Waldman Atlas Of Pain Management Injestion Techniques

Atlas of

Pain Management Injection Techniques THIRD EDITION Steven D. Waldman, MD, JD Clinical Professor of Anesthesiology Professor of Medical Humanities and Bioethics University of Missouri–Kansas City School of Medicine Kansas City, Missouri

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1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899 ATLAS OF PAIN MANAGEMENT INJECTION TECHNIQUES Copyright © 2013, 2007, 2000 by Saunders, an imprint of Elsevier Inc.

ISBN: 978-1-4377-3793-6

All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the ­Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

Notices Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the author assumes any liability for any injury and/ or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or ­operation of any methods, products, instructions, or ideas contained in the material herein. Library of Congress Cataloging-in-Publication Data Waldman, Steven D. Atlas of pain management injection techniques / Steven D. Waldman. — 3rd ed. p. ; cm. Includes bibliographical references and index. ISBN 978-1-4377-3793-6 (hardcover : alk. paper) I. Title. [DNLM: 1. Pain—drug therapy—Atlases. 2. Injections—methods—Atlases. WL 17] 615ˈ.6—dc23

Content Strategist: Pamela Hetherington Content Development Specialist: Sabina Borza Publishing Services Manager: Patricia Tannian Senior Project Manager: Claire Kramer Designer: Louis Forgione Illustrator: Jennifer C. Darcy

Printed in China Last digit is the print number:  9  8  7  6  5  4  3  2  1

2012012534

To E. Grey Dimond, MD Clinician, Educator, Visionary, Mentor, and Friend

PREFACE

One hundred twenty-seven years have passed since Carl Koller first used cocaine to perform an eye operation without pain. Although Koller’s landmark discovery forever changed how surgery is performed and he unwittingly created a cottage industry in regional anesthesia drugs, needles, and, of course, regional anesthesia textbooks, a careful analysis of the ensuing 127 years reveals that most of the advances in regional anesthesia drugs have centered around the development of safer local anesthetics and improved needles. The landmark texts by Pitkin, DeJong, Moore, and others helped make the use of regional anesthesia drugs accessible to the general practitioner. These early books standardized techniques, needle sizes and lengths, and, perhaps most important, the dosages of local anesthetics for the common techniques. Lofgren’s discovery of lidocaine in 1943 moved regional anesthesia drugs into the operating room and obstetric suite, as well as into doctors’ and dentists’ offices. Much safer than ester local anesthetics such as procaine, the most widely used local anesthetic up to that time, lidocaine’s larger therapeutic window was much more forgiving of clinical missteps when nerve blocks were performed, and lidocaine has been the mainstay of regional anesthesia drugs ever since. In the 1980s, pain medicine came into its own as practitioners tested and applied the simple hypothesis that the cause of pain must be diagnosed first to ensure a successful treatment. Along with the birth of this new subspecialty came a new set of “bibles” by Raj and by Cousins and Bridenbaugh and the first edition of

Atlas of Pain Management Injection Techniques, which was first published in 2000. I think that the field of pain management is entering a new and exciting era, now that ultrasound guidance has become increasingly utilized when regional anesthesia drugs are administered. Only time will tell whether ultrasound guidance is a true “moment” or merely a passing fancy that will go the way of nesacaine and succinylcholine drips, but my clinical impression is that ultrasound guidance represents an important advance in regional anesthesia and pain management that I think will stand the test of time. In addition to presenting the fundamentals of ultrasound guidance in the how-to-do-it format that has made previous editions of this book so popular, I have included many new color figures and ultrasound, fluoroscopic, and magnetic resonance images, along with new full-color, clinically relevant anatomic drawings to make the techniques described even more accessible to my readers. With the able assistance of Sabina Borza, Content Development Specialist, we have added clear, concise captions to every figure and strived to improve the layout of the book to make it even more readable than previous editions. I sincerely hope that you will enjoy using this book as much as I enjoyed writing it. Steven D. Waldman, MD, JD 2012

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ACKNOWLEDGMENTS

I would like to thank my editor, Pamela Hetherington, for her wisdom, hard work, and patience and Sabina Borza, who worked tirelessly to improve the content and layout of this book. SDW

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SECTION 1  •  Head and Neck

Chapter 1 TEMPOROMANDIBULAR JOINT INJECTION Indications and Clinical Considerations Injection of the temporomandibular joint is indicated as an important component in the management of temporomandibular joint dysfunction, in the palliation of pain secondary to internal derangement of the joint, and in the treatment of pain secondary to arthritis of the joint. Temporomandibular joint dysfunction (also known as myofascial pain dysfunction of the muscles of mastication) is characterized by pain in the joint itself that radiates into the mandible, ear, neck, and tonsillar pillars. Headache often accompanies the pain of temporomandibular joint dysfunction and is clinically indistinguishable from tension-type headache. Stress is often the precipitating or exacerbating factor in the development of temporomandibular joint dysfunction. Dental malocclusion may also play a role in the evolution of temporomandibular joint dysfunction. Internal derangement and arthritis of the temporomandibular joint may manifest as clicking or grating when the joint is opened and closed (Figure 1-1). If the condition is not treated, the patient may experience increasing pain in the just-mentioned areas and limitation of jaw movement and opening. Recently the injection of autologous blood into the temporomandibular joint has gained popularity in the treatment of recurrent temporomandibular joint hypermobility dislocation (Figure 1-2). This injection technique is also useful in the injection of other substances into the temporomandibular joint such as hyaluronic acid derivatives and tenoxicam.

A

Clinically Relevant Anatomy The temporomandibular joint is a true joint that is divided into an upper and a lower synovial cavity by a fibrous articular disk. Internal derangement of this disk may result in pain and temporomandibular joint dysfunction, but extracapsular causes of temporomandibular joint pain are much more common. The joint space between the mandibular condyle and the glenoid fossa of the zygoma may be injected with small amounts of local anesthetic and corticosteroid. The temporomandibular joint is innervated by branches of the mandibular nerve. The muscles involved in temporomandibular joint dysfunction often include the temporalis, masseter, and external pterygoid and internal pterygoid and may include the trapezius and sternocleidomastoid. Trigger points may be identified when these muscles are palpated.

B Figure 1-1  Osteoarthritis compared in a specimen radiograph (A) and photograph (B) of a sagittally sectioned specimen. The joint space is narrow and the disk is dislocated anteriorly, with thinning and fraying of the meniscal (m) posterior attachment or bilaminar zone. The condylar head cortex is thickened, with small osteophytes (arrows). The mandibular fossa is sclerotic and remodeled, and only a shallow concavity is seen where the articular eminence once was. (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

1

2        SECTION 1  •  Head and Neck

Figure 1-2  Injection of autologous blood into the temporomandibular joint. (From Daif ET: Autologous blood injection as a new treatment modality for chronic recurrent temporomandibular joint dislocation, Oral Surg Oral Med Oral Pathol Oral Radiol Endod 109:31-36, 2010.)

Technique The patient is placed in the supine position with the cervical spine in the neutral position. The temporomandibular joint is identified by asking the patient to open and close his or her mouth several times and by palpating the area just anterior and slightly inferior to the acoustic auditory meatus. After the joint has been identified, the patient is asked to hold his or her mouth in a neutral position. A total of 0.5 mL of local anesthetic is drawn up in a 3-mL sterile syringe. When temporomandibular joint dysfunction, internal derangement of the temporomandibular joint, arthritis pain of the temporomandibular joint, or other painful conditions involving the temporomandibular joint are treated, a total of 20 mg of depot corticosteroid is added to the local anesthetic with the first block, and 10 mg of depot corticosteroid is added to the local anesthetic with subsequent blocks. After the skin overlying the temporomandibular joint has been prepared with antiseptic solution, a 25-gauge, 1-inch styletted needle is inserted just below the zygomatic arch directly in the middle of the joint space. The needle is advanced ½ to ¾ inch in a plane perpendicular to the skull until a “pop” is felt that indicates the joint space has been entered (Figure 1-3). After careful aspiration, 1 mL of solution is slowly injected. Injection of the joint may be repeated at 5- to 7-day intervals if the symptoms persist.

Side Effects and Complications This anatomic region is highly vascular. This vascularity and proximity to major blood vessels also give rise to an increased incidence of postblock ecchymosis and hematoma formation, and the patient should be warned of such. In spite of the vascularity of this anatomic region, this technique can be performed safely in the presence of anticoagulation by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation

Temporomandibular joint External auditory meatus

Torn and inflamed articular surface Figure 1-3  Needle placement into the temporomandibular joint is simplified by having the patient open and close the mouth to facilitate identification of the joint.

dictates a favorable risk-to-benefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-­minute periods after the block will also decrease the amount of postprocedure pain and bleeding the patient may experience. Additional side effects that occur with sufficient frequency include inadvertent block of the facial nerve with associated facial weakness. When this occurs, protection of the cornea with sterile ophthalmic lubricant and patching is mandatory.

1  •  Temporomandibular Joint Injection        3

Clinical Pearls Pain from temporomandibular joint dysfunction requires careful evaluation to design an appropriate treatment plan. Infection and inflammatory causes including collagen vascular diseases first must be ruled out. When temporomandibular joint pain occurs in older patients, the pain must be distinguished from the jaw claudication associated with temporal arteritis. Stress and anxiety often accompany temporomandibular joint dysfunction; these factors must be addressed and treated. The myofascial pain component of temporomandibular joint dysfunction is best treated with tricyclic antidepressant compounds such as amitriptyline. Dental malocclusion and nighttime bruxism should be treated with an acrylic bite appliance. Narcotic analgesics and benzodiazepines should be avoided in patients with temporomandibular joint dysfunction.

SUGGESTED READINGS Daif ET: Autologous blood injection as a new treatment modality for chronic recurrent temporomandibular joint dislocation, Oral Surg Oral Med Oral Pathol Oral Radiol Endod 109:31–36, 2010. Mountziaris PM, Kramer PR, Mikos AG: Emerging intra-articular drug delivery systems for the temporomandibular joint, Methods 47:134–140, 2009. Sidebottom AJ: Current thinking in temporomandibular joint management, Br J Oral Maxillofac Surg 47:91–94, 2009. Waldman SD: Temporomandibular joint dysfunction. In Pain review, ­Philadelphia, 2009, Saunders–Elsevier. Waldman SD: Temporomandibular joint injection. In Pain review, Philadelphia, 2009, Saunders–Elsevier.

Chapter 2 SUPRAORBITAL NERVE BLOCK

Indications and Clinical Considerations Supraorbital nerve block is useful in the diagnosis and treatment of swimmer’s headache and supraorbital neuralgia. Swimmer’s headache is the result of compression of the supraorbital nerves by swimming goggles that fit poorly or are worn too tightly, exerting pressure on the supraorbital nerves as they exit the supraorbital foramen. Repetitive microtrauma from wearing swim goggles may also cause swimmer’s headache. The pain of swimmer’s headache is characterized as persistent pain in the supraorbital region and forehead with occasional sudden, shocklike paresthesias in the distribution of the supraorbital nerves. Sinus headache involving the frontal sinuses, which is much more common than swimmer’s headache, occasionally mimics the pain of swimmer’s headache. Occasionally, a patient with swimmer’s headache will complain that the hair on the front of the head “hurts.”

Referred pain

Clinically Relevant Anatomy The supraorbital nerve arises from fibers of the frontal nerve, which is the largest branch of the ophthalmic nerve. The frontal nerve enters the orbit via the superior orbital fissure and passes anteriorly beneath the periosteum of the roof of the orbit. The frontal nerve gives off a larger lateral branch, the supraorbital nerve, and a smaller medial branch, the supratrochlear nerve. Both exit the orbit anteriorly. The supraorbital nerve sends fibers all the way to the vertex of the scalp and provides sensory innervation to the forehead, upper eyelid, and anterior scalp (Figure 2-1).

Technique The patient is placed in a supine position. A total of 3 mL of local anesthetic is drawn up in a 10-mL sterile syringe. When swimmer’s headache is treated with supraorbital nerve block, a total of 80 mg of depot corticosteroid is added to the local anesthetic with the first block, and 40 mg of depot corticosteroid is added with subsequent blocks. The supraorbital notch on the affected side is then identified by palpation. The skin overlying the notch is prepared with antiseptic solution, with care being taken to avoid spillage into the eye. A 25-gauge, 1½-inch needle is inserted at the level of the supraorbital notch and is advanced medially approximately 15 degrees off the perpendicular to avoid entering the foramen. The needle is advanced until it approaches the periosteum of the underlying bone (Figure 2-2). A paresthesia may be elicited, and the patient should be warned of such. The needle should not enter 4

Figure 2-1  Swimmer’s headache is characterized by persistent pain in the supraorbital region with associated intermittent shocklike paresthesias.

the supraorbital foramen; should this occur, the needle should be withdrawn and redirected slightly more medially. Because of the loose alveolar tissue of the eyelid, a gauze sponge should be used to apply gentle pressure on the upper eyelid and supraorbital tissues before injection of solution to prevent the injectate from dissecting inferiorly into these tissues. This pressure should be maintained after the procedure to avoid periorbital hematoma and ecchymosis. After gentle aspiration, 3 mL of solution is injected in a fanlike distribution. If blockade of the supratrochlear nerve is also desired, the needle is then redirected medially; after careful aspiration, an additional 3 mL of solution is injected in a fanlike manner.

Side Effects and Complications The forehead and scalp are highly vascular, and the pain specialist should carefully calculate the total milligram dose of local anesthetic that may be safely given, especially if bilateral nerve blocks are being performed. This vascularity gives rise to an increased incidence of postblock ecchymosis and hematoma formation.

2  •  Supraorbital Nerve Block        5

is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block also decreases the amount of postprocedure pain and bleeding the patient may experience. Supraorbital n. Supraorbital notch

Clinical Pearls Supraorbital nerve block is especially useful in the diagnosis and palliation of pain secondary to swimmer’s headache and supraorbital neuralgia. The first step in the management of the unusual cause of headache is the correct fitting of swim goggles that do not compress the supraorbital nerves. Coexistent frontal sinusitis should be ruled out in patients who do not respond rapidly to a change in swim goggles and a series of the just-described nerve blocks. Any patient with headaches severe enough to require neural blockade as part of the treatment plan should undergo computed tomography (CT) or magnetic resonance imaging (MRI) of the head to rule out unsuspected intracranial pathology.

SUGGESTED READINGS Figure 2-2  When the needle is placed for supraorbital nerve block, care should be taken to avoid advancing the needle into the supraorbital foramen.

In spite of the vascularity of this anatomic region, this technique can be safely performed in the presence of anticoagulation by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable risk-to-benefit ratio. These complications can be decreased if manual pressure

Levin M: Nerve blocks in the treatment of headache, Neurotherapeutics 7: 197–203, 2010. O’Brien JC Jr: Swimmer’s headache, or supraorbital neuralgia, Proc (Bayl Univ Med Cent) 17:418–419, 2004. Pareja JA, Caminero AB: Supraorbital neuralgia, Curr Pain Headache Rep 10: 302–305, 2006. Sharma RR, Pawar SJ, Lad SD, et  al: Frontal intraosseous cryptic hemangioma presenting with supraorbital neuralgia, Clin Neurol Neurosur 101:215–219, 1999. Sjaastad O, Stolt-Nielsen A, Pareja JA, et al: Supraorbital neuralgia. On the clinical manifestations and a possible therapeutic approach, Headache 39:204–212, 1999.

Chapter 3 TROCHLEAR NERVE BLOCK

Indications and Clinical Considerations Trochlear injection is useful in the diagnosis and treatment of primary trochlear headache. As with most headache syndromes, the exact cause of the pain of primary trochlear headache is unknown, and whether the trochlear nerve plays a role in pathogenesis of this uncommon source of head and face pain is the subject of ongoing debate. In patients with primary trochlear headache the presenting symptom is unilateral periorbital pain radiating from the trochlear area with associated headache. The pain of primary trochlear headache is exacerbated by supraduction of the affected eye, although no limitation of range of motion of the superior oblique should be noted. The pain of this uncommon headache syndrome is often worse at night, and whereas initially the pain is characterized by remissions and exacerbations, without treatment it can become chronic. As the name implies, primary trochlear headache is a diagnosis of exclusion because it occurs in the absence of primary orbital, retro-orbital, or ocular pathology. Often confused with acute ocular diseases such as glaucoma or herpes zoster of the first division of the trigeminal nerve or Charlin syndrome, pathology of the orbit and the retro-orbital region must be ruled out before the diagnosis of primary trochlear headache can be made. Inflammatory and autoimmune conditions involving the trochlear nerve anywhere along its path such as multiple sclerosis, cranial neuritis, and Tolosa-Hunt syndrome, as well as compromise of the trochlear nerve by tumor, abscess, or vascular abnormality must be carefully sought before the diagnosis of primary trochlear can be considered (Figures 3-1 and 3-2). The diagnosis of primary trochlear headache is then confirmed by injection of the trochlear region with local anesthetic and antiinflammatory steroid. Primary trochlear headache will uniformly respond to this injection.

Clinically Relevant Anatomy The trochlear nerve (cranial nerve IV) is composed of somatic general efferent motor fibers. It innervates the superior oblique extraocular muscle of the contralateral orbit (Figure 3-3). Contraction of the superior oblique extraocular muscle intorts (rotates inward), depresses, and abducts the globe. The superior oblique extraocular muscle works in concert with the five other extraocular muscles to allow the eye to perform its essential functions of tracking and fixation on objects. The fibers of the trochlear nerve originate from the trochlear nucleus, which is just ventral to the cerebral aqueduct in the 6

Figure 3-1  Axial, T1-weighted, contrast-enhanced image demonstrates soft tissue in the left cavernous sinus, which has enhanced markedly. The enhancement extends along the free edge of the tentorium cerebelli. Imaging is nonspecific, but after exclusion of other conditions this patient was diagnosed with Tolosa-Hunt syndrome. (From Tang Y, Booth T, Steward M, et al: The imaging of conditions affecting the cavernous sinus, Clin Radiol 65:937-945, 2010.)

tegmentum of the midbrain at the level of the inferior colliculus. As the trochlear nerve leaves the trochlear nucleus, it travels dorsally, wrapping itself around the cerebral aqueduct to then decussate in the superior medullary velum. The decussated fibers of the trochlear nerve then exit the dorsal surface of the brainstem just below the contralateral inferior colliculus, where they then curve around the brainstem, leaving the subarachnoid space along with the oculomotor nerve (cranial nerve III) between the superior cerebellar and posterior cerebral arteries. The trochlear nerve then enters the cavernous sinus and runs anteriorly along the lateral wall of the sinus with the oculomotor nerve (cranial nerve III), trigeminal nerve (cranial nerve V), and abducens nerve (cranial nerve VI).

3  •  Trochlear Nerve Block        7

After exiting the cavernous sinus, the trochlear nerve enters the orbit via the superior orbital fissure. Unlike the oculomotor nerve, the trochlear nerve does not pass through the tendinous ring of the extraocular muscles but passes just above the ring. The trochlear nerve then crosses medially along the roof of the orbit above the levator palpebrae and superior rectus muscles to innervate the superior oblique muscle (see Figure 3-3). Disorders of the trochlear nerve can be caused by central lesions that affect the trochlear nucleus such as stroke or space-occupying lesions such as tumor, abscess, or aneurysm. Increased intracranial pressure from subdural hematoma, sagittal sinus thrombosis, or abscess can compromise the nucleus and/or the efferent fibers of the trochlear nerve as they exit the brainstem and travel toward the orbit, with resultant abnormal nerve function. Traction on the trochlear nerve from loss of cerebrospinal fluid has also been implicated in cranial nerve IV palsy. Small vessel disease from diabetes or vasculitis associated with temporal arteritis may cause ischemia and even infarction of the trochlear nerve with resultant pathologic symptoms. In almost all disorders of the trochlear nerve, symptoms will take the form of a palsy of the superior oblique muscle, most commonly manifesting as an inability to look inward and downward. Often the patient will report difficulty in walking down stairs owing to the inability to depress the affected eye or eyes. On physical examination the clinician may note extorsion (outward rotation) of the affected eye as a result of the unopposed action of the inferior oblique muscle (Figure 3-4, A). In an effort to compensate, the patient may deviate his or her face forward and downward with the chin rotated toward the affected side to look downward (Figure 3-4, B). However, it should be remembered that isolated trochlear nerve palsy is the least common of the ocular motor palsies, and its presence should be viewed as an ominous warning sign.

Technique The patient is placed in a supine position. A total of 2 mL of local anesthetic is drawn up in a 10-mL sterile syringe. When primary trochlear headache is treated with trochlear region block, a total of 80 mg of depot corticosteroid is added to the local anesthetic with the first block, and 40 mg of depot corticosteroid is added with subsequent blocks. For trochlear region block to be performed, the medial canthus is identified and a line is drawn superiorly to a point just below the eyebrow. The skin at the midpoint of this line is prepared with antiseptic solution, with care being taken to avoid spillage into the eye. A 25-gauge, 1½-inch needle is inserted at this point and advanced until the tip of the needle makes contact with the bony surface of the orbit. After careful gentle aspiration, the contents of the syringe are slowly injected as the needle is slowly directed superiorly and inferiorly (Figure 3-5). Because of the loose alveolar tissue of the eyelid, a gauze sponge should be used to apply gentle pressure on the upper eyelid and supraorbital tissues before injection of solution to prevent the injectate from dissecting inferiorly into these tissues. This pressure should be maintained after the procedure to avoid periorbital hematoma and ecchymosis. When trochlear region block is used to treat the pain and symptoms associated with primary trochlear headache, 8 to 10 daily nerve blocks with local anesthetic may be required. If daily blocks are being performed, as a general rule the total dose of depot corticosteroids included in these blocks should not exceed 360 to 400 mg.

Figure 3-2  Axial T1-weighted image with gadolinium and fat saturation. This 55-year-old man had painful ophthalmoplegia (III, IV, VI, and VI) and slight proptosis of the right eye. Magnetic resonance imaging shows an enhancing ill-defined process in the right orbital apex. Cavernous sinus not involved (Tolosa-Hunt syndrome). (From Ferreira T, Verbist B, van Buchem M, et  al: Imaging the ocular motor nerves, Eur J Radiol 74:314-322, 2010.)

Superior oblique

Medial rectus Levator palpebrae superioris

Superior rectus

Lateral

Trochlear nerve [IV]

Figure 3-3  Trochlear nerve (IV) in the orbit. (From Drake RL, Vogl W, Mitchell AWM: Gray’s anatomy for students, ed 2, Philadelphia, 2010, Churchill Livingstone.)

8        SECTION 1  •  Head and Neck

Figure 3-4  A, The unopposed action of the inferior oblique muscle in the presence of trochlear nerve palsy results in extorsion of the globe and associated weak downward gaze. B, To compensate for the unopposed action of the inferior oblique muscle in the presence of trochlear palsy, the patient deviates his face forward and downward with the chin rotated toward the affected side.

A

B

Clinical Pearls

Medial canthus

Trochlear nerve block is especially useful in the diagnosis and palliation of pain secondary to primary trochlear headache. The first step in the care of patients thought to have this unusual cause of headache is ruling out more common types of headache that may mimic primary trochlear headache. Any patient with headaches bad enough to require neural blockade as part of the treatment plan should undergo computed tomography (CT) or magnetic resonance imaging (MRI) of the head to rule out unsuspected intracranial pathologic conditions.

SUGGESTED READINGS Figure 3-5  For trochlear block to be performed, the medial canthus is identified, and a line is drawn superiorly to a point just below the eyebrow.

Side Effects and Complications The major complication of this procedure is inadvertent injury to the eye. Failure to maintain bony contact while advancing the needle will greatly increase the risk of the devastating complication. The practitioner should also remember that this area is highly vascular and the potential for intravascular injection of local anesthetic with its attendant risks remains an ever-present possibility. This vascularity gives rise to an increased incidence of postblock ecchymosis and hematoma formation. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block also decreases the amount of postprocedure pain and bleeding.

Becker M, Kohler R, Vargas MI, et al: Pathology of the trigeminal nerve, Neuroimaging Clin N Am 18:283–307, 2008. Ferreira T, Verbist B, van Buchem M, et al: Imaging the ocular motor nerves, Eur J Radiol 74:314–322, 2010. Lin CM, Hseu IH: Isolated trochlear nerve palsy associated with carotid-cavernous sinus fistula, Int J Gerontol 3:129–132, 2009. Rait J: Ocular causes of headache. In Selvaratnam P, Niere K, Zuluaga M, ­editors: Headache, orofacial pain and bruxism, New York, 2009, Churchill Livingstone, pp 127–138. Waldman SD: The trochlear nerve—cranial nerve IV. In Pain review, ­Philadelphia, 2009, Saunders–Elsevier. Yangüela J, Sánchez-del-Rio M, Bueno A, et al: Primary trochlear headache: a new cephalgia generated and modulated on the trochlear region, Am J Ophthalmol 138:703, 2004. Yangüela J, Sánchez-del-Rio M, Bueno A, et  al: Primary trochlear headache: a new cephalgia generated and modulated on the trochlear region, Neurology 62:1134–1140, 2004.

Chapter 4 BUCCAL FOLD INJECTION FOR INCISORS AND CANINE TEETH Indications and Clinical Considerations The buccal fold injection technique is useful in the diagnosis and treatment of pain involving the incisors or canine teeth of the upper jaw. This technique can provide much-needed emergency relief of dental pain while the patient is waiting for definitive dental treatment. It can also serve as a useful diagnostic maneuver when the clinician is trying to localize the nidus of pain that the patient perceives as dental in origin. Dental pain is the result of irritation or inflammation of the nerves of the pulp and/or root of the tooth. Common causes of irritation or inflammation responsible for dental pain include infection, decay with resultant nerve exposure, gingival disease, plaque at or below the gum line, bruxism, injury, tumor, and tooth extractions (Figure 4-1). Less common causes include chemotherapy-induced odontalgia and barodontalgia. Pain involving the incisors or canine teeth may also be referred from other anatomic areas. Such referred pain may be indicative of temporomandibular joint dysfunction, sinus disease, abnormalities of the trigeminal nerve and its branches, and coronary artery stenosis.

A

C

Dental pain may range from a dull ache to severe, unremitting pain. Its onset may be insidious or acute. Dental pain is often worse when the affected tooth or teeth are exposed to hot or cold temperatures as well as when direct pressure is applied to the tooth or teeth when chewing. Tapping on the affected tooth or teeth may elicit an acute exacerbation of the pain. If significant inflammation or infection is present, rubor and color may be present, as well as swelling. Gingival bleeding or purulent drainage may also be present. It should be remembered that on occasion a severely compromised tooth that is causing a patient significant pain may appear completely normal.

Clinically Relevant Anatomy The incisor and canine and surrounding periosteum and buccal and gingival tissue are innervated by the superior alveolar nerve, which is a branch of the inferior alveolar nerve just before it exits from the infraorbital canal below the orbit (Figure 4-2). Fibers of the ipsilateral superior alveolar nerve may cross the midline and may anastomose with fibers of the contralateral nerve, although medial spread of injected local anesthetics may be limited by the attachments of the labial frenulum at the midline. The periosteum

B

D

Figure 4-1  Intruded primary incisor. A, Day of injury. B, Radiograph on day of injury. C, Three weeks postinjury. D, Five months postinjury. (From McTigue DJ: Managing injuries to the primary dentition, Dent Clin North Am 53:627-638, 2009.)

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10        SECTION 1  •  Head and Neck

Infraorbital foramen Infraorbital nerve Superior alveolar nerve

Figure 4-2  The relationship of the superior alveolar nerve to the incisor and canine. Figure 4-4  Proper needle placement with needle tip in good position. Green area indicates the initial flow of local anesthetic. Supporting structures

target area. The anesthetic will rapidly diffuse and anesthetize the pulp of the affected tooth (Figure 4-4). It should be remembered that the root of the canine tooth is longer than the root of the incisor and the apical portion of the root is often slightly more distally oriented. Apical region

Canine tooth

Figure 4-3  Lateral view of the canine demonstrating relationship of the supporting structures and apical region.

and bone that surround and support the root of the tooth are relatively thin and readily allow diffusion of local anesthetics injected in this region (Figure 4-3).

Technique The patient is placed in a supine position. A total of 1 to 2 mL of local anesthetic is drawn up in a 3-mL sterile syringe. The lip overlying the affected tooth is retracted, and a small amount of topical anesthetic such as viscous lidocaine or EMLA cream is applied to the alveolar sulcus with a cotton-tipped applicator. After topical anesthesia has been achieved, a 25-gauge, 11⁄2-inch needle is inserted through the previously anesthetized area and advanced axially and slightly medially toward the apex of the affected tooth. When the needle tip impinges on bone, it is withdrawn slightly out of the periosteum, and after gentle aspiration the local anesthetic is slowly injected around the apex

Side Effects and Complications In general, the use of nerve blocks in dentistry has enjoyed an amazing track record of utility and safety. Most side effects and complications are related to inadvertent intravascular injection, the use of local anesthetics containing epinephrine, and vasovagal syncope. Occasional hematoma and ecchymosis formation after dental nerve block is encountered, especially in patients taking anticoagulants or antiplatelet drugs. Pitfalls in needle placement include decreased diffusion of local anesthetic resulting from placement that is too superficial or positioning of the needle tip between the relatively impermeable fascia and labial muscle. Excessive pain from overly rapid injection of local anesthetic should also be avoided. The clinician is reminded that severe dental abscess can be life-threatening, and emergency incision and drainage combined with aggressive antibiotic therapy may be required to avoid disaster. Referred pain as well as pain from tumor should always be considered when evaluating a patient with dental pain.

Clinical Pearls Traumatic or nontraumatic dental pain is an increasingly frequent reason for adult and pediatric patients to visit urgent care and emergency room facilities. Often, urgent care or emergency room physicians have little or no training in the treatment of painful dental conditions. The use of dental nerve blocks with long-acting local anesthetics can provide excellent palliation of pain while the patient waits to obtain emergent dental care.

4  •  Buccal Fold Injection for Incisors and Canine Teeth        11 SUGGESTED READINGS Abt E: Topical anesthetics are more effective in diminishing pain from needle stick insertion alone compared to reducing pain from insertion with anesthetic injection, J Evid Based Dent Pract 10:160–161, 2010. Kato T, Lavigne GJ: Sleep bruxism: a sleep-related movement disorder, Sleep Med Clin 5:9–35, 2010. McTigue DJ: Managing injuries to the primary dentition, Dent Clin North Am 53:627–638, 2009.

van Wijk AJ, Hoogstraten J: Anxiety and pain during dental injections, J Dent 37:700–704, 2009. Zadik Y: Barodontalgia: what have we learned in the past decade? Oral Surg Oral Med Oral Pathol Oral Radiol Endod 109:e65–e69, 2010. Zadik Y, Vainstein V, Heling I, et al: Cytotoxic chemotherapy-induced odontalgia: a differential diagnosis for dental pain, J Endod 36:1588–1592, 2010.

Chapter 5 BUCCAL FOLD INJECTION TECHNIQUE FOR UPPER PREMOLAR TEETH

Indications and Clinical Considerations The buccal fold injection technique is useful in the diagnosis and treatment of pain involving the premolar teeth of the upper jaw. This technique can provide much-needed emergency relief of dental pain while the patient is waiting for definitive dental treatment. It can also serve as a useful diagnostic maneuver when the clinician is trying to localize the nidus of pain that the patient perceives as dental in origin. Dental pain is the result of irritation or inflammation of the nerves of the pulp and/or root of the tooth. Common causes of irritation or inflammation responsible for dental pain include infection, decay with resultant nerve exposure, gingival disease, plaque at or below the gum line, bruxism, injury, tumor, and tooth extraction. Less common causes include chemotherapyinduced odontalgia and barodontalgia. Pain involving the incisors or canine teeth may also be referred from other anatomic areas. Such referred pain may be indicative of temporomandibular joint dysfunction, sinus disease, abnormalities of the trigeminal nerve and its branches, and coronary artery stenosis. Dental pain may range from a dull ache to severe, unremitting pain. Its onset may be insidious or acute. Dental pain is often worse when the affected tooth or teeth are exposed to hot or cold temperatures as well as when direct pressure is applied to the tooth or teeth when chewing. Tapping on the affected tooth or teeth may elicit an acute exacerbation of the pain. If significant inflammation or infection is present, rubor and color may be present, as well as swelling. Gingival bleeding or purulent drainage may also be present. It should be remembered that on occasion a severely compromised tooth that is causing a patient significant pain may appear completely normal.

Technique The patient is placed in a supine position. A total of 1 to 2 mL of local anesthetic is drawn up in a 3-mL sterile syringe. The lip overlying the affected tooth is retracted, and a small amount of topical anesthetic such as viscous lidocaine or EMLA cream is applied to the alveolar sulcus with a cottontipped applicator. After topical anesthesia has been achieved, a 25-gauge, 1½-inch needle is inserted through the previously anesthetized area and advanced axially toward the apex of the affected tooth (Figure 5-4). If the needle tip impinges on bone, it is withdrawn slightly out of the periosteum, and after gentle aspiration the local anesthetic is slowly injected around the apex target area. The anesthetic will rapidly diffuse and anesthetize the pulp of the affected tooth. Supplemental block of the greater palatine nerve is carried out by placing the needle at right angles to the mucosa at a point approximately half the height of the affected premolar (Figure 5-5).

Side Effects and Complications In general, the use of nerve blocks in dentistry has enjoyed an amazing track record of utility and safety. Most side effects and complications are related to inadvertent intravascular injection, the use of local anesthetics containing epinephrine, and vasovagal

Clinically Relevant Anatomy The upper premolar is innervated by the superior dental plexus, which is composed of convergent fibers from the superior, posterior, and anterior alveolar nerves (Figure 5-1). In some patients the premolars are innervated from fibers from the middle superior alveolar nerve. The periosteum and bone that surround and support the root of the tooth are relatively thin and readily allow diffusion of local anesthetics injected in this region (Figure 5-2). The adjacent palate is innervated by the greater palatine nerve and occasionally fibers of the nasopalatine nerve (Figure 5-3). Supplemental blockade of these nerves will often be required to completely relieve upper premolar pain. 12

Infraorbital foramen Infraorbital nerve Anterior alveolar nerve Superior posterior alveolar nerve Figure 5-1  Innervation of the upper premolars.

5  •  Buccal Fold Injection Technique for Upper Premolar Teeth        13

syncope. Occasional hematoma and ecchymosis formation after dental nerve block is encountered, especially in patients taking anticoagulants or antiplatelet drugs. Pitfalls in needle placement include decreased diffusion of local anesthetic as a result of placement that is too superficial placement or positioning of the needle tip between the relatively impermeable fascia and labial muscle.

Excessive pain caused by overly rapid injection of local anesthetic should also be avoided. The clinician is reminded that severe dental abscess can be life-threatening, and emergency incision and drainage combined with aggressive antibiotic therapy may be required to avoid disaster. Referred pain as well as pain from tumor should always be considered when evaluating a patient with dental pain.

Figure 5-2  Spread of local anesthetic with blockade of upper premolar. Green indicates spread of local anesthetic.

Figure 5-4  Needle placement for block of the upper premolars.

Greater palatine nerve Greater palatine foramen Figure 5-3  Anatomy of the greater palatine nerve.

Figure 5-5  Needle placement for greater palatine nerve block.

14        SECTION 1  •  Head and Neck

Clinical Pearls Traumatic or nontraumatic dental pain is an increasingly frequent reason for adult and pediatric patients to visit urgent care and emergency room facilities. Often, urgent care or emergency room physicians have little or no training in the treatment of painful dental conditions. The use of dental nerve blocks with long-acting local anesthetics can provide excellent palliation of pain while the patient waits to obtain emergent dental care.

SUGGESTED READINGS Abt E: Topical anesthetics are more effective in diminishing pain from needle stick insertion alone compared to reducing pain from insertion with anesthetic injection, J Evid Based Dent Pract 10:160–161, 2010. Kato T, Lavigne GJ: Sleep bruxism: a sleep-related movement disorder, Sleep Med Clin 5:9–35, 2010.

McTigue DJ: Managing injuries to the primary dentition, Dent Clin North Am 53:627–638, 2009. van Wijk AJ, Hoogstraten J: Anxiety and pain during dental injections, J Dent 37:700–704, 2009. Zadik Y: Barodontalgia: what have we learned in the past decade? Oral Surg Oral Med Oral Pathol Oral Radiol Endod 109:e65–e69, 2010. Zadik Y, Vainstein V, Heling I, et al: Cytotoxic chemotherapy-induced odontalgia: a differential diagnosis for dental pain, J Endod 36:1588–1592, 2010.

Chapter 6 BUCCAL FOLD INJECTION FOR UPPER MOLAR TEETH Indications and Clinical Considerations The buccal fold injection technique is useful in the diagnosis and treatment of pain involving the molars of the upper jaw. This technique can provide much-needed emergency relief of dental pain while the patient is waiting for definitive dental treatment. It can also serve as a useful diagnostic maneuver when the clinician is trying to localize the nidus of pain that the patient perceives as dental in origin. Dental pain is the result of irritation or inflammation of the nerves of the pulp and/or root of the tooth. Common causes of irritation or inflammation responsible for dental pain include infection, decay with resultant nerve exposure, gingival disease, plaque at or below the gum line, bruxism, injury, tumor, and tooth extraction. Less common causes include chemotherapyinduced odontalgia and barodontalgia. Pain involving the incisors or canine teeth may also be referred from other anatomic areas. Such referred pain may be indicative of temporomandibular joint dysfunction, sinus disease, abnormalities of the trigeminal nerve and its branches, and coronary artery stenosis. Dental pain may range from a dull ache to severe, unremitting pain. Its onset may be insidious or acute. Dental pain is often worse when the affected tooth or teeth are exposed to hot or cold temperatures as well as when direct pressure is applied to the tooth or teeth when chewing. Tapping on the affected tooth or teeth may elicit an acute exacerbation of the pain. If significant inflammation or infection is present, rubor and color may be present, as well as swelling. Gingival bleeding or purulent drainage may also be present. It should be remembered that on occasion a severely compromised tooth that is causing a patient significant pain may appear completely normal.

innervated by the greater palatine nerve and in some patients by small anastomosing branches of the nasopalatine nerve (see Figure 5-3). The periosteum and bone that surround and support the roots of the molars are relatively thin and readily allow diffusion of local anesthetics injected in this region. For satisfactory anesthesia to be provided to the upper molars, three separate injections are usually required: (1) the buccal fold injection, (2) the tuberosity injection, and (3) the supplemental greater palatine nerve injection. Each injection is described in the following sections.

Technique Buccal Fold Injection The patient is placed in a supine position. If the more distal molars are to be blocked, it is important not to have the patient open the mouth too widely, or the coronoid process of the mandible will move ventrally and block the injection site. A total of 4 mL of local anesthetic is drawn up in a 5-mL sterile syringe. The lip overlying the affected tooth is retracted, and a small amount of topical anesthetic such as viscous lidocaine or EMLA cream is applied to the alveolar sulcus with a cotton-tipped applicator. After topical anesthesia has been achieved, a 25-gauge, ­11⁄2-inch needle is inserted through the previously anesthetized area and advanced axially and slightly posteriorly toward the apex of the

Clinically Relevant Anatomy The upper molars and surrounding periosteum and buccal and gingival tissue are innervated by the superior alveolar nerve, which branches from the infraorbital nerve before it enters the orbital cavity. These branches travel downward along the maxillary tuberosity to provide innervation for the upper molars and the buccal gingiva and associated periosteum. The gingiva, mucosa, and periosteum of the adjacent palate are innervated by the greater palatine nerve (Figure 6-1). The greater palatine nerve passes from the pterygopalatine fossa via the pterygopalatine canal through the pterygopalatine foramen (see Figure 5-3). In some patients an anatomic variation occurs, and the upper molars are innervated primarily by the middle alveolar nerves. This variation has little clinical import insofar as the success of this block is concerned. The palate adjacent to the molars is

Superior poster alveolar nerve Infraorbital nerve

Greater palatine nerve Pterygopalatine fossa Figure 6-1  Innervation of the upper molars.

15

16        SECTION 1  •  Head and Neck

affected tooth. When the needle tip impinges on bone, it is withdrawn slightly out of the periosteum, and after gentle aspiration 1 to 2 mL of local anesthetic is slowly injected around the apex target area; the anesthetic will rapidly diffuse and anesthetize the pulp of the affected tooth (Figures 6-2 and 6-3). It should be noted that unlike the previously described buccal fold injection techniques for the incisors, canines, and premolars, this technique yields relatively little anesthesia of the adjacent lip (Figure 6-4).

Side Effects and Complications In general, the use of nerve blocks in dentistry has enjoyed an amazing track record of utility and safety. Most side effects and complications are related to inadvertent intravascular injection, the use of local anesthetics containing epinephrine, and vasovagal

Tuberosity Injection The lip overlying the affected tooth is retracted, and the infrazygomatic crest is palpated with the gloved index finger, which also gently retracts the corner of the mouth posteriorly. A 25-gauge, 11⁄2-inch needle is inserted slightly distal to the second molar and; while it is kept close to the maxillary tuberosity, it is advanced in a superior and posterior trajectory (Figure 6-5). After gentle aspiration, an additional 2 mL of local anesthetic is slowly injected around the apex target area; the anesthetic will rapidly diffuse and anesthetize the pulp of the affected tooth (Figure 6-6). This injection will augment the anesthesia of the second and third molars (Figure 6-7). Supplemental Greater Palatine Nerve Injection Most patients with significant molar pain or those undergoing major procedures on the molars (e.g., root canals, extractions) will require supplementation of the anesthesia, obtained with upper molar dental block with injection of the fibers of the greater palatine nerve. This technique is carried out through injection of 0.1 to 0.2 mL of local anesthetic at right angles to the affected tooth at a point approximately one half of the tooth height (Figures 6-8 and 6-9).

Figure 6-3  Needle trajectory for buccal fold injection for the upper molars.

Figure 6-2  Buccal fold injection for the upper molars.

Figure 6-4  Spread of anesthesia after buccal fold injection for the upper molars. Note the relative lack of lip anesthesia.

6  •  Buccal Fold Injection for Upper Molar Teeth        17

syncope. Occasional hematoma and ecchymosis formation after dental nerve block is encountered, especially in patients taking anticoagulants or antiplatelet drugs. Pitfalls in needle placement include decreased diffusion of local anesthetic as a result of placement that is too superficial placement or positioning of the needle tip between the relatively impermeable fascia and labial muscle.

Excessive pain caused by overly rapid injection of local anesthetic should also be avoided. The clinician is reminded that severe dental abscess can be life-threatening, and emergency incision and drainage combined with aggressive antibiotic therapy may be required to avoid disaster. Referred pain as well as pain from tumor should always be considered when evaluating a patient with dental pain.

Figure 6-5  Tuberosity injection for the upper molars.

Figure 6-7  Spread of anesthesia after tuberosity injection for the upper molars.

Figure 6-6  Needle trajectory for tuberosity injection for the upper molars.

Figure 6-8  Injection of the greater palatine nerve for anesthesia of the upper molars.

18        SECTION 1  •  Head and Neck

Clinical Pearls Traumatic or nontraumatic dental pain is an increasingly frequent reason for adult and pediatric patients to visit urgent care and emergency room facilities. Often, urgent care or emergency room physicians have little or no training in the treatment of painful dental conditions. The use of dental nerve blocks with long-acting local anesthetics can provide excellent palliation of pain while the patient waits to obtain emergent dental care.

SUGGESTED READING

Figure 6-9  Spread of anesthesia after greater palatine nerve injection for the upper molars.

Abt E: Topical anesthetics are more effective in diminishing pain from needle stick insertion alone compared to reducing pain from insertion with anesthetic injection, J Evid Based Dent Pract 10:160–161, 2010. Kato T, Lavigne GJ: Sleep bruxism: a sleep-related movement disorder, Sleep Med Clin 5:9–35, 2010. McTigue DJ: Managing injuries to the primary dentition, Dent Clin North Am 53:627–638, 2009. Mylonas AI, Tzerbos FH, Mihalaki M, et al: Cerebral abscess of odontogenic origin, J Craniomaxillofac Surg 35:63–67, 2007. van Wijk AJ, Hoogstraten J: Anxiety and pain during dental injections, J Dent 37:700–704, 2009. Zadik Y: Barodontalgia: what have we learned in the past decade? Oral Surg Oral Med Oral Pathol Oral Radiol Endod 109:e65–e69, 2010. Zadik Y, Vainstein V, Heling I, et al: Cytotoxic chemotherapy-induced odontalgia: a differential diagnosis for dental pain, J Endod 36:1588–1592, 2010.

Chapter 7 INCISIVE NERVE BLOCK

Indications and Clinical Considerations This injection technique is useful in the diagnosis and treatment of pain involving the incisors or canine teeth of the lower jaw. This technique can provide much-needed emergency relief of dental pain while the patient is waiting for definitive dental treatment. It can also serve as a useful diagnostic maneuver when the clinician is trying to localize the nidus of pain that the patient perceives as dental in origin. Dental pain is the result of irritation or inflammation of the nerves of the pulp and/or root of the tooth. Common causes of irritation or inflammation responsible for dental pain include infection, decay with resultant nerve exposure, gingival disease, plaque at or below the gum line, bruxism, injury, tumor, and tooth extraction (Figure 7-1). Less common causes include ­chemotherapy-induced odontalgia and barodontalgia. Pain involving the incisors or canine teeth may also be referred from other

anatomic areas. Such referred pain may be indicative of temporomandibular joint dysfunction, sinus disease, abnormalities of the trigeminal nerve and its branches, and coronary artery stenosis. Dental pain may range from a dull ache to severe, unremitting pain. Its onset may be insidious or acute. Dental pain is often worse when the affected tooth or teeth are exposed to hot or cold temperatures as well as when direct pressure is applied to the tooth or teeth when chewing. Tapping on the affected tooth or teeth may elicit an acute exacerbation of the pain. If significant inflammation or infection is present, rubor and color may be present, as well as swelling. Gingival bleeding or purulent drainage may also be present. It should be remembered that on occasion a severely compromised tooth that is causing a patient significant pain may appear completely normal.

Clinically Relevant Anatomy The lower incisors and canine teeth are innervated by a branch of the incisive nerve, which is a distal branch of the inferior dental

A

C

B

D

Figure 7-1  Right lower gingival carcinoma in a 45-year-old man with histopathologically confirmed alveolar bone invasion (A, arrow). A, Cropped panoramic image. B to D, Cone-beam computed tomography (CT) images (B, horizontal; C, parallel; D, cross section). Cone-beam CT images reveal alveolar bone destruction of the right mandible (B, C, and D, arrow), whereas corresponding bone destruction cannot be seen on panoramic image. (From Momin MA, Okochi K, Watanabe H, et al: Diagnostic accuracy of cone-beam CT in the assessment of mandibular invasion of lower gingival carcinoma: comparison with conventional panoramic radiography, Eur J Radiol 72:75-81, 2009.)

19

20        SECTION 1  •  Head and Neck

Mental foramen Mental nerve Incisive nerve Figure 7-2  The incisive nerve provides innervations to the lower incisors and canines.

Figure 7-4  Buccal fold injection for the lower incisors and canine teeth.

Technique Lingual nerve

Figure 7-3  The relationship of the lingual nerve to the lower incisors and canines.

nerve. In most patients the nerve is covered by a thin layer of osseous lamina that allows easy diffusion of local anesthetic ­(Figure 7-2). Occasionally the bone is too thick to allow rapid diffusion of local anesthetic, and a mental or mandibular nerve block will be required. It should be noted that fibers of the contralateral incisive nerve may cross the midline and confuse the clinical picture. The buccal soft issues in this region are innervated by branches of the mental nerve, whereas the lingual gingiva and associated periosteum are innervated by branches of the sublingual nerve (Figure 7-3). Supplemental blockade of the mental and sublingual nerves may be required to provide complete anesthesia for the lower incisors and canine teeth.

The patient is placed in a supine position. A total of 1 to 2 mL of local anesthetic is drawn up in a 3-mL sterile syringe. The lip overlying the affected tooth is retracted, and a small amount of topical anesthetic such as viscous lidocaine or EMLA cream is applied to the buccal fold with a cotton-tipped applicator. After topical anesthesia has been achieved, a 25-gauge, 11⁄2-inch needle is inserted through the previously anesthetized area and advanced toward the apex of the affected tooth. When the needle tip impinges on bone, it is withdrawn slightly out of the periosteum, and after gentle aspiration the local anesthetic is slowly injected around the apex target area; the anesthetic will rapidly diffuse and anesthetize the pulp of the affected tooth (Figure 7-4). To perform the supplemental lingual nerve block, the needle is advanced just under the attached gingiva; after careful aspiration, 1.0 mL of local anesthetic is slowly injected (Figure 7-5).

Side Effects and Complications In general, the use of nerve blocks in dentistry has enjoyed an amazing track record of utility and safety. Most side effects and complications are related to inadvertent intravascular injection, the use of local anesthetics containing epinephrine, and vasovagal syncope. Occasional hematoma and ecchymosis formation after dental nerve block is encountered, especially in patients taking anticoagulants or antiplatelet drugs. Pitfalls in needle placement include decreased diffusion of local anesthetic from placement that is too superficial or positioning of the needle tip between the relatively impermeable fascia and labial muscle. Excessive pain from overly rapid injection of local anesthetic should also be avoided. The clinician is reminded that severe dental abscess can be life-threatening, and emergent incision and drainage combined with aggressive antibiotic therapy may be required to avoid

7  •  Incisive Nerve Block        21 SUGGESTED READINGS Abt E: Topical anesthetics are more effective in diminishing pain from needle stick insertion alone compared to reducing pain from insertion with anesthetic injection, J Evid Based Dent Pract 10:160–161, 2010. Kato T, Lavigne GJ: Sleep bruxism: a sleep-related movement disorder, Sleep Med Clin 5:9–35, 2010. McTigue DJ: Managing injuries to the primary dentition, Dent Clin North Am 53:627–638, 2009. van Wijk AJ, Hoogstraten J: Anxiety and pain during dental injections, J Dent 37:700–704, 2009. Zadik Y: Barodontalgia: what have we learned in the past decade? Oral Surg Oral Med Oral Pathol Oral Radiol Endod 109:e65–e69, 2010. Zadik Y, Vainstein V, Heling I, et al: Cytotoxic chemotherapy-induced odontalgia: a differential diagnosis for dental pain, J Endod 36:1588–1592, 2010.

Figure 7-5  Lingual nerve block for lower incisor and canine tooth dental pain.

disaster. Referred pain as well as pain from tumor should always be considered when evaluating a patient with dental pain.

Clinical Pearls Traumatic or nontraumatic dental pain is an increasingly frequent reason for adult and pediatric patients to visit urgent care and emergency room facilities. Often, urgent care or emergency room physicians have little or no training in the treatment of painful dental conditions. The use of dental nerve blocks with long-acting local anesthetics can provide excellent palliation of pain while the patient waits to obtain emergent dental care.

Chapter 8 INFERIOR ALVEOLAR NERVE BLOCK FOR LOWER PREMOLAR TEETH Indications and Clinical Considerations The inferior alveolar nerve block is useful in the diagnosis and treatment of pain involving the premolars of the lower jaw. This technique can provide much-needed emergency relief of dental pain while the patient is waiting for definitive dental treatment. It can also serve as a useful diagnostic maneuver when the clinician is trying to localize the nidus of pain that the patient perceives as dental in origin. Dental pain is the result of irritation or inflammation of the nerves of the pulp and/or root of the tooth. Common causes of irritation or inflammation responsible for dental pain include infection, decay with resultant nerve exposure, gingival disease, plaque at or below the gum line, bruxism, injury, tumor, or tooth extraction. Less common causes include chemotherapy-induced odontalgia and barodontalgia. Pain involving the incisors or canine teeth may also be referred from other anatomic areas. Such referred pain may be indicative of temporomandibular joint dysfunction, sinus disease, abnormalities of the trigeminal nerve and its branches, and coronary artery stenosis. Dental pain may range from a dull ache to severe, unremitting pain. Its onset may be insidious or acute. Dental pain is often worse when the affected tooth or teeth are exposed to hot or cold temperatures as well as when direct pressure is applied to the tooth or teeth when chewing. Tapping on the affected tooth or teeth may elicit an acute exacerbation of the pain. If significant inflammation or infection is present, rubor and color may be present, as well as swelling. Gingival bleeding or purulent drainage may also be present. It should be remembered that on occasion a severely compromised tooth that is causing a patient significant pain may appear completely normal.

foramen is identified, and the lower lip overlying the lower premolars is retracted. A small amount of topical anesthetic such as ­viscous lidocaine or EMLA cream is then applied to the alveolar sulcus just superior to the mental foramen with a cotton-tipped applicator. After topical anesthesia has been achieved, a 25-gauge, 11⁄2-inch needle is inserted through the previously anesthetized area and advanced toward the mental foramen (Figure 8-3). Care should be taken to avoid inserting the needle directly into the mental foramen to avoid inadvertent injection into the blood vessels or damage to the mental nerve. When the needle tip impinges on bone, it is withdrawn slightly out of the periosteum, and after gentle aspiration the local anesthetic is slowly injected around the apex target area; the anesthetic will rapidly diffuse and anesthetize the pulp of the affected tooth (Figure 8-4). Some spillover of local anesthetic may result in blockade of some fibers of the buccal nerve, resulting in large areas of anesthesia of the buccal soft tissues. Supplemental blockade of the lingual nerve is often required to provide complete anesthesia of the premolars. To block the lingual nerves, simply place the needle just beneath the surface of the lingual mucosa adjacent to the affect premolar. After careful aspiration, 0.5 mL of local anesthetic per premolar is injected (Figures 8-5 and 8-6).

Mental nerve Mental foramen

Clinically Relevant Anatomy The lower premolars are innervated primarily by the inferior alveolar nerve (Figure 8-1). Fibers of the buccal nerve innervate the buccal gingiva; the lingual gingiva is innervated by the sublingual nerve. Because of the thicker mandibular bone which supports the premolars, diffusion of local anesthetic with the buccal fold block is limited, and mental or mandibular nerve block is required. The mental foramen lies just inferior to and between the lower premolars (Figure 8-2).

Technique The patient is placed in a supine position. A total of 1 to 2 mL of local anesthetic is drawn up in a 3-mL sterile syringe. The mental 22

Branches of the inferior alveolar nerve Figure 8-1  The lower premolars are innervated primarily by branches of the inferior alveolar nerve. Note the dense mandibular bone surrounding the premolars as well as the relationship of the mental foramen to the premolars.

8  •  Inferior Alveolar Nerve Block for Lower Premolar Teeth        23

Side Effects and Complications In general, the use of nerve blocks in dentistry has enjoyed an amazing track record of utility and safety. Most side effects and complications are related to inadvertent intravascular injection, the use of local anesthetics containing epinephrine, and vasovagal syncope. Occasional hematoma and ecchymosis formation after dental nerve block is encountered, especially in patients taking anticoagulants or antiplatelet drugs. Pitfalls in needle placement

include decreased diffusion of local anesthetic because placement is too superficial or positioning of the needle tip between the relatively impermeable fascia and labial muscle. Excessive pain caused by overly rapid injection of local anesthetic should also be avoided. The clinician is reminded that severe dental abscess can be life-threatening, and emergency incision and drainage combined with aggressive antibiotic therapy may be required to avoid disaster. Referred pain as well as pain from tumor should always be considered when evaluating a patient with dental pain.

Mental nerve Figure 8-2  The relationship of the mental nerve to the premolars.

Figure 8-4  Area of anesthesia after mental nerve block.

Lingual nerve

Figure 8-3  Mental nerve block for lower premolar dental pain.

Figure 8-5  Relationship of the lingual nerve to the lower premolars.

24        SECTION 1  •  Head and Neck

Clinical Pearls Traumatic or nontraumatic dental pain is an increasingly frequent reason for adult and pediatric patients to visit urgent care and emergency room facilities. Often, urgent care or emergency room physicians have little or no training in the treatment of painful dental conditions. The use of dental nerve blocks with long-acting local anesthetics can provide excellent palliation of pain while the patient waits to obtain emergent dental care.

SUGGESTED READINGS Abt E: Topical anesthetics are more effective in diminishing pain from needle stick insertion alone compared to reducing pain from insertion with anesthetic injection, J Evid Based Dent Pract 10:160–161, 2010. Kato T, Lavigne GJ: Sleep bruxism: a sleep-related movement disorder, Sleep Med Clin 5:9–35, 2010. McTigue DJ: Managing injuries to the primary dentition, Dent Clin North Am 53:627–638, 2009. van Wijk AJ, Hoogstraten J: Anxiety and pain during dental injections, J Dent 37:700–704, 2009. Zadik Y: Barodontalgia: what have we learned in the past decade? Oral Surg Oral Med Oral Pathol Oral Radiol Endod 109:e65–e69, 2010. Zadik Y, Vainstein V, Heling I, et al: Cytotoxic chemotherapy-induced odontalgia: a differential diagnosis for dental pain, J Endod 36:1588–1592, 2010. Figure 8-6  Lingual nerve block for the premolars.

Chapter 9 INFERIOR ALVEOLAR NERVE BLOCK FOR LOWER MOLAR TEETH Indications and Clinical Considerations The inferior alveolar nerve block is useful in the diagnosis and treatment of pain involving the molars of the lower jaw. This technique can provide much-needed emergency relief of dental pain while the patient is waiting for definitive dental treatment. It can also serve as a useful diagnostic maneuver when the clinician is trying to localize the nidus of pain that the patient perceives as dental in origin. Dental pain is the result of irritation or inflammation of the nerves of the pulp and/or root of the tooth. Common causes of irritation or inflammation responsible for dental pain include infection, decay with resultant nerve exposure, gingival disease, plaque at or below the gum line, bruxism, injury, tumor, or tooth extraction. Less common causes include chemotherapy-induced odontalgia and barodontalgia. Pain involving the incisors or canine teeth may also be referred from other anatomic areas. Such referred pain may be indicative of temporomandibular joint dysfunction, sinus disease, abnormalities of the trigeminal nerve and its branches, and coronary artery stenosis. Dental pain may range from a dull ache to severe, unremitting pain. Its onset may be insidious or acute. Dental pain is often worse when the affected tooth or teeth are exposed to hot or cold temperatures as well as when direct pressure is applied to the tooth or teeth when chewing. Tapping on the affected tooth or teeth may elicit an acute exacerbation of the pain. If significant inflammation or infection is present, rubor and color may be present, as well as swelling. Gingival bleeding or purulent drainage may also be present. It should be remembered that on occasion a severely compromised tooth that is causing a patient significant pain may appear completely normal.

Technique Both the mandibular and lingual nerves can be blocked with one needle stick and minor repositioning of the needle. For the mandibular and lingual nerves to be blocked, the patient is placed in a supine position and a total of 3 mL of local anesthetic is drawn up in a 3-mL sterile syringe. The patient is then asked to open his or her mouth widely, and the coronoid notch is palpated with the index finger of the left hand (Figure 9-4). The syringe with an attached 25-gauge, 1½-inch needle is then directed from between the contralateral premolars toward an area approximately 1 cm above the level of the occlusal surface of the molars to be blocked just in front of the palpating index finger (Figure 9-5). The patient is then asked to slightly close his or her mouth to decrease tension of the pterygoid muscles. With the decrease of tension on the tightly stretched pterygoid muscles, the lateral margin of the pterygoid muscle relaxes, allowing the displaced nerve to return to its proper anatomic position.

Mandibular nerve Mandibular foramen

Clinically Relevant Anatomy The lower molars are innervated primarily by the mandibular (inferior alveolar) nerve (Figure 9-1). Because of the thicker mandibular bone which supports the premolars, diffusion of local anesthetic with buccal fold block is limited, and blockade of the mandibular nerve before it enters the mandibular canal is required (Figure 9-2), The lingual gingiva in the region of the lower molars is innervated by the lingual nerve (see Figure 9-2). Terminal branches of the buccal nerve pass through the buccinator muscles and provide innervations for the buccal mucosa in the region of the lower molars (see Figure 9-2). For satisfactory anesthesia to be provided to the lower molars, both the mandibular and lingual nerves need to be blocked, as well as the buccal nerve (Figure 9-3).

Mandibular canal

Figure 9-1  Anatomy of the mandibular nerve and lower molars.

25

26        SECTION 1  •  Head and Neck

Buccal nerve Mandibular nerve Lingual nerve

Figure 9-4  Palpating the coronoid notch.

Figure 9-2  Anatomy of the mandibular nerve and its relationship to the lingual and buccal nerves.

Buccal nerve Mandibular nerve Lingual nerve

Figure 9-5  Injection site for mandibular nerve block lies at the level of the finger palpating the coronoid notch, which is approximately 1 cm above the occlusal surfaces of the lower molars.

Figure 9-3  Relationship of the mandibular lingual and buccal nerves.

The needle is now advanced dorsally approximately 1.5 to 2.0 cm along the medial aspect of the mandibular ramus, with the trajectory of needle advancement horizontal to the occlusal plane of the molars (Figure 9-6). When the needle impinges onto the middle portion of the mandibular ramus, it is withdrawn slightly, and after careful aspiration 1.5 mL of local anesthetic is injected.

9  •  Inferior Alveolar Nerve Block for Lower Molar Teeth        27

Figure 9-6  Advancement of the needle for mandibular nerve block with the needle shaft in contact with the mandibular ramus and the trajectory in the horizontal plane of the occlusal surfaces of the molars being blocked.

Figure 9-8  Needle trajectory for buccal nerve injection for lower molar dental pain.

ramus (Figure 9-8). After careful aspiration, 0.5 mL of additional local anesthetic is then slowly injected.

Side Effects and Complications In general, the use of nerve blocks in dentistry has enjoyed an amazing track record of utility and safety. Most side effects and complications are related to inadvertent intravascular injection, the use of local anesthetics containing epinephrine, and vasovagal syncope. Occasional hematoma and ecchymosis formation after dental nerve block is encountered, especially in patients taking anticoagulants or antiplatelet drugs. Pitfalls in needle placement include decreased diffusion of local anesthetic caused by placement that is too superficial or positioning of the needle tip between the relatively impermeable fascia and labial muscle. Excessive pain from overly rapid injection of local anesthetic should also be avoided. The clinician is reminded that severe dental abscess can be life-threatening, and emergency incision and drainage combined with aggressive antibiotic therapy may be required to avoid disaster. Referred pain as well as pain from tumor should always be considered when evaluating a patient with dental pain.

Clinical Pearls Figure 9-7  Needle trajectory for lingual nerve block for lower molar dental pain.

The needle is then withdrawn into the soft tissue and the trajectory is redirected medially and ventrally toward the mandibular crest to block the lingual nerve (Figure 9-7). The buccal nerve is then blocked by inserting the needle just above the buccal fold at the third molar and advancing it toward the ipsilateral mandibular

Traumatic or nontraumatic dental pain is an increasingly frequent reason for adult and pediatric patients to visit urgent care and emergency room facilities. Often, urgent care or emergency room physicians have little or no training in the treatment of painful dental conditions. The use of dental nerve blocks with long-acting local anesthetics can provide excellent palliation of pain while the patient waits to obtain emergency dental care.

28        SECTION 1  •  Head and Neck SUGGESTED READINGS Abt E: Topical anesthetics are more effective in diminishing pain from needle stick insertion alone compared to reducing pain from insertion with anesthetic injection, J Evid Based Dent Pract 10:160–161, 2010. Kato T, Lavigne GJ: Sleep bruxism: a sleep-related movement disorder, Sleep Med Clin 5:9–35, 2010. McTigue DJ: Managing injuries to the primary dentition, Dent Clin North Am 53:627–638, 2009.

Mylonas AI, Tzerbos FH, Mihalaki M, et al: Cerebral abscess of odontogenic origin, J Craniomaxillofac Surg 35:63–67, 2007. van Wijk AJ, Hoogstraten J: Anxiety and pain during dental injections, J Dent 37:700–704, 2009. Zadik Y: Barodontalgia: what have we learned in the past decade? Oral Surg Oral Med Oral Pathol Oral Radiol Endod 109:e65–e69, 2010. Zadik Y, Vainstein V, Heling I, et al: Cytotoxic chemotherapy-induced odontalgia: a differential diagnosis for dental pain, J Endod 36:1588–1592, 2010.

Chapter 10 STYLOID PROCESS INJECTION

Indications and Clinical Considerations Eagle syndrome (also known as stylohyoid syndrome) is caused by pressure on the internal carotid artery and surrounding structures including branches of the glossopharyngeal nerve by an abnormally elongated styloid process or a calcified stylohyoid ligament (Figure 10-1). The pain of Eagle syndrome is sharp and stabbing and occurs with movement of the mandible or with turning of the neck. The pain starts below the angle of the mandible and radiates into the tonsillar fossa, the temporomandibular joint, and the base of the tongue. A trigger point may be present in the tonsillar fossa. Injection of the attachment of the stylohyoid ligament to the styloid process with local anesthetic and corticosteroid serves as both a diagnostic and a therapeutic maneuver. Rarely, the elongated styloid process or calcified stylohyoid ligament may actually cause vascular occlusion (Figure 10-2).

Clinically Relevant Anatomy The styloid process extends in a caudal and ventral direction from the temporal bone from its origin just below the auditory meatus. The stylohyoid ligament’s cephalad attachment is to the styloid process, and its caudal attachment is to the hyoid bone. In Eagle syndrome the styloid process is abnormally elongated, either alone or in combination with calcification of the stylohyoid ligament. The elongated process or calcified ligament impinges on the internal carotid artery and branches of the glossopharyngeal nerve (Figure 10-3). The glossopharyngeal nerve exits from the jugular foramen in proximity to the vagus and accessory nerves and the internal jugular vein and passes just inferior to the styloid process (see Figure 10-3). All three nerves lie in the groove between the internal jugular vein and the internal carotid artery. The key landmark for injection when treating Eagle syndrome is the styloid process of the temporal bone. This osseous process represents the calcification of the cephalad end of the stylohyoid ligament. Although the styloid process is usually easy to identify, if ossification is limited it may be difficult to locate with the exploring needle.

Technique

Figure 10-1  Ossification of the stylohyoid ligament (Eagle syndrome). Note the large ossified structure (arrows), which represents an elongated styloid process or ossified stylohyoid ligament or both. (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, ­Saunders.)

The patient is placed in the supine position. An imaginary line that runs from the mastoid process to the angle of the mandible (Figure 10-4) is visualized. The styloid process should lie just below the midpoint of this line. The skin is prepared with antiseptic solution. A 22-gauge, 1½-inch needle attached to a 10-mL syringe is advanced at this midpoint location in a plane perpendicular to the skin. The styloid process should be encountered 29

A

B

C

D

E Figure 10-2  A, Axial computed tomography angiography (CTA) with right sigmoid sinus occlusion (black arrow) and dye present in the left sigmoid sinus (white arrow). B, Computed tomography (CT) venogram confirming the left internal jugular vein compressed between the styloid process (black arrow) and lateral mass of C1 (white arrow). C, Three-dimensional CTA demonstrating the left internal jugular vein compressed between the styloid process (black arrow) and lateral mass of C1 (white arrow). D, Left internal jugular vein, both compressed between the styloid and C1 lateral mass. E, Sagittal view of subsequent CTA demonstrating compression of the right internal jugular vein but some early recanalization. (From Callahan B, Kang J, Dudekula A, et al: New Eagle’s syndrome variant complicating management of intracranial pressure after traumatic brain injury, Inj Extra 41:41-44, 2010.)

10  •  Styloid Process Injection        31

Styloid process

Styloid process Accessory nerve

Accessory nerve Hypoglossal nerve

Hypoglossal nerve

Glossopharyngeal nerve

o&

ric Car

vell Sha

Hyoid bone

Jugular vein Vagus nerve Calcified stylohyoid ligament

Internal carotid artery

Glossopharyngeal nerve

o&

ric Car

vell Sha

Hyoid bone

Jugular vein Vagus nerve Stylohyoid ligament

Internal carotid artery

Figure 10-3  In patients with Eagle syndrome, the abnormally elongated styloid process impinges on the internal carotid artery and glossopharyngeal nerve.

Figure 10-4  For proper needle placement when Eagle syndrome is treated, an imaginary line is drawn from the mastoid process to the angle of the mandible to facilitate locating the styloid process.

within 10 cm. After contact has been made, the needle is withdrawn slightly out of the periosteum or substance of the calcified ligament. After careful aspiration reveals no blood or cerebrospinal fluid, 5 mL of 0.5% preservative-free lidocaine combined with 80 mg of methylprednisolone is injected in incremental doses. Subsequent daily nerve blocks are carried out in a similar manner, substituting 40 mg of methylprednisolone for the initial 80-mg dose.

artery. Hematoma formation and intravascular injection of local anesthetic with subsequent toxicity are not uncommon complications. Inadvertent blockade of the motor portion of the glossopharyngeal nerve can result in dysphagia secondary to weakness of the stylopharyngeus muscle. If the vagus nerve is inadvertently blocked, dysphonia secondary to paralysis of the ipsilateral vocal cord may occur. A reflex tachycardia secondary to vagal nerve block is also observed in some patients. Inadvertent block of the hypoglossal and spinal accessory nerves during glossopharyngeal nerve block will result in weakness of the tongue and trapezius muscle.

Side Effects and Complications The major complications associated with this injection technique are related to trauma to the internal jugular vein and carotid

32        SECTION 1  •  Head and Neck

Clinical Pearls This injection technique for Eagle syndrome is a simple technique that can produce dramatic relief for patients reporting the just-described types of pain. The proximity of the styloid process to major vasculature makes the presence of postblock hematoma and ecchymosis a distinct possibility. Although these complications are usually transitory, their dramatic appearance can be quite upsetting to the patient; therefore the patient should be warned of this possibility before the procedure. The vascularity of this region also increases the incidence of inadvertent intravascular injection. Even small amounts of local anesthetic injected into the carotid artery at this level will result in local anesthetic toxicity and seizures. Incremental administration while carefully monitoring the patient for signs of local anesthetic toxicity helps avoid this complication. Glossopharyngeal neuralgia can be distinguished from Eagle syndrome in that the pain of glossopharyngeal neuralgia is characterized by paroxysms of shocklike pain as in trigeminal neuralgia, rather than the sharp, shooting pain on movement that is associated with Eagle syndrome. Because glossopharyngeal neuralgia may be associated with serious cardiac bradyarrhythmias and syncope, the clinician must distinguish between the two syndromes. The clinician should always evaluate the patient with pain in this anatomic region for occult malignancy. Tumors of the larynx, hypopharynx, and anterior triangle of the neck may manifest as clinical symptoms identical to hyoid syndrome. Given the low incidence of Eagle syndrome relative to pain secondary to malignancy in this anatomic region, Eagle syndrome must be considered a diagnosis of exclusion.

SUGGESTED READINGS Andrade MG, Marchionni AM, Rebello IC, et al: Three-dimensional identification of vascular compression in Eagle’s syndrome using computed tomography: case report, J Oral Maxillofac Surg 66:169–176, 2008. Callahan B, Kang J, Dudekula A, et al: New Eagle’s syndrome variant complicating management of intracranial pressure after traumatic brain injury, Inj Extra 41:41–44, 2010. Lee S, Hillel A: Three-dimensional computed tomography imaging of eagle’s syndrome, Am J Otolaryngol 25:109, 2004. Mendelsohn AH, Berke GS, Chhetri DK: Heterogeneity in the clinical presentation of Eagle’s syndrome, Otolaryngol Head Neck Surg 134:389–393, 2006. Olusesi AD: More on heterogeneity of clinical presentation of Eagle’s syndrome, Otolaryngol Head Neck Surg 135:488, 2006.

Chapter 11 STYLOHYOID LIGAMENT INJECTION

Indications and Clinical Considerations Hyoid syndrome is caused by calcification and inflammation of the attachment of the stylohyoid ligament to the hyoid bone. Tendinitis of the other muscular attachments to the hyoid bone also may contribute to this painful condition. Hyoid syndrome also may be seen in conjunction with Eagle syndrome or as a sequela of traumatic injuries of the hyoid (Figure 11-1). The pain of hyoid syndrome is sharp and stabbing and occurs with movement of the mandible, turning of the neck, or swallowing. The pain starts below the angle of the mandible and radiates into the anterolateral neck. The pain of hyoid syndrome often is referred to the ipsilateral ear. Some patients also may report a foreign body sensation in the pharynx. Injection of the attachment of the stylohyoid ligament to the greater cornu of hyoid bone with local anesthetic and corticosteroid will serve as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The styloid process extends in a caudal and ventral direction from the temporal bone from its origin just below the auditory meatus. The stylohyoid ligament’s cephalad attachment is to the styloid process, and its caudal attachment is to the hyoid bone. In hyoid syndrome, the stylohyoid ligament becomes calcified at its caudal attachment to the hyoid bone (Figure 11-2). Tendinitis of the other muscular attachments to the hyoid bone may also occur, contributing to the pain symptomatology.

The key landmark for injection when treating hyoid syndrome is the cornu of the hyoid bone at a point between the mandible and the larynx. This osseous process is more easily identified if the greater cornu of the hyoid on the opposite side is steadied. Given the relationship of the great vessels of the neck to the greater cornu of the hyoid, care must be taken when placing needles in this anatomic area.

Technique The patient is placed in the supine position. The angle of the mandible on the affected side is then identified. The greater cornu of the hyoid bone should lie approximately 1 inch inferior to the angle of the mandible. Gentle pressure at the same point on the contralateral side of the neck will steady the hyoid bone and make identification of the greater cornu and subsequent injection easier (Figure 11-3). The skin is prepared with antiseptic solution. A 22-gauge, 1½-inch needle attached to a 10-mL syringe is advanced at the point 1 inch inferior to the angle of the mandible in a plane perpendicular to the skin. The greater cornu of the hyoid bone should be encountered within 2.5 to 3 cm (see Figure 11-2). After contact has been made, the needle is withdrawn slightly out of the periosteum or substance of the calcified ligament. After careful aspiration reveals no blood or cerebrospinal fluid, 5 mL of 0.5% preservative-free lidocaine combined with 80 mg of methylprednisolone is injected in incremental doses. Subsequent daily nerve blocks are carried out in a similar manner, substituting 110 mg of methylprednisolone for the initial 80-mg dose.

Side Effects and Complications

Figure 11-1  Bilateral hyoid bone fracture with disarticulation of the greater horns from the body, thyroid cartilage injury, mandibular symphyseal fracture, and left condyle fracture. (From Badiali G, Pasquini E, Piccin O, Marchetti C: Injury risk related to the helmet strap: mandible and hyoid bone fractures with a hyoepiglottic ligament lesion, Inj Extra 41: 89-91, 2010.)

This anatomic region is highly vascular, and because of the proximity of major vessels, the pain specialist should carefully observe the patient for signs of local anesthetic toxicity during injection. This vascularity and proximity to major blood vessels also give rise to an increased incidence of postblock ecchymosis and hematoma formation; the patient should be warned of such. In spite of the vascularity of this anatomic region, this technique can be safely performed in the presence of anticoagulation by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable risk-to-benefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block also will decrease the amount of postprocedure pain and bleeding the patient may experience. Because of the proximity to the spinal column, it also is possible to inadvertently inject the local anesthetic solution into the 33

34        SECTION 1  •  Head and Neck

Trachea Hyoid bone

Internal carotid artery

External carotid artery

Internal jugular vein Carrico & Shavell

Figure 11-2  Hyoid syndrome is usually caused by calcification of the stylohyoid ligament at its caudal attachment to the hyoid bone.

Gentle pressure on greater cornu

Figure 11-3  The hyoid bone can be stabilized by placing gentle pressure on the contralateral side of the hyoid bone, which will facilitate injection of the calcified ligamentous attachment.

epidural, subdural, or subarachnoid space. At this level, even small amounts of local anesthetic placed into the subarachnoid space may result in total spinal anesthesia. If needle placement is too inferior, pneumothorax is possible because the dome of the lung lies at the level of the C7-T1 interspace. Additional side effects associated with the injection of local anesthetic and corticosteroid in the treatment of hyoid syndrome include inadvertent block of the recurrent laryngeal nerve with associated hoarseness and dysphagia and the sensation that there is a lump in the throat when swallowing. Horner syndrome occurs when the superior cervical sympathetic ganglion is inadvertently blocked during this technique. The patient should be warned of the possibility of these complications before injection of local anesthetic and corticosteroid in the region of the greater cornua of the hyoid bone.

11  •  Stylohyoid Ligament Injection        35

Clinical Pearls This injection technique for hyoid syndrome is a simple one that can produce dramatic relief for patients experiencing the just-described types of pain. The proximity of the greater cornu of the hyoid bone to major vasculature makes postblock hematoma and ecchymosis a distinct possibility. Although these complications are usually transitory, their dramatic appearance can be quite upsetting to the patient; therefore the patient should be warned of such a possibility before the procedure. The vascularity of this region also increases the incidence of inadvertent intravascular injection. Even small amounts of local anesthetic injected into the carotid artery at this level will result in local anesthetic toxicity and seizures. Incremental administration while carefully monitoring the patient for signs of local anesthetic toxicity will help avoid this complication. Glossopharyngeal neuralgia can be distinguished from hyoid syndrome in that the pain of glossopharyngeal neuralgia is characterized by paroxysms of shocklike pain as in trigeminal neuralgia, rather than the sharp, shooting pain that occurs on movement associated with hyoid syndrome. Because glossopharyngeal neuralgia may be associated with serious cardiac bradyarrhythmias and syncope, the clinician must distinguish the two syndromes. The clinician should always evaluate the patient with pain in this anatomic region for occult malignancy. Tumors of the larynx, hypopharynx, and anterior triangle of the neck may cause clinical symptoms identical to those of hyoid syndrome. Given the low incidence of hyoid syndrome relative to pain secondary to malignancy in this anatomic region, hyoid syndrome must be considered a diagnosis of exclusion.

SUGGESTED READINGS Badiali G, Pasquini E, Piccin O, Marchetti C: Injury risk related to the helmet strap: mandible and hyoid bone fractures with a hyoepiglottic ligament lesion, Inj Extra 41:89–91, 2010. Ernest EA 3rd, Salter EG: Hyoid bone syndrome: a degenerative injury of the middle pharyngeal constrictor muscle with photomicroscopic evidence of insertion tendinosis, J Prosthet Dent 66:78–83, 1991. Nir D, Hefer T, Joachims HZ: Hyoid bone syndrome and its treatment with nonsteroidal anti-inflammatory drugs, Am J Otolaryngol 19:296–300, 1998. Rubin MM, Sanfilippo RJ: Osteomyelitis of the hyoid caused by Torulopsis glabrata in a patient with acquired immunodeficiency syndrome, J Oral Maxillofac Surg 48:1217–1219, 1990. Waldman SD: Hyoid syndrome. In Waldman SD, editor: Atlas of uncommon pain syndromes, ed 2, Philadelphia, 2008, Saunders.

Chapter 12 NASOCILIARY NERVE BLOCK

Indications and Clinical Considerations Nasociliary nerve block is useful in the diagnosis and treatment of Charlin syndrome, which is also known as nasociliary neuralgia. Although as with most headache syndromes the exact cause of the pain of Charlin syndrome is unknown, the pathogenesis of this uncommon source of head and face pain is thought to be dysfunction of the nasociliary ganglion in a manner analogous to the dysfunction of the sphenopalatine ganglion that is thought to be the source of cluster headache. The presenting symptom of patients with Charlin syndrome is severe paroxysms of ocular or retro-orbital pain that radiates into the ipsilateral forehead, nose, and maxillary region. This pain is associated with voluminous ipsilateral rhinorrhea and congestion of the nasal mucosa as well as significant inflammation of the affected eye. The pain of Charlin syndrome has a rapid onset to peak, with attacks lasting 45 to 60 minutes. In some patients these attacks can be triggered by sensory stimulation of the affected areas. Although in many ways similar to cluster headache (e.g., the retro-orbital location of pain, profuse unilateral rhinorrhea, the rapid onset to peak, and the short duration of attacks), there are many dissimilarities. Unlike in cluster headache, alcohol does not seem to trigger attacks of Charlin syndrome, and the seasonal and chronobiologic patterns so characteristic of cluster headache appear to be absent (Table 12-1). Furthermore, blockade of the sphenopalatine ganglion, which is so effective in the treatment of cluster headache, is of little value in the treatment of Charlin syndrome, whereas patients with Charlin syndrome uniformly respond to daily nasociliary nerve blocks with local anesthetic, as described later.

Clinically Relevant Anatomy The first division of the trigeminal nerve is the ophthalmic nerve, which provides sensory innervation to the cornea, iris, ciliary body, conjunctiva, and associated lacrimal gland. Branches of the ophthalmic nerve provide sensory innervation to the skin of the eyelid, forehead, and nose, as well as providing sensory innervation to portions of the nasal mucosa. The ophthalmic nerve arises from the superior portion of the gasserian ganglion and passes forward along the lateral wall of the cavernous sinus. Just before entering the orbit via the superior orbital fissure, the ophthalmic nerve divides into the lacrimal, frontal, and nasociliary branches (Figure 12-1). The nasociliary branch enters the orbit between the two heads of the rectus lateralis muscle and between the superior or inferior rami of the oculomotor nerve. The nasociliary nerve then passes across the ipsilateral optic nerve to the medial wall of the orbital cavity to pass through the anterior ethmoidal foramen to cross the lateral 36

margin of the cribriform plate of the ethmoid bone into the nasal cavity, where the internal nasal branch provides sensory innervation to the anterior nasal septum and lateral wall of the nasal cavity. The external nasal branch of the nasociliary nerve provides sensory innervation to the skin of the ala and apex of the nose. In addition to the internal and external nasal branches, the nasociliary nerves give off branches including the long ciliary branch; the long root of the ciliary ganglion branch is intimately involved with sympathetic fibers from the deep cervical plexus and ciliary ganglion. Some investigators believe that there are also small intercommunications between these branches and the sphenopalatine ganglion.

Technique The patient is placed in a supine position. A total of 2 mL of local anesthetic is drawn up in a 10-mL sterile syringe. When treating Charlin syndrome with nasociliary nerve block via the medial orbital approach, a total of 80 mg of depot corticosteroid is added to the local anesthetic with the first block, and 40 mg of depot corticosteroid is added with subsequent blocks.

TABLE 12-1

Comparison of Cluster Headache and Charlin Syndrome Cluster Headache

Charlin Syndrome

Ocular and retro-orbital location

Yes

Yes

Unilateral

Yes

Yes

Rapid onset to peak

Yes

Yes

Severe intensity

Yes

Yes

Attacks occur in paroxysms

Yes

Yes

Duration of attacks is short

Yes

Yes

Pain free between attacks

Yes

Yes

Significant rhinorrhea during attacks

Yes

Yes

Alcohol triggers attacks

Yes

No

Tactile trigger areas

No

Yes

Seasonal pattern of attacks

Yes

No

Chronobiologic pattern of attacks

Yes

Yes

Significant eye inflammation

No

Yes

Responds to sphenopalatine ­ anglion block g

Yes

No

Responds to nasociliary block

No

Yes

12  •  Nasociliary Nerve Block        37

Eyeball

Optic n. Nasociliary n.

Ciliary ganglion

Ophthalmic n. (V1) Oculomotor n. (III) Trochlear n. (IV) Trigeminal (V)

Optic chiasma

Figure 12-1  Just before entering the orbit, the ophthalmic nerve divides into the lacrimal, frontal, and nasociliary branches.

To perform blockade of the nasociliary nerve, the medial canthus is identified and a line is drawn superiorly to a point just below the eyebrow (Figure 12-2). The skin overlying this area is prepared with antiseptic solution, with care being taken to avoid spillage into the eye. A 22-gauge, 1½-inch needle is inserted at this point, and, with close contact kept with the bony surface of the orbit, the needle is carefully advanced posteroinferiorly approximately 35 degrees off the perpendicular to a depth of approximately 1¼ inches (Figure 12-3). After careful gentle aspiration, the contents of the syringe are slowly injected. Because of the loose alveolar tissue of the eyelid, a gauze sponge should be used to apply gentle pressure on the upper eyelid and supraorbital tissues before injection of solution to prevent the injectate from dissecting inferiorly into these tissues. This pressure should be maintained after the procedure to avoid periorbital hematoma and ecchymosis. When nasociliary nerve block is used to treat the pain and symptoms associated with Charlin syndrome, 8 to 10 daily nerve blocks with local anesthetic may be required. If daily blocks are being performed, as a general rule the total dose of depot corticosteroids included in these blocks should not exceed 360 to 400 mg.

Side Effects and Complications The major complication of this procedure is inadvertent injury to the eye. Failure to maintain bony contact while the needle is advanced will greatly increase the risk of the devastating complication. The practitioner should also remember that this area is highly vascular, and the potential for intravascular injection of local anesthetic with its attendant risks remains an ever-present possibility. This vascularity gives rise to an increased incidence of

Medial canthus

Figure 12-2  For identification of the nasociliary nerve, an imaginary line is drawn from the medial canthus to a point just below the eyebrow.

postblock ecchymosis and hematoma formation. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block also decreases the amount of postprocedure pain and bleeding.

38        SECTION 1  •  Head and Neck

Clinical Pearls Nasociliary nerve block via the medial orbital approach is especially useful in the diagnosis and palliation of pain secondary to Charlin syndrome. Given the uncommon nature of this headache syndrome and its overlap with the symptoms of cluster headache as well as other neurologic problems, including multiple sclerosis, cavernous sinus thrombosis, and intracranial and retro-orbital tumors, Charlin syndrome must remain a diagnosis of exclusion (Figure 12-4). All patients suspected of having Charlin syndrome require magnetic resonance imaging (MRI) of the brain with and without gadolinium contrast as well as thorough ophthalmologic and neurologic evaluation. Nasociliary nerve block via the medial orbital approach should be performed only by those familiar with the regional anatomy.

Supraorbital nerve Supraorbital foramen

Figure 12-3  When a nasociliary nerve block is performed, the needle tip is advanced while close contact is maintained with the bony surface of the orbit to avoid trauma to the globe.

A

B

C Figure 12-4  A 20-year-old man with known multiple sclerosis and hypoesthesia and pain in the distribution of the left trigeminal nerve. A, T2-weighted axial image shows an area of increased signal intensity (arrow) involving the left lateral pons and extending into the root entry zone of the left trigeminal nerve. B, Unenhanced T1-weighted image shows that the hypointense lesion is well defined (arrow). C, Contrast-enhanced T1-weighted image shows no enhancement (arrow), suggesting an inactive plaque. (From Becker M, Kohler R, Vargas MI, et al: Pathology of the trigeminal nerve, Neuroimaging Clin N Am 18:283-307, 2008.)

12  •  Nasociliary Nerve Block        39 SUGGESTED READINGS Baker BL, Fosko SW: The nose: principles of surgical treatment, Adv Dermatol 24:112–132, 2008. Becker M, Kohler R, Vargas MI, et al: Pathology of the trigeminal nerve, Neuroimaging Clin N Am 18:283–307, 2008. Huibin Q, Jianxing L, Guangyu H, Dianen F: The treatment of first division idiopathic trigeminal neuralgia with radiofrequency thermocoagulation of the peripheral branches compared to conventional radiofrequency, J Clin Neurosci 16:14212–1429, 2009.

Rait J: Ocular causes of headache. In Selvaratnam P, Niere K, Zuluaga M, ­editors: Headache, orofacial pain and bruxism, New York, 2009, Churchill Livingstone, pp 127–138. Rozen T: Post-traumatic external nasal pain syndrome (a trigeminal based pain disorder), Headache 49:1223–1228, 2009.

Chapter 13 AURICULOTEMPORAL NERVE BLOCK

Indications and Clinical Considerations Frey syndrome is a constellation of symptoms including unilateral hyperhidrosis and flushing of the malar region and pinna of the ear that occurs when eating or drinking anything that stimulates the parotid gland to produce saliva (Figure 13-1). Also known as auriculotemporal syndrome, Baillarger syndrome, Dupuy syndrome, salivosudoriparous syndrome, and gustatory sweating syndrome, this disorder usually occurs 2 to 13 months after surgery, open trauma, or infection of the parotid gland. It is thought to be caused by improper regeneration of the sympathetic and parasympathetic nerves subserving the parotid gland and affected anatomic areas. The severity of symptoms associated with Frey syndrome can range from mild to debilitating. Although the incidence of Frey syndrome after parotid surgery can be decreased by careful

attention to surgical technique, including careful identification and preservation of auriculotemporal nerve and creation of a thick skin flap when performing parotidectomy, approximately 5% of patients undergoing parotid surgery will experience some degree of symptomatology. For patients with mild symptoms, reassurance and the use of topical antiperspirants such as 20% aluminum chloride in alcohol or topical scopolamine cream may be all that is required. For more severe symptoms, blockade of the auriculotemporal nerve may provide significant relief. Auriculotemporal nerve block may also be combined with intradermal injection of botulinum toxin A in the areas of hyperhidrosis.

Clinically Relevant Anatomy The auriculotemporal nerve arises from fibers of the mandibular nerve. The auriculotemporal nerve courses upward through the parotid gland, passing between the temporomandibular joint and the external auditory meatus, where it gives off branches that provide sensory innervation to the temporomandibular joint and portions of the pinna of the ear and the external auditory meatus. Ascending over the origin of the zygomatic arch, the auriculotemporal nerve continues upward along with the temporal artery, providing sensory innervation to the temporal region and lateral scalp.

Technique The patient is placed in the supine position with the head turned away from the side to be blocked. A total of 5 mL of local anesthetic is drawn up in a 12-mL sterile syringe. When painful conditions involving the auriculotemporal nerve that may have an inflammatory component are treated, a total of 80 mg of depot corticosteroid is added to the local anesthetic with the first block, and 40 mg of depot corticosteroid is added with subsequent blocks. The temporal artery is identified at a point just above the origin of the zygoma on the affected side. After preparation of the skin with antiseptic solution, a 25-gauge, 1½-inch needle is inserted at this point and is advanced perpendicularly until the needle approaches the periosteum of the underlying bone (Figure 13-2). A paresthesia may be elicited, and the patient should be warned of this possibility. After gentle aspiration, 3 mL of solution is injected. The needle is then redirected in a cephalad trajectory; after careful aspiration, the remaining 2 mL of solution is injected in a fanlike manner.

Side Effects and Complications Figure 13-1  Patients with Frey syndrome experience unilateral hyperhidrosis and flushing of the malar region.

40

The scalp is highly vascular, and the auriculotemporal nerve is in proximity to the temporal artery at the point at which the nerve is blocked. Therefore the pain specialist should carefully calculate

13  •  Auriculotemporal Nerve Block        41

Temporal branches

Posterior auricular n.

Figure 13-2  The auriculotemporal nerve arises from fibers of the mandibular nerve and is blocked at the point just above the origin of the zygoma.

the total milligram dose of local anesthetic that may be safely given, especially if bilateral nerve blocks are being performed. This vascularity gives rise to an increased incidence of postblock ecchymosis and hematoma formation. Despite the vascularity of this anatomic region, this technique can be safely performed in the presence of anticoagulation by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable risk-to-benefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-­minute periods after the block also decreases the amount of postprocedure pain and bleeding the patient may experience.

Clinical Pearls Auriculotemporal block is a useful technique in the management of the symptoms of Frey syndrome that fail conservative therapy, including reassurance and topical antiperspirants. The exact mechanism of how auriculotemporal nerve block relieves the symptoms of Frey syndrome is unknown, but it is plausible to ascribe a neuroanatomic basis for this technique’s efficacy given the interrelation of the auriculotemporal nerve with the abundant sympathetic and parasympathetic fibers that may serve as the nidus of this unusual syndrome. The concomitant use of interdermal injections of botulinum toxin A may further improve symptom relief if auriculotemporal nerve block alone fails to provide satisfactory results.

SUGGESTED READINGS Cantarella G, Berlusconi A, Mele V, et  al: Treatment of Frey’s syndrome with botulinum toxin type B, Otolaryngol Head Neck Surg 143:214–218, 2010. Hoff SR, Mohyuddin N, Yao M: Complications of parotid surgery, Oper Tech Otolaryngol Head Neck Surg 20:123–130, 2009. Moreno-Arias GA, Grimalt R, Llusa M, et al: Frey’s syndrome, J Pediatr 138:294, 2001. O’Neill JP, Condron C, Curran A, Walsh M: Lucja Frey—historical relevance and syndrome review, Surgeon 6:178–181, 2008. Rustemeyer J, Eufinger H, Bremerich A: The incidence of Frey’s syndrome, J ­Craniomaxillofac Surg 36:34–37, 2008.

Chapter 14 OMOHYOID MUSCLE INJECTION

Indications and Clinical Considerations Omohyoid syndrome is caused by trauma to the fibers of the inferior belly of the omohyoid muscle. The syndrome is seen most often in patients who have recently experienced a bout of intense vomiting or sustained a flexion-extension injury to the cervical spine and to the musculature of the anterior neck. Concurrent trauma to the brachial plexus with upper extremity symptomatology also may accompany trauma-induced omohyoid syndrome. The pain of omohyoid syndrome manifests as myofascial pain. It is constant and exacerbated with movement of the affected muscle. A trigger point in the inferior belly of the omohyoid muscle is often present and provides a basis for treatment. The pain of omohyoid syndrome starts just above the clavicle at the lateral aspect of the clavicular attachment of the sternocleidomastoid muscle. The pain may radiate into the anterolateral neck. Injection of the trigger point in the inferior muscle of the omohyoid muscle with local anesthetic and corticosteroid serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The omohyoid muscle extends from the hyoid bone laterally and inferiorly to the insertion at the upper margin of the scapula (Figure 14-1). The intermediate tendon of the omohyoid muscle that runs from the muscle inferiorly to attach at the clavicle tethers the muscle down, and the point of musculotendinous insertion is susceptible to trauma. The inferior portion of the omohyoid muscle is further confined by the overlying attachment of the sternocleidomastoid to the clavicle. The omohyoid muscle also is susceptible to trauma at this point. The internal jugular vein and common carotid artery lie deep to the omohyoid muscle. The brachial plexus lies more lateral. The key landmark for injection when treating omohyoid syndrome is the lateral aspect of the clavicular head of the sternocleidomastoid muscle (see Figure 14-1). The omohyoid muscle is located slightly lateral and deep to the clavicular head of the sternocleidomastoid muscle, ½ to 1 inch above the superior margin of the clavicle. Given the relationship of the great vessels of the neck to the omohyoid muscle, care must be taken when placing needles in this anatomic area.

Splenius capitis m. Levator scapulae m. Trapezius m. Scalenus medius m. Trapezius m.

Hyoid bone Superior belly of the omohyoid m. Internal jugular vein Sternocleidomastoid m. Upper trunk of brachial plexus Inferior belly of the omohyoid muscle External jugular vein Clavicle

Carrico & Shavell

Figure 14-1  The omohyoid muscle extends from the hyoid bone laterally and inferiorly to its insertion at the upper margin of the scapula.

42

14  •  Omohyoid Muscle Injection        43

Technique The patient is placed in a supine position with the head turned away from the side to be blocked. A total of 3.0 mL of local anesthetic is drawn up in a 5.0-mL sterile syringe. When omohyoid syndrome is treated, a total of 80 mg of depot corticosteroid is added to the local anesthetic with the first block, and 40 mg of depot corticosteroid is added with subsequent blocks. The patient is then asked to raise his or her head against the resistance of the pain specialist’s hand to aid in identification of the posterior border of the sternocleidomastoid muscle. The point at which the lateral border of the sternocleidomastoid attaches to the clavicle is then identified. At this point, slightly lateral and approximately 1 inch above the clavicle, after preparation of the skin with antiseptic solution, a 11⁄2-inch needle is inserted directly perpendicular to the tabletop (see Figure 14-1). The needle should be advanced quite slowly because of proximity of the great vessels and brachial plexus. A pop is often felt as the fascia of the omohyoid muscle is pierced. This should occur at a depth of 1⁄2 to 3⁄4 inch. If strict attention to technique is observed and the needle has not been placed or directed too laterally, the brachial plexus should not be encountered. However, because of the proximity of the brachial plexus, the patient should be warned that a paresthesia could occur and to say “there!” should a paresthesia be felt. The needle should never be directed in a more inferomedial trajectory, or pneumothorax is likely to occur. After the muscle has been identified, gentle aspiration is carried out to identify blood or cerebrospinal fluid. If the aspiration test result is negative and no paresthesia into the distribution of the brachial plexus is encountered, 3.0 mL of solution is slowly injected, with the patient being monitored closely for signs of local anesthetic toxicity or inadvertent neuraxial injection.

Side Effects and Complications The proximity to the great vessels of the neck suggests the potential for inadvertent intravascular injection or local anesthetic toxicity from intravascular absorption. This vascularity also gives rise to an increased incidence of postblock ecchymosis and hematoma formation. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block will also decrease the amount of postprocedure pain and bleeding the patient may experience. In addition to the potential for complications involving the vasculature, should the needle be placed too laterally, the proximity of the brachial plexus, the central neuraxial structures, and the phrenic nerve can result in side effects and complications. Although these complications should be rare if proper

technique is observed, the potential for inadvertent epidural, subdural, or subarachnoid injection remains. If the local anesthetic used for this block is accidentally placed in any of these spaces, significant motor and sensory block may result. If unrecognized, these complications could be fatal. Phrenic nerve block also can occur when this injection technique is used to treat omohyoid syndrome if the needle placement is too posterolateral. In the absence of significant pulmonary disease, unilateral phrenic nerve block rarely should create respiratory embarrassment. However, blockade of the recurrent laryngeal nerve with its attendant vocal cord paralysis, combined with paralysis of the diaphragm, may make the clearing of pulmonary and upper airway secretions difficult. Because of the proximity of the apex of the lung, pneumothorax is a distinct possibility and the patient should be informed of this.

Clinical Pearls The key to safely performing this injection technique is a clear understanding of the anatomy and careful identification of the anatomic landmarks necessary to perform the block. The clinician should remember that the brachial plexus is quite superficial at the level at which this block is performed. The needle should rarely be inserted deeper than ¾ inch in all but the most obese patients. If strict adherence to technique is observed and the needle is never advanced medially from the lateral border of the insertion of the sternocleidomastoid muscle on the clavicle, the incidence of pneumothorax should be less than 0.5%. In the absence of well-documented trauma to the anterior neck, omohyoid syndrome is a diagnosis of exclusion. The clinician should always evaluate the patient with pain in this anatomic region for occult malignancy. Tumors of the larynx, hypopharynx, and anterior triangle of the neck may cause clinical symptoms identical to omohyoid syndrome. In the setting of flexion-extension injuries or other forceful trauma to the soft tissues of the neck or cervical spine, the clinician also should evaluate the patient for trauma to the brachial plexus by careful physical examination and the use of electromyography.

SUGGESTED READINGS Kim L, Kwon H, Pyun SB: Pseudodysphagia due to omohyoid muscle syndrome, Dysphagia 24:357–361, 2009. Waldman SD: Omohyoid syndrome. In Waldman SD, editor: Atlas of uncommon pain syndromes, ed 2, Philadelphia, 2008, Saunders. Wong DS, Li JH: The omohyoid sling syndrome, Am J Otolaryngol 21:318–322, 2000. Zachary RB, Young A, Hammond JD: The omohyoid syndrome, Lancet 294:104– 105, 1969.

Chapter 15 TRIGEMINAL NERVE BLOCK

Indications and Clinical Considerations Trigeminal neuralgia is an episodic pain that affects the areas of the face supplied by the trigeminal nerve. The pain is unilateral in 97% of cases reported. When it does occur bilaterally, it is in the same division of the nerve. The second or third division of the nerve is affected in the majority of patients, with the first division affected less than 5% of the time. The pain develops on the right side of the face in unilateral disease 57% of the time. The pain is characterized by paroxysms of electric shock–like pain lasting from several seconds to less than 2 minutes. The progression from onset to peak is essentially instantaneous. The patient with trigeminal neuralgia will go to great lengths to avoid any contact with trigger areas. Persons with other types of facial pain, such as temporomandibular joint dysfunction, tend to constantly rub the affected area or apply heat or cold to it. Patients with uncontrolled trigeminal neuralgia frequently require hospitalization for rapid control of pain. Between attacks, the patient is relatively pain free. A dull ache remaining after the intense pain subsides may indicate a persistent compression of the nerve by a structural lesion. This disease is almost never seen in people younger than 30 unless it is associated with multiple sclerosis. The patient with trigeminal neuralgia will often have severe and at times even suicidal depression with high levels of superimposed anxiety during acute attacks. Both of these problems may by exacerbated by the sleep deprivation that often occurs during episodes of pain. Patients with coexisting multiple sclerosis may exhibit the euphoric dementia characteristic of that disease. The mainstay of the treatment of trigeminal neuralgia is pharmacologic, with carbamazepine and baclofen being drugs of first choice. Other anticonvulsants, including pregabalin, gabapentin, and oxcarbazepine, may also be beneficial. For patients whose condition fails to respond to pharmacologic treatment, trigeminal nerve block via the coronoid approach may be a next reasonable step. If conservative treatment fails, more invasive options including radiofrequency lesioning, balloon compression, Gamma Knife radiosurgery, and microvascular decompression may be considered with a careful assessment of the risk-to-benefit ratio for each procedure.

Clinically Relevant Anatomy The maxillary division (V2) of the trigeminal nerve is a pure sensory nerve (Figure 15-1). It exits the middle cranial fossa via the foramen rotundum and crosses the pterygopalatine fossa (Figure 15-2). Passing through the inferior orbital fissure, it enters the orbit, emerging on the face via the infraorbital foramen. The 44

maxillary nerve can be selectively blocked by placing a needle just above the anterior margin of the lateral pterygoid plate. The maxillary nerve provides sensory innervation for the dura of the middle cranial fossa, the temporal and lateral zygomatic region, and the mucosa of the maxillary sinus. The nerve also provides sensory innervation for the upper molars, premolars, incisors, canines, and associated oral gingiva as well as the mucous membranes of the

V1

V2

V3

V1, Ophthalmic nerve V2, Maxillary nerve V3, Mandibular nerve Figure 15-1  The trigeminal nerve is divided into three divisions. (From Waldman SD: Atlas of Interventional Pain Management, ed 2, Philadelphia, 2003, Saunders.)

15  •  Trigeminal Nerve Block        45

cheek. The nasal cavity, lower eyelid, skin of the side of the nose, and the upper lip are also subserved by the maxillary nerve. The mandibular division (V3) is composed of a large sensory root and smaller motor root. Both leave the middle cranial fossa together via the foramen ovale and join to form the mandibular nerve. Branches of the mandibular nerve provide sensory innervation to portions of the dura mater and the mucosal lining of the mastoid sinus. Sensory innervation to the skin overlying the muscles of mastication, the tragus and helix of the ear, the posterior temporomandibular joint, the chin, and the dorsal aspect of the anterior two thirds of the tongue and associated mucosa of the oral cavity is also provided by the mandibular nerve (see Figure 15-1). The smaller motor branch provides innervation to the masseter, external pterygoid, and temporalis muscles.

Technique The patient is placed in the supine position with the cervical spine in the neutral position. The coronoid notch is identified by ­asking the patient to open and close the mouth several times and palpating the area just anterior and slightly inferior to the acoustic auditory meatus. After the notch has been identified, the patient is asked to hold his or her mouth in neutral position. A total of 7 mL of local anesthetic is drawn up in a 12-mL sterile syringe. When trigeminal neuralgia, atypical facial pain, or other painful conditions involving the maxillary and mandibular nerve are treated, a total of 150 mg of depot corticosteroid are added to the local anesthetic with the first block, and 40 mg of depot corticosteroid is added with subsequent blocks. After the skin overlying the coronoid notch has been prepared with antiseptic solution, a 22-gauge, 3½-inch styletted needle is inserted just below the zygomatic arch directly in the middle of the coronoid notch. The needle is advanced 1½ to 2 inches in a plane perpendicular to the skull until the lateral pterygoid plate is encountered (Figure 15-3). At this point, if blockade of both the maxillary and mandibular nerves is desired, the needle is withdrawn slightly. After careful aspiration, 7 to 15 mL of solution is injected in incremental doses. During the injection procedure the patient must be observed carefully for signs of local anesthetic toxicity.

Side Effects and Complications

Figure 15-2  T1-weighted image through left face medial to the mandible, demonstrating the maxillary sinus (M), orbital surface of the maxilla (open white arrow), medial aspect of the pterygopalatine fossa (white arrowhead), retroantral fat pad (solid white arrow), lateral pterygoid muscle fibers coursing to the proximal mandible (L), marrow in the maxilla (solid white arrow 1) and mandible (solid white arrow 2), sublingual space (small black arrow), geniohyoid muscle (G), and hyoid bone (large black arrow). (From Stark DD, Bradley WG Jr: Magnetic resonance imaging, ed 3, St Louis, 1999, Mosby.)

Because of the highly vascular nature of the pterygopalatine fossa, significant facial hematoma may occur after trigeminal nerve block via the coronoid approach. This vascularity means that the pain specialist should use small, incremental doses of local anesthetic to avoid local anesthetic toxicity. Postprocedure dysesthesia, including anesthesia dolorosa, may occur in a small number of patients who undergo neurodestructive procedures of the branches of the trigeminal nerve in an effort to palliate the pain of trigeminal neuralgia. These dysesthesias can range from mild pulling or burning sensations to severe postprocedure pain called anesthesia dolorosa. These postprocedure

Lateral pterygoid plate

V2

Needle entry point

V3 Coronoid notch Figure 15-3  For trigeminal nerve block to be performed, the needle is inserted in the middle of the coronoid notch and advanced toward the lateral pterygoid plate. (From Waldman SD: Atlas of Interventional Pain Management, ed 2, Philadelphia, 2003, Saunders.)

46        SECTION 1  •  Head and Neck

symptoms are thought to be caused by incomplete destruction of the neural structures. Sloughing of skin in the area of anesthesia may also occur. In addition to disturbances of sensation, blockade or destruction of the branches of the trigeminal nerve may result in abnormal motor function, including weakness of the muscles of mastication and secondary facial asymmetry caused by muscle weakness or loss of proprioception. The patient should be warned that all of these complications may occur.

Clinical Pearls Trigeminal nerve block via the coronoid approach with local anesthetic and corticosteroid represents an excellent option for patients with uncontrolled pain from trigeminal neuralgia that has not responded to pharmacologic management or for palliation of the acute pain of trigeminal neuralgia while waiting for drugs to take effect. The major side effects of this block are related to the vascular nature of the pterygopalatine fossa, and care must be taken to avoid local anesthetic toxicity. In spite of this vascularity, if a 25- or 27-gauge needle is used, this technique can safely be performed in the presence of anticoagulation, albeit at increased risk of facial hematoma, should the clinical situation dictate a favorable risk-to-benefit ratio. Because repeated needle punctures of daily or everyother-day blocks may result in small punctate facial scars, patients should be warned of this possibility. Infection, although rare, remains an ever-present possibility, especially in immunocompromised patients. Early detection of infection is crucial to avoid potentially life-threatening sequelae.

SUGGESTED READINGS Borges A, Casselman J: Imaging the trigeminal nerve, Eur J Radiol 74:323–340, 2010. Dubey A, Sung WS, Shaya M, et al: Complications of posterior cranial fossa surgery—an institutional experience of 500 patients, Surg Neurol 72:369–375, 2009. Martin T, Mark R, Smith H, et  al: Gamma Knife radiosurgery (GKRS) in the management of trigeminal neuralgia: long-term follow-up report of 511 cases, Int J Radiat Oncol Biol Phys 75(3 Suppl 1):S128–S129, 2009. Waldman SD: The trigeminal nerve—cranial nerve V. In Pain review, ­Philadelphia, 2009, Saunders, pp 15–16. Waldman SD: Trigeminal neuralgia. In Atlas of common pain syndromes, ed 2, Philadelphia, 2008, Saunders, pp 29–32. Waldman SD: Trigeminal neuralgia. In Pain review, Philadelphia, 2009, Saunders, pp 220–222.

Chapter 16 INJECTION TECHNIQUE FOR TRAPEZIUS SYNDROME Indications and Clinical Considerations The muscles of the posterior neck are particularly susceptible to the development of myofascial pain syndrome. Flexion-extension injuries to the neck or repeated microtrauma secondary to pressure from the straps of purses, backpacks, or laptop computer cases may result in the development of myofascial pain in the trapezius. Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body. The sine qua non of myofascial pain syndrome is the finding of myofascial trigger points on physical examination. Although these trigger points generally are localized to the regional part of the body affected, the pain of myofascial pain syndrome often is referred to other anatomic areas. This referred pain maybe misdiagnosed or attributed to other organ systems, thereby leading to extensive evaluations and ineffective treatment. Patients with myofascial pain syndrome involving the trapezius frequently have referred pain into the neck, mastoid region, angle of the jaw, and upper extremity—the last leading the patient to believe he or she is having a heart attack. The trigger point is the pathognomonic lesion of myofascial pain and is thought to be the result of microtrauma to the affected muscles. This pathologic lesion is characterized by a local point of exquisite tenderness in affected muscle. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain but also referred pain. In addition to this local and referred pain, often there is an involuntary withdrawal of the stimulated muscle, called a “jump sign.” This sign is also characteristic of myofascial pain syndrome. Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. In spite of this consistent physical finding in patients with myofascial pain syndrome, the pathophysiology of the myofascial trigger point remains elusive, although many theories have been advanced. Common to all of these theories is the belief that trigger points are a result of microtrauma to the affected muscle. This microtrauma may occur as the result of a single injury to the affected muscle or as the result of repetitive microtrauma or chronic deconditioning of the agonist and antagonist muscle unit. In addition to muscle trauma, a variety of other factors seem to predispose the patient to the development of myofascial pain syndrome. The weekend athlete who subjects his or her body to unaccustomed physical activity may develop myofascial pain syndrome. Poor posture while sitting at a computer keyboard or while watching television also has been implicated as a predisposing factor to the development of myofascial pain syndrome. Previous injuries may result in abnormal muscle function and predispose to the subsequent development of myofascial pain syndrome. All of these predisposing

factors may be intensified if the patient also has poor nutritional status or coexisting psychological or behavioral abnormalities, including chronic stress and depression. The trapezius muscle seems to be particularly susceptible to stress-induced myofascial pain syndrome. Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or in conjunction with other painful conditions, including radiculopathy and chronic regional pain syndromes. Psychological or behavioral abnormalities including depression frequently coexist with the muscle abnormalities associated with myofascial pain syndrome. Treatment of these psychological and behavioral abnormalities must be an integral part of any successful treatment plan for myofascial pain syndrome.

Clinically Relevant Anatomy The muscles of the neck work together as a functional unit to stabilize and allow coordinated movement of the head and associated sense organs. Trauma to an individual muscle can result in dysfunction of the entire functional unit. The trapezius is a primary extensor of the neck as well as part of the group of muscles known as the axioscapular group, which is involved in stabilization and movement of the scapula (Figure 16-1). The upper trapezius

Referred pain Splenius capitis m. Ligamentum nuchae

Sternocleidomastoid m. Trapezius m. Trigger points

Figure 16-1  The trapezius muscle is a primary extensor of the neck and is subject to the development of myofascial trigger points.

47

48        SECTION 1  •  Head and Neck

originates at the ligamentum nuchae and the spinous processes of the cervical and upper thoracic spine and attaches to the upper margin of the scapula. The middle portion of the trapezius originates from the spinous processes of the upper thoracic spine and attaches to the medial border of the scapula. The lower fibers of the trapezius originate from the spinous processes of the lower thoracic spine and attach to the medial portion of the scapular spine. These points of origin of the trapezius and attachments are particularly susceptible to trauma and the subsequent development of myofascial trigger points (see Figure 16-1). Injection of these trigger points serves as both a diagnostic and a therapeutic maneuver.

Technique Careful preparation of the patient before trigger point injection helps optimize results. Trigger point injections are directed at the primary trigger point rather than in the area of referred pain. It should be explained to the patient that the goal of trigger point injection is to block the trigger of the persistent pain and thus, it is hoped, provide long-lasting relief. It is important that the patient understand that for most patients with myofascial pain syndrome, more than one treatment modality will be required for optimal pain relief. The use of the recumbent or lateral position when identifying and marking trigger points as well as when performing the actual trigger point injection helps decrease the incidence of vasovagal reactions. The skin overlying the trigger point to be injected should always be prepared with antiseptic solution before injection to avoid infection. After the goals of trigger point injection have been explained to the patient and proper preparation of the patient has been carried out, the trigger point to be injected is reidentified by palpation with the sterilely gloved finger. A syringe containing 10 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 25- or 27-gauge needle of a length adequate to reach the trigger point. Except for the muscles of posture in the low back, a 11⁄2-inch needle is adequate. A volume of 0.5 to 1.0 mL of solution is then injected into each trigger point. A series of two to five treatment sessions may be required to completely abolish the trigger point; the patient should be informed of this.

Side Effects and Complications The proximity to the spinal cord and exiting nerve roots makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing interventional pain management techniques. The proximity to the vertebral artery combined with the vascular nature of this anatomic region makes the potential for intravascular injection high. Even small amounts of injection of local anesthetic into the vertebral arteries will result in seizures. Given the proximity

of the brain and brainstem, ataxia caused by vascular uptake of local anesthetic after trigger point injection is not an uncommon occurrence. Many patients also report a transient increase in pain after injection of trigger points in the trapezius. If long needles are used, pneumothorax also may occur.

Clinical Pearls Trigger point injections are an extremely safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of trigger point injection are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after trigger point injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid pneumothorax when injecting trigger points in proximity to the underlying pleural space. The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators believe that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as amitriptyline and nortriptyline represent good first choices and should be given as a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow. Pregabalin may also be of value in the pharmacologic management of myofascial pain syndromes.

SUGGESTED READINGS Baldry P: Acupuncture treatment of fibromyalgia and myofascial pain. In Chaitow L, editor: Fibromyalgia syndrome, ed 3, Oxford, 2010, Churchill Livingstone, pp 145–159. Ge HY, Nie H, Madeleine P, et al: Contribution of the local and referred pain from active myofascial trigger points in fibromyalgia syndrome, Pain 147: 233–240, 2009. Ge HY, Wang Y, Danneskiold-Samsøe B, et al: The predetermined sites of examination for tender points in fibromyalgia syndrome are frequently associated with myofascial trigger points, J Pain 11:644–651, 2010. LeBlanc KE, LeBlanc LL: Musculoskeletal disorders, Prim Care 37:389–406, 2010. Lucas KR, Rich PA, Polus BI: Muscle activation patterns in the scapular positioning muscles during loaded scapular plane elevation: the effects of latent myofascial trigger points, Clin Biomech (Bristol, Avon) 25:765–770, 2010. Partanen JV, Ojala TA, Arokoski JP: Myofascial syndrome and pain: a neurophysiological approach, Pathophysiology 17:19–28, 2010.

Chapter 17 INJECTION TECHNIQUE FOR CERVICAL STRAIN

Indications and Clinical Considerations The muscles of the posterior neck are particularly susceptible to the development of acute and chronic pain symptomatology after acute flexion, extension, or lateral bending injuries to the neck or repeated microtrauma secondary to pressure from the straps of purses, backpacks, or laptop computer cases. These muscles also are adversely affected by chronic stress, a behavioral abnormality that may manifest itself clinically as cervical strain. Myofascial pain syndrome with its pathognomonic myofascial trigger points also may occur, either alone or in combination with cervical strain. Cervical strain is the result of microtrauma or macrotrauma to the muscle fibers or the musculotendinous unit of the trapezius and the deep muscles of the posterior neck, including the splenius capitis and splenius cervicis. Clinically, cervical strain manifests as aching, tightness, stiffness, and pain in the neck and upper back, with pain radiating into the ipsilateral shoulder. As mentioned previously,

Occipital tuberance Semispinalis capitis m. Rectus capitis posterior major m. Oblique capitis inferior m. Sternocleidomastoid m. Semispinalis cervicis m. Trapezius m.

cervical strain may coexist with myofascial pain syndrome, and trigger points also may be present. Symptoms of cervical strain can be reproduced with ipsilateral rotation and contralateral bending of the cervical spine. Tenderness to deep palpation is present, but unless myofascial pain syndrome is also present, trigger points should be absent. The pain, spasm, and other associated symptoms of cervical strain are aggravated with physical or emotional stress.

Clinically Relevant Anatomy The muscles of the neck work together as a functional unit to stabilize and allow coordinated movement of the head and associated sense organs. Trauma to an individual muscle can result in dysfunction of the entire functional unit. The trapezius, splenius capitis, splenius cervicis, and semispinalis capitis are the primary extensors of the neck, as well as part of the group of muscles known as the axioscapular group, which is involved in stabilization and movement of the scapula (Figure 17-1). The upper trapezius

Trapezius m. Splenius capitis m. Sternocleidomastoid m. Semispinalis cervicis m. Splenius cervicis m. Multifidus m. Longissimus capitis m. Levator scapulae m.

Carrico & Shavell

Figure 17-1  The primary extensor muscles of the neck are susceptible to the development of acute and chronic pain syndromes.

49

50        SECTION 1  •  Head and Neck

originates at the ligamentum nuchae and the spinous processes of the cervical and upper thoracic spine and attaches to the upper margin of the scapula. The middle portion of the trapezius originates from the spinous processes of the upper thoracic spine and attaches to the medial border of the scapula. The lower fibers of the trapezius originate from the spinous processes of the lower thoracic spine and attach to the medial portion of the scapular spine. The splenius capitis arises from the lower part of the ligamentum nuchae and the upper four thoracic spinous processes and inserts into the superior nuchal line of the occipital bone. The splenius cervicis has a similar origin but inserts into the upper transverse process of the upper cervical vertebrae. These points of origin and attachments of these muscles are particularly susceptible to trauma and the subsequent development of strain or myofascial trigger points (see Figure 17-1). The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Technique The goals of this injection technique are explained to the patient, and proper preparation with antiseptic solution of the skin overlying the affected muscles is carried out. A syringe containing 17 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 25- or 27-gauge needle of a length adequate to reach the affected muscle. The needle is then inserted into the body of the muscle (see Figure 17-1). A “pop” will usually be felt when the needle pierces the fascia. After careful aspiration, a volume of 5 to 7 mL is then gently injected in a fanlike fashion throughout the affected muscle. If myofascial trigger points are also present, a volume of 0.5 to 1.0 mL of solution is then injected into each trigger point. A series of two to five treatment sessions may be required to completely abolish the symptoms of cervical strain and coexisting trigger points; the patient should be informed of this.

Side Effects and Complications The proximity to the spinal cord and exiting nerve roots makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing interventional pain management techniques. The proximity to the vertebral artery combined with the vascular nature of this anatomic region makes the potential for intravascular injection high. Even small amounts of injection of local anesthetic into the vertebral arteries will result in seizures. Given the proximity of the brain and brainstem, ataxia caused by vascular uptake of local anesthetic after this injection technique is not an uncommon occurrence. Many patients also report a transient increase in pain after injection of the just-mentioned muscles. If long needles are used, pneumothorax may also occur.

Clinical Pearls This injection technique is extremely effective in the treatment of cervical strain. Trigger point injections should be added if there is coexistent myofascial pain. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of the injection technique for cervical strain are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after this injection technique. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid pneumothorax when injecting muscles or myofascial trigger points in proximity to the underlying pleural space. The use of physical modalities, including local heat and gentle stretching exercises, should be introduced several days after the patient has undergone this injection technique for cervical strain. Vigorous exercise should be avoided because it will exacerbate the patient’s symptomatology. Simple analgesics, nonsteroidal antiinflammatory agents, and antimyotonic agents such as tizanidine may be used concurrently with this injection technique. If myofascial pain coexists with the symptoms of cervical strain, tricyclic antidepressants should be considered. The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators believe that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as amitriptyline and nortriptyline are good first choices and should be given in a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow.

SUGGESTED READINGS Chen HB, Yang KH, Wang ZG: Biomechanics of whiplash injury, Chin J Traumatol 12:305–314, 2009. Cho CH, Song KS, Min BW, et  al: Musculoskeletal injuries in break-dancers, Injury 40:1207–1211, 2009. Opper SE: Neck pain. In Smith HS, editor: Current therapy in pain, Philadelphia, 2009, Saunders, pp 137–147. White K, Hudgins TH, Alleva JT: Cervical sprain/strain definition, Dis Mon 55:724–728, 2009. Zmurko MG, Tannoury TY, Tannoury CA, Anderson DG: Cervical sprains, disc herniations, minor fractures, and other cervical injuries in the athlete, Clin Sports Med 22:513–521, 2003.

Chapter 18 INJECTION TECHNIQUE FOR STERNOCLEIDOMASTOID SYNDROME Indications and Clinical Considerations The sternocleidomastoid is particularly susceptible to the development of myofascial pain syndrome. Flexion-extension and lateral motion stretch injuries to the neck or repeated microtrauma secondary to jobs that require working overhead for long periods such as painting ceilings, reading in bed, or watching television while reclining on a couch may result in the development of myofascial pain in the sternocleidomastoid muscle. Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body. The sine qua non of myofascial pain syndrome is the finding of myofascial trigger points on physical examination. Although these trigger points generally are localized to the regional part of the body affected, the pain of myofascial pain syndrome often is referred to other anatomic areas. This referred pain often is misdiagnosed or attributed to other organ systems, thereby leading to extensive evaluations and ineffective treatment. Patients with myofascial pain syndrome involving the sternocleidomastoid often have referred pain into the upper neck, face, angle of the mandible, and temporal region. The trigger point is the pathognomonic lesion of myofascial pain and is thought to be the result of microtrauma to the affected muscles. This pathologic lesion is characterized by a local point of exquisite tenderness in affected muscle. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain but also referred pain. In addition to this local and referred pain, there often is an involuntary withdrawal of the stimulated muscle, called a “jump sign.” This jump sign also is characteristic of myofascial pain syndrome. Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. In spite of this consistent physical finding in patients with myofascial pain syndrome, the pathophysiology of the myofascial trigger point remains elusive, although many theories have been advanced. Common to all of these theories is the belief that trigger points are the result of microtrauma to the affected muscle. This microtrauma may occur as a single injury to the affected muscle or may occur as the result of repetitive microtrauma or chronic deconditioning of the agonist and antagonist muscle unit. In addition to muscle trauma, various other factors seem to predispose the patient to develop myofascial pain syndrome. The weekend athlete who subjects his or her body to unaccustomed physical activity may develop myofascial pain syndrome. The poor posture of someone sitting at a computer keyboard or watching television has also been implicated as a predisposing factor to the development of myofascial pain syndrome. Previous injuries may result in abnormal muscle function and predispose

to the subsequent development of myofascial pain syndrome. All of these predisposing factors may be intensified if the patient also has poor nutritional status or coexisting psychological or behavioral abnormalities, including chronic stress and depression. The sternocleidomastoid muscle seems to be particularly susceptible to stress-induced myofascial pain syndrome. Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or in conjunction with other painful conditions, including radiculopathy and chronic regional pain syndromes. Psychological or behavioral abnormalities, including depression, frequently coexist with the muscle abnormalities associated with myofascial pain syndrome. Treatment of these psychological and behavioral abnormalities must be an integral part of any successful treatment plan for myofascial pain syndrome.

Clinically Relevant Anatomy The muscles of the neck work together as a functional unit to stabilize and allow coordinated movement of the head and associated sense organs. Trauma to an individual muscle can result in dysfunction of the entire functional unit. The sternocleidomastoid extends the head at the atlantooccipital joint and rotates the head to the contralateral side. The origin of the sternocleidomastoid is by a muscular head from the medial third of the clavicle and a rounded tendon from the front of the sternal manubrium (Figure 18-1). The muscle inserts into the mastoid process of the temporal bone and the occipital bone. These points of origin of the sternocleidomastoid and attachments are particularly susceptible to trauma and the subsequent development of myofascial trigger points (see Figure 18-1). Injection of these trigger points serves as both a diagnostic and a therapeutic maneuver.

Technique Careful preparation of the patient before trigger point injection helps to optimize results. Trigger point injections are directed at the primary trigger point rather than in the area of referred pain. It should be explained to the patient that the goal of trigger point injection is to block the trigger of the persistent pain and thus, it is hoped, provide long-lasting relief. It is important that the patient understand that for most patients with myofascial pain syndrome, more than one treatment modality is required for optimal pain relief. The use of the recumbent or lateral position when identifying and marking trigger points, as well as when performing the actual trigger point injection, helps decrease the incidence 51

52        SECTION 1  •  Head and Neck

after trigger point injection is not an uncommon occurrence. Many patients also complain of a transient increase in pain after injection of trigger points in the sternocleidomastoid. If long needles are used, pneumothorax may also occur. Referred pain

Sternocleidomastoid Trigger point

Figure 18-1  Patients with sternocleidomastoid pain syndrome often experience referred pain to the upper neck, face, angle of the mandible, and temporal region.

of vasovagal reactions. The skin overlying the trigger point to be injected should always be prepared with antiseptic solution before injection to avoid infection. After the goals of trigger point injection have been explained to the patient and proper preparation of the patient has been carried out, the trigger point to be injected is reidentified by palpation with the sterilely gloved finger. A syringe containing 10 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 25- or 27-gauge needle of a length adequate to reach the trigger point. Except for the muscles of posture in the low back, a 1½-inch needle will be adequate. A volume of 0.5 to 1.0 mL of solution is then injected into each trigger point. A series of two to five treatment sessions may be required to completely abolish the trigger point; the patient should be informed of this.

Side Effects and Complications The proximity to the spinal cord and exiting nerve roots, as well as the great vessels of the neck, makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing interventional pain management techniques. The proximity to the carotid artery and jugular vein, combined with the vascular nature of this anatomic region, makes the potential for intravascular injection high. Even small amounts of injection of local anesthetic into the carotid artery will result in seizures. Given the proximity of the brain and brainstem, ataxia caused by vascular uptake of local anesthetic

Clinical Pearls Trigger point injections are extremely safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of trigger point injection are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after trigger point injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid pneumothorax when injecting trigger points in proximity to the underlying pleural space. The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators believe that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as amitriptyline and nortriptyline are good first choices and should be given as a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow. Pregabalin may also be of value in the pharmacologic management of myofascial pain syndromes.

SUGGESTED READINGS Baldry P: Acupuncture treatment of fibromyalgia and myofascial pain. In Chaitow L, editor: Fibromyalgia syndrome, ed 3, Oxford, 2010, Churchill Livingstone, pp 145–159. Ge HY, Nie H, Madeleine P, et al: Contribution of the local and referred pain from active myofascial trigger points in fibromyalgia syndrome, Pain 147:233– 240, 2009. Ge HY, Wang Y, Danneskiold-Samsøe B, et al: The predetermined sites of examination for tender points in fibromyalgia syndrome are frequently associated with myofascial trigger points, J Pain 11:644–651, 2010. LeBlanc KE, LeBlanc LL: Musculoskeletal disorders, Prim Care 37:389–406, 2010. Lucas KR, Rich PA, Polus BI: Muscle activation patterns in the scapular positioning muscles during loaded scapular plane elevation: the effects of latent myofascial trigger points, Clin Biomech (Bristol, Avon) 25:765–770, 2010. Partanen JV, Ojala TA, Arokoski JP: Myofascial syndrome and pain: a neurophysiological approach, Pathophysiology 17:19–28, 2010.

Chapter 19 OCCIPITAL NERVE BLOCK

Indications and Clinical Considerations Occipital nerve block is useful in the diagnosis and treatment of occipital neuralgia. Occipital neuralgia is usually the result of blunt trauma to the greater and lesser occipital nerves. Repetitive microtrauma from working with the neck hyperextended (e.g., painting ceilings or working for prolonged periods with computer monitors whose focal point is too high, causing extension of the cervical spine) also may cause occipital neuralgia. The pain of occipital neuralgia is characterized as persistent pain at the base of the skull with occasional sudden, shocklike paresthesias in the distribution of the greater and lesser occipital nerves. Tensiontype headache, which is much more common than occipital neuralgia, occasionally mimics the pain of occipital neuralgia, as can intracranial neoplasms (Figure 19-1).

Clinically Relevant Anatomy The greater occipital nerve arises from fibers of the dorsal primary ramus of the second cervical nerve and, to a lesser extent, fibers from the third cervical nerve. The greater occipital nerve pierces the fascia just below the superior nuchal ridge along with the occipital artery. It supplies the medial portion of the posterior scalp as far anterior as the vertex (Figure 19-2). The lesser occipital nerve arises from the ventral primary rami of the second and third cervical nerves. The lesser occipital nerve passes superiorly along the posterior border of the sternocleidomastoid muscle, dividing into cutaneous branches that innervate the lateral portion of the posterior scalp and the cranial surface of the pinna of the ear (see Figure 19-2).

Technique The patient is placed in a sitting position with the cervical spine flexed and the forehead on a padded bedside table. A total of 8 mL of local anesthetic is drawn up in a 19-mL sterile syringe. When occipital neuralgia or other painful conditions involving the greater and lesser occipital nerve are treated, a total of 80 mg of methylprednisolone is added to the local anesthetic with the first block, and 40 mg of methylprednisolone is added with subsequent blocks. The occipital artery is then palpated at the level of the superior nuchal ridge. After preparation of the skin with antiseptic solution, a 22-gauge, 1½-inch needle is inserted just medial to the artery and is advanced perpendicularly until the needle approaches the periosteum of the underlying occipital bone. A paresthesia may be elicited; the patient should be warned of this. The needle is then redirected superiorly, and after gentle aspiration 5 mL of solution is injected in a fanlike distribution with care being taken to avoid the foramen magnum, which is located medially (see Figure 19-2). The lesser occipital nerve and a number of superficial branches of the greater occipital nerve are then blocked by directing the needle laterally and slightly inferiorly. After gentle aspiration, an additional 3 to 4 mL of solution is injected. Recently, the use of ultrasound guidance for needle placement has been used in selected patients undergoing occipital nerve block (Figure 19-3). In the rare patient with intractable occipital neuralgia, stimulation of the affected occipital nerves via implanted electrode may be of value.

Side Effects and Complications The scalp is highly vascular and this, coupled with the fact that both nerves are in proximity to arteries, means that the pain

Figure 19-1  Preoperative computed tomography three-dimensional reconstruction reveals a multiloculated cystic mass in the lower portion of the occipital bone, characterized by an increased volume of the dipole with eggshell-like outer and inner plates. (From Han X, Dong Y, Sun K, Lu Y: A huge occipital osteoblastoma accompanied with aneurysmal bone cyst in the posterior cranial fossa, Clin Neurol Neurosurg 110:282-285, 2008.)

53

54        SECTION 1  •  Head and Neck

External occipital protuberance

Greater occipital nerve

Lesser occipital nerve

Superior nuchal line

Figure 19-2  When the occipital nerve is injected, care must be taken to avoid entering the foramen magnum.

Carrico & Shavell

of the vascularity of this anatomic region, this technique can be safely performed in the presence of anticoagulation with a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable risk-to-benefit ratio. Application of cold packs for 20-minute periods after the block also decreases the amount of postprocedure pain and bleeding the patient may experience. As mentioned previously, care must be taken to avoid inadvertent needle placement into the foramen magnum because subarachnoid administration of local anesthetic in this region will result in immediate total spinal anesthesia.

SC Trap

Spl

Splenius capitis m. Sternocleidomastoid m. Trapezius m.

SSC > IOM

Clinical Pearls

Lat.

Med. C1

Figure 19-3  Ultrasound short-axis view at the first cervical nerve (C1) level showing the greater occipital nerve (arrowhead). IOM, Inferior oblique muscle; SSC, semispinalis capitis; Spl, splenius muscle; Trap, trapezius muscle; SC, subcutaneous tissue; Med., medial; Lat., lateral. Note: At this level, the greater occipital nerve is more than 1 cm deep to the subcutaneous tissue (separated by the semispinalis capitis muscle). (From Narouze S: Ultrasound in chronic pain management, Tech Reg Anesth Pain Manag 13:198-202, 2009.)

specialist should carefully calculate the total milligram dose of local anesthetic that may be safely given, especially if bilateral nerve blocks are being performed. This vascularity and proximity to the arterial supply gives rise to an increased incidence of postblock ecchymosis and hematoma formation. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. In spite

The most common reason that greater and lesser occipital nerve block fails to relieve headache pain is that the headache syndrome being treated has been misdiagnosed as occipital neuralgia. Occipital neuralgia is an infrequent cause of headaches and rarely occurs in the absence of trauma to the greater and lesser occipital nerves. More often, the patient with headaches that involve the occipital region is in fact experiencing tension-type headaches. Tension-type headaches do not respond to occipital nerve blocks but are very amenable to treatment with antidepressant compounds (such as amitriptyline) in conjunction with cervical steroid epidural nerve blocks. Therefore the clinician should reconsider the diagnosis of occipital neuralgia in patients whose symptoms are consistent with occipital neuralgia but fail to respond to greater and lesser occipital nerve blocks. Any patient with headaches severe enough to require neural blockade as part of the treatment plan should undergo magnetic resonance imaging of the head to rule out unsuspected intracranial pathology. Furthermore, cervical spine radiographs should be considered to rule out congenital abnormalities such as Arnold-Chiari malformation, which may be the hidden cause of the patient’s occipital headaches.

19  •  Occipital Nerve Block        55 SUGGESTED READINGS Fernández-de-Las-Peñas C, Alonso-Blanco C, Cuadrado ML, Pareja JA: Myofascial trigger points in the suboccipital muscles in episodic tension-type headache, Man Ther 11:225–230, 2006. Levin M: Nerve blocks in the treatment of headache, Neurotherapeutics 7:197– 203, 2010. Paemeleire K, Bartsch T: Occipital nerve stimulation for headache disorders, Neurotherapeutics 7:213–219, 2010.

Waldman SD: Greater and lesser occipital nerve block. In Pain review, Philadelphia, 2009, Saunders, pp 393–394. Waldman SD: Occipital neuralgia. In Atlas of common pain syndromes, ed 2, ­Philadelphia, 2008, Saunders, pp 23–25. Waldman SD: The greater and lesser occipital nerves. In Pain review, Philadelphia, 2009, Saunders, pp 41–42.

