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a LANGE medical book

Clinical Anesthesiology Morgan & Mikhail’s

F I F T H

E D I T I O N

John F. Butterworth IV, MD Professor and Chairman Department of Anesthesiology Virginia Commonwealth University School of Medicine VCU Health System Richmond, Virginia

David C. Mackey, MD Professor Department of Anesthesiology and Perioperative Medicine University of Texas M.D. Anderson Cancer Center Houston, Texas

John D. Wasnick, MD, MPH Steven L. Berk Endowed Chair for Excellence in Medicine Professor and Chair Department of Anesthesia Texas Tech University Health Sciences Center School of Medicine Lubbock, Texas

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

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Morgan & Mikhail’s Clinical Anesthesiology, Fifth Edition Copyright © 2013, 2006, 2002 by The McGraw-Hill Companies, Inc. All rights reserved. Printed in the United States. Except as permitted under the United States Copyright Act of 1976, no part of this publication may be reproduced or distributed in any form or by any means, or stored in a data base or retrieval system, without the prior written permission of the publisher. Previous editions copyright © 1996, 1992 by Appleton & Lange. 1 2 3 4 5 6 7 8 9 0 WCT/WCT

18 17 16 15 14 13

ISBN 978-0-07-162703-0 MHID 0-07-162703-0 ISSN 1058-4277

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.

This book was set in Minion Pro by Thomson Digital. The editors were Brian Belval and Harriet Lebowitz. The production supervisor was Sherri Souffrance. Project management was provided by Charu Bansal, Thomson Digital. The illustration manager was Armen Ovsepyan; illustrations were provided by Electronic Publishing Services. The designer was Elise Lansdon; the cover designer was Anthony Landi; cover illustration by Elizabeth Perez. Quad Graphics was printer and binder.

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International Edition ISBN 978-0-07-181669-4 ; MHID 0-07-181669-0. Copyright © 2013. Exclusive rights by The McGraw-Hill Companies, Inc., for manufacture and export. This book cannot be re-exported from the country to which it is consigned by McGraw-Hill. The International Edition is not available in North America.

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Contents Chapter Authors v | Contributors vii Research and Review ix | Foreword xi | Preface xiii

1 The Practice of Anesthesiology 1 SECTION

I

15 Hypotensive Agents 255 16 Local Anesthetics 263

Anesthetic Equipment & Monitors

2 The Operating Room Environment 9 Charles E. Cowles, MD

3 Breathing Systems 29

17 Adjuncts to Anesthesia 277 SECTION

III

Anesthetic Management

4 The Anesthesia Machine 43

18 Preoperative Assessment, Premedication, & Perioperative Documentation 295

5 Cardiovascular Monitoring 87

19 Airway Management 309

6 Noncardiovascular Monitoring 123

20 Cardiovascular Physiology & Anesthesia 343

SECTION

II

Clinical Pharmacology

7 Pharmacological Principles 143 8 Inhalation Anesthetics 153 9 Intravenous Anesthetics 175

21 Anesthesia for Patients with Cardiovascular Disease 375 22 Anesthesia for Cardiovascular Surgery 435 23 Respiratory Physiology & Anesthesia 487

10 Analgesic Agents 189

24 Anesthesia for Patients with Respiratory Disease 527

11 Neuromuscular Blocking Agents 199

25 Anesthesia for Thoracic Surgery 545

12 Cholinesterase Inhibitors & Other Pharmacologic Antagonists to Neuromuscular Blocking Agents 223

26 Neurophysiology & Anesthesia 575

13 Anticholinergic Drugs 233

28 Anesthesia for Patients with Neurologic & Psychiatric Diseases 613

14 Adrenergic Agonists & Antagonists 239

27 Anesthesia for Neurosurgery 593

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iv

CONTENTS

29 Renal Physiology & Anesthesia 631 30 Anesthesia for Patients with Kidney Disease 653 31 Anesthesia for Genitourinary Surgery 671 32 Hepatic Physiology & Anesthesia 691 Michael Ramsay, MD, FRCA

33 Anesthesia for Patients with Liver Disease 707 Michael Ramsay, MD, FRCA

34 Anesthesia for Patients with Endocrine Disease 727 35 Anesthesia for Patients with Neuromuscular Disease 747 36 Anesthesia for Ophthalmic Surgery 759

SECTION

IV

Regional Anesthesia & Pain Management

45 Spinal, Epidural, & Caudal Blocks 937 46 Peripheral Nerve Blocks 975 Sarah J. Madison, MD and Brian M. Ilfeld, MD, MS

47 Chronic Pain Management 1023 Richard W. Rosenquist, MD and Bruce M. Vrooman, MD

48 Perioperative Pain Management & Enhanced Outcomes 1087 Francesco Carli, MD, MPhil and Gabriele Baldini, MD, MSc

SECTION

V

Perioperative & Critical Care Medicine

37 Anesthesia for Otorhinolaryngologic Surgery 773

49 Management of Patients with Fluid & Electrolyte Disturbances 1107

38 Anesthesia for Orthopedic Surgery 789

50 Acid–Base Management 1141

Edward R. Mariano, MD, MAS

39 Anesthesia for Trauma & Emergency Surgery 805 Brian P. McGlinch, MD

40 Maternal & Fetal Physiology & Anesthesia 825 Michael A. Frölich, MD, MS

41 Obstetric Anesthesia 843 Michael A. Frölich, MD, MS

42 Pediatric Anesthesia 877 43 Geriatric Anesthesia 907 44 Ambulatory, Nonoperating Room, & Office-Based Anesthesia 919

51 Fluid Management & Blood Component Therapy 1161 52 Thermoregulation, Hypothermia, & Malignant Hyperthermia 1183 53 Nutrition in Perioperative & Critical Care 1193 54 Anesthetic Complications 1199 55 Cardiopulmonary Resuscitation 1231 Martin Giesecke, MD and Srikanth Hosur, MBBS, MD

56 Postanesthesia Care 1257 57 Critical Care 1277 58 Safety, Quality, & Performance Improvement 1325 Index 1331

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Chapter Authors Gabriele Baldini, MD, MSc Assistant Professor Department of Anesthesia McGill University Montreal, Quebec John F. Butterworth IV, MD Professor and Chairman Department of Anesthesiology Virginia Commonwealth University School of Medicine VCU Health System Richmond, Virginia Francesco Carli, MD, MPhil Professor Department of Anesthesia McGill University Montreal, Quebec Charles E. Cowles, Jr, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Chief Safety Officer Perioperative Enterprise University of Texas MD Anderson Cancer Center Houston, Texas Michael A. Frölich, MD, MS Associate Professor Department of Anesthesiology University of Alabama at Birmingham Birmingham, Alabama Martin Giesecke, MD M.T. “Pepper” Jenkins Professor in Anesthesiology Vice Chair, University Hospitals Department of Anesthesiology and Pain Management University of Texas Southwestern Medical Center Dallas, Texas

Srikanth Hosur, MBBS, MD Consultant in Intensive Care QuestCare Intensivists Dallas, Texas Brian M. Ilfeld, MD, MS Professor, In Residence Department of Anesthesiology University of California, San Diego San Diego, California David C. Mackey, MD Professor Department of Anesthesiology and Perioperative Medicine University of Texas M.D. Anderson Cancer Center Houston, Texas Sarah J. Madison, MD Assistant Clinical Professor of Anesthesiology Department of Anesthesiology University of California, San Diego San Diego, California Edward R. Mariano, MD, MAS (Clinical Research) Associate Professor of Anesthesia Stanford University School of Medicine Chief, Anesthesiology and Perioperative Care Service VA Palo Alto Health Care System Palo Alto, California Brian P. McGlinch, MD Associate Professor Department of Anesthesiology Mayo Clinic Rochester, Minnesota Colonel, United States Army Reserve, Medical Corps 452 Combat Support Hospital Fort Snelling, Minnesota

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vi

CHAPTER AUTHORS

Michael Ramsay, MD, FRCA Chairman Department of Anesthesiology and Pain Management Baylor University Medical Center President Baylor Research Institute Clinical Professor University of Texas Southwestern Medical School Dallas, Texas Richard W. Rosenquist, MD Chair, Pain Management Department Anesthesiology Institute Cleveland Clinic Cleveland, Ohio

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Bruce M. Vrooman, MD Department of Pain Management Anesthesiology Institute Cleveland Clinic Cleveland, Ohio John D. Wasnick, MD, MPH Steven L. Berk Endowed Chair for Excellence in Medicine Professor and Chair Department of Anesthesia Texas Tech University Health Sciences Center School of Medicine Lubbock, Texas

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Contributors Kallol Chaudhuri, MD, PhD Professor Department of Anesthesia Texas Tech University Health Sciences Center Lubbock, Texas

Robert Johnston, MD Associate Professor Department of Anesthesia Texas Tech University Health Sciences Center Lubbock, Texas

Swapna Chaudhuri, MD, PhD Professor Department of Anesthesia Texas Tech University Health Sciences Center Lubbock, Texas

Sanford Littwin, MD Assistant Professor Department of Anesthesiology St. Luke’s Roosevelt Hospital Center and Columbia University College of Physicians and Surgeons New York, New York

John Emhardt, MD Department of Anesthesia Indiana University School of Medicine Indianapolis, Indiana Suzanne N. Escudier, MD Associate Professor Department of Anesthesia Texas Tech University Health Sciences Center Lubbock, Texas Aschraf N. Farag, MD Assistant Professor Department of Anesthesia Texas Tech University Health Sciences Center Lubbock, Texas Herbert Gonzalez, MD Assistant Professor Department of Anesthesia Texas Tech University Health Sciences Center Lubbock, Texas Kyle Gunnerson, MD Department of Anesthesiology VCU School of Medicine Richmond, Virginia

Alina Nicoara, MD Assistant Professor Department of Anesthesiology Duke University Medical Center Durham, North Carolina Bettina Schmitz, MD, PhD Associate Professor Department of Anesthesia Texas Tech University Health Sciences Center Lubbock, Texas Steven L. Shafer, MD Department of Anesthesia Stanford University School of Medicine Palo Alto, California Christiane Vogt-Harenkamp, MD, PhD Assistant Professor Department of Anesthesia Texas Tech University Health Sciences Center Lubbock, Texas Gary Zaloga, MD Global Medical Affairs Baxter Healthcare Deerfield, Illinois

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Research and Review Jacqueline E. Geier, MD Resident, Department of Anesthesiology St. Luke’s Roosevelt Hospital Center New York, New York

Cecilia N. Pena, MD Resident, Department of Anesthesiology Texas Tech University Medical Center Hospital Lubbock, Texas

Brian Hirsch, MD Resident, Department of Anesthesiology Texas Tech University Medical Center Lubbock, Texas

Charlotte M. Walter, MD Resident, Department of Anesthesiology Texas Tech University Medical Center Lubbock, Texas

Shane Huffman, MD Resident, Department of Anesthesiology Texas Tech University Medical Center Lubbock, Texas

Karvier Yates, MD Resident, Department of Anesthesiology Texas Tech University Medical Center Lubbock, Texas

Rahul K. Mishra, MD Resident, Department of Anesthesiology Texas Tech University Medical Center Lubbock, Texas

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Foreword A little more than 25 years ago, Alexander Kugushev, then the editor for Lange Medical Publications, approached us to consider writing an introductory textbook in the specialty of anesthesiology that would be part of the popular Lange series of medical books. Mr. Kugushev proved to be a convincing salesman, in part by offering his experience with scores of authors, all of whom opined that their most satisfying career achievement was the fathering of their texts. We could not agree more. Now in its fifth edition, the overall stylistic goal of Clinical Anesthesiology remains unchanged: to be written simply enough so that a third year medical student can understand all essential basic concepts, yet comprehensively enough to provide a strong foundation for a resident in anesthesiology. To quote C. Philip Larson, Jr, MD from the Foreword of the first edition: “The text is complete; nothing of consequence is omitted. The writing style is precise, concise and highly readable.”

The fifth edition features three new chapters: Ambulatory, Nonoperating Room, and Officebased Anesthesia; Perioperative Pain Management and Enhanced Outcomes; and Safety, Quality, and Performance Improvement. There are approximately 70 new figures and 20 new tables. The adoption of full color dramatically improves the aesthetic appeal of every page. However, the biggest and most important change in the fifth edition is the “passing of the baton” to a distinguished and accomplished team of authors and editors. We were thrilled to learn that Drs. Butterworth, Mackey, and Wasnick would be succeeding us. The result of their hard work proves our enthusiasm was justified as they have taken Clinical Anesthesiology to a new level. We hope you, the readers, agree! G. Edward Morgan, Jr, MD Maged S. Mikhail, MD

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Preface Authors should be proud whenever a book is sufficiently successful to require a new edition. This is especially true when a book’s consistent popularity over time leads to the succession of the original authors by a new set of authors. This latter circumstance is the case for the fifth edition of what most of us call “Morgan and Mikhail.” We hope that you the reader will find this new edition as readable and useful as you have found the preceding four editions of the work. This fifth edition, while retaining essential elements of its predecessors, represents a significant revision of the text. Only those who have written a book of this size and complexity will understand just how much effort was involved. Entirely new subjects (eg, Perioperative Pain Management and Enhanced Outcomes) have been added, and many other topics that previously lived in multiple chapters have been moved and consolidated. We have tried to eliminate redundancies and contradictions. The number of illustrations devoted to regional anesthesia and analgesia has been greatly increased to adequately address the rapidly growing importance of this perioperative management topic. The clarity of the illustrations is also enhanced by the widespread use of color throughout the book. We hope the product of this endeavor provides readers with as useful an exercise as was experienced by the authors in composing it. • Key Concepts are listed at the beginning of each chapter and a corresponding numbered icon identifies the section(s) within the chapter in which each concept is discussed. These should help the reader focus on important concepts that underlie the core of anesthesiology.

• Case Discussions deal with clinical problems of current interest and are intended to stimulate discussion and critical thinking. • The suggested reading has been revised and updated to include pertinent Web addresses and references to clinical practice guidelines and practice parameters. We have not tried to provide a comprehensive list of references: we expect that most readers of this text would normally perform their own literature searches on medical topics using Google, PubMed, and other electronic resources. Indeed, we expect that an ever-increasing segment of our readers will access this text in one of its several electronic forms. • Multiple new illustrations and images have been added to this edition. Nonetheless, our goal remains the same as that of the first edition: “to provide a concise, consistent presentation of the basic principles essential to the modern practice of anesthesia.” We would like to thank Brian Belval, Harriet Lebowitz, and Marsha Loeb for their invaluable assistance. Despite our best intentions, various errors may have made their way into the fifth edition. We will be grateful to readers who report these to us at [email protected] so that we can correct them in reprints and future editions. John F. Butterworth IV, MD David C. Mackey, MD John D. Wasnick, MD, MPH

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SECTION II

Clinical Pharmacology C

Pharmacological Principles

H

A

P

T

E

R

7

KEY CONCEPTS 1

Drug molecules obey the law of mass action. When the plasma concentration exceeds the tissue concentration, the drug moves from the plasma into tissue. When the plasma concentration is less than the tissue concentration, the drug moves from the tissue back to plasma.

2

Most drugs that readily cross the blood–brain barrier (eg, lipophilic drugs like hypnotics and opioids) are avidly taken up in body fat.

3

Biotransformation is the chemical process by which the drug molecule is altered in the body. The liver is the primary organ of metabolism for drugs.

4

Small unbound molecules freely pass from plasma into the glomerular filtrate. The nonionized (uncharged) fraction of drug is

The clinical practice of anesthesiology is connected more directly than any other specialty to the science of clinical pharmacology. One would think, therefore, that the study of pharmacokinetics and pharmacodynamics would receive attention comparable to that given to airway assessment, choice of inhalation anesthetic for ambulatory surgery, or neuromuscular blockade in anesthesiology curricula and examinations. The frequent

reabsorbed in the renal tubules, whereas the ionized (charged) portion is excreted in urine. 5

Elimination half-life is the time required for the drug concentration to fall by 50%. For drugs described by multicompartment pharmacokinetics (eg, all drugs used in anesthesia), there are multiple elimination half-lives.

6

The offset of a drug’s effect cannot be predicted from half-lives. The contextsensitive half-time is a clinically useful concept to describe the rate of decrease in drug concentration and should be used instead of half-lives to compare the pharmacokinetic properties of intravenous drugs used in anesthesia.

misidentification or misuse of pharmacokinetic principles and measurements suggests that this is not the case.

PHARMACOKINETICS Pharmacokinetics defines the relationships among drug dosing, drug concentration in body fluids and tissues, and time. It consists of four linked 143

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SECTION II

Clinical Pharmacology

processes: absorption, distribution, biotransformation, and excretion.

Absorption Absorption defines the processes by which a drug moves from the site of administration to the bloodstream. There are many possible routes of drug administration: oral, sublingual, rectal, inhalational, transdermal, transmucosal, subcutaneous, intramuscular, and intravenous. Absorption is influenced by the physical characteristics of the drug (solubility, pKa, diluents, binders, and formulation), dose, and the site of absorption (eg, gut, lung, skin, muscle). Bioavailability is the fraction of the administered dose reaching the systemic circulation. For example, nitroglycerin is well absorbed by the gastrointestinal tract but has low bioavailability when administered orally. The reason is that nitroglycerin undergoes extensive first-pass hepatic metabolism as it transits the liver before reaching the systemic circulation. Oral drug administration is convenient, inexpensive, and relatively tolerant of dosing errors. However, it requires cooperation of the patient, exposes the drug to first-pass hepatic metabolism, and permits gastric pH, enzymes, motility, food, and other drugs to potentially reduce the predictability of systemic drug delivery. Nonionized (uncharged) drugs are more readily absorbed than ionized (charged) forms. Therefore, an acidic environment (stomach) favors the absorption of acidic drugs (A– + H+ → AH), whereas a more alkaline environment (intestine) favors basic drugs (BH+ → H+ + B). Most drugs are largely absorbed from the intestine rather than the stomach because of the greater surface area of the small intestine and longer transit duration. All venous drainage from the stomach and small intestine flows to the liver. As a result, the bioavailability of highly metabolized drugs may be significantly reduced by first-pass hepatic metabolism. Because the venous drainage from the mouth and esophagus flows into the superior vena cava rather than into the portal system, sublingual or buccal drug absorption bypasses the liver and first-pass metabolism. Rectal administration partly bypasses the portal system, and represents an alternative route in small children or patients who are unable to tolerate oral ingestion.

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However, rectal absorption can be erratic, and many drugs irritate the rectal mucosa. Transdermal drug administration can provide prolonged continuous administration for some drugs. However, the stratum corneum is an effective barrier to all but small, lipid-soluble drugs (eg, clonidine, nitroglycerin, scopolamine, fentanyl, and free-base local anesthetics [EMLA]). Parenteral routes of drug administration include subcutaneous, intramuscular, and intravenous injection. Subcutaneous and intramuscular absorption depend on drug diffusion from the site of injection to the bloodstream. The rate at which a drug enters the bloodstream depends on both blood flow to the injected tissue and the injectate formulation. Drugs dissolved in solution are absorbed faster than those present in suspensions. Irritating preparations can cause pain and tissue necrosis (eg, intramuscular diazepam). Intravenous injections completely bypass the process of absorption.

Distribution Once absorbed, a drug is distributed by the bloodstream throughout the body. Highly perfused organs (the so-called vessel-rich group) receive a disproportionate fraction of the cardiac output (Table 7–1). Therefore, these tissues receive a disproportionate amount of drug in the first minutes following drug administration. These tissues approach equilibration with the plasma concentration more quickly than less well perfused tissues due to the differences in

TABLE 71 Tissue group composition, relative body mass, and percentage of cardiac output. Tissue Group

Composition

Body Mass (%)

Cardiac Output (%)

Vessel-rich

Brain, heart, liver, kidney, endocrine glands

10

75

Muscle

Muscle, skin

50

19

Fat

Fat

20

6

Vessel-poor

Bone, ligament, cartilage

20

0

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CHAPTER 7 Pharmacological Principles

blood flow. However, less well perfused tissues such as fat and skin may have enormous capacity to absorb lipophilic drugs, resulting in a large reservoir of drug following long infusions. 1 Drug molecules obey the law of mass action. When the plasma concentration exceeds the concentration in tissue, the drug moves from the plasma into tissue. When the plasma concentration is less than the concentration in tissue, the drug moves from the tissue back to plasma. Distribution is a major determinant of endorgan drug concentration. The rate of rise in drug concentration in an organ is determined by that organ’s perfusion and the relative drug solubility in the organ compared with blood. The equilibrium concentration in an organ relative to blood depends only on the relative solubility of the drug in the organ relative to blood, unless the organ is capable of metabolizing the drug. Molecules in blood are either free or bound to plasma proteins and lipids. The free concentration equilibrates between organs and tissues. However, the equilibration between bound and unbound molecules is instantaneous. As unbound molecules of drug diffuse into tissue, they are instantly replaced by previously bound molecules. Plasma protein binding does not affect the rate of transfer directly, but it does affect relative solubility of the drug in blood and tissue. If the drug is highly bound in tissues, and unbound in plasma, then the relative solubility favors drug transfer into tissue. Put another way, a drug that is highly bound in tissue, but not in blood, will have a very large free drug concentration gradient driving drug into the tissue. Conversely, if the drug is highly bound in plasma and has few binding sites in the tissue, then transfer of a small amount of drug may be enough to bring the free drug concentration into equilibrium between blood and tissue. Thus, high levels of binding in blood relative to tissues increase the rate of onset of drug effect, because fewer molecules need to transfer into the tissue to produce an effective free drug concentration. Albumin binds many acidic drugs (eg, barbiturates), whereas α1-acid glycoprotein (AAG) binds basic drugs (local anesthetics). If the concentrations of these proteins are diminished or (typically less important) if the protein-binding sites are occupied

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by other drugs, then the relative solubility of the drugs in blood is decreased, increasing tissue uptake. Kidney disease, liver disease, chronic congestive heart failure, and malignancies decrease albumin production. Trauma (including surgery), infection, myocardial infarction, and chronic pain increase AAG levels. Pregnancy is associated with reduced AAG concentrations. Note that these changes will have very little effect on propofol, which is administered with its own binding molecules (the lipid in the emulsion). Lipophilic molecules can readily transfer between the blood and organs. Charged molecules are able to pass in small quantities into most organs. However, the blood–brain barrier is a special case. Permeation of the central nervous system by ionized drugs is limited by pericapillary glial cells and endo2 thelial cell tight junctions. Most drugs that readily cross the blood–brain barrier (eg, lipophilic drugs like hypnotics and opioids) are avidly taken up in body fat. The time course of distribution of drugs into peripheral tissues is complex and can only be assessed with computer models. Following intravenous bolus administration, rapid distribution of drug from the plasma into peripheral tissues accounts for the profound decrease in plasma concentration observed in the first few minutes. For each tissue, there is a point in time at which the apparent concentration in the tissue is the same as the concentration in the plasma. The redistribution phase (for each tissue) follows this moment of equilibration. During redistribution, drug returns from peripheral tissues back into the plasma. This return of drug back to the plasma slows the rate of decline in plasma drug concentration. Distribution generally contributes to rapid emergence by removing drug from the plasma for many minutes following administration of a bolus infusion. Following prolonged infusions, redistribution generally delays emergence as drug returns from tissue reservoirs to the plasma for many hours. The complex process of drug distribution into and out of tissues is one reason that half-lives are clinically useless. The offset of a drug’s clinical actions are best predicted by computer models using the context-sensitive half-time or decrement times. The context-sensitive half-time is the time required

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SECTION II

Clinical Pharmacology

for a 50% decrease in plasma drug concentration to occur following a pseudo steady-state infusion (in other words, an infusion that has continued long enough to yield nearly steady-state concentrations). Here the “context” is the duration of the infusion. The context-sensitive decrement time is a more generalized concept referring to any clinically relevant decreased concentration in any tissue, particularly the brain or effect site. The volume of distribution, Vd, is the apparent volume into which a drug has “distributed” (ie, mixed). This volume is calculated by dividing a bolus dose of drug by the plasma concentration at time 0. In practice, the concentration used to define the Vd is often obtained by extrapolating subsequent concentrations back to “0 time” when the drug was injected, as follows: Vd =

Bolus dose Concentration time0

The concept of a single Vd does not apply to any intravenous drugs used in anesthesia. All intravenous anesthetic drugs are better modeled with at least two compartments: a central compartment and a peripheral compartment. The behavior of many of these drugs is best described using three compartments: a central compartment, a rapidly equilibrating peripheral compartment, and a slowly equilibrating peripheral compartment. The central compartment may be thought of as including the blood and any ultra-rapidly equilibrating tissues such as the lungs. The peripheral compartment is composed of the other body tissues. For drugs with two peripheral compartments, the rapidly equilibrating compartment comprises the organs and muscles, while the slowly equilibrating compartment roughly represents distribution of the drug into fat and skin. These compartments are designated V1 (central), V2 (rapid distribution), and V3 (slow distribution). The volume of distribution at steady state, Vdss is the algebraic sum of these compartment volumes. V1 is calculated by the above equation showing the relationship between volume, dose, and concentration. The other volumes are calculated through pharmacokinetic modeling. A small Vdss implies that the drug has high aqueous solubility and will remain largely within the intravascular space. For example, the Vdss of

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pancuronium is about 15 L in a 70-kg person, indicating that pancuronium is mostly present in body water, with little distribution into fat. However, the typical anesthetic drug is lipophilic, resulting in a Vdss that exceeds total body water (approximately 40 L). For example, the Vdss for fentanyl is about 350 L in adults, and the Vdss for propofol may exceed 5000 L. Vdss does not represent a real volume but rather reflects the volume into which the drug would need to distribute to account for the observed plasma concentration given the dose that was administered.

Biotransformation 3 Biotransformation is

the chemical process by which the drug molecule is altered in the body. The liver is the primary organ of metabolism for drugs. The exception is esters, which undergo hydrolysis in the plasma or tissues. The end products of biotransformation are often (but not necessarily) inactive and water soluble. Water solubility allows excretion by the kidneys. Metabolic biotransformation is frequently divided into phase I and phase II reactions. Phase I reactions convert a parent compound into more polar metabolites through oxidation, reduction, or hydrolysis. Phase II reactions couple (conjugate) a parent drug or a phase I metabolite with an endogenous substrate (eg, glucuronic acid) to form watersoluble metabolites that can be eliminated in the urine or stool. Although this is usually a sequential process, phase I metabolites may be excreted without undergoing phase II biotransformation, and a phase II reaction can precede or occur without a phase I reaction. Hepatic clearance is the volume of blood or plasma (whichever was measured in the assay) cleared of drug per unit of time. The units of clearance are units of flow: volume per unit time. Clearance may be expressed in milliliters per minute, liters per hour, or any other convenient unit of flow. If every molecule of drug that enters the liver is metabolized, then hepatic clearance will equal liver blood flow. This is true for very few drugs, although it is very nearly the case for propofol. For most drugs, only a fraction of the drug that enters the liver is removed. The fraction removed is called the extraction ratio. The hepatic clearance can therefore be expressed as the liver blood flow times the

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CHAPTER 7 Pharmacological Principles

extraction ratio. If the extraction ratio is 50%, then hepatic clearance is 50% of liver blood flow. The clearance of drugs efficiently removed by the liver (ie, having a high hepatic extraction ratio) is proportional to hepatic blood flow. For example, because the liver removes almost all of the propofol that goes through it, if the hepatic blood flow doubles, then the clearance of propofol doubles. Induction of liver enzymes has no effect on propofol clearance, because the liver so efficiently removes all of the propofol that goes through it. Even severe loss of liver tissue, as occurs in cirrhosis, has little effect on propofol clearance. Drugs such as propofol have flow-dependent clearance. Many drugs have low hepatic extraction ratios and are slowly cleared by the liver. For these drugs, the rate-limiting step is not the flow of blood to the liver, but rather the metabolic capacity of the liver itself. Changes in liver blood flow have little effect on the clearance of such drugs. However, if liver enzymes are induced, then clearance will increase because the liver has more capacity to metabolize the drug. Conversely, if the liver is damaged, then less capacity is available for metabolism and clearance is reduced. Drugs with low hepatic extraction ratios thus have capacity-dependent clearance. The extraction ratios of methadone and alfentanil are 10% and 15% respectively, making these capacitydependent drugs.

