Office orthopedics for primary care: diagnosis issue orthopedics, general practice

Office Orthopedics for Primary Care: Diagnosis Copyright © 2006 Elsevier Inc. All rights reserved Author(s): Bruce Carl...

Author: Bruce Carl Anderson | MD

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Office Orthopedics for Primary Care: Diagnosis Copyright © 2006 Elsevier Inc. All rights reserved Author(s): Bruce Carl Anderson, MD ISBN: 978-1-4160-2207-7

Table of Contents Copyright ,

Dedication ,

Preface ,

Page iv

Page v

Pages vii-viii

Acknowledgments ,

Chapter 1 - ,Neck

Chapter 2 - Shoulder ,

Page ix

Pages 1-18

Pages 19-49

Chapter 3 - Upper Back Pages 50-65 Chapter 4 - Elbow ,

Pages 66-81

Chapter 5 - Wrist ,

Pages 82-100

Chapter 6 - Thumb

Pages 101-117

Chapter 7 - Hand

Pages 118-136

Chapter 8 - Chest

Pages 137-148

Chapter 9 - Lumbosacral , Spine

Pages 149-171

Chapter 10 ,- Hip

Pages 172-194

Chapter 11 - ,Knee

Pages 195-221

Chapter 12 - Ankle

Pages 222-249

Chapter 13 - Foot

Pages 250-276

References ,

Pages 277-293

Index ,

Pages 295-301

1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103–2899

OFFICE ORTHOPEDICS FOR PRIMARY CARE: DIAGNOSIS Copyright © 2006 by Elsevier Inc.

ISBN 987-1-4160-2207-7 ISBN 1-4160-2207-4

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. Permissions may be sought directly from Elsevier’s Health Sciences Rights Department in Philadelphia, PA, USA: phone: (+1) 215 239 3804, fax: (+1) 215 239 3805, e-mail: [email protected]. You may also complete your request on-line via the Elsevier homepages (http://www.elsevier.com), by selecting ‘Customer Support’ and then ‘Obtaining Permissions’.

Notice Knowledge and best practice in this field are constantly changing. As new research and experience broaden our knowledge, changes in practice, treatment and drug therapy may become necessary or appropriate. 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 the practitioners, relying on their own experience and knowledge of the 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 Editors assumes any liability for any injury and/or damage to persons or property arising out or related to any use of the material contained in this book. Library of Congress Cataloging-in-Publication Data Anderson, Bruce Carl. Office orthopedics for primary care: diagnosis / Bruce Carl Anderson.—1st ed. p. ; cm. ISBN 1-4160-2207-4 1. Orthopedics—Diagnosis. 2. Primary care (Medicine) I. Title. [DNLM: 1. Musculoskeletal diseases--diagnosis. 2. Family Practice—methods. 3. Fractures—diagnosis. WE 141 A545oa 2006] RD732.A52 2006 616.7′075—dc22 2005049901

Acquisitions Editor: Rolla Couchman Developmental Editor: Dylan Parker Design Direction: Karen O’Keefe Owens

Printed in the United States of America Last digit is the print number:

9

8

7

6

5

4

3

2

1

To the pioneering work of E C Kendall, biochemist and researcher at the Mayo Clinic of Rochester, Minnesota, and winner of the 1950 Nobel Prize in Biochemistry for the synthesis of cortisone from bile acids.

PREFACE

This is the first edition of Office Orthopedics for Primary Care: Diagnosis, the companion book to Office Orthopedics for Primary Care: Treatment. This two-volume set provides the clinician with the concise information to diagnose, treat, and determine the need for surgical referral on the most common conditions affecting the musculoskeletal system. Emphasis has been placed on those conditions that are most likely to present to the primary care physician, including the most common joint and soft tissue diagnoses as well as the noncatastrophic, uncomplicated fractures that frequently present to the primary care office. The book has been formatted in a unique manner, depending on the needs of the clinician and the time allotted for evaluation of the musculoskeletal complaints. For the clinician interested only in screening the patient, each section begins with the most effective maneuvers that allow a rapid and effective triage of the patient to radiographic or laboratory testing or general treatment guidelines. By contrast, for the clinician interested in the complete management of the patient’s musculoskeletal complaints, the screening maneuvers of each section are followed by the de-

TABLE 1

tailed examinations that allows for a definitive diagnosis and subsequent specific treatment guidelines. Traditionally local musculoskeletal diagnosis has relied upon combining the patient’s description of pain, the demonstration of loss of function, and the results of physical examination with the changes either on plain radiographs or specialized imaging (MRI, CT, bone scanning) to distinguish involvement of the joint from involvement of the soft tissues or bone. In general, this is an effective approach when evaluating patients with degenerative arthritis or advanced tendon and ligament injuries where characteristic changes on plain radiographs or special imaging are unequivocal. However, the combination of history, examination, and imaging fails to accurately diagnosis up to one-third of joint and soft tissue conditions (see the table below) because of the nonspecific nature of the complains, the overlap of physical signs, and the lack of diagnostic changes on radiographic testing. Previous publications have failed to address this inadequacy by failing to emphasize the importance of diagnostic local anesthetic block and synovial and bursal fluid aspiration

SUMMARY: DIAGNOSTIC TESTING FOR 183 LOCAL MUSCULOSKELETAL CONDITIONS

JOINT

X-RAY

CT/MRI

BONE SCAN

EXAM

LOCAL ANESTHESIA

ASPIRATION

SURGERY

Neck

3

Shoulder

6

4

—

2

—

3

1

—

—

3

3

3

—

Upper Back Elbow

3

3

3

1

—

3

1

—

—

—

2

3

6

Wrist

4

—

1

1

2

2

5

Thumb

—

2

—

—

2

3

—

—

Hand

3

—

1

8

1

—

1

Chest

1

—

1

1

4

2

—

Back

4

5

1

2

2

—

— —

Hip

5

1

3

2

4

2

Knee

5

2

—

1

5

5

2

Ankle

7

—

2

8

2

1

—

TOTALS

47

21

10

40

37

25

3

26%

11%

5%

22%

20%

14%

2%

This table summarizes the diagnostic testing used to confirm the most common musculoskeletal conditions described in this book, the conditions that present to the primary physician in an outpatient setting. When more than one method of confirming the diagnosis is possible, the most reliable method was chosen. Local anesthesia refers to confirming the diagnosis by the accurate placement of lidocain or bipivacaine within the joint, bursa, or along the tissue plane adjacent to the tendon, ligament, or nerve. Aspiration uniformly refers to the removal of joint or bursal fluid for laboratory analysis.

VIII PREFACE

and analysis. For example, anserine bursitis frequently complicates medial compartment osteoarthritis of the knee. Both conditions are characterized by impaired gait, medial knee pain, and medial knee tenderness. Neither plain radiographs or special imaging effectively distinguishes one from another. However, pain relief and improved ambulation after placing local anesthetic either intra-articularly or intrabursal is the only means of effectively distinguishing the role of each. Similarly, local anesthetic block is often necessary to distinguish trochanteric bursitis from L4-5 radiculopathy, rotator cuff tendonitis from the referred pain of C4-5 radiculopathy, de Quervain’s tenosynovitis from carpometacarpal osteoarthritis, and so forth.

Table 1 also emphasizes the relative infrequent need to refer to the orthopedic surgical service for specific diagnostic testing. Only 2 percent of diagnoses require surgical intervention to complete the diagnostic workup; namely those conditions that require arthroscopy for confirmation (meniscal tear, ACL tear, and osteochondritis dissecans). Hopefully, this new edition will provide the practitioner with the means to manage the wide range of conditions that commonly affect the musculoskeletal system. With a more accurate means of diagnosis available to the clinician more effective and timely provided treatment will result in better patient outcomes. Bruce Carl Anderson, MD

CHEST IX

ACKNOWLEDGMENTS

This book represents the outgrowth of 27 years of postresidency education and clinical experience with over 50,000 local procedures that would not have been possible without the support and encouragement from many sources. I wish to thank all the members of the departments of medicine, family practice, physiatry, neurosurgery, and surgical orthopedics at the Sunnyside Medical Center, especially Dr. Ian MacMillan of the department of medicine for his support and assistance in developing the medical orthopedic department and the surgeons of the department of orthopedics, Dr. Steven Ebner, Dr. Edward Stark, and Dr. Stephen Groman, for their stimulating feedback. I also wish to thank my extremely capable physician assistant, Linda Onheiber, for her steady contributions to the medical orthopedic department, and all the medical residents of the graduating classes of 2003 and 2004 at Oregon Health Sciences University,

Eastmoreland Osteopathic Hospital, and Emmanual-Legacy and Providence teaching hospitals, for their constant encouragement, contributions, and critical appraisal of the content of the book. I also wish to thank the medical directors of the various Portland, Oregon, teaching hospitals for their support; namely, Dr. Nancy Loeb at Sisters of Providence St. Vincents hospital, Dr. Steven Jones at Emmanual-Legacy hospital, and Dr. Don Girard at the Oregon Health Sciences University. Lastly, I wish to thank Dr. David Gilbert, director emeritus of the Sisters of Providence Glisan hospital—my internal medicine residency director—for his stimulation to excellence, his encouragement to examine ever deeper into clinical problems, and his support and inspiration in my return to clinical research. Bruce Carl Anderson, MD

CHAPTER 1: NECK DIFFERENTIAL DIAGNOSIS Diagnoses Cervical strain (most common diagnosis) Stress Whiplash and related injuries Dorsokyphotic posture Fibromyalgia Osteoarthritis of the neck Reactive cervical strain Radiculopathy Vertebral body fracture Spinal cord injury or tumor

Cervical radiculopathy Foraminal encroachment Herniated nucleus pulposus Epidural process

Confirmations

Socioeconomic or psychological issues Motor vehicle accident or head and neck trauma Typical in older adults or in patients with depression Confirmation by exam: multiple trigger points, normal lab X-ray: cervical series (lateral view) Underlying spinal column, nerves, or cord are threatened Neurologic testing Bone scan or magnetic resonance imaging (MRI) MRI

X-ray: cervical spine x-rays (oblique views); electromyography (EMG) MRI MRI

Thoracic outlet syndrome Cervical rib

Nerve conduction velocity (NCV) and EMG X-ray: cervical series (anteroposterior view)

Greater occipital neuralgia

Local anesthetic block

Temporomandibular joint syndrome

Exam or local anesthetic block

Referred pain Coronary arteries Takayasu’s arteritis Thoracic aortic aneurysm Thyroid disease

Electrocardiogram, creatine phosphokinase, angiogram Erythrocyte sedimentation rate (ESR), angiogram Chest x-ray Thyroid-stimulating hormone, thyroxine, ESR, thyroid scan