Chapter 20 INJECTION TECHNIQUE FOR SPLENIUS CERVICIS SYNDROME Indications and Clinical Considerations The splenius cervicis is susceptible to the development of myofascial pain syndrome. Flexion-extension and lateral motion stretch injuries to the neck and upper back or repeated microtrauma secondary to jobs that require working overhead or looking to one side for long periods such as painting ceilings or to activities such as reading in bed or watching television while reclining on a couch may result in the development of myofascial pain in the splenius cervicis muscle. Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body. The sine qua non of myofascial pain syndrome is the finding of myofascial trigger points on physical examination. Although these trigger points generally are localized to the regional part of the body affected, the pain of myofascial pain syndrome often is referred to other anatomic areas. This referred pain often is misdiagnosed or attributed to other organ systems, thereby leading to extensive evaluations and ineffective treatment. Patients with myofascial pain syndrome involving the splenius cervicis often have referred pain into the occipital and temporal regions as well as circumferential pain that may mimic tension-type headache. The trigger point is the pathognomonic lesion of myofascial pain and is thought to be the result of microtrauma to the affected muscles. This pathologic lesion is characterized by a local point of exquisite tenderness in affected muscle. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain but also referred pain. In addition to local and referred pain, there often is an involuntary withdrawal of the stimulated muscle, called a “jump sign.” This jump sign also is characteristic of myofascial pain syndrome. Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. In spite of this consistent physical finding in patients with myofascial pain syndrome, the pathophysiology of the myofascial trigger point remains elusive, although many theories have been advanced. Common to all of these theories is the belief that trigger points are the result of microtrauma to the affected muscle. This microtrauma may occur as a single injury to the affected muscle or as a result of repetitive microtrauma or chronic deconditioning of the agonist and antagonist muscle unit. In addition to muscle trauma, a variety of other factors seem to predispose the patient to develop myofascial pain syndrome. The weekend athlete who subjects his or her body to unaccustomed physical activity may develop myofascial pain syndrome. The poor posture of someone sitting at a computer keyboard or watching television has also been implicated as a predisposing factor to the development of myofascial pain syndrome. Previous 56

injuries may result in abnormal muscle function and predispose to the subsequent development of myofascial pain syndrome. All of these predisposing factors may be intensified if the patient also has poor nutritional status or coexisting psychological or behavioral abnormalities, including chronic stress and depression. The splenius cervicis muscle seems to be particularly susceptible to stress-induced myofascial pain syndrome. Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or in conjunction with other painful conditions, including radiculopathy and chronic regional pain syndromes. Psychological or behavioral abnormalities, including depression, frequently coexist with the muscle abnormalities associated with myofascial pain syndrome. Treatment of these psychological and behavioral abnormalities must be an integral part of any successful treatment plan for myofascial pain syndrome.

Clinically Relevant Anatomy The muscles of the neck work together as a functional unit to stabilize and allow coordinated movement of the head and associated sense organs. Trauma to an individual muscle can result in dysfunction of the entire functional unit. The splenius cervicis muscle begins as a narrow tendinous band that attaches to the spinous processes of the third through sixth thoracic vertebra (Figure 20-1). The muscle extends upward and inserts via the tendinous fasciculi into the posterior tubercles of the transverse processes of the second and third cervical vertebrae. The splenius cervicis muscles are innervated by the respective lateral branches of the posterior divisions of the middle and lower cervical nerves. The muscle on each side of the neck can act independently to assist in lateral rotation and bending of the neck. The splenius cervicis muscles act together to help extend the cervical spine and pull the head posteriorly. A secondary function of these muscles is to help support and strengthen the deeper muscles of the posterior neck. The points of insertion of the splenius cervicis on the cervical vertebra are particularly susceptible to trauma and the subsequent development of myofascial trigger points (see Figure 20-1). Injection of these trigger points serves as both a diagnostic and a therapeutic maneuver.

Technique Careful preparation of the patient before trigger point injection helps to optimize results. Trigger point injections are directed at

20  •  Injection Technique for Splenius Cervicis Syndrome        57

Referred pain

Splenius cervicis m.

Trigger point

Figure 20-1  The splenius cervicis muscle begins as a fibrous tendon that attaches to the spinous processes of the third through sixth thoracic vertebra.

the primary trigger point rather than in the area of referred pain. It should be explained to the patient that the goal of trigger point injection is to block the trigger of the persistent pain and thus, it is hoped, provide long-lasting relief. It is important for the patient to understand that for most patients with myofascial pain syndrome, more than one treatment modality is required for optimal pain relief. The use of the recumbent or lateral position when identifying and marking trigger points, as well as when performing the actual trigger point injection, helps decrease the incidence of vasovagal reactions. The skin overlying the trigger point to be injected should always be prepared with antiseptic solution before injection to avoid infection. After the goals of trigger point injection have been explained to the patient and proper preparation of the patient has been carried out, the trigger point is reidentified by palpation with the sterilely gloved finger. A syringe containing 10 mL of 0.25% preservativefree bupivacaine and 40 mg of methylprednisolone to be injected is attached to a 25- or 27-gauge needle of a length adequate to reach the trigger point. Except for the muscles of posture in the low back, a 1½-inch needle will be adequate. A volume of 0.5 to 1.0 mL of solution is then injected into each trigger point. A series of two to five treatment sessions may be required to completely abolish the trigger point; the patient should be informed of this.

Side Effects and Complications The proximity to the spinal cord and exiting cervical nerve roots makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing interventional pain management techniques. Given the proximity of the brain and brainstem, ataxia caused by vascular uptake of local anesthetic after trigger point injection is not an uncommon occurrence. Many patients also complain of

a transient increase in pain after injection of trigger points in the splenius cervicis.

Clinical Pearls Trigger point injections are extremely safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of trigger point injection are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after trigger point injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid pneumothorax when injecting trigger points in proximity to the underlying pleural space. The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators believe that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as amitriptyline and nortriptyline represent good first choices and should be given as a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow. Pregabalin may also be of value in the pharmacologic management of myofascial pain syndromes.

58        SECTION 1  •  Head and Neck SUGGESTED READINGS Baldry P: Acupuncture treatment of fibromyalgia and myofascial pain. In Chaitow L, editor: Fibromyalgia syndrome, ed 3, Oxford, 2010, Churchill Livingstone, pp 145–159. Ge HY, Nie H, Madeleine P, et al: Contribution of the local and referred pain from active myofascial trigger points in fibromyalgia syndrome, Pain 147: 233–240, 2009. Ge HY, Wang Y, Danneskiold-Samsøe B, et al: The predetermined sites of examination for tender points in fibromyalgia syndrome are frequently associated with myofascial trigger points, J Pain 11:644–651, 2010.

LeBlanc KE, LeBlanc LL: Musculoskeletal disorders, Prim Care 37:389–406, 2010. Lucas KR, Rich PA, Polus BI: Muscle activation patterns in the scapular positioning muscles during loaded scapular plane elevation: the effects of latent myofascial trigger points, Clin Biomech (Bristol, Avon) 25:765–770, 2010. Partanen JV, Ojala TA, Arokoski JP: Myofascial syndrome and pain: a neurophysiological approach, Pathophysiology 17:19–28, 2010.

SECTION 2  •  Shoulder

Chapter 21 INTRAARTICULAR INJECTION OF THE SHOULDER JOINT Indications and Clinical Considerations The shoulder joint is susceptible to the development of arthritis from a variety of conditions that have in common the ability to damage the joint cartilage. Osteoarthritis of the joint is the most common form of arthritis that results in shoulder joint pain. However, rheumatoid arthritis, posttraumatic arthritis, and rotator cuff tear arthropathy are also common causes of shoulder pain secondary to arthritis. Less common causes of arthritis-induced shoulder pain include the collagen vascular diseases, infection, villonodular synovitis, and Lyme disease. Acute infectious arthritis usually is accompanied by significant systemic symptoms, including fever and malaise, and should be easily recognized by the astute clinician and treated appropriately with culture and antibiotics rather than with injection therapy. The collagen vascular diseases generally manifest as a polyarthropathy rather than a monoarthropathy limited to the shoulder joint, although shoulder pain secondary to collagen vascular disease responds exceedingly well to the intraarticular injection technique described later. In most patients with shoulder pain secondary to osteoarthritis, rotator cuff arthropathy, and posttraumatic arthritis pain, the pain is localized around the shoulder and upper arm. Activity makes the pain worse, and rest and heat provide some relief. The pain is constant and characterized as aching. The pain may interfere with sleep. Some patients report a grating or popping sensation with use of the joint, and crepitus may be present on physical examination. In addition to the just-described pain, patients with arthritis of the shoulder joint often experience a gradual decrease in functional ability with decreasing shoulder range of motion, making simple everyday tasks, such as hair combing, fastening a bra, or reaching overhead, difficult. With continued disuse, muscle wasting may occur, and a frozen shoulder may develop. Plain radiographs are indicated for all patients with shoulder pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the shoulder is indicated if a rotator cuff tear is suspected.

Clinically Relevant Anatomy The rounded head of the humerus articulates with the pearshaped glenoid fossa of the scapula (Figure 21-1). The articular surface is covered with hyaline cartilage, which is susceptible to arthritis. The rim of the glenoid fossa is composed of a fibrocartilaginous layer called the glenoid labrum, which is susceptible to trauma should the humerus be subluxed or dislocated. The joint is surrounded by a relatively lax capsule that allows the wide range of motion of the shoulder joint at the expense of decreased joint stability. The joint capsule is lined with a synovial membrane that attaches to the articular cartilage. This membrane gives rise to

A

Tg

Na

B Tl

C G

Ns

Figure 21-1  Normal anatomy of the shoulder. A, Acromion; B, intertubercular groove (bicipital groove); C, coracoid; G, glenoid; Na, anatomic neck; Ns, surgical neck; Tg, greater tubercle; Tl, lesser tubercle. (From Houston JD, Davis M: Fundamentals of fluoroscopy, Philadelphia, 2001, Saunders.)

59

60        SECTION 2  •  Shoulder

Worn arthritic cartilage

Glenoid fossa Figure 21-3  Proper ultrasound transducer placement for intraarticular injection of the glenohumeral joint.

Figure 21-2  The rounded head of the humerus articulates with the pear-shaped glenoid fossa of the scapula.

synovial tendon sheaths and bursae that are subject to inflammation. The shoulder joint is innervated by the axillary and suprascapular nerves. The major ligaments of the shoulder joint are the glenohumeral ligaments in front of the capsule, the transverse humeral ligament between the humeral tuberosities, and the coracohumeral ligament, which stretches from the coracoid process to the greater tuberosity of the humerus (Figure 21-2). Along with the accessory ligaments of the shoulder, these major ligaments provide strength to the shoulder joint. The strength of the shoulder joint also is dependent on short muscles that surround the joint: the subscapularis, the supraspinatus, the infraspinatus, and the teres minor. These muscles and their attaching tendons are susceptible to trauma and to wear and tear from overuse and misuse.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the shoulder, subacromial region, and joint space is carried out. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 11⁄2-inch, 25-gauge needle with strict aseptic technique. With strict aseptic technique the midpoint of the acromion is identified, and at a point approximately 1 inch below the midpoint the shoulder joint space is identified. The needle is then carefully advanced through the skin and subcutaneous tissues and through the joint capsule into the joint (see Figure 21-2). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected superiorly and slightly more medially. After the joint space has been entered,

Figure 21-4  Intraarticular injection of the shoulder (arrowheads). Note the bare humeral head with cortical irregularity indicative of osteoarthritis (arrow).

the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced slightly into the joint space until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. In patients in whom the anatomic landmarks are difficult to identify, fluoroscopic or ultrasound guidance for needle placement may be beneficial (Figures 21-3 and 21-4).

Side Effects and Complications The major complication of intraarticular injection of the shoulder is infection. This complication should be exceedingly rare if strict aseptic technique is followed. Approximately 25% of patients report a transient increase in pain after intraarticular injection of the shoulder joint; the patient should be warned of this.

21  •  Intraarticular Injection of the Shoulder Joint        61

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to the previously mentioned causes of arthritis of the shoulder joint. Coexistent bursitis and tendinitis also may contribute to shoulder pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for shoulder pain. Vigorous exercise should be avoided because it will exacerbate the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READING Andrews JR: Diagnosis and treatment of chronic painful shoulder: Review of nonsurgical interventions, Arthroscopy 21:333–347, 2005. Cheng PH, Modir JG, Kim HJ, Narouze S: Ultrasound-guided shoulder joint injections, Tech Reg Anesth Pain Manag 13:184–190, 2009. Dalton SE: Clinical examination of the painful shoulder, Baillieres Clin Rheumatol 3:453–474, 1989. Davies AM: Imaging the painful shoulder, Curr Orthop 6:32–38, 1992. Monach PA: Shoulder pain. In Mushlin SB, Greene HL, editors: Decision making in medicine: an algorithmic approach, ed 3, Philadelphia, 2010, Mosby, pp 522–523. Reutter TRC : Shoulder pain. In Ramamurthy S, Rogers J N, Alanmanou E , ­editors: Decision making in pain management, ed 2, Philadelphia, 2006, Mosby, pp 160–162.

Chapter 22 ACROMIOCLAVICULAR JOINT INJECTION Indications and Clinical Considerations The acromioclavicular joint is vulnerable to injury from both acute trauma and repetitive microtrauma. Acute injuries frequently take the form of falls directly onto the shoulder when playing sports or falling from a bicycle. Repeated strain from throwing injuries

or working with the arm raised across the body also may result in trauma to the joint. After trauma the joint may become acutely inflamed, and if the condition becomes chronic, arthritis of the acromioclavicular joint may develop. The patient with acromioclavicular joint pain frequently reports increased pain when reaching across the chest. Often the patient is unable to sleep on the affected shoulder and may report a grinding sensation in the joint, especially on first awakening. Physical examination may reveal enlargement or swelling of the joint with tenderness to palpation. Downward traction or passive adduction of the affected shoulder may cause increased pain. The chin adduction test will also help confirm the diagnosis. This test is performed by having the patient abduct the affected arm to 90 degrees and then adduct the arm across the chest just under the chin with the objective of grasping the contralateral shoulder (Figure 22-1). Patients with acromioclavicular joint dysfunction will experience severe pain and often will be unable to repeat the maneuver. Furthermore, if there is disruption of the ligaments of the acromioclavicular joint, these maneuvers may reveal joint instability. Plain radiographs of the joint may reveal narrowing or sclerosis of the joint consistent with osteoarthritis or widening of the joint consistent with ligamentous injury (Figure 22-2). Magnetic resonance imaging (MRI) is indicated if disruption of the ligaments is suspected or if a clear cause of the patient’s pain has not been found (Figure 22-3). The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy

Figure 22-1  The chin adduction test for acromioclavicular joint dysfunction. (From Waldman SD: Physical Diagnosis of Pain, ed 2, Philadel­ phia, 2010, Saunders.)

Figure 22-2  Widening of the acromioclavicular joint after disruption of the acromioclavicular ligament (arrow). (From Res­ nick D, Kang HS: Internal derangements of joints: emphasis on MR imaging, Philadelphia, 1997, Saunders.)

62

The acromioclavicular joint is formed by the distal end of the clavicle and the anterior and medial aspects of the acromion (Figure 22-4). The strength of the joint arises in large part from the dense coracoclavicular ligament, which attaches the bottom of the distal end of the clavicle to the coracoid process. A small indentation can be felt where the clavicle abuts the acromion. The joint is completely surrounded by an articular capsule. The superior portion of the joint is covered by the superior acromioclavicular ligament, which attaches the distal clavicle to the upper surface of

22  •  Acromioclavicular Joint Injection        63

the acromion. The inferior portion of the joint is covered by the inferior acromioclavicular ligament, which attaches the inferior portion of the distal clavicle to the acromion. Both of these ligaments further add to the joint’s stability. The acromioclavicular joint may or may not contain an articular disk. The volume of the acromioclavicular joint space is small, and care must be taken not to disrupt the joint by forcefully injecting large volumes of local anesthetic and corticosteroid into the intraarticular space when performing this injection technique.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the superior shoulder and distal clavicle is carried out. A sterile syringe containing 1.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 11⁄2-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique the top of the acromion is identified, and at a point approximately 1 inch medially the acromioclavicular joint space is identified. The needle is then carefully advanced through the skin and subcutaneous tissues medially at a 20-degree angle through the joint capsule into the joint (see Figure 22-4). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected slightly more medially. After the joint space has been entered, the contents of the syringe are gently injected. There should be some resistance to injection, because the joint space is small and the joint capsule is dense. If significant resistance is encountered, the needle is probably in a ligament and should be advanced or withdrawn slightly into the joint space until the injection proceeds

Figure 22-3  Osteoarthritis of the acromioclavicular joint: synovial cyst formation. An oblique coronal fat-suppressed fast spin-echo (TR/ TE, 2750/100) magnetic resonance image shows deformity of the distal portion of the clavicle related to osteoarthritis and a synovial cyst (arrow) containing fluid derived from the acromioclavicular joint. (From ­Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, ­Saunders.)

Acromioclavicular ligament

Figure 22-4  The acromioclavicular joint is located approximately 1 inch medial to the acromion.

64        SECTION 2  •  Shoulder

fluoroscopic or ultrasound guidance for needle placement may be beneficial (Figures 22-5 and 22-6).

Side Effects and Complications The major complication of intraarticular injection of the acromioclavicular joint is infection. This complication should be exceedingly rare if strict aseptic technique is followed. As mentioned previously, forceful injection into the joint may disrupt the joint capsule and should be avoided. Approximately 25% of patients report a transient increase in pain after intraarticular injection of this joint; the patient should be warned of this.

Clinical Pearls

Figure 22-5  Proper transducer positioning for ultrasound-guided acromioclavicular joint injection.

This injection technique is extremely effective in the treatment of pain secondary to the just-described causes of arthritis of the acromioclavicular joint. Coexistent bursitis and tendinitis also may contribute to shoulder pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for shoulder pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Andrews JR: Diagnosis and treatment of chronic painful shoulder: Review of nonsurgical interventions, Arthroscopy 21:333–347, 2005. Cheng PH, Modir JG, Kim HJ, Narouze S: Ultrasound-guided shoulder joint injections, Tech Reg Anesth Pain Manag 13:184–190, 2009. Dalton SE: Clinical examination of the painful shoulder, Baillieres Clin Rheumatol 3:453–474, 1989. Davies AM: Imaging the painful shoulder, Curr Orthop 6:32–38, 1992. Monach PA: Shoulder pain. In Mushlin SB, Greene HL, editors: Decision making in medicine: an algorithmic approach, ed 3, Philadelphia, 2010, Mosby, pp 522–523. Reutter TRC: Shoulder pain. In Ramamurthy S, Rogers JN, Alanmanou E, editors: Decision making in pain management, ed 2, Philadelphia, 2006, Mosby, pp 160–162. Figure 22-6  Ultrasound-guided intraarticular needle placement in the acromioclavicular joint. The bright spot indicates the tip of the needle (circle). (From Sabeti-Aschraf M, Ochsner A, Schueller-Weidekamm C, et al: The infiltration of the AC joint performed by one specialist: ultrasound ­versus palpation a prospective randomized pilot study, Eur J Radiol 75: e37-e40, 2010.)

with only limited resistance. If no resistance is encountered on injection, the joint space is probably not intact and MRI of the joint is recommended. The needle is then removed and a sterile pressure dressing and ice pack are placed at the injection site. In patients in whom the anatomic landmarks are difficult to identify,

Chapter 23 SUPRASPINATUS TENDON INJECTION Indications and Clinical Considerations The musculotendinous unit of the shoulder joint is susceptible to the development of tendinitis for several reasons. First, the joint is subjected to a wide range of motions that are often repetitive. Second, the space in which the musculotendinous unit functions is restricted by the coracoacromial arch, making impingement a likely possibility with extreme movements of the joint. Third, the blood supply to the musculotendinous unit is poor, making healing of microtrauma more difficult. All of these factors can contribute to tendinitis of one or more of the tendons of the shoulder joint. Calcium deposition around the tendon may occur if the inflammation continues, making subsequent treatment more difficult (Figure 23-1). Tendinitis of the musculotendinous unit of the shoulder frequently coexists with bursitis of the associated bursae of the shoulder joint, creating additional pain and functional disability. The supraspinatus tendon of the rotator cuff is particularly prone to the development of tendinitis. The onset of supraspinatus tendinitis is usually acute, occurring after overuse or misuse of the shoulder joint. Inciting factors may include carrying heavy loads in front and away from the body or the vigorous use of exercise equipment. The pain is constant and severe, with sleep disturbance often reported. The patient may attempt to splint the inflamed tendon by elevating the scapula to remove tension

A

from the ligament, giving the patient a “shrugging” appearance. Patients with supraspinatus tendinitis exhibit a positive Dawbarn sign—pain on palpation over the greater tuberosity of the humerus when the arm is hanging down that disappears when the arm is fully abducted. In addition to the just-described pain, patients with supraspinatus tendinitis often experience a gradual decrease in functional ability with decreasing shoulder range of motion, making simple everyday tasks, such as hair combing, fastening a bra, or reaching overhead, difficult. With continued disuse, muscle wasting may occur and a frozen shoulder may develop. Plain radiographs are indicated for all patients with shoulder pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the shoulder is indicated if a rotator cuff tear is suspected. Ultrasound evaluation of the affected area may also help delineate the presence of calcific tendinitis or other shoulder disease (Figure 23-2). The injection technique presented later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The supraspinatus muscle is the most important muscle of the rotator cuff. It provides joint stability and, with the deltoid

B

Figure 23-1  Intervertebral osteochondrosis: Pathologic abnormalities. Four coronal sections reveal the varied pathologic changes of intervertebral osteochondrosis. In the initial stages of the disease (A), cracks or crevices in the nucleus pulposus become evident (arrows). With progression (B), the fissures enlarge and involve portions of the nucleus pulposus and anulus fibrosus (arrows). Intervertebral disk space loss and condensation of bone in the vertebral bodies (arrowheads) become evident. With the onset of abnormalities of the anulus fibrosus, triangular osteophytes may be seen (open arrows). (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

65

66        SECTION 2  •  Shoulder

Humerus

A

B

Figure 23-2  Examples of “hard calcification” that typify the formative phase of calcific tendinosis. A, The anteroposterior radiograph of patient A shows a large, sharply circumscribed calcification within the infraspinatus tendon (solid arrow). B, In patient B, the supraspinatus tendon is imaged longitudinally. A large intratendinous calcification (open arrow) produces significant posterior acoustic shadowing artifact. (From Louis LJ: Musculo­ skeletal ultrasound intervention: principles and advances, Ultrasound Clin 4:217–236, 2009.)

Inflamed tendon Subacromial bursa Deltoid muscle

Supraspinatus muscle

Figure 23-3  The supraspinatus tendon of the rotator cuff is particularly prone to the development of tendinitis.

muscle, adducts the arm at the shoulder by fixing the head of the humerus firmly against the glenoid fossa. The supraspinatus muscle is innervated by the suprascapular nerve, has its origin from the supraspinous fossa of the scapula, and inserts into the upper facet of the greater tuberosity of the humerus (Figure 23-3). The muscle passes across the superior aspect of the shoulder joint, with the inferior portion of the tendon intimately involved with the joint capsule. The supraspinatus muscle and tendons are susceptible to trauma and to wear and tear from overuse and misuse, as mentioned previously.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position with the forearm medially rotated behind the back. If the patient cannot tolerate this position, the injection alternatively may be done with the patient in the sitting position, albeit with greater risk of vasovagal attack. This positioning of the upper extremity places the lateral epicondyle of the elbow in an anterior position and makes its identification easier. After the lateral epicondyle of

the elbow has been identified, the humerus is traced superiorly to the anterior edge of the acromion. A slight indentation just below the anterior edge of the acromion marks the point of insertion of the supraspinatus tendon into the upper facet of the greater tuberosity of the humerus. The point is marked with a sterile marker. Proper preparation with antiseptic solution of the skin overlying the shoulder, subacromial region, and joint space is then carried out. A sterile syringe containing 1.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 11⁄2-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the previously marked point is palpated and the indentation indicating the insertion of the supraspinatus tendon is reidentified with the gloved finger. The needle is then carefully advanced perpendicularly at this point through the skin and subcutaneous tissues, through the joint capsule, until it impinges on bone (see Figure 23-2). The needle is then withdrawn 1 to 2 mm out of the periosteum of the humerus, and the contents of the syringe are gently injected. There should be slight resistance to injection. If no resistance is encountered, either the needle tip is in the joint space itself or the supraspinatus tendon is ruptured. If there is significant resistance to injection, the needle tip is probably in the substance of a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is infection. This complication should be exceedingly rare if strict aseptic technique is followed. Trauma to the supraspinatus tendon from the injection itself remains an ever-present possibility. Tendons that are highly inflamed or previously damaged are subject to rupture if they are directly injected. This risk of this complication can be greatly decreased if the clinician uses gentle technique and stops injecting immediately if significant resistance to injection is encountered. Approximately 25% of patients report a transient increase in pain after this injection technique; the patient should be warned of this.

23  •  Supraspinatus Tendon Injection        67

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to the just-described causes of shoulder pain. Coexistent bursitis and arthritis also may contribute to shoulder pain and may require additional treatment with a more localized injection of local anesthetic and depot corticosteroid. This technique is a safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for shoulder pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Andrews JR: Diagnosis and treatment of chronic painful shoulder: Review of nonsurgical interventions, Arthroscopy 21:333–347, 2005. Cheng PH, Modir JG, Kim HJ, Narouze S: Ultrasound-guided shoulder joint injections, Tech Reg Anesth Pain Manag 13:184–190, 2009. Dalton SE: Clinical examination of the painful shoulder, Baillieres Clin Rheumatol 3:453–474, 1989. Davies AM: Imaging the painful shoulder, Curr Orthop 6:32–38, 1992. Monach PA: Shoulder pain. In Mushlin SB, Greene HL, editors: Decision making in medicine: an algorithmic approach, ed 3, Philadelphia, 2010, Mosby, pp 522–523. Reutter TRC: Shoulder pain. In Ramamurthy S, Rogers JN, Alanmanou E, ­editors: Decision making in pain management, ed 2, Philadelphia, 2006, Mosby, pp 160–162. Yoo JC, Koh KH, Park WH, et  al: The outcome of ultrasound-guided needle decompression and steroid injection in calcific tendinitis, J Shoulder Elbow Surg 19:596–600, 2010.

Chapter 24 INFRASPINATUS TENDON INJECTION Indications and Clinical Considerations The musculotendinous unit of the shoulder joint is susceptible to the development of tendinitis for several reasons. First, the joint is subjected to a wide range of motions, which are often repetitive. Second, the space in which the musculotendinous unit functions is restricted by the coracoacromial arch, making impingement a likely possibility with extreme movements of the joint. Third, the blood supply to the musculotendinous unit is poor, making healing of microtrauma more difficult. All of these factors can contribute to tendinitis of one or more of the tendons of the shoulder joint. Calcium deposition around the tendon may occur if the inflammation continues, making subsequent treatment more difficult. Tendinitis of the musculotendinous unit of the shoulder frequently coexists with bursitis of the associated bursae of the shoulder joint, creating additional pain and functional disability. The infraspinatus tendon of the rotator cuff is particularly prone to the development of tendinitis (Figure 24-1). The onset of infraspinatus tendinitis is usually acute, occurring after overuse or misuse of the shoulder joint. Inciting

factors may include activities that require repeated abduction and lateral rotation of the humerus, such as installing brake pads during assembly line work. The vigorous use of exercise equipment also has been implicated. The pain of infraspinatus tendinitis is constant, severe, and localized in the deltoid area. Significant sleep disturbance is often reported. The patient may attempt to splint the inflamed infraspinatus tendon by rotating the scapula anteriorly to remove tension from the tendon. Patients with infraspinatus tendinitis exhibit pain with lateral rotation of the humerus and on active abduction (Figure 24-2). In addition to the just-described pain, patients with infraspinatus tendinitis often experience a gradual decrease in functional ability with decreasing shoulder range of motion, making simple everyday tasks, such as hair combing, fastening a bra, or reaching overhead, difficult. With continued disuse, muscle wasting may occur, and a frozen shoulder may develop. Plain radiographs are indicated for all patients with shoulder pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and/or ultrasound imaging of the shoulder is indicated if a rotator cuff tear is suspected. The injection technique presented later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The infraspinatus muscle is part of the rotator cuff. It provides shoulder joint stability and, along with the teres minor muscle, externally rotates the arm at the shoulder. The infraspinatus muscle is innervated by the suprascapular nerve. The infraspinatus muscle has its origin in the infraspinous fossa of the scapula and inserts into the middle facet of the greater tuberosity of the humerus. It is at this insertion that infraspinatus tendinitis most commonly occurs (Figure 24-3). The infraspinatus muscle and tendons are susceptible to trauma and to wear and tear from overuse and misuse, as mentioned previously.

Technique Figure 24-1  Magnetic resonance image showing severe tendinosis of the infraspinatus tendon. (From Adler RS, Finzel KC: The complementary roles of MR imaging and ultrasound of tendons, Radiol Clin North Am 34:771–807, 2005, with permission.)

68

The goals of this injection technique are explained to the patient. The patient is placed in the sitting position with the arm supported on a bedside table and flexed to 90 degrees at the elbow. The arm is then externally rotated, which brings the insertion of the infraspinatus tendon out from under the deltoid muscle. The infraspinatus muscle can be felt to contract

24  •  Infraspinatus Tendon Injection        69

Supraspinatus m.

Infraspinatus m. Teres minor m.

A

Figure 24-3  Patients with infraspinatus tendinitis will often experience excellent pain relief with injection of the tendon with steroid and local anesthetic.

B Figure 24-2  A and B, The mid-arc abduction test for infraspinatus tendinitis will reveal the onset of severe pain in the middle range of the arc with the pain improving as the patient reaches the top of the arc of abduction. (From Waldman SD: Physical diagnosis of pain, Philadelphia, 2005, Saunders.)

with this maneuver. The posterior angle of the acromion is then identified, as is the lateral epicondyle at the elbow. In this position the insertion of the infraspinatus tendon is in a direct line with the lateral epicondyle of the elbow. The insertion should be approximately 45 degrees inferior to the posterior angle of the acromion. The point is marked with a sterile marker. Proper preparation with antiseptic solution of the skin overlying the posterior shoulder, acromial region, and joint space is then carried out. A sterile syringe containing 1.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 11⁄2-inch, 25-gauge needle with strict ­aseptic technique. With strict aseptic technique, the previously marked point is palpated and the insertion of the infraspinatus tendon is reidentified with the gloved finger. The needle is then carefully advanced at this point through the skin and subcutaneous tissues, as well as through the margin of the deltoid

muscle and underlying infraspinatus muscle, until it impinges on bone (see Figure 24-3). The needle is then withdrawn 1 to 2 mm out of the periosteum of the humerus, and the contents of the syringe are gently injected. There should be slight resistance to injection. If no resistance is encountered, either the needle tip is in the joint space itself or the infraspinatus tendon is ruptured. If there is significant resistance to injection, the needle tip is probably in the substance of a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Trauma to the infraspinatus tendon from the injection itself remains an ever-present possibility. Tendons that are highly inflamed or previously damaged are subject to rupture if they are injected directly. The risk of this complication can be greatly decreased if the clinician uses gentle technique and stops injecting immediately if significant resistance to injection is encountered. Approximately 25% of patients note a transient increase in pain after this injection technique; the patient should be warned of this.

70        SECTION 2  •  Shoulder

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to the just-described causes of shoulder pain. Coexistent bursitis and arthritis also may contribute to shoulder pain and may require additional treatment with a more localized injection of anesthetic and depot corticosteroid. This technique is a safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for shoulder pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Andrews JR: Diagnosis and treatment of chronic painful shoulder: Review of nonsurgical interventions, Arthroscopy 21:333–347, 2005. Cheng PH, Modir JG, Kim HJ, Narouze S: Ultrasound-guided shoulder joint injections, Tech Reg Anesth Pain Manag 13:184–190, 2009. Dalton SE: Clinical examination of the painful shoulder, Baillieres Clin Rheumatol 3:453–474, 1989. Davies AM: Imaging the painful shoulder, Curr Orthop 6:32–38, 1992. Monach PA: Shoulder pain. In Mushlin SB, Greene HL, editors: Decision ­making in medicine: an algorithmic approach, ed 3, Philadelphia, 2010, Mosby, pp 522–523. Reutter TRC: Shoulder pain. In Ramamurthy S, Rogers JN, Alanmanou E, ­editors: Decision making in pain management, ed 2, Philadelphia, 2006, Mosby.

Chapter 25 SUBSCAPULARIS TENDON INJECTION Indications and Clinical Considerations The musculotendinous unit of the shoulder joint is susceptible to the development of tendinitis for several reasons. First, the joint is subjected to a wide range of motions that are often repetitive. Second, the space in which the musculotendinous unit functions is restricted by the coracoacromial arch, making impingement a likely possibility with extreme movements of the joint. Third, the blood supply to the musculotendinous unit is poor, making healing of microtrauma more difficult. All of these factors can contribute to tendinitis of one or more of the tendons of the shoulder joint. Calcium deposition around the tendon may occur if the inflammation continues, making subsequent treatment more difficult. Tendinitis of the musculotendinous unit of the shoulder frequently coexists with bursitis of the associated bursae of the shoulder joint, creating additional pain and functional disability. The subscapularis tendon of the rotator cuff is particularly prone to the development of tendinitis and associated bursitis. The onset of subscapularis tendinitis is usually acute, occurring after overuse or misuse of the shoulder joint. Inciting factors may include activities that require repeated adduction and medial rotation of the humerus, such as repetitive motions during assembly line work. The pain of subscapularis tendinitis is constant, severe, and localized in the anterior deltoid and shoulder. Significant sleep disturbance is often reported. The patient may attempt to splint the inflamed subscapularis tendon by limiting medial rotation of the humerus. Patients with subscapularis tendinitis experience pain on resisted medial rotation and in active rotation and adduction. As mentioned earlier, bursitis often accompanies subscapularis tendinitis. In addition to the just-described pain, patients with subscapularis tendinitis often experience a gradual decrease in functional ability with decreasing shoulder range of motion, making simple everyday tasks, such as hair combing, fastening a bra, or reaching overhead, difficult. With continued disuse, muscle wasting may occur and a frozen shoulder may develop. Plain radiographs are indicated for all patients with shoulder pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) or ultrasound imaging of the shoulder is indicated if a rotator cuff tear is suspected. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The subscapularis muscle is part of the rotator cuff. It provides shoulder joint stability along with the supraspinatus, infraspinatus,

and teres minor muscle (Figure 25-1). The subscapularis muscle medially rotates the arm at the shoulder. The subscapularis muscle is innervated by branches of the posterior cord of the brachial plexus and the upper and lower subscapular nerves. The subscapularis muscle has its origin in the subscapular fossa of the anterior scapula and inserts into the lesser tuberosity of the humerus. It is at this insertion that subscapularis tendinitis most commonly occurs (Figure 25-2). The subscapularis muscle and tendons are susceptible to trauma and to wear and tear from overuse and misuse, as mentioned previously.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the prone position. The arm is then externally rotated approximately 45 degrees. The coracoid process is then identified anteriorly. Just lateral to the coracoid process is the lesser tuberosity. The lesser tuberosity is more easily palpated if the arm is passively rotated. The point overlying the tuberosity is marked with a sterile marker.

S

I SC

t

Figure 25-1  Oblique sagittal T1-weighted magnetic resonance imaging scan at level of coracoid process. Supraspinatus (S), infraspinatus (I), and subscapular muscle (SC) are shown, as well as attachment of triceps tendon (t) to inferior glenoid. (From De Maeseneer M, Van Roy P, Shahabpour M: Normal MR imaging anatomy of the rotator cuff tendons, glenoid fossa, labrum, and ligaments of the shoulder, Radiol Clin North Am 44:479–487, 2006.)

71

72        SECTION 2  •  Shoulder

Side Effects and Complications

Subscapularis m.

The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is followed. Trauma to the subscapularis tendon from the injection itself remains an ever-present possibility. Tendons that are highly inflamed or previously damaged are subject to rupture if they are directly injected. The risk of this complication can be greatly decreased if the clinician uses gentle technique and stops injecting immediately if significant resistance to injection is encountered. Approximately 25% of patients note a transient increase in pain after this injection technique; the patient should be warned of this.

Clinical Pearls

Figure 25-2  The subscapularis tendon is susceptible to tendinitis at its insertion on the lesser tuberosity of the humerus.

Proper preparation with antiseptic solution of the skin overlying the posterior shoulder is carried out. A sterile syringe containing 1.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 11⁄2-inch, 25-gauge needle with strict aseptic technique. With strict aseptic technique, the previously marked point is palpated and the insertion of the subscapularis tendon is reidentified with the gloved finger. The needle is then carefully advanced at this point through the skin and subcutaneous tissues and underlying subscapularis tendon until it impinges on bone (see Figure 25-2). The needle is then withdrawn 1 to 2 mm out of the periosteum of the humerus, and the contents of the syringe are gently injected. There should be slight resistance to injection. If no resistance is encountered, either the needle tip is in the joint space itself or the subscapularis tendon is ruptured. If there is significant resistance to injection, the needle tip is probably in the substance of a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed and a sterile pressure dressing and ice pack are placed at the injection site.

This injection technique is extremely effective in the treatment of pain secondary to the just-described causes of shoulder pain. Coexistent bursitis and arthritis also may contribute to shoulder pain and may require additional treatment with a more localized injection of local anesthetic and depot corticosteroid. This technique is a safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for shoulder pain. Vigorous exercise should be avoided because it exacerbates the patient’ symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS De Maeseneer M, Van Roy P, Shahabpour M: Normal MR imaging anatomy of the rotator cuff tendons, glenoid fossa, labrum, and ligaments of the shoulder, Radiol Clin North Am 44:479–487, 2006. Ingber RS: Shoulder impingement in tennis/racquetball players treated with subscapularis myofascial treatments, Arch Phys Med Rehabil 81:679–682, 2000. Peidro L, Serra A, Suso S: Subcoracoid impingement after ossification of the subscapularis tendon, J Shoulder Elbow Surg 8:170–171, 1999. Waldman SD: The subscapularis muscle. In Pain review, Philadelphia, 2009, ­Saunders, pp 88.

Chapter 26 INJECTION TECHNIQUE FOR DELTOID SYNDROME Indications and Clinical Considerations The deltoid muscle is susceptible to the development of myofascial pain syndrome. Prolonged lifting or repetitive tasks involving moving the shoulder and arm forward and backward may cause repeated microtrauma to the deltoid muscle and may result in the development of myofascial pain. The deltoid muscle is also susceptible to the development of deltoid myofascial pain syndrome after blunt trauma to the muscle, such as that occurring after falls onto the shoulder from a horse or repeated hits to the deltoid muscle during football. Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body. The sine qua non of myofascial pain syndrome is the finding of myofascial trigger points on physical examination. Although these trigger points generally are localized to the regional part of the body affected, the pain of myofascial pain syndrome often is referred to other anatomic areas. This referred pain often is misdiagnosed or attributed to other organ systems, thereby leading to extensive evaluations and ineffective treatment. Patients with myofascial pain syndrome involving the deltoid often have referred pain into the shoulder radiating down into the upper extremity. The trigger point is the pathognomonic lesion of myofascial pain and is thought to be the result of microtrauma to the affected muscles. This pathologic lesion is characterized by a local point of exquisite tenderness in affected muscle. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain but also referred pain. In addition to this local and referred pain, there often is an involuntary withdrawal of the stimulated muscle, called a “jump sign.” This jump sign also is characteristic of myofascial pain syndrome. Patients with deltoid syndrome will exhibit trigger points in both the anterior and posterior fibers of the muscle (Figure 26-1). Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. In spite of this consistent physical finding in patients with myofascial pain syndrome, the pathophysiology of the myofascial trigger point remains elusive, although many theories have been advanced. Common to all of these theories is the belief that trigger points are the result of microtrauma to the affected muscle. This microtrauma may occur as a single injury to the affected muscle or as a result of repetitive microtrauma or chronic deconditioning of the agonist and antagonist muscle unit. In addition to muscle trauma, a variety of other factors seem to predispose the patient to develop myofascial pain syndrome. The weekend athlete who subjects his or her body to unaccustomed physical activity may develop myofascial pain syndrome.

The poor posture of someone sitting at a computer keyboard or watching television has also been implicated as a predisposing factor to the development of myofascial pain syndrome. Previous injuries may result in abnormal muscle function and predispose to the subsequent development of myofascial pain syndrome. All of these predisposing factors may be intensified if the patient also has poor nutritional status or coexisting psychological or behavioral abnormalities, including chronic stress and depression. The deltoid muscle seems to be particularly susceptible to stress-induced myofascial pain syndrome. Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or may occur in conjunction with other painful conditions, including radiculopathy and chronic regional pain syndromes. Psychological or behavioral abnormalities, including depression, frequently coexist with the muscle abnormalities associated with myofascial pain syndrome. Treatment of these psychological and behavioral abnormalities must be an integral part of any successful treatment plan for myofascial pain syndrome.

Clinically Relevant Anatomy The muscles of the shoulder work together as a functional unit to stabilize and allow coordinated movement of the upper extremity. Trauma to an individual muscle can result in dysfunction of the entire functional unit. The deltoid muscle works to stabilize and help attach the shoulder girdle to the arm. The fibers of the deltoid muscle originate from the acromion, the spine of the scapula, and the inferior surface of the lateral third of the clavicle inserting into the deltoid tuberosity. The deltoid muscle helps abduct the upper extremity at the glenohumeral joint, with the anterior muscle fibers helping flex and medially rotate the upper extremity and the posterior muscle fibers helping extend and laterally rotate the upper extremity. The deltoid muscle is innervated by the axillary nerve (see Figure 26-1). The deltoid muscle and tendons are susceptible to trauma and to wear and tear from overuse and misuse as well as tendinitis.

Technique Careful preparation of the patient before trigger point injection helps to optimize results. Trigger point injections are directed at the primary trigger point rather than in the area of referred pain. It should be explained to the patient that the goal of trigger point injection is to block the trigger of the persistent pain and thus, it is hoped, provide long-lasting relief. It is important that the 73

74        SECTION 2  •  Shoulder

Trigger point Deltoid m. Referred pain

Figure 26-1  Deltoid syndrome often develops after blunt trauma to the muscle.

patient understand that for most patients with myofascial pain syndrome, more than one treatment modality is required for optimal pain relief. The use of the recumbent or lateral position when identifying and marking trigger points as well as when performing the actual trigger point injection helps decrease the incidence of vasovagal reactions. The skin overlying the trigger point to be injected should always be prepared with antiseptic solution before injection to avoid infection. After the goals of trigger point injection have been explained to the patient and proper preparation of the patient has been carried out, the trigger point to be injected is reidentified by palpation with the sterilely gloved finger. A syringe containing 10 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 25- or 27-gauge needle of a length adequate to reach the trigger point. Except for the muscles of posture in the

low back, a 1½-inch needle will be adequate. A volume of 0.5 to 1.0 mL of solution is then injected into each trigger point. A series of two to five treatment sessions may be required to completely abolish the trigger point; the patient should be informed of this.

Side Effects and Complications The proximity to the spinal cord and exiting cervical nerve roots makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing interventional pain management techniques. Given the proximity of the brain and brainstem, ataxia caused by vascular uptake of local anesthetic after trigger point injection is not an uncommon occurrence. Many patients also note a transient increase in pain after injection of trigger points in the deltoid muscle.

26  •  Injection Technique for Deltoid Syndrome        75

Clinical Pearls Trigger point injections are extremely safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of trigger point injection are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after trigger point injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid pneumothorax when injecting trigger points in proximity to the underlying pleural space. The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators believe that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as amitriptyline and nortriptyline are good first choices and should be given as a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow. Pregabalin and milnacipran have also been shown to be effective in the management of fibromyalgia and may be worth a try if the condition fails to respond to more established treatments.

SUGGESTED READINGS Baldry P: Acupuncture treatment of fibromyalgia and myofascial pain. In Chaitow L, editor: Fibromyalgia syndrome, ed 3, Oxford, 2010, Churchill Livingstone, pp 145–159. Ge HY, Nie H, Madeleine P, et al: Contribution of the local and referred pain from active myofascial trigger points in fibromyalgia syndrome, Pain 147: 233–240, 2009. Ge HY, Wang Y, Danneskiold-Samsøe B, et al: The predetermined sites of examination for tender points in fibromyalgia syndrome are frequently associated with myofascial trigger points, J Pain 11:644–651, 2010. Hains G, Descarreaux M, Hains F: Chronic shoulder pain of myofascial origin: a randomized clinical trial using ischemic compression therapy, J Manipulative Physiol Ther 33:362–369, 2010. LeBlanc KE, LeBlanc LL: Musculoskeletal disorders, Prim Care 37:389–406, 2010. Partanen JV, Ojala TA, Arokoski JP: Myofascial syndrome and pain: a neurophysiological approach, Pathophysiology 17:19–28, 2010.

Chapter 27 INJECTION TECHNIQUE FOR PECTORALIS MAJOR SYNDROME Indications and Clinical Considerations The pectoralis major muscle is susceptible to the development of myofascial pain syndrome. Prolonged lifting of heavy objects held in front of the body or sustained lifting with the arms held in a fixed position, as in the use of a chain saw, may result in the development of myofascial pain in the pectoralis major muscle. The pectoralis major muscle is also susceptible to the development of myofascial pain syndrome after blunt trauma to the muscle, such as the trauma that occurs to the anterolateral chest during motor vehicle accidents or from sports injuries such as spearing injuries during football. Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body. The sine qua non of myofascial pain syndrome is the finding of myofascial trigger points on physical examination. Although these trigger points generally are localized to the regional part of the body affected, the pain of myofascial pain syndrome often is referred to other anatomic areas. This referred pain often is misdiagnosed or attributed to other organ systems, thereby leading to extensive evaluations and ineffective treatment. Patients with myofascial pain syndrome involving the pectoralis major often have referred pain into the anterior shoulder radiating into the upper chest wall. The trigger point is the pathognomonic lesion of myofascial pain and is thought to be a result of microtrauma to the affected muscles. This pathologic lesion is characterized by a local point of exquisite tenderness in affected muscle. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain but also referred pain. In addition to this local and referred pain, there often is an involuntary withdrawal of the stimulated muscle, called a “jump sign.” This jump sign also is characteristic of myofascial pain syndrome. Patients with pectoralis major syndrome will exhibit trigger points in the clavicular as well as sternal portions of the muscle (Figure 27-1). Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. In spite of this consistent physical finding in patients with myofascial pain syndrome, the pathophysiology of the myofascial trigger point remains elusive, although many theories have been advanced. Common to all of these theories is the belief that trigger points are a result of microtrauma to the affected muscle. This microtrauma may occur as a single injury to the affected muscle or as a result of repetitive microtrauma or chronic deconditioning of the agonist and antagonist muscle unit. In addition to muscle trauma, a variety of other factors seem to predispose the patient to develop myofascial pain syndrome. 76

The weekend athlete who subjects his or her body to unaccustomed physical activity may develop myofascial pain syndrome. The poor posture of someone sitting at a computer keyboard or watching television has also been implicated as a predisposing factor to the development of myofascial pain syndrome. Previous injuries may result in abnormal muscle function and predispose to the subsequent development of myofascial pain syndrome. All of these predisposing factors may be intensified if the patient also has poor nutritional status or coexisting psychological or behavioral abnormalities, including chronic stress and depression. The pectoralis major muscle seems to be particularly susceptible to stressinduced myofascial pain syndrome. Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or may occur in conjunction with other painful conditions, including radiculopathy and chronic regional pain syndromes. Psychological or behavioral abnormalities, including depression, frequently coexist with the muscle abnormalities associated with myofascial pain syndrome. Treatment of these psychological and behavioral abnormalities must be an integral part of any successful treatment plan for myofascial pain syndrome.

Clinically Relevant Anatomy Working with the other muscles of the shoulder and anterior chest wall, the pectoralis major muscle helps adduct and medially rotate the humerus and helps to stabilize the scapula by drawing it anteriorly and inferiorly. The pectoralis major muscle, via its clavicular head, flexes the humerus, with the sternocostal head of the muscle helping to extend the humerus. The muscle is innervated by the lateral and medial pectoral nerves (see Figure 27-1). The pectoralis major muscle and tendons are susceptible to trauma and to wear and tear from overuse and misuse and may develop myofascial pain syndrome as well as tendinitis.

Technique Careful preparation of the patient before trigger point injection helps to optimize results. Trigger point injections are directed at the primary trigger point rather than in the area of referred pain. It should be explained to the patient that the goal of trigger point injection is to block the trigger of the persistent pain and thus, it is hoped, provide long-lasting relief. It is important that the patient understand that for most patients with myofascial pain syndrome, more than one treatment modality is required for optimal pain relief. The use of the recumbent or lateral position when

27  •  Injection Technique for Pectoralis Major Syndrome        77

0.5 to 1.0 mL of solution is then injected into each trigger point (see Figure 27-1). A series of two to five treatment sessions may be required to completely abolish the trigger point; the patient should be informed of this.

Side Effects and Complications The proximity to the spinal cord and exiting cervical nerve roots makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing interventional pain management techniques. Given the proximity of the brain and brainstem, ataxia caused by vascular uptake of local anesthetic after trigger point injection is not an uncommon occurrence. Many patients also note a transient increase in pain after injection of trigger points in the pectoralis major muscle.

Clinical Pearls

Referred pain Pectoralis major m. Trigger point

Figure 27-1  Patients with pectoralis major syndrome often experience referred pain in the anterior shoulder radiating into the chest wall.

identifying and marking trigger points as well as when performing the actual trigger point injection helps decrease the incidence of vasovagal reactions. The skin overlying the trigger point to be injected should always be prepared with antiseptic solution before injection to avoid infection. After the goals of trigger point injection have been explained to the patient and proper preparation of the patient has been carried out, the trigger point to be injected is reidentified by palpation with the sterilely gloved finger. A syringe containing 10 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 25- or 27-gauge needle of a length adequate to reach the trigger point. Except for the muscles of posture in the low back, a 1½-inch needle will be adequate. A volume of

Trigger point injections are extremely safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of trigger point injection are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after trigger point injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid pneumothorax when injecting trigger points in proximity to the underlying pleural space. The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators believe that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as amitriptyline and nortriptyline are good first choices and should be given as a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow. Pregabalin and milnacipran have also been shown to be effective in the management of fibromyalgia and may be worth a try if the condition fails to respond to more established treatments.

SUGGESTED READING Baldry P: Acupuncture treatment of fibromyalgia and myofascial pain. In ­Chaitow L, editor: Fibromyalgia syndrome, ed 3, Oxford, 2010, Churchill ­Livingstone, pp 145–159. Ge HY, Nie H, Madeleine P, et al: Contribution of the local and referred pain from active myofascial trigger points in fibromyalgia syndrome, Pain 147: 233–240, 2009. Ge HY, Wang Y, Danneskiold-Samsøe B, et al: The predetermined sites of examination for tender points in fibromyalgia syndrome are frequently associated with myofascial trigger points, J Pain 11:644–651, 2010. LeBlanc KE, LeBlanc LL: Musculoskeletal disorders, Prim Care 37:389–406, 2010. Partanen JV, Ojala TA, Arokoski JP: Myofascial syndrome and pain: a neurophysiological approach, Pathophysiology 17:19–28, 2010.

Chapter 28 INJECTION TECHNIQUE FOR PECTORALIS MAJOR TEAR SYNDROME Indications and Clinical Considerations The pectoralis major muscle is susceptible to trauma ranging from microscopic tears of the muscle substance caused by heavy exertion to macroscopic partial tearing of the muscle or in extreme cases full-thickness tearing with associated hematoma formation and cosmetic deformity (Figure 28-1). In addition, the pectoralis major tendon can rupture at its point of insertion into the crest of the greater tubercle of the humerus (Figure 28-2). The clinical presentation of pectoralis major tear syndrome is varied owing to its several causes, with the severity of symptomatology directly proportional to the amount of trauma sustained by the muscle and/or its tendons. The presenting symptom of pectoralis major tear syndrome is the acute onset of anterior chest wall pain after trauma to the muscle sustained while carrying out such activities as bench pressing or repelling down cliffs. The severity of pain will be proportional to the amount of trauma sustained. The patient with pectoralis muscle tear syndrome may

also report varying degrees of weakness with internal rotation of the humerus. If a complete tear of the muscle or rupture of the tendon occurs, acutely there will be bulging of the anterior chest wall with contraction of the muscle in a manner analogous to the Popeye bulge or Ludington sign associated with rupture of the biceps tendon. If the complete rupture is not promptly repaired, further muscle retraction and calcification will occur, worsening the functional disability and cosmetic deformity. The patient with pectoralis major tear syndrome will report the acute onset of pain in the anterior chest after trauma to the pectoralis major muscle and/or tendon. If the trauma is significant, hematoma formation will be clearly visible; with rupture of the tendon at its insertion site into the humerus, impressive ecchymosis of the arm and anterior chest wall that may seem out of proportion to the amount of trauma perceived by the patient will be present. Active internal rotation of the humerus against examiner resistance may reveal weakness. If there is significant disruption of the muscle or rupture of the tendon, the patient will be unable to reach behind his or her back. As mentioned

Pectoralis major muscle tear

Characteristic cosmetic deformity

Figure 28-1  Complete tear of the pectoralis major with characteristic cosmetic deformity.

78

28  •  Injection Technique for Pectoralis Major Tear Syndrome        79

Complete rupture of tendon

Figure 28-2  Pectoralis major tendon rupture at the point where it inserts into the crest of the greater tubercle of the humerus.

previously, if complete tear of the muscle or rupture of the tendon has occurred, there will be bulging of the anterior chest wall with contraction of the pectoralis major against the unopposed torn distal muscle and/or tendon. Loss of the axillary fold may also be present. Although not completely diagnostic of pectoralis major tear syndrome, this physical finding should prompt the examiner to obtain a magnetic resonance imaging (MRI) or ultrasound scan of the affected proximal humerus and shoulder as well as the anterior chest wall to further clarify and strengthen the diagnosis. MRI and ultrasound imaging of the shoulder, proximal humerus, and anterior chest wall provides the clinician with the best information regarding any pathology of these anatomic regions. MRI is highly accurate and helps to identify abnormalities that may require urgent surgical repair, such as large complete muscle tears and/or tendon rupture (Figure 28-3). MRI and ultrasound imaging of the affected anatomy will also help the clinician rule out unsuspected pathology that may harm the patient, such as primary and metastatic tumors. In patients who cannot undergo MRI scanning, such as a patient with a pacemaker, computed tomography is a reasonable second choice. Radionuclide bone scanning and plain radiography are indicated if fracture or bony abnormality such as metastatic disease of the proximal humerus, shoulder, or anterior chest wall is being considered in the differential diagnosis. Screening laboratory testing consisting of complete blood cell count, erythrocyte sedimentation rate, and automated blood chemistry testing should be performed if the diagnosis of pectoralis major tear syndrome is in question.

Clinically Relevant Anatomy A broad, thick, fanlike muscle, the pectoralis major arises from the anterior surface of the proximal clavicle, the anterior surface of the sternum, the cartilaginous attachments of the second through sixth and occasionally seventh ribs, and the aponeurotic band of the obliquus externus abdominis muscle. These muscle fibers

Figure 28-3  Axial T2-weighted magnetic resonance image of the chest. White arrow highlights the pectoralis major tendon, which has detached from the humerus and retracted medially. Dark arrow demonstrates local hematoma. (From Hasegaw K, Schofer JM: Rupture of the pectoralis major: a case report and review, J Emerg Med 38:196-200, 2010.)

overlap, with some running upward and laterally, others running horizontally, and others running downward and laterally, all ending in a broad flat tendon that inserts into the crest of the greater tubercle of the humerus.

Technique The pain and functional disability associated with mild microscopic tears of the pectoralis major muscle may be treated conservatively with a combination of the nonsteroidal antiinflammatory agents or cyclooxygenase-2 (COX-2) inhibitors and gentle physical therapy. Patients with partial tears of the pectoralis major also often respond to a gentle injection of local anesthetic and steroid to provide palliation of pain. A complete tear or rupture will require surgical repair. To perform injection of the pectoralis major muscle, the goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the area of the tear is carried out. A sterile syringe containing 4.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique the injection site is identified. At this point the needle is then carefully advanced in a slightly cephalad trajectory through the skin, through the subcutaneous tissues, and into the area of the tear (Figure 28-4). After the needle is in place, the contents of the syringe are gently injected. There should be minimal resistance to injection. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Differential Diagnosis Pectoralis major tear syndrome is a clinical diagnosis that is supported by a combination of clinical history, physical examination, radiography, and MRI. Pain syndromes that may mimic pectoralis major tear syndrome include injuries to the pectoralis minor, subscapularis, or latissimus dorsi muscles and/or inferior glenohumeral ligament injuries. Dislocation of the manubrium from the body of the sternum after acceleration-deceleration injuries

80        SECTION 2  •  Shoulder

Microscopic muscle tears

that may result in ongoing damage to the shoulder or lead to overlooked pathology in this anatomic region that may harm the patient, such as Pancoast tumor or primary or metastatic tumors of the shoulder, humerus, or anterior chest wall. MRI is indicated for all patients thought to have pectoralis major tear syndrome, and aggressive treatment of surgically correctible causes of the patient’s symptoms is indicated on an urgent basis to avoid irreversible cosmetic deformity and functional disability. The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is followed. Trauma to the rotator cuff from the injection itself remains an ever-present possibility. Tendons that are highly inflamed or previously damaged are subject to rupture if they are directly injected. This could convert a partial tear into a complete tear. The risk of this complication can be greatly decreased if the clinician uses gentle technique and stops injecting immediately if significant resistance to injection is encountered. Approximately 25% of patients note a transient increase in pain after this injection technique; the patient should be warned of this.

Clinical Pearls Figure 28-4  Patients with partial tears of the pectoralis major will often respond to a gentle injection of local anesthetic and steroid to provide palliation of pain.

may also confuse the diagnosis. Factures of all of the bony origins of the pectoralis major muscles, for example, the sternum and ribs, as well as fractures of the anatomic or surgical neck of the humerus may mimic the clinical presentation of pectoralis major tear syndrome. Primary and metastatic tumors of the shoulder, humerus, and anterior chest wall and their surrounding structures remain an ever-present possibility and should always be included as part of the differential diagnosis of patients with symptoms thought to be pectoralis major tear syndrome.

Side Effects and Complications Failure to correctly diagnose pectoralis major tear syndrome will put the patient at risk for the missed diagnosis of other syndromes

Pectoralis major tear syndrome is an uncommon but easily recognized cause of anterior chest wall and shoulder pain. Patients with complete pectoralis major muscle tear and/or tendon rupture may have very impressive hematoma and ecchymosis formation that will seem out of proportion to the patient’s perception of the amount of trauma he or she sustained; patients often require reassurance that they will not bleed to death. Such patients should undergo urgent surgical repair and careful postoperative rehabilitation to avoid permanent cosmetic deformity and functional ­disability.

SUGGESTED READINGS Beloosesky Y, Grinblat J, Katz M, et al: Pectoralis major rupture in the elderly: clinical and sonographic findings, Clin Imaging 27:261–264, 2003. Hasegawa K, Schofer JM: Rupture of the pectoralis major: a case report and review, J Emerg Med 38:196–200, 2010. Mellado JM, Calmet J, Giné J, Saurí A: Pectoralis major muscle and tendon tears: report of two cases with surgical correlation and postoperative follow-up, Eur J Radiol Extra 50:101–104, 2004.

Chapter 29 INJECTION TECHNIQUE FOR TERES MAJOR SYNDROME Indications and Clinical Considerations The teres major muscle is susceptible to the development of myofascial pain syndrome. Prolonged lifting of heavy objects held in front of the body or repetitive activities that require medial rotation of the humerus, such as using a screwdriver, may cause the development of teres major syndrome. The teres major muscle is also susceptible to the development of myofascial pain after blunt trauma to the muscle, such as during trauma to the posterolateral chest in motor vehicle accidents or from sports injuries such as spearing injuries in football or falls onto the lateral scapula. Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body. The sine qua non of myofascial pain syndrome is the finding of myofascial trigger points on physical examination. Although these trigger points generally are localized to the regional part of the body affected, the pain of myofascial pain syndrome often is referred to other anatomic areas. This referred pain often is misdiagnosed or attributed to other organ systems, thereby leading to extensive evaluations and ineffective treatment. Patients with myofascial pain syndrome involving the teres major often have referred pain into the ipsilateral shoulder and upper extremity. The trigger point is the pathognomonic lesion of myofascial pain and is thought to be a result of microtrauma to the affected muscles. This pathologic lesion is characterized by a local point of exquisite tenderness in affected muscle. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain but also referred pain. In addition to this local and referred pain, there often is an involuntary withdrawal of the stimulated muscle, called a “jump sign.” This jump sign also is characteristic of myofascial pain syndrome. Patients with teres major syndrome will exhibit trigger points in the axillary or posterior portion of the muscle (Figure 29-1). Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. In spite of this consistent physical finding in patients with myofascial pain syndrome, the pathophysiology of the myofascial trigger point remains elusive, although many theories have been advanced. Common to all of these theories is the belief that trigger points are a result of microtrauma to the affected muscle. This microtrauma may occur as a single injury to the affected muscle or as a result of repetitive microtrauma or chronic deconditioning of the agonist and antagonist muscle unit. In addition to muscle trauma, a variety of other factors seem to predispose the patient to develop myofascial pain syndrome. The weekend athlete who subjects his or her body to unaccustomed physical activity may develop myofascial pain syndrome. The poor posture of someone sitting at a computer keyboard or

watching television has also been implicated as a predisposing factor to the development of myofascial pain syndrome. Previous injuries may result in abnormal muscle function and predispose to the subsequent development of myofascial pain syndrome. All of these predisposing factors may be intensified if the patient also has poor nutritional status or coexisting psychological or behavioral abnormalities, including chronic stress and depression. The teres major muscle seems to be particularly susceptible to stressinduced myofascial pain syndrome.

Trigger point Teres major m. Referred pain

Figure 29-1  Patients with teres major syndrome have referred pain into the ipsilateral shoulder and upper extremity.

81

82        SECTION 2  •  Shoulder

Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or may occur in conjunction with other painful conditions, including radiculopathy and chronic regional pain syndromes. Psychological or behavioral abnormalities, including depression, frequently coexist with the muscle abnormalities associated with myofascial pain syndrome. Treatment of these psychological and behavioral abnormalities must be an integral part of any successful treatment plan for myofascial pain syndrome.

Clinically Relevant Anatomy Working with the other muscles of the shoulder and posterior chest wall, the teres major muscle helps stabilize the shoulder as well as adduct and medially rotate the humerus. The teres major is a thick, flat muscle that arises from the dorsal surface of the inferior angle of the scapula and finds its insertion via a flat tendon onto the crest of the lesser tubercle of the humerus. The muscle is innervated by the subscapular nerve. The teres major muscle and tendons are susceptible to trauma and to wear and tear from overuse and misuse and may develop myofascial pain syndrome as well as tendinitis.

Technique Careful preparation of the patient before trigger point injection helps to optimize results. Trigger point injections are directed at the primary trigger point rather than in the area of referred pain. It should be explained to the patient that the goal of trigger point injection is to block the trigger of the persistent pain and thus, it is hoped, provide long-lasting relief. It is important that the patient understand that for most patients with myofascial pain syndrome, more than one treatment modality is required for optimal pain relief. The use of the recumbent or lateral position when identifying and marking trigger points as well as when performing the actual trigger point injection helps decrease the incidence of vasovagal reactions. The skin overlying the trigger point to be injected should always be prepared with antiseptic solution before injection to avoid infection. After the goals of trigger point injection have been explained to the patient and proper preparation of the patient has been carried out, the trigger point to be injected is reidentified by palpation with the sterilely gloved finger. A syringe containing 10 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 25- or 27-gauge needle of a length adequate to reach the trigger point. Except for the muscles of posture in the low back, a 1½-inch needle will be adequate. A volume of 0.5 to 1.0 mL of solution is then injected into each trigger point (see Figure 29-1). A series of two to five treatment sessions may be required to completely abolish the trigger point; the patient should be informed of this.

Side Effects and Complications The proximity to the spinal cord and exiting cervical nerve roots makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in

performing interventional pain management techniques. Given the proximity of the brain and brainstem, ataxia caused by vascular uptake of local anesthetic after trigger point injection is not an uncommon occurrence. Many patients also note a transient increase in pain after injection of trigger points in the teres major muscle.

Clinical Pearls Trigger point injections are extremely safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of trigger point injection are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after trigger point injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid pneumothorax when injecting trigger points in proximity to the underlying pleural space. The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators believe that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as amitriptyline and nortriptyline are good first choices and should be given as a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow. Pregabalin and milnacipran have also been shown to be effective in the management of fibromyalgia and may be worth a try if the condition fails to respond to more established treatments.

SUGGESTED READINGS Baldry P: Acupuncture treatment of fibromyalgia and myofascial pain. In Chaitow L, editor: Fibromyalgia syndrome, ed 3, Oxford, 2010, Churchill Livingstone, pp 145–159. Ge HY, Nie H, Madeleine P, et al: Contribution of the local and referred pain from active myofascial trigger points in fibromyalgia syndrome, Pain 147: 233–240, 2009. Ge HY, Wang Y, Danneskiold-Samsøe B, et al: The predetermined sites of examination for tender points in fibromyalgia syndrome are frequently associated with myofascial trigger points, J Pain 11:644–651, 2010. Hains G, Descarreaux M, Hains F: Chronic shoulder pain of myofascial origin: a randomized clinical trial using ischemic compression therapy, J Manipulative Physiol Ther 33:362–369, 2010. LeBlanc KE, LeBlanc LL: Musculoskeletal disorders, Prim Care 37:389–406, 2010. Leland JM, Ciccotti MG, Cohen SB, et al: Teres major injuries in two professional baseball pitchers, J Shoulder Elbow Surg 18:e1–e5, 2009. Partanen JV, Ojala TA, Arokoski JP: Myofascial syndrome and pain: a neurophysiological approach, Pathophysiology 17:19–28, 2010.

Chapter 30 BICIPITAL TENDON INJECTION

Indications and Clinical Considerations The musculotendinous unit of the shoulder joint is susceptible to the development of tendinitis for several reasons. First, the joint is subjected to a wide range of motions that are often repetitive. Second, the space in which the musculotendinous unit functions is restricted by the coracoacromial arch, making impingement a likely possibility with extreme movements of the joint. Third, the blood supply to the musculotendinous unit is poor, making the healing of microtrauma more difficult. All of these factors can contribute to tendinitis of one or more of the tendons of the shoulder joint. Calcium deposition and bone spurs around the tendon may occur if the inflammation continues, making subsequent treatment more difficult (Figure 30-1). Tendinitis of the biceps tendon frequently coexists with bursitis of the associated bursae of the shoulder joint, creating additional pain and functional disability. The tendons of the long and short heads of the biceps, either alone or together, are particularly prone to the development of tendinitis, which is known as bicipital tendinitis. The cause of this syndrome is usually, at least in part, impingement on the

biceps tendons at the coracoacromial arch. The onset of bicipital tendinitis is usually acute, occurring after overuse or misuse of the shoulder joint. Inciting factors may include activities such as trying to start a recalcitrant lawn mower, practicing an overhead tennis serve, or overaggressive follow-through when driving golf balls. The pain of bicipital tendinitis is constant, severe, and localized in the anterior shoulder over the bicipital groove. A “catching” sensation also may accompany the pain. Significant sleep disturbance is often reported. The patient may attempt to splint the inflamed tendons by internal rotation of the humerus, which moves the biceps tendon from beneath the coracoacromial arch. Patients with bicipital tendinitis exhibit a positive Yergason sign, which is production of pain on active supination of the forearm against resistance with the elbow flexed at a right angle (Figure 30-2). Bursitis often accompanies bicipital tendinitis. In addition to the just-described pain, patients with bicipital tendinitis often experience a gradual decrease in functional ability with decreasing shoulder range of motion, making simple everyday tasks, such as hair combing, fastening a bra, or reaching overhead, difficult. With continued disuse, muscle wasting may occur and a frozen shoulder may develop.

A

C

B

D

Figure 30-1  Degenerative disease of the shoulder: bicipital groove enthesophytes. A and B, Medial wall enthesophyte. Photograph (A) and radiograph (B) reveal a large bone enthesophyte (arrows) arising from the medial wall of the intertubercular sulcus at the level of attachment of the transverse humeral ligament. C and D, Enthesophyte in the bicipital floor. In a different specimen, note the small bone enthesophyte (arrows) arising from the floor of the intertubercular sulcus. (A and B from Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders; C and D from Cone RO, Danzig L, Resnick D, Goldman AB: The bicipital groove: radiographic, anatomic, and pathologic study, AJR Am J Roentgenol 141:781, 1983. Copyright 1983, American Roentgen Ray Society.)

83

84        SECTION 2  •  Shoulder

Plain radiographs are indicated for all patients with shoulder pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and ultrasound of the shoulder are indicated if a tendon rupture is suspected and to help identify tendinitis (Figure 30-3). The injection technique presented later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy

Figure 30-2  Yergason test for bicipital tendinitis. (From Waldman SD: Physical diagnosis of pain, ed 2, Philadelphia, 2010, Saunders.)

The biceps tendon, along with conjoined tendons of the rotator cuff, aids in the stability of the shoulder joint. The biceps muscle, which is innervated by the musculocutaneous nerve, supinates the forearm and flexes the elbow joint. The biceps muscle has a long and a short head (Figure 30-4). The long head has its origin in the supraglenoid tubercle of the scapula, and the short head has its origin from the tip of the coracoid process of the scapula. The long head exits the shoulder joint via the bicipital groove, where it is susceptible to tendinitis. The long head is joined by the short head in the middle portion of the upper arm. The insertion of the biceps muscle is into the posterior portion of the radial tuberosity. The biceps muscle and tendons are susceptible to trauma and to wear and tear from overuse and misuse, as mentioned previously. If the damage becomes severe enough, the tendon of the long head of the biceps can rupture, leaving the patient with a telltale “Popeye” biceps (Figure 30-5). This deformity can be accentuated by having the patient perform the Ludington maneuver, which is having the patient place his or her hands behind the head and flex the biceps muscle.

+ +

Medial

Lateral

A

Proximal

Distal

B

+ +

+ +

Distal

C

Proximal

Proximal

Distal

D

Figure 30-3  A, Presence of hypoechoic thickening around the tendon in the biceps tendon sheath (arrow), noncompressible, representing synovial hypertrophy. B, Sagittal view (between the + symbols). C, Hyperechoic thickening of biceps tendon sheath (between the + symbols) signifying synovial hypertrophy. D, Image of hypoechoic thickening around the tendon in the biceps tendon sheath, compressible, reflecting presence of synovial fluid (between the + symbols). (From Chen HS, Lin SH, Hsu YH, et al: A comparison of physical examinations with musculoskeletal ultrasound in the diagnosis of biceps long head tendinitis, Ultrasound Med Biol 37:1392–1398, 2011.)

30  •  Bicipital Tendon Injection        85

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position. The arm is then externally rotated approximately 45 degrees. The coracoid process then is identified anteriorly. Just lateral to the coracoid process is

Biceps brachii long head Biceps brachii short head

the lesser tuberosity. The lesser tuberosity is more easily palpated if the arm is passively rotated. The point overlying the tuberosity is marked with a sterile marker. Proper preparation with antiseptic solution of the skin overlying the anterior shoulder is carried out. A sterile syringe containing 1.0 mL of 0.33% preservative-free bupivacaine and 40  mg of methylprednisolone is attached to a 1½-inch, 33-gauge needle using strict aseptic technique. With strict aseptic technique, the previously marked point is palpated and the insertion of the bicipital tendon is reidentified with the gloved finger. The needle is then carefully advanced at this point through the skin and subcutaneous tissues and underlying tendon until it impinges on bone (Figure 30-6). The needle is then withdrawn 1 to 2 mm out of the periosteum of the humerus, and the contents of the syringe are gently injected. There should be slight resistance to injection. If no resistance is encountered, the needle tip is either in the joint space itself or the tendon is ruptured. If there is significant resistance to injection, the needle tip is probably in the substance of a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is followed. Trauma to the bicipital tendon from the injection itself remains an ever-present possibility. Tendons that are highly inflamed or previously damaged are subject to rupture if they are directly injected (see Figure 30-5). The risk of this complication can be greatly decreased if the clinician uses gentle technique and stops injecting immediately if significant resistance to injection is encountered. Approximately 33% of patients note a transient increase in pain after this injection technique; the patient should be warned of this. Figure 30-4  The biceps muscle has a long and a short head, both of which are susceptible to tendinitis.

Frayed and ruptured biceps brachii long head

Tendon frayed and inflamed

Carrico & Shavell

Figure 30-5  Patients with rupture of the long head of the biceps will demonstrate a positive “Popeye” deformity when the biceps muscle is actively flexed.

Figure 30-6  Care must be taken not to inject directly into the damaged tendon or it may rupture.

86        SECTION 2  •  Shoulder

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to the just-described causes of shoulder pain. Coexistent bursitis and arthritis also may contribute to shoulder pain and may require additional treatment with a more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for shoulder pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Karistinos A, Paulo LE: Anatomy and function of the tendon of the long head of the biceps muscle, Oper Tech Sports Med 15:2–6, 2007. Ott JW, Clancy WG Jr, Wilk KE: Soft tissue injuries of the shoulder. In Wilk KE, Reinold MM, Andrews JR, editors: The athlete’s shoulder, ed 2, Philadelphia, 2009, Churchill Livingstone, pp 283–292. Patton WC, McCluskey GM 3rd: Biceps tendinitis and subluxation, Clin Sports Med 20:505–529, 2001. Travis RD, Doane R, Burkhead WZ Jr: Tendon ruptures about the shoulder, Orthop Clin North Am 31:313–330, 2000. Waldman SD: Bicipital tendinitis. In Atlas of common pain syndromes, ed 2, Philadelphia, 2008, Saunders, pp 84–86.

Chapter 31 INJECTION TECHNIQUE FOR SUBACROMIAL IMPINGEMENT SYNDROME Indications and Clinical Considerations Patients with subacromial impingement syndrome have diffuse shoulder pain with an associated feeling of weakness combined with loss of range of motion. The pain is often worse at night; patients often report that they are unable to sleep on the affected shoulder. Although subacromial impingement syndrome can occur as a result of acute trauma, the usual clinical presentation is more insidious without a clear-cut history of trauma to the affected shoulder. Untreated, subacromial impingement syndrome can lead to progressive tendinopathy of the rotator cuff as well as gradually increasing shoulder instability and functional disability. In patients over 50 years of age, progression of impingement often leads to rotator cuff tear. The patient with subacromial impingement syndrome will report increasing shoulder pain with any activities that abduct and/or forward flex the shoulder, such as putting in a lightbulb or reaching for dishes in a cabinet above shoulder height. Patients with subacromial impingement syndrome will demonstrate a positive Neer test result. The Neer test is performed by having the patient assume a sitting position; then the examiner applies firm forward pressure on the patient’s scapula and simultaneously raises the patient’s arm to an overhead position. The Neer test result is considered positive when the patient exhibits pain or apprehension when the arm moves about 60 degrees. Although not completely diagnostic of subacromial impingement syndrome, a positive Neer test result should prompt the examiner to obtain a magnetic resonance imaging (MRI) scan of the affected shoulder to further clarify and strengthen the diagnosis. MRI of the shoulder provides the clinician with the best information regarding any disease of the shoulder. MRI is highly accurate and helps to identify abnormalities that may put the patient at risk for continuing damage to the rotator cuff and the humeral head (Figure 31-1). MRI of the shoulder will also help the clinician rule out unsuspected disease that may harm the patient, such as primary and metastatic tumors of the shoulder joint and surrounding structures. In patients who cannot undergo MRI scanning, such as a patient with a pacemaker, computed tomography is a reasonable second choice. Radionuclide bone scanning and plain radiography are indicated if fracture or bony abnormality such as metastatic disease is considered in the differential diagnosis. Screening laboratory testing consisting of complete blood cell count, erythrocyte sedimentation rate, and automated blood chemistry testing should be performed if the diagnosis of subacromial impingement syndrome is in question. Arthrocentesis of the glenohumeral joint may be indicated if septic arthritis or crystal arthropathy is suspected.

Subacromial impingement syndrome is a clinical diagnosis that is supported by a combination of clinical history, physical examination, radiography, and MRI. Pain syndromes that may mimic subacromial impingement syndrome include subacromial bursitis, tendinopathy and tendonitis of the rotator cuff, calcification and thickening of coracoacromial ligament, and arthritis affecting any of the shoulder joints. Adhesive capsulitis or frozen shoulder may confuse the diagnosis, as may idiopathic brachial plexopathy (Parsonage-Turner syndrome). The presence of primary and metastatic tumors of the shoulder and surrounding structures remains an ever-present possibility and should always remain as part of the differential diagnosis of patients with shoulder pain.

Clinically Relevant Anatomy The subacromial space lies directly inferior to the acromion, the coracoid process, the acromioclavicular joint, and the coracoacromial ligament. Lubricated by the subacromial bursa, the subacromial space in health is narrow, and the anatomic structures surrounding it are responsible for maintaining both static and dynamic shoulder stability. The space between the acromion and the superior aspect of the humeral head is called the impingement interval, and abduction of the arm will further narrow the space (Figure 31-2). Any pathologic condition that further narrows this space (e.g., osteophyte, abnormal acromial anatomy, ligamentous calcification, or congenital defects of the acromion) will increase the incidence of impingement (Table 31-1). Much as the congenital anatomic variant of the trefoil spinal canal is associated with a statistically significantly higher incidence of spinal stenosis, there are several common normal anatomic variants of the acromion that often contribute to the development of subacromial impingement syndrome. These include type 2 and type 3 acromia (Figure 31-3). Whereas the “normal” type 1 acromion is relatively flat, the type 2 acromion curves downward, and the type 3 acromion hooks downward in a shape reminiscent of a scimitar. The downward curves of the type 2 and type 3 acromia markedly narrow the subacromial space (Figure 31-4). In addition to these anatomic variations, a congenitally unfused acromial apophysis termed os acromiale is often associated with subacromial impingement syndrome (see Chapter 32).

Technique The goals of this injection technique are explained to the patient. The patient is placed in the sitting position, and proper preparation with antiseptic solution of the skin overlying the posterior shoulder and distal clavicle is carried out. A sterile syringe containing 1.0 mL of 0.25% preservative-free bupivacaine and 40 mg of 87

88        SECTION 2  •  Shoulder

a a

c

A

B

C Figure 31-1  Shoulder external subacromial impingement syndrome: magnetic resonance (MR) imaging abnormalities. A, On a sagittal oblique T1-weighted (TR/TE, 800/20) spin-echo MR image, a subacromial enthesophyte (solid arrow) containing marrow projects from the anterior surface of the acromion (a) toward the coracoid process (c). Note the enthesophyte’s relationship to the coracoacromial ligament (open arrows) and supraspinatus tendon (arrowhead). B, In a second patient, a sagittal oblique T1-weighted (TR/TE, 800/12) spin-echo MR image shows a large subacromial enthesophyte (arrows). The acromion (a) is indicated. C, In a third patient, a coronal oblique intermediate-weighted (TR/TE, 2000/30) spin-echo MR image reveals the flattened contour and low signal intensity characteristic of a subacromial enthesophyte (arrows). Also observe osteoarthritis of the acromioclavicular joint manifested as osteophytosis (arrowhead) and an elevated position of the humeral head, indicative of a rotator cuff tear. The tear was demonstrated better on other MR images (not shown). (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique the top of the acromion is identified, and at a point approximately 1 inch posteriorly the acromioclavicular joint space is identified. The needle is then carefully advanced through the skin and subcutaneous tissues medially at a 20-degree angle through the joint capsule into the joint (Figure 31-5). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected slightly more medially. After the joint space has been entered, the contents of the syringe are gently injected. There should be some resistance to injection, because the joint space is small and the joint capsule is dense. If significant resistance is encountered, the needle is probably in a ligament and should be advanced or withdrawn slightly into the joint space until the injection proceeds with only limited resistance. If no resistance is encountered on injection, the joint space is probably not intact and MRI of the joint is recommended. The needle is then

removed and a sterile pressure dressing and ice pack are placed at the injection site. In patients in whom the anatomic landmarks are difficult to identify, fluoroscopic or ultrasound guidance for needle placement may be beneficial (Figures 31-6, 31-7, and 31-8).

Side Effects and Complications Failure to correctly diagnose subacromial impingement syndrome will put the patient at risk for missed diagnosis of other syndromes that may result in ongoing damage to the shoulder or lead to overlooked disease in this anatomic region that may harm the patient, such as Pancoast tumor or primary or metastatic tumors of the shoulder. MRI is indicated for all patients thought to have subacromial impingement syndrome, and aggressive treatment of surgically correctible causes of such impingement is generally indicated sooner rather than later to avoid ongoing irreversible shoulder damage.

31  •  Injection Technique for Subacromial Impingement Syndrome        89 Acromioclavicular ligament

Coracoclavicular ligament

Coracoacromial ligament Inflamed supraspinatus tendon Subacromial bursa

Biceps brachii m. Long head Short head

Subscapularis m.

Subacromial bursa impinged

Figure 31-2  Anatomy of the subacromial space and impingement of structures within.

TABLE 31-1

Causes of Subacromial Impingement Syndrome • Subacromial osteophytes • Rotator cuff tears • Abnormal acromial anatomy • Type 2 acromion • Type 3 acromion • Congenital acromial defect (e.g., os acromiale) • Acquired acromial defect (e.g., displaced fracture) • Inflammatory arthritis of the acromioclavicular joint • Abnormalities of the superior aspect of the humeral head • Glenohumeral joint instability • Crystal arthropathies of the acromioclavicular joint • Frozen shoulder (adhesive capsulitis) • Tendinopathy of the coracoacromial ligament

Type I

Type II

Type III Figure 31-4  Lateral downsloping acromion. Coronal oblique PDweighted fat-suppressed image in a patient with clinical subacromial impingement shows lateral downsloping of the acromion (arrow) narrowing the subacromial space. (From Fitzpatrick D, Walz DM: Shoulder MR imaging normal variants and imaging artifacts, Magn Reson Imaging Clin N Am 18:615–632, 2010.)

Figure 31-3  Anatomic variants of the acromion.

90        SECTION 2  •  Shoulder

Posterior acromion

Humerus

Figure 31-5  Injection of subacromial bursa and rotator cuff tendons (posterior subacromial approach). (From Beuerlein MJS, McKee MD, Fam AG: The shoulder. In Lawry GV, Kreder HJ, Hawker GA, Jerome D, editors: Fam’s musculoskeletal examination and joint injection techniques, ed 2, Philadelphia, 2010, Mosby, pp 7–20.)

+ *

Figure 31-6  Proper ultrasound transducer position for subacromial injection.

Figure 31-7  Fluid-filled subacromial bursa (arrowheads). Underlying supraspinatus is thickened and tendinopathic (cross). The asterisk denotes the humeral head.

Figure 31-8  Ultrasound-guided needle placement into subacromial space. Note artifact from needle.

31  •  Injection Technique for Subacromial Impingement Syndrome        91

Clinical Pearls The musculotendinous unit of the shoulder joint is susceptible to the development of tendinitis for several reasons. First, the joint is subjected to a wide range of motions that are often repetitive in nature. Second, the space in which the musculotendinous unit functions is restricted by the coracoacromial arch, making impingement a likely possibility with extreme movements of the joint. Third, the blood supply to the musculotendinous unit is poor, making healing of microtrauma more difficult. All of these factors can contribute to tendinitis of one or more of the tendons of the shoulder joint. Calcium deposition around the tendon may occur if the inflammation continues, making subsequent treatment more difficult. Tendinitis of the musculotendinous unit of the shoulder frequently coexists with bursitis of the associated bursae of the shoulder joint, creating additional pain and functional disability. Patients with untreated subacromial impingement syndrome will continue to experience pain and functional disability, and the condition may well continue to cause ongoing irreversible shoulder damage culminating in damage to the humeral head and rotator cuff tear. Initial treatment of the pain and functional disability associated with subacromial impingement syndrome should include a combination of nonsteroidal antiinflammatory agents or cyclooxygenase-2 (COX-2) inhibitors and gentle physical therapy. The local application of heat and cold may also be beneficial. For patients who do not respond to these treatment modalities, injection of the subacromial space with local anesthetic and steroid is a reasonable next step while performing MRI and other appropriate testing to further clarify the working clinical diagnosis. The use of physical therapy, including gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for shoulder pain. Vigorous exercises should be avoided because they will exacerbate the patient’s symptoms. For patients who do not respond to the previously mentioned treatment modalities or who have radiographically demonstrated anatomic subacromial impingement that is producing ongoing damage to the rotator cuff, open or arthroscopic acromioplasty is required.

SUGGESTED READINGS Edwards SL, Bell JE, Bigliani LU: Subacromial impingement. In Wilk KE, Reinold MM, Andrews JR, editors: The athlete’s shoulder, ed 2, Philadelphia, 2009, Churchill Livingstone, pp 115–122. Lewis J, Green A, Yizhat Z, Pennington D: Subacromial impingement syndrome: has evolution failed us? Physiotherapy 87:191–198, 2001. Lewis JS, Green AS, Dekel S: The aetiology of subacromial impingement syndrome, Physiotherapy 87:458–469, 2001. Michener LA, Walsworth MK, Doukas WC, Murphy KP: Reliability and diagnostic accuracy of 5 physical examination tests and combination of tests for subacromial impingement, Arch Phys Med Rehabil 90:1898–1903, 2009. Neagle CE, Bennett JB: Subacromial anatomy and biomechanics related to the impingement syndrome, Oper Tech Sports Med 2:82–88, 1994.

Chapter 32 INJECTION TECHNIQUE FOR OS ACROMIALE PAIN SYNDROME Indications and Clinical Considerations Patients with os acromiale pain syndrome will have diffuse shoulder pain with an associated feeling of weakness combined with loss of range of motion. The pain is often worse at night; patients often report that they are unable to sleep on the affected shoulder. The clinical presentation is usually insidious without a clear-cut history of trauma to the affected shoulder. Untreated, os acromiale pain syndrome can lead to progressive tendinopathy of the rotator cuff as well as gradually increasing shoulder instability and functional disability (Figure 32-1). In patients over 50 years of age, progression of impingement often leads to rotator cuff tear. The patient with os acromiale pain syndrome will report increasing shoulder pain with any activities that abduct and/or forward flex the shoulder, such as putting in a lightbulb or reaching for dishes in a cabinet above shoulder height. Patients with os acromiale pain syndrome will demonstrate a positive Neer or Hawkins test result. Although not completely diagnostic of subacromial impingement syndrome, a positive Neer or Hawkins test result should prompt the examiner to obtain a magnetic resonance imaging (MRI) scan of the affected shoulder to further clarify and strengthen the diagnosis. MRI of the shoulder provides the clinician with the best information regarding any disease of the shoulder. MRI is highly accurate in the identification of os acromiale and helps to identify abnormalities that may put the patient at risk for continuing damage to the rotator cuff and the humeral head (see Figure 31-1). MRI of the shoulder will also help the clinician rule out unsuspected disease that may harm the patient, such as primary and metastatic tumors of the shoulder joint and surrounding structures. In patients who cannot undergo MRI scanning, such as a patient with a pacemaker, computed tomography is a reasonable second choice. Radionuclide bone scanning and plain radiography are indicated if fracture or bony abnormality such as metastatic disease is considered in the differential diagnosis. Screening laboratory testing consisting of complete blood cell count, erythrocyte sedimentation rate, and automated blood chemistry testing should be performed if the diagnosis of subacromial impingement syndrome is in question. Arthrocentesis of the glenohumeral joint may be indicated if septic arthritis or crystal arthropathy is suspected. Os acromiale pain syndrome is a clinical diagnosis that is supported by a combination of clinical history, physical examination, radiography, and MRI. Pain syndromes that may mimic os acromiale pain syndrome include subacromial impingement syndrome, subacromial bursitis, tendinopathy and tendonitis of the 92

rotator cuff, calcification and thickening of coracoacromial ligament, and arthritis affecting any of the shoulder joints. Adhesive capsulitis or frozen shoulder may confuse the diagnosis, as may idiopathic brachial plexopathy (Parsonage-Turner syndrome). The presence of primary and metastatic tumors of the shoulder and surrounding structures remains an ever-present possibility and should always remain as part of the differential diagnosis of patients with shoulder pain.

Clinically Relevant Anatomy The subacromial space lies directly inferior to the acromion, the coracoid process, the acromioclavicular joint, and the coracoacromial ligament. Lubricated by the subacromial bursa, the subacromial space in health is narrow, and the anatomic structures surrounding it are responsible for maintaining both static and dynamic shoulder stability. The space between the acromion and the superior aspect of the humeral head is called the impingement interval, and abduction of the arm will further narrow the space (see Figure 31-2). Any pathologic condition that further narrows this space (e.g., osteophyte, abnormal acromial anatomy, ligamentous calcification, or congenital defects of the acromion) will increase the incidence of impingement (see Table 31-1). Os acromiale is a congenital defect that is a result of the failure of the distal ossification center of the acromion. The failure of the distal acromion to fuse essentially results in a second acromial joint, which can foster shoulder instability and impingement. Much as the congenital anatomic variant of the trefoil spinal canal is associated with a statistically significantly higher incidence of spinal stenosis, there are several common normal anatomic variants of the acromion that often contribute to the development of subacromial impingement syndrome. These include type 2 and type 3 acromia (see Figure 31-3). Whereas the “normal” type 1 acromion is relatively flat, the type 2 acromion curves downward, and the type 3 acromion hooks downward in a shape reminiscent of a scimitar. The downward curves of the type 2 and type 3 acromia markedly narrow the subacromial space (see Figure 31-4). In addition to these anatomic variations, a congenitally unfused acromial apophysis termed os acromiale is often associated with subacromial impingement syndrome ­(Figure 32-1).

Technique The goals of this injection technique are explained to the patient. The patient is placed in the sitting position, and proper

32  •  Injection Technique for Os Acromiale Pain Syndrome        93 Unfused distal acromion consistent with os acromiale

Inflamed contents of subacromial space

Figure 32-1  Untreated os acromiale can lead to significant shoulder disease, including tendinopathy, shoulder irritability, and bursitis.

preparation with antiseptic solution of the skin overlying the ­posterior shoulder and distal clavicle is carried out. A sterile syringe containing 1.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique the top of the acromion is identified, and at a point approximately 1 inch posteriorly the acromioclavicular joint space is identified. The needle is then carefully advanced through the skin and subcutaneous tissues medially at a 20-degree angle through the joint capsule into the joint (see Figure 31-5). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected slightly more medially. After the joint space has been entered, the contents of the syringe are gently injected. There should be some resistance to injection, because the joint space is small and the joint capsule is dense. If significant resistance is encountered, the needle is probably in a ligament and should be advanced or withdrawn slightly into the joint space until the injection proceeds with only limited resistance. If no resistance is encountered on injection, the joint space is probably not intact and MRI of the joint is recommended. The needle is then removed and a sterile pressure dressing and ice pack are placed at the injection site. In patients in whom the anatomic landmarks are difficult to identify, fluoroscopic or ultrasound guidance for needle placement may be beneficial.

Side Effects and Complications Failure to correctly diagnose os acromiale pain syndrome will put the patient at risk for missed diagnosis of other syndromes that may result in ongoing damage to the shoulder or lead to overlooked disease in this anatomic region that may harm the patient, such as Pancoast tumor or primary or metastatic tumors of the shoulder. MRI is indicated in all patients thought to have os acromiale pain syndrome, and aggressive treatment of surgically correctible causes of such impingement is generally indicated sooner rather than later to avoid ongoing irreversible shoulder damage.

Clinical Pearls The musculotendinous unit of the shoulder joint is susceptible to the development of tendinitis for several reasons. First, the joint is subjected to a wide range of motions that are often repetitive in nature. Second, the space in which the musculotendinous unit functions is restricted by the coracoacromial arch, making impingement a likely possibility with extreme movements of the joint. Third, the blood supply to the musculotendinous unit is poor, making healing of microtrauma more difficult. All of these factors can contribute to tendinitis of one or more of the tendons of the shoulder joint. Calcium deposition around the tendon may occur if the inflammation continues, making subsequent treatment more difficult. Tendinitis of the musculotendinous unit of the shoulder frequently coexists with bursitis of the associated bursae of the shoulder joint, creating additional pain and functional disability. Patients with untreated os acromiale pain syndrome will continue to experience pain and functional disability, and the condition may well continue to cause ongoing irreversible shoulder damage culminating in damage to the humeral head and rotator cuff tear. Initial treatment of the pain and functional disability associated with os acromiale pain syndrome should include a combination of nonsteroidal antiinflammatory agents or cyclooxygenase-2 (COX-2) inhibitors and gentle physical therapy. The local application of heat and cold may also be beneficial. For patients who do not respond to these treatment modalities, injection of the subacromial space with local anesthetic and steroid is a reasonable next step while performing MRI and other appropriate testing to further clarify the working clinical diagnosis. The use of physical therapy, including gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for shoulder pain. Vigorous exercises should be avoided because they will exacerbate the patient’s symptoms. For patients who do not respond to the previously mentioned treatment modalities or who have radiographically demonstrated anatomic subacromial impingement that is producing ongoing damage to the rotator cuff, open or arthroscopic acromioplasty is required.

94        SECTION 2  •  Shoulder SUGGESTED READINGS Edwards SL, Bell JE, Bigliani LU: Subacromial impingement. In Wilk KE, Reinold MM, Andrews JR, editors: The athlete’s shoulder, ed 2, Philadelphia, 2009, Churchill Livingstone, pp 115–122. Lewis J, Green A, Yizhat Z, Pennington D: Subacromial impingement syndrome: has evolution failed us? Physiotherapy 87:191–198, 2001. Lewis JS, Green AS, Dekel S: The aetiology of subacromial impingement syndrome, Physiotherapy 87:458–469, 2001.

Michener LA, Walsworth MK, Doukas WC, Murphy KP: Reliability and diagnostic accuracy of 5 physical examination tests and combination of tests for subacromial impingement, Arch Phys Med Rehabil 90:1898–1903, 2009. Neagle CE, Bennett JB: Subacromial anatomy and biomechanics related to the impingement syndrome, Oper Tech Sports Med 2:82–88, 1994.

Chapter 33 INJECTION TECHNIQUE FOR BICEPS BRACHII SYNDROME Indications and Clinical Considerations The biceps brachii muscle is susceptible to the development of myofascial pain syndrome. Prolonged lifting of heavy objects held close to the body or repetitive activities that require repeated flexion of the upper extremity such as repeated use of exercise weight may cause the development of biceps brachii syndrome. The biceps brachii muscle is also susceptible to the development of myofascial pain after blunt trauma to the muscle, such as during blunt trauma to the humerus and anterior elbow and forearm in motor vehicle accidents or from sports injuries such as spearing injuries in football. Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body. The sine qua non of myofascial pain syndrome is the finding of myofascial trigger points on physical examination. Although these trigger points generally are localized to the regional part of the body affected, the pain of myofascial pain syndrome often is referred to other anatomic areas. This referred pain often is misdiagnosed or attributed to other organ systems, thereby leading to extensive evaluations and ineffective treatment. Patients with myofascial pain syndrome involving the biceps brachii often have referred pain into the ipsilateral upper extremity. The trigger point is the pathognomonic lesion of myofascial pain and is thought to be a result of microtrauma to the affected muscles. This pathologic lesion is characterized by a local point of exquisite tenderness in affected muscle. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain but also referred pain. In addition to this local and referred pain, there often is an involuntary withdrawal of the stimulated muscle, called a “jump sign.” This jump sign also is characteristic of myofascial pain syndrome. Patients with biceps brachii syndrome will exhibit trigger points in the lower third of the bellies of the muscle (Figure 33-1). Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. In spite of this consistent physical finding in patients with myofascial pain syndrome, the pathophysiology of the myofascial trigger point remains elusive, although many theories have been advanced. Common to all of these theories is the belief that trigger points are a result of microtrauma to the affected muscle. This microtrauma may occur as a single injury to the affected muscle or as a result of repetitive microtrauma or chronic deconditioning of the agonist and antagonist muscle unit. In addition to muscle trauma, a variety of other factors seem to predispose the patient to develop myofascial pain syndrome. The weekend athlete who subjects his or her body to unaccustomed

physical activity may develop myofascial pain syndrome. The poor posture of someone sitting at a computer keyboard or watching television has also been implicated as a predisposing factor to the development of myofascial pain syndrome. Previous injuries may result in abnormal muscle function and predispose to the subsequent development of myofascial pain syndrome. All of these predisposing factors may be intensified if the patient also has poor nutritional status or coexisting psychological or behavioral abnormalities, including chronic stress and depression. The biceps brachii muscle seems to be particularly susceptible to stressinduced myofascial pain syndrome.

Biceps m. Referred pain Trigger point

Figure 33-1  Patients with biceps brachii syndrome will often experience referred pain into the ipsilateral upper extremity.

95

96        SECTION 2  •  Shoulder

Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or may occur in conjunction with other painful conditions, including radiculopathy and chronic regional pain syndromes. Psychological or behavioral abnormalities, including depression, frequently coexist with the muscle abnormalities associated with myofascial pain syndrome. Treatment of these psychological and behavioral abnormalities must be an integral part of any successful treatment plan for myofascial pain syndrome.

Clinically Relevant Anatomy The biceps brachii muscle helps to stabilize the elbow as well as supinate the forearm and, in the supine position, flex the forearm. The biceps brachii muscle has two heads, with the origin of the short head at the tip of the coracoid process of the scapula and the long head at the supraglenoid tubercle of the scapula (see Figure 33-1). The muscle inserts onto the tuberosity of the radius and fascia of the forearm via the bicipital aponeurosis. The biceps brachii muscle is innervated by the musculocutaneous nerve.

Technique Careful preparation of the patient before trigger point injection helps to optimize results. Trigger point injections are directed at the primary trigger point rather than in the area of referred pain. It should be explained to the patient that the goal of trigger point injection is to block the trigger of the persistent pain and thus, it is hoped, provide long-lasting relief. It is important that the patient understand that for most patients with myofascial pain syndrome, more than one treatment modality is required for optimal pain relief. The use of the recumbent or lateral position when identifying and marking trigger points, as well as when performing the actual trigger point injection, helps decrease the incidence of vasovagal reactions. The skin overlying the trigger point to be injected should always be prepared with antiseptic solution before injection to avoid infection. After the goals of trigger point injection have been explained to the patient and proper preparation of the patient has been carried out, the trigger point to be injected is reidentified by palpation with the sterilely gloved finger. A syringe containing 10 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 25- or 27-gauge needle of a length adequate to reach the trigger point. Except for the muscles of posture in the low back, a 1½-inch needle will be adequate. A volume of 0.5 to 1.0 mL of solution is then injected into each trigger point (see Figure 33-1). A series of two to five treatment sessions may be required to completely abolish the trigger point; the patient should be informed of this.

Side Effects and Complications The proximity to the spinal cord and exiting cervical nerve roots makes it imperative that this procedure be carried out only by

those well versed in the regional anatomy and experienced in ­performing interventional pain management techniques. Given the proximity of the brain and brain stem, ataxia caused by vascular uptake of local anesthetic after trigger point injection is not an uncommon occurrence. Many patients also note a transient increase in pain after injection of trigger points in the biceps ­brachii muscle.

Clinical Pearls Trigger point injections are extremely safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of trigger point injection are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after trigger point injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators believe that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as amitriptyline and nortriptyline are good first choices and should be given as a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow. Pregabalin and milnacipran have also been shown to be effective in the management of fibromyalgia and may be worth a try if the condition fails to respond to more established treatments.

SUGGESTED READINGS Baldry P: Acupuncture treatment of fibromyalgia and myofascial pain. In Chaitow L, editor: Fibromyalgia syndrome, ed 3, Oxford, 2010, Churchill Livingstone, pp 145–159. Ge HY, Nie H, Madeleine P, et al: Contribution of the local and referred pain from active myofascial trigger points in fibromyalgia syndrome, Pain 147:233–240, 2009. Ge HY, Wang Y, Danneskiold-Samsøe B, et al: The predetermined sites of examination for tender points in fibromyalgia syndrome are frequently associated with myofascial trigger points, J Pain 11:644–651, 2010. Hains G, Descarreaux M, Hains F: Chronic shoulder pain of myofascial origin: a randomized clinical trial using ischemic compression therapy, J Manipulative Physiol Ther 33:362–369, 2010. Landin D, Myers J, Thompson M, Castle R, Porter J: The role of the biceps brachii in shoulder elevation, J Electromyogr Kinesiol 18:270–275, 2008. LeBlanc KE, LeBlanc LL: Musculoskeletal disorders, Prim Care 37:389–406, 2010. Partanen JV, Ojala TA, Arokoski JP: Myofascial syndrome and pain: a neurophysiological approach, Pathophysiology 17:19–28, 2010.

Chapter 34 INJECTION TECHNIQUE FOR TRICEPS BRACHII SYNDROME Indications and Clinical Considerations The triceps brachii muscle is susceptible to the development of myofascial pain syndrome. Prolonged activities that require holding the elbow in front of the chest such as driving or knitting or repetitive strenuous activities requiring forearm extension such as pushups or the overuse of exercise equipment may result in triceps brachii syndrome. The triceps brachii muscle is also susceptible to the development of myofascial pain after blunt trauma to the muscle such as during the blunt trauma to the humerus sustained in motor vehicle accidents or from sports injuries such as spearing injuries in football. Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body. The sine qua non of myofascial pain syndrome is the finding of myofascial trigger points on physical examination. Although these trigger points generally are localized to the regional part of the body affected, the pain of myofascial pain syndrome often is referred to other anatomic areas. This referred pain often is misdiagnosed or attributed to other organ systems, thereby leading to extensive evaluations and ineffective treatment. Patients with myofascial pain syndrome involving the triceps brachii often have referred pain into the back of the ipsilateral arm and forearm. The trigger point is the pathognomonic lesion of myofascial pain and is thought to be a result of microtrauma to the affected muscles. This pathologic lesion is characterized by a local point of exquisite tenderness in affected muscle. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain but also referred pain. In addition to this local and referred pain, there often is an involuntary withdrawal of the stimulated muscle, called a “jump sign.” This jump sign also is characteristic of myofascial pain syndrome. Patients with triceps brachii syndrome will exhibit trigger points throughout the triceps muscle (Figure 34-1). Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. In spite of this consistent physical finding in patients with myofascial pain syndrome, the pathophysiology of the myofascial trigger point remains elusive, although many theories have been advanced. Common to all of these theories is the belief that trigger points are a result of microtrauma to the affected muscle. This microtrauma may occur as a single injury to the affected muscle or may occur as a result of repetitive microtrauma or chronic deconditioning of the agonist and antagonist muscle unit. In addition to muscle trauma, a variety of other factors seem to predispose the patient to develop myofascial pain syndrome. The weekend athlete who subjects his or her body to unaccustomed

physical activity may develop myofascial pain syndrome. The poor posture of someone sitting at a computer keyboard or watching television has also been implicated as a predisposing factor to the development of myofascial pain syndrome. Previous injuries may result in abnormal muscle function and predispose to the subsequent development of myofascial pain syndrome. All of these predisposing factors may be intensified if the patient also has poor nutritional status or coexisting psychological or behavioral abnormalities, including chronic stress and depression. The triceps brachii muscle seems to be particularly susceptible to stressinduced myofascial pain syndrome. Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or may occur in conjunction with other painful conditions, including radiculopathy and chronic regional pain syndromes. Psychological or behavioral abnormalities, including depression, frequently coexist with the muscle abnormalities associated with myofascial pain syndrome. Treatment of these psychological and behavioral abnormalities must be an integral part of any successful treatment plan for myofascial pain syndrome.

Clinically Relevant Anatomy The triceps brachii muscle helps stabilize the abducted head of the humerus and serves as the primary extensor of the forearm. The triceps has its origin in three heads, with the long head arising from the infraglenoid tubercle of scapula, the lateral head from the posterior surface of humerus, and the medial head from the posterior surface of the humerus, inferior to the radial groove (see Figure 34-1). The triceps brachii muscle is innervated by the radial nerve.

Technique Careful preparation of the patient before trigger point injection helps to optimize results. Trigger point injections are directed at the primary trigger point rather than in the area of referred pain. It should be explained to the patient that the goal of trigger point injection is to block the trigger of the persistent pain and thus, it is hoped, provide long-lasting relief. It is important that the patient understand that for most patients with myofascial pain syndrome, more than one treatment modality is required for optimal pain relief. The use of the recumbent or lateral position when identifying and marking trigger points as well as when performing the actual trigger point injection helps decrease the incidence of vasovagal reactions. The skin overlying the trigger point to be 97

98        SECTION 2  •  Shoulder

Triceps muscle Trigger point Referred pain

Figure 34-1  Patients with triceps brachii syndrome will often experience pain referred into the ipsilateral forearm.

injected should always be prepared with antiseptic solution before injection to avoid infection. After the goals of trigger point injection have been explained to the patient and proper preparation of the patient has been carried out, the trigger point to be injected is reidentified by palpation with the sterilely gloved finger. A syringe containing 10 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone to be injected is attached to a 25- or 27-gauge needle of a length adequate to reach the trigger point. Except for the muscles of posture in the low back, a 1½-inch needle will be adequate. A volume of 0.5 to 1.0 mL of solution is then injected into each trigger point (see Figure 34-1). A series of two to five treatment sessions may be required to completely abolish the trigger point; the patient should be informed of this.

Side Effects and Complications The proximity to the spinal cord and exiting cervical nerve roots makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing interventional pain management techniques. Given the proximity of the brain and brainstem, ataxia caused by vascular uptake of local anesthetic after trigger point injection is not an uncommon occurrence. Many patients also note a transient increase in pain after injection of trigger points in the triceps brachii muscle.

Clinical Pearls Trigger point injections are extremely safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of trigger point injection are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after trigger point injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators believe that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as amitriptyline and nortriptyline are good first choices and should be given as a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow.

34  •  Injection Technique for Triceps Brachii Syndrome        99 SUGGESTED READINGS Baldry P: Acupuncture treatment of fibromyalgia and myofascial pain. In Chaitow L, editor: Fibromyalgia syndrome, ed 3, Oxford, 2010, Churchill Livingstone, pp 145–159. Ge HY, Nie H, Madeleine P, et al: Contribution of the local and referred pain from active myofascial trigger points in fibromyalgia syndrome, Pain 147: 233–240, 2009. Ge HY, Wang Y, Danneskiold-Samsøe B, et al: The predetermined sites of examination for tender points in fibromyalgia syndrome are frequently associated with myofascial trigger points, J Pain 11:644–651, 2010. Hains G, Descarreaux M, Hains F: Chronic shoulder pain of myofascial origin: a randomized clinical trial using ischemic compression therapy, J Manipulative Physiol Ther 33:362–369, 2010.

Keener JD, Chafik D, Kim HM, et al: Insertional anatomy of the triceps brachii tendon, J Shoulder Elbow Surg 19:399–405, 2010. LeBlanc KE, LeBlanc LL: Musculoskeletal disorders, Prim Care 37:389–406, 2010. Matsuura S, Kojima T, Kinoshita Y: Cubital tunnel syndrome caused by abnormal insertion of triceps brachii muscle, J Hand Surg Br 19:38–39, 1994. Partanen JV, Ojala TA, Arokoski JP: Myofascial syndrome and pain: a neurophysiological approach, Pathophysiology 17:19–28, 2010.

Chapter 35 INJECTION TECHNIQUE FOR ROTATOR CUFF TEAR

Indications and Clinical Considerations Rotator cuff tears frequently occur after seemingly minor trauma to the musculotendinous unit of the shoulder. However, the disease responsible for the tear is usually a long time in the making and is most often the result of ongoing tendinitis. The supraspinatus and infraspinatus muscle tendons are particularly susceptible to the development of tendinitis for several reasons. First, the joint is subjected to a wide range of motions, which are often repetitive. Second, the space in which the musculotendinous unit functions is restricted by the coracoacromial arch, making impingement a likely possibility with extreme movements of the joint. Third, the blood supply to the musculotendinous unit is poor, making healing of microtrauma more difficult. All of these factors can contribute to tendinitis of one or more of the tendons of the shoulder joint. Calcium deposition around the tendon may occur if the inflammation continues, making subsequent treatment more difficult. Tendinitis of the musculotendinous unit of the shoulder frequently coexists with bursitis of the associated bursae of the shoulder joint, creating additional pain and functional disability. This ongoing pain and functional disability can cause the patient to splint the shoulder group, with resultant abnormal movement of the shoulder, which puts additional stress on the rotator cuff. This can lead to further trauma to the rotator cuff. Because rotator cuff tears may occur after seemingly minor trauma, the diagnosis often is delayed. The tear may be either partial or complete, further confusing the diagnosis, although careful physical examination and the use of MRI can help distinguish the two (Figure 35-1). The patient with a rotator cuff tear frequently complains that he or she cannot lift the arm above the level of the shoulder without using the other arm to lift it. On physical examination, the patient has weakness on external rotation if the infraspinatus is involved and weakness in abduction above the level of the shoulder if the supraspinatus is involved. Tenderness on palpation in the subacromial region often is present. Patients with partial rotator cuff tears exhibit loss of the ability to smoothly reach overhead. Patients with complete tears exhibit anterior migration of the humeral head, as well as a complete inability to reach above the level of the shoulder. A positive result of the drop-arm test, which is the inability to hold the arm abducted at the level of the shoulder after the supported arm is released, often is present with compete tears of the rotator cuff (Figure 35-2). The Moseley test for rotator cuff tear, which is performed by having the patient actively abduct the arm to 80 degrees and then adding gentle resistance, which will force the 100

arm to drop if complete rotator cuff tear is present, also will yield a positive result. Passive range of motion of the shoulder is normal, but active range of motion is limited. The pain of a rotator cuff tear is constant and severe and is made worse with abduction and external rotation of the shoulder. Significant sleep disturbance is often reported. The patient may attempt to splint the inflamed subscapularis tendon by limiting medial rotation of the humerus. Bursitis often accompanies rotator cuff tears and may require specific treatment. In addition to the just-mentioned pain, patients with a rotator cuff tear often experience a gradual decrease in functional ability with decreasing shoulder range of motion, making simple everyday tasks such as hair combing, fastening a bra, or reaching overhead quite difficult. With continued disuse, muscle wasting may occur and a frozen shoulder may develop. Plain radiographs are indicated for all patients with shoulder pain. Based on the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and/or ultrasound imaging of the shoulder is indicated if a rotator cuff tear is suspected (see Figure 35-1).

Figure 35-1  Disruption of the rotator cuff. In young persons, routine radiographs typically are normal in patients with acute tears of the rotator cuff. Magnetic resonance imaging (MRI) is a sensitive method for detection of these tears. This oblique coronal T2-weighted (TR/ TE, 1800/90) spin-echo MR image shows fluid of high signal intensity (arrow) at the site of disruption of the supraspinatus tendon. Fluid in the subacromial-subdeltoid bursa is also evident. (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

35  •  Injection Technique for Rotator Cuff Tear        101

POSTERIOR VIEW

Supraspinatus muscle

Infraspinatus muscle torn and frayed Teres minor muscle

ANTERIOR VIEW

Supraspinatus m. torn and frayed Subacromial bursa Subscapularis m.

Figure 35-3  The rotator cuff is made up of the supraspinatus, infraspinatus, teres minor, and subscapularis musculotendinous units. Figure 35-2  A patient with a complete rotator cuff tear will be unable to hold the arm in the abducted position, and it will fall to the patient’s side. The patient will often shrug or hitch the shoulder forward to use the intact muscles of the rotator cuff and the deltoid to keep the arm in the abducted position. (From Waldman SD: Physical diagnosis of pain, Philadelphia, 2005, Saunders.)

Clinically Relevant Anatomy The rotator cuff is made up of the subscapularis, supraspinatus, infraspinatus, and teres minor muscles and associated tendons (Figure 35-3). The function of the rotator cuff is to rotate the arm and to help provide shoulder joint stability along with the other muscles, tendons, and ligaments of the shoulder. A rotator cuff tear usually involves the supraspinatus or infraspinatus musculotendinous unit, but the other muscles of the rotator cuff can also be involved.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the superior shoulder, acromion, and distal clavicle is carried out. A sterile syringe containing 4.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique the lateral edge of the acromion is identified, and at the midpoint of the lateral edge the injection site is identified. At this point the needle is then carefully advanced in a slightly

cephalad trajectory through the skin, subcutaneous tissues, and deltoid muscle beneath the acromion process (see Figure 35-3). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected slightly more inferiorly. After the needle is in place, the contents of the syringe are gently injected. There should be minimal resistance to injection unless calcification of the subacromial bursal sac is present. Calcification of the bursal sac is identified as a resistance to needle advancement with an associated gritty feel. Significant calcific bursitis ultimately may require surgical excision to effect complete relief of symptoms. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. Ultrasound guidance may be useful in patients in whom the anatomic landmarks are hard to identify (Figures 35-4 and 35-5).

Side Effects and Complications The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is followed. Trauma to the rotator cuff from the injection itself remains an ever-present possibility. Tendons that are highly inflamed or previously damaged are subject to rupture if they are directly injected. This could convert a partial rotator cuff tear into a complete tear. The risk of this complication can be greatly decreased if the clinician uses gentle technique and stops injecting immediately if significant resistance to injection is encountered. Approximately 25% of patients note a transient increase in pain after this injection technique; the patient should be warned of this.

102        SECTION 2  •  Shoulder

Clinical Pearls

Figure 35-4  Percutaneous treatment of shoulder calcific tendinitis in the supraspinatus tendon. Reverberation artifacts (arrows) can be observed behind the needle. (From del Cura JL: Ultrasound-guided therapeutic procedures in the musculoskeletal system, Curr Probl Diagn Radiol 37:203–218, 2008.)

This injection technique is extremely effective in the treatment of pain secondary to the rotator cuff tears. This technique is not a substitute for surgery but can be used to palliate the pain of partial tears and complete tears when surgery is not contemplated. Coexistent bursitis and arthritis also may contribute to shoulder pain and may require additional treatment with a more localized injection of local anesthetic and depot corticosteroid. This technique is a safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for shoulder pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms and may lead to complete tendon rupture. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique. With rotator cuff tears, passive range of motion is normal but active range of motion is limited. This is in contradistinction to frozen shoulder, in which both passive and active range of motion are limited. Rotator cuff tear rarely occurs in individuals younger than 40 years of age, except in cases of severe acute trauma to the shoulder.

SUGGESTED READINGS

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* Figure 35-5  Ultrasound image of 79-year-old woman with a full-thickness rotator cuff tear. Crosses mark the ends of the retracted tendon, with debris in the intervening space. The asterisk marks the humeral head.

Bruyn GA, Schmidt WA: How to perform ultrasound-guided injections, Best Pract Res Clin Rheumatol 23:269–279, 2009. Cheng PH, Modir JG, Kim HJ, Narouze S: Ultrasound-guided shoulder joint injections, Tech Reg Anesth Pain Manag 13:184–190, 2009. Opsha O, Malik A, Baltazar R, et al: MRI of the rotator cuff and internal derangement, Eur J Radiol 68:36–56, 2008. SooHoo NF, Rosen P: Diagnosis and treatment of rotator cuff tears in the emergency department, J Emerg Med 14:309–317, 1996. van der Heijden GJ: Shoulder disorders: a state-of-the-art review, Baillieres Best Pract Res Clin Rheumatol 13:287–309, 1999. Waldman SD: Functional anatomy of the rotator cuff. In Pain review, Philadelphia, 2009, Saunders, pp 85–86.

Chapter 36 INJECTION TECHNIQUE FOR QUADRILATERAL SPACE SYNDROME Indications and Clinical Considerations Quadrilateral space syndrome is an uncommon cause of shoulder and posterior upper arm pain that was first described in by Cahill and Palmer in 1983 and is now being encountered more frequently in clinical practice as magnetic resonance imaging (MRI) makes confirmation of the clinical diagnosis much easier than the previous required arteriography of the shoulder and upper extremity. Quadrilateral space syndrome is caused by compression of the axillary nerve as it passes through the quadrilateral space (Figure 36-1). The onset of quadrilateral space syndrome is usually insidious, with the patient often not reporting any obvious antecedent trauma. The patient with quadrilateral space syndrome will report ill-defined pain in the shoulder with paresthesias radiating into the posterior upper arm and lateral shoulder. This pain and associated paresthesia will frequently be made worse with abduction and external rotation of the affected upper extremity. As the syndrome progresses, the patient may note increasing weakness of the affected arm with difficulty with abduction and external rotation. Most cases of quadrilateral space syndrome have occurred in young athletes in their early second decade to third decade who are involved in throwing activities. The syndrome may occasionally be seen in older patients as a result of other causes of compression of the axillary nerve as it travels through the quadrilateral space such as glenolabral cysts or tumor (Figure 36-2). Mild cases of quadrilateral space syndrome will resolve over time, but more severe cases, if left untreated, will result in permanent atrophy of the deltoid and teres minor muscles. The most important finding in patients with quadrilateral space syndrome is weakness of the supraspinatus and infraspinatus muscles. This weakness manifests itself as weakness of abduction and external rotation of the ipsilateral shoulder ( Figure 36-3). With significant compromise of the axillary nerve, atrophy of the deltoid and teres minor muscle will be readily apparent on physical examination. The pain of quadrilateral space syndrome can be exacerbated by abducting and externally rotating the ipsilateral upper extremity. There often is tenderness to palpation of the quadrilateral space. Electromyography may help identify entrapment of the axillary nerve, although the test result may be normal in mild cases even though significant neuropraxia is present. Electromyography helps to distinguish cervical radiculopathy and Parsonage-Turner syndrome from quadrilateral space syndrome. Plain radiographs are indicated for all patients with quadrilateral space syndrome to rule out occult bony disease. On the basis of the patient’s clinical presentation, additional testing including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody testing may be indicated. MRI and ultrasound imaging of the shoulder

is indicated for all patients suspected of having quadrilateral space syndrome, as this test is highly specific for this disorder. In the rare patient in whom MRI and ultrasound imaging is nondiagnostic, subclavian arteriography to demonstrate occlusion of the posterior humeral circumflex artery may be considered, as this finding is highly suggestive of a diagnosis of quadrilateral space syndrome.

Clinically Relevant Anatomy The quadrilateral space is a four-sided space that is bounded superiorly by the subscapularis and teres minor muscles, medially by the long head of the triceps brachii, laterally by the surgical neck of the humerus, and inferiorly by the teres major muscle (see ­Figure 36-1). Contained within the quadrilateral space is the axillary nerve, which is a branch of the brachial plexus and the posterior circumflex humeral artery. Compromise of either of these structures by tumor, hematoma, aberrant muscle, or heterotopic bone can produce clinical symptoms.

Technique The goals of this injection technique are explained to the patient. A sterile syringe containing 15.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a Acromion

Surgical neck of humerus Axillary nerve Posterior circumflex humeral artery Quadrilateral space

Figure 36-1  Anatomy of the quadrilateral space.

103

104        SECTION 2  •  Shoulder

A

A

B

B Figure 36-2  A, Fast spin-echo T2-weighted oblique sagittal magnetic resonance (MR) image shows extension of the paralabral cyst (large arrow) inferiorly into the quadrilateral space. The axillary nerve and posterior humeral circumflex artery (small arrow) are surrounded and compressed by the cyst. Loss of bulk and fatty infiltration of the teres minor muscle is again noted (open arrows). B, Fast spin-echo T2-weighted coronal oblique MR image shows a large paralabral cyst and labral tear. The labral tear is clearly seen as a band of high signal extending through the inferior labrum and connecting with the paralabral cyst (arrow). (From Sanders TG, Tirman PF: Paralabral cyst: an unusual cause of quadrilateral space syndrome, Arthroscopy 15:632–637, 1999.)

C Figure 36-3  A, Active range of motion showing markedly decreased abduction. B, Paresthesia in the axillary nerve distribution (dotted line area). Point tenderness with compression over the quadrilateral space (looped line area) and deltoid atrophy. C, One of the wounds from the operation (third intercostal space midaxillary line) is shown. (From Nishimura M, Kobayashi M, Hamagashira K, et al: Quadrilateral space syndrome: a rare complication of thoracic surgery, Ann Thorac Surg 86:1350– 1351, 2008.)

36  •  Injection Technique for Quadrilateral Space Syndrome        105

Side Effects and Complications Olecran of the elbow

Axillary fold 2 cm

90°

Neromion’s lateral-posterior corner

The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is followed. Trauma to the axillary nerve and/or posterior circumflex humeral artery from the injection itself remains an ever-present possibility. The risk of this complication can be greatly decreased if the clinician uses gentle technique and stops injecting immediately if significant resistance to injection is encountered or if signs of local anesthetic toxicity are observed. Approximately 25% of patients note a transient increase in pain after this injection technique; the patient should be warned of this.

Clinical Pearls Figure 36-4  Anatomic landmarks for the axillary nerve block. A line is drawn between the lateral-posterior angle of the acromion and the olecranon tip of the elbow. The location is about 2 cm cranial to the convergence of this line, with the perpendicular line originating from the axillary fold. The needle is introduced about 2 cm cranial to this crossing point to elicit deltoid muscle contraction. (From Checcucci G, Allegra A, Bigazzi P, et  al: A new technique for regional anesthesia for arthroscopic shoulder surgery based on a suprascapular nerve block and an axillary nerve block: an evaluation of the first results, Arthroscopy 24:689–696, 2008.)

1½-inch, 25-gauge needle using strict aseptic technique. The patient is placed in the lateral decubitus position, and proper preparation with antiseptic solution of the skin overlying the superior shoulder and proximal affected upper extremity to just below the elbow is carried out. With a sterile marker a line is drawn between the lateral-posterior angle of the acromion and the tip of the ipsilateral olecranon process. A perpendicular line is then drawn from the axillary fold anteriorly until it crosses the line between the acromial tip and olecranon. At a point 2 cm above the point at which the two lines intersect, with strict aseptic technique, the needle is then carefully advanced through the skin and subcutaneous tissues in a perpendicular trajectory until a paresthesia is elicited as the needle tip impinges on the ancillary nerve as it passes through the quadrilateral space (Figure 36-4). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected. After careful aspiration the contents of the syringe are slowly injected while the patient is monitored closely for signs of local anesthetic toxicity. There should be minimal resistance to injection unless calcification of the subacromial bursal sac is present. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. Ultrasound guidance or the use of a nerve stimulator may be useful in patients in whom the anatomic landmarks are hard to identify.

Failure to correctly diagnose quadrilateral space syndrome will put the patient at risk for the missed diagnosis of other syndromes that may result in ongoing damage to the shoulder or lead to overlooked disease in this anatomic region that may harm the patient such as Pancoast tumor or primary or metastatic tumors of the shoulder. MRI is indicated for all patients thought to have quadrilateral space syndrome, and aggressive treatment of surgically correctible causes is generally indicated sooner rather than later to avoid ongoing irreversible shoulder damage. The nonsteroidal antiinflammatory agents or cyclooxygenase-2 (COX-2) inhibitors represent a reasonable first step in the treatment of mild self-limited quadrilateral space syndrome. The use of a tricyclic antidepressant such as nortriptyline at a single bedtime dose of 25 mg and titrated upward as side effects allow will also be useful, especially if sleep disturbance is also present, and gabapentin or carbamazepine may be useful in the treatment of neuritic pain. Avoidance of repetitive trauma thought to be contributing to this entrapment neuropathy is also important, especially in professional athletes. If these maneuvers fail to produce rapid symptomatic relief, surgical exploration and release of the axillary nerve are indicated.

SUGGESTED READINGS Chautems RC, Glauser T, Waeber-Fey MC, et al: Quadrilateral space syndrome: case report and review of the literature, Ann Vasc Surg 14:673–676, 2000. Ishima T, Usui M, Satoh E, et al: Quadrilateral space syndrome caused by a ganglion, J Shoulder Elbow Surg 7:80–82, 1998. McClelland D, Paxinos A: The anatomy of the quadrilateral space with reference to quadrilateral space syndrome, J Shoulder Elbow Surg 17:162–164, 2008. Nishimura M, Kobayashi M, Hamagashira K, et al: Quadrilateral space syndrome: a rare complication of thoracic surgery, Ann Thorac Surg 86:1350–1351, 2008. Sanders TG, Tirman PF: Paralabral cyst: an unusual cause of quadrilateral space syndrome, Arthroscopy 15:632–637, 1999.

Chapter 37 SUBDELTOID BURSA INJECTION

Indications and Clinical Considerations Bursae are formed from synovial sacs that allow easy sliding of muscles and tendons across one another at areas of repeated movement. These synovial sacs are lined with a synovial membrane, which is invested with a network of blood vessels that secrete synovial fluid. Inflammation of the bursa results in an increase in the production of synovial fluid with swelling of the bursal sac. With overuse or misuse, these bursae may become inflamed, enlarged, and, on rare occasions, infected. Although there is significant intrapatient variability as to the number, size, and location of bursae, anatomists have identified a number of clinically relevant bursae, including the subdeltoid bursa. The subdeltoid bursa lies primarily under the acromion, extending laterally between the deltoid muscle and joint capsule under the deltoid muscle. It may exist as a single bursal sac or, in some patients, as a multisegmented series of sacs that may be loculated. The subdeltoid bursa is vulnerable to injury from both acute trauma and repeated microtrauma. Acute injuries frequently take the form of direct trauma to the shoulder when playing sports or falling from bicycles. Repeated strain from throwing injuries, bowling, carrying a heavy briefcase, working with the arm raised across the body, rotator cuff injuries, or repetitive motion associated with assembly line work may result in inflammation of the subdeltoid bursa. If the inflammation of the subdeltoid bursa becomes chronic, calcification of the bursa may occur. The patient with subdeltoid bursitis frequently reports pain with any movement of the shoulder, but especially with abduction. The pain is localized to the subdeltoid area, with referred pain often noted at the insertion of the deltoid at the deltoid tuberosity on the upper third of the humerus. Often the patient is unable to sleep on the affected shoulder and may note a sharp, “catching” sensation when abducting the shoulder, especially on first awakening. Physical examination may reveal point tenderness over the acromion, and occasionally swelling of the bursa gives the affected deltoid muscle an edematous feel. Passive elevation and medial rotation of the affected shoulder reproduces the pain, as does resisted abduction and lateral rotation. Sudden release of resistance during this maneuver markedly increases the pain. Plain radiographs and magnetic resonance imaging (MRI) of the shoulder may reveal calcification of the bursa and associated structures consistent with chronic inflammation (Figure 37-1). Ultrasound imaging of the shoulder may also help diagnose subdeltoid bursitis and associated tendinopathy of the shoulder (­Figure 37-2). MRI is also indicated if disruption of the ligaments of the shoulder is suspected. The injection technique described later serves as both a diagnostic and a therapeutic maneuver. 106

Clinically Relevant Anatomy The acromial arch covers the superior aspect of the shoulder joint and articulates with the clavicle at the acromioclavicular joint. The acromioclavicular joint is formed by the distal end of the clavicle and the anterior and medial aspect of the acromion (see Figure 37-2). The strength of the joint is a result of the dense coracoclavicular ligament, which attaches the bottom of the distal end of the clavicle to the coracoid process. The superior portion of the joint is covered by the superior acromioclavicular ligament, which attaches the distal clavicle to the upper surface of the acromion. The inferior portion of the joint is covered by the inferior acromioclavicular ligament, which attaches the inferior portion of the distal clavicle to the acromion. The subdeltoid bursa lies primarily under the acromion, extending laterally between the deltoid muscle and joint capsule (see Figures 37-1; Figure 37-3).

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the superior shoulder, acromion, and distal clavicle is carried out. A sterile syringe containing 4.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique the lateral edge of the acromion is identified, and at the midpoint of the lateral edge the injection site is identified. At this point the needle is then carefully advanced in a slightly cephalad trajectory through the skin and subcutaneous tissues beneath the acromion capsule into the bursa (see Figure 37-3). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected slightly more inferiorly. After the bursa has been entered, the contents of the syringe are injected gently while the needle is slowly withdrawn. There should be minimal resistance to injection unless calcification of the bursal sac is present. Calcification of the bursal sac is identified as a resistance to needle advancement with an associated gritty feel. Significant calcific bursitis ultimately may require surgical excision to effect complete relief of symptoms. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of injection of the subdeltoid bursa is infection, which should be exceedingly rare if strict aseptic technique is followed. Approximately 25% of patients note a transient increase in pain after injection of the subdeltoid bursa; the patient should be warned of this.

37  •  Subdeltoid Bursa Injection        107

a ss

d

A

B

C

D

Figure 37-1  Subacromial (subdeltoid) bursa: normal anatomy. A, A diagram of a coronal section of the shoulder shows the glenohumeral joint (arrow) and subacromial (subdeltoid) bursa (arrowhead), separated by a portion of the rotator cuff (i.e., supraspinatus tendon). The supraspinatus (ss) and deltoid (d) muscles and the acromion (a) are indicated. B, A subdeltoid-subacromial bursogram, accomplished with the injection of both radiopaque contrast material and air, shows the bursa (arrowheads) sitting like a cap on the humeral head and greater tuberosity of the humerus. Note that the joint is not opacified, indicative of an intact rotator cuff. C, In a different cadaver, a subacromial-subdeltoid bursogram shows much more extensive structure as a result of opacification of the subacromial, subdeltoid, and subcoracoid (arrow) portions of the bursa. D, A radiograph of a transverse section of the specimen illustrated in C shows both the subdeltoid (arrowheads) and subcoracoid (arrow) portions of the bursa. The glenohumeral joint is not opacified. (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

Deltoid muscle displaced Inflamed subdeltoid bursa Supraspinatus muscle

Figure 37-2  Transverse ultrasound—long head of biceps tendon sheath fluid (long arrow) with fluid in the adjacent subdeltoid bursa (short arrow). (From Allen GM: Shoulder ultrasound imaging-integrating anatomy, biomechanics and disease processes, Eur J Radiol 68:137–146, 2008.)

Figure 37-3  The subdeltoid bursa lies primarily under the acromion, extending laterally between the deltoid muscle and joint capsule.

108        SECTION 2  •  Shoulder

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to subdeltoid bursitis. Coexistent arthritis and tendinitis may also contribute to shoulder pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for shoulder pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Allen GM: Shoulder ultrasound imaging-integrating anatomy, biomechanics and disease processes, Eur J Radiol 68:137–146, 2008. Chartash EK, Good PK, Gould ES, Furie RA: Septic subdeltoid bursitis, Semin Arthritis Rheum 22:25–29, 1992. Lento PH, Strakowski JA: The use of ultrasound in guiding musculoskeletal interventional procedures, Phys Med Rehabil Clin N Am 21:559–583, 2010. Waldman SD: Injection technique for subdeltoid bursitis pain. In Pain review, Philadelphia, 2009, Saunders, p 456. Waldman SD: The subdeltoid bursa. In Pain review, Philadelphia, 2009, ­Saunders, p 83.

Chapter 38 SUBCORACOID BURSA INJECTION

Indications and Clinical Considerations Bursae are formed from synovial sacs whose purpose is to allow easy sliding of muscles and tendons across one another at areas of repeated movement. These synovial sacs are lined with a synovial membrane that is invested with a network of blood vessels that secrete synovial fluid. Inflammation of the bursa results in an increase in the production of synovial fluid with swelling of the bursal sac. With overuse or misuse, these bursae may become inflamed, enlarged, and, on rare occasions, infected. Although there is significant intrapatient variability as to the number, size, and location of bursae, anatomists have identified a number of clinically relevant bursae, including the subcoracoid bursa. The subcoracoid bursa lies between the joint capsule and the coracoid process (Figure 38-1). It may exist as a single bursal sac or in some patients as a multisegmented series of sacs that may be loculated. The subcoracoid bursa is vulnerable to injury from both acute trauma and repeated microtrauma. Acute injuries frequently take the form of direct trauma to the shoulder that occurs when playing sports or from falling on the shoulder. The repeated strain associated with repetitive motion may result in inflammation of the subcoracoid bursa. If the inflammation of the subcoracoid bursa becomes chronic, calcification of the bursa may occur. The patient with subcoracoid bursitis frequently notes pain with forward movement and adduction of the shoulder. The pain is localized to the area over the coracoid process, with referred pain noted at the medial shoulder. Often, the patient is unable to sleep on the

affected shoulder, and he or she may report a sharp, “catching” sensation when abducting the shoulder, especially on first awakening. Physical examination may reveal point tenderness over the coracoid process (Figure 38-2). Passive elevation and active internal rotation of the affected shoulder will reproduce the pain of subcoracoid bursitis, as do resisted adduction and internal rotation (Figure 38-3). The abduction release test is also highly diagnostic for subcoracoid bursitis. For this test the patient is asked to adduct the affected arm against the examiner’s resistance (Figure 38-4). The examiner without warning suddenly releases the resistance, which should result in a marked increase in pain symptoms (Figure 38-5). Plain radiographs of the shoulder may reveal calcification of the bursa and associated structures consistent with chronic inflammation. Magnetic resonance imaging (MRI) and/or ultrasound imaging will help identify the presence of subcoracoid bursitis and coexistent shoulder disease (Figure 38-6). Ultrasound imaging may also be helpful in identifying the inciting factors responsible for subcoracoid bursitis. MRI and/or ultrasound imaging is also indicated if disruption of the ligaments is suspected. The injection technique described later serves as both a diagnostic and a therapeutic maneuver. Subcoracoid bursitis Coracoid process Subdeltoid bursitis

Acromioclavicular joint

Coracoid process Subcoracoid bursa

Figure 38-1  The subcoracoid bursa lies between the joint capsule and the coracoid process.

Figure 38-2  Subcoracoid bursitis can be reproduced with palpation directly over the coracoid process. (From Waldman SD: Physical diagnosis of pain, Philadelphia, 2005, Saunders.)

109

110        SECTION 2  •  Shoulder

Figure 38-3  The adduction release test for subcoracoid bursitis. The patient is asked to internally rotate the affected arm until the pain is reproduced. (From Waldman SD: Physical diagnosis of pain, Philadelphia, 2005, Saunders.)

Figure 38-5  The adduction release test for subcoracoid bursitis. If the patient has subcoracoid bursitis, he or she will experience a marked increase in pain symptoms after a sudden release of the resistance to adduction. (From Waldman SD: Physical diagnosis of pain, Philadelphia, 2005, Saunders.)

arm movement or when previous damage to the musculotendinous unit of the shoulder allows abnormal movement of the head of the humerus in the glenoid fossa.