Excretion Some drugs and many drug metabolites are excreted by the kidneys. Renal clearance is the rate of elimination of a drug from the body by kidney excretion. This concept is analogous to hepatic clearance, and similarly, renal clearance can be expressed as the renal blood flow times the renal extraction ratio. 4 Small unbound drugs freely pass from plasma into the glomerular filtrate. The nonionized (uncharged) fraction of drug is reabsorbed in the renal tubules, whereas the ionized (charged) portion is excreted in urine. The fraction of drug ionized depends on the pH; thus renal elimination of drugs that exist in ionized and nonionized forms depends in part on urinary pH. The kidney actively secretes some drugs into the renal tubules. Many drugs and drug metabolites pass from the liver into the intestine via the biliary system. Some

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drugs excreted into the bile are then reabsorbed in the intestine, a process called enterohepatic recirculation. Occasionally metabolites excreted in bile are subsequently converted back to the parent drug. For example, lorazepam is converted by the liver to lorazepam glucuronide. In the intestine, β-glucuronidase breaks the ester linkage, converting lorazepam glucuronide back to lorazepam.

Compartment Models Multicompartment models provide a mathematical framework that can be used to relate drug dose to changes in drug concentrations over time. Conceptually, the compartments in these models are tissues with a similar distribution time course. For example, the plasma and lungs are components of the central compartment. The organs and muscles, sometimes called the vessel-rich group, could be the second, or rapidly equilibrating, compartment. Fat and skin have the capacity to bind large quantities of lipophilic drug but are poorly perfused. These could represent the third, or slowly equilibrating, compartment. This is an intuitive definition of compartments, and it is important to recognize that the compartments of a pharmacokinetic model are mathematical abstractions that relate dose to observed concentration. A one-to-one relationship does not exist between any compartment and any organ or tissue in the body. Many drugs used in anesthesia are well described by a two-compartment model. This is generally the case if the studies used to characterize the pharmacokinetics do not include rapid arterial sampling over the first few minutes (Figure 7–1). Without rapid arterial sampling the ultra-rapid initial drop in plasma concentration immediately after a bolus injection is missed, and the central compartment volume is blended into the rapidly equilibrating compartment. When rapid arterial sampling is used in pharmacokinetic experiments, the results are generally a three-compartment model. In these cases the number of identifiable compartments is a function of the experimental design and not a characteristic of the drug. In compartmental models the instantaneous concentration at the time of a bolus injection is assumed to be the amount of the bolus divided by the central compartment volume. This is not

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Plasma concentration

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Distribution phase

Elimination phase

Time after dose IV bolus

FIGURE 71 Two-compartment model demonstrates the distribution phase (α phase) and the elimination phase (β phase). During the distribution phase, the drug moves from the central compartment to the peripheral compartment. The elimination phase consists of metabolism and excretion.

equilibrating compartment is no longer removing drug from the plasma. Instead, drug returns to the plasma from the rapidly equilibrating compartment. The reversed role of the rapidly equilibrating tissues from extracting drug to returning drug accounts for the slower rate of decline in plasma concentration in this intermediate phase. Eventually there is an even slower rate of decrease in plasma concentration, which is log-linear until the drug is completely eliminated from the body. This terminal log-linear phase occurs after the slowly equilibrating compartment shifts from net removal of drug from the plasma to net return of drug to the plasma. During this terminal phase the organ of elimination (typically the liver) is exposed to the body’s entire body drug load, which accounts for the very slow rate of decrease in plasma drug concentration during this final phase. The mathematical models used to describe a drug with two or three compartments are, respectively: Cp(t) = Ae − αt + Be−βt and

correct. If the bolus is given over a few seconds, the instantaneous concentration is 0, because the drug is all in the vein, still flowing to the heart. It takes only a minute or two for the drug to mix in the central compartment volume. This misspecification is common to conventional pharmacokinetic models. More physiologically based models, sometimes called front-end kinetic models, can characterize the initial delay in concentration. These models are useful only if the concentrations over the first few minutes are clinically important. After the first few minutes, front-end models resemble conventional compartmental models. In the first few minutes following initial bolus administration of a drug, the concentration drops very rapidly as the drug quickly diffuses into peripheral compartments. The decline is typically an order of magnitude over 10 minutes. For drugs with very rapid hepatic clearance (eg, propofol) or those that are metabolized in the blood (eg, remifentanil), metabolism contributes significantly to the rapid initial drop in concentration. Following this very rapid drop there is a period of slower decrease in plasma concentration. During this period, the rapidly

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Cp(t) = Ae −αt + Be −βt + Ce −γ t where Cp(t) equals plasma concentration at time t, and α, β, and γ are the exponents that characterize the very rapid (ie, very steep), intermediate, and slow (ie, log-linear) portions of the plasma concentration over time, respectively. Drugs described by two-compartment and three-compartment models will have two or three half-lives. Each half-life is calculated as the natural log of 2 (0.693), divided by the exponent. The coefficients A, B, and C represent the contribution of each of the exponents to the overall decrease in concentration over time. The two-compartment model is described by a curve with two exponents and two coefficients, whereas the three-compartment model is described by a curve with three exponents and three coefficients. The mathematical relationships among compartments, clearances, coefficients, and exponents are complex. Every coefficient and every exponent is a function of every volume and every clearance. 5 Elimination half-life is the time required for the drug concentration to fall by 50%. For drugs described by multicompartment pharmacokinetics

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CHAPTER 7 Pharmacological Principles

scale (Figure 7–2B), while the response is typically plotted either as the actual measured response (Figure 7–2A) or as a fraction of the baseline or maximum physiological measurement (Figure 7–2B). For our purposes here, basic pharmacodynamic properties are described in terms of concentration, but any metric of drug exposure (dose, area under the curve, etc) could be used. The shape of the relationship is typically sigmoidal, as shown in Figure 7–2. The sigmoidal

A 20 Drop in MAP (mm Hg)

(eg, all drugs used in anesthesia), there are multiple elimination half-lives, in other words the elimination 6 half-time is context dependent. The offset of a drug’s effect cannot be predicted from halflives. Moreover, one cannot easily determine how rapidly a drug effect will disappear simply by looking at coefficients, exponents, and half-lives. For example, the terminal half-life of sufentanil is about 10 h, whereas that of alfentanil is 2 h. This does not mean that recovery from alfentanil will be faster, because clinical recovery from clinical dosing will be influenced by all half-lives, not just the terminal one. Computer models readily demonstrate that recovery from an infusion lasting several hours will be faster when the drug administered is sufentanil than it will be when the infused drug is alfentanil. The time required for a 50% decrease in concentration depends on the duration or “context” of the infusion. The context-sensitive half-time, discussed earlier, captures this concept and should be used instead of half-lives to compare the pharmacokinetic properties of intravenous drugs used in anesthesia.

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Exposure–Response Relationships As the body is exposed to an increasing amount of a drug, the response to the drug similarly increases, typically up to a maximal value. This fundamental concept in the exposure versus response relationship is captured graphically by plotting exposure (usually dose or concentration) on the x axis as the independent variable, and the body’s response on the y axis as the dependent variable. Depending on the circumstances, the dose or concentration may be plotted on a linear scale (Figure 7–2A) or a logarithmic

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10

20 30 Dose (mg)

40

B 100 % of maximal response

Pharmacodynamics, the study of how drugs affect the body, involves the concepts of potency, efficacy, and therapeutic window. Pharmacokinetic models can range from entirely empirical dose versus response relationships to mechanistic models of ligand–receptor binding. The fundamental pharmacodynamic concepts are captured in the relationship between exposure to a drug and physiological response to the drug, often called the dose–response or concentration–response relationship.

75

50

25

1

10 Dose (mg)

100

1000

FIGURE 72 The shape of the dose–response curve depends on whether the dose or steady-state plasma concentration (Ccpss) is plotted on a linear A: or logarithmic B: scale. MAP, mean arterial pressure.

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shape reflects the observation that often a certain amount of drug must be present before there is any measurable physiological response. Thus, the left side of the curve is flat until the drug concentration reaches a minimum threshold. The right side is also flat, reflecting the maximum physiological response of the body, beyond which the body simply cannot respond to additional drug (with the possible exception of eating and weight). Thus, the curve is flat on both the left and right sides. A sigmoidal curve is required to connect the baseline to the asymptote, which is why sigmoidal curves are ubiquitous when modeling pharmacodynamics The sigmoidal relationship between exposure and response is defined by one of two interchangeable relationships: Effect = E0 + E max

Cγ C50γ + C γ

or Effect = E0 + (E max − E 0 )

Cγ C + Cγ γ 50

In both cases, E0 is the baseline effect in the absence of drug, C is drug concentration, C50 is the concentration associated with half-maximal effect, and γ describes the steepness of the concentration versus response relationship. For the first equation, Emax is the maximum change from baseline. In the second equation, Emax is the maximum physiological measurement, not the maximum change from baseline. Once defined in this fashion, each parameter of the pharmacodynamic model speaks to the specific concepts mentioned earlier. Emax is related to the intrinsic efficacy of a drug. Highly efficacious drugs have a large maximum physiological effect, characterized by a large Emax. For drugs that lack efficacy, Emax will equal E0. C50 is a measure of drug potency. Highly potent drugs have a low C50; thus small amounts produce the drug effect. Drugs lacking potency have a high C50, indicating that a large amount of drug is required to achieve the drug effect. The parameter γ indicates steepness of the relationship between concentration and effect. A γ value less than 1 indicates a very gradual increase in drug effect with increasing concentration. A

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γ value greater than 4 suggests that once drug effect is observed, small increases in drug concentration produce large increases in drug effect until the maximum effect is reached. The curve described above represents the relationship of drug concentration to a continuous physiological response. The same relationship can be  used to characterize the probability of a binary (yes/no) response to a drug dose: Probability = P0 + (P max − P 0 )

Cγ C + Cγ γ 50

In this case, the probability (P) ranges from 0 (no chance) to 1 (certainty). P0 is the probability of a “yes” response in the absence of drug. Pmax is the maximum probability, necessarily less than or equal to 1. As before, C is the concentration, C50 is the concentration associated with half-maximal effect, and γ describes the steepness of the concentration versus response relationship. Half-maximal effect is the same as 50% probability of a response when P0 is 0 and Pmax is 1. The therapeutic window for a drug is the range between the concentration associated with a desired therapeutic effect and the concentration associated with a toxic drug response. This range can be measured either between two different points on the same concentration versus response curve, or the distance between two distinct curves. For a drug such as sodium nitroprusside, a single concentration versus response curve defines the relationship between concentration and decrease in blood pressure. The therapeutic window might be the difference in the concentration producing a desired 20% decrease in blood pressure and a toxic concentration that produces a 60% decrease in blood pressure. However, for a drug such as lidocaine, the therapeutic window might be the difference between the C50 for local anesthesia and the C50 for lidocaineinduced seizures, the latter being a separate concentration versus response relationship. The therapeutic index is the C50 for toxicity divided by the C50 for the desired therapeutic effect. Because of the risk of ventilatory and cardiovascular depression (even at concentrations only slightly greater than those producing anesthesia), most inhaled and intravenous hypnotics are considered to have very low therapeutic indices relative to other drugs.

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CHAPTER 7 Pharmacological Principles

then we can solve for receptor occupancy as:

Drug Receptors Drug receptors are macromolecules, typically proteins, that bind a drug (agonist) and mediate the drug response. Pharmacological antagonists reverse the effects of the agonist but do not otherwise exert an effect of their own. Competitive antagonism occurs when the antagonist competes with the agonist for the binding site, each potentially displacing the other. Noncompetitive antagonism occurs when the antagonist, through covalent binding or another process, permanently impairs the drug’s access to the receptor. The drug effect is governed by the fraction of receptors that are occupied by an agonist. That fraction is based on the concentration of the drug, the concentration of the receptor, and the strength of binding between the drug and the receptor. This binding is described by the law of mass action, which states that the reaction rate is proportional to the concentrations of the reactants: [D][RU]

k on

[DR]

koff where [D] is the concentration of the drug, [RU] is the concentration of unbound receptor, and [DR] is the concentration of bound receptor. The rate constant kon defines the rate of ligand binding to the receptor. The rate constant koff defines the rate of ligand unbinding from the receptor. According to the law of mass action, the rate of receptor binding, d[DR]/dt is: d[DR] = [D][RU] k on − [DR]k off dt Steady state occurs almost instantly. Because the rate of formation at steady state is 0, it follows that: [D][RU] k on = [DR]k off In this equation, kd is the dissociation rate constant, defined as kon /koff . If we define f, fractional receptor occupancy, as: [DR] [DR] + [RU]

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151

f=

[D] kd + [D]

The receptors are half occupied when [D] = kd. Thus, kd is the concentration of drug associated with 50% receptor occupancy. Receptor occupancy is only the first step in mediating drug effect. Binding of the drug to the receptor can trigger a myriad of subsequent steps, including opening or closing of an ion channel, activation of a G protein, activation of an intracellular kinase, direct interaction with a cellular structure, or direct binding to DNA. Like the concentration versus response curve, the shape of the curve relating fractional receptor occupancy to drug concentration is intrinsically sigmoidal. However, the concentration associated with 50% receptor occupancy and the concentration associated with 50% of maximal drug effect are not necessarily the same. Maximal drug effect could occur at very low receptor occupancy, or (for partial agonists) at greater than 100% receptor occupancy. Prolonged binding and activation of a receptor by an agonist may lead to hyporeactivity (“desensitization”) and tolerance. If the binding of an endogenous ligand is chronically blocked, then receptors may proliferate resulting in hyperreactivity and increased sensitivity.

SUGGESTED READING Bauer LA (Ed): Applied Clinical Pharmacokinetics, 2nd ed. McGraw-Hill, 2008: Chaps 1, 2. Brunton LL, Chabner BA, Knollman BC (Eds): Goodman & Gilman’s The Pharmacological Basis of Therapeutics, 12th ed. McGraw-Hill, 2010: Chap 2. Keifer J, Glass P: Context-sensitive half-time and anesthesia: How does theory match reality? Curr Opin Anaesthesiol 1999;12:443. Shargel L, Yu AB, Wu-Pong S (Eds): Applied Biopharmaceutics & Pharmacokinetics, 6th ed. McGraw-Hill, 2012.

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C

Peripheral Nerve Blocks Sarah J. Madison, MD and Brian M. Ilfeld, MD, MS

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KEY CONCEPTS 1

In addition to potent analgesia, regional anesthesia may lead to reductions in the stress response, systemic analgesic requirements, opioid-related side effects, general anesthesia requirements, and possibly the incidence of chronic pain.

6

The axillary, musculocutaneous, and medial brachial cutaneous nerves branch from the brachial plexus proximal to the location in which local anesthetic is deposited during an axillary nerve block, and thus are usually spared.

2

Regional anesthetics should be administered in an area where standard hemodynamic monitors, supplemental oxygen, and resuscitative medications and equipment are readily available.

7

3

Local anesthetic may be deposited at any point along the brachial plexus, depending on the desired block effects: interscalene for shoulder and proximal humerus surgical procedures; and supraclavicular, infraclavicular, and axillary for surgeries distal to the mid-humerus.

Often it is necessary to anesthetize a single terminal nerve, either for minor surgical procedures with a limited field or as a supplement to an incomplete brachial plexus block. Terminal nerves may be anesthetized anywhere along their course, but the elbow and the wrist are the two most favored sites.

8

Intravenous regional anesthesia, also called a Bier block, can provide intense surgical anesthesia for short surgical procedures (45–60 min) on an extremity.

9

A femoral nerve block alone will seldom provide surgical anesthesia, but it is often used to provide postoperative analgesia for hip, thigh, knee, and ankle procedures.

4

5

A properly performed interscalene block invariably blocks the ipsilateral phrenic nerve, so careful consideration should be given to patients with severe pulmonary disease or preexisting contralateral phrenic nerve palsy. Brachial plexus block at the level of the cords provides excellent anesthesia for procedures at or distal to the elbow. The upper arm and shoulder are not anesthetized with this approach. As with other brachial plexus blocks, the intercostobrachial nerve (T2 dermatome) is spared.

10 Posterior lumbar plexus blocks are useful

for surgical procedures involving areas innervated by the femoral, lateral femoral cutaneous, and obturator nerves. Complete anesthesia of the knee can be attained with a proximal sciatic nerve block. 11 Blockade of the sciatic nerve may occur

anywhere along its course and is indicated for surgical procedures involving the hip, thigh, knee, lower leg, and foot. —Continued next page 975

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Continued— 12 Popliteal nerve blocks provide excellent

coverage for foot and ankle surgery, while sparing much of the hamstring muscles, allowing lifting of the foot with knee flexion, thus easing ambulation. All sciatic nerve blocks fail to provide complete anesthesia for the cutaneous medial leg and ankle joint capsule, but when a saphenous (or femoral) block is added, complete anesthesia below the knee is provided. 13 A complete ankle block requires a series of

five nerve blocks, but the process may be streamlined to minimize needle insertions. All five injections are required to anesthetize the entire foot; however, many surgical procedures involve only a few terminal nerves, and only affected nerves should be blocked.

An understanding of regional anesthesia anatomy and techniques is required of the well-rounded anesthesiologist. Although anatomic relationships have not changed over time, our ability to identify them has evolved. From the paresthesia-seeking techniques described by Winnie in the mid-twentieth century, to the popularization of the nerve stimulator, to the introduction of ultrasound guidance, anesthesiologists and their patients have benefitted from technology’s evolution. The field of regional anesthesia has accordingly expanded to one that addresses not only the intraoperative concerns of the anesthesiologist, but also longer term perioperative pain management. 1 In addition to potent analgesia, regional anesthesia may lead to reductions in the stress response, systemic analgesic requirements, opioid-related side effects, general anesthesia requirements, and possibly the development of chronic pain.

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14 Intercostal blocks result in the highest

blood levels of local anesthetic per volume injected of any block in the body, and care must be taken to avoid toxic levels of local anesthetic. 15 The thoracic paravertebral space is

defined posteriorly by the superior costotransverse ligament, anterolaterally by the parietal pleura, medially by the vertebrae and the intervertebral foramina, and inferiorly and superiorly by the heads of the ribs. 16 The subcostal (T12), ilioinguinal (L1),

and iliohypogastric (L1) nerves are targeted in the transversus abdominus plane block, providing anesthesia to the ipsilateral lower abdomen below the umbilicus.

PATIENT SELECTION The selection of a regional anesthetic technique is a process that begins with a thorough history and physical examination. Although many patients are candidates for regional anesthesia/analgesia, as with any medical procedure a risk–benefit analysis must be performed. The risk–benefit ratio often favors regional anesthesia in patients with multiple comorbidities for whom a general anesthetic carries a greater risk. In addition, patients intolerant to systemic analgesics (eg, those with obstructive sleep apnea or at high risk for nausea) may benefit from the opioid-sparing effects of a regional analgesic. Patients with chronic pain and opioid tolerance may receive optimal analgesia with a continuous peripheral nerve block (so-called perineural local anesthetic infusion). A comprehensive knowledge of anatomy and an understanding of the planned surgical procedure are

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CHAPTER 46 Peripheral Nerve Blocks

important for selection of the appropriate regional anesthetic technique. If possible, discussion with the surgeon about various considerations (tourniquet placement, bone grafting, projected surgical duration) is ideal. Also, knowing the anticipated course of recovery and anticipated level of postoperative pain will often influence specific decisions regarding a regional anesthetic technique (eg, a single-injection versus continuous peripheral nerve block).

RISKS & CONTRAINDICATIONS Patient cooperation and participation are key to the success and safety of every regional anesthetic procedure; patients who are unable to remain still for a procedure may be exposed to increased risk. Examples include younger pediatric patients and some developmentally delayed individuals, as well as patients with dementia or movement disorders. Bleeding disorders and pharmacological anticoagulation heighten the risk of local hematoma or hemorrhage, and this risk must be balanced against the possible benefits of regional block. Specific peripheral nerve block locations warranting the most concern are posterior lumbar plexus and paravertebral blocks owing to their relative proximity to the retroperitoneal space and neuraxis, respectively. Placement of a block needle through a site of infection can theoretically track infectious material into the body, where it poses a risk to the target nerve tissue and surrounding structures. Therefore, the presence of a local infection is a relative contraindication to performing a peripheral nerve block. Indwelling perineural catheters can serve as a nidus of infection; however, the risk in patients with systemic infection remains unknown. Although nerve injury is always a possibility with a regional anesthetic, some patients are at increased risk. Individuals with a preexisting condition (eg, peripheral neuropathy or previous nerve injury) may have a higher incidence of complications, including prolonged or permanent sensorimotor block. The precise mechanisms have yet to be clearly defined but may involve local ischemia from high injection pressure or vasoconstrictors, a neurotoxic effect of local anesthetics, or direct trauma to nerve tissue.

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Other risks associated with regional anesthesia include local anesthetic toxicity from intravascular injection or perivascular absorption. In the event of a local anesthetic toxic reaction, seizure activity and cardiovascular collapse may occur. Supportive measures should begin immediately, including solicitation of assistance with a code blue, the initiation of cardiopulmonary resuscitation, lipid emulsion administration to sequester local anesthetic, and preparation for cardiopulmonary bypass. Site-specific risks should also be considered for each individual patient. In a patient with severe pulmonary compromise or hemidiaphragmatic paralysis, for example, a contralateral interscalene or deep cervical plexus block with resultant phrenic nerve block could be disastrous.

CHOICE OF LOCAL ANESTHETIC The decision about which local anesthetic to employ for a particular nerve block depends on the desired onset, duration, and relative blockade of sensory and motor fibers. Potential for toxicity should be considered, as well as site-specific risks. A detailed discussion of local anesthetics is provided elsewhere (see Chapter 16).

PREPARATION 2 Regional anesthetics should be administered

in an area where standard hemodynamic monitors, supplemental oxygen, and resuscitative medications and equipment are readily available. Patients should be monitored with pulse oximetry, noninvasive blood pressure, and electrocardiography; measurement of end-tidal CO2 and fraction of inspired oxygen (Fio2) should also be available. Positioning should be ergonomically favorable for the practitioner and comfortable for the patient. Intravenous premedication should be employed to allay anxiety and minimize discomfort. A relatively short-acting benzodiazepine and opioid are most often used and should be titrated for comfort while ensuring that patients respond to verbal cues. Sterile technique should be strictly observed.

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FIGURE 461 A field block targets terminal cutaneous nerves, such as the intercostobrachial nerve.

BLOCK TECHNIQUES

Paresthesia Technique

Field Block Technique

Formerly the mainstay of regional anesthesia, this technique is now rarely used for nerve localization. Using known anatomic relationships and surface landmarks as a guide, a block needle is placed in proximity to the target nerve or plexus. When a needle makes direct contact with a sensory nerve, a paresthesia (abnormal sensation) is elicited in its area of sensory distribution.

A field block is a local anesthetic injection that targets terminal cutaneous nerves (Figure 46–1). Field blocks are used commonly by surgeons to minimize incisional pain and may be used as a supplementary technique or as a sole anesthetic for minor, superficial procedures. Anesthesiologists often use field blocks to anesthetize the superficial cervical plexus for procedures involving the neck or shoulder; the intercostobrachial nerve for surgery involving the medial upper extremity proximal to the elbow (in combination with a brachial plexus nerve block); and the saphenous nerve for surgery involving the medial leg or ankle joint (in combination with a sciatic nerve block). Field blocks may be undesirable in cases where they obscure the operative anatomy, or where local tissue acidosis from infection prevents effective local anesthetic functioning.

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Nerve Stimulation Technique For this technique, an insulated needle concentrates electrical current at the needle tip, while a wire attached to the needle hub connects to a nerve stimulator—a battery-powered machine that emits a small amount (0–5 mA) of electric current at a set interval (usually 1 or 2 Hz). A grounding electrode is attached to the patient to complete the circuit (Figure 46–2). When the insulated needle is placed in

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CHAPTER 46 Peripheral Nerve Blocks

979

technique, 30–40 mL of anesthetic is usually injected with gentle aspiration between divided doses.

Ultrasound Technique

FIGURE 462 A nerve stimulator delivers a small amount of electric current to the block needle to facilitate nerve localization. proximity to a motor nerve, muscle contractions are induced, and local anesthetic is injected. Although it is common to redirect the block needle until muscle contractions occur at a current less than 0.5 mA, there is scant evidence to support this specific current in all cases. Similarly, although some have suggested that muscle contraction with current less than 0.2 mA implies intraneural needle placement, there is little evidence to support this specific cutoff. Nonetheless, most practitioners inject local anesthetic when current between 0.2 and 0.5 mA results in a muscle response. For most blocks using this

Linear

Ultrasound for peripheral nerve localization is becoming increasingly popular; it may be used alone or combined with other modalities such as nerve stimulation. Ultrasound uses high-frequency (1–20 MHz) sound waves emitted from piezoelectric crystals that travel at different rates through tissues of different densities, returning a signal to the transducer. Depending on the amplitude of signal received, the crystals deform to create an electronic voltage that is converted into a two-dimensional grayscale image. The degree of efficiency with which sound passes through a substance determines its echogenicity. Structures and substances through which sound passes easily are described as hypoechoic and appear dark or black on the ultrasound screen. In contrast, structures reflecting more sound waves appear brighter—or white—on the ultrasound screen, and are termed hyperechoic. The optimal transducer varies depending upon the depth of the target nerve and approach angle of the needle relative to the transducer (Figure 46–3). High-frequency transducers provide a high-resolution picture with a relatively clear image but

Curvilinear

No image Poor Good

FIGURE 463 A linear probe offers higher resolution with less penetration. A curvilinear probe provides better penetration with lower resolution.

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A

B

FIGURE 464 In-plane (A) and out-of-plane (B) ultrasound approaches. offer poor tissue penetration and are therefore used predominantly for more superficial nerves. Lowfrequency transducers provide an image of poorer quality but have better tissue penetration and are therefore used for deeper structures. Transducers with a linear array offer an undistorted image and are therefore often the first choice among practitioners. However, for deeper target nerves that require a more acute angle between the needle and long-axis of the transducer, a curved array (curvilinear) transducer will maximize returning ultrasound waves, providing the optimal needle image (Figure 46–3). Nerves are best imaged in cross-section, where they have a characteristic honeycomb appearance (“short axis”). Needle insertion can pass either parallel (“in plane”) or not parallel (“out of plane”) to the plane of the ultrasound waves (Figure 46–4). Unlike nerve stimulation alone, ultrasound guidance allows for a variable volume of local anesthetic to be injected, with the final amount determined by what is observed under direct vision. This technique usually results in a far lower injected volume of local anesthetic (10–30 mL).