1

2

OFFICE ORTHOPEDICS FOR PRIMARY CARE: DIAGNOSIS

INTRODUCTION Cervical strain and osteoarthritis are the two dominant conditions affecting the neck. Cervical strain caused by tension, stress, dorsokyphotic posture, or whiplash is a nearly universal condition early in life. In later life cervical strain is still common but rivaled by osteoarthritis affecting the facet and paravertebral joints, also a nearly universal condition. In the sixth and seventh decades these two processes combine to cause the progressive stiffness and forward position of the head typical of older adults. The diagnosis of an uncomplicated cervical strain caused by tension, stress, poor posture, or mild whiplash is not difficult. Signs and symptoms are limited to the supporting muscles of the neck, the trapezius and paraspinal muscles. The muscles are tender, the range of motion is reduced by muscular spasm, and there is a conspicuous absence of bony tenderness and radicular signs in the upper extremities. This is in stark contrast to reactive cervical strain, which is the direct result of an underlying threat to the spinal column. Bony disorders, spinal nerve compression, or the rare conditions affecting the spinal cord directly cause severe trapezial and paraspinal muscle spasm. The challenge to the primary care provider is to distinguish simple cervical strain from the severe muscular spasm that is a reaction to a serious underlying neurologic process. Cervical arthritis is the second most common neck condition, increasing in prevalence and degree with advancing age. Symptoms can range from simple stiffness and loss of range of motion to radiculopathy from foraminal encroachment and spinal cord compression from spinal stenosis. Osteoarthritic wear occurs at the paravertebral facet joints and between the lateral margins of the vertebral bodies, the Luschka joints. Both cervical strain and cervical osteoarthritis are involved in the development of cervical radiculopathy, or compression of the spinal roots or nerves. Ninety percent of spinal nerve compression results from neuroforaminal narrowing by osteophyte overgrowth, foraminal encroachment disease. With this threat to the spinal nerve, reactive cervical strain develops, compounding the nerve irritation. Only 10% of cervical radiculopathy is caused by a herniated nucleus pulposus (HNP), whereas 90% of radiculopathy in the lumbar spine is caused by HNP. Spinal stenosis is the most dramatic form of cervical radiculopathy. Upper extremity neurologic impairment can also result from brachial plexus nerve compression or inflammation. Loss of upper extremity sensation or motor function can be caused by thoracic outlet (cervical rib, hypertrophy of the scalenus anticus or pectoralis minor, or Pancoast’s tumor) or brachial plexopathy. Greater occipital neuritis is a unique problem arising from the neck. It is also related directly to cervical strain. The greater occipital nerve must traverse the upper cervical muscles to enter the subcutaneous tissue on its way to innervating the scalp. Persistent muscle spasm is the principal irritation of this nerve. Pain referred to the neck is uncommon. Intrinsic shoulder conditions can incite reactive cervical strain. Diseases of the heart, major vessels of the chest, or thyroid (coronary artery disease, Takayasu’s arteritis, thoracic aortic aneurysm, thyroid disease) will cause pain in the jaw or, rarely, neck pain.

SYMPTOMS Patients complain of neck pain, muscle spasm, stiffness or loss of range of motion, or upper extremity sensorimotor symptoms reflective of radiculopathy. Most patients describe a combination of symptoms. Patients with moderate to severe cervical strain may experience reversible sensory radiculopathy. Conversely, patients with radiculopathy often describe symptoms reflective of the accompanying reactive cervical strain. Neck pain is the most common presenting symptom. It is most often described at the base of the cervical spine or along the upper border of the trapezius muscle. Reactive cervical strain—irritation and spasm of the muscles of the neck or upper back—is the principal cause of this pain. Although cervical strain is most commonly caused by the ordinary emotional and physical stresses of everyday life, poor posture, or poor sleeping habits, it is also the body’s final common pathway for any process that threatens the integrity of the spinal column, spinal nerves, or spinal cord; thus, cervical strain often accompanies whiplash, arthritis of the cervical spine, or radiculopathy. Patients also complain of neck stiffness. Varying degrees of neck stiffness often accompany cervical strain. Moderate to severe neck stiffness is typical of cervical degenerative arthritis; facet and paravertebral joint osteophyte formation and articular cartilage thinning correlate directly with the symptoms of stiffness and the measurable loss of neck flexibility, most notably in rotation and extension. Numbness, tingling, and pain down the arm are the common symptoms of cervical radiculopathy (“I think I have a ‘pinched nerve’”). Cervical radiculopathy is caused by spinal nerve compression due to cervical arthritis in 90% of cases. As the paravertebral and facet joints gradually wear, bony osteophytes gradually enlarge, compromising the exit neuroforamina (foraminal encroachment). If the overall surface area is reduced by 50%, the spinal nerve is at risk. It takes only a small degree of cervical strain to incite (pain and paresthesias) or impair (hypesthesias or motor weakness) the spinal nerve. Cervical radiculopathy is caused by a herniated disk in 10% of cases (younger, more acute, and greater degrees of motor involvement on average), and less than 0.1% is caused by spinal cord encasement by large osteophytic bars (spinal stenosis). Some patients complain of a unilateral headache with numbness or tingling of the scalp. This unique headache pattern is the result of intense or chronic paraspinal muscle pain at the base of the neck. Greater occipital neuralgia results from the irritation of this sensory nerve as it penetrates these paraspinal muscles at the base of the skull. Lastly, involvement of the vertebral bodies by fracture, tumor, or infection typically causes severe localized neck pain and dramatic cervical muscle spasm. EXAMINATION The examination of the neck begins with the observation of the general movement of the head, neck, and eyes. The posture and general movements of the neck, whether rigid and guarded or loose and free, should be consistent during the interview phase as well as during the actual examination. Lack of consistency can be a clue to malingering in the case of whiplash or cervical radiculopathy that is under litigation. Measurement of the range of motion of the neck, especially neck rotation and lateral bending, is

NECK

used to assess the general flexibility of the neck; loss of range of motion in these directions is the best indication of abnormal neck function. For example, when neck movement is impaired, endpoint stiffness is demonstrated, and mild to moderate pain is reproduced, cervical osteoarthritis is the likely diagnosis. Next, the supporting muscles of the neck—the trapezius and paraspinal muscles—are examined for local tenderness, spasm, and their effect on neck flexibility. Finally, the Spurling maneuver, the manual vertical traction maneuver, and a detailed upper extremity neuroBOX 1-1

SCREENING EXAMINATION OF THE NECK 1. Observe the movement of the head, neck, and eyes. 2. Perform and estimate neck rotation and lateral bending. 3. Palpate the paraspinal and upper trapezial muscles for tenderness and spasm. 4. Estimate the degree of reactive cervical muscle. 5. Determine the degree of cervical radiculopathy.

logic exam are performed to determine the presence of cervical radiculopathy. Patients with normal range of motion, normal upper extremity neurologic function, and nontender neck muscles should undergo medical examination of the heart, upper chest, and thyroid to evaluate for possible referred pain to the head and neck area. By contrast, the approach to the patient who has sustained serious head or neck trauma differs dramatically from the typical outpatient evaluation. If the patient has sustained significant head or neck trauma, the integrity of the vertebral column is assessed by testing sensation and movement in all four extremities, palpating the spinous process for alignment and local tenderness, and testing range of motion of the neck. If the traumatized patient has focal abnormalities, aggressive radiographic testing for occult vertebral fracture or subluxation or paravertebral hemorrhage must be performed. ONE-MINUTE SCREENING EXAM: MANEUVERS ASSESSING OVERALL NECK FUNCTION AND DIFFERENTIAL DIAGNOSIS

POSTURE AND GENERAL MOVEMENT SUMMARY: The patient’s posture and general manner of movement of the head, neck, and eyes can be an important clue to underlying neck disorders. MANEUVER: The consistency of the patient’s posture and the general movement of the head, neck, and eyes are noted with and without examiner distraction. INTERPRETATION: Patients with depression and older adults present with a dorsokyphotic posture (forward head position, partially flexed neck, slumped shoulders). Sluggish movement or general stiffness is characteristic of osteoarthritis, cervical strain, and fibromyalgia. Torticollis reflects acute muscular spasm, often from an HNP. Extreme guarding or apprehension is indicative of neck trauma or large disk herniation.

FIGURE 1–1. Posture and general movement of the head and neck.

3

4


PASSIVE ROTATION OF THE NECK SUMMARY: Range of motion testing in rotation is the single most important clue to an underlying neck condition. The paravertebral and facet joints of the vertebral bodies, the odontoid process, and the supporting muscles allow the neck to rotate an average of 90 degrees to either side. MANEUVER: The patient is asked to relax. The examiner places one hand on the shoulder and one hand on the chin. The neck is passively rotated to the affected side, noting the degrees of rotation and endpoint stiffness. INTERPRETATION: Rotation less than 90 degrees is abnormal. X-rays and neurologic testing of the upper extremities are necessary to determine the underlying cause of the loss of flexibility (osteoarthritis, injury to the vertebral column, cervical radiculopathy, and severe cervical strain).

FIGURE 1–2. Measurement of passive rotation of the neck.

PALPATION SUMMARY: The superior portion of the trapezius muscle is the most commonly irritated neck muscle. The upper portion of the trapezius muscle originates from the seven spinous processes and the distal aspect of the acromial process. MANEUVER: The superior trapezial muscle is palpated for local tenderness and spasm approximately halfway between the acromion and spinous processes of the neck. INTERPRETATION: Local muscular tenderness can result from trauma (a direct blow), but the majority of cases are caused by reactive cervical muscular strain (cervical muscular strain, fibromyalgia, whiplash, stress, and poor posture).

FIGURE 1–3. Palpation of the upper trapezial muscle.

NECK

SPURLING MANEUVER SUMMARY: The Spurling maneuver attempts to reproduce the patient’s symptoms by further compression of the nerve as it passes by the vertebral disk or through the neuroforamina. Each spinal nerve must pass by the lateral portion of the cervical disk and through its corresponding bony canal, the neuroforamina. Nerve compression is caused most often by bony osteophytes reducing the neuroforamina opening by 50% or by a herniated nucleus pulposus. MANEUVER: Several positions of the head are used to provoke nerve irritation, starting with the head in neutral position. The examiner taps or presses down on the top of the head. If this is unsuccessful, the maneuver is repeated with the head rotated, hyperextended, or bent to the side. INTERPRETATION: This is the only maneuver that is used to reproduce the patient’s radicular pain. It is very specific but lacks sensitivity.

FIGURE 1–4. Spurling maneuver to reproduce the lancinating pain of cervical radiculopathy.

FOCAL TENDERNESS SUMMARY: The greater occipital nerve is a pure sensory nerve providing sensation to half the scalp. The greater occipital nerve passes through the upper cervical muscles to enter the subcutaneous tissue of the back of the head. Chronic cervical muscle strain causes compression and irritation of the nerve, leading to a unilateral headache with accompanying paresthesias. MANEUVER: Local tenderness is present 1 inch below the base of the skull and 1 inch lateral to the midline. Tapping over the nerve (Tinel sign) may induce paresthesias. INTERPRETATION: Greater occipital neuritis should be considered when patients complain of a unilateral headache that is accompanied by sensory abnormalities of the scalp.

FIGURE 1–5. Focal tenderness of the greater occipital nerve.

