 Daily Awakening Trials—Summary Recommendations

SECTION 5

Components recommended for a daily awakening trial: • Consistency—should follow a standardized nursedriven protocol • Continuity—need to ensure a set time for the patient during daylight hours • Coordination—need to ensure daily awakening trial is coordinated with other disciplines, specifically physical therapy, occupational therapy, and respiratory therapy activities Exclusions to a daily awakening trial: • Increased intracranial pressure issues • Neuromuscular blockade • Pressure-regulated pulmonary ventilation with an inverse ratio • Coronary artery bypass graft immediate postoperation Process for weaning drug (per drug) • Target—use sedation scale targets (1 on the RASS) • Sedatives—decrease by 50% or off • Narcotics—consider reducing narcotics if still sedated (or SAS of 3–4) Assess as part of daily awakening trial: • Pain • Delirium • Spontaneous breathing trial/rapid shallow breathing index If continued sedation required, start at lower dose than previously—50% of original or lowest effective dose during titration (the most recent titration dose [before reaching 1 RASS]) • Bolus and titrate up to reach target goal as appropriate; do not resume at previous rate • Abort daily awakening trial if patient becomes physiologically unstable during procedure

“no sedation” in mechanically ventilated patients.100 In that study, the intervention group patients receiving no sedative medications were compared with control patients on continuous midazolam drips. The majority of the eligible ICU patients could not be enrolled as they had medical indications for deep sedation. Patients in the “no sedation” group were allowed morphine boluses and had frequent nonpharmacologic antianxiety interventions such as reassurance by nurses and reassessment by physicians of pain orders and the need for tubes and catheters. Patients in the “no sedation” group had significantly shorter ventilator days and hospital and ICU length of stay, but did have increased delirium and increased use of haloperidol. Monitoring of sedation with an objective device may be possible with the bispectral index (BIS) monitor. Raw electroencephalographic (EEG) information is obtained through a sensor placed on the forehead. The system processes the EEG information and calculates a number between 0 and 100, which provides a direct measure of the patient’s level of consciousness and

response to sedation. A BIS at the time of 100 indicates that patient is fully awake, and a base level of 0 indicates the absence of electrical brain activity. Sedation may be titrated to a specific index depending on the goals for each patient. BIS correlated directly with commonly used sedation scales.

■ Delirium Delirium is defined as fluctuation in mental status such as inattention, disorganized thinking, hallucinations, disorientation, and an altered level of consciousness. It occurs in up to 65% of hospitalized patients, and up to 87% of patients admitted to the ICU. The outcomes of delirium can be serious for the patient and should be considered as another organ failure that affects patient’s outcome. Delirium can increase the hospital stay and increase health care cost. There has been discussion of ICU delirium rates as being a possible quality measure. Delirium must be considered when assessing pain and sedation in the ICU. It can be further defined as (1) hyperactive delirium: previously referred to as ICU psychosis, includes such symptoms as hypervigilance, restlessness, anger, irritability, and uncooperativeness, and is associated with better overall outcomes; (2) hypoactive delirium: the more common and deleterious, characterized by a lack of awareness, decreased alertness, sparse or slow speech, lethargy, decreased motor activity, and apathy; (3) mixed delirium: apparent in patients with a mixed clinical picture and may occur in up to 54% of patients. Delirium occurs in patients typically 24–72 hours after admission to the ICU. Risk factors existing before hospitalization placing patients at risk for delirium include cognitive impairment, chronic illness (including hypertension), age over 65 years, depression, smoking, alcoholism, and severity of illness. Risk factors arising during hospitalization include congestive heart failure, sepsis, prolonged restraint use, immobility, withdrawal from substance abuse, seizures, dehydration, hyperthermia, head trauma, intracranial mass lesions, and the use of lorazepam, midazolam, morphine, fentanyl, and propofol. Assessment of delirium should be carried out in association with pain and sedation assessments and can be facilitated by the use of a validated delirium score such as the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU) or the Intensive Care Delirium Screening Checklist (ICDSC); these tools may be most usefully administered during a daily awakening.101,102 In addition, the patient should be assessed for QTc prolongation on EKG if therapy is being considered as many antidelirium agents are associated with QTc prolongation and risk of torsade de pointes. CAM-ICU and ISDSC allow rapid consistent assessment for altered level of consciousness, disorganized thinking, inattention, and other delirium features. Nonpharmacologic measures that can be used to manage delirium include daily awakening trials, continuous reorientation of the patient by nursing staff, clocks and calendars visible to the patient, promoting effective sleep/awake cycles, timely removal of restraints and catheters, ensuring use of glasses and hearing aids, minimizing ICU noise and stimulation, and avoiding excessive use of benzodiazepines. Pharmacologic agents used in the management of ICU delirium have not been supported by large clinical trials and agent selection should be based on patient-specific factors (Table 55-10).

TABLE 55-10 Pharmacology of Recommended ICU Antidelirium Agents (San Diego Patient Safety Council) Adverse Effects (Incidence)

Antipsychotic Agent Haloperidol (Haldol) Quetiapined (Seroquel) Risperidone (Risperdal)

Aripiprazole (Abilify)

Dosage Form Tablet, IV injection Tablet Tablet, ODT tablet, solution (1 mg/mL) Tablet, solution (5 mg/mL), IM injection

Metabolizing Metabolism Enzyme

Equivalent Maximum QT Dosages (Approximate) Dose (mg Prolongation Potentiala,b Per Day) (mg) Sedation

Dopaminergic2 Affinity/ Extrapyramidal Effectsb

Anticholinergic Orthostatic Effects Hypotension

T1/2: 21 h, hepatic T1/2: 6 h, hepatic T1/2: 3 h, hepatic

CYP3A4, 2D6

2

20

Low

Low

High

Low

Lowc

CYP3A4

125

400

Moderate

Moderate

Low

Moderate

High

CYP2D6, 3A4

1

4

Moderate

Low

High

Low

Moderate

T1/2: 75 h, hepatic

CYP2D6, 3A4

5

10–30 mg

Low

Low

Low

Low

Low

Black box warning: Increased mortality seen when used in elderly patients with dementia-related psychosis due to cardiovascular or infectious complications. The use of these agents for delirium in ICU patients has not been tested in large, randomized, placebo-controlled trials. a

Low, 3–10 milliseconds; medium, 10–15 milliseconds; high, 15 milliseconds.

b

Dose-related effect. Increased with IV formulation. d Caution: bone marrow suppression; blood dyscrasias. c

Principles of Critical Care 1029

CHAPTER 55

1030

Management of Complications after Trauma

SECTION 5

Intravenous drugs include dexmedetomidine, which may be especially useful in patients scaling spontaneous breathing trials secondary to agitation, and intravenous haloperidol. Intravenous haloperidol achieves peak levels 11 minutes after injection and the half-life of the drug is 10–24 hours. The dose required to control agitation and critically ill patients varies widely; a suggested maximum daily dose in the ICU is 35 mg per day; use of larger doses has been reported. Haloperidol has been associated with a reduced seizure threshold, extrapyramidal reactions (dyskinesia), and laryngeal dystonia. It has also been associated with malignant neuroleptic syndrome. Large doses of intravenous health care should only be administered in a monitored critical care setting and serial EKGs obtained to monitor QTc interval. In patients with hypoactive delirium, the dose of haloperidol may need to be reduced. Oral agents are longer acting and include aripiprazole, risperidone, or oral haloperidol. These agents are associated with QTc prolongation and should only be administered if the measured EKG QTc is less than 440 milliseconds. Another oral delirium agent with greater sedative properties is quetiapine; it is not associated with QTc prolongation.

UTILITY OF REGIONAL ANALGESIA AND ANESTHESIA There is a respiratory deficit following upper bowel and thoracic surgery or blunt thoracic trauma (see Chapter 24). Opioid analgesics may exacerbate this deficit by causing respiratory depression, which can be undesirable in ICU patients. The use of regional analgesic techniques typically reduces opioid-related respiratory depression, but may fail to completely restore respiratory function to pretrauma levels. Multiple studies have demonstrated effectiveness of regional analgesia and improving lung volumes and oxygenation and decreasing point complications following blunt thoracic trauma. Epidural analgesia has been well except modality for the treatment of rib fracture pain and the restoration of ventilatory function; however, not all studies have consistently showed positive results. Even with complete relief of pain, epidural methods may only partially restore FVC and forced expiratory volume, minimally improve functional residual capacity, and modestly increase oxygenation. Thus, the pain is only one of several factors leading to a restrictive pulmonary pattern postoperatively. Diaphragmatic dysfunction has been associated as anterior to the decreased lung volumes observed after blunt thoracic trauma. This diaphragmatic dysfunction has been treated to visceral or somatic reflexes decreasing phrenic nerve activity. Spasm and splinting of the abdominal and intercostal muscles may also be involved. Thoracic epidural local anesthesia decreases diaphragmatic dysfunction, increases tidal volume, and decreases respiratory frequency while spinal opiates do not. These effects of epidural local anesthesia may be indirect or direct. Another option for regional control of pain includes paraspinal or regional administration of local anesthetics, particularly with the use of an indwelling catheter and pump system. Such catheters can be placed close to surgical incisions or rib fractures and continuously dilute local anesthetic agents.

In summary, pain is a significant problem after trauma; its relief is necessary not only for patient comfort but also for efficient respiratory therapy. However, pain is not the only mechanism underlying respiratory muscle dysfunction. Inhibitory reflexes of the phrenic nerve are involved and they do not appear to be blocked by spinal opiates; they are however partially blocked by thoracic epidural local anesthetics. No less the analgesia provided by spinal opiates or local anesthetic solutions improves respiratory function more than systemically to the narcotics and can be expected to reduce morbidity and some situations.

COMPLICATIONS AND PITFALLS IN THE ICU Critical care complications interpose a substantial cost burden to the health care institution and society and worsen patient outcomes. There is increasing public awareness of this issue; preventable complications are often reportable to regulatory authorities and many insurers, including Medicare, may refuse to pay hospital or physician charges in case of patients with certain preventable critical care complications. Health care consumers can readily obtain ICU complication rates for their health care institutions from a variety of media. The need to reduce preventable complications of critical care has resulted in a number of guidelines released by professional and regulatory organizations and local hospitals.11,38 These are typically focused on prophylaxis for common ICU complications. Other measures that may be adopted include use of an ICU database to track outcomes and complications and perform risk adjustment, use of robust quality and process improvement programs to detect complications and change practices, and a continuing education program for ICU staff that includes measures to identify and reduce complications. A complete discussion of critical illness complications is beyond the scope of this chapter; however, selected complications that are unique to critical care or are particularly significant to morbidity are discussed. Specific organ system complications are discussed more completely in other chapters.

■ Infectious Complications Two particularly troublesome and expensive nosocomial infections that occur during critical care after major trauma are CLABSI and VAP. One of the principal issues regarding VAP is its effect on outcome after major injury. There is evidence that pneumonia may exacerbate multiple organ failure and ARDS and should presumably be associated with increased mortality, as has been found in other studies. About 25% of patients who have CVCs placed will develop catheter colonization and 5% will develop a CLABSI after an average of 8 catheter days.103 Both CLABSI and VAP are discussed in detail elsewhere.

CRITICAL ILLNESS POLYNEUROPATHY Prolonged neuromuscular weakness associated with critical illness was reported as early as the 1950s. Found to be associated with sepsis, hypotension, or multiple organ dysfunction, CIP may prolong weaning from mechanical ventilation, delay

Principles of Critical Care

■ The Geriatric Trauma Patient in the ICU Mortality in elderly trauma patients has been associated with cardiovascular and septic complications.28 Therefore, aggressive monitoring is warranted as it may help in diagnosing physiologic deterioration and in assessing the effectiveness of a number of therapies deployed in an attempt to improve outcomes. In addition, aggressive monitoring may allow clinicians early identification of complications. Sepsis and subsequent multiple organ system failure cause most late deaths following trauma in the elderly. Urosepsis and pneumonia are common in elderly trauma patients and what would be otherwise a relatively simple problem to treat in the young healthy individual may be the trigger to a cascade of events in the elderly patient, which may culminate with multiple organ dysfunction and death. For these reasons, aggressive and early treatment of these infections, initially with broadspectrum antibiotics followed by culture-based de-escalation or adjustment of therapy, is a critical determinant of good outcome. One of the most common causes of death in the geriatric trauma population is pneumonia following blunt chest trauma and rib fractures. Due to decreased pulmonary reserve and associated comorbidities, the elderly trauma patient is generally more susceptible to the development of pneumonia due to an inability to effectively clear secretions and take deep breaths. Two aspects in the early initial care in the ICU in these patients

are important: avoidance of fluid overload and adequate analgesia. To this end, patient-controlled narcotic analgesia and/or epidural administration of opiate analgesics or local anesthetics may be helpful in appropriately selected trauma patients. Geriatric patients are also at increased risk for thromboembolic complications following trauma. Patients in the high-risk group for thromboembolic events (traumatic brain injury, spinal cord injury, complex pelvic fractures, bilateral lower extremity fractures, prolonged immobilization, or a previous history of deep venous thrombosis or pulmonary embolism) should receive pharmacologic prophylaxis with low-molecular-weight heparin, and/or inferior vena caval filter placement when indicated. More recently, trauma centers in the United States have experienced an epidemic of elderly falls. Many of these patients are taking antiplatelet agents such as aspirin or clopidogrel and warfarin. Even patients with mild to moderate traumatic brain injury are at a much higher risk of developing fatal intracranial hemorrhage due to the use of these drugs and because of “increased space” for hematoma expansion due to brain atrophy. Rapidly obtaining a brain CT scan and quickly assessing coagulation parameters for reversal of anticoagulation are critical in early management. Those individuals who need an immediate craniotomy may benefit from rapid reversal with recombinant factor VIIa or prothrombin complex.

■ Missed Injuries Missed injuries are the most common cause of preventable death; however, the true incidence of missed injury is difficult to determine. An autopsy review of trauma patients compared their findings with discharge diagnoses and demonstrated that 34% of the patients had missed injuries and in 5%, the missed injury was the cause of death.105 The trauma victim who manifests delayed hypotension, that is, after resuscitation, may be bleeding from an occult injury. The injury can be in the thoracic cavity, the abdominal cavity, the pelvis, or the thigh. The initial evaluation of the trauma patient centers around recognizing abnormal physiology and the pattern of injury. Surgical intensivists caring for trauma patients must recognize potential injuries likely to occur given a particular mechanism. The challenge becomes the rapid identification of occult injuries before the clinical condition of the patient deteriorates. Missed injury is a major pitfall in the care of trauma and an unexpected deterioration in the condition of the patient in the ICU should prompt a reexamination for possible missed injury, among other causes.

■ Postresuscitation Hypotension in the ICU Any patient developing hypotension postresuscitation is bleeding until proven otherwise and aggressive investigation of the etiology is mandatory. Such episodes should prompt a reevaluation of the patient’s workup and raise the specter of a missed intra-abdominal injury or a solid organ injury that rebled due to overresuscitation and dislodgment of the initial hemostatic clot. It is a common pitfall to ignore such an episode as an aberration or, perhaps, to explain it away in an attempt to reassure oneself. A common mistake is to assume that resuscitation has been

CHAPTER 55

return to ambulation, and significantly affect overall recovery from post-traumatic critical illness. The syndrome is characterized by the development of diffuse neurogenic muscle weakness, developing typically over a several-week course of severe critical illness. The neurologic manifestations may include unexplained failure to wean from mechanical ventilation, decreased/absent deep tendon reflexes, tetraparesis, muscle atrophy, decreased fibrillations and compound muscle action potentials, and axonal damage for which evidence is found on electrophysiologic testing. Nerve conduction velocities are near normal, and histologic evaluation of peripheral nerves has shown acute diffuse neurogenic atrophy in muscles and axonal degeneration in nerve tissue. CIP may be far more common than is currently recognized and may commonly affect ventilator weaning and recovery.104 It should be considered as a cause of weaning failures or generalized weakness in the setting of critical illness. Electrophysiologic evaluation of muscle and nerve function is important for the diagnosis. Although not conclusive, available data suggest that the avoidance of long-term agents, particularly in combination with corticosteroids or aminoglycoside antibiotics, may be an important preventative measure. Several factors contributing to CIP and the long-term use of neuromuscular blocking agents (e.g., pancuronium, vecuronium) and amino glycoside antibiotics have been identified. The combination of neuromuscular blocking agents and high-dose steroids may be a particularly important cause. Recovery from CIP, although may be prolonged, may be nearly complete from a clinical standpoint. Follow-up electromyographic studies have shown changes with chronic neurogenic damage, however.

1031

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Management of Complications after Trauma

SECTION 5

completed and hypotension is due to other causes such as traumatic brain injury or bleeding due to long bone fractures. There are certain injuries that may require ongoing resuscitation with blood products, most prominent among them a vertical shear-type posterior element pelvic fracture. However, in the absence of any such known injury, a diligent attempt must be made to exclude a missed injury in the abdomen or perhaps an injury whose magnitude was underestimated. The traditional end points of resuscitation include an adequate urinary output, the trend of the base deficit on the arterial blood gas, and normalization of arterial lactate levels. If one has a PA catheter in place (rarely used nowadays), the oxygen extraction ratio can be used as a gauge of resuscitation. The widening a-v O2 difference or an increasing oxygen extraction ratio is an indicator of inadequate flow, given a certain metabolic demand. There are situations in which the urinary output may be misleading. The intoxicated patient will have good urinary output even in the face of hypovolemia, because alcohol inhibits the release of ADH from the posterior pituitary; in addition, it is hypertonic and leads to peripheral arterial vasodilation. Another situation in which the urinary output will be misleadingly elevated is in the setting of hyperglycemia. Whether the patient is a diabetic or he or she has received high-dose steroids for a spinal cord injury, the resultant hyperglycemia will cause a misleadingly comforting urinary output. A serum blood sugar over approximately 180–190 mg/dL results in glycosuria and this pitfall must be recognized. Similarly, the base deficit can also be misinterpreted. The etiology of metabolic acidosis in the injured patient is, until proven otherwise, due to hypoperfusion from hemorrhagic shock; it must be understood, however, that the base deficit can be due to ketosis, nonanion gap acidosis, and sepsis.

■ Hypoxemia Parenchymal disease is the most common cause of hypoxemia. The causes include aspiration pneumonia, hospital-acquired pneumonia, pulmonary contusion, or the ARDS. Pneumothorax and/or hemothorax may also manifest as hypoxemia but generally occur during the initial phase of the resuscitation and less often in the ICU.

■ Pulmonary Contusion Pulmonary contusion consists of a direct injury to the lung followed by alveolar hemorrhage and edema from the injury. Experimental evidence has demonstrated clearly that the contusion evolves over the first 24 hours following injury, such that the pO2 progressively decreases during that time period.106 The contused lung has leaky capillaries and aggressive fluid resuscitation may result in further deterioration of pulmonary function. In addition, administration of colloid can result in deposition of molecules such as albumin in the interstitial space, where such large molecules are not cleared by the lymphatics. Therefore, judicious administration of crystalloid is likely the best therapy in this circumstance. The pitfall in the management of pulmonary contusion centers around not anticipating the progression of the injury. Above all, the patient with major chest wall trauma, even with the normal chest x-ray

on initial evaluation, must be closely observed for the development of a pulmonary contusion.

■ SIRS, Sepsis, Severe Sepsis, and Septic Shock Injury leads to the activation of the inflammatory response, which may be aggravated by the severity of shock, degree of tissue injury, and secondary insults. To some extent, severely injured patients invariably develop an SIRS. SIRS is defined by manifestation of two or more of the following conditions: (1) temperature 38°C or 36°C; (2) heart rate 90 beats/min, (3) respiratory rate 20 breaths/min or PaCO2 32 mm Hg, and (4) white blood cell count 12,000/mm3, 4,000/mm3, or 10% immature forms. The treatment of SIRS is supportive. Sepsis is defined as the presence of a proven infection in a patient with SIRS. Severe sepsis includes sepsis and organ dysfunction, while septic shock encompasses severe sepsis accompanied by hypotension and hypoperfusion, refractory to volume replacement and requiring inotropes (Table 55-11). Persistent SIRS and sepsis may ultimately lead to multiple organ dysfunction (discussed in another chapter). Typically, the first organ to fail is the lungs. The hemodynamic derangements in sepsis, or, more properly, severe sepsis, are classically hypotension, hyperdynamic cardiac index, a low systemic vascular resistance, and metabolic acidosis. The source of sepsis in the injured patient relates to the type of injuries. It is extremely rare for a patient to have septic shock early after injury, unless there is an obvious infection, such as an aspiration pneumonia or perforated colon. The patient who has leukocytosis with bandemia, fever, and clinical deterioration must be investigated closely for a source of infection. The diagnosis of an infection following major trauma is the biggest pitfall since the cardinal signs of infection such as fever, leukocytosis, and hyperdynamic hemodynamic state can and frequently are the result of the inflammatory cascade, in response to tissue trauma. The pitfall lies in the differentiation between the two entities, sepsis and SIRS. The consequences of liberal use of antibiotics to broadly cover for presumptive sepsis are real, including drug resistance, antibiotic-related colitis, and the risk of fungemia. The consequences of not treating a patient with fever, hyperdynamic state, and signs and symptoms of infection, in the absence of positive cultures or a clear source, are equally daunting, as the patient may indeed be harboring an infection, but the yield of blood cultures and the other surveillance tests are poor. This pitfall is real and common, and, unfortunately, there is no reliable method to clinically distinguish between the entities of sepsis and SIRS until a clear source of infection is identified. The usual sources of infection in the ICU are the lungs, indwelling vascular catheters, the urinary tract, and the wound. Each of these sites must be surveyed for infection.

■ Acalculous Cholecystitis Acalculous cholecystitis is a “hidden” cause of fever in the ICU. Changes in gastrointestinal motility, characterized by increased gastric residuals and intolerance to enteral nutrition, imply the

Principles of Critical Care

1033

TABLE 55-11 Vasopressors and Inotropes Agent

Typical Dosage

3–5 mcg/(kg min) 10–20 mcg/(kg min) Dobutamine 2–20 mcg/(kg min) Epinephrine 0.5–2 mcg/min 2–10 mcg/min Norepinephrine 0.5–30 mcg/min Vasopressin 0.01–0.04 U/min Phosphodiesterase inhibitors Amrinone (inamrinone) 0.75–1.5 mg/kg loading dose 5–10 mcg/(kg min) infusion Milrinone 50 mcg/kg loading dose 0.375–0.75 mcg/(kg min) infusion Nitric oxide donors Nitroglycerin 0.2–1.5 mcg/(kg min) Nitroprusside 0.5–8 mcg/(kg min)

onset of an infection and one potential source of such infection is the gallbladder. Acalculous cholecystitis is a disease of the critically ill patient; most of these patients have had major trauma or extensive burns, or are recovering from major surgery. Patients with acquired immune deficiency syndrome (AIDS) are at a special risk for acalculous cholecystitis. The diagnosis can be difficult because patients who develop acalculous cholecystitis tend to be critically ill or severely injured and are frequently unable to react to physical exam. An ultrasound will typically show a thickened gallbladder wall without stones. The diagnostic test of choice is the HIDA scan, which will demonstrate a lack of emptying of the gallbladder in response to administration of cholecystokinin. The initial treatment for acalculous cholecystitis is conservative (n.p.o., antibiotics, intravenous fluids), although some patients will require operative intervention. Alternatively, for those patients who are too sick to tolerate an operation, a percutaneous cholecystostomy tube placement is the best option.

■ Worsening Intracranial Hypertension The patient who does not have an initial surgically treatable lesion may develop elevated ICPs. The CT finding that correlates best with intracranial hypertension is compression or obliteration of the basilar cisterns and midline shift.107 The level of intracranial hypertension at 72 hours following injury is the primary predictor of outcome in patients with these CT scan findings. It is necessary to anticipate this deterioration and plan on optimization of control of ICP, CPP, and cerebral blood flow. The CPP is calculated by subtracting ICP from the MAP; recent work has shown that the CPP should be maintained at least 60 mm Hg. However, the most important intervention revolves around management of ICP. Aggressive therapy should aim to keep the ICP below 20 mm Hg. The usual adjuncts are

MAP

CO



/



SVR

α1

 

β1

β2



DA1 DA2







 

/ /

 

mannitol, hypertonic saline, ventriculostomy drainage, and sometimes barbiturate administration. Extreme cases of intractable intracranial hypertension may require surgical decompression (decompressive craniectomy). The techniques and the theories underlying the management of intracranial hypertension are beyond the scope of this chapter.

ETHICAL ISSUES IN THE ICU Ethics may be regarded, in part, as a series of societal formulations predicated on moral values designed to produce a theoretical “optimal good.” With the ability of modern ICUs to maintain physiologic support and homeostasis well beyond the bounds of reasonable sentient existence, physicians are increasingly called on to participate in sometimes difficult live-or-die, withdraw/withhold support decisions. While ICU ethics also include other considerations, such as consent issues and donor organ procurement (see Chapter 50), this section focuses on the withdrawal/withholding of physiologic support including the application of do not resuscitate (DNR) orders in the surgical ICU.

ETHICAL PRINCIPLES APPLICABLE TO MEDICAL DECISION MAKING Ethical decision making should involve the careful, considered application of established principles. The temptation to apply one’s individual value system to the decision-making process is strong, but the personal values of the patient are paramount, and the personal judgments of both family members and physicians must be considered in the context of the ethical principles involved. With the possible exception of the principle of

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Beneficence : The principle of “doing good” as applies to a particular patient, individual, or situation. Nonmaleficence : The principle of avoiding harm or wrongdoing, as applied to a particular situation or individual. Autonomy : Perhaps the most important operative principle in critical care ethics is the right of self-determination—the inherent right of individuals to make decisions regarding their own treatment options (or withholding thereof ) and ultimately make decisions that will impact their survival. Full disclosure : The principle of accurate communication of information that will allow individuals (or their surrogates) to exercise autonomy or surrogate decision making. Social (distributive) justice : The principle whereby benefits to an individual, if associated with burdens to another individual or individuals, must be weighed in terms of the most “good” done to the society or group as a whole. This last principle typically involves decisions regarding the distribution of scarce resources to allow the “optimum” treatment of not a single individual, but a population of individuals (society). Such a principle may apply during wartime casualty triage or civilian mass-casualty triage. With respect to ICUs in the United States, it is uncommon, within a given municipality or region, that critical resources are sufficiently scarce so as to result in a denial of treatment opportunities, regardless of the medical conditions involved.

WITHDRAWAL/WITHHOLD SUPPORT DECISIONS Modern ICUs have developed the increasing technical capability to support homeostasis, even in the face of what would otherwise be overwhelming disease. Increasingly in the trauma population of ICU patients, patient demise is the result of a decision to withdraw or withhold life support. The consequences and irreversibility of such withdraw/withhold decisions in the CCU mandate that they be considered very carefully and predicted on the careful application of ethical and legal principles. Physicians often assume that withdrawing and withholding support are fundamentally different actions that require different thresholds and criteria and potentially different legal consequences. Case law has served to clarify this issue, beginning with Barber v Santa Barbara Superior Court.108 In this case, the court considered withdrawal of support to be the equivalent of withholding, equating each milligram of drug infused or each ventilator breath as an active intervention. That withdrawal of this type of intervention required an additional order was immaterial and still considered a passive (vs. active) act equivalent to withholding. This concept has been further supported by the President’s Commission and critical care consensus panels.109 This critical legal precedent, generally upheld since that time, had the effect of making the withdrawal of support for critical illness the equivalent of withholding support, and thereby not subjecting health care providers to subsequent legal action regarding active (vs. passive) interventions acting to hasten demise.

The importance and impact of withdraw/withhold decisions is considerable. In a review of such decision, Smedira et al. found that in a mixed population of surgical and medical ICU patients, support was withheld in 1% and withdrawn in 5%. The resultant deaths accounted for 45% of all ICU deaths in the two institutions under study.110 The general setting under which withdraw/withhold decisions are made is poor prognosis, which would include a low chance of survival and high likelihood of poor cognitive function. Specific criteria that may allow withdrawal/withholding include the following: • Provision of further treatment is considered medically futile with respect to achieving well-defined therapeutic goals. • The patient with decision-making capacity (DMC), in exercising his or her autonomy, chooses to have support withdrawn/withheld. • A legal surrogate decision maker (legal guardian or durable power of attorney) chooses to have support withdrawn/ withheld under medically appropriate circumstances. • The decision is made on the basis of a prior written medical directive stipulating circumstances under which support may be withdrawn/withheld. • The physician, acting as a surrogate decision maker in conjunction with next of kin, other consultants, and possibly an ethics committee, elects to withdraw/withhold support. The decision should be based on the following considerations: ❍ Information regarding the patient’s wishes : What the patient would be likely to decide if he or she had DMC. This may be obtained from family, friends, or other providers with a history of relevant contact with the patient. ❍ The benefits/burdens test : The benefits of continued treatment are outweighed by the burdens to the patient of such treatment in accomplishing the defined therapeutic goals. ❍ Substituted judgment : The “reasonable person test.” In the absence of other available information regarding a patient’s wishes, a withdraw/withhold decision should be regarded as one likely to be made by any “reasonable person.” ❍ Best interests test : The decision to withdraw/withhold must be medically appropriate and should not significantly diminish opportunity for recovery within the bounds of benefits/burdens.

FUTILITY The concept of futility, derived from the Greek word futilis, meaning “to leak” (as in Greek mythology), refers to the inability to accomplish a therapeutic goal through medical interventions regardless of the duration of such interventions or the frequency with which they are repeated. The concept of futility is central to initial withdraw/withhold support decisions. Determination of futility requires two elements: (a) the establishment of an agreed-upon therapeutic goal and (b) determination of the probability, given the application of medical therapy, of reaching these therapeutic goals. Therapeutic goals

Principles of Critical Care In patients with multiple organ dysfunction, determination of futility is often achieved in those with three or more organ failures as mortality in these circumstances approaches 100%.

DECISION-MAKING CAPACITY AND AUTONOMY DMC, which has different implications than the legal term competent, requires the following: • The patient must be able to comprehend and communicate information relevant to making a decision. • The patient must be able to comprehend his or her alternatives and the benefits and burdens (risks) associated with each. • The patient must be able to reason and deliberate about these alternatives against a background of stable personal values. The determination of DMC may generally be made by the primary physician or team, but occasionally, particularly in the presence of underlying psychiatric illness, psychiatric consultation may be of benefit in making this determination. The exercise of autonomy is best accomplished by allowing any patient with DMC to participate in withdraw/withhold or DNR decisions. In many cases, a patient’s specific wishes may not be known and legal surrogates or medical directives may be unavailable. With careful adjustment (lightening to the extent possible) of any conscious sedation and directed efforts made in communicating the alternatives (full disclosure), many patients can make decisions or at least provide valuable information allowing surrogates to do so. The written medical directive provides an alternative means by which a patient may exercise autonomy. Medical directives may be structured in a variety of ways—depending on known medical conditions, age of the patient, and so forth—but they typically contain language stipulating preferences (or not) for life-sustaining treatment as a function of expected physical and cognitive outcomes.

DECISION MAKING IN THE ABSENCE OF DECISION-MAKING CAPACITY In situations where the patient does not have DMC and no specific medical directive is available, a surrogate decisionmaking process is utilized. Participants in the surrogate decision-making process may include family members, friends, other health care providers, clergy, and members of the institutional ethics committee. Family members invested with durable power of attorney may make clinically appropriate decisions independently on behalf of the patient. (Durable refers to power of attorney, including instances in which the patient is incapacitated.) Surrogate decision making should involve close collaboration between health care providers and the family to the extent possible. The specific role of the family, however, in the absence of durable power, is not to actually make withdraw/withhold decisions but to provide information allowing

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should be outlined as specifically as possible and may incorporate elements of both physical and cognitive functions. Patients with DMC must be allowed to define their own therapeutic goals, regardless of how “unreasonable” or stringent these goals may seem. The determination of the probability of medical therapy in achieving those goals should be left to the team of treating physicians. Schneiderman et al. have suggested a numerical definition of futility corresponding to a 1% probability.111 This would imply that medical care was futile if, in the experience of a provider or that reported in the literature, the intervention failed to achieve therapeutic goals in the last 100 cases in which it was applied. Although not all providers may adhere to such rigorous quantitative definitions, the general concept of futility is well recognized and broadly applied in such settings. Futility must always be judged, however, based on defined therapeutic goals. Once a given treatment or treatments are deemed to be futile, based on established therapeutic goals, the physician is under no legal or ethical obligation to provide such treatment. Current writing in medical ethics, public policy, and more recently by case law has supported this perspective, although some ethicists do not support this medical prerogative. Individual circumstances, however, particularly in regard to family considerations and consistent with the principle of beneficence, may occasionally be indications for shortterm delivery of what otherwise would be considered medically futile care. During the early ICU phase of care, determination of futility often is achieved in patients with severe nonsurvivable brain injuries (transaxial gunshot injuries or open skull fractures with loss of brain tissue and GCS  3). Patients with significant comorbidities, particularly those with end-stage liver or renal disease, and those with malignancies are not candidates for extreme resuscitation efforts or massive transfusion. To the same extent, blunt trauma victims with significant intra-abdominal bleeding and associated nonsurvivable brain injury, 60% TBSA burns, and cervical spinal cord transactions should not be aggressively resuscitated. Even if some of these patients survive, they will do so with a very poor quality of life and it is the trauma surgeon’s responsibility to provide the family with such information. Patients who received massive blood transfusions in the OR without complete hemostasis usually present to the ICU as hypothermic, acidotic, and coagulopathic. Although difficult to estimate, the rapidity of bleeding and transfusion requirements greater than two blood volumes have traditionally been used as markers of irreversibility and most surgeons would agree that in these circumstances, if bleeding is nonmechanical and hypothermia and coagulopathy have not improved over a period of 6–8 hours, further resuscitation efforts are probably futile and will serve only to consume precious resources.112 Late in the course of ICU care, defining futility in patients with neurologic injury is difficult, as it is almost impossible to predict those who will not achieve a meaningful recovery. Age and comorbidities should be considered when presenting the facts to family members, and they may facilitate the family’s decision to withdraw care.

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providers to best formulate decisions consistent with what the patient’s desires would be. This information may include knowledge of the patient’s values, goals, religious or philosophical beliefs, or previously expressed wishes with respect to medical care. The importance of this information should not be underestimated; in the absence of durable power of attorney, family members have no recognized legal authority to dictate care or to make decisions that are medically or ethically inappropriate. Health care professionals also have a primary responsibility to act in what they perceive to be the best interests of the patient, which may occasionally be in conflict with wishes expressed by the family or, on rare occasions, the wishes expressed by a durable power agent. In the absence of any information pertaining to the presumptive wishes of the patient, substituted judgment may be applied based on several considerations: • What would a “reasonable” person want under similar circumstances? Physicians should rarely be making this judgment independently, and the involvement of colleagues or a formal ethics committee consultation may be appropriate. • What would the likely benefits of continued treatment be (treatment outcome), weighed against the burdens imposed by both the treatment and the treatment outcome? The anticipated degree of functional recovery and resultant quality of life are important factors in this consideration. Therapeutic intervention designed to prolong life in a setting in which the quality of that life—because of severity of pain, lack of cognitive function, and so forth—is regarded as being excessively burdensome to an individual may not be medically appropriate. • What would, overall, be in the patient’s best interests? In many cases, the outcome from a critical illness and specific degree of disability, at a given point in time, cannot be predicted with any degree of certainty. The best interests test prevents premature withdraw/withhold decisions from being made that might deprive a patient of an opportunity for satisfactory recovery. Substituted judgment involves subjective analysis and is associated with a significant amount of uncertainty. Although the strong tendency may be to continue treatment when therapeutic goals or the patient’s wishes are not known, this course of action may also be inappropriate. Additional professional consultation, including the institutional ethics committee, may help resolve the more difficult cases.

CONFLICT RESOLUTION With good ongoing communication, full disclosure of relevant information and prognosis, and sensitivity to patient/ family dynamics, withdraw/withhold support decisions can generally be made smoothly. The liberal use of consultants, particularly those involving the neurosciences, may be a valuable adjunct under such circumstances. Ethics consultation services have also been shown to affect management outcome when they are made available. Conflicts may arise, however, over issues of futility, therapeutic goals, and the conduct of

surrogate decision making. These conflicts are often based on misunderstanding or mistrust and exacerbated by the lack of good communication. In situations in which conflict between care providers and family members appears to be irreconcilable, even with ethics committee and institutional risk management/legal consultation, a number of alternatives should be offered to the family. These alternatives may include the following: (a) procurement of additional intramural or extramural medical, religious, or ethical consultations; (b) transferring the care of the patient to another provider within the institution; (c) transfer of the patient to another institution, under the care of another provider; and (d) procurement of a court order mandating a course of treatment. In most cases, careful collaboration with next of kin and extensive consultation with subspecialty services and/or ethics committee usually will serve to clarify issues surrounding the withdrawal/withholding of support and allow reasonable decisions to be made.

DO NOT RESUSCITATE ORDERS The institution of DNR medical directives has been primarily based on the desire to avoid the indignity of futile cardiopulmonary resuscitation in the setting of inexorable progression of underlying known disease processes. Such orders are frequently applied to patients with long-standing terminal disease (e.g., cancer, end-stage AIDS, irreversible multiple organ failure). DNR orders are implicitly coupled to futility judgments about the benefit of cardiopulmonary resuscitation to achieve prospectively defined therapeutic goals. Under such circumstances, these orders are entirely appropriate and desirable in the variety of clinical disease states. The practice of DNR suspension has occurred most frequently in the operating room, where the intensity of therapeutic intervention frequently results in iatrogenic complications. Most physicians and ethicists believe these complications should be treated, since they generally do not constitute inexorable progression of a known disease process, for which the DNR order was originally designed. In the ICU, particularly the surgical ICU, similar situations may exist. The intensity of critical care interventions with mechanical ventilators and the use of complex drug regimens, including vasoactive drugs, may lead to unexpected (iatrogenic) complications unrelated directly to the underlying disease process for which a DNR order may have been originally placed. In addition, the critical illness being treated in the surgical ICU, particularly for trauma patients, results from a discreet event (surgery or injury) as opposed to complications or exacerbations of chronic disease, as is often the case for medical patients. The presumed reversibility of the physiologic sequelae constitutes a basis for ICU treatment of the trauma patient. As such, DNR for the trauma patient should be applied very carefully to expected complications, or physiologic changes due to inexorable progression of known underlying disease, as opposed to unexpected, very reversible iatrogenic complications. DNR orders for trauma patients may be more appropriately linked to withdraw/withhold support conditions than more

Principles of Critical Care

PALLIATIVE CARE IN THE ICU ICUs have the expectation of being able to provide innovative, highly complex care to help save the lives and limbs of severe trauma patients. However, with the aging of the population there are increased numbers of geriatric trauma victims, in addition to other cases where medical technology can sustain life but not necessarily return quality of life to the severely injured patient. Elderly patients may have preexisting multiple comorbidities to which trauma may be a final, irrecoverable insult. Patients may have multiple, complex problems and may require multiple ICU admissions over the course of their illness. There are several barriers to providing effective palliative care in ICU setting. A 2006 survey of critical care providers noted that these barriers include: • Insufficient communication skills about end-of-life issues among health care providers • Inability of patients to participate in discussions about their treatment • Unrealistic expectations on the part of patients and families about the prognosis of patients or the effectiveness of ICU treatment • Lack of advance directives from patients about how they wish their care to be handled at the end of life114 Palliative care programs have been instituted at ICUs that focus on effective pain and symptom management whether life-prolonging or curative care is being pursued or is being withheld or withdrawn. They may also ease case management burdens on primary physician and staff and provide assistance with care coordination and time-intensive patient–family communication. Members of the American College of Surgeons Surgical Palliative Care Task Force have identified common criteria where a palliative care consult may be indicated (Table 55-12).115

STRUCTURED MEETINGS WITH FAMILIES OF ICU PATIENTS Family meetings facilitate communication between families of patients and critical care providers. Effective communication improves clinical decision making, patient and family satisfaction, and the psychological well-being of family

TABLE 55-12 Top 10 Criteria for Consultation Identified by Members of American College of Surgeons Surgical Palliative Care Task Force Family request Family disagreement with team, advance directive, or each other lasting 4 days Glasgow Outcome Score 3 (i.e., persistent vegetative state) Futility considered or declared by medical team Death expected during same surgical intensive care unit stay A diagnosis with median survival 6 months Carcinomatosis or unresectable malignancy Presence of an advance directive authorizing withdrawal of care Glasgow Coma Score 8 for 1 week in a patient 55 years old Multisystem organ failure 2 systems

members (Table 55-13). As a result, research agendas and lists of quality indicators are increasingly recognizing the importance of good communication with families. Some practical guidelines for family meetings are shown in Table 55-14.

TABLE 55-13 Talking with ICU Families 1. Communicate regularly, using family meetings prophylactically. Beware of family members who are nonparticipants. Involve the staff, especially the nurse. 2. Listen, listen, for family understanding, affect, and how they make decisions. Establish trust. Acknowledge emotions. Avoid jargon. Lecture less and let the family guide you to further topics. 3. Provide psychosocial and spiritual support. Offer hope, not false hope. Bad news is a shock. Use support from the team. Culture and religion play key roles. 4. Inform family regularly about goals of care and how we know if goals are met. 5. Convey uncertainty; avoid false certainty. Describe treatment as a “therapeutic time trial” aimed at specific short-term goals. 6. “Care” always continues, but treatments may be withdrawn or withheld. 7. Do not ask the family to decide about each diagnostic or treatment option; ask them what the patient would want and allow them to concur with a plan consistent with patient values. Reproduced with permission from the Massachusetts General Hospital Palliative Care Service, http://www.massgeneral. org/palliativecare/assets/3x5guidetofamilymtg.pdf.

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generally to patients with a poor but potentially reversible prognosis. The variability with which DNR orders are interpreted and the “message” such orders send to providers also raises concerns about their applicability for trauma patients. A study by Clemency and Thompson suggests a wide variability in the perception of DNR orders in the perioperative period.113 This variability conceivably would apply to the “peri-injury” period as well. In addition to the potential for the inappropriate application of DNR orders in an ICU, application may result in less aggressive care on the part of ancillary providers. DNR orders constitute the prospective application of a specific “withhold support” decision and should be made with the same care and consideration, as described in the above section, as any decision involving the limitation of critical care.

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TABLE 55-14 Guide to ICU Family Meetings

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1. Prepare agenda and setting Assure team consensus on facts. Decide who comes to the meeting and who leads the discussion 2. Introduce participants 3. Assess family understanding and what they want to know 4. Summarize the patient’s medical condition and key clinical decisions 5. What is it like for the patient now? 6. What was the patient like? What would the patient want in such circumstances ⴝ “substituted judgment” 7. Explore and address family fears and concerns 8. Frame recommendations 9. Plan for follow-up 10. Document meeting and communicate content to team Reproduced with permission from the Massachusetts General Hospital Palliative Care Service, http://www.massgeneral. org/palliativecare/assets/3x5guidetofamilymtg.pdf.

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Principles of Critical Care 68. Soo Hoo GW, Park L. Variations in the measurement of weaning parameters: a survey of respiratory therapists. Chest. 2002;121:1947–1955. 69. Petersen GW, Baier H. Incidence of pulmonary barotrauma in a medical ICU. Crit Care Med. 1983;11:67–69. 70. Webb HH, Tierney DF. Experimental pulmonary edema due to intermittent positive pressure ventilation with high inflation pressures. Protection by positive end-expiratory pressure. Am Rev Respir Dis. 1974;110:556–565. 71. Ricard JD, Dreyfuss D, Saumon G. Production of inflammatory cytokines in ventilator-induced lung injury: a reappraisal. Am J Respir Crit Care Med. 2001;163:1176–1180. 72. Tejeda M, Boix JH, Alvarez F, et al. Comparison of pressure support ventilation and assist-control ventilation in the treatment of respiratory failure. Chest. 1997;111:1322–1325. 73. Betensley AD, Khalid I, Crawford J, et al. Patient comfort during pressure support and volume controlled-continuous mandatory ventilation. Respir Care. 2008;53:897–902. 74. Sternberg R, Sahebjami H. Hemodynamic and oxygen transport characteristics of common ventilatory modes. Chest. 1994;105:1798–1803. 75. Guldager H, Nielsen SL, Carl P, et al. A comparison of volume control and pressure-regulated volume control ventilation in acute respiratory failure. Crit Care. 1997;1:75–77. 76. MacIntyre NR. Respiratory function during pressure support ventilation. Chest. 1986;89:677–683. 77. Esteban A, Frutos F, Tobin MJ, et al. A comparison of four methods of weaning patients from mechanical ventilation. Spanish Lung Failure Collaborative Group. New Engl J Med. 1995;332:345–350. 78. Garner W, Downs JB, Stock MC, et al. Airway pressure release ventilation (APRV). A human trial. Chest. 1988;94:779–781. 79. Fort P, Farmer C, Westerman J, et al. High-frequency oscillatory ventilation for adult respiratory distress syndrome—a pilot study. Crit Care Med. 1997;25:937–947. 80. Bollen CW, van Well GT, Sherry T, et al. High frequency oscillatory ventilation compared with conventional mechanical ventilation in adult respiratory distress syndrome: a randomized controlled trial [ISRCTN 24242669]. Crit Care. 2005;9:R430–R439. 81. Douglas WW, Rehder K, Beynen FM, et al. Improved oxygenation in patients with acute respiratory failure: the prone position. Am Rev Respir Dis. 1977;115:559–566. 82. Taccone P, Pesenti A, Latini R, et al. Prone positioning in patients with moderate and severe acute respiratory distress syndrome: a randomized controlled trial. JAMA. 2009;302:1977–1984. 83. Michael JR, Barton RG, Saffle JR, et al. Inhaled nitric oxide versus conventional therapy: effect on oxygenation in ARDS. Am J Respir Crit Care Med. 1998;157:1372–1380. 84. Yang KL, Tobin MJ. A prospective study of indexes predicting the outcome of trials of weaning from mechanical ventilation. New Engl J Med. 1991;324:1445–1450. 85. Kollef MH, Shapiro SD, Silver P, et al. A randomized, controlled trial of protocol-directed versus physician-directed weaning from mechanical ventilation. Crit Care Med. 1997;25:567–574. 86. Goettler CE, Fugo JR, Bard MR, et al. Predicting the need for early tracheostomy: a multifactorial analysis of 992 intubated trauma patients. J Trauma. 2006 (5):991–996. 87. Rumbak MJ, Newton M, Truncale T, et al. A prospective, randomized, study comparing early percutaneous dilational tracheotomy to prolonged translaryngeal intubation (delayed tracheotomy) in critically ill medical patients. Crit Care Med. 2004;32:1689–1694. 88. Sugerman HJ, Wolfe L, Pasquale MD, et al. Multicenter, randomized, prospective trial of early tracheostomy. J Trauma. 1997;43:741–747. 89. Ahmed N, Kuo YH. Early versus late tracheostomy in patients with severe traumatic head injury. Surg Infect. 2007;8:343–347. 90. de Lassence A, Alberti C, Azoulay E, et al. Impact of unplanned extubation and reintubation after weaning on nosocomial pneumonia risk in the intensive care unit: a prospective multicenter study. Anesthesiology. 2002;97:148–156. 91. Chevron V, Menard JF, Richard JC, et al. Unplanned extubation: risk factors of development and predictive criteria for reintubation. Crit Care Med. 1998;26:1049–1053. 92. Jacobi J, Fraser GL, Coursin DB, et al. Clinical practice guidelines for the sustained use of sedatives and analgesics in the critically ill adult. Crit Care Med. 2002;30:119–141. 93. Vender JS, Szokol JW, Murphy GS, Nitsun M. Sedation, analgesia, and neuromuscular blockade in sepsis: an evidence-based review. Crit Care Med. 2004;32:S554–S561. 94. Sessler CN, Gosnell MS, Grap MJ, et al. The Richmond AgitationSedation Scale: validity and reliability in adult intensive care unit patients. Am J Respir Crit Care Med. 2002;166:1338–1344.

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41. Singh AK, Szczech L, Tang KL, et al. Correction of anemia with epoetin alfa in chronic kidney disease. N Engl J Med. 2006;355: 2085–2098. 42. Pfeffer MA, Burdmann EA, Chen CY, et al. A trial of darbepoetin alfa in type 2 diabetes and chronic kidney disease. N Engl J Med. 2009;361: 2019–2032. 43. Corwin HL, Gettinger A, Rodriguez RM, et al. Efficacy of recombinant human erythropoietin in the critically ill patient: a randomized, doubleblind, placebo-controlled trial. Crit Care Med. 1999;27:2346–2350. 44. Corwin HL, Gettinger A, Pearl RG, et al. Efficacy of recombinant human erythropoietin in critically ill patients: a randomized controlled trial. JAMA. 2002;288:2827–2835. 45. Corwin HL, Gettinger A, Fabian TC, et al. Efficacy and safety of epoetin alfa in critically ill patients. N Engl J Med. 2007;357:965–976. 46. Napolitano LM, Fabian TC, Kelly KM, et al. Improved survival of critically ill trauma patients treated with recombinant human erythropoietin. J Trauma. 2008;65:285–297. 47. Arroliga AC, Guntupalli KK, Beaver JS, Langholff W, Marino K, Kelly K. Pharmacokinetics and pharmacodynamics of six epoetin alfa dosing regimens in anemic critically ill patients without acute blood loss. Crit Care Med. 2009;37:1299–1307. 48. Christmas AB, Camp SM, Barrett MC, et al. Removal of erythropoietin from anaemia trauma practice guideline does not increase red blood cell transfusions and decreases hospital utilization costs. Injury. 2009;40: 1330–1335. 49. Bratton SL, Chestnut RM, Ghajar J, et al. Guidelines for the management of severe traumatic brain injury. VI. Indications for intracranial pressure monitoring. J Neurotrauma. 2007;24(suppl 1):S37–S44. 50. Thomason MH, Rutledge R. A statewide analysis of the use of intracranial pressure monitoring with the outcome of severe head injury in 1,563 patients. J Trauma. 1998;45(1):192. 51. Goel RS, Goyal NK, Dharap SB, Kumar M, Gore MA. Utility of optic nerve ultrasonography in head injury. Injury. 2008;39:519–524. 52. Kimberly HH, Shah S, Marill K, Noble V. Correlation of optic nerve sheath diameter with direct measurement of intracranial pressure. Acad Emerg Med. 2008;15:201–204. 53. Reid CL. Poor agreement between continuous measurements of energy expenditure and routinely used prediction equations in intensive care unit patients. Clin Nutr. 2007;26:649–657. 54. van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in the critically ill patients. N Engl J Med. 2001;345:1359–1367. 55. Vogelzang M, Nijboer JM, van der Horst IC, Zijlstra F, ten Duis HJ, Nijsten MW. Hyperglycemia has a stronger relation with outcome in trauma patients than in other critically ill patients. J Trauma. 2006;60: 873–877. 56. Brunkhorst FM, Engel C, Bloos F, et al. Intensive insulin therapy and pentastarch resuscitation in severe sepsis. N Engl J Med. 2008;358: 125–139. 57. Preiser JC, Devos P, Ruiz-Santana S, et al. A prospective randomised multi-centre controlled trial on tight glucose control by intensive insulin therapy in adult intensive care units: the Glucontrol study. Intensive Care Med. 2009;35:1738–1748. 58. Finfer S, Chittock DR, Su SY, et al. Intensive versus conventional glucose control in critically ill patients. N Engl J Med. 2009;360: 1283–1297. 59. Annane D, Sebille V, Charpentier C, et al. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA. 2002;288:862–871. 60. Sprung CL, Annane D, Keh D, et al. Hydrocortisone therapy for patients with septic shock. N Engl J Med. 2008;358:111–124. 61. Reed RL. Contemporary issues with bacterial infection in the intensive care unit. Surg Clin North Am. 2000;80:895–909. 62. Appelgren P, Hellstrom I, Weitzberg E, Soderlund V, Bindslev L, Ransjo U. Risk factors for nosocomial intensive care infection: a long-term prospective analysis. Acta Anaesthesiol Scand. 2001;45:710–719. 63. Severinghaus JW, Bradley AF. Electrodes for blood pO2 and pCO2 determination. J Appl Physiol. 1958;13:515–520. 64. Soubani AO. Noninvasive monitoring of oxygen and carbon dioxide. Am J Emerg Med. 2001;19:141–146. 65. Vukmir RB, Heller MB, Stein KL. Confirmation of endotracheal tube placement: a miniaturized infrared qualitative CO2 detector. Ann Emerg Med. 1991;20:726–729. 66. Warner KJ, Cuschieri J, Garland B, et al. The utility of early end-tidal capnography in monitoring ventilation status after severe injury. J Trauma. 2009;66:26–31. 67. Meade M, Guyatt G, Cook D, et al. Predicting success in weaning from mechanical ventilation. Chest. 2001;120:400S–424S.

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95. Barrientos-Vega R, Mar Sanchez-Soria M, Morales-Garcia C, RobasGomez A, Cuena-Boy R, Ayensa-Rincon A. Prolonged sedation of critically ill patients with midazolam or propofol: impact on weaning and costs. Crit Care Med. 1997;25:33–40. 96. Aitkenhead AR, Pepperman ML, Willatts SM, et al. Comparison of propofol and midazolam for sedation in critically ill patients. Lancet. 1989;2:704–709. 97. Riker RR, Shehabi Y, Bokesch PM, et al. Dexmedetomidine vs midazolam for sedation of critically ill patients: a randomized trial. JAMA. 2009;301:489–499. 98. Girard TD, Kress JP, Fuchs BD, et al. Efficacy and safety of a paired sedation and ventilator weaning protocol for mechanically ventilated patients in intensive care (Awakening and Breathing Controlled trial): a randomised controlled trial. Lancet. 2008;371:126–134. 99. Schweickert WD, Pohlman MC, Pohlman AS, et al. Early physical and occupational therapy in mechanically ventilated, critically ill patients: a randomised controlled trial. Lancet. 2009;373:1874–1882. 100. Strom T, Martinussen T, Toft P. A protocol of no sedation for critically ill patients receiving mechanical ventilation: a randomised trial. Lancet. 2010;375:475–480. 101. Ely EW, Margolin R, Francis J, et al. Evaluation of delirium in critically ill patients: validation of the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU). Crit Care Med. 2001;29: 1370–1379. 102. Plaschke K, von Haken R, Scholz M, et al. Comparison of the confusion assessment method for the intensive care unit (CAM-ICU) with the Intensive Care Delirium Screening Checklist (ICDSC) for delirium in critical care patients gives high agreement rate(s). Intensive Care Med. 2008;34:431–436. 103. Saint S, Veenstra DL, Lipsky BA. The clinical and economic consequences of nosocomial central venous catheter-related infection: are antimicrobial catheters useful? Infect Control Hosp Epidemiol. 2000;21:375–380.

104. Hund EF, Fogel W, Krieger D, DeGeorgia M, Hacke W. Critical illness polyneuropathy: clinical findings and outcomes of a frequent cause of neuromuscular weaning failure. Crit Care Med. 1996;24:1328–1333. 105. Albreksten S, Thomsen J. Detection of injuries in traumatic deaths: the significance of the medicolegal autopsy. Forensic Sci. 1989;42:135. 106. Fulton RL, Peter ET. Compositional and histologic effects of fluid therapy following pulmonary contusion. J Trauma. 1974;14:783. 107. Patel NY, Hoyt DB, Nakaji P, et al. Traumatic brain injury: patterns of failure of nonoperative management. J Trauma. 2000;48(3): 367–375. 108. Luce JM. Withholding and withdrawing life support from the critically ill: how does it work in clinical practice? Respir Care. 1991;36:417–426. 109. Ethical and moral guidelines for the initiation, continuation, and withdrawal of intensive care. American College of Chest Physicians/ Society of Critical Care Medicine Consensus Panel. Chest. 1990;97: 949–958. 110. Smedira NG, Evans BH, Grais LS, et al. Withholding and withdrawal of life support from the critically ill. N Engl J Med. 1990;322:309–315. 111. Schneiderman LJ, Jecker NS, Jonsen AR. Medical futility: its meaning and ethical implications. Ann Intern Med. 1990;112:949–954. 112. Coimbra R, Lee J, Bansal V, Hollingsworth-Fridlund P. Recognizing/ accepting futility: prehospital, emergency center, operating room and intensive care unit. J Trauma Nurs. 2007;14(2):1–4. 113. Clemency MV, Thompson NJ. “Do not resuscitate” (DNR) orders in the perioperative period—a comparison of the perspectives of anesthesiologists, internists, and surgeons. Anesth Analg. 1994;78: 651–658. 114. Nelson JE, Angus DC, Weissfeld LA, et al. End-of-life care for the critically ill: a national intensive care unit survey. Crit Care Med. 2006; 34:2547–2553. 115. Bradley CT, Brasel KJ. Developing guidelines that identify patients who would benefit from palliative care services in the surgical intensive care unit. Crit Care Med. 2009;37:946–950.

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CHAPTER 56

Cardiovascular Failure Mary Margaret Wolfe and Fred Luchette

INTRODUCTION Cardiovascular failure can be either the end result of multisystem organ failure (MOF) or a precursor to shock and MOF (see Chapter 61). Most often cardiovascular collapse will manifest itself with clinical signs and symptoms of cardiac failure. In trauma, the most common cause of shock is acute blood loss (hypovolemia), which results in decreased preload or decreased right heart filling volumes and manifests as tachycardia and hypotension (see Chapter 12). Although this is the most common type of shock occurring after injury, cardiogenic shock, resulting from impaired myocardial contractility, and septic shock, characterized by failure of the heart to overcome decreased vascular tone and failure of end-organ utilization of delivered oxygen, are also seen. As our population ages, the number of elderly patients in the intensive care unit (ICU) will increase. In fact, the number of elderly patients (65 years old) is expected to double in the next three decades. With an aging population, there are age-related changes in physiology, exacerbations of chronic illnesses, and effects of therapeutic drugs, which need to be taken into consideration when caring for the traumatically injured patient.1–3 Therapy to support the failing cardiovascular system is directed at the etiology of the shock state and includes fluid resuscitation (preload) as well as pharmacologic modulation of vascular tone (afterload), contractility (with inotropes), and heart rate (with chronotropes) (Fig. 56-1).

DETERMINANTS OF CARDIAC OUTPUT Cardiac output is defined as the quantity of blood ejected into the aorta by the heart each minute and is calculated as heart rate multiplied by stroke volume (CO  HR  SV). This is the quantity of blood that flows through the circulation and is responsible for oxygen and nutrient transport to the tissues. The primary determinants of cardiac output are preload (the

venous return to the heart), afterload (the resistance against which the heart must pump), contractility (the extent to which the myocardial cells can contract), and heart rate. The primary determinant of cardiac output is the filling of the heart and the ability to pump that volume effectively. Accordingly, the majority of therapeutic modalities aimed at augmenting cardiac output focus on restoring filling pressures and augmenting ineffective contractility. Multiple studies and textbooks cite 5.6 L/min as a “normal” resting cardiac output as measured in young, healthy males. However, cardiac output varies with the level of activity of the body, and is influenced by level of metabolism, exercise state, age, size of the individual, and other factors. Accordingly, cardiac output in women is generally stated as being 10–20% lower than in men. Additionally, when factoring in age, the average cardiac output for adults is approximated as 5 L/min. Laboratory and clinical research have demonstrated that cardiac output increases in proportion to increasing body surface area. Therefore, to standardize cardiac output measurements between individuals, the parameter of cardiac index (defined as cardiac output divided by body surface area in m2) is employed.4

■ Preload In the discussion of cardiovascular physiology, preload is the force that stretches myocardium prior to contraction. The concept of preload is derived from laboratory experiments in which strips of muscle are stretched by small weights (preload) prior to initiating contraction. In these experiments, contraction is triggered by electrical stimulation and a transducer determines the resultant force. Both in vitro experiments and in vivo correlates have revealed that increasing sarcomere length to a maximum of 0.2 m by the addition of weights results in increased force of contraction. Once stretched beyond this length, the contractility of the muscle decreases. This relationship, the Frank–Starling relationship, was described in

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Management of Complications after Trauma

Hemodynamic in stability or evidence of end-organ hypoperfusion Measure CVP

SECTION 5 X

CVP low (<15 mmHg) Fluid resuscitation with crystalloid or blood products until CVP>15 mmHg or end-organ hypoperfusion resolves (at lower CVP)

PAWP low (<5 mmHg), CI high (>3.8 L/min/m2) Non-cardiac failure

CI improves Continue volume resuscitation until hemodynamically stable

CVP normal/high (>15 mmHg) Insert PA catheter and determine PAWP and CI

PAWP high (>15 mmHg), CI high (>3.8 L/min/m2) Decrease fluid resuscitation and consider diuresis if signs of pulmonary edema

PAWP low (<5 mmHg), CI low (<2 L/min/m2) Fluid resuscitation to increase PAWP by 3-5 mmHg, then re-measure CI

PAWP high (>15 mmHg), CI low (<2 L/min/m2) Measure sBP and calculate SVR

CI remains low (<2 L/min/m2) Measure sBP and calculate SVR

Normotensive or hypertensive (SVR high) Afterload reduction with nitroprusside (start 0.5 μg/kg/min, increase until CI increases, titrate to maintain sBP >80 mmHg)

Improved CI with persistent hypotension Levophed (start 0.5 μg/min, titrate to maintain sBP >80 mmHg), Consider adding vasopressin (0.04 U/min)

Hypotensive or continued low CI Inotropic support with dobutamine (start 5 μg/kg/min, increase until CI increases or until arrythmias develop)

No response Amrinone (load 0.75 mg/kg over 5 minutes, then 5-10 μg/kg/min)

FIGURE 56-1 Clinical decision tree for the diagnosis and management of cardiovascular failure.

amphibian hearts by Otto Frank in 1884 and extended to mammalian hearts by Ernest Starling in 1914. The mechanisms linking preload and contractile force are incompletely understood. Although it was initially thought that increased myocardial stretch optimized the overlap of contractile actin and myosin leading to increased force of contraction, more recent research indicates that contractile force is also dependent on sensitivity of the myocyte to ionized calcium gradients, as determined by sarcomere length.5 The Frank–Starling relationship provides a paradigm by which the cardiovascular system and its derangements can be approached. Hypovolemia, or decreased preload, is the result of hemorrhage, contraction of the intravascular space due to exter-

nal fluid losses such as diarrhea, inappropriate polyuria, or contraction of the intravascular space due to internal sequestration as edema or third-space losses. Additionally, venous return to the heart depends on the vascular tone of the venous system. As will be discussed in the pharmacology portion of this chapter, changes in venous capacitance are often unwanted side effects of pharmacologic agents used in treating the injured patient. Taken together, intravascular volume and venous return determine left ventricular end-diastolic volume (LVEDV), which determines the force of ventricular contraction. The Swan–Ganz catheter is used to measure the pulmonary arterial wedge pressure (PAWP), which approximates left ventricular

Cardiovascular Failure

Cardiovascular failure due to a reduction in afterload is referred to as distributive shock, and has multiple etiologies: septic shock, neurogenic shock, and anaphylactic shock. Afterload is the force that opposes ventricular contraction. Similar to preload, the concept of afterload is derived from in vitro experiments using strips of cardiac muscle. In these experiments, length is held constant while the muscle is given a variable load that must be moved (afterload). These studies have established that increasing afterload decreases the speed and force of contraction. Clinically, vascular input impedance appears to be the best in vivo correlate of ventricular afterload. Unfortunately, vascular input impedance is not a readily assessed clinical quantity, requiring right heart catheterization and continuous

SVR  (MAP  CVP)/CO In this equation, MAP is the mean arterial blood pressure, CVP is the central venous pressure, and CO is the cardiac output. This equation provides an approximation of vascular impedance. Therefore, it is important to realize that the clinical practice of “measuring” afterload or SVR with data from the Swan–Ganz catheter actually provides a calculated value that assumes nonpulsatile flow and does not consider the viscosity of blood, the elastic properties of the arterial walls, or the changes in microvascular resistance. Finally, because SVR is inversely proportional to cardiac output, rather than directly treating an abnormally high SVR, one should first treat the low cardiac output with fluid administration to maximize preload, which will serve to increase CO and decrease SVR.

■ Contractility Contractility, also known as inotropic state, is the force with which the myocardium contracts. The inotropic state of the myocardium, and the stroke work performed, can be visualized by the construction of a left ventricular pressure–volume loop (Fig. 56-2). This loop is bounded by the four phases of the cardiac cycle: isovolemic relaxation, diastolic filling, isovolemic contraction, and systolic ejection. Stroke work is defined as the area bounded by this loop. Instantaneous pressure–volume curves also provide a method to determine both external (stroke work) and internal (loss as heat) work performed by the heart during the cardiac cycle. As described above, the area bounded by the pressure–volume loop defines the external, or stroke work performed by the myocardium. The internal work is defined as the area of the triangle determined graphically by three lines: an extrapolation of the elastance line to the x-intercept, the isovolemic relaxation portion of the pressure–volume loop, and the diastolic filling

Closing of aortic valve Left ventricular pressure

■ Afterload

Doppler readings. Therefore, the clinician must rely on systemic vascular resistance (SVR) as a surrogate. SVR is calculated using the hemodynamic equivalent of Ohm’s law:

Systolic ejection

Opening of aortic valve

Isovolemic contraction

Isovolemic relaxation

Closing of mitral valve Diastolic filling Opening of mitral valve

Left ventricular volume

FIGURE 56-2 The relationship between left ventricular pressure and left ventricular volume during a stylized cardiac cycle.

CHAPTER CHAPTER 56 X

end-diastolic pressure (LVEDP). Assuming unaltered ventricular compliance, LVEDP theoretically approximates the LVEDV. Unfortunately, in the setting of critically ill patients, factors such as myocardial ischemia, heart failure, myocardial edema, endotoxemia, cardiac hypertrophy, and circulating tumor necrosis factor (TNF) can decrease ventricular compliance, rendering measurement of PAWP as a surrogate for LVEDV unreliable. In these situations, normal or elevated PAWP may not eliminate inadequate preload as a cause of low cardiac output. Besides changes in venous capacitance, venous return to the heart can be compromised by increased intrathoracic or intra-abdominal pressure. This is most evident with tension pneumothorax, when the shock state is immediately reversed by decompression of the pleural space. Additionally, in the mechanically ventilated patient, the use of positive-pressure ventilation coupled with positive end-expiratory pressure (PEEP) may impair venous return to the heart (see Chapter 57). In this patient population, when intravascular volume is low, the adverse effects of increased intrathoracic pressure on preload predominate and cardiac output is diminished. Importantly, when an underresuscitated patient is placed on positive-pressure ventilation, this situation may lead to cardiovascular collapse. However, in the reverse scenario, patients with normal-to-high intravascular volume may benefit from the afterload-reducing effects of elevated intrathoracic pressure seen with positivepressure ventilation. Indeed, synchronization of positive-pressure ventilation with the cardiac cycle has been described as a method of afterload reduction and cardiac output augmentation.6 In the normal heart, this decrease in afterload does not usually translate into enhanced cardiac output. However, those patients with heart failure are more sensitive to the concomitant decrease in preload. There may also be a poorly understood vasodilatory reflex and changes in sympathoadrenal function.7 It should be noted that patients in cardiogenic shock could demonstrate sudden cardiovascular collapse upon removal of ventilatory support. This change in venous return to the heart is also seen in abdominal compartment syndrome and pregnancy (see Chapter 37). It is important to note that the net result of these physiologic changes may be hard to predict in clinical practice, but a thorough knowledge of the underlying physiology is the key to prompt diagnosis and management.

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SECTION 5 X

Afterload A

Afterload B

Management of Complications after Trauma

Left ventricular pressure

1044

MYOCARDIAL DYSFUNCTION Extra work due to increased afterload

External work for Cycle B

External work for Cycle A

Left ventricular volume

FIGURE 56-3 The effect of changes in afterload on (external) ventricular stroke work at constant stroke volume. The areas inscribed by the heavy lines represent the external stroke work performed during two representative cardiac cycles. Decreasing afterload (from A to B) decreases stroke work.

portion of the pressure–volume loop extrapolated back to its x-intercept (Fig. 56-3). Under this system, the failing heart with low contractility will demonstrate a shallow elastance line, which translates to low efficiency (more internal work performed for the same external work). Clinically, this points toward manipulation of contractility to balance myocardial oxygen demand and delivery. Finally, the strong influence of changes in afterload are readily appreciated under this model, as increasing afterload at a given stroke volume results in increased external work performed by the heart. Presently, the use of pressure–volume curves in patient care is limited to centers using newer generation pulmonary artery catheters (PACs) that measure ventricular volume as well as pressure.8 More commonly, clinicians rely on Frank–Starling curves to determine myocardial performance and estimate contractility. Finally, contractility can be estimated by angiographic or echocardiographic determination of ventricular ejection fraction, but this method is highly sensitive to changes in afterload, and may be less reliable.

■ Heart Rate Heart rate is a key determinant of cardiac output. In the setting of constant stroke volume, increasing the number of cardiac ejections per unit time results in increased cardiac output. In addition, increasing the heart rate increases contractility, a phenomenon known as the Bowditch effect. This effect is due to increases in calcium concentrations. With increased heart rate, the time for reuptake of calcium decreases. The increased calcium concentrations cause upregulation of cAMP, which enhances contractility. However, in the setting of myocardial failure, it is not uncommon to observe heart rates high enough that the diastolic interval is shortened and ventricular filling is compromised, resulting in decreased cardiac output. Rapid ventricular rates that impair cardiac filling are most commonly seen in patients with preexisting or evolving myocardial ischemia. In this setting, rate control becomes paramount in ensuring matched oxygen delivery and utilization.

Myocardial dysfunction can be defined on the basis of perturbed preload, afterload, contractility, or heart rate. Systemic hypovolemia (e.g., inadequate preload), secondary to hemorrhage or third-space losses, is the most common etiology in the postsurgical or trauma patient. Other causes of decreased cardiac output may arise from failing or decreased contractile function of the heart. Evolving ischemia can lead to areas of heart muscle that lose their ability to contract, leading to decreased cardiac output. The contractility of heart muscle can also become altered following any insult that results in intrinsic metabolic derangements at the cellular level. This typically occurs in the settings of sepsis, postcardiac arrest, or postcardiopulmonary bypass. Direct physical injury to the myocardium, as occurs following blunt chest injury, may produce contused cardiac muscle, which can lead to contractile dysfunction and decreased cardiac output. The optimal modalities to diagnose myocardial dysfunction in critically ill patients are poorly established. In this chapter we discuss the evaluation of cardiac function, focusing on measurement of CVP, the use of pulmonary artery (Swan–Ganz) catheters, echocardiography, and noninvasive techniques (see Chapter 17).

MANAGEMENT OF MYOCARDIAL DYSFUNCTION ■ Preload Augmentation and Rewarming Myocardial dysfunction secondary to hypovolemia may be caused by hemorrhage or other causes of intravascular volume loss. Prior to the development of hypotension, most adult patients will demonstrate a decrease in urine output, indicative of end-organ hypoperfusion. Augmentation of preload, or restoration of intravascular volume, will reverse this dysfunction if instituted promptly. Depending on the degree of volume loss, most patients respond to simple crystalloid solutions. However, if severe or ongoing hemorrhage is present, and the patient is not responding to crystalloid administration, transfusion of blood products may be necessary. Normalization of heart rate and blood pressure, along with adequate urine output are simple and effective measurements of adequate volume restoration. During the period of volume replacement, attention must be given to the temperature status of the patient (see Chapter 49). Multiple studies have clearly demonstrated that hypothermia induces a significant depression of both systolic and diastolic left ventricular function.9 The use of warmed fluids during resuscitation results in rapid restoration of left ventricular diastolic function, whereas recovery of systolic function is prolonged.10 This is likely due to long-lasting effects of hypothermia on the excitation–contraction coupling of the actin–myosin complex.

■ Pharmacologic A multitude of pharmacologic agents are available for the management of myocardial dysfunction. Selection of the appropriate agent (or agents) should be tailored to the specific clinical

Cardiovascular Failure

1045

TABLE 56-1 Dosage, Mechanism, and Actions of Pharmacologic Agents Commonly Used in the Treatment of Cardiovascular Failure Typical Dosage

HR

MAP

CO

Norepinephrine Vasopressin

3–5 μg/kg/min 10–20 μg/kg/min 2–20 μg/kg/min 0.5–2 μg/min 2–10 μg/min 0.5–30 μg/min 0.01–0.04 U/min



/



Phosphodiesterase inhibitors: Amrinone Milrinone

5–10 0.3–1.5

Nitrovasodilators: Sodium nitroprusside Nitroglycerin

0.1–5 μg/kg/min 10–20 μg/min

Catecholamines: Dopamine Dobutamine Epinephrine



SVR

α1

 











 



 

β1

β2



DA1 DA2



CO  cardiac output; HR  heart rate; MAP  mean arterial blood pressure; SVR  systemic vascular resistance.

situation. Broadly, the agents can be classified into those that act directly on the vascular system (vasodilatation or constriction) and those that augment cardiac contractility. Selected agents have multiple mechanisms of action (Table 56-1).

■ Norepinephrine Norepinephrine is an endogenous sympathetic neurotransmitter with α- and β-adrenergic effects. At high doses, α-adrenergic effects predominate and increased SVR and increased blood pressure result. Because of this potent vasoconstriction, norepinephrine is generally reserved for patients who are refractory to both volume resuscitation and other inotropic agents.11,12 However, at low doses, the β-adrenergic actions of norepinephrine predominate, resulting in increased heart rate and contractility. Specifically, in the setting of right ventricular failure, low-dose norepinephrine improves cardiac function without adversely affecting visceral perfusion.13 De Backer et al. found no significant overall change in outcome between patients receiving norepinephrine and dopamine for shock.14 However, in those patients with cardiogenic shock, dopamine was associated with a significant increase in the rate of death. This may be due to the higher increase in heart rate seen with dopamine and subsequent ischemic events.14 Additionally, norepinephrine is widely used in the care of the head-injured patient in shock because its vasoconstrictive effects do not extend to the cerebral vasculature, making it an ideal agent for maintaining cerebral perfusion pressure.15

Vasopressin Arginine vasopressin, or vasopressin, is a potent vasoconstrictor. This natural hormone produced by the posterior pituitary has gained widespread acceptance as a treatment for septic shock refractory to volume resuscitation and conventional

pressor agents. During septic shock, the supply of endogenous vasopressin is quickly depleted, and restoration of this deficiency has shown benefits in the weaning of norepinephrine and other pressor agents and also imparts a short-term survival benefit in this group of patients. When vasopressin is combined with norepinephrine, outcomes in the treatment of catecholamine resistant cardiovascular failure in septic shock are superior to therapy with norepinephrine alone.16 Vasopressin has also emerged as a therapy for cardiac arrest and acute resuscitation.17 Current guidelines for cardiopulmonary resuscitation recommend vasopressin as an alternative to epinephrine for shock resistant ventricular fibrillation. Vasopressin is a superior agent to epinephrine in asystolic patients but is similar to epinephrine alone in the treatment of ventricular fibrillation and pulseless electrical activity.18 In the postoperative cardiotomy patient, vasopressin significantly reduces heart rate and the need for both pressor and inotropic support, with no adverse effect on the heart. A significant reduction in cardiac enzymes and cardioversion of arrhythmias into sinus rhythm has also been demonstrated with the use of vasopressin in these patients.19 Patients undergoing cardiopulmonary bypass often experience hemodynamic disturbances similar to those seen in septic patients, with characteristics of peripheral vasodilatation causing hypotension, and diminished response to conventional pressor agents. Vasopressin has been shown to correct vasodilatory shock following cardiopulmonary bypass regardless of normal circulating vasopressin levels.20

■ Dopamine Dopamine is an endogenous catecholamine that has several cardiovascular effects, including increased heart rate, increased contractility, and peripheral vasoconstriction. It is used primarily

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Agent

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for inotropic support in order to maintain brain, heart, and kidney perfusion. Dopamine acts on α- and β-adrenoreceptors as well as DA1 and DA2 dopamine receptors, and its actions can be classified based on dose. At doses of 1–3 μg/kg/min, dopamine acts at primarily DA1 receptors in renal, mesenteric, coronary, and cerebral vascular beds, resulting in vasodilation. It has long been thought that low-dose dopamine (1–3 μg/ kg/min), also referred to as “renal-dose” dopamine, increases renal blood flow and maintains diuresis via the DA1 and DA2 receptors.21 Two meta-analyses and a large prospective, doubleblinded randomized controlled trial have failed to demonstrate that dopamine protects the kidney in critically ill patients with acute renal failure.22–24 For these reasons, there is insufficient evidence to support the use of low-dose dopamine to maintain renal perfusion in an effort to reduce the incidence of acute renal failure (see Chapter 59). At moderate doses (3–5 μg/kg/ min), dopamine stimulates primarily cardiac β-adrenoreceptor, increasing contractility and thus cardiac output. At higher doses of dopamine (10 μg/kg/min), peripheral vasoconstrictive effects from stimulation of α-adrenergic receptors predominate. This can result in significant coronary vasoconstriction resulting in angina, vasospasm, and increased PAWP.25 Additionally, increasing afterload from vasoconstriction coupled with an increased heart rate seen at this dose, results in increased myocardial oxygen consumption and demand. Recent investigation has revealed that individual variation in the pharmacokinetics of dopamine due to weight-based dosing typically results in poor correlation between blood levels and administered dose. Tachycardia can occur with any dose of dopamine, particularly in the hypovolemic patient. When excessive, the increased heart rate will increase myocardial oxygen demand and worsen cardiovascular failure. Due to the variable effects of dopamine, the dosage ranges used to define which receptors it affects are to be used as broad guidelines only, with the awareness that “low-dose” (1–3 μg/kg/min) dopamine may have the unwanted effects of “medium-” (3–5 μg/kg/minute) or “high-dose” (10 μg/kg/min) dopamine on an individual patient.

■ Dobutamine Dobutamine is a synthetic catecholamine with primarily β-adrenegic effects, although it does possess some α1-adrenergic properties. It is primarily an inotrope, increasing contractility, with minimal chronotropic effects. Dobutamine also possesses mild β2-adrenoreceptor activity, producing peripheral vasodilatation. This combination of increased contractility and reduced afterload results in improved cardiac output. Importantly, the increase in cardiac output occurs without an increase in myocardial oxygen consumption.26 Because of the vasodilatory effects, dobutamine may reduce blood pressure and is ideally suited for use in low-output cardiac states. For these reasons, dobutamine should be considered the first-choice inotrope for patients with low cardiac output in the presence of adequate preload.27 Two large prospective trials in critically ill patients failed to demonstrate a benefit to raising oxygen delivery to supranormal levels with the use of dobutamine,28,29 likely due to an inability of the peripheral tissues to utilize the additional oxygen delivered.

■ Epinephrine Epinephrine is an endogenous catecholamine with α- and β-adrenergic activity. At low doses, epinephrine exerts primarily β-adrenergic effects, increasing contractility and reducing SVR. Despite this, there is little evidence that epinephrine is superior to dobutamine in the treatment of low-output states (e.g., myocardial infarction [MI]). The increases in stroke volume and cardiac output seen with epinephrine have the potential of decreasing blood pressure in patients with inadequate preload. In patients with septic shock that have been adequately fluid resuscitated, epinephrine increases heart rate and stroke volume (and therefore cardiac output) and systemic oxygen delivery without altering vascular tone30 At higher rates of infusion, epinephrine exerts primarily α-adrenergic effects, increasing SVR and blood pressure. It is indicated for patients with ventricular dysfunction refractory to dopamine or dobutamine. Care must be taken when using epinephrine, as renal vasoconstriction, cardiac arrythmias, and increased myocardial oxygen consumption and demand may result. Additionally, metabolic abnormalities are common, including dyskalemias, hyperglycemia, and ketoacidosis.31,32 Finally, epinephrine increases blood lactate levels in patients recovering from cardiopulmonary bypass or those with septic shock, likely through increases in tissue oxygen extraction in the absence of adequate delivery.33–35

■ Amrinone and Milrinone Amrinone and milrinone are synthetic bipyridines that belong to the phosphodiesterase inhibitor class, demonstrating both positive inotropic and vasodilatory actions. Although these agents inhibit phosphodiesterase III, leading to increased intracellular cAMP, their positive inotropic effects are likely related to downstream increases in intracellular calcium.36 These unique cardiac drugs have the theoretical advantage of dual mechanisms of action-augmenting cardiac output while reducing cardiac work by positive inotropic actions and peripheral vasodilatation.36 Both have demonstrated clinical utility in multiple low cardiac output states; however, as single-agent therapy, neither has been proven superior to single inotropes (e.g., dobutamine) in improving ventricular performance. Additionally, the longer half-lives of amrinone and milrinone as compared to that of dobutamine do not permit minute-to-minute titration of their cardiovascular effects. In selected situations, an additive effect in myocardial function is observed when dobutamine and amrinone/milrinone are combined. The phosphodiesterase inhibitors may be used as single-agent therapy in patients with isolated systolic heart failure but are more commonly employed as secondary agents (in addition to dobutamine) in cases of refractory heart failure. In this scenario, the beneficial effects on cardiac output are additive as amrinone and milrinone do not act via the adrenergic receptors. The potent vasodilatory effect of the bypyridines requires careful attention from the clinician to avoid hypotension in hypovolemic patients.

■ Nitrovasodilators The nitrovasodilators are useful agents for reducing vascular tone, allowing manipulation of both preload and afterload. The

Cardiovascular Failure

■ Steroids The use of steroids as replacement therapy for insufficient adrenal production and release of corticosteroids has been proven to be a lifesaving intervention. Their role in septic shock, however, is less clear. The use of steroids in cardiovascular collapse secondary to sepsis has gained renewed interest, with new data suggesting that in adrenal-insufficient patients, low-dose glucocorticoid replacement therapy is beneficial.38,39 However, no survival benefit is seen in patients who are not adrenal-insufficient given the same therapy. In addition to their use as a replacement therapy, steroids are known anti-inflammatory agents. Cardiopulmonary bypass produces a brisk inflammatory response, including the production oxygen free radicals, resulting in hypotension and

arrythmias. The use of steroids to temper the production of free radicals in postbypass patients has been studied. In a prospective, randomized trial there was no improvement in the incidence of cardiac arrythmias.40 Therefore, the use of steroids in the treatment of cardiovascular failure secondary to sepsis in nonadrenal insufficient patients, or as an anti-inflammatory agent in cardiopulmonary bypass patients cannot be recommended.

■ Intra-aortic Balloon Pump Counterpulsation When myocardial failure has an underlying, surgically correctable, anatomic cause (e.g., acute mitral regurgitation, intraventricular septal defect, high-grade coronary artery stenosis) and pharmacologic methods have been ineffective in augmenting cardiac output, the use of intra-aortic balloon counterpulsation (IABP) is indicated. IABP involves placement of a balloon catheter into the proximal descending aorta (distal to the origin of the left subclavian artery) via a femoral arterial approach. The balloon catheter is connected to a pumping device that, in synchrony with the electrocardiogram, inflates the balloon during cardiac diastole and deflates it during systole. By filling during diastole, the balloon displaces ∼40 mL of blood retrograde into the coronary arterial circulation and antegrade into the descending aorta. The balloon is abruptly deflated at the beginning of systole, allowing the left ventricle to eject its stroke volume. These dual functions augment coronary arterial flow while decreasing afterload, thereby reducing myocardial oxygen consumption. Although IABP technology has improved and the risk of complications in cardiac surgical patients has decreased dramatically over the last decade,41 the utility of balloon counterpulsation in trauma patients remains unclear. The use of IABP was independently associated with survival at centers with high IABP use rates, regardless of intervention (percutaneous angioplasty [PTCA], thrombolytics, or platelet GPIIb/IIIa) in a National Registry of Myocardial Infarction trial.42 One study demonstrated improved left ventricular function in dogs sustaining blunt cardiac injury,43 but studies in humans have been limited to case reports. This device should be reserved as a method of last resort in treating myocardial failure. There have been no indications for use of IABP in penetrating trauma except in those cases that proceed to cardiac failure or as an adjunct to weaning from cardiopulmonary bypass.44

EVALUATION OF CARDIAC FUNCTION ■ Central Venous Pressure CVP monitoring has been used for over four decades as a measurement of preload. In the young trauma patient with a normal functioning heart, the CVP monitor provides an adequate assessment of right-sided filling pressure or preload. Usually placed percutaneously into the superior vena cava, adequate assessment of volume status is achieved, and fluid resuscitation guided. Normal CVP is between 0 and 4 mm Hg; however, response to fluid is more useful than an absolute number. A low CVP usually indicates hypovolemia, whereas an elevated CVP may be evidence of volume overload. Increases or decreases in

CHAPTER CHAPTER 56 X

most common scenario for their use is in states of elevated SVR. Sodium nitroprusside acts primarily on arteriolar smooth muscle, reducing afterload. The onset of action of sodium nitroprusside is rapid, and its effects cease within minutes once the infusion is discontinued. When titrating the dose of sodium nitroprusside, SVR should be decreased with a concomitant increase in cardiac output, thereby maintaining a relatively constant systemic arterial pressure. Although the effects of sodium nitroprusside favor arterial dilatation, it does have mild venous dilatory effects that can lead to an increase in venous capacitance and decreased preload. Care must be taken when using sodium nitroprusside, as cyanide toxicity is a known side effect. Briefly, the ferrous iron contained in sodium nitroprusside reacts with sulfhydrylcontaining compounds in erythrocytes, producing cyanide. Toxicity results when the rate of production exceeds the capacity of the liver to metabolize cyanide to thiocyanate. This is generally seen with infusion rates in excess of 10 μg/kg/min or with prolonged therapy (several days). Toxicity manifests as an unexplained rise in mixed venous oxygen tension as a result of reduced oxygen consumption. Treatment is with sodium nitrite and is aimed at providing an alternate substrate for the cyanide ion. Sodium nitrite also converts hemoglobin to methemoglobin, producing a ferric ion that competes with the ferric ion in the cytochrome system for the cyanide ion. Methylene blue can be administered to treat the methemoglobinemia that results from sodium nitrite treatment. Nitroglycerin, a potent arteriolar and venous smooth muscle dilator, is a useful agent when both preload and afterload are elevated. The cardiovascular effects are dose-dependent, with low doses (5–20 μg/min) primarily increasing venous capacitance and higher doses (20 g/min) relaxing arterial tone. Side effects are generally the result of an overly rapid reduction in venous or arterial tone, and are readily reversed by cessation of the medication. Phosphodiesterase type 5 inhibitors, such as sildenafil, have been used with success to treat primary pulmonary hypertension37; however, their use in pulmonary hypertension secondary to acute respiratory distress syndrome or in the acute setting has not been studied adequately to draw conclusions on its benefit in this setting. Further studies in this specific subset of patients with secondary or acute pulmonary hypertension are warranted.

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cardiac output/index may be further used in conjunction with CVP to assess volume status as evidenced by the Frank–Starling curve. CVP and PAWP correlate well in the normal functioning heart (EF  50%), but this correlation is not maintained in patients with cardiac impairment (EF  40%).45 CVP measurement has its limitations and is affected by multiple variables, which may cause an inadequate assessment of true volume status. Misplacement of the catheter, congestive heart failure (CHF; right- or left-sided), pneumothorax, lung recruitment techniques or high PEEP, pulmonary embolus, cardiac tamponade, increased intrathoracic, and/or intra-abdominal pressure may all lead to increases in CVP measurements, which do not reflect the true overall volume status. Marik et al. recommends alternative measurements of fluid status to guide resuscitation.46 Magder cautions the use of CVP alone without other measurements of fluid status such as cardiac output, pulse pressure variation, or stroke volume variation.47 These will be discussed later.

■ Pulmonary Artery Catheters PACs or Swan–Ganz catheters, first introduced for human use in 1970, have been widely accepted as the standard for invasive monitoring of not only volume status but also of cardiac function by measurement and approximation of left-sided cardiac pressures. Continuous monitoring of cardiac output/index along with other information provided by newer PACs may help identify cardiovascular failure early and allow treatment to be adjusted accordingly. Measurement of the PAWP is used as an indirect measurement of LVEDP and LVEDV; however, these measurements often show poor correlation and can be altered by myocardial ischemia, ventricular outflow obstruction, mitral regurgitation, vasodilator therapy or severe heart failure.48 Similar to CVP, PAWP can be affected by decreased pulmonary compliance, high PEEP (as seen in lung recruitment strategies). Commercially available PACs currently incorporate multiple calculations to derive other indices of cardiac function and tissue perfusion such as mixed venous oxygen saturation (SVO2), SVR, oxygen delivery (DO2), and consumption (VO2).49 However, a large National Heart, Lung and Blood Institute randomized clinical trial reported that PAC-guided treatment was not superior to that of CV catheter-guided treatment; mortality and ICU length of stay (LOS) were similar but the PAC group had a higher rate of complications.50 A 2006 Cochrane Review analyzing 12 studies found no difference in mortality, hospital or ICU LOS with the use of PAC and that PAC use was associated with higher costs.51

■ Echocardiography Echocardiography, transthoracic and transesophageal, has gained wide acceptance in the monitoring of cardiac function and has emerged as an effective tool in the ICU as a guide to resuscitation and fluid status. In addition, information about structural abnormalities of the heart, aorta, and main pulmonary arteries can be obtained by this method, along with assessment of ventricular dysfunction, ventricular filling, valvular abnormalities, ventricular hypertrophy, and pulmonary embolus. Transesophageal echocardiography can give accurate measurements of both right- and left-sided filling

volumes of the heart and may provide a better assessment of myocardial preload when compared to CVP or PA catheter measurements.51,52 Placed in the esophagus, Doppler probes can accurately predict cardiac output using the diameter of the aorta and measurements of blood flow velocity. Findings of short mitral deceleration time ( 140 ms) is highly predictive of pulmonary capillary wedge pressure of  20 mm Hg, which is consistent with cardiogenic shock.53 These devices can provide invaluable information in the multiply injured patient with comorbidities that make readings from the PAC difficult to interpret. Transesophageal echocardiography has been found to be a safe procedure that can be done at bedside by intensivists and has been found to affect management of the critically ill patient at least one-third of the time.54

Inferior Vena Caval Ultrasound Ultrasound evaluation of the Inferior Vena Cava (IVC) can give an estimate of the volume status of the patient and predict a beneficial response to fluid. An IVC diameter of 1.5 cm with complete inspiratory collapse is associated with a low CVP (5) and a response to fluid bolus and volume loading. An IVC diameter of 2.5 cm with no inspiratory collapse represents a high CVP and an unlikely to response to fluid loading. In those patients on mechanical ventilation, the IVC with expand with inspiration. The need for fluid loading can be gauged by calculating the difference between the inspiratory and expiratory size of the IVC. However, the patients must be sedated enough to not be taking spontaneous breaths during the time of measurement and the ventilator should deliver 10 mg/kg of tidal volume (for the time of the measurement only, ∼30 s). A delta IVC 12% corresponded to a 15% increase in cardiac output in one study while a delta IVC 18% corresponded to fluid responsiveness with 90% specificity and sensitivity in another. Thus, ultrasound of the IVC is a good noninvasive technique for volume status measurement and fluid responsiveness.55–60

Stroke Volume Variation As discussed above, with CVP validity in question, other measurements of fluid status should be utilized. Excessive variations in arterial blood pressure caused by the specific interactions of the heart and lungs under mechanical ventilation are a clinically well known sign of hypovolemia.61,62 Variations in pulse pressure (PPV) are exaggerated when the left ventricle (LV) is on the steep portion of the Frank–Starling curve; small preload changes cause large stroke volume changes. PPV does not measure preload but rather the responsiveness to fluid in mechanically ventilated patients. Variations in the pulse pressure 11% is indicative of fluid responsiveness.62 PPV is a surrogate of stroke volume variation (SVV).63 Pulse pressure proportional to stroke volume and inversely related to aortic compliance. Therefore, PPV may be more affected by changes in vasomotor tone. In contrast, stroke volume is a volume, not a pressure, measurement. Therefore, SVV may be more accurate than PPV. Studies of SVV have shown improve prediction of fluid responsiveness over CVP and PAWP. These studies have validated SVV and PPV as a marker of fluid responsiveness and improved cardiac output.61,64–66

OPTIMAL ENDPOINTS OF RESUSCITATION ■ Mixed Venous Oxygen Saturation Mixed venous oxygen saturation (SvO2) is a measurement of the oxygen saturation in the venous return to the heart and therefore an indirect measurement of oxygen utilization by the end organs. Normal values are approximately 75–80% and are calculated by taking the difference between measured oxygen delivery and oxygen consumption. During the septic state, the cell’s inability to utilize delivered oxygen may increase SvO2. Cellular destruction from prolonged ischemia or cellular metabolic poisoning following carbon monoxide inhalation often yield normal or increased SvO2 despite inadequate end-organ perfusion because of an inability to utilize the oxygen delivered.