Technique

Figure 38-4  The adduction release test for subcoracoid bursitis. The examiner supports the affected arm and asks the patient to begin adducting the arm against the examiner’s resistance. (From Waldman SD: Physical diagnosis of pain, Philadelphia, 2005, Saunders.)

Clinically Relevant Anatomy The coracoid process of the scapula projects upward and forward above the glenoid fossa (see Figure 38-1; Figure 38-7). The coracoid process provides attachment for the coracoclavicular ligament as well as the short head of the biceps. The long head of the biceps has its origin just inferior to the coracoid process in the supraglenoid tubercle of the scapula. The long head exits the shoulder joint via the bicipital groove, where it is susceptible to tendinitis. The long head is joined by the short head in the middle portion of the upper arm. The insertion of the biceps muscle is into the posterior potion of the radial tuberosity. The subcoracoid bursa lies between the joint capsule and the coracoid process. It is susceptible to irritation by pressure from the coracoid process against the head of the humerus during extreme

The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the anterior shoulder, acromion, and distal clavicle is carried out. A sterile syringe containing 4.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique the anterior surface of the lateral clavicle is identified. Next, the deepest portion of the clavicular concavity is identified. At this point, the palpating finger moves 1 inch below the anterior surface of the clavicle. The coracoid process runs anterolaterally, and the palpating finger should be able to feel the tip and medial surface of the coracoid. This point is marked with a sterile marker. At this point the needle is then carefully advanced posteriorly in a slightly lateral trajectory through the skin and subcutaneous tissues beneath the tip of the coracoid process into the bursa (see Figure 38-7). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected slightly more inferiorly. After the bursa has been entered, the contents of the syringe are gently injected while the needle is slowly withdrawn. There should be minimal resistance to injection unless calcification of the bursal sac is present. Calcification of the bursal sac is identified as a resistance to needle advancement with an associated gritty feel. Significant calcific bursitis ultimately may require surgical excision to effect complete relief of symptoms. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

38  •  Subcoracoid Bursa Injection        111

A

B

Figure 38-6  Axial, T2-weighted, gradient-echo (A) and sagittal, T2-weighted, fat-saturated (B) magnetic resonance images in a patient with anterior shoulder pain demonstrate subcoracoid stenosis with coracohumeral interval of 5.6 mm (white arrows). The subscapularis tendon demonstrates mild to moderate tendinosis (black arrows). There are associated subcortical cysts near the lesser tuberosity (white arrowhead) and subcoracoid bursitis (black arrowheads). (From Mulyadi E, Harish S, O’Neill J, Rebello R: MRI of impingement syndromes of the shoulder, Clin Radiol 64:307–318, 2009.)

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to subcoracoid bursitis. Coexistent arthritis and tendinitis also may contribute to shoulder pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for shoulder pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

Figure 38-7  The needle is placed just beneath the top of the coracoid process to inject the subcoracoid bursa.

Side Effects and Complications The major complication of injection of the subcoracoid bursa is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients note a transient increase in pain after injection of the subcoracoid bursa; the patient should be warned of this.

SUGGESTED READINGS Colas F, Nevoux J, Gagey O: The subscapular and subcoracoid bursae: descriptive and functional anatomy, J Shoulder Elbow Surg 13:454–458, 2004. Cowderoy GA, Lisle DA, O’Connell PT: Overuse and impingement syndromes of the shoulder in the athlete, Magn Reson Imaging Clin N Am 17:577–593, 2009. Mulyadi E, Harish S, O’Neill J, Rebello R: MRI of impingement syndromes of the shoulder, Clin Radiol 64:307–318, 2009. Steven D. Waldman: The subcoracoid bursa. In Pain review, Philadelphia, 2009, Saunders, p 89.

Chapter 39 INJECTION TECHNIQUE FOR FROZEN SHOULDER SYNDROME Indications and Clinical Considerations The term frozen shoulder describes a constellation of clinical symptoms, including the unilateral progressive limitation of passive and active range of motion of the shoulder and pain on range of motion. Usually the patient first notes difficulty in reaching behind to fasten clothing such as a bra. Patients exhibit a positive Apley scratch test result; that is, they are unable to scratch their lower back with the affected extremity. The limitation of shoulder range of motion then progresses to limit the patient’s ability to elevate the shoulder. The pain is constant, with worsening on use of the shoulder group. The pain is localized to the anterolateral aspect of shoulder and may radiate into the lateral neck and upper anterior chest. Some patients report a grating or popping sensation with use of the joint, and crepitus may be present on physical examination. Frozen shoulder is distinguishable from other painful conditions of the shoulder such as tendinitis and bursitis in that the limitation of range of motion associated with frozen shoulder affects both passive and active range of motion, whereas tendinitis and bursitis affect only active range of motion. Frozen shoulder is thought to be caused by a progressive adhesive capsulitis secondary to chronic inflammation of the structures of the shoulder (Figure 39-1). Although coexistent tendinopathy or bursitis may be present, the inflammatory changes associated with frozen shoulder selectively affect the ligaments and joint capsule. Individuals with diabetes are more commonly affected by frozen shoulder than the general population, as are patients with collagen vascular diseases such as polymyalgia rheumatica. The collagen vascular diseases generally manifest as a polyarthropathy rather than as a monoarthropathy limited to the shoulder joint. Frozen shoulder also may be seen after myocardial infarction, fractures of the humeral head, and paralytic stroke. In this setting, untreated frozen shoulder may progress to a reflex sympathetic dystrophy with associated vasomotor, sudomotor, and trophic changes. Plain radiographs are indicated for all patients with shoulder pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and ultrasound imaging of the shoulder is indicated if a rotator cuff tear is suspected.

Clinically Relevant Anatomy The rounded head of the humerus articulates with the pearshaped glenoid fossa of the scapula. The articular surface is 112

covered with hyaline cartilage that is susceptible to arthritis. The rim of the glenoid fossa is composed of a fibrocartilaginous layer called the glenoid labrum, which is susceptible to trauma should the humerus be subluxed or dislocated. The joint is surrounded by a relatively lax capsule that allows the wide range of motion of the shoulder joint at the expense of decreased joint stability. It is this capsule that, along with the shoulder ligaments, is most severely affected in frozen shoulder syndrome. The joint capsule is lined with a synovial membrane that attaches to the articular cartilage. This membrane gives rise to synovial tendon sheaths and bursae that are subject to inflammation. The shoulder joint is innervated by the axillary and suprascapular nerves. The major ligaments of the shoulder joint are the glenohumeral ligaments in front of the capsule, the transverse humeral ligament between the humeral tuberosities, and the coracohumeral ligament, which stretches from the coracoid process to the greater tuberosity of the humerus (Figure 39-2). Along with the accessory ligaments of the shoulder, these major ligaments provide strength to the shoulder joint. The strength of the shoulder joint is also dependent on short muscles that surround the joint: the subscapularis, the supraspinatus, the infraspinatus, and the teres minor. These muscles and their attaching tendons are susceptible to trauma and to wear and tear from overuse and misuse.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the shoulder, subacromial region, and joint space is carried out. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique the midpoint of the acromion is identified, and at a point approximately 1 inch below the midpoint the shoulder joint space is identified. The needle is then carefully advanced through the skin and subcutaneous tissues through the joint capsule into the joint (see Figure 39-2). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected superiorly and slightly more medially. After the joint space has been entered, the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced slightly into the joint space until the injection proceeds without significant resistance. The needle is then removed and a sterile pressure dressing and ice pack are placed at

39  •  Injection Technique for Frozen Shoulder Syndrome        113

Spine of scapula Glenoid cavity

Subacromial bursa

Carrico & Shavell

Greater tubercle

A

B

Figure 39-1  Adhesive capsulitis: arthrography. A, Frontal radiograph obtained after the injection of 5 mL of radiopaque contrast material into the glenohumeral joint reveals a tight-appearing articulation with lymphatic filling (arrow). No axillary pouch is seen. B, In a second patient, incomplete opacification of the glenohumeral joint is indicative of adhesive capsulitis. (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

Torn and inflamed articular capsule Articular capsule Synovial layer Fibrous layer

Biceps brachii tendon Humerus

Figure 39-2  Injection of local anesthetic and steroid is useful in the management of frozen shoulder.

+

Post injection

Injection

LT ISP LONGI

A

B

Figure 39-3  Ultrasound showing (A) the needle tip in the articular capsule and (B) the capsular distention. (From Lee HJ, Lim KB, Kim DY, Lee KT: Randomized controlled trial for efficacy of intra-articular injection for adhesive capsulitis: ultrasonography-guided versus blind technique, Arch Phys Med Rehabil 90:1997–2002, 2009.)

the injection site. Ultrasound guidance for needle placement may be beneficial in those patients in whom anatomic landmarks may be difficult to identify (Figure 39-3). A two-needle ultrasoundguided technique to remove calcium deposits has shown promise when calcific tendinitis is contributing to the patient’s symptoms (Figures 39-4, 39-5, and 39-6).

Side Effects and Complications The major complication of this intraarticular injection technique to treat frozen shoulder is infection, which should be exceedingly rare if strict aseptic technique is followed. Approximately 25% of patients note a transient increase in pain after this injection technique; the patient should be warned of this.

Clinical Pearls This injection technique is extremely effective in the treatment of pain and limited range of motion associated with frozen shoulder. Coexistent bursitis and tendinitis also may contribute to shoulder pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for shoulder pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

114        SECTION 2  •  Shoulder

NaCI 0.9%

B

A

NaCI 0.9%

Triamcinolone Ac.

C

D

Figure 39-4  Diagram showing the main steps of the procedure we have used. After the induction of local and intrabursal anesthesia, two needles are positioned inside the calcification under ultrasound guidance, with their tips facing each other (A). Saline solution is injected through one needle while the calcium-containing lavage solution is aspirated with the other needle (B). When the cavity becomes distended during injection and collapses during aspiration, treatment can be terminated. A hyperechoic cap of fibrotic calcific material remains (C). Before withdrawing the needles, we usually inject 40 mg of triamcinolone acetate into the bursa. (D). (From De Conti G, Marchioro U, Dorigo A, et al: Percutaneous ultrasound-guided treatment of shoulder tendon calcifications: clinical and radiological follow-up at 6 months, J Ultrasound 13:188-198, 2010.)

39  •  Injection Technique for Frozen Shoulder Syndrome        115

A

B

C

D

Figure 39-5  Main steps of the treatment. A, The needle is positioned within the calcification (type 1 with shadow cone). B, The second needle is positioned above the first one so that both can be clearly visualized. C, After lavage and aspiration, the calcification collapses, and its shadow cone disappears. D, The procedure is terminated when the aspirate contains only water without calcium. A hyperechoic, fibrocalcific cap remains. (From De Conti G, Marchioro U, Dorigo A, et al: Percutaneous ultrasound-guided treatment of shoulder tendon calcifications: clinical and radiological follow-up at 6 months, J Ultrasound 13:188–198, 2010.)

116        SECTION 2  •  Shoulder

Figure 39-6  Magnetic resonance imaging: evolving steps after treatments. Immediately after treatment, tendon fibers appear hyperintense in T2 and TIRM sequences, and there are usually signs of inflammation at the level of the subacromial bursa. The calcification itself is no longer visible. Six months or more after treatment, the tendon appears normal, but there are still signs of mild bursitis. In many cases, the patient is asymptomatic at this point. (From De Conti G, Marchioro U, Dorigo A, et al: Percutaneous ultrasound-guided treatment of shoulder tendon calcifications: clinical and radiological follow-up at 6 months, J Ultrasound 13:188–198, 2010.)

SUGGESTED READINGS Cain EL, Kocaj SM, Wilk KE: Adhesive capsulitis of the shoulder. In Wilk KE, Reinold MM, Andrews JR, editors: The athlete’s shoulder, ed 2, Philadelphia, 2009, Churchill Livingstone, pp 293–301. Ingram-Rice B: Adhesive capsulitis: the “frozen shoulder” syndrome—­occupational therapy perspective, J Bodyw Mov Ther 4:20–26, 2000. Jacobs LG, Smith MG, Khan SA, et al: Manipulation or intra-articular steroids in the management of adhesive capsulitis of the shoulder? A prospective randomized trial, J Shoulder Elbow Surg 18:348–353, 2009.

Lee HJ, Lim KB, Kim DY, Lee KT: Randomized controlled trial for efficacy of intra-articular injection for adhesive capsulitis: ultrasonography-guided versus blind technique, Arch Phys Med Rehabil 90:997–2002, 2009. Sheridan MA, Hannafin JA: Upper extremity: emphasis on frozen shoulder, Orthop Clin North Am 37:531–539, 2006. Thomas SJ, McDougall C, Brown ID, et  al: Prevalence of symptoms and signs of shoulder problems in people with diabetes mellitus, J Shoulder Elbow Surg 16:748–751, 2007. Vaughn BF: Adhesive capsulitis: the “frozen shoulder” syndrome—introduction and case history, J Bodyw Mov Ther 4:3–4, 2000.

Chapter 40 INJECTION TECHNIQUE FOR SCAPULOCOSTAL SYNDROME Indications and Clinical Considerations Scapulocostal syndrome describes a constellation of symptoms consisting of unilateral pain and associated paresthesias occurring at the medial border of the scapula, referred pain radiating from the deltoid region to the dorsum of the hand, and decreased range of motion of the scapula (Figure 40-1). Scapulocostal syndrome is commonly referred to as traveling salesman’s shoulder because it frequently is seen in individuals who repeatedly reach backward over a car seat to get something from the back seat of the car. Scapulocostal syndrome is an overuse syndrome caused by repeated improper use of the muscles of scapular stabilization, namely, the levator scapulae, the pectoralis minor, the serratus anterior, the rhomboids, and, to a lesser extent, the infraspinatus and teres minor. Physical examination reveals decreased scapular range of motion on the affected side. Pain is reproduced by reaching backward with the affected extremity. A prominent infraspinatus trigger point is present in almost all patients with scapulocostal syndrome. This infraspinatus trigger point can be demonstrated best by having the patient place the hand of the affected side over the deltoid of the opposite shoulder. This maneuver laterally rotates the affected scapula and allows palpation and subsequent injection of the infraspinatus trigger point. Other trigger areas along the medial border of the scapula also may be present and may be amenable to injection therapy. Plain radiographs are indicated for all patients with suspected scapulocostal syndrome to rule out occult bony pathology, including metastatic lesions. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, prostate-specific antigen, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the shoulder is indicated if a rotator cuff tear is suspected. Electromyography is indicated in patients with scapulocostal syndrome to help rule out cervical radiculopathy or plexopathy. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The levator scapulae, pectoralis minor, serratus anterior, and the rhomboids all help stabilize the scapula and are subject to the development of overuse syndrome. In addition, the infraspinatus muscle also may be affected in patients with scapulocostal syndrome; trigger points in all of these muscles may develop (see Figure 40-1). The infraspinatus muscle provides shoulder joint stability and, along with the teres minor muscle, externally

rotates the arm at the shoulder. The infraspinatus muscle has its origin in the infraspinous fossa of the scapula and inserts into the middle facet of the greater tuberosity of the humerus. All of these muscles are susceptible to trauma and to wear and tear from overuse and misuse, as mentioned previously; the net result may be the clinical constellation of symptoms called scapulocostal syndrome.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the sitting position with the hand of the affected arm holding the opposite deltoid muscle (Figure 40-2). The exposed subscapular area is then palpated to identify an infraspinatus trigger point. A positive “jump” sign should be noted when the trigger point is identified. The point is marked with a sterile marker. Proper preparation with antiseptic solution of the skin overlying the shoulder and posterior subscapular region is then carried out. A sterile syringe containing 1.0 mL of 0.25% preservativefree bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique the previously marked point is palpated, and the infraspinatus trigger point is reidentified with the gloved finger. The needle is then carefully advanced at this point through the skin and subcutaneous tissues into the trigger point in the underlying infraspinatus muscle (see Figure 40-2). The needle is then fixed in place, and the contents of the syringe are gently injected. There should be minimal resistance to injection. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. Other trigger points at the medial border of the affected scapula are identified and injected in an analogous manner.

Side Effects and Complications The major complication of this injection technique is pneumothorax if the needle is placed too deeply and invades the pleural space. Infection, although rare, can occur if strict aseptic technique is not followed. Trauma to the tendons from the injection itself remains an ever-present possibility. Tendons that are highly inflamed or previously damaged are subject to rupture if they are directly injected; the risk of this complication can be greatly decreased if the clinician uses gentle technique and stops injecting immediately if significant resistance to injection is encountered. Approximately 25% of patients report a transient increase in pain after this injection technique; the patient should be warned of this. 117

118        SECTION 2  •  Shoulder

Clinical Pearls

Levator scapulae m. Supraspinatus m. Infraspinatus m. Trigger point Teres minor m. Rhomboid m. Referred pain zone

Patients with scapulocostal syndrome often visit the emergency department fearing that they are having a heart attack. The syndrome is also frequently misdiagnosed as a cervical radiculopathy. Electromyography helps delineate the cause and extent of neural compromise. This injection technique is extremely effective in the treatment of scapulocostal syndrome. Coexistent bursitis and arthritis also may contribute to shoulder and scapular pain and may require additional treatment with a more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Pneumothorax can be avoided if shorter needles are used and the needle is not advanced too deeply. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for shoulder pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptomatology. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS

Figure 40-1  Scapulocostal syndrome is a constellation of symptoms consisting of unilateral pain and paresthesias occurring along the medial border of the scapula, referred pain radiating from the scapula to the dorsum of the hand, and decreased range of motion of the scapula.

Hand grabbing contralateral deltoid m.

Trigger point

Figure 40-2  Injection for scapulocostal syndrome should be carried out at the point at which a subscapular trigger point is identified.

Baldry P: Acupuncture treatment of fibromyalgia and myofascial pain. In Chaitow L, editor: Fibromyalgia syndrome, ed 3, Oxford, 2010, Churchill Livingstone, pp 145–159. Baldry PE, Thompson JW: Pain in the arm. In Baldry PE, editor: Acupuncture, trigger points and musculoskeletal pain, ed 3, London, 2005, Churchill Livingstone, pp 223–249. Ge HY, Nie H, Madeleine P, et al: Contribution of the local and referred pain from active myofascial trigger points in fibromyalgia syndrome, Pain 147:233– 240, 2009. Ge HY, Wang Y, Danneskiold-Samsøe B, et al: The predetermined sites of examination for tender points in fibromyalgia syndrome are frequently associated with myofascial trigger points, J Pain 11:644–651, 2010. Hains G, Descarreaux M, Hains F: Chronic shoulder pain of myofascial origin: a randomized clinical trial using ischemic compression therapy, J Manipulative Physiol Ther 33:362–369, 2010. LeBlanc KE, LeBlanc LL: Musculoskeletal disorders, Prim Care 37:389–406, 2010. Partanen JV, Ojala TA, Arokoski JP: Myofascial syndrome and pain: a neurophysiological approach, Pathophysiology 17:19–28, 2010.

SECTION 3  •  Elbow and Forearm

Chapter 41 INTRAARTICULAR INJECTION OF THE ELBOW JOINT Indications and Clinical Considerations The elbow joint is susceptible to the development of arthritis from a variety of conditions that have in common the ability to damage the joint cartilage. Osteoarthritis of the joint is the most common form of arthritis that results in elbow joint pain. In the elbow, osteoarthritis is usually a result of previous trauma or on-the-job injury (Figure 41-1). However, rheumatoid arthritis, posttraumatic arthritis, and psoriatic arthritis are also common causes of elbow pain secondary to arthritis, with 35% of patients with rheumatoid arthritis affected. Less common causes of arthritis-induced elbow pain include the collagen vascular diseases, infection, and Lyme disease. Acute infectious arthritis usually is accompanied by significant systemic symptoms, including fever and malaise, and should easily be recognized by the astute clinician and treated appropriately with culture and antibiotics, rather than injection therapy. The collagen vascular diseases generally manifest as a polyarthropathy rather than a monoarthropathy limited to the elbow joint, although elbow pain secondary to collagen vascular disease responds exceedingly well to the intraarticular injection technique described later. The majority of patients with elbow pain secondary to osteoarthritis and posttraumatic arthritis pain report pain that is localized around the elbow and forearm. Activity makes the pain worse; rest and heat provide some relief. The pain is constant and characterized as aching. The pain may interfere with sleep. Some patients report a grating or popping sensation with use of the joint, and crepitus may be present on physical examination. In addition to the just-mentioned pain, patients with arthritis of the elbow joint often experience a gradual decrease in functional ability with decreasing elbow range of motion, making simple everyday tasks such as using a computer keyboard, holding a coffee cup, or turning a doorknob quite difficult. With continued disuse, muscle wasting may occur and an adhesive capsulitis with subsequent ankylosis may develop. Plain radiographs are indicated for all patients with elbow pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Computed tomography

(CT) and/or magnetic resonance imaging (MRI) of the elbow is indicated if joint instability or joint mice are suspected (Figure 41-2). Ultrasound imaging may also help clarify the diagnosis.

Clinically Relevant Anatomy The elbow joint is a synovial, hinge-type joint that serves as the articulation among the humerus, radius, and ulna (Figure 41-3). The joint’s primary function is to position the wrist to optimize hand function. The joint allows flexion and extension at the elbow, as well as pronation and supination of the forearm. The joint is lined with synovium, and the resultant synovial space allows intraarticular injection. The entire joint is covered by a dense capsule that thickens medially to form the ulnar collateral ligament and laterally to form the radial collateral ligaments. These dense ligaments, coupled with the elbow joint’s deep bony socket, make this joint extremely stable and relatively resistant to subluxation and dislocation. The anterior and posterior joint capsule is less dense and may become distended if there is a joint effusion. The olecranon bursa lies in the posterior aspect of the elbow joint and may become inflamed as a result of direct trauma or overuse of the joint. Bursae susceptible to the development of bursitis also exist between the insertion of the biceps and the head of the radius, as well as in the antecubital and cubital area. The elbow joint is innervated primarily by the musculocutaneous and radial nerves, with the ulnar and median nerves providing varying degrees of innervation. At the middle of the upper arm, the ulnar nerve courses medially to pass between the olecranon process and medial epicondyle of the humerus. The nerve is susceptible to entrapment and trauma at this point. At the elbow, the median nerve lies just medial to the brachial artery and occasionally is damaged during brachial artery cannulation for blood gases.

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side and the elbow flexed with the dorsum of the hand resting on a folded towel. A total of 5 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 12-mL sterile syringe. 119

120        SECTION 3  •  Elbow and Forearm

A

B

Figure 41-1  Lateral (A) and anteroposterior (B) radiographs of a patient with advanced primary osteoarthritis of the elbow. Osteophytes of the olecranon, coronoid, and radial head are present; joint space narrowing and thickening of the olecranon fossa membrane can be noted, together with cyst formation and calcification within the ulnar collateral ligament. (From Dalal S, Bull M, Stanley D: Radiographic changes at the elbow in primary osteoarthritis: a comparison with normal aging of the elbow joint, J Shoulder Elbow Surg 16:358–361, 2007.)

After sterile preparation of the skin overlying the posterolateral aspect of the joint, the head of the radius is identified. Just superior to the head of the radius is an indentation that represents the space between the radial head and humerus. With strict aseptic technique, a 1-inch, 25-gauge needle is inserted just above the superior aspect of the head of the radius through the skin, subcutaneous tissues, and joint capsule into the joint (see Figure 41-3). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected superiorly. After the joint space has been entered, the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced slightly into the joint space until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. In patients in whom the anatomic landmarks are difficult to identify, ultrasound guidance may be beneficial (Figure 41-4).

Side Effects and Complications

Figure 41-2  Computed tomography image of the elbow showing degenerative arthritis and loose bodies at the olecranon fossa. (From Kokkalis ZT, Schmidt CC, Sotereanos DG: Elbow arthritis: current concepts, J Hand Surg Am 34:761–768, 2009.)

The major complication of intraarticular injection of the elbow is infection, which should be exceedingly rare if strict aseptic technique is adhered to. As mentioned earlier, the ulnar nerve is especially susceptible to damage at the elbow. Approximately 25% of patients report a transient increase in pain after intraarticular injection of the elbow joint; the patient should be warned of this.

41  •  Intraarticular Injection of the Elbow Joint        121

LATERAL VIEW Humerus

Head of radius

Lateral epicondyle

Radial collateral ligament

Olecranon

Annular ligament

Olecranon bursa

MEDIAL VIEW Osteoarthritis

Humerus

Annular ligament

Anterior ulnar collateral ligament

Radius

Posterior ulnar collateral ligament

Ulna

Oblique collateral ligament Olecranon

Figure 41-3  The elbow is a hinge-type joint that serves as the articulation among the humerus, radius, and ulna.

Olecranon

* Trochlea

A

B

Figure 41-4  Elbow joint access from a posterior approach. A, With the patient seated and the affected arm placed across the chest, the posterior joint is examined in a sagittal plane. B, The needle is introduced from a posterosuperior approach (dotted line), passing adjacent to the triceps tendon (open arrow), through the posterior fat pad (asterisk), and into the joint. The concave olecranon fossa of the humerus (solid arrows) provides a useful landmark. (Sterile technique not depicted.) (From Louis LJ: Musculoskeletal ultrasound intervention: principles and advances, Ultrasound Clin 4:217–236, 2009.)

122        SECTION 3  •  Elbow and Forearm

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to the just-mentioned causes of arthritis of the elbow joint. Coexistent bursitis and tendinitis also may contribute to elbow pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat as well as gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for elbow pain. Vigorous exercise should be avoided, because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Dalal S, Bull M, Stanley D: Radiographic changes at the elbow in primary osteoarthritis: a comparison with normal aging of the elbow joint, J Shoulder Elbow Surg 16:358–361, 2007. Gallo RA, Payatakes A, Sotereanos DG: Surgical options for the arthritic elbow, J Hand Surg Am 33:746–759, 2008. Kokkalis ZT, Schmidt CC, Sotereanos DG: Elbow arthritis: current concepts, J Hand Surg Am 34:761–768, 2009. Louis LJ: Musculoskeletal ultrasound intervention: principles and advances, Ultrasound Clin 4:217–236, 2009. Steinbach LS, Fritz RC, Tirman PF, Uffman M: Magnetic resonance imaging of the elbow, Eur J Radiol 25:223–241, 1997. Waldman SD: Functional anatomy of the elbow joint. Pain review. Philadelphia, 2009, Saunders, pp 90–94. Waldman SD: Injection technique for intra-articular injection of the elbow. In Pain review, Philadelphia, 2009, Saunders, pp 457–458.

Chapter 42 INJECTION TECHNIQUE FOR ANCONEUS SYNDROME Indications and Clinical Considerations The anconeus muscle is susceptible to the development of myofascial pain syndrome. Such pain most often occurs as a result of repetitive microtrauma to the muscle from such activities as prolonged ironing, handshaking, or digging. Improper one-handed backhand technique in tennis has also been implicated as an inciting factor for this myofascial pain syndrome, as has blunt trauma to the muscle. Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body. The sine qua non of myofascial pain syndrome is the finding of myofascial trigger points on physical examination. Although these trigger points generally are localized to the regional part of the body affected, the pain of myofascial pain syndrome often is referred to other anatomic areas. This referred pain often is misdiagnosed or attributed to other organ systems, thereby leading to extensive evaluations and ineffective treatment. Patients with myofascial pain syndrome involving the anconeus often have referred pain into the ipsilateral forearm. The trigger point is the pathognomonic lesion of myofascial pain and is thought to be a result of microtrauma to the affected muscles. This pathologic lesion is characterized by a local point of exquisite tenderness in affected muscle. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain but also referred pain. In addition to this local and referred pain, there often is an involuntary withdrawal of the stimulated muscle, called a “jump sign.” This jump sign also is characteristic of myofascial pain syndrome. Patients with anconeus syndrome will exhibit a trigger point over the superior insertion of the muscle (Figure 42-1). Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. In spite of this consistent physical finding in patients with myofascial pain syndrome, the pathophysiology of the myofascial trigger point remains elusive, although many theories have been advanced. Common to all of these theories is the belief that trigger points are a result of microtrauma to the affected muscle. This microtrauma may occur as a single injury to the affected muscle or may occur as a result of repetitive microtrauma or chronic deconditioning of the agonist and antagonist muscle unit. In addition to muscle trauma, a variety of other factors seem to predispose the patient to develop myofascial pain syndrome. The weekend athlete who subjects his or her body to unaccustomed physical activity may develop myofascial pain syndrome. The poor posture of someone sitting at a computer keyboard or watching television has also been implicated as a predisposing

factor to the development of myofascial pain syndrome. Previous injuries may result in abnormal muscle function and predispose to the subsequent development of myofascial pain syndrome. All of these predisposing factors may be intensified if the patient also has poor nutritional status or coexisting psychological or behavioral abnormalities, including chronic stress and depression. The anconeus muscle seems to be particularly susceptible to stress-induced myofascial pain syndrome. Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or in conjunction with other painful conditions, including radiculopathy and chronic regional pain syndromes. Psychological or behavioral abnormalities, including depression, frequently coexist with the muscle abnormalities associated with myofascial pain syndrome. Treatment of these psychological and behavioral abnormalities must be an integral part of any successful treatment plan for myofascial pain syndrome.

Clinically Relevant Anatomy Working with the other muscles of the posterior elbow, the anconeus muscle helps stabilize the elbow by stabilizing the proximal ulna during pronation of the forearm to prevent ulnar subluxation as well as by adducting and medially rotating the humerus. Situated posterior to the elbow joint, the anconeus muscle is a triangular muscle that arises from the lateral epicondyle of the humerus and finds its insertion into the lateral margin of the olecranon and posterior ulna (Figure 42-2). The muscle is innervated by the radial nerve. The anconeus muscle is susceptible to trauma and to wear and tear from overuse and misuse and may develop myofascial pain syndrome as well as epicondylitis at its origin on the lateral epicondyle of the humerus. Occasionally the anconeus muscle can compress the ulnar nerve at the elbow, resulting in an entrapment neuropathy known as anconeus epitrochlearis (see Chapter 43).

Technique Careful preparation of the patient before trigger point injection helps to optimize results. Trigger point injections are directed at the primary trigger point rather than in the area of referred pain. It should be explained to the patient that the goal of trigger point injection is to block the trigger of the persistent pain and thus, it is hoped, provide long-lasting relief. It is important that the patient understand that for most patients with myofascial pain syndrome, more than one treatment modality is required for optimal pain 123

124        SECTION 3  •  Elbow and Forearm

Humerus, head Deltoid m.

••

•

Cephalic v.

•

•

Humerus, shaft

•

Biceps m.

•

•

Brachialis m.

•

•

•

Referred pain

•

Anconeus m. Trigger point

Supraspinatus t.

••

•

••

Deltoid m. Infraspinatus m. Teres minor m. Post humeral circumflex a. Teres major m. Latissimus dorsi m. Triceps m., long head Triceps m., lat head

•

Anterior fat pad

•

Capitulum Radius, head Median antebrachial v. Supinator m.

• • •

•

Posterior fat pad

••

Extensor carpi ulnaris m. Supinator m.

•

• •

Pronator teres m.

Figure 42-2  The anconeus muscle is situated in the posterior elbow and functions as a weak elbow extender and an elbow stabilizer preventing ulnar subluxation during pronation. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, WB Saunders.)

After the goals of trigger point injection have been explained to the patient and proper preparation of the patient has been carried out, the trigger point to be injected is reidentified by palpation with the sterilely gloved finger. A syringe containing 10 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone to be injected is attached to a 25- or 27-gauge needle of a length adequate to reach the trigger point. Except for the muscles of posture in the low back, a 1½-inch needle will be adequate. A volume of 0.5 to 1.0 mL of solution is then injected into each trigger point (see Figure 42-1). A series of two to five treatment sessions may be required to completely abolish the trigger point; the patient should be informed of this. Figure 42-1  Patients with anconeus syndrome experience referred pain to the proximal forearm.

Side Effects and Complications

relief. The use of the recumbent or lateral position when identifying and marking trigger points, as well as when performing the actual trigger point injection, helps decrease the incidence of vasovagal reactions. The skin overlying the trigger point to be injected should always be prepared with antiseptic solution before injection to avoid infection.

The proximity to the ulnar nerve makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing interventional pain management techniques. If there is a significant component of lateral epicondylitis associated with anconeus syndrome, the potential to rupture the tendons of the anconeus muscle remains ever-present. Many patients also report a transient increase in pain after injection of trigger points in the anconeus muscle.

42  •  Injection Technique for Anconeus Syndrome        125

Clinical Pearls Trigger point injections are extremely safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of trigger point injection are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after trigger point injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid trauma to the ulnar nerve when structures of the posterior elbow are injected. The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators believe that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as amitriptyline and nortriptyline represent good first choices and should be given as a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow. Pregabalin and milnacipran have also been shown to provide palliation of the pain of fibromyalgia and should be considered for those patients who do not respond to or tolerate tricyclic antidepressants.

SUGGESTED READINGS Baldry P: Acupuncture treatment of fibromyalgia and myofascial pain. In Chaitow L, editor: Fibromyalgia syndrome, ed 3, Oxford, 2010, Churchill Livingstone, pp 145–159. Ge HY, Nie H, Madeleine P, et al: Contribution of the local and referred pain from active myofascial trigger points in fibromyalgia syndrome, Pain 147:233– 240, 2009. Ge HY, Wang Y, Danneskiold-Samsøe B, et al: The predetermined sites of examination for tender points in fibromyalgia syndrome are frequently associated with myofascial trigger points, J Pain 11:644–651, 2010. LeBlanc KE, LeBlanc LL: Musculoskeletal disorders, Prim Care 37:389–406, 2010. Partanen JV, Ojala TA, Arokoski JP: Myofascial syndrome and pain: a neurophysiological approach, Pathophysiology 17:19–28, 2010. Steinmann SP, Bishop AT: Chronic anconeus compartment syndrome: a case report, J Hand Surg Am 25:959–961, 2000.

Chapter 43 INJECTION TECHNIQUE FOR ANCONEUS EPITROCHLEARIS Indications and Clinical Considerations Anconeus epitrochlearis is an uncommon cause of lateral forearm pain and weakness that can be quite distressing to the patient. Anconeus epitrochlearis is caused by entrapment and compression of the ulnar nerve at the elbow by an accessory anconeus muscle (Figures 43-1 and 43-2). This entrapment neuropathy manifests as pain and associated paresthesias in the lateral forearm that radiates to the wrist and ring and little fingers in a manner analogous to tardy ulnar palsy. The symptoms are often aggravated by prolonged flexion of the elbow. The pain of anconeus epitrochlearis has been characterized as unpleasant and dysesthetic. The onset of symptoms is usually after repetitive elbow motions or from repeated pressure on the elbow such as occurs from using the elbows to arise from bed. Anconeus epitrochlearis is also seen in throwing athletes such as baseball pitchers and quarterbacks. Direct trauma to the ulnar nerve as it enters the cubital tunnel may also result in a similar clinical presentation, as can compression of the ulnar nerve as it passes through the cubital tunnel by osteophytes, lipomas, ganglia, and aponeurotic bands. If the condition is untreated, progressive motor deficit and ultimately flexion contracture of the affected fingers can result. Physical findings include tenderness over the ulnar nerve at the elbow. A positive Tinel sign over the ulnar nerve as it passes beneath the aponeuroses is usually present. Weakness of the intrinsic muscles of the forearm and hand that are innervated by the ulnar nerve may be identified with careful manual muscle testing, although early in the course of the evolution of anconeus epitrochlearis, the only physical finding other than tenderness over the nerve may be the loss of sensation on the ulnar side of the little finger. As the syndrome progresses, the affected hand may take on a clawlike appearance. A positive Wartenberg sign indicative of weakness of the adduction of the fifth digit is often present. A positive Froment sign may also be present. Electromyography helps to distinguish cervical radiculopathy and anconeus epitrochlearis from golfer’s elbow. Plain radiographs are indicated for all patients with anconeus epitrochlearis to rule out occult bony disease, such as osteophytes impinging on the ulnar nerve. On the basis of the patient’s clinical presentation, additional testing including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody testing may be indicated. Magnetic resonance imaging (MRI) and/or ultrasound imaging of the elbow is indicated if joint instability is suspected and will clearly identify if the compression of the ulnar nerve is caused by an accessory anconeus muscle. Injection of the ulnar nerve will serve as both a diagnostic and a therapeutic maneuver. 126

Anconeus epitrochlearis is often misdiagnosed as golfer’s elbow, and this fact accounts for the many patients whose “golfer’s elbow” fails to respond to conservative measures. Anconeus epitrochlearis can be distinguished from golfer’s elbow in that in anconeus epitrochlearis, the maximal tenderness to palpation is over the ulnar nerve 1 inch below the medial epicondyle, whereas with golfer’s elbow the maximal tenderness to palpation is directly over the medial epicondyle. Anconeus epitrochlearis should also be differentiated from cervical radiculopathy involving the C7 or C8 roots and golfer’s elbow. Furthermore, it should be remembered that cervical radiculopathy and ulnar nerve entrapment may coexist as the “double crush” syndrome. The double crush syndrome is seen most commonly with median nerve entrapment at the wrist or carpal tunnel syndrome.

Clinically Relevant Anatomy Working with the other muscles of the posterior elbow, the anconeus muscle helps stabilize the elbow by stabilizing the proximal ulna during pronation of the forearm to prevent ulnar subluxation as well as by adducting and medially rotating the humerus. Situated posterior to the elbow joint, the anconeus muscle is a triangular muscle that arises from the lateral epicondyle of the humerus and finds its insertion into the lateral margin of the olecranon and posterior ulna (see Figure 43-3). The muscle is innervated by the

Figure 43-1  Anconeus epitrochlearis above the cubital tunnel compressing the ulnar nerve. (From Boero S, Sénès FM, Catena N: Pediatric cubital tunnel syndrome by anconeus epitrochlearis: a case report, J Shoulder Elbow Surg 18:e21–e23, 2009.)

43  •  Injection Technique for Anconeus Epitrochlearis        127

Inflamed and compressed ulnar nerve Anconeus epitrochlearis Anconeus

Figure 43-2  Ulnar nerve after muscle excision. (From Boero S, Sénès FM, Catena N: Pediatric cubital tunnel syndrome by anconeus epitrochlearis: a case report, J Shoulder Elbow Surg 18:e21–e23, 2009.)

radial nerve. The anconeus muscle is susceptible to trauma and to wear and tear from overuse and misuse and may develop myofascial pain syndrome as well as epicondylitis at its origin on the lateral epicondyle of the humerus.

Technique Careful preparation of the patient before this injection technique helps to optimize results. The use of the recumbent or lateral position is optimal when performing this injection technique. The patient is placed in a supine position with the arm fully adducted at the patient’s side and the elbow flexed with the palm of the hand resting on the patient’s abdomen. A total of 2 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. After sterile preparation of the skin overlying the posterior aspect of the joint, the lateral margin of the olecranon process and lateral epicondyle of the humerus are identified. With strict aseptic technique, a 1-inch, 25-gauge blunt bevel needle is inserted through the skin and subcutaneous tissues at a point midway between the lateral margin of the olecranon process and lateral epicondyle of the humerus (Figure 43-3). The needle is advanced very slowly into the anconeus muscle, with care being taken not to advance the needle too deeply and risk injuring the ulnar nerve. If bone is encountered or a paresthesia is elicited, the needle is withdrawn back into muscle. After the needle is in satisfactory position, the contents of the syringe are slowly injected. There should be little resistance to injection. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complications associated with anconeus epitrochlearis fall into two categories: (1) iatrogenically induced complications from persistent and overaggressive treatment of “resistant golfer’s elbow” and (2) the potential for permanent neurologic deficits caused by prolonged untreated entrapment of the ulnar nerve. Failure of the clinician to recognize an acute inflammatory or

Figure 43-3  Anconeus epitrochlearis is an uncommon cause of lateral forearm pain and weakness resulting from entrapment and compression of the ulnar nerve by the anconeus muscle.

infectious arthritis of the elbow may result in permanent damage to the joint as well as chronic pain and functional disability. The proximity to the ulnar nerve makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing interventional pain management techniques. If there is a significant component of lateral epicondylitis associated with anconeus epitrochlearis, the potential to rupture the tendons of the anconeus muscle remains everpresent. Many patients also report a transient increase in pain after injection of trigger points in the anconeus muscle.

Clinical Pearls An accessory anconeus muscle is present in approximately 11% of the adult population. Anconeus epitrochlearis is a distinct clinical entity that is often misdiagnosed as golfer’s elbow, and this fact accounts for the many patients whose “golfer’s elbow” fails to respond to conservative measures. Anconeus epitrochlearis can be distinguished from golfer’s elbow in that with anconeus epitrochlearis the maximal tenderness to palpation is over the ulnar nerve and a positive Tinel sign is present, whereas with golfer’s elbow the maximal tenderness to palpation is over the medial epicondyle. If anconeus epitrochlearis is suspected, injection of the radial nerve at the elbow with a local anesthetic and steroid will give almost instantaneous relief. Careful neurologic examination to identify preexisting neurologic deficits that may later be attributed to the nerve block should be performed on all patients before beginning ulnar nerve block at the elbow.

128        SECTION 3  •  Elbow and Forearm SUGGESTED READINGS O’Hara JJ, Stone JH: Ulnar nerve compression at the elbow caused by a prominent medial head of the triceps and an anconeus epitrochlearis muscle, J Hand Surg Br 21:133–135, 1996.

Steinmann SP, Bishop AT: Chronic anconeus compartment syndrome: a case report, J Hand Surg Am 25:959–961, 2000.

Chapter 44 ULNAR NERVE BLOCK AT THE ELBOW Indications and Clinical Considerations Cubital tunnel syndrome is caused by compression of the ulnar nerve by an aponeurotic band that runs from the medial epicondyle of the humerus to the medial border of the olecranon (Figure 44-1). This entrapment neuropathy manifests as pain and associated paresthesias in the lateral forearm that radiate to the wrist and ring and little fingers. If the condition remains untreated, progressive motor deficit and ultimately flexion contracture of the affected fingers can result. The onset of symptoms is usually after repetitive elbow motions or from repeated pressure on the elbow, such as occurs from using the elbows to rise from bed. Direct trauma to the ulnar nerve as it enters the cubital tunnel also may result in a similar clinical presentation. Physical findings include tenderness over the ulnar nerve at the elbow. A positive Tinel sign over the ulnar nerve as it passes beneath

Superficial branch Deep branch

the aponeuroses is usually present (Figure 44-2). Weakness of the intrinsic muscles of the forearm and hand that are innervated by the ulnar nerve may be identified with careful manual muscle testing (Table 44-1). Manual muscle testing that assesses the strength of the adductor pollicis includes the Froment and Jeanne signs (­Figure 44-3). Manual muscle testing that tests the interosseus muscles includes the crossed finger test, the finger flexion test, and the Egawa sign (Figure 44-4). Manual muscle testing that assesses the strength of the lumbar innervated lumbrical muscles includes the Duchenne and André-Thomas signs. Manual muscle testing that assesses the strength of the hypothenar muscles includes the Wartenberg, Masse, and Pitres-Testut signs (Figure 44-5). It should be noted that there is always the possibility that a patient with cubital tunnel syndrome may also have additional ulnar, median, or radial nerve lesions distal to the elbow that may confuse the clinical picture. Furthermore, the clinician should be aware that early in the course of the evolution of cubital tunnel syndrome the only physical finding other than tenderness over the nerve may be the loss of sensation on the ulnar side of the little finger. Cubital tunnel syndrome often is misdiagnosed as golfer’s elbow, and this fact accounts for the many patients whose “golfer’s elbow” fails to respond to conservative measures. Cubital tunnel syndrome can be distinguished from golfer’s elbow in that in cubital tunnel syndrome the maximal tenderness to palpation is over the ulnar nerve 1 inch below the medial epicondyle, whereas in golfer’s elbow the maximal tenderness to palpation is directly over the medial epicondyle (see Figure 52-1). Cubital tunnel syndrome also should be differentiated from cervical radiculopathy

Ulnar nerve

Figure 44-1  In cubital tunnel syndrome, the point of maximal tenderness is 1 inch below the medial epicondyle.

Figure 44-2  Tinel sign at elbow.

129

130        SECTION 3  •  Elbow and Forearm

involving the C7 or C8 roots and golfer’s elbow. Furthermore, it should be remembered that cervical radiculopathy and ulnar nerve entrapment may coexist as the so-called “double crush” syndrome. The double crush syndrome is seen most commonly with median nerve entrapment at the wrist or with carpal tunnel syndrome. Electromyography helps distinguish cervical radiculopathy and cubital tunnel syndrome from golfer’s elbow. Plain radiographs and magnetic resonance imaging (MRI) are indicated for all patients with cubital tunnel syndrome to rule out occult bony disease and to confirm the clinical diagnosis (Figure 44-6). On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood count, uric acid, sedimentation rate, and antinuclear antibody testing. MRI of the elbow is indicated if joint instability is suspected. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The ulnar nerve is made up of fibers from the C6-T1 spinal roots. The nerve lies anterior and inferior to the axillary artery in the 3 o’clock to 6 o’clock quadrant. Exiting the axilla, the ulnar nerve descends into the upper arm along with the brachial artery. At the middle of the upper arm, the nerve courses medially to pass between the olecranon process and medial epicondyle of the humerus. It is at this point that the entrapment of the ulnar nerve responsible for cubital tunnel syndrome occurs. The nerve then enters the cubital tunnel and passes between the heads of the flexor carpi ulnaris muscle, continuing downward, moving radially along with the ulnar artery. At a point approximately 1 inch proximal to the crease of the wrist, the ulnar nerve divides into the dorsal and palmar branches. The dorsal branch provides sensation to the ulnar aspect of the

TABLE 44-1

Summary of Ulnar Nerve Motor Signs and Tests Grouped by Affected Musculature Test Name

Description

Positive Result

Motor Signs Involving the Adductor Pollicis Muscle Froment sign

The patient holds a piece of paper using a lateral pinch. The examiner then pulls the paper distally along the thumb’s longitudinal axis and assesses the patient’s method of stabilization.

Thumb IP flexion compensates for a weak adductor pollicis muscle.

Jeanne sign

The patient holds a piece of paper using a lateral pinch. The examiner then pulls the paper distally along the thumb’s longitudinal axis and assesses the patient’s method of stabilization.

Thumb MP hyperextension compensates for a weak adductor pollicis muscle.

Motor Signs and Tests Involving the Interosseous Muscles Finger flexion sign

Performed bilaterally at the same time. Both forearms and wrists are in neutral. Examiner first places a piece of paper between the middle and ring fingers in both hands and then pulls the paper distally.

The involved side will use MP flexion to compensate for interossei weakness.

Crossed finger test

Examiner asks the patient to cross the middle finger over the index finger.

Inability to cross the fingers. ­ ompare with uninvolved side. C

Egawa sign

Examiner asks the patient to flex the middle finger MP joint and then abduct it to both sides. This can be difficult to perform; therefore, bilateral assessment is recommended.

Inability to perform this action as compared with uninvolved side.

Motor Signs Involving the Ulnar Nerve–Innervated Lumbrical Muscles Duchenne sign

Sign is identified by observing the posture of the small and ring fingers on the involved side.

Clawing posture (MP hyperextension and IP flexion) present in the ring and small fingers.

André-Thomas sign

Sign is identified by observing the compensatory pattern used in the ring and small fingers during actions involving EDC use.

Wrist tends to flex with ring and small finger EDC activation.

Motor Signs Involving the Hypothenar Musculature Wartenberg sign

Patient actively abducts the fingers with the forearm in pronation and the wrist in neutral. Observe the small finger’s ability to fully adduct.

Inability of the small finger to fully adduct and touch the ring finger. Compare with the uninvolved side.

Masse sign

Observe the metacarpal arch as compared with the uninvolved side. The convex nature of the ulnar aspect of the hand is altered owing to hypothenar atrophy.

Flattened metacarpal arch

Pitres-Testut sign

Noted after the examiner asks the patient to shape the hand in the form of a cone. Although present in the literature, this sign is not commonly used in ­clinical practice settings.

Inability to shape the hand in the form of a cone.

Palmaris brevis sign

A rarely observed sign in lower ulnar nerve palsy, in which the lesion selectively affects the deep branch. Determine the presence of this sign by observing and evaluating the palmaris brevis muscle as compared with the uninvolved side.

The sparing of the palmaris brevis muscle as compared with the ­uninvolved side.

Motor Signs Involving the Extrinsic Ulnar Nerve–Innervated Muscles Nail file sign

Patient attempts to make a hook fist. Examiner places an index finger along the volar surface of the patient’s small and ring fingers, leaving the DIPs free to ­contract.

Decreased small and ring finger FDP strength as compared with the uninvolved side.

Modified from Goldman SB, Brininger TL, Schrader JW, Koceja DM: A review of clinical tests and signs for the assessment of ulnar neuropathy, J Hand Ther 22:209-220, 2009. DIP, Distal interphalangeal; EDC, extensor digitorum communis; FDP, flexor digitorum profundus; IP, interphalangeal; MP, metacarpophalangeal.

44  •  Ulnar Nerve Block at the Elbow        131

Figure 44-3  Positive Froment sign on the left, negative Froment sign on the right. It is recommended that the wrist be positioned in slight flexion when this test is performed. (From Goldman SB, Brininger TL, Schrader JW, Koceja DM: A review of clinical tests and signs for the assessment of ulnar neuropathy, J Hand Ther 22:209–220, 2009.)

Figure 44-4  Crossed finger test. The left hand shows a positive crossed finger test result as the index finger is unable to completely cross over the middle finger. The right hand shows a negative crossed finger test result. (From Goldman SB, Brininger TL, Schrader JW, Koceja DM: A review of clinical tests and signs for the assessment of ulnar neuropathy, J Hand Ther 22:209–220, 2009.)

Figure 44-5  Wartenberg sign. The right hand indicates a positive Wartenberg sign because the small finger is unable to fully adduct and touch the ring finger. The left hand indicates a negative Wartenberg sign. (From Goldman SB, Brininger TL, Schrader JW, Koceja DM: A review of clinical tests and signs for the assessment of ulnar neuropathy, J Hand Ther 22:209-220, 2009.)

dorsum of the hand, the dorsal aspect of the little finger, and the ulnar half of the ring finger. The palmar branch provides sensory innervation to the ulnar aspect of the palm of the hand, the palmar aspect of the little finger, and the ulnar half of the ring finger.

slightly cephalad trajectory (Figure 44-7). As the needle advances approximately ½ inch, a strong paresthesia in the distribution of the ulnar nerve is elicited. The patient should be warned that a paresthesia will occur and to say “there!” as soon as the paresthesia is felt. After the paresthesia has been elicited and its distribution identified, gentle aspiration is carried out to identify blood. If the aspiration test result is negative and no persistent paresthesia into the distribution of the ulnar nerve remains, 5 to 7 mL of solution is slowly injected, with the patient being monitored closely for signs of local anesthetic toxicity. If no paresthesia can be elicited, a similar amount of solution is slowly injected in a fanlike manner just proximal to the notch, with care being taken to avoid intravascular injection.

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side and the elbow slightly flexed with the dorsum of the hand resting on a folded towel. A total of 5 to 7 mL of local anesthetic is drawn up in a 12-mL sterile syringe. When treating painful or inflammatory conditions that are mediated via the ulnar nerve, a total of 80 mg of methylprednisolone is added to the local anesthetic with the first block and 40 mg of methylprednisolone is added with subsequent blocks. The clinician then identifies the olecranon process and the medial epicondyle of the humerus. The ulnar nerve sulcus between these two bony landmarks is then identified. After preparation of the skin with antiseptic solution, a ⅝-inch, 25-gauge needle is inserted just proximal to the sulcus and is slowly advanced in a

Side Effects and Complications Ulnar nerve block at the elbow is a relatively safe block, with the major complications being inadvertent intravascular injection into the ulnar artery and persistent paresthesia secondary to needle trauma to the nerve. As the nerve passes through the ulnar nerve

132        SECTION 3  •  Elbow and Forearm

complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block also decreases the amount of postprocedure pain and bleeding the patient may experience.

Clinical Pearls

Figure 44-6  Entrapment neuropathy: cubital tunnel syndrome. A transaxial T2-weighted (TR/TE, 2000/70) spin-echo magnetic resonance image, accomplished with fat suppression, shows increased signal intensity in the ulnar nerve (arrow) within the cubital tunnel. The medial (m) and lateral (l) epicondyles of the humerus and the olecranon process (o) of the ulna are indicated. A joint effusion is present. (Courtesy S. K. Brahme, MD, La Jolla, Calif; from Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

Superficial branch Deep branch

Radius Ulna

Ulnar nerve block at the elbow is a simple and safe technique in the evaluation and treatment of the previously mentioned painful conditions. Careful neurologic examination to identify preexisting neurologic deficits that may later be attributed to the nerve block should be performed on all patients before beginning ulnar nerve block at the elbow, because there seems to be a propensity for the development of persistent paresthesia when the ulnar nerve is blocked at this level. The incidence of persistent paresthesia can be decreased by blocking the nerve proximal to the ulnar nerve sulcus and injecting slowly. Ulnar nerve block at the elbow is especially useful in the treatment of pain secondary to ulnar nerve compression syndromes at the elbow, including cubital tunnel syndrome. Cubital tunnel syndrome is often misdiagnosed as golfer’s elbow, and this fact accounts for the many patients whose “golfer’s elbow” fails to respond to conservative measures. Cubital tunnel syndrome can be distinguished from golfer’s elbow in that in cubital tunnel syndrome the maximal tenderness to palpation is over the ulnar nerve 1 inch below the medial epicondyle, whereas in golfer’s elbow the maximal tenderness to palpation is directly over the medial epicondyle. If cubital tunnel syndrome is suspected, injection of the ulnar nerve at the elbow with local anesthetic and steroid gives almost instantaneous relief. Cubital tunnel syndrome also should be differentiated from cervical radiculopathy involving the C8 spinal root, which may at times mimic ulnar nerve compression. Furthermore, it should be remembered that cervical radiculopathy and ulnar nerve entrapment may coexist in the so-called “double crush” syndrome. The double crush syndrome is seen most commonly with median nerve entrapment at the wrist or with carpal tunnel syndrome. Pancoast tumor invading the medial cord of the brachial plexus may also mimic an isolated ulnar nerve entrapment and should be ruled out by apical lordotic chest radiograph. SUGGESTED READINGS

Ulnar nerve

Medial epicondyle Aponeurotic band Figure 44-7  Compression of the ulnar nerve at the elbow is often caused by an aponeurotic band.

sulcus, it is enclosed by a dense fibrous band, so care should be taken to slowly inject just proximal to the sulcus in order to avoid additional compromise of the nerve. This technique can be performed safely in the presence of anticoagulation by using a 25or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable risk-to-benefit ratio. These

Bencardino JT, Rosenberg ZS: Entrapment neuropathies of the shoulder and elbow in the athlete, Clin Sports Med 25:465–487, 2006. Burge P: Abducted little finger in low ulnar nerve palsy, J Hand Surg Br 11:234– 236, 1986. Waldman SD: Ulnar nerve entrapment at the elbow. In Pain review, Philadelphia, 2009, Saunders. Waldman SD: The little finger adduction test for ulnar nerve entrapment at the elbow. In Physical diagnosis of pain, ed 2, Philadelphia, 2010, Saunders. Waldman SD: The Wartenberg test for ulnar nerve entrapment at the elbow. In Physical diagnosis of pain, ed 2, Philadelphia, 2010, Saunders.

Chapter 45 INJECTION TECHNIQUE FOR DRIVER’S ELBOW Indications and Clinical Considerations The ulnar nerve is susceptible to compression when a driver or passenger rests his or her elbow on the lower sill of the vehicle window while the shoulder is abducted and the elbow flexed. When the elbow is flexed, the proximal edge of the arcuate ligament becomes taut and the total volume of the cubital tunnel is decreased, resulting in increased intratunnel pressure that further compromises the ulnar nerve. Vibration transmitted from the car body to the elbow may also further contribute to compromise of the ulnar nerve. This entrapment neuropathy manifests as pain and associated paresthesias in the lateral forearm that radiate to the wrist and ring and little fingers. If the condition remains untreated, progressive motor deficit and ultimately flexion contracture of the affected fingers can result. Physical findings include tenderness over the ulnar nerve at the elbow. A positive Tinel sign over the ulnar nerve as it passes beneath the aponeuroses is usually present (see Figure 44-2). Weakness of the intrinsic muscles of the forearm and hand that are innervated by the ulnar nerve may be identified with careful manual muscle testing (see Table 44-1). It should be noted that there is always the possibility that a patient with driver’s elbow may also have a coexistent ulnar, median, or radial nerve lesion distal to the elbow that may confuse the clinical picture. Furthermore, it should be remembered that cervical radiculopathy and ulnar nerve entrapment may coexist as the so-called double crush syndrome. The double crush syndrome is seen most commonly with median nerve entrapment at the wrist or with carpal tunnel syndrome. The clinician should be aware that early in the course of the evolution of driver’s elbow the only physical finding other than tenderness over the nerve may be the loss of sensation on the ulnar side of the little finger. Driver’s elbow is an entrapment neuropathy caused by external compression of the ulnar nerve, which clinically mimics cubital tunnel syndrome. It is often is misdiagnosed as golfer’s elbow, and this fact accounts for the many patients whose “golfer’s elbow” fails to respond to conservative measures. Driver’s elbow can be distinguished from golfer’s elbow in that in driver’s elbow the maximal tenderness to palpation is over the ulnar nerve 1 inch below the medial epicondyle, whereas in golfer’s elbow the maximal tenderness to palpation is directly over the medial epicondyle (see Figure 52-1). Driver’s elbow should also be differentiated from cervical radiculopathy involving the C7 or C8 roots and golfer’s elbow. Electromyography helps distinguish cervical radiculopathy and driver’s elbow from golfer’s elbow. Ultrasound imaging of the elbow may be useful in assessing the status of the ulnar nerve and can provide important anatomic information when combined with the neurophysiologic data obtained from

electromyography (Figure 45-1). Plain radiographs and magnetic resonance and ultrasound imaging are indicated in all patients with driver’s elbow to rule out intrinsic disease of the elbow joint (Figure 45-2). On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood count, uric acid, sedimentation rate, and antinuclear antibody testing. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The ulnar nerve is made up of fibers from C6-T1 spinal roots. The nerve lies anterior and inferior to the axillary artery in the 3 o’clock to 6 o’clock quadrant. Exiting the axilla, the ulnar nerve descends into the upper arm along with the brachial artery. At the middle of the upper arm, the nerve courses medially to pass between the olecranon process and medial epicondyle of the humerus. It is at this point that the entrapment of the ulnar nerve responsible for cubital tunnel syndrome occurs. The nerve then enters the cubital tunnel and passes between the heads of the flexor carpi ulnaris muscle, continuing downward, moving radially along with the ulnar artery. At a point approximately 1 inch proximal to the crease of the wrist, the ulnar nerve divides into the dorsal and palmar branches. The dorsal branch provides sensation to the ulnar aspect of the dorsum of the hand, the dorsal aspect

ME

EJ

Figure 45-1  Longitudinal ultrasound image at the medial elbow (ME) demonstrating the ulnar nerve (arrows), which shows focal swelling at the elbow joint level. The arrows define the outline of the swollen nerve section. EJ, Elbow joint. (From Park GY, Kim JM, Lee SM: The ultrasonographic and electrodiagnostic findings of ulnar neuropathy at the elbow, Arch Phys Med Rehabil 85:1000–1005, 2004.)

133

134        SECTION 3  •  Elbow and Forearm

A

B

C

Figure 45-2  A and B, Preoperative radiographs and, C, magnetic resonance image show significant destruction of the left distal humerus by malignant tumor. (From Tang X, Guo W, Yang R, et al: Custom-made prosthesis replacement for reconstruction of elbow after tumor resection, J Shoulder Elbow Surg 18:796–803, 2009.)

of the little finger, and the ulnar half of the ring finger. The palmar branch provides sensory innervation to the ulnar aspect of the palm of the hand, the palmar aspect of the little finger, and the ulnar half of the ring finger.

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side and the elbow slightly flexed with the dorsum of the hand resting on a folded towel. A total of 5 to 7 mL of local anesthetic is drawn up in a 12-mL sterile syringe. When painful or inflammatory conditions that are mediated via the ulnar nerve are treated, a total of 80 mg of methylprednisolone is added to the local anesthetic with the first block and 40 mg of methylprednisolone is added with subsequent blocks. The clinician then identifies the olecranon process and the medial epicondyle of the humerus. The ulnar nerve sulcus between these two bony landmarks is then identified. After preparation of the skin with antiseptic solution, a ⅝-inch, 25-gauge needle is inserted just proximal to the sulcus and is slowly advanced in a slightly cephalad trajectory (see Figure 44-7). As the needle advances approximately ½ inch, a strong paresthesia in the distribution of the ulnar nerve is elicited. The patient should be warned that a paresthesia will occur and to say “there!” as soon as the paresthesia is felt. After the paresthesia has been elicited and its distribution identified, gentle

aspiration is carried out to identify blood. If the aspiration test result is negative and no persistent paresthesia into the distribution of the ulnar nerve remains, 5 to 7 mL of solution is slowly injected, with the patient being monitored closely for signs of local anesthetic toxicity. If no paresthesia can be elicited, a similar amount of solution is slowly injected in a fanlike manner just proximal to the notch, with care being taken to avoid intravascular injection.

Side Effects and Complications Ulnar nerve block at the elbow is a relatively safe block, with the major complications being inadvertent intravascular injection into the ulnar artery and persistent paresthesia secondary to needle trauma to the nerve. Because as the nerve passes through the ulnar nerve sulcus it is enclosed by a dense fibrous band, care should be taken to slowly inject just proximal to the sulcus in order to avoid additional compromise of the nerve. This technique can be performed safely in the presence of anticoagulation with a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable risk-to-benefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block also decreases the amount of postprocedure pain and bleeding the patient may experience.

45  •  Injection Technique for Driver’s Elbow        135

Clinical Pearls Ulnar nerve block at the elbow is a simple and safe technique in the evaluation and treatment of the previously mentioned painful conditions. Careful neurologic examination to identify preexisting neurologic deficits that may later be attributed to the nerve block should be performed for all patients before beginning ulnar nerve block at the elbow, because there seems to be a propensity for the development of persistent paresthesia when the ulnar nerve is blocked at this level. The incidence of persistent paresthesia can be decreased by blocking the nerve proximal to the ulnar nerve sulcus and injecting slowly. Ulnar nerve block at the elbow is especially useful in the treatment of pain secondary to ulnar nerve compression syndromes at the elbow, including driver’s elbow. Ulnar nerve entrapment at the elbow is often misdiagnosed as golfer’s elbow, and this fact accounts for the many patients whose “golfer’s elbow” fails to respond to conservative measures. Driver’s elbow can be distinguished from golfer’s elbow in that in driver’s elbow the maximal tenderness to palpation is over the ulnar nerve 1 inch below the medial epicondyle, whereas in golfer’s elbow the maximal tenderness to palpation is directly over the medial epicondyle. If cubital tunnel syndrome is suspected, injection of the ulnar nerve at the elbow with local anesthetic and steroid gives almost instantaneous relief. Driver’s elbow also should be differentiated from cervical radiculopathy involving the C8 spinal root, which may at times mimic ulnar nerve compression. Furthermore, it should be remembered that cervical radiculopathy and ulnar nerve entrapment may coexist in the so-called double crush syndrome. The double crush syndrome is seen most commonly with median nerve entrapment at the wrist or with carpal tunnel syndrome. Pancoast tumor invading the medial cord of the brachial plexus may also mimic an isolated ulnar nerve entrapment and should be ruled out by apical lordotic chest radiograph.

SUGGESTED READINGS Abdel-Salam A, Eyres KS, Cleary J: Drivers’ elbow: a cause of ulnar neuropathy, J Hand Surg Br 16:436–437, 1991. Palmer BA, Hughes TB: Cubital tunnel syndrome, J Hand Surg Am 35:153–163, 2010. Szabo RM, Kwak C: Natural history and conservative management of cubital ­tunnel syndrome, Hand Clin 23:311–318, 2007. Waldman SD: Golfer’s elbow. In Pain review, Philadelphia, 2009, Saunders, pp 267–268. Waldman SD: The ulnar nerve. In Pain review, Philadelphia, 2009, Saunders, p 76. Waldman SD: Ulnar nerve entrapment at the elbow. In Pain review, Philadelphia, 2009, Saunders, pp 270–271.

Chapter 46 INJECTION TECHNIQUE FOR OS SUPERTROCHLEARE–RELATED ELBOW PAIN Indications and Clinical Considerations Elbow pain secondary to os supratrochleare is being seen with increasing frequency in clinical practice owing to the increased interest in physical fitness and the use of exercise machines. Os supratrochleare is the name given to an accessory ossicle occasionally found in the posterior elbow. This accessory ossicle is often found adjacent to the proximal aspect of the olecranon process. It is thought that accessory ossicles such as os supratrochleare bones serve to decrease friction and pressure of tendons as they pass in proximity to a joint. Similar accessory ossicles are found in the feet, hands, and wrists (Figure 46-1). Elbow pain secondary to os supratrochleare is characterized by tenderness and pain over the posterior elbow. The patient often feels that he or she has gravel in the elbow and may report a severe grating sensation with flexion and extension of the elbow (see Figure 41-1). The pain of os supratrochleare worsens with activities that require repeated flexion and extension of the elbow or with forceful overhead throwing. Os supratrochleare is often associated with loose bodies in the elbow joint and may coexist with olecranon bursitis. On physical examination, pain can be reproduced by pressure on the os supratrochleare. In contradistinction to olecranon

Accessory ossicle

Figure 46-1  Patients with os supratrochleare often report pain and a grating sensation with flexion and extension of the affected elbow.

136

bursitis, in which the tender area remains over the olecranon bursa, in os supratrochleare the area of maximum tenderness will be just above the olecranon process. A creaking or grating sensation may be appreciated by the examiner, and locking or catching on extension and flexion of the elbow may occasionally be present. Plain radiographs are indicated for all patients with os supratrochleare to rule out fractures and to identify accessory ossicles and that may have become inflamed (Figure 46-2). Plain radiographs will also often identify loose bodies or joint mice, which are frequently present in patients with elbow pain secondary to os supratrochleare. On the basis of the patient’s clinical presentation, additional testing including complete blood cell count, sedimentation rate, and antinuclear antibody testing may be indicated. Magnetic resonance imaging (MRI) of the elbow joint is indicated if joint instability, occult mass, or tumor is suspected and to further clarify the diagnosis. Radionuclide bone scanning may be useful in the identification of stress fractures or tumors of the elbow and distal humerus that may be missed on plain radiographs. Screening laboratory testing consisting of complete blood cell count, erythrocyte sedimentation rate, and automated blood chemistry testing should be performed if the diagnosis is in question. Arthrocentesis of the elbow joint may be indicated if septic arthritis or crystal arthropathy is suspected. Os supratrochleare pain syndrome is a clinical diagnosis that is supported by a combination of clinical history, physical examination, radiography, and MRI. Pain syndromes that may mimic os supratrochleare pain syndrome include primary disease of the elbow, including gout and occult fractures as well as bursitis and tendonitis and epicondylitis of the elbow, both of which may coexist with os supratrochleare. Osteochondritis dissecans, Panner disease, and synovial chondromatosis may also mimic the pain associated with os supratrochleare. Primary and metastatic tumors of the elbow may also manifest in a manner analogous to elbow pain secondary to os supratrochleare.

Clinically Relevant Anatomy The elbow joint is a synovial, hinge-type joint that serves as the articulation among the humerus, radius, and ulna (see Figure 41-3). The joint’s primary function is to position the wrist to optimize hand function. The joint allows flexion and extension at the elbow, as well as pronation and supination of the forearm. The joint is lined with synovium, and the resultant synovial space allows intraarticular injection. The entire joint is covered by a dense capsule that thickens medially to form the ulnar collateral ligament and laterally to form the radial collateral ligaments. These dense ligaments, coupled with the elbow joint’s deep bony socket, make this joint extremely stable and relatively resistant to subluxation and dislocation. The

46  •  Injection Technique for Os Supertrochleare–Related Elbow Pain        137

Figure 46-2  Large os supratrochleare dorsale accessory ossicle. (arrow) (From Wood VE, Campbell GS: The supratrochleare dorsale accessory ossicle in the elbow, J Shoulder Elbow Surg 3:395–398, 1994.)

anterior and posterior joint capsule is less dense and may become distended if there is a joint effusion. The olecranon bursa lies in the posterior aspect of the elbow joint and may become inflamed as a result of direct trauma or overuse of the joint. Bursae susceptible to the development of bursitis also exist between the insertion of the biceps and the head of the radius, as well as in the antecubital and cubital area. The elbow joint is innervated primarily by the musculocutaneous and radial nerves, with the ulnar and median nerves providing varying degrees of innervation. At the middle of the upper arm the ulnar nerve courses medially to pass between the olecranon process and medial epicondyle of the humerus. The nerve is susceptible to entrapment and trauma at this point. At the elbow the median nerve lies just medial to the brachial artery and occasionally is damaged during brachial artery cannulation for blood gases.

Technique Careful preparation of the patient before this injection technique helps to optimize results. The use of the recumbent or lateral position is optimal for performing this injection technique. The patient is placed in a supine position with the arm fully adducted at the patient’s side and the elbow flexed with the palm of the hand resting on the patient’s abdomen. A total of 2 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. After sterile preparation of the skin overlying the posterior aspect of the joint, the lateral margin of the olecranon process and lateral epicondyle of the humerus are identified. With strict aseptic technique, a 1-inch, 25-gauge blunt bevel needle is inserted through the skin and subcutaneous tissues at a point midway between the lateral margin of the olecranon process and lateral epicondyle of the humerus (Figure 46-3). The needle is advanced

Figure 46-3  Injection of the elbow.

very slowly approximately 0.5 cm, with care being taken not to advance the needle too deeply and risk injuring the ulnar nerve. If bone is encountered or a paresthesia is elicited, the needle is withdrawn. After the needle is in a satisfactory position, the contents of the syringe are slowly injected. There should be little resistance to injection. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of injection of os supratrochleare is infection. This complication should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients report

138        SECTION 3  •  Elbow and Forearm

a transient increase in pain after injection for os supratrochleare, and the patient should be warned of this. Another potential risk of this injection technique is trauma to the extensor tendons from the injection itself.

Clinical Pearls Pain emanating from the elbow is a common problem encountered in clinical practice. Os supratrochleare must be distinguished from fractures of the elbow, fractures of the os supratrochleare itself, entrapment neuropathies of the ulnar nerve, bursitis, tendonitis, and epicondylitis. Less common causes of posterior elbow pain include osteochondritis dissecans, Panner disease, and synovial chondromatosis.

SUGGESTED READINGS Dalal S, Bull M, Stanley D: Radiographic changes at the elbow in primary osteoarthritis: a comparison with normal aging of the elbow joint, J Shoulder Elbow Surg 16:358–361, 2007. Kokkalis ZT, Schmidt CC, Sotereanos DG: Elbow arthritis: current concepts, J Hand Surg Am 34:761–768, 2009. Steinbach LS, Fritz RC, Tirman PF, Uffman M: Magnetic resonance imaging of the elbow, Eur J Radiol 25:223–241, 1997. Waldman SD: Functional anatomy of the elbow joint. In Pain review, Philadelphia, 2009, Saunders, pp 90–94. Wood VE, Campbell GS: The supratrochleare dorsale accessory ossicle in the elbow, J Shoulder Elbow Surg 3:395–398, 1994.

Chapter 47 LATERAL EPICONDYLE INJECTION

Indications and Clinical Considerations Tennis elbow (also known as lateral epicondylitis) is caused by repetitive microtrauma to the extensor tendons of the forearm. The pathophysiology of tennis elbow is initially caused by microtearing at the origin of the extensor carpi radialis and extensor carpi ulnaris. Secondary inflammation may occur, which can become chronic as a result of continued overuse or misuse of the extensors of the forearm. Coexistent bursitis, arthritis, and gout also may perpetuate the pain and disability of tennis elbow. Tennis elbow occurs in patients engaged in repetitive activities that include hand grasping, such as politicians shaking hands, or high-torque wrist turning, such as scooping ice cream at an ice cream parlor. Tennis players develop tennis elbow by two separate mechanisms: (1) increased pressure grip strain as a result of playing with too heavy a racquet and (2) making backhand shots with a leading shoulder and elbow rather than keeping the shoulder and elbow parallel to the net (Figure 47-1). Other racquet sport players also are susceptible to the development of tennis elbow. The pain of tennis elbow is localized to the region of the lateral epicondyle. It is constant and is made worse with active contraction of the wrist. Patients note the inability to hold a coffee cup or hammer. Sleep disturbance is common. On physical examination there is tenderness along the extensor tendons at or just below

the lateral epicondyle. Many patients with tennis elbow exhibit a bandlike thickening within the affected extensor tendons. Elbow range of motion is normal. Grip strength on the affected side is diminished. Patients with tennis elbow demonstrate a positive tennis elbow test result (Figures 47-2 and 47-3). The test is

Figure 47-2  Test for tennis elbow. (From Waldman SD: Physical diagnosis of pain, Philadelphia, 2005, Saunders.)

Leading shoulder

Heavy racquet Leading elbow Improper wrist position

Excessive grip pressure

Figure 47-1  Causes of tennis elbow.

Figure 47-3  Patients with tennis elbow will exhibit a positive tennis elbow test result.

139

140        SECTION 3  •  Elbow and Forearm

Figure 47-4  In tennis elbow, the maximum tenderness to palpation is over the lateral epicondyle, whereas patients with radial tarsal syndrome will experience maximal tenderness over the radial nerve. (From Waldman SD: Physical diagnosis of pain, Philadelphia, 2005, Saunders.)

Figure 47-5  A 45-year-old man with extensor tendonitis (tennis elbow). Doppler ultrasound shows thickened extensor origin (star) with enthesophyte (arrowheads) and mild neovascularity (arrow) within the common extensor tendon. Note the radiocapitellar joint.

biceps and the head of the radius, as well as in the antecubital and cubital area.

performed by stabilizing the patient’s forearm and then having the patient clench his or her fist and actively extend the wrist. The examiner then attempts to force the wrist into flexion. Sudden, severe pain is highly suggestive of tennis elbow. Radial tunnel syndrome and occasionally C6-C7 radiculopathy can mimic tennis elbow. Radial tunnel syndrome is an entrapment neuropathy that is a result of entrapment of the radial nerve below the elbow. Radial tunnel syndrome can be distinguished from tennis elbow in that in radial tunnel syndrome the maximal tenderness to palpation is distal to the lateral epicondyle over the radial nerve, whereas in tennis elbow the maximal tenderness to palpation is over the lateral epicondyle (Figure 47-4). Electromyography helps distinguish cervical radiculopathy and radial tunnel syndrome from tennis elbow. Plain radiographs are indicated in all patients with tennis elbow to rule out joint mice and other occult bony disease. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the elbow is indicated if joint instability is suspected. Ultrasound evaluation may also aid in diagnosis in questionable cases (Figure 47-5). The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

The patient is placed in a supine position with the arm fully adducted at the patient’s side and the elbow flexed with the dorsum of the hand resting on a folded towel to relax the affected tendons. A total of 1 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. After sterile preparation of skin overlying the posterolateral aspect of the joint, the lateral epicondyle is identified. With strict aseptic technique, a 1-inch, 25-gauge needle is inserted perpendicular to the lateral epicondyle through the skin and into the subcutaneous tissue overlying the affected tendon (Figure 47-8). If bone is encountered, the needle is withdrawn back into the subcutaneous tissue. The contents of the syringe are then gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in the tendon and should be withdrawn back until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. Ultrasound guidance may be beneficial in those patients in whom the anatomic landmarks required to perform this block are difficult to identify (Figures 47-9 and 47-10).

Clinically Relevant Anatomy

Side Effects and Complications

The most common nidus of pain from tennis elbow is the bony origin of the extensor tendon of extensor carpi radialis brevis at the anterior facet of the lateral epicondyle (Figures 47-6 and 47-7). Less commonly, tennis elbow pain can originate from the origin of the extensor carpi radialis longus at the supracondylar crest or, rarely, more distally at the point where the extensor carpi radialis brevis overlies the radial head. As mentioned earlier, bursitis may accompany tennis elbow. The olecranon bursa lies in the posterior aspect of the elbow joint and may also become inflamed as a result of direct trauma or overuse of the joint. Other bursae susceptible to the development of bursitis exist between the insertion of the

The major complications associated with this injection technique are related to trauma to the inflamed and previously damaged tendons. Such tendons may rupture if directly injected, and needle position should be confirmed outside the tendon before injection to avoid this complication. Another complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. The ulnar nerve is especially susceptible to damage at the elbow, and care must be taken to avoid this nerve when injecting in this anatomic region. Approximately 25% of patients note a transient increase in pain after this injection technique; the patient should be warned of this.

Technique

47  •  Lateral Epicondyle Injection        141

••

Triceps m.

•

Brachioradialis m.

•

Brachialis m.

•

Pronator m.

Olecranon

•

Med. epicondyle

•• ••

•

•

•

Supinator m., deep portion Radial n., deep branch

Coronoid

•

•• • ••

Common flexor t. Med. collateral lig.

•

• •

Pronator teres m. Brachialis m. & t.

••

••

Median n. Pronator teres t., ulnar head Ulnar a.

• •

Supinator m., superficial portion Extensor digitorum m.

••

•

Common extensor t. Lat. collateral & annular ligs. Extensor carpi radialis longus & brevis mm. Radius, head

•

Lat. epicondyle

• •

Palmaris longus m. Flexor digitorum superficialis m.

Figure 47-6  Magnetic resonance image illustrating the relationship of the lateral epicondyle and associated muscles. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

142        SECTION 3  •  Elbow and Forearm

••

Triceps m.

•

Brachioradialis m.

••

•

Brachialis m.

•

Olecranon

•

• •

Lat. collateral & annular ligs.

• •

•

• ••

•

Supinator m., deep portion Radial n., deep branch

Pronator teres m. Coronoid Brachiallis m. & t. Pronator teres t., ulnar head

•• •

••

Common flexor t. Med collateral lig.

•

• •

Supinator m., superficial portion

•

Palmaris longus m. Flexor carpi radialis m. Ulnar a.

• •

Extensor digitorum m.

••

••

Radius, head Extensor carpi radialis brevis m.

Med. epicondyle

•

Lat. epicondyle Common extensor t.

•

••

Extensor carpi radialis longus m.

Pronator teres m.

•

Flexor digitorum superficialis m.

Figure 47-7  Anatomic coronal section of the elbow illustrating the relationship of the lateral epicondyle and associated muscles. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

Radial nerve Head of radius Extensor carpi radialis longus m. Extensor carpi radialis brevis m.

Inflamed and torn tendons Figure 47-8  For injection to be performed to treat tennis elbow, the needle is inserted perpendicular to the lateral epicondyle toward the affected tendon.

Figure 47-9  Proper transducer position for injection of the lateral epicondyle to treat tennis elbow.

47  •  Lateral Epicondyle Injection        143 SUGGESTED READINGS

*

Figure 47-10  Injection of corticosteroid in the treatment of lateral epicondylitis. A needle (arrow) is directed to the surface of the inflamed tendon (asterisk). (From del Cura JL: Ultrasound-guided therapeutic procedures in the musculoskeletal system, Curr Probl Diagn Radiol 37:203–218, 2008.)

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to tennis elbow. Coexistent bursitis and tendinitis also may contribute to elbow pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat as well as gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for elbow pain. A Velcro band placed around the extensor tendons also may help relieve the symptoms of tennis elbow. Vigorous exercise should be avoided, because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique. As mentioned previously, cervical radiculopathy and radial tunnel syndrome may mimic tennis elbow and must be ruled out to effectively treat the underlying disease.

del Cura JL: Ultrasound-guided therapeutic procedures in the musculoskeletal ­system, Curr Probl Diagn Radiol 37:203–218, 2008. Faro F, Wolf JM: Lateral epicondylitis: review and current concepts, J Hand Surg Am 32:1271–1279, 2007. Rineer CA, Ruch DS: Elbow tendinopathy and tendon ruptures: epicondylitis, biceps and triceps ruptures, J Hand Surg Am 34:566–576, 2009. Waldman SD: Injection technique for tennis elbow. In Pain review, Philadelphia, 2009, Saunders, pp 458–459. Waldman SD: Tennis elbow. In Pain review, Philadelphia, 2009, Saunders, pp 266–267.

Chapter 48 RADIAL NERVE BLOCK AT THE HUMERUS

Indications and Clinical Considerations Radial tunnel syndrome is an entrapment neuropathy of the radial nerve that is often clinically misdiagnosed as resistant tennis elbow. In radial tunnel syndrome the posterior interosseous branch of the radial nerve is entrapped by a variety of mechanisms that have a similar clinical presentation in common. These mechanisms include aberrant fibrous bands in front of the radial head, anomalous blood vessels that compress the nerve, ganglion cysts, or a sharp tendinous margin of the extensor carpi radialis brevis (Figure 48-1). These entrapments may exist alone or in combination.

Regardless of the mechanism of entrapment of the radial nerve, the common clinical feature of radial tunnel syndrome is pain just below the lateral epicondyle of the humerus. The pain of radial tunnel syndrome may develop after an acute twisting injury or direct trauma to the soft tissues overlying the posterior interosseous branch of the radial nerve, or the onset may be more insidious, without an obvious inciting factor. The pain is constant and is made worse with active supination of the wrist. Patients often note the inability to hold a coffee cup or hammer. Sleep disturbance is common. On physical examination there is tenderness to palpation of the posterior interosseous branch of the radial nerve just below the lateral epicondyle. Elbow range of motion is normal. Grip strength on the affected side may be diminished. Patients

Distal

p.i.n. Proximal

A

r.n.

B

p.i.n. r.n.

C Figure 48-1  A teenage musician was diagnosed with radial tunnel syndrome after seeking treatment for pain over the left proximal, radial forearm with activity and with no neurologic deficit. Despite conservative therapy, her pain persisted, and a decompression of the posterior interosseous nerve was performed. A, The proposed curvilinear incision over the proximal lateral forearm is shown. The radial nerve was exposed at the bifurcation into the superficial radial and posterior interosseous nerves. B, Fibrous bands (arrow) were found overlying the posterior interosseous nerve at the arcade of Fröhse. C, Compression of the posterior interosseous nerve by overlying vasculature (arrow) was also observed. p.i.n., Posterior interosseous nerve; r.n., radial nerve. (From Toussaint CP, Zager EL: What’s new in common upper extremity entrapment neuropathies, Neurosurg Clin N Am 19:573–581, 2008.)

144

48  •  Radial Nerve Block at the Humerus        145

Posterior interosseous nerve

Lateral epicondyle

Deltoid m.

Triceps brachii m. Biceps brachii m. Brachialis m. Brachioradialis m.

Figure 48-2  Patients with radial tunnel syndrome will exhibit maximal tenderness to palpation over the posterior interosseous branch of the radial nerve.

with radial tunnel syndrome exhibit pain on active resisted supination of the forearm. Cervical radiculopathy and tennis elbow can mimic radial tunnel syndrome. Radial tunnel syndrome can be distinguished from tennis elbow in that in radial tunnel syndrome the maximal tenderness to palpation is distal to the lateral epicondyle over the posterior interosseous branch of the radial nerve, whereas in tennis elbow the maximal tenderness to palpation is over the lateral epicondyle (Figure 48-2). Electromyography helps distinguish cervical radiculopathy and radial tunnel syndrome from tennis elbow. Plain radiographs are indicated for all patients with radial tunnel syndrome to rule out occult bony disease. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and/or ultrasound imaging of the elbow and forearm is indicated if joint instability or occult tumor or mass is suspected (Figure 48-3). The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The radial nerve is made up of fibers from C5-T1 spinal roots. The nerve lies posterior and inferior to the axillary artery. Exiting

the axilla, the radial nerve passes between the medial and long heads of the triceps muscle. As the nerve curves across the posterior aspect of the humerus, it supplies a motor branch to the triceps. Continuing its downward path, it gives off a number of sensory branches to the upper arm. At a point between the lateral epicondyle of the humerus and the musculospiral groove, the radial nerve divides into its two terminal branches (see Figure 48-1). The superficial branch continues down the arm along with the radial artery and provides sensory innervation to the dorsum of the wrist and the dorsal aspects of a portion of the thumb, index, and middle fingers. The deep posterior interosseous branch provides the majority of the motor innervation to the extensors of the forearm.

Technique The patient is placed in a supine position with the arm abducted 35 to 45 degrees and the hand resting comfortably on the abdomen. A total of 7 to 10 mL of local anesthetic is drawn up in a 12-mL sterile syringe. When painful or inflammatory conditions that are mediated via the radial nerve are treated, a total of 80 mg of methylprednisolone is added to the local anesthetic with the first block and 40 mg of methylprednisolone is added with subsequent blocks.

146        Section 3  •  Elbow and Forearm

Post-op

Pre-op

Pre-op

A

B

C Pre-op

Post-op

E Post-op

D

F

Figure 48-3  Preoperative and postoperative magnetic resonance imaging (MRI) scans (T2-weighted fast spin-echo sequences with fat saturation). A, Sagittal MRI shows cystic mass anterior to the capitellum. B, Postoperative sagittal MRI scan shows decompression of the cyst. C, Preoperative coronal MRI scan shows cyst communication with the proximal radioulnar joint. D, Postoperative coronal MRI scan after decompression. E, Series of preoperative axial MRI scans showing the cyst from the anterior to the capitellum distally into the proximal radioulnar joint. F, Postoperative axial MRI scans after decompression. (From Mileti J, Largacha M, O’Driscoll SW: Radial tunnel syndrome caused by ganglion cyst: treatment by arthroscopic cyst decompression, Arthroscopy 20:e39–e44, 2004.)

The clinician then identifies the lateral epicondyle of the humerus, and at a point approximately 3 inches above the epicondyle the musculospiral groove is identified by deep palpation between the heads of the triceps muscle. After preparation of the skin with antiseptic solution, a 1-inch, 25-gauge needle is inserted perpendicular to the lateral aspect of the humerus and advanced slowly toward the musculospiral groove (see Figure 48-2). As the needle approaches the humerus, a strong paresthesia in the distribution of the radial nerve is elicited. If no paresthesia is elicited and the needle contacts bone, the needle is withdrawn and redirected slightly more anteriorly or posteriorly until paresthesia is elicited. The patient should be warned that a paresthesia will occur and to say “there!” as soon as the paresthesia is felt. After the paresthesia has been elicited and its distribution identified, gentle aspiration is carried out to identify blood. If the aspiration test result is negative and no persistent paresthesia into the distribution of the radial

nerve remains, 7 to 10 mL of solution is slowly injected, with the patient being monitored closely for signs of local anesthetic toxi­city. Ultrasound guidance may simplify this procedure.

Side Effects and Complications Radial nerve block at the humerus is a relatively safe block, with the major complications being inadvertent intravascular injection and persistent paresthesia secondary to needle trauma to the nerve. This technique can safely be performed in the presence of anticoagulation by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable riskto-benefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block decreases the amount of postprocedure pain and bleeding the patient may experience.

48  •  Radial Nerve Block at the Humerus        147

Clinical Pearls Radial nerve block at the humerus is a simple and safe technique and is extremely useful in the management of radial tunnel syndrome. This painful condition is often misdiagnosed as tennis elbow, and this fact accounts for the many patients whose “tennis elbow” fails to respond to conservative measures. Radial tunnel syndrome can be distinguished from tennis elbow in that in radial tunnel syndrome the maximal tenderness to palpation is over the radial nerve, whereas in tennis elbow the maximal tenderness to palpation is over the lateral epicondyle (see Figures 47-2 and 47-3). If radial tunnel syndrome is suggested, injection of the radial nerve at the humerus with local anesthetic and corticosteroid gives almost instantaneous relief. Careful neurologic examination to identify preexisting neurologic deficits that may later be attributed to the nerve block should be performed on all patients before beginning radial nerve block at the humerus.

SUGGESTED READINGS Lee JT, Azari K, Jones NF: Long term results of radial tunnel release—the effect of co-existing tennis elbow, multiple compression syndromes and workers’ compensation, J Plast Reconstr Aesthet Surg 61:1095–1099, 2008. Mileti J, Largacha M, O’Driscoll SW: Radial tunnel syndrome caused by ganglion cyst: treatment by arthroscopic cyst decompression, Arthroscopy 20:e39–e44, 2004. Nessrine A, Latifa T, Abdelkarim D, et  al: Frohse’s arcade is not the exclusive compression site of the radial nerve in its tunnel, Orthop Traumatol Surg Res 95:114–118, 2009. Tennent TD, Woodgate A: Posterior interosseous nerve dysfunction in the radial tunnel, Curr Orthop 22:226–232, 2008. Toussaint CP, Zager EL: What’s new in common upper extremity entrapment neuropathies, Neurosurg Clin N Am 19:573–581, 2008.

Chapter 49 MEDIAL EPICONDYLE INJECTION

Indications and Clinical Considerations Golfer’s elbow (also known as medial epicondylitis) is caused by repetitive microtrauma to the flexor tendons of the forearm in a manner analogous to tennis elbow. The pathophysiology of golfer’s elbow is initially caused by microtearing at the origin of pronator teres, flexor carpi radialis and flexor carpi ulnaris, and palmaris longus (Figure 49-1). Secondary inflammation may occur, which can become chronic as a result of continued overuse or misuse of the flexors of the forearm. Coexistent bursitis, arthritis, and gout may also perpetuate the pain and disability of golfer’s elbow. Golfer’s elbow occurs in patients engaged in repetitive flexion activities that include throwing baseballs, carrying heavy suitcases, and driving golf balls. These activities have in common repetitive flexion of the wrist and strain on the flexor tendons from excessive weight or sudden arrested motion. Interestingly, many of the activities that can cause tennis elbow can also cause golfer’s elbow. The pain of golfer’s elbow is localized to the region of the medial epicondyle. It is constant and is made worse with active contraction of the wrist. Patients note the inability to hold a coffee cup or hammer. Sleep disturbance is common. On physical examination there is tenderness along the flexor tendons at or just below the medial epicondyle. Many patients with golfer’s elbow exhibit a bandlike thickening within the affected flexor tendons. Elbow range of

A

motion is normal. Grip strength on the affected side is diminished. Patients with golfer’s elbow demonstrate a positive golfer’s elbow test result. The test is performed by stabilizing the patient’s forearm and then having the patient actively flex the wrist. The examiner then attempts to force the wrist into extension (Figure 49-2). Sudden, severe pain is highly suggestive of golfer’s elbow. Occasionally C6-C7 radiculopathy can mimic golfer’s elbow. The patient with cervical radiculopathy usually has neck pain and proximal upper extremity pain in addition to symptoms below the elbow. Electromyography helps distinguish radiculopathy from golfer’s elbow. Plain radiographs are indicated in all patients with golfer’s elbow to rule out joint mice and other occult bony disease. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and ultrasound imaging of the elbow is indicated to determine joint instability and to help confirm the diagnosis (MRI). The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The most common nidus of pain from golfer’s elbow is the bony origin of the flexor tendon of the flexor carpi radialis and the humeral heads of the flexor carpi ulnaris and pronator teres at the

B

Figure 49-1  Flexor tendons: tear. Acute avulsive injury of the common flexor tendons. A, A coronal T1-weighted (TR/TE, 600/30) spin-echo magnetic resonance (MR) image shows avulsion of the flexor tendons (arrow) from the medial epicondyle of the humerus. Abnormal signal intensity is also evident in the common extensor tendons (arrowhead). B, A coronal short tau inversion recovery (STIR) MR image reveals high signal intensity at the site of flexor tendon avulsion (arrows), altered signal intensity in the common extensor tendons (arrowhead), and a joint effusion. (Courtesy C. Ho, MD, Palo Alto, Calif.)

148

49  •  Medial Epicondyle Injection        149

Patient Examiner

Inflamed epicondyle

Frayed and inflamed tendons Pronator teres m. Ulnar n.

Flexor carpi ulnaris m.

Medial epicondyle Flexor carpi ulnaris m.

Figure 49-2  Patients with golfer’s elbow will exhibit a positive golfer’s elbow test result.

medial epicondyle of the humerus (Figures 49-3 to 49-5). Less commonly, golfer’s elbow pain can originate from the ulnar head of the flexor carpi ulnaris at the medial aspect of the olecranon process. As mentioned earlier, bursitis may accompany golfer’s elbow. The olecranon bursa lies in the posterior aspect of the elbow joint and also may become inflamed as a result of direct trauma or overuse of the joint. Other bursae susceptible to the development of bursitis exist between the insertion of the biceps and the head of the radius, as well as in the antecubital and cubital area.

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side and the elbow fully extended with the dorsum of the hand resting on a folded towel to relax the affected tendons. A total of 1 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. After sterile preparation of skin overlying the medial aspect of the joint, the medial epicondyle is identified. With strict aseptic technique, a 1-inch, 25-gauge needle is inserted perpendicular to the medial epicondyle through the skin and into the subcutaneous tissue overlying the affected tendon (see Figure 49-3). If bone is encountered, the needle is withdrawn back into the subcutaneous tissue. The contents of the syringe are then gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in the tendon and should be withdrawn

Palmaris longus m.

Figure 49-3  For the treatment of golfer’s elbow, the injected needle is placed perpendicular to the medial epicondyle and advanced toward the affected tendon.

back until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complications associated with this injection technique are related to trauma to the inflamed and previously damaged tendons. Such tendons may rupture if directly injected, and needle position should be confirmed outside the tendon before injection to avoid this complication. Another complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is followed. The ulnar nerve is especially susceptible to damage at the elbow, and care must be taken to avoid this nerve when injecting the elbow. Approximately 25% of patients report a transient increase in pain after this injection technique; the patient should be warned of this.

150        SECTION 3  •  Elbow and Forearm

•

•

Brachialis m. Extensor carpi radialis longus m.

•

Lateral collateral & annular ligs.

Med. epicondyle

••

•

Common extensor t.

• •

••

Common flexor t. Med. collateral lig

••

•

Radius, head

Coronoid

••

Palmaris longus m. Brachialis t.

••

Pronator teres t., ulnar head

• •

Radial n., deep branch

••

• •

Supinator m., superficial portion

•

•

Olecranon

Extensor digitorum m. Supinator m., deep portion

Triceps m.

•

Flexor digitorum superficialis m. Flexor digitorum profundus m.

Figure 49-4  Magnetic resonance image illustrating the relationship of the medial epicondyle and pronator teres, flexor carpi radialis, and flexor carpi ulnaris muscles. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

49  •  Medial Epicondyle Injection        151

•

•

Brachioradialis m.

•

Brachialis m.

••

•

•

•• •

•

Common extensor t.

••

Lat. collateral & annular ligs. Radius, head

••

•

Coronoid

••

Brachialis m. & t. Palmaris longus m.

Flexor digitorum superficialis m.

• • •

Radial n., deep branch Supinator m., superficial portion

••

•

Extensor digitorum m.

Common flexor t. Med. collateral lig.

•

•• Supinator m., deep portion

Med. epicondyle

•

Olecranon fossa Lat. epicondyle Extensor carpi radalis longus m.

Triceps m.

•

Flexor digitorum profundus m.

•

••

••

Flexor carpi ulnaris m. Ulnar n.

Figure 49-5  Anatomic coronal section of the elbow illustrating the relationship of the medial epicondyle and pronator teres, flexor carpi radialis, and flexor carpi ulnaris muscles. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

152        SECTION 3  •  Elbow and Forearm

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to golfer’s elbow. Coexistent bursitis and tendinitis also may contribute to elbow pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat as well as gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for elbow pain. A Velcro band placed around the flexor tendons also may help relieve the symptoms of golfer’s elbow. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique. As mentioned earlier, cervical radiculopathy may mimic golfer’s elbow and must be ruled out to effectively treat the underlying pathologic process.

SUGGESTED READINGS Ciccotti MC, Schwartz MA, Ciccotti MG: Diagnosis and treatment of medial epicondylitis of the elbow, Clin Sports Med 23:693–705, 2004. Rineer CA, Ruch DS: Elbow tendinopathy and tendon ruptures: epicondylitis, biceps and triceps ruptures, J Hand Surg Am 34:566–576, 2009. Waldman SD: Golfer’s elbow. In Atlas of pain management injection techniques, ed 2, Philadelphia, 2009, pp 148–153. Waldman SD: Golfer’s elbow. In Pain review, Philadelphia, 2009, Saunders, pp 267–268. Waldman SD: Golfer’s elbow. In Waldman SD, editor: Pain management, Philadelphia, 2007, Saunders, pp 637–640.

Chapter 50 TRICEPS TENDON INJECTION

Indications and Clinical Considerations Triceps tendinitis is being seen with increasing frequency in clinical practice as exercising and the use of exercise equipment have increased in popularity. The triceps tendon is susceptible to the development of tendinitis at its distal portion and its insertion on the ulna. The triceps tendon is subject to repetitive motion that may result in microtrauma, which heals poorly owing to the tendon’s avascular nature. Exercise is often implicated as the inciting factor of acute triceps tendinitis. Tendinitis of the triceps tendon frequently coexists with bursitis of the associated bursae of the tendon and elbow joint, creating additional pain and functional disability. Calcium deposition around the tendon may occur if the inflammation continues, making subsequent treatment more difficult (Figure 50-1). Continued trauma to the inflamed tendon may ultimately result in tendon rupture (Figure 50-2). The onset of triceps tendinitis is usually acute, occurring after overuse or misuse of the elbow joint. Inciting factors may include activities such as playing tennis and aggressive use of exercise machines. Improper stretching of the triceps muscle and triceps tendon before exercise has also been implicated in the

development of triceps tendinitis as well as acute tendon rupture. Injuries ranging from partial to complete tears of the tendon can occur when the distal tendon sustains direct trauma while it is fully flexed under load or when the elbow is forcibly flexed while the arm is fully extended. The pain of triceps tendinitis is constant and severe and is localized in the posterior elbow (Figure 50-3). Significant sleep disturbance is often reported. Patients with triceps tendinitis will exhibit pain with resisted extension of the elbow. A creaking or grating sensation may be palpated when passively extending the elbow. As mentioned, the chronically inflamed triceps tendon may suddenly rupture with stress or during vigorous injection procedures inadvertently injected into the substance of the tendon. With triceps tendon rupture, the patient will not be able to fully and forcefully extend the affected arm. Plain radiographs and magnetic resonance imaging (MRI) are indicated for all patients with posterior elbow pain. On the basis of the patient’s clinical presentation, additional testing, including complete blood count, sedimentation rate, and antinuclear antibody testing, may be indicated. MRI of the elbow is indicated if joint instability is suspected and to further confirm the diagnosis. Radionuclide bone scanning is useful to identify stress fractures of the elbow not seen on plain radiographs. Ultrasound imaging may also provide the clinician with useful information regarding the condition of the tendon (Figure 50-4).

Clinically Relevant Anatomy ST

T

Figure 50-1  Tendon and soft tissue calcification. Calcified deposits are visualized in the triceps tendon (T) and soft tissues (ST) around the proximal end of the radius. (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

The triceps brachii muscle is the major extensor muscle of the elbow joint and is the antagonist muscle to the biceps brachii and brachialis muscles. The triceps muscle gains its name from the three bundles of muscles that compose it. Each of the three muscles has a different origin. The long head of the triceps finds its origin at the infraglenoid fossa of the scapula. The medial head finds its origin at the groove of the radial nerve as well as the dorsal surface of the humerus; at the medial intermuscular septum; and from the lateral intermuscular septum. The lateral head finds its origin at the dorsal surface of the humerus at a point lateral and proximal to the groove of the radial nerve as well as the greater tubercle down to the region of the lateral intermuscular septum. All three heads are innervated by the radial nerve, with the long head of the triceps receiving innervation from the axillary nerve in many individuals. The three heads of the triceps muscle coalesce into the triceps tendon, which inserts onto the olecranon process and the posterior wall of the capsule of the elbow joint (Figure  50-5). The tendon is susceptible to the development of tendinitis at its insertion. 153

154        SECTION 3  •  Elbow and Forearm

o

o

A

B

Figure 50-2  Triceps tendon rupture imaged in flexion. This patient was unable to extend the elbow because of discomfort. The images were obtained on a high-field scanner with the patient prone and the arm flexed overhead. Proton density (A) and fat-suppressed T2-weighted (B) coronal images reveal a fluid-filled tear of the distal triceps tendon (arrow) from the olecranon (o). (From Edelman RR, Hesselink JR, Zlatkin MB, et al, editors: Clinical magnetic resonance imaging, ed 3, Philadelphia, 2006, Saunders.)

Inflamed triceps tendon

Figure 50-3  The pain of triceps tendinitis is constant and severe and is located in the posterior elbow. (From Waldman SD: Atlas of uncommon pain syndromes, ed 2, Philadelphia, 2008, Saunders.)

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side and the elbow flexed with the palm of the hand resting on the patient’s abdomen. A total of 2 mL of

local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. After sterile preparation of the skin overlying the posterior aspect of the joint, the olecranon process and overlying bursa are identified. With strict aseptic technique, a 1-inch, 25-gauge needle is inserted through the skin and subcutaneous tissues directly into the bursa in the midline (Figure 50-6). If bone is encountered, the needle is withdrawn back into the bursa. After the bursa has been entered, the contents of the syringe are gently injected. There should be little resistance to injection. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complications associated with this injection technique are related to trauma to the inflamed and previously damaged tendons. Such tendons may rupture if directly injected, and needle position should be confirmed outside the tendon before injection to avoid this complication. Another complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. The ulnar nerve is especially susceptible to damage at the elbow, and care must be taken to avoid this nerve when injecting in this anatomic region. Approximately 25% of patients report a transient increase in pain after this injection technique; the patient should be warned of this.

50  •  Triceps Tendon Injection        155

A

B

C Figure 50-4  A, Lateral elbow x-ray study demonstrating no fracture of joint effusion. B, Ultrasound image in longitudinal orientation at distal humerus showing distal triceps tendon (arrow) and olecranon cortex (arrowhead). C, Ultrasound image in longitudinal orientation at distal humerus showing distal triceps tendon (thin arrow), anechoic area (thick arrow) demonstrating lack of tendon continuity, and olecranon cortex (arrowhead). (From Sisson C, Nagdev A, Tirado A, et al: Ultrasound diagnosis of traumatic partial triceps tendon tear in the emergency department, J Emerg Med 40:436– 438, 2011.)

Medial Superficial triceps tendon Triceps tendon Lateral

Figure 50-5  Posterior view of a left elbow showing superficial triceps tendon anatomy. The angled appearance of the lateral tendon compared with the straight aspect of the medial tendon should be noted. (From Keener JD, Chafik D, Kim HM, et al: Insertional anatomy of the triceps brachii tendon, J Shoulder Elbow Surg 19:399–405, 2010.)

Figure 50-6  Injection technique for triceps tendinitis.

156        SECTION 3  •  Elbow and Forearm

Clinical Pearls The triceps tendon is a very strong tendon, yet it is also susceptible to rupture. Coexistent bursitis and arthritis may also contribute to posterior elbow pain and may require additional treatment with a more localized injection of local anesthetic and methylprednisolone acetate. Injection of the triceps tendon is a safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. The use of physical modalities including local heat as well as gentle range of motion exercises should be introduced several days after the patient has undergone this injection technique for elbow pain. Vigorous exercises should be avoided because they will exacerbate the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory drugs may be used concurrently with this injection technique.

SUGGESTED READINGS Isbell WM: Tendon ruptures. In Brukner P, Khan K, editors: Clinical sports medicine, ed 3, Sydney, 2006, McGraw-Hill Australia, pp 367–370. Jafarnia K, Gabel GT, Morrey BF: Triceps tendinitis, Oper Tech Sports Med 9:217–221, 2001. Keener JD, Chafik D, Kim HM, et al: Insertional anatomy of the triceps brachii tendon, J Shoulder Elbow Surg 19:399–405, 2010. Rineer CA, Ruch DS: Elbow tendinopathy and tendon ruptures: epicondylitis, biceps and triceps ruptures, J Hand Surg Am 34:566–576, 2009.

Chapter 51 OLECRANON BURSA INJECTION

Indications and Clinical Considerations Bursae are formed from synovial sacs whose purpose is to allow easy sliding of muscles and tendons across one another at areas of repeated movement. These synovial sacs are lined with a synovial membrane that is invested with a network of blood vessels that secrete synovial fluid. Inflammation of the bursa results in an increase in the production of synovial fluid with swelling of the bursal sac. With overuse or misuse, these bursae may become inflamed, enlarged, and on rare occasions infected. Although there is significant intrapatient variability as to the number, size, and location of bursae, anatomists have identified a number of clinically relevant bursae, including the olecranon bursa. The olecranon bursa lies in the posterior aspect of the elbow between the olecranon process of the ulna and the overlying skin. It may exist as a single bursal sac or in some patients as a multisegmented series of sacs that may be loculated. The olecranon bursa is vulnerable to injury from both acute trauma and repeated microtrauma. Acute injuries frequently take the form of direct trauma to the elbow when playing sports such as hockey or falling directly onto the olecranon process. Repeated

pressure from leaning on the elbow to rise or from working long hours at a drafting table may result in inflammation and swelling of the olecranon bursa. Gout or bacterial infection rarely may precipitate acute olecranon bursitis (Figure 51-1). If the inflammation of the olecranon bursa becomes chronic, calcification of the bursa may occur with residual nodules, called gravel. The patient with olecranon bursitis frequently complains of pain and swelling with any movement of the elbow, but especially with extension. The pain is localized to the olecranon area, with referred pain often noted above the elbow joint. Often the patient is more concerned about the swelling around the bursa than the pain. Physical examination reveals point tenderness over the olecranon and swelling of the bursa, which at times can be quite extensive (Figure 51-2). Passive extension and resisted shoulder flexion reproduce the pain, as does any pressure over the bursa. Fever and chills usually accompany infection of the bursa. If infection is suspected, then aspiration, Gram stain, and culture of the bursa, followed by treatment with appropriate antibiotics, are indicated on an emergent basis. Plain radiographs of the posterior elbow may reveal calcification of the bursa and associated structures consistent with chronic inflammation (Figure 51-3).

Figure 51-1  Septic olecranon bursitis. Note olecranon swelling (arrows) and soft tissue edema caused by Staphylococcus aureus. Previous surgery and trauma are the causes of the adjacent bony abnormalities. (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

157

158        SECTION 3  •  Elbow and Forearm

Clinically Relevant Anatomy The elbow joint is a synovial, hinge-type joint that serves as the articulation among the humerus, radius, and ulna (Figure 51-4). The joint’s primary function is to position the wrist in order to optimize hand function. The joint allows flexion and extension at the elbow, as well as pronation and supination of the forearm. The joint is lined with synovium. The entire joint is covered by a dense capsule that thickens medially to form the ulnar collateral ligament and laterally to form the radial collateral ligaments. These dense ligaments, coupled with the elbow joint’s deep bony socket, make this joint extremely stable and relatively resistant to subluxation and dislocation. The anterior and posterior joint capsule is less dense

and may become distended if there is a joint effusion. The olecranon bursa lies in the posterior aspect of the elbow joint between the olecranon process of the ulna and the overlying skin. The olecranon bursa may become inflamed as a result of direct trauma or overuse of the joint. The elbow joint is innervated primarily by the musculocutaneous and radial nerves, with the ulnar and median nerves providing varying degrees of innervation. At the middle of the upper arm the ulnar nerve courses medially to pass between the olecranon process and the medial epicondyle of the humerus. The nerve is susceptible to entrapment and trauma at this point. At the elbow the median nerve lies just medial to the brachial artery and occasionally is damaged during brachial artery cannulation for blood gases.

Technique

Figure 51-2  Olecranon bursitis in early rheumatoid arthritis. (From ­Klippel JH, Dieppe PA: Rheumatology, ed 2, St Louis, 1997, Mosby.)

A

The patient is placed in a supine position with the arm fully adducted at the patient’s side and the elbow flexed with the palm of the hand resting on the patient’s abdomen. A total of 2 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. After sterile preparation of the skin overlying the posterior aspect of the joint, the olecranon process and overlying bursa are identified. With strict aseptic technique, a 1-inch, 25-gauge needle is inserted through the skin and subcutaneous tissues directly into the bursa in the midline (see Figure 51-4). If bone is encountered, the needle is withdrawn back into the bursa. After the bursa has been entered, the contents of the syringe are gently injected. There should be little resistance to injection. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

B

Figure 51-3  Bursograms showed the shadow of multiple bodies in the distended olecranon bursa. A, Anteroposterior plane. B, Lateral plane. (From Matsumoto T, Fujita K, Fujioka H, et al: Massive nonspecific olecranon bursitis with multiple rice bodies, J Shoulder Elbow Surg 13:680–683, 2004.)

51  •  Olecranon Bursa Injection        159

Clinical Pearls

Humerus

Radius Ulna Olecranon Inflamed and cystic bursa

Figure 51-4  For the treatment of olecranon bursitis, the needle is placed directly into the inflamed bursa.

Side Effects and Complications The major complication of this technique for injection of the olecranon bursa is infection, which should be exceedingly rare if strict aseptic technique is followed. As mentioned previously, the ulnar nerve is especially susceptible to damage at the elbow. Approximately 25% of patients report a transient increase in pain after injection of the olecranon bursa; the patient should be warned of this.

This injection technique is extremely effective in the treatment of pain and swelling secondary to olecranon bursitis. Coexistent tendinitis and epicondylitis also may contribute to elbow pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected, in particular avoiding the ulnar nerve by keeping the needle trajectory in the midline. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat as well as gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for elbow pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Matsumoto T, Fujita K, Fujioka H, et al: Massive nonspecific olecranon bursitis with multiple rice bodies, J Shoulder Elbow Surg 13:680–683, 2004. McFarland EG, Gill HS, Laporte DM, Streiff M: Miscellaneous conditions about the elbow in athletes, Clin Sports Med 23:743–763, 2004. Waldman SD: Injection technique for olecranon bursitis pain. Pain review, ­Philadelphia, 2009, Saunders, pp 461–462. Waldman SD: Olecranon bursitis. In Pain review, Philadelphia, 2009, Saunders, pp 272–273.

Chapter 52 CUBITAL BURSA INJECTION

Indications and Clinical Considerations Bursae are formed from synovial sacs whose purpose is to allow easy sliding of muscles and tendons across one another at areas of repeated movement. These synovial sacs are lined with a synovial membrane that is invested with a network of blood vessels that secrete synovial fluid. Inflammation of the bursa results in an increase in the production of synovial fluid with swelling of the bursal sac. With overuse or misuse, these bursae may become inflamed, enlarged, and on rare occasions infected. Although there is significant intrapatient variability as to the number, size, and location of bursae, anatomists have identified a number of clinically relevant bursae, including the cubital bursa. The cubital bursa lies in the anterior aspect of the elbow. It may exist as a single bursal sac or in some patients as a multisegmented series of sacs that may be loculated. The cubital bursa, which is also known as the bicipitoradial bursa, is vulnerable to injury from both acute trauma and repeated microtrauma. Acute injuries frequently take the form of direct trauma to the anterior aspect of the elbow. Repetitive movements of the elbow, including throwing javelins and baseballs, may result in inflammation and swelling of the cubital bursa. Activities requiring repetitive supination and pronation have also been implicated in the evolution of cubital bursitis. Gout or rheumatoid arthritis rarely may precipitate acute cubital bursitis. If the inflammation of the cubital bursa becomes chronic, calcification of the bursa may occur.

A

The patient with cubital bursitis frequently reports pain and swelling with any movement of the elbow. The pain is localized to the cubital area, with referred pain often noted in the forearm and hand. Physical examination reveals point tenderness in the anterior aspect of the elbow over the cubital bursa and swelling of the bursa. Passive extension and resisted elbow flexion reproduce the pain, as does any pressure over the bursa. Plain radiographs of the posterior elbow may reveal calcification of the bursa and associated structures consistent with chronic inflammation. Magnetic resonance imaging (MRI) and ultrasound imaging may help distinguish between bursitis and other soft tissue masses in the cubital fossa (Figure 52-1).

Clinically Relevant Anatomy The elbow joint is a synovial, hinge-type joint that serves as the articulation among the humerus, radius, and ulna (Figure 52-2). The joint’s primary function is to position the wrist in order to optimize hand function. The joint allows flexion and extension at the elbow, as well as pronation and supination of the forearm. The joint is lined with synovium. The entire joint is covered by a dense capsule that thickens medially to form the ulnar collateral ligament and laterally to form the radial collateral ligaments. These dense ligaments, coupled with the elbow joint’s deep bony socket, make this joint extremely stable and relatively resistant to subluxation and dislocation. The anterior and posterior joint capsule is less dense and may become distended if there is a joint effusion.

B

Figure 52-1  A, Postcontrast computed tomography scan shows a nonenhancing lesion (arrow) in the left elbow. B, Axial spin echo T2-weighted magnetic resonance image shows the lesion with homogeneous, increased signal intensity, suggesting a fluid collection. An arrowhead indicates the biceps tendon. (From Yamamoto T, Mizuno K, Soejima T, Fujii M: Bicipital radial bursitis: CT and MR appearance, Comput Med Imaging Graph 25:531–533, 2001.)

160

52  •  Cubital Bursa Injection        161

Biceps brachii m.

Brachialis m.

Ca rr

ic o

&S ha vel l

Brachial a. Median n.

Cuboidal bursa

Extensor carpi radialis m.

Radial a.

Brachioradialis m.

Medial epicondyle Pronator teres m. Flexor carpi radialis m. Palmaris longus m. Aponeurotic extension of biceps m. Flexor carpi ulnaris m. Flexor digitorum superficialis m.

Figure 52-2  The cubital bursa lies beneath the aponeurosis of the biceps muscle at the elbow.

The cubital fossa lies in the anterior aspect of the elbow joint and is bounded laterally by the brachioradialis muscle and medially by the pronator teres; it contains the median nerve, which is susceptible to irritation and compression from a swollen, inflamed cubital bursa. The bursa lies between the radial head and the insertion of the biceps tendon. The elbow joint is innervated primarily by the musculocutaneous and radial nerves, with the ulnar and median nerves providing varying degrees of innervation. At the middle of the upper arm, the ulnar nerve courses medially to pass between the olecranon process and medial epicondyle of the humerus. The nerve is susceptible to entrapment and trauma at this point. At the elbow the median nerve lies just medial to the brachial artery and occasionally is damaged during brachial artery cannulation for blood gases. The median nerve also may be injured during injection of the cubital bursa.

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side and the elbow extended with the dorsum of the hand resting on a folded towel. A total of 2 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. After sterile preparation of skin overlying the anterior aspect of the joint, the clinician then identifies the pulsations of the brachial

artery at the crease of the elbow. After preparation of the skin with antiseptic solution, a 1-inch, 25-gauge needle is inserted just lateral to the brachial artery at the crease and slowly advanced in a slightly medial and cephalad trajectory through the skin and subcutaneous tissues (see Figure 52-2). If bone is encountered, the needle is withdrawn back into the subcutaneous tissue. The contents of the syringe are then gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in the tendon and should be withdrawn back until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications Injection of the cubital bursa at the elbow is a relatively safe block, with the major complications being inadvertent intravascular injection and persistent paresthesia secondary to needle trauma to the median nerve. This technique can safely be performed in the presence of anticoagulation by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable risk-to-benefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block also decreases the amount of postprocedure pain and bleeding the patient may experience.

162        SECTION 3  •  Elbow and Forearm

Clinical Pearls This injection technique is extremely effective in the treatment of pain and swelling secondary to cubital bursitis. Coexistent tendinitis and epicondylitis also may contribute to elbow pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected, in particular avoiding the median nerve by keeping the needle lateral to the brachial artery. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat as well as gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for elbow pain. Vigorous exercise should be avoided, because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Potter HG, Schachar J, Jawetz S: Imaging of the elbow, Oper Tech Orthop 19:199–208, 2009. Qureshi F, Stanley D: The painful elbow, Surgery (Oxford) 24:368–372, 2006. Waldman SD: Functional anatomy of the elbow joint. In Pain review, Philadelphia, 2009, Saunders, pp 90–94. Waldman SD: Injection technique for cubital bursitis pain. In Pain review, Philadelphia, 2009, Saunders, pp 463–464. Yamamoto T, Mizuno K, Soejima T, Fujii M: Bicipital radial bursitis: CT and MR appearance, Comput Med Imaging Graph 25:531–533, 2001.

Chapter 53 INJECTION TECHNIQUE FOR SUPINATOR SYNDROME Indications and Clinical Considerations The supinator muscle is susceptible to the development of myofascial pain syndrome. Such pain most often occurs as a result of repetitive microtrauma to the muscle from such activities as turning a screwdriver, prolonged ironing, handshaking, or digging with a trowel or garden shovel. An improper one-handed backhand technique in tennis has also been implicated as an inciting factor for this myofascial pain syndrome, as has blunt trauma to the muscle. Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body. The sine qua non of myofascial pain syndrome is the finding of myofascial trigger points on physical examination. Although these trigger points generally are localized to the regional part of the body affected, the pain of myofascial pain syndrome often is referred to other anatomic areas. This referred pain often is misdiagnosed or attributed to other organ systems, thereby leading to extensive evaluations and ineffective treatment. Patients with myofascial pain syndrome involving the supinator often have referred pain into the ipsilateral forearm. The trigger point is the pathognomonic lesion of myofascial pain and is thought to be a result of microtrauma to the affected muscles. This pathologic lesion is characterized by a local point of exquisite tenderness in affected muscle. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain but also referred pain. In addition to this local and referred pain, there often is an involuntary withdrawal of the stimulated muscle, called a “jump sign.” This jump sign also is characteristic of myofascial pain syndrome. Patients with supinator syndrome will exhibit a trigger point over the superior portion of the muscle (Figure 53-1). Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. In spite of this consistent physical finding in patients with myofascial pain syndrome, the pathophysiology of the myofascial trigger point remains elusive, although many theories have been advanced. Common to all of these theories is the belief that trigger points are a result of microtrauma to the affected muscle. This microtrauma may occur as a single injury to the affected muscle or may occur as a result of repetitive microtrauma or chronic deconditioning of the agonist and antagonist muscle unit. In addition to muscle trauma, a variety of other factors seem to predispose the patient to develop myofascial pain syndrome. The weekend athlete who subjects his or her body to unaccustomed physical activity may develop myofascial pain syndrome. The poor posture of someone sitting at a computer keyboard or

Trigger point Referred pain Supinator m.

Figure 53-1  Patients with supinator syndrome will exhibit a trigger point over the superior aspect of the supinator muscle.

163

164        SECTION 3  •  Elbow and Forearm

Humerus

•

••

Brachialis m.

•• Radial n. Brachioradialis m.

• • Anterior fat pad

• ••

• •

•

• •• ••

•

• •

Trochlea Pronator teres m. Brachialis m. & t. Median n.

•

• • •

Capitulum Common extensor t. Lat. collateral & annular ligs. Radius, head Extensor carpi radialis longus m. Radial n., deep branch Radius, tuberosity Supinator m.

• •• ••

Ulnar a. Biceps t. Flexor carpi ulnaris m. Palmaris longus m.

Figure 53-2  The supinator muscle and its relationship to the radius. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

watching television has also been implicated as a predisposing factor to the development of myofascial pain syndrome. Previous injuries may result in abnormal muscle function and predispose to the subsequent development of myofascial pain syndrome. All of these predisposing factors may be intensified if the patient also has poor nutritional status or coexisting psychological or behavioral abnormalities, including chronic stress and depression. The supinator muscle seems to be particularly susceptible to stress-induced myofascial pain syndrome. Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or may occur in conjunction with other painful conditions, including radiculopathy and chronic regional pain syndromes. Psychological or behavioral abnormalities, including depression, frequently coexist with the muscle abnormalities associated with myofascial pain syndrome. Treatment of these psychological and behavioral abnormalities must be an integral part of any successful treatment plan for myofascial pain syndrome.

Clinically Relevant Anatomy The supinator muscle, as its name implies, supinates the forearm. Curving around the upper third of the radius, the supinator muscle is made of a superficial and deep layer, with the superficial layer finding its origin via a tendinous insertion from the lateral epicondyle of the humerus, the radial collateral ligament of the elbow,

and the annular ligament of the supinator crest of the ulna (Figure 53-2). The deep layer has the same origins but attaches directly via muscle fibers. The muscle is innervated by the deep branch of the radial nerve (Figure 53-3). The supinator muscle is susceptible to trauma and to wear and tear from overuse and misuse and may develop myofascial pain syndrome as well as epicondylitis at its origin on the lateral epicondyle of the humerus. Tumors of the muscle in this region can cause compression of the radial nerve and forearm pain (Figure 53-4).

Technique Careful preparation of the patient before trigger point injection helps to optimize results. Trigger point injections are directed at the primary trigger point rather than in the area of referred pain. It should be explained to the patient that the goal of trigger point injection is to block the trigger of the persistent pain and thus, it is hoped, provide long-lasting relief. It is important that the patient understand that for most patients with myofascial pain syndrome, more than one treatment modality is required for optimal pain relief. The use of the recumbent or lateral position when identifying and marking trigger points as well as when performing the actual trigger point injection helps decrease the incidence of vasovagal reactions. The skin overlying the trigger point to be injected should always be prepared with antiseptic solution before injection to avoid infection. After the goals of trigger point injection are explained to the patient and proper preparation of the patient has been carried out,

53  •  Injection Technique for Supinator Syndrome        165

Supinator

Supinator

Supinator

Radius Ulna

A

B

Figure 53-3  The supinator muscle arises from the epicondyle, the radial collateral ligament of the elbow, the radial annular ligament, and the supinator crest of the ulna. It encloses the proximal third of the radius and is inserted to the anterior and lateral profile of the radius. The muscle belly is traversed by the posterior interosseous nerve, a branch of the radial nerve, which perforates it proximally, passing through the fibrous arch of Fröhse to emerge in the deep layers and reach the back of the elbow. (A, Magnetic resonance imaging. B, Ultrasound.) (From Precerutti M, Garioni E, Ferrozzi G: Dorsal forearm muscles: US anatomy pictorial essay, J Ultrasound 13:66–69, 2010.)

A

B

C

Figure 53-4  A, Axial spin-echo T1-weighted image at the level of the proximal radial diaphysis shows a severely attenuated supinator muscle, which contains significant areas of fatty infiltration (arrows). This finding suggests chronic compromise of the innervation to this muscle. B, Axial, fat-suppressed fast spin-echo (FSE) T2-weighted image at the level of the radial head reveals a lobulated cystic lesion (arrows) in the expected area of the posterior interosseous nerve. The cystic lesion is likely causing mass effect against this deep branch of the radial nerve, resulting over time in the atrophic, fatty infiltration involving the supinator muscle seen on the T1-weighted images. C, Sagittal, fat-suppressed FSE T2-weighted image at the level of the radial-capitellar articulation demonstrates the extent and lobulated shape of the complex-appearing cystic lesion, which is located directly anterior to the anterior aspect of the radial head. (From Ly JQ, Barrett TJ, Beall DP, Bertagnolli R: MRI diagnosis of occult ganglion compression of the posterior interosseous nerve and associated supinator muscle pathology, Clin Imaging 29:362–363, 2005.)

the trigger point to be injected is reidentified by palpation with the sterilely gloved finger. A syringe containing 10 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone to be injected is attached to a 25- or 27-gauge needle of a length adequate to reach the trigger point. Except for the muscles of posture in the low back, a 1½-inch needle will be adequate. A volume of 0.5 to 1.0 mL of solution is then injected into each trigger point (see Figure 53-1). A series of two to five treatment sessions may be required to completely abolish the trigger point; the patient should be informed of this.

Side Effects and Complications The proximity to neurovascular structures makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing interventional pain management techniques. If there is a significant component of epicondylitis associated with supinator syndrome, the potential to rupture the tendons and insertional fibers of the supinator muscle remains ever-present. Many patients also note a transient increase in pain after injection of trigger points in the supinator muscle.

166        SECTION 3  •  Elbow and Forearm

Clinical Pearls Trigger point injections are extremely safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of trigger point injection are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after trigger point injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid trauma to the neurovascular structures of the elbow when injecting the supinator muscle. The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators believe that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as amitriptyline and nortriptyline represent good first choices and should be given as a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow.

SUGGESTED READINGS Erak S, Day R, Wang A: The role of supinator in the pathogenesis of chronic lateral elbow pain: a biomechanical study, J Hand Surg Br 29:461–464, 2004. Ly JQ, Barrett TJ, Beall DP, Bertagnolli R: MRI diagnosis of occult ganglion compression of the posterior interosseous nerve and associated supinator muscle pathology, Clin Imaging 29:362–363, 2005. Precerutti M, Garioni E, Ferrozzi G: Dorsal forearm muscles: US anatomy pictorial essay, J Ultrasound 13:66–69, 2010. Thomas SJ, Yakin DE, Parry BR, Lubahn JD: The anatomical relationship between the posterior interosseous nerve and the supinator muscle, J Hand Surg Am 25:936–941, 2000.

Chapter 54 INJECTION TECHNIQUE FOR EXTENSOR CARPI ULNARIS SYNDROME Indications and Clinical Considerations The extensor carpi ulnaris muscle is susceptible to the development of myofascial pain syndrome. Such pain most often occurs as a result of repetitive microtrauma to the muscle from such activities as hammering, turning a screwdriver, and repeated extending of the hand at the wrist or other repetitive activities that require ulnar wrist deviation. Blunt trauma to the muscle may also incite extensor carpi ulnaris myofascial pain syndrome. Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body. The sine qua non of myofascial pain syndrome is the finding of myofascial trigger points on physical examination. Although these trigger points generally are localized to the regional part of the body affected, the pain of myofascial pain syndrome often is referred to other anatomic areas. This referred pain often is misdiagnosed or attributed to other organ systems, thereby leading to extensive evaluations and ineffective treatment. Patients with myofascial pain syndrome involving the extensor carpi ulnaris often have primary pain in the forearm that is referred into the ulnar aspect of the forearm and on occasion into the hand. The trigger point is the pathognomonic lesion of myofascial pain and is thought to be a result of microtrauma to the affected muscles. This pathologic lesion is characterized by a local point of exquisite tenderness in affected muscle. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain but also referred pain. In addition to this local and referred pain, there often is an involuntary withdrawal of the stimulated muscle, called a “jump sign.” This jump sign also is characteristic of myofascial pain syndrome. Patients with extensor carpi ulnaris syndrome will exhibit a trigger point over the superior aspect of the muscle (Figure 54-1). Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. In spite of this consistent physical finding in patients with myofascial pain syndrome, the pathophysiology of the myofascial trigger point remains elusive, although many theories have been advanced. Common to all of these theories is the belief that trigger points are a result of microtrauma to the affected muscle. This microtrauma may occur as a single injury to the affected muscle or as a result of repetitive microtrauma or chronic deconditioning of the agonist and antagonist muscle unit. In addition to muscle trauma, a variety of other factors seem to predispose the patient to develop myofascial pain syndrome. The weekend athlete who subjects his or her body to unaccustomed physical activity may develop myofascial pain syndrome. The poor posture of someone sitting at a computer keyboard or

Trigger point Extensor carpi ulnaris m.

Referred pain

Figure 54-1  Patients with extensor carpi ulnaris syndrome will exhibit a positive trigger point over the superior aspect of the extensor carpi ulnaris muscle.

167

168        SECTION 3  •  Elbow and Forearm

base of the fifth metacarpal. The muscle is innervated by the posterior interosseous nerve, which is a branch of the radial nerve. The extensor carpi ulnaris muscle is susceptible to trauma and to wear and tear from overuse and misuse and may develop myofascial pain syndrome, which also may be associated with lateral epicondylitis.

watching television has also been implicated as a predisposing factor to the development of myofascial pain syndrome. Previous injuries may result in abnormal muscle function and predispose to the subsequent development of myofascial pain syndrome. All of these predisposing factors may be intensified if the patient also has poor nutritional status or coexisting psychological or behavioral abnormalities, including chronic stress and depression. The extensor carpi ulnaris muscle seems to be particularly susceptible to stress-induced myofascial pain syndrome. Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or in conjunction with other painful conditions, including radiculopathy and chronic regional pain syndromes. Psychological or behavioral abnormalities, including depression, frequently coexist with the muscle abnormalities associated with myofascial pain syndrome. Treatment of these psychological and behavioral abnormalities must be an integral part of any successful treatment plan for myofascial pain syndrome.

Technique Careful preparation of the patient before trigger point injection helps to optimize results. Trigger point injections are directed at the primary trigger point rather than in the area of referred pain. It should be explained to the patient that the goal of trigger point injection is to block the trigger of the persistent pain and, it is hoped, provide long-lasting relief. It is important that the patient understand that for most patients with myofascial pain syndrome, more than one treatment modality is required for optimal pain relief. The use of the recumbent or lateral position when identifying and marking trigger points as well as when performing the actual trigger point injection helps decrease the incidence of vasovagal reactions. The skin overlying the trigger point to be injected should always be prepared with antiseptic solution before injection to avoid infection. After the goals of trigger point injection have been explained to the patient and proper preparation of the patient has been carried out, the trigger point to be injected is reidentified by palpation with the sterilely gloved finger. A syringe containing 8 mL of 0.25% preservative-free bupivacaine and 58 mg of methylprednisolone to be injected is attached to a 25- or 27-gauge needle of a

Clinically Relevant Anatomy The extensor carpi ulnaris muscle extends the hand at the wrist and provides ulnar deviation of the hand at the wrist. The extensor carpi ulnaris muscle finds its origin at the lateral epicondyle via the common extensor tendon, the body of the ulna, and the antebrachial fascia (Figure 54-2). The muscle inserts on the medial side of the

Brachialis m.

Brachial a. Median n. Pronator teres m.

• •

Med. epicondyle

Biceps m. & t.

••

••

Brachioradialis m. •

•

•

Ulnar n. Olecranon

••

••

•

• •

Ant. fat pad Extensor carpi radialis longus m. Post. fat pad Lat. epicondyle

•

••

•

•

••

Triceps m. & t.

•

Brachial a.

Brachialis m. ••

Median n.

••

Pronator teres m.

••

•

•

•

• •

•

•

•

••

Triceps m. & t.

Biceps m. & t.

•

•

••

Ulnar n. Olecranon

••

•

Med. epicondyle

Radial n.

•

Brachioradalis m. Radial n. Ant. fat pad Extensor carpi radialis longus m. Post. fat pad Lat. epicondyle

Figure 54-2  The extensor carpi ulnaris muscle and its relationship to the ulnar nerve. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

54  •  Injection Technique for Extensor Carpi Ulnaris Syndrome        169

length adequate to reach the trigger point. Except for the muscles of posture in the low back, a 1½-inch needle will be adequate. A volume of 0.5 to 1.0 mL of solution is then injected into each trigger point (see Figure 54-1). A series of two to five treatment sessions may be required to completely abolish the trigger point; the patient should be informed of this.

Side Effects and Complications The proximity to neurovascular structures including the ulnar nerve makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing interventional pain management techniques. Many patients also report a transient increase in pain after injection of trigger points in the extensor carpi ulnaris muscle.

Clinical Pearls Trigger point injections are extremely safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of trigger point injection are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after trigger point injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid trauma to the neurovascular structures, including the ulnar nerve of the elbow, when injecting the extensor carpi ulnaris muscle. The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators believe that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as amitriptyline and nortriptyline are good first choices and should be given as a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow.

SUGGESTED READINGS Baldry P: Acupuncture treatment of fibromyalgia and myofascial pain. In Chaitow L, editor: Fibromyalgia syndrome, ed 3, Oxford, 2010, Churchill Livingstone, pp 145–159. Ge HY, Nie H, Madeleine P, et al: Contribution of the local and referred pain from active myofascial trigger points in fibromyalgia syndrome, Pain 147: 233–240, 2009. Ge HY, Wang Y, Danneskiold-Samsøe B, et al: The predetermined sites of examination for tender points in fibromyalgia syndrome are frequently associated with myofascial trigger points, J Pain 11:644–651, 2010. LeBlanc KE, LeBlanc LL: Musculoskeletal disorders, Prim Care 37:389–406, 2010. Partanen JV, Ojala TA, Arokoski JP: Myofascial syndrome and pain: a neurophysiological approach, Pathophysiology 17:19–28, 2010.

Chapter 55 INJECTION TECHNIQUE FOR EXTENSOR CARPI RADIALIS LONGUS SYNDROME Indications and Clinical Considerations The extensor carpi radialis longus muscle is susceptible to the development of myofascial pain syndrome. Such pain most often occurs as a result of repetitive microtrauma to the muscle from activities such as hammering, turning a screwdriver, and repeated extending of the hand at the wrist or other repetitive activities that require radial wrist deviation. Blunt trauma to the muscle may also incite extensor carpi radialis longus myofascial pain syndrome. Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body. The sine qua non of myofascial pain syndrome is the finding of myofascial trigger points on physical examination. Although these trigger points generally are localized to the regional part of the body affected, the pain of myofascial pain syndrome often is referred to other anatomic areas. This referred pain often is misdiagnosed or attributed to other organ systems, thereby leading to extensive evaluations and ineffective treatment. Patients with myofascial pain syndrome involving the extensor carpi radialis longus often have primary pain in the forearm that is referred into the radial aspect of the base of the thumb. The trigger point is the pathognomonic lesion of myofascial pain and is thought to be a result of microtrauma to the affected muscles. This pathologic lesion is characterized by a local point of exquisite tenderness in affected muscle. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain but also referred pain. In addition to this local and referred pain, there often is an involuntary withdrawal of the stimulated muscle, called a “jump sign.” This jump sign also is characteristic of myofascial pain syndrome. Patients with extensor carpi radialis longus syndrome will exhibit a trigger point over the superior belly of the muscle (Figure 55-1). Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. In spite of this consistent physical finding in patients with myofascial pain syndrome, the pathophysiology of the myofascial trigger point remains elusive, although many theories have been advanced. Common to all of these theories is the belief that trigger points are a result of microtrauma to the affected muscle. This microtrauma may occur as a single injury to the affected muscle or as a result of repetitive microtrauma or chronic deconditioning of the agonist and antagonist muscle unit. In addition to muscle trauma, a variety of other factors seem to predispose the patient to develop myofascial pain syndrome. The weekend athlete who subjects his or her body to unaccustomed physical activity may develop myofascial pain syndrome. 170

The poor posture of someone sitting at a computer keyboard or watching television has also been implicated as a predisposing factor to the development of myofascial pain syndrome. Previous injuries may result in abnormal muscle function and predispose to the subsequent development of myofascial pain syndrome. All of these predisposing factors may be intensified if the patient also has poor nutritional status or coexisting psychological or behavioral abnormalities, including chronic stress and depression. The extensor carpi radialis longus muscle seems to be particularly susceptible to stress-induced myofascial pain syndrome. Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or in conjunction with other painful conditions, including radiculopathy and chronic regional pain syndromes. Psychological or behavioral abnormalities, including depression, frequently coexist with the muscle abnormalities associated with myofascial pain syndrome. Treatment of these psychological and behavioral abnormalities must be an integral part of any successful treatment plan for myofascial pain syndrome.