5

6


PALPATION OF THE TMJ SUMMARY: Local tenderness can be elicited either in front of the tragus of the ear or in the external canal. In order to distinguish the pain arising from the TMJ from disorders of the ear, the patient is asked to open and close the jaw. MANEUVER: Local tenderness is palpated either just anterior to the tragus or with the examiner’s finger placed in the outer aspect of the external canal. Firm pressure is applied, and the patient is asked to open and close the jaw. INTERPRETATION: The pain and local tenderness of otitis externa and otitis media should not be aggravated by jaw movement. Sialadenitis of the parotid gland is characterized by diffuse tenderness and swelling in a triangular area anterior and inferiorly to the ear.

FIGURE 1–6. Palpation of the TMJ comparing one side with the other.

ONE-MINUTE SCREENING EXAM: MANAGEMENT OPTIONS TRIAGE TO X-RAY For patients with a history of trauma, those who are at risk of bony injury, those in whom radiculopathy is suspected, or those who have had chronic cervical strain: • Order a cross-table lateral with the patient left in the neck collar if there has been a severe injury to the head or neck or the patient has sustained a concussion (fracture or dislocation). Complement this with an MRI if there has been severe neck trauma and the exam demonstrates either focal neurologic deficits or focal bony tenderness (occult vertebral fracture). • Order routine cervical spine series for patients with more than 25% loss of range of motion (osteoarthritis, severe cervical strain, early radiculopathy). • Order routine cervical spine series for all patients with radiculopathy (90% of cervical radiculopathy is caused by narrowing of the exit foramina [foraminal encroachment disease]). • Order a lateral view of the neck to assess the alignment of the cervical spine in patients with chronic cervical strain, fibromyalgia, and persistent whiplash symptoms. TRIAGE TO THE LAB For the rare patient with fever, acute pain, exquisite tenderness, and signs of upper extremity neurologic abnormalities (i.e., acute onset of radicu-

lopathy), order a complete blood cell count, blood cultures, and ESR (possible osteomyelitis or epidural abscess). CONSIDER A BONE SCAN For patients with localized vertebral body tenderness, a recent history of injury, and equivocal cervical spine x-rays (acute vertebral compression fractures). CONSIDER AN MRI For patients with acute cervical radiculopathy and rapidly developing neurodeficit (epidural abscess), for patients with cervical radiculopathy with normal cervical series x-rays (disk herniation), and for patients with cervical radiculopathy and a known history of metastatic disease (epidural metastasis). RECOMMEND EMPIRICAL TREATMENT For patients with mild to moderate neck pain, neck stiffness but preserved rotation to 90 degrees (able to look down the shoulder), tightness and spasm of the paraspinal or trapezial muscles, but no radicular complaints (radicular pain, paresthesias, or loss of upper extremity strength). • • • • • •

Avoid stressful situations. Attend to improved posture. Apply ice to the muscle groups in spasm. Perform daily passive stretching exercises in rotation. Recommend a muscle relaxer over 7 consecutive nights. Use a soft Philadelphia collar during the daytime (optional).

NECK

DETAILED EXAMINATION: SPECIFIC NECK DIAGNOSES Perform a detailed examination of the neck if the patient has persistent or chronic symptoms and one or more of the following signs are present: moderate to severe neck pain and stiffness, focal spinous process tenderness, 40% to 50% loss of range of motion, intense paraspinal or trapezial muscle spasm (torticollis), or radiculopathy with motor involvement.

REACTIVE CERVICAL STRAIN The primary function of the paracervical and trapezial muscles is to support and provide movement for the head and neck. However, their secondary function is to react to any threat to the integrity of the cervical column, spinal cord, or spinal nerves; reactive cervical strain is the neck’s protective mechanism whenever the structures of the neck are in jeopardy.

PALPATION SUMMARY: The superior portion of the trapezial muscle is the most common neck muscle involved in acute and chronic cervical strain. MANEUVER: Palpate the superior trapezial muscle along its entire superior border, with emphasis halfway between the acromion and spinous processes of the neck. Assess the degree of local tenderness, focal muscle spasm (“knots”), and its overall tone (soft, moderate tension, hard). ADDITIONAL SIGNS: Palpate the paraspinal muscles 1 to 2 inches from the midline for tenderness. Palpate the levator scapula and rhomboid muscles for tenderness. Palpate the subscapular bursa at the superomedial angle of the scapula for tenderness.

FIGURE 1–7. Palpation of the upper trapezial muscle in reactive cervical strain.

INTERPRETATION: Cervical muscular strain resulting from poor posture, stress, or unaccustomed use can be graded by the number of muscle groups affected. Fibromyalgia, whiplash, and reactive cervical strain secondary to an underlying process affecting the spinal column involve multiple muscle groups.

LOCAL INTRAMUSCULAR ANESTHETIC BLOCK SUMMARY: A tentative diagnosis of an uncomplicated case of cervical strain is based on the palpation of the supporting muscles of the neck. In order to distinguish simple cervical strain from subscapular bursitis or radicular pain referred from the lower cervical roots, local intramuscular anesthetic block is performed. NEEDLE: DEPTH:

11⁄2 inch, 22 gauge. 1 to 11⁄2 inches.

VOLUME:

FIGURE 1–8. Local intramuscular anesthetic block of the trapezius to confirm of cervical strain.

7

3 to 4 cc anesthetic, 1 mL D80, or both.

NOTE: Lightly advance the needle until the firm, rubbery tension of the outer fascia of the trapezius muscle is encountered. Place 1 cc anesthetic at the interface of the subcutaneous fat and the fascia before entering the body of the muscle. If corticosteroid is used, avoid the triamcinolone derivatives. Kenalog and Aristospan are much more likely to cause atrophy of the muscle or the overlying subcutaneous tissue than methylprednisolone.

8


Age takes its toll on the facet and the paravertebral joints of the neck, leading to a variety of conditions, including the characteristic dorsokyphotic posture,

OSTEOARTHRITIS OF THE NECK

simple stiffness and pain from a gradual loss of rotation, osteoarthritis, and cervical radiculopathy caused by foraminal encroachment or spinal stenosis.

PASSIVE ROTATION OF THE NECK SUMMARY: The paravertebral and facet joints of the vertebral bodies, the odontoid process, and the supporting muscles allow the neck to rotate an average of 90 degrees. Progressive osteoarthritic wear of the paravertebral joints of Luschka and facet joints causes a gradual loss of rotation. MANEUVER: The patient is asked to relax. The examiner places one hand on the shoulder and one hand on the chin. The neck is passively rotated to the affected side, and the examiner notes the degrees of rotation and endpoint stiffness.

FIGURE 1–9. Passive rotation of the neck to estimate the degree of osteoarthritis of the facet joints and the paravertebral joints of Luschka.

ADDITIONAL SIGNS: The patient may describe grinding or crunching with the back and forth rotation of the neck. With progressive impairment, lateral bending and neck extension may be impaired. Signs of radiculopathy may be present with foraminal encroachment. Manual vertical traction typically affords symptom relief. Vertebral artery flow may be impaired with severe arthritic changes, causing the patient to feel dizzy with passive extension of the neck. INTERPRETATION: Rotation less than 90 degrees is abnormal. X-rays and neurologic testing of the upper extremities are necessary to determine the exact cause of the loss of flexibility. Osteoarthritis and severe cervical strain are the two most common causes of loss of rotation.

LATERAL VIEW OF THE NECK CASE: This is the lateral neck x-ray of a 77-year-old former pilot whose sole complaint was neck stiffness. He denied experiencing pain down the arm, numbness or tingling of the fingers, or loss of strength in the upper extremities. Neck rotation measured 60 to 65 degrees (30% loss) with endpoint stiffness. The Spurling maneuver was negative, and the neurologic examination of the upper extremities was normal. DIAGNOSIS:

Uncomplicated cervical osteoarthritis.

DISCUSSION: The lateral view demonstrates an exaggerated cervical lordosis, corresponding to the forward position of the head seen on exam. The disk spaces are uniformly narrowed and mildly irregular. The facet joints are narrowed, hypertrophic, and sclerotic. The posterior aspects of the vertebral bodies (the joints of Luschka) are hypertrophic and sclerotic. The bony osteophytes that form here are responsible for the foraminal encroachment of cervical radiculopathy. FIGURE 1–10. Lateral view of the neck to confirm the degree of osteoarthritis.

NECK

The diagnosis of cervical radiculopathy is most often suggested by the patient’s description of a lancinating pain that crosses at least two major joints and the description of abnormal sensations (paresthesias or hypesthe-

CERVICAL RADICULOPATHY

sias) involving selected digits. The neurologic examination is used to define the degree of nerve impairment. Radiographic studies (plain radiographs or MRI) are used to define the exact anatomic cause.

SPURLING MANEUVER SUMMARY: The Spurling maneuver attempts to reproduce the patient’s symptoms by further compressing the spinal nerve as it passes by the vertebral disk or through the neuroforamina. MANEUVER: Several positions of the head are used to provoke nerve irritation, starting with the head in neutral position. The examiner taps or presses down on the top of the head. If this is unsuccessful, the maneuver is repeated with the head rotated, hyperextended, or bent to the side. ADDITIONAL SIGNS: Manual cervical traction—the opposite of the Spurling maneuver—may reduce the patient’s pain and sensory complaints. The nerve root may be tender when one firmly palpates between the transverse and spinous processes. Sensation, reflex asymmetry, muscle tone, endurance, strength, or bulk may be impaired on neurologic examination of the upper extremities. Signs of reactive cervical strain are nearly always present. FIGURE 1–11. Spurling maneuver to reproduce the lancinating pain of cervical radiculopathy.

INTERPRETATION: This is the only maneuver that is used to reproduce the patient’s radicular pain. It is very specific but rarely positive.

MANUAL CERVICAL TRACTION SUMMARY: If the Spurling maneuver is negative or equivocal, the diagnosis of cervical radiculopathy is enhanced if manually applied vertical traction alleviates the patient’s radicular pain. In addition, this maneuver can be used to assess the patient’s tolerance of therapeutic traction. MANEUVER: The head is grasped at the midjaw and occiput. The patient is asked to relax the neck muscles. Gentle vertical traction is performed to assess the effect on the patient’s neck pain, stiffness, and radicular pain. ADDITIONAL SIGNS:

FIGURE 1–12. Manual cervical traction to assist in the diagnosis of cervical radiculopathy and to assess the patient’s tolerance to therapeutic home traction.

See Figure 1–11.

INTERPRETATION: The response to traction is most important in determining the role of physical therapy based on traction. A positive response is nonspecific. This maneuver will reduce the pain and stiffness of osteoarthritis and cervical strain and the radicular pain of cervical radiculopathy caused by foraminal encroachment.