Continuous Peripheral Nerve Blocks Also termed perineural local anesthetic infusion, continuous peripheral nerve blocks involve the

Morg_Ch46_0975-1022.indd 980

placement of a percutaneous catheter adjacent to a peripheral nerve, followed by local anesthetic administration to prolong a nerve block (Figure 46–5). Potential advantages appear to depend on successfully improving analgesia and include reductions in resting and dynamic pain, supplemental analgesic requirements, opioid-related side effects, and sleep disturbances. In some cases patient satisfaction, ambulation, and functioning may be improved; an accelerated resumption of passive joint range-of-motion realized; and reduced time until discharge-readiness as well as actual discharge from the hospital or rehabilitation center achieved. There are many types of catheters, including nonstimulating and stimulating, flexible and more rigid, through-the-needle and over-the-needle. Currently, there is little evidence that a single design results in superior effects. Local anesthetic is the primary medication infused, as adjuvants do not add benefits to perineural infusions (unlike single-injection peripheral nerve blocks). Longacting local anesthetics (eg, ropivacaine) are more commonly used as they provide a more favorable sensory-to-motor block ratio (optimizing analgesia while minimizing motor block). In an attempt to further minimize any induced motor block, dilute

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FIGURE 465 Placement of a percutaneous catheter adjacent to a peripheral nerve.

local anesthetic (0.1–0.2%) is often infused; however, recent evidence suggests that it is the total dose, and not concentration, that determines the majority of block effects. Unlike single-injection peripheral nerve blocks, no adjuvant added to a perineural local anesthetic infusion has been demonstrated to be of benefit. The local anesthetic may be administered exclusively as repeated bolus doses or a basal infusion, or as a combination of the two methods. Using a small, portable infusion pump (Figure 46–6), continuous peripheral nerve blocks may be provided on an ambulatory basis. As with all medical procedures, there are potential risks associated with continuous peripheral nerve blocks. Therefore, these infusions are usually reserved for patients having procedures expected to result in postoperative pain that is difficult to control with oral analgesics and will not resolve in less time than the duration of a singleinjection peripheral nerve block. Serious complications, which are relatively rare, include systemic local anesthetic toxicity, catheter retention, nerve injury, infection, and retroperitoneal hematoma

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formation. In addition, a perineural infusion affecting the femoral nerve increases the risk of falling, although to what degree and by what specific mechanism (eg, sensory, motor, or proprioception deficits) remain unknown.

UPPER EXTREMITY PERIPHERAL NERVE BLOCKS Brachial Plexus Anatomy The brachial plexus is formed by the union of the anterior primary divisions (ventral rami) of the fifth through the eighth cervical nerves and the first thoracic nerves. Contributions from C4 and T2 are often minor or absent. As the nerve roots leave the intervertebral foramina, they converge, forming trunks, divisions, cords, branches, and then finally terminal nerves. The three distinct trunks formed between the anterior and middle scalene muscles are termed superior, middle, and inferior based on their vertical orientation. As the trunks pass over the lateral border of the first rib

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B

FIGURE 466 Elastomeric (A) and electronic (B) portable infusion pumps.

and under the clavicle, each trunk divides into anterior and posterior divisions. As the brachial plexus emerges below the clavicle, the fibers combine again to form three cords that are named according to their relationship to the axillary artery: lateral, medial, and posterior. At the lateral border of the pectoralis minor muscle, each cord gives off a large branch before ending as a major terminal nerve. The lateral cord gives off the lateral branch of the median nerve and terminates as the musculocutaneous nerve; the medial cord gives off the medial branch of the median nerve and terminates as the ulnar nerve; and the posterior cord gives off the axillary nerve and terminates as the 3 radial nerve. Local anesthetic may be deposited at any point along the brachial plexus, depending on the desired block effects (Figure 46–7): interscalene for shoulder and proximal humerus surgical procedures; and supraclavicular, infraclavicular, and axillary for surgeries distal to the mid-humerus.

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Interscalene Block An interscalene brachial plexus block is indicated for procedures involving the shoulder and upper arm (Figure 46–8). Roots C5–7 are most densely blocked with this approach; and the ulnar nerve originating from C8 and T1 may be spared. Therefore, interscalene blocks are not appropriate for surgery at or distal to the elbow. For complete surgical anesthesia of the shoulder, the C3 and C4 cutaneous branches may need to be supplemented with a superficial cervical plexus block or local infiltration. Contraindications to an interscalene block include local infection, severe coagulopathy, local 4 anesthetic allergy, and patient refusal. A properly performed interscalene block invariably blocks the ipsilateral phrenic nerve (completely for nerve stimulation techniques; unclear for ultrasound-guided techniques), so careful consideration should be given to patients with severe pulmonary disease or preexisting contralateral phrenic nerve palsy. The hemidiaphragmatic paresis may result in

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CHAPTER 46 Peripheral Nerve Blocks

Anterior (palmar) view

Supraclavicular nerves (from cervical plexus)

Axillary nerve Superior lateral brachial cutaneous nerve

Suprascapular nerve

Radial nerve Inferior lateral brachial cutaneous nerve

Intercostobrachial and medial brachial cutaneous nerve

Lateral antebrachial cutaneous nerve (terminal part of musculocutaneous nerve)

Radial nerve Superficial branch Median nerve Palmar and palmar digital branches

Posterior (dorsal) view

Medial antebrachial cutaneous nerve

Ulnar nerve Palmar and palmar digital branches

Ulnar nerve Dorsal branch, dorsal digital branches, and proper palmar digital branches

Axillary nerve Superior lateral brachial cutaneous nerve Radial nerve Posterior brachial cutaneous nerve, inferior lateral brachial cutaneous nerve, and posterior antebrachial cutaneous nerve Lateral antebrachial cutaneous nerve (terminal part of musculocutaneous nerve) Radial nerve Superficial branch and dorsal digital branches Median nerve Proper palmar digital branches

FIGURE 467 The location of local anesthetic deposition along the brachial plexus depends on the desired effects of the block.

dyspnea, hypercapnia, and hypoxemia. A Horner’s syndrome (myosis, ptosis, and anhidrosis) may result from proximal tracking of local anesthetic and blockade of sympathetic fibers to the cervicothoracic ganglion. Recurrent laryngeal nerve involvement often induces hoarseness. In a patient with contralateral vocal cord paralysis, respiratory distress may ensue. Other site-specific risks include vertebral artery injection (suspect if immediate seizure activity is observed), spinal or epidural injection, and pneumothorax. Even 1 mL of local anesthetic delivered into the vertebral artery may induce a seizure. Similarly, intrathecal, subdural, and epidural local anesthetic spread is possible.

Morg_Ch46_0975-1022.indd 983

Lastly, pneumothorax is possible due to the close proximity of the pleura. The brachial plexus passes between the anterior and middle scalene muscles at the level of the cricoid cartilage, or C6 (Figure 46–9). Palpation of the interscalene groove is usually accomplished with the patient supine and the head rotated 30° or less to the contralateral side. The external jugular vein often crosses the interscalene groove at the level of the cricoid cartilage. The interscalene groove should not be confused with the groove between the sternocleidomastoid and the anterior scalene muscle, which lies further anterior. Having the patient lift and turn the head against resistance often helps delineate the

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Regional Anesthesia & Pain Management

Interscalene

Nerves or plexus roots C4 Trunks C5

Divisions C6 Cords Upper trunk

Main branches ord ral c

Late

ior ster

cord

k

C7

run

et ddl

Mi

C8

Po

Lower trunk ord

T1

lc edia

M

FIGURE 468 An interscalene block is appropriate for shoulder and proximal humerus procedures. The ventral rami of C5–C8 and T1 form the brachial plexus.

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CHAPTER 46 Peripheral Nerve Blocks

985

Cricoid cartilage

FIGURE 469 The brachial plexus passes between the anterior and middle scalene muscles at the level of the cricoid cartilage, or C6.

anatomy. If surgical anesthesia is desired for the entire shoulder, the intercostobrachial nerve must usually be targeted separately with a field block since it originates from T2 and is not affected with an interscalene block. Interscalene perineural infusions provide potent analgesia following shoulder surgery.

A. Nerve Stimulation A relatively short (5-cm) insulated needle is usually employed. The interscalene groove is palpated using the nondominant hand, pressing firmly to stabilize the skin against the underlying structures (Figure 46–10). After the skin is anesthetized, the block needle is inserted at a slightly medial and caudad angle and advanced to optimally elicit a motor response of the deltoid or biceps muscles (suggesting stimulation of the superior trunk). A motor response of the diaphragm indicates that the needle is placed in too anterior a direction; a motor response of the trapezius or serratus anterior muscles indicates that the needle is placed in too posterior a direction. If bone (transverse process) is contacted, the needle should be redirected more anteriorly. Aspiration of arterial blood should raise concern for vertebral or carotid artery puncture; the needle should be

Morg_Ch46_0975-1022.indd 985

FIGURE 4610 Interscalene block using nerve stimulation.

withdrawn, pressure held for 3–5 min, and landmarks reassessed.

B. Ultrasound A needle in-plane or out-of-plane technique may be used, and an insulated needle attached to a nerve stimulator can be used to confirm the accuracy of the targeted structure. For both techniques, after identification of the sternocleidomastoid muscle and interscalene groove at the approximate level of C6, a high-frequency linear transducer is placed perpendicular to the course of the interscalene muscles (short axis; Figure 46–11). The brachial plexus and anterior and middle scalene muscles should be visualized in cross-section (Figure 46–12). The brachial plexus at this level appears as three to five hypoechoic circles. The carotid artery and internal jugular vein may be seen lying anterior to the anterior scalene muscle; the sternocleidomastoid is visible superficially as it tapers to form its lateral edge. For an out-of-plane technique, the block needle is inserted just cephalad to the transducer and advanced in a caudal direction toward the visualized plexus. After careful aspiration for nonappearance of blood, local anesthetic (hypoechoic) spread

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middle scalene muscle until it has passed through the fascia anteriorly into the interscalene groove. The needle tip and shaft should be visualized during the entire block performance. Depending on visualized spread relative to the target nerve(s), a lower volume (10 mL) may be employed for postoperative analgesia, whereas a larger volume (20–30 mL) is commonly used for surgical anesthesia.

Supraclavicular Block

Clavicle

FIGURE 4611 Ultrasound-guided interscalene block (in-plane technique). should occur adjacent to (sometimes surrounding) the plexus. For an in-plane technique, the needle is inserted just posterior to the ultrasound transducer in a direction exactly parallel to the ultrasound beam. A longer block needle (8 cm) is usually necessary. It may be helpful to have the patient turn slightly laterally with the affected side up to facilitate manipulation of the needle. The needle is advanced through the

Once described as the “spinal of the arm,” a supraclavicular block offers dense anesthesia of the brachial plexus for surgical procedures at or distal to the elbow (Figure 46–13). Historically, the supraclavicular block fell out of favor due to the high incidence of complications (namely, pneumothorax) that occurred with paresthesia and nerve stimulator techniques. It has seen a resurgence in recent years as the use of ultrasound guidance has theoretically improved safety. The supraclavicular block does not reliably anesthetize the axillary and suprascapular nerves, and thus is not ideal for shoulder surgery. Sparing of distal branches, particularly the ulnar nerve, may occur. Supraclavicular perineural catheters provide inferior analgesia compared with infraclavicular infusion and are often displaced due to a lack of muscle mass to aid catheter retention.

SCM N ASM

N

MSM

N

FIGURE 4612 Interscalene block. Ultrasound image of the brachial plexus in the interscalene groove. ASM, anterior scalene muscle; MSM, middle scalene muscle; SCM, sternocleidomastoid; N, brachial plexus nerve roots in cross-section.

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987

CHAPTER 46 Peripheral Nerve Blocks

Supraclavicular

Nerves or plexus roots C4 Trunks C5

Divisions C6 Cords Upper trunk

Main branches ord ral c

Late

ior ster

cord

Po

k

C7

run

et ddl

Mi

C8 Lower trunk

ord

T1

lc edia

M

FIGURE 4613 A supraclavicular block can provide dense anesthesia for procedures at or distal to the elbow. Light blue shading indicates regions of variable blockade; purple shading indicates regions of more reliable blockade.

Morg_Ch46_0975-1022.indd 987

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SECTION IV

Regional Anesthesia & Pain Management

Many of the same precautions that are taken with patient selection for an interscalene block should be exercised with a supraclavicular block. Nearly half of patients undergoing supraclavicular block will experience ipsilateral phrenic nerve palsy, although this incidence may be decreased by using ultrasound guidance, allowing use of a minimal volume of local anesthetic. Horner’s syndrome and recurrent laryngeal nerve palsy may also occur. Pneumothorax and subclavian artery puncture, although theoretically less likely under ultrasound guidance, remain potential risks.

A. Ultrasound The patient should be supine with the head turned 30o toward the contralateral side. A linear, highfrequency transducer is placed in the supraclavicular fossa superior to the clavicle and angled slightly toward the thorax (Figure 46–14). The subclavian artery should be easily identified. The brachial plexus appears as multiple hypoechoic disks just superficial and lateral to the subclavian artery (Figure 46–15). The first rib should also be identified as a hyperechoic line just deep to the artery. Pleura may be identified adjacent to the rib, and can be distinguished from bone by its movement with breathing. For an out-of-plane technique, a short, 22-gauge blunt-tipped needle is used. The skin is anesthetized, and the needle inserted just cephalad to the ultrasound transducer in a posterior and caudad

FIGURE 4614 Ultrasound probe placement for supraclavicular block (in-plane technique). direction. After careful aspiration for the nonappearance of blood, 30–40 mL of local anesthetic s injected in 5-mL increments while visualizing local anesthetic spread around the brachial plexus. For an in-plane technique, a longer needle may be necessary. The needle is inserted lateral to the transducer in a direction parallel to the ultrasound beam. The needle is advanced medially toward the subclavian artery until the tip is visualized near the brachial plexus just lateral and superficial to the

N N SA

N R

FIGURE 4615 Supraclavicular block. Ultrasound image of the brachial plexus in the supraclavicular fossa. SA, subclavian artery; R, rib; N, brachial plexus in cross-section.

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CHAPTER 46 Peripheral Nerve Blocks

artery. Local anesthetic spread should be visualized surrounding the plexus after careful aspiration and incremental injection, which often requires injections in multiple locations and a highly variable volume (20–30 mL).

Infraclavicular Block 5 Brachial plexus block at the level of the

cords provides excellent anesthesia for procedures at or distal to the elbow (Figure 46–16). The upper arm and shoulder are not anesthetized with this approach. As with other brachial plexus blocks, the intercostobrachial nerve (T2 dermatome) is spared. Site-specific risks of the infraclavicular approach include vascular puncture and pneumothorax (although less common than with supraclavicular block). It is often prudent to avoid this approach in patients with vascular catheters in the subclavian region, or patients with an ipsilateral pacemaker. As the brachial plexus traverses beyond the first rib and into the axilla, the cords are arranged around the axillary artery according to their anatomic position: medial, lateral, and posterior.

A. Nerve Stimulation The patient is positioned supine with the head turned to the contralateral side, and the coracoid process is identified (a bony prominence of the scapula that can be palpated between the acromioclavicular joint and the deltopectoral groove). The subclavian artery and brachial plexus run deep to the coracoid process and can be found approximately 2 cm medial and 2 cm caudad to it, about 4–5 cm deep in the average patient (Figure 46–17). A relatively long (8 cm) insulated needle is placed perpendicular to the skin and advanced directly posterior until a motor response is elicited. An acceptable motor response is finger flexion or extension at a current less than 0.5 mA, but not elbow flexion/extension. B. Ultrasound With the patient in the supine position, a small curvilinear transducer is placed in the parasagittal plane over the point 2 cm medial and 2 cm caudad to the coracoid process (Figure 46–18A). (Abducting the arm 90o improves axillary artery imaging.) A high-frequency linear transducer will

Morg_Ch46_0975-1022.indd 989

989

often provide inadequate needle visualization due to the relatively acute needle-to-transducer angle. The axillary artery and vein are identified in crosssection (Figure 46–18B). The medial, lateral, and posterior cords appear as hyperechoic bundles positioned caudad, cephalad, and posterior to the artery, respectively. A relatively long needle is inserted 2–3 cm cephalad to the transducer. Optimal needle positioning is between the axillary artery and the posterior cord. Three randomized, controlled trials have demonstrated equivalent results with a single 30-mL injection adjacent to the posterior cord or divided among each of the cords. Insertion of a perineural catheter should always be in the same location posterior to the axillary artery, and infraclavicular infusion has been shown to provide superior analgesia to both supraclavicular and axillary catheters.

Axillary Block At the lateral border of the pectoralis minor muscle, the cords of the brachial plexus form large terminal 6 branches. The axillary, musculocutaneous, and medial brachial cutaneous nerves branch from the brachial plexus proximal to the location in which local anesthetic is deposited during an axillary nerve block, and thus are usually spared (Figure 46–19). At this level, the major terminal nerves often are separated by fascia; therefore multiple injections (10-mL each) may be required to reliably produce anesthesia of the entire arm distal to the elbow (Figure 46–20). There are few contraindications to axillary brachial plexus blocks. Local infection, neuropathy, and bleeding risk must be considered. Because the axilla is highly vascularized, there is a risk of local anesthetic uptake through small veins traumatized by needle placement. The axilla is also a suboptimal site for perineural catheter placement because of greatly inferior analgesia versus an infraclavicular infusion, as well as theoretically increased risks of infection and catheter dislodgement. All of the numerous axillary block techniques require the patient to be positioned supine, with the arm abducted 90o and the head turned toward the contralateral side (Figure 46–20). The axillary artery pulse should be palpated and its location marked as a reference point.

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SECTION IV

Regional Anesthesia & Pain Management

Infraclavicular

Nerves or plexus roots C4 Trunks C5

Divisions C6 Cords Upper trunk

Main branches ord ral c

Late

ior ster

cord

Po

k

C7

run

et ddl

Mi

C8 Lower trunk

ord

T1

lc edia

M

FIGURE 4616 Infraclavicular block coverage and anatomy. Light blue shading indicates regions of variable blockade; purple shading indicates regions of more reliable blockade.

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CHAPTER 46 Peripheral Nerve Blocks

991

2 cm 2 cm

FIGURE 4617 Infraclavicular block using nerve stimulation: coracoid technique.

PMa PMi

AV

N N AA N N

B

A

Morg_Ch46_0975-1022.indd 991

FIGURE 4618 Infraclavicular block. A: Use a small curvilinear probe in a parasagittal plane to visualize the brachial plexus. B: Ultrasound image of the brachial plexus surrounding the axillary artery. AA, axillary artery; N, medial, lateral, and posterior cords of the brachial plexus; AV, axillary vein; PMa, pectoralis major muscle; PMi, pectoralis minor muscle. The red dot indicates the location of local anesthetic deposition.

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A. Transarterial Technique This technique has fallen out of favor due to the trauma of twice purposefully penetrating the axillary artery along with a theoretically increased risk of inadvertent intravascular local anesthetic injection. The nondominant hand is used to palpate and immobilize the axillary artery, and a 22-gauge needle is inserted high in the axilla (Figure 46–20) until bright red blood is aspirated. The needle is then slightly advanced until blood aspiration ceases. Injection can be performed posteriorly, anteriorly, or in both locations in relation to the artery. A total of 30–40 mL of local anesthetic is typically used. B. Nerve Stimulation Again the nondominant hand is used to palpate and immobilize the axillary artery. With the arm abducted and externally rotated, the terminal nerves usually lie in the following positions relative to

the artery (Figure 46–21, although variations are common): median nerve superior (wrist flexion, thumb opposition, forearm pronation); ulnar nerve inferior (wrist flexion, thumb adduction, fourth/ fifth digit flexion); and radial nerve inferior–posterior (digit/wrist/elbow extension, forearm supination). The musculocutaneous nerve (elbow flexion) is separate and deep within the coracobrachialis muscle, which is more superior (lateral) in this position and, as a consequence, is often not blocked with this procedure (Figure 46–21). A 2-in., 22-gauge insulated needle is inserted proximal to the palpating fingers to elicit muscle twitches in the hand. Once an acceptable muscle response is identified, and after reducing the stimulation to less than 0.5 mA, careful aspiration is performed and local anesthetic is injected. Although a single injection of 40 mL may be used, greater success will be seen with multiple nerve stimulations (ie, two or three nerves) and divided doses of local anesthetic.

Musculocutaneous n. Axillary n.

Medial brachial cutaneous n.

FIGURE 4619 Axillary block. The axillary, musculocutaneous, and medial brachial cutaneous nerves are usually spared with an axillary approach.

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CHAPTER 46 Peripheral Nerve Blocks

A

993

B

FIGURE 4620 A: Patient positioning and needle angle for axillary brachial plexus block. B: A multiple injection technique is more effective because of fascial separation between nerves.

Subcutaneous tissue

Skin

Intercostobrachial n. Median n. Brachial plexus

Ulnar n. Axillary a. Radial n.

Biceps m. Musculocutaneous n. Axillary v.

Triceps m.

Coracobrachialis m.

FIGURE 4621 Positioning of terminal nerves about the axillary artery (variations are common).

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SECTION IV

Regional Anesthesia & Pain Management

U AV TM

R

M AA

BM MC CB

Median n. Brachial a.

FIGURE 4622 Ultrasound image of axillary brachial plexus block. AA, Axillary artery; AV, axillary vein; U, ulnar nerve; M, median nerve; MC, musculocutaneous nerve; R, radial nerve; CB, coracobrachialis muscle; TM, triceps muscle; BM, biceps muscle.

C. Ultrasound Using a high-frequency linear array ultrasound transducer, the axillary artery and vein are visualized in cross-section. The brachial plexus can be identified surrounding the artery (Figure 46–22). The needle is inserted superior (lateral) to the transducer and advanced inferiorly (medially) toward the plexus under direct visualization. Ten milliliters of local anesthetic is then injected around each nerve (including the musculocutaneous, if indicated).

Biceps tendon

Flexor carpi radialis Palmaris longus Flexor digitorum superficialis

Flexor digitorum profundus

Palmar branch

Palmar digital nerves

Blocks of the Terminal Nerves 7 Often it is necessary to anesthetize a single ter-

minal nerve, either for minor surgical procedures with a limited field or as a supplement to an incomplete brachial plexus block. Terminal nerves may be anesthetized anywhere along their course, but the elbow and the wrist are the two most favored sites.

FIGURE 4623 Median nerve course.

A. Median Nerve Block The median nerve is derived from the lateral and medial cords of the brachial plexus. It enters the arm and runs just medial to the brachial artery

(Figure 46–23). As it enters the antecubital space, it lies medial to the brachial artery near the insertion of the biceps tendon. Just distal to this point, it gives off numerous motor branches to the wrist and finger

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995

CHAPTER 46 Peripheral Nerve Blocks

flexors and follows the interosseous membrane to the wrist. At the level of the proximal wrist flexion crease, it lies directly behind the palmaris longus tendon in the carpal tunnel. To block the median nerve at the elbow, the brachial artery is identified in the antecubital crease just medial to the biceps insertion. A short 22-gauge  insulated needle is inserted just medial to the artery and directed toward the medial epicondyle until wrist flexion or thumb opposition is elicited (Figure 46–24); 3–5 mL of local anesthetic is then injected. If ultrasound is used, the median nerve may be identified in cross-section just medial to the brachial artery and local anesthetic injected to surround it (Figure 46–25). To block the median nerve at the wrist, the palmaris longus tendon is first identified by asking the patient to flex the wrist against resistance. A short 22-gauge needle is inserted just medial and deep to the palmaris longus tendon, and 3–5 mL

Lateral

Medial Brachial artery Median nerve

Biceps

Medial epicondyle Bicipital aponeurosis Flexors

Dorsal

Palmar

FIGURE 4624 Median nerve block at the elbow.

Skin

Subcutaneous tissue

Biceps m.

Median n. Brachial a.

Brachioradialis m. Radial n. Triceps m. Brachialis m. Humerus

FIGURE 4625 Cross-sectional anatomy of median nerve at the elbow.

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SECTION IV

Regional Anesthesia & Pain Management

Brachial a. Ulnar n. Medial epicondyle

Biceps tendon

Arcuate ligament Ulnar a. Radial a. Flexor carpi ulnaris

Flexor digitorum profundus Palmar branch

Palmar retinaculum Median n. Flexor carpi radialis m.

Dorsal branch

Deep branch Superficial branch

Palmaris longus tendon

FIGURE 4626 Median nerve block at the wrist. FIGURE 4627 Ulnar nerve course. of local anesthetic is injected (Figure 46–26). With ultrasound, the median nerve may be identified at the level of the mid-forearm between the muscle bellies of the flexor digitorum profundus, flexor digitorum superficialis, and flexor pollicis longus (transducer faces perpendicular to the trajectory of the nerves).

B. Ulnar Nerve Block The ulnar nerve is the continuation of the medial cord of the brachial plexus and maintains a position medial to the axillary and brachial arteries in the upper arm (Figure 46–27). At the distal third of the humerus, the nerve moves more medially and passes under the arcuate ligament of the medial epicondyle. The nerve is frequently palpable just proximal to the medial epicondyle. In the mid-forearm, the nerve

Morg_Ch46_0975-1022.indd 996

lies between the flexor digitorum profundus and the flexor carpi ulnaris. At the wrist, it is lateral to the flexor carpi ulnaris tendon and medial to the ulnar artery. To block the ulnar nerve at the level of the elbow, an insulated 22-gauge needle is inserted approximately one fingerbreadth proximal to the arcuate ligament (Figure 46–28), and advanced until fourth/fifth digit flexion or thumb adduction is elicited; 3–5 mL of local anesthetic is then injected. To block the ulnar nerve at the wrist, the ulnar artery pulse is palpated just lateral to the flexor carpi ulnaris tendon. The needle is inserted just medial to the artery (Figure 46–29) and 3–5 mL of local anesthetic is injected. If ultrasound is used, the ulnar nerve may be identified just medial to the ulnar artery.

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CHAPTER 46 Peripheral Nerve Blocks

997

Ulnar nerve

Medial epicondyle Olecranon process

Arcuate ligament

Dorsal

Palmar

FIGURE 4628 Ulnar nerve block at the elbow with region of anesthesia illustrated on the hand.

Ulnar a. Ulnar n. Palmaris longus tendon Flexor carpi ulnaris tendon

FIGURE 4629 Ulnar nerve block at the wrist.

Morg_Ch46_0975-1022.indd 997

C. Radial Nerve Block The radial nerve—the terminal branch of the posterior cord of the brachial plexus—courses posterior to the humerus, innervating the triceps muscle, and enters the spiral groove of the humerus before it moves laterally at the elbow (Figure 46–30). Terminal sensory branches include the lateral cutaneous nerve of the arm and the posterior cutaneous nerve of the forearm. After exiting the spiral groove as it approaches the lateral epicondyle, the radial nerve separates into superficial and deep branches. The deep branch remains close to the periosteum and innervates the postaxial extensor group of the forearm. The superficial branch becomes superficial and follows the radial artery to innervate the radial aspects of the dorsal wrist and the dorsal aspect of the lateral three digits and half of the fourth. To block the radial nerve at the elbow, the biceps tendon is identified in the antecubital fossa. A short 22-gauge insulated needle is inserted just lateral to the tendon and directed toward the lateral

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SECTION IV

Regional Anesthesia & Pain Management

Radial n. Radial a. Brachioradialis m. Lateral epicondyle Deep branch

Flexor carpi radialis m.

Posterior interosseous n. Superficial branch

Dorsal digital nerves

FIGURE 4630 Radial nerve course.

epicondyle (Figure 46–31) until wrist or finger extension is elicited; 5 mL of local anesthetic is then injected. With ultrasound, the radial nerve can be identified in cross-section just proximal to the antecubital fossa between the biceps and brachioradialis muscles. At the wrist, the superficial branch of the radial nerve lies just lateral to the radial artery, which can be easily palpated lateral to the flexor carpi radialis tendon (Figure 46–32). Using a short 22-gauge needle, 3–5 mL local anesthetic is injected lateral to the artery. Ultrasound may be used at the level of the wrist or mid-forearm to identify the radial nerve just lateral to the radial artery.