■ Lactate and Base Deficit Elevated serum lactate, or lactic acidosis, may be an indicator of cellular hypoxia or shock. When cells can no longer function normally due to hypoxia or decreased blood flow, the normal mechanism of ATP generation by aerobic metabolism is shifted to anaerobic metabolism. This inefficient method of ATP production yields increased amounts of pyruvate, which is converted to lactate. Therefore, increased levels of lactate may be a reflection of ongoing tissue hypoxia. Hepatic dysfunction may increase serum lactate levels due to inability of the liver to transform lactate to carbon dioxide. The use of serum lactate measurements as a guide to resuscitation is limited due to the time necessary for laboratory results to return. However, in critically ill patients past the acute resuscitation phase of treatment, serum lactate levels may be useful in determining the onset of organ dysfunction.70 In clinical practice, multiple other factors may also affect lactate production. Following severe injury, increased circulating epinephrine may cause an increase in lactate production by anaerobic glycolysis in response to increased activity of the Na /K -ATPase despite adequate tissue perfusion.71 The base deficit is the difference between the standard value of 24 mEq/L and the serum bicarbonate level. This value is typically negative in hemorrhagic shock and therefore the term base deficit is widely used. The magnitude of the base deficit has been used to quantify the magnitude of acidosis, with mild acidosis having a base deficit of −3 to −5 mEq/L, moderate acidosis −6 to −10 mEq/L, and severe acidosis less than 10 mEq/L.72 As the

1049

magnitude of the base deficit increases, the resuscitation volumes of both blood and fluid increases, as does mortality.73 Patients who are able to clear their base deficits in less than 48 hours have decreased mortality when compared to patients whose base deficits persist beyond this time frame.74 Persistent base deficits despite normal vital signs may be a signal of compensated shock requiring further resuscitation, and if left untreated may lead to MOF and increased morbidity and mortality. New-onset lactic acidosis and increasing base deficit in the critically ill patient may be early signs of a low flow state, cellular hypoxia, and/or endorgan injury, therefore every effort should be made to find the cause and address it as quickly as possible.

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Arterial pulse contour analysis has been clinically validated for continuous CO measurement and is now available for the real-time quantification of left ventricular stroke volume variation and cardiac output.63 Despite the promise of encouraging initial results in intraoperative patients, the use of stroke volume variation has its limitations. These studies have been small patient populations under the very strict conditions of nonspontaneous breathing, mechanical ventilation at high tidal volumes, and the absence of arrhythmia. In addition, there are questions of validity at high respiratory rates, with tachycardia, in the presence of β-adrenergic blockade, as well as in an over- or underdampened arterial curve.66–69

Cardiovascular Failure

■ Capnography Defined as the measurement of carbon dioxide, capnography is most commonly used during endotracheal intubation to ensure proper placement of the endotracheal tube. Recent studies have reported its use to predict prognosis following cardiopulmonary arrest, to assess resuscitation efforts, to detect alveolar dead space changes, and to monitor sedation and paralytic therapy.75,76 Under normal conditions, exhaled carbon dioxide closely correlates with arterial blood CO2 levels. Due to unmatched areas of ventilation and perfusion in the lungs, the arterial PaCO2 will usually be slightly higher than the exhaled CO2. End-tidal CO2 has been shown to predict resuscitation efforts during cardiopulmonary arrest.75 In one study higher ETCO2 levels correlated with increased survival after cardiac arrest.77 Nonsurvivors with prehospital arrests after 20 minutes of ACLS were found to have an average ETCO2 of 3.9 mm Hg, whereas survivors had ETCO2 values of 31 mm Hg.78 An ETCO2 value of 10 mm Hg has been determined to provide a 100% sensitivity to predict return of spontaneous circulation.79 Measuring tissue pH to study the adequacy of perfusion is an extremely attractive concept. Tonometric determination of mucosal carbon dioxide tension can be used to calculate pHi by use of the Hendereson–Hasselbalch equation. Although gastric tonometry and measurement of submucosal pH has its merits in determining ongoing tissue hypoxia in the ICU setting, it has not gained wide use in the initial assessment of patients due to the need for serum HCO3 measurement with each tonometric reading. Gastric pHi has proven to be a remarkable reliable predictor of outcome in critically it individuals: general medical ICU patients, multiply injured trauma patients, patients with sepsis, and patients undergoing major surgical procedures. Studies have shown that sublingual CO2 (SLCO2) yielded measurements equivalent with gastric tonometry80 and is a reliable marker of tissue perfusion, with impaired circulatory blood flow correlating with high levels of SLCO2.81 In a prospective observational cohort study, SLCO2 correlated with blood loss in penetrating trauma patients and may be superior to gastric tonometry in its noninvasive nature.82

MYOCARDIAL PROTECTION Patients at high risk for cardiac events during noncardiac surgery have been the topic of discussion for years due to the increased mortality from perioperative arrythmias and MI.

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MI or cardiac death occurs in 1–5% of unselected patients undergoing noncardiac surgery and is the most common reason for preoperative evaluation.83 The pathophysiology of MI in the perioperative setting differs from that seen in nonsurgical patients. In the nonsurgical setting, MI usually follows rupture of atherosclerotic plaques in the coronary arteries leading to platelet aggregation and thrombus formation.84 MI in the perioperative setting is due to plaque rupture approximately 50% of the time, with the remainder resulting from myocardial ischemia from decreased myocardial oxygen supply and increased demand in the face of atherosclerotic coronary artery disease. These demands are usually exacerbated by anemia, hypotension, hypoxia, hypertension, and tachycardia. Shifts in intravascular volume, withdrawal of anesthesia, and postoperative pain are all factors that may contribute to the increased demand of oxygen in the perioperative setting. Postoperative tachycardia, arrhythmias, and MI most commonly occur 3 days after an operation, when fluid shifts are at their greatest.85 Until recently, reduction in the occurrence of these events centered on preoperative risk assessment with clinical recommendations and often cancellation or postponement of procedures.86 Medical strategies have been proposed to reduce perioperative ischemia, as this has been linked to postoperative MI with a 21-fold increase in risk.87 Mixed results have been obtained in studies using intraoperative calcium channel blockers88 and nitroglycerin.89 Two randomized controlled trials have shown that β-blocker therapy reduces perioperative cardiac complications.89,90 Mangano and colleagues performed a randomized, double-blinded, placebo-controlled trial using atenolol in 200 patients with known coronary artery disease and/or risk factors for atherosclerosis who underwent noncardiac surgery. Although acute perioperative mortality did not differ between the two groups at 6 months, eight deaths occurred in the placebo group and none in the atenolol group (P  0.001), with the difference being sustained at the 2-year follow-up period.90 In another study, patients with clinical risk factors and ischemia demonstrated by dobutamine stress echo who were to undergo major vascular procedures were randomly assigned to bisoprolol or placebo.91 The study was terminated early when investigators noted that bisoprolol markedly reduced perioperative mortality (17% vs. 3.4%; P  0.02) and MI (17% vs. 0%; P  0.001). A recent meta-analysis of randomized, controlled trials concluded that β-blockade may be beneficial in preventing perioperative cardiac morbidity despite the heterogeneity of the trials.92 Therefore, it seems that β-blockade reduces the risk of perioperative morbidity and mortality in patients at increased risk and is effective in patients with inducible ischemia by dobutamine stress echo.93 Subsequent studies have shown that withdrawal of β-blockers increased the risk of morbidity and mortality and that initiation of β-blockers preoperatively requires titration to blood pressure and heart rate control. Therefore, current ACCF/AHA recommendations are aimed at continuation of β-blocker therapy in the perioperative period and initiation of β-blockade should be instituted in high-risk patients and titrated to effect prior to surgery.94

CURRENT TREATMENT OF ACUTE MYOCARDIAL INFARCTION The definition of acute MI encompasses a range of clinical entities ranging from non-ST-segment elevation MI (also known as acute coronary syndrome [ACS] or unstable angina) to acute ST-segment elevation MI. The pathophysiology for ACS differs from that of ST-segment elevation MI, as does the treatment. Whereas ACS are commonly due to a partial occlusion of the coronary arteries or transient ischemia (due to plaque rupture with platelet aggregation), in the surgical patient ACS is more commonly secondary to decreased oxygen supply or increased demand due to anemia, tachycardia, intravascular fluid shifts, hypotension, or arrhythmias. Acute ST-segment elevation MI refers to complete occlusion of the coronary arteries with myocardial injury. Despite marked advances in diagnosis and treatment, there is still a 10% mortality associated with acute MI.95 Reduced mortality has been shown to result from adherence to three basic tenets of treatment for acute MI: (1) prompt diagnosis, (2) immediate aspirin therapy, and (3) rapid restitution of blood flow to the infarcted myocardium. Whereas prompt diagnosis and institution of aspirin therapy are relatively straight forward, the reestablishment of blood flow to the affected myocardium has evolved into two primary therapies, pharmacologic therapy with thrombolytics and interventional therapy with PTCA. With its ease of administration, early studies on the use of thrombolytic therapy consistently showed decreased mortality and improved myocardial performance compared with placebo.96 However, thrombolytic therapy has well-documented limitations and contraindications. Intracranial bleeding resulting in death or stroke occurs in 0.6–1.4% of patients who receive thrombolytic therapy.96 Thrombolytic therapy is also associated with a reocclusion rate of 30%, resulting in reinfarction of the affected area within 3 months.97 In the multiply injured patient with an increased risk of bleeding, head injury, or multivessel disease, thrombolytic therapy is contraindicated. Patients who are not candidates for thrombolytic therapy have been shown to benefit from PTCA.98 This invasive therapy has been shown to result in better clinical outcomes when compared to thrombolysis.99 In addition to improved outcomes, PTCA offers direct visualization of the affected anatomy, gives specific hemodynamic and functional data that can be used to guide further therapy. It can also quickly identify those patients who should not undergo reperfusion therapy, which include patients with minimal residual stenosis, spontaneous reperfusion, coronary vasospasm, myocarditis, and aortic dissection involving the ostia.100 Unfortunately, PTCA is not available in all medical centers and there is wide variability in the use of PTCA even in those centers that are PTCA capable.101 Complications from PTCA include major bleeding (7%), vascular complications that require surgical repair (2%), and renal failure (13%). The incidence of renal failure rises with increasing age, volume of contrast material, decreased baseline renal function, and hypovolemia. When comparing thrombolytic therapy to PTCA, primary PTCA had been found to be more effective in reducing both short- and long-term outcomes,

Cardiovascular Failure

MANAGEMENT OF DIASTOLIC DYSFUNCTION The syndrome of CHF typically brings to mind an enlarged heart and decreased systolic function. However, when systolic function is normal or near-normal, as is the case in nearly 50% of patients diagnosed with CHF, and the other clinical manifestations of CHF exist, such as orthopnea, dyspnea, increased jugular venous pressure, and abnormal heart sounds on auscultation, the diagnosis of diastolic dysfunction (DD) or, more accurately, diastolic heart failure is made. DD is associated with hypertension (HTN), diabetes, female gender, coronary artery disease, and chronic atrial fibrillation. Aging itself has been associated with decreases in elastic properties of the great vessels, decreased ventricular filling, decreased relaxation, and compliance and decreased β-adrenergic receptor density. DD should be described as CHF with normal or preserved EF.108 The diagnosis of DD is generally made clinically and is often one of exclusion. Objective testing should include echocardiography or cardiac catheterization. Because the normal ejection fraction is not a standardized number, and given that systolic dysfunction often accompanies DD, the diagnosis of DD is often not clear-cut. Therefore, the diagnostic “gold standard” for DD is cardiac catheterization demonstrating increased ventricular diastolic pressure with normal systolic function and volumes. Echocardiography, being noninvasive and practical, can be used to exclude systolic dysfunction. Although the majority of clinical studies focus on systolic dysfunction, few exist that specifically target DD.

In general, the treatment principles for patients diagnosed with DD include antihypertensive therapy, reduction of volume overload, decreasing heart rate (especially those with atrial fibrillation), and the reduction of ischemia.108 With hypertension being the primary predisposing factor for CHF, neurohormonal regulation has been shown to play a role in CHF and DD. The renin–angiotensin system influences CHF indirectly by causing hypertension and left ventricular hypertrophy (LVH), and directly by both angiotensin II and endothelin contributing to LVH and impaired myocardial relaxation.109,110 Blockade of the renin–angiotensin system improves diastolic distensibility in both human and animal studies.110 Volume overload can be reduced with diuretics or renal replacement therapy in renal failure patients. In DD, the use of β-adrenergic blockade or calcium channel blockade to reduce heart rate and increase left ventricular filling time reduces mortality.111 Digoxin decreases hospitalization of patients with CHF with and without systolic dysfunction; however, since digoxin is a negative chronotrope the benefit may be due to the rate-lowering effect of the drug rather than to its other properties.112 Patients with rate-altering arrhythmias such as atrial flutter or fibrillation show increased filling times once normal sinus rhythm is restored and may also benefit from rate control. Aldosterone has also been shown to contribute to CHF with detrimental effects on endothelial function as well as inducing a vasculopathy.113 Infusion of aldosterone into healthy volunteers for 1-hour results in endothelial dysfunction with a notably reduced vascular response to acetylcholine. Patients with mild CHF treated with β-blocker therapy, ACE inhibitors, and statins show an improvement in acetylcholine-mediated endothelium-dependent vasodilatation.114

■ Pulmonary Hypertension Another recognized cause of right heart dysfunction is pulmonary arterial hypertension (PH). This is defined as systolic Ppa 25 mm Hg at rest and diagnosed by right heart catheterization. Other diagnostic modalities used in the workup of PH is chest radiograph, ECG, echocardiography, pulmonary function tests and arterial blood gases, V/Q scan, high-resolution computed tomography, ultrasonography of the abdomen, and biopsy. These diagnostic modalities are used not only for diagnosis of PH but also to determine etiology and functional impairment.115 Acute PH occurring in the critically ill is most commonly recognized by PAC or echocardiogram (tranthoracic or esophageal). Echocardiographic signs of PH include right ventricular dilation and hypertrophy, septal bowing into the left ventricle during late systole to early diastole (D-shaped left ventricle), right ventricular hypokinesis, tricuspid regurgitation, right atrial enlargement, and a dilated IVC. Primary considerations when managing a critically ill patient with PH in the ICU include the diagnosis which then allows for specific treatment. Hemodynamic goals are to reduce the PVR, augment cardiac output, and resolve systemic hypotension while avoiding tachyarrhythmias. Avoidance of hypoxia and hypercapnea will minimize pulmonary vasoconstriction and thus are simple measures to avoid exacerbation of

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including death.100 Recent trials of PTCA with or without stent placement show no difference in mortality, but stented vessels had a decreased rate of restenosis and reocclusion over 6 months. The use of platelet glycoprotein (GP) IIb/IIIa inhibitors (e.g., abciximab) at the time of PTCA reduces the rates of subacute thrombosis, recurrent ischemia, and need for repeat revascularization procedures during the first month after PTCA with or without stents.102 However, clinical outcomes do not differ at 6-month follow-up. Despite the heterogeneity of these trials, including whether stents were used or not and the use of platelet GP IIb/IIIa inhibitors versus the various thrombolytic agents, the accumulated data appear to favor primary PTCA in the treatment of acute ST-segment MI. The addition of platelet GP IIb/IIIa inhibitors should be based on clinical judgment in the multiply injured trauma patient.103 For those patients with non-ST-segment elevation MI, treatment centers on the presence or absence of hemodynamic instability. In the presence of hemodynamic instability, treatment includes aspirin (ASA), vasopressors, and IABP as needed and cardiac catheterization  PTCA. In those patients with no hemodynamic instability and minimal risk factors for recurrence, medical management with ASA, β-blockers, angiotensin converting enzyme inhibitors (ACE inhibitors), and statins is first line. The use of statins in those patients with AMI showed reduced 1 year mortality, and statins introduced within 24 hours of AMI showed decreased early complications and in-hospital mortality.104,105 For those patients with multiple risk factors, cardiac catheterization may be indicated when the patient is able to be systemically anticoagulated.106,107

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the PH. Dobutamine in doses up to 5 μg/kg/min significantly decreases PVR while slightly increasing cardiac output.116,117 Doses higher than this cause significant tachycardia without improvement in the PVR. When combined with inhaled nitric oxide (iNO), dobutamine improved cardiac index, decreased PVR and significantly increased the PaO2/FiO2 Milrinone significantly reduces PVR and improves right ventricular function. However, its use is limited due to the high incidence of systemic hypotension. Dopamine, phenylephrine, isoproterenol, epinephrine, and vasopressin cannot be recommended for use in management of PH due to the limited studies. Inhaled nitric oxide increases production of both cyclic guanosine monophosphate and cyclic adenosine monophosphate. It is the most commonly utilized pulmonary vasodilator in the critical care setting for the management of acute pulmonary hypertension. Sildenafil is a specific phosphodiesterase-5 inhibitor recently approved for treatment of PH. In stable patients, when it is used alone or in combination with iNO, the cardiac output will increase.118,119 It is contraindicated in patients receiving nitrates because of the potential for severe systemic hypotension. Although use of calcium channel blockers in the management of chronic PH is effective for control of heart rate, there are no studies of their use in the critically ill patient with PH. Because of their negative inotrophic effects, they may precipitate fatal worsening of right ventricular failure.

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Cardiovascular Failure 69. Marik PE, Cavallazzi R, Vasu T, Harani A. Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: a systematic review of the Literature. Crit Care Med. 2009;37:2642–2647. 70. Benedict CR, Rose JA. Arterial norepinephrine changes in patients with septic shock. Circ Shock. 1992;38:165–172. 71. Luchette FA, Jenkins WA, Friend LA, et al. Hypoxia is not the sole cause of lactate production during shock. J Trauma. 2002;52:415–419. 72. Davis JW, Parks SN, Kaups KL, et al. Admission base deficit predicts transfusion requirements and risk of complications. J Trauma. 1996;41:769–774. 73. Moomey CB Jr, Melton SM, Croce MA, et al. Prognostic value of blood lactate, base deficit, and oxygen-derived variables in an LD50 model of penetrating trauma. Crit Care Med. 1999;27:154–161. 74. Davis JW, Shackford SR, Mackersie RC, et al. Base deficit as a guide to volume resuscitation. J Trauma. 1988;28:1464–1467. 75. Ahrens T, Schallom L, Bettorf K, et al. End-tidal carbon dioxide measurements as a prognostic indicator of outcome in cardiac arrest. Am J Crit Care. 2004;10:391–398. 76. Bilkovski RN, Rivers EP, Horst HM. Targeted resuscitation strategies after injury. Curr Opin Crit Care. 2004;10:529–538. 77. Sanders AB, Kern KB, Otto CW, et al. End-tidal carbon dioxide monitoring during cardiopulmonary resuscitation. A prognostic indicator for survival. JAMA. 1989; 262:1347–1351. 78. Wayne MA, Levine RL, Miller CC. Use of end-tidal carbon dioxide to predict outcome in prehospital cardiac arrest. Ann Emerg Med. 1995;25:762–767. 79. Cantineau JP, Lambert Y, Merckx P, et al. End-tidal carbon dioxide during cardiopulmonary resuscitation in humans presenting mostly with asystole: a predictor of outcome. Crit Care Med. 1996;24:791–796. 80. Povoas HP, Weil MH, Tang W, Moran B, Kamohara T, Bisera J. Comparisons between sublingual and gastric tonometry during hemorrhagic shock. Chest. 2000;118:1127–1132. 81. Rackow EC, O’Neil P, Astiz ME, et al. Sublingual capnometry and indexes of tissue perfusion in patients with circulatory failure. Chest. 2001;120:1633–1638. 82. Baron BJ, Sinert R, Zehtabchi S, et al. Diagnostic utility of sublingual PCO2 for detecting hemorrhage in penetrating trauma patients. J Trauma. 2004;57:69–74. 83. Khuri SF, Daley J, Henderson W, et al. The National Veterans Administration Surgical Risk Study: risk adjustment for the comparative assessment of the quality of surgical care. J Am Coll Surg. 1995;180: 519–531. 84. Fuster V, Badimon L, Badimon JJ, et al. The pathogenesis of coronary artery disease and the acute coronary syndromes (1). N Engl J Med. 1992;326:242–250. 85. Raby KE, Barry J, Creager MA, et al. Detection and significance of intraoperative and postoperative myocardial ischemia in peripheral vascular surgery. JAMA. 1992;268:222–227. 86. Guidelines for assessing and managing the perioperative risk from coronary artery disease associated with major noncardiac surgery. American College of Physicians. Ann Intern Med. 1997;127:309–312. 87. Landesberg G, Luria MH, Cotev S, et al. Importance of long-duration postoperative ST-segment depression in cardiac morbidity after vascular surgery. Lancet. 1993;341:715–719. 88. Godet G, Coriat P, Baron JF, et al. Prevention of intraoperative myocardial ischemia during noncardiac surgery with intravenous diltiazem: a randomized trial versus placebo. Anesthesiology. 1987;66: 241–245. 89. Coriat P. Intravenous nitroglycerin dosage to prevent intraoperative myocardial ischemia during noncardiac surgery. Anesthesiology. 1986;64:409–410. 90. Mangano DT, Layug EL, Wallace A, et al. Effect of atenolol on mortality and cardiovascular morbidity after noncardiac surgery. Multicenter Study of Peri-operative Ischemia Research Group. N Engl J Med. 1996;335:1713–1720. 91. Poldermans D, Boersma E, Bax JJ, et al. The effect of bisoprolol on perioperative mortality and myocardial infarction in high-risk patients undergoing vascular surgery. Dutch Echocardiographic Cardiac Risk Evaluation Applying Stress Echocardiography Study Group. N Engl J Med. 1999;341:1789–1794. 92. Auerbach AD, Goldman L. Beta-blockers and reduction of cardiac events in noncardiac surgery: Scientific review. JAMA. 2002;287: 1435–1444. 93. Grayburn PA, Hillis LD. Cardiac events in patients undergoing noncardiac surgery: shifting the paradigm from noninvasive risk stratification to therapy. Ann Intern Med. 2003;138:506–511.

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41. Elahi MM, Chetty GK, Kirke R, et al. Complications related to intraaortic balloon pump in cardiac surgery: a decade later. Eur J Vasc Endovasc Surg. 2005;29:591–594. 42. Chen EW. Relation between hospital intra-aortic balloon counterpulsation volume and mortality in acute myocardial infarction complicated by cardiogenic shock. Circulation. 2003;108:951–957. 43. Saunders CR, Doty DB. Myocardial contusion: effect of intra-aortic balloon counterpulsation on cardiac output. J Trauma. 1978;18:706–708. 44. Wall MJ, Mattox K L, Chen CD, Baldwin JC. Acute management of complex cardiac injuries. J Trauma. 1997;42:905–912. 45. Mangano DT. Monitoring pulmonary arterial pressure in coronaryartery disease. Anesthesiology. 1980;53:364–370. 46. Marik PE, Baram M, Vahid B. Does central venous pressure predict fluid responsiveness? Chest. 2008;134:172–178. 47. Madger S. Central venous pressure: a useful but not so simple measurement. Crit Care Med. 2006;34:2224–2227. 48. Raper R, Sibbald WJ. Misled by the wedge? The Swan-Ganz catheter and left ventricular preload. Chest. 1986;89:427–434. 49. Girolami A, Little RA, Foex BA, et al. Hemodynamic responses to fluid resuscitation after blunt trauma. Crit Care Med. 2002;30:385–392. 50. The NHLBI Acute Respiratory Distress Syndrome (ARDS) Clinical Trial Network. Pulmonary artery versus central venous catheter to guide treatment of acute lung injury. N Engl J Med. 2006;354:2213–2224. 51. Harvey S, Young D, Brampton W, et al. Pulmonary artery catheters for adult patients in intensive care. Cochrane Database Syst Rev. 2006;(3):CD003408. doi:10.1002-14651858.CD003408.pub2. 52. Madan AK, UyBarreta VV, Aliabadi S-Wahle, et al. Esophageal Doppler ultrasound monitor versus pulmonary artery catheter in the hemodynamic management of critically ill surgical patients. J Trauma. 1999;46: 607–611. 53. Reynolds HR, Anand SK, Fox JM, et al. Restrictive physiology in cardiogenic shock: observation from echocardiography. Am Heart J. 2006;151:890.e9–890.e15. 54. Colreavy FB, Donovan K, Lee KY, Weekes J. Transesophageal echocardiography in critically ill patients. Crit Care Med. 2002;30: 989–996. 55. Adler C, Buttner W, Veh R. Relations of the ultrasonic image of the inferior vena cava and central venous pressure. Aktuelle Gerontol. 1983; 13:209–213. 56. Kircher BJ, Himelman RB, Schiller NB. Noninvasive estimation of right atrial pressure from the inspiratory collapse of the inferior vena cava. Am J Cardiol. 1990;66:493–496. 57. Simonson JS, Schiller NB. Sonospirometry: a new method for noninvasive estimation of mean right atrial pressure based on two-dimensional echographic measurements of the inferior vena cava during measured inspiration. J Am Coll Cardiol. 1988;11:557–564. 58. Minutiello L. Non-invasive evaluation of central venous pressure derived from respiratory variations in the diameter of the inferior vena cava. Minerva Cardioangiol. 1993;41:433–437. 59. Barbier C, Loubières Y, Schmit C, et al. Respiratory changes in inferior vena cava diameter are helpful in predicting fluid responsiveness in ventilated septic patients. Intensive Care Med. 2004;30:1740–1746. 60. Feissel M, Michard F, Faller JP, et al. The respiratory variation in inferior vena cava diameter as a guide to fluid therapy. Intensive Care Med. 2004;30:1834–1837. 61. Berkenstadt H, Nevo M, Hadani M, et al. Stroke volume variation as a predictor of fluid responsiveness in patients undergoing brain surgery. Anesth Analg. 2001;92:984–989. 62. Kramer A, Zygun D, Hawes H, et al. Pulse pressure variation predicts fluid responsiveness following coronary artery bypass surgery. Chest. 2004;126:1563–1568. 63. Hofer CK, Muller SM, Zollinger A, et al. Stroke volume and pulse pressure variation for prediction of fluid responsiveness in patients undergoing off-pump coronary artery bypass grafting. Chest. 2005;128:848–854. 64. Pinsky MR. Probing the limits of arterial pulse contour analysis to predict preload responsiveness. Anesth Analg. 2003;96:1245–1247. 65. Reuter DA, Kirchner A, Felbinger TW, et al. Usefulness of left ventricular stroke volume variation to assess fluid responsiveness in patients with reduced cardiac function. Crit Care Med. 2003;31:1399–1404. 66. De Backer D, Taccone GS, Holsten R, Ibrahimi F, Vincent JL. Influence of respiratory rate on stroke volume variation in mechanically ventilated patients. Anesthesiology. 2009;110:1092–1097. 67. Michard F. Pulse contour analysis: fairy tale or new reality? Crit Care Med. 2007;35:1791–1792. 68. Kim HK, Pinsky MR. Effect of tidal volume, sampling duration and cardiac contractility on pulse pressure and stroke volume variation during positive-pressure ventilation. Crit Care Med. 2008;36:2858–2862.

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94. Fleischmann KE. 2009 ACCF/AHA focused update on perioperative beta blockade: a report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines. Circulation. 2009;120(21):2123–2151. 95. Rogers WJ, Canto JG, Lambrew CT, et al. Temporal trends in the treatment of over 1.5 million patients with myocardial infarction in the US from 1990 through 1999: The National Registry of Myocardial Infarction 1, 2 and 3. J Am Coll Cardiol. 2000;36:2056–2063. 96. Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients. Fibrinolytic Therapy Trialists’ (FTT) Collaborative Group. Lancet. 1994;343: 311–322. 97. Gibson CM, Karha J, Murphy SA, et al. Early and long-term clinical outcomes associated with reinfarction following fibrinolytic administration in the thrombolysis in myocardial infarction trials. J Am Coll Cardiol. 2003;42:7–16. 98. Grzybowski M, Clements EA, Parsons L, et al. Mortality benefit of immediate revascularization of acute ST-segment elevation myocardial infarction in patients with contraindications to thrombolytic therapy: A propensity analysis. JAMA. 2003;290:1891–1898. 99. Keeley EC, Boura JA, Grines CL. Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised trials. Lancet. 2003;361:13–20. 100. Keeley EC, Grines CL. Primary coronary intervention for acute myocardial infarction. JAMA. 2004;291:736–739. 101. Fazel, R, Krumholz HM, Bates ER, et al. Choice of reperfusion strategy at hospital with primary percutaneous coronary intervention, A National Registry of Myocardial Infarction Analysis. Circulation. 2009;120: 2455–2461. 102. Dangas G, Aymong ED, Mehran R, et al. Predictors of and outcomes of early thrombosis following balloon angioplasty versus primary stenting in acute myocardial infarction and usefulness of abciximab (the CADILLAC trial). Am J Cardiol. 2004;94:983–988. 103. Adesanya AO, de Lemos JA, Greilich NB, Whitten CW. Management of Perioperative Myocardial Infarction in Noncardiac Surgical Patients. Chest. 2006;130:584–596. 104. Stenestrand U, Wallentin L. Early statin treatment following acute myocardial infarction and 1-year survival. JAMA. 2001;285:430–436. 105. Fonarow GC, Wright RS, Spencer FA, et al. Effect of statin use within the first 24 hours of admission for acute myocardial infarction on early morbidity and mortality. Am J Cardiol. 2005;96:611–616. 106. Eagle KA, Berger PB, Calkins H, et al. ACC/AHA guideline update for perioperative cardiovascular evaluation for noncardiac surgery—executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1996 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). J Am Coll Cardiol. 2002;39:542–553.

107. Kushner FG, Hand M, Smith SC Jr, et al. 2009 Focused updates: ACC/ AHA guidelines for the management of patients with ST-elevation myocardial infarction (updating the 2004 guideline and 2007 focused update) and ACC/AHA/SCAI guidelines on percutaneous coronary intervention (updating the 2005 guideline and 2007 focused update): a report of the American College of Cardiology Foundation/American heart Association Task force on Practice guidelines. Circulation. 2009;120:2271–2306. 108. Wang J, Nagueh SF. Current perspectives on cardiac function in patients with diastolic heart failure. Circulation. 2009;119:1146–1157. 109. Flesch M, Schiffer F, Zolk O, et al. Angiotensin receptor antagonism and angiotensin converting enzyme inhibition improve diastolic dysfunction and Ca (2)-ATPase expression in the sarcoplasmic reticulum in hypertensive cardiomyopathy. J Hypertens. 1997;15:1001–1009. 110. Friedrich SP, Lorell BH, Rousseau MF, et al. Intracardiac angiotensinconverting enzyme inhibition improves diastolic function in patients with left ventricular hypertrophy due to aortic stenosis. Circulation. 1994;90:2761–2771. 111. Banerjee P, Banerjee T, Khand A, et al. Diastolic heart failure: neglected or misdiagnosed? J Am Coll Cardiol. 2002;39:138–141. 112. The effect of digoxin on mortality and morbidity in patients with heart failure. The Digitalis Investigation Group. N Engl J Med. 1997;336: 525–533. 113. Struthers AD. Aldosterone: cardiovascular assault. Am Heart J. 2002; 144(suppl 5):S2–S7. 114. Farquharson CA, Struthers AD. Aldosterone induces acute endothelial dysfunction in vivo in humans: evidence for an aldosterone-induced vasculopathy. Clin Sci (Lond). 2002;103:425–431. 115. McLaughlin VV, Archer SL, Badesch DB, et al. ACCF/AHA 2009 expert consensus document on pulmonary hypertension: a report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents and the American Heart Association. Circulation. 2009;119:2250–2294. 116. Bradford KK, Deb B, Pearl RG. Combination therapy with inhaled nitric oxide and intravenous dobutamine during pulmonary hypertension in the rabbit. J Cardiovasc Pharmacol. 2000;36:146–151. 117. Vizza CD, Rocca GD, Roma AD, et al. Acute hemodynamic effects of inhaled nitric oxide, dobutamine, and a combination of the two in patients with mild to moderate secondary pulmonary hypertension. Crit Care. 2001:5:355–361. 118. Krowka JM, Mandell MS, Ramsay MA, et al. Hepatopulmonary syndrome and portopulmonary hypertension: a report of the multicenter liver transplant data base. Liver Transplantation. 2004;10:174–182. 119. Rafanan AL, Maurer J, Mehta AC, et al. Progressive portopulmonary hypertension after liver transplantation treated with epoprostenol. Chest. 2000;188:1497–1500.

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Respiratory Insufficiency Jeffrey L. Johnson and James B. Haenel

The maintenance of gas exchange may be tenuous in the injured patient because of dysfunction in three key elements of the respiratory system. First, the central nervous system may be impaired, resulting in inadequate respiratory drive, or inability to maintain patent proximal airways. Second, injury to the torso can produce changes in compliance, ineffective respiratory effort, and pain that impact the patient’s ability to complete the work of breathing. Third, primary and secondary insults to the lung result in ineffective gas exchange. In practice, it is common for patients to suffer simultaneous insults, affecting all three elements. Impaired airway patency (e.g., diminished level of consciousness), increased work of breathing (e.g., multiple rib fractures), and impaired gas exchange (e.g., pulmonary contusion, fat emboli syndrome) often coexist in the same patient. Respiratory failure that relates primarily to CNS injury is discussed at length in other chapters and will not be extensively covered here. This chapter will focus on insults that affect work of breathing and gas exchange. The syndrome of postinjury acute respiratory distress syndrome (ARDS) is a major focus.

HYPERCAPNIC PULMONARY FAILURE The neurohormonal response to injury (Chapter 61) results in a remarkable increase in cellular metabolism. This creates a substantial increase in carbon dioxide (CO2) production that must be matched by increased elimination from the lungs. While a resting adult eliminates 200 cm3/(kg min) of CO2, postinjury hypermetabolism results in CO2 production in the range of 425 cm3/(kg min).1 Thus, the minute ventilation required to maintain eucapnia may rise from a resting rate of approximately 5 L/min to more than 10 L/min. This represents a 100% increase in the work of breathing simply to meet metabolic demands. Additionally, injured patients typically have an increase in physiologic and anatomic dead space—ventilated regions that

do not participate in gas exchange. In a normal adult, the proportion of each breath that is dead space (Vd/Vt) is approximately 0.35. In the intubated, ventilated patient, the Vd/Vt can be calculated by a number of techniques including the Bohr– Enghoff method (Vd/Vt  [{PaCO2  mean expired CO2}/ PaCO2]).2 For practical purposes (since mean expired CO2 is not commonly measured), this is a reflection of the minute volume required to achieve a given PaCO2. In ventilated patients with pulmonary failure, the Vd/Vt often exceeds 0.6. Simply put, this extra dead space is a burden because each breath is less effective at eliminating CO2, and therefore minute ventilation requirements in the 12–20 L/min range are not uncommon in the postinjury setting. The above increase in respiratory demand might be met by a healthy adult; however, the injured patient faces several challenges in completing this additional work. CNS dysfunction from injury impairs respiratory drive, as do many medications routinely used for sedation and analgesia. Decreased thoracic compliance from abdominal distension (e.g., as part of the abdominal compartment syndrome, Chapter 41), chest wall edema, and recumbent positioning increases the energy required to complete a respiratory cycle. Decreased pulmonary compliance from an increase in extravascular lung water and pleural collections (effusions/hemothorax) also contribute. Muscular weakness from impaired energetics (acidosis, cardiovascular failure, mitochondrial dysfunction, oxidant stress) or fatigue may be an insurmountable challenge. Finally, pain from torso injuries or operative interventions make the increased ventilatory demand a substantial burden to the patient. The net effect of increased demand and diminished capacity to execute the work of breathing is hypercapnic respiratory failure. In the early postinjury period, patients most commonly present with a mixed acid–base picture where ventilation is inadequate to maintain physiologic pH in the face of a metabolic acidosis. This frequently occurs in the absence of major hypoxia, and therefore caution is warranted in relying

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on oximetry alone to assess adequacy of pulmonary function. Particularly in patients with tachypnea, blood gas analysis is optimal to quickly identify patients who are not meeting their ventilatory demands. While efforts to diminish the work of breathing should be routine, most patients with hypercapnic failure require some form of mechanical ventilation to meet their demands. Approaches to invasive and noninvasive ventilation are covered extensively in Chapter 55. One approach to addressing the challenge of increased CO2 production in the injured patient is to blunt the hypermetabolic response. Simple maneuvers such as maintenance of euthermia, delivery of nutrition, and minimizing pain-induced stress are warranted but may not affect the incidence or outcome of hypercapnic respiratory failure. A more novel approach is delivery of beta-adrenergic blockade, which, in a retrospective analysis, improves outcomes in injured patients. There are reasonably compelling data in the burn population and the acutely brain injured that blunting of hypermetabolism is beneficial.3 A prospective safety and efficacy evaluation of this approach in injured adults is needed before it can be recommended as routine practice. Two injury patterns that precipitate hypercapnic respiratory failure are worthy of special mention: spinal cord injury and flail chest/pulmonary contusion. In spinal cord injury, conventional wisdom asserts that lesions below C5 should not result in pulmonary failure, because innervation to the diaphragm remains intact. In practice, however, most complete cord lesions in the cervical and upper thoracic regions routinely result in failure requiring mechanical ventilation.4,5 The genesis is multifactorial, including delays in patient mobilization, ineffective cough due to loss of innervation of intercostal and abdominal musculature, pneumonia in the setting of multiple injuries, and aspiration at the time of the initial insult. Furthermore, unopposed vagal stimulation results in early bronchorrhea and bronchospasm. This patient population requires aggressive mobilization and pulmonary care as recurrent lobar collapse and pneumonia are the rule. Early operative stabilization of the spine can be recommended as it has been shown to decrease the need for mechanical ventilation and ICU stay.6 Other adjuncts such as noninvasive ventilation, bronchodilators, mucolytics, and percussion should be considered, although most of these have not been studied in a fashion that permits a firm recommendation. Laparoscopic placement of diaphragmatic pacers is a benefit in select patients.7 Specifically, improvement in spirometry and some liberation from mechanical ventilation occurs in most patients evaluated thus far. Largely, this has been studied in the rehabilitation setting, and therefore a role for this approach in the acute setting remains to be defined. Flail chest and pulmonary contusion can be thought of as a single entity. This is a challenging injury pattern, because it impacts both the patient’s ability to execute the work of breathing (from pain and mechanical instability of the thoracic) and gas exchange (from the pulmonary contusion). Isolated pulmonary contusion rarely requires mechanical ventilation. Since minor contusions are frequently identified by computed tomography (CT), it is important to realize that this tends to take a relatively benign course (see Chapter 26). It is clear that

the number of rib fractures is strongly associated with pulmonary failure, ARDS, and mortality, and that this effect is more dramatic in the elderly population.8 This may in part be a marker of energy applied to the chest and injury to the underlying lung. Early pain control, preferably beginning in the emergency department with regional anesthesia, has been shown to be effective in reducing the impact of multiple rib fractures and should be routinely applied. Admission to a high-volume trauma center, use of patient-controlled analgesia, tracheostomy, and an algorithm-driven approach are associated with improved survival.9,10

HYPOXIC PULMONARY FAILURE Hypoxic pulmonary failure is a substantial co-contributor in the trauma setting. The etiologies are diverse including aspiration pneumonitis, pneumonia, pulmonary embolism, acute lung injury (ALI), and ARDS. Most of these entities are discussed elsewhere—ALI and ARDS will be the focus of this chapter. Indeed, the mechanisms at work in ALI and ARDS share many common features with these other processes that affect the alveolar–capillary interface.

ALI AND ARDS ALI and ARDS are clinical syndromes of inflammatory lung injury that can be thought of as a common final pathway of diverse systemic processes. In the past two decades, there has been major progress in defining the underlying pathophysiology and optimal supportive care. Specific therapy for the underlying mechanisms, however, remains an elusive goal.

CURRENT DEFINITIONS AND THEIR LIMITATIONS The recognition of ARDS as a distinct clinical entity resulted from the description by Ashbaugh et al. in 1967.11 Subsequent descriptions include five principal criteria: (1) hypoxemia refractory to oxygen administration; (2) diffuse, bilateral infiltrates on chest radiograph; (3) low static lung compliance; (4) absence of congestive heart failure; and (5) presence of an appropriate at-risk diagnosis. The current standard definitions were developed in 1994, after a Consensus Conference of American and European investigators (AECC) agreed that ARDS should be viewed as the most severe end of a spectrum of ALI. It also recommended diagnostic criteria for ALI and ARDS (Table 57-1). The diagnostic criteria for ARDS include acute onset, the PaO2/FiO2 200 mm Hg or less (300 for ALI), bilateral infiltrates on chest radiograph, and no evidence of left arterial hypertension (either clinical or with direct measurement). Moreover, the committee recognized that ARDS is most often associated with sepsis syndrome, aspiration, primary pneumonia, trauma, cardiopulmonary bypass, multiple blood transfusions, fat embolism, and pancreatitis. Although debate exists as to the usefulness of the AECC diagnostic criteria, they have promoted study of reasonably homogeneous populations, are largely accepted by clinical investigators, and are likely to be used for some time.12

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Acute lung injury criteria Timing: acute onset Oxygenation: PaO2/FiO2 300 mm Hg (regardless of positive end-expiratory pressure) Chest radiograph: bilateral infiltrates on anteroposterior chest radiograph Pulmonary artery occlusion pressure: 18 mm Hg or no clinical evidence of left atrial hypertension ARDS criteria Same as acute lung injury except: Oxygenation: PaO2/FiO2 200 mm Hg (regardless of positive end-expiratory pressure)

One concern about the standard definitions is substantial limitations to bedside application. For example, transient hypoxemia from mucus plugging is common in an ICU setting, and it is unclear that a patient who only transiently meets P/F criteria should be grouped with patients who have ongoing poor oxygenation. Additionally, recruitment of collapsed alveoli may result in a remarkable improvement in P/F ratio in a short period of time—does this patient no longer have ARDS? Lastly, while the AECC definition excludes patients with left atrial pressure (LAP) 18, Ferguson et al.13 showed that patients with no risk factors for congestive heart failure commonly had LAP 18 during a clinical course consistent with ARDS. Whether the current definition is too broad also remains a matter of debate. For example, a 2004 study compared postmortem analysis of lung tissue with the AECC definition. This investigation found the latter to be only 84% specific and 75% sensitive for the pathologic lung lesions characteristic of ARDS.14 It is clear, then, that the AECC definition, while useful for studies of populations, should be applied with caution to individual patients. It is also worthwhile to know its limitations and consider some alternative methods for objectively assessing lung injury. An alternative that remains useful is the Murray lung injury score (LIS). This was proposed in 1988 and is based on four components: chest radiograph, hypoxemia, positive end-expiratory pressure (PEEP), and respiratory compliance (Table 57-2).15 Each component is scored from 0 to 4. The LIS is calculated by summing the scores of the available components and dividing by the number of components used. ARDS (or severe lung injury) is defined as an LIS greater than 2.5. Zero represents no lung injury and 0.1–2.5 represents mild to moderate lung injury. A more recent definition makes a simple adjustment to the AECC definition and appears to approve diagnostic accuracy when compared with pathologic lesions found at autopsy. It may be more suitable for bedside evaluation of the individual patient (Table 57-3).16 Briefly, the authors include PEEP in the consideration of hypoxia and require either the absence of CHF or the presence of a recognized risk factor for ARDS. The degree of hypoxia required is a P/F less than 200 with PEEP

TABLE 57-2 Lung Injury Scorea Chest radiograph score No alveolar consolidation Alveolar consolidation confined Alveolar consolidation confined two quadrants Alveolar consolidation confined three quadrants Alveolar consolidation confined four quadrants

to one quadrant to

0 1 2

to

3

to

4

Hypoxemia score PaO2/FiO2 300 PaO2/FiO2 225–299 PaO2/FiO2 175–224 PaO2/FiO2 100–174 PaO2/FiO2 100

0 1 2 3 4

PEEP score (when ventilated) PEEP 5 cm H2O PEEP 6–8 cm H2O PEEP 9–11 cm H2O PEEP 12–14 cm H2O PEEP 15 cm H2O

0 1 2 3 4

Respiratory system compliance score (when available) Compliance 80 mL/cm H2O Compliance 60–79 mL/cm H2O Compliance 40–59 mL/cm H2O Compliance 20–39 mL/cm H2O Compliance 19 mL/cm H2O

0 1 2 3 4

a

The final value is obtained by dividing the aggregate sum by the number of components that were used: no lung injury, 0; mild to moderate lung injury, 0.1–2.5; severe lung injury (ARDS), 2.5. Source: Murray JF, Matthay MA, Luce JM, Flick MR. Pulmonary perspectives: an expanded definition of the adult respiratory distress syndrome. Am Rev Respir Dis. 1988;138:720. Official journal of the American Thoracic Society. Copyright © American Lung Association. With permission. 10; therefore, it excludes patients who are hypoxic purely because of derecruitment or suboptimal PEEP. By allowing patients with high filling pressures in the presence of a recognized ARDS risk factor, the definition recognizes the prevalence TABLE 57-3 The “Delphi” Definition of ARDS Timing: acute onset Oxygenation: PaO2/FiO2 200 with PEEP 10 Chest radiograph: bilateral infiltrates Absence of CHF or presence of recognized risk factor for ARDS

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TABLE 57-1 American–European Consensus Conference Definitions of Acute Lung Injury and Acute Respiratory Distress Syndrome

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EPIDEMIOLOGY AND RISK FACTORS The estimated incidence of ARDS in population-based studies is on the order of 40 cases per 100,000 person-years.17–19 In the United States, this represents about 200,000 cases per year, and about 15% of ICU admissions. With modern mortality rates (see below), one can estimate this entity is responsible for about 50,000 deaths per year in the United States.

RISK FACTORS Several studies demonstrate that age is a risk factor for ARDS, although it is unclear whether this simply represents diminished physiologic reserve in older patients. Hudson et al. documented an increasing incidence of ARDS with increasing age. Subgroup analysis, however, showed that this was largely due to the group with postinjury ARDS who were significantly older (44 years vs. 36 years).20 These authors also observed that a higher Injury Severity Score (ISS) was a risk factor for ARDS. Genetic variability between patients may also contribute to risk for ARDS (for a discussion of genomics relevant to trauma, see Chapter 53). Polymorphisms in genes encoding cytokines, vasomotor regulators, antioxidants, and surfactant proteins have all been associated with altered risks for either the development of ALI/ARDS or the outcome. Specific candidate genes have included angiotensin-converting enzyme, mannose-binding lectin, extracellular superoxide dismutase, surfactant protein B, and interleukin (IL)-10. Many of these studies are difficult to interpret because the reported effect is modified by gender, disease process (e.g., septic vs. traumatic ARDS), or the patient population studied (e.g., Caucasian vs. Asian). Of potential particular interest in trauma is a polymorphism in the promoter region of the NADPH:qunione oxidoreductase 1 gene (NQO1). This is an inducible gene that when activated regulates generation of oxidant species. In 2009, Reddy et al. completed an analysis demonstrating that critically injured patients (ISS 16, ICU admission) with the variant gene were about half as likely to develop ALI compared with patients homozygous for the wild-type gene. This effect was independent of race, mechanism of injury, and severity of illness score (Apache III).21 Clinical risk factors for ARDS can be broadly categorized into direct and indirect groups (Table 57-4). Direct factors are those primarily associated with local pulmonary parenchymal injury and include pulmonary contusion, aspiration, and pulmonary infection. Indirect factors are those thought to be associated with systemic inflammation and resultant lung injury. These include severe sepsis, transfusion of banked red cells, transfusion of FFP, and multiple long bone fractures. Unless shock is associated with significant tissue injury or other known risk factors, it has not been shown to result in ARDS.22

TABLE 57-4 Clinical Risk Factors for ARDS Risk Factor Direct Aspiration Pneumonia Pulmonary contusion Toxic inhalation Indirect Sepsis syndrome Multiple transfusions Multiple fractures Pancreatitis Disseminated intravascular coagulation

Frequency of ARDS (%) 12–36 12–31 5–22 2–17 11–80 5–36 2–21 7–18 23

PATHOLOGY The current paradigm of systemic inflammation leading to ALI and ARDS posits that a variety of insults, both infectious and noninfectious, can result in an unbridled hyperinflammatory response. This leads to organ injury from indiscriminate activation of effector cells that subsequently release oxidants, proteinases, and other potentially autotoxic compounds. If the initial insult is severe enough, early organ dysfunction results (“onehit” or single insult model). More often, a less severe insult results in a systemic inflammatory response that is not by itself injurious. These patients appear, however, to be primed such that they have an exaggerated response to a second insult, which leads to an augmented/amplified systemic inflammatory response and multiple organ dysfunction (“two-hit” or sequential insult model, see Chapter 61).23 Inflammatory models provide a unifying hypothesis for ARDS and MOF; however, the precise relationship between ARDS and MOF remains to be defined. MOF is a frequent occurrence and the most common cause of mortality in patients with ARDS.24 Indeed, postinjury ARDS appears to be an obligate precursor of other organ failures.25 This may be because the lung is a primary target of the inflammatory process, or because the resultant pulmonary damage impairs the lung’s ability to metabolize inflammatory mediators and control cellular effectors of injury.26 It is also now clear that ventilator strategies that inadvertently promote lung injury may produce systemic inflammation, perhaps leading to other organ failures.27 Inflammatory lung injury leads to the pathologic lesion of diffuse alveolar damage. This prototypic lesion of ARDS is at the alveolocapillary interface, which results in epithelial and endothelial damage as well as high-permeability pulmonary edema. The histologic appearance of this lesion can be divided into three overlapping phases: (1) the exudative phase, with edema and hemorrhage; (2) the proliferative phase, with organization and repair; and (3) the fibrotic phase.28 The exudative phase generally encompasses the first 3–5 days but may last up to a week. The initial histologic changes include interstitial edema, proteinaceous alveolar edema, and

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PATHOGENESIS Lung injury in ARDS involves components of inflammation, coagulation, vasomotor tone, and other systems (see Chapter 57). The pivotal cellular mediators appear to be leukocytes, with both local and humoral mediators orchestrating their function. Activation of these leukocytes results in release or activation of multiple cytokines, chemokines, oxidants, and proteases that result in the final common pathway of tissue injury in ARDS.

■ Neutrophils A consistent histopathologic feature of ARDS is neutrophil infiltration of the pulmonary microvasculature, interstitium, and alveoli. Neutrophils are well equipped to cause damage through the release of reactive oxygen species and proteases.30 Furthermore, neutrophils may be an important source of proinflammatory cytokines. Persistence of neutrophils in serial BAL fluid samples from patients with ARDS suggests unbridled inflammation and portends poor prognosis. In animal models, neutrophil depletion prior to an insult markedly attenuates resulting lung injury.31

The lung normally contains a significant number of sequestered neutrophils, and their mere presence is not sufficient to cause tissue injury. A long-standing model suggests that after a “priming” stimulus, neutrophils firmly adhere to endothelium and accumulate in the lungs; however, lung injury does not occur unless a second activating stimulus is applied. Thus, for neutrophils to cause tissue damage, there must be adherence to the endothelium, transmigration to the interstitium, and subsequent activation. Adherence and transmigration create a toxic microenvironment that is protected from endogenous antioxidants and antiproteases normally present in the plasma. Both cellular biomechanical and adhesive mechanisms are operative in the process of neutrophil sequestration. The initial phase is thought to result from a change in the cytoskeleton of the neutrophil that increases rigidity. This change impedes flow through the pulmonary microvasculature.32 A second, more prolonged phase is related to increased adhesive forces between neutrophils and endothelial cells. Initially, neutrophils “roll” and then “tether” to the endothelium as a result of the interaction of selections (L, E, and P) on the neutrophil and endothelial surfaces. This is followed by firm adhesion or “capture” of the PMN on the endothelial surface, which is mediated by β2 integrins on the neutrophil. These adhere to intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule (VCAM), and MADCAM. Once adherent, PMNS can transmigrate into the subendothelial space via paracellular or transcellular routes, again via surface integrins, adhering to platelet–endothelial cell adhesion molecule-1 (PECAM-1) or junctional adhesion molecules.33

MACROPHAGES The lung contains large numbers of fixed tissue macrophages that are a critical component of the inflammatory response in ALI. Activated macrophages can cause tissue injury by releasing the same toxic mediators as neutrophils (reactive oxygen species and proteases). Probably more important is the macrophage capability to synthesize multiple proinflammatory mediators, such as complement fragments, cytokines, and chemokines. Thus, macrophages are thought to have a major role in amplifying and perpetuating the inflammatory response. This is exacerbated by the long half-life of the macrophage, which is measured in days rather than hours as in the neutrophil. The alveolar macrophage has two additional key functions: control of local infection and modulation of fibrosis.34 Alveolar macrophage from ARDS patients demonstrates defective phagocytosis and bacterial killing, reflecting an increased risk for infection in these patients.

ENDOTHELIUM The pulmonary endothelium is not a passive bystander in the pathogenesis of ARDS, but actively participates in initiating and perpetuating the inflammatory response. Endothelial cells increase the expression of adhesion molecules (ICAM-1, ICAM-3, and E-selectin) following exposure to an activating stimulus. These ligands serve as tethering and signaling

CHAPTER CHAPTER 57 X

intra-alveolar hemorrhage. The exudative phase is characterized by the appearance of hyaline membranes, which are composed of plasma proteins mixed with cellular debris. Electron microscopy reveals endothelial injury with cell swelling, widening intercellular junctions, and increased pinocytotic vesicles. In addition, there is disruption of the basement membrane. The alveolar epithelium usually exhibits extensive loss of type I cells, which slough and leave a denuded basement membrane. While some loss may be from necrosis, it appears that apoptosis contributes substantially. Activation of matrix metalloproteinases, Toll-like receptors, and oxidative stress pathways initiate programmed cell death in these cells. Demonstration of soluble Fas ligand in bronchoalveolar lavage (BAL) fluid early in ARDS supports this concept.29 Loss of the alveolar epithelial barrier results in alveolar edema, as the remaining cells are unable to drive sodium from the alveolar into the interstitial compartment. During the proliferative phase, type II cells divide and cover the denuded basement membrane along the alveolar wall. This process may be seen as early as 3 days after the onset of clinical ARDS. Type II cells are also capable of differentiating into type I epithelial cells. Fibroblasts and myofibroblasts proliferate and migrate into the alveolar space in the third phase. Fibroblasts change the alveolar exudate into granulation tissue, which subsequently organizes and forms dense fibrous tissue. Eventually, epithelial cells cover the granulation tissue. This whole process is called fibrosis by accretion and is important in lung remodeling. Septal collagen deposition by fibroblasts and “collapse induration” also contribute to fibrous remodeling of the lung in ARDS. The fibrotic stage is characterized by thickened, collagenous connective tissue in the alveolar septa and walls. Pulmonary vascular changes occur as well, with intimal thickening and medial hypertrophy of the pulmonary arterioles. Complete obliteration of portions of the pulmonary vascular bed is the end result.

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molecules by binding to their cognate leukocyte membrane proteins. Thus, the endothelial cell actively coordinates trafficking, firm adhesion, and transmigration. In the setting of systemic inflammation, inappropriate endothelial cell activation may lead to indiscriminate leukocyte recruitment and parenchymal inflammation. Moreover, endothelial cells produce and release vasoactive substances, such as prostacyclin, nitric oxide (NO), and endothelins. These substances may mediate much of the pulmonary vascular dysfunction characteristic of ARDS. Activated endothelium also expresses procoagulant activity, which contributes to intravascular coagulation and microvascular dysfunction.35 Thrombin, in turn, has proinflammatory effects on leukocytes. Endothelial injury, then, may be both a proximate cause and a marker for ALI.

THE GUT LYMPH HYPOTHESIS It has long been understood that reperfusion of the ischemic gut can lead to lung injury.36 Because gut ischemia/reperfusion is an established phenomenon in the injured patient with hemorrhagic shock, this remains a tantalizing hypothesis for the development of inflammatory injury to the lung. Curiously, however, convincing evidence of inflammatory mediators leaving the gut into the portal circulation has been lacking in humans. This led Deitch37 to hypothesize that the egress of proinflammatory substances from the gut may be via lymph, not venous blood. This intriguing hypothesis has substantial support in animal models, including the finding that diversion of gut lymph abrogates lung injury. While the precise mediators of this phenomenon are as yet unknown, changes in posthemorrhagic shock lymph flow, lipid content, and protein content are an active area of investigation.38,39

■ Mediators and Markers of Acute Respiratory Distress Syndrome Complement Systemic complement activation secondary to trauma or sepsis is considered a major early factor in ARDS.40 C5a, a product of complement activation, is a powerful neutrophil chemoattractant. Moreover, C5a induces neutrophil aggregation and activation leading to pulmonary neutrophil sequestration and lung injury. Clinically, plasma and bronchoalveolar C3a levels correlate with the development of ARDS.41

Lipid Mediators Phospholipids are potent inflammatory mediators that are formed by the action of phospholipase A2 (PLA2) on membrane phospholipids. PLA2 contributes to the inflammatory response by two separate pathways, catalyzing the production of both plateletactivating factor (PAF) and arachidonic acid. Arachidonic acid metabolism results in release of eicosanoids such as leukotrienes, thromboxane, and prostaglandins. Each of these is a pivotal mediator in the inflammatory cascade and has been implicated in the pathogenesis of ARDS.42

PAF is a phospholipid with potent vasoactive and inflammatory properties. It is produced by a number of cell types including macrophages, neutrophils, endothelial cells, and type II pneumocytes. PAF production is stimulated by endotoxin, tumor necrosis factor (TNF), and leukotrienes, and exerts diverse biologic actions, including neutrophil activation and adherence, platelet aggregation and degranulation, and macrophage production of inflammatory mediators. Infusion of PAF in animals results in increased vascular permeability and neutrophil-mediated ALI.43 Lysophosphatidyl cholines are another class of bioactive lipids that may play a significant role in lung injury after trauma. These compounds accumulate during routine storage of packed red blood cells and have been shown to cause lung injury in isolated perfused rodent lungs.44 These or related compounds from transfusion of banked red cells may provide a second insult leading to inflammatory organ injury in the injured patient. As mentioned above, the pulmonary endothelium is recognized as an active participant in the development of ALI. As such, markers of endothelial activation or injury have been investigated as predictors of the development of ARDS. von Willebrand factor antigen (vWF:Ag) has been studied fairly extensively as a marker of endothelial dysfunction. vWF:Ag is synthesized largely by vascular endothelial cells and has been shown to be a sensitive marker of endothelial injury or activation.45 This antigen was studied prospectively in 45 patients to determine whether elevated levels of vWF:Ag are predictive for the development of ALI.46 Only patients with nonpulmonary sepsis were included, and one third developed ALI. Elevated plasma levels of vWF:AG (45% above controls) were 87% sensitive and 77% specific for development of ALI. Positive predictive value was 65%. Following activation, endothelial expression of adhesion molecules, including ICAM-1, VCAM-1, E-selectin, and P-selectin, is upregulated. These compounds are susceptible to proteolytic cleavage and may exist in the circulation in a soluble form. Therefore, these molecules represent a measure of endothelial activation or damage. We and others have demonstrated elevated ICAM-1 levels in severely injured patients who subsequently developed MOF.47,48 In contrast, plasma levels of soluble E- and P-selectins measured at admission were not useful in predicting ALI. The maintenance of a functioning alveolar epithelium is important for recovery from ALI.49 Unlike the endothelium, there is a lack of specific histologic markers of alveolar epithelial injury. Surfactant abnormalities have been noted in the earliest reports of ARDS. Surfactant lipids and proteins are synthesized and released by alveolar epithelial type II cells. The surfactantassociated proteins SP-A and SP-B are decreased in BAL fluid from patients with ARDS and at risk for ARDS.50 Markers of leukocyte activation have also been measured in plasma and BAL fluid of patients in an attempt to predict development of ARDS. Gordon et al. noted markedly elevated plasma elastase levels very early after multisystem trauma.51 Subsequent studies supported a causative role for neutrophil elastase in ARDS,52 and have led to the clinical development of human elastase inhibitor.53 Increased expression of β2 integrins

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A

B

FIGURE 57-1 (A) Normal admission chest x-ray in a 27-year-old trauma patient with multiple lower extremity fractures. (B) Chest x-ray from the same patient following onset of respiratory insufficiency. Note the bilateral, dense pulmonary infiltrates consistent with severe ARDS.

has been observed on the surface of circulating pulmonary artery neutrophils in patients at risk for postinjury ARDS.54 Circulating and BAL fluid levels of cytokines are also inherently attractive as predictors of ARDS; whether they are markers or mediators remains an important question. TNF-α, IL-1β, IL-6, and IL-8 have been the most intensely investigated in relation to the development of ARDS. Studies examining the predictive value of cytokines central to sepsis (TNF-α, IL-1β) levels in ARDS have had negative or mixed results.55 IL-8 is a neutrophil chemoattractant that has been studied in both plasma and BAL fluid. It is elevated in the plasma following injury but does not appear to consistently predict development of ARDS. Donnelly et al. studied 29 patients at risk for developing ARDS and observed that IL-8 levels in BAL fluid were significantly higher in patients who later progressed to ARDS.56

however, it was already recognized that in the heterogeneously injured lung, airway pressure or stretch may be damaging to the healthy zone. This ventilator-induced lung injury was thought to be responsible for severe protracted ARDS, as well as perpetuation of systemic inflammation and MOF.58,59 A standard method used to describe the mechanical properties of the lung is to determine the static pressure–volume curve during inflation and deflation (Fig. 57-3). In early ARDS, the lower inflection point represents the airway pressure at which considerable alveolar recruitment occurs. The upper inflection

PATHOPHYSIOLOGY ARDS is characterized by diffuse, patchy, panlobular pulmonary infiltrates on plain chest radiograph (Fig. 57-1). CT of the chest will demonstrate that the parenchymal changes are inhomogeneous with the dependent lung regions most affected (Fig. 57-2). The inhomogeneous distribution of parenchymal densities led to the concept of a three-compartment model of the lung in ARDS.57 One compartment is substantially normal (healthy zone), one is fully diseased without any possibility of recruitment (diseased zone), and, finally, the third compartment is composed of collapsed alveoli potentially recruitable with increasing pressure (recruitable zone). Increased airway pressure is necessary to recruit collapsed alveoli. In the 1990s,

FIGURE 57-2 Chest CT scan of a patient with ARDS shows marked inhomogeneity of the process with areas of dense consolidation and essentially normal intervening pulmonary parenchyma.

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Zone of overdistention

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“Safe” window

Volume Zone of derecruitment and atelectasis

Pressure

FIGURE 57-3 Idealized static pressure–volume curve of the lungs in ARDS. At low pressures and volumes, derecruitment, atelectasis, and lung injury from repetitive opening and closing of gas exchange units are a concern. At high pressures and volumes, overdistention, increased shunt, and lung injury from excessive stretch predominate. In between these two extremes is the optimal zone where lung stays recruited but is not overstretched.

point is where near maximal inflation occurs such that further increases in airway pressure result in alveolar overdistension and little change in volume. The “open lung approach” to mechanical ventilation in ARDS advocates setting PEEP at or just above the lower inflection point to avoid repetitive alveolar recruitment and collapse with each breath. In practice, however, inflection points in individual patients have been difficult to consistently measure.

■ Pulmonary Edema Increased pulmonary capillary permeability is a consistent feature. Increased permeability promotes alveolar flooding with protein-rich edema fluid, as well as release of proteins generally confined to the lung into the systemic circulation. Multiple studies have documented elevated total protein concentrations in BAL fluid from patients with established ARDS.60 One study observed higher BAL fluid protein concentrations in nonsurvivors, suggesting that more severe lung injury is associated with greater endothelial and epithelial permeability.61

GAS EXCHANGE Hypoxemia in ARDS results from ventilation–perfusion mismatching and intrapulmonary shunting of blood flow. Shunting results from blood that passes through the systemic venous to pulmonary arterial system without going through the normal gas exchange units in the lung (i.e., right–left shunt). Normally, the shunt fraction is less than 5%; however, in ARDS, it may exceed 25%. Because blood flowing through a shunt is not exposed to alveoli participating in gas exchange, supplemental oxygen is ineffective in increasing arterial oxygen concentration. Other techniques designed to restore ventilation to diseased

lung regions, such as PEEP or continuous positive airway pressure (CPAP), are thus necessary to improve oxygenation. Hypoxic pulmonary vasoconstriction is a protective mechanism that limits perfusion to poorly ventilated alveoli and minimizes shunting. In ARDS, hypoxic pulmonary constriction is impaired, resulting in greater intrapulmonary shunt. Multiple factors may contribute to loss of hypoxic pulmonary vasoconstriction in ALI, including local prostaglandin or NO production.62 In early ARDS, most patients are tachypneic from hypoxemia and are secondarily hypocapneic. With disease progression, hypercapnia may become a prominent feature because of physiologic dead space and CO2 production. Increased dead space ventilation is invariably present. As discussed earlier, the normal dead space to tidal volume ratio is approximately 35%, but in ARDS, it can approach 60%.

PULMONARY MECHANICS Lung compliance is defined as the change in lung volume per change in transpulmonary pressure. Normal lung compliance in a mechanically ventilated patient ranges from 60 to 80 mL/cm H2O. With ARDS, it is not unusual to see greatly diminished lung compliance on the order of 10–30 mL/cm H2O. Initially, reduced compliance is the result of interstitial and alveolar edema with alveolar flooding. Surfactant dysfunction and terminal bronchiolar spasm contribute to loss of ventilated alveoli. In later ARDS, interstitial fibrosis and parenchymal loss further reduce pulmonary compliance.

HEMODYNAMICS Pulmonary hypertension is a frequent finding in patients with ARDS and can lead to increased interstitial pulmonary edema, right ventricular dysfunction, and impaired cardiac output. When severe, pulmonary hypertension has been observed to be a marker of poor outcome. The etiology of pulmonary hypertension in ARDS is multifactorial. Early in ARDS, the predominant mechanism is most likely impaired vasorelaxation related to hypoxemia, acidosis, and vasoactive mediators, in concert with obstruction from microvascular coagulation. In late ARDS, fibrosis and obliteration of the pulmonary vascular bed are most likely responsible. Steltzer et al. noted markedly depressed right ventricular function in nonsurvivors of ARDS.63 The authors related this to reduced myocardial contractility and not to pulmonary hypertension. They also noted that oxygen delivery was more related to cardiac performance than to pulmonary gas exchange.

PRESENTATION The diagnosis of ARDS is based on the criteria used to define the syndrome and has historically been divided into four clinical phases with radiographic, clinical, physiologic, and pathologic correlates (Table 57-5). In the initial phase, dyspnea and tachypnea are evident, with a remarkably normal chest examination (radiographically and clinically). Arterial oxygen saturation is preserved, and hypocapnia from hyperventilation is frequently noted.

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TABLE 57-5 Pathophysiologic Changes of Modern Adult Respiratory Distress Syndrome (Low-Pressure Pulmonary Edema) Phase 1 (early change) Normal radiograph

Clinical Finding

Physiologic Change

Pathologic Change

Dyspnea, tachypnea, normal chest examination

Mild pulmonary hypertension, normoxemic or mild hypoxemia and hypocarbia

Neutrophil sequestration, no clear tissue damage

Pulmonary hypertension, normal wedge pressure, increased lung permeability, increased lung increasing shunt, progressive decrease in compliance, moderateto-serve hypoxemia

Neutrophil infiltration, vascular congestion, fibrin strands, platelet clumps, alveolar septal edema, intra-alveolar protein, white cells, type 1 epithelial damage

Phase 2 (onset of parenchymal changes)a Patchy alveolar infiltrates Dyspnea, tachypnea, beginning in dependent cyanosis, tachycardia, lung coarse rales No perivascular cuffs (unless a component of water, highpressure edema is present) Normal heart size

Phase 3 (acute respiratory failure with progression, 2–10 days) Phase 2 changes persist, Diffuse alveolar infiltrates Tachypnea, progression of symptoms, tachycardia, Air bronchograms increasing shunt fraction, Decreased lung volume hyperdynamic No bronchovascular cuffs state, sepsis further decrease in syndrome, signs compliance, increased Normal heart size minute ventilation, of consolidation, impaired oxygen extraction diffuse rhonchi of hemoglobin Phase 4 (pulmonary fibrosis—pneumonia with progression, .10 days)b Persistent diffuse infiltrates Symptoms as above, Phase 3 changes persist, Superimposed new recurrent sepsis, recurrent pneumonia, pneumonic infiltrates evidence of multiple progressive lung Recurrent pneumothorax system organ failure restriction, impaired tissue Normal heart size oxygenation, impaired Enlargement with pulmonale oxygen extraction, multiple system organ failure

Increased interstitial and alveolar inflammatory exudate with neutrophil and mononuclear cells, type II cell proliferation, beginning fibroblast proliferation, thromboembolic occlusion Type II cell hyperplasia, interstitial thickening, infiltration of lymphocytes, macrophages, fibroblasts, loculated pneumonia and/or interstitial fibrosis, medial thickening and remodeling of arterioles

a

Process readily reversible at this stage if initiating factor controlled.

Multiple system organ failure, common mortality rate 80% at this stage, as resolution is more difficult. Source: From Demling RH. Adult respiratory distress syndrome: current concepts. New Horiz. 1993;1:388. b

The second phase quickly follows (12–24 hours), with physiologic and pathologic evidence of lung injury. The chest x-ray now shows bilateral patchy alveolar infiltrates with hypoxemia evident on arterial blood gas (ABG) determination. If ARDS persists and progresses, the third clinical phase becomes evident. Acute respiratory failure necessitates mechanical ventilation with increasing inspired oxygen concentrations. There is an increase in physiologic dead space and rising minute ventilation. Patients at this point may develop sepsis syndrome with a hyperdynamic hemodynamic pattern. The radiographic picture worsens with more diffuse infiltrates, consolidation, and air bronchograms. Without resolution, progressive pulmonary failure and fibrosis characterize the fourth phase. Pneumonia, often recurrent,

is frequent (see Chapter 18). Hypercapnia may worsen and become more difficult to control. MOF commonly develops and is the most common cause of death (see Chapter 61).

MANAGEMENT Because there is no proven specific treatment for ARDS, therapy primarily involves supportive measures to maintain life while the lung injury resolves. Such measures include identifying and treating predisposing conditions, mechanical ventilatory support with oxygen, nutritional support, nonpulmonary organ support, and hemodynamic monitoring as necessary. Attention to detail is necessary to avoid nosocomial infection and iatrogenic complications.

CHAPTER CHAPTER 57 X

Radiographic Change

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FLUID MANAGEMENT AND HEMODYNAMIC SUPPORT SECTION 5 X

Given the central role of alveolar flooding in ARDS, the appropriate use of fluids and diuretics in managing patients has been a matter of debate since the description of this syndrome. In large part, the discussion centers on whether hydrostatic forces, changes in membrane permeability, or dysfunction of the lung epithelial barrier are the prime contributors to pulmonary edema in ARDS. Some investigators believe that hydrostatic intravascular forces contribute significantly to pulmonary edema in ARDS and favor early diuresis and fluid restriction to minimize interstitial and alveolar edema. If necessary, cardiac output and blood pressure are supported with vasopressors. Potential problems with this approach include decreased end-organ perfusion with precipitation of MOF, and an increased shunt fraction. Some studies observe that increased extravascular lung water does not correlate with oxygenation or outcome in ARDS patients, and calls into question the physiologic basis for this approach.64 Because hypovolemia may be uniquely dangerous in the resuscitation of the injured patient, caution should be exercised before adopting such an approach. Two landmark trials published by the ARDS network in 2006 attempted to address appropriate fluid management in this group of patients. In one study, a total of 1,000 patients were randomized to either liberal or conservative fluid strategies over a period of 7 days.65 The conservative group received approximately a net 1 L less per day, and spent 2.5 fewer days on the ventilator. There was no mortality difference, and no increase in other organ failures in the conservative group. In the second study, care was based on either CVP measurements or pulmonary artery catheter measurements. This study also showed no difference in mortality. Overall, these studies do not show a profound effect of a specific invasive monitor or the amount of fluid administered. It may be that the uniform application of pressurelimited ventilation trumps any major effect of fluid balance in this patient population. With respect to colloids, there is no evidence that their use for acute resuscitation improves outcome. A recent study in hypoproteinemic patients suggests that gas exchange can be improved in late ALI by using colloid in concert with diuretics to mobilize interstitial fluid and promote diuresis.66 A 2006 randomized study also suggested that critically ill patients with profound hypoproteinemia have fewer organ failures (by SOFA score) when given colloid therapy.67 Short-term improvement in physiology is not, however, accompanied by an improved outcome in these investigations. The very large Australian SAFE study suggests that routine use of albumin cannot be supported.68 Thus, outside of the profoundly hypoproteinemic patient, it is difficult to argue that colloids are of any benefit.

MECHANICAL VENTILATION Respiratory support with a mechanical ventilator is a cornerstone in the supportive management of patients with or at risk for ARDS. It has become increasingly clear, however, that

mechanical ventilation can perpetuate or worsen lung injury, as well as result in more readily recognized forms of barotrauma (mediastinal emphysema, pneumothorax, etc.). This recognition has led to the concept of lung-protective strategies in mechanical ventilation.69 Most patients with ARDS require endotracheal intubation for mechanical ventilation. Patients with mild ALI may occasionally be managed initially with noninvasive positive pressure mask ventilation. This technique reduces shunt physiology and administers high concentrations of oxygen. It requires an alert and cooperative patient to tolerate the tightfitting mask and avoid complications (in particular, vomiting and aspiration). Patients with multisystem injuries are frequently poor candidates for this approach. Emergent intubation is associated with significantly higher morbidity and mortality. Accordingly, early elective intubation should be considered in all patients with deteriorating gas exchange or mental status. Historically, large tidal volumes (10–15 mL/kg) were used to achieve normal ABG values while avoiding microatelectasis and patient discomfort. With little modification and the addition of PEEP, this approach was applied as the standard for most critically ill patients. In the setting of ARDS, the conventional goals of mechanical ventilation have been to achieve adequate oxygenation using the least PEEP possible and a nontoxic FiO2 while at the same time maintaining normocarbia. This strategy was intended to minimize or avoid hyperoxic lung injury and the adverse effects of PEEP. The primary priority has shifted from maximizing tissue oxygen delivery to ensuring adequate lung protection (Table 57-6).

TABLE 57-6 Ventilatory Strategies in ARDS Goals

Conventional Normal arterial blood gases Nontoxic FiO2 ( 0.50) Adequate O2 delivery

Ventilator mode Settings tidal volume PEEP

Volume cycled

I:E ratio Plateau airway pressure

1:2 to 1:4 As required by PEEP and tidal volume

10–15 mL/kg 5–20 cm H2O as needed

Lung Protective Acceptable arterial blood gases Prevent alveolar damage Facilitate healing Nontoxic FiO2 ( 0.50) Pressure limited 4–8 mL/(kg IBW) Sufficient to prevent tidal recruitment/ derecruitment Achieve acceptable PaO2/FiO2 ratio 1:1 to 1:4 30 cm H2O

Respiratory Insufficiency

POSITIVE END-EXPIRATORY PRESSURE

PRESSURE-LIMITED VENTILATORY SUPPORT In patients with ARDS, the aerated lung volume able to participate in gas exchange is markedly reduced to one third of the original volume. Thus, in nonfibrotic stages of ARDS, the lungs may be thought of as small rather than stiff. There is accumulating evidence that pulmonary gas exchange may be essentially normal in the aerated portion of the injured lung. The use of conventional tidal volumes in this setting would be expected to result in alveolar overdistention with further impairment of gas exchange, frequent barotrauma, and ventilator-induced lung injury. One approach is to reduce tidal volume in order to limit airway pressures while maintaining adequate alveolar ventilation with an increased respiratory rate. While the safe upper limit of airway pressure is not precisely known, pressures in excess of 35–40 cm H2O are associated with lung injury in animal models. A benchmark clinical trial of low-volume, pressure-limited ventilation in established ARDS forms the basis for modern ventilator management in ALI and ARDS.75 In this study, patients ventilated using smaller (6 cm3/kg) tidal volume had a mortality of 31% versus a 40% mortality in a group ventilated with a larger (12 cm3/kg) tidal volumes. This

CHAPTER CHAPTER 57 X

PEEP is one of several methods of increasing mean airway pressure and improving oxygenation. It improves oxygenation by enhancing lung volume, and increasing functional residual capacity (FRC) through recruitment of collapsed alveoli. Lung compliance may also be improved. The use of PEEP in patients with ARDS has two primary goals: adequate tissue oxygen delivery and the reduction of FiO2 to nontoxic (generally below 0.6) levels. Increasing PEEP above a certain level, however, may have significant adverse effects. By raising intrathoracic pressure, PEEP may significantly reduce venous return and cardiac output.70 This may result in decreased tissue oxygen delivery despite improvement in arterial oxygen saturation. This effect is accentuated in the hypovolemic patient, and can usually be reversed with intravascular volume expansion. Cardiac depression is rarely seen with PEEP levels less than or equal to 10 cm H2O. If PEEP 10 cm H2O is required, assessment of intravascular volume status and cardiac function is warranted. PEEP may also result in alveolar overdistention with compression and obliteration of surrounding pulmonary capillaries. This alveolar overdistention may actually worsen oxygenation by increasing the shunt fraction. Moreover, dead space ventilation may be increased, resulting in a higher minute ventilation requirement. Finally, PEEP may cause a maldistribution of tidal volumes and pressures, creating overdistension of normally aerated lung regions. This hyperinflated form of lung injury may result in barotrauma referred to as “volutrauma.” The optimal approach to PEEP for ARDS remains a matter of debate. Early on, several strategies were proposed for determining optimal PEEP.71 “Best PEEP” sought the greatest static lung compliance. “Optimal” PEEP sought lowest shunt fraction. In “preferred” PEEP, the goal is maximal oxygen delivery. Today, many centers have adopted the algorithm-driven approach adopted by the ARDSNet investigators that is based on a ratio of PEEP to FiO2. In one trial by these investigators comparing “high” with “low” PEEP in a lung-protective strategy, there was no clear difference in outcomes.72 The advantage of a ratio approach is that it can be done without measurement of pulmonary compliance curves or invasive hemodynamic monitoring. One disadvantage is that it is not necessarily applicable to an individual patient with individual physiology. In the individual patient, the application of PEEP needs to be balanced between providing a sufficient inspiratory plateau pressure (peak alveolar pressure) to maintain adequate oxygenation and at the same time avoiding derecruitment of the alveoli during exhalation. Fig. 57-3 demonstrates the area on the pressure–volume curve where optimal ventilation occurs. With recent ventilatory strategies emphasizing pressure-limiting techniques, the “least” PEEP method seemed logical. This approach has been associated with less barotrauma and cardiac compromise.73 The use of minimal PEEP, however, does not address the potential damage from repeated alveolar opening and collapse with each breath.74 This forms the basis for the “open lung” ventilation strategy. Static pressure–volume curves are used to select a PEEP level above the lower infection point

to prevent alveolar end-expiratory collapse. Although this approach is intriguing, static pressure–volume curves can be difficult to obtain as well as to implement. Practically speaking, bedside PEEP trials are frequently initiated in response to worsening hypoxemia. We identify the optimal or least PEEP in the following manner. Baseline PEEP is set at 10 cm H2O, with a Vt of 6 mL/kg ideal body weight. If the patient desaturates, then the patient is recruited for 2 minutes using pressure-controlled ventilation with a PIP of 20 cm H2O, a respiratory rate of 10 breaths/min, and an I:E of 1:1 with PEEP raised to 25–40 cm H2O. The patient is monitored for cardiopulmonary instability during recruitment because this maneuver results in substantial hypoventilation for the period of recruitment. The patient is returned to his or her previous settings and if desaturation reoccurs, the recruitment maneuver is repeated for 2 minutes and the patient is returned to his or her previous ventilator settings except the PEEP is increased by 2.5–5 cm H2O. This process is repeated as needed until oxygen saturation remains stable. With improvement in the patient’s lung injury, PEEP should be withdrawn as the pulmonary compliance, shunt fraction, and dead space ventilation improve. Premature attempts at PEEP reduction, however, will only delay resolution of lung injury and prolong the need for ventilatory support. PEEP weaning should be performed in an orderly fashion. PEEP is reduced slowly in 2.5–5 cm H2O increments, with serial monitoring of arterial oxygen saturation using ABG or oximetry. In general, tidal volumes should be increased to both maintain mean airway pressure and allow respiratory rates associated with greater patient comfort. A significant decrease in PaO2 should prompt a quick return to previous levels of PEEP. Once alveolar collapse and loss of FRC occur, higher levels of PEEP for more prolonged periods may be needed. Generally, PEEP should not be reduced by more than 3–5 cm H2O in a 12-hour period.

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SECTION 5 X

PERMISSIVE HYPERCAPNIA Now that the importance of defending airway pressures has been highlighted, the maintenance of eucapnia is no longer stressed. Controlled hypoventilation (relative to CO2 production) with increased PaCO2 is referred to as permissive hypercapnia. Gradual increases in PaCO2 are usually well tolerated, provided renal compensation is adequate (see Chapter 60) and severe acidosis (pH 7.1) does not occur. Respiratory acidosis has a myriad of physiologic effects that may be relevant to the critical care physician. Because CO2 diffuses freely across cell membranes, an increase in extracellular PCO2 will result in intracellular acidosis. The pathologic effects of this hypercapnia are related to the severity and duration of any resultant intracellular acidosis. Cytosolic pH is normally tightly regulated between 6.9 and 7.2.76 Three mechanisms are responsible for this regulation: (1) physiochemical buffering, mainly due to proteins and phosphates; (2) reduced intracellular generation of protons; and (3) changes in transmembrane ion exchange. Physiochemical buffering is immediate, while the other mechanisms require 1–3 hours. These regulatory mechanisms are remarkably powerful and efficient. As a result, normoxic hypercapnia has only limited potential for resulting in intracellular acidosis, and is generally well tolerated. Hypercapnia has multiple cardiovascular effects. Acute respiratory acidosis results in reversible impairment of myocardial contractility. The principal mechanism for this decrease in cardiac contractility is intracellular acidosis, which interferes with myofilament responsiveness to activator calcium.77 Hypercapnia may lead to a substantial increase in coronary flow and a rise in coronary sinus oxygen tension. The overall hemodynamic response to acute hypercapnia in human experiments is increased cardiac output, heart rate, and stroke volume, with decreased systemic vascular resistance. This reflects the net result of the myocardial depressive effects of CO2, as well as indirect effects with stimulation of the sympathetic nervous system and catecholamine release. In some patients, however, hypercapnia may adversely affect right ventricular function. It results in pulmonary vasoconstriction and may lead to pulmonary hypertension with right ventricular dysfunction.78 Increased PCO2 produces a rightward shift of the oxygen– hemoglobin dissociation curve by two mechanisms. This increases the P50 and facilitates unloading of oxygen at the tissue level, which may be beneficial. Hypercapnia has multiple effects on the central nervous system. Similar acid–base changes to those described above also occur in the brain. Preliminary studies suggest a decrease in the oxygen demand of the brain.79 However, it has long been recognized that hypercarbia increases cerebral blood flow and intracranial pressure. Increased intracranial pressure results from enlargement of cerebral blood volume secondary to diminished vascular tone.

Contraindications to permissive hypercapnia include increased intracranial pressure or other cerebral disorders in which intracranial hypertension may be detrimental. Uncorrected hypovolemia and significant cardiac disease are relative contraindications due to the negative inotropic effects of permissive hypercarbia. Several reports document that permissive hypercapnia in the setting of ARDS is remarkably well tolerated.80 Ideally, this strategy should be implemented slowly over several hours to allow compensatory mechanisms to act. The role of sodium bicarbonate infusion is unclear. In most institutions, sodium bicarbonate would not be administered unless the pH was less than 7.2. With increased experience, however, many centers reserve bicarbonate infusion for pH less than 7.0. An alternative is to use tris-hydroxymethyl aminomethane (THAM), which does not increase CO2 production but is not specifically labeled for this use.81 Sedation is mandatory with permissive hypercapnia in mechanically ventilated patients in order to control respiratory drive and prevent discomfort. Even with heavy sedation, however, respiratory drive may be insufficiently suppressed, resulting in patient–ventilator dyssynchrony. Neuromuscular blockade is often necessary in these patients.

PRONE VENTILATION There continues to be great interest in mechanical ventilation of ARDS patients in the prone position. Bryan described the beneficial effects of the prone position on arterial oxygenation more than 30 years ago.82 Other investigators subsequently confirmed these findings.83 Although large controlled studies are lacking, it appears that at least 50% of patients show improved oxygenation with prone positioning. Pappert et al. used the multiple inert gas elimination technique and showed that the improvement in oxygenation was the result of decreased intrapulmonary shunt fraction.84 Albert and coworkers have investigated the mechanism of prone ventilation in a canine oleic acid model of ARDS. The prone position consistently reduced shunt fraction compared with the supine position. The improvement in gas exchange was independent of changes in cardiac output or FRC between the two positions. Subsequently, pulmonary blood flow was shown to be distributed preferentially to dorsal lung regions in the supine and prone positions.85 In supine animals, pleural pressure increases from nondependent to dependent regions. This may lead to dependent atelectasis in the highly perfused dorsal lung regions, resulting in intrapulmonary shunt and hypoxemia. In the prone position, the pleural pressure gradient is less, and the dorsal (now nondependent) regions are exposed to a lower pleural pressure. This results in opening of previously atelectatic alveoli. Intrapulmonary shunting is reduced because perfusion of the dorsal lung regions is maintained. Lamm et al. recently confirmed this mechanism in a canine oleic acid lung injury model.86 The investigators used single photon emission computed tomography (SPECT) scanning to quantitate regional ventilation and perfusion. Supine animals had markedly reduced or absent ventilation to the

Respiratory Insufficiency

HIGH-FREQUENCY VENTILATION Recognition of the impact of mechanical ventilation on furthering lung injury has been an impetus to revisit high-frequency modes of ventilation (HFV). After all, this might be considered the ultimate in “low tidal volume ventilation.” Several modes of high-frequency ventilation have been available over the last 20 years, including high-frequency jet ventilation, high-frequency positive pressure ventilation, ultrahigh-frequency ventilation, and high-frequency oscillatory ventilation. These techniques use very small tidal volumes (1–5 mL/kg) delivered at rates of 60–3,600 cycles/min. To date there are a number of prospective clinical studies that have failed to demonstrate any meaningful benefit of high-frequency ventilation over conventional modes of positive pressure ventilation in patients with ARDS.93 Although peak airway pressures are reduced compared with conventional modes, mean airway pressures, barotrauma, and hemodynamic compromise appear unchanged. Proponents of high-frequency ventilation argue that it provides the ideal approach to lung-protective ventilation. By definition, HFV delivers an extremely low tidal volume in concert with a relatively high mean airway pressure using a piston pump. Mean airway pressures of 25–45 cm H2O are not unusual. Delivery of plateau pressures in this range with tidal volumes that may be just larger than dead space ventilation, perhaps as high as 5 mL/kg, may not be equally protective in all settings of lung injury. For example, will ARDS that is caused by a direct pulmonary insult such as aspiration respond the same as an injured lung from a nonpulmonary cause of ARDS such as pancreatitis? In an effort to answer these types of questions recently investigators from the Multicenter Oscillatory Ventilation for Acute Respiratory Distress Syndrome Trial (MOAT) published the results of a randomized controlled study comparing HFV with a CV arm in adults with early ARDS.94 One hundred and forty-eight patients were enrolled with 75 randomized to HFV and 73 to CV. The primary study end point was safety and effectiveness of HFV compared with CV. Tidal volume in the CV group was based on actual weight and averaged 10.2 mL/kg, while peak airway pressures were 38 cm H2O. As expected, mean airway pressures were significantly higher at 29 cm H2O versus 23 cm H2O in the HFV group. Oxygenation, as evidenced by the PaO2/FiO2 ratio, was higher in the initial 16 hours in the HFV group but was subsequently decreased and the p/f ratio was no longer significantly different between the two groups. While not statistically significant, there was a clear trend toward a better outcome in the HFV group; mortality was 37% in the FHO group and 52% in the CV group (P  .12). It is regrettable, however, that this trial failed to provide a lung-protective approach for the CV group. So, until a true, randomized, prospective trial comparing HFV with CV using a lung-protective strategy is performed, all we really know is that HFV is safe and effective when compared with CV. Currently, the primary clinical indications for high-frequency ventilation include treatment of neonatal respiratory distress syndrome and ventilatory support during proximal airway procedures.