9

10


OBLIQUE VIEWS OF THE NECK CASE: This radiograph is from a 54-year-old patient who presented with a gradual onset of numbness and tingling of the middle fingers of the right hand. Symptoms waxed and waned over a period of several months. The triceps reflex and muscular strength were preserved. DIAGNOSIS: Cervical radiculopathy caused by C6–C7 foraminal encroachment. DISCUSSION: The spinal nerve is approximately one third the size of the foraminal opening. When bony osteophytes from the joints of Luschka (arrow) reduce the overall size of the foramina by 50%, nerve compression and irritation are possible. This potential nerve irritation is further aggravated by the accompanying reactive cervical strain (muscle spasm generated by the threat to the nerve) or simple strain induced by posture or unaccustomed use. Most cases of reversible radiculopathy probably result from the accompanying cervical strain.

FIGURE 1–13. Oblique views of the neck to confirm foraminal encroachment (osteophytes reducing the overall diameter of the neuroforamina).

MRI CASE: This 43-year-old woman complained of an acute onset of arm pain, numbness of the fingers, and stiffness of the neck. The pain radiated from the base of the neck, through the shoulder, down the arm, and into the hand. She experienced constant numbness and tingling of the first three digits. Her examination showed paraspinal tenderness between the spinous and transverse processes of the lower neck, endpoint stiffness with guarding when the neck was rotated to the affected side, weakness of elbow flexion, and a diminished bicipital reflex. DIAGNOSIS: Cervical radiculopathy caused by a C5–C6 disk herniation.

FIGURE 1–14. MRI to evaluate the cervical spine for occult fracture, radiculopathy caused by herniated disk, epidural abscess or tumor, or spinal cord disorder.

DISCUSSION: Cervical radiculopathy caused by disk herniation should be suspected in the younger patient with acute symptoms, patients with sensorimotor findings on neurologic examination, or patients with cervical radiculopathy who have a poor response to empirical treatment with cervical traction.

NECK

GREATER OCCIPITAL NEURALGIA Irritation or inflammation of the greater occipital nerve is characterized by intense local tenderness at the base of the skull, a unilateral headache, and ipsilateral skin sensitivity or paresthesias over the scalp.

PALPATION SUMMARY: Headaches are a very common accompaniment of most conditions affecting the cervical spine, especially cervical strain, osteoarthritis, and radiculopathy. Greater occipital neuralgia presents with a unique headache pattern characterized by pain and paresthesias limited to one side of the head. MANEUVER: The greater occipital nerve is palpated 1 inch off the midline and approximately 1⁄2 to 1 inch below the base of the skull. ADDITIONAL SIGNS: Tapping over the nerve (Tinel sign) may induce the scalp paresthesias. Sensory testing over the scalp may be impaired. Signs of cervical strain invariably are present with local muscular tenderness, particularly in the paraspinal muscles. INTERPRETATION: The unilateral headache of greater occipital neuritis must be distinguished from migraine and the headache that accompanies foraminal encroachment involvement of the upper three cervical roots.

FIGURE 1–15. Palpation of the greater occipital nerve.

LOCAL ANESTHETIC BLOCK SUMMARY: Local anesthetic placed just above and just below the level of the cervical fascia is used to confirm the direct involvement of the greater occipital nerve and distinguish this unique headache from migraine and the headache that accompanies upper cervical root foraminal encroachment. Enter 1 inch lateral to the midline and 1 inch caudal to the superior nuchal line of the skull (the base of the skull). NEEDLE:

11⁄2 inch, 22 gauge.

DEPTH: 1⁄2 to 3⁄4 inch down to the fascia and then an additional 1⁄4 inch into the muscle. VOLUME:

FIGURE 1–16. Local anesthetic block to confirm greater occipital neuralgia.

3 to 4 cc anesthetic, 1 mL D80, or both.

NOTE: Lightly advance the needle to feel the outer fascia, then enter the body of the muscle. Avoid triamcinolone because it increases the risk of muscle or subcutaneous atrophy.

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TEMPOROMANDIBULAR JOINT SYNDROME The tem-

poromandibular joint ( TMJ) can be injured by trauma to the jaw or face, inflammed in the patient with hematoid arthritis, or irritated by the chronic effects of stress (high muscle tone, clenching

of teeth, or grinding of the jaw at night). Patients complain of jaw pain, ear pain, or difficulties with mastication. The diagnosis is always suggested when the patient describes pain located at or near the ear that is aggravated by opening and closing the jaw.

PALPATION SUMMARY: The TMJ is located directly anterior to the tragus of the ear and is palpated either at this point or from the entrance to the external ear canal. MANEUVER: The patient is asked to open and close the jaw as the examiner palpates the area just anterior to the tragus and then palpates the joint from within the entrance of the external ear canal. Tenderness and clicking are noted. ADDITIONAL SIGNS: The maximum mouth opening (measurement between the upper and lower teeth) may be restricted. The pterygoid muscles along the posterior aspect of the alveolar ridge may be tender and in spasm. Evidence of abnormal teeth wear (grinding) may be present. Anxiety or other signs of situational stress may be present.

FIGURE 1–17. Palpation of the TMJ.

INTERPRETATION: Acute TMJ syndrome typically results from trauma or unusual degrees of chewing. Chronic TMJ syndrome is a manifestation of anxiety and situational stress.

LOCAL ANESTHETIC BLOCK SUMMARY: Ear or facial pain aggravated by chewing or opening and closing the jaw does not pose a diagnostic challenge. Occasionally, in patients with subtle pain, concurrent ear disorders, or other causes of lateral facial pain, anesthesia is needed to confirm involvement of the joint. With the jaw fully opened, enter the joint 1⁄4 to 3⁄8 inch directly anterior to the tragus in the depression formed over the joint; angle perpendicular to the skin. NEEDLE: DEPTH:

⁄8 inch, 25 gauge.

5

VOLUME:

FIGURE 1–18. Local anesthetic block to distinguish TMJ involvement from primary involvement of the ear or parotid gland.

⁄4 to 1⁄2 inch into the joint.

1

⁄2 to 1 cc anesthetic, 1⁄2 mL K40, or both.

1

NOTE: Identify and mark the course of the temporal artery and then lightly advance the needle into joint. If arterial blood enters the syringe, exit the skin, hold pressure for 5 minutes, and reenter either slightly anterior or posterior to the artery.

NECK

THORACIC OUTLET SYNDROME The diagnosis of thoracic

outlet syndrome should be considered in patients presenting with paresthesias in the upper extremity that are not arising from a pathologic process in the neck (normal neck examination and radiographs) or from a peripheral compression neuropathy. Cervical

ribs, hypertrophy of the scalenus anticus or pectoralis minor muscles, Pancoast’s tumor of the chest, or brachial plexopathy cause paresthesias and variable degrees of muscular impairment of the upper extremity. In most cases the lower trunk of the brachial plexus is most vulnerable (ulnar or C8 radicular patterns).

ADSON MANEUVER SUMMARY: After leaving the cervical spine, the roots form the brachial plexus, which traverses the base of the neck, through the muscles of the anterior cervical triangles, under the clavicle, and through the axilla. Compression or traction of the plexus anywhere along this path can lead to neurologic impairment of the upper extremity. MANEUVER: The head and neck are positioned in extension and ipsilateral rotation. The patient is asked to shrug the shoulder and take a deep breath. The examiner palpates the radial pulse and notes any decrease when performing the maneuver. In addition, the patient is asked whether this position reproduces the pain down the arm. ADDITIONAL SIGNS: A full neurologic examination of the upper extremity is necessary. Symptoms can also be brought out by an exaggerated military posture (shoulders held back). INTERPRETATION: A decrease in the radial pulse and a reproduction of the C8 radiculopathy suggests thoracic outlet syndrome that must be confirmed by NCV EMG. FIGURE 1–19. Adson maneuver to screen for thoracic outlet syndrome.

EMG OF THE UPPER EXTREMITY SUMMARY: Patients presenting with ulnar or C8 root distribution paresthesias, motor loss, or both but an absence of signs suggesting a neck or peripheral compression neuropathy should undergo EMG to evaluate for thoracic outlet.

FIGURE 1–20. EMG of the upper extremity to confirm thoracic outlet syndrome.

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1–1

DETAILED EXAMINATION SUMMARY

EXAMINATION MANEUVERS

DIAGNOSIS

CONFIRMATION PROCEDURES

Trapezial or paracervical muscle local tenderness and spasm

1. Cervical strain

Pain with passive neck rotation, local anesthetic placed in the affected muscle (optional)

2. Osteoarthritis

Cervical series x-ray (the lateral view can be used for screening)

Torticollis

Cervical series x-ray (the posteroanterior view can be used for screening)

Cervical radiculopathy

Cervical series, MRI, or EMG

Greater occipital neuralgia

Local anesthetic placed over the outer fascia of the paraspinal muscle

TMJ syndrome

Local anesthetic placed in the synovial cavity

Suspect vertebral fracture or dislocation

Cross-table lateral x-ray, cervical series x-ray, or MRI

Thoracic outlet syndrome

Confirmation with EMG

Painful or limited rotation and lateral bending Trapezial or paracervical muscle stiffness Fixed loss of rotation and lateral bending with stiff endpoints Loss of conjugate movement of the eyes and head Dorsokyphotic posture Head and neck locked in the lateral bent position Local tenderness and spasm in the trapezium muscle ⫹ Spurling sign Improvement with manual traction Paraspinal or spinous process tenderness Abnormal UE neurologic exam; abnormal threshold of reflexes; weakness of grip, biceps, or triceps Tenderness at the base of the skull 1 inch from the midline Paraspinal or trapezial muscle tenderness and spasm Abnormal sensory testing over the scalp TMJ local tenderness Restricted opening of the mouth Clicking or crepitation Pterygoid muscle spasm Signs of anxiety or stress Signs of abnormal teeth wear Rigidity of the trapezial or paraspinal muscles Apprehension with any attempts at passive movement Spinous process tenderness Positive Adson maneuver Symptoms reproduced by exaggerated military posture Abnormalities on neurologic testing of the upper extremity

NECK

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FOR THE TRAUMA PATIENT SUMMARY The guidelines for the emergency room evaluation of the head and neck trauma patient must be strictly adhered to. A step-by-step method to ensure the integrity of the spinal column, spinal nerves, and spinal cord must be followed until the provider is assured that the patient’s neurological status is not in jeopardy. BOX 1-2

EVALUATION OF HEAD AND NECK TRAUMA PATIENTS Examination of the trauma patient focuses on the integrity of the vertebral column. 1. Evaluate the patient’s mental status. 2. Assess the patient’s airway and cardiovascular stability. 3. Check sensation of the four extremities. 4. Check motor strength in the hands and feet. 5. Obtain a cross-table lateral x-ray of the cervical and further radiographic studies if there is any sign of fracture or potential dislocation. 6. If cervical alignment is preserved and there is no obvious fracture, palpate the spinous process for tenderness and alignment (normal cervical lordosis).

7. Obtain an MRI of the cervical spine if focal tenderness is present at any spinous process. 8. Assess range of motion of the neck and palpate the paraspinal muscles. 9. If the patient has extreme muscle guarding, remains apprehensive with any movement of the neck, and has focal tenderness, obtain a neurosurgical consultation to observe for possible occult fracture of the cervical spine, despite “normal” radiographic studies.