D. Musculocutaneous Nerve Block A musculocutaneous nerve block is essential to complete the anesthesia for the forearm and wrist and is commonly included when performing the axillary block. The musculocutaneous nerve is the terminal branch of the lateral cord and the most proximal of the major nerves to emerge from the brachial plexus (Figure 46–33). This nerve innervates the biceps and brachialis muscles and distally terminates as the lateral antebrachial cutaneous nerve, supplying sensory input to the lateral aspect of the forearm and wrist.

Lateral

Medial

Brachialis m.

Biceps

Lateral epicondyle

Median n. Brachial a.

Radial n. Brachioradialis m.

FIGURE 4631 Radial nerve block

Dorsal

Palmar

at the elbow.

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999

CHAPTER 46 Peripheral Nerve Blocks

the coracobrachialis muscle is pierced, and 5–10 mL of local anesthetic is injected, with or without elicitation of elbow flexion. (Simple infiltration may be used, although the success rate using this technique is questionable.) Ultrasound may be used to confirm the location of the musculocutaneous nerve in the coracobrachialis muscle or between this muscle and the biceps (see Figure 46–22). Alternatively, the block can be performed at the elbow as the nerve courses superficially at the interepicondylar line. The insertion of the biceps tendon is identified, and a short 22-guage needle is inserted 1–2 cm laterally; 5–10 mL of local anesthetic is then injected as a field block.

Radius Radial nerve Flexor carpi radialis tendon

Ulnar styloid process Palmar longus tendon

Radial artery

FIGURE 4632 Radial nerve block at the wrist.

To target the musculocutaneous nerve following an axillary block, the needle is redirected superior and proximal to the artery (see Figure 46–21),

E. Digital Nerve Blocks Digital nerve blocks are used for minor operations on the fingers and to supplement incomplete brachial plexus and terminal nerve blocks. Sensory innervation of each finger is provided by four small digital nerves that enter each digit at its base in each of the four corners (Figure 46–34). A small-gauge needle is inserted at the medial and lateral aspects of the base of the selected digit, and 2–3 mL of local anesthetic

Dorsal

Digital Palmar nerve Musculocutaneous nerve

Biceps muscle

Lateral antebrachial cutaneous nerve

Coracobrachialis muscle

Brachialis muscle

Anterior branch Posterior branch

FIGURE 4633 Musculocutaneous nerve course.

Morg_Ch46_0975-1022.indd 999

FIGURE 4634 Sensory innervation of the fingers is provided by the digital nerves.

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SECTION IV

Regional Anesthesia & Pain Management

Skin wheal

T2

FIGURE 4636 Intercostobrachial nerve block.

FIGURE 4635 Intercostobrachial nerve cutaneous innervation.

is inserted without epinephrine. Addition of a vasoconstrictor (epinephrine) has been claimed to seriously compromise blood flow to the digit; however, there are no case reports involving lidocaine or other modern local anesthetics to confirm this claim.

F. Intercostobrachial Nerve Block The intercostobrachial nerve originates in the upper thorax (T2) and becomes superficial on the medial upper arm. It supplies cutaneous innervation to the medial aspect of the proximal arm and is not anesthetized with a brachial plexus block (Figure 46–35). The patient should be supine with the arm abducted and externally rotated. Starting at the deltoid prominence and proceeding inferiorly, a field block is performed in a linear fashion using 5 mL of local anesthetic, extending to the most inferior aspect of the medial arm (Figure 46–36).

intravenous catheter is usually inserted on the dorsum of the hand (or foot) and a double pneumatic tourniquet is placed on the arm or thigh. The extremity is elevated and exsanguinated by tightly wrapping an Esmarch elastic bandage from a distal to proximal direction. The proximal tourniquet is inflated, the Esmarch bandage removed, and 0.5% lidocaine (25 mL for a forearm, 50 mL for an arm, and 100 mL for a thigh tourniquet) injected over 2– 3 min through the catheter, which is subsequently removed (Figure 46–37). Anesthesia is usually established after 5–10 min. Tourniquet pain usually develops after 20–30 min, at which time the distal tourniquet is inflated and the proximal tourniquet subsequently deflated. Patients usually tolerate the distal tourniquet for an additional 15–20 min because it is inflated over an anesthetized area. Even

Intravenous Regional Anesthesia 8 Intravenous regional anesthesia, also called

a Bier block, can provide surgical anesthesia for short surgical procedures (45–60  min) on an extremity (eg, carpal tunnel release). An

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FIGURE 4637 Intravenous regional anesthesia provides surgical anesthesia for procedures of short duration.

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for surgical procedures of a very short duration, the tourniquet must be left inflated for a total of at least 15–20 min to avoid a rapid intravenous systemic bolus of local anesthetic resulting in toxicity. Slow deflation is also recommended to provide an additional margin of safety.

LOWER EXTREMITY PERIPHERAL NERVE BLOCKS Lumbar & Sacral Plexus Anatomy The lumbosacral plexus provides innervation to the lower extremities (Figure 46–38). The lumbar plexus is formed by the ventral rami of L1–4, with occasional contribution from T12. It lies within the psoas muscle with branches descending into the proximal thigh. Three major nerves from the

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lumbar plexus make contributions to the lower limb: the femoral (L2–4), lateral femoral cutaneous (L1–3), and obturator (L2–4). These provide motor and sensory innervation to the anterior portion of the thigh and sensory innervation to the medial leg. The sacral plexus arises from L4–5 and S1–4. The posterior thigh and most of the leg and foot are supplied by the tibial and peroneal portions of the sciatic nerve. The posterior femoral cutaneous nerve (S1–3), and not the sciatic nerve, provides sensory innervation to the posterior thigh; it travels with the sciatic nerve as it emerges around the piriformis muscle.

Femoral Nerve Block The femoral nerve innervates the main hip flexors, knee extensors, and provides much of the sensory

L1 L2 Inguinal nerve

L3

Genitofemoral nerve

L4

Lumbar plexus

L5

Lateral femoral cutaneous nerve

S1

Femoral nerve

S3 S4

Sacral plexus

S2

Inguinal ligament

Sciatic nerve Obturator nerve

FIGURE 4638 The ventral rami of L1–5 and S1–4 form the lumbosacral plexus, which provides innervation to the lower extremities.

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Lateral femoral cutaneous nerve Femoral nerve

Femoral nerve

Articular branch Anterior femoral cutaneous nerve Quadriceps femoris muscle

Obturator nerve

Rectus femoris muscle (cut and reflected) Vastus intermedius muscle Vastus medialis muscle Vastus lateralis muscle

Saphenous nerve

FIGURE 4639 The femoral nerve provides sensory innervation to the hip and thigh, and to the medial leg via its terminal branch, the saphenous nerve.

innervation of the hip and thigh (Figure 46–39). Its most medial branch is the saphenous nerve, which innervates much of the skin of the medial leg and ankle joint. The term 3-in-1 block refers to anesthetizing the femoral, lateral femoral cutaneous, and obturator nerves with a single injection below the inguinal ligament; this term has largely been abandoned as evidence accumulated demonstrating the failure of most single injections to consistently affect

Morg_Ch46_0975-1022.indd 1002

9 all three nerves. A femoral nerve block alone

will seldom provide surgical anesthesia, but it is often used to provide postoperative analgesia for hip, thigh, knee, and ankle (for the saphenous nerve) procedures. Femoral nerve blocks have a relatively low rate of complications and few contraindications. Local infection, previous vascular grafting, and local adenopathy should be carefully considered in patient selection.

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Anterior superior iliac spine

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Femoral vein Femoral artery

Lateral femoral cutaneous nerve

Femoral nerve Genitofemoral nerve Inguinal ligament Pubic symphysis

FIGURE 4640 Femoral block using nerve stimulation.

A. Nerve Stimulation With the patient positioned supine, the femoral artery pulse is palpated at the level of the inguinal ligament. A short (5-cm) insulated needle is inserted at a 45° angle to the skin in a cephalad direction (Figure 46–40) until a clear quadriceps twitch is elicited at a current below 0.5 mA (look for patella motion). B. Ultrasound A high-frequency linear ultrasound transducer is placed over the area of the inguinal crease parallel to the crease itself, or slightly more transverse (Figure 46–41). The femoral artery and femoral vein are visualized in cross-section, with the overlying fascia iliaca. Just lateral to the artery and deep to the fascia iliaca, the femoral nerve appears in crosssection as a spindle-shaped structure with a “honeycomb” texture (Figure 46–42). For an out-of-plane technique, the block needle is inserted just lateral to where the femoral nerve is seen, and directed cephalad at an angle approximately 45° to the skin. The needle is advanced until

Morg_Ch46_0975-1022.indd 1003

it is seen penetrating the fascia iliaca, or (if using concurrent electrical stimulation) until a motor response is elicited. Following careful aspiration for the nonappearance of blood, 30–40 mL of local anesthetic is injected. For an in-plane technique, a longer needle may be used. The needle is inserted parallel to the ultrasound transducer just lateral to the outer edge. The needle is advanced through the sartorius muscle, deep to the fascia iliaca, until it is visualized just lateral to the femoral nerve. Local anesthetic is injected, visualizing its hypoechoic spread deep to the fascia iliaca and around the nerve.

C. Fascia Iliaca Technique The goal of a fascia iliaca block is similar to that of a femoral nerve block, but the approach is slightly different. Without use of a nerve stimulator or ultrasound machine, a relatively reliable level of anesthesia may be attained simply with anatomic landmarks and tactile sensation. Once the inguinal ligament and femoral artery pulse are identified,

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SM

FV

FA

FN

IM

FIGURE 4642 Femoral nerve block. Ultrasound image of the femoral nerve. FA, femoral artery; FV, femoral vein; FN, femoral nerve; SM, Sartorius muscle; IM, iliacus muscle. local anesthetic is deposited under the fascia iliaca between the two nerves which run in the same plane between the fascia and underlying muscle.

Lateral Femoral Cutaneous Nerve Block

FIGURE 4641 Ultrasound-guided femoral nerve block (in-plane technique). the length of the inguinal ligament is divided into thirds (Figure 46–43). Two centimeters distal to the junction of the middle and outer thirds, a short, blunt-tipped needle is inserted in a slightly cephalad direction. As the needle passes through the two layers of fascia in this region (fascia lata and fascia iliaca), two “pops” will be felt. Once the needle has passed through the fascia iliaca, careful aspiration is performed and 30–40 mL of local anesthetic is injected. This block usually anesthetizes both the femoral nerve and lateral femoral cutaneous nerves, since the

Morg_Ch46_0975-1022.indd 1004

The lateral femoral cutaneous nerve provides sensory innervation to the lateral thigh (see Figure 46–39). It may be anesthetized as a supplement to a femoral nerve block or as an isolated block for limited anesthesia of the lateral thigh. As there are few vital structures in proximity to the lateral femoral cutaneous nerve, complications with this block are exceedingly rare. The lateral femoral cutaneous nerve (L2–3) departs from the lumbar plexus, traverses laterally from the psoas muscle, and courses anterolaterally along the iliacus muscle (see Figure 46–38). It emerges inferior and medial to the anterior superior iliac spine to supply the cutaneous sensory innervation of the lateral thigh. The patient is positioned supine or lateral, and the point 2 cm medial and 2 cm distal to the anterior superior iliac spine is identified. A short 22-gauge block needle is inserted and directed laterally, observing for a “pop” as it passes through the fascia lata. A field block is performed with 10–15 mL of local anesthetic, which is deposited above and below the fascia (Figure 46–44).

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Needle insertion point

FIGURE 4643 Fascia iliaca block.

2 cm

Femoral nerve

Anterior superior iliac spine

Femoral vein Femoral artery

Lateral femoral cutaneous nerve Genitofemoral nerve Inguinal ligament

FIGURE 4644 Lateral femoral cutaneous nerve block.

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L2 L3 L4

Obturator externus muscle

Adductor brevis muscle Adductor longus muscle

Adductor magnus muscle Gracilis muscle

FIGURE 4645 Obturator nerve innervation.

Obturator Nerve Block A block of the obturator nerve is usually required for complete anesthesia of the knee and is most often performed in combination with femoral and sciatic nerve blocks for this purpose. The obturator nerve contributes sensory branches to the hip and knee joints, a variable degree of sensation to the medial thigh, and innervates the adductors of the hip (Figure 46–45). This nerve exits the pelvis and enters the medial thigh through the obturator foramen, which lies beneath the superior pubic ramus. After identification of the pubic tubercle, a long (10-cm) block needle is inserted 1.5 cm inferior and 1.5 cm lateral to the tubercle. The needle is advanced

Morg_Ch46_0975-1022.indd 1006

posteriorly until bone is contacted (Figure 46–46). Redirecting laterally and caudally, the needle is advanced an additional 2–4 cm until a motor response (thigh adduction) is elicited and maintained below 0.5 mA. Following careful aspiration for the nonappearance of blood, 15–20 mL of local anesthetic is injected.

Posterior Lumbar Plexus (Psoas Compartment) Block 10 Posterior lumbar plexus blocks are useful for

surgical procedures involving areas innervated by the femoral, lateral femoral cutaneous, and obturator nerves (Figure 46–47). These include

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1007

Obturator nerve Pubic ramus

Obturator foramen

External obturator muscle

2 1

Obturator nerve, anterior branch

Obturator nerve, posterior branch

FIGURE 4646 Obturator nerve block. Contact pubic tubercle (1), then redirect laterally and caudally (2) until a motor response is elicited.

Femoral nerve, lateral cutaneous nerve of thigh, obturator nerve Sciatic nerve, posterior femoral cutaneous nerve

Needle insertion point Lateral femoral cutaneous n.

Femoral n.

Obturator n.

FIGURE 4647 Lumbar plexus blocks provide anesthesia to the femoral, lateral femoral cutaneous, and obturator nerves.

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Inferior vena cava

Ureter Testicular/ovarian vein and artery Psoas muscle

FIGURE 4648 The lumbar plexus lies in close proximity to several important structures.

procedures on the hip, knee, and anterior thigh. Complete anesthesia of the knee can be attained with a proximal sciatic nerve block. The lumbar plexus is relatively close to multiple sensitive structures (Figure 46–48) and reaching it requires a very long needle. Hence, the posterior lumbar plexus block has one of the highest complication rates of any peripheral nerve block; these include retroperitoneal hematoma, intravascular local anesthetic injection with toxicity, intrathecal and epidural injections, and renal capsular puncture with subsequent hematoma. Lumbar nerve roots emerge into the body of the psoas muscle and travel within the muscle compartment before exiting as terminal nerves (see Figure 46–38). Modern posterior lumbar plexus blocks deposit local anesthetic within the body of the psoas muscle. The patient is positioned in lateral

Morg_Ch46_0975-1022.indd 1008

Lumbar plexus Spinal cord

decubitus with the side to be blocked in the nondependent position (Figure 46–49). The midline is palpated, identifying the spinous processes if possible. A line is first drawn through the lumbar spinous processes, and both iliac crests are identified and connected with a line to approximate the level of L4. The posterior superior iliac spine is then palpated and a line is drawn cephalad, parallel to the first line. If available, ultrasound imaging of the transverse process may be helpful to estimate lumbar plexus depth. A long (10- to 15-cm) insulated needle is inserted at the point of intersection between the transverse (intercristal) line and the intersection of the lateral and middle thirds of the two sagittal lines. The needle is advanced in an anterior direction until a femoral motor response is elicited (quadriceps contraction). If the transverse process is contacted, the needle should be withdrawn slightly

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Curvilinear array ultrasound transducer

Iliac crest

Posterior superior iliac spine

Needle entry point 1/3 2/3 L4 L5

FIGURE 4649 Patient positioning and surface landmarks for posterior lumbar plexus block.

and “walked off ” the transverse process in a caudal direction, maintaining the needle in the parasagittal plane. The needle should never be inserted more than 3 cm past the depth at which the transverse process was contacted. Local anesthetic volumes greater than 20 mL will increase the risk of bilateral spread and contralateral limb involvement.

Morg_Ch46_0975-1022.indd 1009

Saphenous Nerve Block The saphenous nerve is the most medial branch of the femoral nerve and innervates the skin over the medial leg and the ankle joint (see Figure 46–39). Therefore, this block is used mainly in conjunction with a sciatic nerve block to provide complete anesthesia/analgesia below the knee.

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11 (see Figure 46–38). Blockade of the sciatic

Tibial tuberosity Line of injection Lateral

Medial

FIGURE 4650 Proximal saphenous nerve block.

A. Trans-Sartorial Technique The saphenous nerve may be accessed proximal to the knee, just deep to the sartorius muscle. A high-frequency linear probe is used to identify the junction between the sartorius, vastus medialis, and adductor muscles in cross-section just distal to the adductor canal. A long needle is inserted from medial to lateral (in-plane) or angled cephalad (outof-plane) and 5–10 mL of local anesthetic deposited within this fascial plane.

nerve may occur anywhere along its course and is indicated for surgical procedures involving the hip, thigh, knee, lower leg, and foot. The posterior femoral cutaneous nerve is variably anesthetized as well, depending on the approach. If sacral plexus or posterior femoral cutaneous nerve anesthesia is required, the parasacral approach is used (a technique that is beyond the scope of this chapter).

A. Posterior (Classic or Labat) Approach The patient is positioned laterally with the side to be blocked in the nondependent position. The patient is asked to bend the knee of the affected leg and tilt the pelvis slightly forward (Sim’s position; Figure 46–51). The greater trochanter, posterior superior iliac spine (PSIS), and sacral hiatus are then identified. A line is drawn from the greater trochanter to the PSIS, its midpoint identified, and a perpendicular line extended in a caudal direction. Next, a line is drawn from the greater trochanter to the

B. Proximal Saphenous Technique A short block needle is inserted 2 cm distal to the tibial tuberosity and directed medially, infiltrating 5–10  mL of local anesthetic as the needle passes toward the posterior aspect of the leg (Figure 46–50). Ultrasound may be used to identify the saphenous vein near the tibial tuberosity, facilitating a perivascular technique with infiltration about the vein. C. Distal Saphenous Technique The medial malleolus is identified, infiltrating 5 mL of local anesthetic in a line running anteriorly around the ankle (see Ankle Block below).

Sciatic Nerve Block The sciatic nerve originates from the lumbosacral trunk and is composed of nerve roots L4–5 and S1–3

Morg_Ch46_0975-1022.indd 1010

Posterior superior iliac spine 5 cm

Sacral hiatus

Greater trochanter

FIGURE 4651 Patient positioning, surface landmarks, and needle positioning for proximal sciatic nerve block (classic approach).

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sacral hiatus and the intersection point is marked; this is the initial needle insertion point. A long (10-cm) insulated needle is inserted at an angle perpendicular to all planes to the skin (Figure 46–51). The needle is advanced through the gluteal muscles (a motor response of these muscles may be encountered) until plantar- or dorsiflexion is elicited (plantarflexion or foot inversion is preferred for surgical anesthesia). A local anesthetic volume of 25 mL provides surgical anesthesia.

B. Anterior Approach After leaving the sciatic notch, the sciatic nerve descends behind the lesser trochanter to a position posterior to the femur. It can be accessed from the anterior thigh just medial to the lesser trochanter. Lateral or prone positioning may present a challenge for some patients requiring a sciatic nerve block (ie, elderly patients, pediatric patients under general anesthesia). An anterior approach can be technically challenging but offers an alternative path to the sciatic nerve. Before proceeding with this block, which carries a risk of vascular puncture (femoral artery and vein), patient-specific risks should be considered (eg, coagulopathy and vascular grafting). In

1011

addition, if combining this block with the femoral nerve block in an unanesthetized patient, performing the sciatic block first is recommended to avoid passing the block needle through a previously anesthetized femoral nerve. A local anesthetic volume of 25 mL provides surgical anesthesia. 1. Nerve stimulation—With the patient positioned supine, a line is drawn along the inguinal ligament, from the anterior superior iliac spine to the pubic tubercle (Figure 46–52). A second line is drawn parallel to the first that traverses the greater trochanter (intertrochanteric line). Next, these two lines are connected with a third line drawn from the point between the medial one third and lateral two thirds of the first line, at a 90° angle, and extended caudally to intersect with the intertrochanteric line. A long (10- to 15-cm) needle is inserted through this intersection and directly posterior until foot inversion or plantarflexion is elicited (dorsiflexion is acceptable for postoperative analgesia). Often with this approach, the femur is contacted before the needle reaches the sciatic nerve. When this occurs, the needle should be withdrawn 2–3 cm, the patient should be asked to internally rotate the leg, and then the needle should be advanced. If the femur is contacted

Femoral artery and vein Anterior superior iliac spine Pubic tubercle Greater trochanter

Lesser trochanter

Needle insertion point

FIGURE 4652 Anatomy and surface landmarks for anterior sciatic nerve block.

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Greater trochanter 4 cm Ischial tuberosity

FIGURE 4653 Patient positioning and surface landmarks for subgluteal sciatic block.

again, the landmarks may require reassessment. A local anesthetic volume of 25 mL provides surgical anesthesia. 2. Ultrasound—With the patient positioned supine and the leg externally rotated, a low-frequency curvilinear transducer is placed transversely over the medial thigh, approximately at the level of the lesser trochanter. The femur, femoral vessels, adductor muscles, and gluteus maximus are identified in crosssection. The elliptical, hyperechoic sciatic nerve is found in the fascial plane between adductors and gluteus muscles, posterior to the femur. Using a long (10-cm) needle, the nerve is approached in-plane (anterior to posterior) or out-of-plane (cephalad to caudad), taking care to avoid femoral vessels, until the needle tip lies in this muscle plane and a local anesthetic injection can be observed as hypoechoic spread surrounding the sciatic nerve.

C. Subgluteal Approach A subgluteal approach to the sciatic nerve is a useful alternative to the traditional posterior approach. In many patients the landmarks are more easily identified, and less tissue is traversed. With the sciatic nerve at a more superficial location, the exclusive use of ultrasound becomes far more practical, as well. If sciatic nerve block is being combined with a femoral block and ambulation is desired within the local anesthetic duration, consider a popliteal approach (below) that will not affect the hamstring muscles to the same degree, allowing knee flexion to lift the foot with the use of crutches. 1. Nerve stimulation—With the patient in Sim’s position, the greater trochanter and ischial

Morg_Ch46_0975-1022.indd 1012

tuberosity are identified and a line drawn between them (Figure 46–53). From the midpoint of this line, a second line is drawn perpendicularly and extended caudally 4 cm. Through this point a long (10-cm) insulated needle is inserted directly slightly cephalad until foot plantarflexion or inversion is elicited (dorsiflexion is acceptable for analgesia). A local anesthetic volume of 25 mL provides surgical anesthesia. 2. Ultrasound—Using the same positioning and landmarks (Figure 46–53), a linear or low-frequency curvilinear (best) ultrasound transducer is placed over the midpoint between the ischial tuberosity and the greater trochanter in a transverse orientation. Both bony structures should be visible in the ultrasound field simultaneously. Gluteal muscles are identified superficially, along with the fascial layer defining their deep border. The triangular sciatic nerve should be visible in cross-section just deep to this layer in a location approximately midway between the ischial tuberosity and the greater trochanter, superficial to the quadratus femoris muscle. For an out-of-plane ultrasound-guided sciatic block, the block needle is inserted just caudad to the ultrasound transducer and advanced in an anterior and cephalad direction. Once the needle passes through the gluteus muscles with the tip next to sciatic nerve, careful aspiration for the nonappearance of blood is performed and local anesthetic is injected, visualizing spread around the nerve. For an in-plane technique, the block needle is inserted just lateral to the ultrasound transducer near the greater trochanter. It is advanced through

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Semitendinosus m.

1013

Sciatic n.

Semimembranosus m. Common peroneal n.

Tibial n.

Sural n. Common peroneal nerve Saphenous nerve Medial calcaneal branches of tibial nerve

Superficial peroneal nerve Sural nerve

Deep peroneal nerve

FIGURE 4654 The sciatic nerve divides into tibial and peroneal branches just proximal to the popliteal fossa and provides sensory innervation to much of the lower leg.

the field of the ultrasound beam until the tip is visible deep to the gluteus maximus, next to the sciatic nerve. Again, local anesthetic spread around the nerve should be visualized.

D. Popliteal Approach 12 Popliteal nerve blocks provide excellent coverage for foot and ankle surgery, while sparing much of the hamstring muscles, allowing lifting of the foot with knee flexion, thus easing ambulation. All sciatic nerve blocks fail to provide complete anesthesia for the cutaneous medial leg and ankle joint capsule, but when a saphenous (or femoral)

Morg_Ch46_0975-1022.indd 1013

block is added, complete anesthesia below the knee is provided. The major site-specific risk of a popliteal block is vascular puncture, owing to the sciatic nerve’s proximity to the popliteal vessels at this location. The sciatic nerve divides into the tibial and common peroneal nerves within or just proximal to the popliteal fossa (Figure 46–54). The upper popliteal fossa is bounded laterally by the biceps femoris tendon and medially by the semitendinosus and semimembranosus tendons. Cephalad to the flexion crease of the knee, the popliteal artery is immediately lateral to the semitendinosus tendon. The popliteal vein is lateral to the artery, and the tibial and

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common peroneal nerves are just lateral to the vein and medial to the biceps tendon, 2–6 cm deep to the skin. The tibial nerve continues deep behind the gastrocnemius muscle, and the common peroneal nerve leaves the popliteal fossa by passing between the head and neck of the fibula to supply the lower leg. The sciatic nerve is approached by either a posterior or a lateral approach. For posterior approaches, the patient is usually positioned prone with the knee slightly flexed by propping the ankle on pillows or towels. For lateral approaches, the patient may be in the lateral or supine position. 1. Nerve stimulation (posterior approach)—With the patient in the prone position, the apex of the popliteal fossa is identified. The hamstring muscles are palpated to locate the point where the biceps femoris (lateral) and the semimembranosus/semitendinosus complex (medial) join (Figure 46–55). Having the patient flex the knee against resistance facilitates recognition of these structures. The needle entry point is 1 cm caudad from the apex. An insulated needle (5–10 cm) is advanced until foot plantarflexion or inversion is elicited (dorsiflexion is acceptable for analgesia). A volume of 30–40 mL of local anesthetic is often required for single-injection popliteal–sciatic nerve block. 2. Nerve stimulation (lateral approach)—With the patient in the supine position and the knee fully extended, the intertendinous groove is palpated between the vastus lateralis and biceps femoris muscles approximately 10 cm proximal to the superior notch of the patella. A long (10-cm) insulated needle is inserted at this point and advanced at a 30° angle posteriorly until an appropriate motor response is elicited. If bone (femur) is contacted, the needle is withdrawn and redirected slightly posteriorly until an acceptable motor response is encountered. 3. Ultrasound—With the patient positioned prone, the apex of the popliteal fossa is identified, as described above. Using a high-frequency linear ultrasound transducer placed in a transverse orientation, the femur, biceps femoris muscle, popliteal vessels, and sciatic nerve or branches are identified in cross-section (Figure 46–55). The nerve is usually posterior and lateral (or immediately posterior) to the vessels and is often located in close

Morg_Ch46_0975-1022.indd 1014

Proximal

Medial

Lateral

Distal

BFM N

PV PA

F

FIGURE 4655 Anatomy and sonoanatomy of the sciatic nerve in the popliteal fossa. PA, popliteal artery; PV, popliteal vein; N, sciatic nerve; BFM, biceps femoris muscle; F, femur.

relationship to the biceps femoris muscle, just deep to its medial edge. For an out-of-plane technique, the needle is inserted just caudad to the ultrasound transducer and directed anteriorly and slightly cephalad. When the needle is positioned in proximity to the sciatic nerve, and following careful aspiration, local anesthetic injected, observing for spread around the nerve.