Clinically Relevant Anatomy The extensor carpi radialis longus muscle extends the hand at the wrist and provides radial deviation of the hand at the wrist as well as weakly flexing the forearm at the elbow and weakly supinating the forearm. The extensor carpi radialis longus muscle finds its origin at the lower lateral supracondylar ridge just below the brachioradialis muscle and the lateral intermuscular septum of the humerus (Figure 55-2). The muscle inserts on the base of the second metacarpal. The muscle is innervated by the radial nerve. The extensor carpi radialis longus muscle is susceptible to trauma and to wear and tear from overuse and misuse and may develop myofascial pain syndrome that also may be associated with lateral epicondylitis.

Technique Careful preparation of the patient before trigger point injection helps to optimize results. Trigger point injections are directed at the primary trigger point rather than in the area of referred pain. It should be explained to the patient that the goal of trigger point injection is to block the trigger of the persistent pain and thus, it is hoped, provide long-lasting relief. It is important that the patient understand that for most patients with myofascial pain syndrome, more than

55  •  Injection Technique for Extensor Carpi Radialis Longus Syndrome        171

one treatment modality is required for optimal pain relief. The use of the recumbent or lateral position when identifying and marking trigger points as well as when performing the actual trigger point injection helps decrease the incidence of vasovagal reactions. The skin overlying the trigger point to be injected should always be prepared with antiseptic solution before injection to avoid infection. After the goals of trigger point injection have been explained to the patient and proper preparation of the patient has been carried out, the trigger point to be injected is reidentified by palpation with the sterilely gloved finger. A syringe containing 10 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone to be injected is attached to a 25- or 27-gauge needle of a length adequate to reach the trigger point. Except for the muscles of posture in the low back, a 1½-inch needle will be adequate. A volume of 0.5 to 1.0 mL of solution is then injected into each trigger point (see Figure 55-1). A series of two to five treatment sessions may be required to completely abolish the trigger point; the patient should be informed of this.

Trigger point Extensor carpi radialis longus m.

Referred pain

Side Effects and Complications The proximity to neurovascular structures including the superficial and deep branches of the radial nerve and the radial artery makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing interventional pain management techniques. Many patients also complain of a transient increase in pain after injection of trigger points in the extensor carpi radialis longus muscle.

Figure 55-1  Patients with extensor carpi radialis longus syndrome will exhibit a positive trigger point over the superior belly of the muscle.

172        SECTION 3  •  Elbow and Forearm Ulnar a.

Pronator teres m., ulnar head Pronator teres m. Flexor carpi radialis m. Palmaris longus m.

Radial a.

••

• • ••

•

•• •

•

•

•

•• •

•

Flexor carpi ulnaris m. Flexor digitorum profundus m. Ulna

Brachioradialis m.

•

•

Median n. Ant. ulnar recurrent a. Flexor digitorum superficialis m. Brachialis m. & t. Ulnar n.

••

•

•

••

• •

• •

• •

Radial n., superficial branch Biceps t. Supinator m., superficial portion Extensor carpi radialis longus m. Radial n., deep branch Extensor carpi radialis brevis m. Supinator m., deep portion Extensor digitorum m.

••

••

Radius Anconeus m.

Extensor carpi ulnaris m.

Pronator teres m., ulnar head Palmaris longus m. Flexor carpi radialis m. Pronator teres m.

Radial a.

••

•

•

Biceps t.

•

••

•• ••

•

••

•• •

•

•• •

••

••

Radial n., superficial branch

••

•

•

••

Brachioradialis m.

••

••

••

Ulna

•

•

Median n. Flexor digitorum superficialis m. Ant. ulnar recurrent a. Ulnar n. Flexor carpi ulnaris m. Brachialis t. Flexor digitorum profundus m.

Ulnar a.

• •

Anconeus m. Extensor carpi ulnaris m.

Radius Supinator m., superficial portion Extensor carpi radialis longus m. Radial n., deep branch Extensor carpi radialis brevis m. Extensor digitorum m.

Supinator m., deep portion

Figure 55-2  The extensor carpi radialis longus muscle and its relationship to the deep branch of the radial nerve and surrounding structures. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

55  •  Injection Technique for Extensor Carpi Radialis Longus Syndrome        173

Clinical Pearls Trigger point injections are extremely safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of trigger point injection are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after trigger point injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid trauma to the neurovascular structures including the superficial and deep branches of the radial nerve and the radial artery when injecting the extensor carpi radialis longus muscle. The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators believe that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as amitriptyline and nortriptyline are good first choices and should be given as a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow.

SUGGESTED READINGS Baldry P: Acupuncture treatment of fibromyalgia and myofascial pain. In Chaitow L, editor: Fibromyalgia syndrome, ed 3, Oxford, 2010, Churchill Livingstone, pp 145–159. Ge HY, Nie H, Madeleine P, et al: Contribution of the local and referred pain from active myofascial trigger points in fibromyalgia syndrome, Pain 147: 233–240, 2009. Ge HY, Wang Y, Danneskiold-Samsøe B, et al: The predetermined sites of examination for tender points in fibromyalgia syndrome are frequently associated with myofascial trigger points, J Pain 11:644–651, 2010. LeBlanc KE, LeBlanc LL: Musculoskeletal disorders, Prim Care 37:389–406, 2010. Partanen JV, Ojala TA, Arokoski JP: Myofascial syndrome and pain: a neurophysiological approach, Pathophysiology 17:19–28, 2010.

Chapter 56 INJECTION TECHNIQUE FOR FLEXOR CARPI ULNARIS SYNDROME Indications and Clinical Considerations The flexor carpi ulnaris muscle is susceptible to the development of myofascial pain syndrome. Such pain most often occurs as a result of repetitive microtrauma to the muscle from activities such as keyboarding and repeatedly flexing the hand at the wrist or other repetitive activities that require ulnar wrist deviation. Blunt trauma to the muscle may also incite flexor carpi ulnaris myofascial pain syndrome. Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body. The sine qua non of myofascial pain syndrome is the finding of myofascial trigger points on physical examination. Although these trigger points generally are localized to the regional part of the body affected, the pain of myofascial pain syndrome often is referred to other anatomic areas. This referred pain often is misdiagnosed or attributed to other organ systems, thereby leading to extensive evaluations and ineffective treatment. Patients with myofascial pain syndrome involving the flexor carpi ulnaris often have primary pain in the ulnar aspect of the forearm that is referred into the palmar surface of the wrist and hand toward the base of the little finger. The trigger point is the pathognomonic lesion of myofascial pain and is thought to be a result of microtrauma to the affected muscles. This pathologic lesion is characterized by a local point of exquisite tenderness in affected muscle. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain but also referred pain. In addition to this local and referred pain, there often is an involuntary withdrawal of the stimulated muscle, called a “jump sign.” This jump sign also is characteristic of myofascial pain syndrome. Patients with flexor carpi ulnaris syndrome will exhibit a trigger point over the superior belly of the muscle (Figure 56-1). Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. In spite of this consistent physical finding in patients with myofascial pain syndrome, the pathophysiology of the myofascial trigger point remains elusive, although many theories have been advanced. Common to all of these theories is the belief that trigger points are a result of microtrauma to the affected muscle. This microtrauma may occur as a single injury to the affected muscle or as a result of repetitive microtrauma or chronic deconditioning of the agonist and antagonist muscle unit. In addition to muscle trauma, a variety of other factors seem to predispose the patient to develop myofascial pain syndrome. The weekend athlete who subjects his or her body to unaccustomed physical activity may develop myofascial pain syndrome. 174

The poor posture of someone sitting at a computer keyboard or watching television has also been implicated as a predisposing factor to the development of myofascial pain syndrome. Previous injuries may result in abnormal muscle function and predispose to the subsequent development of myofascial pain syndrome. All of these predisposing factors may be intensified if the patient also has poor nutritional status or coexisting psychological or behavioral abnormalities, including chronic stress and depression. The flexor carpi ulnaris muscle seems to be particularly susceptible to stress-induced myofascial pain syndrome. Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or in conjunction with other painful conditions, including radiculopathy and chronic regional pain syndromes. Psychological or behavioral abnormalities including depression frequently coexist with the muscle abnormalities associated with myofascial pain syndrome. Treatment of these psychological and behavioral abnormalities must be an integral part of any successful treatment plan for myofascial pain syndrome.

Clinically Relevant Anatomy The flexor carpi ulnaris muscle flexes the hand at the wrist and provides ulnar deviation of the hand at the wrist as well as stabilizing the wrist to allow strong thumb motion. The flexor carpi ulnaris muscle finds its origin at the medial epicondyle via the common flexor tendon as well as the head of the ulna (see Figure 55-2). The muscle inserts on the pisiform and hamate bones via the pisohamate ligament as well as the base of the fifth metacarpal via the pisohamate ligament. The muscle is innervated by the ulnar nerve. The flexor carpi ulnaris muscle is susceptible to trauma and to wear and tear from overuse and misuse and may develop myofascial pain syndrome that also may be associated with medial epicondylitis.

Technique Careful preparation of the patient before trigger point injection helps to optimize results. Trigger point injections are directed at the primary trigger point rather than in the area of referred pain. It should be explained to the patient that the goal of trigger point injection is to block the trigger of the persistent pain and thus, it is hoped, provide long-lasting relief. It is important that the patient understand that for most patients with myofascial pain syndrome, more than one treatment modality is required for optimal pain

56  •  Injection Technique for Flexor Carpi Ulnaris Syndrome        175

Trigger point Flexor carpi ulnaris m.

0.25% preservative-free bupivacaine and 40 mg of methylprednisolone to be injected is attached to a 25- or 27-gauge needle of a length adequate to reach the trigger point. Except for the muscles of posture in the low back, a 11⁄2-inch needle will be adequate. A volume of 0.5 to 1.0 mL of solution is then injected into each trigger point (see Figure 56-1). A series of two to five treatment sessions may be required to completely abolish the trigger point; the patient should be informed of this.

Side Effects and Complications

Referred pain

The proximity to neurovascular structures including the ulnar nerve and the recurrent ulnar artery makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing interventional pain management techniques. Many patients also report a transient increase in pain after injection of trigger points in the flexor carpi ulnaris muscle.

Clinical Pearls Trigger point injections are extremely safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of trigger point injection are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after trigger point injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid trauma to the neurovascular structures including the ulnar nerve and the recurrent ulnar artery when injecting the flexor carpi ulnaris muscle. The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators believe that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as amitriptyline and nortriptyline are good first choices and should be given as a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow.

Figure 56-1  Patients with flexor carpi ulnaris syndrome will exhibit a positive trigger point over the superior belly of the muscle.

relief. The use of the recumbent or lateral position when identifying and marking trigger points as well as when performing the actual trigger point injection helps decrease the incidence of vasovagal reactions. The skin overlying the trigger point to be injected should always be prepared with antiseptic solution before injection to avoid infection. After the goals of trigger point injection have been explained to the patient and proper preparation of the patient has been carried out, the trigger point to be injected is reidentified by palpation with the sterilely gloved finger. A syringe containing 10 mL of

SUGGESTED READINGS Baldry P: Acupuncture treatment of fibromyalgia and myofascial pain. In Chaitow L, editor: Fibromyalgia syndrome, ed 3, Oxford, 2010, Churchill Livingstone, pp 145–159. Budoff JE, Kraushaar BS, Ayala G: Flexor carpi ulnaris tendinopathy, J Hand Surg Am 30:125–129, 2005. Ge HY, Nie H, Madeleine P, et al: Contribution of the local and referred pain from active myofascial trigger points in fibromyalgia syndrome, Pain 147: 233–240, 2009. Ge HY, Wang Y, Danneskiold-Samsøe B, et al: The predetermined sites of examination for tender points in fibromyalgia syndrome are frequently associated with myofascial trigger points, J Pain 11:644–651, 2010. LeBlanc KE, LeBlanc LL: Musculoskeletal disorders, Prim Care 37:389–406, 2010. Partanen JV, Ojala TA, Arokoski JP: Myofascial syndrome and pain: a neurophysiological approach, Pathophysiology 17:19–28, 2010.

Chapter 57 INJECTION TECHNIQUE FOR FLEXOR CARPI RADIALIS SYNDROME Indications and Clinical Considerations The flexor carpi radialis muscle is susceptible to the development of myofascial pain syndrome. Such pain most often occurs as a result of repetitive microtrauma to the muscle from activities such as keyboarding, using a screwdriver, and repeatedly flexing the hand at the wrist or other repetitive activities that require radial wrist deviation. Blunt trauma to the muscle may also incite flexor carpi radialis myofascial pain syndrome. Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body. The sine qua non of myofascial pain syndrome is the finding of myofascial trigger points on physical examination. Although these trigger points generally are localized to the regional part of the body affected, the pain of myofascial pain syndrome often is referred to other anatomic areas. This referred pain often is misdiagnosed or attributed to other organ systems, thereby leading to extensive evaluations and ineffective treatment. Patients with myofascial pain syndrome involving the flexor carpi radialis often have primary pain in the radial aspect of the forearm that is referred into the palmar surface of the wrist and hand toward the base of the thumb. The trigger point is the pathognomonic lesion of myofascial pain and is thought to be a result of microtrauma to the affected muscles. This pathologic lesion is characterized by a local point of exquisite tenderness in affected muscle. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain but also referred pain. In addition to this local and referred pain, there often is an involuntary withdrawal of the stimulated muscle, called a “jump sign.” This jump sign also is characteristic of myofascial pain syndrome. Patients with flexor carpi radialis syndrome will exhibit a trigger point over the superior belly of the muscle (Figure 57-1). Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. In spite of this consistent physical finding in patients with myofascial pain syndrome, the pathophysiology of the myofascial trigger point remains elusive, although many theories have been advanced. Common to all of these theories is the belief that trigger points are a result of microtrauma to the affected muscle. This microtrauma may occur as a single injury to the affected muscle or as a result of repetitive microtrauma or chronic deconditioning of the agonist and antagonist muscle unit. In addition to muscle trauma, a variety of other factors seem to predispose the patient to develop myofascial pain syndrome. The weekend athlete who subjects his or her body to unaccustomed physical activity may develop myofascial pain syndrome. 176

The poor posture of someone sitting at a computer keyboard or watching television has also been implicated as a predisposing factor to the development of myofascial pain syndrome. Previous injuries may result in abnormal muscle function and predispose to the subsequent development of myofascial pain syndrome. All of these predisposing factors may be intensified if the patient also has poor nutritional status or coexisting psychological or behavioral abnormalities, including chronic stress and depression. The flexor carpi radialis muscle seems to be particularly susceptible to stress-induced myofascial pain syndrome. Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or in conjunction with other painful conditions, including radiculopathy and chronic regional pain syndromes. Psychological or behavioral abnormalities, including depression, frequently coexist with the muscle abnormalities associated with myofascial pain syndrome. Treatment of these psychological and behavioral abnormalities must be an integral part of any successful treatment plan for myofascial pain syndrome.

Clinically Relevant Anatomy The flexor carpi radialis muscle flexes the hand at the wrist, ­provides radial deviation of the hand at the wrist, and helps to pronate the forearm. The flexor carpi radialis muscle finds its origin at the medial epicondyle via the common flexor tendon as well as the antebrachial fascia. The muscle inserts on the base of the second and sometimes the third metacarpals. The muscle is innervated by the median nerve. The flexor carpi radialis muscle is susceptible to trauma and to wear and tear from overuse and misuse and may develop myofascial pain syndrome that may also be associated with medial epicondylitis.

Technique Careful preparation of the patient before trigger point injection helps to optimize results. Trigger point injections are directed at the primary trigger point rather than in the area of referred pain. It should be explained to the patient that the goal of trigger point injection is to block the trigger of the persistent pain and thus, it is hoped, provide long-lasting relief. It is important that the patient understand that for most patients with myofascial pain syndrome, more than one treatment modality is required for optimal pain relief. The use of the recumbent or lateral position when identifying and marking trigger points as well as when performing the

57  •  Injection Technique for Flexor Carpi Radialis Syndrome        177

Trigger point Flexor carpi radialis m.

to be injected is attached to a 25- or 27-gauge needle of a length adequate to reach the trigger point. Except for the muscles of posture in the low back, a 11⁄2-inch needle will be adequate. A volume of 0.5 to 1.0 mL of solution is then injected into each trigger point (see Figure 57-1). A series of two to five treatment sessions may be required to completely abolish the trigger point; the patient should be informed of this.

Side Effects and Complications

Referred pain

The proximity to neurovascular structures including the median and ulnar nerve as well as the recurrent anterior ulnar artery makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing interventional pain management techniques. Many patients also report a transient increase in pain after injection of trigger points in the flexor carpi radialis muscle.

Clinical Pearls Trigger point injections are extremely safe if careful ­attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of trigger point injection are related to needle-induced trauma to the ­injection site and underlying tissues. The incidence of ­ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after trigger point injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying ­structures. Special care must be taken to avoid trauma to the neurovascular structures including the median and ulnar nerve as well as the recurrent anterior ulnar artery when injecting the flexor carpi radialis muscle. The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more ­effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators believe that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as ­amitriptyline and nortriptyline are good first choices and should be given as a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow.

Figure 57-1  Patients with flexor carpi radialis syndrome will exhibit a positive trigger point over the superior belly of the flexor carpi radialis muscle.

actual trigger point injection helps decrease the incidence of vasovagal reactions. The skin overlying the trigger point to be injected should always be prepared with antiseptic solution before injection to avoid infection. After the goals of trigger point injection have been explained to the patient and proper preparation of the patient has been carried out, the trigger point to be injected is reidentified by palpation with the sterilely gloved finger. A syringe containing 10 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone

SUGGESTED READINGS Bradley LA: Pathophysiology of fibromyalgia, Am J Med 122:S22–S30, 2009. Ge HY, Nie H, Madeleine P, et al: Contribution of the local and referred pain from active myofascial trigger points in fibromyalgia syndrome, Pain 147: 233–240, 2009. Ge HY, Wang Y, Danneskiold-Samsøe B, et al: The predetermined sites of examination for tender points in fibromyalgia syndrome are frequently associated with myofascial trigger points, J Pain 11:644–651, 2010. Hayter CL, Giuffre BM: Overuse and traumatic injuries of the elbow, Magn Reson Imaging Clin N Am 17:617–638, 2009. LeBlanc KE, LeBlanc LL: Musculoskeletal disorders, Prim Care 37:389–406, 2010. Partanen JV, Ojala TA, Arokoski JP: Myofascial syndrome and pain: a neurophysiological approach, Pathophysiology 17:19–28, 2010. Waldman SD: Painful conditions of the wrist and hand. In Physical diagnosis of pain: an atlas of signs and symptoms, ed 2, Philadelphia, 2010, Saunders, pp 153–154.

Chapter 58 MEDIAN NERVE BLOCK AT THE ELBOW

Indications and Clinical Considerations The injection technique for pronator syndrome is useful in the treatment of pain secondary to median nerve compression syndromes at the elbow, including pronator syndrome and compression of the median nerve by the ligament of Struthers. The pronator syndrome is caused by median nerve compression by the pronator teres muscle (Figure 58-1). The onset of symptoms is usually after repetitive elbow motions such as in chopping wood, sculling, and cleaning fish (Figure 58-2). Clinically, pronator syndrome manifests as a chronic aching sensation localized to the forearm, with pain occasionally radiating into the elbow. Patients with pronator syndrome may complain about a tired or heavy sensation in the forearm with minimal activity, as well as clumsiness of the affected extremity. In contradistinction to carpal

tunnel syndrome, nighttime symptoms are unusual with pronator syndrome. Physical findings include tenderness over the forearm in the region of the pronator teres muscle. Unilateral hypertrophy of the pronator teres muscle may be identified. A positive Tinel sign over the median nerve as it passes beneath the pronator teres muscle also may be present. Weakness of the intrinsic muscles of the forearm and hand that are innervated by the median nerve may be identified with careful manual muscle testing. A positive pronator syndrome test result—pain on forced pronation of the

Enlarged pronator teres m.

Brachialis muscle Median nerve

Pronator teres muscle: superficial head

Deep head

Supinator muscle Figure 58-1  Cadaver specimen: anterior view of the elbow region. This is a deep dissection showing the median nerve as it passes between the superficial and deep heads of the pronator teres muscle. Note the sharp proximal edge of the deep head. (From Pratt N: Anatomy of nerve entrapment sites in the upper quarter, J Hand Ther 18:216-229, 2005.)

178

Figure 58-2  Pronator syndrome is caused by compression of the median nerve by the pronator muscle often following repetitive activities such as cleaning fish.

58  •  Median Nerve Block at the Elbow        179

the axilla, the median nerve descends into the upper arm along with the brachial artery. At the level of the elbow, the brachial artery is just medial to the biceps muscle. At this level the median nerve lies just medial to the brachial artery. As the median nerve proceeds downward into the forearm, it gives off numerous branches that provide motor innervation to the flexor muscles of the forearm. These branches are susceptible to nerve entrapment by aberrant ligaments, muscle hypertrophy, and direct trauma. The nerve approaches the wrist overlying the radius. It lies deep to and between the tendons of the palmaris longus muscle and the flexor carpi radialis muscle at the wrist. The terminal branches of the median nerve provide sensory innervation to a portion of the palmar surface of the hand, as well as the palmar surface of the thumb, the index and middle fingers, and the radial portion of the ring finger. The median nerve also provides sensory innervation to the distal dorsal surface of the index and middle fingers and the radial portion of the ring finger.

Technique

Figure 58-3  The forced pronation test for pronator syndrome. (From Waldman SD: Physical diagnosis of pain, ed 2, Philadelphia, 2010, ­Saunders.)

patient’s fully supinated arm—is highly suggestive of compression of the median nerve by the pronator teres muscle (Figure 58-3). Median nerve entrapment by the ligament of Struthers appears clinically as unexplained persistent forearm pain caused by compression of the median nerve by an aberrant ligament that runs from a supracondylar process to the medial epicondyle. Clinically, it is difficult to distinguish from pronator syndrome. The diagnosis is made by electromyography and nerve conduction velocity testing, which demonstrate compression of the median nerve at the elbow, combined with the radiographic finding of a supracondylar process. Both of these entrapment neuropathies can be differentiated from isolated compression of the anterior interosseous nerve, which occurs 6 to 8 cm below the elbow. These syndromes also should be differentiated from cervical radiculopathy involving the C6 or C7 roots, which may at times mimic median nerve compression. Furthermore, it should be remembered that cervical radiculopathy and median nerve entrapment may coexist as the so-called double crush syndrome. The double crush syndrome is seen most commonly with median nerve entrapment at the wrist or with carpal tunnel syndrome.

Clinically Relevant Anatomy The median nerve is made up of fibers from C5-T1 spinal roots. The nerve lies anterior and superior to the axillary artery. Exiting

The patient is placed in a supine position with the arm fully adducted at the patient’s side and the elbow slightly flexed with the dorsum of the hand resting on a folded towel. A total of 5 to 7  mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 12-mL sterile syringe. The clinician then identifies the pulsations of the brachial artery at the crease of the elbow. After preparation of the skin with antiseptic solution, a 11⁄2-inch, 25-gauge needle is inserted just medial to the brachial artery at the crease and slowly advanced in a slightly medial and cephalad trajectory (Figure 58-4). As the needle advances 1⁄2 to 3 ⁄4 inch, a strong paresthesia in the distribution of the median nerve will be elicited. If no paresthesia is elicited and the needle contacts bone, the needle is withdrawn and redirected slightly more medially until a paresthesia is elicited. The patient should be warned that a paresthesia will occur and to say “there!” as soon as the paresthesia is felt. After a paresthesia has been elicited and its distribution identified, gentle aspiration is carried out to identify blood. If the aspiration test result is negative and no persistent paresthesia into the distribution of the median nerve remains, 5 to 7 mL of solution is slowly injected, with the patient being monitored closely for signs of local anesthetic toxicity. If no paresthesia can be elicited, a similar amount of solution is injected in a fanlike manner just medial to the brachial artery, with care being taken not to inadvertently inject into the artery.

Side Effects and Complications Median nerve block at the elbow is a relatively safe block, with the major complications being inadvertent intravascular injection and persistent paresthesia secondary to needle trauma to the nerve. This technique can safely be performed in the presence of anticoagulation by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable riskto-benefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block also decreases the amount of postprocedure pain and bleeding the patient may experience.

180        SECTION 3  •  Elbow and Forearm

Biceps brachii m.

Brachial a. Median n.

Ligament of Struthers Brachialis m. Medial epicondyle Extensor carpi radialis m. Radial a.

Brachioradialis m.

Enlarged pronator teres m. Palmaris longus m. Aponeurotic extension of biceps Flexor carpi radialis m. Flexor carpi ulnaris m. Flexor digitorum superficialis m.

Figure 58-4  For injection of the medial nerve at the elbow, the needle is placed just medial to the brachial artery.

Clinical Pearls Median nerve block at the elbow is a simple and safe technique in the evaluation and treatment of the just-mentioned painful conditions. Careful neurologic examination to identify preexisting neurologic deficits that later may be attributed to the nerve block should be performed on all patients before beginning median nerve block at the elbow. This technique is especially useful in the treatment of pain secondary to median nerve compression syndromes at the elbow, including compression by the ligament of Struthers and the pronator syndrome. Median nerve compression by the ligament of Struthers manifests clinically as unexplained, persistent forearm pain caused by compression of the median nerve by an aberrant ligament that runs from a supracondylar process to the medial epicondyle. The diagnosis is made by electromyography and nerve conduction velocity testing, which demonstrate compression of the median nerve at the elbow, combined with the radiographic finding of a supracondylar process. The pronator syndrome is characterized by unexplained, persistent forearm pain with tenderness to palpation over the pronator teres muscle. A positive Tinel sign also may be present. Median nerve compression by the ligament of Struthers and pronator syndrome must be differentiated from isolated compression of the anterior interosseous nerve, which occurs 6 to 8 cm below the elbow. These syndromes also should be differentiated from cervical radiculopathy involving the C6 or C7 roots, which may at times mimic median nerve compression. Furthermore, it should be remembered that cervical radiculopathy and median nerve entrapment may coexist as the so-called double crush syndrome. The double crush syndrome is seen most commonly with median nerve entrapment at the wrist or with carpal tunnel syndrome.

SUGGESTED READINGS Dang AC, Rodner CM: Unusual compression neuropathies of the forearm, part ii: median nerve, J Hand Surg Am 34:1915–1920, 2009. De Jesus R, Dellon AL: Historic origin of the “Arcade of Struthers,” J Hand Surg Am 28:528–531, 2003. Gross PT, Tolomeo EA: Proximal median neuropathies, Neurol Clin 17:425–445, 1999. Horak BT, Kuz JE: An unusual case of pronator syndrome with ipsilateral supracondylar process and abnormal muscle mass, J Hand Surg Am 33:79–82, 2008. McCue FC, Alexander EJ, Baumgarten TE: Median nerve entrapment at the elbow in athletes, Oper Tech Sports Med 4:21–27, 1996.

Chapter 59 MEDIAN NERVE BLOCK BELOW ELBOW Indications and Clinical Considerations The injection technique for anterior interosseous syndrome is useful in the treatment of pain and muscle weakness secondary to median nerve compression syndrome below the elbow by the tendinous origins of the pronator teres muscle and flexor digitorum superficialis muscle of the long finger or by aberrant blood vessels (Figure 59-1). The onset of symptoms is usually after acute trauma to the forearm or after repetitive forearm and elbow motions, as in using an ice pick. An inflammatory cause analogous to ParsonageTurner syndrome also has been suggested as a cause of anterior interosseous syndrome. Other causes of anterior interosseous syndrome are listed in Table 59-1. Clinically, anterior interosseous syndrome manifests as an acute pain in the proximal forearm. As the syndrome progresses, patients with anterior interosseous syndrome may report a tired or heavy sensation in the forearm with minimal activity, as well as the inability to pinch items between the thumb and index finger owing to paralysis of the flexor pollicis longus and the

UL

flexor digitorum profundus (Figure 59-2). Positive “Playboy Bunny” and Spinner signs may also be present (Figures 59-3 and 59-4). Physical findings include the inability to flex the interphalangeal joint of the thumb and the distal interphalangeal joint of the index finger owing to paralysis of the flexor pollicis longus and the flexor digitorum profundus (see Figure 59-4). Tenderness over the forearm in the region of the pronator teres muscle is seen in some patients with anterior interosseous syndrome. A positive Tinel sign over the anterior interosseous branch of the median nerve 6 to 8 cm below the elbow also may be present. The anterior interosseous syndrome also should be differentiated from cervical radiculopathy involving the C6 or C7 roots, which may at times mimic median nerve compression. TABLE 59-1

Causes of Anterior Interosseous Syndrome • Direct trauma to nerve • Compression by pronator teres musculotendinous unit • Compression by the flexor digitorum muscle • Compression by fibrous bands • Compression by aberrant median artery • Compression by enlargement of the median artery • Compression by tumor • Compression by soft tissue mass • Compression by hematoma, especially after radius or supracondylar humeral fractures or arterial puncture in the antecubital fossa • Anterior interosseous neuropathies • Inflammatory neuropathies • Compartment syndromes

RA

Patient Figure 59-1  Magnetic resonance imaging demonstrates a focal area of edema (arrowhead) at the myotendinous junction of the flexor digitorum profundus muscle in the proximal forearm adjacent to the anterior interosseous neurovascular bundle (arrow). RA, Radius; UL, ulna. (From Feldman MI, Muhammad K, Beltran J: Preoperative diagnosis of anterior interosseous nerve syndrome resulting in complete recovery, Eur J Radiol Extra 69:e73–e76, 2009.)

Examiner

Figure 59-2  Patients with anterior interosseous syndrome demonstrate an inability to pinch items between the thumb and index fingers owing to paralysis of the flexor pollicis longus and the flexor digitorum profundus muscles.

181

182        SECTION 3  •  Elbow and Forearm Anterior–interosseous nerve syndrome

Anterior interosseous neuropathy

Pseudo–anterior interosseous neuropathy

Lesion of the AIN

Lesion of fibers that ultimately constitute the AIN

• Weakness of FPL, PQ, FDP index • May have weakness of intrinsics, middle finger FDP, and even FDS • Normal sensibility • Normal shoulder girdle

Figure 59-3  The “Playboy Bunny” sign is positive when instead of the classic OK sign as seen on the right, the extension of the distal interphalangeal joint and thumb interphalangeal joint on the right forms the elongated nose of a bunny.

• Weakness of FPL, PQ, FDP index (may be only finding) • May have weakness of intrinsics, middle finger FDP, and even FDS • +/– weakness of shoulder girdle • +/– weakness of thenar muscles • +/– weakness of other muscles • +/– abnormal sensibility (median)

Figure 59-5  Differential diagnosis of anterior interosseous neuropathy compared with pseudo–anterior interosseous neuropathy. AIN, Anterior interosseous neuropathy; FDP, flexor digitorum profundus; FDS, flexor digitorum superficialis; FPL, flexor pollicis longus; PQ, pronator quadratus. (Modified from Chin D, Meals RA: Anterior interosseous nerve syndrome, J Hand Surg Am 1:249-257, 2001.)

Clinically Relevant Anatomy

Figure 59-4  The Spinner sign is positive when the index finger of the affected extremity cannot achieve flexion to the palmar crease as the little, ring, and middle fingers can.

Furthermore, it should be remembered that cervical radiculopathy and median nerve entrapment may coexist as the so-called double crush syndrome. The double crush syndrome is seen most commonly with median nerve entrapment at the wrist or with carpal tunnel syndrome. Anterior interosseous syndrome must also be differentiated from what has been termed “pseudo–anterior interosseous syndrome,” which encompasses pathologic processes that occur above the site of anterior interosseous nerve entrapment that mimic the clinical syndrome of true anterior interosseus nerve entrapment (Figure 59-5). The differential diagnosis will be added by careful physical examination, electromyography and nerve conduction testing, and magnetic resonance imaging.

The median nerve is made up of fibers from C5-T1 spinal roots. The nerve lies anterior and superior to the axillary artery. Exiting the axilla, the median nerve descends into the upper arm along with the brachial artery. At the level of the elbow, the brachial artery is just medial to the biceps muscle. At this level the median nerve lies just medial to the brachial artery. As the median nerve proceeds downward into the forearm, it gives off numerous branches, which provide motor innervation to the flexor muscles of the forearm, including the anterior interosseous nerve (Figure 59-6). These branches are susceptible to nerve entrapment by aberrant ligaments, muscle hypertrophy, and direct trauma. The nerve approaches the wrist overlying the radius. It lies deep to and between the tendons of the palmaris longus muscle and the flexor carpi radialis muscle at the wrist. The terminal branches of the median nerve provide sensory innervation to a portion of the palmar surface of the hand, as well as the palmar surface of the thumb, the index and middle fingers, and the radial portion of the ring finger. The median nerve also provides sensory innervation to the distal dorsal surface of the index and middle fingers and the radial portion of the ring finger.

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side and the elbow slightly flexed with the dorsum of the hand resting on a folded towel. A total of 5 to 7 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 12-mL sterile syringe. The patient is then asked to flex his or her forearm against resistance to identify the biceps tendon at the crease of the elbow. A point 6 to 8 cm below the biceps tendon is then identified and marked with a sterile skin marker. After preparation of the skin with antiseptic solution, a 11⁄2inch, 25-gauge needle is inserted at the previously marked point

59  •  Median Nerve Block Below Elbow        183

Median n. Humerus

Brachial a.

Radius Radial a. Anterior interosseous n.

Ulna

Anterior interosseous a.

Ulnar a.

Pronator quadratus m.

Figure 59-6  A paresthesia is often elicited when the medial nerve is injected in the forearm.

and slowly advanced in a slightly cephalad trajectory (see Figure 59-6). As the needle advances 1⁄2 to 3⁄4 inch, a strong paresthesia in the distribution of the median nerve is elicited. If no paresthesia is elicited and the needle contacts bone, the needle is withdrawn and redirected slightly more medially until a paresthesia is elicited. The patient should be warned that a paresthesia will occur and to say “there!” as soon as the paresthesia is felt. After a paresthesia has been elicited and its distribution identified, gentle aspiration is carried out to identify blood. If the aspiration test is negative and no persistent paresthesia into the distribution of the median nerve remains, 5 to 7 mL of solution is slowly injected, with the patient being monitored closely for signs of local anesthetic toxicity. If no paresthesia can be elicited, a similar amount of solution is injected in a fanlike manner, with care being taken not to inadvertently inject into the anterior interosseous artery.

Side Effects and Complications Median nerve block below the elbow is a relatively safe block, with the major complications being inadvertent intravascular injection and persistent paresthesia secondary to needle trauma to the nerve. This technique can safely be performed in the presence of anticoagulation by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable riskto-benefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block also decreases the amount of postprocedure pain and bleeding the patient may experience.

Clinical Pearls Median nerve block below the elbow is a simple and safe technique in the evaluation and treatment of anterior interosseous syndrome. Careful neurologic examination to identify preexisting neurologic deficits that may later be attributed to the nerve block should be performed on all patients before beginning median nerve block at the elbow. This technique is especially useful in the treatment of pain secondary to anterior interosseous syndrome. Anterior interosseous syndrome can be distinguished from pronator syndrome and median nerve compression by the ligament of Struthers in that the pain of anterior interosseous syndrome occurs more distally and is accompanied by the characteristic loss of ability to pinch items between the thumb and index finger. These entrapment neuropathies also should be differentiated from cervical radiculopathy involving the C6 or C7 roots, which may at times mimic median nerve compression. Furthermore, it should be remembered that cervical radiculopathy and median nerve entrapment may coexist as the so-called double crush syndrome. The double crush syndrome is seen most commonly with median nerve entrapment at the wrist or with carpal tunnel syndrome.

SUGGESTED READINGS al-Qattan MM, Robertson GA: Pseudo–anterior interosseous nerve syndrome: a case report, J Hand Surg Am 18:440–442, 1993. Feldman MI, Muhammad K, Beltran J: Preoperative diagnosis of anterior interosseous nerve syndrome resulting in complete recovery, Eur J Radiol Extra 69:e73–e76, 2009. Kara M, Malas FU, Kaymak B, Ozçakar L: Anterior interosseous syndrome vs flexor pollicis longus tendon rupture: electrodiagnosis or sonography? Surg Neurol 72:647–648, 2009. Proudman TW, Menz PJ: An anomaly of the median artery associated with the anterior interosseous nerve syndrome, J Hand Surg Br 17:507–509, 1992. Waldman SD: Anterior interosseous syndrome. In Pain review, Philadelphia, 2009, Saunders, pp 271–272.

Chapter 60 LATERAL ANTEBRACHIAL CUTANEOUS NERVE BLOCK Indications and Clinical Considerations Lateral antebrachial cutaneous nerve entrapment syndrome is caused by entrapment of the lateral antebrachial cutaneous nerve by the biceps tendon, the brachialis muscle, or the antebrachial superficial fascia. Clinically, the patient with lateral antebrachial cutaneous nerve entrapment syndrome reports pain and paresthesias radiating from the elbow to the base of the thumb. Dull aching of the radial aspect of the forearm is also a common symptom. The pain of lateral antebrachial cutaneous nerve entrapment syndrome may develop after an acute twisting injury to the elbow, hematoma formation in the antecubital fossa and forearm after venous or arterial puncture, or direct trauma to the soft tissues overlying the lateral antebrachial cutaneous nerve; or the onset of pain may be more insidious, without an obvious inciting factor. The pain is constant and is made worse with use of the elbow. Patients with lateral antebrachial cutaneous nerve entrapment syndrome often note increasing pain while keyboarding or playing the piano. Sleep disturbance is common. On physical examination, there is tenderness to palpation of the lateral antebrachial cutaneous nerve at the elbow at a point just lateral to the biceps tendon. Elbow range of motion is normal. Patients with lateral antebrachial cutaneous nerve entrapment syndrome exhibit pain on active resisted flexion or rotation of the forearm. Cervical radiculopathy and tennis elbow can mimic lateral antebrachial cutaneous nerve entrapment syndrome. Lateral antebrachial cutaneous nerve entrapment syndrome can be distinguished from tennis elbow in that in lateral antebrachial cutaneous nerve entrapment syndrome the maximal tenderness to palpation is at the level of the biceps tendon, whereas in tennis elbow the maximal tenderness to palpation is over the lateral epicondyle (see Chapter 47). Electromyography helps distinguish cervical radiculopathy and lateral antebrachial cutaneous nerve entrapment syndrome from tennis elbow. Plain radiographs are indicated for all patients with lateral antebrachial cutaneous nerve entrapment syndrome to rule out occult bony disease. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, uric acid level, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the elbow is indicated if joint instability is suspected. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

continues into the forearm as the lateral antebrachial cutaneous nerve (Figure 60-1). The nerve is susceptible to entrapment at this point. The lateral antebrachial cutaneous nerve passes behind the cephalic vein, where it divides into a volar branch that continues along the radial border of the forearm, providing sensory innervation to the skin over the lateral half of the volar surface of the forearm. It passes anterior to the radial artery at the wrist to provide sensation to the base of the thumb. The dorsal branch provides sensation to the dorsal lateral surface of the forearm.

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side and the elbow slightly flexed with the dorsum of the hand resting on a folded towel. A total of 5 to 7 mL of local anesthetic is drawn up in a 12-mL sterile syringe. When entrapment of the lateral antecubital cutaneous nerve is treated, a total of 80 mg of methylprednisolone is added to the

Biceps tendon

Median n. Brachial a. Biceps brachii m. Brachialis m. Pronator teres m.

Radial a.

Lateral antebrachial cutaneous nerve

Clinically Relevant Anatomy The lateral antebrachial cutaneous nerve is a continuation of the musculocutaneous nerve. The musculocutaneous nerve passes through the fascia lateral to the biceps tendon before it 184

Figure 60-1  The lateral antebrachial cutaneous nerve is a continuation of the musculocutaneous nerve.

60  •  Lateral Antebrachial Cutaneous Nerve Block        185

local anesthetic with the first block and 40 mg of methylprednisolone is added with subsequent blocks. The clinician then identifies the biceps tendon. After preparation of the skin with antiseptic solution, a 11⁄2-inch, 25-gauge needle is inserted just lateral to the biceps tendon at the crease and slowly advanced in a slightly lateral and cephalad trajectory (see Figure 60-1). As the needle advances 1⁄2 to 3⁄4 inch, a strong paresthesia in the distribution of the lateral antebrachial cutaneous nerve is elicited. If no paresthesia is elicited and the needle contacts bone, the needle is withdrawn and redirected slightly more medially until a paresthesia is elicited. The patient should be warned that a paresthesia will occur and to say “there!” as soon as the paresthesia is felt. After the paresthesia has been elicited and its distribution identified, gentle aspiration is carried out to identify blood. If the aspiration test result is negative and no persistent paresthesia into the distribution of the lateral antebrachial cutaneous nerve remains, 5 to 7 mL of solution is slowly injected, with the patient being monitored closely for signs of local anesthetic toxicity. If no paresthesia can be elicited, a similar amount of solution is injected in a fanlike manner just medial to the brachial artery, with care being taken not to inadvertently inject into the artery.

Side Effects and Complications Lateral antebrachial cutaneous nerve block at the elbow is a relatively safe block, with the major complications being inadvertent intravascular injection and persistent paresthesia secondary to needle trauma to the nerve. This technique can safely be performed in the presence of anticoagulation by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable risk-to-benefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block also decreases the amount of postprocedure pain and bleeding the patient may experience.

Clinical Pearls Lateral antebrachial cutaneous nerve block at the elbow is a simple and safe technique. It is extremely useful in the management of lateral antebrachial cutaneous nerve entrapment syndrome. This painful condition may be misdiagnosed as cervical radiculopathy and occasionally as tennis elbow. Lateral antebrachial cutaneous nerve entrapment syndrome can be distinguished from tennis elbow in that in lateral antebrachial cutaneous nerve entrapment syndrome the maximal tenderness to palpation is over the lateral antebrachial cutaneous nerve, whereas in tennis elbow the maximal tenderness to palpation is over the lateral epicondyle. If lateral antebrachial cutaneous nerve entrapment syndrome is suggested, injection of the lateral antebrachial cutaneous nerve at the elbow with local anesthetic and steroid gives almost instantaneous relief. Careful neurologic examination to identify preexisting neurologic deficits that may later be attributed to the nerve block should be performed on all patients before beginning lateral antebrachial cutaneous nerve block at the elbow.

SUGGESTED READINGS Allen DM, Nunley JA: Lateral antebrachial cutaneous neuropathy, Oper Tech Sports Med 9:222–224, 2001. Belzile E, Cloutier D: Entrapment of the lateral antebrachial cutaneous nerve exiting through the forearm fascia, J Hand Surg Am 26:64–67, 2001. Gillingham BL, Mack GR: Compression of the lateral antebrachial cutaneous nerve by the biceps tendon, J Shoulder Elbow Surg 5:330–332, 1996. Waldman SD: The lateral antebrachial cutaneous nerve. In Pain review, Philadelphia, 2009, Saunders, p 99.

SECTION 4  •  Wrist and Hand

Chapter 61 INTRAARTICULAR INJECTION OF THE WRIST JOINT Indications and Clinical Considerations The wrist joint is susceptible to the development of arthritis from a variety of conditions that have in common the ability to damage the joint cartilage. Osteoarthritis of the joint is the most common form of arthritis that results in wrist joint pain. However, rheumatoid arthritis, posttraumatic arthritis, and psoriatic arthritis also are common causes of wrist pain secondary to arthritis. Less common causes of arthritis-induced wrist pain include the collagen vascular diseases, infection, and Lyme disease. Acute infectious arthritis usually is accompanied by significant systemic symptoms, including fever and malaise, and should easily be recognized by the astute clinician and treated appropriately with culture and antibiotics, rather than injection therapy. The collagen vascular diseases generally manifest as a polyarthropathy rather than a monoarthropathy limited to the wrist joint, although wrist pain

A

secondary to collagen vascular disease responds exceedingly well to the intraarticular injection technique described later. The majority of patients with wrist pain secondary to osteoarthritis and posttraumatic arthritis pain complain of pain that is localized around the wrist and hand (Figure 61-1). Activity makes the pain worse; rest and heat provide some relief. The pain is constant and is characterized as aching. The pain may interfere with sleep. Some patients report a grating or “popping” sensation with use of the joint, and crepitus may be present on physical examination. In addition to the just-mentioned pain, patients with arthritis of the wrist joint often experience a gradual decrease in functional ability with decreasing wrist range of motion, making simple everyday tasks such as using a computer keyboard, holding a coffee cup, or turning a doorknob quite difficult. With continued disuse, muscle wasting may occur and an adhesive capsulitis with subsequent ankylosis may develop (Figure 61-2).

B

Figure 61-1  Osteoarthritis of the wrist related to trauma: radial fracture. Posttraumatic alterations in the radiograph (A) and photograph (B) of a coronal section of the wrist relate to a previous fracture of the distal portion of the radius (solid arrows). Findings include irregularity of the radiocarpal compartment related to cartilage loss (arrowheads) and a cyst of the capitate (open arrows). Of interest, minute calcific deposits (related to calcium pyrophosphate dihydrate crystal deposition) can be seen in the triangular fibrocartilage and the space between scaphoid and capitate. (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

186

61  •  Intraarticular Injection of the Wrist Joint        187

Plain radiographs are indicated for all patients with wrist pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Ultrasound and Doppler imaging may help identify wrist disease responsible for the patient’s pain (Figures 61-3 and 61-4). Magnetic resonance imaging (MRI) of the wrist is indicated if joint instability is suspected.

Clinically Relevant Anatomy The wrist joint is a biaxial, ellipsoid-type joint that serves as the articulation between the distal end of the radius and the articular disk above and the scaphoid, lunate, and triquetral bones below (Figures 61-5 and 61-6). The joint’s primary role is to optimize hand function. The joint allows flexion and extension as well as

abduction, adduction, and circumduction. The joint is lined with synovium, and the resultant synovial space allows intraarticular injection, although the septa within the synovial space may limit the flow of injectate. The entire joint is covered by a dense capsule that is attached above to the distal ends of the radius and ulna and below to the proximal row of metacarpal bones. The anterior and posterior joint is strengthened by the anterior and posterior ligaments, with the medial and lateral ligaments strengthening the medial and lateral joint, respectively. The wrist joint also may become inflamed as a result of direct trauma or overuse of the joint. The wrist joint is innervated primarily by the deep branch of the ulnar nerve, as well as by the anterior and posterior interosseous nerves. Anteriorly, the wrist is bounded by the flexor tendons and the median and ulnar nerves. Posteriorly, the wrist is bounded by the extensor tendons. Laterally, the radial artery can be found. The dorsal branch of the ulnar nerve runs medial to the joint; frequently this nerve is damaged when the distal ulna is fractured.

Rad Lun

Figure 61-2  Lunate-hamate arthrosis: accessory lunate facet. A second articular facet of the lunate (arrowhead) articulates with the hamate, and bone sclerosis and widening at this articulation are evident. Osteoarthritis of the trapezioscaphoid and first carpometacarpal joint is apparent. (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

Figure 61-4  Forty-seven–year-old man with rheumatoid arthritis. Ultrasound shows synovial hypertrophy (red star) arising from the radiocarpal joint.

Figure 61-3  Doppler imaging showing increased vascularity within the synovium of the joint.

Figure 61-5  Normal anatomy of the wrist. (From Houston JD, Davis M: Fundamentals of fluoroscopy, Philadelphia, 2001, Saunders.)

188        SECTION 4  •  Wrist and Hand

Figure 61-7  Proper transducer placement for intraarticular injection of the wrist. Capitate Lunate

Scaphoid S SS

Figure 61-6  For an intraarticular injection of the wrist to be performed, the needle is placed in the indentation just proximal to the capitate bone.

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side and the elbow slightly flexed with the palm of the hand resting on a folded towel. A total of 1.5 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. After sterile preparation of skin overlying the dorsal joint, the midcarpus proximal to the indentation of the capitate bone is identified. Just proximal to the capitate bone is an indentation that allows easy access to the wrist joint. With strict aseptic technique, a 1-inch, 25-gauge needle is inserted in the center of the midcarpal indentation through the skin, subcutaneous tissues, and joint capsule into the joint (see Figure 61-6). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected superiorly. After the joint space has been entered, the contents of the syringe are injected gently. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament

R L

Figure 61-8  Ultrasound-guided wrist injection. Figure shows a longitudinal image with proximal oriented left. The needle tip (arrow) is visible with comet-tail artifact between radius (R) and lunate (L). The injected fluid is seen as a hyperechoic cloud (arrowheads) spreading distally from the needle tip into the synovial duplication of the radiocarpal joint (S). On ultrasound, the fluid does not continue into the synovial duplication of the intercarpal joint cavity (SS). (From Boesen M, Jensen KE, TorpPedersen S, et al: Intra-articular distribution pattern after ultrasound-guided injections in wrist joints of patients with rheumatoid arthritis, Eur J Radiol 69:331-338, 2009.)

or tendon and should be advanced slightly into the joint space until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. Ultrasound guidance for needle placement may be useful if the anatomic landmarks necessary for safe intraarticular injection of the wrist are difficult to identify (Figures 61-7 and 61-8).

Side Effects and Complications The major complication of intraarticular injection of the wrist is infection, which should be exceedingly rare if strict aseptic technique is adhered to. As mentioned earlier, the ulnar nerve is especially susceptible to damage at the wrist. Approximately 25% of patients note a transient increase in pain after intraarticular injection of the wrist joint; the patient should be warned of this.

61  •  Intraarticular Injection of the Wrist Joint        189

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to the just-mentioned causes of arthritis of the wrist joint. Coexistent bursitis and tendinitis also may contribute to wrist pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat as well as gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for wrist pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Boesen M, Jensen KE, Torp-Pedersen S, et al: Intra-articular distribution pattern after ultrasound-guided injections in wrist joints of patients with rheumatoid arthritis, Eur J Radiol 69:331–338, 2009. Malfair D: Therapeutic and diagnostic joint injections, Radiol Clin N Am 46:439– 453, 2008. Taylor-Jones LL, Alanmanou E: Steroid joint injections. In Ramamurthy S, ­Rogers JN, Alanmanou E, editors: Decision making in pain management, ed 2, Philadelphia, 2006, Mosby, pp 300–301. Waldman SD: Functional anatomy of the wrist. In Pain review, Philadelphia, 2009, Saunders, pp 100–102. Waldman SD: Technique for intra-articular injection of the wrist joint. In Pain review, Philadelphia, 2009, Saunders, pp 464–465.

Chapter 62 INTRAARTICULAR INJECTION OF THE RADIOULNAR JOINT Indications and Clinical Considerations The radioulnar joint is susceptible to the development of arthritis from a variety of conditions that have in common the ability to damage the joint cartilage. Osteoarthritis of the joint is the most common form of arthritis that results in radioulnar joint pain. However, rheumatoid arthritis, posttraumatic arthritis, and psoriatic arthritis also are common causes of radioulnar pain secondary to arthritis. Less common causes of arthritis-induced radioulnar pain include the collagen vascular diseases, infection, and Lyme disease. Acute infectious arthritis usually is accompanied by significant systemic symptoms, including fever and malaise, and should easily be recognized by the astute clinician and treated appropriately with culture and antibiotics rather than injection therapy. The collagen vascular diseases generally manifest as a polyarthropathy rather than a monoarthropathy limited to the radioulnar joint, although radioulnar pain secondary to collagen vascular disease responds exceedingly well to the intraarticular injection technique described later. The majority of patients with radioulnar pain secondary to osteoarthritis and posttraumatic arthritis pain report pain that is localized to the distal forearm. Activity, especially pronation and supination of the joint, makes the pain worse; rest and heat provide some relief. The pain is constant and is characterized as aching. The pain may interfere with sleep. Some patients note a grating or “popping” sensation with use of the joint. Instability of the distal ulna and crepitus may be present on physical examination and can be identified by performing a distal radioulnar joint stress test (Figure 62-1). In addition to the just-mentioned pain, patients with arthritis of the radioulnar joint often experience a gradual decrease in functional ability with decreasing radioulnar range of motion, making simple everyday tasks, such as using a screwdriver, using a corkscrew, or turning a doorknob, difficult. With continued disuse, muscle wasting may occur and an adhesive capsulitis with subsequent ankylosis may develop. Plain radiographs are indicated for all patients with radioulnar pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and/or ultrasound imaging of the radioulnar joint is indicated if joint instability or damage to the soft tissues is suspected (Figure 62-2).

Clinically Relevant Anatomy The radioulnar joint is a synovial, pivot-type joint that serves as the articulation between the rounded head of the ulna and the 190

ulnar notch of the radius (Figure 62-3). The joint’s primary role is to optimize hand function. The joint allows pronation and supination of the forearm. The joint is lined with synovium, and the resultant synovial space allows intraarticular injection. The entire joint is covered by a relatively weak capsule that surrounds the entire joint. The radioulnar joint also may become inflamed as a result of direct trauma or overuse of the joint. The radioulnar joint is innervated primarily by the anterior and posterior interosseous nerves. The joint is bounded anteriorly by the flexor digitorum profundus and posteriorly by the extensor digiti minimi.

Figure 62-1  The distal radioulnar joint stress test to identify joint instability is performed by firmly grasping and stabilizing the radius with the patient’s forearm in neutral position. The distal ulna is then grasped between the examiner’s thumb and index finger and moved in dorsal and palmar directions relative to the radius. The test result is positive if the ulna was conspicuously displaced relative to the contralateral side. Pain and/or apprehension is often also present.

62  •  Intraarticular Injection of the Radioulnar Joint        191

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side and the elbow slightly flexed with the palm of the hand resting on a folded towel. A total of 1.5 mL

of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. After sterile preparation of skin overlying the dorsal joint, the ulnar styloid is identified. Medially, the radioulnar joint lies approximately one third of the way across the wrist. The joint

A

B

C

D

E

F

G Figure 62-2  This 15-year-old girl injured the ulnar side of the wrist and heard a clicking sound when hitting a tennis ball. A to C, Coronal proton density-weighted images. D to F, T2-weighted images show discontinuity of the ulnar attachment of the triangular fibrocartilage complex (white arrowheads). G, The triangular ligament attachment to the fovea is not identified on the sagittal view. (From Tanaka T, Yoshioka H, Ueno T, et al: Comparison between high-resolution MRI with a microscopy coil and arthroscopy in triangular fibrocartilage complex injury, J Hand Surg Am 31:1308–1314, 2006.)

192        SECTION 4  •  Wrist and Hand

Side Effects and Complications The major complication of intraarticular injection of the radioulnar joint is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients note a transient increase in pain after intraarticular injection of the radioulnar joint; the patient should be warned of this.

Clinical Pearls

Inflamed articular joint

Figure 62-3  The radioulnar joint can be easily identified as the distal radius and ulna are glided together.

can be more easily identified by gliding the distal radius and ulna together. With strict aseptic technique, a 1-inch, 25-gauge needle is inserted in the center of the joint through the skin, subcutaneous tissues, and joint capsule into the joint (see Figure 62-3). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected medially. After the joint space has been entered, the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced slightly into the joint space until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

This injection technique is extremely effective in the treatment of pain secondary to the just-mentioned causes of arthritis of the radioulnar joint. Coexistent bursitis and tendinitis also may contribute to radioulnar joint pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat as well as gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for radioulnar joint pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Boesen M, Jensen KE, Torp-Pedersen S, et al: Intra-articular distribution pattern after ultrasound-guided injections in wrist joints of patients with rheumatoid arthritis, Eur J Radiol 69:331–338, 2009. Katolik LI, Trumble T: Distal radioulnar joint dysfunction, J Hand Surg Am 5:8–29, 2005. Malfair D: Therapeutic and diagnostic joint injections, Radiol Clin North Am 46:439–453, 2008. Steinbach LS, Smith DK: MRI of the wrist, Clin Imaging 24:298–322, 2000. Waldman SD: Functional anatomy of the wrist. Pain review, Philadelphia, 2009, Saunders, pp 100–102. Waldman SD: Technique for intra-articular injection of the inferior radioulnar joint. Pain review, Philadelphia, 2009, Saunders, pp 466–467. Waldman SD: Technique for intra-articular injection of the wrist joint. Pain review, Philadelphia, 2009, Saunders, pp 464–465.

Chapter 63 FLEXOR CARPI RADIALIS TENDON INJECTION

Indications and Clinical Considerations Flexor carpi radialis tendinitis is being seen with increasing frequency in clinical practice as golf and racquet sports have increased in popularity. The flexor carpi radialis tendon is susceptible to the development of tendinitis at the distal portion. The flexor carpi radialis tendon is subject to repetitive motion that may result in microtrauma, which heals poorly owing to the tendon’s avascular nature. Exercise and repetitive trauma are often implicated as the inciting factor of acute flexor carpi radialis tendinitis, with improper grip of golf clubs and tennis racquets and the prolonged use of a heavy hammer being common inciting causes. Tendinitis of the flexor carpi radialis tendon frequently coexists with bursitis, creating additional pain and functional disability. Calcium deposition around the tendon may occur if the inflammation continues, making subsequent treatment more difficult. Continued trauma to the inflamed tendon may ultimately result in tendon rupture (Figure 63-1). The onset of flexor carpi radialis tendinitis is usually acute, occurring after overuse or misuse of the wrist joint. Inciting factors may include activities such as playing tennis or golf and prolonged use of a heavy hammer. Injuries ranging from partial to complete tears of the tendon can occur when the distal tendon sustains direct trauma while the wrist is in full ulnar deviation under load or when the wrist is forced into full ulnar deviation while under load. The pain of flexor carpi radialis tendinitis is constant and severe and is localized in the dorsoradial aspect of the wrist. Significant sleep disturbance is often reported. Patients with flexor carpi radialis tendinitis will exhibit pain with resisted ulnar deviation of the wrist. A creaking or grating may be palpated when passively radially deviating the wrist. As mentioned, the chronically inflamed flexor carpi radialis tendon may suddenly rupture with stress or during vigorous injection procedures when inadvertent injection into the substance of the tendon occurs. Plain radiographs and magnetic resonance scanning are indicated for all patients with radial-sided wrist pain. Ultrasound imaging may also be useful in further delineating the cause of the patient’s wrist pain and functional disability (Figure 63-2). On the basis of the patient’s clinical presentation, additional testing, including complete blood count, sedimentation rate, and antinuclear antibody testing, may be indicated. Magnetic resonance and/or ultrasound imaging of the wrist is indicated if tendon rupture is suspected and to further confirm the diagnosis (Figure 63-2). Radionuclide bone scanning is useful to identify stress fractures of the wrist not seen on plain radiographs.

Clinically Relevant Anatomy The flexor carpi radialis muscle is located in the forearm. Its primary action is to flex and abduct the hand. The muscle finds its origin at the medial epicondyle of the humerus and traverses the forearm just lateral to the flexor digitorum superficialis to insert on the anterior aspect of the base of the second metacarpal. The muscle also has secondary insertions on the third metacarpal and the tuberosity of the trapezium. The flexor carpi radialis muscle is innervated by the median nerve and receives its blood supply from the ulnar artery.

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side and the elbow slightly flexed with the dorsum of the hand resting on a folded towel. A total of 3 mL

Figure 63-1  Clinical photograph demonstrating the defect in the tendon of the flexor carpi radialis muscle lateral to the intact palmaris longus tendon. (From Cowey AJ, Carmont MR, Tins B, Ford DJ: Palmaris longus. Flexor carpi radialis rupture reined in, Inj Extra 38:90–93, 2007.)

193

194        SECTION 4  •  Wrist and Hand

of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. The clinician then has the patient make a fist and at the same time flex his or her wrist to aid in identification of the flexor carpi radialis tendon. After preparation of the skin with antiseptic solution, a 5⁄8-inch, 25-gauge needle is inserted on the ulnar side of the tendon and just proximal to the crease of the wrist at a 30-degree angle (Figure 63-3). The needle is slowly advanced until the tip is just adjacent to the middle of the tendon. If a paresthesia is elicited, the needle is withdrawn slightly away from the median nerve. Gentle aspiration is then carried out to identify blood. If the aspiration test result is negative and no persistent paresthesia into the distribution of the median nerve remains, 3 mL of solution is slowly injected, with the patient being monitored closely for signs of local anesthetic toxicity. If no paresthesia is elicited and the needle tip hits bone, the needle is withdrawn out of the periosteum, and after careful aspiration 3 mL of solution is slowly injected.

RT- FLEX CARP RAD LS Figure 63-2  Ultrasound static image of the longitudinal section of the right forearm. The arrow pointer indicates the fascial sheath; the triangle pointer, the flexor carpi radialis (FCR) tendon; and the double pointer, the striated muscle bulk of flexor digitorum superficialis as compared with the muscle bulk of the FCR, the triple pointer, which is not under tension and has lost its striated appearance. (From Cowey AJ, Carmont MR, Tins B, Ford DJ: Palmaris longus. Flexor carpi radialis rupture reined in, Inj Extra 38:90-93, 2007.)

Side Effects and Complications The major complications associated with this injection technique are related to trauma to the inflamed and previously damaged tendons. Such tendons may rupture if directly injected, and needle position should be confirmed outside the tendon before injection to avoid this complication. Another complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients report a transient increase in pain after this injection technique; the patient should be warned of this.

Clinical Pearls The flexor carpi radialis tendon is a very strong tendon, yet it is also very susceptible to rupture. Coexistent bursitis and arthritis may also contribute to wrist pain and may require additional treatment with a more localized injection of local anesthetic and methylprednisolone acetate. Injection of the flexor carpi radialis tendon is a safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. The use of physical modalities including local heat as well as gentle range of motion exercises should be introduced several days after the patient has undergone this injection technique for elbow pain. Vigorous exercises should be avoided because they will exacerbate the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory drugs may be used concurrently with this injection technique. Inflamed flexor carpi radialis tendon SUGGESTED READINGS

Figure 63-3  Injection technique for flexor carpi radialis tendon.

Akahane T, Nakatsuchi Y, Tateiwa Y: Recurrent granulomatous tenosynovitis of the wrist and finger caused by Mycobacterium intracellulare: a case report, Diagn Microbiol Infect Dis 56:99–101, 2006. Cowey AJ, Carmont MR, Tins B, Ford DJ: Palmaris longus. Flexor carpi radialis rupture reined in, Inj Extra 38:90–93, 2007. Siegal DS, Wu JS, Newman JS, et al: Calcific tendinitis: a pictorial review, Can Assoc Radiol J 60:263–272, 2009. Waldman SD: Functional anatomy of the wrist. In Pain review, Philadelphia, 2009, Saunders, pp 100–102. Wessely MA, Grenier JM: MR imaging of the wrist and hand—a review of the normal imaging appearance with an illustration of common disorders affecting the wrist and hand, Clin Chiropr 10:156–164, 2007.

Chapter 64 FLEXOR CARPI ULNARIS TENDON INJECTION Indications and Clinical Considerations Flexor carpi ulnaris tendinitis is being seen with increasing frequency in clinical practice as golf and racquet sports have increased in popularity. The flexor carpi ulnaris tendon is susceptible to the development of tendinitis at the distal portion. The flexor carpi ulnaris tendon is subject to repetitive motion that may result in microtrauma, which heals poorly owing to the tendon’s avascular nature. Exercise and repetitive trauma are often implicated as the inciting factors of acute flexor carpi ulnaris tendinitis, with improper grip of golf clubs and tennis racquets and the prolonged use of a heavy hammer being common inciting causes. Tendinitis of the flexor carpi ulnaris tendon frequently coexists with bursitis, creating additional pain and functional disability. Calcium deposition around the tendon may occur if the inflammation continues, making subsequent treatment more difficult (Figure 64-1). Continued trauma to the inflamed tendon may ultimately result in tendon rupture. The onset of flexor carpi ulnaris tendinitis is usually acute, occurring after overuse or misuse of the wrist joint. Inciting factors may include activities such as playing tennis or golf and prolonged use of a heavy hammer. Injuries ranging from partial to complete tears of the tendon can occur when the distal tendon sustains direct trauma while the wrist is in full radial deviation under load or when the wrist is forced into full radial deviation

A

while under load. The pain of flexor carpi ulnaris tendinitis is constant and severe and is localized in the dorsoulnar aspect of the wrist. Significant sleep disturbance is often reported. Patients with flexor carpi ulnaris tendinitis will exhibit pain with resisted radial deviation of the wrist. A creaking or grating may be palpated when passively radially deviating the wrist. As mentioned, the chronically inflamed flexor carpi ulnaris tendon may suddenly rupture with stress or during vigorous injection procedures when inadvertent injection into the substance of the tendon occurs. Plain radiographs and magnetic resonance scanning are indicated for all patients with radial-sided wrist pain. Ultrasound imaging may also be useful in further delineating the cause of the patient’s wrist pain and functional disability. On the basis of the patient’s clinical presentation, additional testing, including complete blood count, sedimentation rate, and antinuclear antibody testing, may be indicated. Magnetic resonance imaging of the wrist is indicated if tendon rupture is suspected and to further confirm the diagnosis (Figure 64-2). Radionuclide bone scanning is useful to identify stress fractures of the wrist not seen on plain radiographs.

Clinically Relevant Anatomy The flexor carpi ulnaris muscle is located in the forearm. Its primary action is to flex and adduct the wrist. The muscle has two heads, which find their finds its origins at the medial epicondyle

B

Figure 64-1  A 43-year-old woman with volar wrist pain. A, Anteroposterior and, B, lateral views of the wrist demonstrate several small calcifications (arrows) anterior to the pisiform at the distal attachment of the flexor carpi ulnaris tendon. (From Siegal DS, Wu JS, Newman JS, et al: Calcific tendinitis: a pictorial review, Can Assoc Radiol J 60:263–272, 2009.)

195

196        SECTION 4  •  Wrist and Hand

Figure 64-2  Tenosynovitis of the extensor carpi ulnaris tendon sheath: magnetic resonance (MR) imaging. A transaxial T1-weighed (TR/TE, 600/20) spin-echo MR image of the wrist at the level of the radiocarpal joint shows fluid of intermediate signal intensity (arrows) about the extensor carpi ulnaris tendon in the sixth extensor compartment. (Courtesy S. K. Brahme, MD, La Jolla, Calif; from Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

of the humerus and the medial margin of the olecranon process of the ulna. These heads are connected by a tendinous arch. Beneath this arch pass the ulnar nerve and ulnar artery. The flexor carpi ulnaris muscle traverses the forearm to insert on the pisiform bone and has secondary insertions via ligaments to the hamate and fifth metatarsal. The muscle also has secondary insertions on the third metacarpal and the tuberosity of the trapezium. The flexor carpi ulnaris muscle is innervated by the median nerve and receives its blood supply from the ulnar artery.

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side and the elbow slightly flexed with the dorsum of the hand resting on a folded towel. A total of 3 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. The clinician then has the patient make a fist and at the same time flex his or her wrist to aid in identification of the flexor carpi ulnaris tendon. After preparation of the skin with antiseptic solution, a ⅝-inch, 25-gauge needle is inserted on the ulnar side of the tendon and just proximal to the crease of the wrist at a 30-degree angle (Figure 64-3). The needle is slowly advanced until the tip is just adjacent to the middle of the tendon. If a paresthesia is elicited, the needle is withdrawn slightly away from the median nerve. Gentle aspiration is then carried out to identify blood. If the aspiration test result is negative and no persistent paresthesia into the distribution of the median nerve remains, 3 mL of solution is slowly injected, with the patient being monitored closely for signs of local anesthetic toxicity. If no paresthesia is elicited and the needle tip hits bone, the needle is withdrawn out of the periosteum, and after careful aspiration 3 mL of solution is slowly injected.

Side Effects and Complications The major complications associated with this injection technique are related to trauma to the inflamed and previously

Inflamed flexor carpi ulnaris tendon

Figure 64-3  Injection technique for the flexor carpi ulnaris tendon.

damaged tendons. Such tendons may rupture if directly injected, and needle position should be confirmed outside the tendon before injection to avoid this complication. Another complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients report a transient increase in pain after this injection technique; the patient should be warned of this.

Clinical Pearls The flexor carpi ulnaris tendon is a very strong tendon, yet it is also very susceptible to rupture. Coexistent bursitis and arthritis may also contribute to wrist pain and may require additional treatment with a more localized injection of local anesthetic and methylprednisolone acetate. Injection of the flexor carpi ulnaris tendon is a safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. The use of physical modalities including local heat as well as gentle range of motion exercises should be introduced several days after the patient has undergone this injection technique for elbow pain. Vigorous exercises should be avoided because they will exacerbate the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory drugs may be used concurrently with this injection technique.

64  •  Flexor Carpi Ulnaris Tendon Injection        197 SUGGESTED READINGS Akahane T, Nakatsuchi Y, Tateiwa Y: Recurrent granulomatous tenosynovitis of the wrist and finger caused by Mycobacterium intracellulare: a case report, Diagn Microbiol Infect Dis 56:99–101, 2006. Ankarath S: Chronic wrist pain: diagnosis and management, Curr Orthop 20:141–151, 2006.

Siegal DS, Wu JS, Newman JS, et al: Calcific tendinitis: a pictorial review, Can Assoc Radiol J 60:263–272, 2009. Waldman SD: Functional anatomy of the wrist. In Pain review, Philadelphia, 2009, Saunders, pp 100–102. Wessely MA, Grenier JM: MR imaging of the wrist and hand—a review of the normal imaging appearance with an illustration of common disorders affecting the wrist and hand, Clin Chiropr 10:156–164, 2007.

Chapter 65 RADIAL NERVE BLOCK AT THE WRIST Indications and Clinical Considerations The sensory branch of the radial nerve is particularly susceptible to trauma at the wrist. Fractures or lacerations frequently completely disrupt the nerve, resulting in sensory deficit in the distribution of the radial nerve. The sensory branch of the radial nerve also may be damaged during surgical treatment of de Quervain tenosynovitis. Radial nerve dysfunction secondary to compression by tight handcuffs, wristwatch bands, or casts commonly occurs (Figure 65-1). This entrapment neuropathy is called cheiralgia paresthetica and manifests as pain and associated paresthesias and numbness of the radial aspect of the dorsum of the hand to the base of the thumb. Because there is significant interpatient variability in the distribution of the sensory branch of the radial nerve owing to overlap of the lateral antebrachial cutaneous nerve, the signs and symptoms of cheiralgia paresthetica may vary from patient to patient. The onset of symptoms of cheiralgia paresthetica usually occurs after compression of the sensory branch of the radial nerve, as mentioned earlier. Direct trauma to the nerve also may result in a similar clinical presentation, as can tumors involving or compressing the nerve (Figure 65-2). Physical findings include tenderness over the radial nerve at the wrist. A positive Tinel sign over the radial nerve at the distal forearm usually is present (Figure 65-3). Decreased sensation in the distribution of the sensory branch of the radial nerve often is present, although, as mentioned earlier, the overlap of the lateral antebrachial cutaneous nerve may result in a confusing

clinical presentation. Flexion and pronation of the wrist, as well as ulnar deviation, often cause paresthesias in the distribution of the sensory branch of the radial nerve in patients with cheiralgia paresthetica. A positive wristwatch test result is highly suggestive of the diagnosis of cheiralgia paresthetica. The wristwatch test is performed by having the patient fully deviate his or her wrist to the ulnar side. The examiner then exerts firm pressure on the skin overlying the ulnar nerve (Figure 65-4). The patient is then instructed to fully flex the wrist. The result is considered positive if this maneuver elicits a paresthesia, pain, or numbness. Cheiralgia paresthetica often is misdiagnosed as lateral antebrachial cutaneous nerve syndrome. Electromyography can help identify the exact source of neurologic dysfunction. Cheiralgia paresthetica also should be differentiated from cervical radiculopathy that involves the C6 or C7 roots, although cervical radiculopathy generally causes not only pain and numbness but also reflex and motor changes. Furthermore, cervical radiculopathy and radial nerve entrapment may coexist as the so-called “double crush syndrome.” The double crush syndrome is seen most commonly with median nerve entrapment at the wrist or with carpal tunnel syndrome. Plain radiographs are indicated for all patients with cheiralgia paresthetica to rule out occult bony disease. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody testing. MRI of the wrist is indicated if joint instability is suspected. The injection technique described later serves as both a diagnostic and a therapeutic maneuver and

Superficial branch of the radial nerve Figure 65-1  Cheiralgia paresthetica is caused by compression of the superficial sensory branch of the radial nerve.

198

Figure 65-2  Tumor involving the superficial radial nerve. (From Stuart JE, Smith AC: Plasmacytoma of the superficial radial nerve, J Hand Surg Am 26:776–780, 2001.)

65  •  Radial Nerve Block at the Wrist        199

may be used as an anatomic differential neural blockade to distinguish lesions of the sensory branch of the radial nerve from lesions involving the lateral antebrachial cutaneous nerve.

Clinically Relevant Anatomy The radial nerve is made up of fibers from C5-T1 spinal roots. The nerve lies posterior and inferior to the axillary artery in the 6 o’clock to 9 o’clock quadrant. Exiting the axilla, the radial nerve passes between the medial and long heads of the triceps muscle. As the nerve curves across the posterior aspect of the humerus, it supplies a motor branch to the triceps. Continuing its downward path, it gives off a number of sensory branches to the upper arm. At a point between the lateral epicondyle of the humerus and the musculospiral groove, the radial nerve divides into its two terminal branches. The superficial branch continues down the arm along with the radial artery and provides sensory innervation to the dorsum of the wrist and the dorsal aspects of a portion of the thumb and the index and middle fingers (Figure 65-5). The deep branch provides the majority of the motor innervation to the extensors of the forearm. The major portion of the superficial branch passes between the flexor carpi radialis tendon and the radial artery. However, there are a significant number of small branches that ramify to provide sensory innervation of the dorsum of the hand. These small branches also must be blocked to provide complete blockade of the radial nerve.

Technique

Figure 65-4  The wristwatch test for cheiralgia paresthetica. (From Waldman SD: Physical diagnosis of pain, ed 2, Philadelphia, 2010, Saunders.)

The patient is placed in a supine position with the arm fully adducted at the patient’s side and the elbow slightly flexed with the dorsum of the hand resting on a folded towel. A total of 7 to 8 mL

Distal radial prominence Superficial branch of the radial nerve

Figure 65-3  The positive Tinel sign over the radial nerve in cheiralgia paresthetica. (From Waldman SD: Physical diagnosis of pain, ed 2, Philadelphia, 2010, Saunders.)

Figure 65-5  The superficial branch of the radial nerve is injected at the level of the radial styloid at a point just lateral to the flexor carpi radialis tendon and medial to the radial artery.

200        SECTION 4  •  Wrist and Hand

of local anesthetic is drawn up in a 12-mL sterile syringe. When cheiralgia paresthetica is treated, a total of 80 mg of methylprednisolone is added to the local anesthetic with the first block and 40 mg of methylprednisolone is added with subsequent blocks. The patient is instructed to flex his or her wrist to allow the pain specialist to identify the flexor carpi radialis tendon. The distal radial prominence is then identified. After preparation of the skin with antiseptic solution, a 1½-inch, 25-gauge needle is inserted in a perpendicular trajectory just lateral to the flexor carpi radialis tendon and just medial to the radial artery at the level of the distal radial prominence (see Figure 65-5). The needle is slowly advanced. As the needle approaches the radius, a strong paresthesia in the distribution of the radial nerve will be elicited. The patient should be warned that a paresthesia will occur and to say “there!” as soon as the paresthesia is felt. After the paresthesia has been elicited and its distribution identified, gentle aspiration is carried out to identify blood. If the aspiration test result is negative and no persistent paresthesia into the distribution of the radial nerve remains, 3 to 4 mL of solution is slowly injected, with the patient being monitored closely for signs of local anesthetic toxicity. If no paresthesia is elicited and the needle contacts bone, the needle is withdrawn out of the periosteum, and after careful aspiration 3 to 4 mL of solution is injected. The patient is then asked to fully adduct the wrist, and an additional 3 to 4 mL of solution is injected in a subcutaneous bead, starting at the anatomical snuff box and carrying the injection subcutaneously to just past the midline of the dorsum of the wrist.

Side Effects and Complications Radial nerve block at the wrist is relatively safe, with the major complications being inadvertent intravascular injection and persistent paresthesia secondary to needle trauma to the nerve. This technique can safely be performed in the presence of anticoagulation

by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable risk-to-benefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block will also decrease the amount of postprocedure pain and bleeding the patient may experience.

Clinical Pearls Radial nerve block at the wrist is an effective treatment for the symptoms of cheiralgia paresthetica. Careful neurologic examination to identify preexisting neurologic deficits that may later be attributed to the nerve block should be performed on all patients before beginning radial nerve block at the wrist when treating cheiralgia paresthetica. If cheiralgia paresthetica is identified early, removal of the offending pressure as well as radial nerve block with local anesthetic and corticosteroid should lead to marked improvement in the vast majority of patients.

SUGGESTED READINGS Buttaravoli P: Cheiralgia paresthetica: (handcuff neuropathy). In Minor emergencies, ed 2, Philadelphia, 2007, Mosby, pp 430–431. Dang AC, Rodner CM: Unusual compression neuropathies of the forearm, part I: radial nerve, J Hand Surg Am 34:1906–1914, 2009. Kaufman DM: Peripheral nerve disorders. In Clinical neurology for psychiatrists, ed 6, Philadelphia, 2007, Saunders, pp 61–85. Markiewitz AD, Merryman J: Radial nerve compression in the upper extremity, J Hand Surg Am 5:87–99, 2005. Waldman SD: Cheiralgia paresthetica. In Pain review, Philadelphia, 2009, Saunders, pp 275–276.

Chapter 66 INJECTION TECHNIQUE FOR DE QUERVAIN TENOSYNOVITIS Indications and Clinical Considerations de Quervain tenosynovitis is caused by an inflammation and swelling of the tendons of the abductor pollicis longus and extensor pollicis brevis at the level of the radial styloid process. The inflammation and swelling are usually a result of trauma to the tendon from repetitive twisting motions. If the inflammation and swelling become chronic, a thickening of the tendon sheath occurs, with a resulting constriction of the sheath (Figures 66-1 and 66-2). A triggering phenomenon may result with the tendon catching within the sheath, causing the thumb to lock or “trigger.” Arthritis and gout of the first metacarpal joint also may coexist with and exacerbate the pain and disability of de Quervain tenosynovitis. de Quervain tenosynovitis occurs in patients engaged in repetitive activities that include hand grasping, such as politicians shaking hands, or high-torque wrist turning, such as scooping ice cream at an ice cream parlor. de Quervain tenosynovitis also may develop without obvious antecedent trauma in the parturient. The pain of de Quervain tenosynovitis is localized to the region of the radial styloid. It is constant and is made worse with active pinching activities of the thumb or ulnar deviation of the wrist. Patients note the inability to hold a coffee cup or turn a screwdriver. Sleep disturbance is common. Physical examination reveals tenderness and swelling over the tendons and tendon sheaths along the distal radius, with point tenderness over the radial styloid. Many patients with de Quervain tenosynovitis exhibit a creaking sensation with flexion and extension of the thumb. Range of motion of the thumb may be decreased because of the pain, and a trigger thumb phenomenon may be noted. Patients with

de Quervain tenosynovitis demonstrate a positive Finkelstein test result (Figure 66-3). The Finkelstein test is performed by stabilizing the patient’s forearm, having the patient fully flex his or her thumb into the palm, and then actively forcing the wrist toward the ulna. Sudden severe pain is highly suggestive of de Quervain tenosynovitis. Entrapment of the lateral antebrachial cutaneous nerve, arthritis of the first metacarpal joint, gout, cheiralgia paresthetica, and occasionally C6-C7 radiculopathy can mimic de Quervain tenosynovitis. Cheiralgia paresthetica is an entrapment neuropathy, a result of entrapment of the superficial branch of the radial nerve at the wrist. Electromyography helps distinguish cervical radiculopathy and cheiralgia paresthetica from de Quervain tenosynovitis. Plain radiographs are indicated for all patients with de Quervain tenosynovitis to rule out occult bony disease. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the wrist is indicated if joint instability is suspected.

Tendon, extensor pollicis longus m. Tendon, extensor pollicis brevis m.

Tendon, abductor pollicis longus m.

Extensor retinaculum Radial artery Superficial branches of the radial nerve Figure 66-1  de Quervain tenosynovitis. (From Klippel JH, Dieppe PA: Rheumatology, ed 2, St Louis, Mosby, 1997.)

Figure 66-2  Proper needle placement for treatment of de Quervain tenosynovitis.

201

202        SECTION 4  •  Wrist and Hand

Tendon, extensor pollicis brevis m. Tendon, abductor pollicis longus m. Figure 66-3  The Finkelstein test is performed with the patient fully flexing his or her thumb into the palm and then actively forcing the wrist toward the ulna.

The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The nidus of pain from de Quervain tenosynovitis is the tendons and tendon sheaths of the abductor pollicis longus and extensor pollicis brevis at the level of the radial styloid process (see Figures 66-1 and 66-2). As mentioned earlier, arthritis and gout of the first metacarpal joint may accompany de Quervain tenosynovitis and exacerbate the patient’s pain symptoms. The radial artery and the superficial branch of the radial nerve are in proximity to the injection site for de Quervain tenosynovitis and may be traumatized if the needle is placed too medially.

Figure 66-4  Proper transducer position for injection for de Quervain tenosynovitis.

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side with the ulnar surface of the wrist and hand resting on a folded towel to relax the affected tendons. A total of 2 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. After sterile preparation of the skin overlying the affected tendons, the radial styloid is identified. With strict aseptic technique, a 1-inch, 25-gauge needle is inserted at a 45-degree angle toward the radial styloid through the skin and into the subcutaneous tissue overlying the affected tendon (see Figure 66-2). If bone is encountered, the needle is withdrawn back into the subcutaneous tissue. The contents of the syringe are then gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in the tendon and should be withdrawn back until the injection proceeds without significant resistance. The needle is then removed and a sterile pressure dressing and ice pack are placed at the injection site. Ultrasound guidance may aid in accurate needle placement in patients in whom anatomic landmarks are difficult to identify (Figures 66-4 and 66-5).

Side Effects and Complications The major complications associated with this injection technique are related to trauma to the inflamed and previously damaged tendons. Such tendons may rupture if directly injected, and needle

Figure 66-5  Ultrasound-guided injection into the tendon sheath. Arrowheads indicate needle, and the red star indicates tendon.

position should be confirmed outside the tendon before injection to avoid this complication. Another complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. The radial artery and superficial branch of the radial nerve are susceptible to damage if the needle is placed too medially, and care must be taken to avoid these structures when performing this injection technique. Approximately 25% of patients report a transient increase in pain after this injection technique; the patient should be warned of this.

66  •  Injection Technique for de Quervain Tenosynovitis        203

Clinical Pearls This injection technique is extremely effective in the ­treatment of pain secondary to de Quervain tenosynovitis. Coexistent arthritis and gout also may contribute to the pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is a safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat as well as gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for wrist and thumb pain. A hand splint to immobilize the thumb also may help relieve the symptoms of de Quervain tenosynovitis. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique. As mentioned earlier, arthritis of the first metacarpal joint, gout, cheiralgia paresthetica, and cervical radiculopathy may mimic de Quervain tenosynovitis and must be ruled out to effectively treat the underlying disease.

SUGGESTED READINGS Buttaravoli P: de Quervain’s paratenonitis: (thumb tenosynovitis). In Minor emergencies, ed 2, Philadelphia, 2005, Mosby, pp 438–440. Ilyas AM: Nonsurgical treatment for de Quervain’s tenosynovitis, J Hand Surg Am 34:928–929, 2009. Kay NR: De Quervain’s disease. Changing pathology or changing perception? J Hand Surg Br 25:65–69, 2000. Lane LB, Boretz RS, Stuchin SA: Treatment of de Quervain’s disease: role of ­conservative management, J Hand Surg Br 26:258–260, 2001. McAuliffe JA: Tendon disorders of the hand and wrist, J Hand Surg Am 35:846– 853, 2010. Waldman SD: de Quervain’s tenosynovitis. In Pain review, Philadelphia, 2009, Saunders, pp 276–277.

Chapter 67 INJECTION TECHNIQUE FOR INTERSECTION SYNDROME Indications and Clinical Considerations Intersection syndrome gets its name from the fact that it is caused by tenosynovitis at the intersection of the first and second extensor compartments (Figure 67-1). The tendons within these compartments that become inflamed include the extensor carpi radialis longus, the extensor carpi radialis brevis, the extensor pollicis brevis, and the abductor pollicis longus tendons and associated muscles. This inflammation can be a result of direct trauma to the musculotendinous units or a result of overuse or misuse during activities that require repetitive flexion and extension of the wrist. Rowers, scullers, and weightlifters are at risk for developing intersection syndrome owing to the repetitive flexion and extension of the wrist required for these activities. Other pain syndromes that cause radialsided wrist pain and must be ruled out when considering the diagnosis of intersection syndrome include de Quervain tenosynovitis,

arthritis of the carpometacarpal joint of the thumb, tendinitis of the extensor pollicis longus, and Wartenberg syndrome. Although the pain of intersection syndrome occurs more dorsally than the more radially located pain of de Quervain tenosynovitis, the two are frequently confused (Figure 67-2). Table 67-1 compares and contrasts these two painful conditions of the radial side of the wrist. Patients with intersection syndrome will complain bitterly of radial sided wrist pain that is made worse with wrist flexion or extension. The examiner may be able to elicit a positive creaking tendon test result if the tendons are acutely inflamed (Figure 67-3). The examiner may also able to identify what has been described as wet leather crepitus by careful palpation of the point of intersection during passive or active range of motion of the wrist. As the disease progresses, swelling at the site of intersection is invariably present. On the basis of the patient’s clinical presentation, additional testing, including complete blood count, sedimentation rate, and antinuclear antibody testing, may be indicated. Magnetic resonance imaging of the wrist is indicated if tendon rupture is suspected and to further confirm the diagnosis if de Quervain tenosynovitis is suspected. Radionuclide bone scanning is useful to identify stress fractures of the wrist not seen on plain radiographs. Ultrasound imaging may also help confirm the diagnosis as well as aid in needle placement when performing this injection technique (Figure 67-4).

Extensor carpi radialis brevis Extensor carpi radialis longus Extensor pollicis brevis Abductor pollicis longus

de Quervain Figure 67-1  The site of intersection of the tendons involved in intersection syndrome.

204

Intersection syndrome

Figure 67-2  The site of pain in de Quervain tenosynovitis and intersection syndrome.

67  •  Injection Technique for Intersection Syndrome        205 TABLE 67-1

Comparison of Intersection Syndrome with de Quervain Tenosynovitis de Quervain Tenosynovitis

Intersection Syndrome Tendons involved

Extensor carpi radialis longus Extensor carpi radialis brevis Extensor pollicis brevis Abductor pollicis longus

Abductor pollicis longus Extensor pollicis brevis

Alternate names

Washerwoman’s wrist

Oarsman’s wrist

Clinical signs

Creaking tendon sign Wet leather crepitus

Finkelstein sign

Location of pain

7 cm above radial styloid

At the radial styloid

Site of injection

Above radial styloid at point of maximal ­tenderness

At the radial styloid

Frequency

Rare

Common

Ext. carpi radialis brevis m. Ext. carpi radialis long m.

Abductor pollicis longus m. Ext. pollicis brevis m.

Figure 67-3  Intersection syndrome. Relevant soft tissue anatomy. (From Waldman SD: Physical diagnosis of pain, ed 2, Philadelphia, 2010, Saunders.)

Clinically Relevant Anatomy Intersection syndrome involves the first two compartments of the six compartments that house the extensor tendons of the distal dorsal forearm and dorsal wrist. Passing obliquely over the extensor carpi radialis brevis and extensor carpi radialis longus tendons of the second compartment, the abductor pollicis longus and extensor pollicis brevis of the first compartment intersect at their musculotendinous junctions. This intersection is just proximal to the extensor retinaculum, which serves to tether down the tendons and may contribute to the evolution of intersection syndrome (Figure 67-5).

styloid through the skin and into the subcutaneous tissue overlying the affected tendon (Figure 67-6). If bone is encountered, the needle is withdrawn back into the subcutaneous tissue. The contents of the syringe are then gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in the tendon and should be withdrawn back until the injection proceeds without significant resistance. The needle is then removed and a sterile pressure dressing and ice pack are placed at the injection site. Ultrasound guidance may aid in accurate needle placement in patients in whom anatomic landmarks are difficult to identify.

Technique

Side Effects and Complications

The patient is placed in a supine position with the arm fully adducted at the patient’s side with the ulnar surface of the wrist and hand resting on a folded towel to relax the affected tendons. A total of 2 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. After sterile preparation of the skin overlying the affected tendons, the radial styloid is identified. With strict aseptic technique, a 1-inch, 25-gauge needle is inserted at a point approximately 7 cm above the radial styloid at a 45-degree angle toward the radial

The major complications associated with this injection technique are related to trauma to the inflamed and previously damaged tendons. Such tendons may rupture if directly injected, and needle position should be confirmed outside the tendon before injection to avoid this complication. Another complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients note a transient increase in pain after this injection technique; the patient should be warned of this.

206        SECTION 4  •  Wrist and Hand

EPB-APL EPB ECRB

ECRL

APL

ECRL

Radius

Radius

B A EPL ECRB ECRB

ECRL

ECRL

Radius Radius

C

D

Figure 67-4  A 28-year-old man with the intersection syndrome. Ultrasound shows (proximal to distal) A, proximal crossover point with the abductor pollicis longus (APL) and extensor pollicis brevis (EPB), which pass over the extensor carpi radialis longus (ECRL) and extensor carpi radialis brevis (ECRB) tendons; B, synovitis of the tendons of the first (APL to EPB) and second (ECRL) osteofibrous extensor compartments; C, synovitis of the ECRL and ECRB; D, distal cross-over point with the extensor pollicis longus (EPL) that passes over the ECRL and ECRB; and distal to the intersection with the EPL, absence of fluid in the extensor tendon sheaths of the second compartment. (From Montechiarello S, Miozzi F, D’Ambrosio I, Giovagnorio F: The intersection syndrome: ultrasound findings and their diagnostic value, J Ultrasound 13:70–73, 2010.)

Extensor indicis Extensor pollicis longus Extensor carpi radialis longus Extensor carpi radialis brevis Extensor pollicis brevis

Extensor carpi ulnaris Extensor digiti minimi Extensor digitorum

Abductor pollicis longus

Figure 67-5  The relationship of the extensor retinaculum to the tendons involved in intersection syndrome.

Figure 67-6  Injection technique for intersection syndrome.

67  •  Injection Technique for Intersection Syndrome        207

Clinical Pearls The extensor tendons are very strong structures yet also very susceptible to rupture. Coexistent bursitis, arthritis, and tenosynovitis including de Quervain tenosynovitis may also contribute to wrist pain and may require additional treatment with a more localized injection of local anesthetic and methylprednisolone acetate. The injection technique described earlier is a safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. The use of physical modalities including local heat as well as gentle range-ofmotion exercises should be introduced several days after the patient undergoes this injection technique for wrist pain. Vigorous exercises should be avoided because they will exacerbate the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory drugs may be used concurrently with this injection technique.

SUGGESTED READINGS Descatha A, Leproust H, Roure P, et al: Is the intersection syndrome is an occupational disease? Joint Bone Spine 75:329–331, 2008. Hanlon DP, Luellen JR: Intersection syndrome: a case report and review of the literature, J Emerg Med 17:969–971, 1999. Montechiarello S, Miozzi F, D’Ambrosio I, Giovagnorio F: The intersection syndrome: ultrasound findings and their diagnostic value, J Ultrasound, 13: 70–73, 2010. Waldman SD: Functional anatomy of the wrist. In Pain review, Philadelphia, 2009, Saunders, pp 100–102. Wessely MA, Grenier JM: MR imaging of the wrist and hand—a review of the normal imaging appearance with an illustration of common disorders affecting the wrist and hand, Clin Chiropr 10:156–164, 2007.

Chapter 68 INTRAARTICULAR INJECTION OF THE CARPOMETACARPAL JOINT OF THE THUMB Indications and Clinical Considerations The carpometacarpal joint is susceptible to the development of arthritis from a variety of conditions that have in common the ability to damage the joint cartilage. Osteoarthritis of the joint is the most common form of arthritis that results in carpometacarpal joint pain. Osteoarthritis occurs more commonly in females. However, rheumatoid arthritis, posttraumatic arthritis, and psoriatic arthritis are also common causes of carpometacarpal pain secondary to arthritis. Less common causes of arthritis-induced carpometacarpal pain include the collagen vascular diseases, infection, and Lyme disease. Acute infectious arthritis usually is accompanied by significant systemic symptoms, including fever and malaise, and should easily be recognized by the astute clinician and treated appropriately with culture and antibiotics rather than injection therapy. The collagen vascular diseases generally manifest as a polyarthropathy rather than a monoarthropathy limited to the carpometacarpal joint, although carpometacarpal pain secondary to collagen vascular disease responds exceedingly well to the intraarticular injection technique described later. The clinician should be aware that the carpometacarpal joint of the thumb is susceptible to trauma, and occult ligamentous injuries, dislocations, and fractures should be included in the differential diagnosis of patients with persistent pain in this joint after trauma (Figures 68-1 and 68-2).

The majority of patients with carpometacarpal pain secondary to osteoarthritis and posttraumatic arthritis pain report pain that is localized to the base of the thumb. Activity, especially with pinching and gripping motions, exacerbates the pain; rest and heat provide some relief. The pain is constant and is characterized as aching. The pain may interfere with sleep. Some patients note a grating or “popping” sensation with use of the joint, and crepitus may be present on physical examination. The Watson stress test result is positive in patients with inflammation and arthritis of the carpometacarpal joint of the thumb. This test is performed by having the patient place the dorsum of the hand against a table with the fingers fully extended and then pushing the thumb back toward the table (Figure 68-3). The test result is positive if the patient’s pain is reproduced. In addition to the just-mentioned pain, patients with arthritis of the carpometacarpal joint often experience a gradual decrease in functional ability, with decreasing pinch and grip strength, thereby making everyday tasks such as using a pencil or opening a jar quite difficult. With continued disuse, muscle wasting may occur and an adhesive capsulitis with subsequent ankylosis may develop. Plain radiographs are indicated for all patients with carpometacarpal pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the carpometacarpal joint is indicated if joint instability is suspected.

Clinically Relevant Anatomy

Figure 68-1  An 18-year-old man fell on his left hand from his motorcycle. His thumb carpometacarpal joint appeared unstable. The clinical diagnosis of thumb carpometacarpal joint dislocation was confirmed by computed tomography (reconstructed image). The thumb carpometacarpal joint was stabilized by plication of the dorsal capsule and was placed in a thumb plaster cast for 4 weeks. At follow-up after 4 months, the patient had completely recovered without any pain. Reexamination of the thumb carpometacarpal joint 3 years later showed normal joint stability with a complete range of motion in all directions with normal strength. (From Bosmans B, Verhofstad MJH, Gosens T: Traumatic thumb carpometacarpal joint dislocations, J Hand Surg Am 33:438–441, 2008.)

208

The carpometacarpal joint is a synovial, saddle-shaped joint that serves as the articulation between the trapezium and the base of the first metacarpal (Figure 68-4). The joint’s primary function is to optimize the pinch function of the hand. The joint allows flexion, extension, abduction, adduction, and a small amount of rotation. The joint is lined with synovium, and the resultant synovial space allows intraarticular injection. The entire joint is covered by a relatively weak capsule that surrounds the entire joint and is susceptible to trauma if the joint is subluxed. The carpometacarpal joint may also become inflamed as a result of direct trauma or overuse of the joint.

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side with the hand in neutral position

68  •  Intraarticular Injection of the Carpometacarpal Joint of the Thumb        209

A

B

Figure 68-2  A 25-year-old platform diver after injury to the thumb carpometacarpal joint. A, Coronal fast-spin-echo (FSE) image (TR/TE 4000/30) showing high-grade partial tearing of the anterior oblique ligament (large arrow) with periosteal stripping (small arrows) from the base of the thumb metacarpal. B, Axial FSE image (TR/TE 4000/30) showing the periosteal stripping (open arrow) and the torn anterior oblique ligament (white arrow). (From Connell DA, Pike J, Koulouris G, et al: MR imaging of thumb carpometacarpal joint ligament injuries, J Hand Surg Br 29:46–54, 2004.)

Trapezium

Metacarpal I

Scaphoid

Radius

Trapezoid

Figure 68-4  Gentle traction on the thumb will help open the joint space when an intraarticular injection is performed.

Figure 68-3  The Watson test is performed with the patient placing the dorsum of the hand against a table with the fingers fully extended and then pushing the thumb back toward the table.

with the ulnar aspect against the table. Traction is then placed on the affected thumb to open the joint space (see Figure 68-4). A total of 1.5 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. After sterile preparation of the skin overlying the carpometacarpal joint of thumb, the space between the metacarpal and trapezium is identified. The joint can be more easily identified by abducting and adducting the thumb. With strict aseptic technique, a 1-inch, 25-gauge needle is inserted in the center of the joint through the skin, subcutaneous tissues, and joint capsule into the joint (see Figure 68-4). If bone is encountered, the

needle is withdrawn into the subcutaneous tissues and redirected medially. After the joint space has been entered, the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a tendon and should be advanced slightly into the joint space until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. Ultrasound or fluoroscopic guidance should be considered if the anatomic landmarks necessary to perform this block are difficult to identify (Figures 68-5 and 68-6).

Side Effects and Complications The major complication of intraarticular injection of the carpometacarpal joint of the thumb is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients note a transient increase in pain after intraarticular injection of the carpometacarpal joint; the patient should be warned of this.

210        SECTION 4  •  Wrist and Hand

1st MC

1st MC

Trapezium

A

Trapezium

B

Figure 68-5  A, Injection of the first carpometacarpal joint. The tip of the needle is located superficially to the joint in the muscle (arrow). B, Ultrasound guides the procedure, and in this image the tip of the needle can be appreciated in the intraarticular space (arrow). 1st MC, First metacarpal bone. (From De Zordo T, Mur E, Bellmann-Weiler R, et al: US guided injections in arthritis, Eur J Radiol 71:197–203, 2009.)

SUGGESTED READINGS Day CS, Gelberman R, Patel AA, et al: Basal joint osteoarthritis of the thumb: a prospective trial of steroid injection and splinting, J Hand Surg Am 29:247–251, 2004. Fontana L, Neel S, Claise JM, et al: Osteoarthritis of the thumb carpometacarpal joint in women and occupational risk factors: a case-control study, J Hand Surg Am 32:459–465, 2007. Waldman SD: Technique for intra-articular injection of the carpometacarpal joint of the thumb. In Pain review, Philadelphia, 2009, Saunders, pp 470–471. Yao J, Park MJ: Early treatment of degenerative arthritis of the thumb carpometacarpal joint, Hand Clin 24:251–261, 2008.

Figure 68-6  Proper transducer position for ultrasound guided intraarticular injection of the carpometacarpal joint of the thumb.

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to the just-mentioned causes of arthritis of the carpometacarpal joint. Coexistent tendinitis also may contribute to carpometacarpal joint pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat as well as gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for carpometacarpal joint pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

Chapter 69 INTRAARTICULAR INJECTION OF THE CARPOMETACARPAL JOINT Indications and Clinical Considerations The carpometacarpal joints are susceptible to the development of arthritis from a variety of conditions that have in common the ability to damage the joint cartilage. Osteoarthritis of the joint is the most common form of arthritis that results in carpometacarpal joint pain. It occurs more commonly in females. Although the carpometacarpal joint of the thumb is most commonly affected, the other carpometacarpal joints also may develop arthritis, especially after trauma. Rheumatoid arthritis, posttraumatic arthritis, and psoriatic arthritis also are common causes of carpometacarpal pain secondary to arthritis. Less common causes of arthritis-induced carpometacarpal pain include the collagen vascular diseases, infection, and Lyme disease. Acute infectious arthritis usually is accompanied by significant systemic symptoms, including fever and malaise, and should easily be recognized by the astute clinician and treated appropriately with culture and antibiotics rather than injection therapy. The collagen vascular diseases generally manifest as a polyarthropathy rather than a monoarthropathy limited to the carpometacarpal joint, although carpometacarpal pain secondary to collagen vascular disease responds exceedingly well to the intraarticular injection technique described later. The majority of patients with carpometacarpal pain secondary to osteoarthritis and posttraumatic arthritis pain report pain that is localized to the dorsum of the wrist. Activity associated especially with flexion, extension, and ulnar deviation of the carpometacarpal joints exacerbates the pain; rest and heat provide some relief. The pain is constant and is characterized as aching. The pain may interfere with sleep. Some patients note a grating or “popping” sensation with use of the joint, and crepitus may be present on physical examination. In addition to the just-mentioned pain, patients with arthritis of the carpometacarpal joint often experience a gradual decrease in functional ability with decreasing pinch and grip strength, making everyday tasks such as using a pencil or opening a jar quite difficult. With continued disuse, muscle wasting may occur and an adhesive capsulitis with subsequent ankylosis may develop. Plain radiographs are indicated for all patients with carpometacarpal pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the carpometacarpal joint is indicated if joint instability is suspected.

metacarpals and also allow articulation of the bases of the metacarpal bones with one another (Figure 69-1). Movement of the joints is limited to a slight gliding motion, with the carpometacarpal joint of the little finger possessing the greatest range of motion. The joint’s primary function is to optimize the grip function of the hand. In most patients there is a common joint space. The joint is strengthened by anterior, posterior, and interosseous ligaments.

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side with the hand in neutral position with the palmar aspect resting on a folded towel. A total of 1.5 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. After sterile preparation of the skin overlying the affected carpometacarpal joint, the space between the carpal and metacarpal is identified. The joint can be more easily identified by gliding the joint back and forth. With strict aseptic technique, a 1-inch, 25-gauge needle is inserted in the center of the joint through the skin, subcutaneous tissues, and joint capsule into the joint (see Figure 69-1). If bone is encountered, the needle is withdrawn

Metacarpal IV Capitate

Hamate

Clinically Relevant Anatomy The carpometacarpal joints of the fingers are synovial plane joints that serve as the articulation between the carpals and the

Figure 69-1  Proper needle position for intraarticular injection of the carpometacarpal joint.

211

212        SECTION 4  •  Wrist and Hand

Side Effects and Complications

2nd MC

The major complication of intraarticular injection of the carpometacarpal joints is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients note a transient increase in pain after intraarticular injection of the carpometacarpal joint; the patient should be warned of this.

Clinical Pearls

PP

A

2nd MC PP

B Figure 69-2  A, Longitudinal scan of second metacarpophalangeal joint with rheumatoid arthritis. Tip of the needle (arrow) is placed inside the large amount of synovitis (stars). B, During injection, distension of the joint capsule and hyperechoic drug accumulation can be observed. Stars indicate synovitis; arrow indicates needle. 2nd MC, Second metacarpal bone; PP, proximal phalanx. (From De Zordo T, Mur E, Bellmann-Weiler R, et al: US guided injections in arthritis, Eur J Radiol 71:197-203, 2009.)

This injection technique is extremely effective in the treatment of pain secondary to the just-mentioned causes of arthritis of the carpometacarpal joint. Coexistent tendinitis also may contribute to carpometacarpal joint pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat as well as gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for carpometacarpal joint pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS

into the subcutaneous tissues and redirected medially. After the joint space has been entered, the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a tendon and should be advanced slightly into the joint space until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. Ultrasound or fluoroscopic guidance should be considered if the anatomic landmarks necessary to perform this block are difficult to identify (Figure 69-2).

Alemohammad AM, Nakamura K, El-Sheneway M, Viegas SF: Incidence of carpal boss and osseous coalition: an anatomic study, J Hand Surg Am 34:1–6, 2009. De Zordo T, Mur E, Bellmann-Weiler R, et al: US guided injections in arthritis, Eur J Radiol 71:197–203, 2009. Hunt TR 3rd: Degenerative and post-traumatic arthritis affecting the carpometacarpal joints of the fingers, Hand Clin 22:221–228, 2006. Nakamura K, Patterson RM, Viegas SF: The ligament and skeletal anatomy of the second through fifth carpometacarpal joints and adjacent structures, J Hand Surg Am 26:1016–1029, 2001. Yoshida R, Shah MA, Patterson RM, et al: Anatomy and pathomechanics of ring and small finger carpometacarpal joint injuries, J Hand Surg Am 28:1035–1043, 2003.

Chapter 70 FLEXOR POLLICIS LONGUS TENDON INJECTION Indications and Clinical Considerations Trigger thumb is caused by an inflammation and swelling of the tendon of the flexor pollicis longus as a result of compression by the head of the first metacarpal bone. Sesamoid bones in this region also may cause compression and trauma to the tendon. The inflammation and swelling of the tendon are usually a result of trauma to the tendon from repetitive motion or pressure overlying the tendon as it passes over these bony prominences. If the inflammation and swelling become chronic, a thickening and deterioration of the tendon sheath occurs with a resulting constriction of the sheath (Figures 70-1 and 70-2). Frequently, a nodule develops on the tendon owing to chronic pressure and irritation. These nodules often can be palpated when the patient flexes and extends the thumb. Such nodules may catch in the tendon sheath and cause a triggering phenomenon, thereby causing the thumb to catch or lock. Arthritis and gout of the first metacarpal joint also may coexist with and exacerbate the pain and disability of trigger thumb. Trigger thumb occurs in patients engaged in repetitive activities that include hand grasping, such as politicians shaking hands, or activities that require repetitive pinching movements of the thumb. Video games and frequent card playing also have been implicated in the evolution of trigger thumb.

The pain of trigger thumb is localized to the palmar aspect of the base of the thumb in contradistinction to the pain of de Quervain tenosynovitis, in which the pain is most pronounced more proximally over the radial styloid. The pain of trigger thumb is constant and is made worse with active pinching activities of the thumb. Patients note the inability to hold a coffee cup or a pen. Sleep disturbance is common, and often patients awaken to find that the thumb has become locked in a flexed position during sleep. Physical examination reveals tenderness and swelling over the tendon with maximal point tenderness over the base of the thumb. Many patients with trigger thumb exhibit a “creaking” sensation with flexion and extension of the thumb. Range of motion of the thumb may be decreased owing to the pain, and a trigger thumb phenomenon may be noted. Patients with trigger thumb often demonstrate a nodule on the tendon of the flexor pollicis longus. Plain radiographs are indicated for all patients with trigger thumb to rule out occult bony disease. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the hand is indicated if first metacarpal joint instability is suspected. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Tendon, flexor pollicis longus m.

Synovial sheath Nodule Annular pulley

Figure 70-1  Proper needle position for injection of the flexor pollicis longus tendon.

Figure 70-2  A pathologic pulley. Fragmentation of the coating layer of the gliding surface with detachment of parts of this coating layer, unmasking the underlying collagenous network (scanning electron microscope, ×200). (From Sbernardori MC, Mazzarello V, Tranquilli-Leali P: Scanning electron microscopic findings of the gliding surface of the A1 pulley in trigger fingers and thumbs, J Hand Surg Eur Vol 32:384–387, 2007.)

213

214        SECTION 4  •  Wrist and Hand

Clinically Relevant Anatomy The nidus of pain from trigger thumb is the tendon of the flexor pollicis longus at the level of the base of the first metacarpal (see Figure 70-1). Sesamoid bones present in this region may also impinge on the tendon and tendon sheath, causing inflammation and swelling. As mentioned earlier, arthritis and gout of the first metacarpal joint may accompany trigger thumb and may exacerbate the patient’s pain symptoms. The radial artery and the superficial branch of the radial nerve are in proximity to the injection site for trigger thumb and may be traumatized if the needle is placed too medially.

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side with the dorsal surface of the hand resting on a folded towel. A total of 2 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. After sterile preparation of the skin overlying the affected tendon, the metacarpophalangeal joint of the thumb is identified. With strict aseptic technique, at a point just proximal to the joint, a 1-inch, 25-gauge needle is inserted at a 45-degree angle parallel to the affected tendon, through the skin and into the subcutaneous tissue overlying the affected tendon (see Figure 70-1). If bone is encountered, the needle is withdrawn back into the subcutaneous tissue. The contents of the syringe are then gently injected. The tendon sheath distends as the injection proceeds. There should be little resistance to injection. If resistance is encountered, the needle is probably in the tendon and should be withdrawn back until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complications associated with this injection technique are related to trauma to the inflamed and previously damaged tendon. Such tendons may rupture if directly injected, and needle position should be confirmed outside the tendon before injection to avoid this complication. Another complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. The radial artery and superficial branch of the radial nerve are susceptible to damage if the needle

is placed too medially, and care must be taken to avoid these structures when performing this injection technique. Approximately 25% of patients note a transient increase in pain after this injection technique; the patient should be warned of this.

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to the trigger thumb. Coexistent arthritis and gout also may contribute to the pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat as well as gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique. A quilter’s glove to protect the thumb also may help relieve the symptoms of trigger thumb. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique. de Quervain tenosynovitis may be confused with trigger thumb but can be distinguished by the location of pain and the motions that cause the triggering phenomenon (see Chapter 66).

SUGGESTED READINGS Bodor M, Fullerton B: Ultrasonography of the hand, wrist, and elbow, Phys Med Rehabil Clin N Am 21:509–531, 2010. Kikuchi N, Ogino T: Incidence and development of trigger thumb in children, J Hand Surg Am 31:541–543, 2006. Maneerit J, Sriworakun C, Budhraja N, Nagavajara P: Trigger thumb: results of a prospective randomised study of percutaneous release with steroid injection versus steroid injection alone, J Hand Surg Br 28:586–589, 2003. Ragheb D, Stanley A, Gentili A, et al: MR imaging of the finger tendons: normal anatomy and commonly encountered pathology, Eur J Radiol 56:296–306, 2005. Ryzewicz M, Wolf JM: Trigger digits: principles, management, and complications, J Hand Surg Am 31:135–146, 2006.

Chapter 71 FLEXOR DIGITORUM SUPERFICIALIS INJECTION Indications and Clinical Considerations Trigger finger is an inflammation and swelling of the tendons of the flexor digitorum superficialis caused by compression by the heads of the metacarpal bones. Sesamoid bones in this region also may cause compression and trauma to the tendons (see Chapter 73). The inflammation and swelling of the tendon are usually a result of trauma to the tendon from repetitive motion or pressure overlying the tendon as it passes over these bony prominences. If the inflammation and swelling become chronic, a thickening of the tendon sheath occurs, with a resulting constriction of the sheath. Frequently a nodule develops on the tendon owing to chronic pressure and irritation. These nodules often can be palpated when the patient flexes and extends the fingers. Such nodules may catch in the tendon sheath as the nodule passes under a restraining tendon pulley and cause a triggering phenomenon, causing the finger to catch or lock as the nodule catches on the pulley (Figures 71-1 and 71-2). Coexistent arthritis and gout of the metacarpal and interphalangeal joints may also exacerbate the pain and disability of trigger finger. Trigger finger occurs in patients engaged in repetitive activities that include hand clenching, such as gripping a steering wheel or holding a horse’s reins too tightly.

The pain of trigger finger is localized to the distal palm, with tender tendon nodules often palpated. The pain of trigger finger is constant and is made worse with active gripping activities of the hand. Patients note significant stiffness when flexing the fingers. Sleep disturbance is common, and the patient often awakens to find that the finger has become locked in a flexed position during sleep. Physical examination reveals tenderness and swelling over the tendon with maximal point tenderness over the heads of the metacarpals. Many patients with trigger finger exhibit a “creaking” with flexion and extension of the fingers. Range of motion of the fingers may be decreased owing to the pain, and a trigger finger phenomenon may be noted. Patients with trigger finger often demonstrate nodules on the tendons of the flexor digitorum superficialis. Plain radiographs are indicated for all patients with trigger finger to rule out occult bony disease. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the hand is indicated if joint instability or tendinopathy is suspected. Ultrasound imaging may also help identify soft tissue abnormalities that may be responsible for the triggering phenomenon (Figure 71-3). The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy

Inflamed nodule distal to pulley Inflamed nodule proximal to pulley

Figure 71-1  The mechanism of trigger finger.

The nidus of pain from trigger finger is the tendon flexor digitorum superficialis at the level of the head of the metacarpals (see Figure 71-1). Sesamoid bones present in this region also may impinge on the tendon and tendon sheath and cause inflammation and swelling. As mentioned earlier, arthritis and gout of the metacarpal joints may accompany trigger finger and exacerbate the patient’s pain symptoms.

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side with the dorsal surface of the hand resting on a folded towel. A total of 2 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. After sterile preparation of the skin overlying the affected tendon, the head of the metacarpal beneath the tendon is identified. With strict aseptic technique, at a point just proximal to the joint, a 1-inch, 25-gauge needle is inserted at a 45-degree angle parallel to the affected tendon, through the skin and into the subcutaneous tissue overlying the affected tendon (Figure 71-4). If bone is encountered, the needle is withdrawn back into the subcutaneous 215

216        SECTION 4  •  Wrist and Hand

A

B

Figure 71-2  Clinical photos of the patient’s affected hand at time of presentation to our institution, showing A, the 55-degree flexion contracture and, B, the limitation of active composite flexion. (From Gyuricza C, Umoh E, Wolfe SW: Multiple pulley rupture following corticosteroid injection for trigger digit: case report, J Hand Surg Am 34:1444–1448, 2009.)

Pulley Flexor tendons

MC

A

B Released pulley Flexor tendons

MC

C

D

Figure 71-3  Clinical picture (A) and transverse sections of sonograms (B) of the long finger with grade IV trigger digit before the procedure. Clinical picture (C) and transverse sections of sonograms (D) of the long finger with grade IV trigger digit after the procedure. (From Jou IM, Chern TC: Sonographically assisted percutaneous release of the a1 pulley: a new surgical technique for treating trigger digit, J Hand Surg Br 31:191–199, 2006.)

71  •  Flexor Digitorum Superficialis Injection        217

Inflamed nodule distal to pulley

Figure 71-6  In-plane view of needle in position for injection of the flexor digitorum tendon.

placed at the injection site. Ultrasound guidance may be beneficial if the anatomic landmarks necessary for needle placement are difficult to identify (Figures 71-5 and 71-6).

Side Effects and Complications Figure 71-4  Proper needle placement for injection of the flexor digitorum superficialis tendon.

The major complications associated with this injection technique are related to trauma to the inflamed and previously damaged tendon (Figure 71-7). Such tendons may rupture if they are directly injected; needle position should be confirmed outside the tendon before injection to avoid this complication. Another complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is followed. Approximately 25% of patients report a transient increase in pain after this injection technique; the patient should be warned of this.

Clinical Pearls

Figure 71-5  Trigger finger injection with short-axis view of the needle tip within the target triangle. The tip of a 30-gauge needle (arrow) is the hyperechoic dot next to the flexor digitorum profundus (FDP) tendon and volar plate. The angle of the arrow reflects the trajectory of the needle in the coronal plane. (From Bodor M, Fullerton B: Ultrasonography of the hand, wrist, and elbow, Phys Med Rehabil Clin N Am 21:509–531, 2010.)

tissue. The contents of the syringe are then gently injected. The tendon sheath distends as the injection proceeds. There should be little resistance to injection. If resistance is encountered, the needle is probably in the tendon and should be withdrawn back until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are

This injection technique is extremely effective in the treatment of pain secondary to trigger finger. Coexistent arthritis and gout also may contribute to the pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique. A hand splint to protect the fingers also may help relieve the symptoms of trigger finger. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

218        SECTION 4  •  Wrist and Hand

A

B

Figure 71-7  A, Axial image at the level of the A2 pulley from magnetic resonance imaging of the middle digit. There is complete disruption of the A2 pulley (arrows), with palmar displacement of the flexor tendon. The intact pulley is present in adjacent digits. B, Sagittal image of the middle digit demonstrating palmar displacement of the flexor tendon. (From Gyuricza C, Umoh E, Wolfe SW: Multiple pulley rupture following corticosteroid injection for trigger digit, case report, J Hand Surg Am 34:1444-1448, 2009.)

SUGGESTED READINGS Bodor M, Fullerton B: Ultrasonography of the hand, wrist, and elbow, Phys Med Rehabil Clin N Am 21:509–531, 2010. Brito JL, Rozental TD: Corticosteroid injection for idiopathic trigger finger, J Hand Surg Am 35:831–833, 2010. Ragheb D, Stanley A, Gentili A, et al: MR imaging of the finger tendons: normal anatomy and commonly encountered pathology, Eur J Radiol 56:296–306, 2005.

Ryzewicz M, Wolf JM: Trigger digits: principles, management, and complications, J Hand Surg Am 31:135–146, 2006. Sbernardori MC, Bandiera P: Histopathology of the A1 pulley in adult trigger fingers, J Hand Surg Eur Vol 32:556–559, 2007. Wang AA, Hutchinson DT: The effect of corticosteroid injection for trigger finger on blood glucose level in diabetic patients, J Hand Surg Am 31:979–981, 2006.

Chapter 72 DIGITAL NERVE BLOCK OF THE THUMB Indications and Clinical Considerations Bowler’s thumb is an entrapment neuropathy of the digital nerve on the ulnar side at the base of the thumb that may manifest in either an acute or a chronic form. In bowler’s thumb, compression by the edge of the thumb hole of the bowling ball is the inciting cause (Figure 72-1). The common clinical feature of bowler’s thumb is a painful digital nerve at the point at which the bowling ball compresses it. The nerve may be thickened, and inflammation of the nerve and overlying soft tissues may be seen. In addition to pain, the patient with bowler’s thumb may also report paresthesias and numbness just below the point of nerve compromise. Other causes of compression of the digital nerve on the ulnar side at the base of the thumb have been identified, such as overuse of scissors by dressmakers, compression of the nerve by overuse of jeweler’s pliers, and cherry pitting. The pain of bowler’s thumb may develop after an acute bowling injury or direct trauma to the soft tissues overlying the digital nerve if the thumb gets stuck in the bowling ball, damaging the nerve. The pain is constant and is made worse with compression of the digital nerve. Patients often also note the inability to hold or close a pair of scissors with the affected thumb. Sleep disturbance is common. On physical examination there is tenderness to palpation of the digital nerve on the ulnar side at the base of the thumb. Range of motion of the thumb is normal. Palpation of the affected nerve can cause paresthesias, and continued pressure on the nerve may induce numbness distal to the point of compression. Electromyography helps distinguish other causes of hand numbness from bowler’s thumb. Plain radiographs are indicated for all patients with bowler’s thumb to rule out occult bony disease such as bone spurs or cysts that may be compressing the digital nerve. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the hand can be done to rule out soft tissue tumors such as ganglia that may be compressing the digital nerve. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Compression of palmar digital n.

Figure 72-1  Bowler’s thumb is an entrapment neuropathy caused by compression of the digital nerve on the ulnar side of the thumb.

Clinically Relevant Anatomy The common digital nerves arise from fibers of the median and ulnar nerves. The thumb also has contributions from superficial branches of the radial nerve. The common digital nerves pass along the metacarpal bones and divide as they reach the distal palm. The volar digital nerves supply the majority of sensory

innervation to the fingers and run along the ventrolateral aspect of the finger beside the digital vein and artery. The smaller dorsal digital nerves contain fibers from the ulnar and radial nerves and supply the dorsum of the fingers as far as the proximal joints. 219

220        SECTION 4  •  Wrist and Hand

Side Effects and Complications Palmar digital n.

Needle entry point

Digital nerve block of the thumb is a relatively safe block, with the major complications being inadvertent intravascular injection and persistent paresthesia secondary to needle trauma to the nerve. This technique can safely be performed in the presence of anticoagulation by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable riskto-benefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block decreases the amount of postprocedure pain and bleeding the patient may experience. Under no circumstance should local anesthetics containing epinephrine be used for digital nerve block because gangrene of the digit has been reported.

Clinical Pearls Median n.

Figure 72-2  Proper needle placement for injection of the digital nerve.

Technique The patient is placed in a supine position with the arm fully abducted and the elbow slightly flexed with the palm of the hand resting on a folded towel. A total of 3 mL per digit of non– epinephrine-­containing local anesthetic is drawn up in a 12-mL sterile syringe. After preparation of the skin with antiseptic solution, at a point at the base of the finger, a 25-gauge, 1½-inch needle is inserted on each side of the bone of the digit to be blocked (Figure 72-2). While the anesthetic is slowly injected, the needle is advanced from the dorsal surface of the hand toward the palmar surface. The same technique can be used to block the thumb. The needle is removed, and pressure is placed on the injection site to avoid hematoma formation.

Digital block of the thumb is a safe and simple technique and is extremely useful in the management of bowler’s thumb. If bowler’s thumb is suspected, injection of the digital nerve on the ulnar side of the base of the thumb with local anesthetic and corticosteroid gives almost instantaneous relief of the pain, although numbness may persist. Careful neurologic examination to identify preexisting neurologic deficits that may later be attributed to the nerve block should be performed on all patients before beginning diagnostic and/or therapeutic digital nerve blocks.

SUGGESTED READINGS Dobyns JH, O’Brien ET, Linscheid RL, Farrow GM: Bowler’s thumb: diagnosis and treatment. A review of seventeen cases, J Bone Joint Surg Am 54:751–755, 1972. Hug U, Burg D, Baldi SV, Meyer VE: Compression neuropathy of the radial palmar thumb nerve, Chir Main 23:49–51, 2004. Izzi J, Dennison D, Noerdlinger M, et al: Nerve injuries of the elbow, wrist, and hand in athletes, Clin Sports Med 20:203–217, 2001. Toth C: Peripheral nerve injuries attributable to sport and recreation, Phys Med Rehabil Clin N Am 20:77–100, 2009. Watson J, Gonzalez M, Romero A, Kerns J: Neuromas of the hand and upper extremity, J Hand Surg Am 35:499–510, 2010.

Chapter 73 SESAMOID JOINT INJECTION OF THE HAND Indications and Clinical Considerations Sesamoiditis is a relatively uncommon pain syndrome that affects the hand. Sesamoiditis is characterized by tenderness and pain over the flexor aspect of the thumb and, much less commonly, the index finger. The patient often feels that he or she has a stone or foreign body embedded in the affected digit when grasping things. The pain of sesamoiditis worsens with repeated flexion and extension of the affected digits. When the thumb is affected, the sesamoiditis usually occurs on the radial side, where the condyle of the adjacent metacarpal is less obtrusive. Patients with psoriatic arthritis may have a higher incidence of sesamoiditis of the hand (Figure 73-1). On physical examination, pain can be reproduced by pressure on the sesamoid bone. In contradistinction to occult bony disease of the phalanges in which the tender area remains over the area of disease, with sesamoiditis the tender area moves with the flexor tendon when the patient actively flexes his or her thumb or finger. With acute trauma to the sesamoid, ecchymosis over the flexor surface of the affected digit may be present. Plain radiographs are indicated for all patients with sesamoiditis to rule out fractures, tumors, and avascular necrosis and to identify sesamoid bones that may have become inflamed. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the fingers and bones of the wrist is indicated if joint instability, occult mass, occult fracture, infection, or tumor is suspected. Radionuclide bone scanning may be useful in identifying stress fractures of the thumb and fingers or sesamoid bones that may be missed on plain radiographs of the hand.

Figure 73-1  At the first metacarpophalangeal joint, irregular bone formation in the metacarpal head, proximal phalanx, and adjacent sesamoid (arrow) can be seen. Periostitis of the metacarpal diaphysis is also evident (arrowhead). (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

Clinically Relevant Anatomy The sesamoid bones are small, rounded structures that are embedded in the flexor tendons of the hand and usually are in close proximity to the joints. Sesamoid bones of the thumb occur in almost all patients with sesamoiditis, with sesamoid bones being present in the flexor tendons of the index finger in a small number of patients (Figure 73-2). These sesamoid bones serve to decrease friction and pressure of the flexor tendon as it passes in proximity to a joint.

Inflamed sesamoid bone and flexor pollicis longus tendon

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position with the palmar surface

Figure 73-2  Proper needle placement for injection for sesamoiditis of the hand.

221

222        SECTION 4  •  Wrist and Hand

of the hand exposed. Proper preparation with antiseptic solution of the skin overlying the tender sesamoid bone is then carried out. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a ­⅝-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique the affected sesamoid bones are identified. At this point, the needle is carefully advanced through the palmar surface of the affected digit until the needle tip rests against the sesamoid bone (see Figure 73-2). The needle is withdrawn slightly out of the periosteum and substance of the tendon. After the needle is in the correct position next to the affected sesamoid bone and aspiration for blood is negative, the contents of the syringe are gently injected. There may be slight resistance to injection, given the closed nature of the space. If significant resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. The ice should not be left on for more than 10 minutes to avoid freezing injuries.

Side Effects and Complications The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is followed. Approximately 25% of patients report a transient increase in pain after injection of sesamoid bones; the patient should be warned of this.

Clinical Pearls Pain emanating from the hand is a common problem that is encountered in clinical practice. Sesamoiditis must be distinguished from stress fractures and other occult disease of the phalanges as well as fractures of the sesamoid bones. Although the just-described injection technique provides palliation of the pain of sesamoiditis, the patient often also requires resting hand splints to aid in rehabilitation of the affected finger. Padded gloves may be useful to help take pressure off the affected sesamoid bone and overlying soft tissue. Coexistent bursitis and tendinitis also may contribute to the patient’s hand pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for sesamoiditis pain. Vigorous exercise should be avoided, because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Havulinna J, Parkkinen J, Laitinen M: Aneurysmal bone cyst of the index sesamoid, J Hand Surg Am 30:1091–1093, 2005. Louaste J, Amhajji L, Eddine EC, Rachid K: Chondroma in a sesamoid bone of the thumb: case report, J Hand Surg Am 33:1378–1379, 2008. Shaw M, Lyburn ID, Torreggiani WC, Watura R: Comminuted fracture of the ulnar sesamoid of the metacarpophalangeal joint of the thumb: an uncommon injury, J Emerg Med 24:437–439, 2003. Van Asch Y, Vreugde M, Brabants K: Atraumatic avascular necrosis of an index sesamoid, Chir Main 24:251–253, 2005.

Chapter 74 INTRAARTICULAR INJECTION OF THE METACARPOPHALANGEAL JOINTS Indications and Clinical Considerations The metacarpophalangeal joint is susceptible to the development of arthritis from a variety of conditions that have in common the ability to damage the joint cartilage. Osteoarthritis of the joint is the most common form of arthritis that results in metacarpophalangeal joint pain. However, rheumatoid arthritis, posttraumatic arthritis, and psoriatic arthritis also are common causes of metacarpophalangeal pain secondary to arthritis

A

(Figure 74-1). Less common causes of arthritis-induced metacarpophalangeal pain include the collagen vascular diseases, infection, and Lyme disease. Acute infectious arthritis usually is accompanied by significant systemic symptoms, including fever and malaise, and should easily be recognized by the astute clinician and treated appropriately with culture and antibiotics rather than injection therapy. The collagen vascular diseases generally manifest as a polyarthropathy rather than a monoarthropathy limited to the metacarpophalangeal joint, although metacarpophalangeal pain secondary to collagen vascular disease responds

B

C Figure 74-1  Rheumatoid arthritis: abnormalities of synovial joints. Sequential radiographic changes in metacarpophalangeal joints. A, The earliest abnormalities consist of soft tissue swelling (solid arrows), periarticular osteoporosis, loss of a portion of the subchondral bone plate on the metacarpal head (open arrow), and minimal joint space narrowing. B, With progression, increases in soft tissue swelling (arrows) and osteoporosis are associated with marginal erosions of the metacarpal heads (open arrow). C, The later stages of rheumatoid arthritis are characterized by complete obliteration of the articular space and large central and marginal osseous erosions (open arrows). (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

223

224        SECTION 4  •  Wrist and Hand

t1

* S

* PP

S

MC

A

t2

MC

B

PP

MC

C

MC

D

Figure 74-2  Hand involvement in rheumatoid arthritis. A, Metacarpophalangeal joint synovitis on longitudinal dorsal view. B, Tenosynovitis of the finger flexor tendons on transverse volar view. C and D, Bone erosion at the lateral aspect of the second metacarpal head, depicted on longitudinal (C) and transverse (D) views. *, Synovial fluid; MC, metacarpus; PP, proximal phalanx; S, synovial hypertrophy; t1, superficial finger flexor tendon; t2, deep finger flexor tendon. (From Grassi W, Salaffi F, Filippucci E: Ultrasound in rheumatology, Best Pract Res Clin Rheumatol 19:467–485, 2005.)

exceedingly well to the intraarticular injection technique described later. The majority of patients with metacarpophalangeal pain secondary to osteoarthritis and posttraumatic arthritis pain report pain that is localized to the bases of the proximal phalanges and the heads of the metacarpal bones. Activity, especially with gripping motions, exacerbates the pain; rest and heat provide some relief. The pain is constant and is characterized as aching. The pain may interfere with sleep. Some patients report a grating or “popping” sensation with use of the joint; crepitus may be present on physical examination. Swelling of the joints commonly occurs. In addition to the just-mentioned pain, patients with arthritis of the metacarpophalangeal joint often experience a gradual decrease in functional ability with decreasing grip strength, making everyday tasks such as turning a doorknob or opening a jar quite difficult. With continued disuse, muscle wasting may occur and an adhesive capsulitis with subsequent ankylosis may develop. Plain radiographs are indicated for all patients with metacarpophalangeal joint pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and/or ultrasound of the metacarpophalangeal joints is indicated if joint instability or abnormality is suspected (Figure 74-2).

Clinically Relevant Anatomy The metacarpophalangeal joint is a synovial, ellipsoid joint that serves as the articulation between the base of the proximal

phalanges and the head of its respective metacarpal (Figure 74-3). The joint’s primary role is to optimize the gripping function of the hand. The joint allows flexion, extension, abduction, and adduction. The joint is lined with synovium, and the resultant synovial space allows intraarticular injection. The joint is covered by a capsule that surrounds the entire joint and is susceptible to trauma if the joint is subluxed. Ligaments help strengthen the joints; the palmar ligaments are particularly strong.

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side with the hand in neutral position with the palmar aspect resting on a folded towel. A total of 1.5 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. After sterile preparation of the skin overlying the affected metacarpophalangeal joint, the space between the base of the proximal phalanges and the head of the respective metacarpal is identified. The joint can be identified more easily by flexing and extending the joint. With strict aseptic technique, a 1-inch, 25-gauge needle is inserted in the center of the joint through the skin, subcutaneous tissues, and joint capsule into the joint (see Figure 74-3). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected medially. After the joint space has been entered, the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a tendon and should be advanced slightly into the joint space until injection proceeds without significant

74  •  Intraarticular Injection of the Metacarpophalangeal Joints        225

Clinical Pearls

Inflamed and arthritic joint

This injection technique is extremely effective in the treatment of pain secondary to the just-mentioned causes of arthritis of the metacarpophalangeal joint. Coexistent tendinitis also may contribute to metacarpophalangeal joint pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for metacarpophalangeal joint pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Splinting the hand in neutral position also may provide symptomatic relief. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique. SUGGESTED READINGS

Figure 74-3  Proper needle placement for intraarticular injection of the metacarpophalangeal joint.

resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. Ultrasound guidance may be useful if the anatomic landmarks necessary to perform this technique are difficult to identify (see Figure 74-2).

Side Effects and Complications The major complication of intraarticular injection of the metacarpophalangeal joints is infection, which should be exceedingly rare if strict aseptic technique is followed. Approximately 25% of patients report a transient increase in pain after intraarticular injection of the metacarpophalangeal joint; the patient should be warned of this.

Armbruster EJ, Tan V: Carpometacarpal joint disease: addressing the metacarpophalangeal joint deformity, Hand Clin 24:295–299, 2008. Chen YG, McClinton MA, DaSilva MF, Shaw Wilgis EF: Innervation of the metacarpophalangeal and interphalangeal joints: a microanatomic and histologic study of the nerve endings, J Hand Surg Am 25:128–133, 2000. De Zordo T, Mur E, Bellmann-Weiler R, et al: US guided injections in arthritis, Eur J Radiol 71:197–203, 2009. Grassi W, Salaffi F, Filippucci E: Ultrasound in rheumatology, Best Pract Res Clin Rheumatol 19:467–485, 2005. Waldman SD: Intra-articular injection of the metacarpophalangeal joints. In Pain review, Philadelphia, 2009, Saunders, pp 473–474. Waldman SD: The metacarpophalangeal joints. In Pain review, Philadelphia, 2009, Saunders, p 107.

Chapter 75 INTRAARTICULAR INJECTION OF THE INTERPHALANGEAL JOINTS Indications and Clinical Syndromes The interphalangeal joint is susceptible to the development of arthritis from a variety of conditions that have in common the ability to damage the joint cartilage. Osteoarthritis of the joint is the most common form of arthritis that results in interphalangeal joint pain. However, rheumatoid arthritis, posttraumatic arthritis, and psoriatic arthritis also are common causes of interphalangeal pain secondary to arthritis. Less common causes of arthritisinduced interphalangeal joint pain include the collagen vascular diseases, infection, and Lyme disease. Acute infectious arthritis usually is accompanied by significant systemic symptoms, including fever and malaise, and should easily be recognized by the astute clinician and treated appropriately with culture and antibiotics rather than injection therapy. The collagen vascular diseases generally manifest as a polyarthropathy rather than a monoarthropathy limited to the interphalangeal joint, although interphalangeal pain secondary to collagen vascular disease responds exceedingly well to the intraarticular injection technique described later. The majority of patients with interphalangeal joint pain secondary to osteoarthritis and posttraumatic arthritis pain report pain that is localized to the region of the interphalangeal joints. Activities, especially those with gripping and pinching motions, will exacerbate the pain; rest and heat provide some relief. The pain is constant and is characterized as aching. The pain may interfere with sleep. Some patients note a grating or “popping” sensation with use of the joint; crepitus may be present on physical examination. Swelling of the joints commonly occur, with enlargement of the distal interphalangeal joints (called Heberden nodes) and enlargement of the proximal interphalangeal joints (called Bouchard nodes) (Figure 75-1). In addition to the just-mentioned pain, patients with arthritis of the interphalangeal joint often experience a gradual decrease in functional ability with decreasing grip strength, making everyday tasks such as turning a doorknob or opening a jar quite difficult. With continued disuse, muscle wasting may occur and an adhesive capsulitis with subsequent ankylosis may develop. Plain radiographs are indicated for all patients with interphalangeal pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the interphalangeal joints is indicated if joint instability is suspected.