SENSORY TESTING SUMMARY: Sensory testing is used to determine the integrity of the sensory nerve pathways from spinal cord via the spinal nerves to the peripheral skeleton. A normal sensory exam indicates an intact nervous system. MANEUVER: Light touch or pain sensation is tested in all four extremities (at the fingertips and the tips of the toes). INTERPRETATION: Loss of sensation in all four extremities indicates midneck spinal cord injury. Loss of sensation in the legs indicates lower neck spinal cord injury.

FIGURE 1–21. Sensory testing to assess the integrity of the cervical spine.

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MOTOR TESTING OBJECTIVE: To determine the integrity of the motor nerve pathways from the spinal cord via the spinal nerves to the peripheral motor nerves. MANEUVER: Grip strength and the strength of dorsiflexion and plantarflexion are tested on the right and left sides of the body. ANATOMY: Normal strength testing in all four extremities indicates an intact nervous system. INTERPRETATION: Loss of strength in all four extremities indicates midneck spinal cord injury. Loss of strength in the legs indicates lower neck spinal cord injury.

FIGURE 1–22. Motor testing to assess the integrity of the cervical spine.

PALPATION OBJECTIVE: Palpation of each of the seven spinous processes is used to determine the degree of tenderness of the vertebral bodies and assess their alignment. The seven spinous processes form a smooth lordotic curve (similar to the lower back). The seventh spinous process at the base is the most prominent. MANEUVER: Each spinous process must be palpated, lightly at first, to assess alignment, followed by a greater degree of pressure to assess local tenderness. INTERPRETATION: Any degree of focal spinous process tenderness is significant. Involvement of the underlying bone is assumed until proven otherwise. The differential diagnosis includes vertebral column injury, bony tumor, spondylolisthesis, and osteomyelitis. FIGURE 1–23. Palpation of the spinous processes of the vertebral bodies.

NECK

CROSS-TABLE LATERAL X-RAY CASE: This 19-year-old hockey player was hard checked into the rink wall. He suffered a mild concussion and severe neck pain. He was transferred to the emergency room in a hard collar. His mental status, cardiovascular exam, airway, and screening neurologic exam were normal. This cross-table lateral x-ray was obtained while the patient was still in the hard cervical collar. DIAGNOSIS: Severe reactive cervical strain with straightening of the cervical lordotic curve. No evidence of fracture or dislocation. DISCUSSION: Further examination of the patient after the collar was removed showed intense muscle spasm, focal tenderness at C4, and great apprehension with any attempt to rotate the neck. Initial MRI to define an occult fracture was negative. Follow-up MRI at 10 days showed a healing fracture of the lamina of C4. The suspicion for fracture remained high because of the focal vertebral spinous process tenderness and the severe reactive cervical muscle spasm. FIGURE 1–24. Cross-table lateral x-ray to assess the alignment of the cervical spine.

PALPATION SUMMARY: The paraspinal muscles and the superior portion of the trapezial muscle react with severe spasm when the spinal column has been traumatized. MANEUVER: Palpate the paraspinal muscles and the superior trapezial muscle along the entire length of the cervical spine. Compare the muscle tenderness and degree of muscle spasm on either side of the spine. INTERPRETATION: The most severe reactive cervical muscular strain occurs when the neck has been traumatized. Muscle spasms are extreme with fracture, fracture with dislocation, occult fracture, and malignancy-associated fracture.

FIGURE 1–25. Palpation of the paraspinal muscles in reactive cervical strain.

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CLINICAL PEARLS • Loss of rotation can be considered the universal sign of the conditions that are intrinsic to the neck. Rotation is impaired in the early stages of nearly all conditions that affect the neck; for this reason, it is the best maneuver to use to screen for neck conditions (i.e., more sensitive than changes in flexion, lateral bending, and extension). • Acute muscular spasm associated with acute cervical strain causes a loss of full rotation. • Loss of rotation is the hallmark of osteoarthritis of the neck and correlates directly with its severity. • Trapezius muscle irritation and spasm is a common presenting sign of conditions that are intrinsic to the neck, second only to the changes in the normal range of motion of the neck. Of the three divisions of the trapezius muscle (superior, middle, and lower), selective tenderness, spasm, and irritability of the superior portion correlate highly with an intrinsic neck process. By contrast, involvement of all three divisions with tenderness, spasm, and irritability is seen with fibromyalgia, scoliosis, and poor posture. • Cervical radiculopathy is classified according to the degree of nerve impairment as sensory, sensorimotor, or sensorimotor with spinal cord compression; 80% to 85% of patients have sensory impairment only. The prognosis in these cases is uniformly good; treatment consists of rest, stress reduction, attention to posture, a muscle relaxer taken at night, and gentle stretching exercises in rotation over a period of 4 to 6 weeks. • The prognosis of patients with radiculopathy involving both sensory and motor nerves is less predictable. Patients with motor involvement are more likely to have larger disk herniations, are at higher risk for nerve damage, and are more likely to need neurosurgical intervention. For these reasons, subtle motor involvement should be sought through examination for variability in the thresholds of the neuroreflexes, muscular fatigue when individual muscles are repeated tested for strength, and the loss of bulk in the arms and forearms. • Although the routine cervical series of x-rays consists of five views, including the odontoid, lateral, posteroanterior, and two oblique views, the lateral view provides the most useful clinical information. It can be

•

•

•

• • •

used to screen for loss of alignment (e.g., cervical strain, whiplash), the degree of osteoarthritis (at the facet and paravertebral joints), disk space narrowing (osteoarthritis or radiculopathy), or bony disorders (compression fracture). All patients who present with symptoms and signs of radiculopathy should undergo a cervical series of radiographs. Foraminal encroachment is the underlying cause of cervical radiculopathy in 90% of cases. If the oblique views of the neck do not disclose at least 50% narrowing of the foramina at the appropriate spinal level, MRI should be performed to evaluate for herniated disk. Every patient who has sustained severe trauma to the head or neck must be cleared neurologically before proceeding to special radiographic studies. The first priority is to perform a screening neurologic exam. Next, a cross-table lateral x-ray is obtained to assess the alignment of the vertebral bodies (with the patient in the transport collar). Next, the collar is removed, the spinous processes are palpated, and the neck muscles are assessed for irritability. Once the patient is cleared neurologically, special studies are obtained to further determine alignment and evaluate for fracture, dislocation, or epidural bleeding. Caution: Injury to the vertebral column must be assumed if the patient manifests anxiety when one attempts to remove the transport collar, guarding when one attempts to move the neck in any direction, or rigidity of the paraspinal muscles. For instance, the body interprets even a small, nondisplaced vertebral body or laminar fracture as a potential threat to the spinal cord and nerves. This threat generates severe reactive muscle spasm. For major trauma with signs of neurologic compromise, consult the neurosurgeon. For major trauma without signs of neurologic compromise, proceed cautiously to radiographic studies to exclude occult neck fracture and epidural bleeding. Rotating the neck is nearly impossible in patients who have sustained significant neck trauma. Vertebral body subluxation or fracture leads to neck rigidity from intense muscle spasm.

CHAPTER 2: SHOULDER DIFFERENTIAL DIAGNOSIS Confirmations

Diagnoses Rotator cuff syndromes (most common) Impingement syndrome Rotator cuff tendonitis Rotator cuff tendon thinning Rotator cuff tendon tear Frozen shoulder

Examination, passive painful arc Lidocaine injection test X-ray: shoulder series showing a narrow subacromial space Magnetic resonance imaging (MRI) arthrography Examination showing a loss of range of motion, normal x-ray

Acromioclavicular (AC) joint Osteoarthritis AC separation Osteolysis of the clavicle

X-ray: shoulder series X-ray: weighted views of the shoulder X-ray: shoulder series

Subscapular bursitis


Sternoclavicular joint Strain or inflammatory arthritis Septic arthritis (intravenous drug abuse)

Local anesthetic block Aspiration and culture

Glenohumeral joint Osteoarthritis Inflammatory arthritis Septic arthritis

X-ray: shoulder series (axillary view) Synovial fluid analysis Synovial fluid culture

Multidirectional instability of the shoulder Dislocation Subluxation Glenoid labral tear

X-ray: shoulder series Abnormal sulcus sign Double contrast arthrography

Referred pain Cervical spine Lung Diaphragm Upper abdomen

Neck rotation, x-ray, MRI Chest x-ray Chest x-ray, computed tomography scan Chemistries, ultrasound

.

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INTRODUCTION The unique anatomy of the shoulder allows the greatest range of motion of all of the joints of the body, but at a tremendous price: The vital rotator cuff tendons that are responsible for the support and movement of the shoulder joint are susceptible to the compression forces between the undersurface of the acromion and the top of the humeral head. Specifically, the supraspinatus and infraspinatus tendons are the only tendons in the body that must perform their vital functions while being subjected to the compressive forces between these two bony surfaces. Every time the arm is raised to shoulder level or above, these tendons are compressed and are subject to friction in this subacromial space, a force called subacromial impingement. The largest lubricating sac in the body, the subacromial bursa, attempts to counter these forces but often fails to keep up with the demands; subacromial bursitis results. If the subacromial bursa does not effectively counter the friction and compression caused by overhead reaching, inflammation is carried over to the tendons, and rotator cuff tendonitis results. Inflammation of the supraspinatus and infraspinatus tendons is the most common condition affecting the shoulder, a problem that affects nearly everyone at least once in their lifetime. Left unrecognized and untreated, subacromial impingement can persist and progress over months and years. The repeated mechanical irritation of impingement and the relentless deleterious effects of inflammation lead to recurrent and chronic subacromial bursitis and rotator cuff tendonitis. This in turn can lead to degenerative thinning of the tendon and ultimately to rotator cuff tendon tear with accompanying muscle atrophy. When approaching the patient presenting with upper arm pain and shoulder dysfunction, the provider must view the conditions that affect the subacromial area and rotator cuff tendons, in particular, as a continuum of pathological states: from the earliest stage of mechanical impingement through active subacromial bursitis and uncomplicated rotator cuff tendonitis to the degenerative rotator cuff tendon thinning and the final result of rotator cuff tendon tear. The challenge to the provider is to determine where on this continuum the patient falls. Frozen shoulder, the reversible loss of glenohumeral range of motion, is another complication of impingement and rotator cuff tendonitis. At least 10% of patients with active rotator cuff tendonitis develop frozen shoulder or adhesive capsulitis. Although rotator cuff tendonitis is its most common cause, frozen shoulder can also result from stroke, shoulder surgery, or bony fracture. The second most common condition affecting the shoulder involves the acromioclavicular (AC) joint. The clavicle juts out from the bony thorax and abuts the acromial process of the scapula. The joint is susceptible to wear-andtear and injury with repetitive overhead reaching, to-and-fro movement across the chest, and compression from lateral shoulder pressure. Degenerative osteoarthritis of the AC joint is nearly universal, although not every patient develops symptoms. AC separation is another common condition that occurs after direct blows to the shoulder or falls on an outstretched arm. Glenohumeral osteoarthritis is surprisingly uncommon given the wide range of motion the shoulder is capable of. Unlike degenerative osteoarthritis of the AC joint, osteo-