CHAPTER CHAPTER 57 X

dorsal lung regions while maintaining perfusion to those areas. With prone positioning, ventilation of dorsal regions improved significantly and perfusion was maintained. Using chest CT, Gattinoni et al. showed that in the supine position, gasless lung was found predominantly in the dorsal regions.87 With prone positioning, densities redistributed to the ventral areas and dorsal regions were well aerated. Thus, prone positioning results in recruitment of previously atelectatic dorsal lung regions. Although prone positioning appears to improve oxygenation in many patients with ARDS, a significant number of patients have no response. In a small number of patients, gas exchange actually deteriorates. Currently, responders to prone positioning cannot be reliably predicted while in the supine positions. Despite early reports documenting improved gas exchange in approximately two thirds of patients, it is remarkable that it took 20 years for the first prospective, randomized trial to be performed. The trial, reported by Gattinoni et al.,88 consisted of 152 patients randomized to a prone group and 152 patients to a supine group. Patients randomized to the prone arm were followed for the first 10 days and turned prone for at least 6 hours each day if they met the necessary criteria. Regrettably, no differences in mortality rates were noted between the two groups after a 10-day period (21.1% vs. 25%), and the study was underpowered to detect a statistical difference. A post hoc analysis revealed that in patients with severe hypoxemia, defined as a p/f ratio 90, an APACHE score 49, or having been exposed to high Vt (12 mL/kg) mortality was significantly lower in the prone group than that in the supine group (20.5% vs. 40.00%). Retrospective analysis of these data in a separate report indicated that the best predictor of improved outcome during prone ventilation was a decrease in the PaCO2 and not the response to arterial oxygenation. Since the Gattinoni trial there have been three other randomized trials of prone ventilation. Unfortunately, these studies do not strongly suggest that prone positioning affects survival.89–91 Prone positioning must be performed with care to avoid inadvertent extubation or loss of intravenous lines or chest tubes. Transient hemodynamic instability and desaturation also may occur during repositioning. Cardiopulmonary resuscitation is difficult, if not impossible, in the prone position. Placement of multifunction electrode pads, which allow defibrillation, cardioversion, and pacing, has been recommended to facilitate cardiopulmonary resuscitation in the prone position. Other areas of concern that accompany prone positioning include facial and eyelid edema, peripheral nerve injury, tongue injuries, and skin necrosis. Multiply injured patients may present unique problems due to the presence of incisions, drainage tubes, extremity fractures, cervical spine or facial fractures, and the like. Additional vexing questions remain. In patients who respond, how long should prone positioning be maintained? Some suggest that it be limited to 8–12 hours to allow for patient care; however, it is patients who are maintained prone for more than 20 hours who appear to benefit.92

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EXTRACORPOREAL LIFE SUPPORT SECTION 5 X

Extracorporeal life support (ECLS) is the new term for what was previously called extracorporeal membrane oxygenation (ECMO). ECLS also encompasses the technique of extracorporeal carbon dioxide removal (ECCO2R). It is a modified form of cardiopulmonary bypass that allows for oxygenation and CO2 removal while “resting” the lungs. During ECLS, gas exchange occurs independent of the lungs. Therefore, the lungs are not exposed to potential barotrauma from mechanical ventilation or to oxygen toxicity from exposure to toxic FiO2 levels. Theoretically, the lung is better able to heal during this period of rest and support. A multicenter, prospective trial of ECLS using venoarterial bypass in the late 1970s did not demonstrate improved survival in patients with severe ARDS.95 In contrast, this modality has achieved success in managing neonates with persistent pulmonary hypertension and is considered the standard of care in this group. The technology has changed considerably and more recent studies in adults with ARDS suggest better survival rates compared with historical controls.96 The lack of both concurrent control groups and randomization makes these studies difficult to interpret. The principal complication of ECLS is hemorrhage due to the need for systemic heparinization and frequent thrombocytopenia. Moreover, ECLS is extremely labor intensive and costly. Technical advancements, such as heparin-bonded circuits, may alleviate many of these problems. In a recent randomized study in the United Kingdom, transfer of ARDS patients to a regional center specializing in ECLS resulted in improved outcomes; however, almost one third of the patients did not receive ECLS after transfer and care delivery in patients not referred was not protocolized; it is therefore difficult to make firm conclusions from this study.97

PHARMACOLOGIC THERAPY ■ Inhaled Nitric Oxide NO is responsible for regulation of basal vascular tone. When delivered by the inhaled route, NO is a selective pulmonary vasodilator with no systemic side effects. Moreover, delivery of NO by the inhaled route exposes only ventilated alveoli to its vasodilatory effects. Selective vasodilation of pulmonary vessels in ventilated areas diverts blood away from nonventilated areas, improving ventilation–perfusion matching and hypoxemia. NO decreases mean pulmonary artery pressure, and in doing so, lessens the hydrostatic pressure for pulmonary edema.98 For all of these reasons, inhaled NO has seemed very attractive for use in severely hypoxemic patients. At least 12 prospective randomized clinical trials of inhaled NO versus placebo or standard therapy have been reported. The results are remarkably similar and not encouraging. The largest trial was a multicenter study and was placebo controlled and blinded.99 Results from this study used fixed doses of NO at 0, 1.25, 5, 20, and 40 ppm delivered to patients with ARDS from causes other than sepsis. Only at doses at 5 ppm were there decreases (not statistically significant) in the oxygenation

index and duration of mechanical ventilation. As a result of this trial, the investigators went on to perform a low-dose trial using 5 ppm of NO versus a placebo. The primary end points were days alive and off-assisted ventilation. Mortality was actually a secondary outcome variable, as was meeting extubation criteria. Not surprisingly, there was a statistically significant increase in PaO2, but this diminished after 48 hours. Unfortunately, inhaled NO at 5 ppm had no substantial effect on duration of mechanical ventilation or mortality. Currently, the role of NO should be limited to those patients with severe, refractory hypoxemia or pulmonary hypertension in whom inhaled NO may act as a “bridge” allowing short-term physiologic support. Application of NO in these situations may allow for possible patient survival until other therapies may be employed such as pronation or alternative modes of ventilation. Most studies observe that inhaled NO resulted in only modest improvements in oxygenation that were not sustained beyond 24 hours and frequently did not allow significant reduction in the intensity of ventilatory support. There were no differences in mortality in any of the studies. The multicenter trial also noted no differences in the number of days alive and the number of days off mechanical ventilation. Finally, a metaanalysis of published trials has suggested harm in the cohort of patients given NO.100

CORTICOSTEROIDS The ability of corticosteroids to attenuate the inflammatory response would seem to make them ideal treatment for ARDS. From the first description of ARDS, corticosteroids were suggested as possible therapeutic agents. Large prospective clinical trials, however, showed no survival benefit with high-dose steroids in early ARDS.101 These initial studies focused only on early ARDS and utilized a short course (less than 48 hours) of high-dose steroids. It has become increasingly clear that pathogenetic mechanisms initiating ARDS are different from those that perpetuate late ARDS. The fibroproliferative phase of ARDS is particularly critical. Why lung injury completely resolves in one patient and extensive fibrosis develops in another is unknown. The extent of initial injury, especially the amount of basement membrane disruption, may be an important factor.102 Another important factor is ongoing injury or inflammation. Histologic evidence of continued endothelial injury has been described in patients with advanced fibroproliferation.103 Meduri et al. provide evidence suggesting a link between ongoing fibroproliferation and persistent inflammation.104 The authors measured plasma and BAL fluid cytokine levels following initiation of steroid rescue treatment in patients with late ARDS. They noted a significant reduction in plasma TNF-α and IL-6 levels in patients who responded compared with those who did not. Several anecdotal reports support the use of steroids in late ARDS.105–108 Most of these investigators used methylprednisolone (or its equivalent) in doses ranging from 2 to 8 mg/kg per day for at least 2 weeks. Survival ranged from 76% to 83%, well exceeding that expected in this group of patients. Meduri et al. reported results from a prospective, randomized trial of steroids

Respiratory Insufficiency end point was 60-day mortality, and secondary end points were ventilator-free days, organ failure, and various biomarkers. There was no difference in 60-day mortality except in those patients who received methylprednisolone after ARDS day 14, and then mortality significantly increased. Methylprednisolone did increase the number of ventilator-free days, improved oxygenation and respiratory compliance, and resulted in less vasopressor use. Interestingly, the rate of infectious complications was no different between the groups, but the methylprednisolone group had a higher incidence of neuromuscular weakness. Given the challenges of this patient group, any use of steroids for late ARDS must be individualized and, optimally, delivered before disease day 14.

■ Nutritional Support Overfeeding patients or administering excess carbohydrates can lead to excess production of CO2. In the setting of marginal ability to execute work of breathing, this may, in theory,

Denver health SICU mechanical ventilation protocol Secretions Oxygenation Airway Alertness Parameters

Full support

Initiation of mechanical ventilation

A/C VT R.R. Flow PEEP

Sedation/ Analgesia 6–10 ml/Kg/IBW Plateau < 25 pH 7.40 ± 0.5 Pco2 35–45 1:E 1:3–1:4 +5 if tolerated

Clinically stable

Yes No

T-piece or extubate

Yes All okay? No

Continue F.V.S. Reassess q Day

Recruitment maneuver • Press control vent • PIP 20 cm H2O • I:E ratio 1:1 (3 sec I.T.) • R.R. 10/Min • PEEP 25–40 cm H2O • 2 minute duration • Monitor vital signs B.P.F. • Remove from positive pressure, if possible • PVS – SIMV/PSV • Limit VT to <10 ml/Kg • RR (Accept higher PcO2) • Minimize Insp. time • Paw/use square flow wave • D/C PEEP • Tx airflow obstruction • Consider unconventional therapies – ILV, PL PEEP • Fibrin glue • Consider HcO3 Drip for Ph £7.20

PaO2 Y/FiO2 > 300 P/F 200–300 < 200 = ARDs

Diffuse Auto PEEP Intrinsic Treat cause: • Excessive secretions • Bronchospasm • Pulmonary contusion • ARDS • COPD/Asthma

Focal airspace Dz FiO2 > 40 • Increase FiO2 • Small increases in PEEP • Positional changes • CPT/Bronchoscopy • ? Independent lung ventilation

Extrinsic Treat cause: • High VE • Small E.T.T. • Low flows • Mode of ventilation

* • Acute onset • Bilat infiltrates on CXR • PCWP £18 MMHg • AL IPaO2 /FiO2 £300 ARDS: PaO2 /FiO2 <200

Partial support SIMV/P.S.V PEEP to maintain Lung volume

Lung protective Lung protective ** • A/C (Volume ventilation) • VT = 6 ml/Kg/IBW • Plat press <25 cm H2O • PH ≥7.25 • I:E ratio to 1:1 • Decelerating flow wave form • PEEP 12.5 cm H2O ± 2.5 Consider • Tracheal gas insufflation • Prone ventilation • Steroid “rescue” therapy • Recruitment maneuver for hypoxemia/identify optimal PEEP

** • Include Pts at risk MOF • ISS > 25 or ISS > 15 + 6 units PRBC/12 Hr • Significant pulm contusion • Sepsis • Witnessed aspiration

Abbreviation ALI: Acute lung injury; A/C: Assist/Control; ARDS: Acute respiratory distress syndrome; BPF: Bronchopleural fistula; CPT: Chest physical therapy; E.T.T.: Endotracheal tube; FiO2 : Fraction of inspired oxygen; FVS: Full ventilatory support; IE: Inspiratory to expiratory ratio; ILV: Independent lung ventilation; PAW: Peak airway pressure; PEEP: Positive end expiratory pressure; PIP: Peak inspiratory pressure; PLAT PRESS: Plateau pressure; PL PEEP: Pleural positive end expiratory pressure; PVS: Partial ventilator support; R.R.: Respiratory rate; SIMV: Synchronized intermittent mandatory ventilation; Vt: Tidal volume.

FIGURE 57-4 Denver Health SICU mechanical ventilation protocol.

CHAPTER CHAPTER 57 X

in late ARDS.109 Twenty-four patients were randomized to receive methylprednisolone 2 mg/kg per day for 32 days or placebo. Patients treated with steroids had reduced LISs, increased PaO2 to FiO2 ratios, and greater extubation success 10 days after treatment. ICU and hospital mortality were significantly reduced (0% vs. 62% and 12% vs. 62%, respectively). This study can be criticized for the small number of control patients (n  8) and the crossover of patients from the placebo group to the steroid group (four out of eight). A subsequent publication demonstrated that patients treated with methylprednisolone have a rapid reduction in the proinflammatory cytokines IL-1, IL-6, and TNF, supporting the hypothesis that ongoing ARDS represents a pathologically persistent inflammatory state. Recently, the NIH ARDS Clinical Trials Network reported the results of a multicenter, randomized controlled trial of corticosteroids in patients with persistent ARDS.110 One hundred and eighty patients with ARDS of at least 7-day duration were assigned either methylprednisolone or placebo. The primary

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precipitate or prolong hypercapnic pulmonary failure. Careful monitoring of nutritional support may be necessary in patients with tenuous respiratory status. An indirect calorimeter can be helpful in providing estimates of CO2 production and the respiratory quotient. The respiratory quotient should be kept below 0.9 by appropriate adjustment of the proportion of lipid and total calories administered. Our goals for nutritional support are to deliver 21–25 nonprotein cal/kg per day and 0.25–0.30 g of nitrogen/kg per day. The primary goal of carbohydrate administration should be a rate of less than 5 mg/(kg min).

OUTCOME Mortality associated with ARDS has historically been reported from 30% to 60%. The majority of deaths are related to sepsis and MOF (see Chapter 61). Respiratory failure is a cause of death in only 15% of patients.111 The principal therapy that improves outcome in patients with ARDS appears to be low tidal volume ventilation; however, a gradual improvement in crude mortality from 1996 to 2005 was observed in the ARDS network, with a low 26% in 2004–2005.112 This suggests that other improvements in critical care delivery are at work as well (Fig. 57-4).

REFERENCES 1. Uehara M, Plank LD, Hill GL. Components of energy expenditure in patients with severe sepsis and major trauma: a basis for clinic care. Crit Care Med. 1999;27:1295. 2. Tang Y, Turnery MJ, Baker AB. A new equal area method to calculate and represent physiologic, anatomical and alveolar dead spaces. Anesthesiology. 2006;104:696. 3. Williams FN, Jeschke MG, Chinkes DL, et al. Modulation of the hypermetabolic response to trauma: temperature, nutrition, and drugs. JACS. 2009;208:489. 4. Como JJ, Sutton ER, McCunn M, et al. Characterizing the need for mechanical ventilation following cervical spinal cord injury with neurologic deficit. J Trauma. 2005;59:912. 5. Harrop JS, Sharan AD, Scheid EH Jr, et al. Tracheostomy placement in patients with complete cervical spinal cord injuries: American Spinal Injury Association grade A. J Neurosurgery. 2004;100(suppl 1):20. 6. Schinkel C, Frangen TM, Kmetic A, et al. Timing of thoracic spine stabilization in trauma patients: impact on clinical course and outcome. J Trauma. 2006;61:156. 7. Onders RP, Elmo M, Khansarinia S, et al. Complete worldwide operative experience in laparoscopic diaphragm pacing: results and differences in spinal cord injured patients and amyotrophic lateral sclerosis patients. Surg Endosc. 2009;23:1433. 8. Bulger EM, Arneson MA, Mock CN, Jurkovich GJ. Rib fractures in the elderly. J Trauma. 2000;48:1040. 9. Harrington DT, Phillips B, Machan J, et al. Factors associated with survival following blunt chest trauma in older patients: results from a large regional trauma cooperative. Arch Surg. 2010;145:432. 10. Todd SR, McNally MM, Holcomb JB, et al. A multidisciplinary clinical pathway decreases rib fracture-associated infectious morbidity and mortality in high-risk trauma patients. Am J Surg. 2006;192:806. 11. Ashbaugh DG, Bigelow DB, Petty TL. Acute respiratory distress in adults. Lancet. 1967;2:319. 12. Bernard GR, Artigas A, Brigham KL. The American–European Consensus Conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med. 1994;149:818. 13. Ferguson ND, Meade MO, Hallett DC, Stewart TE. High values of the pulmonary artery wedge pressure in patients with acute lung injury and acute respiratory distress syndrome. Int Care Med. 2002;28:1073.

14. Esteban A, Fernandez-Segoviano P, Frutos-Vivar F, et al. Comparison of clinical criteria for the acute respiratory distress syndrome with autopsy findings. Ann Intern Med. 2004;141:440. 15. Murray JF, Matthay MA, Luce JM, et al. An expanded definition of the adult respiratory distress syndrome. Am Rev Respir Dis. 1988; 138:720. 16. Ferguson ND, Frutos-Vivar F, Esteban A, et al. Acute respiratory distress syndrome: underrecognition by clinicians and diagnostic accuracy of three clinical definitions. Crit Care Med. 2005;33:2228. 17. Frutos-vivar F, Ferguson ND, Esteban A. Epidemiology of acute lung injury and acute respiratory distress syndrome. Semin Respir Crit Care Med. 2006;27:327. 18. Goss CH, Brower RG, Hudson LD, et al. Incidence of acute lung injury in the United States. Crit Care Med. 2003;31:1607. 19. Rubenfeld GD, Caldwell E, Peabody E, et al. Incidence and outcomes of acute lung injury. N Engl J Med. 2005;353(16):1685–1693. 20. Hudson LD, Milberg JA, Anardi D. Clinical risks for development of the acute respiratory distress syndrome. Am J Respir Crit Care Med. 1995; 151:293. 21. Reddy AJ, Christie JD, Aplenc R, et al. Association of human NAD(P) H:quinone oxidoreductase 1 (NQO1) polymorphism with development of acute lung injury. J Cell Mol Med. 2009;13:1784. 22. Norwood SH, Civetta JM. The adult respiratory syndrome. Surg Gynecol Obstet. 1985;161:497. 23. Moore EE, Moore FA, Harken AH, et al. The two-event construct of postinjury multiple organ failure. Shock. 2005;24(suppl 1):71. 24. Stapleton RD, Wang BM, Hudson LD, et al. Causes and timing of death in patients with ARDS. Chest. 2005;128:525. 25. Ciesla DJ, Moore EE, Johnson JL, et al. The role of the lung in postinjury multiple organ failure. Surgery. 2005;138:749. 26. Wiedemann HP, Matthay MA, Gillis CN. Pulmonary endothelial cell injury and altered lung metabolic function. Early detection of the adult respiratory distress syndrome and possible functional significance. Clin Chest Med. 1990;11:723. 27. Tremblay LN, Slutsky AS. Ventilator-induced lung injury: from bench to the bedside. Intensive Care Med. 2006;32:24. 28. Ware LB. Pathophysiology of acute lung injury and the acute respiratory distress syndrome. Semin Respir Crit Care Med. 2006;27:337. 29. Mancione AM. Role of the pulmonary epithelium and inflammatory signals in acute lung injury. Expert Rev Clin Immunol. 2009;5:63. 30. Sibille Y, Reynolds HY. Macrophages and polymorphonuclear neutrophils in lung defense and injury. Am Rev Respir Dis. 1990;141:471. 31. Heflin AC Jr, Brigham KL. Prevention by granulocyte depletion of increased vascular permeability of sheep lung following endotoxemia. J Clin Invest. 1981;68:1253. 32. Worthen GS, Schwab B III, Elson EL, et al. Mechanics of stimulated neutrophils: cell stiffening induces retention in capillaries. Science. 1989; 245:183. 33. Ley K, Laudanna C, Cybulsky MI, Nourshargh S. Getting to the site of inflammation: the leukocyte adhesion cascade updated. Nat Rev Immunol. 2007;7:678. 34. Demling RH. Adult respiratory distress syndrome: current concepts. New Horiz. 1993;1:388. 35. Welty-Wolf KE, Carraway MS, Ortel TL, Piantadosi CA. Coagulation and inflammation in acute lung injury. Thromb Haemost. 2002; 88:17. 36. Hassoun HT, Kone BC, Mercer DW, et al. Post-injury multiple organ failure: the role of the gut. Shock. 2001;15:1. 37. Magnotti LJ, Upperman JS, Xu DZ, et al. Gut-derived mesenteric lymph but not portal blood increases endothelial cell permeability and promotes lung injury after hemorrhagic shock. Ann Surg. 1998;228:518. 38. Peltz ED, Moore EE, Zurawel AA, et al. Proteome and system ontology of hemorrhagic shock: exploring early constitutive changes in postshock mesenteric lymph. Surgery. 2009;146:347. 39. Jordan JR, Moore EE, Sarin EL, et al. Arachidonic acid in postshock mesenteric lymph induces pulmonary synthesis of leukotriene B4. J Appl Physiol. 2008;104:1161. 40. Fosse E, Pillgram-Larsen J, Svennevig JL, et al. Complement activation in injured patients occurs immediately and is dependent on the severity of the trauma. Injury. 1998;29:509. 41. Gama de Abreu M, Kirschfink M, Quintel M, Albrecht DM. White blood cell counts and plasma C3a have synergistic predictive value in patients at risk for acute respiratory distress syndrome. Crit Care Med. 1998;26:1040. 42. Edelson JD, Vadas P, Villar J, et al. Acute lung injury induced by phospholipase A2. Structural and functional changes. Am Rev Respir Dis. 1991;143:1102.

Respiratory Insufficiency 68. Finfer S, Bellomo R, Boyce N, et al. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med. 2004; 350:2247. 69. Marini JJ. New options for the ventilatory management of acute lung injury. New Horiz. 1993;1:489. 70. Van Hook CJ, Carilli AD, Haponik EF. Hemodynamic effects of positive end-expiratory pressure. Historical perspective. Am J Med. 1986; 81:307. 71. Stoller JK, Kacmarek RM. Ventilatory strategies in the management of the adult respiratory distress syndrome. Clin Chest Med. 1990; 11:755. 72. Brower RG, Lanken PN, MacIntyre N, et al. Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med. 2004;351:327. 73. Carroll GC, Tuman KJ, Braverman B, et al. Minimal positive end-expiratory pressure (PEEP) may be “best PEEP.” Chest. 1988; 93:1020. 74. Muscedere JG, Mullen JB, Gan K, et al. Tidal ventilation at low airway pressures can augment lung injury. Am J Respir Crit Care Med. 1994; 149:1327. 75. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342:1301. 76. Dries DJ. Permissive hypercapnia. J Trauma. 1995;39:984. 77. Orchard CH, Kentish JC. Effects of changes of pH on the contractile function of cardiac muscle. Am J Physiol. 1990;258:C967. 78. Viitanen A, Salmenpera M, Heinonen J. Right ventricular response to hypercarbia after cardiac surgery. Anesthesiology. 1990;73:393. 79. Prough DS, Rogers AT, Stump DA, et al. Hypercarbia depresses cerebral oxygen consumption during cardiopulmonary bypass. Stroke. 1990; 21:1162. 80. McIntyre RC Jr, Haenel JB, Moore FA, et al. Cardiopulmonary effects of permissive hypercapnia in the management of adult respiratory distress syndrome. J Trauma. 1994;37:433. 81. Kallet RH, Jasmer RM, Luce JM, et al. The treatment of acidosis in acute lung injury with tris-hydroxymethyl aminomethane (THAM). Am J Respir Crit Care Med. 2000;161:1149. 82. Bryan AC. Conference on the scientific basis of respiratory therapy. Pulmonary physiotherapy in the pediatric age group. Comments of a devil’s advocate. Am Rev Respir Dis. 1974;110:143. 83. Douglas WW, Rehder K, Beynen FM, et al. Improved oxygenation in patients with acute respiratory failure: the prone position. Am Rev Respir Dis. 1977;115:559. 84. Pappert D, Rossaint R, Slama K, et al. Influence of positioning on ventilation–perfusion relationships in severe adult respiratory distress syndrome. Chest. 1994;106:1511. 85. Wiener CM, Kirk W, Albert RK. Prone position reverses gravitational distribution of perfusion in dog lungs with oleic acid–induced injury. J Appl Physiol. 1990;68:1386. 86. Lamm WJ, Graham MM, Albert RK. Mechanism by which the prone position improves oxygenation in acute lung injury. Am J Respir Crit Care Med. 1994;150:184. 87. Gattinoni L, Pelosi P, Vitale G, et al. Body position changes redistribute lung computed-tomographic density in patients with acute respiratory failure. Anesthesiology. 1991;74:15. 88. Gattinoni L, Tognoni G, Pesenti A, et al. Effect of prone positioning on the survival of patients with acute respiratory failure. N Engl J Med. 2001;345:568. 89. Curley MA, Hibbard PL, Fineman LD. Effect of prone positioning on clinical outcomes in children with acute lung injury. A randomized, controlled trial. JAMA. 2005;294:229. 90. Guerine E, Gaillard S, Lemasson S, et al. Effects of systematic prone positioning in hypoxemia acute respiratory failure: a randomized controlled trial. JAMA. 2004;19:2379. 91. Mancebo JM, Fernandez R, Blanch L, et al. A multicenter trial of prolonged prone ventilation in severe acute respiratory distress syndrome. Am J Respir Crit Care Med. 2006;173:1233. 92. Diaz JV, Brower R, Calfee CS, Matthay MA. Therapeutic strategies for severe acute lung injury. Crit Care Med. 2010;38:1644. 93. Hurst JM, Branson RD, Davis K Jr, et al. Comparison of conventional mechanical ventilation and high-frequency ventilation: a prospective, randomized trial in patients with respiratory failure. Ann Surg. 1990; 211:486. 94. Derdak S, Mehta S, Stewart T, et al. High-frequency oscillatory ventilation for acute respiratory distress syndrome in adults: a randomized, controlled trial. Am J Respir Crit Care Med. 2002;166:801.

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43. Zimmerman GA, McIntyre TM, Prescott SM, Stafforini DM. The platelet-activating factor signaling system and its regulators in syndromes of inflammation and thrombosis. Crit Care Med. 2002;30(5 suppl):S294. 44. Silliman CC, Voelkel NF, Allard JD, et al. Plasma and lipids from stored packed red blood cells cause acute lung injury in an animal model. J Clin Invest. 1998;101:1458. 45. Pittet JF, Mackersie RC, Martin TR, et al. Biological markers of acute lung injury: prognostic and pathogenetic significance. Am J Respir Crit Care Med. 1997;155:1187. 46. Rubin DB, Wiener-Kronish JP, Murray JF, et al. Elevated von Willebrand factor antigen is an early plasma predictor of acute lung injury in nonpulmonary sepsis syndrome. J Clin Invest. 1990;86:474. 47. Partrick DA, Moore FA, Moore EE. The inflammatory profile of interleukin-6, interleukin-8, and soluble intercellular adhesion molecule-1 in postinjury multiple organ failure. Am J Surg. 1996;172:425. 48. Law MM, Cryer HG, Abraham E. Elevated levels of soluble ICAM-1 correlate with the development of multiple organ failure in severely injured trauma patients. J Trauma. 1994;37:100. 49. Matthay MA, Wiener-Kronish JP. Intact epithelial barrier function is critical for the resolution of alveolar edema in humans. Am Rev Respir Dis. 1990;142:1250. 50. Gregory TJ, Longmore WJ, Moxley MA, et al. Surfactant chemical composition and biophysical activity in acute respiratory distress syndrome. J Clin Invest. 1991;88:1976. 51. Gordon MW, Robertson CE, Dawes J. Neutrophil elastase levels and major trauma in man. Intensive Care Med. 1989;15:543. 52. Moraes TJ, Chow CW, Downey GP. Proteases and lung injury. Crit Care Med. 2003;31(4 suppl):S189. 53. Okayama N, Kakihana Y, Setoguchi D, et al. Clinical effects of a neutrophil elastase inhibitor, sivelestat, in patients with acute respiratory distress syndrome. J Anesth. 2006;20:6. 54. Simms HH, D’Amico R. Increased PMN CD11b/CD18 expression following post-traumatic ARDS. J Surg Res. 1991;50:362. 55. Donnelly TJ, Meade P, Jagels M, et al. Cytokine, complement, and endotoxin profiles associated with the development of the adult respiratory distress syndrome after severe injury. Crit Care Med. 1994;22:768. 56. Donnelly SC, Strieter RM, Kunkel SL. Interleukin-8 and development of adult respiratory distress syndrome in at-risk patient groups. Lancet. 1993;341:643. 57. Gattinoni L, Pesenti A, Avalli L, et al. Pressure–volume curve of total respiratory system in acute respiratory failure: computed tomographic scan study. Am Rev Respir Dis. 1987;136:730. 58. Slutsky AS, Tremblay LN. Multiple system organ failure. Is mechanical ventilation a contributing factor? Am J Respir Crit Care Med. 1998; 157:1721. 59. Finfer S, Rocker G. Alveolar overdistension is an important mechanism of persistent lung damage following severe protracted ARDS. Anaesth Intensive Care. 1996;24:569. 60. Holter JF, Weiland JE, Pacht ER, et al. Protein permeability in the adult respiratory distress syndrome: loss of size selectivity of the alveolar epithelium. J Clin Invest. 1986;78:1513. 61. Clark JG, Milberg JA, Steinberg KP, et al. Type III procollagen peptide in the adult respiratory distress syndrome. Association of increased peptide levels in bronchoalveolar lavage fluid with increased risk for death. Ann Intern Med. 1995;122:17. 62. Marshall BE, Hanson CW, Frasch F, et al. Role of hypoxic pulmonary vasoconstriction in pulmonary gas exchange and blood flow distribution. 2. Pathophysiology. Intensive Care Med. 1994;20:379. 63. Steltzer H, Krafft P, Fridrich P, et al. Right ventricular function and oxygen transport patterns in patients with acute respiratory distress syndrome. Anaesthesia. 1994;49:1039. 64. National Heart, Lung and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network. Comparison of two fluidmanagement strategies in acute lung injury. N Engl J Med. 2006; 354(24):2564. 65. Brigham KL, Kariman K, Harris TR, et al. Correlation of oxygenation with vascular permeability–surface area but not with lung water in humans with acute respiratory failure and pulmonary edema. J Clin Invest. 1983;72:339. 66. Martin GS, Moss M, Wheeler AP, et al. A randomized, controlled trial of furosemide with or without albumin in hypoproteinemic patients with acute lung injury. Crit Care Med. 2005;183:1681. 67. Dubois MJ, Orellana-Jimenez C, Melot C, et al. Albumin administration improves organ function in critically ill hypoalbuminemic patients: a prospective, randomized, controlled pilot study. Crit Care Med. 2006; 34:2536.

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95. Zapol WM, Snider MT, Hill JD, et al. Extracorporeal membrane oxygenation in severe acute respiratory failure: a randomized prospective study. JAMA. 1979;242:2193. 96. Anderson H III, Steimle C, Shapiro M, et al. Extracorporeal life support for adult cardiorespiratory failure. Surgery. 1993;114:161. 97. Peek GJ, Mugford M, Tiruvoipati R, et al. Efficacy and economic assessment of conventional ventilatory support versus extracorporeal membrane oxygenation for sever adult respiratory failure (CESAR): a multicentre randomized controlled trial. Lancet. 2009;374:1351. 98. Benzing A, Brautigam P, Geiger K, et al. Inhaled nitric oxide reduces pulmonary transvascular albumin flux in patients with acute lung injury. Anesthesiology. 1995;83:1153. 99. Taylor RW, Zimmerman JL, Dellinger RP, et al. Low-dose inhaled nitric oxide in patients with acute lung injury: a randomized, controlled trial. JAMA. 2004;291:1603. 100. Adhikari NK, Burns KE, Friedrich JO, et al. Effect of nitric oxide on oxygenation and mortality in acute lung injury: systematic review and meta-analysis. BMJ. 2007;334:779. 101. Bernard GR, Luce JM, Sprung CL, et al. High-dose corticosteroids in patients with the adult respiratory distress syndrome. N Engl J Med. 1987;317:1565. 102. Crouch E. Pathobiology of pulmonary fibrosis. Am J Physiol. 1990; 259:L159. 103. Bachofen A, Weibel E. Alterations of the gas exchange apparatus in adult respiratory insufficiency associated with septicemia. Am Rev Respir Dis. 1977;116:589.

104. Meduri GU, Chinn AJ, Leeper KV, et al. Corticosteroid rescue treatment of progressive fibroproliferation in late ARDS: patterns of response and predictors of outcome. Chest. 1994;105:1516. 105. Ashbaugh DG, Maier RV. Idiopathic pulmonary fibrosis in adult respiratory distress syndrome: diagnosis and treatment. Arch Surg. 1985; 120:530. 106. Hooper RG, Kearl RA. Established ARDS treated with a sustained course of adrenocortical steroids. Chest. 1990;97:138. 107. Biffl WL, Moore FA, Moore EE, et al. Are corticosteroids salvage therapy for refractory acute respiratory distress syndrome? Am J Surg. 1995; 170:591. 108. Meduri GU, Headley AS, Golden E, et al. Effect of prolonged methylprednisolone therapy in unresolving acute respiratory distress syndrome: a randomized controlled trial. JAMA. 1998;280:159. 109. Meduri GU, Tolley EA, Chrousos GP, et al. Prolonged methylprednisolone treatment suppresses systemic inflammation in patients with unresolving acute respiratory distress syndrome: evidence for inadequate endogenous glucocorticoid secretion and inflammation-induced immune cell resistance to glucocorticoids. Am J Respir Crit Care Med. 2002;165:983. 110. Steinberg KP, Hudson LB, Goodman RB, et al. Efficacy and safety of corticosteroids for persistent acute respiratory distress syndrome. New Engl J Med. 2006;354:1671. 111. Ferring M, Vincent JL. Is outcome from ARDS related to the severity of respiratory failure? Eur Respir J. 1997;10:1297. 112. Erickson SE, Martin GS, Davis JL, et al. Recent trends in acute lung injury mortality: 1996–2005. Crit Care Med. 2009;37:1574.

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CHAPTER 58

Gastrointestinal Failure Rosemary A. Kozar and Frederick A. Moore

INTRODUCTION For patients who survive the first 48 hours of intensive care, sepsisrelated multiple organ failure (MOF) is the leading cause for prolonged intensive care unit (ICU) stays and deaths. Several lines of clinical evidence convincingly link gut injury and subsequent dysfunction to MOF.1 First, patients who experience persistent gut hypoperfusion after resuscitation are at high risk for abdominal compartment syndrome (ACS), MOF, and death.2 Second, epidemiologic studies have consistently shown that the normally sterile proximal gut becomes heavily colonized with a variety of organisms. These same organisms have been identified to be pathogens that cause late nosocomial infections. Third, gutspecific therapies (selective gut decontamination, early enteral nutrition, and most recently immune-enhancing enteral diets [IEDs]) have been shown to reduce these nosocomial infections.3–5 The purpose of this chapter will be to first provide a brief overview of why critically injured trauma patients develop gut dysfunction and how gut dysfunction contributes to adverse outcomes. The discussion will then focus on the pathogenesis and clinical monitoring of specific gut dysfunctions. Based on this information, potential therapeutic strategies to prevent and/or treat gut dysfunction to enhance patient outcome will be discussed.

HOW GUT DYSFUNCTION CONTRIBUTES TO ADVERSE PATIENT OUTCOME ■ Multiple Organ Failure MOF occurs as a result of a dysfunctional inflammatory response and in two different patterns (i.e., early vs. late) (see Chapter 55). After a traumatic insult, patients are resuscitated into a state of systemic hyperinflammation, now referred to as the systemic inflammatory response syndrome (SIRS). The intensity of SIRS is dependent upon (1) inherent host factors, (2) the degree of shock, and (3) the amount of tissue injured.

Of the three, shock is the predominant factor.6 Mild-tomoderate SIRS is most likely beneficial, whereas severe SIRS can result in early MOF. As time proceeds, negative feedback systems downregulate certain aspects of acute SIRS to restore homeostasis and limit potential autodestructive inflammation (see Chapter 67). This latter response has been dubbed the compensatory anti-inflammatory response syndrome (CARS) and results in delayed immunosuppression.7 Mild-to-moderate delayed immunosuppression is clinically insignificant, but severe immunosuppression is associated with late infections. These late infections can worsen early MOF or precipitate late MOF. Over the last decade, late CARS was characterized to include (a) apoptotic loss of intestinal lymphocytes and epithelial cells, (b) PMN and monocytic deactivation, (c) anergy characterized by suppressed T-cell proliferative responses, and (d) a shift from a TH1 to a TH2 phenotype.8,9 More recently, it has been hypothesized that SIRS and CARS are present concurrently following injury. With time though, SIRS ceases to exist and CARS is the predominant force. Debate exists over whether CARS is truly a compensatory response. In the laboratory, CARS does not occur unless preceded by SIRS.10 However, although the intensity of SIRS predicts early adverse outcomes, it does not predict late adverse outcome. CARS appears to occur in response to the injury (not to SIRS) (Fig. 58-1). This is consistent with clinical observations that early MOF and late MOF have different early clinical predictors and biomarkers.11 Additionally, shock insults have been shown to initiate simultaneous proinflammation and antiinflammation.12 We believe that the balance of proinflammation versus anti-inflammation determine clinical trajectory.13 We still see shock-induced severe SIRS that causes fuminant proinflammatory MOF and death. We believe patients are genetically preprogramed for this trajectory or alternatively have been exposed to appropriately timed second hits. Fortunately, most patients survive early SIRS but some appear to be protected (i.e., preconditioned) against further insult and

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Shock

Severe SIRS

Early MOF

Moderate SIRS Moderate CARS

Gut Ischemia

Reperfusion Severe CARS Resuscitation Laparotomy ICU therapies Gut disuse

Progressive gut dysfunction

Aspiration

Infections toxins

Late MOF

Translocation SEPSIS

FIGURE 58-1 Role of compensatory anti-inflammatory response syndrome (CARS) after injury.

recover while others develop unbalanced anti-inflammation. They progress into severe CARS associated with apoptosis and depression in adaptive immunity. This sets the stage for immunoparalysis, poor nutrition status, impaired wound healing, recurrent nosocomial infections, late MOF, and an indolent death. The gut is believed to be both an instigator and victim of this dysfunctional inflammatory response.1 Shock is associated with obligatory gut ischemia. With resuscitation, reperfusion results in a local inflammatory response that can injure the gut, setting the stage for ACS. Additionally, the reperfused gut releases mediators, including proteins such as cytokines and lipid such as those derived from phospholipase A2, via the mesenteric lymph, that amplify SIRS.14 Moreover, for patients undergoing laparotomy, bowel manipulation and anesthetics cause further gut dysfunction.15 Finally, standard ICU therapies (morphine, H2-antagonists, catecholamines, and broad-spectrum antibiotics) and intentional disuse (use of total parenteral nutrition rather than enteral nutrition) promote additional gut dysfunction. The end result is progressive dysfunction (Table 58-1) characterized by gastroesophageal reflux (GER), gastroparesis, duodenogastric reflux, gastric alkalinization,

TABLE 58-1 Progressive Gut Dysfunction in Critically Injured Patients Gastroesophageal reflux Gastroparesis and duodenogastric reflux Gastric alkalinization Decreased mucosal perfusion Impaired intestinal transit Impaired gut absorptive capacity Increased gut permeability Decreased gut mucosal immunity Increased gut colonization Gut edema

decreased mucosal perfusion, impaired intestinal transit, impaired absorptive capacity, increased permeability, decreased mucosal immunity, increased colonization, and gut edema. As time proceeds, the normally sterile upper gut becomes heavily colonized, mucosal permeability increases, and local mucosal immunity decreases. Intraluminal contents (e.g., bacteria and their toxic products) then disseminate by aspiration or translocation to cause systemic sepsis, which then promotes further gut dysfunction.

■ Abdominal Compartment Syndrome Intra-abdominal pressure (IAP) is monitored by urinary bladder pressure measurements. When these pressures exceed 25 cm H2O, extra-abdominal organ functions may become impaired (see Chapter 41). By definition, this is ACS. There are two types of ACS: primary (1°) and secondary (2°).2 Primary ACS occurs in patients with abdominal injuries that typically have undergone “damage control” laparotomy (where obvious bleeding is rapidly controlled and the abdomen is packed) and have entered the “bloody viscus cycle” of coagulopathy, acidosis, and hypothermia, which promotes ongoing bleeding (see Chapter 61). Accumulation of blood, worsening bowel edema from resuscitation, and the presence of intra-abdominal packs all contribute to increasing IAP that causes ACS. Secondary ACS occurs when extra-abdominal bleeding (e.g., mangled extremity or pulmonary hilar gun shot wound) requires massive resuscitation that causes bowel edema, thus increasing IAP and eventually ACS. Markedly elevated IAP also decreases gut perfusion that may adversely affect a variety of gut functions. Clinical studies have clearly documented the poor outcome of patients developing ACS and the frequent association of ACS and MOF.16

■ Nonocclusive Small Bowel Necrosis (NOBN) NOBN is a relatively rare, but frequently fatal, entity that is associated with the use of enteral nutrition in critically ill

Gastrointestinal Failure

Metabolic stress

Impaired intestinal transit

Bacterial colonization

Intraluminal fluid shifts

Intraluminal toxins

Hypoperfusion

Abdominal distention

NOBN

Mucosal injury and inflammation

FIGURE 58-2 Proposed pathogenesis of nonocclusive bowel necrosis (NOBN).

patients.17 Patients typically present with complaints of cramping abdominal pain and progressive abdominal distention associated with SIRS. Computed tomography (CT) may reveal pneumatosis intestinalis or thickened dilated bowel in more advanced stages. For those who progress and require exploratory celiotomy, extensive patchy necrosis of the small bowel is found. Pathologic analysis of the resected specimens yields a spectrum of findings from acute inflammation with mucosal ulceration to transmural necrosis and multiple perforations. The consistent association with enteral nutrition indicates that inappropriate administration of nutrients into a dysfunctional gut plays a pathogenic role. There are three popular hypotheses (Fig. 58-2).17 First, metabolically compromised enterocytes become ATP depleted as a result of increased energy demands induced by the absorption of intraluminal nutrients, leading to hypoperfusion and subsequent NOBN.18 The second hypothesis is that when nutrients are delivered into the dysmotile small bowel, fluid shifts into the lumen as a result of the presence of hyperosmolar enteral formula, leading to abdominal distention, which when severe progresses to NOBN. Third, bacterial colonization leads to intraluminal toxin accumulation, which can result in mucosal injury and inflammation, and if significant, NOBN.

SPECIFIC GUT DYSFUNCTIONS The gut is a complex organ that performs a variety of functions, some of which are vital for ultimate survival of critically ill patients (e.g., barrier function, immune competence, and metabolic regulation). Unfortunately, gut dysfunction in critically injured patients is poorly characterized and routine monitoring of gut function is crude. Currently, the best parameter of gut function is tolerance to enteral nutrition (see Chapter 66). For several reasons, this is an attractive parameter to monitor and potentially modulate. First, tolerance to enteral nutrition requires integrative gut functioning (e.g., secretion, digestion, motility, and absorption). Second, locally administered nutrients may improve perfusion and optimize the recovery of other vital gut functions (e.g., motility, barrier function, mucosal immunity). Third, tolerance correlates with patient

outcome and improving tolerance will likely improve patient outcome. Fourth, refined therapeutic interventions to improve enteral nutrition tolerance will lessen the need to use parenteral nutrition and decrease its associated complications (see Chapter 61). Parameters of gut dysfunctions are outlined in Table 58-1 and are likely contributors to intolerance to enteral nutrition. A brief overview of the pathogenesis of each of these dysfunctions and how they are monitored clinically will be reviewed to provide the rationale for proposed therapeutic strategies to improve tolerance to enteral nutrition.

■ Gastroesophageal Reflux GER is an important contributing factor to aspiration of enteral feedings, which is a common cause of pneumonia in ICU patients. Reflux will occur whenever the pressure difference between the stomach and esophagus is great enough to overcome the resistance offered by the lower esophageal sphincter. Increases in gastric pressure can be due to distention with fluids and failure of the stomach to relax to accommodate fluid. Decreases in resistance at the lower esophageal sphincter can be due to relaxation of the sphincter muscle in response to many stimuli including mediators released during injury and resuscitation. Additional contributing factors include (a) forced supine position, (b) the presence of a nasoenteric tube, (c) hyperglycemia, and (d) morphine. Commonly used clinical monitors include laboratory testing for presence of glucose in tracheal secretions or by observing blue food dye, which has been added to the enteral formula in tracheal aspirates. Detection of glucose lacks specificity. Falsepositive results can occur with high serum glucose levels or presence of blood in tracheal secretions. The use of blue food dye is poorly standardized and lacks sensitivity. More importantly, however, several reports document absorption of blue food dye in critically ill patients that is associated with death. This is presumably due to a toxic effect that blue food dye has on mitochondrial function. A recent consensus conference recommended that both these techniques be abandoned.19 Unfortunately, there are no simple monitors of GER other than

CHAPTER CHAPTER 58 X

Enteral nutrition

Increased energy demands and ATP depletion

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observing for vomiting or regurgitation, which are not very sensitive. The head of the bed should be elevated 30° to 45° to decrease the risk that when GER occurs that it is less likely to result in pulmonary aspiration (see Chapter 60). Gastric residual volumes (GRVs) should be monitored with the presumption that a distended stomach will lead to higher volume GER (see Chapter 66).

■ Gastroparesis and Duodenogastric Reflux Gastroparesis is common in ICU patients and predisposes to increased duodenogastric reflux (a potential contributing factor for gastric alkalinization) and GER (a contributing factor for aspiration). The mechanisms responsible for gastroparesis in critical illness have not been well studied. Potential factors include (a) medications (e.g., morphine, dopamine), (b) sepsis mediators (e.g., nitric oxide), (c) hyperglycemia, and (d) increased intracranial pressure. The common clinical monitors for gastroparesis are intermittent measurement of GRVs when feeding into the stomach or measurement of continuous suction nasogastric tube output when feeding postpyloric. The practice of using GRV is poorly standardized and is a major obstacle to advancing the rate of enteral nutrition.20 GRVs appear to correlate poorly with gastric function and GRVs 200 cc generally are well tolerated. GRVs of 200–500 cc should prompt careful clinical assessment and the initiation of a prokinetic agent. With GRVs 500 cc, enteral nutrition should be stopped. After clinical assessment excludes small bowel ileus or obstruction, placement of a postligament of Treitz feeding tube should be considered (see Chapter 66). Although not well studied in trauma specifically, critically ill patients are known to have a high incidence of gastroduodenal reflux. In a study of antral, duodenal, and proximal jejunal motility, Tournadre et al. demonstrated that postoperative gastroparesis occurs after major abdominal surgery and is associated with discoordinated duodenal contractions of which 20% migrated in a retrograde fashion.21 Heyland et al. administered radio-labeled enteral formulas through a standard postpyloric nasoenteric feeding tube in ventilated ICU patients and documented an 80% rate of radio isotope label reflux into the stomach, 25% reflux rate into the esophagus, and a 4% reflux rate into the lung.22 Finally, Wilmer et al. reported monitoring bile reflux in the esophagus of ventilated ICU patients using a fiberoptic spectrophotometer that detects and quantifies bilirubin concentration.23 Endoscopy was performed and documented erosive esophagitis in half of the patients of which 15% had pathologic acid reflux and 100% had pathologic bile reflux. These studies provide convincing evidence that duodenogastric reflux is a common event in ICU patients.

■ Gastric Alkalinization The stomach, through secretion of hydrochloric acid, normally has a pH below 4.0. This acid environment has been correlated with the relatively low bacterial counts found in the stomach. Reviews of several studies have shown that alkalinization of the stomach through the use of antacids, H2 antagonists, and proton pump inhibitors results in gastric colonization by bacteria not

normally found in the stomach; and several, but not all, studies have shown that gastric colonization predispose patients to ventilator-associated pneumonia,24 and can increase the risk of community-acquired Clostridium difficile–associated disease.25 Several animal studies conducted recently by our group have shown that both lipopolysaccharide administration and mesenteric ischemia/reperfusion result in the gastric accumulation of an alkaline fluid.26 This most likely results from a decrease in gastric acid secretion with continued gastric bicarbonate secretion and the reflux of duodenal contents into the stomach. Even more recently, we have reported that the pH of gastric contents in trauma patients also is elevated, possibly due to similar events.27 Thus, even without the administration of antacids or inhibitors of acid secretion, gastric alkalinization and bacterial colonization of the stomach are likely in this group of patients. When this is combined with the gastroparesis often seen in these patients (see above), it is easy to envision the stomach becoming a major source of bacteria for ventilatorassisted pneumonia and perhaps translocation to other organs.

■ Impaired Mucosal Perfusion Shock results in disproportionate splanchnic vasoconstriction. The gut mucosa appears to be especially vulnerable to injury during hypoperfusion. The arterioles and venules in the small bowel mucosal villi form “hairpin loops.” This anatomic arrangement improves absorptive function, but it also permits a countercurrent exchange of oxygen from the arterioles to the venules in the proximal villus. Under hypoperfused conditions, a proximal “steal” of oxygen is believed to reduce the pO2 at the tip of the villi to zero. The gut mucosa is further injured during reperfusion by reactive oxygen metabolites and recruitment of activated neutrophils (see Chapter 67). This mucosal injury, however, appears to quickly repair. Mucosal blood flow does not always, though, return to baseline with resuscitation and this is in part due to defective vasorelaxation. The gut mucosa is also vulnerable to recurrent episodes of hypoperfusion from ACS, sepsis, and use of vasoactive drugs. Whether recurrent hypoperfusion results in additional ischemia/reperfusion injury is not known, but it is reasonable to assume that hypoperfusion would decrease gut nutrient absorption and render the patient more susceptible to NOBN. Monitoring gastric mucosal perfusion in the clinical setting can be done by gastric tonometry. With hypoperfusion, intramucosal CO2 increases due to insufficient clearance of CO2 produced by aerobic metabolism or due to buffering of extra hydrogen ions produced in anaerobic metabolism. As intramucosal CO2 accumulates, it diffuses into the lumen of the stomach. The tonometer measures the CO2 that equilibrates in a saline filled balloon (newer monitor uses air filled balloon) that sits in the stomach. This is the regional CO2 tension (PrCO2) and is assumed to equal the intramucosal CO2 tension. Using this measured PrCO2 and assuming that arterial bicarbonate equals intramucosal bicarbonate, the intramucosal pH (pHi) is calculated by using the Henderson–Hasselbalch equation. Numerous studies have documented that a persistently low pHi (or high PrCO2 level) despite effective systemic resuscitation predicts adverse outcomes and that attempts to resuscitate to

Gastrointestinal Failure

■ Impaired Intestinal Transit Laboratory models of shock, bowel manipulation, and sepsis demonstrate that small bowel transit is impaired.29 This impairment in turn is expressed as a decrease in the number and/or force of contractions, or as an abnormal pattern of contractions. Although the results in animal models are convincing, surprisingly, clinical studies indicate that small bowel motility and transit are more often than not well preserved after major elective and emergency laparotomies.30 This observation coupled with the observation that small bowel absorption of simple nutrients is relatively intact provided the rationale for early jejunal feeding. Clinical studies have documented that the majority of critically ill patients tolerate early jejunal feeding.31 In a recent study, severely injured patients had jejunal manometers and feeding tubes placed at secondary laparotomy.30 Surprisingly, 50% had fasting patterns of motility that included components of the normal migrating motor complexes (MMCs). These patients tolerated advancements of enteral nutrition without problems. The other 50% who did not have fasting MMCs did not tolerate early advancement of enteral nutrition. Of note, none of the patients converted to a normal-fed pattern of motility once they reached full-dose enteral feeding. This could be due to infusion of caloric loads insufficient to bring about conversion. On the other hand, the failure to develop fed activity, a pattern of motility promoting mixing and absorption, might explain why diarrhea is a common problem in this patient group. Although manometry can be used to monitor motility, it is not practical. Unfortunately, simpler indicators of motility such as the presence of bowel sounds or the passing of flatus are unreliable. Other minimally invasive methods to monitor transit are needed. Contrast studies through the feeding tubes are relatively simple, but not validated.

■ Impaired Gut Absorptive Capacity (GAC) Small bowel absorption of glucose and amino acids is depressed after trauma and sepsis. Multiple factors have been identified including (a) cytosolic calcium overload, (b) ATP depletion, (c) diminished brush border enzyme activity, (d) decreased carrier activity, (e) decreased absorptive epithelial surface area, and (f ) hypoalbuminemia. In a recent animal study, intestinal ischemia/reperfusion caused significant mucosal injury and significant depletion of mucosal ATP.18 When this was combined with exposure of the bowel to a nonmetabolizable nutrient, the damage and ATP depletion were more severe and the absorption of glucose was impaired. In contrast, exposure of the bowel to metabolizable nutrients preserved ATP levels, protected against mucosal injury, and improved GAC. The clinical significance of these observations remains unclear because most patients tolerate enteral nutrition when delivered into the small bowel. However, decreased GAC may be a cause for diarrhea and may explain why patients commonly

experience diarrhea with reinstitution of enteral nutrition after prolonged bowel rest. Unfortunately, there are no easily performed clinical monitors for GAC. D-Xylose absorption is clinically available but is used most frequently to diagnose chronic malabsorption. Diarrhea may be indicative of depressed GAC, but there are other causes for diarrhea in the critically ill including impaired transit, bacterial overgrowth (e.g., presence of C. difficile), contaminated enteral formulas, abnormal colonic responses to enteral nutrition (e.g., ascending colon secretion rather than absorption, or impaired distal colon motor activity), and administration of drugs, which contain sorbitol (e.g., medication elixirs) or magnesium (e.g., antacids).

■ Increased Gut Permeability Enhanced paracellular permeability represents a type of barrier dysfunction that allows increased passage between viable cells and may induce an inflammatory cascade. The major components of the epithelial barrier are tight junctions, which bind cells together and serve as the gateways to the underlying paracellular spaces. The integrity of the tight junctions is modulated by the actin cytoskeleton. Under conditions of ATP depletion, such as would occur during shock, disruption of the actin cytoskeleton with consequent opening of the tight junctions and loss of the integrity of the permeability barrier can occur.18 Intestinal barrier dysfunction has been suggested as a means by which inflammatory cytokines can lead to the SIRS and MOF. Additionally, increased intestinal permeability has been documented in high-risk patients after burns, sepsis, and shock, in most but not all studies.32

■ Decreased Gut Mucosal Immunity During periods of intestinal disuse, critically injured patients are subject to a reduction in gut mucosal immunity. Lack of enteral stimulation (such as during starvation or with use of parenteral nutrition) quickly leads to lack of immunologic protection by mucosal-associated lymphoid tissue (MALT), which normally provides protection for both the gastrointestinal (GI) and respiratory tracts against microbial flora and infectious pathogens. Kudsk has demonstrated a link between intestinal IgA, intestinal cytokine production, and the vascular endothelium of the GI tract. With enteral stimulation, IL-4 and IL-10 production from the lamina propria of the small intestine stimulate production of IgA on the mucosal surface and inhibit intracellular adhesion molecule-1 (ICAM-1) of the vascular endothelium and subsequent neutrophil-associated inflammation and injury.33

■ Increased Gut Colonization With progressive gut dysfunction, the normally sterile upper GI tract becomes colonized with organisms that become pathogens in nosocomial infections. Gastric alkalinization, paralytic ileus, loss of colonization resistance due to broad-spectrum antibiotics, and decreased local gut immunity have all been proposed mechanisms by which the upper GI tract becomes colonized. In an effort to decrease the incidence of infectious complications, selective digestive decontamination (SDD) has been proposed.

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correct a low pHi do not favorably influence mortality.28 Unfortunately, alternative resuscitation strategies have not been able to increase pHi to improve outcome and thus this monitoring tool is in search of a novel application (see Chapter 60).

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Crystalloid resuscitation

CO

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IV oncotic pressure Hydrostatic pressure Capillary leak

Preload CO

Bowel edema CO

IAP

Impaired venous return

UO Airway pressures ACS

FIGURE 58-3 Crystalloid viscious cycle leading to abdominal compartment syndrome. ACS, abdominal compartment syndrome; CO, cardiac output; IAP, intra-abdominal pressure; IV, intravenous; UO, urine output.

SDD generally consists of topical nonabsorbed antibiotics along with a short course of parenteral antibiotics. There have been numerous clinical trials and at least six meta-analyses addressing this practice. Most studies have examined the incidence of ventilator-associated pneumonias and mortality and, in general, have demonstrated a decrease in both. Despite rather impressive results of these trials, most of which have been performed in Europe, intensivists in the United States have generally avoided use of SDD due to reports of antimicrobial resistance.34

■ Gut Edema Aggressive fluid resuscitation can result in significant bowel edema and altered intestinal function. Both in the laboratory and clinically, significant bowel edema following resuscitation can lead to elevated intra-abdominal pressure and potentially to ACS. The precise mechanisms by which bowel edema adversely effects bowel function, however, have not been fully elucidated. Laboratory investigations by Moore-Olufemi et al. have shown that bowel edema alone (not associated with gut ischemia/ reperfusion or hemorrhagic shock) is associated with impaired intestinal transit and this can be reversed with enteral feeding.35 A number of clinical studies, even though not in resuscitated trauma patients, have demonstrated the benefit of fluid restriction on postoperative bowel function and complications.36

STRATEGIES TO IMPROVE GUT DYSFUNCTION ■ Gut-specific Resuscitation and Monitoring for Abdominal Compartment Syndrome If shock-induced gut hypoperfusion is assumed to be a primeinciting event for gut dysfunction, then resuscitation protocols need to be devised to optimize early gut perfusion and prevent reperfusion injury. Traditional resuscitation is aimed at optimizing systemic perfusion, and the standard of care is to first administer 2 L of isotonic crystalloids and then add packed red blood cells to the regimen at a ratio of 3 to 1 crystalloid to blood (see

Chapter 13). Although this approach is effective in most patients, it is associated with problematic bowel edema in patients at high risk for MOF. As edema worsens and intra-abdominal pressure increases, bowel perfusion becomes impaired, setting up a vicious cycle that leads to ACS (Fig. 58-3).37 The hypovolemic trauma patient is volume loaded with crystalloid infusions that decrease intravascular colloid oncotic pressure, increase hydrostatic pressure, and increase capillary leak. Although this intervention can be beneficial in increasing cardiac output through increased preload, it can also have a detrimental effect through increased edema of the reperfused gut. Bowel edema causes intra-abdominal pressure to increase, which impairs venous return and may further worsen bowel edema. As abdominal pressures increase, cardiac output is impeded and patients can enter the futile crystalloid preloading cycle, during which further crystalloid infusion worsens bowel edema, and increases intra-abdominal pressure until full-blown ACS has developed. Intra-abdominal pressures should be measured routinely in patients in whom significant resuscitation is anticipated as ACS can be predicted early in at-risk patients.2 A high index of suspicion and knowledge of these predictors is warranted. In the past, surgeons have not decompressed the abdomen until clear signs of organ dysfunction were present (e.g., decreased urine output, decreased PaO2/FIO2 ratio, decreased cardiac output despite volume loading) in part because of fear of creating an open abdomen with consequent need for planned ventral hernia and delayed reconstruction (see Chapter 41). However, with the advent of vacuum-assisted wound closure of open abdomens this long-term problem is unlikely. As IAP approaches 25 mm Hg, the abdomen is on the steep portion of its compliance curve and additional fluid pushes IAP into pathologic ranges. Thus, based on prediction models,2 those patients who meet defined high-risk criteria and are requiring ongoing aggressive resuscitation may be considered for a “presumptive” decompressive laparotomy. In fact, a recent prospective study demonstrated that early decompression in at-risk patients reduced mortality from intra-abdominal hypertension/ACS.38

Gastrointestinal Failure

■ Analgesics and Sedatives There are three types of opioid receptors, δ, κ, μ, and all have been identified as having GI side effects including delayed gastric emptying and delayed transit time in both the small bowel and colon. One major cause of ileus is stress-related stimulation of opioid receptors. In animal models and humans, both endogenously released and exogenously administered opioids act on receptors in both the central nervous system and in the enteric nervous system to alter intestinal function, especially motility. Although actions at both the central nervous system and enteric nervous system are involved, recent studies indicate that if opioid actions at the enteric nervous system are blocked, ileus may be prevented or resolved without interfering with the desired opioid actions on the central nervous system and other systems. An investigational opioid receptor antagonist that has limited systemic absorption after oral administration and minimal access to the central nervous system has been shown to speed recovery of bowel function and shorten the duration of hospitalization after surgery.40 There is also a peripherally acting μ-receptor antagonist, alvimopan, that has recently been shown in a prospective, randomized controlled trial to accelerate time to recovery of GI function in patients undergoing elective major abdominal surgery.41 μ-Receptor antagonists are attractive agents for postoperative patients in that they are peripherally acting (gut specific), thereby maintaining centrally mediated pain reduction. A recent Cochrane review on μ-opioid antagonists for opioid-induced bowel dysfunction concluded that both alvimopan and methylnaltrexone were effective in reversing increased transit time and constipation. Additionally, alvimopan is safe and efficacious in treating postoperative ileus.42 However, long-term data are lacking and further studies are indicated. Both these agents need to be studied in patients at high risk for postoperative bowel dysfunction, particularly patients who have undergone major resuscitation from shock. Ketamine, an antagonist of the N-methyl-D-aspartate receptor, combines both analgesic and sedative effects and may represent an alternative to benzodiazepines for sedation and opioids for pain control in ICU patients. There are reports in burn patients of the opiate-sparing effect of ketamine minimizing prolonged gut dysfunction and ileus.43 Additionally, both proinflammatory cytokines and mediators have been suppressed in laboratory models of sepsis following ketamine administration.44

ENTERAL AGENTS ■ Benefits of Enteral Versus Parenteral Nutrition Several prospective randomized controlled trials (PRCTs) performed in the late 1980s and early 1990s had significant impact on clinical practice in surgical, and particularly trauma ICUs. These single institutional trials all randomized trauma patients

to early enteral nutrition or parenteral nutrition and all demonstrated that patients receiving early enteral nutrition had significantly fewer infectious complications (see Chapter 66). A meta-analysis that combined data from eight PRCTs (six published, two not published) was then conducted to assess the nutritional equivalence of enteral nutrition compared to parenteral nutrition in high-risk trauma and/or postoperative patients.4 Similar to the single institutional trials, fewer infectious complications developed in patients receiving enteral nutrition. Even when patients with catheter-related sepsis were removed from the analysis, a significant difference in infections between groups remained. Taken together, these trials provide convincing evidence that enteral nutrition is preferred to parenteral nutrition in patients sustaining major torso trauma. A recent meta-analysis evaluating the effect of early versus delayed enteral nutrition in acutely ill (medical and surgical) patients also confirmed a decrease in infectious complications in patients receiving early enteral nutrition.45 Based on available data, we can now explain how enteral nutrition interrupts this sequence of events to prevent late nosocomial infections and MOF. In a variety of models (i.e., sepsis, hemorrhagic shock, and gut I/R), intraluminal nutrients have been shown to reverse shock-induced mucosal hypoperfusion.46 In the laboratory, we have also shown that enteral nutrition reverses impaired intestinal transit when given after a gut I/R insult.47 Improved transit should decrease ileus-induced bacterial colonization. Moreover, enteral nutrition attenuates the gut permeability defect that is induced by critical illness.48 Finally, and most important, the gut is a very important immunologic organ and infections may be lessened by feeding the gut. Dr. Kudsk has performed a series of laboratory studies that have nicely elucidated a mechanistic explanation of how this occurs.49 enteral nutrition supports the function of the MALT that produces 70% of the body’s secretory IgA. Naive T and B cells target and enter the gut-associated lymphoid tissue (GALT) where they are sensitized and stimulated by antigens sampled from the gut lumen and thereby become more responsive to potential pathogens in the external environment. These stimulated T and B cells then migrate via mesenteric lymph nodes to the thoracic duct and into the vascular tree for distribution to GALT and extra intestinal sites of MALT. Lack of enteral stimulation (i.e., use of TPN) causes a rapid and progressive decrease in T and B cells within GALT and simultaneous decreases in intestinal and respiratory IgA levels. Previously resistant TPN-fed laboratory animals, when challenged with pathogens via respiratory tree inoculation, succumb to overwhelming infections. These immunologic defects and susceptibility to infection are reversed within 3 to 5 days after initiating enteral nutrition.

■ Modified Enteral Formulas Recent basic and clinical research suggests that the beneficial effects of enteral nutrition can be amplified by supplementing specific nutrients that exert pharmacologic immune-enhancing effects beyond the prevention of acute protein malnutrition. There are at least 18 PRCT and 3 meta-analyses where an IED is compared with a standard enteral diet or no diet and where the patient outcome was a predetermined end point. Of the

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Alternative resuscitation strategies are under investigation, which may lessen bowel edema and therefore reduce the incidence of ACS and include the earlier use of blood products and more aggressive use of coagulation products.39

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18 PRCTs, 11 trials demonstrated improved outcome, 4 trials were highly suggestive of improved outcome, and 3 trials did not demonstrate any clinical outcome advantage. The majority of trials are in trauma and cancer patients, although a few trials include mixed ICU and septic ICU patients. The proposed immune-enhancing agents include glutamine, arginine, omega-3 polyunsaturated fatty acids (PUFAs), and nucleotides, although the individual contributions of each have not been well investigated. Glutamine is actively absorbed across the intestinal epithelium and then metabolized in the small bowel to ammonia, citrulline, alanine, and proline, and serves as an energy source for the enterocyte. Glutamine is therefore acknowledged to be the preferred fuel of the enterocyte, and stimulates lymphocyte and monocyte function. The demand for glutamine is increased during stressed states and supplementation at pharmacologic doses may be required. Glutamine also promotes protein synthesis, is a precursor for nucleotides as well as glutathione, and is thought to play a role in maintaining gut integrity. In a recent meta-analysis, glutamine (parenteral and enteral) administered to critically ill and surgical patients resulted in a lower mortality, less infectious complications, and shorter hospital stay.50 High-dose and parenteral glutamine had the greatest effect, although the study was not designed to examine these parameters. Additionally, a mixed patient population was included with limited (randomized) studies and clinical endpoints. A randomized trial of glutamine-enriched enteral nutrition in severely injured patients demonstrated a decrease in pneumonia, sepsis, and bacteremia.51 One proposed mechanism by which enteral nutrients may be beneficial is via prevention or reduction of increased intestinal permeability. Glutamine, in particular, has been suggested as an important nutritional supplement with beneficial effects related to intestinal permeability.52 Arginine is a semiessential amino acid that is important for T-cell function and wound healing. Endogenous production is insufficient during periods of metabolic stress (such as illness) and exogenous supplementation is required for maximal function of the immune system. It also is a powerful secretagogue, increasing the production of growth hormone, prolactin, somatostatin, insulin, and glucagon. Additionally, arginine is the chief precursor of nitric oxide and has been shown to increase protein synthesis and improve wound healing. It is the association with nitric oxide production that has led to speculation that arginine may enhance the systemic inflammatory response and therefore be potentially harmful, particularly in the septic patient.53 Sepsis increases levels of inducible nitric oxide synthetase (iNOS). Arginine is a substrate for iNOS and in its presence, arginine combines with molecular oxygen to produce citrulline and nitric oxide. The resulting nitric oxide could have numerous adverse effects in sepsis including vasodilation, cardiac dysfunction, and direct cytotoxic injury by generating potent reactive oxygen species. Increased mortality has been demonstrated in some critically ill septic patients when receiving an immune-enhancing diet, and arginine has been implicated as the causative agent.53 However, Ochoa and others have examined arginine metabolism in trauma patients and demonstrated induction of systemic arginase 1, an enzyme that shunts arginine away from the iNOS pathway.54 Although increased

arginine at the systemic level does not appear to be problematic for trauma patients, its effects at the gut level are largely unknown. Although traditional enteral products contain a high proportion of omega-6 PUFAs, diets with a low omega-6 PUFA and high omega-3 PUFA content more favorably alter the fatty acid composition of membrane phospholipids toward reduced inflammation. Finally, nucleotides (purines and pyrimidines) are needed for DNA and RNA synthesis and may be necessary in stressed states to maintain rapid cell proliferation and responsiveness. In the setting of increased demand, most tissues can increase intracellular de novo synthesis of nucleotides. Lymphocytes, macrophages, and enterocytes, however, rely on increased salvage from the extracellular pool that may be depleted during stress.

Enteral Glutamine During Shock Resuscitation Shock patients are generally not given enteral nutrition. Although there is controversy over the safety of feeding the hypoperfused small bowel, evidence supports the feasibility of enteral nutrition in this setting.55 An alternative concept that we have studied in the laboratory and then pursued clinically is enteral administration of glutamine in the setting of shock.56 There are several reasons why this would be beneficial. First, intraluminal glutamine infusion reverses shock-induced splanchnic vasoconstriction. Second, glutamine is a preferred fuel source and promotes protein synthesis in the gut mucosa. Glutamine is also a preferred fuel for lymphocytes and is a precursor for glutathione and nucleotides. Glutathione protects against oxidant stress and nucleotides are required for rapid cellular proliferation of enterocytes and lymphocytes under stressful conditions. Third, glutamine induces a variety of protective mechanisms. Glutamine protects against oxidant and cytokineinduced apoptosis.57 Glutamine has also been shown to induce antioxidant enzymes (e.g., heat shock protein and heme-oxgenase-1). In our rodent gut IR model, we recently showed that intraluminal glutamine provides protection via a novel molecular mechanism of activating the anti-inflammatory transcription factor peroxisome proliferator activator receptor gamma (PPARγ).56 Of note, enteral glutamine favorably modulates SIRS. In a well-established model in which manipulation of the small bowel initiates local gut inflammation and dysfunction that ultimately causes remote lung inflammation and dysfunction, pretreatment with oral glutamine abrogates both local and remote events.58 Finally, glutamine plays a crucial regulatory role in enterocyte proliferation, which restores villous surface area. This is critical in restoring gut digestive and absorptive capacity, and the ability to tolerate enteral nutrition.

Enteral Glutamine Has Been Used in Critically Ill Patients Of the additives in IEDs, enteral glutamine has been the most tested as monotherapy in critically ill patients. It has proven to be a safe, inexpensive intervention. In recent years, there have been eight published PRCTs that tested high-dose (0.3–0.5 g/kg) enteral glutamine in critically ill patients, the majority demonstrating improved clinical outcomes (principally decreased

Gastrointestinal Failure

■ Prokinetic Agents Because gastroparesis and ileus are commonly seen postoperatively and following resuscitation, and because they can complicate initiation of enteral feeding, agents to restore motility have been sought. Evaluation of such prokinetic agents is difficult because it is not enough to just stimulate contractions, but contractions at adjacent sites must be coordinated in order for normal digestion, absorption, and transit to take place. Coordinated contractions are under the control of hormonal and neural, both central and peripheral, pathways and it is these pathways that are affected by the cytokines and other mediators that are upregulated following a traumatic insult. Prokinetic strategies are aimed at either blocking these mediators or overriding them by stimulating normal pathways. Agents such as erythromycin that act on receptors for motilin, the naturally occurring hormone responsible in part for regulating normal GI motility, have been shown to enhance gastric emptying and intestinal transit in animal models and in some clinical trials. Although clinical studies have documented their effectiveness in promoting gastric emptying their effectiveness in reducing postoperative ileus has been disappointing.59 A promising new peptide, ghrelin, has been shown in a rodent model to not only accelerate gastric emptying and small intestinal transit in unoperated animals but also reverse postoperative gastric ileus.60 Clinical trials examining the efficacy in postoperative and critically injured patients have yet to be performed. A recent Cochrane review of systemic acting prokinetic agents to treat postoperative ileus after abdominal surgery failed to recommend any of the currently available agents.61 Erythromycin showed uniform absence of effect while there was insufficient evidence to recommend cholecystokinin-like drugs, dopamine-antagonists, propanolol, or vasopressin. Most trials had small sample size and inadequate reporting of methods to draw meaningful conclusions.

■ Serotonin Antagonists One of the major transmitters within the enteric nervous system is serotonin. By acting at various serotonin receptors, serotonin can either enhance or inhibit intestinal contractions and transit. Although studies were never overwhelmingly convincing or consistent that serotonin antagonists enhanced motility, a few agents have been used in clinical situations. Side effects, however, have resulted in their being removed from the market. This may be an area for future research.

■ Antioxidants The cycle of organ hypoperfusion during shock followed by reperfusion during resuscitation results in the formation of detrimental reactive oxygen species. Thus, it is logical to pro-

pose that administration of antioxidants could prove beneficial. In many animal models, administration of agents such as superoxide dismutase, ethyl pyruvate, and melatonin limit damage induced by ischemia/reperfusion.29 In a recent animal study, administration of alpha-melanocyte-stimulating hormone preserved both the function and the structural integrity of the intestine following mesenteric ischemia/reperfusion.29 Clinically, antioxidant replacement strategies have demonstrated overall reduction in mortality and specific end-organ protection. A randomized, prospective trial of antioxidant supplementation with vitamins C and E to critically ill surgical patients, primarily trauma patients, demonstrated a significant reduction in organ failure.62 Likewise, Collier et al. demonstrated a significant risk reduction in mortality in severely injured patients who received highdose antioxidants compared to historical controls.63 A systemic review of aggregated clinical trials in critically ill patients demonstrated an overall reduction in mortality with antioxidant supplementation.64 After subgroup analysis, selenium appeared to be the predominant antioxidant responsible for the positive effects. The REDOX trial is a large prospective, randomized, double blinded multicenter trial currently in progress that is designed to evaluate mortality in critically ill patients with evidence of hypoperfusion receiving supplementation with antioxidants alone, glutamine alone, or a combination of glutamine and antioxidants. Results of the phase I dose-escalating study failed to show any adverse effect on organ function from the nutrients but did show a reduction in markers of oxidative stress, greater preservation of glutathione levels, and an improvement in mitochondrial function.65 This important study should provide definitive data on the efficacy of glutamine and antioxidant supplementation in critically ill patients.

■ Probiotics and Prebiotics A probiotic is defined as a live microbial feed supplement that improves the host’s intestinal microbial balance. Commonly utilized probiotics include lactobacilli, bifidobacteria, and saccharomyces. A prebiotic is defined as a nondigestible food ingredient that beneficially affects the host by selectively stimulating the growth and/or activity of specific bacteria in the colon. Probiotics are usually nondigestible oligosaccharides. The most extensively studied are the fructooligosaccharides (FOS) such as oligofructose. FOS are fermented in the colon, which promotes the proliferation of bifidobacteria with a reduction in clostridia and fusobacteria. Manipulation of the colonic microflora may reduce the incidence of enteral nutrition-associated diarrhea by suppressing enteropathogens. Clinically, enteric formulas containing probiotics have shown a significant reduction in a variety of postoperative complications. A recent randomized clinical trials have demonstrated a significant decrease in postoperative infections in patients who have undergone major abdominal surgery and received postoperative enteral formulas containing probiotics.66 Results of recent clinical trials employing probiotics, prebiotics, or a combination, in critically ill and burn patients, however, have been disappointing.67

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infection). Additionally, findings associated with enteral glutamine were decreases in (a) urinary lactulose/mannitol ratios, (b) serum diamine oxidase levels, (c) circulating endotoxin levels, and (d) gram-negative bacteremias, all of which suggest that glutamine is achieving these benefits through a gut-specific mechanism.

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Synbiotics are a combination of pro- and prebiotics, and the combination is postulated to improve the survival of the probiotic organism by having a specific substrate readily available for probiotic fermentation. In a study in trauma patients receiving symbiotic supplementation had decreased intestinal permeability and lower combined infection rates than those receiving other immunomodulating formulas. The authors postulated that the presence of synbiotics in the GI tract reduced pathogenic flora and thereby decreased the incidence of pneumonia.68 These findings represent the immunomodulatory potential for synbiotic enteral formulas in the setting of severe systemic inflammation. However, a meta-analysis failed to demonstrate sufficient evidence to recommend prebiotic, probiotics, or synbiotics to critically ill patients.69 In summary, ACS and nonocclusive bowel necrosis are two extreme outcomes of gut dysfunction that can directly contribute to MOF and mortality. Newer modalities to monitor and modulate gut dysfunction need to be developed and appropriate measures taken to reduce its occurrence. The use gut-specific resuscitants, opioid antagonists, alternative sedatives, and early use of enteral nutrients with select supplements such as glutamine or antioxidants, may all assist in preventing the untoward effects of gut dysfunction in critically injured patients.

REFERENCES 1. Hassoun HH, Kone BC, Mercer DW, Moody FG, Weisbrodt NW, Moore FA. Post-injury multiple organ failure: the role of the gut. Shock. 2001; 15:1–10. 2. Balogh Z, McKinley BA, Holcomb JB, et al. Both primary and secondary abdominal compartment syndrome can be predicted early and are harbingers of multiple organ failure. J Trauma. 2003;54:848–859. 3. Heyland DK, Cook DJ, Jaeschke R, Griffith L, Lee HN, Guyatt GH. Selective decontamination of the digestive tract: an overview. Chest. 1994; 105:1221–1229. 4. Moore FA, Feliciano DV, Andrassy R, et al. Enteral feeding reduces postoperative septic complications: a meta-analysis. Ann Surg. 1992;216: 172–183. 5. Moore FA. Effects of immune-enhancing diets in infectious morbidity and multiple organ failure. JPEN. 2001;25:S36–S42. 6. Sauaia A, Moore FA, Moore EE, Norris JM, Lezotte DC, Hamman RE. Multiple organ failure can be predicted as early as 12 hours postinjury. J Trauma. 1998;45:291–301. 7. Bone RC. Sir Isaac Newton, sepsis, SIRS, and CARS. Crit Care Med. 1996;24:1125–1128. 8. Oberholzer A, Oberholzer C, Moldawer LL. Sepsis syndromes: understanding the role of innate and acquired immunity. Shock. 2001; 16:83–96. 9. Hotchkiss RS, Karl IE. The pathophysiology and treatment of sepsis. N Engl J Med. 2003;348:138–150. 10. Osuchowski MF, Welch K, Siddiqui J, Remick DG. Circulating cytokine/ inhibitor profiles reshape the understanding of the SIRS/ CARS continuum in sepsis and predict mortality. J Immunol. 2006;177:1967–1974. 11. Maier B, Lefering R, Lehnert M, et al. Early versus late onset of multiple organ failure is associated with differing patterns of plasma cytokine biomarker expression and outcome after severe trauma. Shock. 2007;28: 668–674. 12. Rivers EP, Kruse JA, Jacobsen G, et al. The influence of early hemodynamic optimization on biomarker patterns of severe sepsis and septic shock. Crit Care Med. 2007;35:2016–2024. 13. Suliburk J, Helmer K, Moore F, Mercer D. The gut in systemic inflammatory response syndrome and sepsis. Enzyme systems fighting multiple organ failure. Eur Surg Res. 2008;40(2):184–189. 14. Davidson MT, Deitch EA, Lu Q, et al. A study of the biologic activity of trauma-hemorrhagic shock mesenteric lymph over time and the relative role of cytokines. Surgery. 2004;136:32–41.

15. Schwarz NT, Beer-Stolz D, Simmons RL, Bauer AJ. Pathogenesis of paralytic ileus: intestinal manipulation opens a transient pathway between the intestinal lumen and the leukocytic infiltrate of the jejunal muscularis. Ann Surg. 2002;235:31–40. 16. Balogh Z, McKinley BA, Cox CS Jr, et al. Abdominal compartment syndrome: The cause of effect of postinjury multiple organ failure. Shock. 2003;20:483–892. 17. Marvin RG, McKinley BA, McQuiggan M, Cocanour CS, Moore FA. Nonocclusive bowel necrosis which occurs in critically ill trauma patients receiving enteral nutrition manifests no reliable clinical signs for early detection. Am J Surg. 2000;179:7–12. 18. Kozar RA, Schultz SG, Hassoun HT, et al. The type of sodium-coupled solute modulates small bowel mucosal injury, transport function and ATP after ischemia/reperfusion injury in rats. Gastroenterology. 2002;123: 810–816. 19. McClave SA, Demeo MT, Delegge MH, et al. North American Summit on Aspiration in the critically ill patient: consensus statement. JPEN. 2002;26:S80–S85. 20. McClave SA, Snider HL. Clinical use of gastric residual volumes as a monitor for patients on enteral tube feeding. JPEN. 2002;26:S43–S48. 21. Tournadre JP, Barclay M, Fraser R, et al. Small intestinal motor patterns in critically ill patients after major abdominal surgery. Am J Gastroenterol. 2001;96:2418–2426. 22. Heyland DK, Drover JW, MacDonald S, Novak F, Lam M. Effect of postpyloric feeding on gastroesophageal regurgitation and pulmonary microaspiration: results of a randomized controlled trial. Crit Care Med. 2001;29:1495–1501. 23. Wilmer A, Tack J, Frans E, et al. Duodenogastroesophageal reflux and esophageal mucosal injury in mechanically ventilated patients. Gastroenterology. 1999;116:1293–1299. 24. Torres A, El-Ebiary M, Soler N, Monton C, Fabregas N, Hernandez C. Stomach as a source of colonization of the respiratory tract during mechanical ventilation: association with ventilator-associated pneumonia. Eur Respir J. 1996;9:1729–1935. 25. Dial S, Delaney JA, Barkun AN, Suissa S. Use of gastric acid-suppressive agents and the risk of community-acquired Clostridium difficile-associated disease. JAMA. 2005;294:2989–2995. 26. Castaneda A, Vilela R, Chang L, Mercer DW. Effects of intestinal ischemia/reperfusion injury on gastric acid secretion. J Surg Res. 2000; 90:88–93. 27. Cocanour CS, Dial ED, Lichtenberger LM, et al. Gastric alkalinization after major trauma. J Trauma. 2008;64(3):681–687. 28. Levy B, Gawalkiewicz P, Vallet B, Briancon S, Nace L, Bollaert PE. Gastric tonometry with air-automated tonometry predicts outcome in critically ill patients. Crit Care Med. 2003;31:474–480. 29. Hassoun HT, Zou L, Moore FA, Kozar RA, Weisbrodt NW, Kone BC. Alpha-melanocyte stimulating hormone protects against mesenteric ischemia/reperfusion injury. Am J Physiol. 2002;282:G1059–G1068. 30. Moore FA, Cocanour CS, McKinley BA, et al. Migrating motility complexes persist after severe traumatic shock in patients who tolerate enteral nutrition. J Trauma. 2001;51:1075–1082. 31. Kozar RA, McQuiggan MM, Moore EE, Kudsk KA, Jurkovich GJ, Moore FA. Postinjury enteral tolerance is reliably achieved by a standardized protocol. J Surg Res. 2002;104:70–75. 32. Sun Z, Wang X, Deng X, et al. The influence of intestinal ischemia and reperfusion on bi-directional intestinal barrier permeability, cellular membrane integrity, proteinase inhibitors, and cell death in rats. Shock. 1998;19:203–212. 33. Kudsk KA. Effect of route and type of nutrition on intestine-derived inflammatory responses. Am J Surg. 2003;185:16–21. 34. Kollef MH. Selective digestive decontamination should not be routinely employed. Chest. 2003;123:464S–468S. 35. Moore-Olufemi SD, Padalecki J, Olufemi SE, et al. Intestinal edema: effect of enteral feeding on motility and gene expression. J Surg Res. 2009; 155(2):283–292. 36. Brandstrup B, Tonnesen H, Beier-Holgersen R, et al. Danish Study Group on Perioperative Fluid Therapy. Effects of intravenous fluid restriction on postoperative complications: comparison of two perioperative fluid regimens: a randomized assessor-blinded multicenter trial. Ann Surg. 2003;238:641–648. 37. Balogh Z, McKinley BA, Cocanour CS, et al. Supra-normal trauma resuscitation causes more cases of abdominal compartment syndrome. Arch Surg. 2003;138:637–642. 38. Cheatham ML, Safcsak K. Is the evolving management of intra-abdominal hypertension and abdominal compartment syndrome improving survival? Crit Care Med. 2010;38:402–407.

Gastrointestinal Failure 56. Sato N, Moore FA, Cone, BC, et al. Differential induction of PPARγ by luminal glutamine and iNOS by luminal arginine in the rodent post ischemic small bowel. Am J Physiol Gastrointest Liver Physiol. 2006;290: G616–G623. 57. Larson SD, Li J, Chung DH, Evers BM. Molecular mechanisms contributing to glutamine-mediated intestinal cell survival. Am J Physiol Gastrointest Liver Physiol. 2007;293:G1262–G271. 58. Thomas S, Prabhu R, Balasubramanian KA. Surgical manipulation of the intestine and distant organ damage-protection by oral glutamine supplementation. Surgery. 2005;137:48–55. 59. Smith AJ, Missan A, Lanouette NM, et al. Prokinetic effect of erythromycin after colorectal surgery: randomized, placebo-controlled, double-blind study. Dis Colon Rectum. 2000;43:333–337. 60. Trudel L, Tomasetto C, Rio MC, et al. Ghrelin/motilin-related protein is a potent prokinetic to reverse gastric postoperative ileus in rat. Am J Physiol Gastrointest Liver Physiol. 2002;282: 948–952. 61. Traut U, Brugger L, Kunz R, et al. Systemic prokinetic pharmacologic treatment for postoperative adynamic ileus following abdominal surgery. Cochrane Database Syst Rev. 2008;(1):CD004930. 62. Nathens AB, Neff MJ, Jurkovich GJ, et al. Randomized, prospective trial of antioxidant supplementation in critically ill surgical patients. Ann Surg. 2002;236:814–822. 63. Collier BR, Giladi A, Dossett LA, Dyer L, Flaming SB, Cotton BA. Impact of High-dose antioxidants on outcomes in acutely injured patients. J Parenter Enteral Nutr. 2008;32:384–388. 64. Heyalnd DK, Dhaliwal R, Suchner U, Berger MM. Antioxidant nutrients: a systemic review of trace elements and vitamins in the critically ill patient. Intensive Care Med. 2005;31:327–337. 65. Heyland DK, Dhaliwalm R, Day A, Drover J, Cote H, Wischmeyer P. Optimizing the dose of glutamine dipeptides and antioxidants in critically ill patients: a phase I dose-finding study. J Parenter Enteral Nutr. 2007;31: 109–118. 66. Correia MI, Nicoli JR. The role of probiotics in gastrointestinal surgery. Curr Opin Clin Nutr Metab Care. 2006;9:618–621. 67. McNaught CE, Woodcock NP, Anderson AD, MacFie J. A prospective randomized trial of probiotics in critically ill patients. Clin Nutr. 2005;24: 211–219. 68. Spindler-Vesel A, Bengmark S, Vovk I, Cerovic O, et al. Synbiotics, prebiotics, glutamine, or peptide in early enteral nutrition: a randomized study in trauma patients. J Parenter Enteral Nutr. 2007;31(2):119–126. 69. Watkinson PJ, Barber VS, Dark P, Young JD. The use of pre- proand symbiotic in adult intensive care unit patients: systematic review. Clin Nutr. 2007;26:182–192.

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39. Holcomb JB, Wade CE, Michalek JE, et al. Increased plasma and platelet to red blood cell ratios improves outcome in 466 massively transfused civilian trauma patients. Ann Surg. 2008;248:447–458. 40. Taguchi A, Sharma N, Saleem RM, et al. Selective postoperative inhibition of gastrointestinal opioid receptors. N Engl J Med. 2001;345:935–940. 41. Wolff BG, Michelassi F, Gerkin TM, et al. Alvimopan, a novel, peripherally acting mu opioid antagonist: results of a multicenter, randomized, double-blind, placebo-controlled, phase III trial of major abdominal surgery and postoperative ileus. Ann Surg. 2004;240: 728–734. 42. McNicol ED, Boyce D, Schumann, Carr DB. Mu-opioid antagonists for opioid-induced bowel dysfunction. Cochrane Database Syst Rev. 2008;(2): CD006332. 43. Edrich T, Friedrich AD, Eltzschig HK, Felbinger TW. Ketamine for longterm sedation and analgesia of a burn patient. Anesth Analg. 2004;99: 893–895. 44. Adams SD, Radhakrishnan RS, Helmer KS, Mercer DW. Effects of anesthesia on lipopolysaccharide-induced changes in serum cytokines. J Trauma. 2008;65:170–174. 45. Marik PE, Zaloga P. Early enteral nutrition in acutely ill patients: a systematic review. Crit Care Med. 2002;29:2264–2270. 46. Flynn WJ, Jr, Gosche JR, Garrison RN. Intestinal blood flow is restored with glutamine or glucose suffusion after hemorrhage. J Surg Res. 1992;52: 499–504. 47. Grossie VB, Jr., Weisbrodt NW, Moore FA, Moody F. Ischemia/ reperfusion-induced disruption of rat small intestine transit is reversed by total enteral nutrition. Nutrition. 2001;17:939–943. 48. De-Souza DA, Greene LJ. Intestinal permeability and systemic infections in critically ill patients: effect of glutamine. Crit Care Med. 2005;33: 1125–1135. 49. Kang W, Kudsk KA. Is there evidence that the gut contributes to mucosal immunity in humans? JPEN. 2007;31:246–258. 50. Novak F, Heyland DK, Avenell A, Drover JW, Su X. Glutamine supplementation in serious illness: a systematic review of the evidence. Crit Care Med. 2002;30(9):2022–2029. 51. Houdijk APJ, Rijnsburger ER, Jansen J, et al. Randomized trial of glutamine-enriched enteral nutrition on infectious morbidity in patients with multiple trauma. Lancet. 1998;352:772–776. 52. Peng X, Yan H, You Z, Wang P, Wang S. Effects of enteral supplementation with glutamine granules on intestinal mucosal barrier function in severe burns. Burns. 2004;30:135–139. 53. Suchner U, Heyland DK, Peter K. Immune-modulatory actions of arginine in the critically ill. Br J Nutr. 2002;87:S121–S132. 54. Ochoa JB, Bernard AC, O’Brien WE, et al. Arginase 1 expression and activity in human mononuclear cells after injury. Ann Surg. 2001;233: 393–399. 55. Zaloga GP, Roberts PR, Marik P. Feeding the hemodynamically unstable patient: a critical evaluation of the evidence. Nutr Clin Pract. 2003;18: 285–293.

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CHAPTER 59

Renal Failure Charles E. Lucas, Michael T. White, and Anna M. Ledgerwood

The human body is a complex organism composed, primarily, of water and its contained solutes. A 70-kg person has 42 L of water divided into the intracellular space (ICF) of 28 L and the extracellular space (ECF) of 14 L. The ICF is subdivided into the red blood cell (RBC) mass of 2 L and the visceral mass of 26 L; the ECF is subdivided into a plasma volume (PV) of 3 L and an interstitial fluid space (IFS) of 11 L. The cardiac output (CO) in the 70-kg person is 5 L/min with 20% of this flow going to kidneys; the kidneys, with a combined weight of about 600 g, have a renal blood flow (RBF) of 1,250 mL/min or more than 2 mL/(min g) of renal parenchymal. This unusually large ratio of RBF reflects their vital role in regulating the ICF and ECF, controlling fluid and electrolyte balance, modulating acid–base balance, and excreting undesirable catabolyes.1,2 Protection of renal function is essential for recovery after a shock or septic. This chapter reviews normal renal physiology, the renal response to shock and sepsis, guidelines for prevention of acute renal failure (ARF), and treatment of ARF.