The interphalangeal joint’s primary role is to optimize the gripping function of the hand. The joint allows flexion and extension. The joint is lined with synovium, and the resultant synovial space allows intraarticular injection. The joint is covered by a capsule that surrounds the entire joint and is susceptible to trauma if the joint is subluxed. Volar and collateral ligaments help strengthen the joints; the palmar ligaments are particularly strong.

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side and the hand in neutral position with the palmar aspect resting on a folded towel. A total of 1.0 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. After sterile preparation of the skin overlying the affected interphalangeal joint, the space between the affected phalanges is identified. The joint can be identified more easily by flexing and extending the joint. With strict aseptic technique, a 1-inch, 25-gauge needle is inserted in the center of the joint through the skin, subcutaneous tissues, and joint capsule into the joint (see Figure 75-1). If bone is encountered, the needle is withdrawn

Bouchard node

Heberden node

Clinically Relevant Anatomy The interphalangeal joints are synovial hinge-shaped joints that serve as the articulation between the phalanges (see Figure 75-1). 226

Figure 75-1  Proper needle placement for intraarticular injection of the interphalangeal joint.

75  •  Intraarticular Injection of the Interphalangeal Joints        227

Clinical Pearls MP PP

Figure 75-2  Ultrasound-guided joint injection of the third interphalangeal joint in rheumatoid arthritis. In general, only a small amount of synovitis is present in these joints, but with ultrasound it can be detected and the needle can be directed towards the synovitis. The arrow indicates the needle. MP, Middle phalanx; PP, proximal phalanx. (From De Zordo T, Mur E, Bellmann-Weiler R, et al: US guided injections in arthritis, Eur J Radiol 71:197–203, 2009.)

into the subcutaneous tissues and redirected medially. After the joint space has been entered, the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a tendon and should be advanced slightly into the joint space until the injection proceeds without significant resistance. The needle is then removed and a sterile pressure dressing and ice pack are placed at the injection site. Ultrasound guidance may aid in performing this procedure if the anatomic landmarks are difficult to identify (Figure 75-2).

Side Effects and Complications The major complication of intraarticular injection of the interphalangeal joints is infection, which should be exceedingly rare if strict aseptic technique is followed. Approximately 25% of patients note a transient increase in pain after intraarticular injection of the interphalangeal joint; the patient should be warned of this.

This injection technique is extremely effective in the treatment of pain secondary to the just-mentioned causes of arthritis of the interphalangeal joint. Coexistent tendinitis also may contribute to interphalangeal joint pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for interphalangeal joint pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Splinting the hand in neutral position also may provide symptomatic relief. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS De Zordo T, Mur E, Bellmann-Weiler R, et al: US guided injections in arthritis, Eur J Radiol 71:197–203, 2009. Grassi W, Salaffi F, Filippucci E: Ultrasound in rheumatology, Best Pract Res Clin Rheumatol 19:467–485, 2005. Waldman SD: Intra-articular injection of the interphalangeal joints. In Pain review, Philadelphia, 2009, Saunders, pp 475–476. Waldman SD: The interphalangeal joints. In Pain review, Philadelphia, 2009, ­Saunders, p 108.

Chapter 76 INJECTION TECHNIQUE FOR CARPAL TUNNEL SYNDROME Indications and Clinical Considerations Carpal tunnel syndrome is caused by compression of the median nerve as it passes through the carpal canal at the wrist (Figures 76-1 and 76-2). The most common causes of compression of the median nerve at this anatomic location include flexor tenosynovitis, rheumatoid arthritis, pregnancy, amyloidosis, and other space-occupying lesions that compromise the median nerve as it passes through this closed space (Figure 76-3). This entrapment neuropathy manifests as pain, numbness, paresthesias, and associated weakness in the hand and wrist that radiates to the thumb, the index and middle fingers, and the radial half of the ring finger. These symptoms also may radiate proximal to the entrapment into the forearm. If the condition is not treated, progressive motor deficit and ultimately flexion contracture of the affected fingers can result. The onset of symptoms is usually after repetitive wrist motions or from repeated pressure on the wrist, as occurs when resting the wrists on the edge of a computer keyboard. Direct trauma to the median nerve as it enters the carpal tunnel also may result in a similar clinical presentation.

Median nerve Flexor retinaculum Tubercle of trapezium

Pisiform Hook of hamate

Physical findings include tenderness over the median nerve at the wrist. A positive Tinel sign over the median nerve as it passes beneath the flexor retinaculum usually is present (Figure 76-4). A positive Phalen test result is highly suggestive of carpal tunnel syndrome. The Phalen test is performed by having the patient place the wrists in complete unforced flexion for at least 30 seconds (Figure 76-5). If the median nerve is entrapped at the wrist, this maneuver reproduces the symptoms of carpal tunnel syndrome. Weakness of thumb opposition and wasting of the thenar eminence often are seen in advanced carpal tunnel syndrome, although because of the complex motion of the thumb, subtle motor deficits easily may be missed. Early in the course of the evolution of carpal tunnel syndrome, the only physical finding other than tenderness over the nerve may be the loss of sensation in the just-mentioned fingers. Carpal tunnel syndrome often is misdiagnosed as arthritis of the carpometacarpal joint of the thumb, cervical radiculopathy, or diabetic polyneuropathy. Patients with arthritis of the carpometacarpal joint of the thumb have a positive Watson test result and radiographic evidence of arthritis (Figure 76-6). Most patients with cervical radiculopathy have reflex, motor, and sensory changes associated with neck pain, whereas patients with carpal tunnel syndrome have no reflex changes and motor and sensory changes are limited to the distal median nerve. Diabetic polyneuropathy generally manifests as symmetric sensory deficit involving the entire hand rather than being limited to the distribution of the median nerve. Cervical radiculopathy and median nerve entrapment may coexist as the so-called double crush syndrome. Furthermore, because carpal tunnel syndrome commonly is seen in patients with diabetes, it is not surprising that diabetic polyneuropathy usually is present in diabetic patients with carpal tunnel syndrome. Electromyography helps distinguish cervical radiculopathy and diabetic polyneuropathy from carpal tunnel syndrome. Plain radiographs are indicated for all patients with carpal tunnel syndrome to rule out occult bony disease. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) or ultrasound imaging of the wrist is indicated if joint instability or a space-­ occupying lesion is suspected. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy Figure 76-1  Proper needle position for injection of the carpal tunnel.

228

The median nerve is made up of fibers from C5-T1 spinal roots. The nerve lies anterior and superior to the axillary artery in the 12 o’clock to 3 o’clock quadrant. Exiting the axilla, the median

76  •  Injection Technique for Carpal Tunnel Syndrome        229 Lumbricalis mm.

••

•

5th Metacarpal

••

•• ••

••

••

•• •

•

Hypothenar mm.

Flexor digitorum tt.

•

•

Ulnar a.

••

••

••

• ••

•

••

•

Ulnar n.

••

•• ••

Flexor retinaculum 1st Metacarpal Median n.

••

Pisiform.

Thenar mm.

Trapezium Flexor carpi radialis t. Flexor pollicis longus Flexor digitorum tt.

Figure 76-2  Carpal tunnel syndrome. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, ­Saunders.)

nerve descends into the upper arm along with the brachial artery. At the level of the elbow, the brachial artery is just medial to the biceps muscle. At this level, the median nerve lies just medial to the brachial artery. As the median nerve proceeds downward into the forearm, it gives off numerous branches that provide motor innervation to the flexor muscles of the forearm. These branches are susceptible to nerve entrapment by aberrant ligaments, muscle hypertrophy, and direct trauma. The nerve approaches the wrist overlying the radius. It lies deep to and between the tendons of the palmaris longus muscle and the flexor carpi radialis muscle at the wrist. The median nerve then passes beneath the flexor retinaculum and through the carpal tunnel, with the nerve’s terminal branches providing sensory innervation to a portion of the palmar surface of the hand as well as the palmar surface of the thumb, index finger, and middle finger and the radial portion of the ring finger (see Figure 76-1). The median nerve also provides sensory innervation to the distal dorsal surface of the index and middle finger and the radial portion of the ring finger. The carpal tunnel is bounded on

three sides by the carpal bones and is covered by the transverse carpal ligament. In addition to the median nerve, it contains a number of flexor tendon sheaths, blood vessels, and lymphatics.

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side and the elbow slightly flexed with the dorsum of the hand resting on a folded towel. A total of 3 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. The clinician then has the patient make a fist and at the same time flex his or her wrist to aid in identification of the palmaris longus tendon. After preparation of the skin with antiseptic solution, a 5⁄8-inch, 25-gauge needle is inserted just medial to the tendon and just proximal to the crease of the wrist at a 30-degree angle (see Figure 76-1). The needle is slowly advanced until the tip is just beyond the tendon. A paresthesia in the distribution of the median nerve often is elicited, and the patient should be warned of this. The patient should be warned

230        SECTION 4  •  Wrist and Hand

A

B

Figure 76-3  Carpal tunnel syndrome related to fibrolipomatous hamartoma of the median nerve: magnetic resonance (MR) imaging. A, A transaxial T1-weighted (TR/TE, 500/15) spin-echo MR image of the wrist at the level of the base of the first metacarpal bone shows a large mass (large arrow) in the median nerve that has led to dorsal displacement of the flexor tendons (small arrows) and volar bowing of the flexor retinaculum (arrowheads). Note the inhomogeneous signal intensity of the tumor as a result of its fibrous and fatty components. B, A coronal T1-weighted (TR/TE, 500/15) spin-echo MR image of the volar aspect of the wrist shows a mass (arrow) composed of longitudinally oriented cylindric regions of low and high signal intensity. (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

Figure 76-5  The Phalen test is performed by the patient placing the wrists in complete unforced flexion for at least 30 seconds.

Figure 76-6  The Watson stress test for arthritis of the carpometacarpal joint of the thumb. (From Waldman SD: Physical diagnosis of pain, ­Philadelphia, 2005, Saunders.)

Figure 76-4  The Tinel sign for carpal tunnel syndrome. (From Waldman SD: Physical diagnosis of pain, Philadelphia, 2005, Saunders.)

that should a paresthesia occur, he or she is to say “there!” as soon as the paresthesia is felt. If a paresthesia is elicited, the needle is withdrawn slightly away from the median nerve. Gentle aspiration is then carried out to identify blood. If aspiration is negative and no persistent paresthesia into the distribution of the median nerve remains, 3 mL of solution is slowly injected, with the patient

being monitored closely for signs of local anesthetic toxicity. If no paresthesia is elicited and the needle tip hits bone, the needle is withdrawn out of the periosteum, and after careful aspiration 3 mL of solution is slowly injected. Ultrasound guidance may be beneficial if the anatomic landmarks necessary to perform this technique are difficult to identify (Figure 76-7).

Side Effects and Complications Injection of the carpal tunnel is a relatively safe technique, with the major complications being inadvertent intravascular injection and persistent paresthesia secondary to needle trauma to the nerve.

76  •  Injection Technique for Carpal Tunnel Syndrome        231 SUGGESTED READINGS MN

FCR

FDS

FDS

UA

UN

FPL

Figure 76-7  Short-axis view of the distal wrist during injection for carpal tunnel syndrome. The open arrow shows the needle trajectory through cleft between middle and ring finger flexor digitorum superficialis tendons. The hyperechoic oval below the open arrow is the needle tip. FCR, Flexor carpi radialis; FDS, flexor digitorum superficialis; FPL, flexor pollicis longus; MN, median nerve; UA, ulnar artery; UN, ulnar nerve. (From Bodor M, Fullerton B: Ultrasonography of the hand, wrist, and elbow, Phys Med Rehabil Clin N Am 21:509–531, 2010.)

This technique can be performed safely in the presence of anticoagulation by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable riskto-benefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block also decreases the amount of postprocedure pain and bleeding the patient may experience.

Clinical Pearls Carpal tunnel injection is a simple and safe technique in the evaluation and treatment of the just-mentioned painful conditions. Careful neurologic examination to identify preexisting neurologic deficits that may later be attributed to the nerve block should be performed on all patients before beginning median nerve block at the wrist, especially in those patients with clinical symptoms of diabetes or clinically significant carpal tunnel syndrome. Care should be taken to place the needle just beyond the flexor retinaculum and to inject slowly to allow the solution to flow easily into the carpal tunnel without further compromising the median nerve. Carpal tunnel syndrome also should be differentiated from cervical radiculopathy involving the cervical nerve roots, which at times may mimic median nerve compression. Furthermore, cervical radiculopathy and median nerve entrapment may coexist in the socalled double crush syndrome. The double crush syndrome is seen most commonly with median nerve entrapment at the wrist or carpal tunnel syndrome.

Jayaraman S, Naidich TP: The carpal tunnel: ultrasound display of normal imaging anatomy and pathology, Neuroimaging Clin N Am 14:103–113, 2004. Martins RS, Siqueira MG, Simplício H, et  al: Magnetic resonance imaging of idiopathic carpal tunnel syndrome: correlation with clinical findings and electrophysiological investigation, Clin Neurol Neurosurg 110:38–45, 2008. Seror P: Sonography and electrodiagnosis in carpal tunnel syndrome diagnosis, an analysis of the literature, Eur J Radiol 67:146–152, 2008. Waldman SD: Carpal tunnel syndrome. In Pain review, Philadelphia, 2009, Saunders, pp 273–275. Waldman SD: Functional anatomy of the wrist. In Pain review, Philadelphia, 2009, Saunders, pp 100–102. Watts AC, McEachan J: Carpal tunnel syndrome in men, Curr Orthop 20: 294–298, 2006.

Chapter 77 ULNAR NERVE BLOCK AT THE WRIST Indications and Clinical Considerations Ulnar tunnel syndrome is caused by compression of the ulnar nerve as it passes through the Guyon canal at the wrist (Figure 77-1). The most common causes of compression of the ulnar nerve at this anatomic location are space-occupying lesions, including ganglion cysts and ulnar artery aneurysms, fractures of the distal ulna and carpals, and repetitive motion injuries that compromise the ulnar nerve as it passes through this closed space. This entrapment neuropathy manifests most commonly as a pure motor neuropathy without pain, which is caused by compression of the deep palmar branch of the ulnar nerve as it passes through the Guyon canal (see Figure 77-1). This pure motor neuropathy manifests as painless paralysis of the intrinsic muscles of the hand. Ulnar tunnel syndrome may also occur as a mixed sensory and motor neuropathy. Clinically, this mixed neuropathy manifests as pain, numbness, and paresthesias of the wrist that radiate into the ulnar aspect of the palm and dorsum of the hand and the little finger, as well as the ulnar half of the ring finger. These symptoms also may radiate proximal to the nerve entrapment into the forearm. Like carpal tunnel syndrome, the pain of ulnar tunnel syndrome is frequently worse at night and made worse by vigorous flexion and extension of the wrist. If the condition is not treated, progressive motor deficit and ultimately flexion contracture of the affected fingers can result. The onset of symptoms is usually after repetitive wrist motions or from direct trauma to the wrist, such as wrist fractures or direct trauma to the proximal hypothenar eminence, which may occur when the hand is used to hammer on hubcaps or from handlebar compression during long-distance cycling (Figure 77-2). Physical findings include tenderness over the ulnar nerve at the wrist. A positive Tinel sign over the ulnar nerve as it passes beneath the transverse carpal ligament is usually present. If the sensory branches are involved, there is decreased sensation into the ulnar aspect of the hand and the little finger, as well as the ulnar half of the ring finger. Depending on the location of neural compromise, the patient may have weakness of the intrinsic muscles of the hand, as evidenced by the inability to spread the fingers, or weakness of the hypothenar eminence. Ulnar tunnel syndrome is often misdiagnosed as arthritis of the carpometacarpal joints, cervical radiculopathy, or diabetic polyneuropathy. Patients with arthritis of the carpometacarpal joint usually have radiographic evidence and physical findings suggestive of arthritis. Most patients with cervical radiculopathy have reflex, motor, and sensory changes associated with neck pain, whereas patients with ulnar tunnel syndrome have no reflex changes and motor and sensory changes are limited to the distal ulnar nerve. Diabetic polyneuropathy generally manifests as symmetrical sensory 232

deficit involving the entire hand rather than being limited just to the distribution of the ulnar nerve. Cervical radiculopathy and ulnar nerve entrapment may coexist as the so-called double crush syndrome. Furthermore, because ulnar tunnel syndrome is commonly seen in patients with diabetes, it is not surprising that diabetic polyneuropathy is usually present in diabetic patients with ulnar tunnel syndrome. Pancoast tumor invading the medial cord of the brachial plexus also may mimic an isolated ulnar nerve entrapment and should be ruled out by apical lordotic chest radiography. Electromyography helps distinguish cervical radiculopathy, diabetic polyneuropathy, and Pancoast tumor from ulnar tunnel syndrome. Plain radiographs are indicated for all patients with ulnar tunnel syndrome to rule out occult bony disease. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody testing. Magnetic

Ulnar artery Ulnar nerve

Figure 77-1  Proper needle placement for injection of the ulnar nerve at the wrist.

77  •  Ulnar Nerve Block at the Wrist        233

resonance imaging (MRI) or ultrasound imaging of the wrist is indicated if joint instability or a space-occupying lesion is suspected (Figure 77-3). The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The ulnar nerve is made up of fibers from C6-T1 spinal roots. The nerve lies anterior and inferior to the axillary artery in the 3 o’clock to 6 o’clock quadrant. Exiting the axilla, the ulnar nerve descends into the upper arm along with the brachial artery. At the middle of the upper arm, the nerve courses medially to pass between the olecranon process and medial epicondyle of the humerus. The nerve then passes between the heads of the flexor carpi ulnaris muscle, continuing downward, moving radially along with the ulnar artery. At a point approximately 1 inch proximal to the crease of the wrist, the ulnar nerve divides into the dorsal and palmar branches (Figure 77-4). The dorsal branch provides sensation to the ulnar aspect of the dorsum of the hand, the dorsal aspect of the little finger, and the ulnar half of the ring finger (see Figure 77-2). The palmar branch provides sensory innervation to the ulnar aspect of the palm of the hand, the palmar aspect of the little finger, and the ulnar half of the ring finger. Like the carpal tunnel, the ulnar tunnel is a closed space and is bounded on one side by the pisiform and on the other side by the hook of the hamate (Figure 77-5). The ulnar nerve must pass between the transverse carpal ligament and the volar carpal ligament. In addition to the ulnar nerve, the ulnar tunnel contains

Ulnar nerve

Figure 77-2  Ulnar tunnel syndrome is caused by compression of the ulnar nerve as it passes through the Guyon canal.

P S T

A

L

B

C Figure 77-3  A, Axial T2-weighted magnetic resonance (MR) image through the level of the proximal carpal row in a patient with symptoms of ulnar nerve compression. A lesion with high signal intensity (white arrow) adjacent to the ulnar artery and vein (broken white arrows) displaces the ulnar nerve (curved white arrow). B, The postcontrast (obtained after administration of a contrast agent) T1-weighted MR image shows low signal intensity within the lesion (white arrow) without enhancement, and the displaced ulnar nerve is again demonstrated. The appearances are consistent with a ganglion within the Guyon canal. C, The cystic nature of the lesion is further confirmed on the transverse Doppler ultrasound image, on which the ganglion can be seen as an anechoic mass (white arrow) with flow evident in the ulnar artery and vein (black arrows). L, Lunate; P, pisiform; S, scaphoid; T, triquetrum. (From Spratt JD, Stanley AJ, Grainger AJ, et al: The role of diagnostic radiology in compressive and entrapment neuropathies, Eur Radiol 12:2352–2364, 2002.)

234        SECTION 4  •  Wrist and Hand

Figure 77-4  The ulnar nerve can be divided into sensory (palmar) and motor (dorsal) branches. Note the fibrous arch of the hypothenar muscles under which the deep motor branch passes on its way out of the ulnar tunnel. The ulnar artery travels along the radial side of the nerve through the tunnel, after which it splits and becomes the deep and superficial palmar arches. Blue tag, sensory branch; black tag, motor branch; red tag, ulnar artery. (From Waugh RP, Pellegrini VD Jr: Ulnar tunnel syndrome, Hand Clin 23:301–310, 2007.)

the ulnar artery, which may compress the nerve. Unlike the carpal tunnel, the ulnar tunnel does not contain flexor tendon sheaths.

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side and the elbow slightly flexed with the dorsum of the hand resting on a folded towel. A total of 3 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. The clinician then has the patient make a fist and at the same time flex his or her wrist to aid in identification of the flexor carpi ulnaris tendon. After preparation of the skin with antiseptic solution, a 5⁄8-inch, 25-gauge needle is inserted on the radial side of the tendon and just proximal to the crease of the wrist at a 30-degree angle (see Figure 77-1). The needle is slowly advanced until the tip is just beyond the tendon. A paresthesia in the distribution of the ulnar nerve is often elicited, and the patient should be warned of this. The patient also should be warned that should a paresthesia occur, he or she is to say “there!” as soon as the paresthesia is felt. If a paresthesia is elicited, the needle is withdrawn slightly away from the ulnar nerve. Gentle aspiration is then carried out to identify blood. If the aspiration test result is negative and no persistent paresthesia into the distribution of the ulnar nerve remains, 3 mL of solution is slowly injected, with the patient being monitored closely for signs of local anesthetic toxicity. If no paresthesia is elicited and the needle tip hits bone, the needle is withdrawn out of the periosteum, and after careful aspiration 3 mL of solution is slowly injected.

Side Effects and Complications Injection of the ulnar nerve at the wrist to treat ulnar tunnel syndrome is a relatively safe procedure, with the major complications being inadvertent intravascular injection into the ulnar artery and persistent

Figure 77-5  The middle compartment, which is the fibro-osseous tunnel along the length of the pisiform. The Freer elevator is placed deep to the pisohamate arcade and the ulnar nerve on a retractor. The extent of this compartment is shown between the two arrows. (From Ombaba J, Kuo M, Rayan G: Anatomy of the ulnar tunnel and the influence of wrist motion on its morphology, J Hand Surg Am 35:760–768, 2010.)

paresthesia secondary to needle trauma to the nerve. Like the carpal tunnel, the Guyon canal is a closed space and care should be taken to inject slowly to avoid additional compromise of the nerve. This technique can be performed safely in the presence of anticoagulation by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable risk-to-benefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block also decreases the amount of postprocedure pain and bleeding the patient may experience.

Clinical Pearls This injection is a simple and safe technique in the evaluation and treatment of ulnar tunnel syndrome. Careful neurologic examination to identify preexisting neurologic deficits that may later be attributed to the nerve block should be performed on all patients before beginning ulnar nerve block at the wrist. Ulnar tunnel syndrome also should be differentiated from cervical radiculopathy involving the C8 spinal root, which may at times mimic ulnar nerve compression. Furthermore, it should be remembered that cervical radiculopathy and ulnar nerve entrapment may coexist in the so-called double crush syndrome. The double crush syndrome is seen most commonly with ulnar nerve entrapment at the wrist or carpal tunnel syndrome. Pancoast tumor invading the medial cord of the brachial plexus may also mimic an isolated ulnar nerve entrapment and should be ruled out by apical lordotic chest radiography.

77  •  Ulnar Nerve Block at the Wrist        235 SUGGESTED READINGS Murata K, Shih JT, Tsai TM: Causes of ulnar tunnel syndrome: a retrospective study of 31 subjects, J Hand Surg Am 28:647–651, 2003. Nakamichi K, Tachibana S, Kitajima I: Ultrasonography in the diagnosis of ulnar tunnel syndrome caused by an occult ganglion, J Hand Surg Br 25:503–504, 2000.

Waldman SD: Functional anatomy of the wrist. In Pain review, Philadelphia, 2009, Saunders, pp 100–102. Waldman SD: Injection technique for ulnar tunnel syndrome. In Pain review, Philadelphia, 2009, Saunders, pp 469–470. Waugh RP, Pellegrini VD Jr: Ulnar tunnel syndrome, Hand Clin 23:301–310, 2007.

Chapter 78 CARPAL BOSS INJECTION

Indications and Clinical Considerations Carpal boss is a relatively uncommon pain syndrome that affects the dorsum of the hand. Carpal boss is characterized by localized tenderness and sharp pain over the junction of the second and/ or third metacarpal joints (Figure 78-1). The pain of carpal boss is caused by an exostosis of the second and/or third metacarpal joints or, more uncommonly, a loose body involving the intraarticular space (Figure 78-2). The patient often feels that the pain is worse in the area of the carpal boss after rigorous physical activity involving the hand rather than during the activity itself. The pain of carpal boss may also radiate locally, confusing the clinical presentation. On physical examination, pain can be reproduced by pressure on the soft tissue overlying the carpal boss. Patients with carpal boss will demonstrate a positive hunchback sign with the examiner appreciating a bony prominence under the palpating finger when he or she palpates the carpal boss (Figures 78-3 and 78-4). The carpal boss may become more evident when the affected wrist is flexed (Figure 78-5). With acute trauma to the dorsum of the hand, ecchymosis over the carpal boss of the affected joint or joints may be present. Plain radiographs are indicated for all patients with carpal boss to rule out fractures and identify exostoses responsible for the patient’s symptoms. A characteristic volcano-type appearance of the bone is pathognomonic for carpal boss (Figure 78-6). Based on the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, uric acid, and antinuclear antibody testing to rule out inflammatory arthritis. Magnetic resonance imaging (MRI) of the fingers and bones of the wrist is indicated if joint instability, occult mass, occult fracture, infection, or tumor is suspected. Radionuclide bone scanning may be useful in identifying stress fractures of this region as well as carpal boss that may be missed on plain radiographs of the hand (see Figure 78-2).

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position with the dorsal surface of the hand exposed. Proper preparation with antiseptic solution of the skin overlying the tender area is then carried out. A sterile syringe containing 2.0 mL of 0.25% preservative-free

Carpal boss Inflamed tendon and joint meta

Trapezoid Extensor indicis

carpa

l2

Figure 78-1  Proper needle placement for injection of a carpal boss.

Clinically Relevant Anatomy The carpometacarpal joints of the fingers are synovial plane joints that serve as the articulation between the carpals and the metacarpals and also allow articulation of the bases of the metacarpal bones with one another. Movement of the joints is limited to a slight gliding motion, with the carpometacarpal joint of the little finger possessing the greatest range of motion. The joint’s primary function is to optimize the grip function of the hand. In most patients there is a common joint space. The joint is strengthened by anterior, posterior, and interosseous ligaments. 236

A

B

Figure 78-2  Carpal boss (os styloideum). A, Increased accumulation of a bone-seeking radionuclide (arrow) is evident at the side of the carpal boss, at the base of the second and third metacarpal bones. B, In different patient, a typical os styloideum (arrow) is seen. (Courtesy J. Spaeth, MD, Minneapolis, Minn, and G. Greenway, MD, Dallas, Tex; from ­Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, ­Saunders.)

78  •  Carpal Boss Injection        237

Figure 78-3  The hunchback carpal sign for carpal boss. (From Waldman SD: Physical diagnosis of pain, ed 2, Philadelphia, 2010, Saunders.)

Figure 78-5  With wrist flexion, the prominence of the carpal boss becomes strikingly evident (arrow). (From Park MJ, Namdari S, Weiss AP: The carpal boss: review of diagnosis and treatment, J Hand Surg Am 33:446–449, 2008.)

Figure 78-6  Radiograph demonstrating traumatic metacarpal boss characterized by periarticular hypertrophic volcano-shaped spur formation with concomitant articular degeneration. (From Melone CP Jr, Polatsch DB, Beldner S: Disabling hand injuries in boxing: boxer’s knuckle and traumatic carpal boss, Clin Sports Med 28:609–621, 2009.)

Figure 78-4  The carpal boss is frequently confused initially with a dorsal ganglion on viewing the dorsal wrist. The carpal boss generally feels harder with palpation, is positioned more distally than wrist ganglia, and overlies the index and middle finger carpometacarpal joints (arrow). (From Park MJ, Namdari S, Weiss AP: The carpal boss: review of diagnosis and treatment, J Hand Surg Am 33:446–449, 2008.)

bupivacaine and 40 mg of methylprednisolone is attached to a 5 ⁄8-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the carpal boss is identified. At this point, the needle is carefully advanced through the dorsal surface of the wrist until the needle tip rests against the carpal boss (see Figure 78-1). The needle is withdrawn slightly out of the periosteum and substance of the tendon. After the needle is in the correct position adjacent to the carpal boss and aspiration for blood is negative, the contents of the syringe are gently

238        SECTION 4  •  Wrist and Hand

injected. There may be slight resistance to injection, given the closed nature of the space. If significant resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. The ice should not be left on for more than 10 minutes to avoid freezing injuries.

Side Effects and Complications The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is followed. Approximately 25% of patients report a transient increase in pain after injection of sesamoid bones; the patient should be warned of this.

Clinical Pearls Pain emanating from the hand is a common problem that is encountered in clinical practice. Carpal boss must be distinguished from stress fractures, arthritis, and other occult pathology of the wrist and hand. Although the justdescribed injection technique provides palliation of the pain of carpal boss, the patient may ultimately require surgical removal of the exostosis to provide long-lasting relief. Coexistent bursitis and tendinitis also may contribute to the patient’s hand pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for carpal boss pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptomatology. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Alemohammad AM, Nakamura K, El-Sheneway M, Viegas SF: Incidence of carpal boss and osseous coalition: an anatomic study, J Hand Surg Am 34:1–6, 2009. Capo JT, Orillaza NS, Lim PK: Carpal boss in an adolescent: case report, J Hand Surg Am 34:1808–1810, 2009. Melone CP Jr, Polatsch DB, Beldner S: Disabling hand injuries in boxing: boxer’s knuckle and traumatic carpal boss, Clin Sports Med 28:609–621, 2009. Park MJ, Namdari S, Weiss AP: The carpal boss: review of diagnosis and treatment, J Hand Surg Am 33:446–449, 2008.

Chapter 79 INJECTION TECHNIQUE FOR SECRETAN SYNDROME Indications and Clinical Considerations Secretan syndrome is caused by a peritendinous fibrosis that occurs after trauma to the dorsum of the hand. Often the traumatic event is seemingly minor, such as hitting the back of the hand on the corner of a desk. Initially the swelling and tenderness may be attributed to the trauma, but instead of improving with time, the dorsum of the hand becomes more indurated, with the edema becoming brawny. If the syndrome is not treated, peritendinous fibrosis and an almost myxedematous hardening of the soft tissues of the dorsum of the hand occur (Figures 79-1 and 79-2). Like the pain of Dupuytren contracture, the pain of Secretan syndrome seems to burn itself out as the disease progresses. Arthritis, gout of the metacarpal and interphalangeal joints, and tendinitis may coexist with and exacerbate the pain and disability of Secretan syndrome. Reflex sympathetic dystrophy may manifest in a similar clinical manner but can be distinguished from Secretan syndrome by the fact that the pain of reflex sympathetic dystrophy responds to sympathetic neural blockade and the pain of Secretan syndrome does not.

Plain radiographs are indicated for all patients with Secretan syndrome to rule out underlying occult bony disease. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the hand is indicated if joint instability or tumor is suspected. Electromyography is indicated if coexistent ulnar or carpal tunnel syndrome is suspected. The injection technique described later provides improvement of the pain and disability of this disease if implemented early.

Clinically Relevant Anatomy Secretan syndrome is a result of the thickening and fibrosis of the extensor tendons (see Figure 79-1). The primary function of the extensor tendons is to optimize hand grip.

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side with the palmar surface of the hand resting on a folded towel. A total of 2 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. Sterile preparation of the skin overlying the fibrous tissue is carried out. At a point just lateral to the fibrosis, a 1-inch, 25-gauge needle is inserted at a 45-degree angle parallel to the fibrosis through the skin and into the subcutaneous tissue overlying the fibrotic area (see Figure 79-1). If bone is encountered, the needle is withdrawn back into the subcutaneous tissue and again advanced in proximity to the fibrosis. The contents of the syringe are then gently injected. There may be some resistance to injection because of fibrosis of the surrounding tissue. If significant resistance is encountered, the

Peritendinous fibrosis

Figure 79-1  Proper needle placement for injection for Secretan syndrome.

Figure 79-2  Secretan syndrome and complex regional pain syndrome share many clinical characteristics. (From Albrecht PJ, Hines S, Eisenberg E, et al: Pathologic alterations of cutaneous innervation and vasculature in affected limbs from patients with complex regional pain syndrome, Pain 120:244–266, 2006.)

239

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needle is probably in the tendon or fibrotic nodule and should be withdrawn back until the injection proceeds without significant resistance. The needle is then removed and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complications associated with this injection technique are related to trauma to an inflamed or previously damaged tendon. Such tendons may rupture if directly injected, and needle position should be confirmed outside the tendon before injection to avoid this complication. Another complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is followed. Approximately 25% of patients report a transient increase in pain after this injection technique; the patient should be warned of this.

Clinical Pearls This injection technique is extremely effective in the treatment of pain and dysfunction secondary to Secretan syndrome. Coexistent arthritis, tendinitis, and gout also may contribute to the pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. Carpal boss should also be considered in the differential diagnosis (see Chapter 78). This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat, massage, and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Fam AG: The wrist and hand. In Fam AG, Lawry GV, Kreder HJ, editors: Musculoskeletal examination and joint injection techniques, Philadelphia, 2005, Mosby, pp 33–45. Moretta DN, Cooley RD Jr: Secrétan’s disease: a unique case report and literature review, Am J Orthop (Belle Mead NJ) 31:524–527, 2002. Ramos JA, Bush D, Harrington TM: Secretan’s syndrome, Orthopedics 30:239–240, 2007. Saferin EH, Posch JL: Secretan’s disease: post-traumatic hard edema of the dorsum of the hand, Plast Reconstr Surg 58:703–707, 1976.

Chapter 80 INJECTION TECHNIQUE FOR OS CENTRALE CARPI Indications and Clinical Considerations Accessory bones of the wrist are relatively uncommon, with a reported incidence of 0.75% to 2.0%. They are thought to be a remnant of separate ossification centers found in the human embryo and in some other but not all African primates. The most common of these accessory bones of the wrist is called os centrale carpi. In most humans this ossification center fuses with the scaphoid bone by 8 weeks of gestation. In the gibbon and orangutan it remains a separate distinct bone that does not fuse with the scaphoid until old age. Located among the capitates, scaphoid, and trapezium bones, os centrale carpi is often mistaken for a scaphoid fracture or a bipartite scaphoid, or it is simply identified as a serendipitous finding on imaging of the wrist (Figures 80-1 and 80-2; Table 80-1). It may be either unilateral or bilateral, further adding to the clinician’s confusion. The key to differentiating os centrale carpi from a scaphoid fracture is the characteristic smoothness of the borders of the accessory ossicle in relationship to the other carpal bones. In questionable cases, radionuclide scanning, computerized tomography, and magnetic resonance imaging (MRI) may be helpful in making the differential diagnosis. Os centrale carpi may exist as an isolated asymptomatic or symptomatic abnormality or may occur in conjunction with a number of heritable syndromes (Table 80-2). Wrist pain secondary to os centrale carpi is characterized by tenderness and pain over the dorsoradial wrist. The patient often feels as though he or she has gravel in the wrist and may report a severe grating sensation with range of motion of the wrist. The pain of os centrale carpi worsens with activities that required repeated twisting motions such as tightening lids on jars. Os centrale carpi may coexist with tendinitis of the wrist. On physical examination, pain can be reproduced by pressure on the os centrale carpi. In contradistinction to the pain of acute scaphoid fracture, in which the tender area is localized over the anatomic snuffbox, with os centrale carpi the area of maximum tenderness will be just above the accessory ossicle. A creaking or grating may be appreciated by the examiner, and locking or catching on range of motion of the wrist may occasionally be present. Plain radiographs are indicated for all patients with os centrale carpi to rule out fractures and to identify other accessory ossicles that may have become inflamed (Figure 80-3). Plain radiographs will also often identify loose bodies or joint mice that may also be present. On the basis of the patient’s clinical presentation, additional testing including complete blood cell count, sedimentation rate, and antinuclear antibody testing may be indicated. MRI of the wrist joint is indicated if joint instability, occult mass, or

tumor is suspected and to further clarify the diagnosis. Radionuclide bone scanning may be useful in the identification of stress fractures or tumors of the wrist that may be missed on plain radiographs. Arthrocentesis of the wrist joint may be indicated if septic arthritis or crystal arthropathy is suspected. Os centrale carpi pain syndrome is a clinical diagnosis that is supported by a combination of clinical history, physical examination, radiography, and MRI. Pain syndromes that may mimic os centrale carpi pain syndrome include primary disease of the wrist, including gout and occult fractures, and bursitis and tendonitis of the wrist, both of which may coexist with os centrale carpi. Osteochondritis dissecans, carpal coalition syndrome, and synovial chondromatosis may also mimic the pain associated with os centrale carpi. Primary and metastatic tumors of the wrist may also manifest in a manner analogous to wrist pain secondary to os centrale carpi.

Figure 80-1  Standard radiograph of the right wrist showing the os centrale carpi between the distal ulnar pole of the scaphoid and the capitate and trapezoid bones. (From Adolfsson L: Arthroscopic removal of os centrale carpi causing wrist pain, Arthroscopy 16:537–539, 2000.)

241

242        SECTION 4  •  Wrist and Hand

Acute fracture

After 6 weeks in plaster

At 39 months

Figure 80-2  Apparent union after 6 weeks in plaster. Nonunion is identified 39 months later when the patient reinjures his wrist. (From Prosser GH, Isbister ES: The presentation of scaphoid non-union, Injury 34:65–67, 2003.)

TABLE 80-1

Differential Diagnosis of Os Centrale Carpi Os Centrale Carpi

Acute Scaphoid Fracture

Old Scaphoid Fracture

Bipartate Scaphoid

Smooth ­borders

Irregularly ­irregular borders

Demineralization and cystic degeneration

Radiolucency at waist of scaphoid rather than its borders

TABLE 80-2

Heritable Conditions Associated with Os Centrale Carpi • Hand-foot-uterus syndrome • Holt-Oram syndrome • Larsen syndrome • Taybi otopalatodigital syndrome

Clinically Relevant Anatomy

Figure 80-3  This acute scaphoid fracture was identified in a 29-yearold man who fell from a ladder, injuring his nondominant hand. (From Adams JE, Steinmann SP: Acute scaphoid fractures, Hand Clin 25:97–103, 2010.)

The wrist joint is a biaxial, ellipsoid-type joint that serves as the articulation between the distal end of the radius and the articular disk above and the scaphoid, lunate, and triquetral bones below (Figure 80-4). The joint’s primary role is to optimize hand function. The joint allows flexion and extension as well as abduction, adduction, and circumduction. The joint is lined with synovium, and the resultant synovial space allows intraarticular injection,

80  •  Injection Technique for Os Centrale Carpi        243

tender area is then carried out. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a ⅝-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the carpal boss is identified. At this point, the needle is carefully advanced through the dorsal surface of the wrist until the needle tip rests against the os centrale carpi (see Figure 80-4). The needle is withdrawn slightly out of the periosteum and substance of the tendon. After the needle is in the correct position adjacent to the carpal boss and aspiration for blood is negative, the contents of the syringe are gently injected. There may be slight resistance to injection, given the closed nature of the space. If significant resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. The ice should not be left on for more than 10 minutes to avoid freezing injuries. Os centrale carpi

Side Effects and Complications

Figure 80-4  Injection technique for os centrale carpi–related wrist pain.

although septa within the synovial space may limit the flow of injectate. The entire joint is covered by a dense capsule that is attached above to the distal ends of the radius and ulna and below to the proximal row of metacarpal bones. The anterior and posterior joint is strengthened by the anterior and posterior ligaments, with the medial and lateral ligaments strengthening the medial and lateral joint, respectively. The wrist joint also may become inflamed as a result of direct trauma or overuse of the joint. The wrist joint is innervated primarily by the deep branch of the ulnar nerve, as well as by the anterior and posterior interosseous nerves. Anteriorly, the wrist is bounded by the flexor tendons and the median and ulnar nerves. Posteriorly, the wrist is bounded by the extensor tendons. Laterally, the radial artery can be found. The dorsal branch of the ulnar nerve runs medial to the joint; frequently this nerve is damaged when the distal ulna is fractured.

Technique Careful preparation of the patient before this injection technique helps to optimize results. The patient is placed in the supine position with the dorsal surface of the wrist and hand exposed. Proper preparation with antiseptic solution of the skin overlying the

The major complication of injection of os centrale carpi is infection. This complication should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients report of a transient increase in pain after injection of the os centrale carpi and should be warned of such. Another potential risk of this injection technique is trauma to the extensor tendons from the injection itself.

Clinical Pearls Pain emanating from the wrist is a common problem encountered in clinical practice. Os centrale carpi must be distinguished from fractures of the wrist, particularly of the scaphoid, entrapment neuropathies, bursitis, tendonitis, and synovitis. Careful differential diagnosis will help the clinician distinguish os centrale carpi from fractures of the scaphoid, which if undiagnosed can result in significant pain and functional disability.

SUGGESTED READINGS Ankarath S: Chronic wrist pain: diagnosis and management, Curr Orthop 20:141–151, 2006. Greenspan A, Gerscovich EO: Bilateral os centrale carpi: a rare congenital variant, J Hand Surg Am 18:586–587, 1993. Hsu PA, Light TR: Disorders of the immature carpus, Hand Clin 22:447–463, 2006. Lane LB, Gould ES, Stein PD, Coffey E: Unilateral osteonecrosis in a patient with bilateral os centrale carpi, J Hand Surg Am 15:751–754, 1990. Yang ZY, Gilula LA, Jonsson K: Os centrale carpi simulating a scaphoid waist fracture, J Hand Surg Br 19:754–756, 1994.

Chapter 81 INJECTION TECHNIQUE FOR GANGLION CYSTS OF THE WRIST AND HAND Indications and Clinical Considerations The dorsum of the wrist is especially susceptible to the development of ganglion cysts. These cysts are thought to form as a result of herniation of synovial-containing tissues from joint capsules or tendon sheaths. This tissue may then become irritated and begin producing increased amounts of synovial fluid, which can pool in cystlike cavities overlying the tendons and joint space. A oneway valve phenomenon may cause these cystlike cavities to expand because the fluid cannot flow freely back into the synovial cavity. Ganglion cysts may also occur on the volar aspect of the wrist (Figure 81-1). Activity, especially extreme flexion and extension, makes the pain worse; rest and heat provide some relief. The pain is constant and is characterized as aching. It is often the unsightly nature of the ganglion cyst, rather than the pain, that causes the patient to seek medical attention. The ganglion is smooth to palpation and transilluminates with a penlight in contradistinction to solid tumors, which do not transilluminate. Palpation of the ganglion may increase the pain. Plain radiographs of the wrist are indicated for all patients with ganglion cysts to rule out bony abnormalities, including tumors. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and/or ultrasound imaging of the wrist is indicated if the cause of the wrist mass is suspect (Figure 81-2).

of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. After sterile preparation of skin overlying the ganglion, a 1-inch, 22-gauge needle is inserted in the center of the ganglion and the contents of the cyst are aspirated (see Figure 81-4). If bone is encountered, the needle is withdrawn back into the ganglion cyst and aspiration is carried out. After the ganglion cyst has been aspirated, the contents of the syringe are gently injected. There should be little resistance to injection. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. Ultrasound guidance for needle placement may be beneficial if the anatomic landmarks necessary to safely perform this procedure are difficult to identify (Figures 81-5 and 81-6). If the ganglion reappears, surgical treatment ultimately may be required.

Side Effects and Complications The major complication of injection of a ganglion is infection, which should be exceedingly rare if strict aseptic technique is followed. Care must be taken to avoid injecting directly into tendons that may already be inflamed from irritation caused by the ganglion rubbing against the tendon.

Clinically Relevant Anatomy Ganglion cysts usually appear on the dorsum of the wrist, in the area overlying the extensor tendons or the joint space, with a predilection for the joint space of the lunate or from the tendon sheath of the extensor carpi radialis (Figures 81-3 and 81-4).

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side and the elbow slightly flexed with the palm of the hand resting on a folded towel. A total of 1.5 mL

244

Figure 81-1  A ganglion on the volar aspect of the wrist. (From Klippel JH, Dieppe PA: Rheumatology, ed 2, Philadelphia, 1997, Mosby.)

81  •  Injection Technique for Ganglion Cysts of the Wrist and Hand        245

*

* S

A

L

B

S

L

C Figure 81-2  A, Coronal fast spin-echo (FS) T2-weighted magnetic resonance (MR) image of the dorsal compartment of the wrist. A ganglion cyst with high signal intensity (SI) arises between the extensor tendons. B, The axial T1-weighted MR image shows the low-SI cyst (white arrows) lying superficial to the scapholunate joint and deep to the extensor carpi radialis brevis and longus tendons (asterisks). C, The cyst has high SI on the comparative axial FS T2-weighted MR image and is partially loculated. L, Lunate; S, scaphoid. (From Waldman SD, Campbell RS: Imaging of pain, Philadelphia, 2011, Saunders.)

Capitate

Lunate

Figure 81-3  A 65-year-old man with dorsal ganglion cyst (star) arising from the midcarpal joint.

246        SECTION 4  •  Wrist and Hand

Ganglion

Figure 81-5  Proper transducer position for injection or aspiration of a dorsal ganglion cyst of the wrist.

Figure 81-4  Proper needle placement for injection of dorsal ganglion cysts of the wrist.

UA

*

HAM HAM

A

B

Figure 81-6  Aspiration of ganglion cyst causing ulnar nerve palsy. Transverse sonograms of the palmar ulnar wrist. A, A lobulated ganglion cyst (asterisk) is seen extending superficial to the hamate (HAM) to abut the ulnar nerve (arrow). B, A needle (open arrow) has partially decompressed the ganglion, which has receded from the ulnar nerve (solid arrow) and ulnar artery (UA). The patient’s symptoms resolved slowly over the course of several weeks after aspiration. (From Louis LJ: Musculoskeletal ultrasound intervention: principles and advances, Radiol Clin North Am 46:515-533, 2008.)

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to ganglion cysts. Coexistent bursitis and tendinitis also may contribute to wrist pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is a safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Dias JJ, Dhukaram V, Kumar P: The natural history of untreated dorsal wrist ganglia and patient reported outcome 6 years after intervention, J Hand Surg Eur Vol 32:502–508, 2007. Louis LJ: Musculoskeletal ultrasound intervention: principles and advances, Radiol Clin North Am 46:515–533, 2008. Minotti P, Taras JS: Ganglion cysts of the wrist, J Hand Surg Am 2:102–107, 2002. Nahra ME, Bucchieri JS: Ganglion cysts and other tumor related conditions of the hand and wrist, Hand Clin 20:249–260, 2004. Waldman SD: Functional anatomy of the wrist. In Pain review, Philadelphia, 2009, Saunders, pp 100–102.

Chapter 82 DUPUYTREN CONTRACTURE INJECTION Indications and Clinical Considerations Dupuytren contracture is caused by a progressive fibrosis of the palmar fascia. Initially the patient may notice fibrotic nodules that are tender to palpation along the course of the flexor tendons of the hand. These nodules arise from the palmar fascia and initially do not involve the flexor tendons. As the disease advances, these fibrous nodules coalesce and form fibrous bands that gradually thicken and contract around the flexor tendons; the result is that the affected fingers are drawn into flexion. Although all fingers can develop Dupuytren contracture, the ring and little fingers are most commonly affected (Figure 82-1). If untreated, the fingers will develop permanent flexion contractures. The pain of Dupuytren contracture seems to burn itself out as the disease progresses. Dupuytren contracture is thought to have a genetic basis and occurs most frequently in males of northern Scandinavian descent. The disease also may be associated with trauma to the palm, diabetes, alcoholism, and chronic barbiturate use. The disease rarely occurs before the fourth decade. The plantar fascia also may be concurrently affected. In the early stages of the disease, hard, fibrotic nodules may be palpated along the path of the flexor tendons. These nodules often are misdiagnosed as calluses or warts. At this early stage, pain is invariably present. As the disease progresses, the clinician notes taut, fibrous bands that may cross the metacarpophalangeal joint and ultimately the proximal interphalangeal joint. These bands

are not painful to palpation, and, although they limit finger extension, finger flexion remains relatively normal. It is at this point that patients often seek medical advice, as they begin having difficulty putting on gloves and reaching into their pockets to retrieve keys. It is important to note that although the primary pathologic process associated with Dupuytren contracture involves the palmar surface of the hand, changes involving the dorsum of the hand are also common (Figure 82-2). In the final stages of the disease, the flexion contracture develops with its attendant negative impact on function. Arthritis, gout of the metacarpal and interphalangeal joints, and trigger finger may coexist with and exacerbate the pain and disability of Dupuytren contracture. Plain radiographs are indicated in all patients with Dupuytren contracture to rule out underlying occult bony disease. Ultrasound imaging will also provide valuable information regarding the condition of the tendon. Although as the disease progresses the diagnosis of Dupuytren contracture is usually straightforward, the condition can mimic other diseases as listed in Table 82-1. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the hand is indicated if joint instability or tumor is suspected. Electromyography is indicated if coexistent ulnar or carpal tunnel syndrome is suspected. The injection technique described later provides transient improvement of the pain and disability of this disease, but surgical treatment may ultimately be required to restore function.

Figure 82-1  Dupuytren contracture. (From Klippel JH, Dieppe PA: Rheumatology, ed 2, Philadelphia, 1997, Mosby.)

247

248        SECTION 4  •  Wrist and Hand

A

B

Figure 82-2  A and B, Knuckle pads on the dorsum of the hand. (From Kakar S, Giuffre J, Skeete K, Elhassan B: Dupuytren’s disease, Orthop Trauma 24:197–206, 2010.)

TABLE 82-1

Diseases That May Mimic Dupuytren Disease • Ganglion cysts • Callus formation • Hyperkeratosis • Rheumatoid nodules • Palmar fibromatosis • Pigmented villonodular synovitis • Giant cell tumors • Epithelioid sarcomas

Clinically Relevant Anatomy

Fibrotic nodules

Dupuytren contracture is the result of the thickening of the palmar fascia and its effect on the flexor tendons (Figure 82-3). The primary function of the palmar fascia is to provide firm support to the overlying skin to aid the hand in gripping, as well as to protect the underlying tendons.

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side with the dorsal surface of the hand resting on a folded towel. A total of 2 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. Sterile preparation of the skin overlying the fibrous band or nodule is carried out. At a point just lateral to the fibrosis, a 1-inch, 25-gauge needle is inserted at a 45-degree angle parallel to the fibrosis through the skin and into the subcutaneous tissue overlying the fibrotic area (see Figure 82-3). If bone is encountered, the needle is withdrawn back into the subcutaneous tissue and again advanced in proximity to the fibrosis. The contents of the syringe are then gently injected. There may be some resistance to injection owing to fibrosis of the surrounding tissue. If significant resistance is encountered, the needle is probably in the tendon or fibrotic nodule and should be withdrawn back until the injection proceeds without significant resistance. Ultrasound guidance for needle placement may be beneficial if the anatomic landmarks necessary to safely perform this procedure are difficult to identify.

Figure 82-3  Proper needle placement for injection of Dupuytren contracture.

The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complications associated with this injection technique are related to trauma to an inflamed or previously damaged tendon. Such tendons may rupture if directly injected, and needle position should be confirmed outside the tendon before injection to avoid this complication. Another complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients note a transient increase in pain after this injection technique; the patient should be warned of this.

82  •  Dupuytren Contracture Injection        249

Clinical Pearls This injection technique is extremely effective in the treatment of pain and dysfunction secondary to the Dupuytren contracture. Coexistent arthritis and gout also may contribute to the pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat, massage, and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Birks M: Dupuytren’s disease, Surgery (Oxford) 28:85–88, 2010. Geoghegan JM, Forbes J, Clark DI, et al: Dupuytren’s disease risk factors, J Hand Surg Br 29:423–426, 2004. Hayton MJ: Gray ICM: Dupuytren’s contracture: a review, Curr Orthop 171:2003. Waldman SD: Dupuytren’s contracture. In Pain review, Philadelphia, 2009, Saunders, pp 277–278.

Chapter 83 DIGITAL NERVE BLOCK OF THE FINGER

Indications and Clinical Considerations

described later serves as both a diagnostic and a therapeutic maneuver.

Plastic bag palsy is an entrapment neuropathy of the digital nerves caused by compression of the nerves against the bony phalanges by the handles of a plastic bag. Occurring with increasing frequency as stores have switched from paper bags to smaller plastic bags, plastic bag palsy may occur in either an acute or a chronic form. In plastic bag palsy, compression by the handle of a heavy plastic bag is the inciting cause (Figure 83-1). The common clinical feature of plastic bag palsy is the presence of painful digital nerves at the point at which the plastic bag handles compress the nerves. Occasionally seen in the homeless who carry the same plastic bag of their possessions in the same hand each day, the affected nerves may be thickened, and inflammation of the nerve and overlying soft tissues may be seen. In addition to pain, the patient with plastic bag palsy may also report paresthesias and numbness just below the point of nerve compromise. Pain may also increase with exposure to cold. Other causes of compression of the digital nerve have been identified, such as bowling (bowler’s thumb), overuse of scissors by dressmakers, compression of the nerve by overuse of jeweler’s pliers, and cherry pitting. The pain of plastic bag palsy may develop after an acute injury to the nerves after carrying too heavy a bag on too few fingers or from direct trauma to the soft tissues overlying the digital nerve if the affected digits get caught in a bag handle that has twisted around the fingers. The pain of plastic bag palsy is constant and is made worse with compression of the affected digital nerves. Patients often also note the inability to hold objects with the affected fingers. Sleep disturbance is common. On physical examination there is tenderness to palpation of the affected digital nerve. Range of motion of the thumb is normal. Palpation of the affected nerve can cause paresthesias, and continued pressure on the nerve may induce numbness distal to the point of compression. Exploration of the affected nerve may reveal neuroma formation at the site of previous trauma (Figure 83-2). Electromyography helps distinguish other causes of hand numbness from plastic bag palsy. Plain radiographs are indicated for all patients with plastic bag palsy to rule out occult bony disease such as bone spurs or cysts that may be compressing the digital nerve. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the hand can be done to rule out soft tissue tumors such as ganglion cysts that may be compressing the digital nerve. The injection technique

Clinically Relevant Anatomy

250

The common digital nerves arise from fibers of the median and ulnar nerves. The thumb also has contributions from superficial branches of the radial nerve. The common digital nerves pass along the metacarpal bones and divide as they reach the distal palm. The volar digital nerves supply the majority of sensory innervation to the fingers and run along the ventrolateral aspect of the finger beside the digital vein and artery. The smaller dorsal digital nerves contain fibers from the ulnar and radial nerves and supply the dorsum of the fingers as far as the proximal joints.

Technique The patient is placed in a supine position with the arm fully abducted and the elbow slightly flexed with the palm of the hand resting on a folded towel. A total of 3 mL per digit of non– epinephrine-containing local anesthetic is drawn up in a 12-mL sterile syringe. After preparation of the skin with antiseptic solution, at a point at the base of the finger, a 1½-inch, 25-gauge needle is inserted on each side of the bone of the digit to be blocked (Figure 83-3). While the anesthetic is slowly injected, the needle is advanced from the dorsal surface of the hand toward the palmar surface. The same technique can be used to block the thumb. The needle is removed, and pressure is placed on the injection site to avoid hematoma formation.

Side Effects and Complications Digital nerve block is a relatively safe procedure, with the major complications being inadvertent intravascular injection and persistent paresthesia secondary to needle trauma to the nerve. This technique can be safely performed in the presence of anticoagulation by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable riskto-benefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block decreases the amount of postprocedure pain and bleeding the patient may experience. Under no circumstance should local anesthetics containing epinephrine be used for digital nerve block because gangrene of the digit has been reported.

83  •  Digital Nerve Block of the Finger        251

Palmar digital n.

Flexor digitorum profundus

Figure 83-2  Painful neuroma of the radial digital nerve of the left middle finger. (From Thomsen L, Bellemere P, Loubersac T, et al: Treatment by collagen conduit of painful post-traumatic neuromas of the sensitive digital nerve: a retrospective study of 10 cases, Chir Main 29:255–262, 2010.)

Figure 83-1  Plastic bag palsy is caused by compression of the palmar digital nerve.

Needle entry sites

Dorsal digital n. Proper palmar digital n.

Figure 83-3  Proper needle placement for digital nerve block of the finger.

252        SECTION 4  •  Wrist and Hand

Clinical Pearls Digital nerve block is a safe and simple technique and is extremely useful in the management of plastic bag palsy. If plastic bag palsy is suspected, injection of the affected digital nerves with local anesthetic and corticosteroid gives almost instantaneous relief of the pain, although numbness may persist. Careful neurologic examination to identify preexisting neurologic deficits that may later be attributed to the nerve block should be performed on all patients before beginning diagnostic and/or therapeutic digital nerve blocks.

SUGGESTED READINGS Boscheinen-Morrin J, Connolly WB: Peripheral nerve entrapment. In The hand, ed 3, Butterworth-Heinemann, 2001, Oxford, pp 83–98. Cunningham ME, Bueno R, Potter HG, Weiland AJ: Closed partial rupture of a common digital nerve in the palm: a case report, J Hand Surg Am 30:100–104, 2005. Hug U, Burg D, Baldi SV, Meyer VE: Compression neuropathy of the radial palmar thumb nerve, Chir Main 23:49–51, 2004. Izzi J, Dennison D, Noerdlinger M, et al: Nerve injuries of the elbow, wrist, and hand in athletes, Clin Sports Med 20:203–217, 2001. Spaans F: Neurographic assessment of lesions of single proper digital nerves, Clin Neurophysiol 112:2113–2117, 2001. Waldman SD: Metacarpal and digital nerve block. In Pain review, Philadelphia, 2009, Saunders, pp 451–452.

SECTION 5  •  Chest Wall, Trunk, Back, and Abdomen

Chapter 84 INJECTION TECHNIQUE FOR STERNOCLAVICULAR JOINT PAIN Indications and Clinical Considerations The sternoclavicular joint can serve as a source of pain that often may mimic pain of cardiac origin. The sternoclavicular joint is a true joint and is susceptible to the development of arthritis, including osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, Reiter syndrome, and psoriatic arthritis (Figure 84-1). The joint is often traumatized during acceleration-deceleration injuries and blunt trauma to the chest. With severe trauma the joint may sublux or dislocate. Overuse or misuse can also result in acute inflammation of the sternoclavicular joint, which can be quite debilitating. The joint is also subject to invasion by tumor from primary malignancies, including thymoma, or from metastatic disease. Physical examination reveals that the patient will vigorously attempt to splint the joint by keeping the shoulders stiffly in neutral position. Pain is reproduced by active protraction or retraction of the shoulder, as well as full elevation of the arm. Shrugging of the shoulder may also reproduce the pain. The sternoclavicular joint may be tender to palpation and feel hot and swollen if acutely inflamed. The patient may also report a clicking sensation with movement of the joint.

A

Plain radiographs are indicated for all patients with pain thought to be emanating from the sternoclavicular joint to rule out occult bony disease, including tumor. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, prostate-specific antigen, sedimentation rate, and antinuclear antibody testing. MRI of the joint is indicated if joint instability is suspected. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The sternoclavicular joint is a double gliding joint with an actual synovial cavity (Figure 84-2). Articulation occurs among the sternal end of the clavicle, the sternal manubrium, and the cartilage of the first rib. The clavicle and sternal manubrium are separated by an articular disk. The joint is reinforced in front and back by the sternoclavicular ligaments. Additional support is provided by the costoclavicular ligament, which runs from the junction of the first rib and its costal cartilage to the inferior surface of the clavicle. The joint is dually innervated by both the supraclavicular nerve and the nerve supplying the subclavius muscle. Posterior to the joint are a number of large arteries and veins, including the

B

Figure 84-1  Osteoarthritis of the sternoclavicular joint. Radiographs of coronal sections through the sternoclavicular joints in two different cadavers demonstrate the spectrum of osteoarthritis. Changes include subchondral osseous irregularity and osteophytosis of the medial ends of the clavicle and sternum. Note the large excrescences extending laterally from the inferior aspect of the clavicular heads. (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

253

254        SECTION 5  •  Chest Wall, Trunk, Back, and Abdomen Interclavicular ligament Inflamed articular disk Inflamed and arthritic articular surface

Anterior sternoclavicular ligament Costoclavicular ligament Radiate sternocostal ligament

Figure 84-2  Proper needle placement for intraarticular injection of the sternoclavicular joint.

left common carotid and brachiocephalic vein and, on the right, the brachiocephalic artery. These vessels are susceptible to needleinduced trauma if the needle is placed too deeply. The serratus anterior muscle produces forward movement of the clavicle at the sternoclavicular joint, with backward movement at the joint produced by the rhomboid and trapezius muscles. Elevation of the clavicle at the sternoclavicular joint is produced by the sternocleidomastoid, rhomboid, and levator scapulae. Depression of the clavicle at the joint is produced by the pectoralis minor and subclavius muscle.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the root of the neck anteriorly as well as the skin overlying the proximal clavicle is carried out. A sterile syringe containing 1.0 mL of 0.25% preservativefree bupivacaine and 40 mg of methylprednisolone is attached to a 11⁄2-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the sternal end of the clavicle is identified. The sternoclavicular joint should be easily palpable as a slight indentation at the point where the clavicle meets the sternal manubrium. The needle is then carefully advanced through the skin and subcutaneous tissues medially at a 45-degree angle from the skin, through the joint capsule into the joint (see ­Figure 84-2). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected slightly more medially. After the joint space has been entered, the contents of the syringe are gently injected. There should be some resistance to injection because the

joint space is small and the joint capsule is dense. If significant resistance is encountered, the needle is probably in a ligament and should be advanced or withdrawn slightly into the joint space until the injection proceeds with only limited resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is pneumothorax if the needle is placed too laterally or deeply and invades the pleural space. Infection, although rare, can occur if strict aseptic technique is not followed. Trauma to the large arteries and veins in proximity to the sternoclavicular joint remains an ever-present possibility; the risk of this complication can be greatly decreased if the clinician pays close attention to accurate needle placement.

Clinical Pearls Patients with pain emanating from the sternoclavicular joint often attribute their pain symptoms to a heart attack. Reassurance often is required, although it should be remembered that this musculoskeletal pain syndrome and coronary artery disease can coexist. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for sternoclavicular joint pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique. Laboratory evaluation for collagen vascular disease is indicated for patients with sternoclavicular joint pain with other joints involved.

SUGGESTED REMADINGS Crisostomo RA, Laskowski ER, Bond JR, Agerter DC: Septic sternoclavicular joint: a case report, Arch Phys Med Rehabil 89:884–886, 2008. Ferrera PC, Wheeling HM: Sternoclavicular joint injuries, Am J Emerg Med Medicine 18:58–61, 2000. Hamilton RJ, Wylie R: Sternoclavicular pyarthrosis, J Emerg Med 24:327–328, 2003. Noble JS: Degenerative sternoclavicular arthritis and hyperostosis, Clin Sports Med 22:407–422, 2003. Waterman J, Emery R: The diagnosis and treatment of disorders of the sternoclavicular joint, Curr Orthop 16:368–373, 2002.

Chapter 85 LONG THORACIC NERVE BLOCK

Indications and Clinical Considerations Long thoracic nerve entrapment syndrome is caused by compression or stretching of the long thoracic nerve as it passes beneath the subscapularis muscle to innervate the serratus anterior muscle (Figure 85-1). The most common causes of compression of the long thoracic nerve at this anatomic location include direct trauma to the nerve during surgical procedures, such as radical mastectomy and surgery for thoracic outlet syndrome. Direct blunt trauma from heavy items falling from shelves also can cause long thoracic nerve entrapment syndrome. Damage to the long thoracic nerve after first rib fracture also has been reported. Stretch injuries to the long thoracic nerve often occur from wearing improperly fitting heavy backpacks or doing prolonged heavy labor. Clinically, the patient exhibits painless paralysis of the serratus anterior muscle that results in the classic finding of winged scapula (Figure 85-2). The winging of the scapula is the result of the inability of the serratus anterior muscle to hold the scapula firmly against the posterior chest wall. The winged scapula can be identified by having the patient press both hands against the wall and press outward. The clinician, by observing the patient from behind, identifies the affected scapula projecting posteriorly or winging away from the posterior chest wall (see Figure 85-1). The patient with long thoracic nerve syndrome also is unable to fully extend the upper extremity overhead on the affected side, with the last 25 to 30 degrees of extension being lost. Electromyography helps diagnose long thoracic nerve entrapment syndrome. Plain radiographs are indicated for all patients with long thoracic nerve entrapment syndrome to rule out occult bony disease, including scapular and first rib fractures.

and 40 mg of methylprednisolone is drawn up in a 10-mL sterile syringe. The clinician identifies the supraclavicular fossa and then follows the posterior border of the clavicle laterally toward the shoulder. At the most lateral point within the supraclavicular fossa, the skin is prepped with antiseptic solution. A 11⁄2-inch, 25-gauge needle is inserted at this point at a right angle to the clavicle (Figure 85-4). The needle is slowly advanced until the tip is just beyond the inferior margin of the clavicle. If the aspiration test result is negative and there is no persistent paresthesia into the distribution of the brachial plexus, the solution is slowly injected, with the patient being monitored closely for signs of local anesthetic toxicity. If the needle tip hits the bone of the first rib, the needle is withdrawn out of the periosteum, and after careful aspiration the solution is slowly injected.

Long thoracic n.

Clinically Relevant Anatomy The long thoracic nerve is made up of fibers from C5-C7 spinal roots (see Figure 85-1). The nerve passes over the lateral border of the first rib to enter the axilla (Figure 85-3). It is susceptible to injury at this point. The nerve passes behind the axillary artery and brachial plexus. Exiting the axilla, the long thoracic nerve descends over the lateral surface of the serratus anterior muscle, which it innervates.

Technique The patient is placed in a supine position with the arm fully adducted at the patient’s side. A total of 7 mL of local anesthetic

Serratus anterior m. Figure 85-1  Winged scapula is caused by dysfunctions of the long thoracic nerve of bell.

255

256        SECTION 5  •  Chest Wall, Trunk, Back, and Abdomen

Figure 85-2  Photograph showing the prominent, right winged scapula as the patient attempted to push forward against resistance. (From Uerpairojkit C, Leechavengvongs S, Witoonchart K, et al: Nerve transfer to serratus anterior muscle using the thoracodorsal nerve for winged scapula in C5 and C6 brachial plexus root avulsions, J Hand Surg Am 34:74–78, 2009.)

the pleural space. Infection, although rare, can occur if strict aseptic technique is not followed. Trauma to the contents of the mediastinum remains a possibility if the needle is placed too medially. The risk of these complications can be greatly decreased if the clinician pays close attention to accurate needle placement.

Clinical Pearls

Superior angle UP

SSC

Figure 85-4  Proper needle placement for injection of the long thoracic nerve.

This injection technique is a simple and safe technique in the evaluation and treatment of long thoracic nerve entrapment syndrome. Careful neurologic examination to identify preexisting neurologic deficits that may later be attributed to the nerve block should be performed on all patients before beginning long thoracic nerve block.

Middle LTN

2nd rib SUGGESTED READINGS

Figure 85-3  Anatomy of upper part (UP) of the serratus anterior muscle and long thoracic nerve (LTN). The upper part of the serratus anterior muscle, a large and powerful mass, cylindric in shape, is raised from the first and second ribs. The long thoracic nerve runs over the upper part, which covers as a soft tissue to the second rib. SSC, Subscapularis muscle; Superior angle, superior angle of scapula. (From Hamada J, Igarashi E, Akita K, Mochizuki T: A cadaveric study of the serratus anterior muscle and the long thoracic nerve, J Shoulder Elbow Surg 17:790–794, 2008.)

Side Effects and Complications The major complication of this injection technique is pneumothorax if the needle is placed too medially or deeply and invades

Belsh JM: Thoracic nerve. In Aminoff ME, Doroff RB, editors: Encyclopedia of the neurological sciences, ed 2, Waltham, MA, 2003, Academic Press, pp 524–526. Hamada J, Igarashi E, Akita K, Mochizuki T: A cadaveric study of the serratus anterior muscle and the long thoracic nerve, J Shoulder Elbow Surg 17:790–794, 2008. Krasna MJ, Forti G: Nerve injury: injury to the recurrent laryngeal, phrenic, vagus, long thoracic, and sympathetic nerves during thoracic surgery, Thorac Surg Clin 16:267–275, 2006. Novak CB, Mackinnon SE: Surgical treatment of a long thoracic nerve palsy, Ann Thorac Surg 73(5):1643–1645, 2002. Wilbourn AJ, Ferrante MA: Upper limb neuropathies: long thoracic (nerve to the serratus anterior), suprascapular, axillary, musculocutaneous, radial, ulnar, and medial antebrachial cutaneous. In Dyck PJ, Thomas PK, editors: Peripheral neuropathy, ed 4, Philadelphia, 2005, Saunders, pp 1463–1486.

Chapter 86 SUPRASCAPULAR NERVE BLOCK

Indications and Clinical Considerations Suprascapular nerve entrapment syndrome is caused by compression of the suprascapular nerve as it passes through the suprascapular notch (Figure 86-1). The most common causes of compression of the suprascapular nerve at this anatomic location include the prolonged wearing of heavy backpacks and direct blows to the nerve, such as occur in football injuries and in falls from trampolines. This entrapment neuropathy manifests most commonly as a severe, deep, aching pain that radiates from the top of the scapula to the ipsilateral shoulder. Tenderness over the suprascapular notch is usually present. Shoulder movement, especially reaching across the chest, may increase the pain symptoms. If the condition is not treated, weakness and atrophy of the supraspinatus and infraspinatus muscles will occur. Suprascapular nerve entrapment syndrome is often misdiagnosed as bursitis, tendinitis, or arthritis of the shoulder. Cervical radiculopathy of the C5 nerve root also may mimic the ­clinical presentation of suprascapular nerve entrapment syndrome. ­Parsonage-Turner syndrome (idiopathic brachial neuritis) also may manifest as a sudden onset of shoulder pain and can be confused with suprascapular nerve entrapment. Tumor or ganglion cysts involving the superior scapular region or shoulder also should be considered in the differential diagnosis of suprascapular nerve entrapment syndrome (Figure 86-2). Electromyography helps distinguish cervical radiculopathy and Parsonage-Turner syndrome from suprascapular nerve entrapment syndrome. Plain radiographs are indicated for all patients with suprascapular nerve entrapment syndrome to rule out occult bony disease. On the basis of on the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and/or ultrasound of the shoulder is indicated if primary disease or a space-occupying lesion is suggested (see Figure 86-2). The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The suprascapular nerve is formed from fibers originating from the C5 and C6 nerve roots of the brachial plexus, with some contribution of fibers from the C4 root in most patients. The nerve passes inferiorly and posteriorly from the brachial plexus to pass underneath the coracoclavicular ligament through the suprascapular notch. The suprascapular artery and vein accompany the nerve through the suprascapular notch. The suprascapular nerve

provides much of the sensory innervation to the shoulder joint and provides innervation to two of the muscles of the rotator cuff, the supraspinatus and infraspinatus.

Technique The patient is placed in the sitting position with the arms hanging loosely at the patient’s side. A total of 10 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 20-mL sterile syringe. The spine of the scapula is identified, and the clinician then palpates along the length of the scapular spine laterally to identify the acromion. At the point at which the thicker acromion fuses with the thinner scapular spine, the skin is prepared with antiseptic solution. At this point, the skin and subcutaneous tissues are anesthetized using a 1½-inch needle. After adequate anesthesia has been achieved, a 3½-inch, 25-gauge needle is inserted in an inferior trajectory toward the body of the scapula (see Figure 86-1). The needle should make contact with the body of the scapula at a depth of about 1 inch. The needle is then gently “walked” superiorly and medially until the needle tip walks off the scapular body into the suprascapular notch. If the notch is not identified, the same maneuver is repeated, directing the needle superiorly and laterally until the needle tip walks off the scapular body into the suprascapular notch. A paresthesia is

Suprascapular nerve Infraspinatus m. Suprascapular notch

Infraspinatus m.

Figure 86-1  Proper needle placement for suprascapular nerve block.

257

258        SECTION 5  •  Chest Wall, Trunk, Back, and Abdomen

A

B

Figure 86-2  Spinoglenoid notch ganglion. A, T2-weighted (TR 2500 ms, TE 70 ms) sagittal oblique image. A single, rounded, hyperintense mass (asterisk) is present in the spinoglenoid notch of this young man with shoulder pain. B, Gradient-echo axial image. At this level, the lesion is composed of multiple smaller masses. On proton-density images, this mass was intermediate in signal, approximately isointense with muscle. This location and appearance are typical of a spinoglenoid notch ganglion. (From Haaga JR, Lanzeri CF, Gilkerson RC: CT and MR imaging of whole body, ed 4, Philadelphia, 2002, Mosby.)

often encountered as the needle tip enters the notch, and the patient should be warned of this. If a paresthesia is not elicited after the needle has entered the suprascapular notch, advance the needle an additional ½ inch to place the needle tip beyond the substance of the coracoclavicular ligament. The needle should never be advanced deeper or pneumothorax is likely to occur. After paresthesia is elicited or the needle has been advanced into the notch as described earlier, gentle aspiration is carried out to identify blood or air. If the aspiration test result is negative, the solution is slowly injected, with the patient being monitored closely for signs of local anesthetic toxicity. Ultrasound guidance may be beneficial if the anatomic landmarks necessary to safely perform this technique are difficult to identify.

Clinical Pearls

Side Effects and Complications

Gebauer G, Cosgarea AJ: Suprascapular nerve entrapment. In Wilk KE, Reinold MM, Andrews JR, editors: The athlete’s shoulder, ed 2, Philadelphia, 2000, Churchill Livingstone, pp 343–350. Pratt N: Anatomy of nerve entrapment sites in the upper quarter, J Hand Ther 18:216–229, 2005. Toussaint CP, Zager EL: What’s new in common upper extremity entrapment neuropathies, Neurosurg Clin N Am 19:573–581, 2008. Waldman SD: Suprascapular nerve block. Pain review, Philadelphia, 2009, Saunders, pp 494–495. Zylicz Z, Rozenheuvel H: Suprascapular nerve entrapment: a neglected cause of shoulder pain in cachectic patients? J Pain Symptom Manage 20:315–317, 2000.

The proximity to the suprascapular artery and vein suggests the potential for inadvertent intravascular injection or local anesthetic toxicity from intravascular absorption. The clinician should carefully calculate the total milligram dosage of local anesthetic that may be safely given when performing this injection technique. Because of the proximity of the lung, pneumothorax is a possibility if the needle is advanced too deeply through the suprascapular notch.

This injection technique renders the shoulder joint insensate. Therefore it is important that the clinician be sure that the physical and occupational therapists caring for the patient who has undergone suprascapular nerve block understand that not only the shoulder girdle but also the shoulder joint has been rendered insensate. This means that deep heat modalities and range-of-motion exercises must be carefully monitored to avoid burns or damage to the shoulder, respectively.

SUGGESTED READINGS

Chapter 87 COSTOSTERNAL JOINT INJECTION

Indications and Clinical Considerations The costosternal joints can serve as a source of pain that may often mimic the pain of cardiac origin. The costosternal joints are susceptible to the development of arthritis, including osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, Reiter syndrome, and psoriatic arthritis. The joints often are traumatized during acceleration-deceleration injuries and blunt trauma to the chest. With severe trauma, the joints may sublux or dislocate. Overuse or misuse also can result in acute inflammation of the costosternal joint, which can be quite debilitating. The joints also are subject to invasion by tumor either from primary malignancies, including thymoma, or from metastatic disease. Physical examination reveals that the patient will vigorously attempt to splint the joints by keeping the shoulders stiffly in neutral position. Pain is reproduced with active protraction or retraction of the shoulder, deep inspiration, and full elevation of the arm. Shrugging of the shoulder may also reproduce the pain. Coughing may be difficult, and this may lead to inadequate pulmonary toilet in patients who have sustained trauma to the anterior chest wall. The costosternal joints and adjacent intercostal muscles may also be tender to palpation. The patient may also report a clicking sensation with movement of the joint. Plain radiographs are indicated for all patients with pain thought to be emanating from the costosternal joints to rule out occult bony disease, including tumor. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, prostate-specific antigen, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the joints is indicated if joint instability or an occult mass is suggested. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

joint are the structures of the mediastinum. These structures are susceptible to needle-induced trauma if the needle is placed too deeply. The pleural space may be entered if the needle is placed too deeply and laterally; pneumothorax may result.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the affected costosternal joints is carried out. A sterile syringe containing 1.0 mL of 0.25% preservative-free bupivacaine for each joint to be injected and 40 mg of methylprednisolone is attached to a 11⁄2-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the costovertebral joints are identified. The costosternal joints should be easily palpable as a slight bulging at the point where the rib attaches to the sternum. The needle is then carefully advanced through the skin and subcutaneous tissues medially with a slight cephalad trajectory into

Third costochondral junction

Clinically Relevant Anatomy The cartilage of the true ribs articulates with the sternum via the costosternal joints (Figure 87-1). The cartilage of the first rib articulates directly with the manubrium of the sternum and is a synarthrodial joint, which allows a limited gliding movement. The cartilage of the second through sixth ribs articulates with the body of the sternum via true arthrodial joints. These joints are surrounded by a thin articular capsule. The costosternal joints are strengthened by ligaments but can be subluxed or dislocated by blunt trauma to the anterior chest. Posterior to the costosternal

Carrico & Shavell

Figure 87-1  Proper needle placement for costosternal nerve block.

259

260        SECTION 5  •  Chest Wall, Trunk, Back, and Abdomen

proximity with the joint (see Figure 87-1). If bone is encountered, the needle is withdrawn out of the periosteum. After the needle is in proximity to the joint, 1 mL of solution is gently injected. There should be limited resistance to injection. If significant resistance is encountered, the needle should be withdrawn slightly until the injection proceeds with only limited resistance. This procedure is repeated for each affected joint. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is pneumothorax if the needle is placed too laterally or deeply and invades the pleural space. Infection, although rare, can occur if strict aseptic technique is not followed. Trauma to the contents of the mediastinum remains an ever-present possibility. The risk of this complication can be greatly decreased if the clinician pays close attention to accurate needle placement.

Clinical Pearls Patients with pain emanating from the costosternal joint often attribute their pain symptoms to a heart attack. Reassurance is required, although it should be remembered that this musculoskeletal pain syndrome and coronary artery disease can coexist. Tietze syndrome—painful enlargement of the upper costochondral cartilage associated with viral infections—can be confused with costosternal syndrome, although both respond to this injection technique. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for costosternal joint pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique. Laboratory evaluation for collagen vascular disease is indicated for patients with costosternal joint pain with other joints involved.

SUGGESTED READINGS Ramamurthy S: Chronic chest wall pain. In Ramamurthy S, Rogers JN, Alanmanou E, editors: Decision making in pain management, ed 2, Philadelphia, 2006, Mosby, pp 176–177. Stochkendahl MJ, Christensen HW: Chest pain in focal musculoskeletal disorders, Med Clin North Am 94:259–273, 2010. Waldman SD: Costosternal joint injection. In Pain review, Philadelphia, 2009, Saunders, pp 495–496. Waldman SD: Costosternal syndrome. In Pain review, Philadelphia, 2009, Saunders, pp 246–247.

Chapter 88 COSTOVERTEBRAL JOINT INJECTION Indications and Clinical Considerations

and strengthened by the superior and lateral costotransverse ligaments.

The costovertebral joint can serve as a source of pain that often may mimic pain of pulmonary origin. The costovertebral joint is a true joint and is susceptible to the development of arthritis, including osteoarthritis, rheumatoid arthritis, psoriatic arthritis, Reiter syndrome, and, in particular, ankylosing spondylitis (Figure 88-1). The joint is often traumatized during acceleration-deceleration injuries and blunt trauma to the chest and to the dorsal spine. With severe trauma the joint may sublux or dislocate. Overuse or misuse can also result in acute inflammation of the costovertebral joint, which can be quite debilitating. The joint is also subject to invasion by tumor either from primary malignancies, including lung cancer, or from metastatic disease. Physical examination reveals that the patient will attempt to splint the affected joint or joints by splinting that area of the back to avoid flexion, extension, or lateral bending of the spine. The patient may retract the scapulas in an effort to gain relief of the pain emanating from this joint. The costovertebral joint may be tender to palpation and feel hot and swollen if acutely inflamed. The patient may also report a clicking sensation with movement of the joint. Plain radiographs are indicated for all patients with pain thought to be emanating from the costovertebral joint to rule out occult bony disease, including tumor. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, prostate-specific antigen, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the joint is indicated if primary joint disease is suspected. The injection technique presented later serves as both a diagnostic and a therapeutic maneuver.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the prone position, and proper preparation with antiseptic solution of the skin overlying the affected joints is carried out. A fluoroscopic view of the joint and adjacent rib is then obtained, and the skin overlying the adjacent rib of the affected joint or joints is marked with a sterile marker to aid in identification. A sterile syringe containing 1.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 31⁄2-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the margins of the rib adjacent to the affected joint are identified by palpation. The needle is then carefully advanced through the skin and subcutaneous tissues at a point lateral to the joint and in the middle of the rib until the needle impinges on the periosteum of the rib. The needle is then carefully withdrawn out of the periosteum and “walked” medially along the course of the rib until the needle tip enters the costovertebral joint

Clinically Relevant Anatomy The costovertebral joint is a synovial plane-type joint with an actual synovial cavity (Figure 88-2). Articulation occurs between the ribs and the vertebrae. The joint is composed of two elements that articulate with the vertebrae: the head of the ribs and the costotransverse joint. The head of each individual rib articulates with the superior facet of its corresponding vertebral body as well as the inferior facet of the vertebral body just above it. The head of the rib also articulates with the intervertebral disk that is interposed between the two adjacent vertebral bodies. These articulations are supported by the radiate and intraarticular ligaments. The costotransverse joint is made up of the articulation of the tubercle and its adjacent vertebral body. The joint is supported

Figure 88-1  Costovertebral joint ankylosis. A transaxial computed tomography scan of a thoracic vertebra in a patient with ankylosing spondylitis reveals bone erosions and partial ankylosis (arrowhead) of the costovertebral joints on one side. Note the involvement of the ipsilateral rib with cortical thickening (arrows). (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

261

262        SECTION 5  •  Chest Wall, Trunk, Back, and Abdomen

Radiate ligament

T6-T7 vertebra

Costovertebral joint

Anterior costotransverse ligament

Ne

ck o

Ligament of the tubercle

fr

ib

Figure 88-2  Anatomy of the costovertebral joint.

T6-T7 vertebra

Costovertebral joint

Ne

ck o

fr

ib

Figure 88-3  Proper needle placement for intraarticular costovertebral joint injection.

(Figure 88-3). After the joint space has been entered, the contents of the syringe are gently injected. There should be some resistance to injection because the joint space is small and the joint capsule is dense. If significant resistance is encountered, the needle is probably in a ligament and should be advanced or withdrawn slightly into the joint space until the injection proceeds with only limited resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is pneumothorax if the needle is placed too laterally or deeply and invades the pleural space. Infection, although rare, can occur if strict aseptic technique is not followed. Trauma to the large arteries and veins in proximity to the costovertebral joint remains an everpresent possibility; the risk of this complication can be greatly decreased if the clinician pays close attention to accurate needle placement.

Clinical Pearls Patients with pain emanating from the costovertebral joint often attribute their pain symptoms to pulmonary disease. Reassurance often is required, although it should be remembered that this musculoskeletal pain syndrome and pulmonary disease can coexist. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for costovertebral joint pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique. Laboratory evaluation for collagen vascular disease and other joint diseases, including ankylosing spondylitis, is indicated for patients with costovertebral joint pain, especially if other joints are involved.

88  •  Costovertebral Joint Injection        263 SUGGESTED READINGS Carrier G, Fréchette E, Ugalde P, Deslauriers J: Correlative anatomy for the sternum and ribs, costovertebral angle, chest wall muscles and intercostal spaces, thoracic outlet, Thorac Surg Clin 17:521–528, 2007. Duprey S, Subit D, Guillemot H, Kent RW: Biomechanical properties of the costovertebral joint, Med Eng Phys 32:222–227, 2010.

Erwin WM, Jackson PC, Homonko DA: Innervation of the human costovertebral joint: implications for clinical back pain syndromes, J Manipulative Physiol Ther 23:395–403, 2000. Illiasch H, Likar R, Stanton-Hicks M: Tech Reg Anesth Pain Manag 11:103–112, 2007. Vallières E: The costovertebral angle, Thorac Surg Clin 17:503–510, 2007.

Chapter 89 COSTOSTERNAL JOINT INJECTION TECHNIQUE FOR TIETZE SYNDROME Indications and Clinical Considerations

occult mass is suspected. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Tietze syndrome is distinct from costosternal syndrome. First described in 1921, Tietze syndrome is characterized by acute painful swelling of the costal cartilages. The second and third costal cartilages are most commonly involved, and, in contradistinction to costosternal syndrome, which usually occurs no earlier than the fourth decade, Tietze syndrome is a disease of the second and third decades. The onset is acute and often is associated with a concurrent viral respiratory tract infection (Figure 89-1). It has been postulated that microtrauma to the costosternal joints from severe coughing or heavy labor may be the cause of Tietze syndrome. Painful swelling of the second and third costochondral joints is the sine qua non of Tietze syndrome. Such swelling is absent in costosternal syndrome, which occurs much more frequently than Tietze syndrome. A variety of other painful conditions affect the costosternal joints and occur with a much greater frequency than Tietze syndrome. The costosternal joints are susceptible to the development of arthritis, including osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, Reiter syndrome, and psoriatic arthritis. The joints often are traumatized during acceleration-deceleration injuries and blunt trauma to the chest. With severe trauma the joints may sublux or dislocate. Overuse or misuse also can result in acute inflammation of the costosternal joint, which can be quite debilitating. The joints also are subject to invasion by tumor either from primary malignancies, including thymoma, or from metastatic disease. Physical examination reveals that the patient with Tietze syndrome will vigorously attempt to splint the joints by keeping the shoulders stiffly in neutral position. Pain is reproduced with active protraction or retraction of the shoulder, deep inspiration, and full elevation of the arm. Shrugging of the shoulder also may reproduce the pain. Coughing may be difficult, and this may lead to inadequate pulmonary toilet in patients with Tietze syndrome. The costosternal joints, especially the second and third, are swollen and exquisitely tender to palpation. The adjacent intercostal muscles also may be tender to palpation. The patient also may report a clicking sensation with movement of the joint. Plain radiographs are indicated for all patients with pain thought to be emanating from the costosternal joints to rule out occult bony disease, including tumor. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, prostate-specific antigen, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the joints is indicated if joint instability or an

Clinically Relevant Anatomy

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The cartilage of the true ribs articulates with the sternum via the costosternal joints (Figure 89-2). The cartilage of the first rib articulates directly with the manubrium of the sternum and is a synarthrodial joint that allows a limited gliding movement. The cartilage of the second through sixth ribs articulates with the body of the sternum via true arthrodial joints. These joints are surrounded by a thin articular capsule. The costosternal joints are strengthened by ligaments but can be subluxed or dislocated by blunt trauma to the anterior chest. Posterior to the costosternal joint are the structures of the mediastinum. These structures are susceptible to needle-induced trauma if the needle is placed too deeply. The pleural space may be entered if the needle is placed too deeply and laterally; pneumothorax may result.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the affected

Figure 89-1  Swelling of the second and third costochondral joints is the sine qua non of Tietze syndrome. (From Waldman SD: Atlas of uncommon pain syndromes, ed 2, Philadelphia, 2008, Saunders.)

89  •  Costosternal Joint Injection Technique for Tietze Syndrome        265

repeated for each affected joint. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is pneumothorax if the needle is placed too laterally or deeply and invades the pleural space. Infection, although rare, can occur if strict aseptic technique is not followed. Trauma to the contents of the mediastinum remains an ever-present possibility; the risk of this complication can be greatly decreased if the clinician pays close attention to accurate needle placement.

Clinical Pearls Swelling of 2nd and 3rd costochondral joints

Figure 89-2  Painful swelling of the second and third costochondral joints is suggestive of Tietze syndrome.

costosternal joints is carried out. A sterile syringe containing 1.0 mL of 0.25% preservative-free bupivacaine for each joint to be injected and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the costovertebral joints are identified. The costosternal joints should be easily palpable as a slight bulging at the point where the rib attaches to the sternum. The needle is then carefully advanced through the skin and subcutaneous tissues medially with a slight cephalad trajectory into proximity with the joint (see Figure 89-2). If bone is encountered, the needle is withdrawn out of the periosteum. After the needle is in proximity to the joint, 1 mL of solution is gently injected. There should be limited resistance to injection. If significant resistance is encountered, the needle should be withdrawn slightly until the injection proceeds with only limited resistance. This procedure is

Patients with pain emanating from the costosternal joint often attribute their pain symptoms to a heart attack. Reassurance is required, although it should be remembered that this musculoskeletal pain syndrome and coronary artery disease can coexist. Tietze syndrome—painful enlargement of the upper costochondral cartilage associated with viral respiratory tract infections—can be confused with the more commonly occurring costosternal syndrome, although both respond to the just-described injection technique. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for costosternal joint pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique. Laboratory evaluation for collagen vascular disease is indicated for patients with costosternal joint pain with other joints involved.

SUGGESTED READINGS Baldry P, Yunus MB, Inanici F: The chest wall. In Baldry P, editor: Myofascial pain and fibromyalgia syndromes: a clinical guide to diagnosis and management, Edinburgh, 2001, Churchill Livingstone, pp 303–327. De Filippo M, Albini A, Castaldi V, et  al: MRI findings of Tietze’s syndrome mimicking mediastinal malignancy on MDCT, Eur J Radiol Extra 65:33–35, 2008. Stochkendahl MJ, Christensen HW: Chest pain in focal musculoskeletal disorders, Med Clin North Am 94:259–273, 2010. Waldman SD: Tietze’s syndrome. In Pain review, Philadelphia, 2009, Saunders, p 282.

Chapter 90 MANUBRIOSTERNAL JOINT INJECTION Indications and Clinical Considerations The manubriosternal joint can serve as a source of pain that often may mimic pain of cardiac origin. The manubriosternal joint is susceptible to the development of arthritis, including osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, Reiter syndrome, and psoriatic arthritis (Figure 90-1). The joint is often traumatized during acceleration-deceleration injuries and blunt trauma to the chest. With severe trauma the joint may sublux or dislocate (Figures 90-2 and 90-3). Overuse or misuse also can result in acute inflammation of the manubriosternal joint, which can be quite debilitating. The joint also is subject to invasion by tumor either from primary malignancies, including thymoma, or from metastatic disease. Rarely, the manubriosternal joint can become infected (Figure 90-4). Physical examination reveals that the patient will vigorously attempt to splint the joint by keeping the shoulders stiffly in neutral position. Pain is reproduced by active protraction or retraction of the shoulder, deep inspiration, and full elevation of the arm. Shrugging of the shoulder may also reproduce the pain. The manubriosternal joint may be tender to palpation and feel hot and

Figure 90-1  Computed tomography scan of the manubriosternal joint showing osteoarthritic changes. (From Al-Dahiri A, Pallister I: Arthrodesis for osteoarthritis of the manubriosternal joint, Eur J Cardiothorac Surg 29:119–121, 2006.)

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swollen if acutely inflamed. The patient also may report a clicking sensation with movement of the joint. Plain radiographs are indicated for all patients with pain thought to be emanating from the manubriosternal joint to rule out occult bony disease, including tumor. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, prostate-specific antigen, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the joint is indicated if joint instability is suspected. The following injection technique serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The manubrium articulates with the body of the sternum via the manubriosternal joint. The joint articulates at an angle called the angle of Louis, which allows for easy identification. The joint is a fibrocartilaginous joint or synchondrosis, which lacks a true joint cavity. The manubriosternal joint allows protraction and retraction of the thorax (Figure 90-5). Above, the manubrium articulates with the sternal end of the clavicle and the cartilage of the first rib. Below, the body of the sternum articulates with the xiphoid process. Posterior to the manubriosternal joint are the structures of the mediastinum. These structures are susceptible to needle-induced trauma if the needle is placed too deeply. The pleural space may be entered if the needle is placed too deeply and laterally; pneumothorax may result.

Figure 90-2  Photograph showing obvious step in manubriosternal joint following dislocation. (From Lyons I, Saha S, Arulampalam T.: Manubriosternal joint dislocation: an unusual risk of trampolining, J Emerg Med 39:596–598, 2010.)

90  •  Manubriosternal Joint Injection        267

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the angle of the sternum is carried out. A sterile syringe containing 1.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the angle of the sternum is identified. The manubriosternal joint should be easily palpable as a slight indentation at this point. The needle is then carefully advanced through the skin and subcutaneous tissues medially, with a slight cephalad trajectory into the joint (see Figure 90-5).

If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected slightly more cephalad. After the joint has been entered, the contents of the syringe are gently injected. There should be some resistance to injection owing to the fibrocartilaginous nature of the joint. If significant resistance is encountered, the needle should be advanced or withdrawn slightly into the joint until the injection proceeds with only limited resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is pneumothorax if the needle is placed too laterally or deeply and invades the pleural space. Infection, although rare, can occur if strict aseptic technique is not followed. Trauma to the contents of the mediastinum remains an ever-present possibility; risk of this complication can be greatly decreased if the clinician pays close attention to accurate needle placement.

Arthritic and inflamed manubriosternal joint

Figure 90-3  Lateral chest computed tomography scan showing posterior dislocation of the sternum. (From Lyons I, Saha S, Arulampalam T.: Manubriosternal joint dislocation: an unusual risk of trampolining, J Emerg Med 39:596–598, 2010.)

Figure 90-5  Proper needle placement for intraarticular injection of the manubriosternal joint.

Figure 90-4  Computed tomography scan shows an inflammatory mass centered on the manubriosternal joint with mixed fluid and gas density. Posteriorly, this soft tissue collection was related to the periosteum and was pushing the mediastinum rather than directly infiltrating it (axial view, left). The manubriosternal joint looked irregular and widened, with some irregularity of the cortical margin and a small fleck of bone posteriorly (sagittal reconstruction, right). (From Peng EW, McKillop G, Prasad S, Walker WS: Septic arthritis of the manubriosternal joint, Ann Thorac Surg 83:1190–1194, 2007.)

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Clinical Pearls Patients with pain emanating from the manubriosternal joint often attribute their pain symptoms to a heart attack. Reassurance is required, although it should be remembered that this musculoskeletal pain syndrome and coronary artery disease can coexist. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle rangeof-motion exercises, should be introduced several days after the patient has undergone this injection technique for manubriosternal joint pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique. Laboratory evaluation for collagen vascular disease is indicated for patients with manubriosternal joint pain with other joints involved.

SUGGESTED READINGS Ellis H: The superior mediastinum, Anaesth Intensive Care Med 10:360–361, 2009. Peng EW, McKillop G, Prasad S, Walker WS: Septic arthritis of the manubriosternal joint, Ann Thorac Surg 83:1190–1194, 2007. Ramamurthy S: Chronic chest wall pain. In Ramamurthy S, Rogers JN, Alanmanou E, editors: Decision making in pain management, ed 2, Philadelphia, 2006, Mosby, pp 176–177. Stochkendahl MJ, Christensen HW: Chest pain in focal musculoskeletal disorders, Med Clin North Am 94:259–273, 2010. Waldman SD: Manubriosternal joint syndrome. In Pain review, Philadelphia, 2009, Saunders, pp 247–248.

Chapter 91 INJECTION TECHNIQUE FOR STERNALIS SYNDROME Indications and Clinical Considerations Sternalis syndrome is a constellation of symptoms consisting of midline anterior chest wall pain that can radiate to the retrosternal area and the medial aspect of the arm (Figure 91-1). Sternalis syndrome can mimic the pain of myocardial infarction and is frequently misdiagnosed as such. Sternalis syndrome is a myofascial pain syndrome and is characterized by trigger points in the midsternal area. In contradistinction to costosternal syndrome, the pain of sternalis syndrome is not exacerbated by movement of the chest wall and shoulder. Physical examination reveals myofascial trigger points at the midline over the sternum. Occasionally there is a coexistent trigger point in the pectoralis muscle or sternal head of the sternocleidomastoid muscle. Pain is reproduced with palpation of these trigger points rather than movement of the chest wall and shoulders. A positive “jump sign” is present when these trigger points are stimulated. Trigger points at the lateral border of the scapula may also be present and amenable to injection therapy. Plain radiographs are indicated for all patients with suspected sternalis syndrome to rule out occult bony disease, including metastatic lesions. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, prostate-specific antigen, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the chest is indicated if a retrosternal mass such as a thymoma is suspected. Electromyography is indicated in patients with sternalis syndrome to help rule out cervical radiculopathy or plexopathy, which may be considered because of the referred arm pain. The injection technique presented later serves as both a diagnostic and a therapeutic maneuver.

myofascial trigger points in the sternalis muscle. A positive “jump sign” should be noted when a trigger point is identified. Each trigger point is marked with a sterile marker. Proper preparation with antiseptic solution of the skin overlying the trigger points is then carried out. A sterile syringe containing 1.0 mL of 0.25% preservative-free bupivacaine for each trigger point and 40 mg of methylprednisolone is attached to a 11⁄2-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique each previously marked point is palpated, and the trigger point is reidentified with the gloved finger. The needle is then carefully advanced at this point through the skin

Referred pain Trigger point

Sternalis m.

Clinically Relevant Anatomy The sternalis muscle lies anterior to the sternal end of the pectoralis major muscle. The sternalis muscle runs parallel to the sternum and is not present in all individuals. Some anatomists believe that the sternalis muscle is a developmental abnormality and represents an aberrant portion of pectoralis muscle. The sternalis muscle is innervated by the anterior thoracic nerves.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position with the arms resting comfortably at the patient’s side (see Figure 91-1). The midline of the sternum is identified and is then palpated to identify

Figure 91-1  Proper needle placement for injection of the sternalis muscle.

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and subcutaneous tissues into the trigger point in the underlying sternalis muscle (see Figure 91-1). The needle is then fixed in place, and the contents of the syringe are gently injected. There should be minimal resistance to injection. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. Other trigger points at the lateral border of the sternum and pectoralis major are identified and injected in a similar manner.

Side Effects and Complications The major complication of this injection technique is pneumothorax if the needle is placed too deeply and invades the pleural space. Infection, although rare, can occur if strict aseptic technique is not followed. Approximately 25% of patients complain of a transient increase in pain after this injection technique; the patient should be warned of this.

Clinical Pearls Patients with sternalis syndrome often visit the emergency department fearing that they are having a heart attack. The syndrome also is frequently misdiagnosed as a cervical radiculopathy because of the referred arm pain. Electromyography helps delineate the cause and extent of neural compromise. This injection technique is extremely effective in the treatment of sternalis syndrome. Coexistent costosternal or manubriosternal arthritis also may contribute to anterior chest wall pain and may require additional treatment with a more localized injection of local anesthetic and depot corticosteroid. This technique is a safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Pneumothorax can be avoided if shorter needles are used and the needle is not advanced too deeply. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat as well as gentle range-ofmotion exercises, should be introduced several days after the patient has undergone this injection technique for shoulder pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Baldry P: The chest wall. In Baldry P, editor: Myofascial pain and fibromyalgia syndromes: a clinical guide to diagnosis and management, London, 2001, ChurchillLivingstone, pp 303–327. Dommerholt J, Issa TS: Differential diagnosis: myofascial pain syndrome. In Chaitow L, editor: Fibromyalgia syndrome, ed 2, Oxford, 2003, Churchill Livingstone, pp 149–177. Rachlin ES: Injection of specific trigger points. In Rachlin ES, Rachlin I, editors: Myofascial pain and fibromyalgia, ed 2, St. Louis, 2002, Mosby, pp 259–402. Simons DG: Fibrositis/fibromyalgia: a form of myofascial trigger points? Am J Med 81(3 Suppl 1):93–98, 1986.

Chapter 92 XIPHISTERNAL JOINT INJECTION

Indications and Clinical Considerations The xiphisternal joint can serve as a source of pain that may often mimic pain of cardiac and upper abdominal origin. The xiphisternal joint is susceptible to the development of arthritis, including osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, Reiter syndrome, and psoriatic arthritis. The joint is often traumatized during acceleration-deceleration injuries and blunt trauma to the chest. With severe trauma the joint may fracture, sublux, or dislocate (Figure 92-1). The joint also is subject to invasion by tumor either from primary malignancies, including thymoma, or from metastatic disease. This joint appears to serve as the nidus of pain for xiphodynia syndrome. Xiphodynia syndrome is a constellation of symptoms, including severe intermittent anterior chest wall pain in the region of the xiphoid process, that is made worse with overeating, stooping, and bending. The patient may report a nauseated feeling associated with the pain of xiphodynia syndrome. Physical examination reveals that the pain of xiphodynia syndrome is reproduced with palpation or traction on the xiphoid. The xiphisternal joint may feel swollen. Stooping or bending may reproduce the pain. Coughing may be difficult, and this may lead to inadequate pulmonary toilet in patients who have sustained trauma to the anterior chest wall. The xiphisternal joint and adjacent intercostal muscle also may be tender to palpation. The patient also may note a clicking sensation with movement of the joint. Plain radiographs are indicated for all patients with pain thought to be emanating from the xiphisternal joint to rule out occult bony disease, including tumor (Figure 92-2). On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, prostate-specific antigen, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the joint is indicated if joint instability or an occult mass is suspected. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

to needle-induced trauma if the needle is placed too deeply. The pleural space may be entered if the needle is placed too deeply and laterally; pneumothorax may result.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the affected xiphisternal joint is carried out. A sterile syringe containing 1.0  mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the xiphisternal joint is identified. The xiphisternal joint should be easily palpable as a slight indentation at the point where the xiphoid process attaches to the body of the sternum (Figure 92-3). The needle is then carefully advanced at the center of the xiphisternal joint through the skin

Clinically Relevant Anatomy The xiphoid process articulates with the sternum via the xiphisternal joint (see Figure 92-1). The xiphoid process is a plate of cartilaginous bone that becomes calcified in early adulthood. The xiphisternal joint is strengthened by ligaments but can be subluxed or dislocated by blunt trauma to the anterior chest. The xiphisternal joint is innervated by the T4-T7 intercostal nerves as well as by the phrenic nerve. It is thought that this innervation by the phrenic nerve is responsible for the referred pain associated with xiphodynia syndrome. Posterior to the xiphisternal joint are the structures of the mediastinum. These structures are susceptible

Figure 92-1  Avulsion fracture of the xiphoid process. (From Alagha H, Heyes F: Avulsion fracture of xiphoid process, Inj Extra 36:295–296, 2005.)

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and subcutaneous tissues, with a slight cephalad trajectory into proximity with the joint (see Figure 92-3). If bone is encountered, the needle is withdrawn out of the periosteum. After the needle is in proximity to the joint, 1 mL of solution is gently injected. There should be limited resistance to injection. If significant resistance is encountered, the needle should be withdrawn slightly until the

injection proceeds with only limited resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is pneumothorax if the needle is placed too laterally or deeply and invades the pleural space. Infection, although rare, can occur if strict aseptic technique is not followed. Trauma to the contents of the mediastinum remains an ever-present possibility; the risk of this complication can be greatly decreased if the clinician pays close attention to accurate needle placement.

Clinical Pearls

Figure 92-2  Lateral radiograph demonstrating abnormal xiphoid process angle of 135 degrees in patient with xiphodynia. (From Maigne JY, Vareli M, Rousset P, Cornelis P: Xiphodynia and prominence of the xyphoid process. Value of xiphosternal angle measurement: three case reports, Joint Bone Spine 77:474–476, 2010.)

Patients with pain emanating from the xiphisternal joint often attribute their pain symptoms to a heart attack or ulcer disease. Reassurance is required, although it should be remembered that this musculoskeletal pain syndrome, ulcer disease, and coronary artery disease all can coexist. Tietze syndrome—painful enlargement of the upper costochondral cartilage associated with viral infections—can be confused with xiphisternal syndrome, although both respond to the just-described injection technique. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat as well as gentle range-of-motion exercises, should be introduced several days after the patient undergoes this injection technique for xiphisternal joint pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique. Laboratory evaluation for collagen vascular disease is indicated for patients with xiphisternal joint pain with other joints involved.

Arthritic and inflamed joint Xiphoid process

Figure 92-3  Proper needle placement for intraarticular injection of the xiphisternal joint.

92  •  Xiphisternal Joint Injection        273 SUGGESTED READINGS Howell J: Xiphoidynia: an uncommon cause of exertional chest pain, Am J Emerg Med 8:176, 1990. Howell JM: Xiphodynia: a report of three cases, J Emerg Med 10:435–438, 1992. Ramamurthy S: Chronic chest wall pain. In Ramamurthy S, Rogers JN, Alanmanou E, editors: Decision making in pain management, ed 2, Philadelphia, 2006, Mosby, pp 176–177.

Stochkendahl MJ, Christensen HW: Chest pain in focal musculoskeletal disorders, Med Clin North Am 94:259–273, 2010. Waldman SD: Costosternal syndrome. Pain review, Philadelphia, 2009, Saunders, pp 246–247.

Chapter 93 INJECTION TECHNIQUE FOR SLIPPING RIB SYNDROME Indications and Clinical Considerations Slipping rib syndrome is a constellation of symptoms, including severe knifelike pain emanating from the lower costal cartilages associated with hypermobility of the anterior end of the lower costal cartilages. The tenth rib is most commonly involved, but the eighth and ninth ribs also can be affected. This syndrome is also known as rib-tip syndrome. Slipping rib syndrome is almost always associated with trauma to the costal cartilage of the lower ribs. These cartilages often are traumatized during accelerationdeceleration injuries and blunt trauma to the chest. With severe trauma the cartilage may sublux or dislocate from the ribs. Patients with slipping rib syndrome also may report a clicking sensation with movement of the affected ribs and associated cartilage. Physical examination reveals that the patient will vigorously attempt to splint the affected costal cartilage joints by keeping the thoracolumbar spine slightly flexed. Pain is reproduced with pressure on the affected costal cartilage. Patients with slipping rib syndrome exhibit a positive hooking maneuver test result. The hooking maneuver test is performed by having the patient lie in the supine position with the abdominal muscles relaxed while the clinician hooks his or her fingers under the lower rib cage and pulls gently outward (Figure 93-1). Pain and a clicking or snapping sensation of the affected ribs and cartilage indicate a positive test result. Plain radiographs are indicated for all patients with pain thought to be emanating from the lower costal cartilage and ribs to rule out occult bony disease, including rib fracture and tumor. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, ­prostate-specific antigen, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the affected ribs and cartilage is indicated if joint instability or occult mass is suspected (Figure 93-2). The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

attach to the costal cartilage of the rib directly above. The cartilages of the eleventh and twelfth ribs are called floating ribs because they end in the abdominal musculature (see Figure 93-3). The pleural space and peritoneal cavity may be entered when performing the following injection technique if the needle is placed too deeply and laterally; pneumothorax or damage to the abdominal viscera may result.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the affected costal cartilage and rib is done. A sterile syringe containing 1.0 mL of 0.25% preservative-free bupivacaine for each joint to be injected and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the distal rib and costal cartilage are identified. The lower margin of each affected distal rib is identified and marked with a sterile marker. The needle is then carefully advanced at the point marked through the skin and subcutaneous tissues until the needle tip impinges on the periosteum of the underlying rib (see Figure 93-3). The needle is then withdrawn back into the subcutaneous tissues and “walked” inferiorly off the inferior rib margin. The needle should be advanced just beyond the inferior rib margin, but no further or pneumothorax or damage to the abdominal viscera could result. After careful

Hooking maneuver

Clinically Relevant Anatomy The cartilage of the true ribs articulates with the sternum via the costosternal joints (Figure 93-3). The cartilage of the first rib articulates directly with the manubrium of the sternum and is a synarthrodial joint that allows a limited gliding movement. The cartilage of the second through sixth ribs articulates with the body of the sternum via true arthrodial joints. These joints are surrounded by a thin articular capsule. The costosternal joints are strengthened by ligaments. The eighth, ninth, and tenth ribs 274

Figure 93-1  Hooking maneuver for diagnosis of slipping rib syndrome.

93  •  Injection Technique for Slipping Rib Syndrome        275

B

A

D

C

E

Figure 93-2  Rib hemangioma in a 50-year-old woman with a palpable chest wall nodule. A, Frontal chest radiograph shows a sclerotic lesion within the left anterior fourth rib. B, Axial thoracic computed tomography (CT) scan shows a lytic component, with prominent spicules of bone radiating from the center of the lesion. C, Axial T1-weighted, D, axial T2-weighted, and, E, contrast-enhanced T1-weighted images show decreased signal on T1-weighted images, with mixed signal intensity (central areas of low signal related to internal bone) and intense contrast enhancement, the latter sparing the radiating spicules of bone. (From Lee TJ, Collins J: MR Imaging evaluation of disorders of the chest wall, Magn Reson Imaging Clin N Am 16:355–379, 2008.)

aspiration to ensure that the needle tip is not in an intercostal vein or artery, 1 mL of solution is gently injected. There should be limited resistance to injection. If significant resistance is encountered, the needle should be withdrawn slightly until the injection proceeds with only limited resistance. This procedure is repeated for each affected rib and associated cartilage. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is pneumothorax or damage to the abdominal viscera if the needle is placed too medially or deeply and invades the pleural space or peritoneal cavity. Infection, although rare, can occur if strict aseptic technique is not followed. The risk of these complications can be greatly decreased if the clinician pays close attention to accurate needle placement. Because this technique blocks the intercostal nerve corresponding to the rib injected, the patient should be warned to expect some transient numbness of the chest and abdominal wall, as well as bulging of the abdomen in the subcostal region owing to blockade of the motor innervation to these muscles.

Clinical Pearls Patients with pain emanating from slipping rib often attribute their pain symptoms to a gallbladder attack or ulcer disease. Reassurance is required, although it should be remembered that this musculoskeletal pain syndrome and intraabdominal disease can coexist. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient undergoes this injection technique for slipping rib syndrome. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique. Laboratory evaluation for collagen vascular disease is indicated for patients with costal cartilage pain with other joints involved.

276        SECTION 5  •  Chest Wall, Trunk, Back, and Abdomen SUGGESTED READINGS Baldry P: The anterior abdominal wall and pelvic floor. In Baldry P, editor: Myofascial pain and fibromyalgia syndromes: a clinical guide to diagnosis and management, London, 2001, Churchill Livingstone, pp 329–348. David D: Differential diagnosis of chest pain, Dis Mon 4:1–59, 1958. Griffin JG: Rib dysfunction. In Ramamurthy S, Rogers JN, Alanmanou E, editors: Decision making in pain management, ed 2, Philadelphia, 2006, Mosby, pp 182–183. Stochkendahl MJ, Christensen HW: Chest pain in focal musculoskeletal disorders, Med Clin North Am 94:259–273, 2010.

Costal cartilages and ribs disrupted and ragged

10th rib

Figure 93-3  Proper needle placement for the injection for slipping rib syndrome.

Chapter 94 ANTERIOR CUTANEOUS NERVE BLOCK Indications and Clinical Considerations Anterior cutaneous nerve entrapment syndrome is a constellation of symptoms, including severe, knifelike pain emanating from the anterior abdominal wall associated with point tenderness over the affected anterior cutaneous nerve. The pain radiates medially to the linea alba but in almost all cases does not cross the midline. Anterior cutaneous nerve entrapment syndrome occurs most commonly in young females. The patient can often localize the source of pain quite accurately by pointing to the spot at which the anterior cutaneous branch of the affected intercostal nerve pierces the fascia of the abdominal wall at the lateral border of the rectus abdominis muscle. It is at this point that the anterior cutaneous branch of the intercostal nerve turns sharply in an anterior direction to provide innervation to the anterior wall (Figure 94-1). The nerve passes through a firm, fibrous ring as it pierces the fascia, and it is at this point that the nerve is subject to entrapment. The nerve is accompanied through the fascia by an epigastric artery and vein. There is the potential for small amounts of abdominal

fat to herniate through this fascial ring and become incarcerated, which results in further entrapment of the nerve. Contraction of the abdominal muscles puts additional pressure on the nerve and may elicit sudden, sharp, lancinating pain in the distribution of the affected anterior cutaneous nerve. Physical examination reveals that the patient will attempt to splint the affected nerve by keeping the thoracolumbar spine slightly flexed to avoid increasing tension on the abdominal musculature. Pain is reproduced with pressure on the anterior cutaneous branch of the affected intercostal nerve at the point at which the nerve pierces the fascia of the abdominal wall at the lateral border of the rectus abdominis muscle. Having the patient do a sit-up often reproduces the pain, as will a Valsalva maneuver. Plain radiographs are indicated for all patients with pain thought to be emanating from the lower costal cartilage and ribs to rule out occult bony disease, including rib fracture and tumor. Radiographic evaluation of the gallbladder is indicated if cholelithiasis is suspected. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, rectal examination with stool guaiac,

Fat pad Fibrotic band Anterior cutaneous branch, thoracic n. Intraabdominal pressure

Rectus abdominis m.

Transverse abdominis m. Internal oblique m. External oblique m. Carrico & Shavell

Figure 94-1  Clinically relevant anatomy and pathophysiology of anterior cutaneous nerve entrapment syndrome.

277

278        SECTION 5  •  Chest Wall, Trunk, Back, and Abdomen Double layer

Subcutaneous tissue

A

Loops of bowel

Subcutaneous tissue

Double layer

Medial

Lateral

Medial

Rectus abdominis muscle

Lateral

Rectus abdominis muscle

B

Figure 94-2  A, The double-layer sign indicating presence of the aponeurosis of the transversus abdominis and transversalis fascia in transverse view. B, Closer to the midline, loops of bowel are visualized. (From Gray AT: Atlas of ultrasound-guided regional anesthesia, Philadelphia, 2009, Elsevier.)

sedimentation rate, and antinuclear antibody testing. Computed tomography of the abdomen is indicated if intraabdominal disease or an occult mass is suspected. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The intercostal nerves arise from the anterior division of the thoracic paravertebral nerve. A typical intercostal nerve has four major branches. The first branch is the unmyelinated postganglionic fibers of the gray rami communicantes, which interface with the sympathetic chain. The second branch is the posterior cutaneous branch, which innervates the muscles and skin of the paraspinal area. The third branch is the lateral cutaneous division, which arises in the anterior axillary line and provides the majority of the cutaneous innervation of the chest and abdominal wall. The fourth branch is the anterior cutaneous branch, which supplies innervation to the midline of the chest and abdominal wall (see Figure 94-1). The anterior cutaneous branch pierces the fascia of the abdominal wall at the lateral border of the rectus abdominis muscle (Figure 94-2). The nerve turns sharply in an anterior direction to provide innervation to the anterior wall. The nerve passes through a firm fibrous ring as it pierces the fascia, and it is at this point that the nerve is subject to entrapment. The nerve is accompanied through the fascia by an epigastric artery and vein. Occasionally the terminal branches of a given intercostal nerve may actually cross the midline to provide sensory innervation to the contralateral chest and abdominal wall. The twelfth nerve is called the subcostal nerve and is unique in that it gives off a branch to the first lumbar nerve, thus contributing to the lumbar plexus.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the lateral position, and proper preparation with antiseptic solution of the skin overlying the affected

anterior cutaneous branch of the intercostal nerve is carried out. This usually is at approximately the anterior axillary line. A sterile syringe containing 3.0 mL of 0.25% preservative-free bupivacaine for each nerve to be injected and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle with the use of strict aseptic technique. With strict aseptic technique, the rib of the affected intercostal nerve is identified. The lower margin of each affected rib is identified and marked with a sterile marker. The needle is then carefully advanced at the point marked through the skin and subcutaneous tissues until the needle tip impinges on the periosteum of the underlying rib. The needle is then withdrawn back into the subcutaneous tissues and “walked” inferiorly off the inferior rib margin (see Figure 94-1). The needle should be advanced just beyond the inferior rib margin, but no farther or pneumothorax or damage to the abdominal viscera could result. After careful aspiration to ensure that the needle tip is not in an intercostal vein or artery, 1 mL of solution is gently injected. There should be limited resistance to injection. If significant resistance is encountered, the needle should be withdrawn slightly until the injection proceeds with only limited resistance. This procedure is repeated for each affected nerve. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is pneumothorax or damage to the abdominal viscera if the needle is placed too deeply and invades the pleural space or peritoneal cavity. Infection, although rare, can occur if strict aseptic technique is not followed. These complications can be greatly decreased if the clinician pays close attention to accurate needle placement. Because this technique blocks the intercostal nerve corresponding to the rib injected, the patient should be warned to expect some transient numbness of the chest and abdominal wall, as well as bulging of the abdomen in the subcostal region owing to blockade of the motor innervation to these muscles.

94  •  Anterior Cutaneous Nerve Block        279

Clinical Pearls Patients with pain emanating from anterior cutaneous nerve entrapment syndrome often attribute their pain symptoms to a gallbladder attack or ulcer disease. Reassurance is required, although it should be remembered that this musculoskeletal pain syndrome and intraabdominal disease can coexist. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for anterior cutaneous nerve entrapment syndrome. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique. Radiographic evaluation for intraabdominal disease is indicated for patients with anterior abdominal pain of unclear cause.

SUGGESTED READINGS Ellis H: Anterior abdominal wall, Anaesth Intensive Care Med 7:36–37, 2006. Rahn DD, Phelan JN, Roshanravan SM, et  al: Anterior abdominal wall nerve and vessel anatomy: clinical implications for gynecologic surgery, Am J Obstet Gynecol 202:234, e1-234.e5, 2010. Vishy M: Anatomy of the anterior abdominal wall and groin, Surgery (Oxford) 27:251–254, 2009. Waldman SD: Anterior cutaneous nerve block. Pain review, Philadelphia, 2009, Saunders, pp 497–498.

Chapter 95 INJECTION TECHNIQUE FOR LUMBAR MYOFASCIAL PAIN SYNDROME Indications and Clinical Considerations The muscles of the back are particularly susceptible to the development of myofascial pain syndrome. Flexion-extension injuries to the back or repeated microtrauma secondary to improper lifting and bending may result in the development of myofascial pain in the muscles of the back. Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body. The sine qua non of myofascial pain syndrome is the finding of myofascial trigger points on physical examination. Although these trigger points are generally localized to the regional part of the body affected, the pain of myofascial pain syndrome often is referred to other areas. This referred pain often is misdiagnosed or attributed to other organ systems, leading to extensive evaluations and ineffective treatment. Patients with myofascial pain syndrome involving the muscles of the low back often have referred pain into the hips, sacroiliac joint, and buttocks. The trigger point is the pathognomonic lesion of myofascial pain and is thought to be a result of microtrauma to the affected muscles. This pathologic lesion is characterized by a local point of exquisite tenderness in affected muscle. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain but also referred pain. In addition to this local and referred pain, there often is an involuntary withdrawal of the stimulated muscle that is called a “jump sign.” This jump sign is also characteristic of myofascial pain syndrome. Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. In spite of this consistent physical finding in patients with myofascial pain syndrome, the pathophysiology of the myofascial trigger point remains elusive, although many theories have been advanced. Common to all of these theories is the belief that trigger points are a result of microtrauma to the affected muscle. This microtrauma may occur as a single injury to the affected muscle or as a result of repetitive microtrauma or chronic deconditioning of the agonist and antagonist muscle unit. In addition to muscle trauma, a variety of other factors seem to predispose the patient to develop myofascial pain syndrome. The weekend athlete who subjects his or her body to unaccustomed physical activity often develops myofascial pain syndrome. The poor posture of someone sitting at a computer keyboard or watching television also has been implicated as a predisposing factor to the development of myofascial pain syndrome. Previous injuries may result in abnormal muscle function and predispose to the subsequent development of myofascial pain syndrome. All of these predisposing factors may be intensified if the patient also has 280

poor nutritional status or coexisting psychological or behavioral abnormalities, including chronic stress and depression. The muscles of the low back seem to be particularly susceptible to stressinduced myofascial pain syndrome. Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or in conjunction with other painful conditions, including radiculopathy and chronic regional pain syndromes. Psychological or behavioral abnormalities, including depression, frequently coexist with the muscle abnormalities associated with myofascial pain syndrome. Treatment of these psychological and behavioral abnormalities must be an integral part of any successful treatment plan for myofascial pain syndrome.

Clinically Relevant Anatomy The muscles of the back work together as a functional unit to stabilize and allow coordinated movement of the low back and allow one to maintain an upright position. Trauma to an individual muscle can result in dysfunction of the entire functional unit. The rhomboids, latissimus dorsi, iliocostalis lumborum, multifidus, psoas, and quadratus lumborum muscles are frequent sites of myofascial pain syndrome. The points of origin and attachments of these muscles are particularly susceptible to trauma and the subsequent development of myofascial trigger points (Figure 95-1). Injection of these trigger points serves as both a diagnostic and a therapeutic maneuver.

Technique Careful preparation of the patient before trigger point injection helps to optimize results. Trigger point injections are directed at the primary trigger point, rather than in the area of referred pain. It should be explained to the patient that the goal of trigger point injection is to block the trigger of the persistent pain and thus, it is hoped, provide long-lasting relief. It is important that the patient understand that for most patients with myofascial pain syndrome, more than one treatment modality is required for optimal pain relief. The use of the prone or lateral position when identifying and marking trigger points, as well as when performing the actual trigger point injection, helps decrease the incidence of vasovagal reactions. The skin overlying the trigger point should always be prepared with antiseptic solution before injection to avoid infection. After the goals of trigger point injection have been explained to the patient and proper preparation of the patient has been carried

95  •  Injection Technique for Lumbar Myofascial Pain Syndrome        281

report a transient increase in pain after injection of trigger points. If long needles are used, pneumothorax or damage to the retroperitoneal organs, including the kidneys, also may occur. Trapezius m.

Erector spinae m.

Latissimus dorsi m.

Serratus posterior m.

Trigger points

Carrico & Shavell

Figure 95-1  Common point for injection for lumbar myofascial pain syndrome.

out, the trigger point to be injected is reidentified by palpation with the sterilely gloved finger. A syringe containing 10 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 25-gauge needle of a length adequate to reach the trigger point. For the deeper muscles of posture in the low back, a 3½-inch needle is required. A volume of 0.5 to 1.0 mL of solution is then injected into each trigger point. A series of two to five treatment sessions may be required to completely abolish the trigger point; the patient should be informed of this.

Side Effects and Complications The proximity to the spinal cord and exiting nerve roots makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing interventional pain management techniques. Many patients also

Clinical Pearls Trigger point injections are an extremely safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of trigger point injection are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after trigger point injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid pneumothorax when injecting trigger points in proximity to the underlying pleural space. The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators believe that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as amitriptyline and nortriptyline are good first choices and should be given as a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow. Pregabalin, duloxetine, and milnacipran have also been shown to be of benefit in the treatment of myofascial pain syndromes.

SUGGESTED READINGS Baldry P: Acupuncture treatment of fibromyalgia and myofascial pain. In Chaitow L, editor: Fibromyalgia syndrome, ed 3, Oxford, 2010, Churchill Livingstone, pp 145–159. LeBlanc KE, LeBlanc LL: Musculoskeletal disorders, Prim Care 37:389–406, 2010. Marsh W: Milnacipran. In Enna SJ, Bylund DB, editors: xPharm: the comprehensive pharmacology reference, New York, 2008, Elsevier, pp 1–4 . Partanen JV, Ojala TA, Arokoski JP: Myofascial syndrome and pain: a neurophysiological approach, Pathophysiology 17:19–28, 2010.

SECTION 6  •  Hip and Pelvis

Chapter 96 INTRAARTICULAR INJECTION OF THE HIP JOINT Indications and Clinical Considerations The hip joint is susceptible to the development of arthritis from a variety of conditions that have in common the ability to damage the joint cartilage. Osteoarthritis of the joint is the most common form of arthritis that results in hip joint pain (Figure 96-1). ­However, rheumatoid arthritis and posttraumatic arthritis also are common causes of hip pain secondary to arthritis. Less common causes of arthritis-induced hip pain include the collagen

vascular diseases, infection, villonodular synovitis, and Lyme disease. Acute infectious arthritis usually is accompanied by significant systemic symptoms, including fever and malaise, and should be easily recognized by the astute clinician and treated appropriately with culture and antibiotics rather than injection therapy. The collagen vascular diseases generally manifest as a polyarthropathy rather than a monoarthropathy limited to the hip joint, although hip pain secondary to collagen vascular disease responds exceedingly well to the intraarticular injection technique described later. The majority of patients with hip pain secondary to osteoarthritis and posttraumatic arthritis pain report pain that is localized around the hip and upper leg. Activity makes the pain worse; rest and heat provide some relief. The pain is constant and is characterized as aching. The pain may interfere with sleep. Some patients note a grating or popping sensation with use of the joint, and crepitus may be present on physical examination. In addition to the just-mentioned pain, patients with arthritis of the hip joint often experience a gradual decrease in functional ability with decreasing hip range of motion, making simple everyday tasks such as walking, climbing stairs, and getting in and out of cars quite difficult. With continued disuse, muscle wasting may occur and a “frozen hip” caused by adhesive capsulitis may develop. Plain radiographs are indicated for all patients with hip pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the hip is indicated if aseptic necrosis or occult mass or tumor is suggested (Figure 96-2).

Clinically Relevant Anatomy

Figure 96-1  Osteoarthritis of the hip: superolateral migration pattern. Developmental dysplasia of the hip with cyst (or ganglion) formation. In this 40-year-old woman, a frontal radiograph shows a dysplastic hip, flattening and vertical inclination of the acetabulum, lateral displacement with uncovering of the femoral head, bone fragmentation, joint space loss, and a septated acetabular cyst (or ganglion). (From Resnick D: Bone and joint imaging, ed 3, Philadelphia, 2005, Saunders.)

282

The rounded head of the femur articulates with the cup-shaped acetabulum of the hip (see Figure 96-1). The articular surface is covered with hyaline cartilage, which is susceptible to arthritis. The rim of the acetabulum is composed of a fibrocartilaginous layer called the acetabular labrum, which is susceptible to trauma should the femur be subluxed or dislocated. The joint is surrounded by a capsule that allows the wide range of motion of the hip joint. The joint capsule is lined with a synovial membrane that attaches to the articular cartilage. This membrane gives rise

96  •  Intraarticular Injection of the Hip Joint        283

Inguinal ligament Inflamed and arthritic joint Femoral artery

Figure 96-2  Avascular necrosis (AVN) of both femoral heads in a 41-year-old patient receiving corticosteroids for long-standing systemic lupus erythematosus. Coronal T1-weighted magnetic resonance image shows focal crescentic areas of decreased marrow signal typical of AVN in both femoral heads. (From Haaga JR, Lanzieri CF, Gilkeson RC: CT and MR imaging of the whole body, ed 4, Philadelphia, 2002, Mosby.)

to synovial tendon sheaths and bursae that are subject to inflammation. The hip joint is innervated by the femoral, obturator, and sciatic nerves. The major ligaments of the hip joint include the iliofemoral, pubofemoral, ischiofemoral, and transverse acetabular ligaments, which provide strength to the hip joint. The muscles of the hip and their attaching tendons are susceptible to trauma and to wear and tear from overuse and misuse.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the hip, subacromial region, and joint space is done. A sterile syringe containing 4.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 2-inch, 25-gauge needle using strict aseptic technique. The femoral artery is identified. At a point approximately 2 inches lateral to the femoral artery just below the inguinal ligament, the hip joint space is identified. The needle is then carefully advanced through the skin and subcutaneous tissues through the joint capsule into the joint (Figure 96-3). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected superiorly and slightly more medially. After the joint space has been entered, the contents of the syringe are gently injected. There should be

Carrico & Shavell

Figure 96-3  Relationship between the femoral artery, inguinal ligament, and the hip joint.

little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced slightly into the joint space until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. Ultrasound guidance for needle placement may be useful if the anatomic landmarks necessary to safely perform this technique are hard to identity (Figure 96-4).

Side Effects and Complications The major complication of intraarticular injection of the hip is infection, which should be exceedingly rare if strict aseptic technique is followed. Approximately 25% of patients report a transient increase in pain after intraarticular injection of the hip joint; the patient should be warned of this.

284        SECTION 6  •  Hip and Pelvis Representation of needle Ligamentum teres

Iliopsoas Iliofemoral ligament Head of femur

A

B

Figure 96-4  A, Hip injection: anterior longitudinal approach. The transducer is aligned parallel to the neck of the femur. B, Hip injection: anterior longitudinal approach. Ultrasound image with representation of needle targeting the anterior synovial recess located at the neck of the femur. (From Cheng PH, Kim HJ, Ottestad E, Narouze S: Ultrasound-guided injections of the knee and hip joints, Tech Reg Anesth Pain Manag 13:191–197, 2009.)

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to the just-mentioned causes of arthritis of the hip joint. Coexistent bursitis and tendinitis also may contribute to hip pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation (methylprednisolone). This technique is a safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for hip pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Cheng PH, Kim HJ, Ottestad E, Narouze S: Ultrasound-guided injections of the knee and hip joints, Tech Reg Anesth Pain Manag 13:191–197, 2009. Nallamshetty L, Buchowski JM, Nazarian LA, et al: Septic arthritis of the hip following cortisone injection: case report and review of the literature, Clin Imaging 27:225–228, 2003. Villoutreix C, Pham T, Tubach F, et al: Intraarticular glucocorticoid injections in rapidly destructive hip osteoarthritis, Joint Bone Spine 73:66–71, 2006. Waldman SD: Intra-articular injection of the hip joint. Pain review, Philadelphia, 2009, Saunders, pp 546–547.

Chapter 97 ADDUCTOR TENDON INJECTION

Indications and Clinical Considerations

tennis ball between the patient’s knees and asks the patient to hold it there with gentle pressure from the knees (Figure 97-1, A). The patient is then instructed to quickly squeeze the ball between the knees as hard as possible. Patients with adductor tendinitis will reflexively abduct the affected extremity owing to the pain of forced adduction, thereby causing the ball to drop to the floor (Figure 97-1, B). Tendinitis of the musculotendinous unit of the hip frequently coexists with bursitis of the associated bursae of the hip joint, creating additional pain and functional disability. In addition to the just-mentioned pain, patients with adductor tendinitis often experience a gradual decrease in functional ability with decreasing hip range of motion, making simple, everyday tasks such as getting in or out of a car quite difficult. With continued disuse, muscle wasting may occur and an adhesive capsulitis of the hip may develop. Plain radiographs are indicated for all patients with hip pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic

The musculotendinous unit of the hip joint responsible for hip adduction is susceptible to the development of tendinitis from overuse or trauma from stretch injuries. Inciting factors may include the vigorous use of exercise equipment for lower extremity strengthening and acute stretching of the musculotendinous units as a result of sports injuries. The pain of adductor tendinitis is sharp, constant, and severe, with sleep disturbance often reported. The patient may attempt to splint the inflamed tendons by adopting an adductor lurch type of gait (i.e., shifting the trunk of the body over the affected extremity when walking). On physical examination the patient will report pain on palpation of the origins of the adductor tendons. Active resisted adduction reproduces the pain, as does passive abduction. Patients with adductor tendinitis will also exhibit a positive Waldman knee squeeze test result. This test is performed by having the patient sit on the edge of the examination table. The examiner places a

A

B

Figure 97-1  A and B, The Waldman knee squeeze test for adductor tendinitis. (From Waldman SD: Physical diagnosis of pain, Philadelphia, 2005, Saunders.)

285

286        SECTION 6  •  Hip and Pelvis

A

B

C

D

E

F

Figure 97-2  A, Coronal fat-saturated T2-weighted magnetic resonance (MR) image. Bilateral severe adductor longus origin tendinosis (arrows). B, Coronal fat-saturated T2-weighted MR image. Bilateral secondary clefts extending from the pubic symphysis into the adductor attachments, indicating some disruption of the prepubic aponeurotic complex tissue (curved arrows). C, Axial fat-saturated T2-weighted MR image demonstrating bilateral adductor longus tendinosis (arrows). D, Three-dimensional axial fat-saturated T2-weighted MR image. Small tear of the left adductor longus tendon (arrow). E, Sagittal fat-saturated T2-weighted MR image. Small tears of the origin of the left adductor longus tendon (arrow). F, Sagittal fatsaturated T2-weighted MR image. This image demonstrates more severe adductor longus tendinosis that involves the prepubic aponeurotic complex (curved arrow). (From MacMahon PJ, Hogan BA, Shelly MJ, et al: Imaging of groin pain, Magn Reson Imaging Clin N Am 17:655–666, 2009.)

resonance imaging (MRI) of the hip is indicated if tendinitis, aseptic necrosis of the hip, tear of the adductor muscles, or occult mass is suspected (Figures 97-2 and 97-3). The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The adductor muscles of the hip include the gracilis, adductor longus, adductor brevis, and adductor magnus muscles (Figure 97-4). The adductor function of these muscles is innervated by

97  •  Adductor Tendon Injection        287

A

B

Figure 97-3  A, Coronal fat-saturated T2-weighted magnetic resonance (MR) image. Hyperintense signal abnormality at the origin of the right adductor longus tendon (straight arrow) consistent with an acute tear. Chronic tear of left adductor longus as evidenced by thickening and hypointensity with retraction of the tendon and healing with scar formation (curved arrow). B, Axial fat-saturated T2-weighted MR image demonstrating acute right adductor longus tear (arrow). (From MacMahon PJ, Hogan BA, Shelly MJ, et al: Imaging of groin pain, Magn Reson Imaging Clin N Am 17:655-666, 2009.)