arthritis is rare outside the setting of previous bony fracture, dislocation, or complete rotator cuff tendon tear. Hypermobility or multidirectional instability of the glenohumeral joint is also associated with late-onset osteoarthritic change, probably through the complication of glenoid labral tear. The other major bursa affecting the shoulder is the subscapular bursa. Subscapular bursitis, also called costothoracic syndrome, is caused by the exaggerated movement of the scapula across the bony rib cage when normal glenohumeral movement is impaired (frozen shoulder and glenohumeral joint arthritis). This exaggerated degree of shoulder shrugging increases friction between the second and third ribs and the undersurface of the superior medial angle of the scapula. The shoulder is susceptible to trauma, including fractures of the clavicle in early life and humeral head and neck fractures in older adults with advanced osteoporosis. Finally, pain is commonly referred to and through the shoulder from conditions arising in the neck and conditions affecting the heart, lungs, pleura, great vessels, or upper abdomen. SYMPTOMS Conditions intrinsic to the shoulder cause the following symptoms: shoulder pain provoked by specific shoulder movements, loss of mobility (impaired reaching, lifting, pushing, and pulling, pain or stiffness), bony or soft tissue deformity (AC separation and arthritis, dislocation), muscular weakness, or a combination of these symptoms. However, the strongest clue to a specific anatomic diagnosis often is based on the patient’s description and location of their pain. Shoulder pain aggravated by reaching and localized to the lateral deltoid area is the most common pain pattern. This is the classic pain pattern of impingement syndrome and the various stages of rotator cuff tendonitis: simple strain, uncomplicated tendonitis, chronic calcific tendonitis, and tendonitis complicated by tendon tear. When this pain pattern is accompanied by joint stiffness and a measurable loss of movement in external rotation or abduction, frozen shoulder is the most likely diagnosis. When this pain pattern is complicated by weakness and a measurable loss of strength in external rotation or abduction (a loss that cannot be attributed to pain and poor effort), rotator cuff tendonitis complicated by tendon tear is most likely. Shoulder pain localized to the anterior shoulder area is less common and is most characteristic of the conditions affecting the AC joint, glenohumeral joint, or the anterior tendons (long head of the biceps, subscapularis, and rarely the pectoralis major tendon). When this pain is well localized and specifically identified by the patient (often pointing to the distal end of the clavicle), AC separation or osteoarthritis of the AC joint is the most likely diagnosis. When this pain is aggravated by movement of the shoulder in several different directions, involvement of the glenohumeral joint should be suspected. When this pain is aggravated by selective movement in one direction, tendonitis of one of the anterior tendons should be suspected (lifting, the long head of the biceps; reaching, rotator cuff tendonitis, especially when the subscapularis predominates; pushing, pectoralis major).

SHOULDER

Posterior shoulder pain is the least common pain pattern at the shoulder. Rotator cuff tendonitis can refer pain over the broad area of the scapula, the anatomic location of the rotator cuff muscles. However, when the pain localizes to the superior medial angle of the scapula, subscapular bursitis is the more likely diagnosis. Poorly localized posterior shoulder pain is referred from the neck, is caused by compression neuropathy, or arises from the underlying bony structures. Poorly localized and vaguely described posterior shoulder pain may also reflect exaggerated symptoms in patients who are malingering or are involved in worker’s compensation claims or insurance litigation.

BOX 2-1

DIFFERENTIAL DIAGNOSIS OF SHOULDER PAIN BASED ON ANATOMIC AREA Lateral deltoid pain

Anterior shoulder pain

Posterior shoulder pain Referred pain

Impingement syndrome Subacromial bursitis Rotator cuff tendonitis Rotator cuff tendon tear Deltoid tendonitis Acromioclavicular osteoarthritis Acromioclavicular separation Osteolysis of the clavicle Frozen shoulder Glenohumeral osteoarthritis Glenohumeral inflammatory arthritis Glenohumeral septic arthritis Multidirectional instability Sternoclavicular strain Subscapularis tendonitis Subscapular bursitis Cervical strain Cervical radiculopathy Medical causes of shoulder pain

EXAMINATION The examination of the shoulder always begins with assessment of the overall function of the glenohumeral joint followed by a focused evaluation of the most common conditions affecting the surrounding tendons and joints. Functional testing determines the involvement of the glenohumeral joint, readily assesses the severity of the condition, and includes the following maneuvers: range of motion testing in abduction and external rotation (passively performed), estimation of the strength of the infraspinatus muscle (the muscle that is most susceptible to atrophy with disuse), and an assessment of the overall tight-

21

ness of the subacromial space. Next, the painful arc maneuver (passively abducting the glenohumeral joint while simultaneously preventing shoulder shrugging) is combined with the degree of subacromial tenderness to assess the degree of subacromial impingement. If impingement is confirmed, isometric testing of each individual tendon is performed to determine the number of inflamed tendons; for example, subacromial tenderness combined with isometrically resisted external rotation identifies the involvement of the infraspinatus tendon. Pain reproduced by isometrically resisted abduction identifies the involvement of the supraspinatus tendon. Pain reproduced by resisted flexion of the elbow identifies the involvement of the long head of the biceps. To complete the shoulder exam, focal tenderness of the AC joint, sternoclavicular (SC) joint, and subscapular bursa is determined by direct palpation.

BOX 2-2

ESSENTIAL EXAMINATION OF THE SHOULDER 1. Evaluate the general function of the shoulder and glenohumeral joint: Observe the general movement of the shoulder, estimate the tone and strength of the supporting muscles, especially the infraspinatus, and determine the overall tightness of the subacromial space. 2. Perform the painful arc maneuver to determine the degree of subacromial impingement. 3. Palpate the subacromial space, the bicipital groove, and the anterior glenohumeral joint line. 4. Perform isometric testing of the major supporting tendons rotator cuff and biceps. 5. Palpate the AC joint, the SC joint, and the subscapular bursa for tenderness. 6. Perform range of motion of the neck or a general medical exam if a referred source of shoulder pain is suspected.

ONE-MINUTE SCREENING EXAM: MANEUVERS ASSESSING OVERALL SHOULDER FUNCTION AND DIFFERENTIAL DIAGNOSIS The next 10 maneuvers represent the minimal examination of the patient presenting with shoulder symptoms. Function testing, range of motion measurement, and screening maneuvers for tendonitis, the accessory joints, and bursitis provide enough information to triage to x-ray, order appropriate labs, suggest general treatment recommendations, or proceed to more detailed examination and treatment.

22


THE TOUCHDOWN SIGN SUMMARY: Full abduction requires a normal glenohumeral joint, intact rotator cuff tendons, a freely moving AC joint, and well-developed deltoid and rotator cuff muscles. This is the optimal screening maneuver for intact abduction. MANEUVER: The patient is asked to raise both arms directly overhead. The smoothness of the movement, the degree of discomfort, and the ability to complete the maneuver are compared side to side. Similarly, the ability to smoothly control lowering the arm is compared side to side (the latter maneuver is analogous to the drop-arm sign).

FIGURE 2–1. The touchdown sign is used to assess active glenohumeral joint abduction.

INTERPRETATION: Severe pain limits abduction with acute rotator cuff tendonitis, rotator cuff tendonitis with partial tear, the uncommon inflammatory or septic arthritis of the glenohumeral joint, and advanced glenohumeral arthritis. Patients with dislocation or fracture will not attempt the maneuver. Patients with mild glenohumeral osteoarthritis or frozen shoulder have restricted movement with modest pain. Patients with complete rotator cuff tendon tears have impaired movement caused by profound weakness. A diagnosis of polymyalgia rheumatica should be considered in older adults who complain of bilateral stiff shoulders (with or without concurrent hip involvement).

THE APLEY SCRATCH SIGN SUMMARY: Full rotation requires a normal glenohumeral joint, intact rotator cuff tendons, and reasonably well-developed rotator cuff muscles. The Apley scratch maneuver is the most practical means of screening shoulder movement. In addition, it provides the most objective measurement of rotation. MANEUVER: The patient is asked to scratch the lower back and place the thumb as high up on the back in the midline as comfortable. The distance between the thumbs is measured, and the level reached by the thumb is recorded. INTERPRETATION: Rotation is limited with frozen shoulder, arthritis of the glenohumeral joint (osteoarthritis or inflammatory arthritis), and the acute inflammation of rotator cuff tendonitis. The loss of rotation correlates well with the severity of these conditions. Rotation of the shoulder is impossible or the patient refuses to perform the maneuver with dislocation and humeral head fracture.

FIGURE 2–2. The Apley scratch sign is used to screen rotation of the glenohumeral joint.

SHOULDER

ISOMETRIC TESTING SUMMARY: The infraspinatus and teres minor muscles are responsible for external rotation of the shoulder. This is the first muscle to atrophy with any chronic condition affecting the shoulder. It is also the second most common rotator tendon to rupture. In general, testing the strength of external rotation provides the best screening of the shoulder’s overall conditioning. MANEUVER: Using a Theraband, bungee cord, or 10-10 resistance bands (depicted here), the patient is asked to pull the bands apart while keeping the elbows at the sides (pure rotation). The symmetry of motion, strength, and ability to hold the bands steady are compared side to side. FIGURE 2–3. Isometric testing of the external rotation using resistance bands.

INTERPRETATION: Unilateral weakness of external rotation is seen with rotator cuff tendon tear, C5 radiculopathy, and the uncommon suprascapular nerve palsy (hod carrier’s disease). Bilateral weakness of external rotation is seen with poor muscular development, bilateral rotator cuff tears, bilateral glenohumeral arthritis, or any chronic disease.

THE WEIGHTED TOUCHDOWN SIGN SUMMARY: Full abduction requires a normal glenohumeral joint, intact rotator cuff tendons, a functional AC joint, and well-developed deltoid and rotator cuff muscles. The ability to lift progressively heavier weights provides an objective measurement of general, overall shoulder strength. MANEUVER: The patient is asked to raise 1-, 2-, and 5-lb weights overhead. The smoothness of the movement, the degree of discomfort, and the ability to complete the maneuver are compared side to side.

FIGURE 2–4. The weighted touchdown sign to assess overall shoulder strength.

INTERPRETATION: Inability to lift the unweighted arm is seen with a complete rotator cuff tear, severe muscular atrophy, severe C5 radiculopathy, or the rare suprascapular nerve palsy. Ability to lift 1- or 2-lb weights is compatible with a partial rotator cuff tear, poorly developed muscles, or a partial C5 radiculopathy. The ability to lift 5 lb or more is consistent with intact rotator cuff tendon.

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THE SULCUS SIGN SUMMARY: The deltoid muscle arises from the acromion and attaches to the midhumerus. The supraspinatus tendon attaches to the greater tubercle. Downward movement of the humeral head is restricted by the tone and bulk of the deltoid, the tone and thickness of the supraspinatus tendon, and the redundancy of the glenohumeral capsule. This maneuver is used to assess the looseness of the shoulder joint, the subacromial space (subluxation), and the patient’s potential tolerance of the pendulum stretch exercise. MANEUVER: The patient is asked to relax the shoulder. One hand is placed atop the acromion, and one hand is placed in the antecubital fossa. Downward pressure is applied to the arm to open the subacromial space. The examiner assesses the looseness of the shoulder and the discomfort of the maneuver.