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For an in-plane technique, the block needle is inserted lateral to the ultrasound transducer, traversing—or just anterior to—the biceps femoris muscle (Figure 46–56). The needle is advanced in the ultrasound plane, while visualizing its approach either deep or superficial to the nerve. If surgical anesthesia is desired, local anesthetic should be seen surrounding all sides of the nerve, which usually requires multiple needle tip placements with incremental injection. For analgesia alone, a single injection of local anesthetic is acceptable. Ultrasound-guided popliteal sciatic blocks may be performed with the patient in the lateral or supine positions (the latter with leg up-raised on several pillows). These maneuvers are often more technically challenging.

Ankle Block For surgical procedures of the foot, an ankle block is a fast, low-technology, low-risk means of providing anesthesia. Excessive injectate volume and use of vasoconstrictors such as epinephrine must be avoided to minimize the risk of ischemic complications. Since this block includes five separate injections, it is often uncomfortable for patients and adequate premedication is required. Five nerves supply sensation to the foot (Figure 46–57). The saphenous nerve is a terminal branch of the femoral nerve and the only innervation

FIGURE 4656 Patient positioning, probe, and needle orientation for popliteal block.

Common peroneal nerve Saphenous nerve Superficial peroneal nerve Medial calcaneal branches of tibial nerve

Sural nerve

Saphenous nerve

Sural nerve

Deep peroneal nerve

Lateral plantar nerve Medial plantar nerve Medial calcaneal branches

From tibial nerve

FIGURE 4657 Cutaneous innervation of the foot.

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Tibial n. Common peroneal n.

Gastrocnemius m.

Peroneus longus muscle (cut) Extensor digitorum longus m.

Popliteus m.

Soleus m. Superficial peroneal n. Deep peroneal n. Peroneus longus and brevis m. Tibialis posterior m. Extensor hallucis longus m. Tibialis anterior m.

Flexor hallucis longus m. Tibial n.

FIGURE 4658 Tibial and common peroneal nerve courses.

of the foot not a part of the sciatic system. It supplies superficial sensation to the anteromedial foot and is most constantly located just anterior to the medial malleolus. The deep peroneal nerve runs in the anterior leg after branching off the common peroneal nerve, entering the ankle between the extensor hallucis longus and the extensor digitorum longus tendons (Figure 46–58), just lateral to the dorsalis pedis artery. It provides innervation to the toe extensors and sensation to the first dorsal webspace. The superficial peroneal nerve, also a branch of the common peroneal nerve, descends toward the ankle in the lateral compartment, giving motor branches

Morg_Ch46_0975-1022.indd 1016

to the muscles of eversion. It enters the ankle just lateral to the extensor digitorum longus and provides cutaneous sensation to the dorsum of the foot and toes. The posterior tibial nerve is a direct continuation of the tibial nerve and enters the foot posterior to the medial malleolus, branching into calcaneal, lateral plantar, and medial plantar nerves. It is located behind the posterior tibial artery at the level of the medial malleolus and provides sensory innervation to the heel, the medial sole, and part of the lateral sole of the foot, as well as the tips of the toes. The sural nerve is a branch of the tibial nerve and enters the foot between the Achilles tendon

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Tibialis anterior tendon Deep peroneal nerve Saphenous nerve

1017

Extensor hallucis longus tendon Superficial peroneal nerve Tibia Fibula

Posterior tibial nerve Achilles tendon

Sural nerve

A

B

FIGURE 4659 Needle placement for ankle block.

and the lateral malleolus to provide sensation to the lateral foot. 13 A complete ankle block requires a series of five nerve blocks, but the process may be streamlined to minimize needle insertions (Figure 46–59). All five injections are required to anesthetize the entire foot; however, many surgical procedures involve only a few terminal nerves, and only affected nerves should be blocked. In addition, unlike a sciatic nerve block, an ankle block provides no analgesia for (below-the-knee) tourniquet pain, nor does it allow for perineural catheter insertion. To block the deep peroneal nerve, the groove between the extensor hallucis longus and extensor digitorum longus tendons is identified. The dorsalis pedis pulse is often palpable here. A short, small-gauge block needle is inserted perpendicular to the skin just lateral to the pulse, bone is contacted, and 5 mL of local anesthetic is infiltrated as the needle is withdrawn. Continuing from this insertion site, a subcutaneous wheal of 5 mL of local anesthetic is extended toward the lateral malleolus to target the superficial peroneal nerve. The needle is withdrawn and redirected from the same location in a medial direction, infiltrating 5 mL of local anesthetic toward the medial malleolus to target the saphenous nerve. The posterior tibial nerve may be located by identifying the

Morg_Ch46_0975-1022.indd 1017

posterior tibial artery pulse behind the medial malleolus. A short, small-gauge block needle is inserted just posterior to the artery and 5 mL of local anesthetic is distributed in the pocket deep to the flexor retinaculum. To target the sural nerve, 5 mL of local anesthetic is injected subcutaneously posterior to the lateral malleolus.

PERIPHERAL NERVE BLOCKS OF THE TRUNK Superficial Cervical Plexus Block The superficial cervical plexus block provides cutaneous analgesia for surgical procedures on the neck, anterior shoulder, and clavicle. It is helpful to identify and avoid the external jugular vein. The cervical plexus is formed from the anterior rami of C1–4, which emerge from the platysma muscle posterior to the sternocleidomastoid (Figure 46–60). It supplies sensation to the jaw, neck, occiput, and areas of the chest and shoulder. The patient is positioned supine with the head turned away from the side to be blocked. The sternocleidomastoid muscle is identified and its lateral edge marked. At the junction of the upper and middle thirds, a short (5-cm) block needle is inserted,

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C2 C3 C4

FIGURE 4660 Distribution of the superficial cervical plexus.

directed cephalad toward the mastoid process, and 5 mL of local anesthetic is injected in a subcutaneous plane. The needle is turned to advance it in a caudad direction, maintaining a path along the posterior border of sternocleidomastoid. An additional 5 mL of local anesthetic is infiltrated subcutaneously.

Intercostal Block Intercostal blocks provide analgesia following thoracic and upper abdominal surgery, and relief of pain associated with rib fractures, herpes zoster, and cancer. These blocks require individual injections delivered at the various vertebral levels that correspond to the area of body wall to be anesthetized. 14 Intercostal blocks result in the highest blood levels of local anesthetic per volume injected of any block in the body, and care must be taken to avoid toxic levels of local anesthetic. The intercostal block has one of the highest complication rates of any peripheral nerve block due to the close proximity of the intercostal artery and vein (intravascular local anesthetic injection), as well as underlying pleura (pneumothorax). In addition, duration is impressively short due to the high vascular flow, and

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placement of a perineural catheter is tenuous, at best. With the advent of ultrasound guidance, the paravertebral approach is rapidly replacing the intercostal approach. The intercostal nerves arise from the dorsal and ventral rami of the thoracic spinal nerves. They exit from the spine at the intervertebral foramen and enter a groove on the underside of the corresponding rib, running with the intercostal artery and vein; the nerve is generally the most inferior structure in the neurovascular bundle (Figure 46–61). Branches are given off for sensation in a single dermatome from the midline dorsally all the way to across the midline ventrally. With the patient in the lateral decubitus or supine position, the level of each rib in the mid and posterior axillary line is palpated and marked. A small-gauge needle is inserted at the inferior edge of each of the selected ribs, bone is contacted, and the needle is then “walked off ” inferiorly (Figure 46–61). The needle is redirected in a slightly  cephalad direction and advanced approximately 0.25 cm. Following aspiration, observing for blood or air, 3–5 mL of local anesthetic is injected at each desired level.

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Needle insertion point

Intercostal nerve, artery, and vein

FIGURE 4661 Anatomy and needle positioning for intercostal nerve block.

Paravertebral Block Paravertebral blocks provide surgical anesthesia or postoperative analgesia for procedures involving the thoracic or abdominal wall, mastectomy, inguinal or abdominal hernia repair, and more invasive unilateral procedures such as open nephrectomy. Paravertebral blocks usually require individual injections delivered at the various vertebral levels that correspond to the area of body wall to be anesthetized. For example, a simple mastectomy would require blocks at levels T3–6; for axillary node dissection, additional injections should be made from C7 through T2. For inguinal hernia repair, blocks should be performed at T10 through L2. Ventral hernias require bilateral injections corresponding to the level of the surgical site. The major complication of thoracic injections is pneumothorax, whereas retroperitoneal structures may be at risk with lumbar-level injections. Hypotension secondary to sympathectomy can be observed with multilevel thoracic blocks. Unlike the intercostal approach, long-acting local anesthetic will have a nearly 24-hour duration, and perineural catheter

Morg_Ch46_0975-1022.indd 1019

insertion is a viable option (although local anesthetic spread from a single catheter to multiple levels is variable). Each spinal nerve emerges from the intervertebral foramina and divides into two rami: a larger anterior ramus, which innervates the muscles and skin over the anterolateral body wall and limbs, and a smaller posterior ramus, which reflects posteriorly and innervates the skin and muscles of the back 15 and  neck (Figure 46–62). The thoracic paravertebral space is defined posteriorly by the superior costotransverse ligament, anterolaterally by the parietal pleura, medially by the vertebrae and the intervertebral foramina, and inferiorly and superiorly by the heads of the ribs. With the patient seated and vertebral column flexed, each spinous process is palpated, counting from the prominent C7 for thoracic blocks, and the iliac crests as a reference for lumbar levels. From the midpoint of the superior aspect of each spinous process, a point 2.5 cm laterally is measured and marked. In the thorax, the target nerve is located lateral to the spinous process above it, due to the steep

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2 1

Intervertebral foramen

2.5 cm

Spinous process

Transverse process Spinal nerve Spinal cord Pleura Lung

FIGURE 4662 Paravertebral anatomy and traditional approach. Contact transverse process (1), then redirect the needle caudally (2) and advance 1 cm.

angulation of thoracic spinous processes (eg, the T4 nerve root is located lateral to the spinous process of T3).

A. Traditional Technique A pediatric Tuohy needle (20 gauge) is inserted at each point and advanced perpendicular to the skin (Figure 46–62). Upon contact with the transverse process, the needle is withdrawn slightly and redirected caudally an additional 1 cm (0.5 cm for lumbar placement). A “pop” or loss of resistance may be felt as the needle passes through the costotransverse ligament. Some practitioners use a loss-of-resistance syringe to guide placement; others prefer use of a nerve stimulator with chest wall motion for the end point. Inject 5 mL of local anesthetic at each level. The difficulty with this technique is that the depth of the transverse process is simply estimated; thus

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the risk of pneumothorax is relatively high. Using ultrasound to gauge transverse process depth prior to needle insertion theoretically decreases the risk of pneumothorax.

B. Ultrasound An ultrasound transducer with a curvilinear array is used, with the beam oriented in a parasagittal or transverse plane. The transverse process, head of the rib, costotransverse ligament, and pleura are identified. The paravertebral space may be approached from a caudal-to-cephalad direction (parasagittal) or a lateral-to-medial direction (transverse). It is helpful to visualize the needle in-plane as it passes through the costotransverse ligament and observe a downward displacement of the pleura as local anesthetic is injected. At each level 5 mL of local anesthetic is injected.

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External oblique muscle (cut) Transversus abdominis muscle Internal oblique muscle Anterior and lateral cutaneous branches of subcostal nerve (T12) Anterior branch of iliohypogastric nerve (L1) Ilioinguinal nerve (L1) Anterior cutaneous branch of iliohypogastric nerve (L1) Ilioinguinal nerve (L1)

FIGURE 4663 Transversus abdominis plane (TAP) anatomy.

Transversus Abdominis Plane Block The transversus abdominis plane (TAP) block is most often used to provide surgical anesthesia for minor, superficial procedures on the lower abdominal wall, or postoperative analgesia for procedures below the umbilicus. For hernia surgeries, intravenous or local supplementation may be necessary to provide anesthesia during peritoneal traction. Potential complications include violation of the peritoneum with or without bowel perforation, and the use of ultrasound is highly recommended to minimize this risk. 16 The subcostal (T12), ilioinguinal (L1), and iliohypogastric (L1) nerves are targeted in the TAP block, providing anesthesia to the ipsilateral

Morg_Ch46_0975-1022.indd 1021

lower abdomen below the umbilicus (Figure 46–63). For part of their course, these three nerves travel in the muscle plane between the internal oblique and transversus abdominis muscles. Needle placement should be between the two fascial layers of these muscles, with local anesthetic filling the transversus abdominis plane. The patient is ideally positioned in lateral decubitus, but if mobility is limited the block may be performed in the supine position.

A. Ultrasound With a linear or curvilinear array transducer oriented parallel to the inguinal ligament, the layers of the external oblique, internal oblique, and transversus abdominis muscles are identified just superior

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SQ

EO IO TAP TA

FIGURE 4664 Ultrasound image of TAP block. SQ, subcutaneous tissue; EO, external oblique; IO, internal oblique; TA, transversus abdominis; TAP, transversus abdominis plane.

to the anterior superior iliac spine (Figure 46–64). Muscles appear as striated hypoechoic structures with hyperechoic layers of fascia at their borders. A long (10-cm) needle is inserted in-plane just lateral (posterior) to the transducer and advanced, noting tactile feedback from fascial planes, to the hyperechoic effacement of the deep border of internal oblique and the superficial border of transversus abdominis. Following careful aspiration for the nonappearance of blood, 20 mL of local anesthetic is injected, observing for an elliptical separation between the two fascial layers (Figure 46–64).

SUGGESTED READING Capdevila X, Coimbra C, Choquet O: Approaches to the lumbar plexus: Success, risks, and outcome. Reg Anesth Pain Med 2005;30:150.

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Hadzic A (editor): Peripheral Nerve Blocks and Anatomy for Ultrasound-guided Regional Anesthesia, 2nd ed. McGraw-Hill Medical, 2012. Hebl JR, Lennon RL (editors): Mayo Clinic Atlas of Regional Anesthesia and Ultrasound-Guided Nerve Blockade. Oxford University Press, 2010. Heil JW, Ilfeld BM, Loland VJ, et al: Ultrasound-guided transversus abdominis plane catheters and ambulatory perineural infusions for outpatient inguinal hernia repair. Reg Anesth Pain Med 2010;35:556. Horn JL, Pitsch T, Salinas F, Benninger B: Anatomic basis to the ultrasound-guided approach for saphenous nerve blockade. Reg Anesth Pain Med 2009;34:486. Ilfeld BM: Continuous peripheral nerve blocks: A review of the published evidence. Anesth Analg 2011;113:904. Ilfeld BM, Fredrickson MJ, Mariano ER: Ultrasoundguided perineural catheter insertion: Three approaches, but little illuminating data. Reg Anesth Pain Med 2010;35:123. Mariano ER, Loland VJ, Sandhu NS, et al: Ultrasound guidance versus electrical stimulation for femoral perineural catheter insertion. J Ultrasound Med 2009;28:1453. Perlas A, Brull R, Chan VW, et al: Ultrasound guidance improves the success of sciatic nerve block at the popliteal fossa. Reg Anesth Pain Med. 2008;33:259. Perlas A, Chan VW, Simons M: Brachial plexus examination and localization using ultrasound and electrical stimulation: A volunteer study. Anesthesiology 2003;99:429. Sites BD, Brull R, Chan VW, et al: Artifacts and pitfall errors associated with ultrasound-guided regional anesthesia. Part I: Understanding the basic principles of ultrasound physics and machine operations. Reg Anesth Pain Med 2007;32: 412. Sites BD, Brull R, Chan VW, et al: Artifacts and pitfall errors associated with ultrasound-guided regional anesthesia. Part II: A pictorial approach to understanding and avoidance. Reg Anesth Pain Med. 2007;32:419.

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Anesthetic Complications

H

A

P

T

E

R

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KEY CONCEPTS 1

2

The rate of anesthetic complications will never be zero. All anesthesia practitioners, irrespective of their experience, abilities, diligence, and best intentions, will participate in anesthetics that are associated with patient injury. Malpractice occurs when four requirements have been met: (1) the practitioner must have a duty to the patient; (2) there must have been a breach of duty (deviation from the standard of care); (3) the patient (plaintiff ) must have suffered an injury; and (4) the proximate cause of the injury must have been the practitioner’s deviation from the standard of care.

3

Anesthetic mishaps can be categorized as preventable or unpreventable. Of the preventable incidents, most involve human error, as opposed to equipment malfunctions.

4

The relative decrease in death attributed to respiratory rather than cardiovascular damaging events has been attributed to the increased use of pulse oximetry and capnometry.

5

Many anesthetic fatalities occur only after a series of coincidental circumstances, misjudgments, and technical errors coincide (mishap chain).

6

Despite differing mechanisms, anaphylactic and anaphylactoid reactions are typically clinically indistinguishable and equally life-threatening.

7

True anaphylaxis due to anesthetic agents is rare; anaphylactoid reactions are much more common. Muscle relaxants are the most common cause of anaphylaxis during anesthesia.

8

Patients with spina bifida, spinal cord injury, and congenital abnormalities of the genitourinary tract have a very increased incidence of latex allergy. The incidence of latex anaphylaxis in children is estimated to be 1 in 10,000.

9

Although there is no clear evidence that exposure to trace amounts of anesthetic agents presents a health hazard to operating room personnel, the United States Occupational Health and Safety Administration continues to set maximum acceptable trace concentrations of less than 25 ppm for nitrous oxide and 0.5 ppm for halogenated anesthetics (2 ppm if the halogenated agent is used alone).

10 Hollow (hypodermic) needles pose a greater

risk than do solid (surgical) needles because of the potentially larger inoculum. The use of gloves, needleless systems, or protected needle devices may decrease the incidence of some (but not all) types of injury. —Continued next page

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Continued— 11 Anesthesiology is a high-risk medical

specialty for substance abuse. 12 The three most important methods of

minimizing radiation doses are limiting total

1 The rate of anesthetic complications will never

be zero. All anesthesia practitioners, irrespective of their experience, abilities, diligence, and best intentions, will participate in anesthetics that are associated with patient injury. Moreover, unexpected adverse perioperative outcomes can lead to litigation, even if those outcomes did not directly arise from anesthetic mismanagement. This chapter reviews management approaches to complications secondary to anesthesia and discusses medical malpractice and legal issues from an American (USA) perspective. Readers based in other countries may not find this section to be as relevant to their practices.

LITIGATION AND ANESTHETIC COMPLICATIONS All anesthesia practitioners will have patients with adverse outcomes, and in the USA most anesthesiologists will at some point in their career be involved to one degree or another in malpractice litigation. Consequently, all anesthesia staff should expect litigation to be a part of their professional lives and acquire suitably solvent medical malpractice insurance with coverage appropriate for the community in which they practice. When unexpected events occur, anesthesia staff must generate an appropriate differential diagnosis, seek necessary consultation, and execute a treatment plan to mitigate (to the greatest degree possible) any patient injury. Appropriate documentation in the patient record is helpful, as many adverse outcomes will be reviewed by facility-based and practice-based quality assurance and performance improvement authorities. Deviations from acceptable practice will likely be noted in the practitioner’s

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exposure time during procedures, using proper barriers, and maximizing one’s distance from the source of radiation.

quality assurance file. Should an adverse outcome lead to litigation, the medical record documents the practitioner’s actions at the time of the incident. Often years pass before litigation proceeds to the point where the anesthesia provider is asked about the case in question. Although memories fade, a clear and complete anesthesiology record can provide convincing evidence that a complication was recognized and appropriately treated. A lawsuit may be filed, despite a physician’s best efforts to communicate with the patient and family about the intraoperative events, management decisions, and the circumstances surrounding an adverse event. It is often not possible to predict which cases will be pursued by plaintiffs! Litigation may be pursued when it is clear (at least to the defense team) that the anesthesia care conformed to standards, and, conversely, that suits may not be filed when there is obvious anesthesia culpability. That said, anesthetics that are followed by unexpected death, paralysis, or brain injury of young, economically productive individuals are particularly attractive to plaintiff ’s lawyers. When a patient has an unexpectedly poor outcome, one should expect litigation irrespective of one’s “positive” relationship with the patient or the injured patient’s family or guardians. 2 Malpractice occurs when four requirements are met: (1) the practitioner must have a duty to the patient; (2) there must have been a breach of duty (deviation from the standard of care); (3) the patient (plaintiff ) must have suffered an injury; and (4) the proximate cause of the injury must have been the practitioner’s deviation from the standard of care. A duty is established when the practitioner has an obligation to provide care (doctor–patient relationship). The practitioner’s failure to execute that duty

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constitutes a breach of duty. Injuries can be physical, emotional, or financial. Causation is established; if but for the breach of duty, the patient would not have experienced the injury. When a claim is meritorious, the tort system attempts to compensate the injured patient and/or family members by awarding them monetary damages. Being sued is stressful, regardless of the perceived “merits” of the claim. Preparation for defense begins before an injury has occurred. Anesthesiology staff should carefully explain the risks and benefits of the anesthesia options available to the patient. The patient grants informed consent following a discussion of the risks and benefits. Informed consent does not consist of handing the patient a form to sign. Informed consent requires that the patient understand the choices being presented. As previously noted, appropriate documentation of patient care activities, differential diagnoses, and therapeutic interventions helps to provide a defensible record of the care that was provided, resistant to the passage of time and the stress of the litigation experience. When an adverse outcome occurs, the hospital and/or practice risk management group should be immediately notified. Likewise, one’s liability insurance carrier should be notified of the possibility of a claim for damages. Some policies have a clause that disallows the practitioner from admitting errors to patients and families. Consequently, it is important to know and obey the institution’s and insurer’s approach to adverse outcomes. Nevertheless, most risk managers advocate a frank and honest disclosure of adverse events to patients or approved family members. It is possible to express sorrow about an adverse outcome without admitting “guilt.” Ideally, such discussions should take place in the presence of risk management personnel and/or a departmental leader. It must never be forgotten that the tort system is designed to be adversarial. Unfortunately, this makes every patient a potential courtroom adversary. Malpractice insurers will hire a defense firm to represent the anesthesia staff involved. Typically, multiple practitioners and the hospitals in which they work will be named to involve the maximal number of insurance policies that might pay in the

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event of a plaintiff ’s victory, and to ensure that the defendants cannot choose to attribute “blame” for the adverse event to whichever person or entity was not named in the suit. In some systems (usually when everyone in a health system is insured by the same carrier), all of the named entities are represented by one defense team. More commonly, various insurers and attorneys represent specific practitioners and institutional providers. In this instance, those involved may deflect and diffuse blame from themselves and focus blame on others also named in the action. One should not discuss elements of any case with anyone other than a risk manager, insurer, or attorney, as other conversations are not protected from discovery. Discovery is the process by which the plaintiff ’s attorneys access the medical records and depose witnesses under oath to establish the elements of the case: duty, breach, injury, and causation. False testimony can lead to criminal charges of perjury. Oftentimes, expediency and financial risk exposure will argue for settlement of the case. The practitioner may or may not be able to participate in this decision depending upon the insurance policy. Settled cases are reported to the National Practitioner Data Bank and become a part of the physician’s record. Moreover, malpractice suits, settlements, and judgments must be reported to hospital authorities as part of the credentialing process. When applying for licensure or hospital appointment, all such actions must be reported. Failure to do so can lead to adverse consequences. The litigation process begins with the delivery of a summons indicating that an action is pending. Once delivered, the anesthesia defendant must contact his or her malpractice insurer/risk management department, who will appoint legal counsel. Counsel for both the plaintiff and defense will identify “independent experts” to review the cases. These “experts” are paid for their time and expenses and can arrive at dramatically different assessments of the case materials. Following review by expert consultants, the plaintiff ’s counsel may depose the principal actors involved in the case. Providing testimony can be stressful. Generally, one should follow the advice of one’s defense attorney. Oftentimes, plaintiff ’s attorneys will attempt to anger or confuse the deponent,

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hoping to provoke a response favorable to the claim. Most defense attorneys will advise their clients to answer questions as literally and simply as possible, without offering extraneous commentary. Should the plaintiff ’s attorney become abusive, the defense attorney will object for the record. However, depositions, also known as “examinations before trial,” are not held in front of a judge (only the attorneys, the deponent, the court reporter[s], and [sometimes] the videographer are present). Obligatory small talk often occurs among the attorneys and the court reporters. This is natural and should not be a source of anxiety for the defendant, because in most localities, the same plaintiff ’s and defense attorneys see each other regularly. Following discovery, the insurers, plaintiffs, and defense attorneys will “value” the case and attempt to monetize the damages. Items, such as pain and suffering, loss of consortium with spouses, lost wages, and many other factors, are included in determining what the injury is worth. Also during this period, the defense attorney may petition the court to grant defendants a “summary judgment,” dismissing the defendant from the case if there is no evidence of malpractice elicited during the discovery process. At times, the plaintiff ’s attorneys will dismiss the suit against certain named individuals after they have testified, particularly when their testimony implicates other named defendants. Settlement negotiations will occur in nearly every action. Juries are unpredictable, and both parties are often hesitant to take a case to trial. There are expenses associated with litigation, and, consequently, both plaintiff and defense attorneys will try to avoid uncertainties. Many anesthesia providers will not want to settle a case because the settlement must be reported. Nonetheless, an award in excess of the insurance policy maximum may (depending on the jurisdiction) place the personal assets of the defendant providers at risk. This underscores the importance of our advice to all practitioners (not only those involved in a lawsuit) to assemble their personal assets (house, retirement fund, etc.) in a fashion that makes personal asset confiscation difficult in the event of a negative judgment. One should remember that an adverse judgment may arise from a case in which

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most anesthesiologists would find the care to meet acceptable standards! When a case proceeds to trial, the first step is jury selection in the process of voir dire—from the French—“to see, to say.” In this process, attorneys for the plaintiff and defendant will use various profiling techniques to attempt to identify (and remove) jurors who are less likely to be sympathetic to their case, while keeping the jurors deemed most likely to favor their side. Each attorney is able to strike a certain number of jurors from the pool because they perceive an inherent bias. The jurors will be questioned about such matters as their educational level, history of litigation themselves, professions, and so forth. Following empanelment, the case is presented to the jury. Each attorney attempts to educate the jurors—who usually have limited knowledge of healthcare (physicians and nurses will usually be struck from the jury)—as to the standard of care for this or that procedure and how the defendants did or did not breach their duty to the patient to uphold those standards. Expert witnesses will attempt to define what the standard of care is for the community, and the plaintiff and defendant will present experts with views that are favorable to their respective cause. The attorneys will attempt to discredit the opponent’s experts and challenge their opinions. Exhibits are often used to explain to the jury what should or should not have happened and why the injuries for which damages are being sought were caused by the practitioner’s negligence. After the attorneys conclude their closing remarks, the judge will “charge” the jurors with their duty and will delineate what they can consider in making their judgment. Once a case is in the hands of a jury, anything can happen. Many cases will settle during the course of the trial, as neither party wishes to be subject to the arbitrary decisions of an unpredictable jury. Should the case not settle, the jurors will reach a verdict. When a jury determines that the defendants were negligent and negligence was the cause of the plaintiff ’s injuries, the jury will determine an appropriate award. If the award is so egregiously large that it is inconsistent with awards for similar injuries, the judge may reduce its amount. Of course, following any verdict, there are

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numerous appeals that may be filed. It is important to note that appeals typically do not relate to the medical aspects of the case, but are filed because the trial process itself was somehow flawed. Unfortunately, a malpractice action can take years to reach a conclusion. Consultation with a mental health professional may be appropriate for the defendant when the litigation process results in unmanageable stress, depression, increased alcohol consumption, or substance abuse. Determining what constitutes the “standard of care” is increasingly complicated. In the United Sates, the definition of “standard of care” is made separately by each state. The standard of care is NOT necessarily “best practices” or even the care that another physician would prefer. Generally, the standard of care is met when a patient receives care that other reasonable physicians in similar circumstances would regard as adequate. The American Society of Anesthesiologists (ASA) has published standards, and these provide a basic framework for routine anesthetic practice (eg, monitoring). Increasingly, a number of “guidelines” have been developed by the multiple specialty societies to identify best practices in accordance with assessments of the evidence in the literature. The increasing number of guidelines proffered by the numerous anesthesia and other societies and their frequent updating can make it difficult for clinicians to stay abreast of the changing nature of practice. This is a particular problem when two societies produce conflicting guidelines on the same topic using the same data. Likewise, the information upon which guidelines are based can range from randomized clinical trials to the opinion of “experts” in the field. Consequently, guidelines do not hold the same weight as standards. Guidelines produced by reputable societies will generally include an appropriate disclaimer based on the level of evidence used to generate the guideline. Nonetheless, plaintiff ’s attorneys will attempt to use guidelines to establish a “standard of care,” when, in fact, clinical guidelines are prepared to assist in guiding the delivery of therapy. However, if deviation from guidelines is required for good patient care, the rationale for such actions should be documented on the anesthesia record, as plaintiff ’s attorneys will attempt to use the guideline as a de facto standard of care.