Prepubic aponeurotic complex

Pectineus Adductor longus Adductor brevis

Inguinal ligament Symphysis pubis Pectineus m.

Abductor longus m.

Disc Cleft

Hyaline cartilage

Pubic symphysis Obturator externus Figure 97-5  Axial section through the pubic symphysis below the level of the pubic crest, demonstrating the anatomy of the adductor muscles. Note the origin of these muscles from the prepubic aponeurotic complex, which is an extension of the underlying fibrocartilaginous pubic symphysis.

Gracilis m.

Carrico & Shavell

Figure 97-4  Proper needle placement for injection of the adductor tendon.

the obturator nerve, which is susceptible to trauma from pelvic fractures and compression by tumor. The tendons of the adductor muscles of the hip have their origin along the pubis and ischial ramus, and it is at this point that tendinitis frequently occurs (see Figure 97-4; Figure 97-5).

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position with the leg slightly

abducted and externally rotated. This positioning of the lower extremity allows access to the tendinous insertions of the hip adductor muscles. If the patient cannot tolerate this position because of pain and spasm of the adductors, it may be necessary to block the obturator nerve to allow adequate exposure to the origin of the adductor tendons. The origin of the adductor tendons of the hip can be identified at a point 1½ inches lateral from the pubic symphysis along the pubic bone. After the origin of the adductor tendons has been identified, the skin is prepared with antiseptic solution. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. The origin of the adductor tendons is reidentified with the gloved finger. The needle is then carefully advanced perpendicularly to the skin of the affected lower extremity through the skin and subcutaneous tissues until it impinges on bone (see Figure 97-4). The needle is

288        SECTION 6  •  Hip and Pelvis

then withdrawn 1 to 2 mm out of the periosteum of the pubis, and the contents of the syringe are gently injected. There should be slight resistance to injection. If there is significant resistance to injection, the needle tip is probably in the substance of a tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is followed. Trauma to the adductor tendons from the injection itself remains an ever-present possibility. Tendons that are highly inflamed or previously damaged are subject to rupture if they are directly injected. Risk of this complication can be greatly decreased if the clinician uses gentle technique and stops injecting immediately if significant resistance to injection is encountered. Approximately 25% of patients report a transient increase in pain after this injection technique; the patient should be warned of this.

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to the just-mentioned causes of hip pain. Coexistent bursitis and arthritis also may contribute to hip pain and may require additional treatment with a more localized injection of local anesthetic and depot corticosteroid preparation. This technique is a safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for hip pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS MacMahon PJ, Hogan BA, Shelly MJ, et al: Imaging of groin pain, Magn Reson Imaging Clin N Am 17:655–666, 2009. Meyers WC, Greenleaf R, Saad A: Anatomic basis for evaluation of abdominal and groin pain in athletes, Oper Tech Sports Med 13:55–61, 2005. Morelli V, Espinoza L: Groin injuries and groin pain in athletes: part 2, Prim Care 32:185–200, 2005. Morelli V, Weaver V: Groin injuries and groin pain in athletes: part 1, Prim Care 32:163–183, 2005. Topol GA, Reeves KD, Hassanein KM: Efficacy of dextrose prolotherapy in elite male kicking-sport athletes with chronic groin pain, Arch Phys Med Rehabil 86:697–702, 2005.

Chapter 98 ISCHIAL BURSA INJECTION

Indications and Clinical Considerations Bursae are formed from synovial sacs whose purpose is to allow easy sliding of muscles and tendons across one another at areas of repeated movement. These synovial sacs are lined with a synovial membrane that is invested with a network of blood vessels that secrete synovial fluid. Inflammation of the bursa results in an increase in the production of synovial fluid with swelling of the bursal sac. With overuse or misuse, these bursae may become inflamed, enlarged, and on rare occasions infected. Although there is significant intrapatient variability as to the number, size, and location of bursae, anatomists have identified a number of clinically relevant bursae, including the ischial bursa. The ischial bursa lies between the gluteus maximus muscle and the bone of the ischial tuberosity. It may exist as a single bursal sac or in some patients as a multisegmented series of sacs that may be loculated. The ischial bursa is vulnerable to injury from both acute trauma and repeated microtrauma. Acute injuries frequently take the form of direct trauma to the bursa from direct falls onto the buttocks and from overuse, such as prolonged riding of horses or bicycles. Running on uneven or soft surfaces such as sand also may cause ischial bursitis, which is also known as weaver’s bottom. If the inflammation of the ischial bursa becomes chronic, calcification of the bursa may occur. The patient with ischial bursitis frequently reports pain at the base of the buttock with resisted extension off the lower extremity. The pain is localized to the area over the ischial tuberosity, with referred pain noted into the hamstring muscle, which also may develop coexistent tendinitis. Often the patient is unable to sleep on the affected hip and may report a sharp, “catching” sensation when extending and flexing the hip, especially on first awakening. Physical examination may reveal point tenderness over the ischial tuberosity. Passive straight-leg raising and active resisted extension of the affected lower extremity reproduce the pain. Sudden release of resistance during such maneuvers markedly increases the pain (Figure 98-1). Plain radiographs or magnetic resonance imaging (MRI) of the hip may reveal calcification of the bursa and associated structures consistent with chronic inflammation (Figure 98-2). MRI and ultrasound imaging are also indicated to confirm disruption of the hamstring musculotendinous unit and to aid in diagnosis of ischial bursitis. The injection technique described later serves as both a diagnostic and a therapeutic maneuver and also treats hamstring tendinitis.

Clinically Relevant Anatomy The ischial bursa lies between the gluteus maximus muscle and the ischial tuberosity. The action of the gluteus maximus muscle includes the flexion of trunk on thigh when maintaining a sitting

position while riding a horse. This action can irritate the ischial bursa, as can repeated pressure against the bursa that forces it against the ischial tuberosity (Figure 98-3). The hamstring muscles find a common origin at the ischial tuberosity and can be irritated from overuse or misuse. The action of the hamstrings includes flexion of the lower extremity at the knee. Running on soft or uneven surfaces can cause a tendinitis at the origin of the hamstring muscles.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the lateral position with the affected side

Figure 98-1  The resisted hip extension test for ischial bursitis. (From Waldman SD: Physical diagnosis of pain, Philadelphia, 2005, Saunders.)

Figure 98-2  Ischial bursitis: magnetic resonance (MR) imaging. A transaxial T2-weighted (TR/TE, 1500/90) spin-echo MR image shows evidence of bilateral ischial bursitis. (Courtesy J. Dillard, MD, San Diego, Calif; from Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

289

290        SECTION 6  •  Hip and Pelvis

Sciatic nerve Inflamed bursa and tendon

Biceps femoris m. Semitendinosus m.

Figure 98-3  Proper needle placement for injection of the ischial bursa.

up and the affected leg flexed at the knee. Proper preparation with antiseptic solution of the skin overlying the ischial tuberosity is then done. A syringe containing 4.0 mL of 0.25% preservativefree bupivacaine and 40 mg of methylprednisolone is attached to a 11⁄2-inch, 25-gauge needle. The ischial tuberosity is then identified with a sterilely gloved finger. Before needle placement, the patient should be advised to say “there!” as soon as a paresthesia is felt in the lower extremity, indicating that the needle has impinged on the sciatic nerve. Should a paresthesia occur, the needle should be immediately withdrawn and repositioned more medially. The needle is then carefully advanced at that point through the skin, subcutaneous tissues, muscle, and tendon until it impinges on the bone of the ischial tuberosity (see Figure 98-3). Care must be taken to keep the needle in the midline and not to advance it laterally or it could impinge on the sciatic nerve. After careful aspiration and if no paresthesia is present, the contents of the syringe are gently injected into the bursa.

Side Effects and Complications The proximity to the sciatic nerve makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing injection techniques. Many patients also note a transient increase in pain after injection of the just-mentioned bursa and tendons.

Clinical Pearls This injection technique is extremely effective in the treatment of ischial bursitis and hamstring tendinitis. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of this injection technique are related to needleinduced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid trauma to the sciatic nerve. Although the treatment is the same, ischial bursitis can be distinguished from hamstring tendinitis by the fact that ischial bursitis manifests with point tenderness over the ischial bursa, and the tenderness of hamstring bursitis is more diffuse over the upper muscle and tendons of the hamstring. The use of physical modalities, including local heat and gentle stretching exercises, should be introduced several days after the patient has undergone this injection technique. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics, nonsteroidal antiinflammatory agents, and antimyotonic agents such as tizanidine may be used concurrently with this injection technique.

98  •  Ischial Bursa Injection        291 SUGGESTED READINGS Arnold ML: Bursitis: lower extremities. In Ramamurthy S, Rogers JN, ­Alanmanou E, editors: Decision making in pain management, ed 2, Philadelphia, 2006, Mosby, pp 210–211. Hodnett PA, Shelly MJ, MacMahon PJ, et al: MR imaging of overuse injuries of the hip, Magn Reson Imaging Clin N Am 17:667–679, 2009.

Waldman SD: Injection technique for ischial bursitis. In Pain review, Philadelphia, 2009, Saunders, pp 547–549. Waldman SD: The ischial bursa. In Pain review, Philadelphia, 2009, Saunders, pp 138–139. Weiss L, Silver JK, Lennard TA, Weiss JM: Bursae. In Weiss L, Silver JK, ­Lennard TA, Weiss JM, editors: Easy injections, Philadelphia, 2007, Butterworth-­ Heinemann, pp 85–104.

Chapter 99 GLUTEAL BURSA INJECTION

Indications and Clinical Considerations Bursae are formed from synovial sacs whose purpose is to allow easy sliding of muscles and tendons across one another at areas of repeated movement. These synovial sacs are lined with a synovial membrane, which is invested with a network of blood vessels that secrete synovial fluid. Inflammation of the bursa results in an increase in the production of synovial fluid with swelling of the bursal sac. With overuse or misuse, these bursae may become inflamed, enlarged, and on rare occasions infected. Although there is significant intrapatient variability as to the number, size, and location of bursae, anatomists have identified a number of clinically relevant bursae, including the gluteal bursa. The gluteal bursae lie among the gluteal maximus, medius, and minimus muscles, as well as between these muscles and the underlying bone (Figure 99-1). These bursae may exist as a single bursal sac or in some patients as a multisegmented series of sacs that may be loculated. The gluteal bursae are vulnerable to injury from both acute trauma and repeated microtrauma. Acute injuries frequently take the form of direct trauma to the bursa from falls directly onto the buttocks or repeated intramuscular injections, as well as from overuse such as running for long distances, especially on soft or uneven surfaces. If the inflammation of the gluteal bursae becomes chronic, calcification of the bursae may occur.

The patient with gluteal bursitis frequently reports pain at the upper outer quadrant of the buttock and with resisted abduction and extension of the lower extremity. The pain is localized to the area over the upper outer quadrant of the buttock with referred pain noted into the sciatic notch. Often the patient is unable to sleep on the affected hip and may report a sharp, “catching” sensation when extending and abducting the hip, especially on first awakening. Physical examination may reveal point tenderness in the upper outer quadrant of the buttocks. Passive flexion and adduction reproduce the pain, as do active resisted extension and abduction of the affected lower extremity. Sudden release of resistance during such maneuvers markedly increases the pain (Figure 99-2). Plain radiographs of the hip may reveal calcification of the bursa and associated structures consistent with chronic

Inflamed bursa

Gluteus maximus m.

Sciatic nerve

Figure 99-1  The resisted hip abduction test for gluteal bursitis. (From Waldman SD: Physical diagnosis of pain, Philadelphia, 2005, Saunders.)

292

Figure 99-2  Proper needle placement for injection of the gluteal bursa. Note position of the sciatic nerve.

99  •  Gluteal Bursa Injection        293

inflammation. Magnetic resonance imaging (MRI) is indicated if occult mass or tumor of the hip is suspected. The injection technique described later serves as both a diagnostic and therapeutic maneuver.

Clinically Relevant Anatomy There is significant intrapatient variability in the size, number, and location of the gluteal bursae. The gluteal bursae lie among the gluteal maximus, medius, and minimus muscles, as well as between these muscles and the underlying bone. The action of the gluteus maximus muscle includes the rider’s flexion of trunk on thigh when maintaining a sitting position while riding a horse. This action can irritate the gluteal bursae, as can repeated trauma from repetitive activity, including running.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the lateral position with the affected side up and the affected leg flexed at the knee. Proper preparation with antiseptic solution of the skin overlying the upper outer quadrant of the buttocks is then done. A syringe containing 4.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 3½-inch, 25-gauge needle. The point of maximal tenderness within the upper outer quadrant of the buttocks is then identified with a sterilely gloved finger. Before needle placement, the patient should be advised to say “there!” immediately if a paresthesia into the lower extremity is felt, indicating that the needle has impinged on the sciatic nerve. Should a paresthesia occur, the needle should be immediately withdrawn and repositioned more medially. The needle is then carefully advanced perpendicular to the skin at the previously identified point until it impinges on the wing of the ilium (see Figure 99-1). Care must be taken to keep the needle medial and not to advance it laterally or it could impinge on the sciatic nerve. After careful aspiration and if no paresthesia is present, the contents of the syringe are gently injected into the bursa. There should be minimal resistance to injection.

Side Effects and Complications The proximity to the sciatic nerve makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing injection techniques. Many patients also note a transient increase in pain after injection of the just-mentioned bursa.

Clinical Pearls This injection technique is extremely effective in the treatment of gluteal bursitis. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of this injection technique are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid trauma to the sciatic nerve. The use of physical modalities, including local heat and gentle stretching exercises, should be introduced several days after the patient has undergone this injection technique. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics, nonsteroidal antiinflammatory agents, and antimyotonic agents such as tizanidine may be used concurrently with this injection technique.

SUGGESTED READINGS Arnold ML: Bursitis: lower extremities. In Ramamurthy S, Rogers JN, Alanmanou E, editors: Decision making in pain management, ed 2, Philadelphia, 2006, Mosby, pp 210–211. Hodnett PA, Shelly MJ, MacMahon PJ, et al: MR imaging of overuse injuries of the hip, Magn Reson Imaging Clin N Am 17:667–679, 2009. Waldman SD: Injection technique for gluteal bursitis. In Pain review, Philadelphia, 2009, Saunders, pp 549–551. Waldman SD: The gluteal bursa. In Pain review, Philadelphia, 2009, Saunders, pp 139–140.

Chapter 100 PSOAS BURSA INJECTION

Indications and Clinical Considerations Bursae are formed from synovial sacs whose purpose is to allow easy sliding of muscles and tendons across one another at areas of repeated movement. These synovial sacs are lined with a synovial membrane, which is invested with a network of blood vessels that secrete synovial fluid. Inflammation of the bursa results in an increase in the production of synovial fluid with swelling of the bursal sac. With overuse or misuse, these bursae may become inflamed, enlarged, and on rare occasions infected. Although there is significant intrapatient variability as to the number, size, and location of bursae, anatomists have identified a number of clinically relevant bursae, including the psoas bursa. The psoas bursa lies medially in the femoral triangle between the psoas tendon and the anterior aspect of the neck of the femur (Figure 100-1). This bursa may exist as a single bursal sac or in some patients as a multisegmented series of sacs that may be loculated. The psoas bursa is vulnerable to injury from both acute trauma and repeated microtrauma. Acute injuries frequently take the form of direct trauma to the bursa from seat-belt injuries as well as overuse injuries from activities that require repeated hip flexion, such as javelin throwing and ballet. If the inflammation of the psoas bursa becomes chronic, calcification of the bursa may occur. The patient with psoas bursitis frequently reports pain in the groin. The pain is localized to the area just below the crease of the groin anteriorly, with referred pain noted into the hip joint. Often the patient is unable to sleep on the affected hip and may note a sharp, “catching” sensation with range of motion of the hip.

Figure 100-1  Location of needle placement for injection of the psoas bursa.

294

Physical examination may reveal point tenderness in the upper thigh just below the crease of the groin. Passive flexion, adduction, and abduction, as well as active resisted flexion and adduction of the affected lower extremity, reproduce the pain. Sudden release of resistance during this maneuver markedly increases the pain (Figure 100-2). Plain radiographs, computed tomography (CT), magnetic resonance imaging (MRI), or ultrasound imaging of the hip and pelvis may reveal calcification of the bursa and associated structures consistent with chronic inflammation (Figures 100-3 and 100-4). MRI is indicated if occult mass or tumor of the hip or groin is

Figure 100-2  The resisted hip adduction test for iliopsoas bursitis. (From Waldman SD: Physical diagnosis of pain, Philadelphia, 2005, Saunders.)

100  •  Psoas Bursa Injection        295

A

B

C Figure 100-3  Iliopsoas bursitis. A progressively enlarging, painful mass developed in the left inguinal region in a 64-year-old man with longstanding rheumatoid arthritis. A coronal T2-weighted spin-echo magnetic resonance (MR) image (TR/TE, 2000/90) (A) shows the cyst (solid arrows) medial to the psoas muscle (arrowheads) and lateral to the external iliac vessels (open arrow). A transaxial T2-weighted spin-echo MR image (TR/TE, 2000/90) (B) again reveals the cyst (solid arrow) with an opening (arrowhead) to a fluid-filled hip joint (open arrows). At surgery, a grossly dilated fluid-filled iliopsoas bursa with chronically inflamed synovium was identified. C, Subacromial bursitis. In this 34-year-old woman, a transaxial T2-weighted spin-echo MR image (TR/TE, 1800/70) shows the distended bursa (arrows) containing fluid of high signal intensity and areas of low signal intensity, perhaps representing fibrous synovial nodules. (A and B from Lupetin AR, Daffner RH: Rheumatoid iliopsoas bursitis: MR findings, J Comput Assist Tomogr 14:1035, 1990; C courtesy J. Milsap, Jr, MD, Atlanta, Ga.)

suspected. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The psoas bursa lies between the psoas tendon and the anterior aspect of the femoral neck. The bursa lies deep to the femoral artery, vein, and nerve. The psoas muscle arises from the transverse processes, vertebral bodies, and intervertebral disks of the T12-L5 vertebrae and inserts into the lesser trochanter of the femur. The psoas muscle flexes the thigh on the trunk or, if the thigh is fixed, flexes the trunk on the thigh, as when moving from a supine to sitting position (see Figure 100-1). This action can irritate the psoas bursa, as can repeated trauma from repetitive activity, including running up stairs or overuse of exercise equipment for lower-extremity strengthening. The psoas muscle is innervated by the lumbar plexus.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and the pulsation of the femoral artery at the midpoint of the inguinal ligament is identified. At a point 2½ inches down and 2½ inches lateral to these femoral arterial pulsations lies the entry point for the needle. This point should be at the medial edge of the sartorius muscle. Proper preparation with antiseptic solution of the skin overlying this point is then carried out. A syringe containing 9.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 3½-inch, 25-gauge needle. Before needle placement, the patient should be advised to say “there!” as soon as a paresthesia into the lower extremity is felt, indicating that the needle has impinged on the femoral nerve. Should a paresthesia occur, the needle should be immediately

296        SECTION 6  •  Hip and Pelvis

aspiration for blood and if no paresthesia is present, the contents of the syringe are gently injected into the bursa. There should be minimal resistance to injection.

Side Effects and Complications The proximity to the femoral artery, vein, and nerve makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing injection techniques. Many patients also report a transient increase in pain after injection of the just-mentioned bursa.

Clinical Pearls

Figure 100-4  Axial postcontrast computed tomography image shows a distended iliopsoas bursa on the left (arrow), anterior to the left hip. (From MacMahon PJ, Hogan BA, Shelly MJ, et  al: Imaging of groin pain, Magn Reson Imaging Clin N Am 17:655-666, 2009.)

Psoas major m. Femoral n. Femoral a. Femoral v. Inflamed psoas bursa Psoas major m.

This injection technique is extremely effective in the treatment of psoas bursitis. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of this injection technique are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. Special care must be taken to avoid trauma to the femoral nerve. The use of physical modalities, including local heat and gentle stretching exercises, should be introduced several days after the patient has undergone this injection technique. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS

Carrico & Shavell

Figure 100-5  Proper needle placement for injection of the psoas bursa.

withdrawn and repositioned more laterally. The needle is then carefully advanced through the previously identified point at a 45-degree angle medially and cephalad to allow the needle to safely pass beneath the femoral artery, vein, and nerve. The needle is advanced very slowly to avoid trauma to the femoral nerve until it hits the bone of the femoral neck (Figure 100-5). The needle is then withdrawn back out of the periosteum and, after careful

Arnold ML: Bursitis: lower extremities. In Ramamurthy S, Rogers JN, ­Alanmanou E, editors: Decision making in pain management, ed 2, Philadelphia, 2006, Mosby, pp 210–211. Hochman MG, Ramappa AJ, Newman JS, Farraher SW: Imaging of tendons and bursae. In Weissman BN, editor: Imaging of arthritis and metabolic bone disease, Philadelphia, 2009, Saunders, pp 196–238. Hodnett PA, Shelly MJ, MacMahon PJ, et al: MR imaging of overuse injuries of the hip, Magn Reson Imaging Clin N Am 17:667–679, 2009. MacMahon PJ, Hogan BA, Shelly MJ, et al: Imaging of groin pain, Magn Reson Imaging Clin N Am 17:655–666, 2009. Shabshin N, Rosenberg ZS, Cavalcanti CF: MR Imaging of iliopsoas musculotendinous injuries, Magn Reson Imaging Clin N Am 13:705–716, 2005. Waldman SD: Injection technique for psoas bursitis. Pain review, Philadelphia, 2009, Saunders, pp 551–552. Weiss L, Silver JK, Lennard TA, Weiss JM: Bursae. In Weiss L, Silver JK, ­Lennard TA, Weiss JM, editors: Easy injections, Philadelphia, 2007, Butterworth-­ Heinemann, pp 85–104.

Chapter 101 ILIOPECTINEAL BURSA INJECTION

Indications and Clinical Considerations Bursae are formed from synovial sacs whose purpose is to allow easy sliding of muscles and tendons across one another at areas of repeated movement. These synovial sacs are lined with a synovial membrane that is invested with a network of blood vessels that secrete synovial fluid. Inflammation of the bursa results in an increase in the production of synovial fluid with swelling of the bursal sac. With overuse or misuse, these bursa may become inflamed, enlarged, and on rare occasions infected. Although there is significant intrapatient variability as to the number, size, and location of bursa, anatomists have identified a number of clinically relevant bursae, including the iliopectineal bursa. The iliopectineal bursa lies between the psoas and iliacus muscle and the iliopectineal eminence (Figure 101-1). This bursa may exist as a single bursal sac or in some patients as a multisegmented series of sacs that may be loculated. The iliopectineal bursa is vulnerable to injury from both acute trauma and repeated microtrauma. Acute injuries frequently take the form of direct trauma to the bursa via hip injuries, as well as overuse injuries. If the inflammation of the iliopectineal bursa becomes chronic, calcification of the bursa may occur. The patient with iliopectineal bursitis frequently reports pain in the anterior hip and groin. The pain is localized to the area just below the crease of the groin anteriorly, with referred pain noted into the hip joint and anterior pelvis. Often the patient is unable to sleep on the affected hip and may note of a sharp, “catching” sensation with range of motion of the hip. Iliopectinate bursitis often coexists with arthritis of the hip joint. Physical examination may reveal point tenderness in the upper thigh just below the crease of the groin. Passive flexion, adduction, and abduction, as well as active resisted flexion and adduction of the affected lower extremity, reproduce the pain. Sudden release of resistance during this maneuver markedly increases the pain. Plain radiographs of the hip may reveal calcification of the bursa and associated structures consistent with chronic inflammation. Ultrasound imaging may also help identify the presence of bursitis or other painful conditions (Figure 101-2). Magnetic resonance imaging is indicated if occult mass or tumor of the hip or groin is suspected. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The iliopectineal bursa lies between the psoas and iliacus muscles and the iliopectineal eminence. The iliopectineal eminence is the point at which the ilium and the pubis bone merge. The psoas

and iliacus muscles join at the lateral side of the psoas, and the combined fibers are referred to as the iliopsoas muscle. Like the psoas, the iliacus flexes the thigh on the trunk or, if the thigh is fixed, flexes the trunk on the thigh, as when moving from a supine to sitting position. This action can irritate the iliopectineal bursa, as can repeated trauma from repetitive activity including sit-ups or overuse of exercise equipment for lower-extremity strengthening. The iliacus muscle is innervated by the femoral nerve.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and the pulsation of the femoral artery at the midpoint of the inguinal ligament is identified. At a point 2½ inches down and 3½ inches lateral to these femoral arterial pulsations lies the entry point for the needle. This point should be at the lateral edge of the sartorius muscle. Proper preparation with antiseptic solution of the skin overlying

Psoas major m. Femoral n. Femoral a. Inflamed iliopectineal bursa

Psoas major m.

Femoral v.

Figure 101-1  Proper needle placement for injection of the iliopectineal bursa.

297

298        SECTION 6  •  Hip and Pelvis

withdrawn and repositioned more laterally. The needle is then carefully advanced through the previously identified point at a 45-degree angle cephalad to allow the needle to safely pass beneath the femoral artery, vein, and nerve. The needle is advanced very slowly to avoid trauma to the femoral nerve until it hits the bone at the point where the ilium and pubis bones merge (see Figure 101-1). The needle is then withdrawn back out of the periosteum, and after careful aspiration for blood and if no paresthesia is present, the contents of the syringe are gently injected into the bursa. There should be minimal resistance to injection.

Side Effects and Complications The proximity to the femoral artery, vein, and nerve makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing injection techniques. Many patients also report a transient increase in pain after injection of the just-mentioned bursa. A

B Figure 101-2  A and B, Sonography of right groin with large iliopectineal bursitis. (From Weber M, Prim J, Lüthy R: Inguinal pain with limping: iliopectineal bursitis as first sign of polymyalgia rheumatica, Joint Bone Spine 75:332–333, 2008.)

this point is then carried out. A syringe containing 9.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 3½-inch, 25-gauge needle. Before needle placement the patient should be advised to say “there!” as soon as a paresthesia into the lower extremity is felt, indicating that the needle has impinged on the femoral nerve. Should a paresthesia occur, the needle should be immediately

Clinical Pearls This injection technique is extremely effective in the treatment of iliopectineal bursitis. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of this injection technique are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. Special care must be taken to avoid trauma to the femoral nerve. The use of physical modalities, including local heat and gentle stretching exercises, should be introduced several days after the patient has undergone this injection technique. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique. Iliopectinate bursitis frequently coexists with arthritis of the hip, which may require specific treatment to provide palliation of pain and return of function.

SUGGESTED READINGS Farber AJ, Wilckens JH, Jarvis CG: Pelvic pain in the athlete. In Seidenberg PH, Beutler AI, editors: The sports medicine resource manual, Philadelphia, 2008, Saunders, pp 306–327. Gibbons TL: Common orthopaedic hip dysfunction. In Placzek JD, Boyce DA, editors: Orthopaedic physical therapy secrets, ed 2, St. Louis, 2006, Elsevier, pp 523–533. Murphy SB: Iliopectineal bursitis, J R Soc Med 90:359, 1997. Waldman SD: Injection technique for iliopectineal bursitis. In Pain review, Philadelphia, 2009, Saunders, pp 553–554. Weber M, Prim J, Lüthy R: Inguinal pain with limping: iliopectineal bursitis as first sign of polymyalgia rheumatica, Joint Bone Spine 75:332–333, 2008.

Chapter 102 TROCHANTERIC BURSA INJECTION

Indications and Clinical Considerations Bursae are formed from synovial sacs whose purpose is to allow easy sliding of muscles and tendons across one another at areas of repeated movement. These synovial sacs are lined with a synovial membrane that is invested with a network of blood vessels that secrete synovial fluid. Inflammation of the bursa results in an increase in the production of synovial fluid with swelling of the bursal sac. With overuse or misuse, these bursae may become inflamed, enlarged, and on rare occasions infected. Although there is significant intrapatient variability as to the number, size, and location of bursa, anatomists have identified a number of clinically relevant bursae, including the trochanteric bursa. The trochanteric bursa lies among the greater trochanter and the tendon of the gluteus medius and the iliotibial tract (Figure 102-1). This bursa may exist as a single bursal sac or in some patients as a multisegmented series of sacs that may be loculated. The trochanteric bursa is vulnerable to injury from both acute trauma and repeated microtrauma. Acute injuries frequently take the form of direct trauma to the bursa via falls directly onto the greater trochanter or previous hip surgery, as well as overuse injuries, including running on soft or uneven surfaces. If the inflammation of the trochanteric bursa becomes chronic, calcification of the bursa may occur. The patient with trochanteric bursitis frequently reports pain in the lateral hip that can radiate down the leg, mimicking sciatica. The pain is localized to the area over the trochanter. Often the patient is unable to sleep on the affected hip and may note a sharp, “catching” sensation with range of motion of the hip, especially on first rising. The patient may note that walking upstairs is increasingly more difficult. Trochanteric bursitis often coexists

Figure 102-1  Needle entry site for trochanteric bursa injection.

with arthritis of the hip joint, back and sacroiliac joint disease, and gait disturbance. Physical examination may reveal point tenderness in the lateral thigh just over the greater trochanter. Passive adduction and abduction, as well as active resisted abduction of the affected lower extremity, reproduce the pain. Sudden release of resistance during this maneuver markedly increases the pain (Figure 102-2). There should be no sensory deficit in the distribution of the lateral femoral cutaneous nerve, as is seen with meralgia paresthetica, which often is confused with trochanteric bursitis. Plain radiographs, ultrasound imaging, and magnetic resonance imaging (MRI) of the hip may reveal calcification of the bursa and associated structures consistent with chronic inflammation

Figure 102-2  The resisted abduction release test. (From Waldman SD: Physical diagnosis of pain, Philadelphia, 2005, Saunders.)

299

300        SECTION 6  •  Hip and Pelvis

A

B Figure 102-3  Greater trochanteric bursitis and torn gluteus medius tendon. A, Coronal short tau inversion recovery (STIR) image shows focal high signal around the greater trochanter (gt, large arrow). The torn and retracted gluteus medius tendon also is seen (small arrow). B, Axial image shows the well-defined fluid collection that is compatible with greater trochanteric bursitis. The gluteus medius tendon is torn (arrows). Greater trochanteric bursitis often is seen in association with gluteus medius tendon tears. (From Kaplan PA, Helms CA, Dussault R, et al: Musculoskeletal MRI, Philadelphia, 2001, Saunders.)

(Figures 102-3 and 102-4). MRI is indicated if occult mass or tumor of the hip or groin is suspected. Electromyography helps distinguish trochanteric bursitis from meralgia paresthetica and sciatica. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The trochanteric bursa lies between the greater trochanter and the tendon of the gluteus medius and the iliotibial tract. The gluteus medius muscle has its origin from the outer surface of the ilium, and its fibers pass downward and laterally to attach on the lateral surface of the greater trochanter. The gluteus medius locks the pelvis in place when walking and running. This action can irritate the trochanteric bursa, as can repeated trauma from repetitive activity, including jogging on soft or uneven surfaces or overuse of exercise equipment for lower extremity strengthening (see Figure 102-1). The gluteus medius muscle is innervated by the superior gluteal nerve.

*

LT greater trochanter Figure 102-4  Longitudinal ultrasonographic image showing fluid collection in the trochanteric bursa (asterisk). (From Malanga GA, Dentico R, Halperin JS: Ultrasonography of the hip and lower extremity, Phys Med Rehabil Clin N Am 21:533–547, 2010.)

Technique The goals of this injection technique are explained to the patient. The patient is placed in the lateral decubitus position with the

102  •  Trochanteric Bursa Injection        301

affected side up. The midpoint of the greater trochanter is identified. Proper preparation with antiseptic solution of the skin overlying this point is then carried out. A syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 31⁄2-inch, 25-gauge needle. Before needle placement, the patient should be advised to say “there!” as soon as a paresthesia into the lower extremity is felt, indicating that the needle has impinged on the sciatic nerve. Should a paresthesia occur, the needle should be immediately withdrawn and repositioned more laterally. The needle is then carefully advanced through the previously identified point at a right angle to the skin directly toward the center of the greater trochanter. The needle is advanced very slowly to avoid trauma to the sciatic nerve until it hits the bone (Figure 102-5). The needle is then withdrawn back out of the periosteum, and after careful aspiration for blood and if no paresthesia is present, the contents of the syringe are gently injected into the bursa. There should be minimal resistance to injection. Ultrasound guidance for needle placement should be considered if the anatomic landmarks necessary to safely perform this procedure are difficult to identify (Figure 102-6).

Greater trochanter Inflamed trochanteric bursa Gluteus maximus m.

Sciatic nerve

Figure 102-5  Proper needle placement for injection of the trochanteric bursa.

G

GT

GT

A

B

C

T

X

G

GT GT

D

E

Figure 102-6  Greater trochanter evaluation. A, Coronal-oblique imaging over the greater trochanter shows from anterior to posterior (B) the gluteus minimus (arrowheads) insertion on the anterior facet of the greater trochanter (GT) and (C) the gluteus medius (arrows) insertion on the lateral facet of the greater trochanter. Note the iliotibial tract (curved arrow) in C. Transverse images, (D) superior and (E) inferior, show, from anterior to posterior, the gluteus minimus attachment (arrowheads), the gluteus medius attachment (arrows), and the iliotibial tract (curved arrows) (G, gluteus medius muscle; T, tensor fasciae latae; X, gluteus maximus). (From Jacobson JA: Fundamentals of musculoskeletal ultrasound, Philadelphia, 2007, Saunders.)

302        SECTION 6  •  Hip and Pelvis

Side Effects and Complications The proximity to the sciatic nerve makes it imperative that this procedure be carried out only by those well versed in the regional

Clinical Pearls This injection technique is extremely effective in the treatment of trochanteric bursitis. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of this injection technique are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. Special care must be taken to avoid trauma to the sciatic nerve. The use of physical modalities, including local heat and gentle stretching exercises, should be introduced several days after the patient has undergone this injection technique. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique. Trochanteric bursitis frequently coexists with arthritis of the hip, which may require specific treatment to provide palliation of pain and return of function. Occasionally, trochanteric bursitis can be confused with meralgia paresthetica because both manifest with pain in the lateral thigh. The two syndromes can be distinguished in that patients with meralgia paresthetica do not have pain on palpation over the greater trochanter. Electromyography helps sort out confusing clinical presentations.

anatomy and experienced in performing injection techniques. Many patients also note a transient increase in pain after injection of the just-mentioned bursa. Infection, although rare, can occur, and careful attention to sterile technique is mandatory. SUGGESTED READINGS Segal NA, Felson DT, Torner JC, et al: Greater trochanteric pain syndrome: epidemiology and associated factors, Arch Phys Med Rehabil 88:988–992, 2007. Tibor LM, Sekiya JK: Differential diagnosis of pain around the hip joint, Arthroscopy 24:1407–1421, 2008.

Chapter 103 INJECTION TECHNIQUE FOR THIGH SPLINTS Indications and Clinical Considerations The musculotendinous unit of the distal adductor muscles of the hip joint is susceptible to the development of tendinitis and tendinopathy from overuse or trauma from traction injuries at the site of the insertion of these muscles on the femur. Inciting factors may include the vigorous use of exercise equipment for lower-extremity strengthening and acute stretching of the musculotendinous units as a result of sports injuries and/or military training. Analogous to shin splints, the pain of thigh splints is localized to the medial thigh and groin and is described as sharp, constant, and severe. Sleep disturbance is often reported. The patient may attempt to splint the inflamed tendons by adopting an adductor lurch type of gait (i.e., shifting the trunk of the body over the affected extremity when walking). On physical examination the patient will report pain on palpation of the insertion of the adductor tendons. Active resisted adduction reproduces the pain, as does passive abduction. Patients with adductor tendinitis will also exhibit a positive Waldman knee squeeze test result. This test is performed by having the patient sit on the edge of the examination table. The examiner places a tennis ball between the patient’s knees and asks the patient to gently hold

A

it there with gentle pressure from the knees (see Figure 97-1, A). The patient is then instructed to quickly squeeze the ball between the knees as hard as possible. Patients with adductor tendinitis will reflexively abduct the affected extremity owing to the pain of forced adduction, thereby causing the ball to drop to the floor (see Figure 97-1, B). Thigh splints frequently coexist with bursitis of the associated bursae of the hip joint, creating additional pain and functional disability. In addition to the just-mentioned pain, patients with thigh splints often experience a gradual decrease in functional ability with decreasing hip range of motion, making simple everyday tasks, such as getting in or out of a car, difficult. With continued disuse, muscle wasting may occur and an adhesive capsulitis of the hip may develop. Plain radiographs are indicated for all patients with hip, groin, and thigh pain. Patients with thigh splints will demonstrate a periosteal reaction, and an avulsion fracture may be seen ­(Figure 103-1, A). On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the hip, groin, and femur are indicated if tendinitis, aseptic necrosis of the hip, tear

B

Figure 103-1  Adductor insertion avulsion syndrome in a 19-year-old soccer player with left medial thigh pain. A, Anteroposterior radiograph shows focal periosteal reaction along the medial aspect of the midleft femoral diaphysis (arrow). B, Axial T2-weighted image confirms periostitis at the adductor insertion site, with associated thin rim of hyperintensity. There is no accompanying cortical signal abnormality. (From Nelson EN, Kassarjian A, Palmer WE: MR imaging of sports-related groin pain, Magn Reson Imaging Clin N Am 13:727–742, 2005.)

303

304        SECTION 6  •  Hip and Pelvis

or avulsion of the adductor muscles, or occult mass is suspected (Figures 103-1, B, and 103-2). In patients with thigh splints, MRI will reveal increased signal intensity of the proximal and mid shaft of the femur with increased signal on short tau inversion recovery (STIR) images from the periosteum and endosteal surface ­(Figure 103-3). Ultrasound imaging of this area may reveal periosteal edema. Radionuclide scanning may reveal increased uptake at the insertion of the adductor muscles on the femur. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The adductor muscles of the hip include the gracilis, adductor longus, adductor brevis, and adductor magnus muscles (Figure 103-4). The adductor function of these muscles is innervated by the obturator nerve, which is susceptible to trauma from pelvic fractures and compression by tumor. The tendons of the adductor muscles of the hip have their origin along the pubis and ischial ramus and their insertion along the medioposterior aspect of the

mid femur (see Figure 97-4). It is at the point of insertion that the traction injury and resultant tendinopathy and periostitis of the femur occur.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the modified Sims position with the affected leg dependent and fully extended (Figure 103-5). This positioning of the affected lower extremity allows access to the tendinous insertions of the hip adductor muscles on the femur. If the patient cannot tolerate this position because of pain and spasm of the adductors, it may be necessary to block the obturator nerve to allow adequate exposure to the origin of the adductor tendons. The insertion of the adductor tendons on the femur can be identified by palpation along the medioposterior femur. After the site of maximal tenderness has been identified, the skin is prepared with antiseptic solution. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle with the use of strict aseptic technique. The painful insertion of the adductor tendons is reidentified with the gloved finger. The needle is then carefully advanced perpendicularly to the skin of the affected lower extremity through the skin and subcutaneous tissues until it impinges on bone. The needle is then withdrawn 1 to 2 mm out of the periosteum of the femur, and the contents of the syringe are gently injected. There should be slight resistance to injection. If there is significant resistance to injection, the needle tip is probably in the substance of a tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications Figure 103-2  Axial fluid-sensitive images showing abnormal edema and some cortical destruction (arrow) in a 26-year-old recreational hockey player thought to have thigh splints. The injury did not improve after 8 weeks with rest and subsequently was proven to be lymphoma. (From Armfield DR, Kim DH, Towers JD, et al: Sports-related muscle injury in the lower extremity, Clin Sports Med 25:803–842, 2006.)

A

The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is followed. Trauma to the adductor tendons from the injection itself remains an ever-present possibility. Tendons that are highly inflamed or previously damaged are subject to rupture if

B

Figure 103-3  Thigh splints. A, Coronal STIR image of the thighs. Elongated increased signal intensity is present in the proximal to mid femoral shaft (arrow). B, Short tau inversion recovery (STIR) axial image of the right thigh. Abnormal increased signal is seen along the periosteal (long arrow) and endosteal (arrowhead) surfaces of the femur along with similar abnormal signal within the posteromedial cortex (short arrow). Findings are compatible with a developing stress fracture. (From Helms CA, Major NM, Anderson MW, et al: Musculoskeletal MRI, ed 2, Philadelphia, 2009, Saunders.)

103  •  Injection Technique for Thigh Splints        305

Femoral neck Rectus femoris m.

Greater trochanter Quadratus femoris m. Gluteus maximus m. Sciatic n.

Femoral diaphysis Vastus lateralis m.

Vastus intermedius m.

Adductor magnus m.

Deep formula a., perforater branch Adductor magnus m.

Semitendinosus m.

Biceps femoris m., long head Semimembranosus m.

Figure 103-4  Magnetic resonance image of the thigh: sagittal. (From El-Khoury GY, Montgomery WJ, Bergman RA, editors: Sectional anatomy by MRI and CT, ed 3, Philadelphia, 2007, Churchill Livingstone.)

Figure 103-5  Positioning of the patient for injection of thigh splints.

306        SECTION 6  •  Hip and Pelvis

they are directly injected. Risk of this complication can be greatly decreased if the clinician uses gentle technique and stops injecting immediately if significant resistance to injection is encountered. Approximately 25% of patients note a transient increase in pain after this injection technique; the patient should be warned of this.

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to the just-mentioned causes of hip pain. Coexistent bursitis and arthritis also may contribute to hip pain and may require additional treatment with a more localized injection of local anesthetic and depot corticosteroid preparation. This technique is a safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for hip pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Anderson M, Kaplan P, Dussault R: Adductor insertion avulsion syndrome (thigh splints), Am J Roentgenol 177:673–675, 2001. MacMahon PJ, Hogan BA, Shelly MJ, et al: Imaging of groin pain, Magn Reson Imaging Clin N Am 17:655–666, 2009. Meyers WC, Greenleaf R, Saad A: Anatomic basis for evaluation of abdominal and groin pain in athletes, Oper Tech Sports Med 13:55–61, 2005. Morelli V, Espinoza L: Groin injuries and groin pain in athletes: part 2, Prim Care 32:185–200, 2005. Morelli V, Weaver V: Groin injuries and groin pain in athletes: part 1, Prim Care 32:163–183, 2005. Nelson EN, Kassarjian A, Palmer WE: MR imaging of sports-related groin pain, Magn Reson Imaging Clin N Am 13:727–742, 2005. Sofka M, Marx R, Adler RS: Utility of sonography for the diagnosis of adductor avulsion injury (“thigh splints”), J Ultrasound Med 25:913–916, 2006. Weaver JS, Jacobson JA, Jamadar DA, Hayes CW: Sonographic findings of adductor insertion avulsion syndrome with magnetic resonance imaging correlation, J Ultrasound Med 22:403–407, 2003.

Chapter 104 INJECTION TECHNIQUE FOR SNAPPING HIP SYNDROME Indications and Clinical Considerations Snapping hip syndrome is a constellation of symptoms that include a snapping sensation in the lateral hip associated with sudden, sharp pain in the area of the greater trochanter. The snapping sensation and pain are the result of the iliopsoas tendon subluxing over the greater trochanter or iliopectineal eminence (Figure 104-1). The symptoms of snapping hip syndrome occurs most commonly when the patient rises from a sitting to a standing position or walks briskly. Often, trochanteric bursitis coexists with snapping hip syndrome, further increasing the patient’s pain and disability. Physical examination reveals that the patient can re-create the snapping and pain by moving from a sitting to a standing position

and adducting the hip (Figure 104-2). Point tenderness over the trochanteric bursa indicative of trochanteric bursitis also is often present. Plain radiographs are indicated for all patients with pain thought to be emanating from the hip to rule out occult bony disease and tumor. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, prostate-specific antigen, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the affected hip is indicated to help confirm the diagnosis as well as to rule out occult mass or aseptic necrosis of the hip (Figure 104-3). Ultrasound imaging can also help with the diagnosis (Figure 104-4). The following injection technique serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy

Greater trochanter

Iliotibial band

The trochanteric bursa lies between the greater trochanter and the tendon of the gluteus medius and the iliotibial tract (Figure 104-5). The gluteus medius muscle has its origin from the outer surface of the ilium, and its fibers pass downward and laterally to attach on the lateral surface of the greater trochanter. The gluteus medius locks the pelvis in place when walking and running. The gluteus medius muscle is innervated by the superior gluteal nerve. The iliopectineal eminence is the point at which the ilium and the pubic bone merge. The psoas and iliacus muscles join at the lateral side of the psoas, and the combined fibers are referred to as the iliopsoas muscle. Like the psoas muscle, the iliacus flexes the thigh on the trunk or, if the thigh is fixed, flexes the trunk on the thigh, as when moving from a supine to sitting position.

Technique

Figure 104-1  The relationship of the iliotibial band and the greater trochanter.

The goals of this injection technique are explained to the patient. The patient is placed in the lateral decubitus position with the affected side up. The midpoint of the greater trochanter is identified. Proper preparation with antiseptic solution of the skin overlying this point is then carried out. A syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 3½-inch, 25-gauge needle. Before needle placement, the patient should be advised to say “there!” as soon as a paresthesia into the lower extremity is felt; this paresthesia indicates that the needle has impinged on the sciatic nerve. Should a paresthesia occur, the needle should be immediately withdrawn and repositioned more laterally. The needle is then carefully advanced through the previously identified point at a right angle to the skin, directly toward the center of the greater trochanter. The needle is advanced very slowly to avoid trauma 307

308        SECTION 6  •  Hip and Pelvis

Figure 104-2  Eliciting the snap sign. (Waldman SD: Physical diagnosis of pain, Philadelphia, 2005, Saunders.) Figure 104-3  Axial T1-weighted image showing osseous protuberance anteriorly (thin arrow) resulting in intratendinous high signal intensity (tendinosis) within the iliopsoas tendon (thick arrow), also referred to as internal snapping hip syndrome. (From Hodnett PA, Shelly MJ, MacMahon PJ, et al: MR imaging of overuse injuries of the hip, Magn Reson Imaging Clin N Am 17:667–679, 2009.)

to the sciatic nerve until it hits the bone (see Figure 104-1). The needle is then withdrawn back out of the periosteum, and after careful aspiration for blood and if no paresthesia is present, the contents of the syringe are gently injected. There should be minimal resistance to injection.

Side Effects and Complications The proximity to the sciatic nerve makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing injection techniques. Many patients also report a transient increase in pain after the just-mentioned injection technique. Infection, although rare, can occur, and careful attention to sterile technique is mandatory.

104  •  Injection Technique for Snapping Hip Syndrome        309

A

B

Figure 104-4  Normal iliopsoas tendon. A, Transverse sonographic image at the level of the acetabular rim best demonstrates the musculotendinous junction. The iliopsoas tendon (large arrow) has a normal echogenic appearance; the iliopsoas muscle appears normal (small arrow); and acetabular rim (notched arrow) is seen as an echogenic line. B, Longitudinal sonographic image of the iliopsoas tendon (arrows). Note the uniform echogenicity of the tendon. (From Blankenbaker DG, De Smet AA: The role of ultrasound in the evaluation of sports injuries of the lower extremities, Clin Sports Med 25:867–897, 2006.)

Sartorius m.

Rectus femoris t. Rectus femoris m. Lateral femoral circumflex vessel Tensor fasciae latae m. Iliopsoas m. Vastus lateralis m. Femoral neck Iliotibial band Calcar femorale Gluteus medius m. Sciatic n.

Greater saphenous v. Femoral a. Femoral v. Pectineus m. Iliopsoas t. Medial femoral circumflex vessel Obturator externus m. Ischial tuberosity Obturator internus m. Common hamstring t.

Gluteus maximus m.

Figure 104-5  Magnetic resonance image of the hip: axial. (From El-Khoury GY, Montgomery WJ, Bergman RA, editors: Sectional anatomy by MRI and CT, ed 3, Philadelphia, 2007, Churchill Livingstone.)

310        SECTION 6  •  Hip and Pelvis

Clinical Pearls This injection technique is extremely effective in the treatment of snapping hip syndrome. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of this injection technique are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. Special care must be taken to avoid trauma to the sciatic nerve. The use of physical modalities, including local heat and gentle stretching exercises, should be introduced several days after the patient has undergone this injection technique. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics, nonsteroidal antiinflammatory agents, and antimyotonic agents such as tizanidine may be used concurrently with this injection technique. Trochanteric bursitis frequently coexists with snapping hip syndrome, which may require specific treatment for palliation of pain and return of function. Occasionally, coexistent trochanteric bursitis can be confused with meralgia paresthetica because both manifest with pain in the lateral thigh. The two syndromes can be distinguished in that patients with meralgia paresthetica do not have pain on palpation over the greater trochanter. Electromyography helps sort out confusing clinical presentations.

SUGGESTED READINGS Bureau NJ, Cardinal E: Ultrasound examination of the musculoskeletal system: the snapping syndromes, Ultrasound Med Biol 29(5 Suppl 1):S5–S6, 2003. Byrd JWT: Snapping hip, Operative Techniques in Sports Medicine 13:46–54, 2005. Hodnett PA, Shelly MJ, MacMahon PJ, et al: MR imaging of overuse injuries of the hip, Magn Reson Imaging Clin N Am 17:667–679, 2009. Tibor LM, Sekiya JK: Differential diagnosis of pain around the hip joint, Arthroscopy 24:1407–1421, 2008.

Chapter 105 INTRAARTICULAR INJECTION OF THE SACROILIAC JOINT Indications and Clinical Considerations The sacroiliac joint is susceptible to the development of arthritis from a variety of conditions that have in common the ability to damage the joint cartilage. The sacroiliac joint also is susceptible to the development of strain from trauma or misuse. Osteoarthritis of the joint is the most common form of arthritis that results in sacroiliac joint pain. However, rheumatoid arthritis and posttraumatic arthritis are also common causes of sacroiliac pain secondary to arthritis (Figure 105-1). Less common causes of arthritis-induced sacroiliac pain include the collagen vascular diseases, including ankylosing spondylitis, infection, and Lyme disease. Acute infectious arthritis usually is accompanied by significant systemic symptoms, including fever and malaise, and should be easily recognized by the astute clinician and treated appropriately with culture and antibiotics rather than injection therapy. The collagen vascular diseases generally manifest as a polyarthropathy rather than a monoarthropathy limited to the

A

B

sacroiliac joint, although sacroiliac pain secondary to the collagen vascular disease ankylosing spondylitis responds exceedingly well to the intraarticular injection technique described later. Occasionally the clinician encounters patients with iatrogenically induced sacroiliac joint dysfunction caused by overaggressive bone graft harvesting for spinal fusions. The majority of patients with sacroiliac pain secondary to strain or arthritis report pain that is localized around the sacroiliac joint and upper leg. The pain of sacroiliac joint strain or arthritis radiates into the posterior buttocks and the back of the legs. The pain does not radiate below the knees. Activity makes the pain worse; rest and heat provide some relief. The pain is constant and characterized as aching. The pain may interfere with sleep. On physical examination there is tenderness to palpation of the affected sacroiliac joint. The patient often favors the affected leg and exhibits a list to the unaffected side. Spasm of the lumbar paraspinal musculature often is present, as is limitation of range of motion of the lumbar spine in the erect position that improves in the sitting position owing to relaxation of the hamstring muscles.

C

Figure 105-1  Abnormalities of the sacroiliac joint. A, Radiograph of a rheumatoid arthritis patient reveals focal erosions and reactive sclerosis, particularly in the iliac aspect of the sacroiliac joint. The articular space is diminished. These changes can be distributed in a unilateral or bilateral fashion. The degree of bony eburnation that is present in this case is unusual in rheumatoid arthritis. B and C, Coronal sections of the sacroiliac joint of two cadavers with rheumatoid arthritis demonstrate osseous erosions, especially in the ilium (arrows), and segmental intraarticular osseous fusion (arrowheads). (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

311

312        SECTION 6  •  Hip and Pelvis

Patients with pain emanating from the sacroiliac joint exhibit a positive pelvic rock test result. The pelvic rock test is performed by placing the hands on the iliac crests and the thumbs on the anterior superior iliac spine and then forcibly compressing the pelvis toward the midline (Figure 105-2). A positive test result is indicated by the production of pain around the sacroiliac joint. Plain radiographs are indicated for all patients with sacroiliac pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, human leukocyte antigen B27 (HLA-B27) testing, and antinuclear antibody testing.

Clinically Relevant Anatomy The sacroiliac joint is formed by the articular surfaces of the sacrum and iliac bones (Figure 105-3). These articular surfaces have corresponding elevations and depressions, which give the joints their irregular appearance on radiographs. The strength of the sacroiliac joint comes primarily from the posterior and interosseous ligaments rather than from the bony articulations. The sacroiliac joints bear the weight of the trunk and are therefore subject to the development of strain and arthritis. As the joint ages, the intraarticular space narrows, making intraarticular injection more challenging. The ligaments and the sacroiliac joint itself receive their innervation from L3 to S3 nerve roots, with L4 and L5 providing the greatest contribution to the innervation of the joint. This diverse innervation may explain the ill-defined nature of sacroiliac pain. The sacroiliac joint has a very limited range of motion, and that motion is induced by changes in the forces placed on the joint by shifts in posture and joint loading.

Technique

Figure 105-2  The pelvic rock test is performed by placing the hands on the iliac crests and the thumbs on the anterior superior iliac spines and then forcibly compressing the pelvis toward the midline.

The goals of this injection technique are explained to the patient. The patient is placed in the supine position and proper preparation with antiseptic solution of the skin overlying the affected sacroiliac joint space is done. A sterile syringe containing 4.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 3½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the posterior superior spine of the ilium is identified. At this point the needle is carefully advanced through the skin and subcutaneous tissues at a 45-degree angle toward the affected sacroiliac joint (see Figure 105-3). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected superiorly and slightly more laterally. After the joint space has been entered, the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament and should be advanced slightly into the joint space until

Arthritic and inflamed sacroiliac joint

Figure 105-3  Proper needle placement for intraarticular injection of the sacroiliac joint.

105  •  Intraarticular Injection of the Sacroiliac Joint        313

Needle tip

A

B

Contrast spread

Needle tip Arthrogram

C

D

Figure 105-4  Fluoroscopic images from sacroiliac joint (SIJ) injection. A, Needle placement (22 gauge) in illustrative case. B, SIJ arthrogram from illustrative case after injection of 0.5 mL Omnipaque 300. C, Needle placement (22 gauge) in a second, separate subject. D, SIJ arthrogram from second subject after injection of 0.5 mL Omnipaque 300. (From Block BM, Hobelmann JG, Murphy KJ, Grabow TS: An imaging review of sacroiliac joint injection under computed tomography guidance, Reg Anesth Pain Med 30:295–298, 2005.)

the injection proceeds without significant resistance. The needle is then removed and a sterile pressure dressing and ice pack are placed at the injection site. If the physician has difficulty in placing the needle into the sacroiliac joint, fluoroscopic, computed tomography (CT), or ultrasound guidance may be beneficial (Figures 105-4 and 105-5).

Side Effects and Complications The major complication of intraarticular injection of the sacroiliac joint is infection, which should be exceedingly rare if strict

aseptic technique is followed. Approximately 25% of patients report a transient increase in pain after intraarticular injection of the sacroiliac joint; the patient should be warned of this. Care must be taken to avoid injection too laterally or the needle may traumatize the sciatic nerve.

314        SECTION 6  •  Hip and Pelvis

Needle tip

B

A

Arthrogram

C Figure 105-5  Computed tomography (CT) images from sacroiliac joint (SIJ) injection from illustrative case. A, Scout tomogram for planed injection. B, Needle (22 gauge) directly inserted into the SIJ. C, CT image after injection of 1 mL Omnipaque 300. (From Block BM, Hobelmann JG, Murphy KJ, Grabow TS: An imaging review of sacroiliac joint injection under computed tomography guidance, Reg Anesth Pain Med 30:295–298, 2005.)

Clinical Pearls This injection technique is extremely effective in the treatment of the just-mentioned causes of sacroiliac joint pain. Coexistent bursitis and tendinitis also may contribute to sacroiliac pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle rangeof-motion exercises, should be introduced several days after the patient has undergone this injection technique for sacroiliac pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Block BM, Hobelmann JG, Murphy KJ, Grabow TS: An imaging review of sacroiliac joint injection under computed tomography guidance, Reg Anesth Pain Med 30:295–298, 2005. Vydyanathan A, Narouze S: Ultrasound-guided caudal and sacroiliac joint injections, Tech Reg Anesth Pain Manag 13:157–160, 2009. Waldman SD: Functional anatomy of the sacroiliac joint. Pain review, Philadelphia, 2009, Saunders, pp 141–144. Waldman SD: Sacroiliac joint injection. Pain review, Philadelphia, 2009, Saunders, pp 544–545. Waldman SD: Sacroiliac joint pain. Pain review, Philadelphia, 2009, Saunders, pp 251–252.

Chapter 106 INJECTION TECHNIQUE FOR GLUTEUS MAXIMUS SYNDROME Indications and Clinical Considerations The gluteus maximus muscle is susceptible to the development of myofascial pain syndrome. Such pain most often occurs as a result of repetitive microtrauma to the muscle from activities such as running on soft surfaces and overuse of exercise equipment or other repetitive activities that require hip extension. Blunt trauma to the muscle may also incite gluteus maximus myofascial pain syndrome. Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body. The sine qua non of myofascial pain syndrome is the finding of myofascial trigger points on physical examination. Although these trigger points generally are localized to the regional part of the body affected, the pain of myofascial pain syndrome often is referred to other anatomic areas. This referred pain often is misdiagnosed or attributed to other organ systems, thereby leading to extensive evaluations and ineffective treatment. Patients with myofascial pain syndrome involving the gluteus maximus often have primary pain in the medial and lower aspects of the muscle that is referred across the buttocks and into the coccygeal area (Figure 106-1). The trigger point is the pathognomonic lesion of myofascial pain and is thought to be a result of microtrauma to the affected

muscles. This pathologic lesion is characterized by a local point of exquisite tenderness in affected muscle. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain but also referred pain. In addition to this local and referred pain, there often is an involuntary withdrawal of the stimulated muscle, called a “jump sign.” This jump sign also is characteristic of myofascial pain syndrome. Patients with gluteus maximus syndrome will exhibit a trigger point over the upper, medial, and lower aspects of the muscle (see Figure 106-1). Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. In spite of this consistent physical finding in patients with myofascial pain syndrome, the pathophysiology of the myofascial trigger point remains elusive, although many theories have been advanced. Common to all of these theories is the belief that trigger points are a result of microtrauma to the affected muscle. This microtrauma may occur as a single injury to the affected muscle or may occur as a result of repetitive microtrauma or chronic deconditioning of the agonist and antagonist muscle unit. In addition to muscle trauma, a variety of other factors seem to predispose the patient to have myofascial pain syndrome. The weekend athlete who subjects his or her body to unaccustomed physical activity may develop myofascial pain syndrome. The poor posture of someone sitting at a computer keyboard or

Trigger point Referred pain Gluteus maximus m.

Figure 106-1  Location of myofascial trigger points and referred pain in patients with gluteus maximus syndrome.

315

316        SECTION 6  •  Hip and Pelvis

watching television has also been implicated as a predisposing factor to the development of myofascial pain syndrome. Previous injuries may result in abnormal muscle function and predispose to the subsequent development of myofascial pain syndrome. All of these predisposing factors may be intensified if the patient also has poor nutritional status or coexisting psychological or behavioral abnormalities, including chronic stress and depression. The gluteus maximus muscle seems to be particularly susceptible to stress-induced myofascial pain syndrome. Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or may occur in conjunction with other painful conditions, including radiculopathy and chronic regional pain syndromes. Psychological or behavioral abnormalities, including depression, frequently coexist with the muscle abnormalities associated with myofascial pain syndrome. Treatment of these psychological and behavioral abnormalities must be an integral part of any successful treatment plan for myofascial pain syndrome.

Clinically Relevant Anatomy The gluteus maximus muscle’s primary function is hip extension. The gluteus maximus muscle finds its origin at the posterior aspect of dorsal ilium, the posterior superior iliac crest, the posterior inferior aspect of sacrum and coccyx, and the sacrotuberous ligament (see Figure 106-1). The muscle inserts on the fascia lata at the iliotibial band as well as the gluteal tuberosity on the femur. The muscle is innervated by the inferior gluteal nerve. The gluteus maximus muscle is susceptible to trauma and to wear and tear from overuse and misuse and may develop myofascial pain syndrome, which may also be associated with gluteal bursitis.

Technique Careful preparation of the patient before trigger point injection helps to optimize results. Trigger point injections are directed at the primary trigger point rather than in the area of referred pain. It should be explained to the patient that the goal of trigger point injection is to block the trigger of the persistent pain and thus, it is hoped, provide long-lasting relief. It is important that the patient understand that for most patients with from myofascial pain syndrome, more than one treatment modality is required for optimal pain relief. The use of the recumbent or lateral position when identifying and marking trigger points, as well as when performing the actual trigger point injection, helps decrease the incidence of vasovagal reactions. The skin overlying the trigger point should always be prepared with antiseptic solution before injection to avoid infection. After the goals of trigger point injection have been explained to the patient and proper preparation of the patient has been carried out, the trigger point to be injected is reidentified by palpation with the sterilely gloved finger. A syringe containing 10 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 25- or 27-gauge needle of a length adequate to reach the trigger point. Except for the muscles of posture in

the low back, a 1½-inch needle will be adequate. A volume of 0.5 to 1.0 mL of solution is then injected into each trigger point (see Figure 106-1). A series of two to five treatment sessions may be required to completely abolish the trigger point; the patient should be informed of this.

Side Effects and Complications The proximity to neurovascular structures, including the median and ulnar nerve and the recurrent anterior ulnar artery, makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing interventional pain management techniques. Many patients also note a transient increase in pain after injection of trigger points in the gluteus maximus muscle.

Clinical Pearls Trigger point injections are extremely safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of trigger point injection are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after trigger point injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid trauma to the neurovascular structures, including the sciatic nerve, when injecting the gluteus maximus muscle. The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators believe that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as amitriptyline and nortriptyline are good first choices and should be given as a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow. Pregabalin, duloxetine, and milnacipran have also been shown to be of benefit in the treatment of myofascial pain syndromes.

SUGGESTED READINGS Baldry P: Acupuncture treatment of fibromyalgia and myofascial pain. In Chaitow L, editor: Fibromyalgia syndrome, ed 3, 2010, Oxford, Churchill Livingstone, pp 145–159. LeBlanc KE, LeBlanc LL: Musculoskeletal disorders, Prim Care 37:389–406, 2010. Marsh W: Milnacipran. In Enna SJ, Bylund DB, editors: xPharm: the comprehensive pharmacology reference, St. Louis, 2008, Mosby, pp 1–4. Partanen JV, Ojala TA, Arokoski JP: Myofascial syndrome and pain: a neurophysiological approach, Pathophysiology 17:19–28, 2010.

Chapter 107 INJECTION TECHNIQUE FOR GLUTEUS MEDIUS SYNDROME Indications and Clinical Considerations The gluteus medius muscle is susceptible to the development of myofascial pain syndrome. Such pain most often occurs as a result of repetitive microtrauma to the muscle from activities such as running on soft surfaces and overuse of exercise equipment or other repetitive activities that require hip abduction. Blunt trauma to the muscle may also incite gluteus medius myofascial pain syndrome. Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body. The sine qua non of myofascial pain syndrome is the finding of myofascial trigger points on physical examination. Although these trigger points generally are localized to the regional part of the body affected, the pain of myofascial pain syndrome often is referred to other anatomic areas. This referred pain often is misdiagnosed or attributed to other organ systems, thereby leading to extensive evaluations and ineffective treatment. Patients with myofascial pain syndrome involving the gluteus medius often have primary pain along the posterior iliac crest that is referred down the buttocks

across the sacroiliac joint and into the posterior lower extremity (Figure 107-1). The trigger point is the pathognomonic lesion of myofascial pain and is thought to be a result of microtrauma to the affected muscles. This pathologic lesion is characterized by a local point of exquisite tenderness in affected muscle. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain but also referred pain. In addition to this local and referred pain, there often is an involuntary withdrawal of the stimulated muscle, called a “jump sign.” This jump sign also is characteristic of myofascial pain syndrome. Patients with gluteus medius syndrome will exhibit a trigger point along the posterior iliac crest (see Figure 107-1). Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. In spite of this consistent physical finding in patients with myofascial pain syndrome, the pathophysiology of the myofascial trigger point remains elusive, although many theories have been advanced. Common to all of these theories is the belief that trigger points are a result of microtrauma to the affected muscle. This microtrauma may occur as a single injury to the affected muscle or as a result of repetitive

Trigger points Gluteus medius m. Referred pain

Figure 107-1  Trigger point location and pattern of referred pain in patients with gluteus medius syndrome.

317

318        SECTION 6  •  Hip and Pelvis

microtrauma or chronic deconditioning of the agonist and antagonist muscle unit. In addition to muscle trauma, a variety of other factors seem to predispose the patient to develop myofascial pain syndrome. The weekend athlete who subjects his or her body to unaccustomed physical activity may develop myofascial pain syndrome. The poor posture of someone sitting at a computer keyboard or while watching television has also been implicated as a predisposing factor to the development of myofascial pain syndrome. Previous injuries may result in abnormal muscle function and predispose to the subsequent development of myofascial pain syndrome. All of these predisposing factors may be intensified if the patient also has poor nutritional status or coexisting psychological or behavioral abnormalities, including chronic stress and depression. The gluteus medius muscle seems to be particularly susceptible to stressinduced myofascial pain syndrome. Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or in conjunction with other painful conditions, including radiculopathy and chronic regional pain syndromes. Psychological or behavioral abnormalities, including depression, frequently coexist with the muscle abnormalities associated with myofascial pain syndrome. Treatment of these psychological and behavioral abnormalities must be an integral part of any successful treatment plan for myofascial pain syndrome.

Clinically Relevant Anatomy The gluteus medius muscle’s primary function is as a hip abductor, and the muscle also assists in medial and lateral rotation of the hip. The gluteus medius muscle finds its origin at the dorsal ilium just below the iliac crest (see Figure 107-1). The muscle inserts on the greater tuberosity of the femur. The muscle is innervated by the superior gluteal nerve. The gluteus medius muscle is susceptible to trauma and to wear and tear from overuse and misuse and may develop myofascial pain syndrome, which may also be associated with gluteal bursitis.

Technique Careful preparation of the patient before trigger point injection helps to optimize results. Trigger point injections are directed at the primary trigger point rather than in the area of referred pain. It should be explained to the patient that the goal of trigger point injection is to block the trigger of the persistent pain and thus, it is hoped, provide long-lasting relief. It is important that the patient understand that for most patients with myofascial pain syndrome, more than one treatment modality is required for optimal pain relief. The use of the recumbent or lateral position when identifying and marking trigger points, as well as when performing the actual trigger point injection, helps decrease the incidence of vasovagal reactions. The skin overlying the trigger point to be injected should always be prepared with antiseptic solution before injection to avoid infection. After the goals of trigger point injection have been explained to the patient and proper preparation of the patient has been carried out, the trigger point to be injected is reidentified by palpation with the sterilely gloved finger. A syringe containing 10 mL of

0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 25- or 27-gauge needle of a length adequate to reach the trigger point. Except for the muscles of posture in the low back, a 2-inch needle will be adequate except in extremely obese patients. A volume of 0.5 to 1.0 mL of solution is then injected into each trigger point (see Figure 107-1). A series of two to five treatment sessions may be required to completely abolish the trigger point; the patient should be informed of this.

Side Effects and Complications The proximity to neurovascular structures, including the median and ulnar nerve and the recurrent anterior ulnar artery, makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing interventional pain management techniques. Many patients also report a transient increase in pain after injection of trigger points in the gluteus medius muscle.

Clinical Pearls Trigger point injections are extremely safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of trigger point injection are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after trigger point injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid trauma to the neurovascular structures, including the sciatic nerve, when injecting the gluteus medius muscle. The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators think that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as amitriptyline and nortriptyline are good first choices and should be given as a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow. Pregabalin, duloxetine, and milnacipran have also been shown to be of ­benefit in the treatment of myofascial pain syndromes.

SUGGESTED READINGS Baldry P: Acupuncture treatment of fibromyalgia and myofascial pain. In Chaitow L, editor: Fibromyalgia syndrome, ed 3, Oxford, 2010, Churchill Livingstone, pp 145–159. LeBlanc KE, LeBlanc LL: Musculoskeletal disorders, Prim Care 37:389–406, 2010. Marsh W: Milnacipran. In Enna SJ, Bylund DB, editors: xPharm: the comprehensive pharmacology reference, Philadelphia, 2008, Churchill Livingstone. Partanen JV, Ojala TA, Arokoski JP: Myofascial syndrome and pain: a neurophysiological approach, Pathophysiology 17:19–28, 2010.

Chapter 108 INJECTION TECHNIQUE FOR LEVATOR ANI PAIN SYNDROME Indications and Clinical Considerations The levator ani muscle is susceptible to the development of myofascial pain syndrome. Such pain most often occurs as a result of repetitive microtrauma to the muscle from activities such as mountain biking and horseback riding as well as injuries to the muscle during childbirth. Blunt trauma to the muscle may also incite levator ani myofascial pain syndrome. Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body. The sine qua non of myofascial pain syndrome is the finding of myofascial trigger points on physical examination. Although these trigger points generally are localized to the regional part of the body affected, the pain of myofascial pain syndrome often is referred to other anatomic areas. This referred pain often is misdiagnosed or attributed to other organ systems, thereby leading to extensive evaluations

and ineffective treatment. Patients with myofascial pain syndrome involving the levator ani muscle often have primary pain in the pelvic floor that may be referred into the posterior buttocks and posterior lower extremity (Figure 108-1). The trigger point is the pathognomonic lesion of myofascial pain and is thought to be a result of microtrauma to the affected muscles. This pathologic lesion is characterized by a local point of exquisite tenderness in affected muscle. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain but also referred pain. In addition to this local and referred pain there often is an involuntary withdrawal of the stimulated muscle, called a “jump sign.” This jump sign also is characteristic of myofascial pain syndrome. Patients with levator ani syndrome will exhibit a trigger point along the rectum or perineum (see Figure 108-1). Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. In spite of this consistent physical

Inflamed levator ani m.

Trigger point Referred pain

Figure 108-1  Location of trigger point and pattern of referred pain in patient with levator ani pain syndrome.

319

320        SECTION 6  •  Hip and Pelvis

finding in patients with myofascial pain syndrome, the pathophysiology of the myofascial trigger point remains elusive, although many theories have been advanced. Common to all of these theories is the belief that trigger points are a result of microtrauma to the affected muscle. This microtrauma may occur as a single injury to the affected muscle or as a result of repetitive microtrauma or chronic deconditioning of the agonist and antagonist muscle unit. In addition to muscle trauma, a variety of other factors seem to predispose the patient to develop myofascial pain syndrome. The weekend athlete who subjects his or her body to unaccustomed physical activity may develop myofascial pain syndrome. The poor posture of someone sitting at a computer keyboard or while watching television has also been implicated as a predisposing factor to the development of myofascial pain syndrome. Previous injuries may result in abnormal muscle function and predispose to the subsequent development of myofascial pain syndrome. All of these predisposing factors may be intensified if the patient also has poor nutritional status or coexisting psychological or behavioral abnormalities, including chronic stress and depression. The levator ani muscle seems to be particularly susceptible to stressinduced myofascial pain syndrome. Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with

this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or in conjunction with other painful conditions, including radiculopathy and chronic regional pain syndromes. Psychological or behavioral abnormalities, including depression, frequently coexist with the muscle abnormalities associated with myofascial pain syndrome. Treatment of these psychological and behavioral abnormalities must be an integral part of any successful treatment plan for myofascial pain syndrome, especially when pain involves the pelvic region.

Clinically Relevant Anatomy The levator ani is a compound muscle made up of the pubococcygeus and iliococcygeus muscles (Figure 108-2). The levator ani muscle’s primary function is to actively support the pelvic contents as well as compress the urethra and vagina by elevating the pelvic floor and maintaining a physiologic anorectal angle by pulling the anorectal junction forward. The levator ani muscle finds its origin at the posterior surface of the body of the pubis, the fascia of the obturator internus muscle, and the ischial spine (see Figure 108-1). The muscle inserts on the anococcygeal raphe and coccyx. The muscle is innervated by the branches of the ventral primary rami of spinal nerves S3-S4. The levator ani muscle is

L

L

UT OI IC

IC

PR

B

A

L

IC

C Figure 108-2  A, A coronal section through the mid pelvis showing the origin of the iliococcygeus from the fascia of the obturator internus. Gaps are noted at the site of origin of the muscle. Puborectalis lies on a lower plane. B, Measurement of the iliococcygeal angle, indicated by the black arrow, is shown as the angle formed by the iliococcygeus with the horizontal plane of the pelvis. C, The slope of the iliococcygeus decreases as one moves from anterior to posterior and has a horizontal configuration posteriorly. IC, Iliococcygeus; L, levator ani; OI, obturator internus; PR, puborectalis; UT, uterus. (From Singh K, Reid WM, Berger LA: Magnetic resonance imaging of normal levator ani anatomy and function, Obstet Gynecol 99:433–438, 2002.)

108  •  Injection Technique for Levator Ani Pain Syndrome        321

susceptible to trauma and to wear and tear from overuse and misuse and may develop myofascial pain syndrome, which may also be associated with gluteal bursitis and coccydynia and may further confuse the clinical picture.

Technique Careful preparation of the patient before trigger point injection helps to optimize results. Trigger point injections are directed at the primary trigger point rather than in the area of referred pain. It should be explained to the patient that the goal of trigger point injection is to block the trigger of the persistent pain and thus, it is hoped, provide long-lasting relief. It is important that the patient understand that for most patients with myofascial pain syndrome, more than one treatment modality is required to provide optimal pain relief. The use of the recumbent or lateral position when identifying and marking trigger points, as well as when performing the actual trigger point injection, helps decrease the incidence of vasovagal reactions. The skin overlying the trigger point should always be prepared with antiseptic solution before injection to avoid infection. After the goals of trigger point injection have been explained to the patient and proper preparation of the patient has been carried out, the trigger point is reidentified by palpation with the sterilely gloved finger. A syringe containing 10 mL of 0.25% preservativefree bupivacaine and 40 mg of methylprednisolone is attached to a 25- or 27-gauge needle of a length adequate to reach the trigger point. Except for the muscles of posture in the low back, a 2-inch needle will be adequate except in extremely obese patients. A volume of 0.5 to 1.0 mL of solution is then injected into each trigger point (see Figure 108-1). A series of two to five treatment sessions may be required to completely abolish the trigger point; the patient should be informed of this.

Side Effects and Complications The proximity to neurovascular structures of the pelvis and the rectum makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing interventional pain management techniques. Many patients also report a transient increase in pain after injection of trigger points in the levator ani muscle.

Clinical Pearls Trigger point injections are extremely safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of trigger point injection are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after trigger point injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid trauma to the neurovascular structures, including the sciatic nerve, when injecting the levator ani muscle. The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators think that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as amitriptyline and nortriptyline are good first choices and should be given as a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow. Pregabalin, duloxetine, and milnacipran have also been shown to be of benefit in the treatment of myofascial pain syndromes. There is often a psychological component to many pelvic pain syndromes, and failure to fully identify and treat these behavioral issues will result in a less than optimal outcome.

SUGGESTED READINGS Baldry P: Acupuncture treatment of fibromyalgia and myofascial pain. In Chaitow L, editor: Fibromyalgia syndrome, ed 3, Oxford, 2010, Churchill Livingstone, pp 145–159. LeBlanc KE, LeBlanc LL: Musculoskeletal disorders, Prim Care 37:389–406, 2010. Marsh W: Milnacipran. In Enna SJ, Bylund DB, editors: xPharm: the comprehensive pharmacology reference, Philadelphia, 2008, Churchill Livingstone. Partanen JV, Ojala TA, Arokoski JP: Myofascial syndrome and pain: a neurophysiological approach, Pathophysiology 17:19–28, 2010.

Chapter 109 OBTURATOR NERVE BLOCK

Indications and Clinical Considerations Obturator nerve entrapment syndrome is caused by compression of the obturator nerve as it passes through the upper part of the obturator canal (Figures 109-1 and 109-2). The most common causes of compression of the obturator nerve at this anatomic location involve trauma, including gunshot wounds, pelvic fractures, herniation of cement after total hip arthroplasty, endometriosis, tumor, and, rarely, damage during childbirth. Obturator nerve entrapment manifests as paresthesias, pain, and occasionally numbness in the medial thigh. The pain rarely radiates below the knee and is made worse by extension or lateral movement of the lower extremity, which puts traction on the nerve. If it is not treated, progressive motor deficit consisting of hip adductor weakness can lead to significant functional disability owing to the inability to stabilize the hip joint. This instability causes the patient to assume a wide-based gait with the hip held in a fully abducted position. Physical findings include sensory deficit in the medial thigh in the distribution of the obturator nerve (Figure 109-3). Weakness of the hip adductors also may be present. As mentioned earlier, a wide-based gait indicative of adductor muscle paralysis may be seen with advanced cases. Lesions of the lumbar plexus from trauma, hematoma, tumor, diabetic neuropathy, or inflammation are much more common causes of medial thigh pain and hip adductor weakness than isolated lesions of the obturator nerve. Electromyography helps distinguish obturator nerve entrapment from lumbar plexopathy, lumbar radiculopathy, and diabetic polyneuropathy. Plain radiographs of the hip and pelvis are indicated for all patients with obturator nerve entrapment syndrome to rule out occult bony disease. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the lumbar plexus and pelvis is indicated if mass, tumor, or hematoma is suggested (Figure 109-4). The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

entrapment most commonly occurs. The nerve then divides into an anterior and posterior branch. The anterior branch supplies an articular branch to provide sensory innervation to the hip joint, motor branches to the superficial hip adductors, and a cutaneous branch that provides sensory innervation to the medial aspect of the distal thigh. The posterior branch provides motor innervation to the deep hip adductors and an articular branch to the posterior knee joint.

Technique The patient is placed in the supine position with the legs slightly abducted. The pubic tubercle on the involved side is identified by palpation. A point 1 inch lateral and 1 inch inferior to the pubic tubercle is then identified and prepared with antiseptic solution. A 3-inch, 22-gauge needle is then slowly advanced perpendicular to the skin until the needle is felt to impinge on the superior pubic ramus (see Figure 109-1). The depth of bony contact is noted and the needle is withdrawn and redirected laterally and slightly inferiorly. The needle is advanced approximately ¾ to 1 inch deeper to place the needle tip in the obturator canal. A paresthesia in the distribution of the obturator nerve may be elicited. After careful aspiration, a total of 10 mL of 1.0% preservative-free lidocaine

Clinically Relevant Anatomy The obturator nerve provides the majority of innervation to the hip joint. It is derived from the posterior divisions of the L2, L3, and L4 nerves. The nerve leaves the medial border of the psoas muscle and courses inferiorly to pass the pelvis, where it joins the obturator vessels to travel via the obturator canal to enter the thigh (see Figures 109-1 and 109-2; Figure 109-5). It is at this point that 322

Figure 109-1  Anatomy of the bony pelvis.

109  •  Obturator Nerve Block        323

••

•

•

Ext. iliac a. Obturator n.

•

Obturator a.

Inf. gluteal a.

•

Ischium, spine Orturator internus m.

•

Inf. gemellus m.

• •

••

Ischium, tuberosity

•

Adductor brevis m.

• •

Adductor magnus m. Adductor longus m.

•

•

Obturator externus m. Pectineus m.

Piriformis m.

•

•

Pubis

Sciatic n.

•

•

Semimembranosus t.

Figure 109-2  Anatomy of the obturator nerve. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

and 40 mg methylprednisolone is injected. Care must be taken not to place the needle in the obturator artery or vein. Ultrasound guidance may aid in accurate needle placement in those patients in whom the anatomic landmarks are difficult to identify. After injection of the solution, pressure is applied to the injection site to decrease the incidence of postblock ecchymosis and hematoma formation.

Side Effects and Complications The main side effect of obturator nerve block is postblock ecchymosis and hematoma. Because of proximity to the obturator artery and vein, intravascular injection remains an ever-present possibility. As mentioned earlier, pressure should be maintained on the injection site postblock to avoid ecchymosis and hematoma formation.

324        SECTION 6  •  Hip and Pelvis

Obturator nerve

Figure 109-3  Pattern of pain seen in patients with obturator nerve entrapment. (From Waldman SD: Atlas of uncommon pain syndromes, ed 2, Philadelphia, 2008, Saunders.)

Sigmoid colon

Umbilical artery Uterus

Endometriosis tumor in right obturator fossae

Right ext. iliac vessels

Right obturator nerve

Left obturator nerve

Figure 109-4  Transverse magnetic resonance image of the pelvis, with entrapment of the obturator nerve on the right side. (From Langebrekke A, Qvigstad E: Endometriosis entrapment of the obturator nerve after previous cervical cancer surgery, Fertil Steril 91:622–623, 2009.)

Figure 109-5  Overview of the pelvis after laparoscopic lymph node ­dissection. (From Langebrekke A, Qvigstad E: Endometriosis entrapment of the obturator nerve after previous cervical cancer surgery, Fertil Steril 91:622–623, 2009.)

109  •  Obturator Nerve Block        325

Clinical Pearls Obturator nerve block is a simple technique that can produce dramatic relief for patients with obturator nerve entrapment syndrome. Destruction of the obturator nerve by radiofrequency lesion is useful in the palliation of hip adductor spasm after spinal cord injury or stroke that limits the ability to provide perineal care or allow sexual intercourse or urinary catheterization. Botulinum toxin may have an application for this indication. If a patient reports pain that is thought to be mediated via the obturator nerve and does not respond to obturator nerve blocks, a diagnosis of lesions more proximal in the lumbar plexus or an L2-L3-L4 radiculopathy should be considered. Such patients often respond to epidural corticosteroid blocks. Electromyography and MRI of the lumbar plexus are indicated in this patient population to help rule out other causes of hip pain, including malignancy invading the lumbar plexus or epidural or vertebral metastatic disease at L2-L3-L4. Plain radiographs of the hip also should be obtained to rule out local disease.

SUGGESTED READINGS Cardosi RJ, Cox CS, Hoffman MS: Postoperative neuropathies after major pelvic surgery, Obstet Gynecol 100:240–244, 2002. Langebrekke A, Qvigstad E: Endometriosis entrapment of the obturator nerve after previous cervical cancer surgery, Fertil Steril 91:622–623, 2009. Toth C: Peripheral nerve injuries attributable to sport and recreation, Phys Med Rehabil Clin N Am 20:77–100, 2009. Toussaint CP, Perry EC 3rd, Pisansky MT, Anderson DE: What’s new in the diagnosis and treatment of peripheral nerve entrapment neuropathies, Neurol Clin 28:979–1004, 2010. Waldman SD: Obturator nerve block. In Pain review, Philadelphia, 2009, Saunders, pp 565–566.

Chapter 110 LATERAL FEMORAL CUTANEOUS NERVE BLOCK

Indications and Clinical Considerations Meralgia paresthetica is caused by compression of the lateral femoral cutaneous nerve by the inguinal ligament as it passes through or under the inguinal ligament (Figure 110-1). This entrapment neuropathy manifests as pain, numbness, and dysesthesias in the distribution of the lateral femoral cutaneous nerve. These symptoms often begin as a burning pain in the lateral thigh with associated cutaneous sensitivity. Patients with meralgia paresthetica note that sitting, squatting, or wearing wide belts or low-cut trousers that compress the lateral femoral cutaneous nerve causes the symptoms of meralgia paresthetica to worsen. Although traumatic lesions to the lateral femoral cutaneous nerve have been implicated in the onset of meralgia paresthetica, in most patients, no obvious antecedent trauma can be identified. Physical findings include tenderness over the lateral femoral cutaneous nerve at the origin of the inguinal ligament at the anterior superior iliac spine. A positive Tinel sign may be present over the lateral femoral cutaneous nerve as it passes beneath the inguinal ligament. Careful sensory examination of the lateral thigh reveals a sensory deficit in the distribution of the lateral femoral cutaneous nerve (Figure 110-2). No motor deficit should be present. Sitting or the wearing of tight waistbands, especially on

low-cut trousers, or wide belts that compress the lateral femoral cutaneous nerve may exacerbate the symptoms of meralgia paresthetica (Figure 110-3). Meralgia paresthetica often is misdiagnosed as lumbar radiculopathy or trochanteric bursitis or is attributed to primary hip disease. Radiographs of the hip and electromyography help distinguish meralgia paresthetica from radiculopathy or pain emanating from the hip. Most patients with a lumbar radiculopathy have back pain associated with reflex, motor, and sensory changes and lower extremity pain, whereas patients with meralgia paresthetica have no back pain and no motor or reflex changes. The sensory changes of meralgia paresthetica are limited to the distribution of the lateral femoral cutaneous nerve and should not extend below the knee. Lumbar radiculopathy and lateral femoral cutaneous nerve entrapment may coexist as the so-called double crush syndrome. Occasionally, diabetic femoral neuropathy may produce anterior thigh pain, which may confuse the diagnosis. Electromyography helps distinguish lumbar radiculopathy and diabetic femoral neuropathy from meralgia paresthetica. Plain radiographs of the back, hip, and pelvis are indicated in all patients with meralgia paresthetica to rule out occult bony disease. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody testing.

Anterior superior iliac spine

Lateral femoral cutaneous n.

Figure 110-1  Proper needle placement for lateral femoral cutaneous nerve block.

326

110  •  Lateral Femoral Cutaneous Nerve Block        327

Anterior superior iliac spine

Anterior inferior iliac spine

Figure 110-3  Direct compression of the lateral femoral cutaneous nerve occurs by the waistband of low-cut fashion trousers (“taille basse”). (From Moucharafieh R, Wehbe J, Maalouf G: Meralgia paresthetica: a result of tight new trendy low cut trousers (‘taille basse’), Int J Surg 6:164–168, 2008.)

Technique

Figure 110-2  Eliciting the characteristic sensory deficit associated with meralgia paresthetica. (From Waldman SD: Physical diagnosis of pain, Philadelphia, 2005, Saunders.)

Magnetic resonance imaging (MRI) of the spine is indicated if herniated disk, spinal stenosis, or a space-occupying lesion is suspected. MRI and ultrasound of the pelvis are also useful in evaluation of the lateral femoral cutaneous nerve (Figure 110-4). The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The lateral femoral cutaneous nerve is formed from the posterior divisions of the L2 and L3 nerves. The nerve leaves the psoas muscle and courses laterally and inferiorly to pass just beneath the ilioinguinal nerve at the level of the anterior superior iliac spine (see Figure 110-4). The nerve passes under the inguinal ligament and then travels beneath the fascia lata, where it divides into an anterior and posterior branch. The anterior branch provides limited cutaneous sensory innervation over the anterolateral thigh (see Figure 110-1). The posterior branch provides cutaneous sensory innervation to the lateral thigh from just above the greater trochanter to the knee.

The patient is placed in the supine position with a pillow under the knees if lying with the legs extended increases the patient’s pain owing to traction on the nerve. The anterior superior iliac spine is identified by palpation. A point 1 inch medial to the anterior superior iliac spine and just inferior to the inguinal ligament is then identified and prepared with antiseptic solution (see Figure 110-1). A 1½-inch, 25-gauge needle is then slowly advanced perpendicular to the skin until the needle is felt to “pop” through the fascia. A paresthesia is often elicited. After careful aspiration, a total of 5 to 7 mL of 1.0% preservative-free lidocaine and 40 mg of methylprednisolone is injected in a fanlike pattern as the needle pierces the fascia of the external oblique muscle. Care must be taken not to place the needle too deeply and enter the peritoneal cavity and perforate the abdominal viscera. After injection of the solution, pressure is applied to the injection site to decrease the incidence of postblock ecchymosis and hematoma formation, which can be quite dramatic, especially in the anticoagulated patient. Ultrasound guidance may be useful in performing this procedure in patients in whom the anatomic landmarks necessary to safely perform this procedure are difficult to identify (Figure 110-5).

Side Effects and Complications The main side effect of lateral femoral cutaneous nerve block consists of postblock ecchymosis and hematoma. If needle placement is too deep and enters the peritoneal cavity, perforation of the colon may result in the formation of intraabdominal abscess and fistula. Early detection of infection is crucial to avoid potentially lifethreatening sequelae. If the needle is placed too medially, blockade of the femoral nerve may occur and make ambulation difficult.

328        SECTION 6  •  Hip and Pelvis

Iliacus

c Ilia

A

ng

wi

B

Figure 110-4  A, Axial T1-weighted magnetic resonance image demonstrating the lateral cutaneous nerve of the thigh on both sides (white arrows), lying on the surface of the iliacus muscle just proximal to the level of the inguinal ligament. B, An oblique ultrasound image of a different subject shows the round nerve (broken white arrow) lying on the surface of the iliacus muscle immediately deep to the echo-bright inguinal ligament (white arrows). (From Waldman SD, Campbell RSD: Imaging of pain, Philadelphia, 2011, Saunders.)

SUGGESTED READINGS

Left LFC Needle

Post injection

Figure 110-5  Ultrasound image of the lateral femoral cutaneous (LFC) nerve following the injection of 2 mL of local anesthetic. Perineural spread of the local anesthetic can be seen (arrows). The needle is visible as a linear hyperechoic structure deep to the nerve. (From Hurdle MF, ­Weingarten TN, Crisostomo RA, et al: Ultrasound-guided blockade of the lateral femoral cutaneous nerve: technical description and review of 10 cases, Arch Phys Med Rehabil 88:1362–1364, 2007.)

Clinical Pearls Lateral femoral cutaneous nerve block is a simple technique that can produce dramatic relief for patients with meralgia paresthetica. As mentioned previously, pressure should be maintained on the injection site postblock to avoid ecchymosis and hematoma formation. If a patient has pain suggestive of lateral femoral cutaneous neuralgia that does not respond to lateral femoral cutaneous nerve blocks, a diagnosis of lesions more proximal in the lumbar plexus or an L2-L3 radiculopathy should be considered. Pain in such patients often responds to epidural corticosteroid blocks. Electromyography and MRI of the lumbar plexus are indicated in this patient population to help rule out other causes of lateral femoral cutaneous pain, including malignancy invading the lumbar plexus or epidural or vertebral metastatic disease at L2-L3.

Moucharafieh R, Wehbe J, Maalouf G: Meralgia paresthetica: a result of tight new trendy low cut trousers (‘taille basse’), Int J Surg 6:164–168, 2008. Shapiro BE, Preston DC: Entrapment and compressive neuropathies, Med Clin North Am 93:285–315, 2009. Trummer M, Flaschka G, Unger F, Eustacchio S: Lumbar disc herniation mimicking meralgia paresthetica: case report, Surg Neurol 54:80–81, 2000. Waldman SD: Injection technique for meralgia paresthetica. In Pain review, ­Philadelphia, 2009, Saunders, pp 556–557. Waldman SD: Meralgia paresthetica. In Pain review, Philadelphia, 2009, ­Saunders, p 301.

Chapter 111 SCIATIC NERVE BLOCK

Indications and Clinical Considerations Piriformis syndrome is caused by compression of the sciatic nerve by the piriformis muscle as it passes through the sciatic notch (Figure 111-1). This entrapment neuropathy manifests as pain, numbness, paresthesias, and associated weakness in the distribution of the sciatic nerve. These symptoms often begin as severe pain in the buttocks that radiates into the lower extremity and foot. Patients with piriformis syndrome may develop altered gait, which in turn may result in the development of coexistent sacroiliac, back, and hip pain, further confusing the clinical picture. If the condition is not treated, progressive motor deficit of the gluteal muscles and lower extremity can result. The onset of symptoms of piriformis syndrome usually occurs after direct trauma to the sacroiliac and gluteal region and occasionally as a result of repetitive hip and lower extremity motions or repeated pressure on the piriformis muscle and underlying sciatic nerve. Rarely, occult tumors in this anatomic area can also compress the sciatic nerve as it passes through the sciatic notch and produce symptoms identical to piriformis syndrome (Figure 111-2). Anomalous piriformis muscle can also compress the sciatic nerve, as can acute injury to the nerve as it passes through the muscle (Figure 111-3) Physical findings include tenderness over the sciatic notch. A positive Tinel sign over the sciatic nerve as it passes beneath the piriformis muscle often is present. A positive straight-leg raising test is suggestive of sciatic nerve entrapment that may be a result of piriformis syndrome. Palpation of the piriformis muscle reveals tenderness and a swollen, indurated muscle belly. Lifting or bending at the waist and hips increases the pain symptoms in most patients with piriformis syndrome. Weakness of affected gluteal muscles and the lower extremity and, ultimately,

muscle wasting often are seen in advanced untreated piriformis syndrome. Piriformis syndrome often is misdiagnosed as lumbar radiculopathy or is attributed to primary hip disease. Radiographs of the hip and electromyography help distinguish piriformis syndrome from radiculopathy of pain emanating from the hip. Most patients with a lumbar radiculopathy have back pain associated with reflex, motor, and sensory changes that are associated with neck pain, whereas patients with piriformis syndrome have only secondary back pain and no reflex changes. The motor and sensory changes of piriformis syndrome are limited to the distribution of the sciatic nerve below the sciatic notch. Lumbar radiculopathy and sciatic nerve entrapment may coexist as the so-called double crush syndrome. Electromyography helps distinguish lumbar radiculopathy from piriformis syndrome. Plain radiographs of the back, hip, and pelvis are indicated in all patients with piriformis syndrome to rule out occult bony disease. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the back is indicated if a herniated disk, spinal stenosis, or a space-­occupying lesion is suspected. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The piriformis muscle has its origin from the anterior sacrum. It passes laterally through the greater sciatic foramen to insert on the upper border of the greater trochanter of the femur. The piriformis muscle’s primary function is to externally rotate the femur at

Figure 111-1  Proper positioning for sciatic nerve block when piriformis syndrome is treated.

329

330        SECTION 6  •  Hip and Pelvis

say “there!” as soon as the paresthesia is felt. Paresthesia usually is elicited at a depth of 2½ to 3 inches. If the needle is felt to impinge on the bone of the sciatic notch, the needle is withdrawn and redirected laterally and slightly superiorly until a paresthesia is elicited. Once a paresthesia in the distribution of the sciatic

the hip joint. The piriformis muscle is innervated by the sacral plexus. With internal rotation of the femur, the tendinous insertion and belly of the muscle can compress the sciatic nerve and, if this persists, cause entrapment of the sciatic nerve. The sciatic nerve provides innervation to the distal lower extremity and foot with the exception of the medial aspect of the calf and foot, which are subserved by the saphenous nerve. The largest nerve in the body, the sciatic nerve is derived from the L4, L5, and the S1-S3 nerve roots. The roots fuse in front of the anterior surface of the lateral sacrum on the anterior surface of the piriform muscle. The nerve travels inferiorly and leaves the pelvis just below the piriform muscle via the sciatic notch (see Figure 111-1). Just beneath the nerve at this point is the obturator internus muscle. The sciatic nerve lies anterior to the gluteus maximus muscle; at this muscle’s lower border, the sciatic nerve lies halfway between the greater trochanter and the ischial tuberosity. The sciatic nerve courses downward past the lesser trochanter to lie posterior and medial to the femur. In the mid thigh the nerve gives off branches to the hamstring muscles and the adductor magnus muscle. In most patients the nerve divides to form the tibial and common peroneal nerves in the upper portion of the popliteal fossa, although in some patients these nerves can remain separate through their entire course. The tibial nerve continues downward to provide innervation to the distal lower extremity, whereas the common peroneal nerve travels laterally to innervate a portion of the knee joint and, via its lateral cutaneous branch, provide sensory innervation to the back and lateral side of the upper calf.

Technique The patient is placed in the Sims position with the upper leg flexed. The greater trochanter and the ischial tuberosity on the involved side are identified by palpation. Midway between these two bony landmarks lies the sciatic nerve (Figure 111-4). This midpoint is then identified and prepared with antiseptic solution. A 3½-inch, 25-gauge needle is then advanced very slowly perpendicularly to the skin until a paresthesia is elicited. The patient should be warned to expect a paresthesia and should be told to

A

Figure 111-2  Involvement of the sciatic nerve: possible fibrolipomatous hamartoma. A coronal fat-suppressed T1-weighted (TR/TE, 735/17) spin-echo magnetic resonance (MR) image obtained after intravenous gadolinium administration shows gross enlargement and enhancement of signal intensity in the left sciatic nerve (arrow). Transverse MR images (not shown) suggested the presence of a fibrolipomatous hamartoma, although a plexiform neurofibroma was also considered. (Courtesy C. Petersilge, MD, Cleveland, Ohio; from Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

B

Figure 111-3  Sagittal (A) and coronal (B) T1W magnetic resonance images of a patient with sciatic nerve compression symptoms. The piriformis muscle (black arrow) and sciatic nerve (white arrow) are demonstrated. A separate fascicle of the sciatic nerve (broken white arrow) passes between an anomalous slip of the piriformis (broken black arrow) and the main muscle belly. (From Waldman SD, Campbell RSD: Imaging of pain, Philadelphia, 2011, Saunders.)

111  •  Sciatic Nerve Block        331

intraneurally. After injection of the solution, pressure is applied to the injection site to decrease the incidence of postblock ecchymosis and hematoma formation. Ultrasound guidance may be useful in patients in whom the anatomic landmarks necessary to safely perform this procedure are difficult to identify (Figure 111-5). Piriformis m.

Sciatic nerve

Side Effects and Complications The main side effect of this injection technique is formation of postblock ecchymosis and hematoma. As mentioned earlier, pressure should be maintained on the injection site postblock to avoid ecchymosis and hematoma formation. Because a paresthesia is elicited with this technique, the potential for needle-induced trauma to the sciatic nerve remains a possibility. By advancing the needle slowly and withdrawing the needle slightly away from the nerve, needle-induced trauma to the sciatic nerve can be avoided.

Clinical Pearls

Figure 111-4  Proper needle placement for sciatic nerve block.

nerve has been elicited, the needle is withdrawn 1 mm and the patient is observed to be sure that he or she is not experiencing any persistent paresthesia. If no persistent paresthesia is present and after careful aspiration, a total of 8 mL of 1.0% preservativefree lidocaine and 40 mg of methylprednisolone is slowly injected. Care must be taken not to advance the needle into the substance of the nerve during the injection and to thereby inject solution

The just-described injection technique is a simple technique that can produce dramatic relief for patients with piriformis syndrome. The literature has implied that the sciatic nerve is more prone to needle-induced trauma with resultant persistent paresthesia than other peripheral nerves. Whether this is true or simply conjecture remains to be seen. In any event, careful preblock neurologic assessment is important to avoid preexisting neurologic deficits being later attributed to the sciatic nerve block. These assessments are especially important in patients with vulnerable nerves, such as those with diabetes. Gait training and gentle range-of-motion exercises may be introduced several days after this injection technique.

A

Lateral

Medial

Medial

Lateral

332        SECTION 6  •  Hip and Pelvis

B

Medial

Medial

C

Lateral

Sciatic nerve Needle tip

Lateral

Sciatic nerve

D Sciatic nerve Local anesthetic

Distal

Proximal

Sciatic nerve Needle tip Local anesthetic

E Sciatic nerve

Local anesthetic

Figure 111-5  Image sequence showing sciatic nerve block in the subgluteal region. A short-axis view of the sciatic nerve is shown before needle placement (A). An in-plane approach from the lateral aspect of the thigh is demonstrated where the needle tip is placed at the lateral corner of the nerve (B) with injection of local anesthetic (C). After injection, local anesthetic is distributed around the sciatic nerve (D) and tracks along the nerve (E). Note that the fascia that surrounds the sciatic nerve in the subgluteal region is thick, and careful assessment of the local anesthetic distribution is necessary if surgical anesthesia is desired. (From Gray AT: Atlas of ultrasound-guided regional anesthesia, Philadelphia, 2009, Elsevier, 2009.)

SUGGESTED READINGS Ruiz-Arranz JL, Alfonso-Venzalá I, Villalón-Ogayar J: Piriformis muscle syndrome. Diagnosis and treatment. Presentation of 14 cases, Rev Eesp Cir Traumatol Ortop 52:359–365, 2008. Tiel RL: Piriformis and related entrapment syndromes: myth and fallacy, Neurosurg Clin N Am 19:623–627, 2008.

Waldman SD: Injection technique for piriformis syndrome. In Pain review, Philadelphia, 2009, Saunders, pp 558–559. Waldman SD: Piriformis syndrome. In Pain review, Philadelphia, 2009, Saunders, p 310.

Chapter 112 INJECTION TECHNIQUE FOR OSTEITIS PUBIS SYNDROME Indications and Clinical Considerations Osteitis pubis is a constellation of symptoms that includes a localized tenderness over the symphysis pubis, pain radiating into the inner thigh, and a waddling gait. Characteristic radiographic changes of erosion, sclerosis, and widening of the symphysis pubis are pathognomonic for osteitis pubis (Figure 112-1). A disease of the second through fourth decades, osteitis pubis affects women more frequently than men. Osteitis pubis occurs most commonly after bladder, inguinal, or prostate surgery and is thought to be caused by hematogenous spread of infection to the relatively avascular symphysis pubis. It can appear without obvious inciting factors or infection. A pain syndrome clinically similar to osteitis pubis can occur in patients with rheumatoid arthritis and ankylosing spondylitis but without the characteristic radiographic changes of osteitis pubis. On physical examination the patient exhibits point tenderness over the symphysis pubis. The patient may have tenderness over the anterior pelvis and may note that the pain radiates into the inner thigh with palpation of the symphysis pubis. Patients may adopt a waddling gait to avoid movement of the symphysis pubis. This dysfunctional gait may result in lower extremity bursitis and tendinitis, which may confuse the clinical picture and further increase the patient’s pain and disability.

Plain radiographs are indicated for all patients with pain thought to be emanating from the symphysis pubis to rule out occult bony disease and tumor. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, prostate-specific antigen, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the pelvis is indicated if occult mass or tumor is suggested, as well as to confirm the diagnosis (Figure 112-2). Radionuclide bone scanning may be useful to rule out stress fractures not seen on plain radiographs as well as to confirm the diagnosis (Figure 112-3). The injection technique presented later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The symphysis pubis is a cartilaginous joint that provides articulation between the two pubic bones. The interpubic fibroelastic cartilage connects the two opposing articular surfaces of the pubic bones (Figure 112-4). These articular surfaces have thin layers of articular cartilage that are subject to damage or inflammation. The joint is relatively avascular, which accounts for the difficulty in treating joint space infections of the symphysis pubis. The joint is strengthened by a variety of ligaments, including the superior pubic ligament, which connects the top of the joint, and the arcuate ligament, which strengthens the joint from below. These ligaments are subject to disruption from blunt trauma to the pelvis, including seat-belt injuries.

Technique

Figure 112-1  Osteitis pubis. This anteroposterior radiograph of the pelvis shows widening of the symphysis pubis and erosion of bone in the inferior part of the right pubic ramus. (From Crisp AJ: Osteitis pubis. In Klippel JH, Dieppe PA, editors: Rheumatology, ed 2, London, 1998, Mosby.)

The goals of this injection technique are explained to the patient. The patient is placed in the supine position. The midpoint of pubic bones and the symphysis pubis is identified by palpation. Proper preparation of the skin overlying this point with antiseptic solution is then carried out. A syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 3½-inch, 25-gauge needle. The needle is then carefully advanced through the previously identified point at a right angle to the skin, directly toward the center of the pubic symphysis. The needle is advanced very slowly until the needle impinges on the fibroelastic cartilage of the joint (see Figure 112-4). The needle is then withdrawn slightly back out of the joint, and after careful aspiration for blood and if no paresthesia is present, the contents of the syringe are gently injected. There should be minimal resistance to injection. Fluoroscopic or ultrasound imaging may be helpful in patients in whom anatomic landmarks are difficult to identify (Figures 112-5 and 112-6). 333

334        SECTION 6  •  Hip and Pelvis

A

B

C Figure 112-2  A, Coronal fat-saturated T2-weighted magnetic resonance (MR) image. Bilateral osteitis pubis, right worse than left, characterized by bone marrow hyperintensity (arrowheads), with microtearing along the medial right obturator externus attachment and disruption of the prepubic aponeurotic complex causing secondary cleft formation (arrow). B, Axial fat-saturated T2-weighted MR image demonstrating microtearing of the right obturator externus attachment posterior to adductor longus with secondary bony stress reaction (arrow). C, Sagittal fat-saturated T2-weighted MR image. Edema and microtearing of the origin of the obturator externus (short arrow) posterior to adductor longus and brevis, extending posterior to the adductor longus origin from the prepubic aponeurotic complex (long arrow). (From MacMahon PJ, Hogan BA, Shelly MJ, et al: Imaging of groin pain, Magn Reson Imaging Clin N Am 17:655–666, 2009.)

Side Effects and Complications The proximity to the pelvic contents makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing injection techniques. Many patients also note a transient increase in pain after the justmentioned injection technique. Reactivation of latent infection, although rare, can occur; careful attention to sterile technique is mandatory.

Figure 112-3  Isotope bone scan of a 27-year-old soccer player with osteitis pubis shows concentration of radiotracer activity at the symphysis pubis in a patient with increased marginal osteoblastic activity (arrows). (From MacMahon PJ, Hogan BA, Shelly MJ, et al: Imaging of groin pain, Magn Reson Imaging Clin N Am 17:655–666, 2009.)

112  •  Injection Technique for Osteitis Pubis Syndrome        335

Osteitis pubis

Carrico & Shavell

Figure 112-4  Proper needle placement for injection of osteitis pubis.

Figure 112-5  Fluoroscopic needle placement for injection of the symphysis pubis.

Figure 112-6  Ultrasound imaging of the symphysis pubis in a patient with osteitis pubis.

336        SECTION 6  •  Hip and Pelvis

Clinical Pearls This injection technique is extremely effective in the treatment of osteitis pubis. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of this injection technique are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle stretching exercises, should be introduced several days after the patient has undergone this injection technique. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics, nonsteroidal antiinflammatory agents, and antimyotonic agents such as tizanidine may be used concurrently with this injection technique.

SUGGESTED READINGS Garcia-Porrua C, Picallo JA, Gonzalez-Gay MA: Osteitis pubis after MarshallMarchetti-Krantz urethropexy, Joint Bone Spine 70:61–63, 2003. Kai B, Lee KD, Andrews G, et al: Puck to pubalgia: imaging of groin pain in professional hockey players, Can Assoc Radiol J 61:74–79, 2010. MacMahon PJ, Hogan BA, Shelly MJ, et al: Imaging of groin pain, Magn Reson Imaging Clin N Am 17:655–666, 2009. Mandelbaum B, Mora SA: Osteitis pubis, Oper Tech Sports Med 13:62–67, 2005. Morelli V, Espinoza L: Groin injuries and groin pain in athletes: part 2, Prim Care 32:185–200, 2005. Waldman SD: Osteitis pubis. In Pain review, Philadelphia, 2009, Saunders, p 309.

Chapter 113 ILIOINGUINAL NERVE BLOCK

Indications and Clinical Considerations Ilioinguinal nerve entrapment syndrome is caused by compression of the ilioinguinal nerve as it passes through the transverse abdominis muscle at the level of the anterior superior iliac spine (Figure 113-1). The most common causes of compression of the ilioinguinal nerve at this anatomic location involve injury to the nerve induced by trauma, including direct blunt trauma to the nerve, as well as damage during inguinal herniorrhaphy and pelvic surgery. Rarely, ilioinguinal nerve entrapment syndrome occurs spontaneously. Ilioinguinal nerve entrapment syndrome manifests as paresthesias, burning pain, and occasionally numbness over the lower abdomen that radiates into the scrotum or labia and sometimes into the inner upper thigh. The pain does not radiate below the knee. The pain of ilioinguinal nerve entrapment syndrome is made worse by extension of the lumbar spine, which puts traction on the nerve. Patients with ilioinguinal nerve entrapment syndrome often assume a bent-forward novice skier’s position. If the condition is not treated, progressive motor deficit consisting of bulging of the anterior abdominal wall muscles may occur. This bulging may be confused with inguinal hernia. Physical findings include sensory deficit in the inner thigh, scrotum, or labia in the distribution of the ilioinguinal nerve. Weakness of the anterior abdominal wall musculature may be present. A Tinel sign may be elicited by tapping over the ilioinguinal nerve at the point at which it pierces the transverse abdominis muscle. As

mentioned earlier, the patient may assume a bent-forward novice skier’s position (Figure 113-2). Lesions of the lumbar plexus from trauma, hematoma, tumor, diabetic neuropathy, or inflammation can mimic the pain, numbness, and weakness of ilioinguinal neuralgia and must be included in the differential diagnosis. Electromyography helps distinguish ilioinguinal nerve entrapment from lumbar plexopathy, lumbar radiculopathy, and diabetic polyneuropathy. Plain radiographs of the hip and pelvis are indicated for all patients with ilioinguinal nerve entrapment syndrome to rule out occult bony disease. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the lumbar plexus is indicated if tumor or hematoma is suggested. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The ilioinguinal nerve is a branch of the L1 nerve root with contribution from T12 in some patients. The nerve follows a curvilinear course that takes it from its origin of the L1 and occasionally T12 somatic nerves to inside the concavity of the ilium. The ilioinguinal nerve continues anteriorly to perforate the transverse abdominis muscle at the level of the anterior superior iliac spine. The nerve may interconnect with the iliohypogastric nerve as it continues to pass along its course medially and inferiorly where

Anterior superion iliac spine Inguinal ligament Obturator foramen

Figure 113-1  Proper needle placement for ilioinguinal nerve block.

337

338        SECTION 6  •  Hip and Pelvis

Figure 113-2  The patient with ilioinguinal neuralgia will often bend forward in the novice skier’s position to relieve the pain. (From Waldman SD: Atlas of common pain syndromes, Philadelphia, 2002, Saunders.)

Lateral

Medial

4 3 Iliac crest 2 1 5

it accompanies the spermatic cord through the inguinal ring and into the inguinal canal (Figure 113-3). The distribution of the sensory innervation of the ilioinguinal nerves varies from patient to patient because there may be considerable overlap with the iliohypogastric nerve. In general, the ilioinguinal nerve provides sensory innervation to the upper portion of the skin of the inner thigh and the root of the penis and upper scrotum in men or the mons pubis and lateral labia in women (see Figure 113-1).

Technique 6

Figure 113-3  Inguinal sonoanatomy. The lateral arrow points to the ilioinguinal nerve. The medial arrow points to the iliohypogastric nerve. Both are lying between the (1) transverse abdominal and (2) internal oblique abdominal muscles. The arrowhead points to a small vessel next to the ilioinguinal nerve. In contrast to the nerves, the vessel appears completely dark (hypoechogenic). The nerves appear dark with a white horizon and white spots inside (typical sonographic shape of a peripheral nerve). 3, External oblique muscle; 4, subcutaneous tissue; 5, iliac muscle; 6, intraperitoneal space. (From Curatolo M, Eichenberger  U: ­Ultrasound-guided blocks for the treatment of chronic pain, Tech Reg Anesth Pain Manag 11:95–102, 2007.)

The patient is placed in the supine position with a pillow under the knees if lying with the legs extended increases the patient’s pain owing to traction on the nerve. The anterior superior iliac spine is identified by palpation. A point 2 inches medial and 2 inches inferior to the anterior superior iliac spine is then identified and prepared with antiseptic solution. A 1½-inch, 25-gauge needle is then advanced at an oblique angle toward the pubic symphysis (see Figure 113-1), and a total of 5 to 7 mL of 1.0% preservative-free lidocaine and 40 mg of methylprednisolone is injected in a fanlike pattern as the needle pierces the fascia of the external oblique muscle. Care must be taken not to place the needle too deeply and thereby enter the peritoneal cavity and perforate the

113  •  Ilioinguinal Nerve Block        339 Internal oblique muscle

Transversus abdominis muscle

Medial

B

A Ilioinguinal nerves

Needle tip

Ilioinguinal nerves

Internal oblique muscle

Lateral Lateral

External oblique muscle

Transversus abdominis muscle

Medial Medial

Subcutaneous tissue

External Internal oblique muscle oblique muscle

Lateral Lateral

Subcutaneous tissue

Lateral Lateral

External oblique muscle

Medial

Subcutaneous tissue

C Local anesthetic

Ilioinguinal nerves

Transversus abdominis muscle

Figure 113-4  Image sequence showing ilioinguinal nerve block. A, Sonogram demonstrating the ilioinguinal nerves before needle placement. B, An in-plane approach is demonstrated where the needle tip is placed in the fascial layer between the internal oblique and transversus muscles adjacent to the nerves. C, After injection, local anesthetic layers next to the ilioinguinal nerves. (From Gray AT: Atlas of ultrasound-guided regional anesthesia, Philadelphia, 2009, Elsevier, 2009.)

abdominal viscera. Ultrasound guidance for needle placement may be beneficial in patients in whom the anatomic landmarks necessary to safely perform this procedure are difficult to identify (Figure 113-4). Because of overlapping innervation of the ilioinguinal and iliohypogastric nerves, it is not unusual to block branches of each nerve when performing ilioinguinal nerve block. After injection of the solution, pressure is applied to the injection site to decrease the incidence of postblock ecchymosis and hematoma formation, which can be quite dramatic, especially in the anticoagulated patient.

Side Effects and Complications The main side effect of ilioinguinal nerve block is postblock ecchymosis and hematoma formation. If needle placement is too deep and the needle enters the peritoneal cavity, perforation of the colon may result in the formation of intraabdominal abscess and fistula. Early detection of infection is crucial to avoid potentially life-threatening sequelae.

Clinical Pearls Ilioinguinal nerve block is a simple technique that can produce dramatic relief for patients with ilioinguinal nerve entrapment syndrome. As mentioned previously, pressure should be maintained on the injection site postblock to avoid ecchymosis and hematoma formation. If a patient has pain suggestive of ilioinguinal neuralgia that does not respond to ilioinguinal nerve blocks, a diagnosis of lesions more proximal in the lumbar plexus or an L1 radiculopathy should be considered. Such patients often respond to epidural steroid blocks. Electromyography and MRI of the lumbar plexus are indicated in this patient population to help rule out other causes of ilioinguinal pain, including malignancy invading the lumbar plexus or epidural or vertebral metastatic disease at T12-L1.

SUGGESTED READINGS Ellis H: Anatomy of the anterior abdominal wall and inguinal canal, Anaesth Intensive Care Med 10:315–317, 2009. Morelli V, Weaver V: Groin injuries and groin pain in athletes: part 1, Prim Care 32:163–183, 2005. Waldman SD: Ilioinguinal nerve block. In Pain review, Philadelphia, 2009, ­Saunders, pp 510–511. Waldman SD: Ilioinguinal neuralgia. In Pain review, Philadelphia, 2009, ­Saunders, pp 298–299.

Chapter 114 GENITOFEMORAL NERVE BLOCK

Indications and Clinical Considerations Genitofemoral neuralgia is one of the most common causes of lower abdominal and pelvic pain encountered in clinical practice. Genitofemoral neuralgia may be caused by compression of or damage to the genitofemoral nerve anywhere along its path. The most common causes of genitofemoral neuralgia involve injury to the nerve induced by trauma, including direct blunt trauma to the nerve, as well as damage during inguinal herniorrhaphy and pelvic surgery. Rarely, genitofemoral neuralgia will occur spontaneously. Genitofemoral neuralgia manifests as paresthesias, burning pain, and, occasionally, numbness over the lower abdomen that radiates into the inner thigh in both men and women and into the labia majora in women and the bottom of the scrotum and cremasteric muscles in men. The pain does not radiate below the knee. The pain of genitofemoral neuralgia is made worse by extension of the lumbar spine, which puts traction on the nerve. Patients with genitofemoral neuralgia will often assume a bent-forward novice skier’s position. Physical findings include sensory deficit in the inner thigh, base of the scrotum, or labia majora in the distribution of the genitofemoral nerve. Weakness of the anterior abdominal wall musculature may occasionally be present. A Tinel sign may be elicited by tapping over the genitofemoral nerve at the point where it passes beneath the inguinal ligament. As mentioned, the patient may assume a bent-forward novice skier’s position.

then identified and prepared with antiseptic solution. A 1½-inch 25-gauge needle is then advanced at an oblique angle toward the pubic symphysis (see Figure 114-1). A total of 3 to 5 mL of 1.0% preservative-free lidocaine in solution with 80 mg methylprednisolone is injected in a fanlike manner as the needle pierces the inguinal ligament. Care must be taken not to place the needle too deep and thereby enter the peritoneal cavity and perforate the abdominal viscera. The femoral branch of the genitofemoral nerve is blocked by identifying the middle third of the inguinal ligament. After preparation of the skin with antiseptic solution, 3 to 5 mL of 1.0% lidocaine is infiltrated subcutaneously just below the ligament (see Figure 114-1). Care must be taken not to enter the femoral artery or vein or inadvertently block the femoral nerve. The needle must be kept in a subcutaneous location, because placement that is too deep may allow the needle to enter the peritoneal cavity and perforate the abdominal viscera. If there is an

Genitofemoral n.

Inguinal ligament

Clinically Relevant Anatomy The genitofemoral nerve arises from fibers of the L1 and L2 nerve roots. The genitofemoral nerve passes through the substance of the psoas muscle, where it divides into a genital and a femoral branch. The femoral branch passes beneath the inguinal ligament along with the femoral artery and provides sensory innervation to a small area of skin on the inside of the thigh (Figure 114-1). The genital branch passes through the inguinal canal to provide innervation to the round ligament of the uterus and labia majora in women. In men, the genital branch of the genitofemoral nerve passes with the spermatic cord to innervate the cremasteric muscles and provide sensory innervation to the bottom of the scrotum.

Femoral br. of genitofemoral n.

Genital br. of genitofemoral n.

Technique The patient is placed in the supine position with a pillow under the knees if lying with the legs extended increases the patient’s pain owing to traction on the nerve. The pubic tubercle is identified by palpation. A point just lateral to the pubic tubercle is 340

Pubic tubercle Figure 114-1  Proper needle placement for genitofemoral nerve block. (From Waldman SD: Atlas of interventional pain management, ed 2, Philadelphia, 2004, Saunders.)

114  •  Genitofemoral Nerve Block        341

Ce

Ce

FA

FA EIA

A

B

Figure 114-2  A, Ultrasound (US) image of the spermatic cord within the inguinal canal (circumscribed by arrowheads). B, US image after injection within and around the spermatic cord. Ce, Cephalad; EIA, external iliac artery; FA, femoral artery. (From Bellingham GA, Peng PWH: Ultrasound-guided interventional procedures for chronic pelvic pain, Tech Reg Anesth Pain Manag 13:171–178, 2009.)

inflammatory component to the pain, the local anesthetic is combined with 80 mg methylprednisolone and is injected in incremental doses. Subsequent daily nerve blocks are carried out in a similar manner, substituting 40 mg methylprednisolone for the initial 80-mg dose. Ultrasound guidance for needle placement may be beneficial in those patients in whom the anatomic landmarks necessary to perform this technique are difficult to identify (Figures 114-2 and 114-3). Because of overlapping innervation of the ilioinguinal and iliohypogastric nerves, it is not unusual to block branches of each nerve when performing genitofemoral nerve block. After injection of the solution, pressure is applied to the injection site to

decrease the incidence of postblock ecchymosis and hematoma formation, which can be quite dramatic, especially in the anticoagulated patient.

Side Effects and Complications The main side effect of genitofemoral nerve block is postblock ecchymosis and hematoma formation. If needle placement is too deep and the needle enters the peritoneal cavity, perforation of the colon may result in the formation of intraabdominal abscess and fistula. Early detection of infection is crucial to avoid potentially life-threatening sequelae.

342        SECTION 6  •  Hip and Pelvis External oblique muscle

Internal oblique muscle

Transversus abdominis muscle

Medial

Lateral

Subcutaneous tissue

A Ilioinguinal nerves Internal oblique muscle

External oblique muscle

Needle tip

Transversus abdominis muscle

Medial

Lateral

Subcutaneous tissue

B Ilioinguinal nerves Figure 114-3  In rare patients, three nerves (here collectively referred to as ilioinguinal nerves) can be identified between the internal oblique and transversus muscles (A). Corresponding sonogram during regional block (B). The needle tip is placed in the fascial layer between the identified nerves. (From Gray AT: Atlas of ultrasound-guided regional anesthesia, Philadelphia, 2009, Elsevier, 2009.)

Clinical Pearls Genitofemoral neuralgia is a common cause of lower abdominal and pelvic pain. Genitofemoral nerve block is a simple technique that can produce dramatic relief for patients with genitofemoral neuralgia. As mentioned previously, pressure should be maintained on the injection site postblock to avoid ecchymosis and hematoma formation. For patients who do not rapidly respond to genitofemoral nerve block, epidural steroid injection of the L1-2 segments should be considered. If a patient reports pain suggestive of genitofemoral neuralgia that does not respond to genitofemoral nerve blocks, a diagnosis of lesions more proximal in the lumbar plexus or an L1 radiculopathy should be considered. Such patients will often respond to epidural steroid blocks. Electromyography and magnetic resonance imaging of the lumbar plexus are indicated in this patient population to help rule out other causes of genitofemoral pain, including malignancy invading the lumbar plexus or epidural or vertebral metastatic disease at T12-L1.

SUGGESTED READINGS Ferzli GS, Edwards E, Al-Khoury G, Hardin R: Postherniorrhaphy groin pain and how to avoid it, Surg Clin North Am 88:203–216, 2008. Morelli V, Weaver V: Groin injuries and groin pain in athletes: part 1, Prim Care 32:163–183, 2005. Ramamurthy S: Groin pain. In Ramamurthy S, Rogers JN, Alanmanou E, ­editors: Decision making in pain management, ed 2, Philadelphia, 2006, Mosby, pp ­118–119. Waldman SD: Genitofemoral nerve block. In Pain review, Philadelphia, 2009, Saunders, pp 513–514. Waldman SD: Genitofemoral neuralgia. In Pain review, Philadelphia, 2009, ­Saunders, pp 299–300.

Chapter 115 SACROCOCCYGEAL JOINT INJECTION Indications and Clinical Considerations Coccydynia is a common pain syndrome that is characterized by pain localized to the tailbone that radiates into the lower sacrum and perineum. Coccydynia affects females more frequently than males. It occurs most often after direct trauma to the coccyx from a kick or a fall directly onto the coccyx. Coccydynia also can occur after difficult vaginal delivery. The pain of coccydynia is thought to be a result of strain of the sacrococcygeal ligament or occasionally fracture of the coccyx. Less commonly, arthritis of the sacrococcygeal joint can result in coccydynia. On physical examination the patient exhibits point tenderness over the coccyx with the pain being increased with movement of the coccyx. Movement of the coccyx also may cause sharp

paresthesias into the rectum, which can be quite distressing to the patient. On rectal examination, the levator ani, piriformis, and coccygeus muscles may feel indurated and palpation of these muscles may induce severe spasm. Sitting may exacerbate the pain of coccydynia, and the patient may attempt to sit on one buttock to avoid pressure on the coccyx. Plain radiographs are indicated for all patients with pain thought to be emanating from the coccyx to rule out fracture, occult bony disease, and tumor (Figure 115-1). On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, prostatespecific antigen, sedimentation rate, and antinuclear antibody. Magnetic resonance imaging (MRI) of the pelvis is indicated if occult mass or tumor is suspected (Figure 115-2). Radionuclide bone scanning may be useful to rule out stress fractures not seen on plain radiographs. The injection technique presented later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The triangular sacrum consists of the five fused sacral vertebrae that are dorsally convex. The sacrum inserts in a wedgelike manner between the two iliac bones, articulating superiorly with the fifth lumbar vertebra and caudally with the coccyx. On the

Arrow 1

Arrow 2

Figure 115-1  Plain radiograph of the corresponding fractures seen on magnetic resonance imaging. Arrow 1 points to an obvious coccygeal fracture with step-off. Arrow 2 demonstrates a subtle nondisplaced ­fracture.

Figure 115-2  Axial computed tomography reveals a large, lobulated mass posterior to perineal region. (From Kendi ATK, Kendi M, Muhtesem A, Yilmaz S: MR imaging findings of a large epidermal cyst, Eur J Radiol Extra 53:7–9, 2005.)

343

344        SECTION 6  •  Hip and Pelvis

anterior concave surface there are four pairs of unsealed anterior sacral foramina that allow passage of the anterior rami of the upper four sacral nerves. The posterior sacral foramina are smaller than their anterior counterparts. The vestigial remnants of the inferior articular processes project downward on each side of the sacral hiatus. These bony projections are called the sacral cornua and are important clinical landmarks for performing caudal epidural nerve block. The triangular coccyx is made up of three to five rudimental vertebrae. Its superior surface articulates with the inferior articular surface of the sacrum. The sacral hiatus is formed by the incomplete midline fusion of the posterior elements of the lower portion of the S4 and the entire S5 vertebrae. This U-shaped space is covered posteriorly by the sacrococcygeal ligament, which connects the sacrum to the coccyx.

Technique The patient is placed in the prone position with the head placed on a pillow and turned away from the clinician. The legs and heels are abducted to prevent tightening of the gluteal muscles, which can make identification of the sacrococcygeal joint more difficult (Figure 115-3). Preparation of a wide area of skin with antiseptic solution is then carried out, so that all of the landmarks can be palpated aseptically. A fenestrated sterile drape is placed to avoid contamination of the palpating finger. The middle finger of the clinician’s nondominant hand is placed over the sterile drape into the natal cleft, with the fingertip palpating the sacrococcygeal joint at the base of the sacrum. After the sacrococcygeal joint has been located, a 1½-inch, 25-gauge needle is inserted through the skin at a 45-degree angle into the region of the sacrococcygeal joint and ligament (see Figure 115-3). The use of longer needles increases the incidence of complications, including intravascular injection and inadvertent caudal epidural and dural puncture, and adds nothing to the overall success of this technique. If the sacrococcygeal ligament is penetrated, a “pop” will be felt and the needle should be withdrawn back through the ligament. If contact with the bony wall of the sacrum occurs, the needle should be withdrawn slightly. This will disengage the needle tip from the periosteum. When the needle is satisfactorily positioned, a syringe containing 5 mL of 1.0% preservative-free lidocaine and 40 mg of methylprednisolone is attached to the needle. Gentle aspiration is carried out to identify cerebrospinal fluid or blood. Albeit rarely, inadvertent dural puncture can occur and careful observation for cerebrospinal fluid must be carried out. Aspiration of blood occurs more commonly. This can happen either because of damage to veins during inadvertent insertion of the needle too deeply into the caudal canal or, less commonly, because of intravenous placement of the needle. Should the aspiration test result be positive for either cerebrospinal fluid or blood, the injection technique is discontinued and not reattempted for at least 24 hours. If the aspiration test result is negative, the contents of the syringe are slowly injected. There should be little resistance to injection. Any significant pain or sudden increase in resistance during injection suggests incorrect needle placement, and the clinician should stop injecting immediately and reassess the position of the needle. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Figure 115-3  Abducting the legs and heels to prevent tightening of the gluteal muscles can make identification of the sacrococcygeal joint easier.

Side Effects and Complications The major complication of this injection technique is infection caused by proximity to the rectum. This complication should be exceedingly rare if strict aseptic technique is followed. Approximately 25% of patients note a transient increase in pain after this injection technique; the patient should be warned of this. Care must be taken to avoid placing the needle too deeply, or inadvertent caudal epidural placement of the local anesthetic and corticosteroid, with its attendant sensory and motor blockade, could result.

115  •  Sacrococcygeal Joint Injection        345

Sympathetic trunks

Sacral splanchnic nerves

Lumbar ganglia

Sacral ganglia Ganglion impar

A

B

Figure 115-4  A, Anatomic location of the ganglion impar. Ganglion impar represents the termination of the paravertebral sympathetic chains, converging at the sacrococcygeal level. B, Sagittal T2-weighted magnetic resonance image showing the ganglion impar as a small isointense signal structure anterior to the sacrococcygeal level (white arrow). C, Contrast medium outlining the ganglion impar, seen as filling defect (black arrow) in the pool of contrast. (From Datir A, Connell D: CT-guided injection for ganglion impar blockade: a radiological approach to the management of coccydynia, Clin Radiol 65:21–25, 2010.)

C

Clinical Pearls This injection technique is extremely effective in the treatment of coccydynia. In some patients, ganglion impar block is required to provide long-lasting relief (Figure 115-4). Coexistent sacroiliitis may contribute to coccygeal pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat, gentle rangeof-motion exercises, and rectal massage of the affected muscles, should be introduced several days after the patient has undergone this injection technique for coccygeal pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Datir A, Connell D: CT-guided injection for ganglion impar blockade: a radiological approach to the management of coccydynia, Clin Radiol 65:21–25, 2010. Foye PM: Reasons to delay or avoid coccygectomy for coccyx pain, Injury 38:1328–1329, 2007. Hodges SD, Eck JC, Humphreys SC: A treatment and outcomes analysis of patients with coccydynia, Spine J 4:138–140, 2004. Oyelowo T: Coccydynia. In: Mosby’s guide to women’s health: a handbook for health professionals, St. Louis, 2007, Mosby, pp 62–64. Waldman SD: Coccydynia. In: Pain review, Philadelphia, 2009, Saunders, pp 252–253.

SECTION 7  •  Knee and Lower Extremity

Chapter 116 INTRAARTICULAR INJECTION OF THE KNEE JOINT Indications and Clinical Considerations The knee joint is susceptible to the development of arthritis from a variety of conditions that have in common the ability to damage the joint cartilage. Osteoarthritis of the joint is the most common form of arthritis that results in knee joint pain (Figure 116-1). However, rheumatoid arthritis and posttraumatic arthritis also are common causes of knee pain secondary to arthritis. Less common causes of arthritis-induced knee pain include the collagen vascular diseases, infection, villonodular synovitis, and Lyme disease. Acute infectious arthritis usually is accompanied by significant systemic symptoms, including fever and malaise, and should be

easily recognized by the astute clinician and treated appropriately with culture and antibiotics, rather than injection therapy. The collagen vascular diseases generally manifest as a polyarthropathy rather than a monoarthropathy limited to the knee joint, although knee pain secondary to collagen vascular disease responds exceedingly well to the intraarticular injection technique described later. The majority of patients with knee pain secondary to osteoarthritis and posttraumatic arthritis pain report pain that is localized around the knee and distal femur. Activity makes the pain worse; rest and heat provide some relief. The pain is constant and characterized as aching. The pain may interfere with sleep. Some patients note a grating or popping sensation with use of the joint, and crepitus may be present on physical examination.

Figure 116-1  Anteroposterior standing view of both knees in osteoarthritis. There is preferential narrowing of the medial tibiofemoral compartment with slight lateral subluxation of the tibia in relationship to the femur. (From Brower AC, Flemming DJ: Arthritis in black and white, ed 2, Philadelphia, 1997, Saunders.)

346

116  •  Intraarticular Injection of the Knee Joint        347

In addition to the just-mentioned pain, patients with arthritis of the knee joint often experience a gradual decrease in functional ability with decreasing knee range of motion, making simple everyday tasks such as walking, climbing stairs, and getting in and out of cars quite difficult. Morning stiffness and stiffness after sitting for prolonged periods are commonly reported by patients with arthritis of the knee. With continued disuse, quadriceps muscle weakness and wasting may occur and loss of support from the muscles and ligaments eventually makes the knee joint unstable. This instability is most evident when the patient attempts to walk on uneven surfaces or climb stairs. Plain radiographs are indicated for all patients with knee pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the knee is indicated if internal derangement or occult mass or tumor is suspected (Figure 116-2).

Clinically Relevant Anatomy The rounded condyles of the femur articulate with the condyles of the tibia below and the patella anteriorly (Figure 116-3). The articular surface is covered with hyaline cartilage, which is susceptible to arthritis. The joint is surrounded laterally and posteriorly by a capsule that provides support for the joint. The capsule is absent anteriorly, and in its place are the suprapatellar and infrapatellar bursae. Laterally and medially the joint is strengthened by the tendons of the vastus lateralis and medius muscles. Posteriorly, the joint is strengthened by the oblique popliteal ligament. Also adding to the strength of the joint are a variety of extracapsular ligaments, including the medial and lateral collateral ligaments and the ligamentum patellae anteriorly and the oblique popliteal ligament posteriorly. Within the joint capsule there are also a variety of ligaments that add to the strength of the joint, including the anterior and posterior cruciate ligaments.

A

The joint capsule is lined with a synovial membrane that attaches to the articular cartilage and gives rise to a number of bursa, including the suprapatellar and infrapatellar bursae. The knee joint is innervated by the femoral, obturator, common peroneal, and tibial nerves. In addition to arthritis, the knee joint is susceptible to the development of tendinitis, bursitis, and disruption of the ligaments, cartilage, and tendons.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position with a rolled blanket underneath the knee to gently flex the joint. The skin overlying the medial joint is prepared with antiseptic solution. A sterile syringe containing 5.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the joint space is identified. The clinician places his or her thumb on the lateral margin of the patella and pushes it medially. At a point at the middle of the medial edge of the patella, the needle is inserted between the patella and femoral condyles. The needle is then carefully advanced through the skin and subcutaneous tissues through the joint capsule into the joint (Figure 116-4). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected superiorly. After the joint space has been entered, the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced slightly into the joint space until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. Ultrasound guidance for needle placement may be beneficial if the anatomic landmarks necessary to safely perform this procedure are difficult to identify (Figure 116-5).

B

C

D

Figure 116-2  Meniscal tears: abnormalities of intrameniscal signal in­­ tensity and meniscal structure. Sagittal intermediate-weighted (TR/TE, 2200/20) spin-echo magnetic resonance (MR) images (A and C) and sagittal T2-weighted (TR/TE, 2200/60) spin-echo MR images (B and D). A and B, Posterior horn of the medial meniscus. Note the grade 3 pat­ tern of intrameniscal signal intensity (arrows) that increases further in signal intensity in B. The superior portion of the meniscus is irregular. C and D, Posterior horn of the medial meniscus. Note the grade 3 pattern of intrameniscal signal intensity (arrows) that reveals a further increase in signal intensity in D. (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

Tibia Fibula

Figure 116-3  Anatomy of the intraarticular space of the knee.