FIGURE 2–5. The sulcus sign evaluates the looseness or tightness of the shoulder and can be used to determine the appropriateness of the pendulum stretch exercise.

INTERPRETATION: A tight shoulder—no movement with downward pressure—is seen with extreme guarding and tension due to pain, frozen shoulder, fibromyalgia, or an overly developed deltoid. Downward movement of 1⁄4 inch is considered average looseness. Downward movement of more than 1 ⁄2 inch indicates hypermobility (subluxation).

PASSIVE PAINFUL ARC MANEUVER SUMMARY: Several maneuvers are used to define the degree of subacromial impingement, including the Neer and Hawkins maneuvers. The passively performed painful arc maneuver (depicted here) is the easiest maneuver to perform and provides the most reproducible assessment of impingement. The combination of this maneuver with focal tenderness defines the degree of subacromial impingement. MANEUVER: One hand is placed atop the acromion, and one hand grasps the proximal forearm. The patient is asked to relax the shoulder. While applying simultaneously downward pressure on the acromion to prevent the protective effect of shrugging, the arm is carefully raised, and the angle at which pain is reproduced is noted.

FIGURE 2–6. Subacromial impingement is assessed by the passive painful arc maneuver.

INTERPRETATION: Mild impingement is defined by pain reproduced at 90 degrees of abduction. Moderate impingement occurs at an angle of 60 to 70 degrees, and severe impingement is defined by pain at 45 degrees.

SHOULDER

PALPATION OF THE SUBACROMIAL SPACE SUMMARY: The subacromial space is occupied by the subacromial bursa, the rotator cuff tendons, and 1 to 2 mm of articular cartilage. The deltoid muscle is layered over the acromion, the subacromial space, and the greater tubercle of the upper humerus. Subacromial tenderness, just under the lateral edge of the acromion, combined with the passive painful arc maneuver defines the impingement syndrome. MANEUVER: The anterior, lateral, and posterior edges of the acromion are marked with a pen. The subacromial space is palpated just under the lateral edge of the acromion. FIGURE 2–7. Palpation of the subacromial space.

INTERPRETATION: Focal tenderness is typical of impingement syndrome, active rotator cuff tendonitis, rotator cuff tendonitis with tear, and bony lesions of the humerus. Diffuse tenderness is characteristic of acute subacromial bursitis and patients with active shoulder tendonitis with a low pain threshold.

PALPATION OF THE AC JOINT OBJECTIVE: The AC joint is formed by the acromial process of the scapula and the distal end of the clavicle. The joint is held together by the acromioclavicular, coracoacromial, and coracoclavicular ligaments. The joint is susceptible to osteoarthritis and traumatic separation. MANEUVER: The anterior, lateral, and posterior edges of the acromion are marked with a pen. The AC joint is 13⁄4 inches from the lateral edge of the acromion.

FIGURE 2–8. Palpation of the AC joint.

INTERPRETATION: Osteoarthritis of the AC joint is characterized by bony enlargement. An osteoarthritic flare is characterized by bony enlargement combined with local tenderness. Local tenderness with normal-positioned and normal-sized bones is characteristic of a first-degree AC separation. Local tenderness and bony deformity after trauma to the shoulder are seen with second- and third-degree AC separations.

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PALPATION OF THE SUBSCAPULAR BURSA SUMMARY: The levator scapula attaches to the superior medial angle of the scapula. The rhomboid muscles attach to the medial border of the scapula. The middle portion of the trapezius muscle forms the outer muscular layer that covers the muscles and the scapula. The subscapular muscle is located underneath the scapula, acting as a natural protective pad between the ribs and scapula. MANEUVER: The ipsilateral arm is fully abducted. The patient is asked to place the hand on the contralateral shoulder. The superior medial angle of the scapula and the center of the ribs are marked with a pen. Bursal tenderness is palpated directly over the rib closest to the angle of the scapula.

FIGURE 2–9. Palpation of the subscapular bursa.

INTERPRETATION: A half dollar–sized area of tenderness at the superior medial angle is most commonly caused by subscapular bursitis as opposed to the generalized muscular tenderness of the strain of the upper back muscles. Primary involvement of the rib or the scapula must be considered in the case of the patient with a known primary cancer (e.g., breast, lung, prostate).

PALPATION OF THE SC JOINT SUMMARY: The SC joint is formed by the upper portion of the sternum and the proximal clavicle. When the joint swells, the proximal clavicle projects anteriorly. The anterior position of the clavicle causes a pseudoenlargement of the clavicle. MANEUVER: The sternal notch, proximal clavicle, and center of sternum are palpated and marked with a pen. The SC joint is palpated at the junction of the sternum and the proximal clavicle, approximately 3⁄4 to 1 inch from the midline.

FIGURE 2–10. Palpation of the SC joint.

INTERPRETATION: SC joint involvement is uncommon. SC joint strain is characterized solely by local tenderness. SC joint local tenderness and pseudoenlargement of the clavicle are seen with SC joint arthritis, most commonly Reiter’s disease. A red, hot, swollen joint is a unique complication of intravenous drug abuse, acute septic arthritis.

SHOULDER

ONE-MINUTE SCREENING EXAM: MANAGEMENT OPTIONS TRIAGE TO X-RAY The patient has a history of trauma, is at risk of bony injury, has recurrent episodes of rotator cuff tendonitis, has significant loss of range of motion in rotation or abduction, or has an enlarged AC or SC joint by history or exam: • Order three views of the shoulder for patients with a history of fall to an outstretched arm, a severe blow to the shoulder, or a hyperextension injury (humeral or clavicular fracture, AC separation, or glenohumeral joint dislocation). • Order three views of the shoulder for patient with recurrent or chronic rotator cuff tendonitis (narrowing of the subacromial space also known as high-riding humeral head seen with thinning of the rotator cuff tendons). • Order weighted views of the shoulder (traumatic AC separation). • Order three views of the shoulder and an axillary view (glenohumeral joint osteoarthritis or as a part of the workup for frozen shoulder). • Order apical lordotic views of the upper chest (SC joint swelling and subluxation). TRIAGE TO THE LAB For patients suspected of having gout, acute arthritis, or septic arthritis (rare): • Order a complete blood cell count, uric acid, and erythrocyte sedimentation rate for patients with acute pain, exquisite anterior joint line tenderness, signs of active inflammation, and dramatic loss of range of motion in all directions (gout or acute arthritis) and include blood cultures if the acute inflammatory changes are accompanied by significant fever or concurrent signs of infection elsewhere in the body.

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CONSIDER A BONE SCAN For patients with vague pain about the shoulder with a history of previous solid tumor and for patients with osteoporosis, a history of fall, and a high suspicion for occult fracture. CONSIDER MRI For patients with an examination suggestive of rotator cuff tear or glenoid labral tear from previous subluxation or dislocation. RECOMMEND EMPIRICAL TREATMENT For patients with mild to moderate shoulder pain and stiffness, unrestricted movement of the joint, and normal strength in rotation and abduction. • Restrict reaching, lifting, pushing, and pulling. • Apply ice up to four times a day or take a full-strength nonsteroidal anti-inflammatory drug for 10 to 14 days. • Perform the pendulum stretch exercise once or twice daily. • Perform isometric toning exercise of external rotation. DETAILED EXAMINATION: SPECIFIC SHOULDER DIAGNOSES Perform a detailed examination of the shoulder if the patient has persistent or chronic symptoms, has sustained an injury, demonstrates moderate loss of range of motion, or has lost strength in rotation or abduction.

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IMPINGEMENT SYNDROME Shoulder pain and impaired

reaching at or above shoulder level that is caused by the direct bony contact of the undersurface of the acromion and the greater tubercle of the humeral head is called impingement syndrome.

It is the mechanical abnormality of the shoulder that is the principle cause of inflammation of the subacromial bursa—common shoulder bursitis—and rotator cuff tendonitis.

PASSIVE PAINFUL ARC MANEUVER SUMMARY: Several maneuvers are used to define the degree of subacromial impingement, including the Neer and Hawkins maneuvers and the passively performed painful arc maneuver (depicted here). The painful arc maneuver is the easiest to perform and is applicable to most patients with clinically significant impingement. The combination of this maneuver with focal tenderness defines the degree of subacromial impingement.

FIGURE 2–11. Subacromial impingement assessed by the passive painful arc maneuver.

MANEUVER: One hand is placed atop the acromion, and one hand grasps the proximal forearm. The patient is asked to relax the shoulder. While downward pressure is applied on the acromion to prevent the protective effect of shrugging, the arm is carefully raised, and the angle at which pain is reproduced is noted. INTERPRETATION: Mild impingement is defined by pain reproduced at 90 degrees of abduction. Moderate impingement occurs at an angle of 60 to 70 degrees, and severe impingement is defined by pain at 45 degrees.

LIDOCAINE INJECTION TEST SUMMARY: The lidocaine injection test is used to confirm impingement as the primary cause of shoulder pain and to define the various presentations of shoulder tendonitis (rotator cuff tendonitis, rotator cuff tendonitis with tear, and rotator cuff tendonitis complicated by frozen shoulder) and glenohumeral joint arthritis. POSITIONING: Sitting, relaxed shoulder, with or without downward traction applied to the elbow. SURFACE ANATOMY:

Lateral edge of the acromion.

POINT OF ENTRY: 1 to 11⁄2 inches below the midpoint of the acromion. ANGLE OF ENTRY: NEEDLE: DEPTH:

Paralleling the acromion.


1

1 to 11⁄2 inches.

ANESTHESIA: Ethyl chloride, skin: 1 mL, deltoid; 1 to 2 mL, subacromial bursa.

FIGURE 2–12. The lidocaine injection test is used to confirm impingement.

SHOULDER

Rotator cuff tendonitis, inflammation of the important supporting tendons of glenohumeral joint, results from repeated subacromial impingement and a failure of the subacromial bursa to provide adequate lubrication

ROTATOR CUFF TENDONITIS

and protection. Of the four rotator cuff tendons, the supraspinatus tendon is the most susceptible to injury and inflammation because of its vulnerable position just under the acromion process.

ISOMETRIC TESTING SUMMARY: Of the three abductors of the shoulder— the deltoid, supraspinatus, and trapezius—the supraspinatus is responsible for abduction in the midarc. Active shoulder tendonitis is defined by reproducing the patient’s pain with active isometric testing of the actions of the various tendons. Active resisting abduction in the midarc defines the degree of inflammation of the supraspinatus tendon. MANEUVER: The patient’s arm is abducted to 45 degrees. The patient is asked to actively abduct the arm against the resistance of the examiner’s hand placed at the elbow. The effort, strength, and discomfort are noted.

FIGURE 2–13. Isometric testing of the supraspinatus tendon in midarc.