NORMAL RENAL FUNCTION Renal function is affected by general anesthesia, intraoperative manipulation of organs, general stress, hemorrhage, hypovolemia from trauma, postoperative fluid shifts, and sepsis. The 1,250 mL/min of RBF exits the renal artery into the interlobar, the arcuate, and, finally, the intralobar arteries; 85% of the RBF perfuses the outer cortical glomeruli; the remaining 15% of RBF perfuses the juxtamedullary glomeruli (Fig. 59-1). The glomeruli (Bowman’s capsules) are like capillaries except that proteins, normally, are not filtered.2,3 While passing through the glomeruli, 20% of the plasma is filtered as a cell-free, protein-free filtrate. The effective renal plasma flow (ERPF) through these tubular vessels is determined by the clearance of para-aminohippurate (CPAH) that is filtered and secreted but not reabsorbed by the renal tubules. Ninety-one percent of PAH is cleared in one passage; 9% remains bound to the plasma

protein. Renal oxygen consumption parallels ERPF which averages 650 mL/min. True renal plasma flow (TRPF) is calculated by dividing ERPF by 0.91 and averages 710 mL/min. The extraction ratio of PAH (EPAH), however, may vary with injury and sepsis; true EPAH requires renal vein sampling to accurately measure TRPF (TRPF  ERPF/EPAH).2–5 TRBP may be calculated by correcting the TRPF for hematocrit: TRBF  TRPF/ (1  Hct). The distribution of RBF can be measured by isotopic disappearance of radioactive xenon-133 (133Xe) or krypton-85 that can be graphically portrayed as a cumulative slope composed of four separate subslopes reflecting parallel flow in mL/min per 100 g to components CI (outer cortex), CII (juxtamedullary, inner cortex, and outer medulla), CIII (inner medulla), and CIV (renal pelvis and fat) (Fig. 59-1).2,5,6 Blood leaving the juxtamedullary component II glomeruli perfuses the peritubular vessels to the long straight vasa recta in the inner medulla prior to returning to the venous system adjacent to the same glomerulus.2,3 The normal glomerular filtration rate (GFR) averages 125 mL/min (180 L per day) and is measured by the renal clearance (urine concentration  volume/plasma concentration) of exogenous inulin (CIn) or endogenous creatinine (CCr), both of which are completely filtered; the CIn is slightly higher than the CCr since creatinine in humans is partially reabsorbed by the renal tubules.3,7 The work of GFR is performed by the heart. The protein-free filtrate passes through the proximal convoluting tubules where approximately 80% of the sodium and water are reabsorbed by active sodium transport and the passive movement of water, thereby maintaining an isosmolar state. The nonfiltered blood, now protein-rich, perfuses the efferent arterioles and the peritubular vessels, which augment tubular reabsorption and secretion.8 The juxtaglomerular (CII) nephrons that receive 15% of the RBF are unique; each has a loop of Henle with descending and ascending straight segments that pass into the inner medulla.2,3

Renal Failure

1085

Afferent A

CI

CHAPTER CHAPTER 59 X

CORTEX OUTER CORTEX

Glomerulus

Efferent A Proximal tubule

RENIN

Distal tubule

Interlobular A. and V

Arcuate A

Arcua

C II

ADH ALDOSTERONE

MEDULLA INNER MEDULLA OUTER MEDULLA

te V

Collecting tubule

Loop of Henle

C III Vasa recta

FIGURE 59-1 The kidney is divided into three components. The outer cortex (CI) contains 85% of the glomeruli. The inner cortex/outer medulla (CII) contains the remaining juxtamedullary glomeruli whose peritubular vessels extend to the vasa recta in the inner medulla (CIII) that establishes the hyperosmolality within the loops of Henle.

These segments actively reabsorb sodium against a gradient and, thereby, create a hypertonic medullary interstitium (CIII) that facilitates the subsequent concentration of glomerular filtrate and the preservation of salt and water. Glucose and electrolytes, namely, chloride, phosphate, and potassium, are likewise absorbed at this site. This hypertonic medullary interstitium is further regulated by the peritubular vessels and vasa recta passing close to the loop of Henle (Fig. 59-1). Rapid blood flow through these vessels may cause a “washout” of sodium ions and osmoles resulting in transient “paralysis” of the renal concentrating mechanism; inadequate blood flow with ischemia injury to these tubular cells impedes sodium reabsorption against a gradient, thus preventing medullary hypertonicity and normal filtrate preservation.2,3 This is discussed later. Twenty percent (36 L per day) of protein-free filtrate and sodium enters the distal convoluting tubules where additional sodium is reabsorbed by active transport as chloride follows passively.3,8 This process is facilitated by aldosterone. The distal tubular aldosterone effect is estimated by dividing the free water clearance (CH2O) by the CH2O sodium clearance (CNa) in patients with a positive CH2O. When the product is greater than 0.73, the “aldosterone” effect has been blocked. The distal tubule also exchanges sodium for either potassium or hydrogen depending on pH and potassium load. Each distal

tubule returns to its own glomerulus at the afferent arteriole where the macula densa and Polkissen body, known as the juxtaglomerular apparatus (JGA), are located. The JGA serves as a “feedback” loop for each nephron affecting sodium and water balance and mediated by distal tubular sodium concentration, afferent arteriole pressure, afferent arteriole pulse pressure, and others.3,7–9 After passing through the distal convoluted tubules, the remaining hypotonic filtrate (15 mL/min or 31 L per day) enters the collecting ducts where water reabsorption occurs; this is facilitated by antidiuretic hormone (ADH) as the filtrate passes through the hypertonic inner medullary (CIII) interstitium to the renal pelvis.3 The final concentration and urine volume, therefore, vary with PV, serum osmolality, ADH release, and other factors; urine concentration may range from isosmolar to 1,400 mOs/L. Alteration of this highly integrated system occurs with hemorrhagic shock so that the renal concentrating ability may be restricted to 600 mOs/L.4 The collecting ducts normally reabsorb approximately 14 mL/min or 30 L per day with the remaining 1 mL/min (1,440 mL per day) being excreted as urine. The renal handling of sodium, osmoles, and water is expressed as the clearances of sodium (CNa), osmoles (COsm), and free water (UV  COsm).4 With normal water and solute intake, both the CNa and COsm average 1–3% of the GFR; CH2O is usually

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Management of Complications after Trauma

TABLE 59-1 Graded Renal Response to Acute Hypovolemia

SECTION 5 X

Severity of Hemorrhage Normal Class I Class II Class III Class IV

Volume Deficit (mL) 5,000 700 1,200 1,600 2,000

Blood Pressure (torr) 120/80 120/80 115/80 90/70 60/40

Renal Plasma Flow (mL/min) 650 520 260 85 10

Filtration Rate (mL/min) 125 115 60 10 2

negative, reflecting the excretion of concentrated urine. A decrease in RBF or PV causes CNa and COsm to fall, reflecting sodium preservation.3 Likewise, a breakdown in the countercurrent mechanism brought about by a selective insult to the juxtamedullary nephrons and their loops of Henle causes increased CNa and COsm from impaired tubular concentration of sodium.3,4

RENAL RESPONSE TO INJURY AND HEMORRHAGIC SHOCK The very high ratio of RBF to kidney weight allows the kidney to efficiently preserve PV after injury and hemorrhage (Table 59-1).3,10 Renal vasoconstriction at the efferent arteriole permits a rise in renal vascular resistance (RVR) from a normal 5,000 to 8,000 dyne s/cm5 with a concomitant decrease in RBF from 1,250 to 800 mL/min while maintaining a normal GFR (Fig. 59-2). Excretion of metabolites is thus maintained, while 400 mL of blood/min is redirected to core areas. This phenomenon of maintained GFR despite a reduction in RBF is known as autoregulation (Fig. 59-2). Both experimental and clinical studies show that autoregulation allows GFR to be maintained while RBF is decreased to 70% of normal.2,3,11 The filtration fraction (GFR/ERPF) under such circumstances increases from a normal of 20% to as high as 40%.3,11 More severe hypovolemia causes vasoconstriction at both the afferent and efferent arterioles, thus leading to a reduction in GFR (Table 59-1). The mechanism for the rise in RVR is multifactorial due primarily to the renal perfusion of peripherally generated catecholamines that, in turn, activates the JGA to stimulate intrarenal renin release. This, in turn, stimulates the renin–angiotensin–aldosterone system (RAAS) which not only promotes sodium reabsorption but may also increase RVR.7,12,13 When the RVR increases above 14,000 dyne s/cm5, the RBF falls below 500 mL/min, thereby allowing over 700 mL/min to be redirected to core organs. When hypovolemia causes hypotension below 70 mm Hg, GFR ceases and essentially all RBF is redirected to the systemic circuit (Table 59-1). This causes renal injury and potential ARF. During hypoperfusion, the kidney conserves salt and water. This results from decreased GFR, increased ADH, and renin release with aldosterone generation leading to sodium, water,

Sodium Clearance (mL/min) 1.5 1.3 0.7 0.1 0

Osmolar Clearance (mL/min) 2.0 2.0 1.3 0.1 0

Urine Output (mL/min) 1.0 0.9 0.3 0.1 0

Renal Vascular Resistance (dyne s/ cm5) 6,000 5,500 8,000 10,000 12,000

and osmole reabsorption.3,13 When PV and CO are restored, the renal vasoconstriction subsides—first at the preglomerular afferent arteriole and later at the postglomerular efferent arteriole. The increase in RVR, however, may persist for many hours and even days in patients with a severe hemorrhagic shock.3,13,19

■ The Kidney During Operation After Injury During operation, the kidney exerts the same autoregulatory response to a PV deficit as described above. The major difference reflects the altered systemic status brought about by general anesthesia, especially in the marginally volemic patient in whom systemic vasoconstriction was maintaining a blood pressure prior to induction. This was first described in the excellent studies performed by Ladd during the Korean conflict.12 Civilian studies have shown the same phenomenon.2,3 The sudden reduction in protective vasoconstriction plus continued bleeding from injured organs precipitates a marked reduction in PV and CO causing hypotension, increased RVR, and decreased RBF with an abrupt reduction in CI flow; the consequent fall in GFR causes oliguria or anuria, which may persist as ARF after operation.2,12 The prime objective during operation is to correct the depleted PV and ineffective CO while hemostasis is obtained. When hemostasis has been achieved and the blood pressure has been restored, oliguria often persists. Osmotic or loop diuretics, such as mannitol or furosemide, have been advocated in this setting on the assumption that induced diuresis increases RBF, GFR, and urine output, and prevents ARF.2,14,16 Other studies, however, showed that diuresis in this setting provides no renal protection.16,17 Loop diuresis in combination with low-dose dopamine, likewise, affords no renal protection during major surgery.17 Induced diuresis causes a further decrease in effective PV, thus making the likelihood of ARF greater.18 Furthermore, induced diuresis interferes with one of the crucial monitors of effective postoperative PV replacement, namely, uninduced urine output rates.18 Interoperative protection of the kidney in a hypovolemic, hypotensive patient must be directed toward improving the cardiovascular status by PV expansion with fluid, blood, and blood products. Inotropic support should be added when PV

Renal Failure Glomerulus Afferent A 125

CI

CHAPTER CHAPTER 59 X

CORTEX OUTER CORTEX

AUTOREGULATION

Efferent A Proximal tubule 520

Distal tubule

Interlobular A. and V

Arcuate A

Arcua

te V

MEDULLA INNER MEDULLA OUTER MEDULLA

1087

CNa = 1.5

C II

UO = 1.0

COsm = 2.0

Collecting tubule

Loop of Henle

C III Vasa recta

FIGURE 59-2 Mild to moderate hemorrhage causes efferent arteriolar vasoconstriction resulting in reduced RBF (520 mL/min) while maintaining GFR (125 mL/min). This is known as autoregulation that redirects blood flow to the systemic circuit without compromising filtration and excretion.

expansion causes an elevated control pressure despite persistent hypotension and oliguria. Experimental and clinical studies show that a temporary delay in reestablishing urine flow after arterial pressure (MAP) is restored may result from a persistent rise in RVR after hypovolemia is corrected.7,10 Renal vasodilation, experimentally, can reverse this lagging anuria, but such therapy is difficult and hazardous in humans.10 Based on clinical observations, some patients in whom the MAP has been restored are still PV and IFS depleted, resulting in a marked increase in both total peripheral resistance (TPR) and RVR. The persistent elevation in RVR is likely due to the prior ischemic insult and not persistent perfusion by catecholamines in stable patients; measurements of renin and arginine vasopressin (AVP) at this time in stable patients have been normal (C. E. Lucas and I. K. Rosenberg, Surgical renal study unit, unpublished data). Thus, pharmacologic intervention with angiotensin-converting enzyme blockade or nitrous oxide would likely be ineffective.13 Since both peripheral and renal vasoconstriction can lead to a doubling of total resistance, the CO may be reduced by 50% of normal despite a normal MAP. Thus, the PV and IFS deficit may exceed 1,500 mL after the MAP rises to normal. Assuming that concomitant oliguria reflects this vasoconstriction and PV depletion, the rapid infusion of 1 or 2 L of balanced electrolyte

solution plus whole blood, if indicated, will restore RBF, GFR, and urine output. This approach protects renal function in the postoperative period. The few patients who are unresponsive to this regimen may be treated by a loop diuretic, such as furosemide (40 mg), which typically produces a dramatic diuresis. Such patients, however, must be monitored closely since even small dosages of a loop diuretic may induce excessive diuresis, leading to subsequent hypovolemia and hypotension.16–18

■ Early Postoperative Juxtamedullary Washout and Polyuria An interesting, but potentially hazardous, renal response to shock in injured patients is a transient period of polyuria during or immediately after operation (Fig. 59-3).19 This polyuria is not excessive, seldom exceeding 250 mL/30 min, and usually abates by 5 hours following operation (Table 59-2). This phenomenon tends to occur in patients who have had a major hemorrhagic shock insult requiring more than 15 blood transfusions prior to successful hemostasis.19 On arrival to the SICU, the blood pressure and pulse normalize while the urine output exceeds 3 mL/min (180 mL/h) at the expense of effective PV. The urine sodium concentration exceeds 40 mEq/L

Management of Complications after Trauma

SECTION 5 X

CORTEX OUTER CORTEX

1088

Glomerulus MAP = 84 Afferent A CI

OPERATING ROOM

GFR = 36

Efferent A Proximal tubule

Distal tubule

Interlobular A. and V

Arcuate A

Arcua MEDULLA INNER MEDULLA OUTER MEDULLA

te V

C II

CH2O = +0.4 UO = 8.2

CNa –5.9 COsm = 8.5

Collecting tubule

Loop of Henle

C III Vasa recta

FIGURE 59-3 Following restoration of PV during and shortly following operation, a renal concentrating defect may exist whereby a patient may have a low-normal MAP (84 torr) with a markedly reduced GFR (35 mL/min) while excreting a large urine volume (8.2 mL/min; 500 mL/h). This concentrating defect is likely due to inner medullary washout of osmoles, thus impairing reabsorption of sodium and water in response to aldosterone and AVH. This phenomenon seldom lasts more than 5 hours following conclusion of operation.

and the fractional excretion of sodium (FENA) or CNa exceeds 3%. Therapy for this syndrome should be by maintenance of effective PV as judged by vital signs until the polyuric phase subsides, usually within 5 hours of operation.19 The mechanism for early postoperative polyuria is unclear but likely is due to an inner medullary (CIII) washout of osmoles. During shock, the primary reduction in RBF occurs in the outer cortex (CI) with minimal reduction in juxtamed-

ullary (CII) flow; this is referred to as cortical to medullary shunting.2,3 Since the juxtamedullary nephrons have loops of Henle that affect interstitial medullary (CIII) tonicity, a relative increase in RBF to these nephrons may cause a “washout” of osmoles. This disrupts the countercurrent regulatory system and precludes effective sodium and water reabsorption from the collecting ducts when outer cortical flow is first reestablished.19

TABLE 59-2 Impaired Concentration During and Shortly After Operation

Operation Postoperative (5 h) Postoperative (15 h)

MAP (torr) 84 100 98

ERPF (mL/min) — 260 —

GFR (mL/min) 35 90 110

U/O (mL/min) 8.5 3.9 1.6

CNa (mL/min) 5.9 4.3 1.8

COsm (mL/min) 8.1 6.0 3.1

CH2O (mL/min) 0.4 2.0 1.5

The transient period of impaired concentration occurs near the end of operation and in the early postoperative period. This probably reflects inner medullary (CIII) washout, thereby precluding reabsorption of sodium and water in response to aldosterone and ADH. This transient polyuria causes PV depletion but, fortunately, is short lived.

Renal Failure

■ Postoperative Oliguria During Extravascular Fluid Sequestration Phase Following operative control of bleeding after severe hemorrhagic shock, there are major shifts in sodium, water, and protein from the plasma into the IFS. This causes reduced PV, MAP, CO, RBF, GFR, and urine output. This phase of extravascular fluid sequestration lasts about 36 hours in patients who have received an average of 15 RBC transfusions prior to operative control of bleeding.20 Part of the IFS expansion includes intrapulmonary sequestration resulting in respiratory insufficiency.20 Successful therapy mandates a careful balance to maintain perfusion and protect the kidney while not overloading the pulmonary circulation (Fig. 59-4). When the intravenous infusion rate is decreased because of increased weight gain and IFS sequestration, the MAP falls, causing a fall in RBF and potential ARF. This typically occurs during the initial 12 hours after operation and causes decreased ERPF, GFR, UO, CNa, and COsm. During the 36 hours of obligatory IFS expansion, the patient may need 10 L balanced electrolyte solution to maintain kidney function. Inotropes and

ventilator support are often needed during this fluid uptake phase.20 Restoring PV, hemoglobin level, and normal MAP enables the kidney to maintain GFR and urine output even though RBF may be reduced. CNa and COsm during this period reflect the underlying renal circulatory status and are decreased when RBF is lowered but return to normal when the effective circulatory volume is restored; CH2O is negative at this time.11 When a therapeutic decision is made to restrict fluids because of high central pressures, the resultant PV depletion and reduction in RBF often leads to ARF which, in the fluid sequestration phase, usually results in death.2,21 The advocates of fluid restriction ascribe such a death to multiple organ failure not related to ARF since renal function may be maintained by hemodialysis (HD); more likely, multiple organ failure reflects the initial deficiency in circulating volume that led to ARF as part of the multiple organ failure syndrome.2,21,22 The technique used to provide ventilatory support during the fluid uptake phase may also affect kidney function.23,24 When the lungs that are supported by continuous positive pressure breathing with high tidal volumes (above 10 mL/kg body weight), the arterial gases show better saturation but there is a fall in MAP and CO resulting in reduced ERPF, GFR, and urine flow.23 Likewise, the addition of positive end-expiratory pressure (PEEP) above 10 cm H2O causes improved arterial oxygenation but reduction in MAP, CO, ERPF, CNa, COsm, and urine output.24 This response appears to be mediated through sinoaortic baroreceptors, renal innervation, and renal vein pressure changes.25 The reduced ERPF associated with PEEP may also cause renal renin release that causes increased sodium reabsorption.25,26 The SICU team must adjust ventilatory settings with renal function in mind.

Response to Furosemide in Early Sequestration Phase Fluids pushed Furosemide (15 mgm)

Digitalized steroids CaCl 2

Fluids pushed Dopamine

Furosemide (20 mgm)

Systolic 140 pressure (mmHg) 120

Pulse B.P.

100 Pulse rate/min

C.V.P.

25

80 60 400

Urine volume (mL/hr)

5

200 100 50

Urine

1

2

3

4 5 6 7 8 Time (hours after surgery)

9

10

11

12

FIGURE 59-4 Following an operation requiring 23 RBC units and 9 L crystalloid solution, this patient became oliguric (1 hour) and was treated with low-dose furosemide causing prompt diuresis and hypotension. Fluid bolus restored pressure (2 hours) and inotropes were added for rising central pressures (steroid use was part of a prospective randomized trial). Low-dose dopamine was added at 7 hours and this improved perfusion pressure. Furosemide at hour 9 reproduced prompt diuresis and hypotension treated with additional fluid bolus through hour 10. Clearly, loop diuresis during the fluid update phase is hazardous. The patient made a full recovery.

CHAPTER CHAPTER 59 X

Increased osmotic diuresis with polyuria may also be due to the overutilization of solutions containing 5% dextrose. Marked hyperglycemia (500–1,000 mg/100 mL) and hyperosmolemia (310–320 mOs/L) have occurred in patients resuscitated with only crystalloid solutions containing 5% dextrose. This hazard is circumvented by limiting the amount of 5% dextrose in crystalloid solution to 2,000 mL after which a nonglucose balanced electrolyte solution is infused along with whole blood and blood products as needed.2,19

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Management of Complications after Trauma duplicated in a canine model of isolated renal perfusion and had the same effect (C. E. Lucas and I. K. Rosenberg, Surgical renal study unit, unpublished data).21

THE RENAL EFFECTS OF COLLOID RESUSCITATION SECTION 5 X

The type of fluid therapy during the sequestration phase will also affect renal function. Early administration of human serum albumin (HSA) has been recommended to prevent weight gain and IFS expansion during the obligatory fluid uptake phase.27 This recommendation is based on the belief that colloid, such as HSA, will remain within the PV and, by its oncotic effect, cause fluid to return to the PV. Unfortunately, HSA leaves the PV at an increased rate after intravenous administration and causes a prolonged sequestration phase, larger fluids needs, a greater weight gain, and altered renal dynamics.21,28 Patients randomized to receive HSA during the sequestration phase exhibit an increase in PV and RBF but, paradoxically, a reduction in GFR, CNa, COsm, and urine output.28 The reduction in GFR is caused by the HSA oncotic properties within the glomerular tufts where Bowman’s capsule acts like a modified capillary except that it is impervious to protein transmigration. The hyperoncotic blood leaving the glomerular tufts perfuses the vasa recta in the inner medulla (CIII). This hyperoncotic filtrate extracts water and, with it, sodium from the interstices of the inner medulla. The resultant hyperosmolar CIII interstices facilitate the reabsorption of sodium and water from the distal nephrons under the influence of aldosterone and ADH. Both aldosterone and ADH facilitate the reabsorption of sodium and water in direct response to the inner medullary oncotic and osmotic gradients (Table 59-3).2,3,21 Furthermore, almost half of the patients receiving HSA supplementation required loop diuresis compared with only 20% of the non-albumin-supplemented patients.21 Finally, 13 of the 46 albumin-supplemented patients developed some type of renal failure compared with 1 of the 48 nonalbumin patients.21,28 This phenomenon has been

TABLE 59-3 Renal Effects of Randomized Albumin-Supplemented Resuscitation Parameters ERPF (mL/min) GFR (mL/min) U/O (mL/min) CNa (mL/min) COsm (mL/min) CH2O (mL/min) Loop diuretics ARF

Albumin (46 Patients) 477 86 2.4 1.4 3.0 0.35 21 13

Nonalbumin (48 Patients) 403 107 3.2 2.4 3.9 0.37 10 1

Albumin-supplemented resuscitation was associated with an increase in ERPF but a significant decrease in GFR, urine output, and the clearances of sodium and osmoles. Twenty-one of 46 albumin-supplemented patients required loop diuresis and 13 patients developed ARF compared with 10 and 1 patients, respectively, for those not receiving albumin supplementation.

■ Vasopressor Therapy and Renal Function Besides inotropic support, the hypotension associated with IFS expansion after operation often stimulates therapy with vasopressor agents to restore MAP by precapillary vasoconstriction. The resultant rise in MAP may stimulate the baroreceptor response so that the pituitary that decreases the release of ADH promotes increased urine output. This increase in urine volume can be duplicated initially with all vasopressor agents when administered at a low dosage.29 Unfortunately, when tachyphylaxis to the vasopressor agent occurs, increased doses must be administered; this leads to excessive vasoconstriction including the renal circulatory bed resulting in a subsequent oliguria that often progresses to ARF. One of the popular vasopressor agents, dopamine, has been described as having a beneficial effect on the renal circulation when given at low doses (5 μg/(kg min)).29 This salutary effect has been attributed to a dopaminergic-induced reduction in RVR resulting in increased RBF, GFR, and urine output. Clinical studies, however, have not shown renal benefits (C. E. Lucas and I. K. Rosenberg, Surgical renal study unit, unpublished data).30 Prior studies have demonstrated that low-dose dopamine in critically ill trauma and septic patients almost uniformly produces an increase in urine output (C. E. Lucas and I. K. Rosenberg, Surgical renal study unit, unpublished data). These low-dose infusions, however, increased MAP and CO so that the resultant increase in urine output is mediated through baroreceptor responses to the pituitary that blocks ADH release (C. E. Lucas and I. K. Rosenberg, Surgical renal study unit, unpublished data). Similar results have been seen with other vasopressor agents such as norepinephrine and Aramine (C. E. Lucas and I. K. Rosenberg, Surgical renal study unit, unpublished data). More recently, there has been a relook at AVP as a means of restoring peripheral pressure in hypotensive patients and, at the same time, protecting the kidney. AVP exerts its effects at three different receptors. The AVP receptor two (V2R), within the renal collecting tubular cells, responds to minute doses of AVP and facilitates the reabsorption of water from the renal tubule in accordance with the inner medullary (CIII) osmolar gradient.31 V1A acts on the myocardium and will exert an inotropic effect; this increases the MAP and, through the same mechanism as the other low-dose vasopressor agents, stimulates a reduction in ADH release through the baroreceptor stimulation of the pituitary. AVP may be beneficial in patients with hypotension that is refractory to the standard vasopressor agents such as norepinephrine.32 It does not increase renal perfusion so that the temporary improvement in urine output will be followed by oliguria as tachyphylaxis occurs unless the underlying clinical problem is corrected.31,32

■ Fluid Mobilization and Renal Changes After an average of 36 hours of IFS sequestration, patients who receive an average of 15 RBC transfusions segue into a fluid

Renal Failure

TABLE 59-4 The Renal Factor and Postresuscitative Hypertension (PRH) Parameter Measured GFR (mL/min) ERPF (mL/min) RBF (mL/min) RBR (dyne s/cm5) Renal oxygen consumption (mL/min) CNa (mL/min) COsm (mL/min) PV (mL) IFS (mL) PV/IFS

PRH Patients 98 361 602 15,808 5

Non-PRH Patients 112 532 990 8039 18.6

2.9 5.6 3,625 13,971 25.9

2.1 4.0 3,410 16,481 20.7

Hypertension during the fluid mobilization phase was associated with reduced RBF, increased RVR, reduced IFS volume, and increased PV/IFS ratio implying that a renal-mediated reduction in IFS compliance is responsible. Loop diuresis tends to cause hypotension in the hypertensive patients in contrast to normal tensive patients with a larger IFS.

THE RENAL FACTOR IN POSTRESUSCITATIVE HYPERTENSION The mechanism that leads to the PRH syndrome during the fluid mobilization phase is not fully understood but is related to altered renal function. When comparing patients who develop PRH with comparably injured patients without PRH, there is impaired mobilization from the IFS (Table 59-5). The IFS sequestration phase in the PRH patients averages 7 days compared with 5.3 days in comparably injured patients without PRH.33 Despite comparable GFR levels between the two groups of patients (98 mL/min vs. 112 mL/min), the patients with PRH had a marked reduction in TRPF and RBF that averaged 397 and 602 mL/min, respectively, compared with the non-PRH patients in whom the TRPF and RBF averaged 659 and 990 mL/min (Table 59-1). Consequently, there was a marked increase in RVR which averaged 15,808 dyne s/cm5 in the PRH patients compared with 8,039 dyne s/cm5 in

non-PRH patients (C. E. Lucas and I. K. Rosenberg, Surgical renal study unit, unpublished data).33 Renal oxygen consumption was also reduced in PRH patients (Table 59-4). The rise in RVR occurs primarily at the postglomerular level since GFR was maintained. PRH is a problem of fluid maldistribution rather than simple total body fluid overload. The patients with PRH had a higher PV and MAP in comparison to the non-PRH patients but had a lower IFS volume. Thus, the PV/ IFS ratio was markedly increased in the PRH patients compared with those without PRH (C. E. Lucas and I. K. Rosenberg, Surgical renal study unit, unpublished data).33 This combination of increased PV with reduced IFS implies a reduction in the interstitial space compliance.34 Likewise, the PRH patients had a reduction in the total ECF which averaged

TABLE 59-5 Relationship of Serum Creatinine to Renal Hemodynamic Studies in Injured and Septic Patients Serum Creatinine (mg/dL) CCr (mL/min) CPAH (mL/min) CIn (mL/min) Calculated RBF (mL/min) CNa (mL/min) CH2O (mL/min) COsm (mL/min)

N ⴝ 11 (0.1–0.5) 128 606 139 1,070 2.0 ()1.6 4.2

N ⴝ 26 (0.6–1.0) 122 502 116 896 2.5 ()1.2 4.1

N ⴝ 190 (1.1–1.5) 99 390 89 694 2.6 ()1.0 4.3

N ⴝ 46 (1.6–2.0) 60 238 48 420 1.6 ()0.8 3.3

N ⴝ 15 (2.1–2.3) 50 212 55 380 2.5 ()0.7 3.9

Nⴝ7 (2.4–3.0) 37 148 32 269 2.8 ()1.2 4.2

N ⴝ 13 (>3.0) 13 53 6.6 113 0.2 ()0.2 0.9

CHAPTER CHAPTER 59 X

mobilization phase. This process is the result of contraction of the IFS matrix that forces large quantities of salt and water into the adjacent lymphatics for remote delivery into the PV.21,28 The duration of this mobilization phase is documented by determining the time from maximal weight gain during the fluid sequestration phase until maximal weight loss and averages 5.6 days.28 This rate of IFS fluid relocation into the PV may exceed 10 L in 24 hours causing acute hypervolemia associated with impaired renal excretion.20,28 This intravascular flux should be anticipated and treated aggressively with fluid restriction and loop diuresis.20,28 The renal function studies during the first 48 hours of mobilization reflect the increase in MAP and PV so that GFR, CNa, COsm, and urine output increase; RVR, however, continues to be elevated, primarily at the postglomerular level (Table 59-4). Once reverse movement ensues, an increase in MAP follows and hypertension (BP 150/100 torr) often ensues.20 Lack of appreciation of the “new plateau” of MAP in the fluid mobilization phase leads to the “postresuscitative hypertension (PRH) syndrome” with associated respiratory failure, cardiac compromise, confusion, and hematuria.20,28 When loop diuretics do not reverse the acute hypertension, low-dose vasodilators are indicated.

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SECTION 5 X

25% of total body weight compared with 30% of total body weight in the non-PRH patients.33,35 The cause of reduced IFS compliance and hypervolemia with the PRH remains obscure but is likely consequent to a renal tubular ischemic insult.34 The marked increase in RVR was associated with a reduction in the renal perfusion index (RBF/CO). Measurements of renin activity and aldosterone-like effect in the two groups of patients showed no differences (C. E. Lucas and I. K. Rosenberg, Surgical renal study unit, unpublished data). Delays in recovery of renal perfusion following hemorrhagic shock have been demonstrated in both humans and animals.11,36 The mechanisms leading to this delayed restoration of perfusion, however, have never been fully explained. The increase in the IFS in non-PRH patients suggests some mechanism, whereby the kidneys may be responsible for maintenance of the PV/IFS ratio following severe hemorrhagic shock (C. E. Lucas and I. K. Rosenberg, Surgical renal study unit, unpublished data).33 The renal response to loop diuresis was also evaluated in PRH and non-PRH patients.35 Patients without PRH had a much greater increase in CNa, COsm, and urine output in comparison to the non-PRH patients. Another interesting difference between the two groups of patients reflects the changes in blood pressure following the therapeutic administration of loop diuresis.35 The PRH patients often went from hypertension to hypotension within 2 hours after completion of the loop diuresis, whereas the non-PRH patients tolerated the loop diuresis with marked increases in urine output and maintained perfusion pressure suggesting rapid restoration of the PV by the IFS.35 The inability of the expanded IFS to rapidly replenish a depleted PV after loop diuresis can only be caused by an altered IFS compliance.33,34 A reduction in IFS volume due to reduced compliance, as was seen in the PRH patients, would explain the postdiuresis hypotensive response since the IFS is not available for reentry into the PV.33,34 PRH with increased PV has been reproduced in a rodent model of renal insufficiency; these animals have reduced IFS volume and compliance.34 The factor responsible for these changes can be cross-perfused into normal control rats, thus indicating that this is a humeral factor.34 The excessive response to loop diuresis must be carefully monitored to be certain that PRH patients do not rapidly go from hypertension to hypotension. Possibly the renal hypoperfusion causes ischemic injury to the arteriolar walls leading to transmural migration of sodium on to intramural collagen, thus making these vessels in both the periphery and the kidney more sensitive to a normal level of circulating catecholamines.34,36 Following recovery, renal function studies in both groups of patients are normal.

THE RENAL RESPONSE TO SEPSIS Patients with severe multiple injuries often develop sepsis. The renal response to sepsis is, for the most part, a renal adaptation to an altered systemic circulatory status. Those factors that have created the most controversy regarding this response, therefore, are an extension of the controversy regarding the cardiovascular response to sepsis.37 Historically, sepsis has been characterized as a hypodynamic state with increased TPR and

decreased CO; the kidneys, traditionally, shared in this response with increased RVR and decreased RBF, especially outer cortical (CI) flow.38 These traditional concepts, however, reflect endotoxin studies in animals and a poor understanding of fluid shifts in septic patients. The empirical recognition that septic patients respond better to a fluid challenge questioned these traditional views.39 Clinical studies in severely septic patients showed an expanded PV, increased CO, decreased TPR, increased IFS volume, and increased urine volume.37,39 This hemodynamic response has been called the “hyperdynamic state of sepsis”. The kidney often shares in this hyperdynamic state.39 Polyuria exceeding 2 L per day is seen in many severely septic patients if resuscitation is initiated early enough to prevent renal ischemia and shutdown.39,40 Furthermore, polyuria may be inappropriate and persist despite fluid restriction that causes hypovolemia and hypotension.40 Since a vital renal function is regulation of PV by both diuresis and water conservation, this “inappropriate polyuria” soon after a septic insult is an unusual paradox.40 The physiology and danger of this phenomenon are illustrated in the following example (Fig. 59-5). This 27-year-old woman presented with a 3-day history of lower abdominal pain, distention, fever, tenderness, leukocytosis, and a lower quadrant mass. Shortly thereafter, she became hypotensive and agitated; fluids containing vasopressors were administered. Vital signs responded to large-volume intravenous replacement. Laparotomy revealed massive peritoneal spillage from a ruptured viscus. Postoperatively, she exhibited marked fluid sequestration, weight gain, increased CVP (22–25 cm H2O), and polyuria (300 mL/h); she received large volumes of intravenous fluid to prevent hypotension and was given inotropes. Her urine sodium concentration was 47 mEq/L. Despite objections from the surgical team, a fluid restriction regimen was instituted to “protect” the lungs (Fig. 59-5). Within 4 hours, the blood pressure fell to 90/70 mm Hg and the pulse rose to 125/ min as the urine volume decreased from 300 to 50 mL/h. The pooled 4-hour urine specimen, which averaged 140 mL/h, contained 12 mEq sodium. By hour 28, hypotension (80/60 mm Hg) and tachycardia (155/min) worsened and she became anuric; the CVP fell to 21 cm H2O. The urine sodium just prior to ARF was 5 mEq/L. She remained anuric and died of respiratory failure 2 days later (Fig. 59-5). This brief summary shows how the polyuric state of sepsis persists after the initiation of fluid restriction and contributes to hypotension; thus, it is inappropriate polyuria. Studies on patients with inappropriate polyuria of sepsis show an elevated CO, normal GFR, and normal TRPF associated with normal RBF distribution to the outer cortex, inner medulla–outer cortex, and inner medulla.40 Past experiences indicate that fluid restriction leading to ARF in comparable septic patients almost always is fatal despite the availability of HD. Since pulmonary function generally shows little improvement with fluid restriction during the initial 24 hours of a massive septic insult, the pulmonary insufficiency appears to result from the sepsis, per

Renal Failure

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Polyuria of acute sepsis

Pulse rate

160

25 CVP 20 cm H2O 15

140

10

CHAPTER CHAPTER 59 X

120 Systolic pressure 100 mm Hg 80

120 100

Fluid restricted

300 Urine 200 volume mL/hr. 100 0

Na = 47 K = 37 24

Na = 12 K = 94

28

32

36

Time in hours after operation

FIGURE 59-5 This young woman had reoperation for massive peritonitis. Inappropriate polyuria through the first 28 hours after operation persisted despite normal vital signs. Fluid restriction to protect the cardiovascular status led to hypotension, tachycardia, and renal failure within 4 hours resulting in her later demise on day 3.

se, rather than a PV overload. Patients with this inappropriate polyuric syndrome must be monitored closely. When the urine sodium level falls below 10 mEq/L or the FENA is less than 1, expansion of PV to enhance renal perfusion is indicated.39,40

■ Mechanism of Inappropriate Polyuria of Sepsis The polyuria of sepsis was initially observed by Ladd during the Korean conflict; he postulated osmotic diuresis as the etiology.12 Hyperosmolemia (between 290 and 330 mOs/L; normal is 270–278 mOs/L) has been confirmed in septic patients; furthermore, this hyperosmolemia cannot be explained by the combined osmolar effects of serum sodium, blood urea nitrogen (BUN), and serum glucose concentrations that are used to measure calculated serum osmolality (Calc Osm) by the following formula: Calc Osm  serum sodium  1.86 BUN (mg/dL)/2.5 serum glucose (mg/dL)/18. The Calc Osm in septic patients, typically, is normal (250–265 mOs/L).39,40 The osmolar difference (OsmDiff ) equals the actual serum osmolarity minus the Calc Osm and is usually increased in severely septic patients, averaging 47 mOs/L compared with a normal of 15 mOs/L.39 This increased OsmDiff reflects the severity of sepsis and correlates closely with mortality rates and the degree of polyuria. Contrary to Ladd’s theory that the polyuria is due to osmotic diuresis, however, COsm in septic patients averages about 3 mL/min, which is the upper limit of normal.39 The positive correlations between the OsmDiff and polyuria are probably spurious in that both factors are indices of the severity of sepsis. Hyperosmolemia, per se, however, may contribute to the polyuria by a mechanism not related to diuresis. It is a potent vasodilator in many vascular beds, including the kidney, and may facilitate diuresis by renal vasodilatation and its described effects.39,41

The polyuria of sepsis might be due, partially, to a juxtamedullary “washout” secondary to selective decrease of RBF to the outer cortex (CI) with maintained flow to the juxtamedullary nephrons (CII) prior to volume replacement. This reduces the inner medullary interstitial (CIII) osmotic pressure, thereby temporarily “paralyzing” the countercurrent mechanism. This explanation would explain polyuria that occurs during the early postresuscitation interval when the inner medullary osmolar gradient becomes reestablished. Two factors have negated this postulate. First, the period of increased RBF and decreased RVR in septic patients is transient, usually lasting 48–96 hours; in contrast, the polyuria may last beyond that time in patients subjected to a second septic insult that is not associated with hypotension. Second, RBF distribution measurements by 133Xe disappearance during the period of inappropriate polyuria, but 72 hours after the initial insult when the TPR was normal, did not support this conclusion.40 Each patient had normal intrarenal distribution to all three renal components (Fig. 59-6).40 Experimental studies on the effects of sepsis on renal hemodynamics show a decrease in RVR and an increase in RBF.41,42 Hermreck et al. demonstrated that dogs made septic by the introduction of enteric flora into the muscles of the hind limb developed increased RBF as measured by an electromagnetic flow meter.41 Ravikant and Lucas monitored renal circulation with this hind limb sepsis model, using radioactive microspheres; they showed a hyperdynamic state with increased CO and RBF despite a lower MAP and CVP when compared with control animals.42 Ravikant and Lucas also showed a decrease in EPAH indicating that some blood entering the kidney was shunted into the renal vein without actively engaging in renal metabolism.42 The reduced EPAH in septic animals led to clinical studies in which renal vein sampling was used to measure EPAH in septic patients.40 These

1094

Management of Complications after Trauma Glomerulus Afferent A

95

CI 386

Efferent A Proximal tubule

Distal tubule

Interlobular A. and V

Arcuate A

1200

Arcua

te V

MEDULLA INNER MEDULLA OUTER MEDULLA

SECTION 5 X

CORTEX OUTER CORTEX

POLYURIA: Sepsis

C II 72

UO = 6 Collecting tubule

Loop of Henle

C III Vasa recta

13

FIGURE 59-6 This patient with extensive peritonitis had inappropriate polyuria (6 mL/min; 360 mL/h) despite marginal blood pressure and normal RPF (1,200 mL/min), GFR (95 mL/min), and RBF distribution to CI, CII, and CIII. This inappropriate polyuria subsided after 36 hours and he recovered.

measurements showed a significant reduction in EPAH, calculated RBF using measured EPAH, and documented decreased RVR and increased RBF early in the course of septic patients who were fully resuscitated and had normal vital signs.40 Decreased EPAH in septic animals and patients parallels similar findings in human volunteers receiving pyrogens intravenously.43 Both septic patients and volunteers receiving pyrogens have a comparable increase in RBF, urine output, and CNa; the same is seen in animals and humans after vasodilation with phenoxybenzamine administration.43 Hermreck et al. implicated a diabetes insipidus–like syndrome.41 They blocked the polyuria in dogs with infected hind limbs by the systemic administration of ADH. The ADH dosage, however, was greater than that which produces a specific renal effect independent of systemic vasoconstriction. Using renal physiologic dosages of ADH (1–2 μg/kg/h) injected into the renal arteries of septic patients with inappropriate polyuria, no effect was seen on the polyuria.40 This syndrome has also been attributed to a distal tubular blockade of aldosterone receptor sites; calculated aldosterone-like effect on the renal tubules (CH2O/(CH2O CNa) in septic patients with positive free water clearance, however, shows no such impairment. Indeed, most septic patients can reabsorb sodium with great efficiency right up to the development of AORF, and few have a positive

CH2O (C. E. Lucas and I. K. Rosenberg, Surgical renal study unit, unpublished data).39 The therapeutic implications of this syndrome are apparent. Clinicians must recognize that “a good urine output” of 35–50 mL/h in the early septic period may not be adequate and may reflect PV deficiency. Likewise, a large urine output exceeding 200 mL/h need not reflect overload.39 Polyuria, together with large insensible losses, IFS expansion, and increased gastric losses over a period of days, may lead to an incipient hypovolemia that goes unrecognized prior to a “sudden” vascular collapse. Careful monitoring of intake and output provides clues of impending collapse; blood pressure, pulse, pulse pressure, and urine sodium concentration must be monitored closely.39

■ Renal Response to Hypodynamic Sepsis Not all septic patients develop the hyperdynamic state.37,39 Indeed, up to 35% of patients with sepsis develop a low CO and a high TPR. The renal response to “hypodynamic” sepsis consists of increased RVR, decreased RBF, and decreased GFR reflecting, primarily, a decrease in outer cortical (CI) flow. This leads to a low CNa, COsm, and urine output. Therapy for the oliguria must be directed toward supporting the myocardium and maintaining PV. Persistent oliguria in fully

Renal Failure

■ Significance of Free Water Clearance Free water clearance (CH2O) represents the difference between urine output and osmolar clearance (COsm). The addition of CH2O measurements provides more insight into renal concentrating capacity.44 Concentrating impairment, as reflected by the excretion of a dilute urine, is due to an intrinsic renal dysfunction. This defect may proceed azotemia and oliguria by 24–72 hours.45 Excess CH2O (CH2O  0.25 mL/min) in critically ill patients is associated with a reduction in PV, GFR, and ERPF.45 This subgroup of patients has the highest incidence of subsequent renal failure (21%). When the CH2O approaches unity (0.25 mL/min), careful monitoring will help determine whether this is a normal response to increased PV or to an intrinsic tubular defect predicting subsequent ARF.44 Patients with a rising CH2O, without evidence of PV expansion, need to be watched carefully for toxic renal insult, particularly from associated medicines such as renal toxic antimicrobials (C. E. Lucas and I. K. Rosenberg, Surgical renal study unit, unpublished data). The effect of the random addition of albumin (HSA) to a resuscitation regimen also affects CH2O.45 The significant decrease in CNa associated with HSA-supplemented resuscitation causes a rise in CH2O. This is due to both increased peritubular oncotic pressure and decreased filtered sodium load. These changes are mediated through distal nephron sodium–potassium exchange.45

SIGNIFICANCE OF A SERUM CREATININE VALUE The GFR provides the best single study assessment of renal function. Ideally, this is a 24-hour GFR to filter out subtle renal changes during the day. The 24-hour GFR, however, is seldom measured as one relies on 2-hour samplings of GFR using CCr. When a 2-hour GFR is not performed, one has only a static serum creatinine value to estimate the current renal function.46,47 Based on detailed studies of injured and septic patients, one can estimate that approximately 1 million or 50% of the 2 million nephrons are functioning when the serum creatinine is 1.5 mg/dL (Table 59-5).47 Likewise, the ERPF has decreased to about 400 mL/min and the calculated RBF has fallen to less than 700 mL/min. When the serum creatinine level reaches 2.5 mg/dL, the number of functioning nephrons has decreased to about 250,000 with a GFR of about 30 mL/ min (Table 59-1; Fig. 59-1). This, in turn, is associated with an ERPF and RBF of 148/min and 269/min, respectively. This represents severe renal insufficiency and progression to ARF is threatened.47 When the serum creatinine exceeds 3.1 mg/dL, the GFR has fallen to less than 10 mL/min, which is defined as ARF. When this occurs, all nephrotoxic agents

should be discontinued to try to prevent progression to oliguric ARF.47

RIFLE CRITERIA FOR RENAL FAILURE Whereas the serum creatinine provides a static image of renal function, the Risk, Injury, Failure, Loss, and ESKD (RIFLE) criteria emphasize change in function during treatment. The RIFLE criteria focus on changes in GFR, serum creatinine, and urine output.48 Renal risk of ARF is defined when the serum creatinine increases by 1.5 times, the GFR decreases by 35%, or the U/O is less than 0.5 mL/(kg h) (35 mL/(h 70 kg)) for more than 6 hours. Renal injury is defined as an increase in serum creatinine by two times, a fall in GFR by more than 50%, or a fall in U/O to less than 0.5 mL/(kg h) for more than 12 hours. Renal failure is defined as an increase in serum creatinine by three times, a decrease in GFR by 75%, a U/O less than 0.3 mL/(kg h) for 24 hours, or anuria for 12 hours. Renal loss is defined as failure that lasts more than 4 weeks. End-stage renal disease (ESKD) is defined as failure that lasts more than 3 months.48 Recovery from ARF is defined as partial or complete depending on how far the patient reverses the above process of RIFLE. When there is no baseline creatinine or GFR with which ongoing values can be compared, an age-, gender-, and race-based nomogram is used to define what the initial serum creatinine should have been.48 Just as a low serum creatinine will estimate the number of functioning nephrons, so will the RIFLE criteria identify when renal function is worsening so that all nephrotoxic agents can be discontinued.47 The Acute Kidney Injury Network (AKIN) developed a similar system for defining ARF that they referred to as acute kidney injury (AKI).49 The AKIN, like the RIFLE classification, defines three separate levels of AKI with these three levels based on the clinical parameters of urine output and changes in serum creatinine levels. When the AKIN system is compared with the RIFLE system, there appears to be no significant change in sensitivity between the two systems in defining ARF or in the ability of either system to predict the outcome of critically ill patients.49 Advocates for the AKIN or RIFLE system in defining severity stages for ARF point out that creatinine clearance may not be an accurate monitor for renal function in patients with low GFR because the creatinine is both filtered at the glomerulus and secreted by the renal tubules. Comparisons between GFR measured by CCr and CIn that is not secreted by the tubules show that the increase in CCr over CIn is predictable at all ranges of GFR (Fig. 59-7).47,48 Thus, renal function with one test would be the CCr corrected for the known relationship between CCr and CIn (Table 59-5; Fig. 59-7).47

■ Effects of Renal Trauma on Renal Function Injury to the kidney, per se, affects renal function.50 When the renal injury does not require retroperitoneal exploration for hemostasis or correction of a urine leak, the postoperative renal function is comparable to those patients who had similar hemorrhagic shock insult requiring a comparable number of

CHAPTER CHAPTER 59 X

resuscitated patients requires induced diuresis with mannitol or a loop diuretic.35 When oliguric ARF is developing, a loop diuretic, such as furosemide, beginning at 40 mg and doubling this dose every 30–60 minutes to a total of 3,200 mg, may prevent renal shutdown. If a renal response does occur with this regimen, it usually occurs by the time the furosemide dosage has reached 160 mg.35 When there is no response, the end result is oliguric ARF.

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Correlation between SCr and GFR Logarithmic

SECTION 5 X

4.0

3.5

3.0

2.5

SCr (mg/dL) 2.0

1.5

1.0

0.5

0.0 0

25

50

75

100

125

150

175

200

225

250

275

300

GFR (mL/min) FIGURE 59-7 Correlation between SCr and GFR. Measurements made on 289 severely injured patients and 34 septic patients show that, at each level of serum creatinine (SCr), the creatinine clearance (dashed line) is greater than the inulin clearance (solid line). This occurs because creatinine is both filtered and secreted, whereas inulin is only filtered.

RBC transfusions during operation but did not have renal failure.50 Likewise, when renal hemostasis is achieved by means of suture repair, the postoperative renal function is not different from matched controls.50 When nephrectomy is needed, there is a significant reduction in RBF and GFR.50 Furthermore, the incidence of ARF rises when partial or total nephrectomy is required for hemostasis in comparison to comparably injured patients without renal injury. Finally, nephrectomy is associated with an increased mortality due to the underlying trauma/shock insult in comparison to comparably injured patients who receive the same number of RBC transfusions during operation but do not require nephrectomy.50 Consequently, one must emphasize the importance of successful repair of renal injuries without nephrectomy when following a policy for exploration of intermediate severity renal injuries.50,51

CONTRAST-INDUCED RENAL INJURY Most seriously injured patients undergo computed tomography (CT), usually in conjunction with an iodinated intravenous contrast media injection. A major complication is contrastinduced nephropathy. This complication is the third leading cause of hospital-acquired ARF that, in turn, is associated with

significant mortality rates.52,53 This complication occurs even though less toxic, nonionic, iso-osmolar contrast agents have replaced hyperosmolar ionic contrast agents that were associated with red cell crenation and small vascular occlusion.53 Careful restoration of PV and correction of electrolyte abnormalities, particularly hyperchloremia, are important preventative steps.53 Contrast-induced ARF occurs in all age groups.54 The likelihood for contrast-induced ARF increases precipitously when the creatinine is greater than 1.5 mg/dL prior to study; furthermore, the patient with nonoliguric ARF is likely to progress to renal shutdown when the prestudy creatinine exceeds 3.0 mg/dL.53 A rise in the serum creatinine or a fall in urine output prior to study would meet the risk portion of the RIFLE criteria as being another warning for contrast-induced nephrotoxicity.54 Repeat CT studies magnify the risk. The mechanism for contrast-induced ARF is due to reduced RBF and oxygen consumption leading to direct tubular insult.55,56 PV expansion is preventative; the addition of osmotic or loop diuresis does not appear to be helpful and may, in selective circumstances, cause nephrotoxicity.53 The value of adding sodium bicarbonate to the hydration fluid is controversial; Merten and colleagues suggested that the incidence of ARF is lowered in comparison to prestudy resuscitation with sodium chloride.55

The association between ARF and crush injury was made many years ago. This occurred in World War II when citizens of London were trapped in falling buildings during the Nazi blitz. Patients who were safely extracted after limb crush shortly thereafter developed ARF which led to their demise. The mechanism for crush-induced ARF is thought to be a combination of reduced PV due to fluid sequestration in the crushed limb, lowered RBF and GFR, and tubular insult due to the byproducts of rhabdomyolysis.56 The myoglobin that is released from the injured muscle may attach to haptoglobin that lowers GFR. Furthermore, free myoglobin that is filtered may precipitate in the tubule causing obstruction from cast formation; tubular obstruction is aggravated by uric acid cast formation. Both are accelerated by a low pH of the tubular filtrate due to the systemic hypoperfusion.56 Other causes of extensive muscle ischemia causing myoglobin-induced ARF include limb ischemia, cocaine administration, excessive amphetamine exposure, bacterial myonecrosis, and, occasionally, extensive hemolysis from transfusion reactions.57,58 The diagnosis is made from the classical history, an elevated creatinine phosphokinase (CPK), hyperkalemia, and myoglobin in the urine; the urine typically has a deep orange color and likely will contain dark brown granular casts.55 Treatment includes prompt PV expansion, correction of the acidosis, and both osmotic and loop diuresis to unplug the obstructed tubules. An induced urine output of 200 mL/h until the serum creatinine and CPK values have returned toward normal is recommended; this may take 4 or 5 days. Early institution of this regimen helps prevent the progression to ARF. When this therapeutic regimen is delayed and ARF ensues, HD is required. In contrast to patients with ARF due to severe hemorrhagic shock or massive sepsis, the patients with ARF from an isolated crush syndrome will survive.57

■ Intraperitoneal Pressure and the Kidney Increases in the intraperitoneal pressure affect renal function first at the tubular level and subsequently at the glomerulus.9 Patients with abdominal hypertension due to ascites from liver cirrhosis or stage IV malignancies have increased abdominal pressure; the extent of intra-abdominal venous hypertension, as monitored through indwelling catheters, correlates directly with a reduction in CNa, COsm, and urine output (C. E. Lucas and I. K. Rosenberg, Surgical renal study unit, unpublished data).9 When the IVC pressure rises above 20 torr, there is a reduction in ERPF and GFR (C. E. Lucas and I. K. Rosenberg, Surgical renal study unit, unpublished data). The most severe form of abdominal hypertension occurs in patients with the abdominal compartment syndrome (ACS), who have had massive injury or sepsis requiring large-volume fluid and blood product replacement. Intra-abdominal hypertension above 35 torr is associated with renal shutdown; such patients must be rapidly decompressed with some type of abdominal wall pack used to maintain the viscera within the peritoneal cavity while correcting the intra-abdominal hypertension. Renal function is typically promptly restored with abdominal decompression as long as the renal insult was not excessively prolonged (C. E.

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Lucas and I. K. Rosenberg, Surgical renal study unit, unpublished data).9 Similar changes in tubular function were shown in a canine model in which super renal IVC hypertension was created by different stages of venous constriction (C. E. Lucas and I. K. Rosenberg, Surgical renal study unit, unpublished data). When extreme hypertension was created by materializing the left renal vein, all renal perfusion ceased on the left experimental side while the normal kidney continued to function (C. E. Lucas and I. K. Rosenberg, Surgical renal study unit, unpublished data).

CHAPTER CHAPTER 59 X

■ Crush Injury and the Kidney

Renal Failure

■ Differential Diagnosis of Oliguria Oliguria, refractory to initial PV expansion, may be prerenal, intrinsic renal, or postrenal.2 Postrenal oliguria may be due to a plugged, kinked, or malpositioned indwelling catheter, urethral disruption, or unrecognized retroperitoneal bladder injury. Once diagnosed, the mechanical problem can be corrected. Distinguishing between a prerenal and an intrinsic oliguria requires an analysis of the urine (Table 59-6). Prerenal oliguria is due to reduced CO, RBF, and GFR resulting in a urine with a high specific gravity, high osmolality, low sodium concentration, low CNa and FENA, and an elevated urine/ plasma osmolar ratio and urea ratio. The oliguria due to intrinsic renal failure will be dilute with a low specific gravity, osmolality, and urine/plasma osmolar ratio with a urine sodium concentration greater than 40 mEq/L (Table 59-6). When the differential between prerenal and intrinsic oliguria is unclear, a rapid infusion of 500 mL of balanced electrolyte solution over 20 minutes while monitoring central pressures and peripheral pressures should yield a prompt diagnosis that will guide therapy.

■ Nephrotoxic Agents and ARF Many medicines, particularly antimicrobials, used in the critically ill patient cause nephrotoxicity. These agents are best avoided when the serum creatinine exceeds 1.5 mg/dL.59 For

TABLE 59-6 Differential Diagnosis of Oliguria Parameter Measured Urine specific gravity Urine osmolality (mOs/L) Urine (mOs/L): plasma (mOs/L) Urine urea: plasma urea Urine sodium (mEq/L) FENA (%)

Prerenal 1.030

Probable Prerenal 1.020

Intrinsic Renal 1.012

1,000

400

400

1.2

1.4

1.2

—

10

10

20

40

40

1

2–3

3

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SECTION 5 X

example, such patients with yeast infections are best treated with fluconazole and not amphotericin which has significant nephrotoxicity. The aminoglycosides are also notorious for nephrotoxicity, particularly in the patient with marginal renal function. Reduced dosage and single daily dosage based on peak and trough measurements have been purported to circumvent this toxicity.59 Adherence to these recommendations, however, has not prevented ARF.47,59 Peak and trough dosing recommendations are based on serum levels that have been associated with nephrotoxicity. Critically ill patients, however, have expansion of the IFS with free movement of aminoglycoside into the IFS where it has direct contact with the tubular cells. There are no studies on renal dosing of antimicrobials that take into account IFS concentration of antimicrobials (C. E. Lucas and I. K. Rosenberg, Surgical renal study unit, unpublished data).47 Consequently, nephrotoxic agents should be avoided when the serum creatinine is greater than 1.5 mg/dL.

■ Acute Renal Failure ARF may be defined as an abrupt and sustained decline in renal function that leads to the accumulation of nitrogenous waste products and uremic toxins. Many definitions of ARF have been proposed. Risk factors for ARF following injury include advanced age, high injury severity score, shock, multiple fractures, rhabdomyolysis, major head injury, and lung injury requiring mechanical ventilation. All definitions include anuria (renal shutdown) and oliguria (less than 200 mL per day) as ARF. Nonoliguric ARF implies the maintenance of some filtration; when the GFR is less than 10 mL/min the patient has nonoliguric ARF, whereas when the GFR is greater than 10 mL/min but less than 30 mL/min the patient has acute renal insufficiency.7 Although this definition does not get into the many subtleties of tubular dysfunction, reduction in GFR is the prime component for the development of ARF in the critically injured patient. Such patients with increased mortality and length of stay result in exorbitant hospital cost.7

■ Renal Replacement Therapy The standard renal replacement therapy (RRT) for ARF in the critically ill patient is intermittent HD. Questions exist, however, about the timing and frequency.60 There is a general consensus that HD is mandated in patients with increased PV, electrolyte abnormalities, particularly hyperkalemia, symptomatic azotemia such as confusion, circulating toxins, and metabolic acidosis not corrected by hyperventilation.60,61 Retrospective studies suggest that when intermittent HD is begun early in a patient’s course, there is marked increase in survival, whereas other studies show that HD is not benign and is associated with increased need for vasopressor therapy, bleeding, and infections.60,61 HD is also associated with decreased CO and increased intestinal oxygen consumption producing mucosal acidosis.62 Likewise, there may be a fall in urine output in patients with nonoliguric ARF following HD.61 Indeed, increased mortality rates have been described in a randomized controlled trial in patients who have more frequent HD in comparison to the subgroup with less frequent HD.61 Technical

improvements in HD are developing particularly with the use of biocompatible membranes that are associated with less inflammatory reaction than the traditional cellulose-based membranes. A number of techniques for continuous RRT have been described. The most popular is continuous venovenous hemofiltration (CVVH), which is safer for unstable patients who are not candidates for HD. CVVH has better results in those patients who have higher GFR.62 Other forms of continuous RRT include the continuous arterial venous hemofiltration and continuous arterial venous HD that use the patient’s MAP to provide the flow through the membranes. These types of continuous RRT will help remove circulating toxins of low-molecularweight substances including antimicrobials such as gentamycin with molecules less than 500 d. Continuous RRT also helps correct problems with acidosis due to impaired renal tubular function.63 Future advances for making earlier diagnosis of renal injury, such as measurements of neutrophil gelatinase-associated lipocalin and in the development of renal-assisted devices that have a standard hemofiltration cartridge seeded with renal tubular cells await more clinical trials.64,65 Regardless of technique employed, there must be a close working relationship between the RRT team and the primary care team. Injured and septic patients often have IFS expansion that is due to cellular insult and not PV overload or heart failure. Attempts to remove excess fluid in this setting will compromise PV and renal perfusion, thus aggravating the renal insult. For this reason, the authors prefer to limit RRT for the classical indications of PV overload, electrolyte abnormality (mainly hyperkalemia), toxemia, and symptomatic azotemia in patients with altered mental status. Finally, patients who progress from oliguric ARF to nonoliguric ARF may have impaired tubular function and need close monitoring to identify and correct PV deficiency and hypokalemia.

REFERENCES 1. Lameire N, VanBiesen W, Vanholder R. Acute renal failure. Lancet. 2005;365:417. 2. Lucas CE. The renal response to acute injury and sepsis. Surg Clin North Am. 1976;56(4):953–975. 3. Smith HW. Principles of Renal Physiology. New York: Oxford University Press; 1956. 4. Lucas CE, Rector FE, Werner M, et al. Altered renal hemostasis with acute sepsis: clinical significance. Arch Surg. 1973;106:444–449. 5. Birtch AG, Zakheim RM, Jones LG, et al. Redistribution of renal blood flow produced by furosemide and ethacrynic acid. Circ Res. 1967;21:869. 6. Cosgrove MD, Mowat P. Evaluation of xenon133 renal blood flow method. Br J Urol. 1974;46:137. 7. Schirer RW, Wei W. Acute renal failure and sepsis. N Engl J Med. 2004;251:159. 8. Navar G. Integrating multiple paracrine regulators of renal microcirculation dynamics. Am J Physiol. 1998;274:F433. 9. Doty JM, Saggi BH, Sugarman HJ, et al. Effect of increased renal venous pressure on renal function. J Trauma. 1999;47:1000–1003. 10. Rosenberg IK, Gupta SL, Lucas CE, et al. Renal insufficiency after trauma and sepsis: a prospective functional and ultrastructural analysis. Arch Surg. 1971;103:175–183. 11. Hayes DF, Werner MH, Rosenberg IK, et al. Effects of traumatic hypovolemic shock on renal function. J Surg Res. 1974;16:490–497. 12. Ladd M. Renal Function in the Battle Casualty. Army Medical Service Graduate School Report. Washington, DC; 1954:chap 6. 13. Rüster C, Wolf G. Renin–angiotensin–aldosterone-system and progression of renal disease. J Am Soc Nephrol. 2006;17:2985–2991.

Renal Failure 40. Cortez A, Zito J, Lucas CE, et al. Mechanism of inappropriate polyuria in septic patients. Arch Surg. 1977;112:471–476. 41. Hermreck AS, Berg RA, Ruhlen JR, et al. The polyuria of sepsis. Surg Forum. 1972;23:53–54. 42. Ravikant T, Lucas CE. Renal blood flow distribution in septic hyperdynamic pigs. J Surg Res. 1977;22(3):294–298. 43. Lathem W. The urinary excretion of sodium and potassium during the pyrogenic reaction in man. J Clin Invest. 1956;35:947–953. 44. Kosinski JP, Lucas CE, Ledgerwood AM. Meaning and value of free water clearance in injured patients. J Surg Res. 1983;33:184–188. 45. Moon MR, Lucas CE, Ledgerwood AM, et al. Free water clearance after supplemental albumin resuscitation for shock. Circ Shock. 1989;28:1–8. 46. Brown VR, Dubose JJ, Hadjizacharia P, et al. Natural history and outcomes of renal failure after trauma. J Am Coll Surg. 2008;206: 426–433. 47. White MJ, Diebel LN, Ledgerwood AM, Lucas CE. The significance of a serum creatinine in defining renal function in seriously injured and septic patients. J Trauma. 2011;70:421–425. 48. Venkataraman R, Kellum JA. Defining acute renal failure: the RIFLE criteria. J Intensive Care Med. 2007;22(4):187–193. 49. Chang CH, Lin CY, Tian YC, et al. Acute kidney injury classification: comparison of Akin and Rifle criteria. Shock. 2010;33:247–252. 50. McGonnigal MD, Lucas CE, Ledgerwood AM. The effects of renal trauma on renal function. J Trauma. 1987;27(5):471–476. 51. McAninch JW, Carroll PR. Renal trauma: kidney preservation through improved vascular control—a refined approach. J Trauma. 1982;22: 285–290. 52. Scwab S, Hlarky MA, Pieper KS, et al. Contrast nephrotoxicity: a randomized controlled trial of a non-ionic and an ionic radiographic contrast agent. N Engl J Med. 1989;320:149–153. 53. Mueller C, Buerkle G, Buettner HJ, et al. Prevention of contrast mediaassociated nephropathy: randomized comparison of 2 hydration regimens in 1620 patients undergoing coronary angiography. Arch Intern Med. 2002;162(3):329–336. 54. McGillicuddy EA, Schuster KM, Kaplan LJ, et al. Contrast induced nephropathy in elderly trauma patients. J Trauma. 2010;68:294. 55. Merten GJ, Burgess P, Gray LV, et al. Prevention of contrast-induced nephropathy with sodium bicarbonate: a randomized clinical trial. JAMA. 2004;291:2328–2334. 56. Singh D, Chander J, Chopra K. Rhabdomyolysis. Methods Find Exp Clin Pharmacol. 2005;27:39–48. 57. Better OS, Rubenstein I. Management of shock and acute renal failure in casualties suffering from the crush syndrome. Ren Fail. 1997;19(5): 647–653. 58. Webber J, Kline R, Lucas CE. Aortic thrombosis associated with cocaine use: report of two cases. Ann Vasc Surg. 1999;13:302–304. 59. Hatala R, Dinh TT, Cook DJ. Single daily dosing of aminoglycosides in immunocompromised adults: a systematic review. Clin Infect Dis. 1997;24:810. 60. Gettings LG, Reynolds HN, Scalea T. Outcome in post-traumatic acute renal failure when continuous renal replacement therapy is applied early vs. late. Intensive Care Med. 1999;25:805. 61. Gillum D, Dixon BS, Yanowver MJ, et al. The role of intensive dialysis in acute renal failure. Clin Nephrol. 1986:25:249. 62. Vanholder R, Van Biesen W, Lamier N. What is the renal replacement method of first choice for intensive care patients? J Am Soc Nephrol. 2001;12:S40. 63. Huyghebaert M, Dhainaut JF, Monsallier JF, et al. Bicarbonate hemodialysis of patients with acute renal failure and severe sepsis. Crit Care Med. 1985;13:840. 64. Makris K, Markou N, Evodia E, et al. Urinary neutrophil gelatinaseassociated lipocalin (NGAL) as an early marker of acute kidney injury in critically ill multiple trauma patients. Clin Chem Lab Med. 2009;47(1):79. 65. Humes HD, Buffington DA, Mackay SM, et al. Replacement of renal function in uremic animals with a tissue engineered kidney. Nat Biotechnol. 1999;17:451.

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14. Brown R. Renal dysfunction in the surgical patient: maintenance of a high output state with furosemide. Crit Care Med. 1979;7:63. 15. Solomon R, Werner C, Mann D, et al. Effects of saline, mannitol, and furosemide on acute decreases in renal function induced by radiocontrast agents. N Engl J Med. 1994;331:1416–1420. 16. Shilliday IR, Quinn KJ, Allison ME. Loop diuretics in the management of acute renal failure: a prospective double blind placebo-controlled randomized study. Nephrol Dial Transplant. 1997;12:2592. 17. Lassnigg A, Donner E, Grubhoffer G, et al. Lack of renal protective effects of dopamine and furosemide during cardiac surgery. J Am Soc Nephrol. 2000;11:97–104. 18. Lucas CE, Zito JG, Carter KM, et al. Questionable value of furosemide in preventing renal failure. Surgery. 1977;82:314–320. 19. Lucas CE, Harrigan C, Denis R, et al. Impaired renal concentrating ability during resuscitation from shock. Arch Surg. 1983:118:642–645. 20. Ledgerwood AM, Lucas CE. Postresuscitation hypertension: etiology, morbidity and treatment. Arch Surg. 1974;108:531–538. 21. Lucas CE. The water of life: a century of confusion. J Am Coll Surg. 2001:192:86–93. 22. Bellomo R, Ronco C, Kellum JA, et al. Acute renal failure—definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care. 2004;8:R204. 23. Harrigan C, Lucas CE, Ledgerwood AM, et al. Effects of altered tidal volume on oxygen dynamics in shock lung. Am Surg. 1983;49(6):304– 309. 24. Lucas CE, Ledgerwood AM, Liebold WC, et al. Effect of end-expiratory pressure on total oxygen dynamics. Surgery. 1983;94(4):643–649. 25. Mullins RJ, Dawe EJ, Lucas CE, et al. Mechanisms of impaired renal function with PEEP. J Surg Res. 1984;37:189–196. 26. Fewell JE, Bond GC. Renal denervation eliminates the renal response to continuous positive-pressure ventilation. Proc Soc Exp Biol Med. 1979;161:574–578. 27. The SAFE Study Investigators. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med. 2004;350: 2247–2256. 28. Lucas CE, Ledgerwood AM. Physiology of colloid-supplemental resuscitation from shock. J Trauma. 2003;54(5):S75–S81. 29. Denton M, Chertow G, Brady H. “Renal-dose” dopamine for the treatment of acute renal failure: scientific rationale experimental studies and clinical trials. Kidney Int. 1996;49:4–14. 30. Bellomo R, Chapman M, Finfur S. Low dose dopamine in patients with early renal dysfunction: a placebo controlled randomized trial. Australian and New Zealand Intensive Care Society (ANZICS) Clinical Trials Group. Lancet. 2000;356:2139–2143. 31. Laugwitz KL, Ungerer M, Schoneberg T, et al. Adenoviral gene transfer of the human V2 vasopressin receptor improves contractile force of the rat cardiomyocytes. Circulation. 1999;99:925–933. 32. Gordon AC, Russell JA, Walley KR, et al. The effects of vasopressin on acute kidney injury in septic shock. Intensive Care Med. 2010;36:83–91. 33. Lucas CE, Ledgerwood AM, Shier MR, et al. The renal factor in the posttraumatic “fluid overload” syndrome. J Trauma. 1977;17(9):667–676. 34. Lucas J, Floyer MA. Changes in body fluid distribution and interstitial space compliance during the development or reversal of experimental renal hypotension in the rat. Clin Sci. 1974;47:1. 35. Lucas CE. The renal response to shock. In: Najarian JS, Delaney JP, eds. Trauma and Critical Care. Chicago: Yearbook Medical Publishers; 1987:201–212. 36. Conger J, Falk S, Robinette J. Cytosolic smooth muscle calcium: kinetics in the 48-hour post-ischemic renal vasculature. J Am Soc Nephrol. 1994;6:895. 37. Wilson RF, Thal AP, Kindling PH, et al. Hemodynamic measurements in septic shock. Arch Surg. 1965;91:121–129. 38. Reddin JL, Starzecki B, Spink WW. Comparative hemodynamic and humeral responses of puppies and adult dogs to endotoxin. Am J Physiol. 1966;210:540–544. 39. Lucas CE, Rector FE, Werner M, et al. Altered renal homeostasis with acute sepsis. Arch Surg. 1973;106:444–449.

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CHAPTER 60

Nutritional Support and Electrolyte Management Kenneth A. Kudsk and Caitlin Curtis

Nutritional therapy is an integral part of the management of severely injured patients. Although malnutrition is a frequent comorbid factor in general hospitalized patients, most trauma patients are young and well nourished. Their nutritional risk is not from preexisting defects in protein stores but due to a hypermetabolic response to injury, inflammation, and sepsis. Rapid mobilization of protein from muscle supports healing, the acute-phase response, and systemic and local host barriers to infection. While tolerated for a limited time, complications during healing, sepsis, and multiple organ dysfunction syndrome (MODS) progressively drain the ability to maintain defenses and heal wounds. This chapter focuses on the role of enteral and parenteral nutritional (PN) support in reducing complications in critically injured patients with particular attention to the identification, institution, and successful management of enteral feeding.

POSTINJURY HYPERMETABOLISM The response to the stress of injury has been classified into “ebb” and “flow” phases, which are influenced by the magnitude of injury. Changes in oxygen consumption, hyperglycemia, and increased vascular tone characterize the “ebb” phase. Epinephrine, norepinephrine, cortisol, aldosterone, and antidiuretic hormone release and exert their central and peripheral effects. Energy expenditure and body temperature are influenced through regulatory changes within the hypothalamus.1 Oxygen consumption and delivery and body temperature increase during the “flow” phase, as amino acids are mobilized into the amino acid pool from peripheral tissues for redistribution for gluconeogenesis, acute-phase protein production, immunologic proliferation, red blood cell production, and fibroblast proliferation. The magnitude of the flow phase correlates with the magnitude and severity of injury but gradually resolves unless a complication intervenes. In uncomplicated cases, diuresis of retained intracellular and extracellular water reflects resolution of this hypermetabolism as stress hormone

levels drop. Appetite and gastrointestinal (GI) function return and positive nitrogen balance reappears with repletion of fat and lean body mass. During this hypermetabolism, patients are usually immobilized and restricted by injuries and the medical therapy. Exercise is a fundamental determinant of muscle mass and immobilization of uninjured patients results in negative nitrogen balance for approximately 3–4 weeks despite adequate nutrition. Except on a very temporary basis, “positive nitrogen balance” cannot be achieved in immobilized injured patients during the first 3 weeks of hospitalization, and attempts to overfeed the negative nitrogen balance must be avoided.

THE ENDOCRINE RESPONSE TO STRESS AND INJURY The hypercatabolism of injury, stress, and sepsis differs from that of starvation where inadequate substrate is available to meet metabolic demands; a comparison is shown in Table 60-1.2 Starvation is characterized by a decrease in metabolic rate, lethargy, a decrease in cardiac output, and a transition to ketone bodies as a major energy source. Within 18–24 hours, glycogen stores are depleted and amino acids provide the substrate for gluconeogenesis. As serum insulin levels drop, fatty acids, ketones, and glycerol become the primary substrate in tissues over 7–10 days. Ketone bodies can meet 70% of the energy requirements of the brain, normally an obligate glucose-requiring tissue. Even at full adaptation, some tissues require glucose for function. This adaptation preserves lean tissue, since amino acid demand drops and protein synthesis and catabolism decrease compared with the fed state. The respiratory quotient (RQ, the ratio of carbon dioxide production to oxygen consumed) is approximately 0.6–0.7 in starvation, indicative of utilization of fat as a primary fuel. During hypermetabolism, the RQ ranges between 0.80 and 0.85. Hyperglycemia and glucose intolerance characterize this condition. Hyperglycemia is due to elevated catecholamines,

Nutritional Support and Electrolyte Management

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TABLE 60-1 Starvation versus Severe Stress Hypercatabolism

which induce hepatic glycogenolysis and gluconeogenesis while inhibiting insulin secretion. Elevated cortisol stimulates glycogenolysis, muscle proteolysis, and gluconeogenesis and induces a peripheral insulin resistance to limit glucose uptake. Cortisol also inhibits gluconeogenic enzymes, potentiates hepatic effects of epinephrine and glucagon, and stimulates muscle proteolysis.3 Overall, the circulating insulin level drops and its anabolic effects are lost, resulting in increased lipolysis, fat oxidation, glucose production,4 and dependence on amino acids for glucose production. Other hormones released with injury include glucagon and arginine vasopressin (AVP) (formerly antidiuretic hormone). Glucagon increases gluconeogenesis, glycolysis, and lipolysis, partly by reducing the insulin to glucagon ratio. AVP stimulates hepatic glycogenolysis and gluconeogenesis. Growth hormone (GH) is normally anabolic and increases glycogen deposition and protein synthesis while mobilizing fatty acids. It is inhibited following injury and during stress, as is insulin-like growth factor I (IGF-I), which is produced by the liver in response to GH. The overall effect is an imbalance in the direction of the counterregulatory hormones, a reduction in the anabolic hormones, and an accelerated loss in lean tissue. If the hypermetabolism remains unchecked, peripheral tissues become incapable of amino acid mobilization for gluconeogenesis or protein synthesis.

CHANGES IN INTERMEDIARY METABOLISM WITH STRESS AND SEPSIS ■ Protein Metabolism Both protein synthesis and catabolism increase after severe trauma. Starvation, immobilization, and the hormonal and cytokine milieu factor in this response.5 Release of 3-methylhistidine, an amino acid derived from actin and myosin metabolism in damaged and undamaged tissues, increases. Essential amino acid levels, especially branched-chain amino acids (BCAA), increase within the cell and levels of nonessential amino acids decrease, primarily through a 50% reduction in intracellular glutamine (GLN). Up to 70% of the amino acids

←Continuum→

Stress ↑↑ High (0.85) ↑↑↑ Fat amino acids ↓↓↓

released by skeletal muscle are alanine and GLN, although they constitute 10–15% of muscle composition. The production and metabolism of these amino acids have been studied extensively.6 During stress, skeletal muscle is capable of utilizing the BCAAs, valine, isoleucine, and leucine. While the non-BCAAs are released into the systemic amino acid pool, waste nitrogen of BCAA is disposed in two ways. In the cell, glucose is metabolized to pyruvate, which accepts a nitrogen molecule from the BCAA via transamination to create alanine. Alanine is released, cleared by the liver, deaminated, and recycled to glucose. The nitrogen is converted to urea. Additional pyruvate is converted to acetyl CoA for entry into the Krebs cycle. The transamination of nitrogen from BCAA onto alpha-ketoglutarate in the Krebs cycle produces glutamate. Transamination of a second nitrogen completes the synthesis of GLN. GLN is released and functions as a primary fuel for enterocytes and various immunologic cells (especially T-lymphocytes), and for conversion to glucose by the kidney. GLN is converted by the gut-associated lymphoid tissue (GALT) and splanchnic tissue to ammonia, ornithine, citrulline, and alanine and released into the portal circulation. Hepatic uptake clears these by-products for entry into appropriate metabolic cycles. Although serum and intracellular levels of GLN drop, overall production is increased. Waste nitrogen in the kidney is excreted as ammonia into the tubules binding hydrogen ion for elimination. Skeletal muscle protein catabolism exceeds synthesis but there are net increases in hepatic protein production and gluconeogenesis in the liver. Synthesis of constitutive transport proteins (e.g., albumin and prealbumin) is depressed while synthesis of acute-phase proteins (e.g., C-reactive protein [CRP] and α2-acid glycoprotein) is increased. This catabolism is tolerated by well-nourished patients for a limited period, but prolonged body protein loss is associated with pulmonary, cardiovascular, metabolic, and immunologic system failure.

■ Glucose Metabolism Hepatic gluconeogenesis remains elevated despite hyperglycemia. After glycogen depletion, protein provides the substrate since fat cannot be converted into glucose. Glucose infusions

CHAPTER CHAPTER 60 X

Resting energy expenditure Respiratory quotient Counterregulatory hormones Primary fuel Proteolysis Branched-chain oxidation Hepatic protein synthesis Acute-phase protein production Constitutive protein production Urinary nitrogen losses Gluconeogenesis Ketone body production

Starvation ↓ Low (0.65)  Fat  ↓

1102

Management of Complications after Trauma

SECTION 5 X

do not inhibit this accelerated gluconeogenesis.7 Alanine, GLN, increased lactate levels released by hypoxic tissues, and glycerol released from adipose tissue can be converted into glucose. Alanine levels increase by 40% while glycerol and lactate increase by as much as 100% in trauma patients.5 Data from burn patients8 suggest that glucose production is controlled by the liver since lowering of insulin and glucagon concentrations by somatostatin reduces hepatic glucose production despite elevated levels of substrate appropriate for gluconeogenesis. There is evidence of less efficient glucose oxidation in both septic and trauma patients that may be secondary to intracellular derangements in control pathways caused by low pyruvate dehydrogenase levels. It is unlikely that reduced glucose oxidation is due only to insulin resistance, since glucose clearance from plasma is unrelated to glucose oxidation. This mobilization of glucose may be protective since experimental infusion of hypertonic glucose following hemorrhage reduces mortality in pigs and increases blood pressure clinically. Some effect may be due to fluid shifts due to hyperglycemia, but a positive pressor effect from increased myocardial glucose uptake has been postulated.

■ Fat Metabolism Fat is the primary fuel during stress and sepsis. Increased levels of epinephrine, glucagon, cortisol, and perhaps GH enhance lipolysis following injury despite increased levels of plasma insulin. Plasma free fatty acid levels do not correlate with the degree of trauma,9 perhaps from shunting of blood from adipose tissue or drops in serum albumin since it is a transport molecule for free fatty acids. Lactic acidosis lowers free fatty acids by augmenting reesterification. The contribution of fat is evident by the depressed RQ in septic patients. As the patient recovers, the RQ increases from 0.7 of fat to 1.0 of carbohydrate, but the RQ remains depressed in septic patients. The type of fat administered influences cellular responses. All forms of intravenous fat currently available in the United States are omega-6 fatty acids derived from vegetable oils. The omega-6 polyunsaturated fatty acid (PUFA) linoleic acid is subsequently incorporated into membranes of both immune and nonimmune cells as arachidonic acid. During stress, increased intracellular calcium releases the fatty acids by activating phospholipase A2. The products are acted upon by cyclooxygenase and lipoxygenase to produce the prostanoid PGE2, a vasodilator prostanoid, while lipoxygenase produces leukotriene B4 and 5-hydroxy-6,8,11,14-eicosatetraenoic acid (5-HETE). At high concentrations PGE2 is immunosuppressive and reduces T-cell function and migration and generation of cytotoxic cells. Leukotrienes are powerful chemoattractants that stimulate aggregation and adherence of leukocytes and natural killer cell activity. Most contemporary enteral formulas contain omega-3 fatty acids from fish and canola oil. After their subsequent release, intracellular enzymes produce prostaglandins of the 3 series (PGE3) and leukotrienes of the 5 series, which are less immunosuppressive and not as proinflammatory as the omega-6 products. Clinically, these cell membrane increases are measurable within a few days of administration.10

■ Current Issues Nutritional support is but one very important aspect in the overall management of the trauma patient. Most trauma patients are well nourished, although geriatric patients and younger patients with histories of substance abuse may have varying degrees of malnutrition. Debridement, drainage, resection of infected tissue, stabilization of fractures, adequate resuscitation, etc., are the priorities in early management, because early control will influence the subsequent metabolic response. If sources of inflammatory mediators are not controlled, nutrition support will not preserve catabolic lean tissue. With control, nutritional support can maintain host defenses, preserve lean body mass, improve patient outcome, and, if administered early via the GI tract, reduce infections. Aggressive nutrition support in critically injured patients is an invasive form of therapy with risks and benefits that cannot be approached casually. In elective surgical patients undergoing general surgical procedures, the risks of therapy can, in some circumstances, outweigh benefits.11 However, in patients who are malnourished or at risk of becoming so, the benefits outweigh the risks if nutritional support is carefully instituted and monitored. There are significant clinical data demonstrating that after gaining hemodynamic stability, severely injured patients who are fed early via the GI tract have a reduced risk of septic complications and, in some circumstances, MODS.12–17 The availability of effective tools to quantitate the magnitude of injury and likelihood of subsequent septic complication allows surgeons to identify patients for whom enteral access is warranted at the time of initial celiotomy. Not all patients can be fed enterally, particularly if enteral access is not obtained at the initial laparotomy. In these situations, intravenous nutrition should be instituted on the fifth day, since there is no evidence that early intravenous nutrition significantly improves clinical outcome. However, when it is clear that the GI tract is not functioning or will not function, PN is indicated.

ENTERAL VERSUS PARENTERAL FEEDING: THE CLINICAL ARGUMENT The preponderance of evidence demonstrates benefits with enteral feeding and the elective use of PN early after trauma is associated with increased infections.38 The most compelling data exist in randomized, prospective clinical studies12–18 of victims of blunt and/or penetrating trauma. After the first clinical data of improved outcome with enteral feeding shown in pediatric burn patients,19 subsequent trauma studies compared various enteral products with either no feeding or intravenous feeding. Most showed reductions in intra-abdominal abscess and pneumonia in the enterally fed group. Moore et al. randomized patients with an abdominal trauma index (ATI) between 15 and 40 to early feeding with a defined-formula diet or no early feeding and showed a 3-fold reduction in sepsis (primarily intra-abdominal abscess) with enteral feeding.13 Subsequently, they showed that enteral feeding significantly reduced pneumonia compared with PN14 consistent with

Nutritional Support and Electrolyte Management

DETERMINING INDICATORS FOR ENTERAL (POSTPYLORIC) ACCESS DURING CELIOTOMY FOR TRAUMA The ATI (Table 60-2) can be rapidly tabulated at the operating table to determine the need for direct small bowel access.24 Patients with an ATI 25 appear to benefit from early enteral nutrition once they are hemodynamically stable. Patients with insignificant intra-abdominal injuries will benefit from early feeding if they sustain significant extra-abdominal injuries such as a severe pulmonary contusion; multiple rib fractures; a closed head injury with a Glasgow Coma Scale (GCS) score 8; a spinal injury; a major soft tissue injury requiring repeated irrigation, debridement, and skin grafts; or multiple extremity fractures necessitating later surgery. In addition, patients with multiple chronic diseases or patients who will require prolonged ventilator support or have delayed resumption of oral intake are appropriate candidates. Most patients with these criteria have an ISS 20 and benefit from the early enteral feeding (Fig. 60-1). Severe intra-abdominal injuries to the colon, pancreas, liver, or duodenum increase the risk of septic complications, but enteral access is usually unnecessary with relatively minor, isolated injuries to these organs.

■ Patients with Closed Head Injury There is little evidence that early nutrition affects outcome after severe head injuries. We wait until GI tract function returns and gastroparesis resolves (generally within 3 days) before instituting intragastric feeding. Prolonged gastroparesis (6 days) unresponsive to gastric motility agents requires that a tube be advanced into the distal duodenum and ideally beyond the ligament of Treitz. Intravenous nutrition should start if this is not possible. This approach stems from a critical review of the head injury studies. Rapp et al.25 randomized 38 patients to PN or delayed enteral feeding (1 week) once gastroparesis resolved. Initial work suggested improved GCS score at 3 months with early PN but no difference after this point. This result was not confirmed in a follow-up study.26 Grahm et al.27 randomized headinjured patients to enteral feeding via nasojejunal tube placed fluoroscopically within 36 hours of injury or via a gastrostomy tube once gastric atony resolved, usually within 5 days. Fewer bacterial infections and fewer ICU days occurred after early enteral feeding. However, bronchitis was the major diagnostic category separating the groups, rather than established infections such as pneumonia or abscess. Borzotta et al.28 randomized patients with severe head injuries to early enteral feeding via nasojejunal tube or delayed enteral feeding and demonstrated no reduction in infections and a slight, perhaps clinically insignificant improvement in neurologic outcome with early feeding. A Memphis study29 found no difference between an early placement of a tube beyond the ligament of Treitz and intragastric feeding, with no improvement in GCS or infectious complications. The failure of enteral nutrition to reduce infections in headinjured patients appears contradictory to multiple trauma results, but the groups differ significantly. Prolonged intubation and pneumonia may be unavoidable after severe closed head injury, since patients with such injuries often remain intubated for weeks, while many multiple trauma patients require support only for several days.

■ Burn Patients Early enteral feeding in burn patients is well established. Alexander et al.19 randomized severely burned children to either a standard enteral diet or a protein-supplemented diet. Patients receiving the high-protein diet had a higher survival rate and a lower sepsis rate but received significantly less PN than control patients. Herndon et al.30 randomized 39 patients with 50% or greater total body burn to early IV or enteral feeding and measured significant decreases in natural killer cell activity and the T-helper/suppressor ratio with PN. Since higher survival rates occurred with enteral feedings, they concluded that PN should be used only with total enteral failure. Intragastric feeding should be started within 12 hours of burn, since this approach reduces gastroparesis. Gastroparesis occurs in 45% of patients with intragastric feeding delayed for 18 hours, but it occurs in less than 5% of patients if feeding is instituted within 8 hours of burn. Laboratory evidence suggests a blunting of the hypermetabolic response after burn by reducing levels of cortisol and catecholamines.

CHAPTER CHAPTER 60 X

prior20 work showing a lower septic rate in patients receiving most of their nutrition enterally. The Memphis group showed that enteral feeding significantly reduced pneumonia (11.8% vs. PN 31%), intraabdominal abscess (1.9% vs. PN 13.3%), and line sepsis (1.9% vs. PN 13.3%).12 Severity of injury influenced the results since the reduced infection rate occurred in patients with an Injury Severity Score (ISS) 20 and an ATI 24 or both, where PN increased infectious rates by 6.3, 7.3, or 11 times, respectively. A few studies produced conflicting data. One group found similar rates of infection in trauma patients receiving intravenous feeding or enteral nutrition with no difference in pneumonia or intra-abdominal infection.21 However, there were nearly twice as many head injuries, three times as many severe thoracic injuries, and three times as many pelvic fractures in the enterally fed patients. The increased incidence of severe chest injuries in the enteral group made the diagnosis of pneumonia suspect, since pneumonia was diagnosed using the standard criteria of fever, leukocytosis, and a new or changing infiltrate on chest x-ray, which overdiagnoses pneumonia in more than two thirds of cases.22 Another study randomized blunt trauma patients requiring intensive care unit (ICU) care to either early (24 hours) or late (72 hours) enteral feeding.23 Total infectious complications—ranging from pneumonia to an eye infection—were significantly greater in the early fed group but there was a very high dropout rate, and the early fed patients had more severe pulmonary injury, as measured by the PaO2/FiO2 ratio. Eleven of 19 patients in the early group had a PaO2/FiO2 ratio 150, while only 4 of 19 patients in the late group had severe pulmonary dysfunction. Pneumonia occurred twice as often in the early fed patients, but results were confounded by the increased chest trauma.

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Management of Complications after Trauma

TABLE 60-2 Calculated Risk of Sepsis by the Abdominal Trauma Index

SECTION 5 X

Organ Injured High risk Pancreas

Risk Factor

Large intestine

(5)

Major vascular

(5)

(5)

Moderately high risk Duodenum (4)

Scoring 1. Tangential 2. Through-and-through (duct intact) 3. Major debridement or distal duct injury 4. Proximal duct injury 5. Pancreaticoduodenectomy 1. Serosal 2. Single wall 3. 25% wall 4.  25% wall 5. Colon wall and blood supply 1. 25% wall 2. 25% wall 3. Complete transection 4. Interposition grafting or bypass 5. Ligation 1. 2. 3. 4.