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ADVERSE ANESTHETIC OUTCOMES Incidence There are several reasons why it is difficult to accurately measure the incidence of adverse anesthesia-related outcomes. First, it is often difficult to determine whether the cause of a poor outcome is the patient’s underlying disease, the surgical procedure, or the anesthetic management. In some cases, all three factors contribute to a poor outcome. Clinically important measurable outcomes are relatively rare after elective anesthetics. For example, death is a clear endpoint, and perioperative deaths do occur with some regularity. But, because deaths attributable to anesthesia are much rarer, a very large series of patients must be studied to assemble conclusions that have statistical significance. Nonetheless, many studies have attempted to determine the incidence of complications due to anesthesia. Unfortunately, studies vary in criteria for defining an anesthesiarelated adverse outcome and are limited by retrospective analysis. Perioperative mortality is usually defined as death within 48 hr of surgery. It is clear that most perioperative fatalities are due to the patient’s preoperative disease or the surgical procedure. In a study conducted between 1948 and 1952, anesthesia mortality in the United States was approximately 5100 deaths per year or 3.3 deaths per 100,000 population. A review of cause of death files in the United States showed that the rate of anesthesia-related deaths was 1.1/1,000,000 population or 1 anesthetic death per 100,000 procedures between 1999 and 2005 (Figure 54–1). These results suggest a 97% decrease in anesthesia mortality since the 1940s. However, a 2002 study reported an estimated rate of 1 death per 13,000 anesthetics. Due to differences in methodology, there are discrepancies in the literature as to how well anesthesiology is doing in achieving safe practice. In a 2008 study of 815,077 patients (ASA class 1, 2, or 3) who underwent elective surgery at US Department of Veterans Affairs hospitals, the mortality rate was 0.08% on the day of surgery. The strongest association with perioperative death was the type of surgery (Figure 54–2). Other factors associated with increased risk of death

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Deaths/million surgical discharges

25

20

15

10

5

0

0–4

5–14

15–24 25–34 35–44 45–54 55–64 65–74 75–84

≥85

Age (years)

FIGURE 541 Annual in-hospital anesthesia-related deaths rates per million hospital surgical discharges and 95% confidence intervals by age, United States, 1999-2005.

(Reproduced, with permission, from Li G, Warner M, Lang B, et al: Epidemiology of anesthesia-related mortality in the United States 1999-2005. Anesthesiology 2009;110:759.)

included dyspnea, reduced albumin concentrations, increased bilirubin, and increased creatinine concentrations. A subsequent review of the 88 deaths that occurred on the surgical day noted that 13 of

the patients might have benefitted from better anesthesia care, and estimates suggest that death might have been prevented by better anesthesia practice in 1 of 13,900 cases. Additionally, this study reported

Spine Intracranial Urologic Abdominal Head/Neck Other Vasc. Aortic Thoracic Bone 0

20

40

60

80

100

120

140

160

Number of deaths

FIGURE 542 Total number of deaths by type of surgery in Veterans Affairs hospitals. (Reproduced, with permission, from Bishop M, Souders J, Peterson C, et al: Factors associated with unanticipated day of surgery deaths in Department of Veterans Affairs hospitals. Anesth Analg 2008;107:1924.)

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that the immediate postsurgical period tended to be the time of unexpected mortality. Indeed, often missed opportunities for improved anesthetic care occur following complications when “failure to rescue” contributes to patient demise.

American Society of Anesthesiologists Closed Claims Project The goal of the ASA Closed Claims Project is to identify common events leading to claims in anesthesia, patterns of injury, and strategies for injury prevention. It is a collection of closed malpractice claims that provides a “snapshot” of anesthesia liability rather than a study of the incidence of anesthetic complications, as only events that lead to the filing of a malpractice claim are considered. The Closed Claims Project consists of trained physicians who review claims against anesthesiologists represented by some US malpractice insurers. The number of claims in the database continues to rise each year as new claims are closed and reported. The claims are grouped according to specific damaging events and complication type. Closed Claims Project analyses have been reported for airway injury, nerve injury, awareness, and so forth. These analyses provide insights into the circumstances that result in claims; however, the incidence of a complication cannot be determined from closed claim data, because we know neither the actual incidence of the complication (some with the complication may not file suit), nor how many anesthetics were performed for which the particular complication might possibly develop. Other similar analyses have been performed in the United Kingdom, where National Health Service (NHS) Litigation Authority claims are reviewed.

Causes

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TABLE 541 Human errors that may lead to preventable anesthetic accidents. Unrecognized breathing circuit disconnection Mistaken drug administration Airway mismanagement Anesthesia machine misuse Fluid mismanagement Intravenous line disconnection

malfunctions (Table 54–2). Unfortunately, some rate of human error is inevitable, and a preventable accident is not necessarily evidence of incompetence. During the 1990s, the top three causes for claims in the ASA Closed Claims Project were death (22%), nerve injury (18%), and brain damage (9%). In a 2009 report based on an analysis of NHS litigation records, anesthesia-related claims accounted for 2.5% of total claims filed and 2.4% of the value of all NHS claims. Moreover, regional and obstetrical anesthesia were responsible for 44% and 29%, respectively, of anesthesia-related claims filed. The authors of the latter study noted that there are two ways to examine data related to patient harm: critical incident and closed claim analyses. Clinical (or critical) incident data consider events that either cause harm or result in a “near-miss.” Comparison between clinical incident datasets and closed claims analyses demonstrates that not all critical events generate claims and that claims may be filed in the absence of negligent care. Consequently, closed claims reports must always be considered in this context.

MORTALITY AND BRAIN INJURY Trends in anesthesia-related death and brain damage have been tracked for many years. In a Closed Claims Project report examining claims in the

3 Anesthetic mishaps can be categorized as

preventable or unpreventable. Examples of the latter include sudden death syndrome, fatal idiosyncratic drug reactions, or any poor outcome that occurs despite proper management. However, studies of anesthetic-related deaths or near misses suggest that many accidents are preventable. Of these preventable incidents, most involve human error (Table 54–1), as opposed to equipment

Morg_Ch54_1199-1230.indd 1205

TABLE 542 Equipment malfunctions that may lead to preventable anesthetic accidents. Breathing circuit Monitoring device Ventilator Anesthesia machine Laryngoscope

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# of claims per year

A 400 300 200 100 0

1975

1980

1985

1975

1980

1985

1990

1995

2000

% per year

B 60 40 20 0 1990 1995 2000 p<0.01 over years (logistic regression)

FIGURE 543 A: The total number of claims by the year of injury. Retrospective data collection began in 1985. Data in this analysis includes data collected through December 2003. B: Claims for death or permanent brain

damage as percentage of total claims per year by year of injury. (Reproduced, with permission, from Cheney FW, Domino KB,

period between 1975 and 2000, there were 6750 claims (Figure 54–3A and B), 2613 of which were for brain injury or death. The proportion of claims for brain injury or death was 56% in 1975, but had decreased to 27% by 2000. The primary pathological mechanisms by which these outcomes occurred were related to cardiovascular or respiratory problems. Early in the study period, respiratory-related damaging events were responsible for more than 50% of brain injury/death claims, whereas cardiovascular-related damaging events were responsible for 27% of such claims; however, by the late 1980s, the percentage of damaging events related to respiratory issues had decreased, with both respiratory and cardiovascular events being equally likely to contribute to severe brain injury or death. Respiratory damaging events included difficult airway, esophageal intubation, and unexpected extubation. Cardiovascular damaging events were usually multifactorial. Closed claims reviewers found that anesthesia care was substandard in 64% of claims in which respiratory complications contributed to brain injury or death, but in only 28% of cases in

which the primary mechanism of patient injury was cardiovascular in nature. Esophageal intubation, premature extubation, and inadequate ventilation were the primary mechanisms by which less than optimal anesthetic care was thought to have contributed to patient injury related to respiratory events. 4 The relative decrease in causes of death being attributed to respiratory rather cardiovascular damaging events during the review period was attributed to the increased use of pulse oximetry and capnometry. Consequently, if expired gas analysis was judged to be adequate, and a patient suffered brain injury or death, a cardiovascular event was more likely to be considered causative. A 2010 study examining the NHS Litigation Authority dataset noted that airway-related claims led to higher awards and poorer outcomes than did nonairway-related claims. Indeed, airway manipulation and central venous catheterization claims in this database were most associated with patient death. Trauma to the airway also generates significant claims if esophageal or tracheal rupture occur. Postintubation mediastinitis should always

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Caplan RA, Posner KL: Nerve injury associated with anesthesia: a closed claims analysis. Anesthesiology 1999;90:1062.)

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1207

Swelling/ inflammation/ infection 17% Nerve damage 17%

Skin slough or necrosis 28%

Burns from treatment of IV infiltration 3% Frivolous 6%

Fasciotomy scar 16%

Miscellaneous 6%

Air embolism 8%

be considered whenever there are repeated unsuccessful airway manipulations, as early intervention presents the best opportunity to mitigate any injuries incurred.

VASCULAR CANNULATION Claims related to central venous access in the ASA database were associated with patient death 47% of the time and represented 1.7% of the 6449 claims reviewed. Complications secondary to guidewire or catheter embolism, tamponade, bloodstream infections, carotid artery puncture, hemothorax, and pneumothorax all contributed to patient injury. Although guidewire and catheter embolisms were associated with generally lower level patient injuries, these complications were generally attributed to substandard care. Tamponade claims following line placement were often for patient death. The authors of a 2004 closed claims analysis recommended reviewing the chest radiograph following line placement and repositioning lines found in the heart or at an acute angle to reduce the likelihood of tamponade. Brain damage and stroke are associated with claims secondary to carotid cannulation. Multiple confirmatory methods should be used to ensure that the internal jugular and not the carotid artery is cannulated. Claims related to peripheral vascular cannulation in the ASA database accounted for 2% of 6849 claims, 91% of which were for complications secondary to the extravasation of fluids or drugs

Morg_Ch54_1199-1230.indd 1207

FIGURE 544 Injuries related to IV catheters (n = 127). (Reproduced, with permission, from Bhananker S, Liau D, Kooner P, et al: Liability related to peripheral venous and arterial catheterization: a closed claims analysis. Anesth Analg 2009;109:124.)

from peripheral intravenous catheters that resulted in extremity injury (Figure 54–4). Air embolisms, infections, and vascular insufficiency secondary to arterial spasm or thrombosis also resulted in claims. Of interest, intravenous catheter claims in patients who had undergone cardiac surgery formed the largest cohort of claims related to peripheral intravenous catheters, most likely due to the usual practice of tucking the arms alongside the patient during the procedure, placing them out of view of the anesthesia providers. Radial artery catheters seem to generate few closed claims; however, femoral artery catheters can lead to greater complications and potentially increased liability exposure.

OBSTETRIC ANESTHESIA Both critical incident and closed claims analyses have been reported regarding complications and mortality related to obstetrical anesthesia. In a study reviewing anesthesia-related maternal mortality in the United States using the Pregnancy Mortality Surveillance System, which collects data on all reported deaths causally related to pregnancy, 86 of the 5946 pregnancy-related deaths reported to the Centers for Disease Control were thought to be anesthesia related or approximately 1.6% of total pregnancy related-deaths in the period 1991–2002. The anesthesia mortality rate in this period was 1.2 per million live births, compared with 2.9 per million live births in the

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period 1979–1990. The decline in anesthesiarelated maternal mortality may be secondary to the decreased use of general anesthesia in parturients, reduced concentrations of bupivacaine in epidurals, improved airway management protocols and devices, and greater use of incremental (rather than bolus) dosing of epidural catheters. In a 2009 study examining the epidemiology of anesthesia-related complications in labor and delivery in New York state in the period 2002–2005, an anesthesia-related complication was reported in 4438 of 957,471 deliveries (0.46%). The incidence of complications was increased in patients undergoing cesarean section, those living in rural areas, and those with other medical conditions. Complications of neuraxial anesthesia (eg, postdural puncture headache) were most common, followed by systemic complications, including aspiration or cardiac events. Other reported problems related to anesthetic dose administration and unintended overdosages. African American women and those aged 40–55 years were more likely to experience systemic complications, whereas Caucasian women and those aged 30–39 were more likely to experience complications related to neuraxial anesthesia. ASA Closed Claims Project analyses were reported in 2009 for the period 1990–2003. Four hundred twenty-six claims from this period were compared with 190 claims in the database prior to 1990. After 1990, the proportion of claims for maternal or fetal demise was lower than that recorded prior to 1990. After 1990, the number of claims for maternal nerve injury increased. In the review of claims in which anesthesia was thought to have contributed to the adverse outcome, anesthesia delay, poor communication, and substandard care were thought to have resulted in poor newborn outcomes. Prolonged attempts to secure neuraxial blockade in the setting of emergent cesarean section can contribute to adverse fetal outcome. Additionally, the closed claims review indicated that poor communication between the obstetrician and the anesthesiologist regarding the urgency of newborn delivery was likewise thought to have contributed to newborn demise and neonatal brain injury. Maternal death claims were secondary to airway difficulty, maternal hemorrhage, and high neuraxial

Morg_Ch54_1199-1230.indd 1208

blockade. The most common claim associated with obstetrical anesthesia was related to nerve injury following regional anesthesia. Nerve injury can be secondary to neuraxial anesthesia and analgesia, but also due to obstetrical causes. Early neurological consultation to identify the source of nerve injury is suggested to discern if injury could be secondary to obstetrical rather than anesthesia interventions.

REGIONAL ANESTHESIA In a closed claims analysis, peripheral nerve blocks were involved in 159 of the 6894 claims analyzed. Peripheral nerve block claims were for death (8%), permanent injuries (36%), and temporary injuries (56%). The brachial plexus was the most common location for nerve injury. In addition to ocular injury, cardiac arrest following retrobulbar block contributed to anesthesiology claims. Cardiac arrest and epidural hematomas are two of the more common damaging events leading to severe injuries related to regional anesthesia. Neuraxial hematomas in both obstetrical and nonobstetrical patients were associated with coagulopathy (either intrinsic to the patient or secondary to medical interventions). In one study, cardiac arrest related to neuraxial anesthesia contributed to roughly one-third of the death or brain damage claims in both obstetrical and nonobstetrical patients. Accidental intravenous injection and local anesthesia toxicity also contributed to claims for brain injury or death. Nerve injuries constitute the third most common source of anesthesia litigation. A retrospective review of patient records and a claims database showed that 112 of 380,680 patients (0.03%) experienced perioperative nerve injury. Patients with hypertension and diabetes and those who were smokers were at increased risk of developing perioperative nerve injury. Perioperative nerve injuries may result from compression, stretch, ischemia, other traumatic events, and unknown causes. Improper positioning can lead to nerve compression, ischemia, and injury, however not every nerve injury is the result of improper positioning. The care received by patients with ulnar nerve injury was rarely judged to be inadequate in the ASA Closed Claims database. Even awake patients undergoing

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CHAPTER 54 Anesthetic Complications

spinal anesthesia have been reported to experience upper extremity injury. Moreover, many peripheral nerve injuries do not become manifest until more than 48 hr after anesthesia and surgery, suggesting that some nerve damage that occurs in surgical patients may arise from events taking place after the patient leaves the operating room setting.

PEDIATRIC ANESTHESIA In a 2007 study reviewing 532 claims in pediatric patients aged <16 years in the ASA Closed Claims database from 1973–2000 (Figure 54–5), a decrease in the proportion of claims for death and brain damage was noted over the three decades. Likewise, the percentage of claims related to respiratory events also was reduced. Compared with before 1990, the percentage of claims secondary to respiratory events decreased during the years 1990–2000, accounting for only 23 % of claims in the latter study years compared with 51% of claims in the 1970s. Moreover, the percentage of claims that could be avoided by better monitoring decreased from 63% in the 1970s to 16% in the 1990s. Death and brain damage constitute the major complications for which claims are filed. In the 1990s, cardiovascular events joined respiratory complications in sharing the primary causes of pediatric anesthesia litigation. In

1209

the study mentioned above, better monitoring and newer airway management techniques may have reduced the incidence of respiratory events leading to litigation-generating complications in the latter years of the review period. Additionally, the possibility of a claim being filed secondary to death or brain injury is greater in children who are in ASA classes 3, 4, or 5. In a review of the Pediatric Perioperative Cardiac Arrest Registry, which collects information from about 80 North American institutions that provide pediatric anesthesia, 193 arrests were reported in children between 1998 and 2004. During the study period, 18% of the arrests were “drug related,” compared with 37% of all arrests during the years 1994–1997. Cardiovascular arrests occurred most often (41%), with hypovolemia and hyperkalemia being the most common causes. Respiratory arrests (27%) were most commonly associated with laryngospasm. Central venous catheter placement with resultant vascular injury also contributed to some perioperative arrests. Arrests from cardiovascular causes occurred most frequently during surgery, whereas arrests from respiratory causes tended to occur after surgery. The reduced use of halothane seems to have decreased the incidence of arrests secondary to medication administration. However, hyperkalemia and electrolyte disturbances

90%

% of alms in time period

80%

Death or permanent brain damage

70% 60%

Preventable by monitoring

50% 40%

Respiratory events

30% 20% 10%

Cardiovascular events

19 7

3– 19 19 77 76 – 19 19 79 78 – 19 19 81 80 – 19 19 83 82 – 19 19 85 84 – 19 19 87 86 – 19 19 89 88 – 19 19 91 90 – 19 19 93 92 – 19 19 95 94 – 19 19 97 96 –2 00 0

0%

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FIGURE 545 Trends over time. Outcome, type of event, and prevention by better monitoring. Years are grouped for illustration. (Reproduced, with permission, from Jimenez N, Posner K, Cheney F, et al: An update on pediatric anesthesia liability: a closed claims analysis. Anesth Analg 2007;104:147.)

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associated with transfusion and hypovolemia also contribute to sources of cardiovascular arrest in children perioperatively. A review of data from the Pediatric Perioperative Cardiac Arrest Registry with a focus on children with congenital heart disease found that such children were more likely to arrest perioperatively secondary to a cardiovascular cause. In particular, children with a single ventricle were at increased risk of perioperative arrest. Children with aortic stenosis and cardiomyopathy were similarly found to be at increased risk of cardiac arrest perioperatively.

OUT OF THE OPERATING ROOM ANESTHESIA AND MONITORED ANESTHESIA CARE Review of the ASA Closed Claims Project database indicates that anesthesia at remote (out of the operating room) locations poses a risk to patients secondary to hypoventilation and excessive sedation. Remote location anesthesia care was more likely than operating room anesthesia care to involve a claim for death (54% vs 29%, respectively). The endoscopy suite and cardiac catheterization laboratory were the most frequent locations from which claims were generated. Monitored Anesthesia Care (MAC) was the most common technique employed in these claims. Overwhelmingly, adverse respiratory events were most frequently responsible for the injury. An analysis of the ASA Closed Claims Project database focusing on MAC likewise revealed that oversedation and respiratory collapse most frequently lead to claims. Claims for burn injuries suffered in operating room fires were also found in the database. Supplemental oxygen, draping, pooling of flammable antiseptic preparatory solutions, and surgical cautery combine to produce the potential for operating room fires.

EQUIPMENT PROBLEMS “Equipment problems” is probably a misnomer; the ASA Closed Claims Project review of 72 claims involving gas delivery systems found that equipment misuse was three times more common than equipment malfunction. The majority (76%) of adverse

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TABLE 543 Factors associated with human errors and equipment misuse. Factor

Example

Inadequate preparation

No machine checkout or preoperative evaluation; haste and carelessness; production pressure

Inadequate experience and training

Unfamilarity with anesthetic technique or equipment

Environmental limitations

Inability to visualize surgical field: poor communication with surgeons

Physical and emotional factors

Fatigue; distraction caused by personal problems

outcomes associated with gas delivery problems were either death or permanent neurological damage. Errors in drug administration also typically involve human error. It has been suggested that as many as 20% of the drug doses given to hospitalized patients are incorrect. Errors in drug administration account for 4% of cases in the ASA Closed Claims Project, which found that errors resulting in claims were most frequently due to either incorrect dosage or unintentional administration of the wrong drug (syringe swap). In the latter category, accidental administration of epinephrine proved particularly dangerous. Another type of human error occurs when the most critical problem is ignored because attention is inappropriately focused on a less important problem or an incorrect solution (fixation error). Serious anesthetic mishaps are often associated with distractions and other factors (Table 54–3). The impact of most equipment failures is decreased or avoided when the problem is identified during a routine preoperative checkout performed by adequately 5 trained personnel. Many anesthetic fatalities occur only after a series of coincidental circumstances, misjudgments, and technical errors coincide (mishap chain).

Prevention Strategies to reduce the incidence of serious anesthetic complications include better monitoring and anesthetic techniques, improved education, more

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comprehensive protocols and standards of practice, and active risk management programs. Better monitoring and anesthetic techniques imply more comprehensive monitoring and ongoing patient assessments and better designed anesthesia equipment and workspaces. The fact that most accidents occur during the maintenance phase of anesthesia— rather than during induction or emergence—implies a failure of vigilance. Inspection, palpation, percussion, and auscultation of the patient provide important information. Instruments should supplement (but never replace) the anesthesiologist’s own senses. To minimize errors in drug administration, drug syringes and ampoules in the workspace should be restricted to those needed for the current specific case. Drugs should be consistently diluted to the same concentration in the same way for each use, and they should be clearly labeled. Computer systems for scanning bar-coded drug labels are available that may help to reduce medication errors. The conduct of all anesthetics should follow a predictable pattern by which the anesthetist actively surveys the monitors, the surgical field, and the patient on a recurrent basis. In particular, patient positioning should be frequently reassessed to avoid the possibility of compression or stretch injuries. When surgical necessity requires patients to be placed in positions where harm may occur or when hemodynamic manipulations (eg, deliberate hypotension) are requested or required, the anesthesiologist should note on the record the surgical request and remind the surgeon of any potential risks to the patient.

QUALITY MANAGEMENT Risk management and continuous quality improvement programs at the departmental level may reduce anesthetic morbidity and mortality rates by addressing monitoring standards, equipment, practice guidelines, continuing education, quality of care, and staffing issues. Specific responsibilities of peer review committees include identifying (and, ideally, preventing) potential problems, formulating and periodically revising departmental policies, ensuring the availability of properly functioning anesthetic equipment, enforcing standards required

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for clinical privileges, and evaluating the appropriateness and quality of patient care. A quality improvement system impartially and continuously reviews complications, compliance with standards, and quality indicators.

AIRWAY INJURY The daily insertion of endotracheal tubes, laryngeal mask airways, oral/nasal airways, gastric tubes, transesophageal echocardiogram (TEE) probes, esophageal (bougie) dilators, and emergency airways all involve the risk of airway structure damage. Common morbid complaints, such as sore throat and dysphagia, are usually self-limiting, but may also be nonspecific symptoms of more ominous complications. The most common persisting airway injury is dental trauma. In a retrospective study of 600,000 surgical cases, the incidence of injury requiring dental intervention and repair was approximately 1 in 4500. In most cases, laryngoscopy and endotracheal intubation were involved, and the upper incisors were the most frequently injured. Major risk factors for dental trauma included tracheal intubation, preexisting poor dentition, and patient characteristics associated with difficult airway management (including limited neck motion, previous head and neck surgery, craniofacial abnormalities, and a history of difficult intubation). Other types of airway trauma are rare. Although there are scattered case reports in the literature, the most comprehensive analysis was performed by the ASA Closed Claims Project. This report describes 266 claims, of which the least serious were temporomandibular joint (TMJ) injuries that were all associated with otherwise uncomplicated intubations and occurred mostly in females younger than age 60 years. Approximately 25% of these patients had previous TMJ disease. Laryngeal injuries included vocal cord paralysis, granuloma, and arytenoid dislocation. Most tracheal injuries were associated with emergency surgical tracheotomy, but a few were related to endotracheal intubation. Some injuries occurred during seemingly easy, routine intubations. Proposed mechanisms include excessive tube movement in the trachea, excessive cuff inflation

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leading to pressure necrosis, and inadequate relaxation. Esophageal perforations contributed to death in 5 of 13 patients. Esophageal perforation often presents with delayed-onset subcutaneous emphysema or pneumothorax, unexpected febrile state, and sepsis. Pharyngoesophageal perforation is associated with difficult intubation, age over 60 years, and female gender. As in tracheal perforation, signs and symptoms are often delayed in onset. Initial sore throat, cervical pain, and cough often progressed to fever, dysphagia, and dyspnea, as mediastinitis, abscess, or pneumonia develop. Mortality rates of up to 50% have been reported after esophageal perforation, with better outcomes attributable to rapid detection and treatment. Minimizing the risk of airway injury begins with the preoperative assessment. A thorough airway examination will help to determine the risk for difficulty Documentation of current dentition (including dental work) should be included. Many practitioners believe preoperative consent should include a discussion of the risk of dental, oral, vocal cord, and esophageal trauma in every patient who could potentially need any airway manipulation. If a difficult airway is suspected, a more detailed discussion of risks (eg, emergency tracheotomy) is appropriate. In such cases, emergency airway supplies and experienced help should be available. The ASA algorithm for difficult airway management is a useful guide. After a difficult intubation, one should seek latent signs of esophageal perforation and have an increased level of suspicion for airway trauma. When intubation cannot be accomplished by routine means, the patient or guardian should be informed to alert future anesthesia providers of potential airway difficulty. Emergent nonoperating room intubations present unique challenges. In a review of 3423 out of the operating room intubations, 10% were considered to be “difficult,” and 4% of these intubations were associated with some form of complication, including aspiration, esophageal intubation, or dental injury. In this report, intubation bougies were employed in 56% of difficult intubations. The increased availability of video laryngoscopes and bougies have made emergent intubations less stressful and less likely to be unsuccessful.

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PERIPHERAL NERVE INJURY Nerve injury is a complication of being hospitalized, with or without surgery, regional, or general anesthesia. Peripheral nerve injury is a frequent and vexing problem. In most cases, these injuries resolve within 6–12 weeks, but some are permanent. Because peripheral neuropathies are commonly associated (often incorrectly!) with failures of patient positioning, a review of mechanisms and prevention is necessary. The most commonly injured peripheral nerve is the ulnar nerve (Figure 54–6). In a retrospective study of over 1 million patients, ulnar neuropathy (persisting for more than 3 months) occurred in approximately 1 in 2700 patients. Of interest, initial symptoms were most frequently noted more than 24 hr after a surgical procedure. Risk factors included male gender, hospital stay greater than 14 days, and very thin or obese body habitus. More than 50% of these patients regained full sensory and motor function within 1 yr. Anesthetic technique was not implicated as a risk factor; 25% of patients with ulnar neuropathy underwent monitored care or lower extremity regional technique. The ASA Closed Claims Project findings support most of these results, including the delayed onset of symptoms and the lack of relationship between anesthesia technique and injury. This study also noted that many neuropathies occurred despite notation of extra padding over the elbow area, further negating compression as a possible mechanism of injury. Finally, the ASA Closed Claims Project investigators found no deviation from the standard of care in the majority of patients who manifested nerve damage perioperatively.