348        SECTION 7  •  Knee and Lower Extremity

Side Effects and Complications Femur

Patella Inflamed and arthritic joint

Figure 116-4  Proper needle position for the intraarticular space.

The major complication of intraarticular injection of the knee is infection, which should be exceedingly rare if strict aseptic technique is followed. Approximately 25% of patients report a transient increase in pain after intraarticular injection of the knee joint; the patient should be warned of this.

Clinical Pearls This injection technique is extremely effective in the treat­ ment of pain secondary to the just-mentioned causes of arthritis of the knee joint. Coexistent bursitis and tendinitis also may contribute to knee pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if care­ ful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be intro­ duced several days after the patient has undergone this injection technique for knee pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Albert C, Brocq O, Gerard D, et al: Septic knee arthritis after intra-articular hyaluronate injection: two case reports, Joint Bone Spine 73:205–207, 2006. Qvistgaard E, Kristoffersen H, Terslev L, et al: Guidance by ultrasound of intraarticular injections in the knee and hip joints, Osteoarthritis Cartilage 9:512– 517, 2001. Schumacher HR, Chen LX: Injectable corticosteroids in treatment of arthritis of the knee, Am J Med 118:1208–1214, 2005. Waldman SD: Functional anatomy of the knee. In Pain review, Philadelphia, 2009, Saunders, pp 144–149. Waldman SD: Intra-articular injection of the knee. In Pain review, Philadelphia, 2009, Saunders. pp 583–584.

Figure 116-5  Corticosteroid injection (triamcinolone)—patient with an undifferentiated oligoarthritis. Ultrasound shows the needle entering the suprapatellar recess and the bubbling effect of the drug. Air bubbles are present in the injection mixture (arrow). (From Gonçalves B, Ambrosio C, Serra S, et al: US-guided interventional joint procedures in patients with rheumatic diseases—when and how we do it? Eur J Radiol 79:407–414, 2010.)

Chapter 117 SUPERIOR TIBIOFIBULAR JOINT INJECTION Indications and Clinical Considerations The tibiofibular joint is susceptible to the development of arthritis from a variety of conditions that have in common the ability to damage the joint cartilage. Osteoarthritis of the joint is the most common form of arthritis that results in tibiofibular joint pain. However, rheumatoid arthritis and posttraumatic arthritis also are common causes of tibiofibular pain secondary to arthritis. The tibiofibular joint frequently is damaged from falls with the foot fully medially rotated and the knee flexed, and such trauma frequently results in posttraumatic arthritis. Less common causes of arthritis-induced tibiofibular pain include the collagen vascular diseases, infection, villonodular synovitis, and Lyme disease. Acute infectious arthritis usually is accompanied by significant systemic symptoms, including fever and malaise, and should be easily recognized by the astute clinician and treated appropriately with culture and antibiotics rather than injection therapy. The collagen vascular diseases generally manifest as a polyarthropathy rather than a monoarthropathy limited to the tibiofibular joint, although tibiofibular pain secondary to collagen vascular disease responds exceedingly well to the intraarticular injection technique described later. The joint can also be affected by ganglion cysts and tumors (Figure 117-1). The majority of patients with tibiofibular pain secondary to osteoarthritis and posttraumatic arthritis report pain that is localized around the tibiofibular joint and the lateral aspect of the knee. Activity, especially involving flexion and medial rotation of the knee, will make the pain worse; rest and heat provide some relief. The pain is constant and is characterized as aching. The pain may interfere with sleep. Some patients note a grating or popping sensation with use of the joint, and crepitus may be present on physical examination. In addition to the just-mentioned pain, patients with arthritis of the tibiofibular joint often experience a gradual decrease in functional ability with decreasing tibiofibular joint range of motion, making simple, everyday tasks such as walking, climbing stairs, and getting in and out of cars quite difficult. Morning stiffness and stiffness after sitting for prolonged periods are commonly reported by patients with arthritis of the tibiofibular joint. With continued disuse, muscle weakness and wasting may occur and loss of support from the muscles and ligaments eventually makes the tibiofibular joint unstable. This instability is most evident when the patient attempts to walk on uneven surfaces or climb stairs. Plain radiographs are indicated for all patients with tibiofibular joint pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell

count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the tibiofibular joint is indicated if internal derangement or occult mass or tumor is suspected (Figure 117-2). Bone scan may be useful to identify occult stress fractures involving the joint, especially if trauma has occurred.

Clinically Relevant Anatomy The lateral epicondyle of the tibia and the head of the fibula articulate at the superior tibiofibular joint (Figure 117-3). The flattened articular surfaces are covered with hyaline cartilage, which is susceptible to arthritis. The joint is surrounded by a capsule that provides support to the joint. Anterior and posterior ligaments strengthen the joint. The joint capsule is lined with a synovial membrane that attaches to the articular cartilage and

Figure 117-1  Magnetic resonance image (coronal T2-weighted gradientecho sequence) showing bilobed ganglion arising from the proximal tibiofibular joint compressing the common peroneal nerve. (From Kapoor V, Theruvil B, Britton JM: Excision arthroplasty of superior tibiofibular joint for recurrent proximal tibiofibular cyst. A report of two cases, Joint Bone Spine 71:427–429, 2004.)

349

350        SECTION 7  •  Knee and Lower Extremity

may give rise to bursae. The tibiofibular joint is innervated by the common peroneal nerves (Figure 117-4). In addition to arthritis, the tibiofibular joint is susceptible to the development of tendinitis, bursitis, and disruption of the ligaments, cartilage, and tendons.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position with a rolled blanket underneath the knee to gently flex the joint. The skin overlying the lateral aspect of the tibiofibular joint is prepared with antiseptic solution. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the head of the fibula is identified. The joint space is identified just medial to the head of the fibula. At a point at the middle of the joint space, the needle is inserted in an oblique trajectory. The needle is then carefully advanced through the skin and subcutaneous tissues through the joint capsule into the joint (Figure 117-5). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected laterally. After the joint space has been entered, the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced slightly into the joint space until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications

Figure 117-2  Magnetic resonance imaging scan of the left knee, sagittal cut, showing fluid at the proximal tibiofibular joint. (From Rethnam U, Sinha A: Instability of the proximal tibiofibular joint: an unusual cause for knee pain, Inj Extra 37:190–192, 2006.)

The major complication of intraarticular injection of the tibiofibular joint is infection, which should be exceedingly rare if strict aseptic technique is followed. Approximately 25% of patients report a transient increase in pain after intraarticular injection of the tibiofibular joint; the patient should be warned of this. Care must be taken to avoid placing the needle too posteriorly or damage to the peroneal nerve could occur.

Patellar lig

Tibia, lat. condyle Sup tibiofibular joint Fibula Biceps femoris t. Peroneus longus m Common peroneal n.

Tibia, med. condyle Sartorius t. Gracilis t. Greater saphenous v. Semitendinosus t. Gastrocnemius m., med. head Popliteus m. Post tibial a. Tibial n.

Soleus m. Gastrocnemius, lat. head and plantaris mm. Ant. tibial a.

Figure 117-3  Anatomy of the knee. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

117  •  Superior Tibiofibular Joint Injection        351

Clinical Pearls

Common peroneal n.

This injection technique is extremely effective in the treatment of pain secondary to the just-mentioned causes of arthritis of the tibiofibular joint. Coexistent bursitis and tendinitis also may contribute to tibiofibular pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is a safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Special attention must be paid to the relative relationship of the tibiofibular joint and the peroneal nerve. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for tibiofibular pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Figure 117-4  Relationship of the common peroneal nerve to the superior tibiofibular joint.

Articular capsule Inflamed and arthritic articular surface

Figure 117-5  Proper needle placement for intraarticular injection of the superior tibiofibular joint.

Bellemans J: Biomechanics of anterior knee pain, Knee 10:123–126, 2003. Crema MD, Roemer FW, Marra MD, Guermazi A: Magnetic resonance imaging assessment of subchondral bone and soft tissues in knee osteoarthritis, Rheum Dis Clin North Am 35(3):557–577, 2009. Kesson M, Atkins E: The knee. In Orthopaedic medicine: a practical approach, ed 2, Oxford, 2005, Butterworth-Heinemann, pp 403–452. Rethnam U, Sinha A: Instability of the proximal tibiofibular joint: an unusual cause for knee pain, Inj Extra 37:190–192, 2006. Waldman SD: Functional anatomy of the knee. In Pain review, Philadelphia, 2009, Saunders, pp 144–149.

Chapter 118 INJECTION TECHNIQUE FOR SEMIMEMBRANOSUS INSERTION SYNDROME Indications and Clinical Considerations

attachment of the semimembranosus muscle at the posterior medial condyle of the tibia (Figures 118-1 and 118-2). Semimembranosus insertion syndrome occurs most commonly after overuse or misuse of the knee, often after overaggressive exercise regimens. Direct trauma to the posterior knee by kicks or tackles during football also may result in the development of semimembranosus insertion syndrome.

Semimembranosus insertion syndrome is a constellation of symptoms including a localized tenderness over the posterior aspect of the medial knee joint with severe pain being elicited on palpation of the

••

Semimembranosus m. & t.

•

Vastus medialis m.

•• Med. sup. genicular a.

•

Adductor magnus t. Med. femoral condyle

• •

•• Tibial collateral lig. & joint capsule

••

••

•

Med. patellar retinaculum

• Semitendinosus t. Gracilis t.

•

Sartorius t. Greater saphenous v.

• ••

Gastrocnemius m., med. head

Figure 118-1  Anatomy of the semimembranosus muscle tendon. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

352

118  •  Injection Technique for Semimembranosus Insertion Syndrome        353

Coexistent inflammation of the semimembranosus bursa, which lies among the medial head of the gastrocnemius muscle, the medial femoral epicondyle, and the semimembranosus tendon, may exacerbate the pain of semimembranosus insertion syndrome. On physical examination the patient exhibits point tenderness over the attachment of the semimembranosus muscle at the posterior medial condyle of the tibia. The patient may have tenderness over the posterior knee and will exhibit a positive twist test for semimembranosus insertion syndrome (Figure 118-3). The twist test is performed by placing the knee in 20 degrees of flexion and passively rotating the flexed knee. The test result is positive if the pain is reproduced. Internal derangement of the knee also may be present and should be searched for on examination of the knee. Plain radiographs are indicated for all patients with pain thought to be emanating from semimembranosus insertion syndrome to rule out occult bony disease, including tibial plateau fractures and tumor. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, prostate-specific antigen, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the knee is indicated if internal derangement, occult mass, or tumor is suspected. Radionuclide bone scanning may be useful to rule out stress fractures not seen on plain radiographs. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

medial condyle of the tibia (Figure 118-4). The semimembranosus muscle flexes and medially rotates the leg at the knee as well as extending the thigh at the hip joint. A fibrous extension of the muscle called the oblique popliteal ligament extends upward and laterally to provide support to the posterior knee joint. This ligament, as well as the tendinous insertion of the muscle, is prone to development of inflammation from overuse, misuse, or trauma. The semimembranosus muscle is innervated by the tibial portion of the sciatic nerve. The common peroneal nerve is in proximity to the insertion of the semimembranosus muscle, with the tibial nerve lying more medially. The popliteal artery and vein also lie in the middle of the joint. Also serving as a source of pain in the posterior knee is the semimembranosus bursa, which lies among the medial head of the gastrocnemius muscle, the medial femoral epicondyle, and the semimembranosus tendon.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the prone position with the

Clinically Relevant Anatomy The semimembranosus muscle has its origin from the ischial tuberosity and inserts into a groove on the medial surface of the

Semimembranosus Femur

Tibia Fibula

Figure 118-2  Clinical relevant anatomy for injection of semimembranosus insertion syndrome.

Figure 118-3  The twist test for semimembranosus insertion syndrome. (From Waldman SD: Physical diagnosis of pain, Philadelphia, 2005, ­Saunders.)

354        SECTION 7  •  Knee and Lower Extremity

A

B

C

D

s bf

sm

g

E

lg

mg

F

Figure 118-4  A, Axial T1-weighted images of proximal thighs. Note how T1-weighted images allow good depiction of muscle fat planes. This image is proximal to the ischial tuberosity and shows the sacrotuberous ligament (white arrow) insertion on the tuberosity. B, Mid-tuberosity level shows the anterior semimembranosus insertion (black arrow) and the posterior conjoined tendon of biceps femoris and semitendinosus (white arrow). C, Inferior aspect of ischial tuberosity shows semimembranosus (black arrow) and conjoined tendon separating (white arrow). Note origin of adductor magnus anteriorly (open arrow). D, Continued separation of the three tendons. E, Distally the semitendinosus has a long tendon (arrow) and lies posterior to the semimembranosus. F, Tendons of the posterior knee: semimembranosus (arrowhead), semitendinosus (white arrow), gracilis (open arrow), biceps femoris (black arrow). bf, Biceps femoris; g, gracilis; lg, lateral gastrocnemius; mg, medial gastrocnemius; s, sartorius; sm, semimembranosus. (From Armfield DR, Kim DH, Towers JD, et al: Sports-related muscle injury in the lower extremity, Clin Sports Med 25:803–842, 2006.)

Semitendinosus m. Semimembranosus m. Popliteal v. Popliteal a. Tibial n.

Common peroneal n.

Carrico & Shavell

Figure 118-5  Proper needle position for injection in semimembranosus insertion syndrome.

anterior ankle resting on a folded towel to slightly flex the knee. The medial condyle of the tibia is then identified, and at a point 2 cm below the medial joint line is the insertion of the semimembranosus muscle. Proper preparation with antiseptic solution of the skin overlying this point is then carried out. A syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 3½-inch, 25-gauge needle. The needle is then carefully advanced through the previously identified point at a right angle to the skin directly toward the insertion point of the semimembranosus muscle. The needle is advanced very slowly until the needle impinges on the medial condyle of the tibia (Figure 118-5). The needle is then withdrawn slightly back out of the periosteum of the tibia. After careful aspiration for blood and if no paresthesia in the distribution of the common peroneal or tibial nerve is present, the contents of the syringe are gently injected. There should be minimal resistance to injection.

118  •  Injection Technique for Semimembranosus Insertion Syndrome        355

Side Effects and Complications The proximity to the common peroneal and tibial nerve as well as the popliteal artery and vein makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing injection techniques. Many patients also report a transient increase in pain after the just-mentioned injection technique. Although rare, infection may occur if careful attention to sterile technique is not followed.

Clinical Pearls This injection technique is extremely effective in the treatment of semimembranosus insertion syndrome. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of this injection technique are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle stretching exercises, should be introduced several days after the patient has undergone this injection technique. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics, nonsteroidal antiinflammatory agents, and antimyotonic agents such as tizanidine may be used concurrently with this injection technique.

SUGGESTED READINGS Boutin RD, Fritz RC, Steinbach LS: Imaging of sports-related muscle injuries, Magn Reson Imaging Clin N Am 11:341–371, 2003. Brockmeier SF, Klimkiewicz JJ: Overuse injuries. In Johnson DL, Mair SD, editors: Clinical sports medicine, St. Louis, 2006, Mosby, pp 625–630. Waldman SD: Functional anatomy of the knee. In Pain review, Philadelphia, 2009, Saunders, pp 144–149.

Chapter 119 CORONARY LIGAMENT INJECTION

Indications and Clinical Considerations The coronary ligaments are thin bands of fibrous tissue that anchor the medial meniscus to the tibial plateau. The coronary ligaments are extensions of the joint capsule (Figure 119-1). These ligaments are susceptible to disruption from trauma from forced rotation of the knee. The medial portion of the ligament is most commonly damaged. Patients with coronary ligament syndrome experience pain over the medial joint and increased pain on passive external rotation of the knee. Activity, especially involving flexion and external rotation of the knee, makes the pain worse; rest and heat provide some relief. The pain is constant and is characterized as aching. The pain may interfere with sleep. Coexistent bursitis, tendinitis, arthritis, or internal derangement of the knee, in particular the medial meniscus, may confuse the clinical picture after trauma to the knee joint. Plain radiographs are indicated for all patients with coronary ligament syndrome pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody

testing. Magnetic resonance imaging (MRI) of the knee is indicated if internal derangement or occult mass or tumor is suspected as well as to confirm the diagnosis of coronary ligament syndrome (Figure 119-2). Bone scan may be useful to identify occult stress fractures involving the joint, especially if trauma has occurred.

Clinically Relevant Anatomy The rounded condyles of the femur articulate with the condyles of the tibia below and the patella anteriorly. The articular surface is covered with hyaline cartilage, which is susceptible to arthritis. The joint is surrounded laterally and posteriorly by a capsule, which provides support for the joint. Extensions of the joint ­capsule, the coronary ligaments are thin bands of fibrous tissue that anchor the medial meniscus to the tibial plateau (see Figure 119-1). The capsule is absent anteriorly and in its place is the suprapatellar and infrapatellar bursa. Laterally and medially, the joint is strengthened by the tendons of the vastus lateralis and medius muscles. Posteriorly, the joint is strengthened by the oblique popliteal ligament. Also adding to the strength of the joint are various extracapsular ligaments, including the medial and lateral collateral ligaments and the ligamentum patellae anteriorly and the oblique popliteal ligament posteriorly. Within the joint

Medial meniscus Torn and inflamed coronary ligament

Figure 119-1  Proper needle placement for injection of the coronary ligament of the knee.

356

Figure 119-2  The medial meniscus in an abnormally elevated position relative to the tibial plateau secondary to coronary ligament rupture. (From Lougher L, Southgate CR, Holt MD: Coronary ligament rupture as a cause of medial knee pain, Arthroscopy 19:e157–e158, 2003.)

119  •  Coronary Ligament Injection        357

capsule there are also various ligaments that add to the strength of the joint, including the anterior and posterior cruciate ligaments. The joint capsule is lined with a synovial membrane that attaches to the articular cartilage and gives rise to a number of bursae, including the suprapatellar and infrapatellar bursae. The knee joint is innervated by the femoral, obturator, common peroneal, and tibial nerves. In addition to arthritis, the knee joint is susceptible to the development of tendinitis, bursitis, and disruption of the ligaments, cartilage, and tendons.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position with the knee flexed and the plantar aspect of the foot fixed firmly against the examination table. The foot is then maximally externally rotated and the tibial plateau is identified. The skin overlying the medial aspect of the knee joint is prepared with antiseptic solution. A sterile syringe containing 1.5 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the tender area of the tibial plateau is palpated. The needle is inserted vertically and is then carefully advanced through the skin and subcutaneous tissues through the joint capsule until it impinges on the tibial plateau (see Figure 119-1). The needle is then withdrawn slightly out of the periosteum, and the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique

is followed. Approximately 25% of patients report a transient increase in pain after injection of the coronary ligaments of the knee; the patient should be warned of this.

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to the just-mentioned causes of coronary ligament syndrome. Coexistent bursitis, tendinitis, arthritis, and internal derangement of the knee also may contribute to the patient’s pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for tibiofibular pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Aichroth P: Degenerative meniscal tears, Knee 1:181–182, 1994. Colletti JE, Kilgore KP, Derrick J: Traumatic knee pain, Ann Emerg Med 53: 403–409, 2009. Drosos GI, Pozo JL: The causes and mechanisms of meniscal injuries in the sporting and non-sporting environment in an unselected population, Knee 11: 143–149, 2004. Loudon JK: Meniscal injuries. In Placzek JD, Boyce DA, editors: Orthopaedic physical therapy secrets, ed 2, St. Louis, 2006, Elsevier, pp 564–569.

Chapter 120 MEDIAL COLLATERAL LIGAMENT INJECTION Indications and Clinical Considerations Medial collateral ligament syndrome is characterized by pain at the medial aspect of the knee joint. It is usually a result of trauma to the medial collateral ligament from falls with the leg in valgus and externally rotated, typically during snow skiing accidents (Figure 120-1). The medial collateral ligament is a broad, flat, bandlike ligament that runs from the medial condyle of the femur to the medial aspect of the shaft of the tibia, where it attaches just above the groove of the semimembranosus muscle attachment. It also attaches to the edge of the medial semilunar cartilage. The ligament is susceptible to strain at the joint line or avulsion at its origin or insertion. Patients with medial collateral ligament syndrome experience pain over the medial joint and increased pain on passive valgus and external rotation of the knee. Activity, especially involving flexion and external rotation of the knee, makes the pain worse; rest and heat provide some relief. The pain is constant and is characterized

as aching. The pain may interfere with sleep. Coexistent bursitis, tendinitis, arthritis, or internal derangement of the knee may confuse the clinical picture after trauma to the knee joint. Plain radiographs are indicated for all patients with medial collateral ligament syndrome pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and/or ultrasound imaging of the knee is indicated if internal derangement or occult mass or tumor is suspected as well as to confirm the diagnosis of suspected medical collateral ligament injury (Figure 120-2). Bone scan may be useful to identify occult stress fractures involving the joint, especially if trauma has occurred.

Clinically Relevant Anatomy The medial collateral ligament is a broad, flat, bandlike ligament that runs from the medial condyle of the femur to the medial aspect of the shaft of the tibia, where it attaches just above the groove of the semimembranosus muscle attachment (Figure 120-3). It also attaches to the edge of the medial semilunar cartilage. The medial collateral ligament is crossed at its lower part by the tendons of the sartorius, gracilis, and semitendinosus muscles. A bursa is between these tendons and the medial collateral ligament and is subject to inflammation if the ligament or tendons are traumatized.

Technique

Medial collateral ligament torn and inflamed

Figure 120-1  Proper needle position for injection of the medial collateral ligament.

358

The goals of this injection technique are explained to the patient. The patient is placed in the supine position with a rolled blanket underneath the knee to gently flex the joint. The skin overlying the lateral aspect of the knee joint is prepared with antiseptic solution. A sterile syringe containing 2.0 mL of 0.25% preservativefree bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the most tender portion of the ligament is identified. At this point the needle is inserted at a 45-degree angle to the skin. The needle is then carefully advanced through the skin and subcutaneous tissues into proximity with the medial collateral ligament (Figure 120-4). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected superiorly. The contents of the syringe are then gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

120  •  Medial Collateral Ligament Injection        359

VM St Gr

Sa

A

B

Figure 120-2  A, Cadaver image of the knee as viewed from the medial side shows the posterior oblique ligament (POL) (isolated with blue tape passed under it), the medial collateral ligament (MCL) (black arrows), the medial head of the gastrocnemius (white arrow), the semitendinosus (St), the gracilis (Gr), the sartorius (Sa), and the vastus medialis (VM). B, Cadaver image of the knee as viewed from the medial side shows the POL (black arrowheads), the MCL (black arrows), and the medial patellofemoral ligament (MPFL) (white arrows). (From Beall DP, Googe JD, Moss JT, et al: Magnetic resonance imaging of the collateral ligaments and the anatomic quadrants of the knee, Radiol Clin North Am 45:983–1002, 2007.)

Figure 120-4  Needle entry point in injection of medial collateral ­ligament.

Clinical Pearls

Figure 120-3  Coronal fat-suppressed (FS) T2-weighted magnetic resonance image of an acute grade II tear of the medial collateral ligament with poorly defined ligament fibers and surrounding soft tissue edema (white arrows). (From Waldman SD, Campbell RSD: Imaging of pain, Philadelphia, 2011, Saunders.)

Side Effects and Complications The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is followed. Approximately 25% of patients report a transient increase in pain after injection of the medial collateral ligament of the knee; the patient should be warned of this.

This injection technique is extremely effective in the treatment of pain secondary to the just-mentioned causes of medial collateral ligament syndrome. Coexistent bursitis, tendinitis, arthritis, and internal derangement of the knee also may contribute to the patient’s pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for tibiofibular pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

360        SECTION 7  •  Knee and Lower Extremity SUGGESTED READINGS Colletti JE, Kilgore KP, Derrick J: Traumatic knee pain, Ann Emerg Med 53:403– 409, 2009. Kastelein M, Wagemakers HP, Luijsterburg PA, et al: Assessing medial collateral ligament knee lesions in general practice, Am J Med 121:982–988.e2, 2008.

Waldman SD: Functional anatomy of the knee. In Pain review, Philadelphia, 2009, Saunders. Wen DY, Propeck T, Kane SM, et al: MRI description of knee medial collateral ligament abnormalities in the absence of trauma: edema related to osteoarthritis and medial meniscal tears, Magn Reson Imaging 25:209–214, 2007.

Chapter 121 INJECTION TECHNIQUE FOR QUADRICEPS EXPANSION SYNDROME Indications and Clinical Considerations The quadriceps expansion syndrome is characterized by pain at the superior pole of the patella. It is usually a result of overuse or misuse of the knee joint, as in running marathons, or direct trauma to the quadriceps tendon from kicks or head butts during football. The quadriceps tendon also is subject to acute calcific tendinitis, which may coexist with acute strain injuries. Calcific tendinitis of the quadriceps has a characteristic radiographic appearance of “whiskers” on the anterosuperior patella. Patients with quadriceps expansion syndrome experience pain over the superior pole of the sesamoid, more commonly on the medial side. The patient notes increased pain on walking down slopes or down stairs. Activity using the knee makes the pain worse; rest and heat provide some relief. The pain is constant and is characterized as aching. The pain may interfere with sleep.

On physical examination there is tenderness under the superior edge of the patella, occurring more commonly on the medial side. Active resisted extension of the knee reproduces the pain (Figure 121-1). Coexistent suprapatellar and infrapatellar bursitis, tendinitis, arthritis, or internal derangement of the knee may confuse the clinical picture after trauma to the knee joint. Plain radiographs are indicated for all patients with quadriceps ligament syndrome pain. On the basis of on the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and ultrasound imaging of the knee are indicated if internal derangement of the joint, complete disruption of the quadriceps tendon, or occult mass or tumor is suspected (Figures 121-2 and 121-3). Bone scan may be useful to identify occult stress fractures involving the joint, especially if trauma has occurred.

Clinically Relevant Anatomy The quadriceps tendon is made up of fibers from the four muscles that make up the quadriceps muscle: the vastus lateralis, the vastus intermedius, the vastus medialis, and the rectus femoris. These muscles are the primary extensors of the lower extremity at the knee. The tendons of these muscles converge and unite to form a single, exceedingly strong tendon (Figure 121-4). The patella functions as a sesamoid bone within the quadriceps tendon, with fibers of the tendon expanding around the patella and forming the medial and lateral patella retinacula, which help strengthen the knee joint. These fibers are called expansions and are subject to strain; the tendon proper is subject to the development of tendinitis. The suprapatellar, infrapatellar, and prepatellar bursae also may concurrently become inflamed with dysfunction of the quadriceps tendon.

Technique

Figure 121-1  The knee extension test for quadriceps expansion syndrome. (From Waldman SD: Physical diagnosis of pain, Philadelphia, 2005, Saunders.)

The goals of this injection technique are explained to the patient. The patient is placed in the supine position with a rolled blanket underneath the knee to gently flex the joint. The skin overlying the medial aspect of the knee joint is prepared with antiseptic solution. A sterile syringe containing 2.0 mL of 0.25% preservativefree bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the medial edge of the superior patella is identified (Figure 121-5). At this point, the needle is inserted horizontally toward the medial edge of the patella. The needle is 361

362        SECTION 7  •  Knee and Lower Extremity

Right leg Tendon Patella

Blood Tendon

Torn quadriceps

A

B

Figure 121-3  Two-dimensional ultrasound of patient’s right knee showing disrupted quadriceps tendon and an acute bleed. (From LaRocco BG, Zlupko G, Sierzenski P: Ultrasound diagnosis of quadriceps tendon rupture, J Emerg Med 35:293–295, 2008.)

then carefully advanced through the skin and subcutaneous tissues until it impinges on the medial edge of the patella (Figure 121-6). The needle is then withdrawn slightly out of the periosteum of the patella, and the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is followed. Approximately 25% of patients report a transient increase in pain after injection of the quadriceps tendon of the knee; the patient should be warned of this. C

D

Figure 121-2  Partial and complete tears of the quadriceps tendon: magnetic resonance (MR) images. A and B, Partial tear. Sagittal intermediateweighted (TR/TE, 2500/20) (A) and T2-weighted (TR/TE, 2500/80) (B) spin-echo MR images show disruption of the normal trilaminar appearance of the quadriceps tendon. The tendon (solid arrows) of the vastus intermedius muscle appears intact. The other tendons have retracted (open arrows). Note the high signal intensity at the site of the tear (arrowhead) and in the soft tissues and muscles in B. C and D, Complete tear. Sagittal intermediate-weighted (TR/TE, 2500/30) (C) and T2-weighted (TR/TE, 2500/80) (D) spin-echo MR images show a complete tear (arrows) of the quadriceps tendon at the tendo-osseous junction. Note the high signal intensity at the site of the tear in D. The patella is displaced inferiorly. (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

121  •  Injection Technique for Quadriceps Expansion Syndrome        363 Patellar lig.

Infrapatellar fat body

••

Lat. patellar retinaculum

•

••

•

Vastus lateralis t.

••

Iliotibial tract

Med. patellar retinaculum

Lat. femoral condyle

Tibial collateral lig.

Ant. cruciate lig.

•

Popliteus t.

•

Fibular collateral lig.

• ••

•• ••

•• • ••

••

•• •

••

Sartorius m. & t. Gracilis t. Semimembranosus t. Semitendinosus t. Gastrocnemius m. & t. med. head

•

••

••

•

•

••

••

••

Post. cruciate lig. Greater saphenous v.

•

• •

Gastrocnemius, lat. head & plantaris mm. Common peroneal n. Lat. sural cutaneous n.

• •

Biceps femoris m. & t.

Med. femoral condyle

••

Oblique popliteal lig. & joint capsule Tibial n. Lesser saphenous v. Popliteal a. & v. Infrapatellar fat body

Quadriceps t. Patella Lat. patellar retinaculum

•• ••

• •

Vastus lateralis t.

•

Lat. femoral condyle

••

••

•

••

•

••

••

•

•• •• ••

•

•

••

••

Tibial collateral lig.

•

••

••

••

Gastrocnemius, lat. head & plantaris mm. Common peroneal n. Lat. sural cutaneous n.

•

•

Iliotibial tract Ant. cruciate lig. Popliteus t. Fibular collateral lig. Biceps femoris m. & t.

Med. patellar retinaculum

•

Oblique popliteal lig. & joint capsule Tibial n. Popliteal a. & v.

•

•• ••

•

•

Med. femoral condyle Post. cruciate lig. Greater saphenous v. Sartorius m. & t. Gracilis t. Semimembranosus t. Semitendinosus t.

Gastrocnemius m. & t. med head

Figure 121-4  Anatomy of the quadriceps tendon and related structures. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

364        SECTION 7  •  Knee and Lower Extremity

Clinical Pearls

Figure 121-5  Needle entry point for injection for quadriceps expansion syndrome.

Rectus femoris m. Vastus medialis m.

Vastus lateralis m.

This injection technique is extremely effective in the treatment of pain secondary to the just-mentioned causes of quadriceps expansion syndrome. Coexistent bursitis, tendinitis, arthritis, and internal derangement of the knee also may contribute to the patient’s pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for tibiofibular pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

Inflamed quadriceps expansion Patellar ligament SUGGESTED READINGS

Carrico & Shavell

Figure 121-6  Proper needle position for quadriceps expansion s­yndrome.

Colletti JE, Kilgore KP, Derrick J: Traumatic knee pain, Ann Emerg Med 53: 403–409, 2009. Kesson M, Atkins E: The knee. In Orthopaedic medicine: a practical approach, ed 2, Oxford, 2005, Butterworth-Heinemann, pp 403–452. LaRocco BG, Zlupko G, Sierzenski P: Ultrasound diagnosis of quadriceps tendon rupture, J Emerg Med 35:293–295, 2008. Waldman SD: Functional anatomy of the knee. In Pain review, Philadelphia, 2009, Saunders, pp 144–149.

Chapter 122 QUADRICEPS TENDON INJECTION

Indications and Clinical Considerations Jumper’s knee is characterized by pain at the inferior or superior pole of the patella that occurs in up to 20% of jumping athletes at some point in their careers. It may affect one or both knees and occurs in males twice as often as in females when just one knee is affected. It is usually a result of overuse or misuse of the knee joint, as in running, jumping, or overtraining on hard surfaces, or of direct trauma to the quadriceps or patellar tendon or from kicks or head butts during football or kick boxing. Weak or poor quadriceps and hamstring muscle flexibility as well as congenital variants of the anatomy of the knee such as patella alta or baja and limb-length discrepancies have also been implicated as risk factors for the development of jumper’s knee. It should be noted that jumper’s knee is a repetitive stress disorder that causes tendinosis of the quadriceps and patellar tendons and is a distinct clinical entity from tendinitis of the quadriceps or patellar tendons or quadriceps expansion syndrome, which may coexist with jumper’s knee and confuse the clinical picture (see Chapter 121). Interestingly, it is postulated that the strong eccentric contraction of the quadriceps muscle to strengthen the knee joint during landing is the inciting factor during jumping rather than the jump itself. The quadriceps tendon also is subject to acute calcific tendinitis, which may coexist with acute strain injuries as well as the more chronic changes of jumper’s knee. Calcific tendinitis of the quadriceps has a characteristic radiographic appearance of “whiskers” on the anterosuperior patella. Patients with jumper’s knee experience pain over the superior and/or inferior pole of the sesamoid; and unlike quadriceps expansion syndrome, which has a predilection for the medial side of the superior pole of the patella, jumper’s knee affects both the medial and lateral sides of both the quadriceps and patellar tendons. The patient notes increased pain on walking down slopes or down stairs. Activity using the knee, especially jumping, makes the pain worse; rest and heat provide some relief. The pain is constant and is characterized as aching and may interfere with sleep. On physical examination there is tenderness of the quadriceps and/or patellar tendons, and a joint effusion may be present. Active resisted extension of the knee reproduces the pain. Coexistent suprapatellar and infrapatellar bursitis, tendinitis, arthritis, or internal derangement of the knee may confuse the clinical picture after trauma to the knee joint. Plain radiographs are indicated for all patients with knee pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and/or ultrasound imaging of the knee

is indicated if jumper’s knee is suggested because it will readily demonstrate the tendinosis of the quadriceps and/or patellar tendons responsible for this common pain syndrome (Figures 122-1 and 122-2). Bone scan may be useful to identify occult stress fractures involving the joint, especially if trauma has occurred.

Clinically Relevant Anatomy The quadriceps tendon is made up of fibers from the four muscles that constitute the quadriceps muscle: the vastus lateralis, the vastus intermedius, the vastus medialis, and the rectus femoris. These muscles are the primary extensors of the lower extremity at the knee. The tendons of these muscles converge and unite to form a single, exceedingly strong tendon (Figures 122-3 and 122-4). The patella functions as a sesamoid bone within the quadriceps

A

B

Figure 122-1  Chronic patellar tendinosis: magnetic resonance (MR) imaging. Sagittal intermediate-weighted (TR/TE, 2200/30) (A) and T2-weighted (TR/TE, 2200/80) (B) spin-echo MR images show marked thickening of the entire patellar tendon, more pronounced in the middle and distal segments, and indistinctness of the anterior margin of the tendon. No increase in signal intensity within the patellar tendon is seen in B. (Courtesy J. Yu, MD, Columbus, Ohio; from Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

365

366        SECTION 7  •  Knee and Lower Extremity

tendon, with fibers of the tendon expanding around the patella and forming the medial and lateral patellar retinacula, which help strengthen the knee joint. These fibers are called expansions and are subject to strain; the tendon proper is subject to the development of tendinitis. The suprapatellar, infrapatellar, and prepatellar bursae also may concurrently become inflamed with dysfunction of the quadriceps tendon. The patellar tendon extends from the patella to the tibial tuberosity. It is also called the patellar ligament (see Figures 122-3 and 122-4).

Technique

Figure 122-2  Longitudinal scan of the insertion of the patellar tendon on tibia. The hypoechoic change is intermixed with hyperechoic areas and takes up most of the insertion. Normal tendon is indicated by n. Power Doppler signals indicate flow inside the tendon and in its immediate surroundings. T, Tibia. (From Terslev L, Qvistgaard E, Torp-Pedersen S, et al: Ultrasound and power Doppler findings in jumper’s knee—preliminary observations, Eur J Ultrasound 13:183–189, 2001.)

The goals of this injection technique are explained to the patient. The patient is placed in the supine position with a rolled blanket underneath the knee to gently flex the joint. If only the quadriceps tendon is affected, the skin overlying the medial aspect of the knee joint is prepared with antiseptic solution. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle

••

Tibial n.

•

Rectus femoris m.

•• • •

Quadriceps t. Suprapatellar bursa Suprapatellar fat body

Femur

••

Prefemoral fat body

Lat. sup. genicular a.

••

•

•

Tibial n. Ant. cruciate lig.

Patella

•

•

••

Post. meniscofemoral lig. of Wrisberg Post. cruciate lig.

•

Patellar lig.

• •

Lat. inf. genicular a. Infrapatellar fat body

•• •

•

Transverse lig.

• ••

•

•

Tibia

Oblique popliteal lig. & joint capsule

•

•

•

Popliteus m. Gastrocnemius, lat. head & plantaris mm. Popliteal v. & tibial n. Soleus m.

Figure 122-3  Radiographic anatomy of the knee. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

122  •  Quadriceps Tendon Injection        367

•• •

Rectus femoris m.

Prefemoral fat body Quadriceps t.

•

Suprapatellar bursa Suprapatellar fat body

Lat. sup. genicular a. Tibial n.

•

Femur

••

••

Oblique popliteal lig. & joint capsule

•

••

••

• •

Patellar lig.

••

••

•

Ant. cruciate lig. Post. meniscofemoral lig. of Wrisberg

•

Post. cruciate lig.

•

Infrapatellar fat body

•

•

Transverse lig. Lat. inf. genicular a.

•

Patella

Tibial n.

••

Gastrocnemius, lat. head & plantaris mm. Popliteal v. & tibial n.

•• •• •

Tibia

••

•

Popliteus m. Soleus m.

Figure 122-4  Anatomy of the knee. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

using strict aseptic technique. With strict aseptic technique, the superior margin of the medial patella is identified (Figure 122-5). Just above this point, the needle is inserted horizontally to slide just beneath the quadriceps tendon (Figure 122-6). If the needle strikes the femur, it is then withdrawn slightly and redirected in a more anterior trajectory. When the needle is in position just below the quadriceps tendon, the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. If only the patellar tendon is affected, the skin overlying the medial portion of the lower margin of the patella is prepared with antiseptic solution. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the medial lower margin of the patella is identified (Figure 122-7). Just below this point, the

Figure 122-5  Needle entry point for injection of the quadriceps tendon.

needle is inserted at a right angle to the patella to slide beneath the ligamentum patellae into the deep infrapatellar bursa (Figure 122-8). If the needle strikes the patella, it is withdrawn slightly and redirected in a more inferior trajectory. When the needle is in position in proximity to the deep infrapatellar bursa, the contents

368        SECTION 7  •  Knee and Lower Extremity

Rectus femoris tendon Inflamed suprapatellar bursa

Inflamed and swollen deep infrapatellar bursa

Figure 122-8  Proper needle placement to inject for jumper’s knee.

Approximately 25% of patients report a transient increase in pain after injection of the quadriceps tendon of the knee; the patient should be warned of this. Figure 122-6  Proper needle position for injection of the quadriceps tendon.

Figure 122-7  Site for needle insertion for injection for jumper’s knee.

of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. If both the quadriceps and patellar tendon are affected, both of these injections should be performed.

Side Effects and Complications The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is followed. Because jumper’s knee is a result of chronic damage and degeneration of the tendons, care must be taken to avoid injecting into the substance of the tendon to avoid tendon rupture.

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to the just-mentioned causes of jumper’s knee. Coexistent bursitis, tendinitis, arthritis, and internal derangement of the knee also may contribute to the patient’s pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for the pain of jumper’s knee. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Benjamin M, Kumai T, Milz S, et al: The skeletal attachment of tendons—tendon “entheses,” Comp Biochem Physiol A Mol Integr Physiol 133:931–945, 2002. Draghi F, Danesino GM, Coscia D, et  al: Overload syndromes of the knee in adolescents: sonographic findings, J Ultrasound 11:151–157, 2008. Kon E, Filardo G, Delcogliano M, et al: Platelet-rich plasma: new clinical application: a pilot study for treatment of jumper’s knee, Injury 40:598–603, 2009. O’Keeffe SA, Hogan BA, Eustace SJ, Kavanagh EC: Overuse injuries of the knee, Magn Reson Imaging Clin N Am 17:725–739, 2009. Terslev L, Qvistgaard E, Torp-Pedersen S, et al: Ultrasound and power Doppler findings in jumper’s knee—preliminary observations, Eur J Ultrasound 13: 183–189, 2001.

Chapter 123 SUPRAPATELLAR BURSA INJECTION Indications and Clinical Considerations

the bursal sac. With overuse or misuse, these bursae may become inflamed, enlarged, and on rare occasions infected. Although there is significant intrapatient variability as to the number, size, and location of bursae, anatomists have identified a number of clinically relevant bursae, including the suprapatellar bursa. The suprapatellar bursa extends superiorly from beneath the patella under the quadriceps femoris muscle (Figures 123-1 and 123-2). This bursa may exist as a single bursal sac or, in some patients, as a multisegmented series of sacs that may be loculated.

Bursae are formed from synovial sacs, whose purpose is to allow easy sliding of muscles and tendons across one another at areas of repeated movement. These synovial sacs are lined with a synovial membrane that is invested with a network of blood vessels that secrete synovial fluid. Inflammation of the bursa results in an increase in the production of synovial fluid with swelling of

•

Rectus femoris m.

•

•

Popliteal a. & v. Joint capsule Post. cruciate lig. Post. meniscofemoral lig. of Wrisberg Post. cruciate lig.

• •

• •

•• •

Tibia

•

•

Patellar lig.

•

•

Infrapatellar synovial fold Med. inf. genicular a. Ant. cruciate lig. Infrapatellar fat body

••

•

Patella

•

•

Quadriceps t. Suprapatellar fat body

••

•

Prefemoral fat body Suprapatellar bursa

••

••

Femur

Popliteal v. Lesser saphenous v. Med. sup. genicular a.

•

••

•• • • ••

Gastrocnemius m. med. head Popliteus m. Popliteal v. & tibial n. Soleus m.

Figure 123-1  Anatomy of the suprapatellar bursa and related structures. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, ­Saunders.)

369

370        SECTION 7  •  Knee and Lower Extremity

The suprapatellar bursa is vulnerable to injury from both acute trauma and repeated microtrauma. Acute injuries frequently take the form of direct trauma to the bursa via falls directly onto the knee or patellar fractures, as well as overuse injuries, as from running on soft or uneven surfaces or from jobs that require crawling on the knees such as carpet laying. If the inflammation of

the suprapatellar bursa becomes chronic, calcification of the bursa may occur. The patient with suprapatellar bursitis frequently reports pain in the anterior knee above the patella that can radiate superiorly into the distal anterior thigh. Often the patient is unable to kneel or walk down stairs. The patient also may note a sharp, “catching” sensation with range of motion of the knee, especially on first rising. Suprapatellar bursitis often coexists with arthritis and tendinitis of the knee joint, and these other pathologic processes may confuse the clinical picture. Physical examination may reveal point tenderness in the anterior knee just above the patella. Passive flexion, as well as active resisted extension of the knee, reproduces the pain. Sudden release of resistance during this maneuver markedly increases the pain. There may be swelling in the suprapatellar region with a “boggy” feeling on palpation. Occasionally, the suprapatellar bursa may become infected, with systemic symptoms, including fever and malaise, as well as local symptoms, with rubor, color, and dolor being present. Plain radiographs of the knee may reveal calcification of the bursa and associated structures, including the quadriceps tendon, consistent with chronic inflammation. Magnetic resonance imaging (MRI) and/or ultrasound imaging is indicated if internal derangement, occult mass, or tumor of the knee is suggested, as well as to help confirm the clinical diagnosis of suprapatellar bursitis (Figure 123-3). Electromyography helps distinguish suprapatellar bursitis from femoral neuropathy, lumbar radiculopathy, and plexopathy. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Rectus femoris tendon Inflamed suprapatellar bursa

Clinically Relevant Anatomy The suprapatellar bursa extends superiorly from beneath the patella under the quadriceps femoris muscle and its tendon (see Figures 123-1 and 123-2). The bursa is held in place by a small portion of

Figure 123-2  Proper needle position for injection of the suprapatellar bursa.

*

P

P

H

* A

B

Figure 123-3  A, Drawing illustrating the suprapatellar bursa. This sagittal view demonstrates the suprapatellar bursa (*) located posteriorly to the quadriceps tendon (arrowheads) and above the patella (P). This bursa usually communicates with the knee joint. Note the infrahoffatic recess (arrow). B, Sagittal T2-weighted magnetic resonance image demonstrating fluid signal intensity within the suprapatellar bursa (arrows). Note the fluid-filled infrahoffatic recess (*). H, Hoffa fat pad; P, patella. (From Marra MD, Crema MD, Chung M, et al: MRI features of cystic lesions around the knee, Knee 15:423-438, 2008.)

123  •  Suprapatellar Bursa Injection        371

is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. Ultrasoundguided needle placement may be beneficial in those patients in whom the anatomic landmarks necessary to safely perform the procedure are difficult to identify.

Side Effects and Complications Figure 123-4  Site of needle entry for injection of the suprapatellar bursa.

the vastus intermedius muscle, called the articularis genus muscle. Both the quadriceps tendon and the suprapatellar bursa are subject to the development of inflammation caused by overuse, misuse, or direct trauma. The quadriceps tendon is made up of fibers from the four muscles that constitute the quadriceps muscle: the vastus lateralis, the vastus intermedius, the vastus medialis, and the rectus femoris. These muscles are the primary extensors of the lower extremity at the knee. The tendons of these muscles converge and unite to form a single, exceedingly strong tendon. The patella functions as a sesamoid bone within the quadriceps tendon, with fibers of the tendon expanding around the patella and forming the medial and lateral patellar retinacula, which help strengthen the knee joint. These fibers are called expansions and are subject to strain; the tendon proper is subject to the development of tendinitis. The suprapatellar, infrapatellar, and prepatellar bursae also may concurrently become inflamed with dysfunction of the quadriceps tendon.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position with a rolled blanket underneath the knee to gently flex the joint. The skin overlying the medial aspect of the knee joint is prepared with antiseptic solution. A sterile syringe containing 2.0 mL of 0.25% preservativefree bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the superior margin of the medial patella is identified (Figure 123-4). Just above this point, the needle is inserted horizontally to slide just beneath the quadriceps tendon (see Figure 123-1). If the needle strikes the femur, it is then withdrawn slightly and redirected in a more anterior trajectory. When the needle is in position just below the quadriceps tendon, the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle

The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is followed. Approximately 25% of patients report a transient increase in pain after injection of the suprapatellar bursa of the knee; the patient should be warned of this.

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to suprapatellar bursitis. Coexistent bursitis, tendinitis, arthritis, and internal derangement of the knee also may contribute to the patient’s pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for suprapatellar bursitis pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Marra MD, Crema MD, Chung M, et al: MRI features of cystic lesions around the knee, Knee 15:423–438, 2008. O’Keeffe SA, Hogan BA, Eustace SJ, Kavanagh EC: Overuse injuries of the knee, Magn Reson Imaging Clin N Am 17:725–739, 2009. Waldman SD: Bursitis syndromes of the knee. In Pain review, Philadelphia, 2009, Saunders, pp 318–322. Waldman SD: Injection technique for suprapatellar bursitis. In Pain review, Philadelphia, 2009, Saunders, pp 584–585. Yamamoto T, Akisue T, Marui T, et al: Isolated suprapatellar bursitis: computed tomographic and arthroscopic findings, Arthroscopy 19:10, 2003.

Chapter 124 PREPATELLAR BURSA INJECTION

Indications and Clinical Considerations Bursae are formed from synovial sacs whose purpose is to allow easy sliding of muscles and tendons across one another at areas of repeated movement. These synovial sacs are lined with a synovial membrane that is invested with a network of blood vessels that secrete synovial fluid. Inflammation of the bursa results in an increase in the production of synovial fluid with swelling of the bursal sac. With overuse or misuse, these bursae may become inflamed, enlarged, and on rare occasions infected. Although there is significant intrapatient variability as to the number, size, and location of bursae, anatomists have identified a number of clinically relevant bursae, including the prepatellar bursa. The prepatellar bursa lies between the subcutaneous tissues and the patella (Figure 124-1). This bursa may exist as a single bursal sac or in some patients as a multisegmented series of sacs that may be loculated. The prepatellar bursa is vulnerable to injury from both acute trauma and repeated microtrauma. Acute injuries frequently take the form of direct trauma to the bursa via falls directly onto the knee or from patellar fractures, as well as from overuse injuries, including running on soft or uneven surfaces. Prepatellar bursitis also may result from jobs that require crawling or kneeling such as carpet laying or scrubbing floors; the other name for prepatellar

bursitis is “housemaid’s knee.” If the inflammation of the prepatellar bursa becomes chronic, calcification of the bursa may occur. The patient with prepatellar bursitis frequently notes pain and swelling in the anterior knee over the patella that can radiate superiorly and inferiorly into the area surrounding the knee. Often the patient is unable to kneel or walk down stairs. The patient also may report a sharp, “catching” sensation with range of motion of the knee, especially on first rising. Prepatellar bursitis often coexists with arthritis and tendinitis of the knee joint, and these other pathologic processes may confuse the clinical picture. Physical examination may reveal point tenderness in the anterior knee just above the patella. Swelling and fluid accumulation surrounding the patella often are present. Passive flexion and active resisted extension of the knee reproduce the pain. Sudden release of resistance during this maneuver markedly increases the pain. The prepatellar bursa may become infected, with systemic symptoms, including fever and malaise, as well as local symptoms, with rubor, color, and dolor, being present. Plain radiographs of the knee may reveal calcification of the bursa and associated structures, including the quadriceps tendon, consistent with chronic inflammation. Magnetic resonance imaging (MRI) and/or ultrasound imaging is indicated if bursitis, internal derangement, occult mass, or tumor of the knee is suggested (Figure 124-2). Electromyography helps distinguish prepatellar bursitis from femoral neuropathy, lumbar radiculopathy, and plexopathy. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy

Inflamed and swollen prepatellar bursa

Figure 124-1  Proper needle position for prepatellar bursa injection.

372

The prepatellar bursa lies between the subcutaneous tissues and the patella (see Figure 124-1). The bursa is held in place by the ligamentum patellae. Both the quadriceps tendon and the prepatellar bursa are subject to the development of inflammation caused by overuse, misuse, or direct trauma. The quadriceps tendon is made up of fibers from the four muscles that constitute the quadriceps muscle: the vastus lateralis, the vastus intermedius, the vastus medialis, and the rectus femoris. These muscles are the primary extensors of the lower extremity at the knee. The tendons of these muscles converge and unite to form a single, exceedingly strong tendon. The patella functions as a sesamoid bone within the quadriceps tendon, with fibers of the tendon expanding around the patella and forming the medial and lateral patellar retinacula, which help strengthen the knee joint. These fibers are called expansions and are subject to strain; the tendon proper is subject to the development of tendinitis. The prepatellar, infrapatellar, and prepatellar bursae also may concurrently become inflamed with dysfunction of the quadriceps tendon.

124  •  Prepatellar Bursa Injection        373

Figure 124-3  Site of needle entry for injection of the prepatellar bursa.

RT prepatellar bursa TR

Figure 124-2  Prepatellar bursitis. A sagittal short tau inversion recovery (STIR) (TR/TE, 5300/30; inversion time, 150 ms) magnetic resonance image shows fluid and synovial tissue in the prepatellar bursa. (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position with a rolled blanket underneath the knee to gently flex the joint. The skin overlying the patella is prepared with antiseptic solution. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the center of the medial patella is identified (Figure 1243). Just above this point, the needle is inserted horizontally to slide subcutaneously into the prepatellar bursa (see Figure 1241). If the needle strikes the patella, it is withdrawn slightly and redirected in a more anterior trajectory. When the needle is in position in proximity to the prepatellar bursa, the contents of the syringe are then gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. Ultrasound guidance may be useful in patients in whom the anatomic landmarks necessary to safely perform this procedure are difficult to identify (Figure 124-4).

Side Effects and Complications The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients report a transient increase in pain after injection of the prepatellar bursa of the knee; the patient should be warned of this.

Figure 124-4  Transverse (axial) view of an ultrasound-guided aspiration for complex prepatellar bursitis. An 18-gauge needle is entering from the medial side of the knee (left screen, lateral; right screen, medial; top screen, superficial; bottom screen, deep). RT, right; TR, transverse. (From Smith J, Finnoff JT: Diagnostic and interventional musculoskeletal ultrasound: part 1. Fundamentals, PM R 1:64–75, 2009.)

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to prepatellar bursitis. Coexistent bursitis, tendinitis, arthritis, and internal derangement of the knee also may contribute to the patient’s pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for prepatellar bursitis pain. Vigorous exercise should be avoided, because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

374        SECTION 7  •  Knee and Lower Extremity SUGGESTED READINGS Marra MD, Crema MD, Chung M, et al: MRI features of cystic lesions around the knee, Knee 15:423–438, 2008. O’Keeffe SA, Hogan BA, Eustace SJ, Kavanagh EC: Overuse injuries of the knee, Magn Reson Imaging Clin N Am 17:725–739, 2009.

Waldman SD: Bursitis syndromes of the knee. In Pain review, Philadelphia, 2009, Saunders. Waldman SD: Prepatellar bursitis. In Pain review, Philadelphia, 2009, Saunders. Wasserman AR, Melville LD, Birkhahn RH: Septic bursitis: a case report and primer for the emergency clinician, J Emerg Med 37:269–272, 2009.

Chapter 125 SUPERFICIAL INFRAPATELLAR BURSA INJECTION Indications and Clinical Considerations Bursae are formed from synovial sacs whose purpose is to allow easy sliding of muscles and tendons across one another at areas of repeated movement. These synovial sacs are lined with a synovial membrane that is invested with a network of blood vessels that secrete synovial fluid. Inflammation of the bursa results in an increase in the production of synovial fluid with swelling of the bursal sac. With overuse or misuse, these bursae may become inflamed, enlarged, and on rare occasions infected. Although there is significant intrapatient variability as to the number, size, and location of bursae, anatomists have identified a number of clinically relevant bursae, including the superficial and deep infrapatellar bursae. The superficial infrapatellar bursa lies between the subcutaneous tissues and the upper part of the ligamentum patellae (Figure 125-1). The deep infrapatellar bursa lies between the ligamentum patellae and the tibia. These bursae may exist as single bursal sacs or in some patients as a multisegmented series of sacs that may be loculated. Both infrapatellar bursae are vulnerable to injury from both acute trauma and repeated microtrauma. Acute injuries frequently take the form of direct trauma to the bursae via falls directly onto the knee or patellar fractures, as well as overuse injuries, as from long-distance running. Infrapatellar bursitis also may result from jobs that require crawling or kneeling, such as laying carpet or scrubbing floors. If the inflammation of the infrapatellar bursae becomes chronic, calcification of the bursae may occur.

Inflamed and swollen superficial infrapatellar bursa

Figure 125-1  Proper needle position for injection of the superficial infrapatellar bursa.

The patient with infrapatellar bursitis frequently notes pain and swelling in the anterior knee below the patella that can radiate inferiorly into the area surrounding the knee. Often the patient is unable to kneel or walk down stairs. The patient also may report a sharp, “catching” sensation with range of motion of the knee, especially on first rising. Infrapatellar bursitis often coexists with arthritis and tendinitis of the knee joint, and these other pathologic processes may confuse the clinical picture. Physical examination may reveal point tenderness in the anterior knee just below the patella. Swelling and fluid accumulation often surround the lower patella. Passive flexion and active resisted extension of the knee reproduce the pain. Sudden release of resistance during this maneuver markedly increases the pain. The superficial infrapatellar bursa may become infected, with systemic symptoms, including fever and malaise, as well as local symptoms, with rubor, color, and dolor, being present. Plain radiographs of the knee may reveal calcification of the bursa and associated structures, including the quadriceps tendon, consistent with chronic inflammation. Magnetic resonance imaging (MRI) and/or ultrasound imaging is indicated if bursitis, internal derangement, occult mass, or tumor of the knee is suggested (Figure 125-2). Electromyography helps distinguish infrapatellar bursitis from neuropathy, lumbar radiculopathy, and plexopathy. The injection technique described later serves as a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The superficial infrapatellar bursa lies between the subcutaneous tissues and the ligamentum patellae (see Figure 125-1). The bursa is held in place by the ligamentum patellae. Both the ligamentum patellae and the superficial infrapatellar bursa are subject to the development of inflammation caused by overuse, misuse, or direct trauma. The ligamentum patella attaches above to the lower patella and below to the tibia. The fibers that make up the ligamentum patellae are continuations of the tendon of the quadriceps femoris muscle. The quadriceps tendon is made up of fibers from the four muscles that constitute the quadriceps muscle: the vastus lateralis, the vastus intermedius, the vastus medialis, and the rectus femoris. These muscles are the primary extensors of the lower extremity at the knee. The tendons of these muscles converge and unite to form a single, exceedingly strong tendon. The patella functions as a sesamoid bone within the quadriceps tendon, with fibers of the tendon expanding around the patella, thereby forming the medial and lateral patellar retinacula, which help strengthen the knee joint. These fibers are called expansions and are subject to strain; the tendon proper is subject to the development of tendinitis. 375

376        SECTION 7  •  Knee and Lower Extremity

P

PT T

A

B

Figure 125-2  A, Drawing illustrating superficial infrapatellar bursitis. This sagittal view demonstrates a fluid collection within the superficial infrapatellar bursa (blue), located anteriorly to the distal part of the patellar tendon (arrowheads), near its insertion at the tibia (T). B, Sagittal T2-weighted magnetic resonance image demonstrating a collection anterior to the distal patellar tendon (PT) consistent with superficial infrapatellar bursitis (arrowheads). Note the fluid-fluid level within the collection consistent with hemorrhage. P, Patella. (From Marra MD, Crema MD, Chung M, et al: MRI features of cystic lesions around the knee, Knee 15:423–438, 2008.)

or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients report a transient increase in pain after injection of the superficial infrapatellar bursa of the knee; the patient should be warned of this. Figure 125-3  Needle entry site for injection of the superficial infrapatellar bursa.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position with a rolled blanket underneath the knee to gently flex the joint. The skin overlying the patella is prepared with antiseptic solution. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the center of the lower pole of the patella is identified (Figure 125-3). Just below this point, the needle is inserted at a 45-degree angle to slide subcutaneously into the superficial infrapatellar bursa (see Figure 125-1). If the needle strikes the patella, it is then withdrawn slightly and redirected in a more inferior trajectory. When the needle is in position in proximity to the superficial infrapatellar bursa, the contents of the syringe are then gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to superficial infrapatellar bursitis. Coexistent bursitis, tendinitis, arthritis, and internal derangement of the knee also may contribute to the patient’s pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for superficial infrapatellar bursitis pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

125  •  Superficial Infrapatellar Bursa Injection        377 SUGGESTED READINGS Marra MD, Crema MD, Chung M, et al: MRI features of cystic lesions around the knee, Knee 15:423–438, 2008. O’Keeffe SA, Hogan BA, Eustace SJ, Kavanagh EC: Overuse injuries of the knee, Magn Reson Imaging Clin N Am 17:725–739, 2009. Waldman SD: Bursitis syndromes of the knee. In Pain review, Philadelphia, 2009, Saunders.

Waldman SD: Injection technique for superficial infrapatellar bursitis. In Pain review, Philadelphia, 2009, Saunders. Wasserman AR, Melville LD, Birkhahn RH: Septic bursitis: a case report and primer for the emergency clinician, J Emerg Med 37:269–272, 2009.

Chapter 126 DEEP INFRAPATELLAR BURSA INJECTION Indications and Clinical Considerations Bursae are formed from synovial sacs whose purpose is to allow easy sliding of muscles and tendons across one another at areas of repeated movement. These synovial sacs are lined with a synovial membrane that is invested with a network of blood vessels that secrete synovial fluid. Inflammation of the bursa results in an increase in the production of synovial fluid with swelling of the bursal sac. With overuse or misuse, these bursae may become inflamed, enlarged, and on rare occasions infected. Although there is significant intrapatient variability as to the number, size, and location of bursae, anatomists have identified a number of clinically relevant bursae, including the superficial and deep infrapatellar bursae. The superficial infrapatellar bursa lies between the subcutaneous tissues and the upper part of the ligamentum patellae (Figure 126-1). The deep infrapatellar bursa lies between the ligamentum patellae and the tibia. These bursae may exist as single bursal sacs or in some patients as a multisegmented series of sacs that may be loculated. The infrapatellar bursa is vulnerable to injury from both acute trauma and repeated microtrauma. Acute injuries frequently take the form of direct trauma to the bursae via falls directly onto the knee or patellar fractures, as well as overuse injuries, as from long-distance running. Infrapatellar bursitis also may result from jobs that require crawling or kneeling, such as laying carpet or scrubbing floors. If the inflammation of the infrapatellar bursae becomes chronic, calcification of the bursae may occur. The patient with deep infrapatellar bursitis frequently reports pain and swelling in the anterior knee below the patella that can radiate inferiorly into the area surrounding the knee. Often the patient is unable to kneel or walk down stairs. The patient also may report a sharp, “catching” sensation with range of motion of the knee, especially on first rising. Infrapatellar bursitis often coexists with arthritis and tendinitis of the knee joint, and these other pathologic processes may confuse the clinical picture. Physical examination may reveal point tenderness in the anterior knee just below the patella. Swelling and fluid accumulation often surround the lower patella. Passive flexion as well as active resisted extension of the knee reproduce the pain. Sudden release of resistance during this maneuver markedly increases the pain. The deep infrapatellar bursa is not as susceptible to infection as the superficial infrapatellar bursa. Plain radiographs of the knee may reveal calcification of the bursa and associated structures, including the quadriceps tendon, consistent with chronic inflammation. Magnetic resonance imaging (MRI) and/or ultrasound imaging is indicated if bursitis, internal derangement, occult mass, or tumor of the knee is suggested 378

Inflamed and swollen deep infrapatellar bursa

Figure 126-1  Proper needle position for injection of deep infrapatellar bursa.

(Figure 126-2). Electromyography helps distinguish infrapatellar bursitis from neuropathy, lumbar radiculopathy, and plexopathy. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The deep infrapatellar bursa lies between the ligamentum patellae and the tibia (see Figure 126-1). The bursa is held in place by the ligamentum patellae. Both the ligamentum patellae and the deep infrapatellar bursa are subject to the development of inflammation after overuse, misuse, or direct trauma. The ligamentum patella attaches above to the lower patella and below to the tibia. The fibers that make up the ligamentum patellae are continuations of the tendon of the quadriceps femoris muscle. The quadriceps tendon is made up of fibers from the four muscles that constitute the quadriceps muscle: the vastus lateralis, the vastus intermedius, the vastus medialis, and the rectus femoris. These muscles are the primary extensors of the lower extremity at the knee. The tendons of these muscles converge and unite to form a single, exceedingly strong tendon. The patella functions as a sesamoid bone within the quadriceps tendon, with fibers of the tendon expanding around the patella and thereby forming the medial and lateral patellar retinacula, which help strengthen the knee joint. These fibers are called expansions and are subject to strain; the tendon proper is subject to the development of tendinitis.

126  •  Deep Infrapatellar Bursa Injection        379

P

PT T

A

*

T

B

Figure 126-2  A, Drawing illustrating a deep infrapatellar bursitis. This sagittal view demonstrates a fluid collection within the deep infrapatellar bursa (blue), located posterior to the distal part of the patellar tendon (arrowheads), and anterior to the anterior aspect of the tibia (T). B, Sagittal proton density (PD)–weighted fat-suppressed magnetic resonance image showing a fluid collection (*) between the distal patellar tendon (PT) and the tibia (T), consistent with deep infrapatellar bursitis. P, Patella. (From Marra MD, Crema MD, Chung M, et al: MRI features of cystic lesions around the knee, Knee 15:423–438, 2008.)

tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients report a transient increase in pain after injection of the deep infrapatellar bursa of the knee; the patient should be warned of this. Figure 126-3  Needle entry site for injection of deep infrapatellar bursa.

Clinical Pearls Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position with a rolled blanket underneath the knee to gently flex the joint. The skin overlying the medial portion of the lower margin of the patella is prepared with antiseptic solution. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the medial lower margin of the patella is identified (Figure 126-3). Just below this point the needle is inserted at a right angle to the patella to slide beneath the ligamentum patellae into the deep infrapatellar bursa (see Figure 126-1). If the needle strikes the patella, it is withdrawn slightly and redirected in a more inferior trajectory. When the needle is in position in proximity to the deep infrapatellar bursa, the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or

This injection technique is extremely effective in the treatment of pain secondary to deep infrapatellar bursitis. Coexistent bursitis, tendinitis, arthritis, and internal derangement of the knee also may contribute to the patient’s pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for deep infrapatellar bursitis pain. Vigorous exercise should be avoided, because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

380        SECTION 7  •  Knee and Lower Extremity SUGGESTED READINGS Marra MD, Crema MD, Chung M, et al: MRI features of cystic lesions around the knee, Knee 15:423–438, 2008. O’Keeffe SA, Hogan BA, Eustace SJ, Kavanagh EC: Overuse injuries of the knee, Magn Reson Imaging Clin N Am 17:725–739, 2009.

Waldman SD: Bursitis syndromes of the knee. In Pain review, Philadelphia, 2009, Saunders. Wasserman AR, Melville LD, Birkhahn RH: Septic bursitis: a case report and primer for the emergency clinician, J Emerg Med 37:269–272, 2009.

Chapter 127 PES ANSERINUS BURSA INJECTION

Indications and Clinical Considerations Bursae are formed from synovial sacs whose purpose is to allow easy sliding of muscles and tendons across one another at areas of repeated movement. These synovial sacs are lined with a synovial membrane that is invested with a network of blood vessels that secrete synovial fluid. Inflammation of the bursa results in an increase in the production of synovial fluid with swelling of the bursal sac. With overuse or misuse, these bursae may become inflamed, enlarged, and on rare occasions infected. Although there is significant intrapatient variability as to the number, size, and location of bursae, anatomists have identified a number of clinically relevant bursae, including the pes anserinus bursa. The pes anserinus bursa lies beneath the pes anserinus tendon, which is the insertional tendon of the sartorius, gracilis, and semitendinosus muscle to the medial side of the tibia (Figure 127-1). This bursa may exist as a single bursal sac or in some patients as a multisegmented series of sacs that may be loculated. Patients with pes anserinus bursitis experience pain over the medial knee joint and increased pain on passive valgus and external rotation of the knee. Activity, especially involving flexion and external rotation of the knee, makes the pain worse; rest and heat provide some relief. Often the patient is unable to kneel or walk down stairs. The pain is constant and is characterized as aching. The pain may interfere with sleep. Coexistent bursitis, tendinitis, arthritis, or internal derangement of the knee may confuse the clinical picture after trauma to the knee joint. Frequently the medial collateral ligament also is involved if the patient has sustained trauma to the medial knee joint. If the inflammation of the pes anserinus bursa becomes chronic, calcification of the bursa may occur.

Figure 127-1  Needle entry site for pes anserinus bursa injection.

Physical examination may reveal point tenderness in the anterior knee just below the medial knee joint at the tendinous insertion of the pes anserinus tendon. Swelling and fluid accumulation often surround the bursa. Active resisted flexion of the knee reproduces the pain. Sudden release of resistance during this maneuver markedly increases the pain. Rarely, the pes anserinus bursa becomes infected in a manner analogous to infection of the prepatellar bursa. Plain radiographs of the knee may reveal calcification of the bursa and associated structures, including the pes anserinus tendon, consistent with chronic inflammation. Magnetic resonance imaging (MRI) is indicated if bursitis, internal derangement, occult mass, or tumor of the knee is suggested (Figure 127-2). Electromyography helps distinguish pes anserinus bursitis from neuropathy, lumbar radiculopathy, and plexopathy. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The pes anserinus bursa lies between the combined tendinous insertion of the sartorius, gracilis, and semitendinosus muscles and the medial tibia (see Figure 127-1). The bursa is subject to

Figure 127-2  Pes anserinus ganglion cyst (bursitis). Magnetic resonance image shows a large, fluid-filled mass adjacent to the anteromedial portion of the tibia. (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

381

382        SECTION 7  •  Knee and Lower Extremity

the development of inflammation after overuse, misuse, or direct trauma. The medial collateral ligament often also is involved if the medial knee has been subjected to trauma. The medial collateral ligament is a broad, flat, bandlike ligament that runs from the medial condyle of the femur to the medial aspect of the shaft of the tibia, where it attaches just above the groove of the semimembranosus muscle. It also attaches to the edge of the medial semilunar cartilage. The medial collateral ligament is crossed at its lower part by the tendons of the sartorius, gracilis, and semitendinosus muscles.

Medial collateral ligament

Inflamed pes anserinus bursa

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position with a rolled blanket underneath the knee to gently flex the joint. The skin just below the medial knee joint is prepared with antiseptic solution. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the pes anserinus tendon is identified by having the patient strongly flex his or her leg against resistance. The point distal to the medial joint space at which the pes anserinus tendon attaches to the tibia is the location of the pes anserinus bursa ­(Figures 127-3 and 127-4). The bursa usually is identified by point tenderness at that spot. At this point the needle is inserted at a 45-degree angle to the tibia to pass through the skin, the subcutaneous tissues, and the pes anserinus tendon into the pes anserinus bursa (see Figure 127-1). If the needle strikes the tibia, it is withdrawn slightly into the substance of the bursa. When the needle is in position in proximity to the pes anserinus bursa, the contents of the syringe are then gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients report a transient increase in pain after injection of the pes anserinus bursa of the knee; the patient should be warned of this.

Figure 127-3  Relationship of the pes anserinus bursa to the medial collateral ligament.

PES

* A

*

MCL

C

A B

B

Figure 127-4  A, Anatomic dissection of the medial knee demonstrating the pes anserinus (asterisk), medial collateral ligament (MCL), and sartorius (A), gracilis (B), and semitendinosus (C) tendons, with a needle placed into the pes anserinus bursa. The black rectangle over the needle demonstrates the orientation of the transducer used for B. Left, distal; right, proximal; top, anterior; bottom, posterior. B, Coronal oblique ultrasound image of a needle (white arrowheads) in the pes anserinus bursa (asterisk) between the MCL (black arrows) and the pes anserinus (PES). Left, proximal; right, distal; top, superficial; bottom, deep. (From Finnoff JT, Nutz DJ, Henning PT, et al: Accuracy of ultrasound-guided versus unguided pes anserinus bursa injections, PM R 2:732–739, 2010.)

127  •  Pes Anserinus Bursa Injection        383

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to pes anserinus bursitis. Coexistent bursitis, tendinitis, arthritis, and internal derangement of the knee, including damage to the medial collateral ligament, also may contribute to the patient’s pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for pes anserinus bursitis pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Marra MD, Crema MD, Chung M, et al: MRI features of cystic lesions around the knee, Knee 15:423–438, 2008. O’Keeffe SA, Hogan BA, Eustace SJ, Kavanagh EC: Overuse injuries of the knee, Magn Reson Imaging Clin N Am 17:725–739, 2009. Waldman SD: Bursitis syndromes of the knee. In Pain review, Philadelphia, 2009, Saunders. Wasserman AR, Melville LD, Birkhahn RH: Septic bursitis: a case report and primer for the emergency clinician, J Emerg Med 37:269–272, 2009.

Chapter 128 ILIOTIBIAL BAND BURSA INJECTION Indications and Clinical Syndromes Bursae are formed from synovial sacs whose purpose is to allow easy sliding of muscles and tendons across one another at areas of repeated movement. These synovial sacs are lined with a synovial membrane that is invested with a network of blood vessels that secrete synovial fluid. Inflammation of the bursa results in an increase in the production of synovial fluid with swelling of the bursal sac. With overuse or misuse, these bursae may become inflamed, enlarged, and on rare occasions infected. Although there is significant intrapatient variability as to the number, size, and location of bursae, anatomists have identified a number of clinically relevant bursae, including the iliotibial band bursa. The iliotibial band bursa lies beneath the iliotibial band tendon, which is an extension of the deep fascia of the thigh that attaches to the lateral condyle of the tibia (Figures 128-1, 128-2, and 128-3). The rubbing back and forth of the iliotibial band across the lateral condyle of the femur during running or bicycling may cause inflammation of the iliotibial bursa as well as the iliotibial band (Figures 128-4 and 128-5). This bursa may exist as a single bursal sac or in some patients as a multisegmented series of sacs that may be loculated in nature. Patients with iliotibial band bursitis experience pain over the lateral side of the distal femur just over the lateral femoral condyle. The onset of iliotibial bursitis frequently occurs after long-distance biking or jogging with worn-out shoes without proper cushioning. Activity, especially that involving resisted abduction and passive adduction of the lower extremity, makes the pain worse; rest and heat provide some relief. Flexion of the affected knee also reproduces the pain in many patients with iliotibial band bursitis. Often the patient is unable to kneel or walk down stairs. The pain is constant and is characterized as aching in nature. The pain may interfere with sleep. Coexistent bursitis, tendinitis, arthritis, or internal derangement of the knee may confuse the clinical picture after trauma to the knee joint. If the inflammation of the iliotibial band bursa becomes chronic, calcification of the bursa may occur. Physical examination may reveal point tenderness over the lateral condyle of the femur just above the tendinous insertion of the iliotibial band (Figure 128-6). Swelling and fluid accumulation often surround the bursa. Palpation of this area while having the patient flex and extend the knee may result in a creaking or “catching” sensation. Active resisted abduction of the lower extremity reproduces the pain, as does passive adduction. Sudden release of resistance during this maneuver markedly increases the pain. Pain is exacerbated by having the patient stand with all the weight on the affected extremity and then flex the affected knee 30 to 40 degrees. 384

Inflamed iliotibial bursa

Inflamed iliotibial band

Figure 128-1  Proper needle position for iliotibial band bursa injection.

Plain radiographs of the knee may reveal calcification of the bursa and associated structures, including the iliotibial band tendon, consistent with chronic inflammation. Magnetic resonance imaging (MRI) and/or ultrasound imaging scan is indicated if bursitis, internal derangement, occult mass, or tumor of the knee is suspected. Electromyography helps distinguish iliotibial band bursitis from neuropathy, lumbar radiculopathy, and plexopathy. The following injection technique serves as a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The iliotibial band bursa lies between the iliotibial band and the lateral condyle of the femur. The iliotibial band is an extension of the fascia lata, which inserts at the lateral condyle of the tibia. The iliotibial band can rub backward and forward over the lateral epicondyle of the femur and irritate the iliotibial bursa beneath it (see Figures 128-1, 128-2, and 128-3). The iliotibial bursa is subject to the development of inflammation caused by overuse, misuse, or direct trauma.

128  •  Iliotibial Band Bursa Injection        385

Iliotibial tract

••

•

Vastus lateralis m.

•

•

•

Infrapatellar fat body

••

Vastus medialis m. & t. (apon)

Femur

••

•

Med. meniscus, ant. horn

•

Iliotibial tract

Med. sup. genicular a.

Tibia

•• •• •

Sartorius, gracilis & semitendinosus tt.

•

••

Ant. tibial recurrent a. Extensor digitorum longus m. Tibialis ant. m.

Figure 128-2  Anatomy of the iliotibial band and adjacent structures. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position with a rolled blanket underneath the knee to gently flex the joint. The skin over the lateral epicondyle of the femur is prepared with antiseptic solution. A sterile syringe containing 2.0 mL of 0.25% preservativefree bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the iliotibial band bursa is identified by locating the point of maximal tenderness over the lateral condyle of the femur (see Figure 128-6). The bursa usually is identified by point tenderness at that spot. At this point, the needle is inserted at a 45-degree angle to the femoral condyle to pass through the skin, the subcutaneous tissues, and the iliotibial band into the iliotibial band bursa (see Figure 128-1). If the needle strikes the femur, it is withdrawn slightly into the

substance of the bursa. When the needle is in position in proximity to the iliotibial band bursa, the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is infection. This complication should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients report a transient increase in pain after injection of the iliotibial band bursa of the knee; the patient should be warned of this.

Med. sup. genicular a.

• •

Vastus lateralis m.

••

•

Iliotibial tract

Vastus medialis m. and t. (apon.)

Femur

• •

Infrapatellar fat body

Med. meniscus, ant. horn

•

•

Iliotibial tract

••

Tibia

••

•• •

Tibialis ant. m.

Sartorius, gracilis and semitendinosus tt.

Figure 128-3  Anatomy of the iliotibial band and adjacent structures. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

A

B

Figure 128-4  Iliotibial band friction syndrome. A, Coronal T2 fat-saturated image demonstrates high signal intensity in the fatty tissue deep to the iliotibial band (arrowhead) with loss of definition of the normally low-signal-intensity band (arrow). B, Axial T2 fat-saturated image demonstrates high signal intensity in the fatty tissue deep to the iliotibial band consistent with replacement by inflammatory tissue (arrowhead). (From O’Keeffe SA, Hogan BA, Eustace SJ, Kavanagh EC: Overuse injuries of the knee, Magn Reson Imaging Clin N Am 17:725–739, 2009.)

128  •  Iliotibial Band Bursa Injection        387

A

B

Figure 128-5  A, Drawing illustrating an iliotibial bursitis. This coronal view demonstrates a fluid collection within the iliotibial bursa (blue), located medial to the iliotibial band (arrowheads). B, Coronal proton density (PD)–weighted magnetic resonance image with fat suppression demonstrating a fluid collection located medial to the distal iliotibial band (arrowheads), consistent with iliotibial bursitis. (From Marra MD, Crema MD, Chung M, et al: MRI features of cystic lesions around the knee, Knee 15:423–438, 2008.)

SUGGESTED READINGS Draghi F, Danesino GM, Coscia D, et  al: Overload syndromes of the knee in adolescents: sonographic findings, J Ultrasound 11:151–157, 2008. Ellis R, Hing W, Reid D: Iliotibial band friction syndrome—a systematic review, Man Ther 12:200–208, 2007. Marra MD, Crema MD, Chung M, et al: MRI features of cystic lesions around the knee, Knee 15:423–438, 2008. O’Keeffe SA, Hogan BA, Eustace SJ, Kavanagh EC: Overuse injuries of the knee, Magn Reson Imaging Clin N Am 17:725–739, 2009. Waldman SD: The iliotibial band bursa. In Pain review, Philadelphia, 2009, ­Saunders, pp 154–155.

Figure 128-6  Needle entry site for iliotibial band bursa injection.

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to iliotibial band bursitis. Coexistent bursitis, tendinitis of the insertion of the iliotibial band, arthritis, and internal derangement of the knee also may contribute to the patient’s pain and may require additional treatment with more localized injection of local anesthetic and depot-steroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique in order to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for iliotibial band bursitis pain. Vigorous exercise should be avoided, because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

Chapter 129 MEDIAL COLLATERAL LIGAMENT BURSA INJECTION Indications and Clinical Considerations Bursae are formed from synovial sacs whose purpose is to allow easy sliding of muscles and tendons across one another at areas of repeated movement. These synovial sacs are lined with a synovial membrane that is invested with a network of blood vessels that secrete synovial fluid. Inflammation of the bursa results in an increase in the production of synovial fluid with swelling of the bursal sac. With overuse or misuse, these bursae may become inflamed, enlarged, and on rare occasions infected. Although there is significant intrapatient variability as to the number, size, and location of bursae, anatomists have identified a number of clinically relevant bursae, including the medial collateral ligament bursa. The medial collateral ligament bursa lies beneath the medial collateral ligament, which is a broad, flat, bandlike ligament that runs from the medial condyle of the femur to the medial aspect of the shaft of the tibia, where it attaches just above the groove of the semimembranosus muscle attachment (Figure 129-1). The medial collateral ligament (which is also known as the tibial collateral ligament) also attaches to the edge of the medial semilunar cartilage (Figure 129-2). The rubbing back and forth

of the medial collateral ligament across the medial condyle of the femur during running or bicycling may cause inflammation of the medial collateral ligament bursa. This bursa may exist as a single bursal sac or in some patients as a multisegmented series of sacs that may be loculated. Patients with medial collateral ligament bursitis experience pain over the medial side of the distal femur just over the medial femoral condyle. The onset of medial collateral ligament bursitis frequently occurs after long-distance biking or jogging with wornout shoes without proper cushioning. Activity, especially that involving resisted adduction and passive abduction of the lower extremity, makes the pain worse; rest and heat provide some relief. Flexion of the affected knee also reproduces the pain in many patients with medial collateral ligament bursitis. Often the patient is unable to kneel or walk down stairs. The pain is constant and is characterized as aching and may interfere with sleep. Coexistent bursitis, tendinitis, arthritis, or internal derangement of the knee may confuse the clinical picture after trauma to the knee joint. If the inflammation of the medial collateral ligament bursa becomes chronic, calcification of the bursa may occur. Physical examination may reveal point tenderness over the medial condyle of the femur just above the tendinous insertion

ITB

A

B

Figure 129-1  A, Drawing illustrating medial collateral ligament (MCL) bursitis. This coronal view demonstrates a fluid collection (blue) between the superficial (arrowheads) and deep (arrows) layers of the MCL. B, Coronal proton density (PD)–weighted magnetic resonance image with fat suppression demonstrating a fluid collection located between the deep (arrows) and superficial (arrowheads) portions of the MCL, consistent with MCL bursitis. ITB, Iliotibial band. (From Marra MD, Crema MD, Chung M, et al: MRI features of cystic lesions around the knee, Knee 15:423–438, 2008.)

388

129  •  Medial Collateral Ligament Bursa Injection        389

of the medial collateral ligament (see Figure 129-1). Swelling and fluid accumulation often surround the bursa. Palpation of this area while having the patient flex and extend the knee may result in a creaking or “catching” sensation. Active resisted adduction of the lower extremity reproduces the pain, as does passive abduction. Sudden release of resistance during this maneuver markedly increases the pain. Pain is exacerbated by having the patient stand with all the weight on the affected extremity and then flex the affected knee 30 to 40 degrees. Plain radiographs of the knee may reveal calcification of the bursa and associated structures, including the medial collateral ligament tendon, consistent with chronic inflammation. Magnetic resonance imaging (MRI) and/or ultrasound imaging is indicated if internal derangement, occult mass, or tumor of the knee is suggested as well as to confirm the diagnosis (see Figure 129-1). Electromyography helps distinguish medial collateral ligament bursitis from neuropathy, lumbar radiculopathy, and plexopathy. The injection technique described later serves as a diagnostic and therapeutic maneuver.

Clinically Relevant Anatomy The medial collateral ligament bursa lies between the medial collateral ligament and the medial condyle of the femur. The medial collateral ligament is a broad, flat, bandlike ligament that runs from the medial condyle of the femur to the medial aspect of the shaft of the tibia, where it attaches just above the groove of the semimembranosus muscle attachment. The medial collateral ligament (which is also known as the tibial collateral ligament) also attaches to the edge of the medial semilunar cartilage. The medial collateral ligament can rub backward and forward over the medial epicondyle of the femur and irritate the iliotibial bursa beneath

Vastus lateralis m. Lat sup genicular a.

it (see Figures 129-1 and 129-2). The medial collateral ligament bursa is subject to the development of inflammation caused by overuse, misuse, or direct trauma.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position with a rolled blanket underneath the knee to gently flex the joint. The skin over the medial epicondyle of the femur is prepared with antiseptic solution. A sterile syringe containing 2.0 mL of 0.25% preservativefree bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the medial collateral ligament bursa is identified by locating the point of maximal tenderness over the medial condyle of the femur (Figure 129-3). The bursa usually is identified by point tenderness at that spot. At this point, the needle is inserted at a 45-degree angle to the femoral condyle to pass through the skin, the subcutaneous tissues, and the medial collateral ligament into the medial collateral ligament bursa. If the needle strikes the femur, it is withdrawn slightly into the substance of the bursa. When the needle is in position in proximity to the medial collateral ligament bursa, the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. Ultrasound guidance may be useful in patients in whom the anatomic landmarks necessary to safely perform this procedure are difficult to identify.

Vastus medialis m. Med. sup genicular a.

Femur

Ant cruciate lig. Infrapatellar fat body Lat. meniscus, ant. horn Iliotibial tract

Extensor digitorum longus m. Ant tibial recurrent a.

Post. cruciate lig. Med. meniscus Tibial collateral lig.

Tibia

Med. inf. genicular a. Sartorius, gracilis and semitendinosus tt.

Figure 129-2  Anatomy of the medial collateral ligament and adjacent structures. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an ­anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

390        SECTION 7  •  Knee and Lower Extremity

Clinical Pearls

Large, swollen, and inflamed bursa Medial collateral ligament

Figure 129-3  Injection technique for medial lateral collateral bursitis.

Side Effects and Complications The major complication of this injection technique is infection. This complication should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients report a transient increase in pain after injection of the medial collateral ligament bursa of the knee; the patient should be warned of this.

This injection technique is extremely effective in the treatment of pain secondary to medial collateral ligament bursitis. Coexistent bursitis, tendinitis of the insertion of the medial collateral ligament, arthritis, and internal derangement of the knee also may contribute to the patient’s pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for medial collateral ligament bursitis pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptomatology. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Marra MD, Crema MD, Chung M, et al: MRI features of cystic lesions around the knee, Knee 15:423–438, 2008. O’Keeffe SA, Hogan BA, Eustace SJ, Kavanagh EC: Overuse injuries of the knee, Magn Reson Imaging Clin N Am 17:725–739, 2009. Waldman SD: Bursitis syndromes of the knee. In Pain review, Philadelphia, 2009, ­Saunders. Wasserman AR, Melville LD, Birkhahn RH: Septic bursitis: a case report and primer for the emergency clinician, J Emerg Med 37:269–272, 2009.

Chapter 130 ILIOTIBIAL BAND INJECTION

Indications and Clinical Considerations Runner’s knee is a common cause of lateral knee pain encountered in clinical practice. Also known as iliotibial band friction syndrome, runner’s knee is an overuse syndrome caused by friction injury to the iliotibial band as it rubs back and forth across the lateral epicondyle of the femur during running (Figures 130-1 and 130-2). Runner’s knee is a distinct clinical entity from iliotibial bursitis, although these two painful conditions frequently coexist. Runner’s knee occurs more often in patients with genu varum and planus feet, although worn-out jogging shoes have also been implicated in the evolution of this painful disorder. Patients with runner’s knee experience pain over the lateral side of the distal femur just over the lateral femoral epicondyle.

The pain tends to be a little less localized than the pain associated with iliotibial bursitis, and there is rarely an effusion as can be seen with iliotibial bursitis. The onset of runner’s knee frequently occurs after long-distance biking or jogging with worn-out shoes without proper cushioning. Activity, especially that involving resisted abduction and passive adduction of the lower extremity, makes the pain worse rest and heat provide some relief. Flexion of the affected knee also reproduces the pain in many patients with runner’s knee. Often the patient is unable to kneel or walk down stairs. The pain is constant and is characterized as aching and may interfere with sleep. Coexistent bursitis, tendinitis, arthritis, or internal derangement of the knee may confuse the clinical picture after trauma to the knee joint. If the inflammation of the iliotibial band becomes chronic, calcification may occur.

Femur Iliotibial band Lateral epicondyle

Figure 130-1  Pathophysiology of iliotibial band syndrome.

391

392        SECTION 7  •  Knee and Lower Extremity

Figure 130-2  Normal iliotibial tract: magnetic resonance (MR) imaging. A coronal intermediate-weighted (TR/TE, 2000/20) spin-echo MR image shows the iliotibial tract (solid arrows) attaching to Gerdy tubercle (open arrow) in the tibia. A small joint effusion is evident just medial to the iliotibial tract (arrowhead). (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

Physical examination may reveal point tenderness over the lateral epicondyle of the femur just above the tendinous insertion of the iliotibial band (see Figure 130-1). If coexistent iliotibial bursitis is present, swelling and fluid accumulation often surround the bursa. Palpation of this area while having the patient flex and extend the knee may result in a creaking or “catching” sensation. Active resisted abduction of the lower extremity reproduces the pain, as does passive adduction. Sudden release of resistance during this maneuver markedly increases the pain. Pain is exacerbated by having the patient stand with all the weight on the affected extremity and then flexing the affected knee 30 to 40 degrees. Plain radiographs of the knee may reveal calcification of the bursa and associated structures, including the iliotibial band tendon, consistent with chronic inflammation. Magnetic resonance imaging (MRI) and ultrasound imaging are indicated if runner’s knee, iliotibial band bursitis, internal derangement, occult mass, or tumor of the knee is suspected (Figures 130-3 and 130-4). Electromyography helps distinguish iliotibial band bursitis from neuropathy, lumbar radiculopathy, and plexopathy. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The iliotibial band bursa lies between the iliotibial band and the lateral condyle of the femur. The iliotibial band is an extension of the fascia lata, which inserts at the lateral condyle of the tibia (see Figures 130-1 to 130-5). The iliotibial band can rub backward and forward over the lateral epicondyle of the femur and become

Figure 130-3  Iliotibial tract syndrome: magnetic resonance (MR) imaging. This coronal fat-suppressed fast spin-echo (TR/TE, 2500/42) MR image shows an abnormal, poorly defined region of high signal intensity deep to the iliotibial tract. (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

–1

Femoral condyle

Tibia

–2

Figure 130-4  Iliotibial band syndrome. Wide longitudinal ultrasound scan along the iliotibial band (arrows): edematous swelling of the soft tissues deep to the iliotibial band, whose fibers do not show any alteration. (From Draghi F, Danesino GM, Coscia D, et al: Overload syndromes of the knee in adolescents: sonographic findings, J Ultrasound 11:151–157, 2008.)

inflamed (see Figure 130-5). This rubbing can also irritate the iliotibial bursa beneath it. The iliotibial bursa is subject to the development of inflammation caused by overuse, misuse, or direct trauma.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position with a rolled blanket underneath the knee to gently flex the joint. The skin over the lateral epicondyle of the femur is prepared with antiseptic solution. A sterile syringe containing 2.0 mL of 0.25% preservativefree bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the iliotibial band bursa is identified by locating the point of maximal tenderness over the lateral condyle of the femur (Figure 130-6). The bursa usually is identified by

130  •  Iliotibial Band Injection        393

Med. sup. genicular a.

• •

Vastus lateralis m.

••

•

Iliotibial tract

Vastus medialis m. & t. (apon)

Femur

•• •

Infrapatellar fat body

Med. meniscus, ant. horn

•

•

Iliotibial tract

••

Tibia

••

Sartorius, gracilis & semitendinosus tt.

•

Tibialis ant. m.

••

Figure 130-5  Anatomy of the iliotibial tract and adjacent structures. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

point tenderness at that spot. At this point, the needle is inserted at a 45-degree angle to the femoral condyle to pass through the skin, subcutaneous tissues, and the iliotibial band into the iliotibial band bursa (see Figure 130-6). If the needle strikes the femur, it is withdrawn slightly into the substance of the bursa. When the needle is in position in proximity to the iliotibial band bursa, the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant

resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is infection. This complication should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients report a transient increase in pain after injection of the iliotibial band of the knee; the patient should be warned of this.

394        SECTION 7  •  Knee and Lower Extremity SUGGESTED READINGS Costa ML, Marshall T, Donell ST, Phillips H: Knee synovial cyst presenting as iliotibial band friction syndrome, Knee 11:247–248, 2004. Ellis R, Hing W, Reid D: Iliotibial band friction syndrome—a systematic review, Man Ther 12:200–208, 2007. Farrell KC, Reisinger KD, Tillman MD: Force and repetition in cycling: possible implications for iliotibial band friction syndrome, Knee 10:103–109, 2003. Rosen AL, Scuderi GR, McCann PD: Running injuries. In Scuderi GR, McCann PD, editors: Sports medicine: a comprehensive approach, ed 2, St. Louis, 2004, Mosby, pp 550–556. Schueller-Weidekamm C, Schueller G, Uffmann M, Bader T: Incidence of chronic knee lesions in long-distance runners based on training level: findings at MRI, Eur J Radiol 58:286–293, 2006. Strakowski JA, Jamil T: Management of common running injuries, Phys Med Rehabil Clin N Am 17:537–552, 2006.

Figure 130-6  Injection technique for runner’s knee.

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to runner’s knee. Coexistent bursitis, tendinitis of the insertion of the iliotibial band, arthritis, and internal derangement of the knee also may contribute to the patient’s pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for runner’s knee pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

Chapter 131 HAMSTRING TENDON INJECTION

Indications and Clinical Considerations The musculotendinous insertion of the hamstring group of muscles is susceptible to the development of tendinitis for two reasons. First, the knee joint is subjected to significant repetitive motion under weight-bearing conditions. Second, the blood supply to the musculotendinous unit is poor, making healing of microtrauma difficult. Calcium deposition around the tendon may occur if the inflammation continues, thereby complicating subsequent treatment. Tendinitis of the musculotendinous insertion of the hamstring frequently coexists with bursitis of the associated bursae of the knee joint, creating additional pain and functional disability. The onset of hamstring tendinitis is usually acute, occurring after overuse or misuse of the muscle group. Inciting factors may include long-distance running, dancing injuries, or the vigorous use of exercise equipment for lower-extremity strengthening. The pain is constant and severe, with sleep disturbance often reported. The patient may attempt to splint the inflamed tendon by holding the knee in a slightly flexed position and assuming a lurch-type antalgic gait. Patients with hamstring tendinitis exhibit severe pain to palpation over the tendinous insertion, with the medial portion of the tendon more commonly affected than the lateral portion. Crepitus or “creaking” may be present when the tendon is palpated while the patient flexes the affected knee. In addition to the just-mentioned pain, patients with hamstring tendinitis often experience a gradual decrease in functional ability with decreasing knee range of motion that makes simple everyday tasks such as walking, climbing stairs, or getting into a car quite difficult. With continued disuse, muscle wasting may occur and a stiff knee may develop. Plain radiographs are indicated for all patients with posterior knee pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the knee is indicated if internal derangement, occult mass, or partial tendon disruption is suspected. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

chronic, they may rupture if subjected to sudden trauma during exercise or injection. The primary innervation of these muscles is the sciatic nerve. Intimately involved with these muscles are a number of bursae located around the knee joint. These bursae also are subject to inflammation and can coexist as sources of knee pain, along with tendinitis of the hamstring tendon insertion.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the prone position with the anterior ankle resting on a folded towel to slightly flex the knee. The hamstring tendon is identified by having the patient flex the affected leg at the knee against resistance. The tendon is traced inferiorly below the joint line to its point of insertion. Proper preparation with antiseptic solution of the skin overlying this point is then done. A syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 2-inch, 25-gauge needle. The needle is then carefully advanced through the previously identified point at a right angle to the skin, directly toward the insertion point of the affected hamstring tendon. The needle is advanced very slowly until the needle impinges on bone (see Figure 131-1). The needle is then withdrawn slightly back out of the periosteum. After careful aspiration for blood is negative and if no paresthesia in the distribution of the common peroneal or tibial nerve is present, the contents of the syringe are gently injected. There should be minimal resistance to injection.

Side Effects and Complications The proximity to the common peroneal and tibial nerves, as well as the popliteal artery and vein, makes it imperative that this Biceps femoris m. Semitendinosus m. Semimembranosus m.

Clinically Relevant Anatomy The hamstring muscle group is made up of the muscles of the posterior fascial compartment of the thigh: the biceps femoris, the semitendinosus, the semimembranosus, and a small part of the adductor magnus muscles. These muscles are the primary knee flexors, and their tendinous insertions on the tibia and fibula are subject to the development of tendinitis (Figures 131-1 and 131-2). If the inflammation of the tendinous insertions of these muscles becomes

Inflamed tendinous insertions

Figure 131-1  Proper needle position for hamstring tendon injection.

395

396        SECTION 7  •  Knee and Lower Extremity

Vastus lateralis m.

Vastus medialis m.and t.(apon.)

Femur Iliotibial tract, vastus lateralis t.(apon.) and lat. patellar retinaculum Infrapatellar fat body

Tibia Lat.patellar retinaculum

Med meniscus, ant.horn

Sartorius, gracilis, and semitendinosus tt. and med. patellar retinaculum

Figure 131-2  Anatomy relevant to hamstring tendon injection. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

procedure be done only by those well versed in the regional anatomy and experienced in performing injection techniques. Trauma to the hamstring tendon from the injection itself remains an everpresent possibility. Tendons that are highly inflamed or previously damaged are subject to rupture if they are directly injected. The risk of this complication can be greatly decreased if the clinician uses gentle technique and stops injecting immediately if significant resistance to injection is encountered. Many patients also report a transient increase in pain after the just-mentioned injection technique. Although rare, infection may occur if careful attention to sterile technique is not followed.

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to hamstring tendinitis. Coexistent bursitis and arthritis also may contribute to knee pain and may require additional treatment with a more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for shoulder pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Donatelli RA: Overuse injury and muscle damage. In Sports-specific rehabilitation, St. Louis, 2006, Churchill Livingstone, pp 97–103. Hoskins W, Pollard H: The management of hamstring injury—part 1: issues in diagnosis, Man Ther 10:96–107, 2005. Miller TT: Common tendon and muscle injuries: lower extremity, Ultrasound Clin 2:595–615, 2007. O’Keeffe SA, Hogan BA, Eustace SJ, Kavanagh EC: Overuse injuries of the knee, Magn Reson Imaging Clin N Am 17:725–739, 2009.

Chapter 132 INJECTION TECHNIQUE FOR BAKER CYST Indications and Clinical Considerations Baker cyst of the knee is the result of an abnormal accumulation of synovial fluid in the medial aspect of the popliteal fossa. Overproduction of synovial fluid from the knee joint results in Semitendinosus m. Semimembranosus m.

Popliteal v. Popliteal a. Tibial n.

Inflamed cyst

Common peroneal n.

Carrico & Shavell

Figure 132-1  Proper needle position for injection of a Baker cyst.

A

the formation of a cystic sac (Figures 132-1 and 132-2). This sac often communicates with the knee joint, with a one-way valve effect causing a gradual expansion of the cyst. Often a tear of the medial meniscus or a tendinitis of the medial hamstring tendon is the inciting factor responsible for the development of a Baker cyst. Patients with rheumatoid arthritis are especially susceptible to the development of Baker cysts (Figure 132-3). Patients with Baker cysts report a feeling of fullness behind the knee. Often they notice a lump behind the knee that becomes more apparent when flexing the affected knee. The cyst may continue to enlarge and may dissect inferiorly into the calf. Patients with rheumatoid arthritis are prone to this phenomenon, and the pain associated with dissection into the calf may be confused with thrombophlebitis and inappropriately treated with anticoagulants (Figure 132-4). Occasionally, the Baker cyst spontaneously ruptures, usually after frequent squatting. On physical examination, the patient with Baker cyst has a cystic swelling in the medial aspect of the popliteal fossa. Baker cysts can become quite large, especially in patients with rheumatoid arthritis. Activity, including squatting or walking, makes the pain of Baker cyst worse; rest and heat provide some relief. The pain is constant and is characterized as aching and may interfere with sleep. Baker cyst may spontaneously rupture, and there may be rubor and color in the calf that may mimic thrombophlebitis. Homans sign is negative, and no cords are palpable. Occasionally,

B

Figure 132-2  Synovial cyst: knee. A, A transaxial multiplanar gradient recalled (MPGR) (TR/TE, 500/15; flip angle, 20 degrees) magnetic resonance (MR) image shows the site of origin of the synovial cyst. Note the fluid of high signal intensity passing posterior to the semimembranosus tendon (open arrow), medial to the tendon (solid arrow) of the medial head of the gastrocnemius muscle, and lateral to the semitendinosus tendon (arrowhead). B, A coronal T2-weighted (TR/TE, 2000/80) spin-echo MR image in the same patient as in A shows the more distal extent of the synovial cyst, which is superficial to the medial head of the gastrocnemius muscle. (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

397

398        SECTION 7  •  Knee and Lower Extremity

Figure 132-3  Arthrogram of knee in patient with rheumatoid arthritis demonstrating communication between the synovial space and the Baker cyst (arrow). (From Torreggiani WC, Al-Ismail K, Munk PL, et al: The imaging spectrum of Baker’s [popliteal] cysts, Clin Radiol 57:681–691, 2002.)

Figure 132-4  Ruptured Baker cyst in patient initially thought to have acute thrombophlebitis. (From Torreggiani WC, Al-Ismail K, Munk PL, et al: The imaging spectrum of Baker’s [popliteal] cysts, Clin Radiol 57:681–691, 2002.)

tendinitis of the medial hamstring tendon may be confused with Baker cyst. Plain radiographs are indicated for all patients with Baker cyst. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and ultrasound imaging of the knee is indicated if internal derangement or occult mass or tumor is suspected and also is useful in confirming the presence of a Baker cyst (see Figure 132-2; Figure 132-5).

Clinically Relevant Anatomy The popliteal fossa is posterior to the knee joint. The fossa contains the popliteal artery and vein, the common peroneal and tibial nerves, and the semimembranosus bursa. The knee joint capsule is lined with a synovial membrane that attaches to the articular cartilage and gives rise to a number of bursae, including the suprapatellar, prepatellar, infrapatellar, and semimembranosus bursae. When these bursae become inflamed, they may overproduce synovial fluid, which can become trapped in saclike cysts because of a one-way valve phenomenon. This occurs commonly in the medial aspect of the popliteal fossa (see Figure 132-1).

Technique The goals of this injection technique are explained to the patient. The patient is placed in the prone position with the anterior ankle resting on a folded towel to slightly flex the knee. The middle of

Cyst SMT

Gastroc MFC

Figure 132-5  Ultrasound image of a Baker cyst arising out of the knee joint between the medial head of the gastrocnemius muscle (Gastroc) and the semimembranosus tendon (SMT). The cyst is anechoic, consistent with simple fluid. The back of the medial femoral condyle (MFC) is also visible. (From Waldman SD, Campbell RSD: Baker cyst. In Imaging of pain, Philadelphia, 2011, Saunders, pp 413–414.)

the popliteal fossa is identified and, at a point two fingers medial and two fingers below the popliteal crease, the skin is prepared with antiseptic solution. A syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 2-inch, 22-gauge needle.

132  •  Injection Technique for Baker Cyst        399

The needle is carefully advanced through the previously identified point at a 45-degree angle from the medial border of the popliteal fossa directly toward the Baker cyst. With continuous aspiration the needle is advanced very slowly to avoid trauma to the tibial nerve or popliteal artery or vein. When the cyst is entered, synovial fluid suddenly aspirates into the syringe. At this point, if there is no paresthesia in the distribution of the common peroneal or tibial nerve, the contents of the syringe are gently injected (see Figure 132-1). There should be minimal resistance to injection. A pressure dressing is then placed over the cyst to prevent fluid reaccumulation.

Side Effects and Complications The proximity to the common peroneal and tibial nerves, as well as the popliteal artery and vein, makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing injection techniques. Many patients also report a transient increase in pain after the just-mentioned injection technique. Although rare, infection may occur if careful attention to sterile technique is not followed.

Clinical Pearls This injection technique is extremely effective in the treatment of pain and swelling secondary to Baker cyst. Coexistent semimembranosus bursitis, medial hamstring tendinitis, or internal derangement of the knee also may contribute to knee pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation, as well as reaccumulation of fluid within the Baker cyst, can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle rangeof-motion exercises, should be introduced several days after the patient has undergone this injection technique for knee pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Lowe G, Tait C: Limb pain and swelling, Medicine 37:96–99, 2009. Ozgocmen S, Kaya A, Kocakoc E, et al: Rupture of Baker’s cyst producing pseudothrombophlebitis in a patient with Reiter’s syndrome, Kaohsiung J Med Sci 20:600–603, 2004. Sansone V, Sosio C, da Gama Malchèr M, de Ponti A: Two cases of tibial nerve compression caused by uncommon popliteal cysts, Arthroscopy 18:8, 2002. Waldman SD: Baker’s cyst of the knee. In Pain review, Philadelphia, 2009, Saunders, p 317. Waldman SD, Campbell RSD: Baker cyst. In Imaging of pain, Philadelphia, 2011, Saunders, p 413.

Chapter 133 FABELLA INJECTION

Indications and Clinical Considerations Accessory bones of the knee are relatively common, with a reported incidence of the fabella of approximately 25%. The fabella, which is Latin for “little bean,” is asymptomatic in the vast majority of patients. However, in some patients the fabella becomes painful owing to repeated rubbing of the fabella on the posterolateral femoral condyle. Located in the lateral head of gastrocnemius, the fabella is often mistaken for a joint mouse or osteophyte, or it is simply identified as a serendipitous finding on imaging of the knee (Figure 133-1). It may be either unilateral or bilateral and may be partite or tripartite, further adding to the clinician’s confusion. The fabella may exist as an isolated asymptomatic or symptomatic finding. There are reports of fracture and dislocation of the fabella as well as hypertrophy of this accessory bone causing compression of the peroneal

Figure 133-1  Plain radiograph of the right knee (lateral). (From Robertson A, Jones SCE, Paes R, Chakrabarty G: The fabella: a forgotten source of knee pain? Knee 11:243–245, 2004.)

400

nerve (Figure 133-2). As the fabella is covered in hyaline cartilage to facilitate its articulation with the femoral condyle, it is subject to chondromalacia as well as the development of osteoarthritis. Knee pain secondary to the fabella is characterized by tenderness and pain over the posterolateral knee. The patient often feels that he or she has gravel in the knee and may report a severe grating sensation with range of motion of the knee. The pain of fabella worsens with activities that require repeated flexion and extension of the knee. Fabella may coexist with tendinitis and bursitis of the knee. On physical examination, pain can be reproduced by pressure on the fabella. A creaking or grating sensation may be appreciated by the examiner, and locking or catching on range of motion of the knee may occasionally be present. Plain radiographs are indicated for all patients with fabella to rule out fractures and to identify other accessory ossicles and that may have become inflamed (see Figure 133-1). Plain radiographs will also often identify loose bodies or joint mice that may also be present. On the basis of the patient’s clinical presentation, additional testing including complete blood cell count, sedimentation

Figure 133-2  Axial computed tomography scan depicts the hypertrophic, dislocated fabella. (From Franceschi F, Longo UG, Ruzzini L, et  al: Dislocation of an enlarged fabella as uncommon cause of knee pain: a case report, Knee 14:330–332, 2007.)

133  •  Fabella Injection        401

Femoral condyle

Lateral gastrocnemius

Figure 133-3  Wide longitudinal ultrasound scan along the lateral gastrocnemius muscle. Ultrasound allows identification of the fabella, which might provoke a typical painful syndrome. (From Draghi F, Danesino GM, Coscia D, et al: Overload syndromes of the knee in adolescents: sonographic findings, J Ultrasound 11:151–157, 2008.)

rate, and antinuclear antibody testing may be indicated. Magnetic resonance imaging (MRI) and ultrasound imaging of the knee joint are indicated if bursitis, tendinitis, Baker cyst, joint instability, occult mass, or tumor is suspected and to further clarify the diagnosis (Figures 133-3 and 133-4). Radionuclide bone scanning may be useful in identifying stress fractures or tumors of the knee that may be missed on plain radiographs. Arthrocentesis of the knee joint may be indicated if septic arthritis or crystal arthropathy is suspected. Fabella pain syndrome is a clinical diagnosis that is supported by a combination of clinical history, physical examination, radiography, ultrasound, radionuclide scanning, and MRI. Pain syndromes that may mimic fabella pain syndrome include primary disease of the knee, including gout and occult fractures as well as bursitis and tendonitis of the knee, both of which may coexist with fabella. Baker cyst rupture may also mimic the pain associated with fabella. Primary and metastatic tumors of the knee may also manifest in a manner analogous to knee pain secondary to fabella pain syndrome.

Clinically Relevant Anatomy The popliteal fossa is posterior to the knee joint. The fossa contains the popliteal artery and vein, the common peroneal and tibial nerves, and the semimembranosus bursa. The knee joint capsule is lined with a synovial membrane that attaches to the articular cartilage and gives rise to a number of bursae, including the suprapatellar, prepatellar, infrapatellar, and semimembranosus bursae. When these bursae become inflamed, they may overproduce synovial fluid, which can become trapped in saclike cysts because of a one-way valve phenomenon. This occurs commonly in the popliteal fossa. The gastrocnemius muscle has two heads, with the lateral head finding its origin on the lateral condyle of the femur and the medial head finding its origin from the medial condyle of the femur. The fabella is located in the lateral portion of the gastrocnemius muscle. The gastrocnemeus muscle coalesces with the soleus muscle to form a common tendon known as the Achilles tendon, which attaches to the posterior calcaneus.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the prone position with the anterior ankle

Figure 133-4  T2 weighted magnetic resonance image, right knee (sagittal). Normal appearances with the fabella posterior to the femoral condyle. (From Robertson A, Jones SCE, Paes R, Chakrabarty G: The fabella: a forgotten source of knee pain? Knee 11:243–245, 2004.)

resting on a folded towel to slightly flex the knee. The popliteal fossa is identified and, at a point two fingers lateral and two fingers below the popliteal crease, the skin is prepared with antiseptic solution. With a sterile gloved finger, the lateral head of the gastrocnemeus is palpated for the point of maximal tenderness. A syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 2-inch, 22-gauge needle. The needle is carefully advanced through the previously identified point at a 45-degree angle from the medial border of the popliteal fossa directly toward the painful area containing the fabella. With continuous aspiration, the needle is advanced very slowly to avoid trauma to the peroneal nerve or popliteal artery or vein. When the needle tip impinges on the fabella, if there is no paresthesia in the distribution of the common peroneal or tibial nerve, the contents of the syringe are gently injected (Figure 133-5). There should be minimal resistance to injection. A pressure dressing is then placed over the cyst to prevent fluid reaccumulation. Occasionally, surgical excision of the fabella will be required for long-lasting pain relief (Figure 133-6).

Side Effects and Complications The proximity to the common peroneal and tibial nerves, as well as the popliteal artery and vein, makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing injection techniques. Many patients also note a transient increase in pain after the justmentioned injection technique. Although rare, infection may occur if careful attention to sterile technique is not followed.

402        SECTION 7  •  Knee and Lower Extremity

Popliteal fossa Medial head of the gastrocnemius

Fabella

Lateral head of the gastrocnemius

Figure 133-6  Surgical excision of a systematic fabella. (From Franceschi F, Longo UG, Ruzzini L, et al: Dislocation of an enlarged fabella as uncommon cause of knee pain: a case report, Knee 14:330–332, 2007.) SUGGESTED READINGS Clark AM, Matthews GJ: Osteoarthritis of the fabella: a fourth knee compartment? J R Coll Surg Edinb 36:58, 1991. Franceschi F, Longo UG, Ruzzini L, et al: Dislocation of an enlarged fabella as uncommon cause of knee pain: a case report, Knee 14:330–332, 2007. Kuur E: Painful fabella: a case report with review of the literature, Acta Orthop Scand 57:453–454, 1986. Robertson A, Jones SCE, Paes R, Chakrabarty G: The fabella: a forgotten source of knee pain? Knee 11:243–245, 2004. Weiner DS, McNab I: The “fabella syndrome”: an update, J Pediatr Orthop 2:405– 408, 1982.

Figure 133-5  Injection technique for painful fabella.

Clinical Pearls Pain emanating from the knee is a common problem encountered in clinical practice. Fabella pain syndrome must be distinguished from other, more common causes of knee pain including Baker cyst, bursitis, tendonitis, and synovitis. Careful differential diagnosis will help the clinician distinguish the symptomatic fabella from other causes of knee pain.

Chapter 134 FASCIA LATA INJECTION

Indications and Clinical Considerations Fascia lata fasciitis syndrome is caused by inflammation of the fascia lata from overuse or misuse. It is characterized by a dull, aching pain in the lateral hip that radiates into the lateral thigh. The pain is frequently worse on rising. The pain improves with initial activity and then again worsens with continued activity, making walking extremely difficult. The patient with fascia lata fasciitis syndrome also may experience pain in the low back at the iliac crest and buttocks on the affected side, caused by muscle spasm. On physical examination there is diffuse tenderness over the fascia lata laterally, with specific areas of point tenderness along the course of the fascia (Figure 134-1). Dimpling caused by adhesions of the subcutaneous tissue to the fascia lata is often present. This dimpling can best be identified by placing the patient on his or her side at the edge of the examination table with the affected extremity on top and then having the patient abduct the leg at the hip with resistance (Figure 134-2). Bursitis of the trochanteric and iliotibial band bursae also may coexist with fascia lata fasciitis syndrome and confuse the clinical picture. Plain radiographs of the hip and knee may reveal calcification of the trochanteric and iliotibial bursae and associated structures, including the iliotibial band tendon, consistent with chronic inflammation. Magnetic resonance imaging (MRI) is indicated if internal derangement, occult mass, or tumor of the hip or knee is suggested. Electromyography helps distinguish fascia lata fasciitis syndrome from diabetic neuropathy, meralgia paresthetica, lumbar radiculopathy, and plexopathy. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The fascia lata, or deep fascia of the thigh, attaches to the iliac crest and covers the gluteus medius muscle. It continues downward, enveloping the thigh, much like a trouser leg (Figure 134-3). The fascia lata thickens laterally to form the iliotibial band, which attaches to the lateral condyle of the tibia (see Figure 134-1). The iliotibial band forms a sheath for the tensor fasciae latae muscle.

The iliotibial band bursa lies between the iliotibial band and the lateral condyle of the femur. The iliotibial band can rub backward and forward over the lateral epicondyle of the femur and become irritated and can irritate the iliotibial bursa beneath it (see Chapter 128). The iliotibial bursa is subject to the development of inflammation caused by overuse, misuse, or direct trauma, as is the trochanteric bursa, which overlies the greater trochanter of the femur.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the lateral position with the affected extremity on top. The patient is asked to abduct his or her leg against resistance, and the clinician palpates the length of the fascia lata to identify points of maximal tenderness along its course, as well as coexistent bursitis. These tender points and bursae are marked with a sterile marker. The skin over these points and inflamed bursae is then prepared with antiseptic solution. A sterile syringe containing 6.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, each of the previously marked points is reidentified and then gently injected with 1 mL of solution, again using strict aseptic technique (see Figure 134-1). If the needle strikes the femur, it is withdrawn slightly. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients report a transient increase in pain after injection of the fascia lata and associated inflamed bursae.

403

404        SECTION 7  •  Knee and Lower Extremity

Sites of tenderness or adhesions along fascia lata

Iliotibial band

Figure 134-1  Sites of tenderness and pain along the fascia lata is characteristic of fascia lata fasciitis syndrome.

Figure 134-2  Patients with fascia lata fasciitis syndrome will often exhibit dimpling over the fascia lata on abduction against resistance.

134  •  Fascia Lata Injection        405

•

Rectus femoris t.

•

•

•

• •

•

• •• ••

•

•

Vastus medialis m. Fascia lata Popliteal a. Adductor magnus m. & t.

• ••

•

Great saphenous v. Sartorius m. Semimembranosus m.

•

•

• ••

Fascia lata

Fascia lata

•• ••

••

•

Semitendinosus m. & tt.

•

• •

Biceps femoris m., long head

•

Common peroneal n. Tibial n.

Gracilis m. & t.

Vastus intermedius t.

•

••

Popliteal v. Biceps femoris m., short head

Great saphenous v. Sartorius m.

Suprapatellar bursa Vastus intermedius m.

•

•

Femur Iliotibial tract

•• ••

••

••

•

Vastus lateralis m. & t. Vastus intermedius m.

••

Semimembranosus m. •

Rectus femoris t.

Vastus medialis m. Fascia lata Popliteal a. Adductor magnus m. & t.

•

Fascia lata

Fascia lata

•

•• ••

Biceps femoris m., long head Semitendinosus m. & tt.

•

•• ••

• •

Common peroneal n. Tibial n.

Suprapatellar bursa Vastus intermedius m.

••

•

Popliteal v. Biceps femoris m., short head

Vastus intermedius t.

•

•

Femur Iliotibial tract

• •

Vastus lateralis m. & t. Vastus intermedius m.

•

•• •

Fascia lata

•• •

Gracilis m. & t. Fascia lata

Figure 134-3  Anatomy of the fascia lata and related structures. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

406        SECTION 7  •  Knee and Lower Extremity

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to fascia lata fasciitis. Coexistent bursitis, tendinitis of the insertion of the iliotibial band, arthritis, and internal derangement of the knee also may contribute to the patient’s pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for fascia lata fasciitis pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Magrum E, Wilder RP: Evaluation of the injured runner, Clin Sports Med 29:331– 345, 2010. Miller TT: Common tendon and muscle injuries: lower extremity, Ultrasound Clin 2:595–615, 2007. Plastaras CT, Rittenberg JD, Rittenberg KE, et al: Comprehensive functional evaluation of the injured runner, Phys Med Rehabil Clin N Am 16:623–649, 2005. Strakowski JA, Jamil T: Management of common running injuries, Phys Med Rehabil Clin N Am 17:537–552, 2006.

Chapter 135 SAPHENOUS NERVE BLOCK

Indications and Clinical Considerations Saphenous neuralgia is caused by compression of the saphenous nerve by the sartorius muscle and the adductor longus and magnus muscles as the nerve passes through the Hunter canal or, more commonly, as the nerve passes over the medial condyle of the femur (Figure 135-1). This entrapment neuropathy manifests as pain, numbness, and dysesthesias in the distribution of the saphenous nerve. These symptoms often begin as a burning pain over the medial knee. Patients with saphenous neuralgia note that sitting or squatting often causes the symptoms of saphenous neuralgia to worsen. Although traumatic lesions to the saphenous nerve

Femoral n.

Saphenous n.

Cut sartorius m.

after vein stripping surgery and vein harvest surgery for coronary artery bypass surgery have been implicated in the onset of saphenous neuralgia, in most patients no obvious antecedent trauma can be identified. Physical findings include tenderness over the saphenous nerve just medial to the midline of the mid thigh. A positive Tinel sign over the saphenous nerve as it passes over the medial femoral condyle may be present. Careful sensory examination of the medial thigh reveals a sensory deficit in the distribution of the saphenous nerve. No motor deficit should be present. Sitting or squatting, which compress the saphenous nerve, may exacerbate the symptoms of saphenous neuralgia. Saphenous neuralgia often is misdiagnosed as lumbar radiculopathy or is attributed to primary knee disease. Radiographs of the knee and electromyography help distinguish saphenous neuralgia from radiculopathy or pain emanating from the knee. Most patients with a lumbar radiculopathy have back pain associated with reflex, motor, and sensory changes and associated with neck pain, whereas patients with saphenous neuralgia have no back pain and no motor or reflex changes. The sensory changes of saphenous neuralgia are limited to the distribution of the saphenous nerve. Lumbar radiculopathy and saphenous nerve entrapment may coexist as the so-called double crush syndrome. Occasionally, diabetic femoral neuropathy may produce anterior thigh pain, which may confuse the diagnosis. Electromyography helps distinguish lumbar radiculopathy and diabetic femoral neuropathy from saphenous neuralgia. Plain radiographs of the back, hip, and pelvis are indicated for all patients with saphenous neuralgia to rule out occult bony disease. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the back is indicated if herniated disk, spinal stenosis, or a space-occupying lesion is suggested. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy

Figure 135-1  Relationship of the saphenous nerve to the surrounding musculature.

The saphenous nerve is the largest sensory branch of the femoral nerve. The saphenous nerve provides sensory innervation to the medial malleolus, medial calf, and a portion of the medial arch of the foot. The saphenous nerve is derived primarily from the fibers of the L3 and L4 nerve roots (Figure 135-2). The nerve travels along with the femoral artery through the Hunter canal and moves superficially as it approaches the knee. It passes over the medial condyle of the femur, splitting into terminal sensory branches (see Figure 135-1; Figure 135-3). The saphenous nerve is subject to trauma or compression anywhere along its course. The 407

408        SECTION 7  •  Knee and Lower Extremity

nerve frequently is traumatized during vein harvest procedures for coronary artery bypass grafting procedures. The saphenous nerve also is subject to compression as it passes over the medial condyle of the femur.

Technique The patient is placed in the lateral position with the leg slightly flexed. The medial condyle of the femur is palpated. A point just in front of the posterior edge of the medial condyle is then identified and prepared with antiseptic solution. A ½-inch, 25-gauge needle is then advanced through this point very slowly toward the medial condyle of the femur until a paresthesia in the Cut sartorius m. Iliacus m. Rectus femoris m.

distribution of the saphenous nerve is elicited (Figure 135-4). The patient should be warned to expect a paresthesia and should be told to say “there!” as soon as the paresthesia is felt. Paresthesia usually is elicited at a depth of ¼ to ½ inch. If a paresthesia is not elicited, the needle is withdrawn and redirected slightly more anteriorly until a paresthesia is obtained. Once a paresthesia in the distribution of the saphenous nerve has been elicited, the needle is withdrawn 1 mm and the patient is observed to be sure that he or she is not experiencing any persistent paresthesia. If no persistent paresthesia is present and after careful aspiration, a total of 5 mL of 1.0% preservative-free lidocaine and 40 mg of methylprednisolone is slowly injected. Care must be taken not to advance the needle into the substance of the nerve during the injection and thereby inject solution intraneurally. Ultrasound guidance may be useful when saphenous nerve blocks are performed on patients in whom the anatomic landmarks are difficult to identify. After injection of the solution, pressure is applied to the injection site to decrease the incidence of postblock ecchymosis and hematoma formation.

Pectineus m. Femoral v. Femoral a. Saphenous n. Hunter’s canal Adductor longus m. Cut sartorius m. Figure 135-2  Relationship of the saphenous nerve to the femoral artery and vein.

Common peroneal n. Tibial n.

Side Effects and Complications The main side effect of saphenous nerve block at the knee is postblock ecchymosis and hematoma formation, because the nerve is in close proximity to the greater saphenous artery. As mentioned earlier, pressure should be maintained on the injection site postblock to avoid ecchymosis and hematoma formation. Because a paresthesia is elicited with this technique, needle-induced trauma to the saphenous nerve remains a possibility. By advancing the needle slowly and then withdrawing the needle slightly away from the nerve, needle-induced trauma to the saphenous nerve can be avoided.

Semimembranosus m. Sartorius m.

Perforating a. Biceps femoris m. Saphenous n. Popliteal a. Gastrocnemius m. & t., lat head Lat. femoral condyle Popliteus t. Biceps femoris t. Arcuate popliteal lig. and joint capsule Lat. tibial plateau

Gastrocnemius m. and t., med. head Joint capsule Med. femoral condyle Oblique popliteal lig. and tibial collateral lig. Sartorius t. Med. tibial plateau Post. cruciate lig. Gracilis t. Semimembranosus t. Semitendinosus t.

Fibula Soleus m. and t. Gastrocnemius m., med. head Figure 135-3  Anatomy of the knee demonstrating saphenous nerve. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

135  •  Saphenous Nerve Block        409 SUGGESTED READINGS

Saphenous n.

Figure 135-4  Proper needle placement for saphenous nerve block.

Clinical Pearls Saphenous nerve block at the knee is a simple technique that can produce dramatic relief for patients with saphenous neuralgia. Careful preblock neurologic assessment is important to avoid preexisting neurologic deficits being later attributed to the saphenous nerve block at the knee. These assessments are especially important in patients who have sustained trauma to the distal femur, have undergone vascular procedures on the lower extremity, or who have diabetic neuropathy in which saphenous nerve block at the knees is being used for acute pain control. Compressive neuropathy of the saphenous nerve at the knee is sometimes seen in musicians who play the cello; this painful syndrome is called viol paresthesia. The most common cause of pain radiating into the lower extremity is herniated lumbar disk or nerve impingement secondary to degenerative arthritis of the spine, not disorders involving the saphenous nerve per se. Other pain syndromes that may be confused with saphenous nerve entrapment include lesions above the origin of the saphenous nerve, such as lesions of the femoral nerve, and lesions of the saphenous nerve at the ankle. Electromyography and MRI of the lumbar spine combined with the clinical history and physical examination can help sort out the cause of distal lower pain.

Candido KD, Benzon HT: Lumbar plexus, femoral, lateral femoral cutaneous, obturator, saphenous, and fascia iliaca blocks. In Benzon HT, Raja SN, Molloy RE, Liu S, Fishman SM, editors: Essentials of pain medicine and regional anesthesia, ed 2, Philadelphia, 2004, Churchill Livingstone, pp 645–658. Dayan V, Cura L, Cubas S, Carriquiry G: Surgical anatomy of the saphenous nerve, Ann Thorac Surg 85:896–900, 2008. Iizuka M, Yao R, Wainapel S: Saphenous nerve injury following medial knee joint injection: a case report, Arch Phys Med Rehabil 86:2062–2065, 2005. Moawad MR, Masannat YA, Alhamdani A, Gibbons CP: Nerve injury in lower limb vascular surgery, Surgeon 6:32–35, 2008. Toussaint CP, Perry EC III, Pisansky MT, Anderson DE: What’s new in the diagnosis and treatment of peripheral nerve entrapment neuropathies, Neurol Clin 28:979– 1004, 2010. Waldman SD: Saphenous nerve block at the knee. In Pain review, Philadelphia, 2009, Saunders, pp 573–574.

SECTION 8  •  Ankle and Foot

Chapter 136 INTRAARTICULAR INJECTION OF THE ANKLE JOINT Indications and Clinical Considerations The ankle joint is susceptible to the development of arthritis from a variety of conditions that have in common the ability to damage the joint cartilage. Osteoarthritis of the joint is the most common form of arthritis that results in ankle joint pain. However, rheumatoid arthritis and posttraumatic arthritis also are common causes of ankle pain secondary to arthritis (Figure 136-1). Less common causes of arthritis-induced ankle pain include the collagen vascular diseases, infection, villonodular synovitis, and Lyme disease. Acute infectious arthritis usually is accompanied by significant systemic symptoms, including fever and malaise, and should be easily recognized by the astute clinician and treated appropriately with culture and antibiotics, rather than injection therapy. The collagen vascular diseases generally manifest as a polyarthropathy rather than a monoarthropathy limited to the ankle joint, although ankle pain secondary to collagen vascular disease responds exceedingly well to the intraarticular injection technique described later. The majority of patients with ankle pain secondary to osteoarthritis and posttraumatic arthritis pain report pain that is localized around the ankle and distal leg. Activity, especially dorsiflexion, makes the pain worse; rest and heat provide some relief. The pain is constant and is characterized as aching and may interfere with sleep. Some patients note a grating or popping sensation with use of the joint, and crepitus may be present on physical examination. In addition to the just-mentioned pain, patients with arthritis of the ankle joint often experience a gradual decrease in functional ability with decreasing ankle range of motion, making simple everyday tasks such as walking and climbing stairs quite difficult. With continued disuse, muscle wasting may occur and a “frozen ankle” caused by adhesive capsulitis may develop. Plain radiographs are indicated for all patients with ankle pain (see Figure 136-1). On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the ankle is indicated if joint instability, occult mass, or tumor is suspected. 410

Figure 136-1  Anteroposterior view of the ankle in rheumatoid arthritis showing uniform narrowing of the joint space with severe osteoporosis of the surrounding bone structures. (From Brower AC, Flemming DJ: Arthritis in black and white, ed 2, Philadelphia, 1997, Saunders.)

136  •  Intraarticular Injection of the Ankle Joint        411

Clinically Relevant Anatomy The ankle is a hinge-type articulation among the distal tibia, the two malleoli, and the talus (Figures 136-2 and 136-3). The articular surface is covered with hyaline cartilage, which is susceptible to arthritis. The joint is surrounded by a dense capsule, which helps strengthen the ankle. The joint capsule is lined with a synovial membrane that attaches to the articular cartilage. The ankle joint is innervated by the deep peroneal and tibial nerves. The major

Figure 136-2  Site of needle insertion for intraarticular injection of the ankle joint.

ligaments of the ankle joint include the deltoid, anterior talofibular, calcaneofibular, and posterior talofibular ligaments, which provide the majority of strength to the ankle joint. The muscles of the ankle and their attaching tendons are susceptible to trauma and to wear and tear from overuse and misuse.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the ankle joint is done. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, with the foot in neutral position, the junction of the tibia and fibula just above the talus is identified. At this point a triangular indentation that indicates the joint space is easily palpable. The needle is then carefully advanced through the skin and subcutaneous tissues, through the joint capsule, and into the joint (Figure 136-4). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected superiorly and slightly more medially. After the joint space has been entered, the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced slightly into the joint space until the injection proceeds without significant resistance. Ultrasound guidance may be useful in facilitating safe needle placement in patients in whom the anatomic landmarks are difficult to identify. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

3 10 Tibia 4

Fibula

5

Inflamed joint

6 1 9

Talus

7 8

2

Figure 136-3  Anteroposterior radiograph of the ankle: 1, medial malleolus; 2, lateral malleolus; 3, tibial diaphysis; 4, tibiofibular syndesmosis; 5, anterior tibial plafond; 6, ankle joint space; 7, talar dome; 8, lateral gutter; 9, medial gutter; 10, fibular diaphysis. (From Waldman SD, Campbell RSD: Anatomy: special imaging considerations of the ankle and foot. In Imaging of pain, Philadelphia, 2011, Saunders.)

Figure 136-4  Proper needle position for intraarticular injection of the ankle joint.

412        SECTION 8  •  Ankle and Foot

Side Effects and Complications The major complication of intraarticular injection of the ankle is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients report a transient increase in pain after intraarticular injection of the ankle joint; the patient should be warned of this.

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to the just-mentioned causes of arthritis of the ankle joint. Coexistent bursitis and tendinitis also may contribute to ankle pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for ankle pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Waldman SD: Functional anatomy of the ankle and foot. In Pain review, Philadelphia, 2009, Saunders, pp 155–156. Waldman SD: Intra-articular injection of the ankle joint. In Pain review, Philadelphia, 2009, Saunders, pp 590–591. Waldman SD, Campbell RSD: Anatomy: special imaging considerations of the ankle and foot. In Imaging of pain, Philadelphia, 2011, Saunders, pp 417–419. Ward ST, Williams PL, Purkayastha S: Intra-articular corticosteroid injections in the foot and ankle: a prospective 1-year follow-up investigation, J Foot Ankle Surg 47:138–144, 2008.

Chapter 137 INTRAARTICULAR INJECTION OF THE SUBTALAR JOINT Indications and Clinical Considerations The subtalar joint is susceptible to the development of arthritis from a variety of conditions that have in common the ability to damage the joint cartilage. Osteoarthritis of the joint is the most common form of arthritis that results in subtalar joint pain. However, rheumatoid arthritis and posttraumatic arthritis also are common causes of subtalar pain secondary to arthritis. Less common causes of arthritis-induced subtalar pain include the collagen vascular diseases, infection, villonodular synovitis, and Lyme disease. Acute infectious arthritis is usually accompanied by significant systemic symptoms, including fever and malaise, and should be easily recognized by the astute clinician and treated appropriately with culture and antibiotics rather than injection therapy. The collagen vascular diseases generally manifest as a polyarthropathy rather than a monoarthropathy limited to the subtalar joint, although subtalar pain secondary to collagen vascular disease responds exceedingly well to the intraarticular injection technique described later. The majority of patients with subtalar joint pain secondary to osteoarthritis and posttraumatic arthritis experience pain that is localized deep within the heel. Activity, especially adduction of the calcaneus, makes the pain worse; rest and heat provide some relief. The pain is constant and is characterized as aching and may interfere with sleep. Some patients report a grating or popping sensation with use of the joint, and crepitus may be present on physical examination. In addition to the just-mentioned pain, patients with arthritis of the subtalar joint often experience a gradual decrease in functional ability with decreasing subtalar range of motion, making simple, everyday tasks such as walking and climbing stairs quite difficult. With continued disuse, muscle wasting may occur and a “frozen subtalar joint” caused by adhesive capsulitis may develop. Plain radiographs are indicated for all patients with subtalar joint pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the subtalar joint is indicated if joint instability, occult mass, or tumor is suggested.

Clinically Relevant Anatomy The subtalar joint is a synovial plane-type articulation between the talus and calcaneus (Figure 137-1). The articular surface is covered with hyaline cartilage, which is susceptible to arthritis. The joint is surrounded by a dense capsule, which helps

Figure 137-1  Needle insertion site for intraarticular injection of the su­btalar joint.

strengthen the subtalar joint. The joint capsule is lined with a synovial membrane that attaches to the articular cartilage. The major ligaments of the subtalar joint include the medial and lateral talocalcaneal ligaments and the interosseous ligament, which provide the majority of strength to the subtalar joint (Figure 137-2). The muscles of the subtalar joint and their attaching tendons are susceptible to trauma and to wear and tear from overuse and misuse.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the subtalar joint is carried out. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, with the lower extremity slightly abducted, the medial malleolus is identified. At a point approximately 1 inch below the medial malleolus lies a bony prominence called the sustentaculum tali. Just above and slightly posterior to the sustentaculum tali lies the subtalar joint. At this point the needle is carefully advanced at a right angle to the ankle through the skin and subcutaneous tissues, through the joint capsule, and into the joint (Figure 137-3). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected superiorly and slightly more anteriorly. After the joint space has been entered, the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced 413

414        SECTION 8  •  Ankle and Foot Extensor digitorum brevis m.

Peroneus tertius m.

Tibia

Extensor digitorum longus t.

Talus Peroneus brevis m. Lat. malleolus

Lat. cuneiform

Post. inf. tibiofibular lig. Post. talofibular lig.

Interosseous cuneocuboid lig.

Interosseous talocalcaneal lig.

3rd metatarsal Cuboid

Calcaneus

4th metatarsal Long plantar lig.

Interosseous mm.

Plantar apon., lat. cord

Peroneus longus t. Abductor digiti minimi m

Figure 137-2  Anatomy of the ankle and foot. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

Medial malleolus Joint inflamed Talus Calcaneus

Sustentaculum tali Figure 137-3  Proper needle position for intraarticular injection of the subtalar joint.

slightly into the joint space until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. Ultrasound or computed tomographic guidance may be beneficial if the anatomic landmarks necessary to safely perform this procedure are difficult to identify (Figures 137-4 and 137-5).

Side Effects and Complications The major complication of intraarticular injection of the subtalar joint is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients report a transient increase in pain after intraarticular injection of the subtalar joint; the patient should be warned of this.