Single wall

25% wall 5% wall Duodenal wall and blood supply 5. Pancreaticoduodenectomy 1. Nonbleeding peripheral 2. Bleeding, central, or minor debridement 3. Major debridement or hepatic artery ligation 4. Lobectomy 5. Lobectomy with caval repair or extensive bilobar debridement

Liver

(4)

Moderate risk Stomach

(3)

1. 2. 3. 4. 5.

Spleen

(3)

1. Nonbleeding

Single wall Through-and-through Minor debridement Wedge resection 35% resection

2. Cautery or hemostatic agent 3. Minor debridement or suturing 4. Partial resection 5. Splenectomy

Organ Injured Low risk Kidney

Risk Factor (2)

1. Nonbleeding 2. Minor debridement or suturing 3. Major debridement 4. Pedicle or major calyceal 5. Nephrectomy

Ureter

(2)

Bladder

(1)

1. 2. 3. 4. 5. 1. 2. 3. 4. 5.

Contusion Laceration Minor debridement Segmental resection Reconstruction Single wall Through-and-through Debridement Wedge resection Reconstruction

Extrahepatic biliary

(1)

1. 2. 3. 4. 5.

Contusion Cholecystectomy

25% wall 25% wall Biliary enteric reconstruction

Bone

(1)

1. 2. 3. 4. 5.

Periosteum Cortex Through-and-through Intra-articular Major bone loss

Small bowel

(1)

1. 2. 3. 4. 5.

Minor vascular

(1)

Scoring

Single wall Through-and-through

25% wall 25% wall Wall and blood supply or 5 injuries 1. Nonbleeding small hematoma 2. Nonbleeding large hematoma 3. Suturing 4. Ligation of isolated vessels 5. Ligation of named vessels

Source: Adapted with permission from Moore EE, Dunn EL, Moore JB, et al. Penetrating abdominal trauma index. J Trauma. 1981;21:440; Data from Borlase BC, Moore EE, Moore FA. The abdominal trauma index—a critical reassessment and validation. J Trauma. 1990;30:1341, with permission, from Lippincott Williams & Wilkins.

Post-ligament-of-Treitz access (at final exploration if multiple surgeries required 2° to packing, etc.)

ATI ≥25

Contraindication to enteral nutrition (rare)

Celiotomy

Hemodynamic stability (1) No pressor agents (excluding renotonic Dopamine) (2) Stabilization of fluid requirements (3) Evidence of adequate perfusion (a) Base deficit clearing and near normal (b) Adequate urine output (unless renal failure) (c) Warm extremities

TPN

Start immune-enhancing diet: Advance as tolerated to 0.32–0.38 gm/kg per day

Improving with ↓ risk of septic complications

TPN

Convert diet Severe trauma

ATI <25 but: (1) Spinal cord injury (2) CHI (GCS ≤ 8) (3) Injuries requiring return trips to operating room (ortho, soft tissue, facial, etc.) (4) Flail chest (5) Severe pulmonary contusion (6) Chronic diseases (7) Elderly

Early (<12 h) intragastric feeding

No celiotomy

Advance as tolerated to 2.0–2.5 g protein/kg per day and consider immune-enhancing diet

Gastroparesis CHI with or without multiple trauma

Initial NG tube

Day 4

Start diet with cal/nit ratio of 80:1 to 120:1 with or without fiber

Post-ligament of Treitz access <250 cc q 8° drainage

Replace NG with small-bore tube

Diet w/ or w/o fiber cal/nit ratio 80 to 120:1

>250 cc q 8° Clamp tube check residuals ATI = Abdominal Trauma Index ISS = Injury Severity Score

CHI = Head injury GCS = Glasgow Coma Scale Score

>250 cc

Post-ligament of Treitz access

Failure by day 6

TPN

Motility agents

FIGURE 60-1 Protocol for nutrition support at the University of Wisconsin-Madison and the Elvis Presley Trauma Center at the University of Tennessee, Memphis.

Nutritional Support and Electrolyte Management

Severe Burns (>15–20% BSA)

Post-ligament of Treitz access

Failure to tolerate 50–75% of goal by day 7

1105

CHAPTER CHAPTER 60 X

1106

Management of Complications after Trauma

INFLUENCE OF THE TYPE OF ENTERAL FEEDING ON INFECTIOUS COMPLICATIONS SECTION 5 X

■ Specialty “Immune-Enhancing” Diets The concept that some nutrients became “conditionally essential” during stress and sepsis (e.g., GLN) or that other substrates such as omega-6 fatty acids could potentially aggravate inflammation through production of proinflammatory products led to the creation of a family of immune-enhancing diets (IEDs). These IEDs contain various combinations of GLN, arginine, omega-3 fatty aids, beta-carotene, and nucleotides. Liquid diets cannot be supplemented with GLN as a free amino acid because of its propensity to degrade into the toxic products pyroglutamate and ammonia after heat sterilization. Free GLN is found only in dry, powdered diets, which require reformulation prior to administration. These diets can be administered via transgastric jejunostomies (TGJs), large-bore (12–18 Fr) jejunostomies, and 7-Fr needle catheter jejunostomies (NCJs), but they tend to clog 5-Fr NCJs. The rationale for these specific nutrient supplementations has been partly discussed above. Although skeletal muscle production of GLN increases during stress and sepsis, serum and intracellular levels decrease. GLN is a substrate for various immunologic cells and for enterocytes in the unfed state.6 Arginine promotes proliferating T cells after mitogen or cytokine stimulation in vitro and increases natural killer cell cytotoxicity, specific cytolytic T-cell activity, and macrophage tumor cytotoxicity. It also exerts a positive effect on wound healing; stimulates pituitary GH, prolactin, insulin, and IGF-I, and acts as a precursor for nitric oxide, nitrites, and nitrates as well as the growth substances putrescine, spermine, and spermidine, which may be involved in GI tract integrity. Omega-3 PUFAs from fish or canola oil can replace omega-6 PUFAs, such as linoleic acid, found mainly in vegetable oils. Omega-6 fatty acids inhibit killer cell activity, antibody formation, and cell-mediated immune response due to the inhibitory nature of their metabolic end products.10 Animal studies have shown that omega-3 supplementation reduces mortality after burn injury, reduces bacterial translocation compared with other lipids, promotes cell-mediated immunity, increases resistance to infection, reduces inflammation, and reduces mortality following bacterial peritonitis. The administration of RNA via nucleotides improves survival to a septic challenge with Candida albicans, and malnourished animals provided RNA during refeeding from a malnourished state had more rapid improvement in immune function.31 Nucleotide deprivation suppresses helper T-cell and interleukin-2 (IL-2) production, largely due to uracil, since adenine does not prevent this immunosuppression. Clinically, various combinations of these nutrients have been made available in specialty nutrient diets. The majority of clinical studies carried out in critically ill patients, general surgical patient populations, trauma patients, and burn patients suggest an additional benefit with the IEDs over unsupplemented diets.16,17,32,33 Gottschlich et al.34 randomized 50 pediatric and adult patients with burns over 10–89% of their body surface area to diets including a modular feeding supplemented with arginine,

cysteine, histidine, and omega-3 fatty acids. A significant reduction in wound infection, length of stay per percent body burn, and total number of infectious complications occurred in this group, with a trend (P  .06) toward reduced pneumonia. More inhalation injuries in the control group as well as more fat and less carbohydrates in the control formula were confounding variables. Patients with an ATI between 18 and 40 randomized to an IED or a chemically defined diet generated significant increases in total lymphocyte count and T-lymphocyte and T-helper cell numbers as well as fewer intra-abdominal abscesses and less multiple organ failure with the supplemented diet.17 Since a higher nitrogen content in the IED was a confounding variable, a subsequent study randomized patients with an ATI 25 or an ISS 20 to an IED or an isonitrogenous, isocaloric diet.16 Unfed cohorts, eligible for the trial entry but without enteral access, were also prospectively followed. The IED resulted in fewer major septic complications, fewer therapeutic antibiotics, and a shorter hospital stay than in the unfed group or those receiving the control diet. The incidence of intra-abdominal abscess, pneumonia, bacteremia, major wound infections, or any major complication was highest in the unfed population. Complications and antibiotic use with the control diet were between the unfed and IED groups. Administration of a GLNsupplemented enteral diet has also been shown to reduce pneumonia, bacteremia, and sepsis.35 Potential negative effects may also occur with these diets. One study noted an increase in respiratory failure with an IED.36 An increased incidence of respiratory failure in the treatment group at baseline limited the ability to implicate the diet, however. We institute an IED in patients with an ATI 25 or an ISS 20 (Fig. 60-1) and convert to a standard high-protein enteral diet once the patients are less vulnerable to septic complications, usually within 7–10 days. Patients with less severe injuries receive a high-protein diet.

POSSIBLE DELETERIOUS EFFECTS OF IMMUNONUTRITION IN THE CRITICALLY ILL Recently published Canadian practice guidelines for nutrition support in mechanically ventilated critically ill patients recommended that arginine-containing diets (oral immunonutrition that contains arginine supplementation) should not be used in critically ill ICU patients.37 The conclusion was reached despite significantly reduced hospital stays and trends toward reduced ventilator days and ICU days noted with these diets in trials. This meta-analysis based these recommendations on three studies. One trial of trauma, surgical, and medical ICU patients randomized patients to a diet enriched in arginine, omega-3 fatty acids, and nucleotides.33 Patients tolerating more than 821 mL per day benefited clinically in a post hoc analysis, but septic patients randomized to the arginine-containing diet had increased mortality, although overall mortality was not affected. A second randomized but unpublished prospective study conducted in 1996 randomized critically ill patients to a specialized diet containing moderate amounts of arginine and omega-3 fatty acids. Mortality increased with this supplemented diet in

Nutritional Support and Electrolyte Management

POTENTIAL REASONS FOR IMPROVED OUTCOME WITH ENTERAL FEEDING The unfed GI tract has altered function and architecture. Decreases in villus height occur in unfed human patients, but to a lesser extent than in rat models of starvation or intravenous feeding, where 40–50% of villus height is lost in the proximal intestine. Changes occur quickly in the GI tract following shock and stress, with rapid decreases in enzymes and motility and temporary increases in permeability. The reduced motility (i.e., ileus) occurs in the stomach and colon, allowing absorption of nutrients delivered into the small intestine. Shock, trauma, and sepsis increase gut permeability, which increases bacterial translocation to mesenteric lymph nodes in animal models and under certain clinical conditions, such as bowel obstruction, inflammatory bowel disease, and shock. This does not appear to be clinically relevant following trauma.43 Increased permeability in trauma patients is unrelated to the magnitude of trauma but does correlate with the IL-6 and acute-phase protein response of severely injured patients. The level of permeability returns to baseline within a week. The well-fed intestine is a metabolically and immunologically active organ that passively and actively maintains a bacterial barrier through peristalsis, IgA, mucin, and mucosal cell integrity. Experimentally, these systems fail in starvation, shock, and sepsis. Approximately 75% of the body’s immunoglobulinproducing cells line the GI and respiratory tracts to produce 70–80% of the immunoglobulin as secretory IgA (SIgA), which is transported across the mucosa.44 The GALT is affected by PN, producing decreases in GALT mass and reductions in intestinal and respiratory IgA. Normally, the IgA coating the surface of the epithelium binds and neutralizes viruses, bacteria, and other pathogenic antigens by trapping them in the mucin layer. As a result, these infective agents cannot attach to the mucosa, a prerequisite to invasive infection. Experimentally, PN-fed animals lose established antibacterial and antiviral

immunity.44 Under conditions of stress, ischemia, and injury, Alverdy and Chang demonstrated that intraluminal bacteria respond to this hostile environment by upregulation of virulence genes and expressing adhesins that render them more virulent in vivo.45 Intraperitoneal protection can also be explained by similar mechanisms. Enteral feeding significantly improves the survival of malnourished or well-nourished animals with septic peritonitis by increasing intraperitoneal tumor necrosis factor (TNF) response, resulting in a lower systemic cytokine response and bacteremia compared with animals fed intravenously. A differential cytokine response has also been confirmed in patients. Normal volunteers administered PN demonstrate an increase in production of TNF compared with enterally fed patients following intravenous injection of endotoxin.46 Since TNF has been considered one of the precipitating stimuli for the subsequent proinflammatory cytokine response, this may be clinically relevant. Exposure of the systemic circulation to bacterial products has been postulated to be a driving force in the development of MODS.47 Enteral stimulation maintains a normal gut cytokine response with high levels of IL-4 and IL-10.44 These cytokines upregulate IgA production from mucosal protection and downregulate adhesion molecule expression on the vascular endothelium. Parenteral feeding reduces these cytokines, leading to an upregulation of vascular adhesion molecules and accumulation of neutrophils within the intestine and priming of these neutrophils to subsequent ischemic events.82 Ischemic events within the gut have been previously related to neutrophil priming as an initial step in MODS development.48 These experimental data are consistent with the reduction in MODS in trauma patients fed enterally.17

THE NUTRIENT PRESCRIPTION: ISSUES COMMON TO ENTERAL OR PARENTERAL FEEDING There are a number of issues common to both enteral and parenteral feedings related to the amount and type of nutrition administered to trauma patients. In the past, calculation of nutrient needs used standard equations, such as the Harris– Benedict equation, multiplied by correction factors. Indirect calorimetry has shown that these correction factors for stress and activity tend to overestimate nutrient needs. Overfeeding leads to increased oxygen consumption, increased CO2 production, hepatic lipogenesis, potential immune suppression secondary to hyperglycemia, and other negative effects without reducing weight loss or lean tissue catabolism.

ESTIMATING NUTRITIONAL NEEDS The most common calculation used to determine basal energy expenditure (BEE) is the Harris–Benedict formula, defined as follows: For males: BEE  66 (13.8  W ) (5  H)  (6.8  A), For females: BEE  665 (9.6  W ) (1.8  H )  (4.7  A), where W is the weight in kilograms, H is the height in centimeters, and A is the age in years. These calculated values

CHAPTER CHAPTER 60 X

elderly male patients admitted with sepsis and pneumonia. However, significantly more patients with pneumonia were randomized to the specialty diet due to a randomization breakdown. Most patients who died either received less than 3 days of feeding or did not receive the specialty diet long after completion of the study period. A third study38 randomized septic patients requiring more than 4 days of nutrition support and a “higher level of care” to PN or an omega-3 fatty acid/argininesupplemented enteral diet. Increased mortality occurred in this group but most deaths occurred in patients septic with pneumonia similar to unpublished trial noted above. Although there are significant reservations regarding the design and implementation of these three trials, septic patients— particularly if septic with pneumonia—may have a poorer outcome with immunonutrition for unknown reasons, although increased nitric oxide production during sepsis, but not stress, has been proposed.39 Two trials noted no increase in mortality with sepsis using similar diets.40,41 With the clinical evidence of improvement in trauma patients, there is no evidence to suggest this population has increased risks with administration of these specialty diets and guidelines have recommended their use.42

1107

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Management of Complications after Trauma ↑ CO2 production CHO >4–5 mg/(kg min)

SECTION 5 X

Serum glucose >220 mg/dL

↑ Ventilation demands

Delayed weaning

↑ Insulin

↓ Serum K+, PO4−3

↓ White blood cell function if prolonged

Exceed energy needs

FAT >1–1.5 g/kg per day

Fat deposition in liver

Cholestasis ↑ SGOT ↑ SGPT ↑ Alk. Phos.

Hyperlipidemia Reticuloendothelial blockade

PROTEIN >1.5–2 g/kg per day

↑ BUN to 70 or greater if renal function impaired

FIGURE 60-2 Complications of overfeeding. (Reproduced with permission from Frankel WL, Evans NJ, Rombeau JL. Scientific rationale and clinical application of parenteral nutrition in critically ill patients. In: Rombeau JL, Caldwell MD, eds. Clinical Nutrition. Vol. 2. Parenteral Nutrition. 2nd ed. Philadelphia: Saunders; 1993:597, © Elsevier.)

have been increased by a stress factor (ranging from 1.25 to 2) and an activity factor to account for the increases in metabolic rate by injury and stress. Indirect calorimetry measures metabolic needs using expired gas analysis to determine overall resting energy expenditure (REE). Carbon dioxide production (VCO2) and oxygen consumption (VO2) are used to calculate the RQ. When VO2 and VCO2 are applied to the Weir equation, REE can be determined. There is an RQ characteristic for each fuel utilized: for example, fat is 0.7, glucose is 1.0, and protein is 0.8. Since fat deposition with overfeeding has an RQ value of approximately 8, an RQ value greater than 1.0 generally means that lipogenesis and overfeeding are occurring. In studies of patients in surgical ICUs, metabolic cart measurements were generally within 5–10% of the energy requirements calculated by the Harris– Benedict equation; addition of stress factors led to unnecessary administration of nutrients.49 There are drawbacks to indirect calorimetry. Since VO2 is an integral part of the measurement, there is loss of accuracy as the FiO2 increases because of the errors between the inspired and expired oxygen consumptions. With an FiO2 of 0.8, a 1% error in measurement of the inspired or expired VO2 leads to 100% error in VO2 calculation. Since air leaks are interpreted as increases in oxygen consumption, critically ill patients requiring a high FiO2 and high positive end-expiratory pressure are most likely to have inaccurate measurements. In addition, these calculations are labor-intensive and results are most reliable when protocols defined by trained technicians are used. Indirect calorimetry measurements only reflect caloric needs over a 20- to 30-minute period. When the patients are turned, suctioned, or receiving physical therapy, those measurements may not represent total energy expenditure. For these reasons, many practitioners increase the REE by 10–15% to calculate

total energy expenditure. Because of the expenses necessary to avoid the pitfalls of indirect calorimetry, its routine use is not recommended. However, data obtained from sites proficient in the technique have provided valuable guidelines to avoid overfeeding, especially in cases of obesity, amputation, or quadriplegia, where traditional calculations are not reliable. Current recommendations for caloric support range between 25 and 30 total kcal/kg per day. While some studies have recommended other values, if 30 kcal/kg is provided, 90% of patients will reach their energy requirement with overfeeding in approximately 15–20% of patients.49 To avoid complications of overfeeding (Fig. 60-2), we administer approximately 25–30 total kcal/kg per day to multiply injured patients initially and decrease this to 22–25 kcal/kg as they improve clinically, with diuresis, ventilator weaning, and discontinuation of antibiotics. Presumed body weight is obtained from family members or the patient, when possible, to avoid overfeeding based on weights increased by edema. As diuresis occurs, weight is rechecked with appropriate adjustments in total caloric load. In general, we withhold nutrition in patients requiring high rates of catecholamine infusion, since there is no evidence that administered glucose or protein (or amino acids) slows lean body tissue mobilization or the rate of gluconeogenesis. Stress induces an increase in both glucose utilization and gluconeogenesis with significant recycling of glucose from lactate (the Cori cycle) and alanine. Lactic acid is produced in the periphery when pyruvate cannot enter the Krebs cycle. As NADPH is converted to NADP, hydrogen ion is transferred to pyruvate creating lactate, which is then released, transported back to the liver, and converted to glucose. Alanine is formed by transamination of pyruvate during BCAA metabolism in skeletal muscle and released for conversion back to pyruvate and glucose by the liver. Hyperglycemia occurs as hepatic

Nutritional Support and Electrolyte Management

ENERGY REQUIREMENTS AND FEEDING RECOMMENDATIONS IN THE MORBIDLY OBESE Morbid obesity is becoming more and more prevalent in the trauma and surgical ICUs. The World Health Organization now classifies obese patients into three categories: Obese Class I are patients with BMIs of 30–34.9, Obese Class II are patients with BMIs of 35–39.9, and Obese Class III are patients with BMIs 40. Current feeding recommendations for morbidly obese trauma or surgical ICU patients are for Class I or Class II obesity, 22 total kcal/kg ideal body weight and 2 g of protein/kg ideal body weight. For patients who are in the Obese Class III category, recommendations are for slightly higher calories of 22–25 total kcal/kg of ideal body weight and 2–2.5 g protein/kg of body weight.51 This is based on observations that nitrogen retention increases as caloric intake increases until caloric intake approaches 50–60% of total energy expenditure. Additional energy further improves nitrogen retention but less efficiently. Although weight loss occurs, this is primarily due to fat loss. In a 2-week study of enteral feeding52 this population received 1.5–1.9 g/kg ideal body weight per day of protein with either 19 kcal/kg actual body weight per day (30 total kcal/kg ideal body weight per day) or 11 total kcal/kg actual body weight per day (hypocaloric group: 22 total kcal/kg ideal body weight per day). Prealbumin increases were similar in the two groups. Both had negative nitrogen balance due to catabolism, but the hypocaloric group had a shorter ICU stay, fewer antibiotic days, and a trend toward reduced ventilator days (P  .09). Hypocaloric, parenteral high-protein feeding of postoperative obese patients with 2.1 g of protein and 20 total/kcal ideal body weight resulted in 1.7 kg per week of weight loss, net protein anabolism (improved serum protein concentration and positive nitrogen balance), and successful wound healing.53 Two other randomized double-blind studies of obese patients compared hypocaloric feeding with higher-calorie regimens. In the first, both groups received 2 g/kg ideal body weight per day but calories were administered at 100% or 50% of the measured

energy expenditure.54 Nitrogen balances were similar. In the second, hypocaloric or higher-calorie parenteral regimens (14  3 total kcal/kg actual weight per day vs. 22  5 total kcal/kg actual weight per day) were given for up to 14 days with both groups receiving 2 g/kg ideal body weight of protein. Nitrogen balances were similar, but glucose control was improved and less exogenous insulin was necessary with the hypocaloric regimen.55

FAT REQUIREMENTS Free fatty acids are the primary energy source utilized during stress and sepsis. Lipolysis and mobilization of free fatty acids is enhanced by beta-adrenergic stimulation of lipases and hormone-sensitive tissues as fatty acid oxidation increases. The administration of glucose as calculated above can provide approximately 50–60% of total caloric requirements; the balance of nonprotein calories (NCPs; 20–30% of total calories) can be met by fat at a dose of 1 g/kg per day. Infusion rate for lipids should not exceed 0.11 g/kg/hr. In patients in whom ventilator weaning is an important issue, administration of fat as total calories up to 50% may be beneficial in selected patients. Increased CO2 production is rarely a cause of weaning problems in trauma patients except, perhaps, in geriatric patients following flail chest injuries or those with prolonged recovery. Trauma patients with moderate to severe chronic obstructive pulmonary disease (COPD) who have trouble weaning from the ventilator may benefit from a diet higher in fat. If overfeeding is suspected, reduction in total calories administered is the most appropriate intervention. Higher doses of fat may also be useful in hyperglycemic patients as a result of diabetes or corticosteroid administration. This may cause hyperlipidemia, cholestasis, increased risk of infection, and perhaps immunosuppression. All lipid emulsions available in the United States are vegetable oils, which provide mainly omega-6 long-chain PUFAs; these may increase production of immunosuppressive prostaglandins and leukotrienes. Currently, structured lipids containing both omega-6 and medium-chain triglycerides as their primary fatty acid side chains are being tested as are intravenous fats with omega-3 fatty acids. Additional immunosuppression may come from blockade of the reticuloendothelial system by lipid particles. Omega-3 fatty acids from canola or fish oil are found in most enteral products; these can be metabolized to the less immunosuppressive 3 or 5 series of prostaglandins. Omega-3 PUFAs may increase the production of lipid peroxidases and inhibit platelet aggregation, but these concerns have not appeared to be of clinical significance. Several investigators have determined the maximum hydrolysis rate for intravenous lipids by LPL in normal adults to be approximately 0.12 g/kg/hr (2.9 g/kg per day); above this infusion rate emulsion triglyceride particles begin to accumulate. Intravenous lipid emulsion in the critically ill adult below this infusion rate is recommended in order to avoid elevated triglyceride concentrations and other metabolic complications. Doses of intravenous lipids should be limited to the provision of essential fatty acids (e.g., 250 mL of 20% lipid emulsion

CHAPTER CHAPTER 60 X

gluconeogenesis increases from 2.0 to 2.5 mg/(kg min) under the normal condition to 4–5 mg/(kg min) in the stressed or septic patient. Given these conditions, high levels of infused glucose aggravate hyperglycemia causing glucosuria, hepatic fatty deposition, increased CO2 production (rarely a significant clinical problem in young trauma victims), and potentially an increased infection rate. Since the maximal rate of glucose oxidation is 5 mg/(kg min) or approximately 7.2 g/kg per day, cumulative glucose administration including enteral and parenteral products as well as intravenous fluids should not exceed these levels. In a 70-kg adult, this is 500 g of glucose at maximum, which is almost completely met by 2 L of a 25% dextrose PN solution. Ideally, blood sugars should be maintained below 180 mg/dL. With insulin, it is usually possible to keep blood sugars below 180 mg/dL except in trauma patients with insulin-dependent diabetes mellitus or those with steroid or high catecholamine needs.50

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SECTION 5 X

once or twice weekly) when triglyceride concentrations rise above 400 mg/dL. Withholding intravenous lipids must be considered when triglyceride concentrations are greater than 500 mg/dL or in the presence of lipemic serum.

PROTEIN REQUIREMENTS Skeletal muscle loses considerable mass as amino acids are redistributed for healing wounds, acute-phase proteins, and substrate for lymphoid tissue and the GI tract. Overall, nitrogen is lost through ureagenesis by the liver and ammonia synthesis by the kidney. Immobilization aggravates the loss. Total protein catabolism exceeds synthesis, which leads to loss of function and potential morbidity and mortality. Unfortunately, this hypercatabolism and lean tissue loss is not blunted by the administration of exogenous calories or amino acids. In general, the recommended dose of amino acid protein for stressed or septic patients without renal dysfunction is 1.5–2 g/kg per day. Although blood urea nitrogen (BUN) may increase to approximately 40 mg/dL, these levels cause no metabolic complications and BUN generally stabilizes at that level. If urea levels climb to greater than 100 mg/dL, protein administration must be reduced. If creatinine levels are low, that is, no evidence of acute renal failure (ARF), and elevated BUN appears due to excessive protein (or amino acid) administration, protein should be decreased to 1.3–1.5 g/kg per day. As the stress phase resolves, 1–1.5 g/kg per day of protein meets nutrient requirements in most patients. In burn patients, administration of 2–2.5 g/kg per day is desirable due to excessive urinary losses and the inability to accurately assess wound losses of nitrogen. Patients who develop ARF secondary to injury/hypotension still require high doses of protein for wound repair; however, it is practical to provide only 0.8–1.0 g/kg per day of protein until a decision on initiation of dialysis is made. Once dialysis has been initiated, the type and frequency will dictate how much the protein dose can be liberalized. Generally, 1.2–1.5 g/kg per day can be administered to a patient receiving hemodialysis three times a week (assuming that the hemodialysis is effective). Patients who cannot tolerate hemodialysis secondary to hypotension may receive continuous arterial venous hemodialysis (CAVHD) or continuous venovenous hemodialysis (CVVHD). These methods of dialysis provide the critical care practitioner volume to administer PN with nonconcentrated formulas, and protein can usually be administered as high as 2.5 g/kg per day if indicated.

THE FORMULA ■ Calorie-to-Nitrogen Ratio Caloric density for nutrients is as follows: 1 g protein equals 4 kcal, 1 g of hydrated glucose equals 3.4 kcal, and 1 g of fat (as an enteral form) equals 9.1 kcal, but 1 g of lipid emulsion contains 10 kcal/g because of glycerol contained within the emulsion. In patients who are not critically ill or septic but at risk of developing starvation-induced malnutrition if not fed

(e.g., small bowel obstruction, prolonged intestinal paresis, multiple small bowel fistulas), a calorie:nitrogen ratio between 130:1 and 160:1 is appropriate, and protein should be administered at a dose of 1–1.5 g/kg per day. In patients who are stressed or septic, however, the calorie:nitrogen ratio should drop to 80:1 to 120:1. The goal in the stressed or septic patient is approximately 30 kcal/kg total with 1.5–2 g/kg per day of protein. In burn patients, protein is administered with approximately the same low calorie:nitrogen ratio, providing 35–40 kcal/kg per day total and 2–2.5 g/kg per day of protein. Refer to Figure 60-3 for sample calculations of a PN formulation involving a 70-kg trauma patient. Fat can be used to displace glucose calories and, in fact, should meet 20–30% of total calories. Figure 60-3 illustrates how intravenous fat would be incorporated into PN formulation for the 70-kg trauma patient used in the first example. The issues are much simpler with enteral formulas, since labels contain the calorie:nitrogen ratio, allowing clinicians to determine the appropriate patient population for use. Enteral products with a calorie:nitrogen ratio between approximately 130:1 and 170:1 should be used in nonstressed patients who are malnourished or at risk of becoming malnourished, while solutions with a calorie:nitrogen ratio of 80:1 to 110:1 should be used in stressed or septic patients. Particular care should be taken, however, with the IEDs, which, because of their supplemental GLN and/or arginine and/or BCAA, have a much lower calorie: nitrogen ratio, in the range of 55:1 to 60:1. Although this would seem to provide either too few total calories or too much nitrogen for the stressed patient, the additional benefits that are gained in severely injured trauma patients with these formulas would warrant their administration in select cases. In these situations, patients are usually provided 2–2.2 g/kg of protein or amino acid (0.32–0.35 g/kg per day of nitrogen), with NCPs of approximately 20 kcal. Using these formulations, BUN often rises to 50 mg/dL but rarely higher unless there is compromised renal function.

■ Acute Renal Failure (ARF) In some patients with climbing BUN and creatinine levels, it is unclear whether the changes are due to volume deficits or renal dysfunction. ARF can be confirmed by calculating the fractional excretion of sodium (FeNa) obtained from a urine specimen in the following equation:









UNa  V UNa  Pcr Ucr  V FeNa (%)  ______  ______  100  _______  100, PNa

Pcr

PNa  Ucr

where UNa is the urine sodium concentration, V is the urine volume, PNa is the plasma sodium concentration, Ucr is the urinary creatinine concentration, and Pcr is the serum creatinine concentration. A FeNa less than 1% reflects a reabsorption of sodium of more than 99%, suggesting an adequate renal response to hypovolemia, renal hypoperfusion, and other nontubular disorders. Damage to the renal tubules reduces the ability of the kidney to resorb sodium, and the FeNa is then usually 2–3% or greater. Calculation of the FeNa minimizes effects of inappropriate ADH, hypovolemia, or low-flow states such as congestive heart failure on variability in water and

Nutritional Support and Electrolyte Management

70 kg 3 5 mg/(kg min) 3 1440 min/day 1000 mg/g 5 504 g or ~500 g dextrose per day Using a 70% dextrose (D70W) stock solution for compounding: 70 g 100 mL

500 g

5

x

Solving for x yields approximately 714 mL of D70W Using a 10% amino acid (AA10) stock solution for compounding: 10 g 100 mL

105 g

5

x

Solving for x yields 1050 mL of AA10% Total kcal from regimen: 500 g 3 3.4 kcal/g 1 105 g 3 4 kcal/g 5 1700 1 420 5 2120 kcal Calculation of administration rate: 714 mL dextrose 1 1050 mL AA 5 1764 mL/day 1 50 mL for additives 5 1814 mL/day 1814 mL 24 h

5 75 mL/h for 2-in-1 solution

OR using final concentrations 30 mL/kg per day 3 70 kg 5 2100 mL/day to meet maintenance IV fluid requirements Dextrose calculation: 500 g 2100 mL

5

x 100 mL

Solving for x yields 23.8% or approximately 25% dextrose. Protein calculation: 105 g 2100 mL

5 50 g/L or AA5%

For 3-in-1 (dextrose, amino acid, lipid) formulation: Estimated kcal: 30 kcal/kg per day 3 70 kg 5 2100 kcal/day Lipid provision 5 20% total kcal 5 0.2 3 (2100–2450) 5 420–490 kcal/day Using a 20% lipid emulsion (which provides 2 kcal/mL): 420 kcal 2 kcal/mL

5 210 mL of 20% lipid emulsion

Solving for total grams of lipid:

20 g 100 mL

5

x 210 mL

Solving for x yields 42 g lipid emulsion Using final concentrations: 42 g 2100 mL

5 20 g/L or 2% lipid

FIGURE 60-3 Calculation of PN formulation.

sodium absorption not due to renal dysfunction. Because of associated injuries, the hormonal milieu, and immobilization, the rate of urea accumulation is increased in these patients, compared with those suffering from chronic renal disease. A convenient method to determine urea loads, the urea nitrogen appearance (UNA), can be calculated by the following equations: UNA (g per day)  urinary urea nitrogen (g per day) change in body urea nitrogen (g per day), Change in body urea nitrogen (g per day)  SUNf  BWf  0.8 (L/kg)  SUNi (g/L)  BWi (kg per day)  0.8 (L/kg), where i and f are the initial and final values for the period of measurement and SUN is the serum urea nitrogen in grams per liter. BW is body weight in kilograms, and although 0.6 is the usual number to estimate the fraction of body weight that is body water in health, following trauma, body water compartments are expanded and as much as 80% can be total body water. When dialysis is started: UNA (g per day)  urinary urea nitrogen (g per day) dialysis urea nitrogen (g per day) change in body urea nitrogen (g per day). In contrast, no benefit has been shown from protein restriction in ARF and prolonged delivery of such regimens may actually increase skeletal muscle protein breakdown. Before dialysis is started, patients should receive a normal dose of total calories and a protein dose ranging from 0.8 to 1 g/kg per day. Specialized, essential amino acid solutions have not been shown to be of benefit, and a standard mixture of amino acids can be used.56 Often both serum potassium and phosphate concentrations drop from abnormal or high normal ranges to normal ranges with the institution of PN; potassium, phosphorus, and magnesium should not be added to PN initially but supplemented as necessary over time. If the ARF is short lived, this therapy may avoid dialysis completely, particularly if the renal failure is nonoliguric. At approximately 90 mg/dL, urea exerts toxic effects on platelets. After hemodialysis is started, protein administration can be increased to 1.2–1.5 g/kg per day. Alternative renal replacement therapies such as continuous venovenous hemofiltration (CVVH), CVVHD, and continuous venovenous hemodiafiltration (CVVHDF) usually necessitate a higher protein intake (1.5–2.5 g/kg per day) due to considerable loss of amino acids with the dialysate. As the kidneys recover, 3–5 L of urine per day may be excreted, and urinary output should be replaced with appropriate fluids. With resolving ARF, urine has 70–80 mEq of sodium/L, and the most commonly used fluid for replacement is 0.45% saline. A urine sample should be sent for electrolyte analysis. As SUN drops to 60 mg/dL or less, urinary replacement can be stopped. The urea has little osmotic effect and renal function has usually recovered adequately. Higher levels of SUN (i.e., greater than 80 mg/dL) act as an osmotic drag and, without fluid replacement, cause hypovolemia and recurrence of oliguric renal failure.

CHAPTER CHAPTER 60 X

Example: 70-kg man sustaining severe multiple long-bone fractures Estimated kcal: 30 kcal/kg per day 3 70 kg 5 2100 kcal/day Protein: 1.5 g/kg per day 3 70 kg 5 105 g/day For 2-in-1 (dextrose/amino acid) formulation:

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Management of Complications after Trauma

PULMONARY FAILURE SECTION 5 X

Although considerable attention has been drawn to avoiding overfeeding of patients with pulmonary dysfunction, overfeeding and lipogenesis with increased CO2 production rarely poses clinically significant problems in trauma patients. Usually, multiple rib fractures, pulmonary contusion, pneumonia, closed head injury, or spinal cord injuries delay weaning. Selected patients, who have been chronically intubated but require a low rate of ventilator support, may benefit by increasing fat as a percentage of total calories. A typical example is a geriatric patient with multiple injuries and chest trauma who has been weaned to a rate of 2–4 over several weeks but cannot tolerate prolonged continuous positive airway pressure or tracheostomy collar. Usually GI function is normal and transitioning to a high-fat enteral formula providing 1 g/kg per day of protein and a calorie:nitrogen ratio of approximately 120:1 with 40–50% of the calories as of fat may help. Several trials support the use of an enteral feeding formula containing eicosapentaenoic acid (EPA), gamma-linolenic acid (GLA), and antioxidants for patients with acute respiratory distress syndrome (ARDS). Omega-3 fatty acids such as EPA have anti-inflammatory effects. GLA may also work to decrease inflammation, by suppressing the synthesis of leukotrienes and pushing the prostaglandin cascade toward less inflammatory compounds. Pacht et al. show that a diet enriched with EPA GLA and antioxidants decreases levels of inflammatory cytokines in the respiratory tract.57 Singer et al. enrolled ventilated patients with acute lung injury and randomized them to receive a standard enteral diet or one enriched with GLA, EPA, and antioxidants.58 The primary outcome measures were oxygenation and respiratory mechanics. Significant results include better oxygenation in the EPA GLA group on days 4 and 7, defined as higher PaO2/FiO2 ratios (day 4 values: 317.3  90.5 in the EPA GLA group vs. 214.3 56.4 in the standard diet group), P  .05. Length of ventilation, in hours, was significantly lower in the EPA GLA group, 160.4  15.2 versus 166.8  5.2 in the standard diet group, P  .03. It is questionable whether this statistical significance translates into clinical significance. Finally, Pontes-Arruda et al. compared a formula with EPA GLA and antioxidants with a standard diet in patients newly diagnosed with sepsis and septic shock requiring ventilator support.59 This trial shows a significant reduction in mortality rate, significant improvements in oxygen status, and more ventilator-free days when EPA GLA is used compared with a standard diet. The EPA GLA diet has promising results, but has not been trialed in large and varied populations of patients.

HEPATIC FAILURE Following trauma, the onset of hepatic failure with MODS carries a dismal prognosis. Very few nutritional manipulations influence outcome. Excessive protein restriction should be avoided. Intravenous amino acid solutions are better tolerated (e.g., 1–1.5 g/kg per day) than the enteral protein, and high levels of glucose should be avoided. The onset of hypoglycemia

with severe hepatic failure represents final stages of systemic failure. Although high branched-chain formulas specific for hepatic dysfunction are commercially available, the desperate clinical situation of severe hepatic failure usually does not warrant their usage. Unless some etiologic cause—such as sepsis, acalculous cholecystitis, or obstructive biliary pathology—can be identified and successfully treated, nutritional support probably has little bearing on the outcome from hepatic failure in trauma patients.

FLUID AND ELECTROLYTES In the first 48 hours, lactated Ringer’s solution is the principal fluid given in the ICU. Initial expansion of both intracellular and extracellular water occurs as part of the neuroendocrine response to injury. During the hypercatabolic phase, the intracellular water and associated electrolytes (in particular potassium, magnesium, and phosphorus) associated with catabolism of protein are released into the extracellular space. As the catabolic phase improves and cells regain the ability to respond to exogenous nutrients, intracellular electrolytes associated with cytosolic fluid expansion must also be replaced or cell growth does not occur and a “refeeding syndrome” develops, which severely depresses serum potassium, phosphate, and magnesium levels. Since many of these severely injured trauma patients are intubated, respiratory muscle weakness may not be noted, but hypokalemia can reduce the effectiveness or increase the toxicity of various cardiac medications. Severe problems rarely develop if electrolytes are closely monitored and can be treated quickly if they occur.

■ Sodium The most common electrolyte problems noted in trauma patients are derangements in sodium. While diabetes insipidus or inappropriate ADH may occur with head injuries, producing hypernatremia and hyponatremia (see Chapter 19), respectively, the most common cause for abnormalities in sodium levels is an excess in sodium administration, fluid restriction in closed head injury patients, or administration of large volumes of fluid containing low sodium. In the first case, prolonged use of normal saline or lactated Ringer’s as a maintenance fluid in association with other hidden sources of sodium administered through multiple antibiotics, H2 blockers, etc., in saline produces a gradual and progressive hypernatremia. Many antibiotics contain large amounts of sodium, and since specific admixtures for medications are rarely ordered, intravenous “piggybacks” can reach 2–2.5 L per day in some patients. If this is administered in normal saline, hypernatremia develops. Likewise, if medications are mixed in 5% dextrose and water, significant hyponatremia develops (probably the most common etiology of hyponatremia in our ICU). Assessment of volume status in concert with the low serum sodium concentration will usually identify the patient as hypovolemic, isovolemic, or hypervolemic. Hypovolemic patients usually respond to normal saline or lactated Ringer’s infusions. If losses of fluid are chronic and similar to serum

Nutritional Support and Electrolyte Management

■ Potassium Hypokalemia is very common after trauma, especially in patients with normal renal function who require aggressive resuscitation with crystalloid. Loss of GI fluids rich in hydrogen and chloride aggravates this hypokalemia. Patients with prolonged nasogastric suction will lose considerable HCl resulting in metabolic alkalosis and substantial renal wasting of potassium. Drug therapy with loop diuretics, amphotericin B,

antipseudomonal penicillins, and corticosteroids has been reported to aggravate renal wasting of potassium. Other drugs, such as inhaled beta-agonists (e.g., albuterol) and insulin, drive potassium into the cell also resulting in hypokalemia in some patients. All the above conditions will require additional potassium added to the nutrient solution above the standard of 30–40 mEq/L that is commonly used in PN or present in enteral formulas. Occasionally, up to 120 mEq of potassium/L must be added to nutrient solutions of patients who were receiving three or four of the above-mentioned drugs to keep them in potassium balance. Body potassium needs are not proportionate to serum levels. Each 0.25-mEq drop in serum potassium levels between 3.0 and 4.0 mEq/L represents a 25- to 50-mEq deficit in total body potassium. Between 2.5 and 3.0 mEq/L, each 0.25-mEq drop represents an additional 100- to 200-mEq deficit, which must be replaced to avoid precipitous drops with refeeding. Hyperkalemia is less common than hypokalemia after trauma, and is usually associated with compromise in renal function. In general, hyperkalemia from ARF warrants potassium removal from the nutrient solution. Once levels have decreased to 4.0 mEq/L, potassium should be added back in modest doses (e.g., 10 mEq/L). Other causes of hyperkalemia are hemolysis of the blood sample and drugs known to cause this disorder, even when renal function is normal. Most laboratories will identify hemolyzed samples that do not require treatment other than repeat analysis. Heparin and trimethoprim have been reported to cause hyperkalemia in patients. Heparin is an aldosterone antagonist that causes sodium wasting and potassium retention. This drug–nutrient interaction occurs with both systemic and low-dose heparin, especially in patients with diabetes and chronic renal dysfunction. Trimethoprim is a component of the combination product of trimethoprim/sulfamethoxazole used frequently for gram-negative systemic infections. It is a weak diuretic with potassium-sparing activities. Patients who experience these interactions should have potassium decreased in the nutrient solution, even when renal function is normal.

■ Phosphorus Hypophosphatemia is a common metabolic complication of critically ill patients receiving nutritional support. While most practitioners add phosphorus to PN solutions routinely, several patient populations require greater amounts, including patients with a history of alcohol abuse, poor nutritional status preinjury, or chronic use of antacids or sucralfate. Even when serum phosphorus concentrations are monitored closely, hypophosphatemia occurs in approximately 30% of patients receiving PN. Treatment of hypophosphatemia is dictated by the severity, and intravenous replacement doses are most frequently used. The enteral route should be considered in mild cases of hypophosphatemia by adding 5–10 mL of Fleet’s phosphosoda to each liter of the enteral formula in patients requiring additional phosphate. In patients requiring both potassium and phosphate, potassium phosphate (usually 15–22.5 mmol/L) can be added to the formula. For isolated potassium depression,

CHAPTER CHAPTER 60 X

(e.g., ileostomy losses), additional sodium may be needed in the nutrient solutions. Isovolemic, hyponatremic patients often need little treatment beyond increasing the sodium content in intravenous fluids. In severe cases where urine sodium is elevated at 100–200 mEq/L, restriction of free water is necessary by decreasing fluid administration and concentrating the nutrient solution. This problem is most commonly seen with severe head injury or pneumonia and resolves as the patient recovers. Hypervolemic, hyponatremic patients should have nutrient formulas concentrated as much as possible. Other therapy such as diuretics may occasionally be needed. A less common cause of hyponatremia after trauma is inappropriate ADH secretion (see Chapter 19). It is usually associated with central nervous system (CNS) effects induced by head injury, meningitis, subarachnoid hemorrhage, anesthetics, meperidine, carbamazepine, or tricyclic drugs. In addition, a decrease in the vascular volume, secondary to use of diuretics in patients who are on high levels of PEEP or have large fluid losses from the GI tract, open abdominal wounds, etc., can also lead to increased ADH secretion and increased sodium loss. Typically, serum chloride concentrations decrease with the hyponatremia, and a hypokalemic metabolic alkalosis with a high serum bicarbonate occurs, especially when diureticinduced. The diagnosis of inappropriate ADH is made by a combination of hyponatremia, a decrease in serum osmolality, a urine osmolality that is elevated relative to serum osmolality, a urine sodium greater than 20, and, if measured, an increase in ADH. Because of the effect of ADH on the kidney, water is absorbed without sodium so that urine sodium and tonicity are high relative to serum. The appropriate therapy is water restriction. Hypernatremia is also relatively common in the critically ill trauma patient, especially in patients with severe head injury, where a mild hyperosmolar state is often used to decrease intracranial pressure (see Chapter 19). After bedside assessment, most of these patients can be categorized as hypovolemic, isovolemic, or hypervolemic. Patients with hypovolemic hypernatremia are usually treated with lactated Ringer’s solution first to ensure adequate organ perfusion, and then with solutions containing substantial free water (e.g., D5W, 0.22% or 0.45% sodium chloride injection). During free water administration, it is appropriate for the sodium to be reduced in the nutrient solution. Patients with isovolemic hypernatremia usually need free water and sodium should be removed from the PN. Patients with hypervolemic hypernatremia should have intake minimized by concentrating the nutrient formula. Exogenous sodium should be eliminated from PN, medications, and other infusions to the extent possible.

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SECTION 5 X

potassium chloride can be added to the enteral formula. Brown et al. have developed a graduated dosing scheme for replacement of phosphorus in patients receiving specialized nutrition support (i.e., either PN, enteral nutrition, or both) based on the serum phosphorus concentration of the patient:60 Serum Phosphorus Concentration (mg/dL)a 2.3–3.0 1.6–2.2 1.5

Phosphorus Dose (mmol/kg) 0.32 over 4 h 0.64 over 4–6 h 1 over 8 h

a

Normal phosphorus concentration is 3.0–4.5 mg/dL.

Additional phosphorus can be added to the PN or enteral formula following correction of initial hypophosphatemia. Hyperphosphatemia is much less prevalent than hypophosphatemia in trauma patients and is usually associated with renal compromise when it does occur. Phosphorus should be decreased or removed from the nutrient solution.

■ Magnesium The development of hypomagnesemia is underappreciated. Magnesium is rapidly depleted in stress, particularly when diuretics and antibiotics such as aminoglycosides are administered. Dysrhythmias, hypocalcemia (an unusual problem in trauma patients), and irritability are avoided with magnesium monitoring and appropriate treatment. Patients with a history of alcohol abuse or lower GI losses, such as diarrhea, are particularly prone to develop hypomagnesemia. Amphotericin B, aminoglycosides, and loop diuretics (and in addition cisplatin and cyclosporine) have all been reported to cause renal wasting of magnesium. Intravenous magnesium replacement therapy is usually necessary in patients with moderate to severe magnesium deficiency due to poor absorption of oral magnesium salts. Magnesium has a renal tubular threshold similar to glucose, so rapid administration over a short period of time will invariably result in high urinary losses. We have developed a weight-based dosing regimen for magnesium deficiency in which intravenous doses are infused slowly over 12–24 hours to facilitate better retention: Serum Magnesium Concentration (mg/dL)a 1.5–1.8 1.1–1.4

1

Magnesium Dose (mEq/kg) 0.5 over 12 h 1 over 24 h 1.5 over 24 h

a

Normal magnesium concentration is 1.7–2.3 mg/dL.

Magnesium status should also be considered in evaluating a hypokalemic patient, as magnesium is an important cofactor for the Na/K-ATPase pump. We often administer magnesium

replacement therapy for low-normal serum magnesium concentrations in the presence of hypokalemia, because magnesium is an intracellular cation and serum concentrations may not accurately reflect intracellular status. Our standard magnesium concentration in PN solutions is 12 mEq/L; however, some patients as described above need increased doses. We have safely administered as high as 28 mEq/L via PN in selected patients. Hypermagnesemia usually occurs in association with renal dysfunction or failure. Magnesium should be removed from the PN of these patients.

■ Electrolyte Management in Severely Injured Trauma Patients Table 60-3 shows the composition of the various GI secretions that must be considered in fluid and electrolyte balance of patients. Two values are given for potassium in gastric drainage, 10 and 40 mEq; NG drainage contains approximately 10 mEq/L, but because of hydrogen loss, gastric loss should be calculated as 40 mEq/L because of increased renal potassium excretion. In the overall management of critically injured patients, unusual fluid losses in significant quantity (500 mL per day) through such sources as duodenal fistulas, pancreatic fistulas, or high small bowel fistulas should be sent for electrolyte analysis and appropriate adjustments made in intravenous nutrition to account for the excessive losses. It is often helpful to calculate sodium balance by comparing losses with administered intake considering all intravenous solutions and admixtures. Most cases of hyponatremia are due to significant discrepancies (often 600–800 mEq per day) between the sodium administered and the sodium lost. There are several rules of thumb in fluid management of complex trauma patients. Gastric drainage should be replaced with 0.45% sodium chloride with 40 mEq of potassium chloride/L to avoid hypokalemia, hypochloremia, and metabolic alkalosis. Fluid losses from the GI tract distal to the pylorus, including the liver and pancreas, have a sodium of approximately 130– 140 mEq/L. Losses of associated bicarbonate and chloride vary, depending on the organ. Bicarbonate is equivalent to serum in bile and small bowel fluids, and the appropriate replacement fluid for them is lactated Ringer’s. High-output pancreatic fistulas produce bicarbonate loss (80–90 mEq/L) and an appropriate replacement fluid (greater than 300 mL per day) is 0.2 sodium chloride with two ampules of sodium bicarbonate. Standard adult electrolyte requirements for PN are provided in Table 60-4 with adjustments as necessary, depending on unusual losses. Sodium can be administered as the chloride, acetate, or phosphate salt depending on needs. Generally, chloride salts are used for patients with metabolic alkalosis and acetate salts for metabolic acidosis. Patients with severe edema or anasarca generally should receive a sodium-free PN solution. Most enteral formulas have 30–40 mEq of sodium/L (i.e., approximately 0.2 saline) that should be considered in the overall fluid management. Like sodium, potassium is available as the chloride, acetate, or phosphate salts. Calcium is usually administered as the gluconate salt in PN because it is more stable and less likely to precipitate with phosphorus. Magnesium is generally given as the sulfate salt in PN. Significant fluid and

Nutritional Support and Electrolyte Management

1115

TABLE 60-3 Electrolyte Composition of Gastrointestinal Secretions: Average (Range) Secretion

K (mEq/L)

Cl (mEq/L)

HCO3 (mEq/L)

70 (60–90) 140 (135–155) 140 (135–145) 130 (120–140)

10 (4–12), 40a 5 (4–6) 5 (4–6) 5 (4–10)

90 (50–150)b 75 (60–110) 100 (90–110) 105 (60–125)

0 80 (70–90) 35 (30–40) 35 (30–40)

a

Includes renal losses. Lower in achlorhydria.

b

electrolyte disorders are unusual unless supplemental fluids administered through admixtures to drugs are ignored.

ISSUES OF RELEVANCE TO ENTERAL FEEDING ■ Patients Requiring Celiotomy Early enteral feeding of severely injured patients reduces septic complications compared with starvation or PN, but several principles (Table 60-5) must be appreciated to avoid unacceptably high complication rates. First, ISS and ATI can identify patients benefiting from early feeding using the previously noted algorithm. Second, safe effective access should be obtained beyond the ligament of Treitz, using an NCJ, TGJ, or nasoenteric tube advanced during celiotomy. While direct small bowel access is usually successful, a recent study showed an unusually high incidence of complications.61 This section details techniques to avoid these complications. Third, an appropriate nutritional regimen should be instituted. Fourth, early small bowel feeding should be started only in hemodynamically stable patients. Finally, close monitoring and gradual advancement is paramount. Multiple tubes are available. In general, a 5- or 7-Fr NCJ can be placed in most patients, but the life span of these devices is only about 3–4 weeks; therefore, their use should be limited to short-term enteral support. For more “permanent” access (e.g., severely injured geriatric or patients with severe closed head injury), placement of a larger (14, 16, or 18 Fr) catheter is

TABLE 60-4 Electrolytes in Total Parenteral Nutrition Electrolyte Sodium Potassium

Usual Requirement Per Day 100–150 mEq 80–100 mEq (more if anabolic)

Magnesium Calcium

8–30 mEq 10–15 mEq

Phosphorus

20–40 mmol

Standard TPN Concentration/L 40–60 mEq/L 20 mEq/L as phosphate 20 mEq/L as acetate 8 mEq/L as sulfate 5 mEq/L as gluconate 15 mmol/L as K salt or Na salt

advisable, since it can be replaced after 5–7 days, if necessary. Finally, a TGJ is helpful in patients requiring prolonged gastric drainage as well as small bowel feedings. They are also useful when surgeons prefer not to cannulate the small bowel directly. Certain instances mandate specific tubes. The 5-Fr NCJ tube tolerates most standard enteral products, including those containing fiber, and its use need not be limited to definedformula elemental diets. Fiber reduces diarrhea in critically ill patients. Bacteria metabolize soluble fiber to short-chain fatty acids that provide energy to the colonocyte for sodium and water reabsorption. 5-Fr NCJ tubes clog if protein supplements are added to standard enteral formulas or when IEDs are used. For these circumstances, a 7-Fr NCJ or larger-diameter catheter should be used. Medications should not be administered via NCJs, since the elixirs containing medication such as theophylline, potassium chloride, etc., coagulate the tube feedings to produce early tube loss. In general, an NCJ should be used only for the enteral formula. Placement of jejunostomies is critically important. A site should be chosen with a long mesenteric loop to avoid traction

TABLE 60-5 Principles of Enteral Feeding Access Determine appropriateness of patient Choose the tube appropriate for expected needs: • Needle catheter: 3–4 weeks • Large-bore tube: chronic needs • Transgastric jejunostomy: if there is a contraindication to direct small bowel access or for simultaneous gastric drain. Read the instructions provided! Obtain safe postpyloric access: • Position jejunostomy to avoid afferent loop tension if distention occurs • Create lax Witzel tunnel • Suture 6–10 cm of jejunum to the anterior abdominal wall with four to five sutures • Position at the lateral aspect of the rectus sheath away from the midline • Examine patient daily with all dressings off prior to advancing feeding rate

CHAPTER CHAPTER 60 X

Gastric Pancreatic fistula Bile New ileostomy

Na (mEq/L)

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by the afferent limb from the fixed ligament of Treitz, should distention occur. In all circumstances, we recommend creating a Witzel tunnel around the tube with five 3-0 silk sutures placed approximately 1 cm apart, leaving the needle on the first, third, or fifth suture. The sutures creating the Witzel tunnel should loosely approximate the bowel around the tube to prevent tearing if significant edema occurs in the bowel wall. If the bowel is too edematous or indurated to create a lax Witzel tunnel around a 16- or 18-Fr tube, an NCJ can be used. Another form of access should be chosen if bowel is too indurated to create a Witzel tunnel around an NCJ. The Witzel tunnel eliminates dislodgment of the tube into the peritoneal cavity. The jejunostomy should exit the peritoneal cavity at the lateral aspect of the rectus sheath. Placement at or lateral to the rectus sheath—most commonly on the left side, but acceptable on the right side if a stoma is necessary in the left upper quadrant—minimizes the chance of volvulus of intestine over the attachment point. Placement near the midline incision also interferes with reexploration. Finally, the jejunostomy itself, particularly an NCJ, should not be brought out at a 90° angle through the abdominal wall to avoid kinking the tube as it exits the fascia. The externalized jejunostomy tube should be kept short, less than 3–4 cm, and anchored securely to the anterior abdominal wall. A transparent dressing over the catheter prevents disoriented patients from pulling and dislodging the jejunostomy. If prolonged gastric drainage is likely, TGJ allows gastric decompression and direct small bowel feeding. The distal limb of the TGJ should lie beyond the ligament of Treitz and not in the duodenum. Intraduodenal feeding with shorter tubes stimulates pancreaticoduodenal and gastric secretions, which can result in fluid and electrolyte problems. Nutrients introduced beyond the ligament of Treitz do not stimulate significant upper GI secretion. A note of caution with TGJs is in order. The gastroesophageal junction is the most dependent part of the stomach in supine patients and the stomach should be decompressed with an NG tube until the patient can be elevated to 30–40° to avoid reflux and aspiration. As a final technique for small bowel access, long tubes can be advanced through the nose or mouth into the proximal small intestine at celiotomy. Although some institutions successfully use this technique, it requires close vigilance by nursing staff during routine patient care, transport, or ambulation.

DIET CHOICE BY THE ENTERAL ROUTE Several clinical trials support the use of an IED in patients at high risk of developing sepsis (ATI 25, ISS 20; Fig. 60-1). Some powdered diets, such as Immunaid, contain free l-GLN in addition to omega-3 fatty acids, nucleotides, BCAAs, and arginine. Liquid diets such as Perative do not contain such free GLN because of the instability of that amino acid in liquid form. A recently introduced enteral liquid product has higher levels of GLN in the protein component. Liquid diets may contain soluble fiber, which serves as an energy source for enterocytes after metabolism by endogenous bacteria to the short-chain fatty acids, acetoacetate, butyrate, and propionate. In our experience, the IEDs should be administered through

larger-bore catheters, such as the 7-Fr or larger NCJ, since increased clogging occurs in the 5-Fr NCJs. In less severely injured patients, a nonprotein calorie:nitrogen (NCP:N) ratio of approximately 80:1 to 120:1 increases the protein loading without a high NPC:N load. Chemically defined diets are not mandatory, although they are still frequently used and provide an adequate nutritional substrate. Chemically defined diets are often associated with a higher incidence of diarrhea due to their high osmolarity and lack of soluble fiber. Fiber-containing diets are not contraindicated in critically ill patients; in our experience, diarrhea is reduced by their use, although impaction may occasionally mimic bowel obstruction. Typically, if intragastric feedings are being given, impaction presents as distention without high gastric residuals. The diagnosis is made by recognizing colonic distention in an x-ray. Most patients respond to colonic stimulation with enemas or suppositories. Recent reports suggest neostigmine to stimulate colonic motility but bradycardia and hypotension may occur. If the patient improves but continued enteral feeding is necessary due to prolonged inability to take an ad libitum diet, the NPC:N should be increased to 130:1 to 160:1 and protein administration reduced to 1.2–1.5 g/kg. Total calories are given in the range of 20–25 kcal/kg per day. In diabetic patients, a formula with a higher percentage of fat may reduce hyperglycemia if hypertriglyceridemia is not a problem. In the occasional, rare patient who cannot be weaned from low levels of ventilator support, transition to a higher-fat diet may improve weaning, although this scenario is very uncommon in young trauma patients.

DIET PROGRESSION Diet advancement requires close monitoring. Direct small intestinal feeding should be delayed if multiple blood transfusions, fluid boluses, or pressor agents (other than low-dose dopamine) are required to maintain hemodynamic stability. Enteral feeding increases splanchnic blood flow and increases splanchnic metabolic rate. Shock, sepsis, and hemodynamic instability shunt blood away from the GI tract, and it is presumed that inability to shunt blood to the mucosa may be the cause of feeding-related small bowel necrosis. Evidence of adequate splanchnic perfusion includes adequate urine output, hemodynamic stability, warm peripheral extremities, etc. Progression is determined by the type of formula. Protocols have been defined for progression of defined-formula diets (Table 60-6). More complex diets should be started at 15 mL/h for the first 6–8 hours in patients who were previously unstable or in shock. Diets can be advanced after 6–8 hours to 25 mL/h and at increments of 25 mL/h per day depending on tolerance. Moore et al.14 advanced patients with less severe injuries (i.e., an ATI 40 and no bowel injury) to goal rate within 48 hours following institution of a chemically defined diet. Patients with an ATI 40 or bowel injuries had increased bloating, cramps, and general intolerance when advanced this quickly and should be advanced more slowly, generally by 25 mL/h per day, up to the calculated goal rate, while being

Nutritional Support and Electrolyte Management

TABLE 60-6 Protocol for Advancement of Chemically Defined Diet by Jones and Moore Rate (mL/h) 50 75 100 100 100 100 125a

Duration (h) 8 8 8 8 8 8

a

If required.

observed for intolerance. In our experience, approximately 50% of severely injured patients can be advanced up to or close to the goal rate within 3–4 days with few, if any, problems. Approximately 10% of patients do not tolerate feedings at all, with intolerance manifest by reflux of feedings into the stomach (which necessitates the immediate discontinuation of direct small bowel feedings), significant bloating, or complaints of cramps. The remaining 40% of patients generally tolerate feedings to approximately 50–75% of goal but develop temporary (2–3 days) intolerance, such as discomfort or diarrhea, at higher rates. Tube feedings should be slowed to the tolerated rate for 24–48 hours and then advanced. If patients tolerate at least 50% of goal rate, we do not add PN. In the minority of patients with complete tolerance, however, PN should be instituted by the fourth or fifth day, with transition to enteral feedings as soon as possible. Once PN is started, it is not weaned until patients tolerate at least 50% of the goal enteral rate and feedings are being advanced to 75% of the calculated rate.

PROKINETIC AGENTS Gastroparesis is manifested by high aspirated residual volume (150 mL) and is one of the more troublesome GI complications. The nurse should check gastric residuals every 4–6 hours to assure that gastric residuals remain low. Acutely elevated residuals in patients who previously tolerated a high rate indicate ileus from a septic process or acute stress ulceration. Evidence of upper GI bleeding (coffee-grounds aspirate or obvious bleeding) warrants early endoscopy because of a high rate of duodenal or gastric ulceration, especially following spinal cord injuries, severe head injuries, or burns. With gastroparesis persistent beyond 3–4 days, most practitioners use a prokinetic agent to enhance gastric emptying. The three drugs used most commonly in the critical care setting are metoclopramide, cisapride, and erythromycin. Metoclopramide is available as a tablet, syrup, or intravenous solution in the United States and is a selective dopamine-2 agonist that enhances peristalsis contractility of the esophagus, gastric antrum, and small intestine. Metoclopramide enhanced gastric emptying of acetaminophen in trauma patients and

DRUG–NUTRIENT INTERACTIONS Critically ill trauma patients receive a large number of pharmacological agents. A few agents influence the designing of the nutritional formula. Propofol, commonly used for sedation, is manufactured in a lipid emulsion that provides 1.1 kcal/mL. Clevidipine, an intravenous calcium channel blocking agent, is also delivered with a lipid emulsion and contains 2 kcal/mL. The caloric contribution from the lipid vehicle is negligible in small doses; however, it becomes very important with higher rates of infusion. The nutritional prescription should be modified by decreasing or eliminating lipids from the parenteral solution or by using a high-protein enteral formula with added protein powder to provide an appropriate mix of carbohydrate, fat, and protein. Enteral nutrition influences effectiveness of drugs such as the antiepileptics, phenytoin, or carbamazepine, when given via the GI tract. Phenytoin interacts with calcium or the caseinates within the formula to decrease drug absorption. Recommendations for phenytoin administration include discontinuation of tube feedings for 2 hours before and after the drug dose, dilution of phenytoin, irrigation of the tube with 60-mL flushes, and increases in the phenytoin dosage as necessary. Serum levels should be monitored during initiation of therapy or with changes in enteral nutrition. Carbamazepine absorption is slower with continuous enteral feeding and monitoring of serum levels is appropriate. Warfarin is commonly used in the treatment of deep venous thrombosis (DVT) prophylaxis, but enteral products can interfere due to the vitamin K in the formula or through physical/ chemical interaction, which impairs drug absorption.

CHAPTER CHAPTER 60 X

Strength 1/4 1/4 1/4 1/2 3/4 Full Full

reduced time to maximal plasma concentration compared with erythromycin or placebo.62 Cisapride is no longer available in the United States because it was associated with events of cardiac arrhythmia. Erythromycin is available as a capsule, suspension, or intravenous solution acting locally to enhance motilin release from enterochromaffin cells of the duodenum. Motilin enhances contractile activity of the gastric antrum and duodenum. Compared with placebo, erythromycin significantly increased the frequency of gastric contractions, amplitude of contractions, and the motility index. The time to reach the maximal concentration of acetaminophen (gastric emptying marker) was also shortened when compared with the placebo group in this one-dose study involving 10 critically ill patients receiving mechanical ventilation.63 In healthy volunteers, both total gastric volume and gastric volume of a continuous liquid meal decreased by 22% in patients receiving erythromycin versus placebo. The most recent data show that using erythromycin and metoclopramide in combination is more effective in improving gastric motility than erythromycin alone. When patients were fed via a nasogastric tube, the combination prokinetic therapy resulted in more calories delivered and less need for placement of postpyloric feeding tubes. The most prominent side effect noted was watery diarrhea. No prolongation of QT interval was seen.64

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TABLE 60-7 Medications Incompatible with Enteral Formulation

TABLE 60-8 Sorbitol Content of Oral Medications

Dimetapp Elixir Dimetane Elixir Sudafed Syrup Thorazine Concentrate

Drug (g Per Day) Acetaminophen Elixir (Roxane) Acetaminophen Suspension (McNeil Children’s) Acetaminophen Liquid (McNeil Adult) Maalox Calcium Carbonate Suspension (Roxane) Tagamet Liquid (SK Beecham) Diphenoxylate and atropine (Lomotil, Searle) Diphenoxylate and atropine (Roxane) Metoclopramide (Reglan, Robins) Theophylline (Rorer) Bactrim (Roche)

Feosol Elixir Robitussin Expectorant Mellaril Oral Solution

Adapted from Cutie AJ, Altman E, Lenkel L. Compatibility of enteral products with commonly employed drug additives. JPEN J Parenter Enteral Nutr. 1983;7; 186–191, with permission from the American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). A.S.P.E.N. does not endorse the use of this material in any form other than its entirety.

Hydralazine, ciprofloxacin, and itraconazole are affected by enteral administration when tube feedings are in progress and necessitate close monitoring. Addition of drugs to the enteral formula can affect stability of the fat, alter viscosity, and change the consistency and particulate size of the formula. Calcium, zinc, and iron produce jelling or curdling and a number of drug products increase clumping and change viscosity due to their acidic nature. Drugs incompatible with enteral products are listed in Table 60-7.65

COMPLICATIONS OF ENTERAL FEEDING

g/5 mL 1.8

Sorbitol Average 29.25 g/2,600 mg

0.84

13.7 g/2,600 mg

0.4

6.2 g/2,600 mg

0.225 1.4

5.4 g/120 mL 4.2 g/3,750 mg

2.52

10 g/1,200 mg

1.05

8.4 g

2.3

18.4 g

2.25

18 g

2.02 0.35

30.2 g 2.8 g/40 mL

Source: Lutomski DM, Gora ML, Wright SM, Martin JE. Sorbitol content of selected oral liquids. Ann Pharmacother. 1993;27:269, with permission.

■ Distention Patients should be examined 6 hours following institution of their feedings and when cramping or diarrhea occurs. Mild abdominal distention is common in fed and unfed trauma patients and discontinuation of the tube feedings for minimal symptoms is not necessary. If, however, alert patients complain of severe discomfort, the rate should be reduced if the pain is not incisional. Colonic distension secondary to constipation or impaction is likely in patients receiving intragastric feeding even with low residuals; it responds to suppositories and/or enemas. The institution and advancement of early enteral feedings into the small bowel requires that patients be examined approximately 6 hours following institution of their feedings as well as if there are any complaints of significant cramping or diarrhea.

■ Diarrhea Diarrhea occurs commonly in fed and unfed critically ill patients. In tube-fed patients, diarrhea occurs from 5% to 25% depending on the definition of diarrhea. Five to six formed or semiformed stools per day are not diarrhea. However, watery stools that constantly soil the patient during turning eventually cause irritation and skin breakdown. While tube feedings are often implicated, diarrhea is more commonly caused by medications. Twenty percent of severely injured trauma patients administered a chemically defined diet developed significant diarrhea in our study,12 which decreased to 4% with a fibercontaining diet.

Approximately three quarters of cases of diarrhea are caused by antibiotic-induced pseudomembranous enterocolitis (see Chapter 18), magnesium medications, or sorbitol.66 Sorbitol is used for sweetness or as a solubilizing agent replacing alcohol. Surprisingly large amounts of sorbitol are present in commonly administered medications (Table 60-8) such as potassium chloride, theophylline medications, phenytoin, and even antidiarrheal drugs. On occasion, prokinetic drugs successfully instituted for gastroparesis cause diarrhea that stops after discontinuation. Multiple antibiotics generate bacterial overgrowth and rarely pseudomembranous colitis. Proctosigmoidoscopy should be performed for suspected Clostridium difficile, particularly in guaiac-positive patients. Specimens should be sent for fecal leukocytes and the mucosa observed for pseudomembranes. In patients receiving antibiotics and enteral nutrition, C. difficile was present in over 50% of patients with diarrhea. Patients with diarrhea should receive an isotonic formula with soluble fiber. Prokinetic agents and enteral medications are immediately discontinued and the rate of feeding reduced to 50% of the current rate. Diarrhea commonly persists for another 12 hours as the GI tract eliminates the fluid. Sigmoidoscopy is performed and stool for C. difficile is sent, if clinically appropriate. If positive, appropriate therapy is started (see Chapter 18). Although hypoalbuminemia was implicated as an important cause of diarrhea in critically ill patients, a prospective study

Nutritional Support and Electrolyte Management

PNEUMATOSIS INTESTINALIS AND NECROSIS Necrosis secondary to direct small bowel feedings seems to occur in hemodynamically unstable patients often on pressor. Tachycardia (160/min), a temperature spike to 103°F, and rapid abdominal distention are hallmarks of this devastating complication. Although the mechanism for necrosis is unclear, potential explanations include bacterial invasion of the bowel wall with mucosal necrosis, abnormal carbohydrate metabolism, or ischemia secondary to low GI blood flow. While spontaneous necrosis has occurred in unfed critically ill patients, enteral feedings are an important factor as shown by the report of necrosis following radical cystectomy and jejunostomy feeding. Necrosis of the entire small intestine developed except for the isolated ileoconduit.69 Pneumatosis intestinalis occurs in both fed and unfed ICU patients and if diagnosed necessitates immediate discontinuation of tube feedings and initiation of antibiotic therapy against both aerobic and anaerobic organisms. The use of antibiotics is debatable but probably should be instituted. Surgery is necessary in rare cases, but if necrosis is found at exploration, immediate anastomosis should be delayed for 24 hours to eliminate progressive necrosis not initially recognized. Tube feedings should never be administered to patients with an obstruction or immediately after release of the obstruction because of the potential for necrosis. Postoperative diuresis and resolution of abdominal distention should be complete prior to instituting enteral nutrition.

ASPIRATION Aspiration occurs in 1–70% of patients who are enterally fed; in our experience, it is uncommon in trauma patients. While some protection is probably provided by direct small bowel feeding, gastric decompression should be continued until gastric residuals drop since mortality with aspiration can be 50% or greater. Tracheostomy or endotracheal intubation with an inflated cuff does not completely protect against lethal aspiration in ventilated patients. Monitoring of residual gastric volumes is the major watchdog to minimize aspiration with intragastric feeding. Unfortunately, the tip of the feeding tube may not lie in the pool of residual tube feeding and the gastroesophageal junction becomes the most dependent area of the stomach in the supine position.

In critically ill patients, many clinicians use gastric residual volumes to gauge patient tolerance of enteral nutrition, although clinical data fail to support this practice. Our institution holds tube feedings for residual volumes of greater than 250 mL in patients with gastrostomy tubes. If a single residual is high, feedings can be replaced into the stomach and residuals checked in 2 hours. If they remain high, feedings should not be restarted. A prokinetic agent should be started if appropriate. Critically ill patients tolerating successful intragastric feeding at goal or near goal rates who suddenly develop high residual volumes may have impending sepsis or have a pyloric channel or duodenal ulcer. This is particularly common in patients with spinal cord injuries, severe closed head injuries, or burns. If the NG aspirate is guaiac-positive, upper endoscopy is warranted, particularly if there is an unexplained drop in hematocrit. More commonly, gastroparesis signals the early onset of sepsis from pneumonia, intra-abdominal abscess, or another cause of sepsis. Patients with direct small bowel access do not need residual volumes checked, but reflux of tube feeding into the stomach require that feeding be discontinued immediately since this is a reliable marker of distal bowel obstruction or significant intolerance.

MECHANICAL COMPLICATIONS Jejunostomy tube dislodgement into the peritoneal cavity or volvulus at the jejunostomy site is avoided by the surgical techniques described earlier. Complete dislodgment can be avoided by secure suture of the tube at the anterior abdominal wall and by keeping the external segment short and covered with an occlusive dressing. While complete dislodgment of a large-bore red rubber feeding tube is considered a minor inconvenience if replaced promptly with an appropriately sized catheter, dislodgment of an NCJ loses the portal for direct small bowel access. Large-bore tubes in place for at least a week can be replaced with a tube of a smaller or similar size. Occlusion of feeding tubes is common, but this is of little significance with a 14- or 16-Fr tube, since it can be replaced. Occlusion may necessitate removal of a 5- or 7-Fr NCJ. If NCJs occlude within the first 24–48 hours, the cause is a kink at the point where the NCJ tube pierces the fascia and enters the bowel. By applying pressure with a 10-mL saline-filled syringe while gently withdrawing the catheter, the flow restarts as soon as the kink is straightened. The catheter should be withdrawn 5 or 6 cm until the catheter can be divided beyond the kink and reattached. This rarely occurs a second time. If an NCJ occludes after 2–3 weeks, flushing may temporarily open the tube, but the life span of the NCJ is limited. Fortunately, since most patients tolerate direct intragastric feeding by this time, the NCJ has served its function. No medications are permitted via an NCJ because elixirs used to solubilize medications coagulate feedings and occlude the tube. Medications given through a larger-bore catheter should be flushed with 15–20 mL fluid prior to and another 40–50 mL water or saline after administering the medication. Use of a guidewire to disimpact a tube is not advisable, since it can perforate the tube or the intestine. Special devices are marketed that can be inserted into clogged tubes. Such a device usually consists

CHAPTER CHAPTER 60 X

using peptide formulas (promoted as a benefit in hypoalbuminemic patients) in standard isotonic formulas produced no benefit in hypoalbuminemic patients67 compared with an intact protein diet. In a very small percentage of patients, many of whom are not being fed, diarrhea persists, and administration of Lactobacillus acidophilus has been successful on occasion. Safety of using probiotics in patients with central lines is controversial, as there have been several case reports of Lactobacillus bacteremia thought to be due to contamination of central catheters when the capsule was opened at the bedside for administration down a feeding tube.68 Antidiarrheal medicines, such as tincture of opium or loperamide, are used only as a last resort.

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of a small catheter fitted with an adapter for connection of a syringe. Water or declogging powder can be instilled by the syringe for irrigation. Although a variety of agents (i.e., carbonated beverages, acidic juices, meat tenderizer) have been tried to restore patency to occluded tubes, a combination of pancreatic enzymes and sodium bicarbonate appears to produce the best results. Other devices resembling soft, threaded screws have been inserted inside a large-bore gastrostomy or jejunostomy tube and rotated to bore through a clog.

PARENTERAL FEEDING ■ Access and Monitoring of Lines The critically ill trauma patient will require reliable venous access at all times. Therefore, most patients who are hospitalized in the ICU will already have central vein access when the decision to start PN is made. This allows for the administration of central PN, which usually includes very hyperosmolar formulas that must be diluted quickly in the vasculature. Peripheral PN has been used with some success in hospitalized patients; however, it is not frequently administered to critically ill trauma patients because of fluid considerations and the resulting thrombophlebitis necessitating frequent vein rotation to maintain the infusion. To administer adequate nonprotein energy with peripheral PN, greater than 50% of energy calories is usually given as intravenous lipid. This may result in a mixture of nutritional substrates that is not optimal for the critically ill patient. The percutaneous subclavian vein approach is the procedure of choice for obtaining central vein access in critically ill trauma patients. Alternative methods, though less desirable, include the internal jugular vein approach and the femoral vein approach. There is an increased rate of catheter sepsis with each of these techniques and a potential risk of DVT with femoral lines. When the decision to start central PN has been made, the critical care practitioner is faced with several choices regarding access: (a) use the current central line for the provision of PN (e.g., triple-lumen catheter, Swan–Ganz catheter), (b) change the present catheter to a new triple-lumen catheter using the modified Seldinger technique with a flexible guidewire, or (c) place an entirely new central line with a triple-lumen catheter dedicating one port for the provision of PN. The method used will depend on the patient’s hemodynamic stability, the length of time the existing catheter has been in place, the condition of the site where the existing central catheter was placed (e.g., redness, swelling, gross pus), and the other fluid requirements of the patient including intravenous fluid, continuous medication drips, electrolyte boluses, and other medications and blood. An open port on the Swan–Ganz catheter can be used for PN in patients who are hemodynamically unstable. This obviates the need to subject the critically ill patient to another procedure, especially one who may have a coagulopathy. Once hemodynamic stability is achieved, the Swan–Ganz catheter should be “changed out” to a triple-lumen catheter using the modified Seldinger technique with a sterile guidewire. If there is purulence present at the central vein site

or a high index of suspicion that the present catheter is infected, access at an alternative site (e.g., the opposite subclavian vein) should be strongly considered. Placement of an indwelling central catheter does include some short- and long-term risks. Pneumothorax, hemothorax, aneurysms, arterial puncture, and nerve injury may all occur during attempted cannulation of a central vein. Subclavian thrombosis and catheter-related sepsis are major problems that occur after placement of a central vein catheter. Patients with subclavian central catheters should be observed frequently for neck swelling or complaints of stiffness to aid in the diagnosis of subclavian thrombosis. Subclavian vein thrombosis may require removal of the catheter and anticoagulation. Also, the use of catheters made of silicone or polyurethane elastomers results in less thrombogenicity than that of ones made of polyvinyl or polyethylene. Catheter-related thrombotic occlusions frequently complicate the care of central venous catheters. Catheter occlusion may occur in the form of thrombotic and nonthrombotic causes. Types of thrombotic catheter occlusions include (a) intraluminal thrombus, (b) mural thrombus, (c) fibrin sheath, and (d) fibrin tail. Intraluminal thrombus development is characterized as occurring within the lumen of the catheter. This usually presents as resistance to infusion or blood aspiration from the catheter. Inadequate flushing or blood reflux may account for this type of occlusion. A mural thrombus refers to the formation of fibrin from vessel wall injury that extends to the surface of the catheter. Clinical symptoms consistent with vascular obstruction, such as neck vein distention, edema, and pain over the ipsilateral neck, may signify the presence of this type of occlusion. Fibrin sheath formation can encase the catheter and occlude the distal tip, whereas a fibrin tail refers to an accumulation of fibrin that surrounds the end of the catheter. Thrombolytic therapy is recommended for all of the preceding types of catheter occlusion that are thrombotic in nature. Due to the unavailability of urokinase, t-PA is now the recommended agent for thrombosed catheters. A 2-mg dose of t-PA administered with a 30-minute to 2-hour dwell time has been shown to restore patency to occluded catheters. Nonthrombotic causes of occlusion can arise from precipitation of drugs, intravenous lipids, and calcium-phosphate complexes. If drug or mineral deposits are suspected, 1–3 mL of 0.1N HCl is recommended for clearance. On the other hand, if waxy lipid deposits are thought to be responsible for impaired catheter flow, 1–3 mL of 70% ethanol can restore patency. Ethanol should only be used in silicone-based catheters, as there is evidence that it might damage catheters made of polyurethane. Other problems such as air embolism may occur at anytime if there is a central catheter present. Catheter-related infection/ sepsis is always a possibility for the critically ill patient with a central vein catheter. Hyperthermia, tachypnea, tachycardia, leukocytosis with “left shift,” and the presence of shaking and chills all may occur in patients who have catheter-related sepsis. With the presence of the above signs, most practitioners would “change out” the central catheter using a sterile guidewire and culture the tip of the removed catheter, as well as a central and peripheral blood culture for definitive diagnosis. If the catheter tip grows a pathologic organism with 15 colony-forming

Nutritional Support and Electrolyte Management

FORMULA PREPARATION ■ Components The PN admixture is made from a complex combination of macronutrients (dextrose, amino acids, and fat emulsion), micronutrients (electrolytes, vitamins, trace elements), and water. Hydrated dextrose is the most frequently used parenteral carbohydrate in the world for the preparation of PN. Fructose, sorbitol, and xylitol are other carbohydrates that have been used with varying success in PN. Each gram of hydrated dextrose yields 3.4 kcal. Stock solutions of dextrose for the preparation of PN come in strengths varying from D10W to D70W. Many institutions that make PN solutions with an automated compounder stock only D70W because it can be diluted with sterile water for injection to make many different final concentrations of dextrose, even odd strengths such as D17W. As previously mentioned, dextrose administration in PN should not exceed 5 mg/(kg min) (approximately 25 kcal/kg per day). Many critical care practitioners administer dextrose at a slightly lower dose routinely (e.g., 3–4 mg/(kg min)) to minimize CO2 production, lipogenesis, and hyperglycemia. Intravenous fat emulsions (IVFE) are used in PN to provide essential fatty acids and to provide another source of NCPs. The commercially available IVFE in the United States are either soybean oil emulsions or a combination of soybean/ safflower oil emulsions. The current products and their pertinent characteristics are listed in Table 60-9. These products are available as 10%, 20%, and 30% IVFE. The 10% and 20% IVFE may be infused directly into a patient’s vein or added to dextrose and amino acids to make a total nutrient admixture (TNA). The 30% IVFE can only be used as part of a TNA in the United States; however, it is approved for direct vein infusion in Europe. Fat is a concentrated calorie source by

providing 10 kcal/g. The maximum dose of IVFE in adults is 0.11 g/kg/hr; however, most clinicians caring for critically ill patients administer approximately 1 g/kg per day as either a continuous infusion or part of a TNA administered over 24 hours in each case. Considerable controversy exists regarding the effects of IVFE on immune function. Bactericidal and migratory functions of polymorphonuclear cells and decreased bacterial clearance have been demonstrated in patients who have received excessively high or rapidly infused doses of IVFE. To date, these changes have not demonstrated significant effects on patient outcome; however, clinicians are usually cautious with the infusion of IVFE in critically ill patients. Patients who have ARDS should have IVFE given in lower doses (0.5–1 g/kg per day as a continuous infusion) because problems with oxygenation have been reported when rapid infusions (3 mg/(kg min)) have been given.71 Currently available forms of IVFE contain mainly omega-6 fatty acids, which result in products that can induce inflammation and immunosuppression. Again, cautious administration of IVFE appears to be safe and efficacious in critically ill trauma patients. Vitamins are necessary for normal metabolism and cellular function. There are currently 13 known vitamins, with vitamin B12 being the last one isolated, in 1948. Trauma patients receiving PN should receive a parenteral multivitamin preparation daily. Most commercially available products for adults contain 12 of the 13 known vitamins (all except vitamin K). In April 2000, the US Food and Drug Administration (FDA) amended requirements for marketing of an “effective” adult parenteral multivitamin formulation and recommended changes to the 12-vitamin formulation that has been available for over 20 years.72 The new requirements for increased dosages of vitamins B1, B6, C, and folic acid as well as addition of vitamin K are based on the recommendations from a 1985 workshop sponsored jointly by the American Medical Association’s (AMA) Division of Personal and Public Health Policy and the FDA’s Division of Metabolic and Endocrine Drug Products. Specific modifications of the previous formulation include increasing the provision of ascorbic acid (vitamin C) from 100 to 200 mg per day, pyridoxine (vitamin B6) from 4 to 6 mg per day, thiamine (vitamin B1) from 3 to 6 mg per day, folic acid from 400 to 600 g per day, and addition of phylloquinone (vitamin K) 150 g per day (Table 60-10). When the 12-vitamin formulation is being used, vitamin K can be given individually as a daily dose (0.5–1 mg) or a weekly dose (5–10 mg given once weekly). Patients who are to receive

TABLE 60-9 Available Intravenous Fat Emulsions in the United States Trade Name Intralipid

Source Soybean

Liposyn II

Soybean/safflower

Liposyn III

Soybean

Strength (%) 10 20 30 10 20 10 20

kcal/ML 1.1 2.0 3.0 1.1 2.0 1.1 2.0

Glycerin (%) 2.25 2.25 2.25 2.5 2.5 2.5 2.5

EGG PHOS (%) 1.2 1.2 1.2 1.2 1.2 1.2 1.2

CHAPTER CHAPTER 60 X

units, the replaced catheter should be removed after obtaining central access at a new site. If catheter removal is undesirable because of limited vascular access, recommendations from the Centers for Disease Control and Prevention (CDC) are available for quantitative blood culturing techniques to assist the clinician in diagnosis of a catheter-related bloodstream infection (CR-BSI).70 Testing of paired blood samples is required. Criteria for the presence of a CR-BSI are met if the colony count obtained via the central catheter is 5- to 10-fold greater than the sample obtained from the peripheral vein.

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TABLE 60-10 Parenteral Vitamins Recommended by New FDA Guidelines

SECTION 5 X

Vitamin Vitamin A Vitamin D2 Vitamin E Thiamin Riboflavin (B2) Pyridoxine (B6) Niacin Pantothenate Biotin Folate Cyanocobalamin (B12) Ascorbic acid (C)

Dose 3,300 IU (1 mg retinol) 200 IU (5 μg cholecalciferol) 10 mg (alpha-tocopherol) 6 mg 3.6 mg 6 mg 40 mg 15 mg 60 μg 600 μg 5 μg 200 mg

warfarin should be monitored more closely when receiving vitamin K to ensure the appropriate level of anticoagulation is maintained. It is reasonable to supplement the PN with thiamine (25–50 mg per day) in trauma patients who have a history of alcohol abuse, especially when they did not receive thiamine at admission, or in times of parenteral multivitamin shortages (common in the United States in the 1990s). The United States has been plagued with two periods of short supply of multiple vitamin products in the 1990s. This has resulted in vitamin deficiencies in patients receiving PN without parenteral vitamins. Several recommendations emanated from the American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.) following the latest parenteral vitamin shortage, which began in 1996: (a) the use of oral multivitamins when possible, especially liquid multivitamins via feeding tubes; (b) restriction of the use of multivitamin products in PN during periods of short supply, such as one infusion three times per week; (3) administration of thiamine, ascorbate, niacin, pyridoxine, and folic acid daily as individual entities in the PN during periods of short supply; and (4) administration of vitamin B12 at least once per month during periods of short supply. The shortage in 1996–1998 was caused by one manufacturer who stopped making its multivitamin product and another who was unable to meet the national demand because of manufacturing difficulties. Trace elements are usually provided daily during PN in trauma patients as a cocktail of four or five separate metals. Trace element cocktails providing zinc, copper, manganese, chromium, and selenium should be given daily to most trauma patients receiving PN. Patients who have sustained small bowel or large bowel fluid losses should receive supplemental zinc (5–10 mg per day) in addition to the amount in the trace element cocktail (3–5 mg per day). Provision of large intakes of trace elements to thermal injury patients may facilitate wound healing and decrease length of hospital stay. Based on exudative losses from burn wounds, one group of investigators increased daily intakes of copper (4.5 mg), selenium (187 μg), and zinc (39 mg). A reduction in grafting requirements and total hospital days (45  16 days vs. 57  27 days, P  .05)

was observed in the supplemented group versus the group receiving standard trace element intakes.73 Patients who have hepatic cholestasis should have copper and manganese withheld from the PN solution because these trace elements are excreted in the bile. Neurologic damage from deposition of manganese in the basal ganglia has been reported in PN patients with chronic liver disease or cholestasis.74 Parenteral molybdenum and iodine are also available; however, these trace elements are usually reserved for long-term PN patients if they are used at all. Water is a vital component for life and an important part of the PN formula. Trauma patients who require PN will vary considerably in their water requirements. Fluid balance should be assessed by intake and output and hemodynamic monitoring as appropriate. In many cases the trauma patient is septic and has difficulty in mobilizing fluid from third spaces. This results in edema and fluid overload. The PN prescription for these patients should be maximally concentrated and be void of free water if possible. This can be accomplished by using only the most concentrated macronutrients (e.g., D70W, 15% amino acids, 30% IVFE) for the preparation of the PN formula. Other patients, such as those with multiple GI drains or fistulas, may have water and salt requirements that exceed those provided by standard PN solutions that can meet nutritional needs. In this case, an additional intravenous fluid such as 0.45% sodium chloride injection will need to be used as a fluid supplement to keep the patient in proper water and sodium balance.

■ Examples of PN Formulas There are several ways in which to prescribe PN formulas. Each institution or health care system will usually have a single method that is preferable for the respective pharmacy. Many health care systems use a preprinted order form to minimize confusion for the prescriber, especially where there are multiple prescribers. The examples used in this chapter are expressed in final concentrations of the respective macronutrients. This appears to be an effective way of teaching these concepts in systems with multiple prescribers or where there are a few prescribers who change services every month. Table 60-11 lists several PN formulas that have been used for critically ill trauma patients. PN formulas containing between D15W and D25W, 4–5% amino acids, and 2–3% lipids are usually suitable for trauma

TABLE 60-11 Examples of TPN Formulas Used in Trauma Patients Type Standard #1 Standard #2 Concentrated ARFb—no dialysis ARFb—dialysis a b

Amino acids.

Acute renal failure.

Carbohydrate Protein D20W AAa 5% D15W AA 5% AA 6% D30W AA 2% D30W AA 4% D30W

Fat Lipids 2% Lipids 3% Lipids 4% Lipids 2% Lipids 2%

Nutritional Support and Electrolyte Management

INSTITUTION OF THERAPY Most patients can be started on PN and advanced to a desired goal over 2–3 days. A reasonable initiation rate is 25–50 mL/h for 12–24 hours. If glucose homeostasis is reasonable, the PN rate can be advanced by 25–40 mL/h per day until the desired goal is reached. For example, an 80-kg critically ill trauma patient with normal organ function and serum electrolyte concentrations may have a PN formula (D15W, amino acids 5%, lipids 2%) started at 50 mL/h, advanced to 85 mL/h on day 2, and then advanced to the desired goal of 115 mL/h on day 3. A different approach would be taken for the fluidoverloaded, hyperglycemic, septic trauma patient with normal renal function. The PN would be concentrated (D30W, amino acids 6%, lipids 4%), undoubtedly have regular insulin added to it (or coinfused with an infusion of insulin), and initiated at a low rate such as 15–25 mL/h. This PN formula would be advanced slowly (e.g., 25 mL/h per day) based on patient clinical status, glucose tolerance, and fluid balance.