The Role of Positioning Other peripheral nerve injuries seem to be more closely related to positioning or surgical procedure. They may involve the peroneal nerve, the brachial plexus, or the femoral and sciatic nerves. External pressure on a nerve could compromise its perfusion, disrupt its cellular integrity, and eventually result in edema, ischemia, and necrosis. Pressure injuries are particularly likely when nerves pass through closed compartments or take a superficial course (eg, the

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Humerus

Ulnar nerve Medial epicondyle

Arcuate ligament Olecranon process

A

Pronation

B

Supination

FIGURE 546 A: Pronation of the forearm can cause external compression of the ulnar nerve in the cubital tunnel. B: Forearm supination avoids this problem.

(Modified and reproduced, with permission, from Wadsworth TG: The cubital tunnel and the external compression syndrome. Anesth Analg 1974;53:303.)

peroneal nerve around the fibula). Lower extremity neuropathies, particularly those involving the peroneal nerve, have been associated with such factors as extreme degrees (high) and prolonged (greater than 2 h) durations of the lithotomy position. But, these nerve injuries also sometimes occur when such conditions are not present. Other risk factors for lower extremity neuropathy include hypotension, thin body habitus, older age, vascular disease, diabetes, and cigarette smoking. An axillary (chest) “roll” is commonly used to reduce pressure on the inferior shoulder of patients in the lateral decubitus position. This roll should be located caudad to the axilla to prevent direct pressure on the brachial plexus and large enough to relieve any pressure from the mattress on the lower shoulder. The data are convincing that some peripheral nerve injuries are not preventable. The risk of peripheral neuropathy should be included in

discussions leading to informed consent. When reasonable, patients with contractures (or other causes of limited flexibility) can be positioned before induction of anesthesia to check for feasibility and discomfort. Final positioning should be evaluated prior to draping. In most circumstances, the head and neck should be kept in a neutral position. Shoulder braces to support patients maintained in a Trendelenberg position should be avoided if possible, and shoulder abduction and lateral rotation should be minimized. The upper extremities should not be extended greater than 90° at any joint. (There should be no continuous external compression on the knee, ankle, or heel.) Although injuries may still occur, additional padding may be helpful in vulnerable areas. Documentation should include information on positioning, including the presence of padding. Finally, patients who complain of sensory or motor dysfunction in the postoperative period should be

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reassured that this is usually a temporary condition. Motor and sensory function should be documented. When symptoms persist for more than 24 hr, the patient should be referred to a neurologist (or a physiatrist or hand surgeon) who is knowledgeable about perioperative nerve damage for evaluation. Physiological testing, such as nerve conduction and electromyographic studies, can be useful to document whether nerve damage is a new or chronic condition. In the latter case, fibrillations will be observed in chronically denervated muscles.

Complications Related to Positioning Changes of body position have physiological consequences that can be exaggerated in disease states. General and regional anesthesia may limit the cardiovascular response to such a change. Even positions that are safe for short periods may eventually lead to complications in persons who are not able to move in response to pain. For example, the alcoholic patient who passes out on a hard floor or a park bench may awaken with a brachial plexus injury. Similarly, regional and general anesthesia abolish protective reflexes and predispose patients to injury.

Complications of postural hypotension, the most common physiological consequence of positioning, can be minimized by avoiding abrupt or extreme position changes (eg, sitting up quickly), reversing the position if vital signs deteriorate, keeping the patient well hydrated, and having vasoactive drugs available to treat hypotension. Whereas maintaining a reduced level of general anesthesia will decrease the likelihood of hypotension, light general anesthesia will increase the likelihood that movement of the endotracheal tube during positioning will cause the patient to cough and become hypertensive. Many complications, including air embolism, blindness from sustained pressure on the globe, and finger amputation following a crush injury, can be caused by improper patient positioning (Table 54–4). These complications are best prevented by evaluating the patient’s postural limitations during the preanesthetic visit; padding pressure points, susceptible nerves, and any area of the body that will possibly be in contact with the operating table or its attachments; avoiding flexion or extension of a joint to its limit; having an awake patient assume the position

TABLE 544 Complications associated with patient positioning. Complication

Position

Prevention

Venous air embolism

Sitting, prone, reverse Trendelenburg

Maintain adequate venous pressure; ligate “open” veins

Alopecia

Supine, lithotomy, Trendelenburg

Avoid prolonged hypotension, padding, and occasional head turning.

Backache

Any

Lumbar support, padding, and slight hip flexion.

Extremity compartment syndromes

Especially lithotomy

Maintain perfusion pressure and avoid external compression.

Corneal abrasion

Any, but especially prone

Taping and/or lubricating eye.

Digit amputation

Any

Check for protruding digits before changing table configuration.

Any Lithotomy, lateral decubitus Any Any Prone, sitting Any

Avoid stretching or direct compression at neck, shoulder, or axilla. Avoid sustained pressure on lateral aspect of upper fibula.

Nerve palsies Brachial plexus Common peroneal Radial Ulnar Retinal ischemia Skin necrosis

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Avoid compression of lateral humerus. Avoid sustained pressure on ulnar groove. Avoid pressure on globe. Avoid sustained pressure over bony prominences.

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to ensure comfort; and understanding the potential complications of each position. Monitors must often be disconnected during patient repositioning, making this a time of greater risk for unrecognized hemodynamic derangement. Compartment syndromes can result from hemorrhage into a closed space following a vascular puncture or prolonged venous outflow obstruction, particularly when associated with hypotension. In severe cases, this may lead to muscle necrosis, myoglobinuria, and renal damage, unless the pressure within the extremity compartment is relieved by surgical decompression (fasciotomy) or in the abdominal compartment by laparotomy.

AWARENESS A continuing series of media reports have imprinted the fear of awareness under general anesthesia into the psyche of the general population. Accounts of recall and helplessness while paralyzed have made unconsciousness a primary concern of patients undergoing general anesthesia. When unintended intraoperative awareness does occur, patients may exhibit symptoms ranging from mild anxiety to posttraumatic stress disorder (eg, sleep disturbances, nightmares, and social difficulties). Although the incidence is difficult to measure, approximately 2% of the closed claims in the ASA Closed Claims Project database relate to awareness under anesthesia. Analysis of the NHS Litigation Authority database from 1995–2007 revealed that 19 of 93 relevant claims were for “awake paralysis.” Clearly, awareness is of great concern to patients and may lead to litigation. Certain types of surgeries are most frequently associated with awareness, including those for major trauma, obstetrics, and major cardiac procedures. In some instances, awareness may result from the reduced depth of anesthesia that can be tolerated by the patient. In early studies, recall rates for intraoperative events during major trauma surgery have been reported to be as frequent as 43%; the incidence of awareness during cardiac surgery and cesarean sections is 1.5% and 0.4%, respectively. As of 1999, the ASA Closed Claims Project reported 79 awareness claims; approximately 20% of the claims were for awake paralysis, and the remainder

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of the claims were for recall under general anesthesia. Most claims for awake paralysis were thought to be due to errors in drug labeling and administration, such as administering paralytics before inducing narcosis. Since the 1999 review, another 71 cases have appeared in the database. Claims for recall were more likely in women undergoing general anesthesia without a volatile agent. Patients with long term substance abuse may have increased anesthesia requirements which if not met can lead to awareness. Other specific causes of awareness include inadequate inhalational anesthetic delivery (eg, from vaporizer malfunction) and medication errors. Some patients may complain of awareness, when, in fact, they received regional anesthesia or monitored anesthesia care; thus, anesthetists should make sure that patients have reasonable expectations when regional or local techniques are employed. Likewise, patients requesting regional or local anesthesia because they want to “see it all” and/ or “stay in control” often can become irate when sedation dulls their memory of the perioperative experience. In all cases, frank discussion between anesthesia staff and the patient is necessary to avoid unrealistic expectations. Some clinicians routinely discuss the possibility of intraoperative recall and the steps that will be taken to minimize it as part of the informed consent for general anesthesia. This makes particular sense for those procedures in which recall is more likely. It is advisable to also remind patients who are undergoing monitored anesthesia care with sedation that awareness is expected. Volatile anesthetics should be administered at a level consistent with amnesia. If this is not possible, benzodiazepines (and/or scopolamine) can be used. Movement of a patient may indicate inadequate anesthetic depth. Documentation should include end-tidal concentrations of anesthetic gases (when available) and dosages of amnesic drugs. Use of a bispectral index scale (BIS) monitor or similar monitors may be helpful although randomized clinical trials have failed to demonstrate a reduced incidence of awareness with use of BIS when compared with a group receiving appropriate concentrations of volatile agents. Finally, if there is evidence of intraoperative awareness during postoperative rounds, the practitioner should obtain a detailed account of the experience, answer patient

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questions, be very empathetic, and refer the patient for psychological counseling if appropriate.

EYE INJURY A wide range of conditions from simple corneal abrasion to blindness have been reported. Corneal abrasion is by far the most common and transient eye injury. The ASA Closed Claims Project identified a small number of claims for abrasion, in which the cause was rarely identified (20%) and the incidence of permanent injury was low (16%). It also identified a subset of claims for blindness that resulted from patient movement during ophthalmological surgery. These cases occurred in patients receiving either general anesthesia or monitored anesthesia care. Although the cause of corneal abrasion may not be obvious, securely closing the eye lids with tape after loss of consciousness (but prior to intubation) and avoiding direct contact between eyes and oxygen masks, drapes, lines, and pillows (particularly during monitored anesthesia care, in transport, and in nonsupine positions) can help to minimize the possibility of injury. Adequate anesthetic depth (and, in most cases, paralysis) should be maintained to prevent movement during ophthalmological surgery under general anesthesia. In patients scheduled for MAC, the patient must understand that movement under monitored care is hazardous and, thus, that only minimal sedation may be administered to ensure that he or she can cooperate. Ischemic optic neuropathy (ION) is a devastating perioperative complication. ION is now the most common cause of postoperative vision loss. Postoperative vision loss is most commonly reported after cardiopulmonary bypass, radical neck dissection, and spinal surgeries in the prone position. Both preoperative and intraoperative factors may be contributory. Many of the case reports implicate preexisting hypertension, diabetes, coronary artery disease, and smoking, suggesting that preoperative vascular abnormalities may play a role. Intraoperative deliberate hypotension and anemia have also been implicated (in spine surgery), perhaps because of their potential to reduce oxygen delivery. Finally, prolonged surgical time in positions that compromise venous outflow (prone, head down, compressed

Morg_Ch54_1199-1230.indd 1216

abdomen) have also been found to be factors in spine surgery. Symptoms are usually present immediately upon awakening from anesthesia, but have been reported up to 12 days postoperatively. Such symptoms range from decreased visual acuity to complete blindness. Analysis of case records submitted to the ASA Postoperative Vision Loss Registry revealed that vision loss was secondary to ION in 83 of 93 cases. Instrumentation of the spine was associated with ION when surgery lasted more than 6 hr and blood loss was more than 1 L. ION can occur in patients whose eyes are free of pressure secondary to the use of pin fixation, indicating that direct pressure on the eye is not required to produce ION. Increased venous pressure in patients in the Trendelenberg position may reduce blood flow to the optic nerve. It is difficult to formulate recommendations to prevent this complication because risk factors for ION are often unavoidable. Steps that might be taken include: (1) limiting the degree and duration of hypotension during controlled (deliberate) hypotension, (2) administering a transfusion to severely anemic patients who seem to be at risk of ION, and (3) discussing with the surgeon the possibility of staged operations in high-risk patients to limit prolonged procedures. Of note, postoperative vision loss can be caused by other mechanisms as well, including angle closure glaucoma or embolic phenomenon to the cortex or retina. Immediate evaluation is advised.

CARDIOPULMONARY ARREST DURING SPINAL ANESTHESIA Sudden cardiac arrest during an otherwise routine administration of spinal anesthetics is an uncommon complication. The initial published report was a closed claims analysis of 14 patients who experienced cardiac arrest during spinal anesthesia. The cases primarily involved young (average age 36 years), relatively healthy (ASA physical status I–II) patients who were given appropriate doses of local anesthetic that produced a high dermatomal level of block prior to arrest (T4 level). Respiratory insufficiency with hypercarbia due to sedatives was thought to be a potential contributing factor. The

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average time from induction of spinal anesthesia to arrest was 36 min, and, in all cases, arrest was preceded by a gradual decline in heart rate and blood pressure. Just prior to arrest, the most common signs were bradycardia, hypotension, and cyanosis. Treatment consisted of ventilatory support, ephedrine, atropine, cardiopulmonary resuscitation (average duration 10.9 min), and epinephrine. Despite these interventions, 10 patients remained comatose and 4 patients regained consciousness with significant neurological deficits. A subsequent study concluded that such arrests had little relationship to sedation, but were related more to extensive degrees of sympathetic blockade, leading to unopposed vagal tone and profound bradycardia. Rapid appropriate treatment of bradycardia and hypotension is essential to minimize the risk of arrest. Early treatment of bradycardia with atropine may prevent a downward spiral. Stepwise doses of ephedrine, epinephrine, and other vasoactive drugs should be given to treat hypotension. If cardiopulmonary arrest occurs, ventilatory support, cardiopulmonary resuscitation, and full resuscitation doses of atropine and epinephrine should be administered without delay.

HEARING LOSS Perioperative hearing loss is usually transient and often goes unrecognized. The incidence of lowfrequency hearing loss following dural puncture may be as high as 50%. It seems to be due to cerebrospinal fluid leak, and, if persistent, can be relieved with an epidural blood patch. Hearing loss following general anesthesia can be due to a variety of causes and is much less predictable. Mechanisms include middle ear barotrauma, vascular injury, and ototoxicity of drugs (aminoglycosides, loop diuretics, nonsteroidal antiinflammatory drugs, and antineoplastic agents). Hearing loss following cardiopulmonary bypass is usually unilateral and is thought to be due to embolism and ischemic injury to the organ of Corti.

ALLERGIC REACTIONS Hypersensitivity (or allergic) reactions are exaggerated immunological responses to antigenic stimulation in previously sensitized persons. The antigen, or

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TABLE 545 Hypersensitivity reactions. Type I (immediate) Atopy Urticaria—angioedema Anaphylaxis Type II (cytotoxic) Hemolytic transfusion reactions Autoimmune hemolytic anemia Heparin-induced thrombocytopenia Type III (immune complex) Arthus reaction Serum sickness Acute hypersensitivity pneumonitis Type IV (delayed, cell-mediated) Contact dermatitis Tuberculin-type hypersensitivity Chronic hypersensitivity pneumonitis

allergen, may be a protein, polypeptide, or smaller molecule. Moreover, the allergen may be the substance itself, a metabolite, or a breakdown product. Patients may be exposed to antigens through the respiratory tract, gastrointestinal tract, eyes, skin and from previous intravenous, intramuscular, or peritoneal exposure. Anaphylaxis occurs when inflammatory agents are released from basophils and mast cells as a result of an antigen interacting with the immunoglobulin (Ig) E. Anaphylactoid reactions manifest themselves in the same manner as anaphylactic reactions, but are not the result of an interaction with IgE. Direct activation of complement and IgG-mediated complement activation can result in similar inflammatory mediator release and activity. Depending on the antigen and the immune system components involved, hypersensitivity reactions are classically divided into four types (Table 54–5). In many cases, an allergen (eg, latex) may cause more than one type of hypersensitivity reaction. Type I reactions involve antigens that cross-link IgE antibodies, triggering the release of inflammatory mediators from mast cells. In type II reactions, complement-fixing (C1-binding) IgG antibodies bind to antigens on cell surfaces, activating the classic complement pathway and lysing the cells. Examples of type II reactions include hemolytic transfusion reactions and heparin-induced thrombocytopenia. Type III reactions occur when antigen–antibody

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(IgG or IgM) immune complexes are deposited in tissues, activating complement and generating chemotactic factors that attract neutrophils to the area. The activated neutrophils cause tissue injury by releasing lysosomal enzymes and toxic products. Type III reactions include serum sickness reactions and acute hypersensitivity pneumonitis. Type IV reactions, often referred to as delayed hypersensitivity reactions, are mediated by CD4+ T lymphocytes that have been sensitized to a specific antigen by prior exposure. Prior TH1 response causes expression of a T-cell receptor protein that is specific for the antigen. Reexposure to the antigen causes these lymphocytes to produce lymphokines—interleukins (IL), interferon (IFN), and tumor necrosis factor-γ (TNF-γ)—that attract and activate inflammatory mononuclear cells over 48–72 hr. Production of IL-1 and IL-6 by antigen-processing cells amplifies clonal expression of the specific sensitized T cells and attracts other types of T cells. IL-2 secretion transforms CD8+ cytotoxic T cells into killer cells; IL-4 and IFN-γ cause macrophages to undergo epithelioid transformation, often producing granuloma. Examples of type IV reactions are those associated with tuberculosis, histoplasmosis, schistosomiasis, and hypersensitivity pneumonitis and some autoimmune disorders, such as rheumatoid arthritis and Wegener’s granulomatosis.

1. Immediate Hypersensitivity Reactions Initial exposure of a susceptible person to an antigen induces CD4+ T cells to lymphokines that activate and transform specific B lymphocytes into plasma cells, producing allergen-specific IgE antibodies (Figure 54–7). The Fc portion of these antibodies then associates with high affinity receptors on the cell surface of tissue mast cells and circulating basophils. During subsequent reexposure to the antigen, it binds the Fab portion of adjacent IgE antibodies on the mast cell surface, inducing degranulation and release of inflammatory lipid mediators and additional cytokines from the mast cell. The end result is the release of histamine, tryptase, proteoglycans (heparin and chondroitin sulfate), and carboxypeptidases. Prostaglandin (mainly prostaglandin

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D2) and leukotriene (B4, C4, D4, E4, and plateletactivating factor) synthesis is also increased. The combined effects of these mediators can produce arteriolar vasodilatation, increased vascular permeability, increased mucus secretion, smooth muscle contraction, and other clinical manifestations of type I reactions. Type I hypersensitivity reactions are classified as atopic or nonatopic. Atopic disorders typically affect the skin or respiratory tract and include allergic rhinitis, atopic dermatitis, and allergic asthma. Nonatopic hypersensitivity disorders include urticaria, angioedema, and anaphylaxis; when these reactions are mild, they are confined to the skin (urticaria) or subcutaneous tissue (angioedema), but when they are severe, they become generalized and a life-threatening medical emergency (anaphylaxis). Urticarial lesions are characteristically well-circumscribed skin wheals with raised erythematous borders and blanched centers; they are intensely pruritic. Angioedema presents as deep, nonpitting cutaneous edema from marked vasodilatation and increased permeability of subcutaneous blood vessels. When angioedema is extensive, it can be associated with large fluid shifts; when it involves the pharyngeal or laryngeal mucosa, it can rapidly compromise the airway.

2. Anaphylactic Reactions Anaphylaxis is an exaggerated response to an allergen (eg, antibiotic) that is mediated by a type I hypersensitivity reaction. The syndrome appears within minutes of exposure to a specific antigen in a sensitized person and characteristically presents as acute respiratory distress, circulatory shock, or both. Death may occur from asphyxiation or irreversible circulatory shock. The incidence of anaphylactic reactions during anesthesia has been estimated at a rate of 1:3500 to 1:20000 anesthetics. Mortality from anaphylaxis can be as frequent as 4% of cases with brain injury, occurring in another 2% of surviving patients. A French study evaluating 789 anaphylactic and anaphylactoid reactions reported that the most common sources of perioperative anaphylaxis were neuromuscular blockers (58%), latex (17%), and antibiotics (15%).

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A

1219

Free drug Fixation of IgE antibodies to mast cells and blood basophils

Carrier (eg, albumin)

Drugcarrier complex

Prednisone blocks

Mitosis Macrophage

B

IgE antibody producing cells

Reaginic (IgE) antibody-forming precursor cell

IgE reaginic antibodies

Binding of allergen to specific IgE antibody on surface of mast cell induces mediator release Antihistamines partially block

Histamine, kinins, leukotrienes (SRS), prostaglandins, serotonin, platelet-activating factor

Degranulation and mediator release

Smooth muscle and other end organs

Isoproterenol, theophylline, epinephrine, and cromolyn partially block

FIGURE 547 A: Induction of IgE-mediated allergic sensitivity to drugs and other allergens. B: Response of IgE-sensitized cells to subsequent exposure to allergens.

Ig, immunoglobulin. (Reproduced, with permission, from Katzung BG [editor]: Basic & Clinical Pharmacology, 8th ed. McGraw-Hill, 2001.)

The most important mediators of anaphylaxis are histamine, leukotrienes, basophil kallikrein (BK-A,) and platelet-activating factor. They increase vascular permeability and contract smooth muscle. H1-receptor activation contracts bronchial smooth muscle, whereas H2-receptor activation causes

vasodilatation, enhanced mucus secretion, tachycardia, and increased myocardial contractility. BK-A cleaves bradykinin from kininogen; bradykinin increases vascular permeability and vasodilatation and contracts smooth muscle. Activation of Hageman factor can initiate intravascular coagulation.

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TABLE 546 Clinical manifestations of anaphylaxis. Organ System

Signs and Symptoms

Cardiovascular

Hypotension,1 tachycardia, arrhythmias

Pulmonary

Bronchospasm,1 cough, dyspnea, pulmonary edema, laryngeal edema, hypoxia

Dermatological

Urticaria,1 facial edema, pruritus

1

Key signs during general anesthesia.

Eosinophil chemotactic factor of anaphylaxis, neutrophil chemotactic factor, and leukotriene B4 attract inflammatory cells that mediate additional tissue injury. Angioedema of the pharynx, larynx, and trachea produce upper airway obstruction, whereas bronchospasm and mucosal edema result in lower airway obstruction. Histamine may preferentially constrict large airways, whereas leukotrienes primarily affect smaller peripheral airways. Transudation of fluid into the skin (angioedema) and viscera produces hypovolemia and shock, whereas arteriolar vasodilatation decreases systemic vascular

resistance. Coronary hypoperfusion and arterial hypoxemia promote arrhythmias and myocardial ischemia. Leukotriene and prostaglandin mediators may also cause coronary vasospasm. Prolonged circulatory shock leads to progressive lactic acidosis and ischemic damage to vital organs. Table 54–6 summarizes important manifestations of anaphylactic reactions. Anaphylactoid reactions resemble anaphylaxis but do not depend on IgE antibody interaction with antigen. A drug can directly release histamine from mast cells (eg, urticaria following high-dose mor6 phine sulfate) or activate complement. Despite differing mechanisms, anaphylactic and anaphylactoid reactions typically are clinically indistinguishable and equally life-threatening. Table 54–7 lists common causes of anaphylactic and anaphylactoid reactions. Factors that may predispose patients to these reactions include pregnancy, known atopy, and previous drug exposure. Such reactions are more common in younger than older patients. Laboratory identification of patients who have experienced an adverse allergic reaction or who may be particularly

TABLE 547 Causes of anaphylactic and anaphylactoid reactions. Anaphylactic reactions against polypeptides

Venoms (Hymenoptera, fire ant, snake, jellyfish) Airborne allergens (pollen, molds, danders) Foods (peanuts, milk, egg, seafood, grain) Enzymes (trypsin, streptokinase, chymopapain, asparaginase) Heterologous serum (tetanus antitoxin, antilymphocyte globulin, antivenin) Human proteins (insulin, corticotropin, vasopressin, serum and seminal proteins) Latex

Anaphylactic reactions against hapten carrier

Antibiotics (penicillin, cephalosporins, sulfonamides) Disinfectants (ethylene oxide, chlorhexidine) Local anesthetics (procaine)

Anaphylactoid reactions

Polyionic solutions (radiocontrast medium, polymyxin B) Opioids (morphine, meperidine) Hypnotics (propofol, thiopental) Muscle relaxants (rocuronium, succinylcholine, cisatracurium) Synthetic membranes (dialysis) Nonsteroidal antiinflammatory drugs Preservatives (sulfites, benzoates) Protamine Dextran Steroids Exercise Idiopathic

Adapted and reproduced, with permission, from Bochner BS, Lichtenstein LM: N Engl J Med 1991;324:1786.

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TABLE 548 Treatment of anaphylactic and anaphylactoid reactions. Discontinue drug administration Administer 100% oxygen Epinephrine (0.01–0.5 mg IV or IM)1 Consider intubation Intravenous fluid bolus Diphenhydramine (50–75 mg IV) Ranitidine (150 mg IV) Hydrocortisone (up to 200 mg IV) or methylprednisolone (1–2 mg/kg) 1 The dose and route of epinephrine depend on the severity of the reaction. An infusion of 1–5 mcg/min may be necessary in adults.

susceptible is often aided by intradermal skin testing, leukocyte or basophil degranulation testing (histamine release test), or radio-allergosorbent testing (RAST). The latter is capable of measuring the level of drug-specific IgE antibody in the serum. Serum tryptase measurement is helpful in confirming the diagnosis of an anaphylactic reaction. Prophylactic pretreatment with histamine receptor antagonists and corticosteroids decreases the severity of the reaction. Treatment must be immediate and tailored to the severity of the reaction (Table 54–8).

3. Allergic Reactions to Anesthetic Agents 7 True anaphylaxis due to anesthetic agents is

rare; anaphylactoid reactions are much more common. Risk factors associated with hypersensitivity to anesthetics include female gender, atopic history, preexisting allergies, and previous anesthetic exposures. Muscle relaxants are the most common cause of anaphylaxis during anesthesia, with an estimated incidence of 1 in 6500 patients. They account for almost 60% of perioperative anaphylactic reactions. In many instances, there was no previous exposure to muscle relaxants. Investigators suggest that over-the-counter drugs, cosmetics, and food products, many of which contain tertiary or quaternary ammonium ions, can sensitize susceptible individuals. A French study found that, in decreasing order of frequency, rocuronium, succinylcholine, and atracurium were most often responsible; this likely reflects the propensity to cause anaphylaxis, together with frequency of use.

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Although rarer, hypnotic agents can also be responsible for some allergic reactions. The incidence of anaphylaxis for thiopental and propofol is 1 in 30,000 and 1 in 60,000, respectively. Allergic reactions to etomidate, ketamine, and benzodiazepines are exceedingly rare. True anaphylactic reactions due to opioids are far less common than nonimmune histamine release. Similarly, anaphylactic reactions to local anesthetics are much less common than vasovagal reactions, toxic reactions to accidental intravenous injections, and side effects from absorbed or intravenously injected epinephrine. IgE-mediated reactions to ester-type local anesthetics, however, are well described secondary to reaction to the metabolite, para-aminobenzoic acid, In contrast, true anaphylaxis due to amidetype local anesthetics is very rare; in some instances, the preservative (paraben or methylparaben) was believed to be responsible for an apparent anaphylactoid reaction to a local anesthetic. Moreover, the cross-reactivity between amide-type local anesthetics seems to be low. There are no reports of anaphylaxis to volatile anesthetics.