137  •  Intraarticular Injection of the Subtalar Joint        415

CALC TAL

A

PSTJ

B

Figure 137-4  A, Sonographic view of anterolateral approach. Peroneal tendons circled. Arrows surround sural nerve. Left, cephalad; right, caudal; top, superficial; bottom, deep. B, Position of transducer and needle relative to the lateral posterior subtalar joint (PSTJ) for the anterolateral approach. Left, posterior; right, anterior; top, cephalad; bottom, caudal. CALC, Calcaneus; PSTJ (with arrow), posterior subtalar joint; TAL, talus. (From Henning T, Finnoff JT, Smith J: Sonographically guided posterior subtalar joint injections: anatomic study and validation of 3 approaches, PM R 1:925–931, 2009.)

A

B

Figure 137-5  A, Foot position for lateral approach into the posterior subtalar joint. B, Computed tomography image demonstrates needle placed in the posterior subtalar joint. (From Saifuddin A, Abdus-Samee M, Mann C, et al: CT guided diagnostic foot injections, Clin Radiol 60:191-195, 2005.)

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to the just-mentioned causes of arthritis of the subtalar joint. Coexistent bursitis and tendinitis also may contribute to subtalar joint pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for subtalar pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Henning T, Finnoff JT, Smith J: Sonographically guided posterior subtalar joint injections: anatomic study and validation of 3 approaches, PM R 1:925–931, 2009. Waldman SD: Functional anatomy of the ankle and foot. In Pain review, Philadelphia, 2009, Saunders, pp 155–156. Waldman SD, Campbell RSD: Anatomy: special imaging considerations of the ankle and foot. Imaging of pain, Philadelphia, 2011, Saunders, pp 417-149. Ward ST, Williams PL, Purkayastha S: Intra-articular corticosteroid injections in the foot and ankle: a prospective 1-year follow-up investigation, J Foot Ankle Surg 47:138–144, 2008.

Chapter 138 INTRAARTICULAR INJECTION OF THE MIDTARSAL JOINTS Indications and Clinical Considerations The midtarsal joint is susceptible to the development of arthritis from a variety of conditions that have in common the ability to damage the joint cartilage. Osteoarthritis of the joint is the most common form of arthritis that results in midtarsal joint pain. However, rheumatoid arthritis and posttraumatic arthritis also are common causes of midtarsal pain secondary to arthritis (Figure 138-1). Less common causes of arthritis-induced midtarsal pain include the collagen vascular diseases, infection, villonodular synovitis, and Lyme disease. Acute infectious arthritis usually is accompanied by significant systemic symptoms, including fever and malaise, and should be easily recognized by the astute clinician and treated appropriately with culture and antibiotics rather than injection therapy. The collagen vascular diseases generally manifest as a polyarthropathy rather than a monoarthropathy limited to the midtarsal joint, although midtarsal joint pain secondary to collagen vascular disease responds exceedingly well to the intraarticular injection technique described later. The majority of patients with midtarsal joint pain secondary to osteoarthritis and posttraumatic arthritis pain experience pain that

A

is localized to the dorsum of the foot. Activity, especially inversion and adduction of the midtarsal joints, makes the pain worse; rest and heat provide some relief. The pain is constant and is characterized as aching and may interfere with sleep. Some patients report a grating or popping sensation with use of the joint, and crepitus may be present on physical examination. In addition to the just-mentioned pain, patients with arthritis of the midtarsal joint often experience a gradual decrease in functional ability with decreasing midtarsal range of motion, making simple everyday tasks such as walking and climbing stairs quite difficult. Plain radiographs are indicated for all patients with midtarsal joint pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Computed tomography (CT), magnetic resonance imaging (MRI), and ultrasound imaging of the midtarsal joints are indicated if joint instability, occult mass, or tumor is suggested.

Clinically Relevant Anatomy Each joint of the midtarsus has its own capsule (Figure 138-2). The articular surface of these joints is covered with hyaline cartilage,

B

Figure 138-1  Posttraumatic avascular necrosis and osteoarthritis 2 years after an undiagnosed navicular injury. (From Makwana NK, van Liefland MR: Injuries of the midfoot, Curr Orthop 19:231–242, 2005.)

416

138  •  Intraarticular Injection of the Midtarsal Joints        417

which is susceptible to arthritis. The midtarsal joint capsules are lined with a synovial membrane that attaches to the articular cartilage and allows the gliding motion of the joints. Various ligaments provide the majority of strength to the midtarsal joints. The muscles of the midtarsal joint and their attaching tendons are susceptible to trauma and to wear and tear from overuse and misuse.

Tibia Fibula

Inflamed and arthitic joint

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the most tender midtarsal joint is done. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a ⅝-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the affected joint space is identified (Figure 138-3). At this point the needle is carefully advanced at a right angle to the dorsal aspect of the ankle through the skin and subcutaneous tissues, through the joint capsule, and into the joint (see Figure 138-2). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected superiorly. After the joint space has been entered, the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced slightly into the joint space until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. Fluoroscopic, ultrasound, or CT guidance may be useful in those patients in whom the anatomic landmarks necessary to perform this procedure are difficult to identify (Figure 138-4).

Talus

Navicular 2nd cuneiform 3rd cuneiform

Figure 138-2  Proper needle position for intraarticular injection of the midtarsal joints.

Side Effects and Complications The major complication of intraarticular injection of the midtarsal joint is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients report a transient increase in pain after intraarticular injection of the midtarsal joint; the patient should be warned of this.

Figure 138-3  Site for needle insertion for intraarticular injection of the midtarsal joints.

A

B

Figure 138-4  A, Foot position for lateral approach into the mid-foot joints. B, Computed tomography image demonstrates needle placed in the severely degenerated talonavicular joint. (From Saifuddin A, Abdus-Samee M, Mann C, et al: CT guided diagnostic foot injections, Clin Radiol 60:191–195, 2005.)

418        SECTION 8  •  Ankle and Foot

Clinical Pearls Pain emanating from the midtarsal joints is commonly seen in football punters and ballet dancers, both of whom forcefully point their toes. This injection technique is extremely effective in the treatment of pain secondary to the justmentioned causes of arthritis of the midtarsal joint. Coexistent bursitis and tendinitis also may contribute to midtarsal joint pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for midtarsal joint pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Reid JJ, Pinney SJ: Midfoot Injuries in athletes: fundamentals of examination and treatment, Oper Tech Sports Med 18:46–49, 2010. Saifuddin A, Abdus-Samee M, Mann C, et al: CT guided diagnostic foot injections, Clin Radiol 60:191–195, 2005. Waldman SD: Functional anatomy of the ankle and foot. In Pain review, Philadelphia, 2009, Saunders, pp 155–156. Waldman SD, Campbell RSD: Anatomy: special imaging considerations of the ankle and foot. In Imaging of pain, Philadelphia, 2011, Saunders, pp 417–419. Ward ST, Williams PL, Purkayastha S: Intra-articular corticosteroid injections in the foot and ankle: a prospective 1-year follow-up investigation, J Foot Ankle Surg 47:138–144, 2008.

Chapter 139 INTRAARTICULAR INJECTION OF THE TOE JOINTS Indications and Clinical Considerations The toe joint is susceptible to the development of arthritis from a variety of conditions that have in common the ability to damage the joint cartilage. Osteoarthritis of the joint is the most common form of arthritis that results in toe joint pain. However, rheumatoid arthritis and posttraumatic arthritis also are common causes of toe joint pain secondary to arthritis. Less common causes of arthritis-induced toe joint pain include the collagen vascular diseases, gout, psoriatic arthritis, infection, and Lyme disease (Figure 139-1). Acute infectious arthritis usually is accompanied by significant systemic symptoms, including fever and malaise, and should be easily recognized by the astute clinician and treated appropriately with culture and antibiotics rather

than injection therapy. The collagen vascular diseases generally manifest as a polyarthropathy rather than a monoarthropathy limited to the toe joint, although toe joint pain secondary to collagen vascular disease responds exceedingly well to the intraarticular injection technique described later. The majority of patients with toe joint pain secondary to osteoarthritis and posttraumatic arthritis pain experience pain that is localized to the affected joint of the foot. The great toe is most commonly affected. Activity, especially flexion of the toe joints, makes the pain worse; rest and heat provide some relief. The pain is constant and is characterized as aching and may interfere with sleep. Some patients note a grating or popping sensation with use of the joint, and crepitus may be present on physical examination. In addition to the just-mentioned pain, patients with arthritis of the toe joint often experience a gradual decrease in functional ability with decreasing toe range of motion, making simple everyday tasks such as walking, standing on tiptoes, and climbing stairs quite difficult. Plain radiographs are indicated for all patients with toe joint pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the toe is indicated if joint instability, occult mass, or tumor is suggested.

Clinically Relevant Anatomy Each toe joint has its own capsule (Figures 139-2, 139-3, and 1394). The articular surface of these joints is covered with hyaline cartilage, which is susceptible to arthritis. The toe joint capsules are lined with a synovial membrane that attaches to the articular cartilage. The deep transverse ligaments connect the joints of the five toes and provide the majority of strength to the toe joints. The muscles of the toe joint and their attaching tendons are susceptible to trauma and to wear and tear from overuse and misuse.

Inflamed and arthritic joint

Figure 139-1  Erosions with “paint brush” appearance along medial aspect of first metatarsophalangeal joint. There is also new bone formation (arrows) at margins of erosions. Note “pencil-in-cup” appearance at first interphalangeal joint in psoriatic arthropathy. (From Brower AC, Flemming DJ: Arthritis in black and white, ed 2, Philadelphia, 1997, Saunders.)

Figure 139-2  The pain associated with arthritis of the toe joints is amenable to treatment with intraarticular injection of the toe joints.

419

420        SECTION 8  •  Ankle and Foot Navicular

Tibialis ant. t. Tibialis post. t. Med. malleolus Flexor digitorum longus t.

Med. cuneiform

Deltoid lig. Tibal n.

Extensor hallucis longus t.

Post. tibal a. Tibialis post. t.

1st metatarsal Flexor hallucis longus t.

Abductor hallucis m.

Flexor hallucis brevis m. Plantar apon. Figure 139-3  Anatomy of the ankle and foot. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

Proximal phalanx

the needle is withdrawn into the subcutaneous tissues and redirected superiorly. After the joint space has been entered, the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced slightly into the joint space until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of intraarticular injection of the toe joint is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients report a transient increase in pain after intraarticular injection of the toe joint; the patient should be warned of this.

Clinical Pearls First metatarsal Figure 139-4  Proper needle position for intraarticular injection of the toe joints.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the affected toe joint is carried out. A sterile syringe containing 1.5 mL of 0.25% preservativefree bupivacaine and 40 mg of methylprednisolone is attached to a ⅝-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the affected toe is distracted to open the joint space. The joint space is then identified. At this point the needle is carefully advanced perpendicular to the joint space just next to the extensor tendons, through the skin and subcutaneous tissues, through the joint capsule, and into the joint (see Figure 139-4). If bone is encountered,

Pain emanating from the toe joints commonly is seen after trauma to the toes. This injection technique is extremely effective in the treatment of pain secondary to the just-mentioned causes of arthritis of the toe joint. Coexistent bursitis and tendinitis also may contribute to toe joint pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for toe joint pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

139  •  Intraarticular Injection of the Toe Joints        421 SUGGESTED READINGS Waldman SD: Functional anatomy of the ankle and foot. In Pain review, Philadelphia, 2009, Saunders, pp 155–156. Waldman SD: Intra-articular injection of the toe joints. In Pain review, Philadelphia, 2009, Saunders, pp 591–592.

Waldman SD, Campbell RSD: Anatomy: special imaging considerations of the ankle and foot. In Imaging of pain, Philadelphia, 2011, Saunders, pp 417–419. Ward ST, Williams PL, Purkayastha S: Intra-articular corticosteroid injections in the foot and ankle: a prospective 1-year follow-up investigation, J Foot Ankle Surg 47:138–144, 2008.

Chapter 140 DELTOID LIGAMENT INJECTION

Indications and Clinical Considerations The deltoid ligament is susceptible to strain from acute injury from sudden overpronation of the ankle or from repetitive microtrauma to the ligament from overuse or misuse, such as in longdistance running on soft or uneven surfaces. Patients with strain of the deltoid ligament experience pain just below the medial malleolus. Plantarflexion and eversion of the ankle joint exacerbate the pain. On physical examination, there is point tenderness over the medial malleolus. With acute trauma, ecchymosis over the ligament may be noted. Passive eversion and plantarflexion of the ankle joint exacerbate the pain. Coexistent bursitis and arthritis of the ankle and subtalar joint also may be present and may confuse the clinical picture. Plain radiographs are indicated for all patients with ankle pain (Figure 140-1). On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and/or ultrasound imaging of the ankle is indicated if disruption of the deltoid ligament, joint instability, occult mass, or tumor is suggested (Figure 140-2).

medial malleolus is done. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, with the lower extremity slightly abducted, the lower margin of the medial malleolus is identified (Figure 140-5). At this point the needle is carefully advanced at a 30-degree angle to the ankle through the skin and subcutaneous tissues to impinge on the lower margin of the medial malleolus (see Figure 140-3). The needle is then withdrawn slightly, and the contents of the syringe are gently injected. There is slight resistance to injection. If significant resistance is encountered, the needle is probably in the ligament and should be withdrawn slightly until the injection proceeds without significant resistance. The needle

Clinically Relevant Anatomy The ankle is a hinge-type articulation among the distal tibia, the two malleoli, and the talus. The articular surface is covered with hyaline cartilage, which is susceptible to arthritis. The joint is surrounded by a dense capsule that helps strengthen the ankle. The joint capsule is lined with a synovial membrane that attaches to the articular cartilage. The ankle joint is innervated by the deep peroneal and tibial nerves. The major ligaments of the ankle joint include the deltoid, anterior talofibular, calcaneofibular, and posterior talofibular ligaments, which provide the majority of strength to the ankle joint. The deltoid ligament is exceptionally strong and is not as subject to strain as the anterior talofibular ligament. The deltoid ligament has two layers (Figure 140-3). Both attach above to the medial malleolus (Figure 140-4). A deep layer attaches below to the medial body of the talus, with the superficial fibers attaching to the medial talus, the sustentaculum tali of the calcaneus, and the navicular tuberosity.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the area of the 422

Figure 140-1  Anteroposterior radiograph of a severe acute eversion ankle injury. There is an oblique fracture of the distal fibula. Disruption of the ankle mortise with widening of the medial joint line (doubleheaded arrow) indicates a tear of the deltoid ligament. This pattern of injury is less common than an avulsion fracture of the entire medial malleolus with an intact ligament. (From Waldman SD, Campbell RSD: Deltoid ligament tear. In Imaging of pain, Philadelphia, 2011, Saunders.)

140  •  Deltoid Ligament Injection        423

B

A

D

C

E

Figure 140-2  A, Sagittal fast spin (FS) T2-weighted magnetic resonance (MR) image of an athlete with a subacute eversion ankle sprain. There is marrow edema in the tip of the medial malleolus (white arrow) and a possible small bony avulsion injury (broken white arrow). B, The coronal FS T2-weighted MR image also shows the marrow edema (white arrow), and there is high signal intensity within the deltoid ligament (curved white arrow) as a result of partial tearing. C and D, Consecutive axial FS T2-weighted MR images more clearly demonstrate the deltoid ligament edema (curved white arrow) anterior to the flexor tendons (white arrows). The bony avulsion fragment is demonstrated as a small round area of low signal intensity (broken white arrow). E, The coronal computed tomography scan confirms the presence of an avulsion fracture of the tip of the medial malleolus. (From Waldman SD, Campbell RSD: Deltoid ligament tear. In Imaging of pain, Philadelphia, 2011, Saunders.)

424        SECTION 8  •  Ankle and Foot

is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique

is adhered to. Approximately 25% of patients report a transient increase in pain after injection of the deltoid ligament; the patient should be warned of this. Injection around strained ligaments should always be done gently to avoid further damage to the already compromised ligament.

Medial malleolus

Deltoid ligament Tibionavicular part Anterior tibiotalar part Inflamed tibiocalcaneal part Posterior tibiotalar part

Figure 140-3  Proper needle placement for injection of the deltoid ligament.

140  •  Deltoid Ligament Injection        425 Navicular

Tibialis ant. t.

•• ••

•

Med. malleolus Flexor digitorum longus t.

•

Deltoid lig.

•• •• ••

•

Tibialis post. t.

•

Med. cuneiform

•

1st metatarsal Flexor hallucis brevis m. Flexor hallucis longus t.

Post. tibial a. & tibial n.

•

Abductor hallucis m.

• • •

Plantar apon.

Navicular

Tibialis ant. t.

• •

Med. malleolus

••

• ••

Med. cuneiform Extensor hallucis longus t.

•

1st metatarsal

••

•

•

Flexor hallucis longus t. Flexor hallucis brevis m. Plantar apon.

••

••

Flexor digitorum longus t. Deltoid lig.

•

•

Tibialis post. t.

•

Tibial n. Post. tibial a. Tibialis post. t.

Abductor hallucis m.

•• •

Figure 140-4  Anatomy of the deltoid ligament and related structures. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

426        SECTION 8  •  Ankle and Foot SUGGESTED READINGS

Figure 140-5  Site of needle insertion for deltoid ligament injection.

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to the deltoid ligament strain. Coexistent arthritis, bursitis, and tendinitis also may contribute to medial ankle pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for ankle pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

Beals TC, Crim J, Nickisch F: Deltoid ligament injuries in athletes: techniques of repair and reconstruction, Oper Tech Sports Med 18:11–17, 2010. Ganjianpour M: Deltoid ligament: a review of normal anatomy with magnetic resonance imaging and arthroscopic correlation (SS-61), Arthroscopy 18(5 Suppl 1):48–49, 2002. Hintermann B, Knupp M, Pagenstert GI: Deltoid ligament injuries: diagnosis and management, Foot Ankle Clin 11:625–637, 2006. Waldman SD: Functional anatomy of the ankle and foot. In Pain review, ­Philadelphia, 2009, Saunders, pp 155–156. Waldman SD: The deltoid ligament. In Pain review, Philadelphia, 2009, ­Saunders, p 157. Waldman SD, Campbell RSD: Deltoid ligament tear. In Imaging of pain, ­Philadelphia, 2011, Saunders.

Chapter 141 ANTERIOR TALOFIBULAR LIGAMENT INJECTION Indications and Clinical Considerations

is indicated if disruption of the talofibular ligament, joint instability, occult mass, or tumor is suggested (Figure 141-1).

The talofibular ligament is susceptible to strain from acute injury from sudden inversion of the ankle or from repetitive microtrauma to the ligament from overuse or misuse, as from longdistance running on soft or uneven surfaces. Patients with strain of the talofibular ligament experience pain just below the lateral malleolus. Inversion of the ankle joint exacerbates the pain. On physical examination, there is point tenderness just below the lateral malleolus. With acute trauma, ecchymosis over the ligament may be noted. Passive inversion of the ankle joint exacerbates the pain. Coexistent bursitis and arthritis of the ankle and subtalar joint also may be present and may confuse the clinical picture. Plain radiographs are indicated for all patients with ankle pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and/or ultrasound imaging of the ankle

Clinically Relevant Anatomy The ankle is a hinge-type articulation among the distal tibia, the two malleoli, and the talus. The articular surface is covered with hyaline cartilage, which is susceptible to arthritis. The joint is surrounded by a dense capsule that helps strengthen the ankle. The joint capsule is lined with a synovial membrane that attaches to the articular cartilage. The ankle joint is innervated by the deep peroneal and tibial nerves. The major ligaments of the ankle joint include the talofibular, anterior talofibular, calcaneofibular, and posterior talofibular ligaments, which provide the majority of strength to the ankle joint (see Figure 141-1). The talofibular ligament is not as strong as the deltoid ligament and is susceptible to strain. The talofibular ligament runs from the anterior border of the lateral malleolus to the lateral surface of the talus (Figures 141-2 and 141-3).

*

A

*

B

Figure 141-1  A and B, Consecutive axial T1-weighted magnetic resonance arthrogram images demonstrating complete rupture of the talofibular ligament with only a small proximal remnant (broken arrows). High–signal intensity fluid has extravasated outside the normal joint recesses (asterisks). (From Waldman SD, Campbell RSD: Anterior talofibular ligament tear. In Imaging of pain, Philadelphia, 2012, Saunders.)

427

428        SECTION 8  •  Ankle and Foot

•

•

Ant. talofibular lig.

Tibia

•

Lat. malleolus

•• •

•

Talus

Post. tibiotalar lig.

• ••

Calcaneofibular lig. Peroneus brevis t.

•

Peroneus longus t.

••

• •• ••

Calcaneus

Plantar apon., lat. cord

• •

Abductor digiti minimi m.

• • •• •

Sural n.

• •

Peroneal retinaculum

Med. malleolus

•

•

Tibialis post. t. Flexor retinaculum Flexor digitorum longus t. Interosseous talocalcaneal lig.

•••

Flexor hallucis longus t. Med. plantar a. & n.

••

Quadratus plantae m. Lat. plantar a. & n. Abductor hallucis m. Flexor digitorum brevis m.

•

Plantar apon.

Figure 141-2  Anatomy of the ankle showing locations of the anterior talofibular ligament. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the area of the lateral malleolus is done. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 11⁄2-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, with the lower extremity slightly adducted, the lower margin of the lateral malleolus is identified (Figure 141-4). At this point the needle is carefully advanced at a 30-degree angle to the ankle through the skin and subcutaneous tissues to impinge on the lower margin of the lateral malleolus (Figure 141-5). The needle is then withdrawn slightly and the contents of the syringe are gently injected. There is slight

resistance to injection. If significant resistance is encountered, the needle is probably in the ligament and should be withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients note a transient increase in pain after injection of the talofibular ligament; the patient should be warned of this. Injection around strained ligaments should always be done gently to avoid further damage to the already compromised ligament.

141  •  Anterior Talofibular Ligament Injection        429

Figure 141-3  Axial T1-weighted magnetic resonance arthrogram image outlining a normal low–signal intensity anterior talofibular ligament (arrow). (From Waldman SD, Campbell RSD: Anterior talofibular ligament tear. In Imaging of pain, Philadelphia, 2011, Saunders.)

Figure 141-4  Site of needle insertion for anterior talofibular ligament injection.

Talus Inflamed anterior talofibular ligament Lateral malleolus Posterior talofibular ligament

Calcaneofibular ligament Calcaneus

Figure 141-5  Proper needle placement for anterior talofibular ligament injection.

430        SECTION 8  •  Ankle and Foot

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to talofibular ligament strain. Coexistent arthritis, bursitis, and tendinitis also may contribute to lateral ankle pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle rangeof-motion exercises, should be introduced several days after the patient has undergone this injection technique for ankle pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Bonnel F, Toullec E, Mabit C, et al: Chronic ankle instability: biomechanics and pathomechanics of ligaments injury and associated lesions, Orthop Traumatol Surg Res 96:424–432, 2010. Haller J, Bernt R, Seeger T, et al: MR-imaging of anterior tibiotalar impingement syndrome: Agreement, sensitivity and specificity of MR-imaging and indirect MR-arthrography, Eur J Radiol 58:450–460, 2006. Waldman SD: Functional anatomy of the ankle and foot. In Pain review, Philadelphia, 2009, Saunders, pp 155–156. Waldman SD: The anterior talofibular ligament. In Pain review, Philadelphia, 2009, Saunders, p 158. Waldman SD, Campbell RSD: Anterior talofibular ligament tear. In Imaging of pain, Philadelphia, 2011, Saunders, pp 437–438.

Chapter 142 DEEP PERONEAL NERVE BLOCK

Indications and Clinical Considerations Anterior tarsal tunnel syndrome is caused by compression of the deep peroneal nerve as it passes beneath the superficial fascia of the ankle (Figures 142-1 and 142-2). The most common cause of compression of the deep peroneal nerve at this anatomic location is trauma to the dorsum of the foot. Severe, acute plantarflexion of the foot has been implicated in anterior tarsal tunnel syndrome, as has the wearing of overly tight shoes or squatting and bending ­forward, as when planting flowers. Anything that has the propensity to impinge on the deep peroneal nerve such as tumor, osteophyte, ganglion, and synovitis can cause anterior tarsal tunnel syndrome (Figure 142-3). Anterior tarsal tunnel syndrome is much less common than posterior tarsal tunnel syndrome. This entrapment neuropathy manifests primarily as pain, numbness, and paresthesias of the dorsum of the foot that radiate into the first dorsal web space. These symptoms also may radiate proximal to the entrapment into the anterior ankle. There is no motor involvement unless the distal lateral division of the deep peroneal nerve is involved. Nighttime foot pain analogous to the nocturnal pain of carpal tunnel syndrome often is present. The

Extensor hallucis longus tendon

Tarsal branch Deep peroneal nerve entrapped under fascia

Figure 142-1  Proper needle placement for deep peroneal nerve block.

patient may report that holding the foot in the everted position may decrease the pain and paresthesias of anterior tarsal tunnel syndrome. Physical findings include tenderness over the deep peroneal nerve at the dorsum of the foot. A positive Tinel sign just medial to the dorsalis pedis pulse over the deep peroneal nerve as it passes beneath the fascia usually is present. Active plantarflexion often reproduces the symptoms of anterior tarsal tunnel syndromes. Weakness of the extensor digitorum brevis may be present if the lateral branch of the deep peroneal nerve is affected. Anterior tarsal tunnel syndrome often is misdiagnosed as arthritis of the ankle joint, lumbar radiculopathy, or diabetic polyneuropathy. Patients with arthritis of the ankle joint have radiographic evidence of arthritis. Most patients with a lumbar radiculopathy have reflex, motor, and sensory changes associated with back pain, whereas patients with anterior tarsal tunnel syndrome have no reflex changes and have motor and sensory changes limited to the distal deep peroneal nerve. Diabetic polyneuropathy generally manifests as symmetrical sensory deficit involving the entire foot, rather than limited just to the distribution of the deep peroneal nerve. Lumbar radiculopathy and deep peroneal nerve entrapment may coexist as the so-called double-crush syndrome. Furthermore, because anterior tarsal tunnel syndrome is seen in patients with diabetes, it is not surprising that diabetic polyneuropathy usually is present in diabetic patients with anterior tarsal tunnel syndrome. Electromyography helps distinguish lumbar radiculopathy and diabetic polyneuropathy from anterior tarsal tunnel syndrome. Plain radiographs are indicated for all patients with anterior tarsal syndrome to rule out occult bony disease. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and/or ultrasound imaging of the ankle and foot is indicated if joint instability or a space-occupying lesion is suspected (Figure 142-4). The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The common peroneal nerve is one of the two major continuations of the sciatic nerve, the other being the tibial nerve. The common peroneal nerve provides sensory innervation to the inferior portion of the knee joint and the posterior and lateral skin of the upper calf. The common peroneal nerve is derived from the posterior branches of the L4, L5, S1, and S2 nerve roots. The nerve splits from the sciatic nerve at the superior margin of the popliteal fossa and descends laterally behind the head of the fibula. 431

432        SECTION 8  •  Ankle and Foot

Extensor hallucis longus m. & t. Ant. tibial a. Deep peroneal n. Extensor digitorum longus m. & t.

••

•• ••

•• •

Talus

•

•

Med. malleolus

••

••

•

••

••

••

•

Peroneus longus t.

Greater saphenous v. Tibionavicular lig.

••

Post. inf. tibiofibular lig. Peroneus brevis m. & t.

• •

•

Lat. malleolus

Tibialis ant. t.

••

Peroneus tertius m.

•

•

••

Tibialis post. t. Flexor digitorum longus t. Post. tibial a. Tibial n. Flexor hallucis longus m. & t.

••

Tendo calcaneus

Figure 142-2  Anatomy of the deep peroneal nerve and related structures. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

The common peroneal nerve is subject to compression at this point by improperly applied casts and tourniquets. The nerve also is subject to compression as it continues its lateral course, winding around the fibula through the fibular tunnel, which is made up of the posterior border of the tendinous insertion of the peroneus longus muscle and the fibula itself. Just distal to the fibular tunnel, the nerve divides into its two terminal branches, the superficial and the deep peroneal nerves. Each of these branches is subject to trauma and may be blocked individually as a diagnostic and therapeutic maneuver. The deep branch continues down the leg in conjunction with the tibial artery and vein to provide sensory innervation to the web space of the first and second toes and adjacent dorsum of the foot (see Figure 142-1). Although this distribution of sensory fibers is small, this area is often the site of Morton neuroma surgery and thus is important to the regional anesthesiologist. The deep peroneal nerve provides motor innervation to all of the toe extensors. The deep peroneal nerve passes beneath the dense superficial fascia of the ankle, where it is subject to entrapment.

Technique The patient is placed in the supine position with the leg extended. The extensor hallucis longus tendon is identified by having the patient extend his or her big toe against resistance. A point just medial to the tendon at the skin crease of the ankle is identified and prepared with antiseptic solution. A 1½-inch, 25-gauge needle is then advanced through this point very slowly toward the tibia until a paresthesia into the web space between the first and second toes is elicited (see Figure 142-1). The patient should be warned to expect a paresthesia and should be told to say “there!” as soon as the paresthesia is felt. Paresthesia usually is elicited at a depth of ¼ to ½ inch. If a paresthesia is not elicited, the needle is withdrawn and redirected slightly more posteriorly until a paresthesia is obtained. Once a paresthesia in the distribution of the deep peroneal nerve has been elicited, the needle is withdrawn 1 mm and the patient is observed to be sure that he or she is not experiencing any persistent paresthesia. If no persistent paresthesia is present and after careful aspiration, a total of 6 mL of 1.0% preservative-free lidocaine and

142  •  Deep Peroneal Nerve Block        433

A

B

C

Figure 142-3  A, Lateral radiograph of a patient with osteoarthritis of the ankle and subtalar joint. There is prominent anterior osteophyte formation at the anterior aspect of the joint with associated soft tissue shadowing (white arrow). The axial T1-weighted (B) and T2-weighted with fat suppression (C) magnetic resonance images show the anterior osteophytosis and associated synovitis (white arrows) impinging on the extensor tendons. The anterior tibial artery is displaced anteriorly (broken white arrows) between the extensor tendons. The deep peroneal nerve is not visualized. (From Waldman SD, Campbell RSD: Anterior tarsal tunnel syndrome. In Imaging of pain, Philadelphia, 2011, Saunders.)

A

B

C

Figure 142-4  Axial T1-weighted (A) and T2-weighted with fat suppression (B) magnetic resonance (MR) images of a patient with ankle pain and paresthesia over the dorsal aspect of the foot. A mass of synovitis arising from the ankle joint surrounds the extensor tendons and the anterior neurovascular bundle. The synovium has intermediate signal intensity on both images and also on the coronal T2-weighted MR image (C). There is also bony erosion. These appearances are typical of pigmented villonodular synovitis. (From Waldman SD, Campbell RSD: Anterior tarsal tunnel syndrome. In Imaging of pain, Philadelphia, 2011, Saunders.)

40 mg of methylprednisolone is slowly injected. Care must be taken not to advance the needle into the substance of the nerve during the injection and thereby inject solution intraneurally. After injection of the solution, pressure is applied to the injection site to decrease the incidence of postblock ecchymosis and hematoma formation.

Side Effects and Complications The main side effects of deep peroneal nerve block are postblock ecchymosis and hematoma. As mentioned earlier, pressure should be maintained on the injection site post block to avoid ecchymosis

434        SECTION 8  •  Ankle and Foot

and hematoma formation. Because a paresthesia is elicited with this technique, needle-induced trauma to the common peroneal nerve remains a possibility. By advancing the needle slowly and then withdrawing the needle slightly away from the nerve, needleinduced trauma to the common peroneal nerve can be avoided.

Clinical Pearls Deep peroneal nerve block is a simple technique that is useful in the treatment of anterior tarsal tunnel syndrome. Anterior tarsal tunnel syndrome is characterized by persistent aching of the dorsum of the foot that is sometimes associated with weakness of the toe extensors. This pain frequently is worse at night and may awaken the patient from sleep. It is relieved by moving the affected ankle and toes. Anterior tarsal tunnel syndrome can occur after squatting and leaning forward for long periods of time, as when planting flowers. People with diabetes or vulnerable nerve syndromes may be more susceptible to the development of this syndrome. Most patients with anterior tarsal tunnel syndrome can be treated with deep peroneal nerve blocks with local anesthetic and corticosteroid combined with avoidance techniques. Careful preblock neurologic assessment is important to avoid preexisting neurologic deficits later being attributed to the deep peroneal nerve block. These assessments are especially important for patients who have sustained trauma to the ankle or foot and for patients with diabetic neuropathy in whom deep peroneal nerve blocks are being used for acute pain control. The most common cause of pain radiating into the lower extremity is a herniated lumbar disk or nerve impingement secondary to degenerative arthritis of the spine, not disorders involving the common or deep peroneal nerve per se. Other pain syndromes that may be confused with deep peroneal nerve entrapment include lesions either above the origin of the common peroneal nerve, such as lesions of the sciatic nerve, or lesions at the point at which the common peroneal nerve winds around the head of the fibula. Electromyography and MRI of the lumbar spine, combined with the clinical history and physical examination, helps sort out the cause of distal lower extremity and foot pain.

SUGGESTED READINGS DiDomenico LA, Masternick EB: Anterior tarsal tunnel syndrome, Clin Podiatr Med Surg 23:611–620, 2006. Kennedy JG, Baxter DE: Nerve disorders in dancers, Clin Sports Med 27:329–334, 2008. Waldman SD: Anterior tarsal tunnel syndrome. In Pain review, Philadelphia, 2009, Saunders, pp 322–323. Waldman SD: Functional anatomy of the ankle and foot. In Pain review, Philadelphia, 2009, Saunders, pp 155–156. Waldman SD, Campbell RSD: Anterior tarsal tunnel syndrome. In Imaging of pain, Philadelphia, 2011, Saunders, pp 421–423.

Chapter 143 TIBIAL NERVE BLOCK AT THE ANKLE Indications and Clinical Considerations Posterior tarsal tunnel syndrome is caused by compression of the posterior tibial nerve as it passes through the posterior tarsal tunnel. The posterior tarsal tunnel is made up of the flexor retinaculum, the bones of the ankle, and the lacunate ligament. In addition to the posterior tibial nerve, the tunnel contains the posterior tibial artery and a number of tendons, which are subject to tenosynovitis (Figures 143-1 and 143-2). The most common cause of compression of the posterior tibial nerve at this anatomic location is trauma to the ankle, including fracture, dislocation, and crush injuries. Thrombophlebitis and aneurysms involving the posterior tibial artery also have been implicated in the evolution of posterior tarsal tunnel syndrome (Figure 143-3). Patients with rheumatoid arthritis have a higher incidence of posterior tarsal tunnel syndrome than the general population. Posterior tarsal tunnel syndrome is much more common than anterior tarsal tunnel syndrome. Posterior tarsal tunnel syndrome manifests in a manner analogous to carpal tunnel syndrome. The patient reports pain, numbness, and paresthesias of the sole of the foot. These symptoms also may radiate proximal to the entrapment into the medial ankle. The medial and lateral plantar divisions of the posterior tibial nerve provide motor innervation to the intrinsic muscles of the foot. The patient may note weakness of the toe flexors and instability of the foot caused by weakness of the lumbrical muscles. Nighttime foot pain analogous to the nocturnal pain of carpal tunnel syndrome often is present.

Physical findings include tenderness over the posterior tibial nerve at the medial malleolus. A positive Tinel sign just below and behind the medial malleolus over the posterior tibial nerve usually is present. Active inversion of the ankle often reproduces the symptoms of the posterior tarsal tunnel syndrome. Weakness of the flexor digitorum brevis and the lumbrical muscles may be present if the medial and lateral branches of the posterior tibial nerve are affected. Posterior tarsal tunnel syndrome often is misdiagnosed as arthritis of the ankle joint, lumbar radiculopathy, or diabetic polyneuropathy. Patients with arthritis of the ankle joint have radiographic evidence of arthritis. Most patients with a lumbar radiculopathy have reflex, motor, and sensory changes associated with back pain, whereas patients with posterior tarsal tunnel syndrome have no reflex changes and have motor and sensory changes limited to the distal posterior tibial nerve. Diabetic polyneuropathy generally manifests as symmetrical sensory deficit involving the entire foot, rather than limited just to the distribution of the posterior tibial nerve. Lumbar radiculopathy and posterior tibial nerve entrapment may coexist as the so-called double crush syndrome. Furthermore, because posterior tarsal tunnel syndrome is seen in patients with diabetes, it is not surprising that diabetic polyneuropathy usually is present in diabetic patients with posterior tarsal tunnel syndrome. Electromyography helps distinguish lumbar radiculopathy and diabetic polyneuropathy from posterior tarsal tunnel syndrome. Plain radiographs are indicated for all patients with posterior tarsal tunnel syndrome to rule out occult bony disease. On the basis of the patient’s clinical presentation, additional testing may be

Tibial n. Tibial v. Flexor digitorum m. Tendon, tibialis posterior m. Medial malleolus

Peroneus longus m. Peroneus brevis m. Lateral malleolus

Tibial a. Flexor retinaculum

Calcaneal tendon

Figure 143-1  Important regional anatomy for performing tibial nerve block at the ankle.

435

436        SECTION 8  •  Ankle and Foot

Extensor hallucis longus t.

••

Extensor digitorum longus & peroneus tertius tt.

•

Tibialis ant. t.

Greater saphenous v.

•

••

••

••

Tibionavicular lig.

• •

Talus

•

Transverse tibiofibular lig.

•

••

• • •

Peroneal retinaculum

•• ••

••

Peroneus brevis m. & t. Peroneus longus t.

•• •

Lat. malleolus Post. inf. tibiofibular lig.

Med. malleolus

••

Tibialis post. t. Flexor digitorum longus t. Post. tibial a. Tibial n. Flexor hallucis longus m. & t.

•• •

Tendo calcaneus

Figure 143-2  Anatomy of the posterior tibial nerve and related structures. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

indicated, including complete blood count, uric acid, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and/or ultrasound imaging of the ankle and foot is indicated if joint instability or a space-occupying lesion is suspected (Figure 143-4). The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The tibial nerve is one of the two major continuations of the sciatic nerve, the other being the common peroneal nerve. The tibial nerve provides sensory innervation to the posterior portion of the calf, the heel, and the medial plantar surface. The tibial nerve splits from the sciatic nerve at the superior margin of the popliteal fossa and descends in a slightly medial course through the popliteal fossa. The tibial nerve at the ankle lies just beneath the popliteal fascia and is readily accessible for neural blockade. The tibial nerve continues its downward course,

running between the two heads of the gastrocnemius muscle, passing deep to the soleus muscle. The nerve courses medially between the Achilles tendon and the medial malleolus, where it divides into the medial and lateral plantar nerves, providing sensory innervation to the heel and medial plantar surface (see Figures 143-1 and 143-2). The tibial nerve is subject to compression at this point as the nerve passes through the posterior tarsal tunnel. The posterior tarsal tunnel is made up of the flexor retinaculum, the bones of the ankle, and the lacunate ligament. In addition to the posterior tibial nerve, the tunnel contains the posterior tibial artery and a number of flexor tendons.

Technique The patient is placed in the lateral position with the affected leg in the dependent position and slightly flexed. The posterior tibial artery at this level is then palpated. The area between the medial malleolus and the Achilles tendon is identified and

143  •  Tibial Nerve Block at the Ankle        437

a

V

V V V

fhl

a

fhl

T

T

B

A

Figure 143-3  Tarsal tunnel syndrome. A, Short-axis, 5- to 14-MHz ultrasound image over the tarsal tunnel shows normal medial and lateral plantar nerves (arrows) trapped below a vascular arch made by a pseudoaneurysm of the posterior tibial artery (a) and tibial veins (V); this compresses the tibial nerve and causes symptoms of tarsal tunnel syndrome without ultrasound nerve abnormalities. B, The corresponding short-axis ultrasound image shows the contralateral, asymptomatic tarsal tunnel with normal vessels. fhl, Flexor policis longus tendon; T, talus bone. (From Michaud J: Peripheral nerves. In Wakefield RJ, D’Agostino MA, editors: Essential applications of musculoskeletal ultrasound in rheumatology, Philadelphia, 2010, Saunders.)

A

B

C

Figure 143-4  Axial proton density (PD) (A) and T2-weighted (T2W) (B) magnetic resonance (MR) images of the ankle in a patient with medial foot pain. There is a discrete rounded lesion (white arrow) within the tarsal tunnel. It has intermediate signal intensity (SI) on the PD MR images and high SI on the T2W MR images consistent with a fluid-filled ganglion cyst. C, The sagittal T1-weighted MR image demonstrates the mass posterior to the talus and the flexor hallucis longus tendon (broken arrow); one of the posterior tibial vessels runs over the superficial surface of the mass (black arrow). The cyst is causing mass effect within the tarsal tunnel, compressing the posterior tibial nerve and producing symptoms of posterior tarsal tunnel syndrome. (Reproduced with permission from Spratt JD, Stanley AJ, Grainger AJ, et al: The role of diagnostic radiology in compressive and entrapment neuropathies, Eur Radiol 12:2352–2364, 2002.)

prepared with antiseptic solutions. A 1½-inch, 25-gauge needle is inserted at this level and directed anteriorly toward the pulsations of the posterior tibial artery. If the arterial pulsations cannot be identified, the needle is directed toward the posterior superior border of the medial malleolus. The needle is then advanced slowly toward the tibial nerve, which lies in the posterior groove of the medial malleolus, until a paresthesia in the distribution of the tibial nerve is elicited (Figure 143-5). The patient should be warned to expect a paresthesia and should be told to say “there!” as soon as the paresthesia is felt. Paresthesia usually is elicited after the needle is advanced ½ to ¾ inch. If a paresthesia is not elicited, the needle is withdrawn and redirected slightly more

cephalad until a paresthesia is achieved. Once a paresthesia in the distribution of the tibial nerve has been elicited, the needle is withdrawn 1 mm and the patient is observed to be sure that he or she is not experiencing any persistent paresthesia. If no persistent paresthesia is present and after careful aspiration, a total of 6 mL of 1.0% preservative-free lidocaine and 40 mg of methylprednisolone is slowly injected. Care must be taken not to advance the needle into the substance of the nerve during the injection and thereby inject solution intraneurally. After injection of the solution, pressure is applied to the injection site to decrease the incidence of postblock ecchymosis and hematoma formation.

438        SECTION 8  •  Ankle and Foot

Clinical Pearls

Medial malleolus Tibial n. Calcaneal tendon

Carrico & Shavell

Figure 143-5  Proper needle placement for tibial nerve block at the ankle.

Side Effects and Complications The main side effect of tibial nerve block at the ankle is postblock ecchymosis and hematoma formation. As mentioned earlier, pressure should be maintained on the injection site postblock to avoid ecchymosis and hematoma formation. Because a paresthesia is elicited with this technique, needle-induced trauma to the tibial nerve remains a possibility. By advancing the needle slowly and then withdrawing the needle slightly away from the nerve, needle-induced trauma to the tibial nerve can be avoided. This technique can safely be performed in the presence of anticoagulation by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable risk-to-benefit ratio.

Tibial nerve block at the ankle is a simple technique that can produce dramatic relief for patients with posterior tarsal tunnel syndrome. Careful preblock neurologic assessment is important to avoid preexisting neurologic deficits later being attributed to the tibial nerve block. These assessments are especially important for patients who have sustained trauma to the foot or ankle and patients with diabetic neuropathy with whom tibial nerve block at the ankle is being used for acute pain control. The most common cause of pain radiating into the lower extremity is a herniated lumbar disk or nerve impingement secondary to degenerative arthritis of the spine, not disorders involving the tibial nerve per se. Other pain syndromes that may be confused with tibial nerve entrapment at the posterior tarsal tunnel include lesions either above the origin of the tibial nerve, such as lesions of the sciatic nerve, or distal lesions of the tibial nerve, such as posterior tarsal tunnel syndrome. Electromyography and MRI of the lumbar spine, combined with the clinical history and physical examination, help sort out the cause of distal lower pain.

SUGGESTED READINGS Cancilleri F, Ippolito M, Amato C, Denaro V: Tarsal tunnel syndrome: four uncommon cases, Foot Ankle Surg 13:214–217, 2007. Fujita I, Matsumoto K, Minami T, et  al: Tarsal tunnel syndrome caused by epineural ganglion of the posterior tibial nerve: report of 2 cases and review of the literature, J Foot Ankle Surg 43:185–190, 2004. Mezrow CK, Sanger JR, Matloub HS: Acute tarsal tunnel syndrome following partial avulsion of the flexor hallucis longus muscle: a case report, J Foot Ankle Surg 41:243–246, 2002. Waldman SD: Posterior tarsal tunnel syndrome. In Pain review, Philadelphia, 2009, Saunders, pp 323–324. Waldman SD, Campbell RSD: Posterior tarsal tunnel syndrome. In Imaging of pain, Philadelphia, 2011, Saunders, pp 425–426.

Chapter 144 ACHILLES TENDON INJECTION

Indications and Clinical Considerations The Achilles tendon is susceptible to the development of tendinitis both at its insertion on the calcaneus and at its narrowest part, at a point approximately 5 cm above its insertion (Figure 144-1). The Achilles tendon is also subject to repetitive motion, which may result in microtrauma that heals poorly owing to the tendon’s avascular nature. Running is often implicated as the inciting factor of acute Achilles tendinitis. Tendinitis of the Achilles tendon frequently coexists with bursitis of the associated bursae of the tendon and ankle joint, creating additional pain and functional disability. Calcium deposition around the tendon may occur if the inflammation continues, making subsequent treatment more difficult. Continued trauma to the inflamed tendon ultimately may result in tendon rupture (Figure 144-2). The onset of Achilles tendinitis usually is acute, occurring after overuse or misuse of the ankle joint. Inciting factors may include activities such as running and sudden stopping and starting, as when playing tennis. Improper stretching of the gastrocnemius

and Achilles tendon before exercise as well as the use of quinolone antibiotics have also been implicated in the development of Achilles tendinitis, as well as acute tendon rupture. The pain of Achilles tendinitis is constant and severe and is localized in the posterior ankle. Significant sleep disturbance often is reported. The patient may attempt to splint the inflamed Achilles tendon by adopting a flat-footed gait to avoid plantarflexing the affected tendon. Patients with Achilles tendinitis exhibit pain with resisted plantarflexion of the foot. Creaking or grating may be palpated when passively plantarflexing the foot (Figure 144-3). As mentioned earlier, the chronically inflamed Achilles tendon may suddenly rupture with stress or during vigorous injection procedures into the tendon itself. Plain radiographs are indicated for all patients with posterior ankle pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and/or ultrasound imaging of the ankle is indicated if Achilles tendinitis or joint instability is suggested (Figures 144-4, 144-5, and 144-6). Radionuclide bone scanning is useful to identify stress fractures of the tibia not seen on plain radiographs. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The Achilles tendon is the thickest and strongest tendon in the body, yet it is also very susceptible to rupture. The common tendon of the gastrocnemius muscle, the Achilles tendon begins at mid calf and continues downward to attach to the posterior calcaneus, where it may become inflamed (see Figure 144-1; Figure 144-7). The Achilles tendon narrows during this downward course, becoming most narrow at approximately 5 cm above its calcaneal insertion. It is at this narrowest point that tendinitis also may occur. A bursa is located between the Achilles tendon and the base of the tibia and the upper posterior calcaneus. This bursa also may become inflamed as a result of coexistent Achilles tendinitis and may confuse the clinical picture. A

B

Figure 144-1  Achilles peritendinitis and paratendinitis: magnetic resonance (MR) imaging. In a soccer player, a sagittal T1-weighted (TR/TE, 700/15) spin-echo MR image (A) shows an irregular region of intermediate signal intensity (arrows) within the pre-Achilles fat body. A sagittal short tau inversion recovery (STIR) (TR/TE, 5000/22; inversion time, 150 ms) MR image (B) shows high signal intensity (arrows) anterior to the Achilles tendon. (Courtesy C. Wakeley, MD, Bristol, England; from Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

Technique The goals of this injection technique are explained to the patient. The patient is placed in the prone position with the affected foot hanging off the end of the table. The foot is gently dorsiflexed to facilitate identification of the margin of the tendon, to aid in avoiding injection directly into the tendon. The tender points at the tendinous insertion or at its most narrow part approximately 5 cm above the insertion are identified and marked with a sterile marker (Figure 144-8). 439

440        SECTION 8  •  Ankle and Foot

A

B

C

D

Figure 144-2  Chronic Achilles tendinosis with a partial or complete tear: magnetic resonance (MR) imaging. A, Partial tear. A sagittal T2-weighted (TR/TE, 2000/70) spin-echo MR image shows an enlarged Achilles tendon containing irregular regions of high signal intensity. B, Complete tear. A sagittal intermediate-weighted (TR/TE, 3000/30) spin-echo MR image shows complete disruption of the Achilles tendon and a proximal segment that is inhomogeneous in signal intensity. Note the edema and hemorrhage of high signal intensity about the acutely torn tendon. C, Complete tear. A sagittal T2-weighted (TR/TE, 1800/80) fat-suppressed spin-echo MR image reveals an acute and complete tear of the Achilles tendon with multiple regions of high signal intensity. D, Complete tear. A sagittal intermediate-weighted (TR/TE, 2000/20) spin-echo MR image reveals a chronic tear characterized by complete disruption of the Achilles tendon. (C courtesy D. Levey, MD, Corpus Christi, Texas; A, B, and D from Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

Figure 144-3  Eliciting the creak sign for Achilles tendinitis. (From Waldman SD: Physical diagnosis of pain, Philadelphia, 2005, Saunders.)

Proper preparation with antiseptic solution of the skin overlying these points is then carried out. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the previously marked points are palpated. The needle is then carefully advanced at this point alongside the tendon, through the skin and subcutaneous tissues, with care being taken not to enter the substance of the tendon (see Figure 144-7). The contents of the syringe are then gently injected while the needle is slowly withdrawn. There should be minimal resistance to injection. If there is significant resistance to injection, the needle tip is probably in

the substance of the Achilles tendon and should be withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. Ultrasound guidance may be beneficial to help avoid injection into the substance of the inflamed tendon (Figure 144-9).

Side Effects and Complications The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Trauma to the Achilles tendon from the injection

144  •  Achilles Tendon Injection        441

* C M

A

Figure 144-6  Longitudinal section ultrasound of the Achilles tendon. Note the nonuniform echotexture of the Achilles tendon in keeping with tendinopathy (red cross). Note the subparatenon position of the needle (red arrowhead) and fluid between the paratenon and tendon (red star).

B Figure 144-4  A, Longitudinal ultrasound image of a patient with Achilles tendinopathy. The tendon (white arrows) inserts on the calcaneus (C), and lies superficial to Kager fat pad and the underlying posterior compartment muscle group (M). The middle portion of the tendon demonstrates fusiform thickening with low-reflective change (asterisk). B, A localized power Doppler image also shows the tendon thickening as well as prominent areas of neovascularization within the tendon substance. (From Waldman SD, Robert SD Campbell: Achilles tendinitis. In Imaging of pain, Philadelphia, 2011, Saunders.) Inflamed Achilles tendon

Calcaneus

Figure 144-7  Proper needle placement for Achilles tendon injection.

Figure 144-5  Transverse ultrasound image of an inflamed Achilles ­tendon.

itself remains an ever-present possibility. Tendons that are highly inflamed or previously damaged are subject to rupture if they are directly injected. The risk of this complication can be greatly decreased if the clinician uses gentle technique and stops injecting immediately if significant resistance to injection is encountered. Approximately 25% of patients report a transient increase in pain after this injection technique; the patient should be warned of this.

442        SECTION 8  •  Ankle and Foot

Clinical Pearls

Figure 144-8  Site of needle insertion for Achilles tendon injection.

This injection technique is extremely effective in the treatment of pain secondary to the just-mentioned causes of posterior ankle pain. Coexistent bursitis and arthritis also may contribute to posterior ankle pain and may require additional treatment with a more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for ankle pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Damuth E, Heidelbaugh J, Malani PN, Cinti SK: An elderly patient with fluoroquinolone-associated Achilles tendinitis, Am J Geriatr Pharmacother 6:264–268, 2008. De Simone C, Guerriero C, Giampetruzzi AR, et al: Achilles tendinitis in psoriasis: clinical and sonographic findings, J Am Acad Dermatol 49:217–222, 2003. Lesic A, Bumbasirevic M: Disorders of the Achilles tendon, Curr Orthop 18:63– 75, 2004. Waldman SD: Achilles tendinitis. In Pain review, Philadelphia, 2009, Saunders, p 325. Waldman SD, Campbell RSD: Achilles tendinitis. In Imaging of pain, Philadelphia, 2011, Saunders, pp 427–428.

Figure 144-9  Proper transducer placement for evaluation and injection of the Achilles tendon.

Chapter 145 ACHILLES BURSA INJECTION

Indications and Clinical Considerations Bursae are formed from synovial sacs whose purpose is to allow easy sliding of muscles and tendons across one another at areas of repeated movement. These synovial sacs are lined with a synovial membrane that is invested with a network of blood vessels that secrete synovial fluid. Inflammation of the bursa results in an increase in the production of synovial fluid with swelling of the bursal sac. With overuse or misuse, these bursae may become inflamed, enlarged, and on rare occasions infected. Although there is significant intrapatient variability as to the number, size, and location of bursae, anatomists have identified a number of clinically relevant bursae, including the Achilles bursa. The Achilles bursa, which is also known as the retrocalcaneal bursa, lies beneath the Achilles tendon, which is the insertional tendon of the gastrocnemius muscle to the posterior calcaneus (Figure 145-1). This bursa may exist as a single bursal sac or in some patients as a multisegmented series of sacs that may be loculated. Patients with Achilles bursitis experience pain over the posterior heel and tenderness anterior to the Achilles tendon itself. The patient with Achilles bursitis may report increased pain on full passive plantarflexion of the foot. Activity, especially involving repetitive plantarflexion, such as running, makes the pain worse, with rest and heat providing some relief. Often the patient is unable to stand on tiptoes or walk up stairs. The pain is constant and is characterized as aching and may interfere with sleep. Coexistent Achilles tendinitis, arthritis, or internal derangement of the ankle may confuse the clinical picture after trauma to the knee joint. If the inflammation of the Achilles bursae becomes chronic, calcification of the bursae may occur.

Physical examination may reveal point tenderness in front of the Achilles tendon, at its insertion at the calcaneus. Swelling and fluid accumulation often surround the bursa. Active resisted plantarflexion of the foot reproduces the pain. Sudden release of resistance during this maneuver markedly increases the pain. Rarely, the Achilles bursa may become infected in a manner analogous to infection of the prepatellar bursa. Plain radiographs of the knee may reveal calcification of the bursa and associated structures, including the Achilles tendon, consistent with chronic inflammation (Figure 145-2). Magnetic resonance imaging (MRI) and/or ultrasound is indicated if bursitis, internal derangement, occult mass, tumor of the ankle, or Achilles tendinopathy is suspected and to help confirm the diagnosis. Electromyography helps distinguish Achilles bursitis from neuropathy, lumbar radiculopathy, and plexopathy. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

C Achilles tendon

Inflamed Achilles bursa

Figure 145-1  Proper needle placement for Achilles bursa injection.

Figure 145-2  Normal retrocalcaneal bursa. Tissue interposed between the posterosuperior calcaneus and distal Achilles tendon is of normal fat density (circle). C, calcaneus. (From Hochman MG, Ramappa AJ, Newman JS, Farraher SW: Imaging of tendons and bursae. In Weissman BN, ­editor: Imaging of arthritis and metabolic bone disease, Philadelphia, 2009, Saunders.)

443

444        SECTION 8  •  Ankle and Foot

Clinically Relevant Anatomy The Achilles bursa lies between the Achilles tendon and the base of the tibia and the posterior calcaneus (Figure 145-3). The bursa is subject to the development of inflammation after overuse, misuse, or direct trauma. The Achilles tendon is the thickest and strongest tendon in the body, yet it is also very susceptible to rupture. The common tendon of the gastrocnemius muscle, the Achilles tendon begins at mid calf and continues downward to attach to the posterior calcaneus, where it may become inflamed (see ­Figure ­145-1). The Achilles tendon narrows during this downward course, becoming most narrow approximately 5 cm above its calcaneal insertion. It is at this narrowest point that tendinitis also may occur. Tendinitis, especially at the calcaneal insertion, may mimic Achilles bursitis and may make diagnosis difficult.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the prone position with the affected foot hanging off the end of the table. The foot is gently dorsiflexed to

facilitate identification of the medial margin of the tendon at its insertion, to aid in avoiding injection directly into the tendon. The tender point in front of the tendon is identified and marked with a sterile marker (Figure 145-4). Proper preparation with antiseptic solution of the skin overlying this point is then carried out. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the previously marked point is palpated. The needle is then carefully inserted at a right angle to the tendon, just anterior to the tendon to place the needle tip in proximity to the Achilles bursa (see Figure 145-1). Care must be taken not to enter the substance of the tendon. The contents of the syringe are then gently injected. There should be minimal resistance to injection. If there is significant resistance to injection, the needle tip is probably in the substance of the Achilles tendon and should be withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications

a

The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Trauma to the Achilles tendon from the injection itself remains an ever-present possibility. Tendons that are highly inflamed or previously damaged are subject to rupture if they are directly injected. The risk of this complication can be greatly decreased if the clinician uses gentle technique and stops injecting immediately if significant resistance to injection is encountered. Approximately 25% of patients report a transient increase in pain after this injection technique; the patient should be warned of this.

C

Figure 145-3  Retrocalcaneal bursitis in patient with rheumatoid arthritis. The retrocalcaneal fat is obscured by fluid in the retrocalcaneal bursa. Owing to the bursitis, an erosion has developed in the calcaneus (arrowhead). a, Achilles tendon; C, calcaneus. (From Hochman MG, Ramappa AJ, Newman JS, Farraher SW: Imaging of tendons and bursae. In Weissman BN, editor: Imaging of arthritis and metabolic bone disease, Philadelphia, 2009, Saunders.)

Figure 145-4  Site of needle insertion for Achilles bursa injection.

145  •  Achilles Bursa Injection        445

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to the just-mentioned causes of posterior ankle pain. Coexistent Achilles tendinitis and arthritis also may contribute to posterior ankle pain and may require additional treatment with a more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient undergoes this injection technique for ankle pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Aronow MS: Posterior heel pain (retrocalcaneal bursitis, insertional and noninsertional Achilles tendinopathy), Clin Podiatr Med Surg 22:19–43, 2005. Hochman MG, Ramappa AJ, Newman JS, Farraher SW: Imaging of tendons and bursae. In Weissman BN, editor: Imaging of arthritis and metabolic bone disease, Philadelphia, 2009, Saunders, pp 196–238. Lesi A, Bumbasirevi M: Disorders of the Achilles tendon, Curr Orthop 18:63–75, 2004. Van der Wall H, Lee A, Magee M, et al: Radionuclide bone scintigraphy in sports injuries, Semin Nucl Med 40:16–30, 2010. Vyce SD, Addis-Thomas E, Mathews EE, Perez SL: Painful prominences of the heel, Clin Podiatr Med Surg 27:443–462, 2010.

Chapter 146 FIBULOCALCANEAL LIGAMENT INJECTION Indications and Clinical Considerations The fibulocalcaneal ligament, which is also known as the calcaneofibular ligament, is susceptible to strain from acute injury from sudden inversion of the ankle, as when stepping off a high curb, or from repetitive microtrauma to the ligament from overuse or misuse, such as in long-distance running on soft or uneven surfaces. Patients with strain of the fibulocalcaneal ligament experience pain anterior and inferior to the lateral malleolus. Inversion of the ankle joint exacerbates the pain. On physical examination there is point tenderness just below the lateral malleolus. With acute trauma, ecchymosis over the ligament may be noted. Passive inversion of the ankle joint exacerbates the pain. Coexistent bursitis and arthritis of the ankle and subtalar joint also may be present and may confuse the clinical picture. Plain radiographs are indicated for all patients with ankle pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and/or ultrasound imaging of the ankle is indicated if disruption of the fibulocalcaneal ligament, joint instability, occult mass, or tumor is suspected (Figure 146-1).

2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 11⁄2-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, with the lower extremity slightly adducted, the lower margin of the lateral malleolus is identified (Figure 146-4). One-half inch below this point, the needle is carefully advanced at a 30-degree angle to the ankle, through the skin and subcutaneous tissues, to impinge on the lower margin of the lateral malleolus (see Figure 146-2). The needle is then withdrawn slightly, and the contents of the syringe are gently injected. There will be slight resistance to injection. If significant resistance is encountered, the needle is probably in the ligament and should be withdrawn

Clinically Relevant Anatomy The ankle is a hinge-type articulation among the distal tibia, the two malleoli, and the talus. The articular surface is covered with hyaline cartilage, which is susceptible to arthritis. The joint is surrounded by a dense capsule that helps strengthen the ankle. The joint capsule is lined with a synovial membrane that attaches to the articular cartilage. The ankle joint is innervated by the deep peroneal and tibial nerves. The major ligaments of the ankle joint include the talofibular, anterior fibulocalcaneal, calcaneofibular, and posterior fibulocalcaneal ligaments, which provide the majority of strength to the ankle joint. The fibulocalcaneal ligament is not as strong as the deltoid ligament and is susceptible to strain. The fibulocalcaneal ligament runs from the anterior border of the lateral malleolus to the lateral surface of the calcaneus (Figure 146-2, Figure 146-3).

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the area of the lateral malleolus is carried out. A sterile syringe containing 446

Figure 146-1  A 43-year-old woman with ankle strain. The oblique coronal (angled 50 degrees), fat-suppressed, proton density weighted (TR/TE = 2800/34) images showed nonvisualization of the hypointense structure between the calcaneus and the fibular malleolus. There were apparent edematous changes of the surrounding soft tissue (arrowheads). The initial interpretation based on plain magnetic resonance imaging findings was calcaneofibular (CF) ligament disruption. (From Chou MC, Yeh LR, Chen CK, et al: Comparison of plain MRI and MR arthrography in the evaluation of lateral ligamentous injury of the ankle joint, J Chin Med Assoc 69:26–31, 2006.)

146  •  Fibulocalcaneal Ligament Injection        447

Talofibular ligament

Lateral malleolus Posterior talofibular ligament Inflamed anterior calcaneofibular ligament Calcaneus

Figure 146-2  Proper needle placement for fibulocalcaneal ligament injection.

Extensor digitorum longus tt. Lat. cuneiform Peroneus tertius t. Extensor digitorum brevis m. Cuboid

2nd metatarsal Interosseous intercuneiform lig. Med. cuneiform Tibialis ant. t. Intermediate cuneiform Navicular Tibialis post. t. Plantar calcaneonavicular lig.

Interosseous talocalcaneal lig. Peroneus brevis t. Peroneus longus t. Calcaneofibular lig.

Sustentaculum tali Flexor digitorum longus t. Calcaneus Flexor hallucis longus t. Med. plantar n. Post. tibial a. Lat. plantar n.

Tendo calcaneus

Figure 146-3  Anatomy of the ankle. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the ­injection site.

Side Effects and Complications The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients note a transient increase in pain after injection of the fibulocalcaneal ligament; the patient should be warned of this. Injection around strained ligaments should always be done gently to avoid further damage to the already compromised ligament. Figure 146-4  Site of needle insertion for fibulocalcaneal ligament ­injection.

448        SECTION 8  •  Ankle and Foot

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to the fibulocalcaneal ligament strain. Coexistent arthritis, bursitis, and tendinitis also may contribute to lateral ankle pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for ankle pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Amaral De, Noronha M, Borges NG Jr: Lateral ankle sprain: isokinetic test reliability and comparison between invertors and evertors, Clin Biomech (Bristol, Avon) 19:868–871, 2004. Chou MC, Yeh LR, Chen CK, et al: Comparison of plain MRI and MR arthrography in the evaluation of lateral ligamentous injury of the ankle joint, J Chin Med Assoc 69:26–31, 2006. Hunt GC: Injuries of peripheral nerves of the leg, foot and ankle: an often unrecognized consequence of ankle sprains, Foot 13:14–18, 2003. van Rijn RM, van Os AG, Bernsen RM, et  al: What is the clinical course of acute ankle sprains? A systematic literature review, Am J Med 121:324–331. e7, 2008. Weber JM, Maleski RM: Conservative treatment of acute lateral ankle sprains, Clin Podiatr Med Surg 19:309–318, 2002.

Chapter 147 PERONEAL TENDON INJECTION

Indications and Clinical Considerations The tendons of the peroneus longus and brevis muscles are susceptible to the development of tendinitis and tenosynovitis. These tendons are subjected to repetitive motion, which may result in microtrauma that heals poorly owing to the tendons’ avascular nature. Eversion injuries during running and tennis often are implicated as the inciting factor of acute peroneal tendinitis. Tendinitis of the peroneal tendons frequently coexists with bursitis of the associated bursae of the ankle joint, creating additional pain and functional disability. Calcium deposition around the tendons and their tendon sheath may occur if the inflammation continues, making subsequent treatment more difficult (Figure 147-1). Continued trauma to the inflamed tendon ultimately may result in tendon rupture (Figure 147-2). The onset of peroneal tendinitis usually is acute, occurring after overuse or misuse of the ankle joint. Inciting factors may include activities such as eversion injuries to the ankle during running or when playing tennis. Improper stretching of the peroneus longus and brevis muscles and tendons before exercise also has been implicated in the development of peroneal tendinitis, as well as acute tendon rupture. The pain of peroneal tendinitis is constant and severe and is localized in the posterior ankle. Significant sleep disturbance often is reported. Patients with peroneal tendinitis exhibit pain in the lateral ankle and foot with resisted eversion of the foot. Creaking or grating may be palpated when passively inverting the foot. As mentioned earlier, the chronically inflamed peroneal tendons may suddenly rupture with stress or during vigorous injection procedures into the tendon itself. Plain radiographs are indicated for all patients with lateral ankle pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) or ultrasound of the ankle is indicated if peroneal tendinitis, tear, rupture, and/or joint instability is suspected (Figures 147-3 and 147-4). Radionuclide bone scanning is useful to identify stress fractures of the tibia not seen on plain radiographs. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The peroneus longus and brevis muscles and their associated tendons run together in a single synovial sheath (Figures 147-5 and 147-6). The tendon of the peroneus longus muscle passes behind

the lateral malleolus and then turns inward on the cubital bone to cross the sole of the foot to insert on the base of the first metatarsal. There may be a sesamoid bone at each turn of the tendon. The tendon of the peroneus brevis also passes behind the lateral malleolus and then turns forward along the lateral calcaneus above the tendon of the peroneus longus muscle to attach at the base of the fifth metatarsal.

A

B Figure 147-1  A, An oblique plain radiograph of the right foot showing a calcific deposit within the peroneus longus tendon. B, Repeat plain radiograph of the right foot at 3 months showing resorption of the intratendinous calcification. (From Brinsden MD, Wilson JH: Acute calcific tendinitis of the peroneus longus tendon, Inj Extra 36:426–427, 2005.)

449

450        SECTION 8  •  Ankle and Foot

A

B

Figure 147-2  A and B, Photos show complete rupture of the peroneus longus at the cuboid tunnel, which required insertion into the cuboid using an interference screw. (From Cerrato RA, Myerson MS: Peroneal tendon tears, surgical management and its complications, Foot Ankle Clin 14:299–312, 2009.)

*

*

A

B

Figure 147-3  A, Coronal magnetic resonance imaging of the right foot and ankle showing the peroneus brevis tendon (black arrows) and the enlarged peroneal tubercle (star). B, Sagittal magnetic resonance imaging of the right foot and ankle showing effusion in the peroneal tendon sheath (asterisk), peroneus brevis tendon increased signal intensity (black arrows), and enlarged peroneal tubercle (star). (From Boya H, Pinar H: Stenosing tenosynovitis of the peroneus brevis tendon associated with hypertrophy of the peroneal tubercle, J Foot Ankle Surg 49:188–190, 2010.)

Technique

Figure 147-4  Ultrasound image after injection of peroneus longus tendinitis showing complete rupture of the tendon. (From Borland S, Jung S, Hugh IA: Complete rupture of the peroneus longus tendon secondary to injection, Foot (Edinb) 19:229–231, 2009.)

The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the area just below the lateral malleolus is done. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 11⁄2-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, with the foot strongly everted, the lower margin of the lateral malleolus is identified and the path of the peroneal tendons is traced anteriorly until the V-shaped division of the tendons is palpated (Figure 147-7). At this point the needle is carefully advanced at a 30-degree angle to the ankle through the skin and subcutaneous tissues toward the lateral malleolus into the combined tendon sheath (see Figure 147-5). The contents of the syringe are then gently injected. There should be minimal resistance to injection. If significant resistance is encountered, the needle is probably in a

147  •  Peroneal Tendon Injection        451

Cuboid Lateral malleolus Peroneus brevis m. Peroneus longus m.

Synovial sheaths inflamed or swollen

5th metatarsal

Figure 147-5  Proper needle placement for peroneal tendon injection.

••

Peroneus brevis m. & t.

••

Tibial n.

•

•

Post. tibial a.

Flexor hallucis longus m. & t.

••

Peroneus longus t.

Lesser saphenous v.

•

••

••

•

Sural n.

Calcaneus

••

•

Abductor hallucis m.

Figure 147-6  Anatomy of the peroneus longus and brevis muscles and related structures. (From Kang HS, Ahn JM, Resnick D: MRI of the extremities: an anatomic atlas, ed 2, Philadelphia, 2002, Saunders.)

452        SECTION 8  •  Ankle and Foot

Clinical Pearls

Figure 147-7  Site of needle insertion for peroneal tendon injection.

tendon and should be withdrawn slightly until the injection proceeds without significant resistance. The solution should distend the tendon sheath, giving it a hot dog–shaped appearance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Trauma to the peroneal tendons from the injection itself remains an ever-present possibility. Tendons that are highly inflamed or previously damaged are subject to rupture if they are directly injected. The risk of this complication can be greatly decreased if the clinician uses gentle technique and stops injecting immediately if significant resistance to injection is encountered. Approximately 25% of patients report a transient increase in pain after this injection technique; the patient should be warned of this.

This injection technique is extremely effective in the treatment of pain secondary to the just-mentioned causes of lateral ankle pain. Coexistent bursitis and arthritis also may contribute to lateral ankle pain and may require additional treatment with a more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for ankle pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Borland S, Jung S, Hugh IA: Complete rupture of the peroneus longus tendon secondary to injection, Foot (Edinb) 19:229–231, 2009. Boya H, Pinar H: Stenosing tenosynovitis of the peroneus brevis tendon associated with hypertrophy of the peroneal tubercle, J Foot Ankle Surg 49:188–190, 2010. Brinsden MD, Wilson JH: Acute calcific tendinitis of the peroneus longus tendon, Inj Extra 36:426–427, 2005. Lamm BM, Myers DT, Dombek M, et al: Magnetic resonance imaging and surgical correlation of peroneus brevis tears, J Foot Ankle Surg 43:30–36, 2004.

Chapter 148 PLANTAR FASCIITIS INJECTION

Indications and Clinical Considerations Plantar fasciitis is characterized by pain and tenderness over the plantar surface of the calcaneus. Occurring twice as often in women, plantar fasciitis is thought to be caused by an inflammation of the plantar fascia. This inflammation can occur alone or be part of a systemic inflammatory condition, such as rheumatoid arthritis, Reiter syndrome, or gout. Obesity also seems to predispose to the development of plantar fasciitis, as does going barefoot or wearing house slippers for prolonged periods. High-impact aerobic exercise also has been implicated. Although plantar fasciitis is usually a straightforward diagnosis, occasional other pathologic processes of the foot can mimic this condition (Table 148-1). The pain of plantar fasciitis is most severe on first walking after having not borne weight and is made worse by prolonged standing or walking. Characteristic radiographic changes are lacking in plantar fasciitis, but radionuclide bone scanning may show increased uptake at the point of attachment of the plantar fascia to the medial calcaneal tuberosity. On physical examination the patient exhibits point tenderness over the plantar medial calcaneal tuberosity. The patient also may have tenderness along the plantar fascia as it moves anteriorly. Pain is increased by dorsiflexing the toes, which pulls the plantar fascia taut, and then palpating along the fascia from the heel to the forefoot. Plain radiographs are indicated for all patients with pain thought to be emanating from plantar fasciitis to rule out occult bony disease and tumor. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, prostate-specific antigen, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and ultrasound imaging of the foot is indicated if plantar fasciitis, occult mass, or tumor is suggested (Figures 148-1, 148-2, and 148-3). Radionuclide bone scanning may be useful to rule

out stress fractures not seen on plain radiographs. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The plantar fascia is made up of thick connective tissue that is tightly attached to the plantar skin. It attaches to the medial calcaneal tuberosity and then runs forward, dividing into five bands, one going to each toe (Figure 148-4).

A

TABLE 148-1

Diseases That May Mimic Plantar Fasciitis Plantar fascial tear Plantar calcaneal bursitis Bone contusion Medial calcaneal nerve entrapment Rheumatoid arthritis Reiter syndrome Ankylosing spondylitis Osteomyelitis Calcaneal stress fracture Tarsal tunnel syndrome

B Figure 148-1  Plantar fasciitis: magnetic resonance (MR) imaging. A, Normal plantar fascia. A sagittal intermediate-weighted (TR/TE, 2000/20) spin-echo MR image shows the normal central portion of the plantar fascia (arrows) and overlying subcutaneous fibrous septa. B, Plantar fasciitis. A sagittal T2-weighted (TR/TE, 2000/80) spin-echo MR image reveals subcutaneous edema (arrowhead) and focally thickened plantar fascia (arrow). A plantar calcaneal enthesophyte is also present. (From Berkowitz JF, Kier R, Rudicel S: Plantar fasciitis: MR imaging, Radiology 179:665, 1991.)

453

454        SECTION 8  •  Ankle and Foot

Figure 148-2  Normal plantar fascia. Longitudinal image of the normal plantar fascia (arrow); note uniform echogenicity. (From Blankenbaker DG, De Smet AA: The role of ultrasound in the evaluation of sports injuries of the lower extremities, Clin Sports Med 25:867–897, 2006.)

Figure 148-5  Site of needle insertion for plantar fasciitis injection.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position. The medial aspect of the heel is identified by palpation (Figure 148-5). Proper preparation with antiseptic solution of the skin overlying this point is then carried out. A syringe containing 2.0 mL of 0.25% preservativefree bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle. The needle is then carefully advanced through the previously identified point at a right angle to the skin, directly toward the center of the medial aspect of the calcaneus. The needle is advanced very slowly until the needle impinges on bone (see Figure 148-4). The needle is then withdrawn slightly back out of the periosteum, and the contents of the syringe are gently injected as the needle is slowly withdrawn. There should be slight resistance to injection, given the closed nature of the heel.

Side Effects and Complications Figure 148-3  Plantar fasciitis. Longitudinal image of the plantar fascia shows a thickened (arrow) hypoechoic plantar fascia (6 mm) in this patient with plantar fasciitis. (From Blankenbaker DG, De Smet AA: The role of ultrasound in the evaluation of sports injuries of the lower extremities, Clin Sports Med 25:867–897, 2006.)

Many patients report a transient increase in pain after the justmentioned injection technique. This side effect can be minimized by injecting gently and slowly. Infection, although rare, may occur if careful attention to sterile technique is not observed.

Clinical Pearls

Plantar fascia Figure 148-4  Proper needle placement for plantar fasciitis injection.

This injection technique is extremely effective in the treatment of plantar fasciitis. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of this injection technique are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle stretching exercises, should be introduced several days after the patient has undergone this injection technique. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Heel pads or molded orthotic devices also may be of value. Extracorporeal shock wave therapy has also been advocated as a treatment for recalcitrant plantar fasciitis. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

148  •  Plantar Fasciitis Injection        455 SUGGESTED READINGS Buccilli TA Jr, Hall HR, Solmen JD: Sterile abscess formation following a corticosteroid injection for the treatment of plantar fasciitis, J Foot Ankle Surg 44:466–468, 2005. Melamed E, Cohen I, Heim M, Robinson D: Soft tissue chondroma of the heel mimicking plantar fasciitis, Foot 16:175–177, 2006.

Puttaswamaiah R, Chandran P: Degenerative plantar fasciitis: a review of current concepts, Foot 17:3–9, 2007. Rajput B, Abboud RJ: Common ignorance, major problem: the role of footwear in plantar fasciitis, Foot 14:214–218, 2004. Toomey EP: Plantar heel pain, Foot Ankle Clin 14:229–245, 2009. Waldman SD: Plantar fasciitis. In Pain review, Philadelphia, 2009, Saunders, p 327.

Chapter 149 INJECTION TECHNIQUE FOR CALCANEAL SPURS Indications and Clinical Considerations Calcaneal spurs are a common cause of heel pain. When symptomatic, they usually are found in association with plantar fasciitis. Calcaneal spurs form most commonly at the insertion of the plantar fascia on the medial calcaneal tuberosity but can occur anywhere along the calcaneal tuberosity (Figures 149-1, 149-2, and 149-3). Calcaneal spurs usually are asymptomatic, but when they cause pain it is usually a result of an inflammation of the insertional fibers of the plantar fascia at the medial tuberosity. As with plantar fasciitis, calcaneal spurs can occur alone or can be part of a systemic inflammatory condition, such as rheumatoid arthritis, Reiter syndrome, or gout. In some patients, the cause seems to be entirely mechanical, and often such patients exhibit an abnormal gait with excessive heel strike. High-impact aerobic exercise also has been implicated in the evolution of calcaneal spurs. The pain of calcaneal spurs is most severe on first walking after not having borne weight and is made worse by prolonged standing or walking. Characteristic radiographic changes are lacking in both calcaneal spurs and plantar fasciitis, but radionuclide bone scanning may show increased uptake at the point of attachment of the plantar fascia to the medial calcaneal tuberosity in both painful conditions. On physical examination the patient exhibits point tenderness over the plantar medial calcaneal tuberosity. The patient also may have tenderness along the plantar fascia as it moves anteriorly. The

Figure 149-2  Closeup view of the heel spur taken from lateral weightbearing radiograph. Dashed arrow indicates a small “saddle injury.” Solid arrow indicates subtle fracture line. (From Smith S, Tinley P, Gilheany M, et  al: The inferior calcaneal spur—anatomical and histological considerations, Foot 17:25–31, 2007.)

pain of calcaneal spurs is increased by weight bearing and relieved by padding of the affected heel. Plain radiographs are indicated for all patients with pain thought to be emanating from calcaneal spurs to rule out occult bony disease and tumor. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, prostate-specific antigen, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the foot is indicated if calcaneal spurs, occult mass, or tumor is suggested. Radionuclide bone scanning may be useful to rule out stress fractures not seen on plain radiographs. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy

Plantar fascia

Bone spur

Figure 149-1  Proper needle position for injection of a calcaneal spur.

456

The calcaneus is the largest of the tarsal bones (see Figure 149-1). The main function of the calcaneus is to transfer the weight of the body to the ground, as well as to serve as a lever for the muscles of the calf. The plantar surface of the calcaneus is elevated posteriorly to form the calcaneal tuberosity. The calcaneal tuberosity is depressed centrally, with a lateral and medial process. It is at the medial process that symptomatic calcaneal spurs most commonly occur. The plantar fascia is made up of thick connective tissue that is tightly attached to the plantar skin. The plantar fascia attaches to the medial calcaneal tuberosity

149  •  Injection Technique for Calcaneal Spurs        457

Figure 149-4  Needle insertion site for injection technique for calcaneal spurs.

Adipose tissue Figure 149-3  Calcaneal enthesophyte: magnetic resonance (MR) imaging. A sagittal T1-weighted (TR/TE, 800/12) spin-echo MR image shows a large marrow-containing calcaneal enthesophyte (arrow) that is arising at the site of insertion of the Achilles tendon. (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

and then runs forward, dividing into five bands, one going to each toe.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position. The painful area of  the heel overlying the calcaneal spur is identified by palpation (Figure 149-4). Proper preparation with antiseptic solution of the skin overlying this point is then done. A syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle. The needle is then carefully advanced through the previously identified point at a right angle to the skin, directly toward the center of the painful area (see Figure 149-4). The needle is advanced very slowly until the needle impinges on bone. The needle is then withdrawn slightly back out of the periosteum and the contents of the syringe are gently injected as the needle is slowly withdrawn. There should be slight resistance to injection, given the closed nature of the heel.

Side Effects and Complications Many patients report a transient increase in pain after the justmentioned injection technique. This side effect can be minimized by injecting gently and slowly. Infection, although rare, may occur if careful attention to sterile technique is not observed.

Tissue of intrinsic musculature

Figure 149-5  The excised spur. Muscle and adipose tissue attached to the calcaneal spur are highlighted. (From Smith S, Tinley P, Gilheany M, et  al: The inferior calcaneal spur—anatomical and histological considerations, Foot 17:25–31, 2007.)

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to calcaneal spurs. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of this injection technique are related to needleinduced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle stretching exercises, should be introduced several days after the patient has undergone this injection technique. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Heel pads or molded orthotic devices may be of value. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique. Occasionally, surgical excision will be required for long-lasting relief in patients with calcaneal spurs whose pain does not respond to the previously mentioned treatment modalities (Figure 149-5).

458        SECTION 8  •  Ankle and Foot SUGGESTED READINGS Irving DB, Cook JL, Menz HB: Factors associated with chronic plantar heel pain: a systematic review, J Sci Med Sport 9:11–22, 2006. Onwuanyi ON: Calcaneal spurs and plantar heel pad pain, Foot 10:182–185, 2000.

Smith S, Tinley P, Gilheany M, et al: The inferior calcaneal spur—anatomical and histological considerations, Foot 17:25–31, 2007. Thomas JL, Christensen JC, Kravitz SR, et al: The diagnosis and treatment of heel pain: a clinical practice guideline—revision 2010, J Foot Ankle Surg 49(3 Suppl 1): S1–S19, 2010.

Chapter 150 SUPERFICIAL EXTENSOR TENDON INJECTION Indications and Clinical Considerations The superficial extensor tendons are susceptible to the development of tendinitis as they pass over the dorsum of the foot. Shoes, boots, or ice skates that are laced too tightly, as well as wrinkles in the tongue of a tightly laced shoe, have been implicated as the inciting factor of acute superficial extensor tendinitis (Figure 150-1). Osteophytes and ganglion cysts have also been reported to cause superficial extensor tendinitis (Figure 150-2). Although usually occurring as an isolated painful condition, altered gait as a result of pain when walking may cause the development of bursitis of the associated bursae of the tendons and ankle joint, creating additional pain and functional disability. Calcium deposition around the extensor tendons may occur if the inflammation continues, making subsequent treatment more difficult. The pain of superficial extensor tendinitis is constant and severe and is localized in the dorsum of the foot. Significant sleep disturbance often is reported. The patient may attempt to splint the inflamed superficial extensor tendons by adopting an antalgic gait to avoid using the affected tendons. Patients with superficial extensor tendinitis exhibit pain with resisted extension of the toes. The dorsum of the foot may feel hot and appear swollen, which may be erroneously attributed to a superficial thrombophlebitis or cellulitis. Creaking or grating may be palpated when passively flexing and extending the toes.

Plain radiographs are indicated for all patients with foot and ankle pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and ultrasound imaging of the foot and ankle are indicated if joint instability is suggested as well as to aid in confirmation of the diagnosis (Figures 150-3 and 150-4). Radionuclide bone scanning is useful to identify stress fractures of the foot and ankle not seen on plain radiographs. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy The superficial extensor tendons of the foot, including the extensor hallucis longus, the extensor digitorum longus, and the extensor digitorum brevis, are susceptible to the development of superficial extensor tendinitis (Figure 150-5). These tendons can be identified

Tight shoe laces squeezing extensor tendons

Figure 150-1  Shoes, boots, or ice skates that are laced too tightly, as well as wrinkles in the tongue of a tightly laced shoe, have been implicated as the inciting factor of acute superficial extensor tendinitis.

Figure 150-2  Dumbbell ganglion of the extensor digitorum longus tendon at the level of the ankle joint. (From Lui TH: Extensor tendoscopy of the ankle, Foot Ankle Surg 17:e1–e6, 2011.)

459

460        SECTION 8  •  Ankle and Foot

A

B

Figure 150-3  Sagittal (A) and transverse (B) views of the magnetic resonance image of the ankle suggest tenosynovitis of the extensor digitorum longus tendon. (From Lui TH: Extensor tendoscopy of the ankle, Foot Ankle Surg 17:e1–e6, 2011.)

T

MT Extensor hallucis longus tendon Dorsalis pedis a.

Figure 150-4  Longitudinal extended field-of-view image of extensor hallucis longus tendon (T) on first metatarsal bone (MT) shows a diffusely thickened, hypoechoic tendon (arrows). (From Lee KT, Choi YS, Lee YK, et al: Extensor hallucis longus tendon injury in taekwondo athletes, Phys Ther Sport 10:101–104, 2009.)

by dorsiflexing the toes. The dorsalis pedis artery can be palpated between the extensor hallucis longus and the extensor digitorum longus and can serve as a reference point when identifying the extensor tendons if swelling over the dorsum of the foot is present.

Inflamed tendons of the extensor digitorum longus m.

Inferior extensor retinaculum

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position with the affected foot in neutral position. The foot is gently dorsiflexed to facilitate identification of the margin of the tendons, to aid in avoiding injection directly into the tendons. The affected tendons are identified by gentle palpation and marked with a sterile marker. Proper preparation with antiseptic solution of the skin overlying these points is then carried out. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg

Figure 150-5  Proper needle position for superficial extensor tendon injection.

of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the previously marked points are palpated. The needle is then carefully advanced at this point alongside the tendons, through the skin and subcutaneous tissues, with care being taken not to enter the substance of the tendons (see Figure 150-5). The contents of

150  •  Superficial Extensor Tendon Injection        461

the syringe are then gently injected while slowly withdrawing the needle. There should be minimal resistance to injection. If there is significant resistance to injection, the needle tip is probably in the substance of the superficial extensor tendons and should be withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Trauma to the superficial extensor tendons from the injection itself remains an ever-present possibility. Tendons that are highly inflamed or previously damaged are subject to rupture if they are directly injected. The risk of this complication can be greatly decreased if the clinician uses gentle technique and stops injecting immediately if significant resistance to injection is encountered. Approximately 25% of patients note a transient increase in pain after this injection technique; the patient should be warned of this.

Clinical Pearls This injection technique is extremely effective in the treatment of pain secondary to the tendinitis of the superficial extensor tendons of the foot. Coexistent bursitis and arthritis also may contribute to foot and ankle pain and may require additional treatment with a more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for ankle pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Cho CH, Song KS, Min BW, et  al: Musculoskeletal injuries in break-dancers, Injury 40:1207–1211, 2009. Pontell D, Hallivis R, Dollard MD: Sports injuries in the pediatric and adolescent foot and ankle: common overuse and acute presentations, Clin Podiatr Med Surg 23:209–231, 2006. Sijbrandij ES, van Gils AP, de Lange EE: Overuse and sports-related injuries of the ankle and hind foot: MR imaging findings, Eur J Radiol 43:45–56, 2002. Wessely MA: MR imaging of the ankle and foot—a review of the normal imaging appearance with an illustration of common disorders, Clin Chiropr 10:101–111, 2007.

Chapter 151 POSTERIOR TIBIALIS TENDON INJECTION Indications and Clinical Considerations The posterior tibialis tendon is susceptible to the development of tendinitis as it curves around the medial malleolus. Acute eversion injury of the ankle is the most common cause of the development of posterior tibialis tendinitis, although running on soft or uneven surfaces also has been implicated. There may be coexistent bursitis of the associated bursae of the tendon and ankle joint, as well as arthritis, creating additional pain and functional disability. Posterior tarsal tunnel syndrome also may occur after acute eversion injuries or fractures to the ankle and may confuse the clinical picture. The pain of posterior tibialis tendinitis is constant and severe and is localized to the inner aspect of the ankle. Patients often report that it feels as though their shoes are rubbing the insides of their ankles raw, although on examination the skin appears normal. Significant sleep disturbance often is reported. The patient may attempt to splint the inflamed posterior tibialis tendon by adopting an antalgic gait to avoid using the affected tendon. Patients with posterior tibialis tendinitis exhibit pain with resisted inversion and passive eversion of the ankle. The inner aspect of the ankle may feel hot and appear swollen, which may be erroneously attributed to a superficial thrombophlebitis or cellulitis. Creaking or grating may be palpated when passively inverting and everting the ankle. The acutely inflamed tendon is susceptible to tear or complete rupture. Plain radiographs are indicated for all patients with foot and ankle pain. On the basis of patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and ultrasound imaging of the foot and ankle are indicated if joint instability is suggested as well as to confirm the diagnosis (Figures 151-1 and 151-2). Radionuclide bone scanning is useful to identify stress fractures of the foot and ankle not seen on plain radiographs. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the area of the medial malleolus is done. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 11⁄2-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, with the lower extremity slightly abducted, the lower margin of the medial malleolus is identified (Figure 151-4). At this point, the needle is carefully advanced at a 30-degree angle to the ankle through the skin and subcutaneous tissues to impinge on the lower margin of the medial malleolus (see Figure 151-3). The needle is then withdrawn slightly, and the contents of the syringe are gently injected. There is slight resistance to injection. If significant resistance is encountered, the needle is probably in the tendon and should be withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

T

Clinically Relevant Anatomy The posterior tibialis muscle has its origin from the posterior tibia and fibula. The tendon of the muscle runs behind the medial malleolus, beneath the flexor retinaculum, and into the sole of the foot and inserts on the navicular bone (Figure 151-3). The tendon is susceptible to the development of tendinitis as it curves around the medial malleolus. The posterior tibialis muscle plantarflexes the foot at the ankle and inverts the foot at the subtalar and transverse tarsal joints. 462

Figure 151-1  Tenosynovitis. T2* axial image of the ankle. The posterior tibial tendon (T) is mildly enlarged but of normal signal intensity. It is surrounded by high-signal intensity fluid, representing tenosynovitis. The thin line within the fluid (arrow) is the mesotendon, where the tendon invaginated the tendon sheath during fetal development. (From Helms CA, Major NM, Anderson MW, et  al: Musculoskeletal MRI, ed 2, Philadelphia, 2009, Saunders.)

151  •  Posterior Tibialis Tendon Injection        463

Clinical Pearls

Talus

N

Figure 151-2  Longitudinal ultrasound image of a complete rupture of the posterior tibial tendon. The proximal and distal tendon (white arrows) is visualized inferior to the level of the medial malleolus, superficial to the talus, and inserting on the navicular (N). The torn ends of the tendon (broken arrows) can be seen, with some anechoic fluid within the tendon sheath. (From Waldman SD, Campbell RSD: Posterior tibial tendon rupture. In Imaging of pain, Philadelphia, 2011, Saunders.)

Navicular 1st cuneiform

Tendon of tibialis posterior Synovial sheath (tibialis posterior) Flexor retinaculum

Inflamed tendon and sheath

Figure 151-3  Proper needle position for posterior tibialis tendon ­injection.

Figure 151-4  Needle insertion site for posterior tibialis tendon injection.

Side Effects and Complications The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Trauma to the posterior tibialis tendon from the injection itself remains an ever-present possibility. Tendons that are highly inflamed or previously damaged are subject to rupture if they are directly injected. The risk of this complication can be greatly decreased if the clinician uses gentle technique and stops injecting immediately if significant resistance to injection is encountered. Approximately 25% of patients report a transient increase in pain after this injection technique; the patient should be warned of this.

This injection technique is extremely effective in the treatment of pain secondary to the tendinitis of the posterior tibialis tendon of the foot. Coexistent bursitis and arthritis also may contribute to foot and ankle pain and may require additional treatment with a more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for ankle pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Bass A, Walsh HPJ, Sills JA: Tibialis posterior tendon dysfunction in childhood, Foot Ankle Surg 5:143–145, 1999. Bowring B, Chockalingam N: Conservative treatment of tibialis posterior tendon dysfunction—a review, Foot 20:18–26, 2010. Edwards MR, Jack C, Singh SK: Tibialis posterior dysfunction, Curr Orthop 22:185–192, 2008. Noon M, Hoch AZ, McNamara L, Schimke J: Injury patterns in female Irish dancers, PM R 2:1030–1034, 2010. Shibuya N, Ramanujam CL, Garcia GM: Association of tibialis posterior tendon pathology with other radiographic findings in the foot: a case-control study, J Foot Ankle Surg 47:546–553, 2008.

Chapter 152 INJECTION TECHNIQUE FOR BUNION PAIN SYNDROME Indications and Clinical Considerations The term bunion refers to a constellation of symptoms including soft tissue swelling over the first metatarsophalangeal joint associated with abnormal angulation of the joint that results in a prominent first metatarsal head with associated overlapping of the first and second toes (Figures 152-1 and 152-2). It is referred to as the hallux valgus deformity and occurs more often in women. The first metatarsophalangeal joint ultimately may sublux, and the overlapping of the first and second toes worsens. The development of an inflamed adventitious bursa may accompany bunion formation. The most common cause of bunion formation is the wearing of narrow-toed shoes. Wearing high-heeled shoes may exacerbate the problem. The majority of patients with bunion pain syndrome experience pain that is localized to the affected first metatarsophalangeal joint and the inability to get shoes to fit. Walking makes the pain worse; rest and heat provide some relief. The pain is constant, is characterized as aching, and may interfere with sleep.

Some patients report a grating or popping sensation with use of the joint, and crepitus may be present on physical examination. In addition to the just-mentioned pain, patients with bunions develop the characteristic hallux valgus deformity, which consists of a prominent first metatarsal head and improper angulation of the joint, with overlapping first and second toes. Plain radiographs are indicated in all patients with bunion pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the toe is indicated if bunion, joint instability, occult mass, or tumor is suggested.

Clinically Relevant Anatomy Each toe joint has its own capsule (see Figure 152-1). The articular surface of these joints is covered with hyaline cartilage that is susceptible to arthritis. The toe joint capsules are lined with a synovial membrane that attaches to the articular cartilage. The deep transverse ligaments connect the joints of the five toes and

Thickened and inflamed bunion

1st metatarsal

Figure 152-1  Proper needle position for injection technique for bunion pain syndrome.

464

152  •  Injection Technique for Bunion Pain Syndrome        465

the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of bunion injection of the toe is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients note a transient increase in pain after this injection technique.

Clinical Pearls

Figure 152-2  Hallux valgus. Abnormalities consist of soft tissue swelling, lateral displacement and rotation of the proximal phalanx and sesamoids (arrows), and bony hypertrophy (arrowhead) on the medial aspect of the metatarsal bone. (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

provide the majority of strength to the toe joints. The muscles of the toe joint and their attaching tendons are susceptible to trauma and to wear and tear from overuse and misuse.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the bunion is done. A sterile syringe containing 1.5 mL of 0.25% preservativefree bupivacaine and 40 mg of methylprednisolone is attached to a 5⁄8-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique the bunion is identified, and at this point the needle is carefully advanced against the first metatarsal head (see Figure 152-1). The needle is then withdrawn slightly out of the periosteum, and the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until

Pain from bunions can be quite debilitating, and the deformity may be cosmetically unacceptable for many patients. This injection technique is extremely effective in the treatment of pain secondary to bunions. Coexistent arthritis, bursitis, and tendinitis also may contribute to bunion pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. Patients with bunions should be advised to avoid tight, narrow-toed shoes. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for toe pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Albert A, Leemrijse T: The dorsal bunion: an overview, Foot Ankle Surg 11:65–68, 2005. Kenned JG, Collumbier JA: Bunions in dancers, Clin Sports Med 27:321–328, 2008. Mann R: Bunion deformity in elite athletes. In Porter DA, Schon LC, editors: Baxter’s the foot and ankle in sport, ed 2, Philadelphia, 2008, Mosby, pp 435–443. Mann RA, Horton GA: Management of the foot and ankle in rheumatoid arthritis, Rheum Dis Clin North Am 22:457–476, 1996. Motta-Valencia K: Dance-related injury, Phys Med Rehabil Clin N Am 17:697–723, 2006.

Chapter 153 INJECTION TECHNIQUE FOR BUNIONETTE PAIN SYNDROME Indications and Clinical Considerations The term bunionette refers to a constellation of symptoms including soft tissue swelling over the fifth metatarsophalangeal joint associated with abnormal angulation of the joint that results in a prominent fifth metatarsal head with associated medial angulation (Figures 153-1 and 153-2). Bunionette is also known as tailor’s bunion because tailors would sit with their legs crossed, putting pressure on the lateral portions of their feet. This deformity is analogous to the hallux valgus deformity and occurs more often in women. The development of an inflamed adventitious bursa may accompany bunionette formation and may contribute to the patient’s pain. A corn overlying the fifth metatarsal head also usually is present. The most common cause of bunionette formation is the wearing of tight, narrow-toed shoes. Wearing high-heeled shoes may exacerbate the problem. The majority of patients presenting with bunionette pain syndrome experience pain that is localized to the affected fifth metatarsophalangeal joint and the inability to get shoes to fit. Walking makes the pain worse; rest and heat provide some relief. The pain is constant, is characterized as aching, and may interfere with sleep. Some patients report a grating or popping sensation with use of the joint, and crepitus may be present on physical examination. In addition to the just-mentioned pain, patients with bunionettes develop a characteristic deformity consisting of a prominent fifth metatarsal head and improper medial angulation of the fifth metatarsal.

Plain radiographs are indicated for all patients with bunionette pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the toe is indicated if joint instability, occult mass, or tumor is suspected.

Clinically Relevant Anatomy Each toe joint has its own capsule (see Figure 153-1). The articular surface of these joints is covered with hyaline cartilage that is susceptible to arthritis. The toe joint capsules are lined with a synovial membrane that attaches to the articular cartilage. The deep transverse ligaments connect the joints of the five toes and provide the majority of strength to the toe joints. The muscles of the toe joint and their attaching tendons are susceptible to trauma and to wear and tear from overuse and misuse.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the bunionette is done. A sterile syringe containing 1.5 mL of 0.25% preservativefree bupivacaine and 40 mg of methylprednisolone is attached to a ⅝-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique the bunionette is identified, and at this point the

Inflamed bunionette

5th metatarsal

Figure 153-1  Proper needle position for injection technique for bunionette pain syndrome.

466

153  •  Injection Technique for Bunionette Pain Syndrome        467

A

B

Figure 153-2  A, Tailor’s bunion deformity may be assessed radiographically with a lateral splaying in the distal fifth metatarsal. B, Clinically, the patient generally has symptoms occurring laterally or plantarlaterally, often with an adduction of the fifth toe. (From Clinical Practice Guideline Forefoot Disorders Panel, Thomas JL, Blitch EL 4th, et al: Diagnosis and treatment of forefoot disorders. Section 4. Tailor’s bunion, J Foot Ankle Surg 48:257–263, 2009.)

needle is carefully advanced against the fifth metatarsal head (see Figure 153-1). The needle is then withdrawn slightly out of the periosteum, and the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of bunionette injection of the toe is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients report a transient increase in pain after this injection technique.

Clinical Pearls Pain from bunionettes can be quite debilitating, and the deformity may be cosmetically unacceptable for many patients. This injection technique is extremely effective in the treatment of pain secondary to bunionettes. Coexistent arthritis, bursitis, and tendinitis also may contribute to bunionette pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. Patients with bunionettes should be advised to avoid tight, narrow-toed shoes. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for toe pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

468        SECTION 8  •  Ankle and Foot SUGGESTED READINGS Ajis A, Koti M, Maffulli N: Tailor’s bunion: a review, J Foot Ankle Surg 44:236–245, 2005. Clinical Practice Guideline Forefoot Disorders Panel, Thomas JL, Blitch EL 4th, et al: Diagnosis and treatment of forefoot disorders. Section 2. Central metatarsalgia, J Foot Ankle Surg 48:239–250, 2009.

Clinical Practice Guideline Forefoot Disorders Panel, Thomas JL, Blitch EL 4th, et al: Diagnosis and treatment of forefoot disorders. Section 5. Trauma, J Foot Ankle Surg 48:264–272, 2009. Roukis TS: The tailor’s bunionette deformity: a field guide to surgical correction, Clin Podiatr Med Surg 22:223–245, 2005.

Chapter 154 INJECTION TECHNIQUE FOR MALLET TOE PAIN SYNDROME Indications and Clinical Considerations The term mallet toe refers to a constellation of symptoms including a painful flexion deformity of the distal interphalangeal joint (Figure 154-1). The second toe is affected most often. Mallet toe is usually a result of a jamming injury to the second toe, although, like bunion, bunionette, and hammer toe, the wearing of tight, narrow-toed shoes also has been implicated. As with bunion and bunionette, the mallet toe deformity occurs more often in women. The development of an inflamed adventitious bursa may accompany mallet toe formation and may contribute to the patient’s pain. A callus or ulcer overlying the tip of the affected toe also may be present (Figure 154-2). Wearing high-heeled shoes may exacerbate the problem. The majority of patients with mallet toe experience pain that is localized to the affected distal interphalangeal joint and the inability to get shoes to fit. Walking makes the pain worse; rest and heat provide some relief. The pain is constant and is characterized as aching. Some patients report a grating or popping sensation with use of the joint, and crepitus may be present on physical examination. In addition to the just-mentioned pain, patients with mallet toe develop a characteristic deformity consisting of a painful flexion deformity of the distal interphalangeal joint. Unlike with bunion and bunionette, alignment of the toes is relatively normal. Plain radiographs are indicated for all patients with mallet toe pain. On the basis of the patient’s clinical presentation, additional

testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the toe is indicated if joint instability, occult mass, or tumor is suggested.

Clinically Relevant Anatomy Each toe joint has its own capsule (see Figure 154-1). The articular surface of these joints is covered with hyaline cartilage that is susceptible to arthritis. The toe joint capsules are lined with a synovial membrane that attaches to the articular cartilage. The deep transverse ligaments connect the joints of the five toes and provide the majority of strength to the toe joints. The muscles of the toe joint and their attaching tendons are susceptible to trauma and to wear and tear from overuse and misuse.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the mallet toe is done. A sterile syringe containing 1.5 mL of 0.25% preservativefree bupivacaine and 40 mg of methylprednisolone is attached to a ⅝-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique the mallet toe is identified, and at this point the needle is carefully advanced against the affected distal phalanges (see Figure 154-1). The needle is then withdrawn slightly

Inflamed distal interphalangeal joint

Mallet toe

Figure 154-1  Proper needle position for injection technique for mallet toe pain syndrome.

469

470        SECTION 8  •  Ankle and Foot

Figure 154-2  Mallet toe deformity. (From Coughlin MJ, Grimes JS, Schenck RC Jr: Lesser-toe disorders. In Porter DA, Schon LC, editors: Baxter’s the foot and ankle in sport, ed 2, Philadelphia, 2008, Mosby.)

out of the periosteum, and the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of mallet toe injection of the toe is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients note a transient increase in pain after this injection technique.

Clinical Pearls Pain from mallet toes can be quite debilitating, and the deformity may be cosmetically unacceptable for many patients. This injection technique is extremely effective in the treatment of pain secondary to mallet toes. Coexistent arthritis, bursitis, and tendinitis also may contribute to mallet toe pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is a safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. Patients with mallet toes should be advised to avoid tight, narrow-toed shoes. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for toe pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Barakat MJ, Gargan MF: Deformities of the lesser toes—how should we describe them? Foot 16:16–18, 2006. Coughlin MJ, Grimes JS, Schenck RC Jr: Lesser-toe disorders. In Porter DA, Schon LC, editors: Baxter’s the foot and ankle in sport, ed 2, Philadelphia, 2008, Mosby, pp 383–409. Good J, Fiala K: Digital surgery: current trends and techniques, Clin Podiatr Med Surg 27:583–599, 2010. Menz HB: Disorders of the toes. In Foot problems in older people: assessment and management, Oxford, 2008, Churchill Livingstone, pp149–177. Mizel MS: Correction of hammertoe and mallet toe deformities, Oper Tech Orthop 2:188–194, 1992. Smith AG: Commentary on: “Athletes foot: when all else fails” by William C.R. Agunwa, [Foot Ankle Surg 12:209–210, 2006], Foot Ankle Surg 14:55, 2008.

Chapter 155 INJECTION TECHNIQUE FOR HAMMER TOE PAIN SYNDROME Indications and Clinical Considerations The term hammer toe refers to a constellation of symptoms including a painful flexion deformity of the proximal interphalangeal joint with the middle and distal phalanges flexed down onto the proximal phalange (Figure 155-1). The second toe is affected most often, and the condition usually is bilateral (Figure 155-2). Like hallux valgus deformity, hammer toe deformity is usually a result of wearing shoes that are too tight, although trauma also has been implicated. As with bunion and bunionette, the hammer toe deformity occurs more often in women. The development of an inflamed adventitious bursa may accompany hammer toe formation and may contribute to the patient’s pain. A callus overlying the plantar surface of these bony prominences also usually is present. Wearing high-heeled shoes may exacerbate the problem. The majority of patients with hammer toe report pain that is localized to the affected proximal interphalangeal joint and the inability to get shoes to fit. Walking makes the pain worse; rest and heat provide some relief. The pain is constant, is characterized as aching, and may interfere with sleep. Some patients report a grating or popping sensation with use of the joint, and crepitus

may be present on physical examination. In addition to the justmentioned pain, patients with hammer toe develop a characteristic deformity consisting of a painful flexion deformity of the proximal interphalangeal joint with the middle and distal phalanges flexed down onto the proximal phalange. Plain radiographs are indicated for all patients with hammer toe pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the toe is indicated if joint instability, occult mass, or tumor is suggested.

Clinically Relevant Anatomy Each toe joint has its own capsule (see Figure 155-1). The articular surface of these joints is covered with hyaline cartilage that is susceptible to arthritis. The toe joint capsules are lined with a synovial membrane that attaches to the articular cartilage. The deep transverse ligaments connect the joints of the five toes and provide the majority of strength to the toe joints. The muscles of the toe joint and their attaching tendons are susceptible to trauma and to wear and tear from overuse and misuse.

Inflamed proximal interphalangeal joint

Figure 155-1  Proper needle position for injection technique for hammer toe pain syndrome.

471

472        SECTION 8  •  Ankle and Foot

Clinical Pearls

Figure 155-2  Bowstringing of the extensor tendon to the fourth digit, with hammer toes and partial subluxation of the second and third metatarsophalangeal joints (MTPJs). Although clinically not symptomatic, extensor tenotomy at the MTPJ level helps to prevent any progression of this deformity postoperatively. (From Good J, Fiala K: Digital surgery: ­current trends and techniques, Clin Podiatr Med Surg 27:583–599, 2010.)

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the hammer toe is done. A sterile syringe containing 1.5 mL of 0.25% preservativefree bupivacaine and 40 mg of methylprednisolone is attached to a ⅝-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the hammer toe is identified, and at this point the needle is carefully advanced against the second metatarsal head (see Figure 155-1). The needle is then withdrawn slightly out of the periosteum, and the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications The major complication of hammer toe injection of the toe is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients note a transient increase in pain after this injection technique.

Pain from hammer toes can be quite debilitating, and the deformity may be cosmetically unacceptable for many patients. This injection technique is extremely effective in the treatment of pain secondary to hammer toes. Coexistent arthritis, bursitis, and tendinitis also may contribute to hammer toe pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. Patients with hammer toes should be advised to avoid tight, narrow-toed shoes. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for toe pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Barakat MJ, Gargan MF: Deformities of the lesser toes—how should we describe them? Foot 16:16–18, 2006. Clinical Practice Guideline Forefoot Disorders Panel, Thomas JL, Blitch EL 4th, et al: Diagnosis and treatment of forefoot disorders. Section 5. Trauma, J Foot Ankle Surg 48:264–272, 2009. Coughlin MJ, Grimes JS, Schenck RC Jr: Lesser-toe disorders. In Porter DA, Schon LC, editors: Baxter’s the foot and ankle in sport, ed 2, Philadelphia, 2008, Mosby, pp 383–409. Good J, Fiala K: Digital surgery: current trends and techniques, Clin Podiatr Med Surg 27:583–599, 2010. Menz HB: Disorders of the toes. In Foot problems in older people: assessment and management, Oxford, 2008, Churchill Livingstone, pp 149–177. Mizel MS: Correction of hammertoe and mallet toe deformities, Oper Tech Orthop 2:188–194, 1992. Smith AG: Commentary on: “Athletes foot: when all else fails” by William C.R. Agunwa [Foot Ankle Surg 12:209–210, 2006], Foot Ankle Surg 14:55, 2008.

Chapter 156 INJECTION TECHNIQUE FOR MORTON NEUROMA SYNDROME Indications and Clinical Considerations Morton neuroma is one of the most common pain syndromes that affects the forefoot. It is characterized by tenderness and burning pain in the plantar surface of the forefoot, with associated painful paresthesias into the affected two toes. This pain syndrome is thought to be caused by perineural fibrosis of the interdigital nerves. There is often coexistent intermetatarsal bursitis, as the pathogenesis of both pathologic conditions is similar. Although the nerves between the third and fourth toes most often are affected, the second and third toes and rarely the fourth and fifth toes can be affected (Figures 156-1 and 156-2). The patient often feels that he or she is walking with a stone in his or her shoe. The pain of Morton neuroma worsens with prolonged standing or walking for long distances and is exacerbated by improperly fitting or padded shoes. As with bunion, bunionette, and hammer toe deformities, Morton neuroma most often is associated with the wearing of tight, narrow-toed shoes. On physical examination, pain can be reproduced by firmly squeezing the two metatarsal heads together with one hand while placing firm pressure on the interdigital space with the other hand. In contradistinction to metatarsalgia, in which the tender area remains over the metatarsal heads, with Morton neuroma the

tender area is localized to only the plantar surface of the affected interspace, with paresthesias radiating into the two affected toes. The patient with Morton neuroma often exhibits an antalgic gait in an effort to reduce weight bearing during walking. Plain radiographs are indicated for all patients with Morton neuroma to rule out fractures and identify sesamoid bones that may have become inflamed. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and ultrasound imaging of the metatarsal bones is indicated if Morton neuroma, joint instability, occult mass, or tumor is suggested (see Figure 156-2; Figures 156-3 and 156-4). Radionuclide bone scanning may be useful in identifying stress fractures of the metatarsal bones or sesamoid bones that may be missed on plain radiographs of the foot.

Clinically Relevant Anatomy In a manner analogous to the digital nerves of the hand, the digital nerves of the foot travel through the intrametatarsal space to provide innervation to each toe (see Figure 156-1). The plantar digital nerves that are derived from the posterior tibial nerve provide sensory innervation to the major portion of the plantar surface. The dorsal aspect of the foot is innervated by terminal branches of the deep and superficial peroneal nerves. There may be considerable overlap in the sensory innervation of these nerves.

Technique The patient is placed in a supine position with a pillow under the knee to slightly flex the leg. A total of 3 mL of non–epinephrine-containing Dorsal digital nerves

A Morton’s neuroma Figure 156-1  Proper needle position for injection technique for Morton neuroma.

B

Figure 156-2  Morton neuroma: magnetic resonance (MR) imaging. Coronal T1-weighted (TR/TE, 450/14) (A) and T2-weighted (TR/TE, 4000/100) (B) spin-echo MR images reveal a mass (arrows) of low signal intensity between the third and fourth metatarsal bones. Such low signal intensity is characteristic of this lesion. (From Resnick D: Diagnosis of bone and joint imaging, ed 4, Philadelphia, 2003, Saunders.)

473

474        SECTION 8  •  Ankle and Foot

A

Figure 156-5  Needle insertion site for injection technique for Morton neuroma.

B Figure 156-3  A and B, Consecutive coronal T1-weighted magnetic resonance images of a low–signal intensity Morton neuroma (white arrows) arising between the third and fourth metatarsal heads. (From Waldman SD, Campbell RSD: Morton neuroma. In Imaging of pain, Philadelphia, 2011, Saunders.)

Figure 156-4  Morton neuroma of the third interspace.

local anesthetic and 40 mg of methylprednisolone is drawn up in a 12-mL sterile syringe. The affected interdigital space is identified, and the dorsal surface of the foot at this point is marked with a sterile marker (Figures 156-5, 156-6, and 156-7). After preparation of the skin with antiseptic solution, at a point proximal to the metatarsal head, a 25-gauge, 1½-inch needle is inserted between the two metatarsal bones to be blocked (see Figure 156-1). While slowly injecting, the clinician advances the needle from the dorsal surface of the foot toward the plantar surface. The plantar digital nerve is situated beneath the intermetarsal transverse ligament, and thus the needle has to be advanced almost to the plantar surface of the foot. The needle is removed,

Figure 156-6  Proper transducer placement for evaluation and injection for Morton neuroma.

and pressure is placed on the injection site to avoid hematoma formation.

Side Effects and Complications Because of the confined nature of the soft tissue surrounding the metatarsals and digits, the potential for mechanical compression of the blood supply after injection of solution must be considered. The clinician must avoid rapidly injecting large volumes of solution into these confined spaces or vascular insufficiency and

156  •  Injection Technique for Morton Neuroma Syndrome        475

Clinical Pearls

Figure 156-7  Ultrasound-guided needle placement for injection for Morton neuroma. Arrowhead indicates needle. Star indicates neuroma.

gangrene may occur. Furthermore, epinephrine-containing solutions must always be avoided because of ischemia and possible gangrene. This technique can be performed safely in the presence of anticoagulation by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable riskto-benefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 10-minute periods after the block also decreases the amount of postprocedure pain and bleeding the patient may experience.

Pain emanating from the forefoot is a common problem encountered in clinical practice. Morton neuroma must be distinguished from stress fractures of the metatarsal bones, metatarsalgia, sesamoiditis, and fractures of the sesamoid bones. Although the just-described injection technique provides palliation of the pain of Morton neuroma, the patient often also requires shoe orthoses and shoes with a wider toe box to help remove pressure from the affected interdigital nerves. Coexistent intermetatarsal bursitis and tendinitis also may contribute to metatarsal pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is a safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for Morton neuroma pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Adams WR 2nd: Morton’s neuroma, Clin Podiatr Med Surg 27:535–545, 2010. Betts RP, Bygrave CJ, Jones S, et al: Ultrasonic diagnosis of Morton’s neuroma: a guide to problems, pointers, pitfalls and prognosis, Foot 13:92–99, 2003. George VA, Khan AM, Hutchinson CE, Maxwell HA: Morton’s neuroma: the role of MR scanning in diagnostic assistance, Foot 15:14–16, 2005. Kay D, Bennett GL: Morton’s neuroma, Foot Ankle Clin 8:49–59, 2003.

Chapter 157 INTERMETATARSAL BURSA INJECTION Indications and Clinical Considerations Bursae are formed from synovial sacs whose purpose is to allow easy sliding of muscles and tendons across one another at areas of repeated movement. These synovial sacs are lined with a synovial membrane that is invested with a network of blood vessels that secrete synovial fluid. Inflammation of the bursa results in an increase in the production of synovial fluid with swelling of the bursal sac. With overuse or misuse, these bursae may become inflamed, enlarged, and on rare occasions infected. Although there is significant intrapatient variability as to the number, size, and location of bursae, anatomists have identified a number of clinically relevant bursae, including the intermetatarsal bursae. The intermetatarsal bursa lies between the metatarsal phalangeal joints in a position that is just dorsal to the deep transverse intermetatarsal ligament. The bursae extend approximately 1 cm beyond the distal border of the ligament in the web spaces between the second and third and third and fourth digits. This bursa may exist as a single bursal sac or in some patients as a multisegmented series of sacs that may be loculated. Most investigators think that intermetatarsal bursitis is a result of repeated microtrauma to the intermetarsal space and that intermetatarsal bursitis, intermetatarsal fibrosis, and the development of Morton’s neuroma all share similar pathogenesis and may all coexist in the same patient (Figures 157-1 and 157-2). Patients with intermetatarsal bursitis experience pain and tenderness over the affected intermetarsal spaces, with the pain made worse by wearing high heels or shoes which are too narrow. Obesity may also predispose to this condition. The pain

A

may radiate distally into the toes, especially if the adjacent interdigital nerve is involved. Often the patient is unable to stand on tiptoes or walk up stairs. Activity makes the pain worse. The pain is constant, is characterized as sharp, and may interfere with sleep. Coexistent neuritis, neuropathy, Morton neuroma, stress fractures, metatarsalgia, and synovitis may confuse the clinical picture. As the bursitis worsens, the affected intermetarsal bursae tend to expand, surrounding the adjacent interdigital nerves and making the patient’s clinical presentation indistinguishable from the pain of Morton neuroma. If the inflammation of the intermetatarsal bursae becomes chronic, calcification of the bursae and fibrosis of the surrounding interdigital space may occur. On physical examination, pain can be reproduced by squeezing the affected web space between the index finger and thumb. If the interdigital nerve is involved or if a Morton neuroma has developed, a positive Mulder sign can be elicited by firmly squeezing the two metatarsal heads together with one hand while placing firm pressure on the interdigital space with the other hand. The patient with intermetatarsal bursitis often exhibits an antalgic gait in an effort to reduce weight bearing during walking. Plain radiographs are indicated for all patients with intermetatarsal bursitis to rule out fractures and identify sesamoid bones that may have become inflamed. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and ultrasound imaging of the metatarsal bones is indicated if Morton neuroma, joint instability, occult mass, or tumor is suggested (Figures 157-3, 157-4, and 157-5). Radionuclide bone scanning

B

Figure 157-1  Intermetatarsal bursitis and fibrosis. A, Coronal image of intermetatarsal fibrosis (arrow). B, Coronal image of third web space intermetatarsal bursitis (arrowhead) and fibrosis (arrow). Fibrous tissue prolapses to the plantar side of the web space. (From Gregg JM, Schneider T, Marks P: MR imaging and ultrasound of metatarsalgia—the lesser metatarsals, Radiol Clin North Am 46:1061–1078, 2008.)

476

157  •  Intermetatarsal Bursa Injection        477

A

B

RT 3 is long non comp

2

RT 3 is long comp

3

C Figure 157-2  Morton neuroma with associated intermetatarsal bursitis. A and B, Longitudinal sonographic images and C, transverse image of the third intermetatarsal space demonstrate a hypoechoic mass measuring 1.0 cm × 0.5 cm (arrows). The patient’s typical pain was produced during this examination. A, Noncompression image and, B, compression image show a change in configuration of the mass representing coexisting bursitis. Overestimation of the size of a Morton neuroma can occur with bursitis. (From Blankenbaker DG, De Smet AA: The role of ultrasound in the evaluation of sports injuries of the lower extremities, Clin Sports Med 25:867–897, 2006.)

A

B

Figure 157-3  Magnetic resonance imaging of the foot, in the short axis plane, T2-weighted (A) and T1-weighted with contrast (A), demonstrating a region of high signal intensity about the inferior aspect of the intermetatarsal space between the second and third metatarsals. This region exhibits a moderate degree of enhancement with the addition of contrast (A) owing to the presence of intermetatarsal bursitis. (From Wessely MA: MR imaging of the ankle and foot—a review of the normal imaging appearance with an illustration of common disorders, Clin Chiropr 10:101–111, 2007.)

may be useful in identifying stress fractures of the metatarsal bones or sesamoid bones that may be missed on plain radiographs of the foot.

Clinically Relevant Anatomy In a manner analogous to the digital nerves of the hand, the digital nerves of the foot travel through the intrametatarsal space beneath the deep transverse intermetatarsal ligament to provide innervation to each toe (Figure 157-6). The plantar digital nerves that are derived from the posterior tibial nerve provide sensory innervation to the major portion of the plantar surface. The dorsal aspect of the foot is innervated by terminal branches of the deep and superficial peroneal nerves. There may be considerable overlap in the sensory innervation of these nerves.

Figure 157-4  Intermetatarsal bursitis. Anechoic compressible fluid collection (arrow) located within the second interspace measuring 1.5 cm × 0.5 cm. (From Blankenbaker DG, De Smet AA: The role of ultrasound in the evaluation of sports injuries of the lower extremities, Clin Sports Med 25:867–897, 2006.)

478        SECTION 8  •  Ankle and Foot

The intermetatarsal bursa lies between the metatarsal phalangeal joints in a position that is just dorsal to the interdigital nerves (see Figure 157-6). The bursae extend approximately 1 cm beyond the distal border of the ligament in the web spaces between the second and third and third and fourth digits.

Technique The patient is placed in a supine position with a pillow placed under the knee to slightly flex the leg. A total of 3 mL of non– epinephrine-containing local anesthetic and 40 mg of methylprednisolone is drawn up in a 12-mL sterile syringe. The affected interdigital space is identified, and the dorsal surface of the foot at this point is marked with a sterile marker. After preparation of the skin with antiseptic solution, at a point proximal to the metatarsal head, a 25-gauge, 1½-inch needle is inserted between the two metatarsal bones to be blocked (see Figure 157-6). While slowly injecting, the clinician advances the needle from the dorsal surface of the foot toward the plantar surface. The intermetatarsal bursa is situated just dorsal to the interdigital nerve, and thus the needle has to be advanced almost to the palmar surface of the foot. The needle is removed, and pressure is placed on the injection site to avoid hematoma formation.

A

Side Effects and Complications

B Figure 157-5  A, Coronal T2-weighted magnetic resonance (MR) image of a patient with rheumatoid arthritis demonstrating an inflammatory bursa in the intermetatarsal space (white arrow). There is associated synovitis in the third metatarsophalangeal joint. B, The corresponding T1-weighted MR image shows the synovial thickening (black arrows) and the associated bony erosions (white arrows). (From Waldman SD, Campbell RSD: Morton neuroma. In Imaging of pain, Philadelphia, 2011, Saunders.)

Because of the confined nature of the soft tissue surrounding the metatarsals and digits, the potential for mechanical compression of the blood supply after injection of solution must be considered. The clinician must avoid rapidly injecting large volumes of solution into these confined spaces or vascular insufficiency and gangrene may occur. Furthermore, epinephrine-containing solutions must always be avoided because of ischemia and possible gangrene. This technique can be performed safely in the presence of anticoagulation by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable

Phalange Deep intermetatarsal ligament Intermetatarsal bursa Metatarsal

Figure 157-6  Injection technique for treatment of intermetatarsal bursitis.

157  •  Intermetatarsal Bursa Injection        479

risk-to-benefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 10-minute periods after the block also decreases the amount of postprocedure pain and bleeding the patient may experience.

Clinical Pearls Pain emanating from the forefoot is a common problem encountered in clinical practice. Morton neuroma must be distinguished from stress fractures of the metatarsal bones, metatarsalgia, sesamoiditis, and fractures of the sesamoid bones. Although the just-described injection technique provides palliation of the pain of intermetatarsal bursitis, the patient often also requires shoe orthoses and shoes with a wider toe box to help remove pressure from the affected interdigital nerves. Coexistent synovitis, tendinitis, and Morton neuroma also may contribute to metatarsal pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is a safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle rangeof-motion exercises, should be introduced several days after the patient has undergone this injection technique for intermetatarsal bursitis pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Adams WR 2nd: Morton’s neuroma, Clin Podiatr Med Surg 27:535–545, 2010. Franson J, Baravarian B: Intermetatarsal compression neuritis, Clin Podiatr Med Surg 23:569–578, 2006. Gregg JM, Schneider T, Marks P: MR imaging and ultrasound of metatarsalgia— the lesser metatarsals, Radiol Clin North Am 46:1061–1078, 2008. Kay D, Bennett GL: Morton’s neuroma, Foot Ankle Clin 8:49–59, 2003. Lento PH, Strakowski JA: The use of ultrasound in guiding musculoskeletal interventional procedures, Phys Med Rehabil Clin N Am 21:559–583, 2010. Menz HB: Disorders of the forefoot. In Foot problems in older people: assessment and management, Oxford, 2008, Churchill Livingstone, pp 179–189. Wessely MA: MR imaging of the ankle and foot—a review of the normal imaging appearance with an illustration of common disorders, Clin Chiropr 10:101–111, 2007.

Chapter 158 SESAMOID BONE INJECTION OF THE FOOT

Indications and Clinical Considerations Sesamoiditis is one of the most common pain syndromes that affects the forefoot. It is characterized by tenderness and pain over the metatarsal heads. Although the first sesamoid bone of the first metatarsal head is affected most commonly, the sesamoid bones of the second and fifth metatarsal heads also are subject to the development of sesamoiditis (Figures 158-1 and 158-2). The patient often feels that he or she is walking with a stone in his or her shoe. The pain of sesamoiditis worsens with prolonged standing or walking for long distances and is exacerbated by improperly fitting or padded shoes. Sesamoiditis is most often associated with pushing-off injuries during football or repetitive microtrauma from running or dancing. On physical examination, pain can be reproduced by pressure on the sesamoid bone. In contradistinction to metatarsalgia, in which the tender area remains over the metatarsal heads, with sesamoiditis the tender area moves with the flexor tendon when the patient actively flexes his or her toe. The patient with sesamoiditis often exhibits an antalgic gait in an effort to reduce weight-bearing during walking. With acute trauma to the sesamoid, ecchymosis over the plantar surface of the foot may be present. Plain radiographs are indicated for all patients with sesamoiditis to rule out fractures and identify sesamoid bones that may have become inflamed. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the metatarsal bones is indicated if sesamoiditis, joint instability, occult mass, or tumor is suggested. Radionuclide bone scanning and ultrasound

imaging may be useful in identifying stress fractures of the metatarsal bones or sesamoid bones that may be missed on plain radiographs of the foot (Figures 158-3 and 158-4).

Clinically Relevant Anatomy The sesamoid bones are small, rounded structures that are embedded in the flexor tendons of the foot and usually are in close proximity to the joints. Sesamoid bones of the first metatarsal occur in almost all patients, with sesamoid bones being present in the flexor tendons of the second and fifth metatarsals in a significant number of patients (see Figures 158-1 and 158-2). These sesamoid bones decrease friction and pressure of the flexor tendon as it passes in proximity to a joint.

Technique The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the tender sesamoid bone is carried out. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a ⅝-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the affected sesamoid bones are identified. At this point, the needle is carefully advanced through the plantar surface of the foot until the needle tip rests against the sesamoid bone (Figure 158-5). The needle is withdrawn slightly out of the periosteum and substance of the tendon. After the needle is in the correct position next to the affected sesamoid bone and aspiration for blood is negative, the contents of the syringe are gently injected. There may be slight resistance to injection, given the closed nature of the space. If significant resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. The ice should not be left on for more than 10 minutes to avoid freezing injuries.

Side Effects and Complications Figure 158-1  Sesamoid bones are small, rounded structures embedded in the flexor tendons of the foot. They decrease friction and pressure of the flexor tendon as it passes in proximity to a joint.

480

The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients note a transient increase in pain after injection of sesamoid bones; the patient should be warned of this.

158  •  Sesamoid Bone Injection of the Foot        481

A

B

Figure 158-2  Sesamoiditis. This 33-year-old man had pain and swelling beneath the great toe, with no history of recent injury. A, Radiograph shows irregularity and flattening of the lateral sesamoid bone (arrow) beneath the first metatarsal head. B, Bone scan documents increased accumulation of the radionuclide (arrow) in this region, as well as laterally in the midfoot. (Courtesy Vint V, MD, San Diego, Calif; from Resnick D: Diagnosis of bone and joint imaging, ed 4, Philadelphia, 2003, Saunders.)

M L

Sesamoids Figure 158-3  Proper transducer position for evaluation of sesamoiditis.

Figure 158-4  Ultrasound imaging of the sesamoids. Lateral (L) and medial (M) sesamoids with traversing flexor hallucis longus (red arrowhead) seen.

482        SECTION 8  •  Ankle and Foot

1st metatarsal

Flexor hallucis longus m. (synovial sheath)

Sesamoid bone and tendon inflamed

Figure 158-5  Proper needle position for sesamoid bone injection of the foot.

Clinical Pearls Pain emanating from the forefoot is a common problem that is encountered in clinical practice. Sesamoiditis must be distinguished from stress fractures of the metatarsal bones, metatarsalgia, Morton neuroma, and fractures of the sesamoid bones. Although the just-described injection technique provides palliation of the pain of sesamoiditis, the patient often also requires shoe orthoses, including padded insoles, to help remove pressure from the affected sesamoid bones. Coexistent bursitis and tendinitis also may contribute to metatarsal pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle rangeof-motion exercises, should be introduced several days after the patient has undergone this injection technique for sesamoiditis pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Anwar R, Anjum SN, Nicholl JE: Sesamoids of the foot, Curr Orthop 19:40–48, 2005. Cohen BE: Hallux sesamoid disorders, Foot Ankle Clin 14:91–104, 2009. Kennedy JG, Hodgkins CW, Columbier JA, Hamilton WG: Foot and ankle injuries in dancers. In Porter DA, Schon LC, editors: Baxter’s the foot and ankle in sport, ed 2, Philadelphia, 2008, Mosby, pp 469–483. Sanders TG, Rathur SK: Imaging of painful conditions of the hallucal sesamoid complex and plantar capsular structures of the first metatarsophalangeal joint, Radiol Clin North Am 46:1079–1092, 2008. Umans HR: Imaging sports medicine injuries of the foot and toes, Clin Sports Med 25:763–780, 2006.

Chapter 159 METATARSAL LIGAMENT INJECTION Indications and Clinical Considerations Metatarsalgia is one of the most common pain syndromes that affect the forefoot. It is characterized by tenderness and pain over the metatarsal heads. The patient often feels that he or she is walking with a stone in his or her shoe. The pain of metatarsalgia worsens with prolonged standing or walking for long distances and is exacerbated by improperly fitting or padded shoes. Often the patient with metatarsalgia develops hard callus formations over the heads of the second and third metatarsals as he or she tries to shift the weight off the head of the first metatarsal to relieve the pain. This callus formation increases the pressure on the metatarsal heads and further exacerbates the patient’s pain and disability (Figure 159-1). On physical examination, pain can be reproduced by pressure on the metatarsal heads. Callus formation often is present and can be distinguished from plantar warts by the lack of thrombosed blood vessels, which appear as small, dark spots through the substance of the wart when the surface is trimmed. The patient with metatarsalgia often exhibits an antalgic gait in an effort to reduce weight-bearing during the static stance phase of walking. Ligamentous laxity and flattening of the transverse arch also may be present, giving the foot a splayed-out appearance. Plain radiographs are indicated for all patients with metatarsalgia to rule out fractures and identify sesamoid bones that may have become inflamed. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the metatarsal bones is indicated if joint instability, fracture, plantar plate abnormality, occult mass, or tumor is suspected (Figure 159-2). Radionuclide bone scanning may be useful in identifying stress fractures that may be missed on plain radiographs of the foot.

Hard callus formation on 1st metatarsal Callus on skin surface Figure 159-1  Hard callus formation over the heads of the second and third metatarsals resulted when the patient attempted to shift weight off the head of the first metatarsal to relieve pain.

via the transverse metatarsal ligaments (see Figure 159-1). The transverse metatarsal ligament is subject to strain, especially in long-distance runners, that may coexist with metatarsalgia. Sesamoid bones beneath the heads of the metatarsal bones are present in some individuals and are subject to the development of inflammation. The muscles of the metatarsal joints and their attaching tendons are susceptible to trauma and to wear and tear from overuse and misuse.

Clinically Relevant Anatomy

Technique

The strength of the foot is based on the arch-type configuration of the bones and ligaments. This configuration gives the foot an amazing amount of strength and resiliency during the stresses of weight-bearing and walking. Anything that alters the structural integrity of the arches or changes the way that stresses are applied to these arches usually results in pain and disability. The first metatarsal bone is similar to the first metacarpal in that it is not connected to the second metatarsal by any ligaments. The bases of the other four metatarsal bones are attached to one another by the dorsal, plantar, and interosseous ligaments. The heads of the metatarsal bones are connected

The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the most tender metatarsal heads is done. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 5⁄8-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the affected metatarsal heads are identified. At this point just next to the tender head, the needle is carefully advanced through the dorsal surface of the foot to a depth of 1⁄2 inch (Figure 159-3). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected 483

484        SECTION 8  •  Ankle and Foot

A

B

C

D

Figure 159-2  A, Proton density and, B, T2 fat-suppressed images of stress fracture of the second metatarsal (arrows). C, Sonogram of the dorsal aspect of a second metatarsal shaft shows a repairing stress fracture. D, Longitudinal sonogram of the dorsum of the fourth metatarsal base shows a stress fracture with hypervascularity. (From Gregg JM, Schneider T, Marks P: MR imaging and ultrasound of metatarsalgia—the lesser metatarsals, Radiol Clin North Am 46:1061–1078, 2008.)

laterally. After the needle is positioned next to the affected metatarsal head and aspiration for blood is negative, the contents of the syringe are gently injected. There may be slight resistance to injection, given the closed nature of the space. If significant resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. The ice should not be left on for more than 10 minutes to avoid freezing injuries.

Side Effects and Complications

Figure 159-3  Proper needle position for metatarsal ligament injection.

The major complication of this injection technique is infection, which should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients report a transient increase in pain after injection of the metatarsal heads; the patient should be warned of this.

159  •  Metatarsal Ligament Injection        485

Clinical Pearls Pain emanating from the forefoot is a common problem that is encountered in clinical practice. Metatarsalgia must be distinguished from stress fractures of the metatarsal bones, Morton neuroma, and sesamoiditis. Although the just-described injection technique provides palliation of the pain of metatarsalgia, the patient often also requires shoe orthoses, including metatarsal bars and padded insoles, to help remove pressure from the metatarsal heads. Coexistent bursitis and tendinitis also may contribute to metatarsal pain and may require additional treatment with more localized injection of anesthetic and depot corticosteroid preparation. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for metatarsalgia pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

SUGGESTED READINGS Armagan OE, Shereff MJ: Injuries to the toes and metatarsals, Orthop Clin North Am 32:1–10, 2001. Bardelli M, Turelli L, Scoccianti G: Definition and classification of metatarsalgia, Foot Ankle Surg 9:79–85, 2003. Gregg JM, Schneider T, Marks P: MR imaging and ultrasound of metatarsalgia— the lesser metatarsals, Radiol Clin North Am 46:1061–1078, 2008. Umans HR: Imaging sports medicine injuries of the foot and toes, Clin Sports Med 25:763–780, 2006. Waldman SD: Metatarsalgia. In Pain review, Philadelphia, 2009, Saunders, p 326.