COMPLICATIONS OF PARENTERAL NUTRITION AND THEIR TREATMENT The complications of PN are often divided into three broad categories: mechanical, metabolic, and infectious. The major mechanical and infectious complications are covered in Section “Access and Monitoring of Lines,” and are therefore not repeated here.

■ Glucose The most common metabolic complication of PN is glucose homeostasis. Hyperglycemia is a common finding in critically ill patients receiving PN not only because of the administered dextrose but also because of the accompanying stress associated with injury (e.g., increased corticosteroids, cytokines), dextrose administration from intravenous fluids and medications, chronic diseases such as diabetes, and coadministration of drugs that can exacerbate glucose homeostasis such as glucocorticosteroids. One recent study correlates hyperglycemia in parenterally fed patients to poor outcomes in hospitalized patients.75 Recent trials have explored the benefits of tighter glucose control in the ICU. The trial by Van den Berghe et al. showed benefits from strict glycemic control in cardiac patients receiving specialized nutrition support (EN and PN).76 This study compared patients with strict glycemic control (keeping blood glucose between 80 and 110 mg/dL) with those treated with conventional treatment (keeping blood glucose between 180 and 200 mg/dL). This trial showed that intensive insulin therapy reduced mortality and morbidity. Limitations of the trial include the large percentage of cardiac surgery patients, large percentage of patients receiving PN, and dedicated

research nursing staff whose only role was to adjust insulin drips. It did not appear that general surgical or trauma patient benefited from this approach. In the most recent glycemic control trial, NICE-SUGAR, the investigators question the need for tight control of blood glucose, and propose that a wider range of blood glucose control (180 mg/dL) will be just as beneficial.50 The NICE-SUGAR trial was a multicenter study involving 42 hospitals and randomizing a population of mixed medical and surgical ICU patients. Patients were randomized to receive an intensive insulin regimen to keep blood glucose between 80 and 108 mg/dL, or a “conventional” insulin regimen to keep blood glucose between 70 and 180. Results showed a mortality benefit in favor of the conventional insulin group. Of the patients in the intensive insulin group, 27.5% of the 3,010 patients died; in comparison, 24.9% of the 3,012 patients in the conventional group died, which is an absolute difference in mortality of 2.6% (95% CI, 0.4–4.8). Also, severe hypoglycemia (defined as blood glucose less than 40 mg/dL) was reported significantly more often in the intensive insulin group at 6.8% than in the conventional insulin group at 0.5% (P  .001). Investigators conclude that the intensive insulin regimen results in a higher mortality rate and do not recommend using it in an ICU setting. The investigators note the differences in the trial, that is, a mixed medical and surgical ICU, more patients receiving enteral nutrition rather than PN, and the use of existing personnel (no research nursing staff ) as reasons for the results. Also, researchers of the NICE-SUGAR trial note that there were excess deaths in the intensive insulin group due to cardiovascular events, and suggest that reducing blood glucose with insulin may affect the cardiovascular system. Most practitioners agree that blood glucose in the ICU should be kept between 70 and 180 mg/dL, and that insulin drips should be initiated for blood glucose levels 200 mg/dL. We administer regular insulin intravenously or subcutaneously when the glucose values exceed 150 mg/dL or glucosuria becomes moderate to severe (500 mg/dL or greater). Table 60-12 contains an algorithm for intravenous or subcutaneous administration of regular insulin. While fingersticks for glucose are routinely checked every 6 hours in most patients, they can be increased to every 3 or 4 hours in patients who need better control. Direct addition of regular human insulin to the PN solution usually begins with 0.1 U of insulin/g of dextrose (i.e., 15 U/L in 15% dextrose, 20 U/L in 20% dextrose). A continuous insulin infusion of regular human insulin is used in patients who continue to be intolerant with the above interventions (see Table 60-13). Strategies other than insulin drips have been recommended for optimizing glycemic control in patients receiving PN. Avoiding overfeeding with hypocaloric regimens for obese patients and limiting caloric goals to 25 total kcal/kg per day for nonobese individuals have been effective. Dextrose should be restricted to less than 200 g on day 1 of PN, with patients at high risk for hyperglycemia (i.e., history of diabetes, corticosteroid use, etc.) receiving no more than 100 g per day. When baseline serum glucose concentrations exceed 300 mg/dL, PN should be instituted when serum glucose concentrations are below 200 mg/dL. Daily intake of dextrose

CHAPTER CHAPTER 60 X

patients with normal organ function and relatively normal fluid balance. Electrolyte components of PN may vary considerably in these types of patients depending on serum concentrations, concomitant drug therapy, acid–base status, pre-injury nutritional status, and extrarenal losses of fluid and electrolytes.

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TABLE 60-12 Algorithm for Regular Insulin Administration

SECTION 5 X

Plasma Glucose (mg/dL) 79c 80–99 101–120 121–150 151–200 201–250 251–300 301–350 351–400 400c

SQ Insulin Dose (U)a 1 ampule D50W No treatment No treatment No treatment 2 4 8 12 16 20

IV Bolus Insulin Dose (U)b 1 ampule D50W No treatment No treatment No treatment 2 4 6 8 10 12

Insulin Infusion Rate (U/h) 1 ampule D50W Discontinue Discontinue 1 2 4 6 8 10 12

a

SQ administration of regular insulin should not be more often than every 4 hours.

b

IV administration of regular insulin should not be more often than every 1 hour.

c

Notify the physician and order a stat serum glucose.

calories should be advanced toward goal only when serum glucose concentrations can be maintained under this level. Patients who have experienced significant glucosuria resulting in an osmotic diuresis will often need to be supplemented with intravenous fluid to prevent dehydration. Intravenous solutions such as 0.45% sodium chloride or 0.22% sodium chloride injection are very effective in these situations.

■ Essential Fatty Acid Deficiency As long as at least 2–4% of total calories from PN are given as essential fatty acids (i.e., linoleic acid and linolenic acid), essential fatty acid deficiency (EFAD) should be prevented. Most trauma patients will receive from 15% to 25% of total calories as IVFE during PN, which easily prevents EFAD and also provides a source of NCPs. Occasionally, a critically ill patient who is receiving PN will have sustained hypertriglyceridemia (e.g., 500 mg/dL). Most practitioners would withhold intravenous lipid in this situation until the serum triglyceride concentration falls below 400 mg/dL. After 2 weeks of fat-free PN in the adult, biochemical evidence of EFAD occurs, with symptoms following as early as 1 week later. Some practitioners have administered small doses of intravenous lipid cautiously to

TABLE 60-13 Equation for Calculating Nitrogen Balance protein intake (g)

Nitrogen balance (g)  _________________  [urinary 6.25 (conversion factor) excrertion of urea nitrogen (g) 4] Note: The 4 g in this equation is used as a “fudge factor” to account for skin, fecal, and non–urea nitrogen losses. The conversion factor for 6.25 g of protein  1 g nitrogen.

prevent EFAD during hypertriglyceridemia, while others have attempted to give essential fatty acids with the topical administration of safflower or sunflower oil.

■ Micronutrient Deficiencies Zinc is a trace element that is concentrated in small and large bowel fluids. Patients who have substantial ostomy losses are prone to develop zinc deficiency and should be supplemented with extra zinc in the PN solution. The stress of injury will cause enhanced urinary excretion of zinc, so the recommendation is to give at least 5 mg per day during PN administration in trauma patients. Trauma patients with a history of alcohol abuse who are to receive PN often need supplemental thiamine and folic acid added to the solution over and above standard vitamin additives. Although not widely appreciated, thermal injury patients experience high rates of postburn bone disease. Klein et al. recently found a defect in the skin conversion of 7-dehydrocholesterol into previtamin D3.77 In children with a mean time of 14 months after their burn injury, skin 7-dehydrocholesterol was significantly lower in the burn scar than in unburned controls, and previtamin D3 was significantly lower than controls in both burn scar and unburned skin adjacent to the scar. Low serum 25-hydroxyvitamin D concentrations were also found. Obviously, adults are at risk for developing postburn bone disease, especially in women after menopause and as both men and women attain ages beyond 50 years. These findings also suggest that vitamin D supplementation should be encouraged to prevent bone disease in this particular population of patients.

TRANSITION TO ENTERAL NUTRITION Most trauma patients who receive PN have a GI tract that becomes functional with recovery. Nasogastric tubes for suction can be removed as the patient regains bowel function. As oral

Nutritional Support and Electrolyte Management

MONITORING THERAPY The fluid administered during PN in critically ill patients provides anywhere from 50% to 95% of the patient’s intake once the goal rate is attained. Therefore, all general monitoring measurements become exceedingly important to the critical care practitioner responsible for prescribing the administration of PN. Fluid status and fluid balance should be assessed each day in critically ill trauma patients. The PN formula should be concentrated and reduced in sodium for the overloaded patients. Patients who are euvolemic but require large volumes of fluid can have the PN solution administered with addition of IVF to keep the patient in proper water balance. Laboratory measurements for glucose, sodium, potassium, acid/base status, and renal function should be done daily in the critically ill trauma patient. Laboratory measurements for calcium, phosphorus, and magnesium should be performed at least three times a week, while triglyceride concentrations should be assessed weekly during the acute phase of injury in this patient population. After collection of a 24-hour urine for volume and urea nitrogen, nitrogen balance can be calculated by finding the difference between nitrogen intake from PN (and enteral tube feeding or oral intake if applicable) and nitrogen output (see Table 60-13). Generally, nitrogen equilibrium in the young, stressed, previously healthy trauma patient is an appropriate goal. Patients who have spinal cord or severe head injuries will remain in negative nitrogen balance even when a dose of protein of 2 g/kg per day is given because of disuse atrophy. Nitrogen equilibrium usually can be attained 3–4 weeks after injury in these cases. Other practitioners favor the serial monitoring of serum proteins during administration of PN. Serum albumin concentration is usually depressed following trauma mainly due to redistribution from the intravascular space to the interstitial space. It takes several months for this protein to normalize, so

it is not a good marker of nutrition support efficacy. Serum proteins with short half-lives such as prealbumin (2 days) and transferrin (7 days) have the potential of rising acutely with adequate nutritional support. They are also very sensitive to the clinical course of the patient and will rise and fall independently of nutrition intake when the patient is recovering or decompensating, respectively. Assessment of CRP will help determine whether the decline in short-term serum proteins (i.e., prealbumin) is associated with an acute-phase response or nutritional deficiency. CRP is recognized as a positive acute-phase protein, defined as one whose plasma concentration increases by at least 25% during inflammatory disorders. If CRP is elevated and prealbumin has fallen, this is more indicative of the systemic response to inflammation. However, a falling prealbumin with a concurrent low CRP concentration may represent an inadequate intake of energy or protein. Use of these basic principles can assist the clinician in determining the appropriate time to alter a patient’s nutritional regimen.

ANABOLIC AGENTS IN TRAUMA PATIENTS It is recognized that standard nutritional support in patients subjected to severe trauma rarely allows them to attain nitrogen equilibrium during the first 2 weeks following injury. In fact, some severely injured patients may lose up to 30–40 g of nitrogen per day during the early flow phase of injury. Because there are toxicities associated with excessive administration of specialized nutrition support, anabolic agents as adjunctive therapy with parenteral or enteral nutrition to enhance recovery have been considered. There are some data supporting the administration of GH, IGF-I, or anabolic steroids to patients with polytrauma. Petersen et al. reported significantly improved nitrogen balance and whole-body protein synthesis following the administration of GH with PN when compared with a group receiving PN alone.78 Our work has shown that GH affects visceral protein status and increases serum albumin in critically injured patients but has relatively little effect on nitrogen retention in severely immobilized patients.79 Unfortunately, patients receiving GH tended to be hyperglycemic, particularly if there were infectious complications. The safety of GH therapy use has been further questioned based on two well-designed multicenter trials conducted in Europe, which reported an increase in mortality among critically ill patients treated with GH. These two independent, prospective, double-blind, randomized trials were conducted in parallel involving 247 Finnish patients and 285 patients from other European countries, and the results were published as one report in the New England Journal of Medicine. A total of 532 critically ill patients received high-dose GH (0.1  0.02 mg/kg per day) or placebo until discharge from the ICU or for a maximum of 21 days. In the Finnish study, mortality rate was significantly higher in the GH group as compared with the placebo group (39% vs. 20%, P  .001).80 A similar finding was observed in the multinational study conducted in other European countries, with a 44% mortality rate in the treatment group versus 18% in the placebo group. Previous trials in ICU patients and thermal injury patients demonstrated improvements in lean tissue mass accretion or wound healing and none demonstrated

CHAPTER CHAPTER 60 X

nutrition is introduced and progressed, weaning of the PN solution becomes an important issue. Generally, weaning of PN only begins when the trauma patient has demonstrated tolerance to at least a full liquid diet (i.e., one that can be nutritionally complete). Once the patient is ingesting at least one half a nutritionally complete diet, the PN can be decreased to a lower rate. As the patient approaches an intake of two thirds to three fourths of the diet, the PN can be discontinued. Many trauma patients will be unable to or will not eat orally when the GI tract is recovering. These patients become excellent candidates for enteral tube feeding, either temporarily until oral intake is established or permanently in the patient in a chronic vegetative state where the decision has been made to provide adequate nutrition. Generally, the PN solution is weaned as the rate of enteral tube feeding is increased. This way the patient continues to receive adequate nutrition during the transition to nutritional support via the GI tract. Once patients are receiving three fourths to complete enteral nutrition, the PN can be discontinued. Most trauma patients eventually progress to an oral diet and ingest sufficient amounts so that the enteral tube feeding can be discontinued as well.

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SECTION 5 X

a decrease in survival. Herndon et al. have demonstrated improved healing of donor sites and shorter length of stay/ percent burn in thermally injured children who received recombinant GH as adjunctive therapy to nutrition support.81 However, the Finnish and multinational studies excluded patients with burns or septic shock and trauma patients accounted for less than 10% of the total population. Demographic data also revealed that 95% of patients from both trials combined had respiratory failure on enrollment and the average age of patients was 60 years. Despite these differences in patient characteristics and study methodology, these results sharply diminished the enthusiasm of practitioners to use recombinant GH therapy in adult trauma patients. Much of the effects of GH occur because of IGF-I. IGF-I is produced by the liver in response to GH but does not have the hyperglycemic effects induced by direct GH administration. In a phase II safety and efficacy trial using IGF-I in patients with moderate or severe head injury, Hatton et al.82 reported that patients receiving the hormone had significantly decreased nitrogen excretion. A subset of patients with GCS scores of 5–7 who received IGF-I demonstrated improved neurologic outcome at 6 months postinjury.83 One group of investigators has published several positive studies evaluating the use of oxandrolone, a newer anabolic agent, in thermal injury patients.84 Reductions in weight loss and net nitrogen loss accompanied by increases in donor site wound healing and rates of weight restoration in the recovery phase have been observed in burn patients (total body surface area burns of 40–70%) receiving oxandrolone 20 mg per day. One study85 evaluated oxandrolone in multiple trauma patients and showed no significant differences in length of hospital stay, length of ICU stay, body cell mass, or infectious complications between oxandrolone 20 mg per day and placebo. Thus, more clinical research with IGF-I and anabolic steroids is needed in trauma patients.

REFERENCES 1. McClave SA, Snider HL. Understanding the metabolic response to critical illness: factors that cause patients to deviate from the expected pattern of hypermetabolism. New Horiz. 1994;2:139. 2. Cerra FB. Metabolic and nutritional support. In: Mattox KL, Feliciano DV, Moore EE, eds. Trauma. 3rd ed. Stamford, CT: Appleton & Lange; 1996:1155. 3. Frankel WL, Evans NJ, Rombeau JL. Scientific rationale and clinical application of parenteral nutrition in critically ill patients. In: Rombeau JL, Caldwell MD, eds. Clinical Nutrition: Vol. 2. Parenteral Nutrition. 2nd ed. Philadelphia: Saunders; 1993:597. 4. Moore FD. Bodily changes during surgical convalescence. Ann Surg. 1953;137:289. 5. Shaw JHF, Wolfe RR. An integrated analysis of glucose, fat and protein metabolism in severely traumatized patients: studies in the basal state and the response to intravenous nutrition. Ann Surg. 1989; 207:63. 6. Souba WW. Glutamine: a key substrate for the splanchnic bed. Annu Rev Nutr. 1991;11:285. 7. Shaw JHF, Wolfe RR. Determination of glucose turnover and oxidation in normal volunteers and septic patients using stable and radioisotopes: the response of glucose infusion and total parenteral nutrition. Aust N Z J Surg. 1986;56:785. 8. Jahoor F, Herndon DN, Wolfe RR. Role of insulin and glucose in the response of glucose and alanine kinetics in burn injured patients. J Clin Invest. 1986;78:807.

9. Stoner HB, Frayn KN, Barton RN, et al. The relationship between plasma substrates and hormone and the severity of injury in 277 recently injured patients. Clin Sci (Lond). 1979;56(6):563–573. 10. Kenler AS, Swails WS, Driscoll DF, et al. Early enteral feeding in postsurgical cancer patients: fish oil structured lipid-based polymeric formula versus a standard polymeric formula. Ann Surg. 1996; 223:316. 11. The Veteran Affairs Total Parenteral Nutrition Cooperative Study Group. Perioperative total parenteral nutrition in surgical patients. N Engl J Med. 1991;325:525. 12. Kudsk KA, Croce MA, Fabian TC, et al. Enteral vs. parenteral feeding: effects on septic morbidity following blunt and penetrating abdominal trauma. Ann Surg. 1992;215:503. 13. Moore FA, Moore EE, Jones TN. Benefits of immediate jejunostomy feeding after major abdominal trauma—a prospective randomized study. J Trauma. 1986;26:874. 14. Moore FA, Moore EE, Jones TN, et al. TEN vs. PN following major abdominal trauma—reduced septic morbidity. J Trauma. 1989;29:916. 15. Moore FA, Feliciano DV, Andrassy RJ, et al. Early enteral feeding, compared with parenteral, reduces postoperative septic complications: the results of a meta-analysis. Ann Surg. 1992;216:172. 16. Kudsk KA, Minard G, Croce MA. A randomized trial of isonitrogenous enteral diets following severe trauma: an immune-enhancing diet (IED) reduces septic complications. Ann Surg. 1996;224:531. 17. Moore FA, Moore EE, Kudsk KA, et al. Clinical benefits of an immuneenhancing diet for early postinjury enteral feeding. J Trauma. 1994; 37:607. 18. Sena MJ, Utter GH, Cuschieri J, et al. Early supplemental parenteral nutrition is associated with increased infectious complications in critically ill trauma patients. J Am Coll Surg. 2008;207(4):459–467. PMID 18926446. 19. Alexander JW, Macmillan BG, Stinnett JD, et al. Beneficial effects of aggressive protein feeding in severely burned children. Ann Surg. 1980; 192:505. 20. Border JR, Hassett J, LaDuca J, et al. The gut origin septic states in blunt multiple trauma (ISS 40) in the ICU. Ann Surg. 1987;206:427. 21. Adams S, Dellinger EP, Wertz MJ, et al. Enteral versus parenteral nutritional support following laparotomy for trauma: a randomized prospective trial. J Trauma. 1986;26:882. 22. Fagon JY, Chastre J, Domart Y, et al. Nosocomial pneumonia in patients receiving continuous mechanical ventilation: prospective analysis of 52 episodes with use of a protected specimen brush and quantitative culture techniques. Am Rev Respir Dis. 1989;139:877. 23. Eyer SD, Micon LT, Konstantinides FN, et al. Early enteral feeding does not attenuate metabolic response after blunt trauma. J Trauma. 1993;34:639. 24. Borlase BC, Moore EE, Moore FA. The abdominal trauma index—a critical reassessment and validation. J Trauma. 1990;30:1340. 25. Rapp RP, Young B, Twymand D, et al. The favorable effect of early parenteral feeding on survival in head injured patients. J Neurosurg. 1983;58:906. 26. Young B, Ott L, Twyman D, et al. The effect of nutritional support on outcome from severe head injury. J Neurosurg. 1987;67:668. 27. Grahm TW, Zadrozny DB, Harrington T. The benefits of early jejunal hyper-alimentation in the head-injured patient. Neurosurgery. 1989; 25:729. 28. Borzotta AP, Pennings J, Papasadero B, et al. Enteral versus parenteral nutrition after severe closed head injury. J Trauma. 1994;37:459. 29. Minard G, Kudsk KA, Melton S, et al. Early versus delayed feeding with an immune-enhancing diet in patients with severe head injuries. JPEN J Parenter Enteral Nutr. 2000;24:145. 30. Herndon DN, Barrow RE, Stein M, et al. Increased mortality with intravenous supplemental feeding in severely burned patients. J Burn Care Rehabil. 1989;10:309. 31. Kulkarni AD, Fanslow WC, Drath DB, et al. Influence of dietary nucleotide restriction on bacterial sepsis and phagocytic cell function in mice. Arch Surg. 1986;121:169. 32. Daly JM, Lieberman MD, Goldfine J, et al. Enteral nutrition with supplemental arginine, RNA, and omega-3 fatty acids in patients after operation: immunologic, metabolic, and clinical outcome. Surgery. 1992; 112:56. 33. Bower RH, Cerra FB, Bershadsky B, et al. Early enteral administration of a formula supplemented with arginine, nucleotides, and fish oil in intensive care unit patients: results of a multicenter prospective, randomized, clinical trial. Crit Care Med. 1995;23:436. 34. Gottschlich MM, Jenkins M, Warden GD, et al. Differential effects of three enteral dietary regimens on selected outcome variables in burn patients. JPEN J Parenter Enteral Nutr. 1990;14:225.

Nutritional Support and Electrolyte Management 60. Brown KA, Dickerson RN, Morgan LM, et al. A new graduated dosing regimen for phosphorus replacement in patients receiving nutrition support. JPEN J Parenter Enteral Nutr. 2006;30:209–214. 61. Holmes JH IV, Brundage SI, Yuen P, et al. Complications of surgical feeding jejunostomy in trauma patients. J Trauma. 1999;47: 1009. 62. MacLaren R, Kuhl DA, Gervasio JM, et al. Sequential single doses of cisapride, erythromycin, and metoclopramide in critically ill patients intolerant to enteral nutrition: a randomized, placebo-controlled, crossover study. Crit Care Med. 2000;28:438. 63. Heyland DK, Tougas G, Cook DJ, et al. Cisapride improves gastric emptying in mechanically ventilated, critically ill patients. A randomized, double-blind trial. Am J Respir Crit Care Med. 1996;154:1678. 64. Nguyen NQ, Chapman M, Fraser RJ, et al. Prokinetic therapy for feeding intolerance in critical illness: on drug or two? Crit Care Med. 2007;35: 2561–2567. 65. Cutie AJ, Altman E, Lenkel L. Compatibility of enteral products with commonly employed drug additives. JPEN J Parenter Enteral Nutr. 1983;7:186. 66. Lutomski DM, Gora ML, Wright SM, et al. Sorbitol content of selected oral liquids. Ann Pharmacother. 1993;27:269. 67. Mowatt-Larssen CA, Brown RO, Wojtysiak SL, et al. Comparison of tolerance and nutritional outcome between a peptide and a standard enteral formula in critically ill, hypo-albuminemic patients. JPEN J Parenter Enteral Nutr. 1992;16:20. 68. Snydman DR. Safety of probiotics. Clin Infect Dis. 2008;46:S104. 69. Brenner DW, Schellhammer PF. Mortality associated with feeding catheter jejunostomy after radical cystectomy. Urology. 1987;30:337. 70. O’Grady N, Alexander M, Dellinger E, et al. Guidelines for prevention of intravascular catheter-related infections. Centers for Disease Control and Prevention. MMWR Recomm Rep. 2002;55(RR10):1. 71. Venus B, Smith RA, Patel CB, et al. Hemodynamic and gas exchange alterations during Intralipid infusion in patients with adult respiratory distress syndrome. Chest. 1989;95:1278. 72. Department of Health and Human Services, Food and Drug Administration. Parenteral multivitamin products, drugs for human use—drug efficacy study implementation amendment. Federal Register 2000;65(77):21200–21201]. 73. Berger MM, Cavadini C, Chiolero R, et al. Influence of large intakes of trace elements on recovery after major burns. Nutrition. 1994;10:327. 74. Fitzgerald K, Mikalunas V, Rubin H, et al. Hypermanganesemia in patients receiving total parenteral nutrition. JPEN J Parenter Enteral Nutr. 1999;23:333. 75. Pasquel FJ, Spiegelman R, McCauley M, et al. Hyperglycemia during total parenteral nutrition: an important marker of poor outcome and mortality in hospitalized patients. Diabetes Care. 2010;33:739. 76. Van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in critically ill patients. N Engl J Med. 2001;345:1359. 77. Klein GL, Chen TC, Hollick MF, et al. Synthesis of vitamin D in skin after burns. Lancet. 2004;363:291. 78. Petersen SR, Holaday NJ, Jeevanandam M. Enhancement of protein synthesis efficiency in parenteral fed trauma victims by adjuvant recombinant human growth hormone. J Trauma. 1994;36:726. 79. Behrman SW, Kudsk KA, Brown RO, et al. The effect of growth hormone on nutritional markers in enterally fed immobilized trauma patents. JPEN J Parenter Enteral Nutr. 1995;19:41. 80. Takala J, Ruokonen E, Webster NR, et al. Increased mortality associated with growth hormone treatment in critically ill adults. N Engl J Med. 1999;341:785. 81. Herndon DN, Barrow RE, Kunkel KR, et al. Effects of recombinant human growth hormone on donor-site healing in severely burned children. Ann Surg. 1990;212:424. 82. Hatton J, Rapp RP, Kudsk KA, et al. Intravenous insulin-like growth factor-I (IGF-1) in moderate-to-severe head injury: a phase II safety and efficacy trial. J Neurosurg. 1997;86:779. 83. Hausmann DF, Nutz V, Rommelsheim K, et al. Anabolic steroids in polytrauma patients. Influence on renal nitrogen and amino acid losses: a double-blind study. JPEN J Parenter Enteral Nutr. 1990;14:111. 84. Demling RH, DeSanti L. Oxandrolone, and anabolic steroid, significantly increases the rate of weight gain in the recovery phase after major burns. J Trauma. 1997;43:47. 85. Gervasio JM, Dickerson RN, Swearingen J, et al. Oxandrolone in trauma patients. Pharmacotherapy. 2000;20:1328.

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35. Houdijk AP, Rijnsburger ER, Jansen J, et al. Randomised trial of glutamine-enriched nutrition on infectious morbidity in patients with multiple trauma. Lancet. 1998;352:772. 36. Mendez C, Jurkovich GJ, Garcia I, et al. Effects of an immune-enhancing diet in critically injured patients. J Trauma. 1997;42:933. 37. Heyland DK, Dhaliwal R, Drover JW, et al. Canadian clinical practice guidelines for nutrition support in mechanically ventilated, critically ill adult patients. JPEN J Parenter Enteral Nutr. 2003;27:355. 38. Bertolini G, Lapichino G, Radrizzani D, et al. Early immunonutrition in patients with severe sepsis: results of an interim analysis of a randomized multicenter clinical trial. Int Care Med. 2003;29:834. 39. Ochoa JB, Makarenkova V, Bansal V. A rational use of immune enhancing diets: when should we use dietary arginine supplementation? Nutr Clin Pract. 2004;19(3):216–225. 40. Galban C, Montejo JC, Mesejo A, et al. An immune-enhancing enteral diet reduces mortality rate and episodes of bacteremia in septic intensive care unit patients. Crit Care Med. 2000;28:643. 41. Atkinson S, Sieffert E, Bihari D. A prospective randomized, double-blind controlled clinical trial of enteral immunonutrition in the critically ill. Crit Care Med. 1998;26:1164. 42. McClave SA, Martindale RG, Vanek VW, et al. Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). JPEN J Parenter Enteral Nutr. 2009;33(3):277–316. 43. Moore FA, Moore EE, Poggetti R, et al. Gut bacterial translocation via the portal vein: a clinical perspective with major torso trauma. Trauma. 1991;31:629. 44. Kudsk KA. 2008 Rhoads lecture: of mice and men … and a few hundred rats. JPEN J Parenter Enteral Nutr. 2008;32(4):460–473. 45. Alverdy JC, Chang EB. The re-emerging role of the intestinal microflora in critical illness and inflammation: why the gut hypothesis of sepsis syndrome will not go away. J Leukoc Biol. 2008;83(3):461–466. 46. Fong Y, Marano MA, Barber E, et al. Total parenteral nutrition and bowel rest modify the metabolic response to endotoxin in humans. Ann Surg. 1989;210:449. 47. Moore FA, Moore EE. The evolving rationale for early enteral nutrition based on paradigms of multiple organ failure: a personal journey. Nutr Clin Pract. 2009;24(3):297–304. 48. Moore EE, Moore FA, Franciose RJ, et al. The postischemic gut serves as a priming bed for circulating neutrophils that provoke multiple organ failure. J Trauma. 1994;37:881. 49. Hwang T-L, Hwang S-L, Chen M-F. The use of indirect colorimetry in critically ill patients—relationship with measured energy expenditure to injury severity score, a septic severity score, and Apache II score. J Trauma. 1993;34:247. 50. The NICE-SUGAR Study Investigators. Intensive versus conventional glucose control in critically ill patients. N Engl J Med. 2009;360:1283. 51. Choban PS, Dickerson RN. Morbid obesity and nutrition support: is bigger different? Nutr Clin Pract. 2005;20:480. 52. Dickerson RN, Boschert KJ, Kudsk KA, et al. Hypocaloric enteral tube feeding in critically ill obese patients. Nutrition. 2002;18:241. 53. Choban PS, Burge JC, Scales D, et al. Hypoenergetic nutrition support in hospitalized obese patients: a simplified method for clinical application. Am J Clin Nutr. 1997;66L:546. 54. Burge JC, Goon A, Choban PS, et al. Efficacy of hypocaloric total parenteral nutrition in hospitalized obese patients: a prospective, doubleblind randomized trial. JPEN J Parenter Enteral Nutr. 1994;18:203. 55. Liu KJ, Cho MJ, Atten MJ, et al. Hypocaloric parenteral nutrition support in elderly obese patients. Am Surg. 2000;66:394. 56. Mirtallo JM, Kudsk KA, Ebbert ML. Nutritional support of patients with renal disease. Clin Pharm. 1984;3(3):253–263. PMID 6428798. 57. Pacht ER, DeMichele S, Nelson J. Enteral nutrition with eicosapentaenoic acid, gamma linolenic acid and antioxidants reduces alveolar inflammatory mediators and protein influx in patients with acute respiratory distress syndrome. Crit Care Med. 2003;31:491. 58. Singer P, Theilla M, Fisher H, et al. Benefit of an enteral diet enriched with eicosapentaenoic acid and gamma-linolenic acid in ventilated patients with acute lung injury. Crit Care Med. 2006;34:1033. 59. Pontes-Arruda A, Aragao A, Albuqerque J. Effects of enteral feeding with eicosapentaenoic acid, gamma linolenic acid, and antioxidants in mechanically ventilated patients with severe sepsis and septic shock. Crit Care Med. 2006;34:2325.

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CHAPTER 61

Multiple Organ Failure Angela Sauaia, Frederick A. Moore, and Ernest E. Moore

HISTORICAL PERSPECTIVE: EVOLVING CONCEPTS ON THE PATHOGENESIS OF MULTIPLE ORGAN FAILURE Our increasing ability to keep severely injured trauma patients alive resulted in the clinical syndrome called postinjury multiple organ failure (MOF). As advances in prehospital and acute hospital care conquered “the golden hour” and the trimodal distribution of trauma deaths described in the 1970s and 1980s slowly flattened its first mode, MOF emerged as the leading cause of late trauma death.1–3 Much of advance in the treatment of trauma and shock has been stimulated by military experience.4 In World War I, soldiers’ death on battle was initially attributed to toxins released by dead or dying tissue (Table 61-1).5 Cannon et al, via their observations on the battlefield in 1917, expanded this concept to question the role of hypovolemia; however, it was not until the 1930s that reduced circulating blood volume was recognized as the cause of shock and mortality.6 Casualties in World War II were initially resuscitated with plasma and later with blood. This continued in Korea where blood and plasma were administered until blood pressure returned to normal. In addition to rapid transport for definitive care in field medical units, blood and plasma resuscitation improved battlefield survival but resulted in late deaths due to oliguric renal failure. In the 1960s, Shires et al. proposed that extracellular fluid deficits (third space losses) compounded traumatic shock and demonstrated in animals that survival improved with balanced salt solutions.7 Consequently, crystalloid resuscitation was added to blood and plasma resuscitation in the Vietnam War and resuscitation end points focused on maintaining adequate urine output. Helicopter evacuation also enabled rapid transport of casualties and the overall mortality rate decreased. Although late deaths from renal failure declined, a new entity termed “shock lung” emerged as the primary cause of late deaths.5 This new disorder became recognized in civilian trauma centers as

the adult respiratory distress syndrome (ARDS).8 In the 1970s, subsequent improvements in advanced organ support such as mechanical ventilation (MV), vasoactive drugs, total parenteral nutrition, and hemodialysis armed physicians with better treatment to sustain the critically ill. Death from isolated pulmonary failure became rare, and a new syndrome of “multiple, progressive, or sequential systems failure” was recognized.9 Eiseman et al. in Denver coined the term “multiple organ failure” in 1977, and provided the first clinical description of 42 patients with progressive organ dysfunction.10 During the late 1970s MOF was thought to be the “fatal expression of uncontrolled infection.”11 In addition, at this time, studies indicated that organ failure was a bimodal phenomenon with distinct patterns: rapid single-phase MOF due to massive tissue injury and shock or delayed two-phase MOF due to moderate trauma and shock followed by delayed sepsis.12,13 While infection remained a frequent cause of organ failure, by the mid1980s it was convincingly shown that organ failure occurred in the absence of infection and the concept of “generalized autodestructive inflammation” emerged.14,15 By the 1990s, noninfectious inflammatory models of MOF became the focus.16 In this conceptual framework, patients are resuscitated into a state of early systemic hyperinflammation, referred to as the systemic inflammation response syndrome (SIRS) (Fig. 61-1). A mild response is presumed to be beneficial and resolves in most patients as they recover. In the “one-event” model, a massive traumatic insult overwhelms the capacity of the patient to respond to resuscitation and precipitates organ failure. In the more common, alternative “two-event” model, patients who are initially resuscitated to a moderate response (primed) are vulnerable to a second (activating) event that can also precipitate hyperinflammation leading to early organ failure. The timing of the second hit may vary from occurring shortly after the first hit, where the two are indistinguishable, to a delay, where the second event is conspicuous 12–36 hours later. Patients who escape early MOF become

Multiple Organ Failure

1129

TABLE 61-1 Historical Perspective of Postinjury Multiple Organ Failure

Mid-1970s Early 1880s Late 1980s

Proposed Etiology Wound toxins ↓ Blood volume ↓ Blood volume ↓ Extracellular fluid Shock Advanced age sepsis Uncontrolled infection Systemic inflammation Bacterial translocation SIRS/CARS

1990s 2000 to present

Cellular and subcellular signaling

Interventions Undefined Resuscitate to normal SBP Resuscitate to normal urine output Crystalloid resuscitation Advanced organ support

Clinical Patterns Cardiac failure Renal failure Respiratory failure

Prevent and treat septic complications Control inciting event Attenuate early inflammation Improved resuscitation end points Avoid secondary events Immunomodulation

Infectious models

susceptible to infection during the so-called compensatory antiinflammatory response syndrome (CARS). If infected during this window, patients are at risk of developing late MOF. Other second hits include abdominal compartment syndrome (ACS), sepsis, fat embolus, MV, blood transfusions, long bone fixation, and secondary surgery.17 More recently, a new model has emerged in which it is believed the injury triggers simultaneous, opposite responses: the proinflammation (SIRS) and the anti-inflammation (CARS)

Multiple organ failure

Inflammatory models Dysfunctional inflammation Decreased MOF incidence and severity

(Fig. 61-1).18 The term compensatory inflammation is in fact considered a misnomer as CARS appears to occur in response to the injury (not to SIRS). In this paradigm, the development of MOF is related to the intensity and the balance between these inflammatory responses to trauma. Severe SIRS, due to unbalanced early proinflammation, causes early MOF and can eventually result in a fulminant proinflammatory death. On the other hand, early anti-inflammation is directed at limiting proinflammation, creating a preconditioned state

Activation 2nd event Pro-inflammation

Early MOF

Injury 1st event

Priming SIRS Innate immune system Adaptive immune system

Recovery

CARS • Tissue disruption • Cellular shock • Blood component transfusion • Coagulation • Genotype FIGURE 61-1 Pathogenesis of multiple organ failure.

Late MOF Infection 2nd event

CHAPTER CHAPTER 61 X

Time Period World War I World War II Vietnam War

Management of Complications after Trauma

SECTION 5 X

where the host is protected against second hits, and hastening the healing process. Anti-inflammation is also associated with apoptosis and depression in adaptive immunity. When countering unbalanced proinflammation, persistent antiinflammation can result in severe CARS. This sets the stage for immunoparalysis, impaired wound healing, recurrent nosocomial infections, and late MOF, which can cause an indolent death.18 This new construct evolved from clinical observations and experimental studies at the bench level, and remains the foundation of contemporary MOF research. Research during the past decade has progressed toward further explaining these inflammatory mechanisms at the cellular and subcellular levels. New strategies to reduce secondary insults and to modulate the inflammatory responses in the early and late postinjury periods are currently undergoing intense clinical investigation. In sum, the presentation and outcome of postinjury MOF has changed considerably over the past 15 years. Yet, as we will describe in the next sections, MOF victims continue to suffer with high morbidity and long hospital stays and consume an inordinate amount of resources.

To determine whether the incidence reduction was due to a decline in disease severity of the patients admitted to our center, we examined changes in the major risk factors of postinjury MOF: age, Injury Severity Score (ISS), and number of RBC units transfused within the first 12 hours.23 Patients’ ISS and age increased over time while the proportion of patients requiring more than 6 U of RBC in the first 12 hours decreased after the implementation of a new protocol of judicious blood product utilization. The decrease in blood products use over time remained statistically significant after adjusting for age and ISS.22 In the early 1990s, about half of the MOF cases presented early (3 days after injury) while the remaining cases presented later, most often around 7 days. This bimodal presentation pattern, first recognized by Faist et al. in 1983,13 seems to be changing in recent years, with the second peak gradually leveling out (Fig. 61-2), possibly as a result of improved prevention and treatment of second insults. The risk factors for early MOF include an ISS 24, emergency department (ED) systolic blood pressure less than 90 mm Hg, blood transfusions 6 U within 12 hours of injury, and a lactate level 2.5 mmol/L measured between 12 and 24 hours after injury.24 Major infections are more likely to be a symptom that followed (sometimes worsening organ dysfunction) than a trigger that precipitated early MOF. Early MOF is typically associated with a higher incidence of heart failure than late MOF. Late MOF (72 hours postinjury), consistent with the distinct two-event construct, appears to be related to the increased risk of infection and systemic sepsis that is attributed to the relative immunosuppression associated with severe trauma. Independent risk factors for late MOF include age over 55 years, blood transfusion more than 6 U within 12 hours of injury, early base deficit more than 8 mEq/L in the first 12 hours postinjury, and a lactate level greater than 2.5 nmol/L measured between 12 and 24 hours postinjury.24 Although the risk factors for both early and late MOF included blood transfusion, base excess, and lactate levels, the shock indices were

EPIDEMIOLOGY AND CLINICAL RELEVANCE The epidemiological descriptions of MOF vary widely. The reported incidence of postinjury MOF varies from as low as single digit numbers to values approaching 40%, with casefatality rates also varying within similarly large ranges.19 Recent studies have been inconsistent regarding changes in the incidence or the mortality associated with postinjury MOF, with some reporting no change in the incidence but a decreased mortality20 while others reporting both decreased incidence and mortality compared with historical controls.21 Reviews of patients prospectively included in our Denver MOF dataset showed a significant reduction in the incidence of MOF, with the most dramatic decrease being observed from 1998 to 2004, while MOF case-fatality rate has not shown a significant decrease.22

12%

1995–1996 1999–2000 1997–1998 2001–2002 2003–2004

10% MOF incidence

1130

8% 6% 4% 2% 0% 2

3

4

5

6

7

Post admission day FIGURE 61-2 Temporal distribution of MOF over time.

8

9

10

11

Multiple Organ Failure

PATHOPHYSIOLOGY ■ The First Hit: Initial Inflammatory, Hormonal, and Immune Responses to Trauma The model of postinjury MOF, described in a previous section, was derived from a two-way translational model in which information was exchanged between epidemiological studies, predictive models, and basic investigations using in vivo and in vitro models. As mentioned above, severe trauma patients are resuscitated into an early state of systemic inflammation or SIRS. The American College of Chest Physicians and the Society of Critical Care Medicine defined SIRS as two or more of the following criteria26: (1) temperature 36.8°C or 38.8°C; (2) heart rate 90/min; (3) respiratory rate 20 breaths/min or pCO2 32 mm Hg; and (4) WBC 4,000/mL or 12,000 mL or greater than 10% immature forms. Figure 61-3 illustrates the current framework for the immunoinflammatory response to trauma. SIRS is the manifestation

of the immunoinflammatory activation that occurs in response to ischemia–reperfusion (I/R) injury and released factors from disrupted tissue, that is, the damage-associated molecular patterns (DAMPs). In trauma, hemorrhagic shock following injury causes whole-body hypoperfusion, followed by subsequent reperfusion during resuscitation, which circulates cytokines, proinflammatory lipids, and proteins that prime polymorphonuclear neutrophils (PMNs) within 3–6 hours after injury.17 The CARS includes (a) apoptotic loss of intestinal lymphocytes and epithelial cells, (b) PMN and monocytic deactivation, (c) anergy characterized by suppressed T-cell proliferative responses, and (d) a shift from a THI to a TH2 phenotype.18 In the past, most studies attributed SIRS to hyperactivity of the innate immune system and CARS to dysfunction of the adaptive immune system, but recent evidence suggests that interactions between the innate and adaptive immune systems induce both SIRS and CARS and that the predominant mechanism for MOF is the balance between proinflammatory and counterinflammatory states.27

Role of the Gut The gut is the last organ to have its circulation restored after ischemia, and is thought to play a pivotal role in the pathogenesis of postinjury MOF.18,28 Initially, the dominant hypothesis linking the gut to MOF was related to bacterial translocation: intestinal mucosa increased permeability allowed gut bacteria and/or endotoxin to be translocated to the circulation leading to sepsis and MOF. However, inconsistent results regarding the role of bacteria and endotoxin in the genesis of MOF led to experiments demonstrating that the mesenteric lymph acted as a bridge between the gut and the systemic circulation, allowing gut-derived inflammatory mediators and primed neutrophils to reach the systemic circulation. Via the thoracic duct, these mediators reach the pulmonary circulation and affect the lungs before any other organ, which is consistent with human studies demonstrating that postinjury respiratory dysfunction is an obligate event that precedes heart, liver, and kidney failure.29,30

Role of the PMN and Other Cells PMN kinetics are different between MOF patients and nonMOF patients. Both groups develop neutrophilia at 3 hours postinjury; however, in patients who develop MOF there is a rapid neutropenia between 6 and 12 hours postinjury suggesting end-organ sequestration.31 PMNs marginated to end organs cause direct local cytotoxic cellular effects via degranulation, and the release of nitric oxide and reactive oxygen species. They also have remote systemic proinflammatory cytokine effects, releasing proinflammatory mediators including IL-8, IL-6, and TNF-α. In non-MOF, neutrophil priming and neutrophilia are not followed by neutropenia, and resolve over the next 36 hours without end-organ damage.32 Following trauma there is an immediate increase in adhesion molecules, including L-selectin and CD18, which allow PMNs to slow and roll along the endothelium and marginate out of circulation.17,33 Antibodies directed against the CD11b/CD18 components of the adhesion receptor complex between leukocytes

CHAPTER CHAPTER 61 X

stronger risk factors for early MOF, whereas major infections were more frequently classified as triggers in patients who developed late MOF. Patients with late MOF also had a higher incidence of liver failure but a lower mortality (16%) than early MOF patients. Mortality is similar for early and late MOF as well as other adverse outcomes such as intensive care unit (ICU) length of stay and ventilation time. Regarding individual organ patterns, the lung is virtually always the first organ to show evidence of dysfunction in the absence of preexisting disease.25 Lung dysfunction precedes heart dysfunction by an average of 0.6  0.2 days, liver dysfunction by 4.8  0.2 days, and kidney dysfunction by 5.5  0.5 days. The number of involved organs and the severity of other organ dysfunction also seemed dependent on the severity of lung impairment. Of course, these conclusions are limited by our measurements of individual organ dysfunctions, that is, our measurements of lung dysfunction are far more sensitive to function changes than our measurements of liver or kidney function. While MOF incidence seems to be decreasing, these patients continue to demand an excessive amount of hospital resources. Among MOF patients, the proportion of patients with less than 21 ventilator-free days (VFD) and less than 14 ICU-free days (IFD) has significantly increased steadily over the past decade from 90% to 100%. Indeed, from 1994 to 1998, there were 138 postinjury MOF patients in our ICU, who required 3,428 ICU days and 2,785 MV days. While from 1999 to 2003, there were less MOF patients (n  123, an 11% decrease), they required 3,548 ICU days and 2,812 MV days. In brief, despite reduction in incidence, MOF patients are responsible for an even larger amount of resources than in the past. Each MOF patient required a median number of 21 ICU days and 17.5 MV days from 1994 to 1998, while in the 1998–2003 period, the median number of ICU days was 26 and that of MV days was 21. Collectively, these numbers strongly support that despite a reduction in the MOF incidence, these patients still suffer through long hospital stays, have high morbidity, and consume an inordinate amount of resources.

1131

1132

Management of Complications after Trauma

Tissue disruption

Tissue ischemia/reperfusion

SECTION 5 X

Blood transfusion

–

+

Cholinergic response

Genetic modification

Immuno inflammatory activation Neutrophils

Platelets

Exaggerated innate immunity

Microvascular thrombosis

Macrophages

Endothelium

Complement

Mediators: Cytokines, Eicosanoids, Nitric oxide, Oxidants, Proteases, DAMPS, Alarmins

Endothelium/ epithelium barrier failure

Mitochondrial dysfunction

Cellular disruption

Coagulation

Toll-like receptors

Suppressed adaptive immunity

Apoptosis

Organ dysfunction

FIGURE 61-3 Immunoinflammatory response to trauma.

and endothelium significantly attenuate lung injury and prevent the neutropenia associated with tissue sequestration during sepsis, further supporting that adherence of neutrophils to endothelium is a critical step in local tissue injury.33 Circulating monocytes and tissue macrophages also become primed after severe injury and most authorities agree that microvascular endothelium has an integral role in postinjury priming of the innate inflammatory response.32 Finally, other studies have demonstrated that the organ damage is also dependent on complement activation through the classical pathway mediated by natural IgM antibody produced by B1 lymphocytes.27

Cytokines The hemodynamic, metabolic, and immune responses are mainly regulated by endogenous mediators referred to as cytokines, produced by diverse cell types at the site of injury and by systemic immune cells.33 Cytokines bind to specific cellular receptors resulting in activation of intracellular signaling pathways that regulate gene transcription and influence immune cell activity, differentiation, proliferation, and survival. They also regulate the production and activity of other cytokines, which may either augment or attenuate the inflammatory response. There is also significant overlap in bioactivity among different cytokines.33 Cytokines can be classified into proinflammatory (TNF-α, MIP, GM-CSF, IFN-γ, IL-1, IL-2, IL-6, IL-8, IL-17, etc.) and anti-inflammatory cytokines (IL-4,

IL-10, IL-13), which downregulate synthesis of the proinflammatory cytokines.33 Recently, Jastrow et al. assessed the temporal cytokine expression (every 4 hours during 24 hours postinjury) during shock resuscitation in severely injured torso trauma patients.34 Median concentrations of IL-1 receptor antagonist (IL-1Ra), IL-8, eotaxin, granulocyte colony-stimulating factor (GCSF), granulocyte-macrophage colony-stimulating factor (CSF), inducible protein 10 (IP-10), monocyte chemotactic protein-1, and macrophage inflammatory protein-1 (MIP-1) were significantly greater in the MOF compared with those in the non-MOF subgroup at each time interval. Adams et al. demonstrated that IL-8 can activate PMNs via two different receptors, and differential early expression of these receptors may provide an explanation for why only selected patients develop MOF.35 The cytokine pattern after trauma also differs for patients developing early (less than 3 days) versus late (3 days) MOF. Analysis of cytokine serum biomarkers revealed that whereas early onset MOF was associated with an initial peak of IL-6 and IL-8 followed by a comparatively rapid return to baseline values, late MOF was characterized by a significant secondary increase of the proinflammatory cytokines IL-6 and IL-8.36 Moreover, plasma levels of soluble tumor necrosis factor-alpha receptors (sTNF-R p55, sTNF-R p75) progressively increased during the 10-day observation period, and higher values were associated with lethal outcome.

Multiple Organ Failure

PAMPS, Alarmins, and DAMPS Pathogen-associated molecular patterns (PAMPs) are exogenous microbial molecules that alert the organism to pathogens and are recognized by cells of the innate and acquired immunity system, primarily through Toll-like receptors (TLRs), and activate several signaling pathways (e.g., NF-κB). A new awareness of the close relationship between trauma- and pathogen-evoked responses recently emerged and the term “alarmin” was proposed to differentiate the endogenous molecules that signal tissue and cell damage.38 Together, alarmins and PAMPs comprise the DAMPs. Alarmins are rapidly released after nonprogrammed cell death but not by apoptotic cells. They recruit and activate receptor-expressing cells of the innate immune system, and also promote adaptive immunity responses. An example of an alarmin is the high-mobility group box 1 (HMGB1), a nuclear protein which binds to nucleosomes and promotes DNA bending. HMGB1 has been associated with SIRS and end-organ damage in animals, and shown to be elevated in trauma patients more than 30-fold above healthy controls as early as 1 hour postinjury.38–40 A recent study by Zhang et al. showed that injury releases mitochondrial DAMPs (MTDs) into the circulation with functionally important immune consequences. The authors suggest that since mitochondria are evolutionary endosymbionts derived from bacteria, the released MTDs have conserved similarities to bacterial PAMPs. Thus, these MTDs signal through innate immune pathways identical to those activated in sepsis to create a sepsis-like state. This mechanism may provide the key link between trauma, inflammation, and SIRS.41

Toll-Like Receptors TLRs are transmembranal proteins present in most body cell types, which form the major pattern recognition receptors that transduce signals in response to DAMPs.42 They were shown to participate in the recognition of endogenous alarmins released from damaged tissues after I/R injuries. Innate immune system responses are then initiated, including NF-αB activation, cell activation, and proinflammatory cytokine production.42 Inhibition of TLR2 or TLR4 seems to be beneficial in I/R injury in certain organs (hepatic, renal, cerebral, and heart) but not in gut I/R injuries. It is conceivable that because the gut mucosa is continuously exposed to local bacterial endotoxins, local TLRs are uniquely regulated to prevent persistent inflammatory activity. In spite of the distinct roles played by TR2 and TR4 in individual organs, our understanding of how the several TLR members interact among each other in I/R injuries is still limited, which may hinder the interpretation of interventions aimed at a specific TLR.42

Heat Shock Proteins (HSPs) HSPs are a family of molecular chaperones (e.g., Hsp70 and Hsp90) necessary for the folding of newly synthesized proteins in the cell and also for the protection of proteins during exposure to stressful situations such as heat shock, which causes proteins folded previously to unfold.43 Extracellular HSPs can interact with several receptors (including TLRs), and have been implicated in inducing secretion of proinflammatory cytokines. However, highly purified HSPs do not show any cytokine effects suggesting recombinant HSP products may be contaminated with PAMPs that appear to be responsible for the reported in vitro cytokine effects of HSPs.43 Thus, the reported HSP’s role in antigen presentation and cross-presentation and in vitro cytokine functions may be attributable to molecules bound to or chaperoned by HSPs.

Complement Complement system activation occurs immediately after trauma leading to production of biologically active peptides.28 Proinflammatory peptides include C3a, C3b, C4b (chemotaxis of leukocytes; degranulation of phagocytic cells, mast cells, and basophils; smooth muscle contraction and increased vascular permeability), and C5b-9 or membrane attack complex that leads to lysis of the target cells at the end stage of the complement activation cascade. Furthermore, complement activation results in the production of oxygen free radicals, arachidonic acid metabolites, and cytokines. Several studies suggest that complement activation, especially serum C3 and C3a levels, reflects severity and treatment of injury.28

Oxidative Stress Oxidative stress occurs when the level of toxic reactive oxygen intermediates (ROIs) overcomes endogenous antioxidant defenses as a result from either oxidant production excess or antioxidant defense depletion.44 ROIs are normally generated by mitochondrial oxidation, metabolism of arachidonic acid, activation of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in phagocytes, and activation of xanthine oxidase (XO) and play important roles in cellular homeostasis, mitosis, differentiation, and signaling.28 Excess ROI, however, causes direct oxidative injury to cellular proteins and nucleic acids, and cell membrane destruction by inducing lipid peroxidation.28,42,44 I/R injury leads to significant disturbances in the production of ROIs.28,42 During ischemia, hypoxemia leads to a shift from aerobic to anaerobic metabolism, with consumption of and decreased production of adenosine triphosphate (ATP). As ATP decreases, changes in cell membrane permeability result in intracellular Na increase causing cellular swelling and cell membrane damage. ATP reduction also alters cytosolic Ca2 levels leading to phospholipase and protease activation and cell damage. Increased ATP hydrolysis is followed by rising levels of AMP and purine metabolites. As reperfusion increases O2 availability, oxidation of purines produces urate and superoxide radicals, which can then produce the toxic hydroxyl radicals. In addition, superoxide radicals may be generated by a plasma membrane–associated NADPH oxidase system, which

CHAPTER CHAPTER 61 X

Although inflammatory mediators’ levels vary greatly according to injury-related factors as well as the patient’s individual characteristics, most studies agree that the changes start very early postinjury. This underscores the importance of measuring inflammatory mediators very early and at short intervals after injury.27 Indeed, a recent German study including 58 multiple injured patients (ISS 16) found that IL-6, IL-8, and IL-10 differentiate patients with MOF (n  43) and those without MOF (n  15) within 90 minutes post trauma.37

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Management of Complications after Trauma

SECTION 5 X

can be activated by macrophages, neutrophils, and other immunologic cells.45 ROI secreted from PMNs after I/R injury induces cytokines, chemokines (IL-8), HSP, and adhesion molecules (P-selectin, ICAM-1) leading to cell and tissue damage.28 Under normal conditions, NO production greatly exceeds O2 production in the endothelial cell (EC). However, with reperfusion, the balance between NO and O2 shifts in favor of O2. The relatively low level of NO by constitutive endothelial nitric oxide synthase (NOS-I) reacts with the now abundant O2 to generate peroxynitrites, leaving little NO available to reduce arteriolar tone, prevent platelet aggregation, and minimize PMN adhesion to EC.46 In addition, NO seems to upregulate the production of proinflammatory cytokines.28 Thus, altering the redox state of the cell may contribute to the ongoing inflammatory cytokine production and progression to MOF.42 ROIs also play a role as second messengers in the intracellular signaling pathways of inflammatory cells, in particular, activation of NF-κB and activator protein 1 (AP-1), which can be activated by both oxidants and antioxidants depending on the cell type and on intracellular conditions.44 Endogenous antioxidant defenses, including enzymatic (superoxide dismutase, catalase, glutathione peroxidase) and nonenzymatic (vitamins E and C, provitamin A, glutathione, bilirubin, urate) groups that combat oxidative stress, have been the focus of interventions to modulate the inflammatory response to critical illness, as detailed later.

Hormones Traditionally, the injury stress response was viewed as a neuroendocrine reflex mediated via counterregulatory hormones (cortisol, glucagon, and epinephrine) that altered substrate metabolism while the body is in a state of repair. Adrenaline is released and suppresses insulin secretion but stimulates secretion of growth hormone and renin, proteolysis and glycogenolysis, enhancing hepatic-mediated gluconeogenesis.33 Glucagon is released by pancreatic islet cells that increase hepatic glucose production from substrate that arises from tissue catabolism. The liver produces acute phase reactants such as opsonins (CRP), protease inhibitors, hemostatic agents (fibrinogen), and transporters (transferrin).33 The hypothalamic–pituitary–adrenal (HPA) axis is activated during stress, stimulating the release of adrenal corticotropic hormone (ACTH) from the pituitary gland, which induces the release of cortisol from the adrenal cortex.47 The HPA axis and the immune response are intrinsically linked in a negative feedback loop in which activated immune cells produce specific cytokines that activate the HPA axis increasing cortisol release that in turn suppresses the immune response and further cytokine release.47 Cytokines also act directly on the adrenal cortex and on glucocorticoid receptors (GR), present in most cells. In addition, different types of stress (sepsis, trauma, elective surgery) seem to be associated with the release of distinct mediators that may inhibit or stimulate cortisol production by acting on the HPA axis, adrenal cortex, and/or GR. The HPA response is pivotal for survival as adrenal insufficiency (AI) increases the mortality of critically ill or injured

patients.47 In the Section “Interventions,” we will return to this important topic in the treatment and prevention of MOF. Less clear is the role of sexual hormones. Choudhry et al. in Alabama have studied extensively the influence of gender in the response to trauma and hemorrhage (TH) in animal models.48 They suggested that immune and cardiac dysfunctions after TH are depressed in adult males and ovariectomized/aged females, while both are maintained in castrated males and in proestrus females. The female reproductive cycle seems to be an important variable in the regulation of lung injury after TH.49 One of their most recent studies showed that enhanced hepatic heme oxygenase (HO-1) in proestrus- and estradiol-pretreated ovariectomized females modulates inflammatory responses and protects liver following TH.49 In contrast with the animal studies, clinical investigations have shown controversial results regarding a protective effect of female gender. In a 2006 study by the Alabama group, female polytrauma victims younger than 50 years with an ISS 25 suffered significantly less MOF and sepsis and had lower plasma cytokines compared with age-matched males.50 This study however included a relatively small number of women (n  37), of whom over half were older than 50 years of age; thus, a type II error in the postmenopausal women was possible. A more recent study by the “Inflammation and the Host Response to Injury Investigators” attempted to characterize the gender dimorphism after injury with specific reference to the reproductive age of the women (young, 48 years of age, vs. old, 52 years of age) in a cohort of 1,036 severely injured trauma patients.51 The independent protective effect of female gender on MOF rates remained significant in both premenopausal and postmenopausal women when compared with similarly aged men suggesting that factors other than sex hormones were responsible for the gender-based differences after injury.

■ The Second Hit Abdominal Compartment Syndrome A hallmark of the postinjury inflammatory state is generalized capillary leak and associated tissue edema. Historically, peripheral edema was considered to be a minimally significant consequence of fluid resuscitation. This view has changed with the resurgent interest in intra-abdominal hypertension that has accompanied the recent widespread application of damage control procedures (DCP). Increased intra-abdominal pressures (IAP) are accompanied by a host of physiologic derangements that include high ventilator pressures, decreased cardiac output, and impaired renal function, a constellation of signs that are named ACS. Usually associated with abdominal injuries (primary ACS), these effects can also be observed following extraabdominal injury or following large-volume resuscitation for nontraumatic or nonsurgical conditions (secondary ACS).52 The incidence of ACS varies greatly according to the resuscitation strategy but is primarily dependent on the severity of injury and the degree of shock. Mesenteric I/R increases microvascular permeability causing bowel wall edema that can directly cause decreased bowel motility, decreased barrier function, and further capillary leak. Splanchnic hypoperfusion

Multiple Organ Failure

Blood Transfusions The goals of transfusion in the injured patient are to maintain adequate oxygen-carrying capacity. However, there is abundant, solid evidence that blood transfusions are a risk factor for the development of MOF independent of shock or injury severity.53,54 Indeed, blood transfusions fit many of the criteria for causation, that is, strength of the association, temporal relationship (risk factor precedes outcome), dose–response relationship, consistency, and reproducibility. Early blood transfusion is indeed the most powerful independent risk factor for postinjury MOF.53 Reductions in blood transfusion in the resuscitation period correlate with improved outcome and less MOF.22 Blood products are immunoactive, contain proinflammatory cytokines and lipids, and have an early immunosuppressive effect predisposing the patient to CARS, infection, and late MOF.54 The age of transfused blood is also important, with progressive daily increases in proinflammatory cytokines in stored blood products. Transfusing packed red blood cells (PRBCs) stored

3 weeks in the first 6 hours postinjury are associated with a higher rate of MOF while PRBC units with shorter storage times are associated with decreased MOF prevalence and less morbidity and mortality.54 Leukodepletion does not remove the potential for blood to act as a second hit, as PRBCs contain proinflammatory cytokines, including IL-8 and IL-6. The mechanism was believed to be related to the generation of the proinflammatory agents PAF, IL-6, and IL-8 during storage. Later studies found that additional biologically active cytokines and lipid mediators (lysophosphatidylcholines) accumulate in stored blood and are capable of PMN priming.54 “Passenger leukocytes” present in stored blood have been implicated as pivotal components by the finding that prestorage leukoreduction decreases the PMN priming and transfusion-mediated lung injury in animal models.54 Proposed mechanisms include induction of T-cell anergy in the recipient, decreased natural killer cell function, altered ratio of T-helper to T-suppressor cells, and soluble proinflammatory cytokines produced by leukocytes during storage.54 Together, these effects can suppress the recipient immune system and promote a worse proinflammatory state leading to increased infection and complications. Other blood-derived products (platelets, plasma, and coagulation factors) are also immunoactive and could act as second hits.17 Indeed, transfusion of fresh frozen plasma (FFP) is associated with MOF, especially among patients who received more than 6 U of PRBCs in the first 12 hours postinjury.55

■ Infections Osler was the first to recognize in 1904 that “except on few occasions, the patient appears to die from the body’s response to infection rather than from the infection.”56 The association of infection and MOF was always strong. In the late 1970s, intra-abdominal abscess (IAA) was the inciting event in half of the cases.11 As a result of the appropriate use of presumptive antibiotics in patients sustaining abdominal trauma and prompt diagnosis of hollow viscus injury, the incidence of postinjury IAA decreased and its progression toward MOF was hindered. The epidemiology of postinjury infections changed and nosocomial pneumonia became the principal infection associated with MOF. While CARS, the anti-inflammatory response, may be protective because it limits unnecessary (potentially autodestructive) inflammation, it is associated with relative immunosuppression predisposing the host to infections.57 Data from both clinical and animal studies suggest diminished production of proinflammatory type 1 and increased production of inhibitory type 2 cytokines by T cells. Monocytes/macrophages and suppressor T lymphocytes have been implicated to be key modulators that downregulate immune functions.57 Another area of research interest has been the potential role of persistent hypercatabolism in the development of infections.33 Although energy expenditure can increase dramatically following injury, the associated hypercatabolism is a critical metabolic alteration. If not supported by exogenous nutrients, the consequent obligatory protein turnover quickly erodes somatic protein stores and then the critical visceral mass. The resulting acute protein malnutrition causes well-documented

CHAPTER CHAPTER 61 X

during shock is compounded by even mild increases in IAP (which can reduce the abdominal perfusion pressure) and low plasma oncotic pressure from crystalloid resuscitation (which worsens edema).52 As with any compartment syndrome, the increased pressure within the compartment rises above postcapillary pressure causing a functional venous and lymphatic obstruction. Under these conditions, the intestinal epithelium microvilli secrete fluid into the gut lumen. Transudation of free fluid into the peritoneal space also contributes to further IAP increases. The combination of bowel wall edema, intraluminal fluid secretion, and fluid accumulation in the peritoneal cavity further increases IAP and gut ischemia, which affects the inflammatory response as described above. While ACS physiologic effects usually reverse on decompression, the immunomodulatory effects may persist and trigger MOF.52 Both primary and secondary ACS can be predicted early. The independent predictors of primary ACS are the indicators of the damage control physiology (transfer to the operating room without further imaging, temperature 34°C, hemoglobin 8 g/dL, base deficit 8 mmol/L), whereas the secondary ACS predictors are markers of uncontrolled resuscitation (7.5 L of crystalloids before ICU admission, no indication for lifesaving surgical intervention, relatively low urine output [ 150 mL/h] on ICU admission [considering the massive resuscitation]). Identification of these independent predictors led to earlier hemorrhage control in orthopedic trauma, abandoning crystalloid-based supranormal resuscitation goals, introduction of hemostatic resuscitation, and the early application of ICU resuscitation protocols.52 The current treatment of full-blown postinjury ACS is surgical decompression. Abdominal decompression may be performed in the ICU, especially in secondary ACS cases, whereas in primary ACS repeated hemorrhage control is usually required, preferably undertaken in the OR. After decompression, open abdomen management starts with the application of temporary abdominal closure followed by timely restoration of the abdominal wall.52

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Management of Complications after Trauma adverse immunologic consequences and is a recognized cofactor for the development of postinjury infection.

SECTION 5 X

■ Secondary Operation The second operation can be considered a controlled traumatic event where surgical trauma takes the place of the initial injury. Additional stresses of secondary operations include higher intraoperative fluid consumption, hypothermia, hypotension, tissue hypoxia, and intraoperative blood loss.33 The timing of the second operation has been variously studied over the last decade mostly as related to operative fracture fixation. While early definitive fracture fixation decreases postinjury morbidity and improves recovery, it is not without consequences when performed within the priming window. A 2003 randomized controlled trial by Pape et al. demonstrated that early external fixation followed by delayed conversion to intramedullary instrumentation was associated with a decreased inflammatory response to the operative fixation.58 The same group compared the inflammatory response of injured patients with femoral shaft fracture who were divided into two groups according to their initial treatment: (1) damage control orthopedics (DCO) group if the femoral fracture was initially stabilized with an external fixator and (2) intramedullary nailing (IMN) group if they underwent primary IMN.59 Despite more severe injuries in the DCO group, patients had a smaller, shorter postoperative SIRS and did not suffer significantly more pronounced organ failure than the IMN group. DCO patients undergoing conversion while their SIRS score was raised suffered the most pronounced subsequent inflammatory response and organ failure. According to these data, DCO treatment was associated with a lesser SIRS than early total care for femur fractures. Our group recently examined outcomes associated with early total care with IMN (ETC group) versus damage control external fixation (DCO group) for 462 multiple injured patients with femoral shaft fractures.60 Although minimal differences were noted between DCO and ETC groups regarding systemic complications, DCO was a safer initial approach, significantly decreasing the initial operative exposure and blood loss. Collectively, these findings strongly suggest that a secondary operation can act as an additional inflammatory insult and amplify the postinjury inflammatory response and precipitate MOF.

DEFINING MOF Defining MOF given the absence of a definitive gold standard is a challenge.19 As a consequence, authors have used disparate definitions and the epidemiological descriptions of this condition vary widely. Indeed, the reported incidence of postinjury MOF varies from as low as single digit numbers to values approaching 40%, with case-fatality rates also varying within similarly large ranges.19 Some studies suggest that MOF is disappearing while other studies have not found a consistent change.19 These disparities are, in large part, due to the difficulty in defining and measuring MOF. The syndrome seems to fit well with Justice Stewart’s famous quote: “I may not be able to define it, but I know it when I see it.”

VALIDATION OF CURRENT SCORES In the absence of a gold standard, validation must be done examining the association of different scores with objective adverse outcomes, reflecting clinical status (VFD, IFD, and death) and resource utilization (length of ICU stay [LOS] and MV days). VFD and IFD have been recently proposed as alternative outcomes for critically ill patients that account for patients who died early and consequently had shorter MV and ICU times.61 In addition, the validation process can be greatly enhanced if conducted on a homogenous population observed for an extended period of time, as in our long-term Denver MOF dataset. Started in 1992, this database contains prospectively collected clinical data on patients at risk for postinjury MOF for the first 28 postinjury days.19 To our knowledge, this is the longest, sustained prospective database on postinjury MOF using standardized data collection methods. Acutely injured patients admitted to the Rocky Mountain Regional Trauma Center surgical intensive care unit (SICU) at the Denver Health Medical Center (DHMC, a state-designated Level I trauma center verified by the American College of Surgeons Committee on Trauma) are studied prospectively. The analytic dataset of 1,480 patients from 1992 to 2004 is summarized in Table 61-2. Our population consisted of mostly young, healthy males, with moderate to severe injuries, mostly due to blunt force in motor vehicle accidents. Mortality and number of VFD days were low, but health care resource utilization was high with over one third of these patients requiring longer than 14 admission days in the surgical ICU (LOS) and/or over 7 days of MV. (Data from additional 1,000 patients admitted since 2005 are still being examined for accuracy and processed into analytic files.) Patients fitting the following criteria are entered in the dataset: 1. ISS greater than 15: patients with this level of injury or worse are all likely to be admitted to the ICU, minimizing selection bias. 2. Survival longer than 48 hours from injury: our studies demonstrate that physiologic derangements prior to 48 hours are not indicative of MOF, but rather reflect the primary injury or inability to respond to resuscitation.62 3. Admission to DHMC within 48 hours of injury: due to delay in admission, early risk factors shown to be associated with MOF were not observed or recorded. 4. Age greater than 15 years: it has been demonstrated that MOF presents differently among children, and that the currently used organ dysfunction measures may not be appropriate to the pediatric population; thus, children are not included in this analysis;63 we are however including children in a specific section of the MOF dataset, which will be used to adapt current scores to pediatric use. In addition, we exclude patients with isolated head injuries because these patients tend to have a lower MOF incidence with distinct presentation, risk factors, and outcomes when compared with torso injury patients. Patients with burn and/or hanging injuries are also excluded, as they are most often treated primarily at other centers and their risk factors for MOF are different from torso blunt and penetrating injuries. Daily physiologic and laboratory data are collected through day 28.

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TABLE 61-2 The Denver MOF Dataset: Characteristics of a Trauma Patient Population at Risk for MOF Admitted from 1992 to 2004 Mean

STD

SEM

Median

Lower Quartile

Upper Quartile

37.5 1,004 (72%)

16.7

0.4

34

24

46

11.3 8.8 5.2 2.3 4.2

0.3 0.2 0.1 0.1 0.1

26 0 0 0 0

22 0 0 0 0

34 6.0 2.0 0 2.0

14.6 7.4 9.3

0.4 0.2 0.2

11 3 25

5 0 15

21 10 28

777 (55%) 401 (29%) 149 (11%)

Comorbid conditions Injury severity Injury mechanism: blunt force Injury Severity Score RBC units/first 12 h FFP units/first 12 h Platelet units/first 12 h Crystalloids/first 12 h (L)

1,059 (76%) 29.5 4.5 2.3 0.4 2.0

Outcomes Length of ICU stay (days) Mechanical ventilation (days) Ventilator-free days Mortality

15 6.2 20.4 116 (8%)

388 (28%)

■ MOF Scores We focused our validation on two widely used scores: the Marshall MOD score (Marshall score) and the Denver MOF score (Denver score), developed by our group. For other scores, the reader is referred to the excellent review by Baue.64 The Denver score, first proposed in 1991, originally included eight organ systems, (cardiovascular, pulmonary, renal, hepatic, gastrointestinal, hematologic, central nervous system [CNS], and metabolic). The score was later revised and gastrointestinal, hematologic, CNS, and metabolic failures were excluded since their addition did not improve the characterization of MOF. In brief, the Denver score grades on a scale from 0 to 3 the dysfunction of four systems (pulmonary, renal, hepatic, and cardiac), evaluated daily throughout the patient’s ICU stay with the total score ranging from 0 to 12 (Table 61-3). The Marshall score was developed in 1994 and validated based on probability of subsequent mortality in a sample of 692 patients from a Canadian ICU.65,66 It grades dysfunction from 0 to 4 and evaluates the same four systems as the Denver score, plus the dysfunctions of the hematologic and neurologic systems (Table 61-4).

■ MOF Classification in the Denver MOF Dataset There were 1,389 patients with complete data in the Denver MOF dataset to calculate both scores (95% of the 1,440 total sample). Tables 61-5 and 61-6 show the risk factors and outcomes

distribution stratified by MOF classification. Patients could be classified into one of the following four potential scenarios: Marshall MOF Score Yes No

Denver MOF Score Yes Scenario a Scenario b

No Scenario c Scenario d

Or: • Scenario a: classified as “MOF” by both scores • Scenario d: classified as “no MOF” by both scores • Scenario b: classified as “MOF” by Denver score but as “no MOF” by Marshall score • Scenario c: classified as “no MOF” by Denver score but as “MOF” by Marshall score Patients in scenarios a and d were those for whom both scores agreed in the classification while scenarios b and c represented the discordant classification. Three major groups of patients emerged: (1) patients classified by both scores as MOF comprised a severe injury group of patients with high rates of risk factors, mortality, and utilization, (2) patients classified as “no MOF” by both scores constituted a mild injury group for whom risk factor rates, utilization, and mortality were all low, and (3) patients for whom the scores disagree in the MOF classification represented a moderate injury group with medium risk factor rates, medium utilization, and low mortality.

CHAPTER CHAPTER 61 X

Variable Demographic characteristics Age (years) Gender: male Race/ethnicity White non-Latino Latino (of any race) Black non-Latino

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TABLE 61-3 Denver Postinjury Multiple Organ Failure Score

SECTION 5 X

Organ System Pulmonary PaO2/FiO2 ratio

Grade 0

Grade 1

Grade 2

Grade 3

250

250–200

200–100

100

Renal Creatinine (mg/dL) Creatinine (μmol/L)

1.8 159

1.9–2.5 160–221

2.51–5.0 222–442

5.0 442

Hepatic Bilirubin (mg/dL) Bilirubin (μmol/L)

2.0 34

2.0–4.0 34–68

4.1–8.0 69–137

8.0 137

Cardiac

a

No inotropes

Only one inotrope at a small dosea

Any inotrope at moderate dose or 1 agent, all at small dosesa

Any inotrope at large dose or 2 agents at moderate dosesa

Inotrope doses (in μg/(kg min)): Small 0.3 0.03 6 6 0.06 0.11 0.6

Milrinone Vasopressin Dopamine Dobutamine Epinephrine Norepinephrine Phenylephrine

Moderate 0.4–0.7 0.03–0.07 6–10 6–10 0.06–0.15 0.11–0.5 0.6–3

Large 0.7 0.07 10 10 0.15 0.5 3

TABLE 61-4 Marshall Multiple Organ Dysfunction Score Dysfunction

Grade 0

Grade 1

Grade 2

Grade 3

Grade 4

Pulmonary PaO2/FiO2 ratio

300

226–300

151–225

76–150

75

Renal Creatinine (μmol/L)

100

101–200

201–350

351–500

500

Hepatic Bilirubin (μmol/L)

20

21–60

61–120

121–240

240

Heart rate 120 PAR 10

Heart rate 120–140 PAR 10.1–15

Heart rate 140 PAR 15.1–20

Inotropesa PAR 20.1–30

Lactate 5 mmol/L PAR 30

15

13–14

10–12

7–9

6

120

81–120

51–80

21–50

20

Cardiac 1994 version 1995 versionb Central nervous system Glasgow Coma Scale Hematologic Platelet count  103/mL a b

Need for inotropes more than dopamine 3 μg/(kg min).

PAR: pressure-adjusted heart rate. PAR  heart rate  central venous pressure/mean arterial blood pressure.

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TABLE 61-5 Risk Factors of Patients Identified as Having or Not MOF Based on the Denver and Marshall MOF Scores

MOF defined as Denver 3, Marshall 5 Denver  Marshall  MOF Denver  Marshall  no MOF Denver  MOF, Marshall  no MOF Denver  no MOF, Marshall  MOF

34.5 26.8 32.5 30.5

304 694 4 387

(0.8) (0.4) (7.3) (0.5)

■ Validation of the Scores Using Receiver Operating Characteristic (ROC) Curves

Mean Age (SEM) 41.6 (1.0) 36.4 (0.6) 27 (5.8) 36.6 (0.9)

Median RBC/ 12 h (IQR)

Blunt Trauma (%)

4 (0–12) 0 (0–2) 0 (0–1) 2 (0–7)

75 78 100 73

■ Protective Resuscitation Techniques

ROC curves were developed during World War II to determine if a blip on a radar screen represented a ship or an extraneous noise. The radar receiver operators used this method to set the threshold for military action. In medicine, ROC curves have gained increasing popularity as a method to evaluate measurements. For every possible boundary between “positive” and “negative,” the ROC plot shows the trade-off between sensitivity (ability to detect disease) and specificity (ability to detect lack of disease). ROCs, by convention, plot the sensitivity in the Y axis and (1−specificity) in the X axis. The best cutoff for a measurement, that is, the cutoff that has the best combination of sensitivity and specificity, is the data point located at the left uppermost position in the ROC curve. In addition, the area under the ROC (AUR) may be used as a measurement of the overall performance of the measurement. To validate the MOF scores, we compared their ROC curves for the outcomes (death, VFD 21 days, LOS 14 days, and MV 7 days) as shown in Figures 61-4 to 61-7. Overall, both scores were associated with areas 80 (ideal value  100). The AUR for the Denver score was slightly greater than that for the Marshall score regarding prediction of death, VFD, and MV. The differences, however, were not significant.

INTERVENTIONS Preventing the onset of MOF through therapies directed at modulating SIRS or blocking CARS is likely to offer more practical benefit to injured patients than efforts to treat MOF once established, when the treatment is largely supportive.27

Certain resuscitative strategies protect against distant organ injury after periods of gut I/R.29 Resuscitation with isotonic crystalloids proposed in the late 1960s contributed to a decrease in mortality and acute renal failure, but was implicated in the emergence of ARDS as a major source of morbidity and mortality in the ICU. There is still controversy about the use of isotonic crystalloids compared with colloids. The multicenter, randomized, double-blind SAFE trial showed no difference in mortality, single organ failure, and MOF between the groups receiving saline and the group receiving albumin.67 A preplanned subgroup analysis of trauma patients, however, seemed to favor the use of crystalloids, although the difference was not significant at the 95% confidence level (relative risk, 1.36, 95% confidence interval, 0.99–1.86, P  .06). In fact, when patients with brain injury were excluded, no difference was detected (death rate in both groups  6.2%, relative risk, 1.0, 95% confidence interval, 0.56–1.79, P  1.00). A recent Cochrane systematic review (published in 2007 and updated in 2009 without any change in conclusions) compared colloids with crystalloids and showed no difference in mortality of trauma patients. The lack of a survival advantage combined with the higher costs of colloids favors the use of crystalloids in trauma resuscitation. A systematic review (published in 2004 and updated in 2007) comparing hypertonic with isotonic crystalloid solutions for the resuscitation of patients with trauma or burns or those undergoing surgery did not provide enough data to determine there was a difference in outcomes.68 The authors, however, pointed out that confidence intervals were wide and recommended further trials were needed. Hypertonic resuscitation (hypertonic saline and 6% Dextran 70) was compared with lactated Ringer’s solution (LRS) in adult, blunt trauma patients

TABLE 61-6 Adverse Outcomes of Patients Identified as Having or Not MOF Based on the Denver and Marshall MOF Scores

MOF defined as Denver 3, Marshall 5 Denver  Marshall  MOF Denver  Marshall  no MOF Denver  MOF, Marshall  no MOF Denver  no MOF, Marshall  MOF

N

Death Rate (%)

304 694 4 387

30 1 0 4

ICU Stay 14 Days (%) 73 15 75 54

Mechanical Ventilation 7 Days (%) 76 9 75 41

Ventilator-Free Days 21 (%) 10 88 25 50

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Mean ISS (SEM)

N

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SECTION 5 X FIGURE 61-4 ROC curves for the Denver and Marshall MOF scores showing prediction of postinjury mortality.

by Bulger et al. in a recent randomized clinical trial.69 The study, stopped for futility after the second interim analysis, demonstrated no significant difference in ARDS-free survival (hazard ratio, 1.01; 95% confidence interval, 0.6–1.6). There was improved ARDS-free survival in the subset requiring massive transfusion (hazard ratio, 2.2; 95% confidence interval, 1.1–4.4), suggesting a benefit may exist in patients at highest risk of ARDS.69 However, this large multicenter clinical trial

was subsequently reactivated, and the preliminary results do not indicate a clinical benefit. In addition to more efficient volume restoration, hypertonicity has an effect on multiple immune response functions, which may someday translate to improved outcome in select populations.70 Similarly, low-dose albumin was shown to protect against shock-induced lung, EC, and red blood cell injury, as was the intraintestinal administration of a pancreatic protease inhibitor.29

FIGURE 61-5 ROC curves for the Denver and Marshall MOF scores showing prediction of postinjury ventilator-free days shorter than 21 days.

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FIGURE 61-6 ROC curves for the Denver and Marshall MOF scores showing prediction of postinjury mechanical ventilation longer than 7 days.

Judicious Use of Blood Transfusions Judicious use of blood products seems to prevent MOF. A 12-year analysis of our MOF dataset suggests that reduction of blood use was implicated in the decreased incidence of MOF in our trauma center.22 Current transfusion guidelines support the safety of restrictive transfusion practices in trauma patients.71,72 Other techniques to reduce the deleterious effects of PRBCs are washed PRBCs and prestorage leukoreduction. Despite the

beneficial effects of washed PRBC units, the preparation time, the lack of apparatus to wash units in many blood banks, and the short outdate of washed units (24 hours) make them impractical in the trauma setting.54 Prestorage leukoreduction may reduce biologically active lipids in stored PRBC; however, trials have shown modest or no improvement in outcomes.54,71 Finally, blood substitutes have offered promising results in trauma populations. Only two hemoglobin substitutes have

FIGURE 61-7 ROC curves for the Denver and Marshall MOF scores showing prediction of postinjury ICU stay longer than 14 days.

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been used extensively in injured patients, the diaspirin crosslinked hemoglobin from the Baxter Corporation and polymerized, pyridoxylated human hemoglobin (PolyHemeTM) from Northfield Laboratories.54 Our experience in the trauma setting with PolyHemeTM suggests it provides an immunologic advantage relative to blood in the injured patient by diminishing PMN priming and decreasing IL-6 and IL-8.54,73 In a recent clinical trial, patients resuscitated with PolyHeme, without stored blood for up to 6 U in12 hours postinjury, had outcomes comparable with those for the standard of care. Although there were more adverse events in the PolyHeme group, the benefitto-risk ratio of PolyHeme was favorable when blood was needed but not available.74 In a recent meta-analysis of blood substitutes, the authors concluded that these products were associated with an increased risk of mortality and myocardial infarction.75 However, because the authors included studies on such diverse populations, the results of the meta-analysis were questionable.76 In fact, in studies with trauma patients, the associations were not significant.

Fracture Management The benefits of early definitive fracture stabilization include early patient mobility, improved pulmonary toilet, and a decrease in systemic inflammation, thromboembolic events, morbidity, mortality, and hospital resource utilization. However, this is not without a price, as operative fracture fixation exposes the patient to an additional inflammatory insult that can precipitate MOF. Consequently, the concept of damage control surgery was extended to major fracture initial management in the severely injured. Damage control external fixation (DCO) is performed in coordination with acute resuscitation and hemodynamic stabilization, and it allows fracture stabilization with minimal blood loss and anesthesia time.58,77 The principle is to provide early fracture stabilization by external fixation as a bridge to definitive fracture care once the patient is more physiologically appropriate. Conversion of external fixation to intramedullary implantation is associated with reduced procedure-related inflammatory response compared with early primary femur fracture fixation.58 When compared with early total care, the damage control approach with delayed conversion to definitive care has been shown to decrease the initial operative time and intraoperative blood loss without increasing the risk of procedure-related complications such as infection and nonunion, and may improve overall survival.77 A recent study examining acute patient outcomes associated with early total care with IMN (ETC group) versus DCO group for multiple injured patients with femoral shaft fractures showed comparable outcomes between the two methods, suggesting that DCO is a safer initial approach, decreasing the initial operative exposure and blood loss, both potential insults that can trigger MOF.60

Protective Lung Ventilation In addition to direct injury and secondary inflammatorymediated injury discussed below, the lung is also subject to ventilator-induced lung injury. While the mechanical ventilator

is an indispensable therapy for lung failure, the administration of positive pressure ventilation can result in lung injury that is functionally and histologically identical to that seen in ARDS. Conversion from negative pressure ventilation to positive pressure ventilation is associated with unequal distribution of tidal volumes to the heterogeneously involved lung parenchyma. Areas of low compliance (as seen in pulmonary contusion, edema, or infection) force tidal volumes to areas of high compliance resulting in increased alveolar pressures, overdistension, and injury to uninvolved lung tissue. Mechanical injuries to the lung (barotraumas, atelectrauma, volutrauma) initiate a local inflammatory reaction and biotrauma with release of inflammatory mediators from damaged cells, recruitment of PMNs to the site of injury, and local inflammatory reaction mediated by circulating leukocytes. Mechanical stresses on the living cell are translated into intracellular inflammatory signal transduction and the combination of mechanical damage from positive pressure ventilation and the inflammation increases pulmonary dysfunction.78 The effects of ventilator-induced lung injury extend beyond the lung. Impaired oxygen delivery amplifies post-traumatic I/R injury. Mechanical disruption of normal lung defense mechanisms increases the infectious potential and the risk of pulmonary sepsis. Inflammatory cytokines generated in the lung spill over into the systemic circulation and have the capacity to increase the inflammatory state (priming) and promote remote organ dysfunction via direct cell signaling (activation). Lung tissue that has undergone a prior stress such as direct injury or I/R is particularly sensitive to further ventilatorinduced lung injury.79 Clinical evidence of the contributing effects of MV on the incidence of MOF was demonstrated in the ARDS Network lung-protective ventilation (LPV) trials.80 A 2007 Cochrane Library systematic review showed that day 28 mortality was significantly reduced by LPV (relative risk, 0.74; 95% confidence interval, 0.61–0.88).81 Current evidence supports PLV as the standard therapy for patients at risk for ARDS.

Adrenal Insufficiency and Cortisol Replacement Therapy Serum cortisol levels in polytrauma patients have been shown to be 30 μg/dL or greater for at least a week.47 Adrenal insufficiency (AI: random serum cortisol 25 μg/dL or stimulation test increase 10 μg/dL), seems to be a frequent occurrence in trauma patients, that if left untreated is associated with increased mortality.82,83 Recent data from our MOF database showed that the relationship between cortisol levels and postinjury MOF is complex with both low and high cortisol values being associated with higher risk of MOF.84 The major limitation of these retrospective reviews, however, is related to patient selection bias, as only patients in whom AI is suspected have cortisol measurements and/or stimulation tests. An RCT in trauma patients is urgently needed to better define whether AI is a risk factor for, or a symptom of, postinjury MOF, and the role of administration of cortisol postinjury. Despite controversies, a recent task force from the Society of Critical Care Medicine and the European Society of Intensive

Multiple Organ Failure

Insulin and Glycemic Control While glycemic control ( 180 mg/dL) is undoubtedly important, tighter glucose control (81–108 mg/dL) in critical care patients has had conflicting results.86–88 The recently published NICE-SUGAR study89 demonstrated an increased death risk associated with intensive glucose control compared with more conventional glycemic goals. Interestingly, in this study, trauma patients were one of two subgroups to exhibit the opposite trend, albeit not statistically significant. A review of our Denver MOF database to evaluate our glucose control protocol is underway, but our preliminary findings are as follows. After exclusion of diabetes patients, there was a significant dose response between mean level of glucose and mortality. Over half of these patients maintained mean levels of glucose 160 mg/dL, with only 22% maintaining mean levels 130 mg/dL. Mean number of required insulin units was also consistently higher among nonsurvivors than among survivors suggesting that the difficulty to achieve normoglycemia (and possibly insulin resistance) may be associated with higher risk of death. We are now evaluating these findings among patients for whom cortisol was measured.