4. Latex Allergy The severity of allergic reactions to latex-containing products ranges from mild contact dermatitis to lifethreatening anaphylaxis. Latex allergy is the second most common cause of anaphylaxis during anesthesia. Most serious reactions seem to involve a direct IgE-mediated immune response to polypeptides in natural latex, although some cases of contact dermatitis may be due to a type IV sensitivity reaction to chemicals introduced in the manufacturing process. Nonetheless, a relationship between the occurrence of contact dermatitis and the probability of future anaphylaxis has been suggested. Chronic exposure to latex and a history of atopy increases the risk of sensitization. Healthcare workers and patients undergoing frequent procedures with latex items (eg, repeated urinary bladder catheterization, barium enema examinations) should therefore be consid8 ered at increased risk. Patients with spina bifida, spinal cord injury, and congenital abnormalities of the genitourinary tract have an increased incidence of latex allergy. The incidence of

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latex anaphylaxis in children is estimated to be 1 in 10,000. A history of allergic symptoms to latex should be sought in all patients during the preanesthetic interview. Foods that cross-react with latex include mango, kiwi, chestnut, avacado, passion fruit, and banana. IL-18 and IL-13 single nucleotide polymorphisms may affect the sensitivity of individuals to latex and promote allergic responses. Anaphylactic reactions to latex may be confused with reactions to other substances (eg, drugs, blood products) because the onset of symptoms can be delayed for more than 1 hr after initial exposure. Treatment is the same as for other forms of anaphylactic reactions. Skin-prick tests, intradermal tests, basophil histamine-release tests, and RAST have been used to evaluate high-risk patients. Preventing a reaction in sensitized patients includes pharmacological prophylaxis and absolute avoidance of latex. Preoperative administration of H1 and H2 histamine antagonists and steroids may provide some protection, although their use is controversial. Although most pieces of anesthetic equipment are now latex-free, some may still contain latex (eg, gloves, tourniquets, some ventilator bellows, intravenous injection ports, and older reusable face masks). An allergic reaction has even been documented from inhalation of latex antigen contained within aerosolized glove powder. Manufacturers of latex-containing medical products must label their products accordingly. Only devices specifically known not to contain latex (eg, polyvinyl or neoprene gloves, silicone endotracheal tubes or laryngeal masks, plastic face masks) can be used in latex-allergic patients. Rubber stoppers should be removed from drug vials prior to use, and injections should be made through plastic stopcocks, if latex has not been eliminated from containers and injection ports.

5. Allergies to Antibiotics Many true drug allergies in surgical patients are due to antibiotics, mainly β-lactam antibiotics, such as penicillins and cephalosporins. Although 1% to 4% of β-lactam administrations result in allergic reactions, only 0.004% to 0.015% of these reactions

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result in anaphylaxis. Up to 2% of the general population is allergic to penicillin, but only 0.01% of penicillin administrations result in anaphylaxis. Cephalosporin cross-sensitivity in patients with penicillin allergy is estimated to be 2% to 7%, but a history of an anaphylactic reaction to penicillin increases the cross-reactivity rate up to 50%. Patients with a prior history of an anaphylactic reaction to penicillin should therefore not receive a cephalosporin. Although imipenem exhibits similar cross-sensitivity, aztreonam seems to be antigenically distinct and reportedly does not cross-react with other β-lactams. Sulfonamide allergy is also relatively common in surgical patients. Sulfa drugs include sulfonamide antibiotics, furosemide, hydrochlorothiazide, and captopril. Fortunately, the frequency of cross-reactivity among these agents is low. Like cephalosporins, vancomycin is commonly used for antibiotic prophylaxis in surgical patients. Unfortunately, it is associated with adverse reactions. An anaphylactoid-type reaction, “red man syndrome,” consists of intense pruritus, flushing, and erythema of the head and upper torso, often with arterial hypotension; this syndrome seems to be related to a rapid rate of administration more than to dose or allergy. Isolated systemic hypotension is a much more frequent side effect and seems to be primarily mediated by histamine release, because pretreatment with H1 and H2 antihistamines can prevent hypotension, even with rapid rates of administration. Immunologic mechanisms are associated with other perioperative pathologies. Transfusion-related lung injury may be secondary to the activity of antibodies in the donor plasma, producing a hypersensitivity reaction that results in lung infiltrates and respiratory failure. IgG antibody formation directed at heparin–PF4 complexes results in platelet activation, thrombosis, and heparin-induced thrombocytopenia.

OCCUPATIONAL HAZARDS IN ANESTHESIOLOGY Anesthesiologists spend much of their workday exposed to anesthetic gases, low-dose ionizing radiation, electromagnetic fields, blood products,

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1223

TABLE 549 Relative rate ratios for drug and suicide deaths comparing anesthesiologists with internists before and after January 1, 1987. Anesthesiologists (N)

Internists (N)

RR1

95% CI

All drug-related deaths

<1987 ≥1987

36 55

14 19

2.65 2.87

1.42–4.91 1.71–4.84

Drug-related suicides

<1987 ≥1987

16 32

11 11

1.48 2.88

0.69–3.20 1.45–5.71

Suicides

<1987 ≥1987

41 62

33 38

1.25 1.60

0.79–1.97 1.07–2.39

Cl, confidence interval. 1 Ratio (RR) of anesthesiologists compared with internists for that time period, RR is adjusted for age, gender, and race. Reproduced, with permission, from Alexander B, Checkoway H, Nagahama S, Domino K: Cause-specific mortality risks of anesthesiologists. Anesthesiology 2000;93:922.

and workplace stress. Each of these can contribute to negative health effects in anesthesia practitioners. A 2000 paper compared the mortality risks of anesthesiologists and internists. Death from heart disease or cancer did not differ between the groups; however, anesthesiologists had an increased rate of suicides and drug-related deaths (Table 54–9). Anesthesiologists also had a greater chance of death from external causes, such as boating, bicycling, and aeronautical accidents compared with internists. Nevertheless, both anesthesiologists and internists had lower mortality than the general population, likely due to their higher socioeconomic status. Anesthesiologists’ access to intravenous opioids likely contributes to a 2.21 relative risk for drugrelated deaths compared with that of internists.

low levels depends on efficient scavenging equipment, adequate operating room ventilation, and conscientious anesthetic technique. Most people cannot detect the odor of volatile agents at a concentration of less than 30 ppm. If there is no functioning scavenging system, anesthetic gas concentrations reach 3000 ppm for nitrous oxide and 50 ppm for volatile agents. Early studies indicated that female operating room staff might be at increased risk of spontaneous abortion compared with other women. It is unclear if other factors related to operating room activity could also contribute to the possibly increased potential for pregnancy loss.

1. Chronic Exposure to Anesthetic Gases

Hospital workers are exposed to many infectious diseases prevalent in the community (eg, respiratory viral infections, rubella, and tuberculosis). Herpetic whitlow is an infection of the finger with herpes simplex virus type 1 or 2 and usually involves direct contact of previously traumatized skin with contaminated oral secretions. Painful vesicles appear at the site of infection. The diagnosis is confirmed by the appearance of giant epithelial cells or nuclear inclusion bodies in a smear taken from the base of a vesicle, the presence of a rise in herpes simplex virus titer, or identification of the virus with antiserum. Treatment is conservative and includes

9 There is no clear evidence that exposure to

trace amounts of anesthetic agents presents a health hazard to operating room personnel. However, because previous studies examining this issue have yielded flawed but conflicting results, the US Occupational Health and Safety Administration continues to set maximum acceptable trace concentrations of less than 25 ppm for nitrous oxide and 0.5 ppm for halogenated anesthetics (2 ppm if the halogenated agent is used alone). Achieving these

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topical application of 5% acyclovir ointment. Prevention involves wearing gloves when contacting oral secretions. Patients at risk of harboring the virus include those suffering from other infections, immunosuppression, cancer, and malnutrition. The risk of this condition has virtually disappeared now that anesthesia personnel routinely wear gloves during manipulation of the airway, which was not the case in the 1980s and earlier. Viral DNA has been identified in the smoke plume generated during laser treatment of condylomata. The theoretical possibility of viral transmission from this source can be minimized by using smoke evacuators, gloves, and appropriate OSHA approved masks. More disturbing is the potential of acquiring serious blood-borne infections, such as hepatitis B, hepatitis C, or human immunodeficiency virus (HIV). Although parenteral transmission of these diseases can occur following mucous membrane, cutaneous, or percutaneous exposure to infected body fluids, accidental injury with a needle contaminated with infected blood represents the most common occupational mechanism. The risk of transmission can be estimated if three factors are known: the prevalence of the infection within the patient population, the incidence of exposure (eg, frequency of needlestick), and the rate of seroconversion after a single exposure. The seroconversion rate after a specific exposure depends on several factors, including the infectivity of the organism, the stage of the patient’s disease (extent of viremia), the size of the inoculum, and the immune status of the healthcare provider. Rates of seroconversion following a single needlestick are estimated to range 10 between 0.3% and 30%. Hollow (hypodermic) needles pose a greater risk than do solid (surgical) needles because of the potentially larger inoculum. The use of gloves, needleless systems, or protected needle devices may decrease the incidence of some (but not all) types of injury. The initial management of needlesticks involves cleaning the wound and notifying the appropriate authority within the health care facility. After an exposure, anesthesia workers should report to their institution’s emergency or employee health department for appropriate counseling on

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postexposure prophylaxis options. All OR staff should be made aware of the institution’s employee health notification pathway for needle stick and other injuries Fulminant hepatitis B (1% of acute infections) carries a 60% mortality rate. Chronic active hepatitis (<5% of all cases) is associated with an increased incidence of cirrhosis of the liver and hepatocellular carcinoma. Transmission of the virus is primarily through contact with blood products or body fluids. The diagnosis is confirmed by detection of hepatitis B surface antigen (HBsAg). Uncomplicated recovery is signaled by the disappearance of HBsAg and the appearance of antibody to the surface antigen (anti-HBs). A hepatitis B vaccine is available and is strongly recommended prophylactically for anesthesia personnel. The appearance of anti-HBs after a three-dose regimen indicates successful immunization. Hepatitis C is another important occupational hazard in anesthesiology; 4% to 8% of hepatitis C infections occur in healthcare workers. Most (50% to 90%) of these infections lead to chronic hepatitis, which, although often asymptomatic, can progress to liver failure and death. In fact, hepatitis C is the most common cause of nonalcoholic cirrhosis in the United States. There is currently no vaccine to protect against hepatitis C infection. Anesthesia personnel seem to be at a low, but measureable, risk for the occupational contraction of HIV. The risk of acquiring HIV infection following a single needlestick contaminated with blood from an HIV-infected patient has been estimated at 0.4% to 0.5%. Because there are documented reports of transmission of HIV from infected patients to healthcare workers (including anesthesiologists), the Centers for Disease Control and Prevention proposed guidelines that apply to all categories of patient contact. These universal precautions, which are equally valid for protection against hepatitis B or C infection, are as follows: • No recapping and the immediate disposal of contaminated needles • Use of gloves and other barriers during contact with open wounds and body fluids • Frequent hand washing

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• Use of proper techniques for disinfection or the disposal of contaminated materials • Particular caution by pregnant healthcare workers, and no contact with patients by workers who have exudative or weeping skin lesions

3. Substance Abuse 11 Anesthesiology is a high-risk medical spe-

cialty for substance abuse. Probable reasons for this include the stress of anesthetic practice and the easy availability of drugs with addiction potential (potentially attracting people at risk of addiction to the field). The likelihood of developing substance abuse is increased by coexisting personal problems (eg, marital or financial difficulties) or a family history of alcoholism or drug addiction. The voluntary use of nonprescribed moodaltering pharmaceuticals is a disease. If left untreated, substance abuse often leads to death from drug overdose—intentional or unintentional. One of the greatest challenges in treating drug abuse is identifying the afflicted individual, as denial is a consistent feature. Unfortunately, changes evident to an outside observer are often both vague and late: reduced involvement in social activities, subtle changes in appearance, extreme mood swings, and altered work habits. Treatment begins with a careful, well-planned intervention. Those inexperienced in this area would be well advised to consult with their local medical society or licensing authority about how to proceed. The goal is to enroll the individual in a formal rehabilitation program. The possibility that one may lose one’s medical license and be unable to return to practice provides powerful motivation. Some diversion programs report a success rate of approximately 70%; however, most rehabilitation programs report a recurrence rate of at least 25%. Long-term compliance often involves continued participation in support groups (eg, Narcotics Anonymous), random urine testing, and oral naltrexone therapy (a longacting opioid antagonist). Effective prevention strategies are difficult to formulate; “better” control of drug availability is unlikely to deter a determined individual. It is unlikely that education about the severe consequences of substance abuse will bring new information to the potential drug-abusing

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physician. There remains controversy regarding the rate at which anesthesia staff will experience recidivism. Many experts argue for a “one strike and you’re out” policy for anesthesiology residents who abuse injectable drugs. The decision as to whether a fully trained and certified physician who has been discovered to abuse injectable drugs should return to anesthetic practice after completing a rehabilitation program varies and depends on the rules and traditions of the practice group, the medical center, the relevant medical licensing board, and the perceived likelihood of recidivism. Physicians returning to practice following successful completion of a program must be carefully monitored over the long term, as relapses can occur years after apparent successful rehabilitation. Alcohol abuse is a common problem among physicians and nurses, and anesthesia personnel are no exception. Interventions for alcohol abuse, as is true for injectable drug abuse, must be carefully orchestrated. Guidance from the local medical society or licensing authority is highly recommended.

4. Ionizing Radiation Exposure The use of imaging equipment (eg, fluoroscopy) during surgery and interventional radiologic procedures exposes the anesthesiologist to the potential 12 risks of ionizing radiation. The three most important methods of minimizing radiation doses are limiting total exposure time during procedures, using proper barriers, and maximizing the distance from the source of radiation. Anesthesiologists who routinely perform fluoroscopic image guided invasive procedures should consider wearing protective eyeware incorporating radiation shielding. Lead glass partitions or lead aprons with thyroid shields are  mandatory protection for all personnel who are exposed to ionizing radiation. The inverse square law states that the dosage of radiation varies inversely with the square of the distance. Thus, the exposure at 4 m will be one-sixteenth that at 1 m. The maximum recommended occupational wholebody exposure to radiation is 5 rem/yr. This can be monitored with an exposure badge. The health impact on operating room personnel of exposure to electromagnetic radiation remains unclear.

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Perioperative & Critical Care Medicine

CASE DISCUSSION Unexplained Intraoperative Tachycardia & Hypertension A 73-year-old man is scheduled for emergency relief of an intestinal obstruction from a sigmoid volvulus. The patient had a myocardial infarction 1 month earlier that was complicated by congestive heart failure. His blood pressure is 160/90 mm Hg, pulse 110 beats/min, respiratory rate 22 breaths/min, and temperature 38.8°C. Why is this case an emergency? Strangulation of the bowel begins with venous obstruction, but can quickly progress to arterial occlusion, ischemia, infarction, and perforation. Acute peritonitis could lead to severe dehydration, sepsis, shock, and multiorgan failure. What special monitoring is appropriate for this patient? Because of the history of recent myocardial infarction and congestive heart failure, an arterial line would be useful. Transesophageal echocardiography and pulse contour analysis monitors of cardiac output could be used. Pulmonary arterial flotation catheters have often been used in the past, but they are associated with significant complications and current evidence does not indicate that their use improves patient outcomes. Large fluid shifts should be anticipated. Furthermore, information regarding myocardial supply (diastolic blood pressure) and demand (systolic blood pressure, left ventricular wall stress, and heart rate) should be continuously available. Central venous pressure may not track left atrial pressure in a patient with significant left ventricular dysfunction. What cardiovascular medications might be useful during induction and maintenance of general anesthesia? Drugs causing severe tachycardia or extremes in arterial blood pressure should be avoided. During the laparotomy, gradual increases in heart rate and blood pressure are noted. ST-segment elevations appear on the electrocardiogram. A nitroglycerin infusion is started. The heart

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rate is now 130 beats/min, and the blood pressure is 220/140 mm Hg. The concentration of volatile anesthetic is increased, and metoprolol is administered intravenously in 1-mg increments. This results in a decline in heart rate to 115 beats/min, with no change in blood pressure. Suddenly, the rhythm converts to ventricular tachycardia, with a profound drop in blood pressure. As amiodarone is being administered and the defibrillation unit prepared, the rhythm degenerates into ventricular fibrillation. What can explain this series of events? A differential diagnosis of pronounced tachycardia and hypertension might include pheochromocytoma, malignant hyperthermia, or thyroid storm. In this case, further inspection of the nitroglycerin infusion reveals a labeling error: although the tubing was labeled “nitroglycerin,” the infusion bag was labeled “epinephrine.” How does this explain the paradoxic response to metoprolol? Metoprolol is a β1-adrenergic antagonist. It inhibits epinephrine’s β1-stimulation of heart rate, but does not antagonize α-induced vasoconstriction. The net result is a decrease in heart rate, but a sustained increase in blood pressure. What is the cause of the ventricular tachycardia? An overdose of epinephrine can cause lifethreatening ventricular arrhythmias. In addition, if the central venous catheter was malpositioned, with its tip in the right ventricle, the catheter tip could have stimulated ventricular arrhythmias. What other factors may have contributed to this anesthetic mishap? Multiple factors will often combine to create an anesthetic misadventure. Incorrect drug labels are but one example of errors that can result in patient injury. Inadequate preparation, technical failures, knowledge deficits, and practitioner fatigue or distraction can all contribute to adverse outcomes. Careful adherence to hospital policies, checklists, patient identification procedures, and surgical and regional block timeouts can all help to prevent iatrogenic complications.

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CHAPTER 54 Anesthetic Complications

GUIDELINES Practice advisory for the prevention of perioperative peripheral neuropathies: a report by the American Society of Anesthesiologists Task Force on prevention of peripheral neuropathies. Anesthesiology 2000;92:1168.

SUGGESTED READING Alexander B, Checkoway H, Nagahama S, Domino K: Cause-specific mortality risks of anesthesiologists. Anesthesiology 2000;93:922. Berge E, Seppala M, Lanier W: The anesthesiology community’s approach to opioid and anesthetic abusing personnel: time to change course. Anesthesiology 2008;109:762. Bhananker S, Posner K, Cheney F, et al: Injury and liability associated with monitored anesthesia care. Anesthesiology 2006;104:228. Bhananker S, Liau D, Kooner P, et al: Liability related to peripheral venous and arterial catheterization; a closed claims analysis. Anesth Analg 2009;109:124. Bishop M, Souders J, Peterson C, et al: Factors associated with unanticipated day of surgery deaths in Department of Veterans Affairs hospitals. Anesth Analg 2008;107:1924. Bowdle TA: Drug administration errors from the ASA closed claims project. ASA Newslett 2003;67:11. Brown RH, Schauble JF, Miller NR: Anemia and hypotension as contributors to perioperative loss of vision. Anesthesiology 1994;80:222. Bryson E, Silverstein J: Addiction and substance abuse in anesthesiology. Anesthesiology 2008;109:905. Caplan RA, Ward RJ, Posner K, Cheney FW: Unexpected cardiac arrest during spinal anesthesia: a closed claims analysis of predisposing factors. Anesthesiology 1988;68:5. Caplan RA, Vistica MF, Posner KL, Cheney FW: Adverse anesthetic outcomes arising from gas delivery equipment: a closed claims analysis. Anesthesiology 1997;87:741. Chadwick HS: An analysis of obstetric anesthesia cases from the American Society of Anesthesiologists closed claims project database. Int J Obstet Anesth 1996;5:258. Cheesman K, Brady J, Flood P, Li G: Epidemiology of anesthesia-related complications in labor and delivery, New York state, 2002-2005. Anesth Analg 2009;109:1174.

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Cheney FW: The American Society of Anesthesiologists closed claims project: what have we learned, how has it affected practice, and how will it affect practice in the future? Anesthesiology 1999;91:552. Cheney FW, Posner KL, Caplan RA, Gild WM: Burns from warming devices in anesthesia. Anesthesiology 1994;80:806. Cheney FW, Domino KB, Caplan RA, Posner KL: Nerve injury associated with anesthesia: a closed claims analysis. Anesthesiology 1999;90:1062. Cheney F, Posner K, Lee L, et al: Trends in anesthesiarelated death and brain damage. Anesthesiology 2006;105:1071. Cook T, Bland L, Mihai R, Scott S: Litigation related to anaesthesia: an analysis of claims against the NHS in England 1995-2007. Anaesthesia 2009;64:706. Cook T, Scott S, Mihai R: Litigation related to airway and respiratory complications of anaesthesia: an analysis of claims against the NHS in England 1995-2007. Anaesthesia 2010;65:556. Coppieters MW, Van De Velde M, Stappaerts KH: Positioning in anesthesiology. Toward a better understanding of stretch-induced perioperative neuropathies. Anesthesiology 2002;97:75. Cranshaw J, Gupta K, Cook T: Litigation related to drug errors in anaesthesia: an analysis of claims against the NHS in England 1995-2009. Anaesthesia 2009;64:1317. Crosby E: Medical malpractice and anesthesiology: literature review and role of the expert witness. Can J Anesth 2007;54:227. Davies J, Posner K, Lee L, et al: Liability associated with obstetric anesthesia. Anesthesiology 2009;110:131. Domino KB, Posner Kl, Caplan RA, Cheney FW: Awareness during anesthesia: a closed claims analysis. Anesthesiology 1999;90:1053. Domino KB, Posner KL, Caplan RA, Cheney FW: Airway injury during anesthesia: a closed claims analysis. Anesthesiology 1999;91:1703. Domino K, Bowdle T, Posner K, et al: Injuries and liability related to central vascular catheters. Anesthesiology 2004;100:1411. Edbril SD, Lagasse RS: Relationship between malpractice litigation and human errors. Anesthesiology 1999;91:848. Fisher DM: New York State guidelines on the topical use of phenylephrine in operating rooms. Anesthesiology 2000;92:858. Fitzgibbon DR, Posner KL, Domino KB, et al: Chronic pain management: American Society of Anesthesiologists Closed Claims Project. Anesthesiology 2004;100:98.

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Gayer S: Prone to blindness: answers to postoperative visual loss. Anesth Analg 2011;112:11. Ghoneim MM: Awareness during anesthesia. Anesthesiology 2000;92:597. Gild WM, Posner KL, Caplan RA, Cheney FW: Eye injuries associated with anesthesia. Anesthesiology 1992;76:204. Hawkins J, Chang J, Palmer S, et al: Anesthesia-related maternal mortality in the United States: 1979-2002. Obstet Gynecol 2011;117:69. Hepner DL, Castells MC: Anaphylaxis during the perioperative period. Anesth Analg 2003;97:1381. Jimenez N, Posner K, Cheney F, et al: An update on pediatric anesthesia liability: a closed claims analysis. Anesth Analg 2007;104:147. Lagasse R: Anesthesia safety: model or myth? Anesthesiology 2002;97:1336. Lagasse R: To see or not to see. Anesthesiology 2006; 105:1971. Lagasse R: Innocent prattle. Anesthesiology 2009;110:698. Lee LA: Postoperative visual loss data gathered and analyzed. ASA Newslett 2000;64:25. Lee L, Posner K, DominoK, et al: Injuries associated with regional anesthesia in the 1980s and 1990s. Anesthesiology 2004;101:143. Lee L, Posner K, Cheney F, et al: Complications associated with eye blocks and peripheral nerve blocks: an American Society of Anesthesiologists Closed Claims analysis. Reg Anesth Pain Med 2008;33:416. Lee LA, Rothe S, Posner KL, et al: The American Society of Anesthesiologists Postoperative Visual Loss Registry: analysis of 93 spine surgery cases with postoperative visual loss. Anesthesiology 2006;105:652. Lesser JB, Sanborn KV, Valskys R, Kuroda M: Severe bradycardia during spinal and epidural anesthesia recorded by an anesthesia information management system. Anesthesiology 2003;99:859. Levy J, Adkinson N: Anaphylaxis during cardiac surgery: implications for clinicians. Anesth Analg 2008;106:392. Li G, Warner M, Lang B, et al: Epidemiology of anesthesia related mortality in the United States 1999-2005. Anesthesiology 2009;110:759. Liang B: “Standards” of anesthesia: law and ASA guidelines. J Clin Anesth 2008;20:393. Lineberger C: Impairment in anesthesiology: awareness and education. Int Anesth Clin 2008;46:151. Marco A: Informed consent for surgical anesthesia care: has the time come for separate consent? Anesth Analg 2009;110:280.

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Martin L, Mhyre J, Shanks A, et al: 3,423 emergency tracheal intubations at a university hospital: airway outcomes and complications. Anesthesiology 2011;114:42. Martin JT: Compartment syndromes: concepts and perspectives for the anesthesiologist. Anesth Analg 1992;75:275. Metzner J, Posner K, Domino K: The risk and safety of anesthesia at remote locations: the US closed claims analysis. Curr Opin Anaesthesiol 2009;22:502. Monitto C, Hamilton R, Levey E, et al: Genetic predisposition to natural rubber latex allergy differs between health care workers and high risk patients. Anesth Analg 2010;110:1310. Morray JP, Geiduschek JM, Caplan RA: A comparison of pediatric and adult anesthesia closed malpractice claims. Anesthesiology 1993;78:461. Newland MC, Ellis SJ, Lydiatt CA, et al: Anestheticrelated cardiac arrest and its mortality. Anesthesiology 2002;97:108. Pollard JB: Cardiac arrest during spinal anesthesia: common mechanisms and strategies for prevention. Anesth Analg 2001;92:252. Ramamoorthy C, Haberkern C, Bhananker S, et al: Anesthesia-related cardiac arrest in children with heart disease: data from the pediatric perioperative cardiac arrest (POCA) registry. Anesth Analg 2010;110:1376. Ranta SOV, Lauila R, Saario J, et al: Awareness with recall during general anesthesia: incidence and risk factors. Anesth Analg 1998;86:1084. Roh J, Kim D, Lee S, et al: Intensity of extremely low frequency electromagnetic fields produced in operating rooms during surgery at the standing position of anesthesiologists. Anesthesiology 2009;111:275. Rose G, Brown R: The impaired anesthesiologist: not just about drugs and alcohol anymore. J Clin Anesthesiol 2010;22:379. Sharma AD, Parmley CL, Sreeram G, Grocott HP: Peripheral nerve injuries during cardiac surgery: risk factors, diagnosis, prognosis, and prevention. Anesth Analg 2000;91:1358. Silverstein JH, Silva DA, Iberti TJ: Opioid addiction in anesthesiology. Anesthesiology 1993;79:354. Sprung J, Bourke DL, Contreras MG, et al: Perioperative hearing impairment. Anesthesiology 2003;98:241. Tait AR: Occupational transmission of tuberculosis: implications for anesthesiologists. Anesth Analg 1997;85:444.

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Warner MA, Warner ME, Martin JT: Ulnar neuropathy. Incidence, outcome, and risk factors in sedated or anesthetized patients. Anesthesiology 1994;81:1332. Warner MA, Warner DO, Harper CM: Lower extremity neuropathies associated with lithotomy positions. Anesthesiology 2000;93:938. Warner ME, Benenfeld SM, Warner MA, et al: Perianesthetic dental injuries. Anesthesiology 1999;90:1302. Weinger MB, Englund CE: Ergonomic and human factors affecting anesthetic vigilance and monitoring

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performance in the operating room environment. Anesthesiology 1990;73:995. Welch M, Brummett C, Welch T, et al: Perioperative nerve injuries: a retrospective study of 380,680 cases during a 10-year period at a single institution. Anesthesiology 2009;111:490. Williams EL, Hart WM Jr, Tempelhoff R: Postoperative ischemic optic neuropathy. Anesth Analg 1995;80:1018. Yuill G, Saroya D, Yuill S: A national survey of the provision for patients with latex allergy. Anaesthesiology 2003;58:775.

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