In addition to its role in glucose control and induction of anabolic processes, one must account for the immunomodulatory effects of insulin, which can attenuate SIRS and modulate the proliferation, apoptosis, differentiation, and immune functions of monocytes/macrophages, neutrophils, and T cells associated with severe trauma, burn injury, or sepsis.90

Immunonutrition Two aspects are relevant in immunonutrition: the delivery route (enteral vs. parenteral) and the diet composition.18 Although controversy exists concerning the safety of feeding the hypoperfused small bowel, evidence supports that early enteral nutrition (EEN) is not only feasible but also associated with decreased incidence of nosocomial infections.18 EEN effects go far beyond mere nourishment; rather EEN induces a complex immunologic response.91 EEN supports the function of the mucosal-associated lymphoid tissue (MALT) that produces 70% of the body’s secretory IgA.92 Naive T and B cells target and enter the gut-associated lymphoid tissue (GALT) where they are sensitized and stimulated by antigens sampled from the gut lumen and thereby become more responsive to potential pathogens in the external environment. These stimulated T and B cells then migrate via mesenteric lymph nodes and the thoracic duct and into the vascular tree for distribution to GALT and extraintestinal sites of MALT. Lack of enteral stimulation (i.e., use of TPN) causes a rapid and progressive decrease in T and B cells within GALT and simultaneous decreases in intestinal and respiratory IgA levels. Previously resistant TPN-fed lab animals, when challenged with pathogens via respiratory tree inoculation, succumb to overwhelming infections. These immunologic defects and susceptibility to infection are reversed within 3–5 days after initiating EN.92 Indeed, feeding the gut in critically ill patients has been shown to reverse shock-induced mucosal hypoperfusion and impaired intestinal transit as well as attenuate gut permeability defects and lessen the severity of CARS.18 Regarding content, to be effective, immunonutritional therapies must ameliorate cellular defense, oxidative stress, and mitochondrial function without increasing SIRS. Previous systematic reviews of immunomodulating diets (IMD) have shown a positive, albeit modest effect in decreasing mortality, infections, and length of stay in trauma patients.93,94 These analyses are hindered by the different content of the studied diets. This remains a major issue in IMD: which nutrients to include? In which dose? In which combination? Specifically regarding the inclusion of antioxidants, supplementation of Se and Zn has shown that early provision of micronutrients improves recovery in trauma and burns.95 Se is important in thyroid hormone activity and its supplementation achieves a more rapid correction of the low triiodothyronine (T3) concentrations, a characteristic post-traumatic thyroid alteration.95 The IV route seems the only way to deliver the doses required to obtain a clinical effect. There is some evidence suggesting that Zn supplementation during the immediate postinjury period is associated with improved neurologic recovery after severe closed head injury.95 The evidence, however, seems to favor using a combination of several antioxidants.45

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Care Medicine appraised the current evidence and delivered general recommendations regarding AI and cortisol replacement therapy in critically ill patients.85 Although the recommendations did not specifically address trauma patients, it is reasonable to assume that AI behaves similarly in trauma as in other SIRSinducing conditions. The task force recommended that AI should be suspected in hypotensive patients who have responded poorly to fluids and vasopressor agents, who present a delta serum cortisol of 9 μg/dL after adrenocorticotrophic hormone (250 μg) administration or a random total cortisol of 10 μg/dL. Although the task force supported the use of stimulation tests in AI diagnosis, the sole use of a random cortisol level has been shown to be sufficient and rarely discordant with the results of the stimulation tests.47,84 In patients most likely to benefit from treatment with glucocorticoid (vasopressor-dependent septic shock and patients with early severe ARDS, i.e., PaO2/FiO2 of 200 and within 14 days of onset), the task force recommended that the decision to treat with corticosteroids be based on the clinical criteria and not on the results of adrenal function. Glucocorticoids should be tapered down slowly, and reinstitution should be considered if there are signs of sepsis, hypotension, or worsening oxygenation. The dose of corticosteroid should be sufficient to downregulate the proinflammatory response without causing immunodeficiency and impaired wound healing. Therapy with high-dose corticosteroids (1,000 mg per day of hydrocortisone or equivalent) has not improved outcomes and was associated with higher complication rates.47 The use of extended course, stressdose corticosteroids (200–350 mg/dL of hydrocortisone or equivalent) in critically ill patients has been associated with improved outcomes (reduction in mortality, length of stay, and MV requirements). A note of caution on the use of etomidate as an anesthetic induction agent in critically ill patients: this agent has been associated with inhibited cortisol production for up to 48 hours, and to be an independent risk factor for death.47

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Intraluminal glutamine seems to have several beneficial effects: (1) reverses shock-induced splanchnic vasoconstriction; (2) preferred fuel source for the gut and lymphocytes; (3) promotes protein synthesis in the gut mucosa; (4) precursor for the antioxidant glutathione and nucleotides (required for rapid cellular proliferation of enterocytes and lymphocytes under stress); (5) protection against oxidant- and cytokineinduced apoptosis (a prominent event in severe CARS); and (6) induction of antioxidant enzymes.18 Indeed, the Houston group has been exploring enteral administration of glutamine in the setting of gut hypoperfusion. Their preliminary results in a small trial with 20 shock resuscitation patients showed that enteral glutamine administered during active shock resuscitation and through the early postinjury period is safe and enhances gastrointestinal tolerance. The results of the REDOXS study, designed to evaluate the effect of multiple antioxidants (Se, Zn, β-carotene, vitamins E and C) combined with high-dose glutamine on mortality in a large-scale randomized trial in critically ill patients, will provide important information on the value of this combination.45 The inclusion of arginine in IMD has been under debate because its use has been associated with gut barrier dysfunction and enhanced early inflammation.18 In addition, arginine is a substrate for inducible nitric oxide synthase (iNOS), which can be pathologically activated if the patient develops septic shock. Recent work by the Pittsburgh group, however, has shown that trauma patients exhibit a dramatic increase in arginase activity leading to arginine deficiency, which depresses T-cell immunity.96 Thus, the role of arginine in IMD for trauma patients needs to be further investigated.

TLR-Directed Interventions Because TLR activation leads to an intense and immediate inflammatory reaction in response to I/R injury, targeting TLRs may be a promising intervention strategy to reduce MOF.42 Yet, because TLR activation occurs through a variety of mechanisms, generating full antagonists is technically difficult. The development of eritoran, a potent and full antagonist of LPS at TLR4, is a significant advance and offers hope that other TLR-selective antagonists may become available in future years.

Continuous Renal Replacement Therapy (CRRT) In addition to the conventional aim of replacing renal function in acute kidney injury (AKI), CRRT may be used to modulate SIRS in sepsis.97 With the intention of influencing circulating levels of inflammatory mediators such as cytokines and chemokines, the complement system, as well as factors of the coagulation system, several modifications of CRRT have been developed over the last years. These include high-volume hemofiltration, high-adsorption hemofiltration, use of high cutoff membranes, and hybrid systems such as coupled plasma filtration absorbance. One of the most promising concepts may be the development of renal assist devices using renal tubular cells for implementing renal tubular function into CRRT.

Immunostimulating Factors In the immunodepression stage of the inflammatory response to injury, it may be useful to enhance immune function to prevent infections that can act as second insults. Although still in its infancy, therapy with immunostimulating factors seems promising. GM-CSF was tested in small trauma populations and shown to counteract trauma-induced monocyte function depression while IFN-γ had the capacity to enhance HLA-DR on B and T lymphocytes.98,99 In conclusion, MOF remains the leading cause of late death among trauma patients. While new therapies seem to have reduced its incidence, its morbidity and mortality remain high. Indeed, despite being fewer, MOF patients are spending even more hospital resources. The latest framework to explain MOF is based on the balance between the initial inflammatory response to injury and the compensatory anti-inflammation that follows.

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21. Durham RM, Moran JJ, Mazuski JE, Shapiro MJ, Baue AE, Flint LM. Multiple organ failure in trauma patients. J Trauma. 2003;55(4):608–616. 22. Ciesla DJ, Moore EE, Johnson JL, Burch JM, Cothren CC, Sauaia A. A 12-year prospective study of postinjury multiple organ failure: has anything changed? Arch Surg. 2005;140(5):432–438. 23. Sauaia A, Moore FAM, Moore EE, Norris JM, Lezotte DC, Hamman RM. Multiple organ failure can be predicted as early as 12 hours after injury. J Trauma Inj Infect Crit Care. 1998;45(2):291–303. 24. Moore FA, Sauaia A, Moore EE, Haenel JB, Burch JM, Lezotte DC. Postinjury multiple organ failure: a bimodal phenomenon. J Trauma. 1996;40(4):501–510. 25. Ciesla DJ, Moore EE, Johnson JL, et al. Decreased progression of postinjury lung dysfunction to the acute respiratory distress syndrome and multiple organ failure. Surgery. 2006;140(4):640–648. 26. Bone RC, Balk RA, Cerra FB, et al. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. Chest. 1992;101(6): 1644–1655. 27. Mannick JA, Rodrick ML, Lederer JA. The immunologic response to injury. J Am Coll Surg. 2001;193(3):237–244. 28. Tsukamoto T, Chanthaphavong RS, Pape HC. Current theories on the pathophysiology of multiple organ failure after trauma. Injury. 2010; 41(1):21–26. 29. Magnotti LJM, Deitch EAM. Burns, bacterial translocation, gut barrier function, and failure. J Burn Care Rehabil. 2005;26(5):383–391. 30. Ciesla DJ, Moore EE, Johnson JL, Burch JM, Cothren CC, Sauaia A. The role of the lung in postinjury multiple organ failure. Surgery. 2005;138(4):749–758. 31. Botha AJ, Moore FA, Moore EE, Sauaia A, Banerjee A, Peterson VM. Early neutrophil sequestration after injury: a pathogenic mechanism for multiple organ failure. J Trauma. 1995;39(3):411–417. 32. Moore EE, Moore FA, Harken AH, Johnson JL, Ciesla D, Banerjee A. The two-event construct of postinjury multiple organ failure. Shock. 2005;24(suppl 1):71–74. 33. Giannoudis PV. Current concepts of the inflammatory response after major trauma: an update. Injury. 2003;34(6):397–404. 34. Jastrow KM III, Gonzalez EA, McGuire MF, et al. Early cytokine production risk stratifies trauma patients for multiple organ failure. J Am Coll Surg. 2009;209(3):320–331. 35. Adams JMM, Hauser CJM, Livingston DHM, Lavery RFM, Fekete ZM, Deitch EAM. Early trauma polymorphonuclear neutrophil responses to chemokines are associated with development of sepsis, pneumonia, and organ failure. J Trauma. 2001;51(3):452–457. 36. Maier B, Lefering R, Lehnert M, et al. Early versus late onset of multiple organ failure is associated with differing patterns of plasma cytokine biomarker expression and outcome after severe trauma. Shock. 2007; 28(6):668–674. 37. Bogner V, Keil L, Kanz KG, et al. Very early posttraumatic serum alterations are significantly associated to initial massive RBC substitution, injury severity, multiple organ failure and adverse clinical outcome in multiple injured patients. Eur J Med Res. 2009;14(7):284–291. 38. Bianchi ME. DAMPs, PAMPs and alarmins: all we need to know about danger. J Leukoc Biol. 2007;81(1):1–5. 39. Levy RM, Mollen KP, Prince JM, et al. Systemic inflammation and remote organ injury following trauma require HMGB1. Am J Physiol Regul Integr Comp Physiol. 2007;293(4):R1538–R1544. 40. Peltz ED, Moore EE, Eckels PC, et al. HMGB1 is markedly elevated within 6 hours of mechanical trauma in humans. Shock. 2009;32(1):17–22. 41. Zhang Q, Raoof M, Chen Y, et al. Circulating mitochondrial DAMPs cause inflammatory responses to injury. Nature. 2010;464(7285):104–107. 42. Arumugam TV, Okun E, Tang SC, Thundyil J, Taylor SM, Woodruff TM. Toll-like receptors in ischemia–reperfusion injury [review]. Shock. 2009;32(1):4–16. 43. Tsan MF, Gao B. Heat shock proteins and immune system. J Leukoc Biol. 2009;85(6):905–910. 44. Bulger EM, Maier RV. Antioxidants in critical illness. Arch Surg. 2001;136(10):1201–1207. 45. Heyland DK, Dhaliwal R, Day AG, et al. REducing Deaths due to OXidative Stress (The REDOXS© Study): rationale and study design for a randomized trial of glutamine and antioxidant supplementation in critically-ill patients. Proc Nutr Soc. 2006;65(03):250–263. 46. Galkina SI, Dormeneva EV, Bachschmid M, Pushkareva MA, Sud′ina GF, Ullrich V. Endothelium–leukocyte interactions under the influence of the superoxide–nitrogen monoxide system. Med Sci Monit. 2004;10(9): BR307–BR316.

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72. West MAM, Shapiro MBM, Nathens ABM, et al. Inflammation and the host response to injury, a large-scale collaborative project: patientoriented research core–-standard operating procedures for clinical care. IV. Guidelines for transfusion in the trauma patient. J Trauma. 2006; 61(2):436–439. 73. Johnson JL, Moore EE, Gonzalez RJ, Fedel N, Partrick DA, Silliman CC. Alteration of the postinjury hyperinflammatory response by means of resuscitation with a red cell substitute. J Trauma. 2003;54(1): 133–139. 74. Moore EE, Moore FA, Fabian TC, et al. Human polymerized hemoglobin for the treatment of hemorrhagic shock when blood is unavailable: the USA multicenter trial. J Am Coll Surg. 2009;208(1):1–13. 75. Natanson C, Kern SJ, Lurie P, Banks SM, Wolfe SM. Cell-free hemoglobin-based blood substitutes and risk of myocardial infarction and death: a meta-analysis. JAMA. 2008;299:2304–2312. 76. Sauaia A, Moore EE, Banerjee A. Hemoglobin-based blood substitutes and risk of myocardial infarction and death. JAMA. 2008;300(11):1297. 77. Pape HC, Tornetta P III, Tarkin I, Tzioupis C, Sabeson V, Olson SA. Timing of fracture fixation in multitrauma patients: the role of early total care and damage control surgery. J Am Acad Orthop Surg. 2009;17(9): 541–549. 78. Dolinay T, Kaminski N, Felgendreher M, et al. Gene expression profiling of target genes in ventilator-induced lung injury. Physiol Genomics. 2006;26(1):68–75. 79. Crimi E, Zhang H, Han RN, Del Sorbo L, Ranieri VM, Slutsky AS. Ischemia and reperfusion increases susceptibility to ventilator-induced lung injury in rats. Am J Respir Crit Care Med. 2006;174(2):178–186. 80. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med. 2000;342(18):1301–1308. 81. Petrucci N, Iacovelli W. Lung protective ventilation strategy for the acute respiratory distress syndrome. Cochrane Database Syst Rev. 2007;(3): CD003844. 82. Offner PJ, Moore EE, Ciesla D. The adrenal response after severe trauma. Am J Surg. 2002;184(6):649–653. 83. Guillamondegui OD, Gunter OL, Patel S, Fleming S, Cotton BA, Morris JR. Acute adrenal insufficiency may affect outcome in the trauma patient. Am Surg. 2009;75(4):287–290. 84. Biffl WL, Johnson JL, Moore EE, Ciesla D, Banerjee A, Sauaia A. Adrenal insufficiency after injury is associated with multiple organ failure. 6th Congress of the International Federation of Shock Societies, Cologne, Germany, 2008. 85. Marik PE, Pastores SM, Annane D, et al. Recommendations for the diagnosis and management of corticosteroid insufficiency in critically ill

86. 87. 88. 89. 90. 91. 92. 93. 94. 95. 96. 97. 98.

99.

adult patients: consensus statements from an international task force by the American College of Critical Care Medicine. Crit Care Med. 2008; 36(6):1937–1949. Sperry JL, Frankel HL, Vanek SL, et al. Early hyperglycemia predicts multiple organ failure and mortality but not infection. J Trauma. 2007; 63(3):487–493. Langley J, Adams G. Insulin-based regimens decrease mortality rates in critically ill patients: a systematic review. Diabetes Metab Res Rev. 2007;23(3):184–192. Wiener RS, Wiener DC, Larson RJ. Benefits and risks of tight glucose control in critically ill adults: a meta-analysis. JAMA. 2008;300(8): 933–944. The NICE-SUGAR Study Investigators. Intensive versus conventional glucose control in critically ill patients. N Engl J Med. 2009;360(13): 1283–1297. Deng HP, Chai JK. The effects and mechanisms of insulin on systemic inflammatory response and immune cells in severe trauma, burn injury, and sepsis. Int Immunopharmacol. 2009;9(11):1251–1259. Kudsk KA. Beneficial effect of enteral feeding. Gastrointest Endosc Clin N Am. 2007;17(4):647–662. Kang W, Kudsk KA. Is there evidence that the gut contributes to mucosal immunity in humans? JPEN J Parenter Enteral Nutr. 2007;31(3): 246–258. Marik P, Zaloga G. Immunonutrition in critically ill patients: a systematic review and analysis of the literature. Intensive Care Med. 2008; 34(11):1980–1990. Moore FA. Effects of immune-enhancing diets on infectious morbidity and multiple organ failure. JPEN J Parenter Enteral Nutr. 2001; 25(2 suppl):S36–S42. Berger MM. Antioxidant micronutrients in major trauma and burns: evidence and practice. Nutr Clin Pract. 2006;21(5):438–449. Bryk JA, Popovic PJ, Zenati MS, Munera V, Pribis JP, Ochoa JB. Nature of myeloid cells expressing arginase 1 in peripheral blood after trauma. J Trauma. 2010;68(4):843–852. Joannidis M. Continuous renal replacement therapy in sepsis and multisystem organ failure. Semin Dial. 2009;22(2):160–164. Flohe SM, Lendemans SM, Selbach C, et al. Effect of granulocytemacrophage colony-stimulating factor on the immune response of circulating monocytes after severe trauma. Crit Care Med. 2003;31(10): 2462–2469. Lendemans S, Kreuzfelder E, Waydhas C, Schade F, Flohé S. Differential immunostimulating effect of granulocyte-macrophage colony-stimulating factor (GM-CSF), granulocyte colony-stimulating factor (G-CSF) and interferon gamma (IFNgamma) after severe trauma. Inflamm Res. 2007; 56(1):38–44.

SECTION 6

ATLAS OF TRAUMA

Introduction to the Atlas........................................ 1148 Head and Neck ...................................................... 1149 FIGURE FIGURE FIGURE FIGURE FIGURE

1 2 3 4 5

Nasal Packing for Hemorrhage Control Steps in Performing a Lateral Parietal Craniectomy Anatomy of the Neck Alternate Neck Incisions Repair Techniques for Injury to the Common Carotid Artery Proximal to the Bifurcation

Thoracic Outlet and Chest ...................................... 1155 FIGURE 6 Alternative Approach to Interposition Grafting for an Injury to the Proximal Internal Carotid Artery FIGURE 7 Repair of a Combined Injury to the Trachea and Esophagus FIGURE 8 Control of Injured Vertebral Artery FIGURE 9 Tube Thoracostomy, the Most Commonly Performed Thoracic (Operative) Procedure FIGURE 10 Thoracic Incision Options FIGURE 11 Technique for Performing Median Sternotomy FIGURE 12 Median Sternotomy With a Neck Extension for Access to the Left Proximal Common Carotid Artery Injury FIGURE 13 Opening the Pericardium to Explore the Heart FIGURE 14 Cardiorrhaphy FIGURE 15 Pulmonary Tractomy FIGURE 16 Anatomy of Left Pulmonary Hilum FIGURE 17 Anatomy of the Right Pulmonary Hilum FIGURE 18 Controlling Intercostal Artery Bleeding FIGURE 19 Exposure and Management of Innominate Artery Injury FIGURE 20 Controlling Hemorrhage From the Subclavian Artery FIGURE 21 Exposure and Repair of a Subclavian Artery Injury FIGURE 22 Anatomy of the Thoracic Duct FIGURE 23 Cross-clamping of the Thoracic Aorta FIGURE 24 Left Heart Bypass FIGURE 25 Hilar “Lung Twist”

Abdomen ............................................................... 1175 FIGURE 26 Pelvic Packing for Grade 5 Fracture With Retroperitoneal Bleeding FIGURE 27 Liver and Biliary Anatomy

FIGURE FIGURE FIGURE FIGURE FIGURE FIGURE FIGURE FIGURE FIGURE

28 29 30 31 32 33 34 35 36

FIGURE FIGURE FIGURE FIGURE

37 38 39 40

FIGURE 41 FIGURE 42 FIGURE 43 FIGURE 44 FIGURE 45 FIGURE 46 FIGURE 47

Hepatorrhaphy Tractotomy Liver Omental Packing Hepatic Balloon Tamponade Liver Packing Pancreaticoduodenal Biliary Anatomy The Pringle Maneuver Pyloric Exclusion Division of Pancreatic Neck to Expose the Portal Vein Distal Pancreatectomy Kocher and Cattell–Braasch Maneuvers Atrial Caval Shunt Exposure and Repair of Injury at the Esophagogastric Junction Celiac Axis Bleeding Mattox Maneuver for Large Central Suprarenal Retroperitoneal Hematoma Repair of the Transected Ureter Temporary Abdominal Wall Closure Following Damage Control Laparotomy Secondary “Damage Control” (if needed) Tertiary “Damage Control” (if needed) Closure for Prior “Damage Control”

Vascular.................................................................. 1192 FIGURE FIGURE FIGURE FIGURE FIGURE FIGURE

48 49 50 51 52 53

FIGURE 54 FIGURE FIGURE FIGURE FIGURE

55 56 57 58

Small Vascular Anastomoses Deliberate Division of the Right Common Iliac Artery Temporary Vascular Shunt Complex Femoral Artery Reconstruction Popliteal Artery Injury Behind the Knee Exposure and Repair of Popliteal Artery and Vein Injuries Exposure and Repair of Popliteal and Tibial Artery Injuries Posterior Exposure of Popliteal Artery Injuries Calf Fasciotomy Forearm Fasciotomy Venous Bypass

1148

Introduction to the Atlas

Each preceding chapter has figures, tables, and drawings that aid the author and the editors in imparting and clarifying the messages of the chapter. In this edition of TRAUMA, the editors have devoted a special section to an atlas. It is not intended to include an exhaustive artistic rendering of every operation, but, rather, to focus on procedures that are commonly used in major trauma operations, along with related anatomical drawings. Some procedures that may have been

commonly practiced in the past but are rarely currently done are not included. However, a few relatively infrequently used concepts and procedures have been included in this section because of sufficient need to clarify the opinions of the editors. The art has been kept in as simple a form as possible, so it is expeditiously available when needed for a quick refresher in anatomy, anatomical relationships, and/or surgical approach in the “heat of battle.”

Head and Neck

1149

Head and Neck SECTION 6 FIGURE 1 Nasal Packing for Hemorrhage Control

A

B

FIGURE 1 Nasal Packing for Hemorrhage Control A. Under general or topical anesthesia, gauze impregnated with Vaseline to facilitate insertion is layered into a bleeding nasal passage to achieve hemostasis B. Balloon devices are commercially available to provide posterior and anterior nasal packing

1150

Atlas of Trauma

SECTION 6

Burr holes

FIGURE 2 Steps in Performing a Lateral Parietal Craniectomy

A

B

Epidural hematoma caused by damaged meningeal arteries Ligated meningeal arteries

C

D

FIGURE 2 Steps in Performing a Lateral Parietal Craniectomy A. The exact location and size of the skin flap vary, depending on extent of the wound but must not extend to the midline at the top of the skull B. Skin clips are placed for hemostasis, and burr holes elevate the skull bone flap C–D. The bone flap is removed, the dura mater is opened to expose and release an epidural hematoma, and bleeding vessels are ligated. In the absence of significant brain swelling, the skull plate is reattached once hemorrhage is controlled and other necessary procedures have been accomplished. With significant brain swelling, the dura is closed, sometime using dural substitutes, and the bone flap is not replaced at initial operation (decompressive craniotomy)

Head and Neck

1151

SECTION 6

Symphysis menti Digastric (anterior belly) Mylohyoid muscle

Hyoid External jugular Sternocleidomastoid Sternohyoid Omohyoid (superior belly)

Internal carotid External carotid Internal jugular Common carotid Thyroid cartilage Vagus nerve Thyroid Trachea

Trapezius

A

FIGURE 3 Anatomy of the Neck A. Anterior Perspective—Although usually approached from incisions just anterior to the sternocleidomastoid muscle, the surgeon must always review the cervical anatomy and its structural relationships prior to incision. The external jugular vein is a subcutaneous structure, and the internal jugular vein and carotid arteries are deep and medial in the neck

FIGURE 3 Anatomy of the Neck

Submandibular gland

Mandible

1152

Atlas of Trauma

SECTION 6 Angle of mandile Messeter Parotid duct Submandibular gland

Parotid gland Digastric Occipital protuberance

FIGURE 3 Anatomy of the Neck (continued)

Facial artery Mandible Hyoid Omohyoid Thyroid cartilage

Internal carotid External carotid Spinal part of accessory nerve Common carotid

Trachea Thymus

Trapezius External jugular vein

Sternocleidomastoid Acromion Clavicle

B

Subclavian artery and vein

FIGURE 3 Anatomy of the Neck (continued) B. Lateral Perspective—The proximal sternocleidomastoid and scalene anticus muscles cover the proximal extrathoracic subclavian artery. Not shown are the almost invisible thoracic ducts (both sides of the neck) that enter at the lateral superior junction of the internal jugular vein and the subclavian vein

Head and Neck

1153

SECTION 6 FIGURE 4 Alternate Neck Incisions

A

B

C

FIGURE 4 Alternate Neck Incisions A. For thoracic outlet injuries (Zone 1 cervical injuries), median sternotomy may be combined with either a right or left classic anterior neck incision, which allows for proximal vascular control B. For injury to the proximal extrathoracic subclavian artery, supraclavicular extension of a median sternotomy allows for proximal control as well as exposure, should division or removal of the clavicle be required for exposure and repair of the injury In some instances, such as an injury to the proximal left carotid artery, it is necessary to extend the median sternotomy into an anterior neck incision C. In some instances of bilateral neck injury, a bilateral anterior neck incision may be made separately or joined to create a skin flap to expose the entire anterior neck

1154

Atlas of Trauma

SECTION 6 A

FIGURE 5 Repair Techniques for Injury to the Common Carotid Artery Proximal to the Bifurcation

B

C

FIGURE 5 Repair Techniques for Injury to the Common Carotid Artery Proximal to the Bifurcation A. The injured vessel is debrided after proximal and distal control is obtained. Local heparinized saline is injected distally B. If the injury is not extensive, end-to-end anastomosis with 5 (0) polypropylene running suture using a “parachuting” technique is possible. Note, with adequate arterial collateral circulation, a temporary carotid artery shunt is not required C. If the artery is going to be under tension or stretched, an interposition graft of Dacron (shown), polytetrafluoroethylene (PTFE), or scavenged vein is inserted Prior to completely releasing the clamps and before prograde flow is reestablished to the brain, any microclots that might have formed during the procedure are adequately flushed out, both proximally and distally

Thoracic Outlet and Chest

1155

Thoracic Outlet and Chest SECTION 6

B

FIGURE 6 Alternative Approach to Interposition Grafting for an Injury to the Proximal Internal Carotid Artery A. Following proximal and distal control and instillation of local heparinized saline, the area of injury is resected, and the external carotid artery is mobilized for a distance sufficient to bridge the gap for the injured internal carotid artery B. The origin of the proximal internal carotid artery is oversewn, and one anastomosis is accomplished using the mobilized external carotid artery branch to beyond the injury on the internal carotid artery. Ligation of one or two branches of the external carotid artery may be required to accomplish significant mobilization

Interposition of sternocleidomastoid

B

Esophageal repair (seen through muscle) Tracheal repair

A

FIGURE 7 Repair of a Combined Injury to the Trachea and Esophagus A. Following repair using interrupted absorbable sutures on the trachea, a vascularized muscle pedicle (such as the sternal head of the sternocleidomastoid muscle) is interposed between these two tubular structures to reduce the postrepair complication of fistula formation B. The procedure demonstrated in cross section

FIGURE 6 Alternative Approach to Interposition Grafting for an Injury to the Proximal Internal Carotid Artery FIGURE 7 Repair of a Combined Injury to the Trachea and Esophagus

A

1156

Atlas of Trauma

SECTION 6

Vertebral artery

FIGURE 8 Control of Injured Vertebral Artery

A

Bone wax

B

FIGURE 8 Control of Injured Vertebral Artery A. The vertebral artery lies deep in the neck inside the transverse foramen of the cervical vertebra. For uncontrolled bleeding from an injured vertebral artery within the transverse foramen of the neck, dissection and unroofing of this bony covering can be difficult and even produce additional injury and complications B. Bone wax pressed into the area of bleeding can rapidly control persistent bleeding

Thoracic Outlet and Chest

1157

SECTION 6

Midaxillary line

B

A

A C

D

FIGURE 9 Tube Thoracostomy, the Most Commonly Performed Thoracic (Operative) Procedure A. The lateral anatomy in the auscultatory triangle at the fourth intercostal space in the midclavicular line is the point for chest tube insertion B. Following adequate anesthesia, skin incision, and dissection of subcutaneous tissue are accomplished, and a large clamp or dissecting scissors are used to spread the intercostal muscles. The pleura is entered with the probing finger. Up to 25% of patients have some element of pleural symphysis, and entering the pleura with a Trocar or other similar instrument risks producing an iatrogenic lung injury. The finger allows digital exploration to discern the pericardium or a diaphragmatic injury and/or release pleural adhesions C. After an appropriately sized hole is created, a chest tube is introduced with the aid of a large curved clamp attached to the tip and directing the tube to the posterior apex location of the pleural space. The tube is attached to an appropriate collection, water seal, and negative pressure device D. The chest tube is aimed toward the apex of the pleura, with the last hole in the tube inside the chest wall

FIGURE 9 Tube Thoracostomy, the Most Commonly Performed Thoracic (Operative) Procedure

4th and 5th ribs

1158

Atlas of Trauma

SECTION 6 FIGURE 10 Thoracic Incision Options

B

A

C

FIGURE 10 Thoracic Incision Options A. The median sternotomy is the standard incision for anterior cardiac and thoracic outlet vascular injury, but is not an appropriate incision for approach to posterior mediastinal structures or the pulmonary hilum B. A median sternotomy with an anterior neck or supraclavicular extension is used for thoracic outlet great vessel injuries to Zone 1 of the neck C. The anterolateral incision, particularly on the left, is the utility emergency thoracotomy for trauma and resuscitation. It is made from the sternal edge, under the mammary fold, and in a curvilinear fashion toward the axilla, staying in close proximity to the fourth or fifth intercostal space. This incision should not be a straight line incision nor be carried through the female breast

Thoracic Outlet and Chest

1159

SECTION 6

Inframammary fold

D

F

E

FIGURE 10 Thoracic Incision Options (continued) D. Bilateral anterolateral incisions may be either separate or combined and transternal. When transternal, the sternum is traversed with a Gigli saw or other cutting device, and the internal thoracic arteries are ligated on both sides on the upper and lower incision sites (four ligatures). Both incisions should be curvilinear, with the transternal cut high enough on the sternum to expose the mid-portion of the heart and also with sufficient sternum to accomplish a solid bony closure. On occasion, when a right-sided injury is suspected high in the pleural cavity, the incision might even be above the right nipple E. In the female, the anterolateral incision is at the inframammary fold and is accomplished by moving the breast tissue cranially F. With the patient in a lateral decubitus position, a posterolateral fourth or fifth interspace incision can be made from near the area of the nipple, laterally around to near the spinal canal. This incision for trauma traverses the latissimus dorsi muscle and portions of other chest muscles. The scapula must be retracted superiorly to achieve fourth or fifth interspace incisions. This incision provides exposure of posterior mediastinal structures, such as the aorta, lung hilum, esophagus, trachea, and azygos vein

FIGURE 10 Thoracic Incision Options (continued)

Reflected breast

1160

Atlas of Trauma

SECTION 6 FIGURE 11 Technique for Performing Median Sternotomy

A

B

C

D

FIGURE 11 Technique for Performing Median Sternotomy A. With the patient appropriately prepped and draped, a skin incision is made from the manubrial notch to below the xiphisternum B. Using blunt dissection, the fingers are inserted just beneath the sternum from below and above, carefully dissecting the pericardium and loose fatty tissue away from the back of the sternum C. Using a sternal saw, keeping in the midline of the sternum, and exerting upward pressure on the saw, the total length of the sternum is cut. Care is taken not to divert to the right or left chest cavity D. A sternal retractor is placed into the incision, first with the two blades touching each other, and then slowly opening the sternum to avoid fracture of the sternum or any ribs. The pericardium, the thoracic vena cava, ascending aorta, pulmonary artery, and lower neck structures are now exposed. The left innominate vein, in the upper extent of the incision, is enclosed in fatty and thymic tissue, and care must be taken not to injure this vein

Thoracic Outlet and Chest

1161

SECTION 6

Vagus

Phrenic Recurrent laryngeal

FIGURE 12 Median Sternotomy With a Neck Extension for Access to the Left Proximal Common Carotid Artery Injury A neck incision or a median sternotomy, alone, is insufficient for control and reconstruction of injury to the left proximal common carotid artery. However, a combined incision, aided by two retractors, affords excellent exposure. The hematoma is often extensive. Note the location of the left vagus nerve, with its recurrent laryngeal nerve, around the aortic arch. Also note the lateral location of the left phrenic nerve. Concomitant venous injury and bleeding is common

FIGURE 12 Median Sternotomy With a Neck Extension for Access to the Left Proximal Common Carotid Artery Injury

Bleeding from carotid

1162

Atlas of Trauma

SECTION 6 FIGURE 13 Opening the Pericardium to Explore the Heart FIGURE 14 Cardiorrhaphy

FIGURE 13 Opening the Pericardium to Explore the Heart Using scissors or a scalpel, the left pericardium is incised, with the lung positioned posteriorly. The incision is made anterior and parallel to the phrenic nerve. With a tense hemopericardium, purchase of the pericardium is difficult, making this maneuver difficult. The ratchet mechanism of the chest wall retractor is positioned posteriorly

A

B

FIGURE 14 Cardiorrhaphy A. Through a median sternotomy, the tense pericardium is incised in the midline and the clot extracted as digital hemorrhage control is accomplished B. Cardiorrhaphy is accomplished by simple direct closure of the penetrating wound using 4(0) polypropylene suture. Repair is accomplished prior to cardiac defibrillation. Often, traction on a figure-of-eight suture will cause all bleeding to stop, and the suture is simply tied

Thoracic Outlet and Chest

1163

SECTION 6 FIGURE 14 Cardiorrhaphy (continued)

C

D

E

FIGURE 14 Cardiorrhaphy (continued) C. Some surgeons prefer to accomplish cardiorrhaphy with pledgets, an adjunct probably most useful on the friable left ventricular muscle tissue D. For injury to the heart, very near a coronary artery, it is possible to use the double needle armed suture to go under the artery with both needles and tie the suture (with or without pledgets) lateral to the injury. For a distal coronary artery injury, simple ligation is sufficient E. Completed closure and ligated distal coronary artery injury F. Cross section demonstrating the coronary artery undercircling technique

F

1164

Atlas of Trauma

SECTION 6 FIGURE 15 Pulmonary Tractomy

A

FIGURE 15 Pulmonary Tractomy A. A through-and-through hole to the lung or even a large tangential laceration might be controlled with clamps or a linear stapler. The linear stapler is inserted into the tract, thereby joining the two holes. The stapler is fired and the lung cut, exposing the base of the tract B. A pulmonary tractotomy can also be accomplished by placing two large vascular clamps through the tract and cutting the lung between clamps. A polypropylene suture is run back and forth under the clamps, and other sutures control the base of the tract in a manner similar to when the stapler is used C. Persistent bleeding points and air leaks are closed with 4(0) polypropylene suture. This nonanatomic procedure is extremely well tolerated

B

C

Thoracic Outlet and Chest

1165

SECTION 6

Sup. pulmonary vein Inf. pulmonary vein

Left main bronchus

Basal pulmonary artery

FIGURE 16 Anatomy of Left Pulmonary Hilum The anatomy of the two pulmonary hila are slightly different. Before performing a trauma lobectomy or even pneumonectomy, a review of the related anatomy can reduce catastrophic iatrogenic bleeding and prevent bronchial injury. With the lung displaced posteriorly and inferiorly, the highest structure in the left pulmonary hilum, the main left pulmonary artery, is exposed and then sharply separated from the aortic arch. This artery goes behind the left superior pulmonary vein (draining the left upper lobe), and the artery continues downward, giving off branches to the left upper lobe and then to its terminal branches to the left lower lobe. The left main stem bronchus is behind the superior pulmonary artery. Both the superior and inferior pulmonary veins drain into the left atrium

FIGURE 16 Anatomy of Left Pulmonary Hilum

L. main pulmonary artery

1166

Atlas of Trauma

SECTION 6 FIGURE 17 Anatomy of the Right Pulmonary Hilum

Pleura R. inf. pulmonary vein R. main pulmonary artery

R. sup. pulmonary vein R. inf. pulmonary artery

Ant. seg. bronchus Basal bronchus

Middle bronchus

FIGURE 17 Anatomy of the Right Pulmonary Hilum The right lung has three lobes, so the anatomy is different from that of the left lung. To expose either hilum, the pleuras covering the vessels and bronchus are mobilized. The highest vessel in the hilum is the right pulmonary artery, giving off branches to the upper and then middle lobes, and then continuing to the arborization into the lower lobe. The middle lobe bronchus and artery come off the bronchus intermedius and right intermedius pulmonary artery in an anterior fashion. The inferior pulmonary vein is in a similar position to that on the left

Thoracic Outlet and Chest

1167

SECTION 6 FIGURE 18 Controlling Intercostal Artery Bleeding

A

B

FIGURE 18 Controlling Intercostal Artery Bleeding A. Bleeding from an intercostal artery, injured by a knife, missile, or fractured rib, can be extremely difficult to expose and control. One approach is a figure-of-eight suture ligation of the bleeding intercostal artery at the inferior border of the rib, where the injury occurred B. Alternatively, absorbable suture can be used to encircle a rib lateral to the bleeding points, pressing the vessel up against the inferior groove of the rib with the encircling suture

1168

Atlas of Trauma

SECTION 6

Hematoma

FIGURE 19 Exposure and Management of Innominate Artery Injury

Pericardium opened

A

FIGURE 19 Exposure and Management of Innominate Artery Injury A. The pericardium is opened vertically via a median sternotomy with the sternal retractor in place to expose the anterior heart and ascending aorta. The source of intrapericardial bleeding must be determined. The pericardial incision extends superior to the ascending aorta near the aortic arch. At the thoracic outlet, note the hematoma, which is encountered with an injury to the innominate artery or vein or proximal internal carotid. In this drawing, the upper limits of the incision are extended into the neck (can be either to right or left of midline) so that the distal control of the thoracic outlet great vessels can be obtained. Note, also, that the innominate vein is in the center of the hematoma B. A blunt injury to the proximal innominate artery is actually a fracture of the aortic arch intima at the takeoff of the innominate artery. The intima of the innominate artery is rolled up with the presentation of the arterial discoloration and injury appears to be in the innominate artery. Through a median sternotomy with a right neck extension, the ascending aorta, aortic arch, innominate vein, innominate artery, subclavian artery, and right and left carotid arteries are exposed C. Without systemic heparinization or hypothermia, a Dacron graft is sutured end to side to the ascending aorta. In some instances the innominate vein might be divided to expose the area of injury. A partially occluding clamp is placed on the aortic arch proximal to the takeoff of the innominate artery and another vascular clamp is placed just proximal to the bifurcation of the innominate artery

B

C

Thoracic Outlet and Chest

1169

SECTION 6

A

B

FIGURE 20 Controlling Hemorrhage From the Subclavian Artery A. Temporary vascular control is achieved via short anterior third interspace incision with a vascular clamp applied to the intrathoracic left subclavian artery B. Alternately, control can be achieved using a Rommel tourniquet Note: In the emergency room, this injury can be immediately temporarily controlled with the tamponading finger or an inflated 30 mL Foley balloon

FIGURE 19 Exposure and Management of Innominate Artery Injury (continued) FIGURE 20 Controlling Hemorrhage From the Subclavian Artery

D

FIGURE 19 Exposure and Management of Innominate Artery Injury (continued) D. The graft is sutured to the distal innominate artery, taking care to back flush and clear the graft of any clot prior to the completion of the suture line. The aortic plate proximal to the injury is oversewn using two pledget strips

1170

Atlas of Trauma

SECTION 6 FIGURE 21 Exposure and Repair of a Subclavian Artery Injury

A

C

B

D

FIGURE 21 Exposure and Repair of a Subclavian Artery Injury A. Although endovascular stent graft options are increasingly being used for injury to the subclavian artery, they are not always available, so direct exposure may be required. With the arm prepped free but positioned at the patient’s side, clavicular division or resection might aid in exposure. A liberal supraclavicular incision is made over the clavicle B. The bone is exposed using a periosteal elevator C. The clavicle is divided in its middle portion, and the proximal end may be retracted medially D. The key to the fossa containing the subclavian artery is to remove the scalene fat pad. The phrenic nerve resides in the middle one-third of the scalene anticus muscle, the lateral half body of which is divided to aid exposure

Thoracic Outlet and Chest

F

FIGURE 21 Exposure and Repair of a Subclavian Artery Injury (continued) E. The subclavian artery is extremely fragile, and a saphenous vein is the preferred conduit to use in an open reconstruction F. Following vascular reconstruction, the clavicle can be reconstructed with orthopedic plating

Thoracic duct

FIGURE 22 Anatomy of the Thoracic Duct At the base of the mesentery, anterior to the abdominal aorta and very near the left renal vein, the cisterna chyli collects lymph from the mesenteric lymphatic channels and carries lymph upward, continuing anterior to the thoracic aorta on to the thoracic outlet, via the lymphatic duct. Other numerous lymphatic collateral channels join this thoracic lymphatic duct, where it bifurcates in the upper posterior chest. Although the left thoracic duct is the larger, a thoracic duct empties into the right superior subclavian vein just as it receives the corresponding internal jugular vein. Note that the thoracic duct is anterior to the subclavian artery and posterior to the subclavian vein. Most injuries to the thoracic duct close spontaneously, but if operative closure with very fine 6(0) polypropylene suture is required. Feeding the patient olive oil or cream at the time of anesthesia induction will help discern specific injury site

FIGURE 21 Exposure and Repair of a Subclavian Artery Injury (continued) FIGURE 22 Anatomy of the Thoracic Duct

A E

SECTION 6

Saphenous vein graft

1171

1172

Atlas of Trauma

Phrenic nerve

SECTION 6 Aorta

FIGURE 23 Cross-clamping of the Thoracic Aorta

A Phrenic nerve

Aorta Esophagus

B

FIGURE 23 Cross-clamping of the Thoracic Aorta A. With the patient in the supine position, a left fourth or fifth interspace curvilinear incision is made beneath the nipple and breast fold aiming to the axilla. The aorta is clamped higher in the chest, at the proximal descending thoracic aorta, using a spring (noncrushing) vascular clamp B. Alternately, the aorta may be cross-clamped low in the chest. The lung pushed upward, showing the heart within the pericardium, the phrenic nerve, the diaphragm, and the aorta. The esophagus is seen anterior to the aorta and the spine, with the segmental arteries coming off at each interspace. The aorta is cross-clamped low in the thorax using a spring vascular (noncrushing) clamp

Thoracic Outlet and Chest

1173

SECTION 6 FIGURE 24 Left Heart Bypass

A

B

FIGURE 24 Left Heart Bypass A. One option in the repair of a transection of the descending thoracic aorta is to use active left heart bypass from the left inferior pulmonary vein to the common femoral artery. This procedure decreases the upper extremity hypertension and increases visceral and spinal cord perfusion associated with simple aortic cross-clamping. Appropriately sized cannulas are inserted using a purse string on the inferior pulmonary vein/left atrial junction, with clamp isolation and a Rommel tourniquet around the upper part of the femoral artery. The cannulas are connected to the active bypass circuit as the aortic repair is accomplished. Use of systemic heparin or heparin-bonded tubing is a surgeon’s choice, but care must be taken to avoid any stasis in the active circuit. Following removal, the arteriotomy is repaired B. A simple femoral vein to femoral artery bypass is occasionally used as an emergency bypass option

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SECTION 6 FIGURE 25 Hilar “Lung Twist” AA

BB

FIGURE 25 Hilar “Lung Twist” A. Through a fifth anterolateral thoracotomy, the “lung twist” procedure is accomplished by first sharply dividing the inferior pulmonary ligament, taking care not to injure the inferior pulmonary vein at the upper extent of this ligament B. With the inferior pulmonary ligament divided, the entire lung can be rotated by moving the upper lobe to the area on top of the diaphragm and the lung diaphragmatic surface to the apex of the pleural space. This maneuver creates a torque with the pulmonary vessels, almost immediately causing a cessation of bleeding. Laparotomy packs are used to secure and maintain the lung in this torqued position until appropriate decisions are made to permanently address bleeding from the hilum of the lung

Abdomen

1175

Abdomen SECTION 6

Hematoma

6-8 cm midline incision

A

Hematoma

Bladder

Laparotomy pad inserted next to bladder

C

FIGURE 26 Pelvic Packing for Grade 5 Fracture With Retroperitoneal Bleeding A–B. Through a low midline incision, the area of the extraperitoneal bladder is approached, taking care to stay outside the peritoneal cavity C. Any free blood is removed, and the sides of the bladder are retracted

FIGURE 26 Pelvic Packing for Grade 5 Fracture With Retroperitoneal Bleeding

B

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SECTION 6 FIGURE 26 Pelvic Packing for Grade 5 Fracture With Retroperitoneal Bleeding (continued)

Three laparotomy pads on each side of bladder

D

FIGURE 26 Pelvic Packing for Grade 5 Fracture With Retroperitoneal Bleeding (continued) D. Three laparotomy pads are placed on each side, lateral and posterior to the bladder. The laparotomy pads are left in place as a damage control tactic (to be removed later), and the lower midline incision is closed. Some surgeons also ligate the internal iliac arteries bilaterally. Others recommend leaving these vessels intact to provide a route for embolization should bleeding continue

Abdomen

Common bile duct

SECTION 6

Proper hepatic artery

1177

Gastroduodenal artery

B

FIGURE 27 Liver and Biliary Anatomy A. This drawing depicts the anatomy of the gallbladder and porta hepatis. Although many variations may exist, review of this area can be helpful prior to operating on an injury in this location B. This drawing illustrates the vascular anatomy of the liver

FIGURE 27 Liver and Biliary Anatomy

Portal vein A

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SECTION 6 FIGURE 28 Hepatorrhaphy FIGURE 29 Tractotomy

FIGURE 28 Hepatorrhaphy Using a large, special “liver” needle on an absorbable suture, a deep figure-of-eight suture can stop troublesome bleeding. Sutures should be tied loosely, rather than snug and tight, since the liver swells postoperatively, and tight sutures can cause liver necrosis

FIGURE 29 Tractotomy Gross, large ligatures to the liver may cause liver necrosis and postoperative fever. The injury is unroofed by performing a tractomy, with direct ligation of the biliary and vascular structures

Abdomen

1179

SECTION 6 FIGURE 31 Hepatic Balloon Tamponade A custom, temporary balloon is fashioned using a Penrose catheter and a rubber catheter, sealing off the ends of the Penrose drain placed over the catheter. After insertion into the body of the liver, the catheter is then filled with saline. Over time, the pressure on the “balloon” can be lost, so that reinflation or a secondary procedure might be necessary following this temporary “damage control” tactic

FIGURE 30 Liver Omental Packing FIGURE 31 Hepatic Balloon Tamponade

FIGURE 30 Liver Omental Packing The left side of the omentum is mobilized off of the transverse colon mesentery, preserving a vascular pedicle from the right side of the transverse mesocolon. The sutures attaching the omentum to the liver are loosely applied, so as not to strangulate the omentum

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SECTION 6 FIGURE 32 Liver Packing FIGURE 33 Pancreaticoduodenal Biliary Anatomy

FIGURE 32 Liver Packing Temporary packing of a bleeding liver is the prime example of damage control. Laparotomy packs are placed above and below a bleeding area in the liver, making a “liver sandwich.” Care is taken not to obstruct the inferior vena cava or to produce too much constriction, leading to liver necrosis

IVC Aorta Common hepatic artery Splenic artery and vein

Pancreas tail Pancreas body Posterior superior pancreaticoduodenal artery

Pancreas neck

Anterior superior pancreaticoduodenal artery

Uncinate process

Pancreas head

Superior mesenteric artery and vein

Duodenum

Anterior inferior pancreaticoduodenal artery

Posterior inferior pancreaticoduodenal artery

FIGURE 33 Pancreaticoduodenal Biliary Anatomy The normal anatomy in the gastroduodenal-pancreatic area of the abdomen is very compact, with many adjacent structures. The superior mesenteric vein is usually to the right of the superior mesenteric artery, and the splenic artery is usually near the superior border of the pancreas, while the splenic vein is posterior to the pancreas and covered by this organ. Note, the collateral arterial circulation in the head of the pancreas, which can be a significant source of bleeding

Abdomen

1181

SECTION 6

A

B

FIGURE 35 Pyloric Exclusion A. For a complex combined injury to the pancreatic head and duodenum, pyloric exclusion is performed to eliminate lateral duodenal fistula formation, should a duodenal leak occur postoperatively. After control of the injury at the duodenum and pancreas has been accomplished, a dependent gastrotomy is made in the antrium of the stomach. The pylorus is palpated and grasped with a Babcock clamp and closed with the suture of choice. Almost most every suture used tends to cut through the pylorus, and the gastroduodenal outlet reopens in 3–6 weeks B. Following closure of the pylorus, a dependent anticolic gastrojejunostomy is created. As this is not an ulcerogenic operation, a truncal vagotomy is not necessary

FIGURE 34 The Pringle Maneuver FIGURE 35 Pyloric Exclusion

FIGURE 34 The Pringle Maneuver Using a noncrushing (vascular) clamp, the entire porta hepatis can be occluded to decrease bleeding from an injured liver. This is a temporary occlusion of the portal vein, hepatic artery, and bile duct. It is accomplished by palpating the Foramen of Winslow and precisely placing the clamp on only the desired structures

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SECTION 6 FIGURE 36 Division of Pancreatic Neck to Expose the Portal Vein FIGURE 37 Distal Pancreatectomy

FIGURE 36 Division of Pancreatic Neck to Expose the Portal Vein The portal vein is formed behind the neck of the pancreas as the superior mesenteric vein is joined by the splenic vein. Bleeding from this area following penetrating trauma presents an exposure problem. As there are very few sizable veins entering the portal vein from the posterior surface of the pancreas, after the superior mesenteric vein is exposed, a dissecting finger can be placed behind the pancreas, and anterior to the superior mesenteric/portal vein. Using scissors or electrocautery, the neck of the pancreas is deliberately divided over the dissecting finger under direct vision. This exposes the extent to the proximal portal vein, and appropriate vascular control and repair can be accomplished. The cut ends of the pancreas are later simply closed with suture or staples

FIGURE 37 Distal Pancreatectomy Whether a blunt transection or a large penetrating injury, if distal pancreatectomy is required in an adult, removal of an uninjured spleen is usually necessary, although occasionally the spleen can be preserved. In this instance, a linear stapler transects the mobilized distal pancreas with the spleen. This area of resection is often drained

Abdomen

1183

SECTION 6

C

FIGURE 38 Kocher and Cattell–Braasch Maneuvers A. These maneuvers expose the area of the infrarenal vena cava. With right-sided retroperitoneal injuries, the Kocher maneuver is made by using sharp and blunt dissection lateral and posterior to the duodenum. Retracting the liver superiorly, the peritoneum, lateral to the duodenum, is sharply and bluntly divided, and the duodenum is mobilized toward the left side. The kidney, right renal vessels, and inferior vena cava are left in situ as the portal triad area is brought anteriorly and to the left B. Exposure of predominately right-sided retroperitoneal vascular injuries can be expedited using a Cattell– Braasch maneuver. First, a Kocher maneuver is performed behind the right colon and lateral to the duodenum, using sharp and blunt dissection. For the Cattell–Braasch maneuver, the Kocher maneuver is extended to the cecum, and then dissection is carried up to the left side of the mesentery attachments, including all mesenteric vessels, with the right colon and small bowel C. Using this maneuver, the small intestines, right colon and mesenteric vessels can be placed on the anterior thorax, exposing the infrarenal retroperitoneal vascular structures

B

FIGURE 38 Kocher and Cattell–Braasch Maneuvers

A

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SECTION 6 FIGURE 39 Atrial Caval Shunt FIGURE 39 Atrial Caval Shunt Isolation of uncontrolled bleeding from the retrohepatic vena cava can be accomplished with an atrial caval shunt. The underlying principle is shunting lower body blood to the right atrium. A large chest tube with an extra hole cut near the base end and clamped at the base is inserted via a purse string suture at the right atrial appendage and advanced into the infrarenal inferior vena cava. Assure the last hole in the tube is below the area of the suprarenal inferior vena cava Rommel tourniquet. A second Rommel tourniquet is placed around the intrathoracic intrapericardial inferior vena cava. Finally, a Pringle maneuver accomplishes virtually total hepatic and retrohepatic vena cava vascular isolation to allow precise repair or reconstruction

Abdomen

1185

SECTION 6

A

D

C

FIGURE 40 Exposure and Repair of Injury at the Esophagogastric Junction A. High gastric injuries can be difficult to expose and repair. Following mobilization of the left lobe of the liver by lysing the left triangular ligament, the liver is retracted and the esophagus encircled with a Penrose drain for downward traction B. Anterior holes can be suture repaired, taking care not to cause a stricture at this location C–D. For an extensive esophagogastric junction injury, the greater curvature of the stomach is mobilized, ligating the vasobrevia vessels, and a fundoplication might be added for a more secure closure

FIGURE 40 Exposure and Repair of Injury at the Esophagogastric Junction

B

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SECTION 6 FIGURE 41 Celiac Axis Bleeding FIGURE 42 Mattox Maneuver for Large Central Suprarenal Retroperitoneal Hematoma

A

B

FIGURE 41 Celiac Axis Bleeding A. Drawing illustrating injury to the celiac axis B. Ligation of celiac axis injury

B

A

FIGURE 42 Mattox Maneuver for Large Central Suprarenal Retroperitoneal Hematoma A. The initial dissection is accomplished by going lateral to the left colon and dividing the line of Toldt, and with blunt dissection, move the spleen, left colon, stomach, pancreas tail, left kidney, and renal vessels and ureter toward the midline B. The viscera is mobilized to the right by dissecting behind the left kidney and anterior to the psoas muscle. Note that the abdominal aorta is exposed from the esophageal hiatus to the abdominal outlet at the iliac arteries. Care is taken to avoid injury to the left renal artery and vein. The esophageal crux is exposed at the area of the celiac axis, and the left crux can be purposefully cut with scissors and extended laterally across the left diaphragm to expose the distal thoracic aorta to as high as T8. Proximal and distal vascular clamps can be applied preparatory to either lateral aortorrhaphy or interposition Dacron graft placement. The surgeon on the right side of the operating room table is retracting and exposing, and the surgeon on the left is best positioned to perform the aortic repair

Abdomen

1187

SECTION 6 FIGURE 43 Repair of the Transected Ureter

A

B

FIGURE 43 Repair of the Transected Ureter A. Drawing of a transected ureter B. Spatulated transected ureter C. Direct repair of transected ureter

C

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SECTION 6 FIGURE 44 Temporary Abdominal Wall Closure Following Damage Control Laparotomy

A

B Black VAC sponges affidex and suction applied

C

D

FIGURE 44 Temporary Abdominal Wall Closure Following Damage Control Laparotomy A. This is the first of a series of drawings demonstrating approaches to management of the abdominal wall after a damage control laparotomy and one in which there is concern for an abdominal compartment syndrome. In this first drawing (44A), a transverse depiction of the abdomen is shown with a plastic drape covering the intestines, a series of cloth packings in the middle of the incision, and a plastic drape covering over the entire abdomen, with this drape resting on the skin. B–D. In the second drawing (44B) the covering is seen from a frontal view and two suction tubes are seen to emerge from the lower abdomen. Alternatively to the drawings using available pads, plastic sheeting, and suction tubing in every operating room, some surgeons, even at the first operation, might choose to use the same principle, but employ a commercially available device (Numbers 44C and 44D). Other surgeons might elect to use such a commercial device at the second or third damage control laparotomy.

Abdomen

1189

White sponges covering bowel Sutures to prevent fascial retraction

SECTION 6

Approximated fascia

B Black VAC sponge affixed and suction applied

C

D

FIGURE 45 Secondary “Damage Control” (if needed) A–D. At a second operation, the abdomen is cleaned of any old blood and appropriate secondary operations are conducted prior to application of new plastic coverings over the intestines, new cloth packing, and new plastic sheeting over the packing as seen here on transverse section (45B) and frontal view (45A). Alternatively, a smaller commercial device can be applied (Number 45C and 45D).

FIGURE 45 Secondary “Damage Control” (if needed)

A

1190

Atlas of Trauma Black VAC sponge affixed and suction applied

SECTION 6

Sutures to prevent fascial retraction

FIGURE 46 Tertiary “Damage Control” (if needed)

A

Skin closed over approximated fascia

B Small black VAC sponge

C

D

FIGURE 46 Tertiary “Damage Control” (if needed) A–D. In patients with significant bowel edema it might require subsequent and planned take-back operations where the wound is systematically closed as much as possible as shown using available material (number 46A–B), or commercial devices (Numbers 46C and D).

Abdomen

1191

Fascia and skin closed

SECTION 6

B

FIGURE 47 Closure for Prior “Damage Control” A–B. When all injuries in the abdomen have been repaired and any abdominal compartment syndrome has resided, the abdomen is formally closed (47 A–B)

FIGURE 47 Closure for Prior “Damage Control”

A

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Atlas of Trauma

Vascular SECTION 6 FIGURE 48 Small Vascular Anastomoses FIGURE 49 Deliberate Division of the Right Common Iliac Artery

A

B

FIGURE 48 Small Vascular Anastomoses A. A triangulated end-to-end vascular anastomoses, a technique initially described by Alexis Carrel B. Three temporary stay sutures may be tied as each section of the anastomosis is completed. Some surgeons prefer an interrupted anastomosis (not shown)

B B

A

A

FIGURE 49 Deliberate Division of the Right Common Iliac Artery A. Exposure of an injury to the right common iliac vein is very difficult. Deliberate division of the right common iliac artery between vascular clamps facilitates exposure and repair of underlying venous injury (right common iliac vein, iliac vein) B. Following venous control, the right common iliac artery is simply re-anastomosed

Vascular

1193

SECTION 6 FIGURE 50 Temporary Vascular Shunt

A

B

FIGURE 50 Temporary Vascular Shunt A. Used in most major named vessels of the body, a temporary intravascular shunt is pictured here in the common femoral artery. This vascular damage control tactic provides oxygenated blood distal to a vascular injury, while other injuries are addressed or, if necessary, the patient is transferred for a higher level of care B. Using appropriately sized plastic tubing, that is, commercially available carotid shunts, the shunt is secured with encircling tapes

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Atlas of Trauma

SECTION 6 FIGURE 51 Complex Femoral Artery Reconstruction

A

B

C

D

FIGURE 51 Complex Femoral Artery Reconstruction A. Drawing illustrating a complex injury to the femoral artery B. Medial and lateral incisions are made in both the profunda femoris and superficial femoral arteries. Suturing these sides together produces a larger opening, which can, at times, be primarily sutured to the distal common femoral artery C. The artery may also be reconstructed using an interposition graft, here depicted with Dacron D. On occasion, a bridge of prosthetic material can be sutured to the proximal superficial femoral artery, with the foreshortened profunda femoris artery sutured end-to-side to a more distal location in the superficial femoral artery

Vascular

1195

SECTION 6

Vein graft AB

B

FIGURE 52 Popliteal Artery Injury Behind the Knee A. Among the several options to reconstruct this injury, ligation of the two ends of the vessel with simple bypass using the saphenous vein from the other leg preserves the muscles and tendons at the medial side of the knee (pes anserinus). Depending on presence of associated injuries, the bypass saphenous graft may be passed subcutaneously or deep in the normal traverse of the popliteal artery. Care must be taken to assure the graft does not kink when the knee is flexed B. In some instances, appropriately sized PTFE graft material may be used

FIGURE 52 Popliteal Artery Injury Behind the Knee

PTFE bypass

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Atlas of Trauma

Popliteal artery and vein

SECTION 6

Cut pes anserinus Soleus Hunter’s canal

FIGURE 53 Exposure and Repair of Popliteal Artery and Vein Injuries FIGURE 54 Exposure and Repair of Popliteal and Tibial Artery Injuries

Cut sartorius and gracilis

Cut gastrocnemius Cut semitendinosus and semimembranosus

FIGURE 53 Exposure and Repair of Popliteal Artery and Vein Injuries Opening the entire medial side of the leg from Hunter’s Canal above, to below the area of the popliteal artery arborization exposes the popliteal artery and vein. Through this incision, the medial head of the gastrocnemius muscle is taken down, and the distal tendinous portions of the semitendinosus and semimembranosus muscles are cut. At the conclusion of the operation and vascular construction, the medial fascial disconnections must be repaired

A

FIGURE 54 Exposure and Repair of Popliteal and Tibial Artery Injuries A. Care is taken that the upper portion of this medial incision does not injure the subcutaneous saphenous vein and that it is sufficiently long enough for exposure of the right proximal tibial artery. The lower extent of the incision should be almost half way down the calf B. The medial head of the gastrocnemius is taken down and the soleus muscle is exposed. The popliteal artery first gives off the anterior tibial artery, which traverses anteriorly through the interosseous membrane. Once precise vascular control is obtained in the area of the injury, reconstruction can be accomplished

Popliteal artery and vein Soleus

B

Retracted gastrocnemius

Vascular

1197

SECTION 6

Popliteal vein

Peroneal nerve Tibial nerve

A

B

FIGURE 55 Posterior Exposure of Popliteal Artery Injuries A. On rare occasion, a posterior approach to the popliteal fossa and its vessels may be desired. This approach prevents access to the groin and often reduces the opportunity for saphenous vein salvage B. Anatomy as seen for posterior approach of popliteal space

FIGURE 55 Posterior Exposure of Popliteal Artery Injuries

Popliteal artery

1198

Atlas of Trauma Anterior compartment

SECTION 6

Deep posterior compartment

Lateral compartment

Superficial posterior compartment A

FIGURE 56 Calf Fasciotomy

Saphenous vein

B

Deep peroneal nerve

C

Superficial peroneal nerve

FIGURE 56 Calf Fasciotomy A. Cross section of the four compartments of the calf B. The lateral skin incision is made over the fibula, curving anterior as the incision reaches its upper extents to avoid injury to the superficial peroneal nerve, which can cause foot drop C. The medial incision is made along the mid-calf, being very careful in the upper extent to avoid iatrogenic injury the subcutaneous saphenous vein, which is a major venous outflow for the foot and calf if the deep tibial veins are ligated

Vascular

1199

SECTION 6

A

FIGURE 57 Forearm Fasciotomy

Superficial volar

Deep volar

B

Dorsal

FIGURE 57 Forearm Fasciotomy A. A simple, single incision, beginning on the radial side of the anticubital fossa and curving downward to the hand on the ulnar surface of the forearm, allows all the forearm compartments to be released, when needed B. After the skin flap is developed just above the muscle compartments, any bulging muscle bundle is released. The incision is extended to beyond the retinaculum at the wrist. Through this flap, the superficial and deep volar compartments can be released

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SECTION 6 FIGURE 58 Venous Bypass FIGURE 58 Venous Bypass A patient may be placed on bypass circuit using a centrifugal pump to achieve the desired rate of bypass for various reasons. The rate of return is equal to the rate of blood collection. Bypass may be used to isolate an injured liver by draining the inferior vena cava and portal vein. Alternately (not shown), a femoral vein to axillary vein bypass technique can be used for rewarming a hypothermic patient

INDEX Note: Page numbers followed by f and t indicate figures and tables, respectively. A AAST Colon Injury Scale, 621, 622t AAST Duodenum Organ Injury Scale, 611t grade I, 610–612 grade II, 610–612 grade III, 612–613 grade IV, 613 grade V, 613 AAST Pancreas Organ Injury Scale, 615t grade I, 613–614 grade II, 613–614 grade III, 614–616 grade IV, 616 grade V, 616 AAST Rectal Organ Injury Scale, 626t abbreviated burn injury severity (ABSI) score, 880 Abbreviated Injury Scale (AIS), 26 abdomen damage control closure for prior, 1191f secondary, 1189f tertiary, 1190f abdominal arteries, damage control operations in, 730 abdominal compartment syndrome classification of, 734, 734t definition of, 733 measurement of IAP and, 733 prevention and management of, 735 subtypes of, 733 abdominal injuries, 581, 867–869, 879. See also abdominal trauma; pancreatic injuries anatomy and physiology, 582 injury/pathophysiology, mechanism of, 582–587 associated with colon injuries, 624 blood supply to small bowel, 584f stomach, 583f blunt intestinal injury, 585f CT few hours after injury, 588f shortly after injury, 588f tangential GSN, 589f diagnosis of, 587–589 enterocutaneous fistula, 599f fistula VAC, 598f gastrointestinal secretions, 597t historical perspective, 581–582 isolated mesenteric injury, 593f jejunum and ileum, 585f lumbar spine, causes, 586f

operative management, 589 small bowel injuries, 591–595 stomach injuries, 590–591 oral contrast extravasation, 588f postoperative management, 595–600 small bowel fistula, 599f small bowel injury handsewn vs. stapled anastomoses, 594t treatment of grade I and II, 592f treatment of grade III and IV, 593f small bowel injury scale, 590t stomach injury, 590t abdominal perfusion pressure, 734–735 abdominal trauma damage control operations for abdominal arteries, 730 abdominal veins, 730–731 gastrointestinal tract, 729 intra-abdominal packing, 731–732 liver, 728–729 pancreas, 729–730 spleen, 729 abdominal vascular injury, 636 classification of, 632, 633t complications of, 649–650 diagnosis of blood pressure examination, 634t history and physical examination, 633–634 endovascular techniques in, 648–649 epidemiology of, 632–633 management celiac axis injuries, 639 exposure and vascular control, 637–638 injuries to proximal renal arteries, 640 injuries to superior mesenteric artery, 639–640, 640f and resuscitation, 635–636 suprarenal aorta, 638, 639t management in inframesocolic region exposure and vascular control, 641–642, 643–644 infrahepatic inferior vena cava, 642–643 infrarenal aorta, 642 management in pelvic retroperitoneum exposure and vascular control, 645 injuries to common or external iliac vein, 646 injury to common or external iliac artery, 645–646

management in upper lateral retroperitoneum exposure and vascular control, 643–644 renovascular injuries, 644 in military conflicts, 632–633 operative preparations for, 636–637 pathophysiology of blunt trauma, 633 penetrating trauma, 633 abdominal veins, damage control operations in, 730–731 abdominal wall closure, damage control laparotomy, 1188f absorbable meshes, 739–741, 740f Accessibility/Remoteness Index of Australia (ARIA+), 141 acetabular fractures, management of, 792–793, 793f acidosis, 727 acromioclavicular dislocation, 764 ACS Field Triage System, 62 acute care surgery, 91–98, 991 academic success, 91 Acute Care Surgery Fellowship, 93 operative management principles and technical procedure, 95t–96t algorithm for making clinical judgments of futility, 887–889 clinical component of fellowships, 97 comet tail artifact, 311f curriculum, 94–98, 94t decision-making algorithm, 888f deep venous thrombosis, sagittal ultrasound image, 318f fascial dehiscence, 315f femoral vein, transducer position, 317f fractured sternum, sagittal view, 312f futility, four concepts of, 886–887 ICP monitoring, 92 intensive care unit, surgeon-performed ultrasound, 315 central venous catheter, insertion, 316–317 common femoral vein, thrombosis, 317–318 educational model, 318–319 inferior venal caval filters (IVCF), insertion, 318 intraperitoneal fluid/blood, 316 pleural effusion, 316 liver, kidney, and diaphragm sagittal view, 307f, 310f

1201

1202

Index acute care surgery (continued ) minimally invasive surgery, 92 normal and abnormal, heart, parasternal view, 307f penetrating chest wounds algorithm, 309f pericardial area, sagittal view, 306f spleen, kidney, and diaphragm sagittal view, 308f sternum, sagittal view, 312f Surgical Council on Resident Education (SCORE), 93 surgical discipline, advancement, 91 surgical disorders, surgeon-performed ultrasound acute abdominal pain, evaluation, 314 stable patient, 314 unstable patient, 314–315 dehiscence and soft tissue infections, 315 surgical training, 93f thoracic ultrasound examination, transducer positions, 310f transducer frequencies, clinical applications, 305t trauma, surgeon-performed ultrasound austere settings, 313–314 in space, 313–314 focused assessment for the sonographic examination of the trauma patient (FAST), 304–306 accuracy, 307–309 advances and organ specificity, 309–310 blood, quantification, 309 technique, 306–307 transducer positions, schematic diagram, 306f in pediatric trauma patients, 313 in penetrating trauma, 313 pneumothorax, 311–312 in pregnant trauma patient, 312–313 sternal fracture, 312 traumatic hemothorax, 310 accuracy, 310–311 technique for examination, 310 ultrasound imaging essential principles, 304f maximizing accuracy, 306t scanning planes, 304t, 305f terminology, 302t–303t, 304t ultrasound physics, 301–302 urinary bladder, coronal view, 308f vein/artery, transverse ultrasound image, 317f Acute Care Surgery Fellowship, 93 Acute Care Surgical service, 95 acute limb ischemia, 820 acute radiation syndrome (ARS), 137 acute respiratory distress syndrome (ARDS), 870, 880 acute traumatic brain injury, 863 advanced automatic crash notification (AACN) equipment, 150

advanced life support (ALS), 100, 141 Advanced Trauma Life Support (ATLS), 55, 141, 154, 859 age-specific hypotension, 861 Agkistrodon, 914, 915 airway, breathing, circulation, disability, exposure/environment (ABCDE), 154 airway management, 167 assessment of, 169 history, 169 physical examination, 169 bag valve mask (BVM), 169 brain laryngeal mask airway (LMA) anterior and lateral photograph, 178f combitube double-lumen tube, lateral photograph, 176f difficult airway, 184–185 algorithm, 185f equipment and technique, 186 emergency airway, complications aspiration, 186 esophageal intubation, 186 failure to intubate, 186 pneumonia, 186 endotracheal intubation esophageal tracheal combitube (ETC), 175–177 gum elastic bougie, 175 nasotracheal intubation (NTI), 174 retrograde intubation, 174–175 equipment, 167 failed airway, algorithm, 184f injured patient, challenges cervical spine trauma, 180–181 closed head injury, 181–182 laryngotracheal trauma, 180 maxillofacial acial trauma, 180 thermal trauma, 181 maxillofacial injury, extreme destructive nature, 180f monitoring/troubleshooting airway maneuvers, manual, 168 capnography, 167–168 chin lift, 168 jaw thrust, 168 pulse oximetry, 167 sellick maneuver, 168 troubleshooting, 168 nasopharyngeal devices, 169 needle cricothyroidotomy, setup, 179f optimal rapid sequence intubation team, 168f oropharyngeal devices, 168–169 pediatric airway airway failure, 183–184 anatomy, 182 equipment, 182 physiology, 182 spontaneous respirations, 184 technique, 182–183 preparation, 167 priority, 167

rapid sequence induction (RSI) overview, 170 pharmacology, 171t preoxygenation, 170–171 preparation, 170 steps and timing, 171t rapid sequence induction (RSI), pharmacology, 171 complications/outcomes, 174 cricoid cartilage pressure, 174 induction agents barbiturates, 173 dissociative agents, 173 etomidate, 172–173 propofol, 173 paralysis neuromuscular blocking agents, 173 nondepolarizing agents, 174 succinylcholine, 173 placement confirmation, 174 premedication agents, 172 antiarrhythmics, 172 benzodiazepines, 172 beta-adrenergic blockers, 172 defasciculation paralytic agents, 172 opioids, 172 retrograde intubation, 175f supralaryngeal airways cricothyroidotomy, 177–179 cricothyroidotomy technique, 179 laryngeal mask airway, 177 laryngeal tube airway (LTA), 177 needle cricothyroidotomy, 179 video laryngoscopy, 177 trachea, intubation guidelines for emergency, 169–170 alcohol and drug use, 893 alcohol dependence syndromes, 853 application of brief intervention, 855–856 evidence of effect in trauma settings, 853 guidelines for brief interventions for trauma patients, 855 magnitude of problem, 851 nature of problem, 851–853 SBIRT program, 856–857 billing for, 857 confidentiality concerns, 857 screening methods, 854–855 alcohol dependence syndromes, 853 Alcohol, Smoking, and Substance Involvement Screening Test (ASSIST), 855 Alcohol Use Disorders Identification Test (AUDIT), 854t algorithm for emergency cesarean section, 720f all-terrain vehicles (ATVs), 142 alternate closures of incisions, indications for, 733 Ambroise Pare, 905 American Academy of Pediatrics (AAP), 40 American Association for the Surgery of Trauma (AAST), 83

Index American Board of Surgery (ABS), 93 American College of Surgeons Committee on Trauma (ACSCOT), 54, 859 American Psychological Association Presidential Task Force on Violence and the Family, 891 amniotic sac, 712 ampicillin, 911 analytic epidemiology, 18 anaphylaxis, treatment for, 917t Anatomic Profile Score (APS), 79 anatomy criteria, trauma systems, 59 direct laryngoscopy and intubation, 170 kinematics, 8 scoring systems, injury severity scores (ISSs), 79–83 anemia, hemorrhagic shock, red blood cell (RBC) transfusion, 216 anesthesia toxicity, 906 angiogenesis, 899 ankle–brachial index, 821 ankle injuries, 809–810 antecolic gastrojejunostomy, 731f anterolateral thoracotomy, 834 antibiotic prophylaxis for colon injuries, 629 for human bites, 911 antibiotic, usage for acute wounds delayed presentation, 908 heavily contaminated extensive soft tissue wounds, 908 host factors, 908 open fractures or open joints, 907–908 anticoagulant medications, 877 anticoagulation, 882 anticoagulation agents, 834 antimicrobial therapy, of wounds, 908 antiplatelet agents, 834 antiplatelet medications, 877 antiplatelet therapy, 882 APC injuries, 657, 658 Apis mellifera, 919 arterial injuries, 503 ascending aorta, 503 descending thoracic aorta, 504–506 foreign body embolism, 509 innominate artery, 503–504 intercostal arteries, 507 internal mammary artery, 507 left carotid artery, 507 mediastinal traverse injuries, 508 postoperative management, 509–510 pulmonary artery, 507 subclavian artery, 506–507 systemic air embolism, 508–509 thoracic duct injury, 508 transverse aortic arch, 503 venous injuries azygos vein, 508 pulmonary veins, 507 subclavian veins, 508 thoracic vena cava, 507

arterial repair, 827 arteriogram time equation, 822 ascorbic acid, 902 asphalt abrasions, 908 atherosclerotic disease, 877 atrial caval shunt, 1184f automatic/semi-automatic external defibrillators (AEDs), 103 automotive safety, 40 axillary artery injury, 833 axonotmesis, 761 azygos vein, thoracic vascular injuries, 508f B Bacteroides spp., 909, 911 bag-valve mask (BVM) device, 102 basic fibroblast growth factor (bFGF), 899 β-blocker therapy, 875 bee and wasp stings, wounds caused by, 919 Bennett’s fracture, 776f benzodiazepines, 853, 881 Betadine®, 905 beta-lactamase inhibitor, 911 bicarbonate secretion and pancreatic secretion, 608 bilateral internal iliac artery embolization, 663f biliary anatomy, 1177f biliary fistulae, 555 biliary tract injury. See extrahepatic biliary tract injury, traumatic bites and stings by marine animals bee and wasp stings, 919 insect and bug bites, 918–919 marine invertebrates, 917–918 piranha attacks, 918 shark bites, 918 spider bites, 919 venomous fish, 918 by terrestrial animals cat bites, 911 dog bites, 911 human bites, 909–911 rabies prophylaxis, 911–912 snakebites, 912–917 treatments for antivenin therapy, 916–917 coral snake envenomation, 917 crotalid envenomation, 914–915 definitive care for, 916 fasciotomy, 917 first aid for, 915–916 identification of the snake for, 913–914 blast injury to colon, 622f blood alcohol concentration (BAC), 29, 41 blood alcohol screening, 41 blood pressure, 158 blood transfusions, and abdominal septic complications, 625 blood typing, 608 blood vessel, injuries to, 869–870

blunt abdominal trauma, 11 in pregnancy, management of, 716 blunt abdominal vascular injury algorithm, 650f blunt diaphragmatic rupture, 867 blunt force injury, 820 blunt trauma, 633, 869 to colon, 620 blunt trauma assessment abdomen, contrast extravasation, 273f acetabulum column fractures, 284f transverse acetabular fracture, 283f anteroposterior (AP) pelvis radiograph, 252f radiograph, 286f recumbent chest radiograph, 252f aortic injury, 268f appendicular skeleton conventional radiography, 282 joint, computed tomography, 282–285 blunt carotid and vertebral injury, 260f blunt head injury, 255f catheter angiography, 285 acute blunt-force traumatic aortic injury, arch angiography, 289–291 blunt-force lacerations hepatic angiography, 291–292 splenic arteriography, 292 blunt pelvic fractures, 293–295 pelvic hemorrhage, 293–295 penetrating pelvic trauma, 295 peripheral vascular injuries, 295–299 renal trauma, interventions, 292–293 transcatheter endovascular therapies, 285–289 cross-table lateral cervical spine radiograph, 252f diaphragmatic rupture, 272f epidural hematoma, 254f esophageal injuries, 258f facial fracture, 257f fatal bleed from internal iliac arteries, 279f flexion–extension radiograph, cervical spine, 266f focused abdominal sonography for trauma (FAST), 253 coronal image of, 252f genitourinary injuries, lower, 278f grade IV renal laceration, 277f gunshot injury of aortic arch, 269f herniation, patterns, 256f imaging for, 251 head, computed tomography of, 254–255 maxillofacial skeleton, computed tomography of, 255–257 multidetector computed tomography (MDCT), 253–254 neck, soft tissue injuries, 257–259 neck, vascular injuries, 259 left superior gluteal artery bleed, 279f

1203

1204

Index blunt trauma assessment (continued ) liver laceration, 291f long-bone fracture, 285f lower cervical spine, sagittal reformations, 263f mediastinal hematoma, caused by nonaortic injury, 270f multimodality correlations, cervical spine, 264f neck, penetrating vascular injuries, 259 abdomen/pelvis CT, 271–276 cervical spine computed tomography, 260–265 flexion/extension X-rays, 266–267 chest CT, 267–271 pelvis/acetabulum CT, 276–282 spine conventional X-rays, 260–265 magnetic resonance imaging, 266 thoracolumbar spine, computed tomography, 265–266 patterns of injury, 274f central package, 274f left package, 275f right package, 276f pelvic fractures, multiple bleeds, 296f pelvic ring fracture, 280f anteroposterior (AP) compression type, 281f lateral compression type, 280f periarticular fractures, 286f intra-articular intercondylar distal femur fracture, 288f midfoot, calcaneus and Lisfranc fractures, 290f tibial plateau fracture, 289f periarticular injury, 287f permanent particulate emboli, microcatheter, 295, 296f popliteal artery minimal injury, 297f thrombosis of, 298f pulmonary contusion and laceration, 271f renal artery injury, 294f shock-bowel syndrome, 280f small bowel perforation, 279f soft tissue neck injury, 258f splenic artery embolization, long-term follow-up, 293f splenic intraparenchymal false aneurysms, 293f splenic laceration and active extravasation, 279f thoracic aorta, blunt traumatic rupture, 267f trauma series, 251–253 traumatic aortic pseudoaneurysm, 291f upper cervical spine, coronal reformations, 261f upper cervical spine, sagittal reformations, 262f vascular isolation by proximal and distal coil occlusion, 298f

vertical shear injury, with unstable sacral fracture, 282f zygomaticomaxillary complex (ZMC) fracture, 257f bone injuries floating elbow, 772 floating shoulder, 769 fractures of capitellum, 771 carpal bones, 774–775 clavicle, 769 distal humerus, 770–771 distal radius, 772–773 head of radius, 772 metacarpal bones, 775–776 phalanges, 776–777 proximal humerus, 769–770 proximal ulna, 771 radius and ulna, 773 scaphoid, 773–774 scapula, 769 shaft of humerus, 770 shaft of radius, 772 shaft of ulna, 772 nightstick fracture, 772 Bothrops atrox, 915 brachial artery injuries, 836 laceration, 820 brachial plexus injuries, 761–763 palsy, 833 brain injury. See traumatic brain injury (TBI) brain laryngeal mask airway (LMA) anterior and lateral photograph, 178f Brain laryngeal mask airway (LMA), anterior and lateral photograph, 178f Brain Trauma Foundation, 864 Broselow Pediatric Resuscitation Measuring Tape, 860 buckle fractures, 870 bulging perineum, 712 bupivacaine, 906, 907t burn injury Berkow chart, 926t burn wound, surgical management of, 929 care of burn wound, 928–929 changes in organ function, 924 chemical burns, 928 control of infection, 930 criteria for referral, 922–923 Curreri formula, 931t definition, 923t depth, determination, 925–926 in elderly population, 879–880 electrical burns, 928 epidemiology, 922 escharotomies, 926–927 fluid resuscitation, 924–925 hypermetabolism, 931 incidence of, 922

inflammatory response, 923 inhalation injury, 927–928 initial care, 924 management of organ systems, 930–931 nutritional management, 931 pathophysiology, 923 pediatric burn patients, estimating caloric requirements, 931t resuscitation formulas, 925t rule of nines, size, 926f size, determination, 926 wound coverings, advantages and disadvantages, 929t zones illustration, 923f BVM device, 116 C CAGE questionnaires, for detection of alcohol problems, 854 calcium gluconate, 918 calf compartment syndrome, 829 calf fasciotomy, 829, 1198f capitellum, fractures of, 771 Capnocytophaga, 911 cardiac enzymes, 159 cardiac toxicity, 906 cardiogenic shock, 159 cardiopulmonary resuscitation (CPR), 102, 871, 886 cardiorrhaphy, 1062f–1063f cardiotocographic strip, 715f cardiovascular comorbidities, 875 cardiovascular effects, rehabilitation aerobic capacity, 952 cardiac effects, 951 orthostatic hypotension, 951–952 prevention and treatment, 952 shift of body fluids, 951 venous thrombosis and pulmonary embolus, 952 cardiovascular failure, 1041 cardiac function, evaluation central venous pressure, 1047–1048 echocardiography, 1048 inferior vena caval ultrasound, 1048 pulmonary artery catheters, 1048 stroke volume variation, 1048–1049 cardiac output, determinants of, 1041 afterload, 1043 contractility, 1043–1044 heart rate, 1044 preload, 1041–1043 diagnosis and management, 1042f diastolic dysfunction, management, 1051 pulmonary hypertension, 1051–1052 left ventricular pressure and left ventricular volume, 1043f myocardial dysfunction, 1044 amrinone and milrinone, 1046 dobutamine, 1046 dopamine, 1045–1046 epinephrine, 1046

Index intra-aortic balloon pump counterpulsation, 1047 nitrovasodilators, 1046–1047 norepinephrine, 1045 pharmacologic, 1044–1045 preload augmentation and rewarming, 1044 steroids, 1047 vasopressin, 1045 myocardial infarction, current treatment of, 1050–1051 myocardial protection, 1049–1050 resuscitation, optimal endpoints capnography, 1049 lactate and base deficit, 1049 mixed venous oxygen saturation, 1049 treatment of, 1045t ventricular stroke, 1044f cardiovascular system, changes in maternal, 711 carotid artery proximal to bifurcation, repair techniques for injury, 1154f carpal bones, fractures of, 774–775 carpal dislocations, 767–768 casualty clearing station, 57 casualty collection areas (CCAs), 130 cat bite wounds, 911 catheter arteriography, 822 Cattell-Braasch maneuvers, 1183f causalgia, 840 CBD curve and duodenum, 607 celiac axis bleeding, 1186f celiac axis injuries, management of, 639 Center for Medicare and Medicaid Services (CMS), 23 Centers for Disease Control and Prevention (CDC), 24, 55 central nervous system (CNS), 61, 906 injury, 20 cerebral atrophy, 877 cerebral edema, 864 cerebral perfusion pressure (CPP), 864 cerebrospinal fluid (CSF), 161 cervical and thoracic nerve roots and function, 749t cervical spine injuries, 864–866. See also thoracic spine injuries; thoracolumbar spine injuries acute atlantoaxial instability, 451–452 extension–distraction injuries, 454 facet fracture and dislocation, 454 flexion–compression fractures, 453–454 fractures of atlas, 451 occipital condyle injuries, 450 occipitocervical instability, acute, 451 odontoid fractures, 452–453 subaxial cervical injuries, 453 traumatic spondylolisthesis of axis, 453 cesarean section following trauma in pregnancy, management of, 719–720

Chance fracture, 867 Charlson Comorbidity Index (CCI), 85 chemical burns, 163 treatment of, 759 chest radiograph, 14 child abuse, 871 Child Protective Services (CPS), 871 Children’s Sleepwear Standard law, 43 ChloraPrep®, 905 chlorhexidine, 905 chronic obstructive pulmonary disease (COPD), 85 clavicle fractures, 769 clinical (overall) futility, 886 Clostridia, 917 coagulopathy, 727–728, 863, 917 cocaine, 906 Cockroft–Gault formula, for estimation of degree of dysfunction, 875 Code of Federal Regulations, 857 collagen-bound von Willebrand factor, 898 collagen synthesis, 902 collagen transcription, 902 collagen type I, 902 colon injuries abdominal complications after, 624–625 diagnosis of, 620–621 epidemiology, 620 grading system for, 621 incidence of abdominal septic complications in, 621t left vs. right, 624 mortality and morbidity, 620 operative management of destructive injuries, 622–624 history of, 621–622 nondestructive injuries, 622 Colon Injury Scale, 621 colon leaks, 625 colostomy closure, timing of, 630 combat casualty care, modern, 964 case fatality rate (CFR), 965–966 CCAT team description, 978t combat application tourniquet, 979f combat casualty calculation(s), explanation, 966f comparative distribution of injuries, 969f critical care aeromedical transport team (CCATT), 985f, 986f damage control packing, 987 damage control temporary closure, 987f definitions, 965 died of wounds, 966–967 mathematical definition, 966f distribution of injuries, 967–970 echelons of care, 977t field care, 970–971 high-energy thermal and penetrating injury, 969f IED explosion, 969f, 970f injury encountered during operation Iraqi freedom and operation enduring freedom, 968t

international normalized ratio, ED and subsequent mortality, 981f Joint Theater Trauma Registry, cumulative data, 989f killed in action, 966 lethal triad, 980f Level IIB surgical augmentation teams, 977t Level III medical facility, 977f aerial depiction of, 978f massive transfusion, risk of, 983f military edition of Pre-Hospital Trauma Life Support (PHTLS), 972f military medical care structure Level I, 971 Level IIA, 971–972 Level IIB, 972–977 Level III, 977–978 Level IV, 978 Level V, 978 military trauma systems, 987 battlefield care—clinical practice guidelines, 988 coordination of care/leadership, 988 prevention, 988 research, 989 mine resistant ambush protected (MRAP), 971f MRAP after IED explosion, 970f energy-displacing effects, 971f multiple penetrating fragmentary injuries, 970f operating room, 965f outside structure, 965f patients movement, overview, 978 plasma: RBC ratio groups, mortality, 983f prehospital care advances, 978 damage control resuscitation, 980 fluid resuscitation, 979 topical hemostatics, 980 tourniquets, 979 protective body armor, typical distribution of, 968f QuikClot Combat Gauze©, 980f recognition of patient at risk, 980 acidosis, 981 coagulopathy, 981 damage control resuscitation (DCR), 982–984 damage control surgery principles, 985–987 en route care, 985 hemoglobin less than 11, 982 hypothermia, 981 systolic hypotension, 981–982 whole blood, transfusion, 984–985 systolic blood pressure and mortality, 982f tactical combat casualty care, logo, 971f tactical combat casualty care, recommendations of committee, 973t–976t

1205

1206

Index combat casualty care, modern (continued ) temporary vascular shunt in superficial femoral artery, 986f trauma epidemiology, 967 US military deaths in historic context, 967t wounded in action (WIA), 965 combination closure, 736 combined pancreatic and duodenal injuries, 616 Combined pancreaticoduodenal trauma, mortality by mechanism of injury, 606t Commission on Accreditation of Allied Health Education Programs (CAAHEP), 102 Committee on Tactical Combat Casualty Care (CoTCCC), 111 common femoral vascular injuries, 837 common or external iliac artery, management of injuries to, 645–646 common or external iliac vein, management of injuries in, 646 Common Procedural Terminology (CPT) codes, 857 community violence history of, 892 risk factors, 893 comparative-effectiveness research (CER), 86 compartment syndrome, 788, 819–820, 821, 829 compensatory anti-inflammatory response syndrome (CARS), 333f complex extremity trauma, 832 complex wounds, treatment of, 754 computed tomography (CT) scanning, 862, 878 of abdominal vascular injury, 634–635 of colon injury, 620–621 of pancreatic and duodenal injuries, 608–609 of pelvic injuries, 658–659, 659f concomitant venous injury, 834 connective tissue disorders, 903 continuous positive airway pressure (CPAP), 102 contrecoup injury, 9 coral snake envenomation, 917 cortisol, 875 creatinine, 875 cricoid cartilage pressure, 174 cricothyroidotomy, 860 critical care intervention, 887 critical care obstetrics, 720–721 critical care, principles, 1006 adrenal insufficiency, 1012 airway pressure release ventilation (APRV), 1019 analgesia and conscious sedation, 1022–1023 assist-control mode ventilation, 1016–1017, 1017f

conflict resolution, 1036 continuous mandatory ventilation (CMV), 1016–1017 criteria for consultation, 1037t extubation, 1022t critical illness polyneuropathy, 1030 acalculous cholecystitis, 1032–1033 hypoxemia, 1032 ICU geriatric trauma patient, 1031 postresuscitation hypotension, 1031–1032 missed injuries, 1031 pulmonary contusion, 1032 SIRS, sepsis, severe sepsis, and septic shock, 1032 worsening intracranial hypertension, 1033 daily awakening trials, 1028t decision-making capacity, 1035–1036 and autonomy, 1035 do not resuscitate orders, 1036–1037 extubation, 1021–1022 factors contributing to respiratory failure, 1020t fever, noninfectious sources, 1013t futility, 1034–1035 gas exchange, monitoring of, 1013–1014 hemodynamic monitoring, 1008, 1009t arterial pressure monitoring, 1008–1009 bioimpedance, 1010 blood transfusions, 1010–1011 central venous pressure monitoring, 1009 echocardiography, 1010 erythropoiesis-stimulating agents (ESAs), 1011 gastric tonometry, 1010 hemoglobin therapies, 1010 near-infrared spectroscopy (NIRS), 1010 pulmonary artery catheters, 1009–1010 ICU antidelirium agents, 1029t complications and pitfalls, 1030 continuous quality improvement, 1007–1008 ethical issues, 1033 family meetings, 1038t organization, 1006–1007 palliative care, 1037 structured meetings with families, 1037–1038 tight glycemic control, 1012 infectious monitoring and surveillance, 1013 intravenous opioid doses for adult ICU patients, 1024t intravenous sedation agents for adult ICU patients, 1026t

lung mechanics/inspiratory/expiratory pressure, assessment dynamic compliance, 1015 pressure–volume curves, 1015 static compliance, 1014 mechanical ventilation, 1013 weaning from, 1020 medical decision making, ethical principles, 1033–1034 “mFASTrHUGS” for SICU TEAM rounding tool, 1008t monitoring/daily awakening, 1027 delirium, 1028–1030 monitoring ventilation, 1014 neurologic monitoring, 1011 intracranial pressure monitoring, 1011–1012 noninfectious sources of fever, 1013t nutritional monitoring, 1012 parenteral agents for anxiety dexmedetomidine, 1027 lorazepam, 1025 midazolam, 1025 propofol, 1025–1027 parenteral opioid for analgesia, 1023 fentanyl, 1024–1025 hydromorphone, 1025 morphine, 1024 physiologic monitoring, 1008 pressure-regulated volume control (PRVC) ventilation, 1017 pressure support ventilation (PSV), 1017–1018, 1018f pressure–volume curves, 1015f protocols for weaning, 1021 regional analgesia and anesthesia, 1030 respiratory therapy, adjuvant therapies pharmacologic agents, 1019–1020 prone positioning, 1019 Richmond Agitation Sedation Scale (RASS), 1027t San Diego Patient Safety Council ICU Sedation Guidelines of Care, 1023f synchronous intermittent mandatory ventilation (SIMV), 1017, 1018f talking with ICU families, 1037t time-cycled pressure-controlled ventilation (TCPV), 1018–1019 tracheostomy, 1022 unplanned extubations, 1022 vasopressors and inotropes, 1033t ventilation, spontaneous breathing mode, 1016f ventilator-induced lung injury, 1015–1016 ventilatory capacity, 1015, 1020–1021 ventilatory modes, 1016 weaning process, 1021 withdrawal/withhold support decisions, 1034 work of breathing, 1020 critical mortality rate (CMR), 127 critical soft tissue injury, 788f

Index CroFab antibody, 916 cross-linked collagen fibers, 902 crotalid venoms, 917 Crotalus atrox, 914, 917 crush wounds, 833 crystalloid infusion, 824 D damage control operations in abdominal trauma abdominal arteries, 730 abdominal veins, 730–731 gastrointestinal tract, 729 intra-abdominal packing, 731–732 liver, 728–729 pancreas, 729–730 spleen, 729 definition, 725 intraoperative indications for, 727t acidosis, 727 coagulopathy, 727–728 hypothermia, 726–727, 727t patients likely to need, 725–726, 726t stages of, 725 in thoracic trauma, 728 in vascular trauma of extremity, 732 damage control resuscitation, 636 damage control shunt placement, 832 dehydroepiandrosterone (DHEA), 874 delirium, 880–881 destructive colon injuries, management of, 623–624, 624t dextran, 826, 834, 839 Diagnostic and Statistics Manual III (DSM III), 851 diagnostic peritoneal lavage (DPL), 862 diaphragm, 529 acute diaphragmatic injuries, repair of, 533–535 anatomy, 529 blunt diaphragmatic injury, 531 chest radiograph, 532f chronic diaphragmatic injuries, repair of, 535–536 algorithm, 537f contrast enema with splenic flexure, 532f CT scan demonstrating herniated viscus, 533f diagnosis/diagnostic tests, 531–533 diagnostic algorithm, 534f grading of, 532t history, 529 incidence, 530–531 injury/pathophysiology, mechanism of, 531 National Trauma Data Bank, 532t outcomes, 536 pericardio-diaphragmatic rupture, 536–537 physiology, 529–530 presentation, 531 Statistics from National Trauma Data Bank, 531t

surgical incisions, 530f technique for repair, 536f two layer repair, 535f view of, 530f diffuse axonal injury (DAI), 9 digestive enzymes, 607 digital block, method of executing, 908 disaster planning, 125 disasters casualties, medical care hospital considerations, 130 prehospital considerations, 130 principles of, 132 resource utilization, 131–132 surge, 130–131 classification, 123–124, 124t command and contro, 126–127 common pitfalls, 125t incident command system, structure, 126f injury following disasters, pathophysiology/patterns biological mass casualty events, 134–135 mycobacterium tuberculosis, 134–135 syndromic surveillance, 135 blast pathophysiology, 133–134 dirty bombs, 134 primary blast injury (PBI), 133 quaternary blast injury, 133–134 secondary blast injury, 133 tertiary blast injury, 133 blast physics, 132–133 chemical mass casualty events, 135–137 blood agents, 136 gross decontamination, 136 nerve agents, 135 off-gassing, 137 potential chemical terrorism agents, 135t vesicants, 136 explosive mass casualty events, 132 mass casualty management, implications, 134 radiological mass casualty events, 137–138 acute radiation syndrome (ARS), 137 contamination/exposure, 137 decontamination, 138 injury severity scores (ISS), graphic comparison, 124f major global terrorist and accidental explosive events, 133t mass casualty hospital influx, computer model, 131f mass casualty hospital management, computer model of, 128f ongoing, 124 overtriage/critical mortality rate

in mass casualties, 129f in survivors, 128t overtriage on hospital capability, 127f planning, 124–126, 125t triage, 127 accuracy, 127–129 decisions, 129–130 dislocation and fracture–dislocation of elbow, 766–767 distal brachial artery, 836 distal humerus, fractures of, 770–771 distal pancreatectomy, 869, 1182f with splenectomy, 732f distal radius, fractures of, 747, 772–773 distal rectal irrigation, 627 dog bite wounds, 911 domestic violence diagnosis of, 891–892 incidence and prevalence of, 890–891 partner violence screen, 891f treatment and referral, documentation, and reporting, 892 don’t feel qualified, 92 dorsal fingertip injuries, 757 double-layer absorbable mesh coverage of open abdomen, 739f draping and incisions, 636 driving under the influence (DUI), 853 drunk-driving laws, 41 ductal stenting, 869 duodenal fistula and stricture, 617 duodenal hematomas diagnosis of, 612 intramural, 610 duodenal injuries, 867 AAST Organ Injury Scale (OIS) for grade I, 610–612 grade II, 610–612 grade III, 612–613 grade IV, 613 grade V, 613 blunt force to epigastrium, 608 diagnosis of, 608–610 history of, 603–605 injuries to nearby organs and vessels in patients with, 605 duodenal lacerations, 611 duodenal rupture, surgical repair of, 603 duodenal trauma associated injuries in, 606t complications of, 616 late deaths in, 605 mortality by mechanism of injury, 603–604 timing of death following, 607t duodenoduodenostomy, 612–613 duodenotomies, 612 duodenum anatomy and physiology, 605–606 blood supply of, 606–607 functions of, 607

1207

1208

Index E Eastern Association for the Surgery of Trauma, 878 E-Codes, 23 Eikenella corrodens, 909 Einstein’s mass–energy equivalency formula, 6 elbow dislocation and fracture-dislocation of, 766–767 trauma to, 765–766 elder abuse diagnosis of, 892 treatment and referral, 892 electrolyte management, in severely injured trauma patients, 1114–1115 emergency department (ED), 131 Emergency Department Approved for Trauma (EDAT), 146 emergency department resuscitation, 635–636 emergency departments (EDs), 20 emergency department thoracotomy (EDT) in adults, 239t aortic cross-clamping, hemodynamic and metabolic consequences, 248 aortic cross-clamp, lung, 246f bronchovenous air embolism, 247f Satinsky clamp, 247f cardiac massage, 246f in children, 241t clamshell/butterfly incision, 243f clinical results, 238–240 definitions, 236–237 historical perspective, 236 indications and contraindications, 240t indications for, 240–241 internal paddles for defibrillation, 245f in multiply injured trauma patient, algorithm, 241f nonsalvageability, definition, 248 optimal application, 236 oxygen-carrying capacity, 248 pericardiotomy with toothed pickups and curved Mayo scissors, 244f physiologic rationale, 237 achieve thoracic aortic cross-clamping, 237–238 control cardiac hemorrhage, 237 control intrathoracic bleeding, 237 evacuate bronchovenous air embolism, 238 perform open cardiac massage, 237 release pericardial tamponade, 237 procedural complications, 247–248 sternum, transverse division of, 243f technical details, 241 advanced cardiac life support interventions, 244–245 metabolic acidosis, 245 pericardiotomy/cardiac hemorrhage control, 244

thoracic acic aortic occlusion/ pulmonary hilar control, 245–247 thoracic incision, 242–244 temporary mechanical cardiac support, concept of, 249 temporary physiologic hibernation, concept of, 248–249 thoracotomy incision, 242f emergency medical condition (EMC), 147 emergency medical services (EMS), 20, 54, 100, 160 Emergency Medical Services (EMS) Systems Act, 100 emergency medical technician (EMT), 55, 100, 144 emotional distress, 860 endocrine cells, 607 endoscopic retrograde cholangiopancreatography (ERCP), 609–610 endotracheal intubation esophageal tracheal combitube (ETC), 175–177 gum elastic bougie, 175 nasotracheal intubation (NTI), 174 retrograde intubation, 174–175 enteral feeding complications of, 1118–1119 diarrhea, 1118–1119 distention, 1118 diet choice, 1116 vs. parenteral feeding, 1102–1103 patients requiring celiotomy, 1115–1116 type of immune-enhancing diets, 1106 immunonutrition, 1106–1107 epidemiology, 18–33 analytic, 18 annual traumatic brain injury, estimated average percentage of, 27f causes of death by age group and rank, 21t data sources, 31–33 firearm-related injury, countermeasures in injury control, 22t gun control laws, positioning, 20f injuries fatal falls, 30–31 firearm-related injuries, 30 traffic-related incidents, 29–30 injuries, confounding factors analysis and interpretation, 28–29 injuries distribution by geographic location, 27–28 by nature and severity, 26–27 injury death rates, 28f injury patterns by age and gender, 20–23 by mechanism and intent, 23–26 temporal distribution of trauma deaths, 24f total of all burden, by body region, 27f

traumatic brain injury death rates, 27f trends in annual rates of death, 22f in US incidence and cost of injury, 25t injuries, 25f overview of, 19–20 violence-related deaths, 28f years of potential life lost (YPLL) before age 65, 23f epidermal growth factor (EGF), 899 esmarch bandage silo closure of bilateral anterolateral thoracotomy, 736f esophagogastric junction, exposure and repair of injury, 1185f esophagus injuries esophageal injury, complications of missed/delayed diagnosis, 482 tracheoesophageal fistula, 483 intercostal musculopleural flap, construction of, 482f necrotic mediastinal pleura, 481f operative treatment, 480–481 outcomes, 481–482 presentation and evaluation, 479–480 single-lumen endotracheal tube, intraoperative airway management, 478f esophagus, trachea, combined injury repair, 1155f euvolemia, 864 exocrine cells, 607 exsanguination, 616 extracorporeal membrane oxygenation (ECMO), 870 extrahepatic biliary tract injury, traumatic, 555 bile duct injury, 556–558 gallbladder, 556 management of, 556 extraperitoneal rectal injuries, 627 eye trauma, 377 chemical injuries, 381–383 classification, 377–378 clinical approach ancillary studies, 380 clinical examination, 379 dilated fundoscopy, 380 external/ocular adnexal examination, 380 history, 378–379 intraocular pressure, 380 motility, 379–380 ocular trauma, patient management, 380–381 pupillary examination, 379 slit lamp biomicroscope, 380 visual acuity, 379 epidemiology, 377 hyphema, 385f and lid lac, 386f hypopyon, 389f injury classification, 378f intraocular foreign body, 392f

Index iris protrusion corneal laceration, 384f lid lac, 390f mechanical injury, 383 chorioretinitis sclopetaria, 388–389 choroidal rupture, 389 conjunctival lacerations, 383 corneal abrasion, 383–384 corneal foreign bodies, 384 corneal lacerations, 384–385 endophthalmitis, 389 eyelid lacerations, 390 intraocular foreign body, 387–388 intraorbital foreign bodies, 391 laser-assisted in situ keratomileusis (LASIK) patients, 385 optic nerve avulsion, 390 orbital compartment syndrome, 391–392 orbital fractures, 390–391 retinal contusion, 388 retinal detachment, 388 sclera laceration/rupture, 385 subconjunctival hemorrhage, 383 traumatic cataracts, 387 traumatic hyphema, 385–386 traumatic iritis/mydriasis/iris sphincter tears/iridodialysis, 386–387 traumatic lens injury lens dislocation/ subluxation, 387 traumatic macular hole, 388 traumatic optic neuropathy, 389–390 vitreous hemorrhage, 387 ocular surface burns by Roper-Hall, severity of, 382t ocular trauma score, determination, 382t open globe, 392f ophthalmology, consultation need, 392 posterior synechiae, 386f prognosis, 381 subconjunctival hemorrhage, 383f F facial skeleton approaches, 403–404 mandibular repair, 406–409 midface, 409–412 rigid fixation, fundamentals, 404–406 facial trauma, 395 autogenous bone graft, orbital floor repair, 409f Champy’s ideal line of osteosynthesis, 407f compression plate fixation, 406f emergency department care primary survey airway, 395 bleeding, 395–396 cervical spine, 396 disability, 396 secondary survey, 396 endoscopic subcondylar fracture repair, 408f

evaluation of bony, 400 mandible, 401 midface, 401 orbit, 401 radiographic evaluation, 401–402 soft tissue injuries, 400 upper face, 401 visceral, 400 eyelids/schematized globe, cross section of, 398f facial skeleton approaches, 403–404 mandibular repair, 406–409 midface, 409–412 rigid fixation, fundamentals, 404–406 infraorbital horizontal buttress, 399f management ear, 403 eyelids, 403 lips, 402–403 low-energy wounds, 402 nose, 403 soft tissue, 402 visceral, 403 mandible fractures, three-dimensional computed tomography scan, 402f manibular angle fracture lag screw fixation, 407f massive full-thickness wounds, 412 maxillofacial and mandibular injury, 411f medial canthal tendon, components, 399f naso-orbito-ethmoid fracture classification, 410f normal anatomy bony, 399–400 soft tissue, 396–398 visceral, 398–399 orbital blowout fracture coronal computed tomography image of, 401f severe panfacial fractures, variation, 410f surgical approaches, 405f temporal scalp/temporalis muscle, fascial planes, 397f vertical maxillary buttresses, 399f zygomaticomaxillary (ZMC) complex, vertical/horizontal arcs, 400f fatal accident reporting system (FARS), 73 fatal analysis reporting system (FARS), 32 fecal contamination, and abdominal sepsis, 625 fecal diversion, 627 Federal Motor Vehicle Safety Standards (FMVSS), 39 femoral artery reconstruction, complex injury, 1194f femoral neck fractures, management of, 795–797, 796f femoral shaft fractures, management of, 800–801 fetal exposure from radiologic procedures, 716t

fetal injuries following blunt trauma, 717–718 in pregnancy, management of, 717–718 fetal outcome following trauma and pregnancy, 721 fetal–placental unit, 712–714 fingertip and nail bed injuries, treatment of, 757–758 floating elbow, 772 floating shoulder, 769 focal axolemmal permeability, 9 focal cerebral injuries, 361 cerebral contusions, 361 epidural hemorrhage, 361–362 intraparenchymal hemorrhage, 361 subarachnoid hemorrhage, 363 subdural hemorrhage, 362–363 Focused Abdominal Sonography for Trauma (FAST) of abdominal vascular injury, 634 of pancreatic or duodenal injuries, 608 focused assessment for the sonographic examination of the trauma patient (FAST), 862 focused assessment sonography in trauma (FAST), 155 Fogarty balloon-tip catheter, 827 foot, fractures and dislocations of, 810–812 forearm and upper arm fasciotomy, 831–832 forearm arterial injuries, 836 forearm fasciotomy, 836, 1199f fractures of distal femur, management of, 801–803, 802f, 803f fractures of head of radius, 772 FRAMES intervention for trauma patients, guidelines for, 855 free fluid seen on ultrasound (FAST), 867 free microvascular fibula transfer, 790f frostbite, 940 cold contact/flash freeze injuries, 941 nonfreezing cold injuries, 941 frostbite/rapid freeze injury, clinical differences, 940t frostbite, treatment of, 758–759 Functional Independence Measure (FIM), 32 Fusobacterium, 911 G Galeazzi fracture–dislocation., 773f gallbladder injury, 555–556 gastric decompression, 861 gastrografin enema, 629f gastrointestinal failure, 1073 compensatory anti-inflammatory response syndrome (CARS), role of, 1074f crystalloid viscious cycle, 1078f enteral agents antioxidants, 1081 enteral glutamine during shock resuscitation, 1080 glutamine, 1080–1081

1209

1210

Index gastrointestinal failure (continued ) modified enteral formulas, 1079–1080 vs. parenteral nutrition, 1079 probiotics and prebiotics, 1081–1082 prokinetic agents, 1081 serotonin antagonists, 1081 gut dysfunction to adverse patient outcome abdominal compartment syndrome, 1074 decreased gut mucosal immunity, 1077 gastric alkalinization, 1076 gastroesophageal reflux, 1075–1076 gastroparesis/duodenogastric reflux, 1076 gut edema, 1078 impaired gut absorptive capacity (GAC), 1077 impaired intestinal transit, 1077 impaired mucosal perfusion, 1076–1077 increased gut colonization, 1077–1078 increased gut permeability, 1077 multiple organ failure, 1073–1074 nonocclusive small bowel necrosis (NOBN), 1074–1075 in critically injured patients, 1074t strategies to improve analgesics and sedatives, 1079 gut-specific resuscitation, 1078–1079 nonocclusive bowel necrosis (NOBN), pathogenesis of, 1075f gastrointestinal injury, 581 gastrointestinal tract, damage control operations in, 729 gastrojejunostomy, 867 genitourinary trauma, 669 anatomy, 669–672 anterior urethral disruption, mechanism of, 681f bladder neck avulsion injury, 698f stress cystograms, 678f–679f blunt renal injury, staging computed tomography scans, 675f complications of, 700–701 consultation and interservice interaction, 702–705 damage control laparotomy, 705f principles, 701–702 Gerota’s fascial envelope, 690f grade V parenchymal injury, 684f gunshot wound to mons pubis region, 702f gunshot wound to penis, 701f injury grading and scoring systems, 672–673 intraperitoneal bladder injury from blunt trauma, 697f

intraperitoneal bladder rupture, computed tomography (CT) cystogram, 680f intrarenal vascular anatomy, 670f manipulating flexible cystoscope, 699f medicolegal considerations, 706 nonoperative management bladder, 685–686 genital injuries, 687–688 kidney, 680–683 ureter, 683–685 urethra, 686–687 operative management bladder, 695–698 kidney, 688–693 penis, testis, and scrotum, 699–700 ureter, 693–695 urethra, 698–699 partial nephrectomy for, 691f pediatric renal trauma, 675–676 penetrating injury, algorithm for management, 705f penetrating renal injury, 685f, 686f penile fracture, 700f renal anatomy, 670f renal artery occlusion, 676f renal autotransplantation, 696f renal trauma clinical presentation/diagnosis, 673 bladder, 677 clinical presentation and evaluation, 673–674 external genitalia, 680 incidence and patterns of injury, 673 radiographic imaging, 674–675 ureteral injuries, 676–677 urethra, 677–680 organ injury scaling system, 673f surgical management, 689f, 692f, 693f retrograde urethrogram, technique of, 682f scrotal exploration and testicular repair, 704f stress cystogram, 677f subtotal penile amputation injury, 703f testicular rupture, 703f transureteroureterostomy, 696f ureter, 687f ureteral anatomy, 671f ureteral blood supply, 671f ureteral reconstruction, techniques, 694f ureteral reimplantation with psoas hitch, 695f urethra, 683f urethral disruption, 671f urologic injury scale, 672t wedge resection of injured parenchyma, 690f genome structure clinical practice, 995–996 definitions, 992 DNA sequence, 991

genetic basis for disease, 993 genetic risk factors, 994–995 sepsis/organ dysfunction, 995 pharmacogenomics, 994–995 trauma/burns, gene expression profiling, 993–994 typical gene, structure, 993f venous thrombosis, genetic causes, 994t geriatric fracture centers, 800 geriatric patient aging process, 874–875 end of life, 883 management of initial assessment, 877–878 triage, 876–877 organ function and aging cardiac, 875 endocrine, 875 functional reserve, 875–876 pulmonary, 875 renal system, 875 skin/soft tissue and musculoskeletal system, 875 organ system changes with aging in, 876t outcomes complications, 881 preexisting conditions (PECs), 881 resource utilization, 881–882 specific injuries abdominal injury, 879 burns, 879–880 critical care, 880–881 pelvic fractures, 879 penetrating trauma, 880 rib fractures, 878–879 traumatic brain injury, 878 strategies for improving outcomes medications, 882 specialists, 882–883 triage, 882 Glasgow Coma Scale (GCS), 61, 84, 140, 864 Glasgow Coma Score (GCS), 156 Glasgow Outcome Scale (GOS), 878 glenohumeral dislocation, 764–765, 765f global positioning satellite (GPS), 142 glomerular filtration rate (GFR), 875 Golgi apparatus, 902 graduated driver licensing (GDL), 42 greenstick fractures, 870 ground zero, 64 gunshot wounds, 763 gut dysfunction to adverse patient outcome abdominal compartment syndrome, 1074 decreased gut mucosal immunity, 1077 gastric alkalinization, 1076 gastroesophageal reflux, 1075–1076 gastroparesis/duodenogastric reflux, 1076 gut edema, 1078

Index impaired gut absorptive capacity (GAC), 1077 impaired intestinal transit, 1077 impaired mucosal perfusion, 1076–1077 increased gut colonization, 1077–1078 increased gut permeability, 1077 multiple organ failure, 1073–1074 nonocclusive small bowel necrosis (NOBN), 1074–1075 in critically injured patients, 1074t strategies to improve analgesics and sedatives, 1079 gut-specific resuscitation, 1078–1079 H Haddon Matrix of injury etiology, 37t motor vehicle crash incident, 19t Haddon’s Matrix, 41 Haemophilus influenzae type B vaccine, 868 hand, infection in, 763 Haplochlaena spp., 918 Harborview Injury Prevention and Research Center (HIPRC), 44 Harlem Hospital Injury Prevention Program (HHIPP), 47 head to neck ratio, 865 Health Insurance Portability and Accountability Act (HIPAA), 165 Health Resources and Services Administration (HRSA), 55 heart bypass, left, 1173f heart injuries bleeding control, temporary techniques, 490f blunt cardiac injury, 486 clinical presentation blunt cardiac injury, 487 cardiac enzymes, 488 echocardiography, 488 electrocardiography, 488 evaluation, 487–488 focused assessment with sonography for trauma (FAST), 488 penetrating cardiac injury, 487 pericardial injury, 487 subxiphoid pericardial window, 488–489 complex cardiac injuries, 491 coronary arteries, 491f dysrhythmias, 491t electrical injury, 487 follow-up, 492 iatrogenic cardiac injury, 486–487 incidence, 485 left anterior thoracotomy, 489f penetrating cardiac injury, 485–486 pericardium , transdiaphragmatic exploration, 489f traumatic heart diseases, etiology of, 486t treatment

blunt cardiac injury, 490–491 penetrating injury, 489–490 heart rate variability (HRV), 159 helicopter EMS (HEMS), 104 helmet promotion, 44 hematoma, 610–611 associated with abdominal vascular injuries, 636 hemithorax, video-assisted thoracoscopic surgery (VATS), port placement, 474f hemodynamic monitoring, 1008, 1009t arterial pressure monitoring, 1008–1009 bioimpedance, 1010 blood transfusions, 1010–1011 central venous pressure monitoring, 1009 echocardiography, 1010 erythropoiesis-stimulating agents (ESAs), 1011 gastric tonometry, 1010 hemoglobin therapies, 1010 near-infrared spectroscopy (NIRS), 1010 pulmonary artery catheters, 1009–1010 hemorrhage, 616, 832, 837 hemostasis, 216 acute endogenous coagulopathy, pathways, 221f antifibrinolytics, 229 blood components, complications, 231–232 bloody vicious cycle, updated, 222f cell-based coagulation construct, 218 coagulation/anticoagulation/fibrinolysis, proteins involved, 219t factor XIIIa, 229–230 management controversies goal-directeded hemostasis, 225–228 hypotensive resuscitation, 223 preemptive blood components, 223–225 trauma, acute coagulopathy, 218–223 MT, literature addressing component transfusion ratios, 224t postinjury coagulopathy perspective, 217–218 postinjury hypercoagulability, 232 pre-injury antithrombotic agents, 230 antiplatelet therapy, 230–231 warfarin, 230 prothrombin complex concentrate (PCC), 230 recombinant factor VIIa (rVIIa), 228–229 red blood cell (RBC) transfusion, 216–217 resuscitation via thrombelastography, 228f thrombelastographic tracings, characteristic, 227f thrombelastography (TEG) instrument and tracing, 226f parameters, 227t hemotherapy, postinjury, 216. See also hemostasis

heparin-induced thrombocytopenia, 839 hepatic artery, management of injury to, 647 hepatic balloon tamponade, 1179f hepatic injuries, nonoperative management of, 868 hepatorrhaphy, 1178f hexachlorophene solution, 905 Hibiclens®, 905 high-energy vs. low-energy trauma, 747 high-pressure injection injuries, treatment of, 758 high-resolution real-time ultrasonography (US), 714 high-speed cine-radiography, 9 high-speed motor vehicle injury with mesocolon avulsion, 621f high-velocity penetrating injuries, 620, 621f hilar, 1174f hip dislocation, management of, 793–795, 794f hip fractures geriatric fracture centers for, 800 management of, 795 rehabilitation of patients with, 799–800 Hosmer–Lemeshow (HL) statistic, 88 human bite wounds, 909–911 human immunodeficiency virus (HIV), 911 human rabies cases in the United States by exposure category, 913t clinical symptoms of, 911 reatment recommendations and estimates of the risk of, 912t hyperglycemia, 863 hyperthermia, 864, 941 exercise, 941 iatrogenic hyperthermia syndromes, 941–942 hypervolemia, 711 hypotension, 821 hypothermia, 141, 726–727, 727t, 826, 862, 903 cardiac function, 940 coagulation, 940 immunity, 940 localized, 940 management algorithm, 939f maneuvers to prevent, 636 and metabolic reserves, 940 primary accidental, 938–939 secondary metabolic, 939 therapeutic, 940 in trauma, 939 hypovolemia, 875, 882 hypoxia-induced factor (HIF), 899 I iliac artery, right common, 1192f immediate amputation, role of, 833 imminent demise futility, 886 immunosuppressant therapy, 944 incisional hernia, late closure of, 741–742 increased intracranial pressure (ICP), 864

1211

1212

Index infection, 330 antibiotic choice recommendations, 339t SIS/IDSA evidence-based guidelines, 341t, 342t antibiotic prophylaxis, evidence-based recommendations, 337t clinical pulmonary infection score (CPIS), 348t microbial contamination, 331f microbial factors, environmental factors, and host defenses, 331f microbiology, 333 marine trauma, 335–336 rabies, 334–335 tetanus, 335 pathogenesis, 330 environmental barriers, 330–331 host defense mechanisms, 332–333 microbial factors, 331–332 pathogenic microorganisms, region, 332t postinjury infections, diagnostic approach, 340f postsplenectomy vaccinations, recommendations, 350t post-traumatic empyema, bacteriology, 342t prevention blood transfusion, 338 double gloving, 337–338 general principles, 336 nutritional support, 338–339 prophylactic antibiotics, 336–337 supplemental oxygen, 338 surgical scrub, 337 suture material, 338 temperature control, 338 tracheostomy, 339 S. aureus bone and joint infections, bacterial determinant, 343t septic joints/osteomyelitic bone infections, 343t septic shock/severe sepsis, infection control priorities, 347t surgical/trauma intensive care unit, nosocomial infections, 346t surgical wounds, classification, 336t trauma-related infections, 339 catheter-related bloodstream infection, 349 chronologic approach to prevention, recognition, and treatment, 344 Clostridium difficile diarrhea, 350 diagnosis, 339–340 empyema, 341–343 environmental pathogens, occupational exposure, 344 ICU and early postoperative period, 346–347 intra-abdominal infections, 340–341 operating room, 345–346 osteomyelitis/septic arthritis, 343

overwhelming postsplenectomy infection (OPSI), 351 postsplenectomy vaccinations, 350 resuscitation bay, 344–345 surgical site infection, after discharge, 351 surgical site infections, 349–350 urinary tract infections, 349 ventilator-associated pneumonia, 347–349 traumatic injuries, immunologic defects, 334t ventilator-associated pneumonia, 334t Vibrio vulnificus Wound Infections, 336t infection in hand, 763 inferior pancreatoduodenal artery, 607 infrahepatic inferior vena cava, management of injuries in, 642–643 inframesocolic region, management of injuries in exposure and vascular control, 641–642, 643–644 infrahepatic inferior vena cava, 642–643 infrarenal aorta, 642 infrarenal aorta, management of injuries in, 642 initial assessment and management, 154 airway maintenance, with cervical spine protection, 156–157 blood loss, 158t breathing, 157 chin lift/jaw thrust, airway, 157f circulation with hemorrhage control, 157–160 stop the bleeding, 158–160 definitive airway, indications, 156t definitive care, 164 disability, neurologic status, 160–161 documentation, medical record, 165 exposure and environmental control, 161 hospital phase, 155 initial fluid resuscitation, responses, 160t intraosseous puncture, demonstration, 160f prehospital phase, 154–155 preparatory phase, 154 primary survey, 155 catheters and tubes, 161 early transfer, decision, 162 geriatric patient, 155–156 monitoring, 161 obese patients, 156 pediatric patients, 155 pregnant women, 156 x-rays and diagnostic studies, 161–162 reevaluation, 164 secondary survey history, 162–163 physical examination abdomen, 164 chest, 163 head and face, 163

musculoskeletal and peripheral vascular system, 164 neck and spine, 163 neurologic assessment, 163 triage, 155 ventilation, 157 initial assessment, of geriatric patient airway, 877 breathing, 877 circulation, 877 disability, 877 exposure, 878 injuries confounding factors, analysis and interpretation, 28–29 death rates, 26f distribution by geographic location, 27–28 by nature and severity, 26–27 fatal falls, 30–31 fatally injured drivers with blood alcohol level, 30f firearm-related injuries, 30 gun control laws, positioning, 20f injury control, 19f patterns by age and gender, 20–23 by mechanism and intent, 23–26 traffic-related incidents, 29–30 injury coding, 77 injury control cube, 18 injury etiology, Haddon Matrix interactions of phases and factors, 37t injury prevention, 36 accomplishment, 38 components, 50t global initiatives, 49–50 importance, 36 intentional injuries, prevention strategies alcohol/firearms, roles of, 48–49 assaultive behavior, 46–47 community-based programs, 47 crisis intervention services, 48 domestic violence, 47 education programs, aimed at general public, 48 high risk of suicide, 48 reducing access to means of suicide, 48 school-based programs, 46–47 suicide, 47–48 scientific approach, 36 ethical issues, 39 historical development, 36–37 political issues, 39–40 practical considerations, 38–39 surgeon’s role, 51 unintentional injuries, prevention strategies, 40 alcohol, 41–42 clothing ignition, 43 distracted driving, 42–43 graduated drivers licensing systems, 42 helmet promotion, 44

Index helmets, 41 house fires, 43 motor vehicle, 40 prevention efforts, nationwide effectiveness, 46 residential safety, 43 safety-related vehicle design/occupant protection, 40–41 scalds, 43 Seattle bicycle helmet campaign, 44–45 speed limits, 41 transportation, 40 Washington State motorcycle helmet law, 45–46 injury prevention during pregnancy, 721–722 injury severity scores (ISSs), 58, 77, 142, 877 AIS components, 79t anatomic scoring systems, 79–83 combined scoring systems, 85–86 comorbidity scoring systems, 85 GCS components, descriptors, 84t ICISS vs. actual mortality, 83f injury coding, 77–79 classification schemes, 78t injury severity scores, 80t–82t ISS vs. actual mortality, 83f NISS vs. actual mortality, 83f physiological scoring systems, 83–85 revised trauma score (RTS) variable breakpoints, 84t TRAIS and ICISS, 84f trauma outcomes research basics, 86 covariates, 86–87 critical variables, identifying, 86–87 database choices, 87–88, 87t injury coding/classification choices, 88 outcome/dependent variables, 86 predictor/independent variables, 86 risk adjustment approaches, analysis, 87 risk adjustment choices, 88 risk of outcome, 79 trauma severityerity codes, evaluation, 88 TRISS equation, 85t innominate artery injury, exposure and management, 1168f–1169f insect and bug bites, wounds caused by, 918–919 insulin-like growth factor-1 (IGF-1), 898 intensive care before reoperation, 737 intensive care unit (ICU), 61, 859, 870 length of stay (LOS), 77 surgeon-performed ultrasound, 315 central venous catheter, insertion, 316–317 common femoral vein, thrombosis, 317–318 educational model, 318–319 inferior venal caval filters (IVCF), insertion, 318

intraperitoneal fluid/blood, 316 pleural effusion, 316 intercellular adhesion molecule-1 (ICAM-1), 898 intercostal artery, controlling, 1167f International Classification of Diseases (ICD), 23, 77 International Classification of Diseases Injury Severity Score (ICISS), 79 ICD-9 codes, 83 International Classification of Disease Version 9 (ICD-9) codes, 852 international normalization ratio (INR), 882 International Trauma Life Support (ITLS), 107 interpersonal violence, 722 interphalangeal joint dislocations, 768–769 intimate partner violence (IPV), 722, 890 intra-abdominal aorta, endovascular intervention in injury to, 648 intra-abdominal hypertension, clinical manifestations of, 734 intra-abdominal packing, damage control operations in, 731–732 intra-abdominal pressure abdominal perfusion pressure, 734–735 clinical and laboratory manifestations of increased, 734t definition, 734 measurement of, 734 intracranial hemorrhage, 877 intraoperative cholangiogram, 610 intraoperative cholangiopancreatogram, 610 intraoperative evaluation of duodenum and pancreas, 608 intraoperative metabolic failure, 733 intraparenchymal bleeding, 869 intraperitoneal injuries, 627 intrathoracic blood loss, 866 ionizing radiation, 137 ischemia, 819 ischemic neurolysis, 819 ISDN lines, 151 isolated ulnar injuries, 836 J Joint Commission on Accreditation of Healthcare Organizations (JCAHO), 890 joint injuries acromioclavicular dislocation, 764 carpal dislocations, 767–768 dislocation and fracture–dislocation of elbow, 766–767 glenohumeral dislocation, 764–765, 765f interphalangeal joint dislocations, 768–769 metacarpophalangeal dislocations, 768 scapulothoracic dissociation, 764, 764f sternoclavicular dislocation, 764 trauma to elbow, 765–766 jugular venous distension (JVD), 159

K Kaplan–Meier trauma, 939f killer T cells, 898 kinematics, 2 anatomic considerations, 8 abdominal injury, 10–11 brain and maxillofacial injury, 8–9 musculoskeletal injury, 11–12 prevention, 12–13 spine and whiplash injuries, 12 thoracic injury, 9–10 basic principles, 2 blast injury and ionizing radiation, 5–6 elastic and inelastic collisions, 3–4 energy and work, 3 impulse, 2 Newton’s law, 2–3 penetrating trauma and ballistics, 4–5 biomaterials, properties elasticity, 6–7 strain, 6–7 stress, 6–7 Young’s modulus, 6–7 biomechanical mechanisms of injury, 6f blast injuries, 14–15 department of defense classification, 15t blunt abdominal trauma, shear strain, 10f blunt trauma mechanisms/ injury patterns falls, 8 motor vehicle crashes, 7–8 pedestrian injuries, 8 bronchial injury, injury mechanisms, 10f explosive blast, physical characteristics of, 5f fracture mechanics, 11f geriatrics, 14 motor vehicle crash scenarios, energy and momentum, 3f pediatrics, 13 pregnancy, 14 pressure-time relationship, 5f stress, strain, elastic modulus, plastic modulus, tensile strength and energy, 7f thoracic aorta injury, 10f velocity and kinetic energy characteristics of guns, 4t Yaw, tumble, deformation, and fragmentation, 5f Kleihauer–Betke (KB) test, 712–713 knee dislocations, 833 management of, 804–805 Kocher maneuvers, 1183f L Lactrodectus macrotans, 919 laparotomy, trauma, 512 abdomen, chest, and groins operative field for torso trauma, 514f abdominal closure at reoperation, 526t

1213

1214

Index laparotomy, trauma (continued ) Cattell–Braasch maneuver, 523f generic sequence, schematic depiction, 515f Kocher maneuver, 522f left upper quadrant to achieve temporary hemostasis, 519f Mattox maneuver, 521f operative profile, factors, 524t penetrating abdominal trauma, 520t peritoneal cavity, 517f principles core mission, 512 operative sequence, 514–515 preparation, 513–514 surgeons, 515–516 surgeon’s support envelope, 513 relaparotomy abdominal infection, 525 planned reoperation, 526 urgent reoperation for bleeding, 524–525 role of, 527–528 small bowel, evisceration of, 518f surgeon’s support envelope, 513t surgical intensive care unit, bedside, 526–527, 527f techniques/maneuvers achieving temporary hemostasis, 517–518 gaining access/exposure, 516–517 intra-abdominal bleeding, 521–522 medial visceral rotations, 520–521 operative profile, choosing, 522–524 peritoneal cavity, 518–520 temporary abdominal closure, 524 uncontrolled abdominal infection, relaparotomy, technical options, 525t laryngeal mask airway (LMA), 110 laryngoscope, 860 late closure of incisional hernia, 741–742 lateral parietal craniectomy, performing steps, 1150f, 1151f–1152f LC injuries, 658 left medial visceral mobilization, 637f leukocytes, 819 lidocaine, 906, 907t ligamentous injuries, management of, 805–806 limb salvage vs. amputation, 791–792 procedure for, 787f limb-threatening ischemia, 821 liver anatomy, 1177f damage control operations in, 728–729 omental packing, 1179f packing, 1180f liver injury, 539 anatomy functional, 539–540 hepatic artery, 540

hepatic veins, 540 ligaments, 540 lobes, 539 portal vein, 540 diagnosis of diagnostic peritoneal lavage, 542–543 focused abdominal sonography for trauma, 543 hemodynamically stable patient, 543 hemodynamically unstable patient, 542 focused abdominal sonography for trauma (FAST) CT scanning, 543–544 laparoscopy, 544 incidence and classification, 540–541 initial management, 541–542 liver trauma, management of, 544 abscesses, 546 anatomic resection, 553 bilomas/bile leak, 546 blunt hepatic injury, follow-up CT scanning of, 547 devascularization, 546 direct venous repair, 552–553 drains, 554 hemobilia, 546 hemodynamically stable patient, 547 hemodynamically stable patient with blunt injury, 545 hemorrhage, 546 nonoperative blunt hepatic injury , complications of, 545–546 operative management, 547–548 with major liver injury, 547–548 with minor liver injury, 547–548 operative management, complications of abdominal compartment syndrome, 554 bilhemia, 554 biliary fistulae, 555 bleeding, 554 fistulae problems, 555 hemobilia, 554 hepatic necrosis, 555 penetrating injury, nonoperative management of, 547 resumption of activity, 547 retrohepatic vena cava/hepatic vein injury, 552 severe parenchymal injury, hemostatic maneuvers direct suture, 549 fibrin sealants and hemostatic devices, 551 finger fracture, 549 hepatic artery ligation, 551–552 hepatic transplantation, 552 omental packing, 549–550 packing, 549 penetrating tract, 550–551 resection, 551 systemic inflammatory response, 546 tamponade with containment, 553–554

unusual complications, 546–547 vena cava stenting, 553 local anesthetic overdose, symptoms of, 906t long bone fractures, 790–791 loop colostomy with diversion, 628f loss of pregnancy after trauma, risk factors for, 721t low- and middle-income countries (LMICs), 49 low-energy vs. high-energy trauma, 747 lower extremity fractures and dislocations, management of acetabular fractures, 792–793, 793f femoral neck fractures, 795–797, 796f femoral shaft fractures, 800–801, 801f fractures of distal femur, 801–803, 802f, 803f hip dislocation, 793–795, 794f hip fractures, 795 knee dislocations, 804–805 ligamentous injuries, 805–806 patellar fractures, 803–804 subtrochanteric fractures, 798–799, 799f tibia fractures, 806–810 trochanteric fractures, 797–798, 798f soft tissue injuries to (See soft tissue injuries) lower extremity injuries associated injuries injury combinations, 786–787 joint dislocation, 787–788 nerve injuries, 786 vascular injuries, 785–786 casues of, 783 challenges and controversies limb salvage vs. amputation, 791–792 long bone fractures, 790–791 replantation, 792 clinical assessment, 784–785 history of, 783–784 late complications of malunion, 812 nonunion, 812 sequelae of joint trauma, 812 mechanism of injury, 784 pathophysiology and biomechanics, 784 radiographic diagnostics, 785 lower extremity vascular injuries, 836 low-velocity gunshot wounds, 621f Loxosceles reclusa, 919 lungs injuries, 468 anterolateral thoracotomy incision, 471f complications chylothorax, 475–476 empyema, 475 lung abscesses, 475 persistent air leak/bronchopleural fistula, 475 pneumatocele/intraparenchymal hematoma, 475 pneumonia, 474 retained hemothorax, 474–475

Index CXR and CT demonstrating right-sided pulmonary contusion, 474f indications for operation, 470–471 mechanism of systemic air embolism, 509f operative techniques, 471–473 outcomes, 474 presentation and evaluation, 469–470 pulmonary tractotomy with exposed hemorrhage sources ligation, 472f sizeable anterior pneumothorax, 469f surgical exposure, 471 tracheal intubation, 472f video-assisted thoracoscopic surgery (VATS) techniques, 473–474 lung twist, 1174f M Major Trauma Outcome Study (MTOS), 58, 880 “mangled limb,” 789 mangled upper extremities, 777 mannitol, 864 marine animals, bites and stings by bee and wasp stings, 919 insect and bug bites, 918–919 marine invertebrates, 917–918 piranha attacks, 918 shark bites, 918 spider bites, 919 venomous fish, 918 marine invertebrates, wounds caused by, 917–918 mass casualty systems, 124, 127, 128 massive transfusion protocol (MTP), and damage control resuscitation, 636 maternal assessment, 712 matrix metalloproteinases (MMPs), 899 Mattox maneuver, for large central suprarenal retroperitoneal hematoma, 1186f maxillofacial injuries, 9 maximum AIS (maxAIS), 79 medial mobilization of right-sided intraabdominal viscera, 641f median nerve block anesthesia, technique of, 907f median sternotomy with neck extension, 1061f technique for performing, 1060f Medicaid, 857 medically reasonable, meaning of, 887 medical screening exam (MSE), 147 meshed split-thickness skin graft, 740f mesocolon and pancreas, 606 metacarpal bones, fractures of, 775–776 metacarpophalangeal (MCP), 911 metacarpophalangeal dislocations, 768 Michigan Alcohol Screening Test (MAST) questionnaires, for detection of alcohol problems, 854 microaerophilic streptococci, 909 Micrurus euryxanthus, 914, 917

Micrurus fulvius, 917 Micrurus fulvius fulvius, 914 Micrurus fulvius tenere, 914 midline bleeds, 663f military antishock trousers (MAST) garment, 660 missile emboli, 820 Mobile Army Surgical Hospital (MASH), 58 Model Trauma Care System Plan, 56 “modicum of benefit” test, of beneficencebased clinical judgment, 887 monocyte chemoattractant protein-1 (MCP-1), 899 Morison’s pouch, 162 motor vehicle collisions (MVCs), 8 rear-end impact, 12 motor vehicle crash incident death rates, 34f Haddon Matrix, 19t multidetector CT (MDCT), 609 multiple organ dysfunction syndrome (MODS), 333f multiple organ failure, 1128 concepts on pathogenesis, 1128–1130 Denver MOF dataset, 1137t Denver Postinjury Multiple Organ Failure Score, 1138t adverse outcomes, 1139t risk factors, 1139t epidemiology and clinical relevance, 1130–1131 immunoinflammatory response to trauma, 1132f interventions adrenal insufficiency/cortisol replacement therapy, 1142–1143 blood transfusions, judicious use of, 1141–1142 continuous renal replacement therapy (CRRT), 1144 fracture management, 1142 immunonutrition, 1143–1144 immunostimulating factors, 1144 insulin/glycemic control, 1143 protective lung ventilation, 1142 protective resuscitation techniques, 1139–1141 TLR-directed interventions, 1144 Marshall Multiple Organ Dysfunction Score, 1138t adverse outcomes, 1139t risk factors, 1139t MOF, definition, 1136 Denver MOF dataset, 1137t MOF classification, 1137–1139 MOF scores, 1137 receiver operating characteristic (ROC) curves, 1139 validation of current scores, 1136 MOF over time, temporal distribution of, 1130f pathogenesis of, 1129f

pathophysiology abdominal compartment syndrome, 1134–1135 blood transfusions, 1135 complement system, 1133 cytokines, 1132–1133 heat shock proteins (HSPs), 1133 hormones, 1134 infections, 1135–1136 inflammatory, hormonal, and immune responses to trauma, 1131 oxidative stress, 1133–1134 PAMPS, alarmins, and DAMPS, 1133 role of gut, 1131 role of PMN, 1131–1132 secondary operation, 1136 toll-like receptors, 1133 postinjury multiple organ failure, historical perspective, 1129t ROC curves for ICU, 1141f mechanical ventilation, 1141f mortality, 1140f ventilator-free days, 1140f multiple organ failure (MOF) score, 881 muscle mass, 875 musculoskeletal effects, rehabilitation contractures, 951 disuse osteoporosis, 951 muscle atrophy and weakness, 950–951 prevention and treatment, 951 musculoskeletal injury, 9 musculoskeletal trauma, 11 Mycobacterium tuberculosis, 134 myocardial dysfunction, 1044 amrinone and milrinone, 1046 dobutamine, 1046 dopamine, 1045–1046 epinephrine, 1046 intra-aortic balloon pump counterpulsation, 1047 nitrovasodilators, 1046–1047 norepinephrine, 1045 pharmacologic, 1044–1045 preload augmentation and rewarming, 1044 steroids, 1047 vasopressin, 1045 myocardial infarction, current treatment of, 1050–1051 N nasal packing for hemorrhage control, 1149f National Center for Injury Prevention and Control (NCIPC), 31 National Crime Victimization Survey (NCVS), 32 National Electronic Injury Surveillance System—All Injury Program (NEISS-AIP), 31 National Health Interview Survey (NHIS), 31

1215

1216

Index National Highway Traffic Safety Administration (NHTSA), 13, 37 National Hospital Discharge Survey (NHDS), 31 National Standard Curriculum (NSC), 101 National Trauma Data Bank (NTDB), 26, 84, 91 National Violent Death Reporting System (NVDRS), 29, 51 navicular fracture–dislocation and metatarsal, 811f neck, 414 anatomy of, 414–415, 1150f arteriography, duplex ultrasonography, color flow doppler, CTA, 419–420 asymptomatic patients computed tomography, 419 modest/moderate symptoms, 419f pellet wound, 420f physical examination, 419 Zone I, 418 Zone II, 418–419 BCVI, screening criteria, 422t blunt cerebrovascular injuries, treatment of, 421 imaging for screening, 422 incidence/screening, 422 injuries, types, 422 management, 422–423 carotid artery, principles of repair, 424t cervical esophagostomy, 426f endotracheal intubation into distal trachea, 417f esophagogram/esophagoscopy/CT, 420–421 esophagus, principles of repair, 425t Fogarty balloon catheter, 418f laryngoscopy/fiber-optic bronchoscopy/ CT, 421 left sternocleidomastoid muscle, sternal head, 426f operative management esophagus, 425 general principles/incisions, 423 injury to carotid artery, 423–424 internal jugular vein, injury, 425 neurological deficit, 424 repair, 424 trachea, 425–426 tracheoesophageal, trachea–carotid artery/esophagus–carotid artery, 426 vertebral artery, injury, 424–425 Zone III injuries, 424 overt symptoms/signs, algorithm for management, 416f patients management , symptoms/signs, 415–418 penetrating vascular injuries, 259 abdomen/pelvis CT, 271–276 cervical spine, computed tomography, 260–265 cervical spine, flexion/extension X-rays, 266–267

chest CT, 267–271 pelvis/acetabulum CT, 276–282 spine, conventional X-rays, 260–265 spine, magnetic resonance imaging, 266 thoracolumbar spine, computed tomography, 265–266 presentation, 415 trachea, principles of repair, 426t Zone II hematoma secondary to gunshot wound of carotid artery, 417f Zone III, 421 zones, 415, 415f neck incisions, alternate, 1153f needle decompression, 116 nerve agents, 135 nerve injuries in upper extremity, 760–763 neurogenic shock, 159 neurologic injury, 666 anterior cord syndrome, 437 Brown-Séquard syndrome, 437 cauda equina syndrome, 438 central cord syndrome, 437 cervical root syndrome, 437 classification, 436–437 conus medullaris syndrome, 438 location, 435 posterior cord syndrome, 437 primary and secondary, 435–436 neurologic injury in pregnancy, management of, 718–719 neuropraxic injury, 761 neurotmesis, 761 neutrophil phagocytic function, 874 neutrophils, 898 New Injury Severity Score (NISS), 66, 79 Newtonian mechanics, 2 nightstick fracture, 772 nondestructive colon injuries, management of, 622 nonocclusive bowel necrosis (NOBN), pathogenesis of, 1075f nutritional therapy, 1100 abdominal trauma index, sepsis risk, 1104t acute renal failure (ARF), 1110–1111 anabolic agents, in trauma patients, 1125–1126 aspiration, 1119 calorie-to-nitrogen ratio, 1110 diet by Jones and Moore, 1117t diet progression, 1116–1117 drug–nutrient interactions, 1117–1118 electrolytes in total parenteral nutrition, 1115t endocrine response to stress/injury, 1100–1101 enteral (postpyloric) access, determining indicators, 1103 burn patients, 1103–1105 patients with closed head injury, 1103 enteral feeding access, 1115t complications of, 1118–1119

diet choice, 1116 patients requiring celiotomy, 1115–1116 enteral feeding, type of immune-enhancing diets, 1106 immunonutrition, 1106–1107 enteral formulation, medications incompatible, 1118t enteral nutrition, 1124–1125 enteral vs. parenteral feeding, 1102–1103 estimating nutritional needs, 1107–1109 fat requirements, 1109–1110 FDA guidelines, parenteral vitamins, 1122t fluid/electrolytes electrolyte management in severely injured trauma patients, 1114–1115 magnesium, 1114 phosphorus, 1113–1114 potassium, 1113 sodium, 1112–1113 formula preparation components, 1121–1122 PN formulas, 1122–1123 gastrointestinal secretions, electrolyte composition, 1115t hepatic failure, 1112 institution of therapy, 1123 intravenous fat emulsions in the United States, 1121t mechanical complications, 1119–1120 monitoring therapy, 1125 morbid obesity, 1109 nitrogen balance, 1124t nutrient prescription, 1107 nutrition support, protocol, 1105f oral medications, sorbitol content, 1118t outcome with enteral feeding, 1107 overfeeding, complications of, 1108f parenteral feeding, 1120 access and monitoring, 1120–1121 parenteral nutrition, complications essential fatty acid deficiency (EFAD), 1124 glucose, 1123–1124 micronutrient deficiencies, 1124 pneumatosis intestinalis and necrosis, 1119 postinjury hypermetabolism, 1100 prokinetic agents, 1117 protein requirements, 1110 protocol for nutrition support, 1105f pulmonary failure, 1112 regular insulin administration, algorithm, 1124t starvation vs. severe stress hypercatabolism, 1101t stress/sepsis, intermediary metabolism current issues, 1102 fat metabolism, 1102 glucose metabolism, 1101–1102 protein metabolism, 1101 TPN formulas, trauma patients, 1122t

Index O on-call practice, 92 open abdomen operative techniques for combination closure, 736 open packing, 737 suture closure of skin, 735 temporary silos, 735 towel clips, 735 vacuum-assisted wound closure, 736–737 at reoperation, techniques for management of absorbable meshes, 739–741, 740f permanent meshes, 739 repeat application of silo, 739 vacuum-assisted fascial closure, 739 zipper closure, 739 open fractures, 789, 907–908 classification of, 789–790 open packing, 737 open pelvic fractures, 665–666 with anorectal injury, 629f open soft tissue injuries, treatment of, 754 operating room (OR), 65 operative techniques for open abdomen combination closure, 736 open packing, 737 suture closure of skin, 735 temporary silos, 735 towel clips, 735 vacuum-assisted wound closure, 736–737 opiod narcotics, 881 organ procurement and transplantation network (OPTN), 944 overtriage, 59 oxygen consumption, 216 P pancreas anatomy and physiology, 606 blood supply of, 606 CT scan of, 609 damage control operations in, 729–730 duct and acinar cells of, 607 and duodenum, anatomic relation of, 605 endocrine and exocrine cells, 607 functions of, 607–608 pancreatic antisecretory medication, 869 pancreatic fistula, 617 pancreatic injuries, 869 AAST Organ Injury Scale (OIS) for grade I, 613–614 grade II, 613–614 grade III, 614–616 grade IV and V, 616 blunt force to epigastrium, 608 diagnosis of, 608–610 history of, 603–605 pancreatic insufficiency, 617 pancreatic neck, division of, 1182f pancreaticoduodenal biliary anatomy, 1180f

pancreatic pseudocyst, 617 pancreatic trauma algorithm for, 615 associated injuries in, 606t complications of, 616 late deaths in, 605 mortality by mechanism of injury, 604 timing of death following, 607t pancreatitis, 617 pancreatoduodenal vessels, 607 papaverine hydrochloride, 826 paper plan syndrome, 125 Parent Teachers Association (PTA), 44 Pasteurella multocida, 911 patellar fractures, management of, 803–804 pediatric airway airway failure, 183–184 anatomy, 182 equipment, 182 physiology, 182 spontaneous respirations, 184 technique, 182–183 Pediatric Glasgow Coma Scale, 864t pediatric patients child abuse, 871 diagnostic assessment of, 862–863 emergency department management and family relations, 871 epidemiology of injured child, 859 initial assessment and resuscitation of injured child, 859–860 airway management, 860–861 restoration of circulation, 861–862 vascular access, 861 laboratory studies, use of, 863 pediatric critical care, 870 rehabilitation of, 870 specific injuries, management of abdomen injuries, 867–869 blood vessel injuries, 869–870 cervical spine injuries, 864–866 head and central nervous system injuries, 863–864 skeletal system injuries, 870 thorax injuries, 866–867 Pediatric Rapid Sequence Intubation (RSI), 860t pediatric vascular access, 861t pelvic anatomy, 655 pelvic binders, 659–660, 659f, 660f pelvic bleeding management, 663f angiographic embolization, 661–663 external fixation, 660–661 hypotensive resuscitation, 659 military antishock trousers (MAST) garment, 660 pelvic binders, 659–660, 659f, 660f preperitoneal pelvic packing, 663–664 pelvic fracture algorithm for management of, 666f associated injuries, 665–666 definitive fixation of, 664–665 Tile classification of, 655–657, 656t

Young–Burgess classification of, 657–658, 658t pelvic fractures, 879 in pregnancy, management of, 716–717 pelvic injuries (PI), 655 diagnosis of, 658–659 pelvic inlet and outlet films, 659 pelvic retroperitoneum, management of injuries in exposure and vascular control, 645 injuries to common or external iliac artery, 645–646 common or external iliac vein, 646 Penetrating Abdominal Trauma Index (PATI), 66 penetrating trauma, 633 of elderly people, 880 in pregnancy, management of, 718 penetrating truncal wounds, 634 penicillin, 868 pericardium, opening, 1062f permanent meshes, 739 petrolatum-impregnated dressing, 908 pfannenstiel incision, 664f phalanges, fractures of, 776–777 pharyngotracheal lumen (PtL) airway, 110 PHisoHex®, 905 phospholipid platelet-activating factor (PAF), 898 physiologic changes during pregnancy, 710–711, 710t physiologic futility, 886 pilon fractures, 808–809 piranha attacks, wounds caused by, 918 placental injury, 709 plain anteroposterior pelvic film, 658 planned reoperation, 733 platelet-derived growth factor (PDGF), 898 platelet plug, 897 P. multocida, 911 pneumococcal vaccine, 868 pneumonia, 878, 881 pneumothorax, 861, 866 poisonous and nonpoisonous snakes, characteristics of, 915f policymakers decide, 151 polyamines, 902 polyvinyl alcohol sponges, 909 popliteal and tibial artery injuries, 839 popliteal arteries, exposure and repair, 1196f popliteal artery injuries behind knee, 1195f posterior exposure, 1197f popliteal/tibial artery injuries, exposure and repair, 1196f porta hepatis, management of injuries in exposure and vascular control, 646–647 injury to hepatic artery, 647 injury to portal vein, 647–648, 648t

1217

1218

Index portal vein, injuries to management, 647–648 survival with, 648t portal vein pancreatic neck, division of, 1182f positive-end expiratory pressure (PEEP), 14 posterior elbow dislocation, 765f, 766f postischemic neuropathic pain, 843 postoperative anticoagulation, 839 postoperative hemorrhage, 616–617 postsplenectomy immunization, 868 posttraumatic coagulopathy, 862 post-traumatic stress disorder (PTSD), 134 povidone–iodine solution, 905 Practice Management Guideline on chest trauma analgesia management, 878 prebiotics, 1081–1082 pregnancy evaluation of state of, 712–713 fetal outcome following trauma and, 721 injury prevention during, 721–722 management of injuries during blunt abdominal trauma, 716 cesarean section following trauma, 719–720 fetal injuries, 717–718 neurologic injury, 718–719 pelvic fractures, 716–717 penetrating trauma, 718 thermal injury, 719 thoracic trauma, 716 physiologic changes during, 710–711, 710t trauma in (See trauma in pregnancy) pregnancy-associated homicide, risk factors for, 710 pregnancy-induced hypervolemia, 711 prehospital care, 711 airway management, 109f assessment and management, 107 abdominal trauma, 117 airway management, 108–110 AMPLE history, 113–115 circulation, 110–111 disability, 111 exposure and environmental control, 112 fluid therapy, 112–113 head-to-toe survey, 115 musculoskeletal trauma, 117 primary survey, 108 resuscitation, 112 safety/standard precaution, 107 scalp wounds, 115 scene, 107 secondary survey, 113 situation, 107–108 spinal trauma, 117 supraglottic airways percutaneous transtracheal ventilation (PTV), 110 surgical cricothyroidotomy, 110 thoracic trauma, 116–117 traumatic brain injury, 115–116

traumatic cardiopulmonary arrest, 111 ventilatory support, 110 communications, 104 critical trauma patient, 113t emergency medical services system, 101 EMS personnel, 101–102 advanced, 102 education and certification, 102 emergency medical responder, 102 emergency medical technician, 102 international trauma life support (ITLS), 107 nurses, 102–103 paramedic, 102 physicians, 103 prehospital trauma life support (PHTLS) program, 107 trauma education, 107 EMS provider levels, 101t EMS unit, equipment, 104 field triage decision scheme, 114f–115f historical perspective, 100–101 medical control, 106 direct (on-line), 106–107 indirect (off-line/protocols), 106 performance improvement (PI) process care rendered, 106 system efficiency, 105–106 prehospital care overview, 112f prehospital trauma care, audit filters, 106t principles, 119t protocol for tourniquet application, 111f research and development, 119 spinal immobilization, indications, 118f system design, 103 advanced life support, 103–104 basic life support, 103 tiered response systems, 104 transport modalities ground units fixed-wing aircraft, 105 rotor-wing aircraft, 104–105 traumatic brain injury prehospital management, algorithm for, 116t triage, 117–119 prehospital fluid therapy, 113 Prehospital Index (PHI), 61 prehospital resuscitation, 635 Prehospital Trauma Life Support (PHTLS) program, 107 preoperative abdominal aortography, 635 presacral drainage, 627 present-on-admission (POA) Codes, 23 preterm labor risk after maternal trauma, 712–713 primary blast injury (PBI), 133 primary survey, 711–712 pringle maneuver, 1181f probiotics, 1081–1082 profunda femoral artery, 837 progressive sclerosis, 875 proteolytic enzymes, 607 proximal humerus, fractures of, 769–770

proximal internal carotid artery, interposition grafting for injury, 1155f proximal interphalangeal (PIP) joints, 911 proximal renal arteries, management of injuries to, 640 proximal tibia fractures, 806–807, 806f proximal ulna, fractures of, 771 Pseudomonas spp., 917 Pterois volitans, 918 pulmonary agents, 136 pulmonary hila, anatomy of left, 1065f right, 1066f pulmonary tractomy, 1064f pulse oximetry, 157 Pygocentrus nattereri, 918 pyloric exclusion, 730f, 1181f Q quality-adjusted life years (QALYs), 86 quality-of-life futility, 887, 889 R rabies prophylaxis, 911–912 schedule recommended in the United States after possible exposure to rabies, 913t treatment recommendations and estimates of the risk of, 912t radial artery injuries, 836 Radiation Emergency Assistance Center/ Training Site (REAC/TS), 138 radiation injuries, 931 absolute lymphocyte count on prognosis, 934t acute radiation syndrome, 933, 933t assessment, 934 decontamination, 934–935 human cell types, radiosensitivity of, 933t incidents, 932 local injuries, management of, 935 measuring exposure, 932 pathophysiology, 932–933 triage, 934 types of, 932t whole-body exposure, 933–934 whole-body injuries, management of, 935 radiographic examination, 714–716 radiological mass casualty events, 137–138 acute radiation syndrome (ARS), 137 contamination/exposure, 137 decontamination, 138 radius and ulna, fractures of, 773 RANGE intervention for trauma patients, guidelines for, 855 rapid resectional debridement technique, 729f rapid sequence intubation (RSI), 108, 860 rapid two-suture splenorrhaphy, 729f Receiver Operating Characteristic (ROC) curve, 88

Index recombinant activated factor VII and coagulopathy, 727 rectal injuries diagnosis of, 626–627 epidemiology of, 626 mortality and morbidity related to, 626 operative management of history of, 627 technical tips for, 627–628 Rectal Organ Injury Scale, 626t rectum anatomy, 626 recurrent (secondary) hemorrhage, 616–617 red blood cell (RBC) transfusion, 216 rehabilitation afferent nociception pathway, 955f cardiovascular effects aerobic capacity, 952 cardiac effects, 951 orthostatic hypotension, 951–952 prevention and treatment, 952 shift of body fluids, 951 venous thrombosis and pulmonary embolus, 952 common pain terminology, 955t gastrointestinal effects appetite and gastric transit time, 953 prevention/treatment, 953 immobility, effects, 950 integumentary system effects decubitus ulcers, 953 prevention/treatment, 953 interdisciplinary team care, functional improvement, 956 case managers and social work services, 957 engineers/AT specialists, 957 mental health professionals, 957 orthotists and prosthetists (O&P), 957 OTs, 956–957 peer support visitors, 957 physical medicine and rehabilitation (PM&R) specialists, 956 PTs, 956 SLPs, 957 vocational rehabilitation specialists, 957 musculoskeletal effects contractures, 951 disuse osteoporosis, 951 muscle atrophy and weakness, 950–951 prevention and treatment, 951 pain management, 954 background, 954 nonpharmacological, 956 pharmacological antidepressant medications, 956 antiseizure medications, 956 continuous infusion analgesia and anesthesia, 956 NSAIDs, 955–956 opioids, 955 sympathetic blockade, 956 terminology and pathophysiology, 954 treatment, 954–955

pulmonary effects lung volume and structural changes, 952 prevention and treatment, 952 Ranchos Los Amigos Scale, 959t trauma patients, unique complications of heterotopic ossification (HO), 953–954 spasticity, 954 traumatic brain injury classification, 959t traumatic injuries amputation, 961 burn injuries, 960–961 peripheral nerve injuries and complications, 961–962 spinal cord injury, 957–959 traumatic brain injury, 959–960 urinary system effects prevention and treatment, 953 urinary retention/stones/urinary tract infection, 952–953 renal failure, 1084 albumin-supplemented resuscitation, renal effects, 1090t colloid resuscitation, renal effects of fluid mobilization and renal changes, 1090–1091 vasopressor therapy and renal function, 1090 contrast-induced renal injury, 1096 crush injury and kidney, 1097 intraperitoneal pressure and kidney, 1097 nephrotoxic agents and ARF, 1097–1098 oliguria, differential diagnosis, 1097 renal replacement therapy (RRT), 1098 graded renal response to acute hypovolemia, 1086t hemorrhagic shock, 1086 kidney during operation after injury, 1086–1087 postoperative juxtamedullary and polyuria, 1087–1089 postoperative oliguria during extravascular fluid sequestration phase, 1089 impaired concentration after operation, 1088t kidney, components, 1085f mild to moderate hemorrhage causes, 1087f normal renal function, 1084–1086 oliguria, differential diagnosis, 1097t patient with extensive peritonitis, 1094f polyuria of acute sepsis, 1093f postresuscitative hypertension (PRH), 1091–1092, 1091t renal response to sepsis, 1092–1095 free water clearance, 1095 hypodynamic sepsis, 1094–1095 polyuria, 1093–1094

response to furosemide in early sequestration phase, 1089f restoration of PV, 1088f rifle criteria, 1095 renal trauma on renal function, 1095–1096 SCr and GFR correlation, 1096f serum creatinine to renal hemodynamic studies, 1091t serum creatinine value, 1095 renal perfusion, 875 renovascular injuries endovascular management of, 649 management of, 644 reoperation emergency, 737–738, 738t intensive care before, 737 routine, 738 repeat application of silo, 739 reperfusion injury, 819 replantation, 792 replantations of upper extremities, 777, 779–780, 779f reproductive system, changes in maternal, 711 Residency Review Committee (RRC), 94 respiratory distress syndrome (RDS), 866 respiratory insufficiency, 1055 acute lung injury, definitions of, 1057t acute respiratory distress syndrome, definitions of, 1057t ALI and ARDS, 1056 ARDS chest CT scan, 1061f clinical risk factors, 1058t Delphi definition, 1057t idealized static pressure–volume curve, 1062f ventilatory strategies, 1064t corticosteroids, 1068–1070 nutritional support, 1069–1070 definitions and limitations, 1056–1058 Denver Health SICU mechanical ventilation protocol, 1069f epidemiology and risk factors, 1058 extracorporeal life support (ECLS), 1068 fluid management/hemodynamic support, 1064 gas exchange, 1062 gut lymph hypothesis, 1060–1061 respiratory distress syndrome, acute, mediators/markers of, 1060–1061 hemodynamics, 1062 high-frequency modes of ventilation (HFV), 1066–1067 hypercapnic pulmonary failure, 1055–1056 hypoxic pulmonary failure, 1056 low-pressure pulmonary edema, 1063t Lung Injury Score, 1057t macrophages, 1059 management, 1063 mechanical ventilation, 1064

1219

1220

Index respiratory insufficiency (continued ) multiple lower extremity fractures., 1061f outcome, 1070 pathogenesis, neutrophils, 1059 pathology, 1058–1059 pathophysiology, 1061–1062 permissive hypercapnia, 1066 pharmacologic therapy, 1068 inhaled nitric oxide, 1068 positive end-expiratory pressure, 1065 presentation, 1062–1063 pressure-limited ventilatory support, 1065–1066 prone ventilation, 1066–1067 pulmonary edema, 1062 pulmonary endothelium, 1059–1060 pulmonary mechanics, 1062 risk factors, 1058 respiratory rate (RR), 83 respiratory system, changes in maternal, 711 resuscitation damage control, 636 emergency department, 635–636 prehospital, 635 Resuscitation Outcomes Consortium (ROC), 66 retained amputated fingertip, 758 retinal hemorrhage, 13 retroperitoneal bleeding, grade 5 fracture, pelvic packing, 1175f–1176f retroperitoneal duodenal perforation, computed tomography (CT) finding of, 609 Revised Trauma Score (RTS), 84, 85 rib calcification, 875 rib fractures, 878–879 ribonucleic acid (RNA), 902 right scaphoid fracture, 774f road rash, 908 roux-en-Y duodenojejunostomy, 612, 613f rural trauma, 140 ambulance to local hospital, 142, 143f communications, 144 education/maintenance of skills, 146–147 environment, 140–141 epidemiology, 141–142 facilities, 145–146 global positioning satellite (GPS), 142 manpower, 143–144 resources and limitations, 142 discovery and access to system, 142–143 rural, definition, 141 telemedicine, 150–151 telepresence surgery, 151 transport systems, 145, 150 trauma systems, 151 treatment options damage control surgery, 148–149 definitive surgery, 148 local definitive care, 149 operative stabilization and transfer, 148 population shifts, 150

stabilization and transfer to definitive care, 147–148 wireless technology, 150 Rural Trauma Subcommittee, 143 S sacral trauma, 456 San Diego Trauma System, 68 saphenous vein interposition graft, for repair of brachial artery laceration, 840f saphenous vein panel interposition graft, 837, 839 scaphoid, fractures of, 773–774 scapula, fractures of, 769 scapulothoracic dissociation, 764, 764f, 833 injury, 833 screening and brief intervention (SBI), 41 Screening, Brief Intervention, and Referral to Treatment (SBIRT), 851 billing for, 857 Common Procedural Terminology (CPT) codes, 857 establishment of, 856–857 “Seat belt aorta,” 648 “secondary” abdominal compartment syndrome, 735 secondary survey, 712 sedative-hypnotics, 853 drugs, 853 Sellick maneuver. See cricoid cartilage pressure septic shock, 204–206 serum osmolarity, 864 shaft of humerus, fractures of, 770 shaft of radius, fractures of, 772 shaft of ulna, fractures of, 772 shark bites, wounds caused by, 918 shock, 189, 624–625 afferent signals, 191 efferent signals cardiovascular response, 191–192 cellular effects, 193–195 immunologic/inflammatory response, 192–193 neuroendocrine response, 192 quantifying cellular hypoperfusion, 195–196 extracellular BEA and mortality, 196f forms of, 190t cardiogenic, 203–204 hypovolemic, 200–202 neurogenic, 202–203 obstructive, 206–207 septic, 204–206 traumatic, 207 hemorrhagic shock, rodent model, 191f mortality and serum lactate levels, 195f pathophysiology, 190–191 tissue hypoperfusion algorithm, 197f, 198f trauma patient, evaluation hypotensive resuscitation, 199–200 overview, 196–197

resuscitation fluids, 199 severe hemorrhage patients, vascular access, 197–199 trauma patient, resuscitation, 207 near-infrared spectroscopy, 208–212 hemorrhagic shock, 209–211 muscle oxidative metabolism measurement, 211–212 StO2, histogram of, 209f StO2 measurements, 208, 212f StO2, ROC curves, 210f Shock Index, 877 shoulder girdle region, imaging examinations for, 750t “single-shot” extremity arteriography, technique for, 822t single-vessel arterial injuries, 827 Sistrurus, 914 skeletal system, injuries to, 870 skin wheals and level of cross-section, position of, 908 small bowel. See abdominal injuries smoke detectors, 43 Snakebite Severity Score (SSS), 915 snakebite wounds, 912–913 algorithm for the treatment of, 914f anaphylaxis, treatment for, 917t antivenin therapy for treatment of, 916–917 coral snake envenomation, 917 CroFab antibody, 916 crotalidae of North America and, 914t crotalid envenomation, assessment of, 914–915 definitive care for treatment of, 916 fasciotomy, 917 first aid for, 915–916 and identification of the snake, 913–914 poisonous and nonpoisonous snakes, characteristics of, 915f Snakebite Severity Score (SSS), 915 social violence community violence history of, 892 risk factors, 893 domestic violence diagnosis of, 891–892 incidence and prevalence of, 890–891 treatment and referral, documentation, and reporting, 892 elder abuse diagnosis of, 892 treatment and referral, 892 surgeon’s role in, 893 soft tissue injuries Hannover classification of, 788t to lower extremity, 788 soft tissue lacerations, 747 soft tissue wounds, 908 Solenopsis invicta, 918 Solenopsis richteri, 918 spider bites, wounds caused by, 919

Index spinal cord injury (SCI), 13, 27, 430. See also cervical spine injuries anatomy and biomechanics, 431–434 anatomy and physiology, 434–435 ASIA classification of neurologic deficit, 436f atlantoaxial subluxation, 452f Atlas fractures, 452f blood supply of, 435f causes of, 431f cervical spine Canadian cervical spine rules, 441f NEXUS low-risk criteria, 440f cervical vertebrae, 433f emergency room, evaluation, 438–439 epidemiology, 430–431 flexion–distraction subaxial cervical spine injury, 454f gunshot wounds, 457–458 Halo pin placement, 448f Halo ring apparatus, 448f Hangman’s fracture, 453f imaging, 439–441 ankylosing spondylitis, 440 cervical spine, clearing, 440–441 lateral cervical spine x-ray, analyzing, 439f lumbar vertebrae, 434f lumbosacral dissociation injury, CT, 457f lumbosacral spine, checklist for the diagnosis, 444t management, 444 spinal stability, 444–446 neurologic injury anterior cord syndrome, 437 Brown-Séquard syndrome, 437 cauda equina syndrome, 438 central cord syndrome, 437 cervical root syndrome, 437 classification, 436–437 conus medullaris syndrome, 438 location, 435 posterior cord syndrome, 437 primary and secondary, 435–436 nonoperative management, 447 cervical traction, 449 halo fixator, 447–449 spinal orthotics, 447 occipital condyle injuries, classification, 450f odontoid fractures, classification, 452f operative management goals of, 449–450 perioperative considerations, 449 spinal fractures, stabilization timing, 450 posterior ligamentous complex (PLC), 433 Power’s ratio, 451f prehospital care, 438 prophylaxis against deep vein thrombosis (DVT), 441 protocol for initial evaluation, 442t rule of 12’s, 451f

spinal cord injury, patterns, 437f subaxial cervical spine injuries based on injury mechanism, 445f Subaxial Injury Classification (SLIC) Scale, 446t surgical decompression, timing, 443 therapeutic intervention decubitus ulcer, prevention, 441–442 oxygenation/hemodynamic parameters, maintenance of, 442 pharmacologic/cellular interventions, 442–443 thoracic/thoracolumbar spine, checklist for the diagnosis, 444t Thoracolumbar Injury Classification and Severity Score (TLICS), 446t thoracolumbar spine burst fracture of, 455f fracture-dislocation of, 457f traumatic spondylolisthesis, classification of, 453f upper cervical spine, midsagittal section, 432f spinal cord injury without radiographic abnormalities (SCIWORA), 13, 865 spleen, damage control operations in, 729 spleen injury, 561 algorithm for diagnosis and management, 569f arterial blood supply, 564f complications nonoperative management, 576–577 operative management, 577–578 computed tomographic findings, 567f diagrammatic representation, 568f, 571f grading systems, 567–568 guidelines for resource utilization, 572t historical perspective, 561–562 imaging and diagnostic peritoneal lavage, 566–567 initial evaluation and management, 565–566 injury scaling system, 568t ligaments, 563f mobilization of, 574f nonoperative management, 568 operative management, 573–576 partial splenectomy, depiction of, 562f pathophysiology of, 564 patient management, 572–573 patient selection, 568–572 postembolization view, 571f postsplenectomy infection, 578 splenic anatomy, 562–564 splenic function, 562 splenic tissue, autotransplantation of, 576f splenectomy, 868 splenic flexure of colon, 626f split-thickness skin graft donor, 908 Stab wounds and colon injuries, 620 Staphylococcus spp., 909, 911, 917 START triage system, 62

sternoclavicular dislocation, 764 stomach. See abdominal injuries STOP THE BLEEDING!!!, 160 Streptococcus viridans, 909 strict futility, 886 subatmospheric sponge dressings, 909 subclavian and axillary vascular injuries, 834–836 subclavian artery, hemorrhage controlling, 1169f subclavian artery injury, 835 exposure and repair, 1170f–1171f subendothelial matrix collagen, 897 subtrochanteric femoral nonunion, salvage procedure of, 813 subtrochanteric fractures, management of, 798–799, 799f SUM intervention for trauma patients, guidelines for, 855 superficial femoral vascular injuries, 837–838 superior mesenteric artery management of injuries to, 639–640, 640f survival with injuries to, 640 supraclavicular subclavian injuries, 834 supracondylar humerus fracture, 836 suprarenal aorta, management of injuries to, 638, 639t Surgical Council on Resident Education (SCORE), 93 surgical intensive care unit (SICU), resuscitation in, 725 survivable vascular injuries, 817 S. viridans, 911 Synanceia spp., 918 syndromic surveillance, 135 systemic inflammatory response syndrome (SIRS), 67, 333f, 898 systolic blood pressure (SBP), 83 T telemedicine, 150–151 telepresence surgery, 151 temporary silos, 735 tendons in distal extremity, treatment of injuries to extensor tendon, 754–755 flexor tendons and “spaghetti wrist,” 756–757 thumb extensor injury, 756 terrestrial animals, bites and stings by cat bites, 911 dog bites, 911 human bites, 909–911 rabies prophylaxis, 911–912 snakebites, 912–917 tetanus prophylaxis, 904t therapeutic anticoagulation, 877 thermal injuries, treatment of, 759–760 thermal injury in pregnancy, management of, 719 thigh fasciotomy, 831

1221

1222

Index thoracic duct anatomy, 1171f cross-clamping of, 1172f thoracic incision, options, 1058f–1059f thoracic (operative) procedure, 1057f thoracic spine injuries, 454–455 thoracic trauma damage control operations in, 728 in pregnancy, management of, 716 thoracic vascular injuries, 492 algorithm, 498f anteroposterior projection, 500f aortic isthmus flow analysis, 497f three-dimensional reconstruction, 496f aortogram demonstrating blunt chest trauma, 505f intimal tear and traumatic pseudoaneurysm, 504f azygos vein, 508f blunt injury, plain chest x-ray, 501f blunt thoracic aortic injury, 501t bullet in left groin, 495f bypass exclusion technique, 504f chest radiograph, 499f diagnostic studies, catheter arteriography, 499–500 emergency center evaluation chest radiography, 494 history, 493 physical examination, 493 etiology and pathophysiology, 492–493 groups of patients, 493t initial evaluation, prehospital management, 493 initial treatment and screening emergency center thoracotomy, 494 impulse therapy/beta-blockade, 495–496 intravenous access and fluid administration, 494–495 screening/planning CT scan, 496–499 tube thoracostomy, 494 innominate artery, blunt injury, 503f lateral chest x-ray, cardiac silhouette, 494f misdiagnosis by aortography, 499f multifactorial development, 506t patient classification, 493 penetrating wound, plain chest x-ray, 500f proximal innominate artery, 503f radiographic clues, 495t recommended incisions, 502t surgical repair, 501–503 damage control, 502–503 therapeutic approaches, management of, 505t thoracic aorta distal, multiplanar, 496f thoracic aortic anomalies, 492t treatment options endograft repair, 500–501 nonoperative management, 500

thoracolumbar spine injuries burst fractures, 455–456 compression fractures, 455 flexion–distraction injuries, 456 fracture–dislocations, 456 isolated injuries, 456 thoracotomy, traumatic incision algorithm, 464f indications, 462 minor therapeutic interventions, 462 patient positions/incisions, 462–463 specific injuries algorithm, 464f thoracic anatomy and physiology, 461 evaluation technology, 461–462 thoracic damage control, 463–464 thoracic incisions, 463f thoracic trauma, complications of, 466 thoracic trauma controversies cardiorrhaphy, pledgets, 465 chest tubes, clamping of, 465 CT scanning, 464–465 pericardiocentesis, 465 pleural cavity, needle decompression of, 465 subxyphoid pericardiotomy, 465 trap door thoracotomy, 465 trocar chest tubes, 465 timing of, 465–466 tube thoracostomy, 462 thorax, injuries to, 866–867 thrombocytopenia, 863 thrombosis of brachial artery, 841f Through the Brazilian Wilderness (1914), 918 tibia fractures, management of, 806–810 ankle injuries, 809–810 pilon fractures, 808–809 proximal, 806–807, 806f tibial shaft, 807–808, 809f tibial shaft fractures, 807–808, 809f tibial vessel injuries, 839 tick-borne encephalitis (TBE) viruses, 134 Tile classification of pelvic fracture, 655–657, 656t tissue coverage, role of, 829 tissue hypoperfusion, 877 tissue inhibitors of matrix metalloproteinases (TIMP-1), 899 total body surface area (TBSA), 879 trachea esophagus, combined injury repair, 1155f tracheobronchial injuries, 476 distal tracheal repair, intraoperative photograph of, 477f operative techniques, 477–478 outcomes, 478–479 presentation and evaluation, 476–477 tracheal injury, preoperative bronchoscopy, 476f tracheal stenosis, 479 tractotomy, 1178f traffic-related injury prevention, 46 transected ureter, repair, 1187f transesophageal ECHO (TEE), 867

transforming growth factor alpha (TGF-α), 899 transforming growth factor beta (TGF-β), 898 transplantation brain death declaration, 946–947 physiologic consequences, 947–948 brain death, defining, 946t donor management, 948 donor screening, 946 donor type, 945f organ donation and allocation, 944–946 contraindications, 946t organ procurement for, 944, 948–949 transscaphoid perilunate dislocation, 767f Trauma and Injury Severity Score (TRISS), 85 Trauma and Injury Severity Score Comorbidity (TRISSCOM), 85 trauma care, 890 trauma in pregnancy causes of, 709 epidemiology of, 709–710 initial assessment and management algorithm for, 713f fetal–placental unit, 712–714 maternal assessment, 712 prehospital care, 711 primary survey, 711–712 radiographic examination, 714–716 secondary survey, 712 ultrasonography, 714 trauma ostomy complications, 630 Trauma Quality Improvement Program (TQIP), 88 Trauma Score (TS), 61 trauma systems ACS Field Triage System, 62 age, comorbid disease, and environmental concerns, 60 anatomic criteria, 59 chain of custody, 1002 classic key points, 997–998 clothing, 1001 combination methods, 62 communications system, 57 components, 56 concepts, principles, and definitions consent, 998–1000 duty to treat, 998 CRAMS scale, 61 critical targets for future development, 75t definition of, 54 development, 55–56 disaster situations, 1002 emergency medical service system components, 55t errors/preventable death, definition of, 72–73 forensic/medical implications, 1000 forensic nursing, 1000 Glasgow Coma Scale (GCS), 61 histories, 54–55

Index human resources, 57 injury identification, classification, and grading, 1000–1001 injury, mechanism, 59 interacting with attorneys hospital bylaws, committees, credentialing, policies, 1002 professional liability, depositions, and testifying in court, 1002–1003 laboratory specimen collection, for law enforcement purposes, 1001–1002 law enforcement, 997 legal considerations, during mass casualty, 1002 limitations of, 73t medical direction, 57 outcome from transfer, 69–70 paramedic judgment, 60 performance analysis, 73–74 physiologic criteria, 59 prehospital, 57 prehospital index, 61 prehospital triage decision scheme, 63f problems and challenges, 74–75, 74t public information, education, and injury prevention, 56–57 quality improvement (QI), 71–72 regional trauma system development, 56f rehabilitation, 71 rural trauma, 151 simple triage and rapid treatment (START), 62 statewide trauma care system, criteria, 55t system evaluation, 71 transport mode , interfacility transfer, 70 trauma care system, diagram, 56f trauma center facilities, and leadership acute care, 71 Level I, 70–71 Level II, 71 Level III, 71 Level IV, 71 specialty trauma centers, 71 trauma index, 61 trauma triage criteria, uses, 60t trauma triage rule, 61–62 triage and transport, 57–58 triage guidelines, 65 field triage riage scores, 66–67 in-hospital, triage, 67–68 interhospital transfer, 68–69 criteria, 69 major trauma patient, 65–66 transfer agreement, 69 transfer methods, 69 transport modality, 69 transport team, 69 undertriage/overtriage, 68 triage principles, application, 62 disaster management, 64–65 mass casualties, 64 multiple casualties, 62–63 single patient, 62

triage, purpose/challenges of, 58–59 triage scoring method, 61 triage tools/decision making, components, 59 wounds from firearms, 1001 Trauma Systems Planning and Development Act, 55 trauma team, 142, 143 trauma team activation (TTA), 876 traumatic aortoiliac disease, endovascular management of, 649 traumatic brain injury (TBI), 26, 110, 356, 877, 878, 944 acute subdural hemorrhage, CT, 362f bilateral hemispheric decompressive craniectomy, CT of, 371f brain death determination, 374 coagulopathy/DVT prophylaxis, 373 concussion grading, 364t diffuse cerebral injuries blast traumatic brain injury, 366–367 child abuse/nonaccidental trauma, 367 concussion, 364 diffuse axonal injury, 364 extracranial vascular injury, 367 penetrating missile injury, 365–366 penetrating nonmissile injury, 364–365 epidemiology, 356 epidural hemorrhage, CT, 362f focal cerebral injuries, 361 cerebral contusions, 361 epidural hemorrhage, 361–362 intraparenchymal hemorrhage, 361 subarachnoid hemorrhage, 363 subdural hemorrhage, 362–363 Glasgow Coma Scale, 358, 358t for children, 358t Glasgow Outcome Score, 374t infection, 372–373 intracranial pressure assessment, 368 cerebral blood flow and metabolism, 369 cerebral perfusion pressure, 369 ICP monitoring, 368–369 intracranial pressure management analgesics and sedatives, 369–370 antiseizure prophylaxis, 372 barbiturates, 371–372 decompressive craniectomy, 371 hyperosmolar therapy, 370 hypertonic saline (HS), 370 hyperventilation, 370–371 hypothermia, 372 steroids, 372 left central sulcus, traumatic subarachnoid hemorrhage CT, 363f medical management, 367–368 blood pressure and oxygenation, 368 multiple sports-related concussions, 365t neurological examination, 357, 357t nutrition, 372 organ donation, 374

outcome, prognosis, 373–374 pathophysiology, 356 penetrating nail-gun injury, intraoperative picture of, 366f ping-pong skull fracture, CT bone windows, 359f pupillary response, 357–358 radiographic diagnosis, 359–361 radiographic evaluation angiography, 359 CT scan, 359 MRI, 359 plain x-rays, 358 SDH on CT/MRI, 363t single sports-related concussion, 365t skull fractures, 359 CT bone windows, 360f differential diagnosis, 360t systemic evaluation and resuscitation, 356–357 trauma to elbow, 765–766 triage guidelines, trauma, 65 field triage riage scores, 66–67 in-hospital, triage, 67–68 interhospital transfer, 68–69 criteria, 69 major trauma patient, 65–66 transfer agreement, 69 transfer methods, 69 transport modality, 69 transport team, 69 undertriage/overtriage, 68 trochanteric fractures, management of, 797–798, 798f tube thoracostomy, 1057f U ulnar nerve block anesthesia, technique of, 907f ultrasonography, 714 ultrasound examination of injured gravid patient, 717f ultrasound imaging essential principles, 304f maximizing accuracy, 306t scanning planes, 304t, 305f terminology, 302t–303t, 304t ultrasound physics, 301–302 undertriage, 58 unhealthy alcohol use, 851 upper extremities fractures and dislocations of, 778–779t injury-specific history of, 747–748 vs. lower extremities, 777 nerve injuries in, 760–763 nerves and muscles of, 748–749t physical examination, 747–748 reconstructive requirements for, 754 replantations of, 777, 779–780 vascular injuries in, 760 x-ray examination, 750 upper extremity arterial injury, guideline for management of, 837f

1223

1224

Index upper extremity injuries classification of, 747–748 clinical presentations, 752–753t compartment syndrome, 751, 753f “fight bite” injuries of head of metacarpal bone, 751–752 joint injuries (See joint injuries) treatment chemical burns, 759 electrical injuries, 759 frostbite, 758–759 high-pressure injection injuries, 758 injuries to fingertip and nail bed, 757–758 injuries to tendons, 754–757 open soft tissue injuries and complex wounds, 754 thermal injuries, 759–760 upper extremity vascular injuries, 834 upper lateral retroperitoneum, management of injuries in exposure and vascular control, 643–644 renovascular injuries, 644 ureteral stenting, for urine leaks, 869 urinary bladder, coronal view, 308f urinary system effects, rehabilitation prevention and treatment, 953 urinary retention/stones/urinary tract infection, 952–953 uterine contraction pattern, assessment of, 712 V vac sponge, 909 V.A.C.® system, 909 vacuum-assisted closure, 741 vacuum-assisted fascial closure, 739 vacuum-assisted wound closure, 736–737 vaginal bleeding, 712 varus malunion of tibia shaft fracture, 809f vascular anastomoses, small, 1192f vascular cell adhesion molecule-1 (VCAM-1), 898 vascular injuries in upper extremity, 760 vascular injury by anatomic region brachial artery injuries, 836 common femoral vascular injuries, 837 forearm arterial injuries, 836 lower extremity vascular injuries, 836 popliteal and tibial artery injuries, 839 subclavian and axillary vascular injuries, 834–836 superficial femoral vascular injuries, 837–838 upper extremity vascular injuries, 834 clinical presentation, 820–821 complications and outcome, 839–840 damage control principles and techniques, 832

decision making in extremity arterial and venous repairs in stable patients, 828f diagnostic evaluation of, 823f arteriography, 822 of combined arterial and skeletal extremity trauma, 832–833 common management errors and pitfalls, 834 early postoperative management, 833–834 noninvasive evaluation, 822 physical examination, 821–822 practice recommendation for extremity vascular, 822–823 and principles of operative management, 826–832 and role of immediate amputation, 833 of vascular damage control, 832 epidemiology of, 817–818 extremity vascular trauma case presentations lower extremity, 842–846 upper extremity, 840–842 four-compartment calf fasciotomy checklist, 831f “hard” and “soft” signs of, 821t indications for arteriography in patients with, 822t lessons of war, 816–817 management of endovascular management, 823–824 endovascular repairs, 824 minimal vascular injury and nonoperative management, 823 operative, 824 preoperative preparation, 824–826 vascular trauma surgery, 824 pathophysiology of, 818–819 compartment syndrome, 819–820 missile emboli, 820 potential errors in the recognition, preoperative preparation, and operative management of, 817t preparation checklist for repair of, 825f prognostic factors, 820 vascular shunt, temporary, 1193f vasoconstriction, 834 vasodilatory shock. See septic shock vein clamping, 837 vein injuries, exposure and repair, 1196f venomous fish, wounds caused by, 918 venous bypass, 1200f venous hypertension, 828 venous injuries azygos vein, 508 pulmonary veins, 507 subclavian veins, 508 thoracic vena cava, 507 venous repairs, 828–829 vertebral artery, injury control, 1056f

vertical shear injuries, 658 vesicants, 136 Vietnam Vascular Registry, 816 violence, definition of, 890 visceral herniation, 867 vital functions for children, 862t volar fingertip injures, 757–758 vscular endothelial growth factor (VEGF), 899 W warfarin therapy, 882 warning signs, 48 war-related colorectal injuries, 628–629 recommendations for, 629 Web-Based Injury Statistics Query and Reporting System (WISQARS), 859 well-trained air medical crews, 110 Western Trauma Association (WTA), 92 World Health Organization (WHO), 49 wound closure, types of, 903 wound management, 629 wounds bites and stings, caused by (See bites and stings) clinical management of antibiotic usage for, 907–908 conditions requiring management in operating room, 905t decision-making for, 903–904 local anesthetics for, 905–907 operative issues and, 905 operative vs. nonoperative, 904–905 subatmospheric sponge dressings, 909 wound closure, types of, 903 wound dressing, 908–909 dressing materials for, 910t dressing of, 908–909 subatmospheric sponge, 909 healing of algorithm for the treatment, 897f cytokines and growth factors, 900t–901t inflammatory phase, 897–898 migratory phase of, 899–900 normal aspect of, 896–897 phases of, 897t proliferative phase of, 900–902 remodeling phase of, 902 threats to infection-free, 904t technique for high-pressure syringe irrigation of, 906f tetanus characteristics, 904t Y Years of Potential Life Lost (YPLL), 850 Young–Burgess classification of pelvic fractures, 657–658, 658t Z zipper closure, 739