ADDITIONAL SIGNS: The diagnosis of rotator cuff tendonitis is suggested when the signs of impingement (local tenderness and the painful arc maneuver) are accompanied by pain reproduced by isometric testing of the rotator cuff tendons. Strength of midarc abduction should be normal unless the tendon has been split or torn. INTERPRETATION: Isometric induced pain and normal strength suggests rotator cuff tendonitis. Pain and weakness of midarc abduction suggests rotator cuff tendonitis with tear. Weakness without pain suggests chronic rotator cuff tear, muscular atrophy, C5 radiculopathy, or suprascapular nerve palsy.

ISOMETRIC TESTING SUMMARY: The infraspinatus is the primary external rotator of the shoulder (the teres minor plays a minor role). This maneuver is performed with the shoulder kept in neutral position. If the patient’s pain is reproduced only by resistance to external rotation, one can assume that the infraspinatus tendon is solely responsible for the active tendonitis. MANEUVER: The elbow is flexed to 90 degrees and held next to the body with one hand. The patient is asked to actively rotate the arm against the resistance of the examiner’s hand placed at the wrist. The effort, strength, and discomfort are noted.

FIGURE 2–14. Isometric testing of the infraspinatus tendon in neutral position.

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ASSOCIATED SIGNS: The diagnosis of rotator cuff tendonitis is suggested when the signs of impingement (local tenderness and the painful arc maneuver) are accompanied by pain reproduced by isometric testing of the rotator cuff tendons. INTERPRETATION: Identical to isometric testing of the supraspinatus tendon (see Figure 2–13).

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NORMAL SUBACROMIAL WIDTH SUMMARY: The subacromial space—the anatomic areas between the superior humeral head and the undersurface of the acromion—contains the subacromial bursa, the rotator cuff tendons, and 2 mm of articular cartilage. Chronic inflammation of the subacromial bursa leads to bursa wall fibrosis and eventual loss of its normal lubricating function. If the bursa cannot protect the rotator cuff tendons from the friction and compressive forces of subacromial impingement, the rotator cuff tendons will be vulnerable to mucinoid degenerative thinning.

FIGURE 2–15. X-rays of the shoulder to determine the normal subacromial width.

CASE: This radiograph demonstrates the normal relationships of the acromion and the humeral head. The normal subacromial space (depicted here) measures 10 to 11 mm. Narrowing of the space correlates directly with thinning of the rotator cuff tendons. Radiologists often refer to a narrowed subacromial space as a “high-riding humeral head” sign.

ABNORMAL SUBACROMIAL WIDTH CASE: This patient had a history of recurrent rotator cuff tendonitis over many years. He worked in construction all his life, performing heavy physical work, including physical work at or above his shoulder level. He was forced to retire because of refractory right shoulder pain. This radiograph demonstrates a near obliteration of the subacromial space, measuring 1 mm or less (loss of the subacromial bursa and complete thinning of the rotator cuff tendons). The greater tubercle of the humeral head shows severe sclerosis caused by the chronic compressive forces of impingement over the years. Patients with loss of the normal subacromial space are at the highest risk for rotator cuff tendon tear. (Radiologists often fail to comment on the sclerotic changes occuring at the greater tubercle, the radiographic signs of impingement.)

FIGURE 2–16. X-rays of the shoulder demonstrating the abnormal subacromial width.

SHOULDER

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LIDOCAINE INJECTION TEST SUMMARY: Patients presenting with severe shoulder pain and severe guarding on examination need local anesthetic block in order to more accurately assess the function of the shoulder. The lidocaine injection test is used to confirm rotator cuff tendonitis, exclude rotator cuff tear (normal strength), exclude glenohumeral joint involvement, and determine the degree of frozen shoulder (persistent loss of range of motion). POSITIONING: Sitting, relaxed shoulder, downward traction applied to the elbow. SURFACE ANATOMY:

Lateral edge of the acromion.

POINT OF ENTRY: 1 to 11⁄2 inches below the midpoint of the acromion. ANGLE OF ENTRY: FIGURE 2–17. The lidocaine injection test confirming rotator cuff tendonitis.

NEEDLE: DEPTH:

Paralleling the acromion.


ANESTHESIA: Ethyl chloride, skin: 1 mL, deltoid; 1 to 2 mL, subacromial bursa. FROZEN SHOULDER Frozen shoulder or adhesive capsulitis, a loss of the normal range of motion of the glenohumeral joint, is a direct result of injury or inflammation of the shoulder. The most common causes are rotator cuff tendonitis, fracture of

the humerus, dislocation of the glenohumeral joint, and shoulder surgery. In 95% of cases the contracture of the glenohumeral capsule is reversible.

APLEY SCRATCH SIGN SUMMARY: Full rotation requires a normal glenohumeral joint, intact rotator cuff tendons, and reasonably well-developed rotator cuff muscles. The Apley scratch sign is the most practical and objective measurement of rotation. MANEUVER: The patient is asked to scratch the lower back and place the thumb as high up on the back in the midline as comfortable. The distance between the thumbs is measured, and the level reached by the thumb is recorded. ADDITIONAL SIGNS: The touchdown sign demonstrating an abnormal abduction range of motion is typically abnormal as well. The passive range of motion of external rotation and abduction are dramatically lower than that of any other direction. Signs of active rotator cuff tendonitis often accompany the exam because it is the most common cause of frozen shoulder.

FIGURE 2–18. The Apley scratch sign to estimate the severity of frozen shoulder.

INTERPRETATION: Rotation is limited with frozen shoulder, arthritis of the glenohumeral joint (osteoarthritis or inflammatory arthritis), and the acute inflammation of rotator cuff tendonitis. The loss of rotation correlates well with the severity of these conditions.

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ARTHROGRAPHY OF THE GLENOHUMERAL JOINT SUMMARY: The diagnosis of frozen shoulder is based on the clinical criteria of preferential loss of external rotation and abduction relative to other directions of motion, no underlying primary involvement of the glenohumeral joint, and no concomitant neurologic disease that would restrict range of motion. Plain radiographs are necessary to exclude an underlying glenohumeral osteoarthritis that can mimic the physical findings of frozen shoulder. Arthrography (depicted here to emphasize the loss of distensibility of the glenohumeral joint) is not necessary to confirm the diagnosis.

FIGURE 2–19. Arthrography of the glenohumeral joint demonstrating loss of the normal synovial cavity distensibility.

CASE: This middle-aged woman with insulin-dependent diabetes developed a painful shoulder 6 months ago. She was treated with restriction in reaching and heavy lifting, ice, ibuprofen, and physical therapy exercises. Her pain gradually improved, but she gradually developed stiffness and lost full range of motion. Her Apley scratch signs were 10 inches apart. Her passive measurements of external rotation and abduction were 15 degrees and 50 degrees, respectively. The arthrogram depicted here demonstrates a poorly filled synovial cavity that accepted only 6 to 7 mL of radiopaque dye.

SHOULDER

ROTATOR CUFF TENDON TEAR In the majority of cases rupture of the rotator cuff tendons occurs as a complication of preexisting rotator cuff tendonitis. Other risk factors include chronic mucinoid degenerative tendon thinning, injury (fall to an out-

stretched arm or direct blow), age greater than 62 years, a history of recurrent tendonitis, a narrowed subacromial space on x-ray, muscular weakness, systemic steroids, concomitant rheumatic disease, and intratendinous injection.

ROTATOR CUFF TENDON WEAKNESS SUMMARY: Approximately 15% of cases of rotator cuff tendonitis are complicated by tear. The hallmark feature of rotator cuff tear is loss of strength in the direction of the affected tendon (external rotation, infraspinatus; midarc abduction, supraspinatus). The diagnostic challenge is to identify the patient at risk and to evaluate the extent of the tear by estimating the degree of weakness and the impact of the tear on overall shoulder function. In many cases, a lidocaine injection test (see Figure 2–17) is necessary to reduce pain to allow completion of the examination. MANEUVER: To assess the impact of a possible rotator cuff tendon tear on overall function, the patient is asked to actively raise the arm overhead. Patients with large complete tears (depicted here) are unable to raise the arm without contralateral arm assist. In order to grade the size of tears and their impact on the shoulder, the patient can be asked to raise progressively heavier weights (see Figure 2–4). FIGURE 2–20. Rotator cuff tendon weakness and inability to lift the arm.

ASSOCIATED SIGNS: Weakness of external rotation (see Figure 2–3), weakness of midarc abduction (see Figure 2–13), bruising of the anterior shoulder or upper arm, previous ruptured biceps tendons (increased risk), and swelling of the glenohumeral joint (depicted here).

HIGH-RIDING HUMERAL HEAD CASE: This 74-year-old woman has a 25-year history of “shoulder bursitis.” She is unable to raise her arm overhead, cannot comb her hair, and cannot reach up to remove dishes from her higher shelves. She uses her left arm to assist with abduction. Her external rotation strength is nonexistent, and her abduction strength is poor. DIAGNOSIS:

Complete rotator tendon tear.

DISCUSSION: The high-riding humeral head sign focuses on the cephalad migration of the humeral head. From a clinical perspective, a more helpful description would be “narrowed subacromial space,” thus shifting the emphasis to the narrowed thickness of the soft tissues located between the humeral head and the undersurface of the acromion. The normal width is 10 to 11 mm (1 mm humeral articular cartilage, 7 mm rotator cuff tendon, 1 mm subacromial bursa). FIGURE 2–21. The high-riding humeral head sign, strongest evidence of mucinoid degenerative thinning of the rotator cuff tendons.

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ARTHROGRAPHY CASE: This 71-year-old woman presented with recurrent rotator cuff tendonitis. She presented with local subacromial tenderness, a painful arc at 70 degrees, and pain and mild weakness when resisting midarc abduction and external rotation. Her strength improved modestly with the lidocaine injection test. Arthrography demonstrated a complex tear (the lower arrow). Dye entered the subacromial bursa (upper arrow) from the glenohumeral joint (the bursa and the synovial cavity to not communicate in the normal shoulder).

FIGURE 2–22. Arthrography to confirm a rotator cuff tendon tear. Hypaque 60 injected into the glenohumeral joint leaks through a tear in the rotator cuff and into the subacromial bursa.

DIAGNOSIS: Full-thickness rotator tendon tear. The subacromial space measures 10 mm (normal 10 to 11 mm), indicating a normal thickness rotator cuff tendon. DISCUSSION: The patient fully recovered with a combination of restricted reaching and lifting, the pendulum stretch exercise, a subacromial injection of Depo-Medrol, and recovery toning exercises. The prognosis for full recovery depends on the thickness of the tendons (normal thickness indicates no mucinoid degenerative thinning).

SHOULDER MRI CASE: This right-handed, 55-year-old construction worker fell 5 to 6 feet onto concrete, striking his right side and right shoulder. He felt immediate pain so severe he could not raise his arm up without the help of his left arm. Testing of midarc abduction and external rotation strength was impossible due to pain. Plain x-rays did not disclose a fracture or dislocation. DIAGNOSIS: Acute rotator cuff tendon rupture with muscle retraction.

FIGURE 2–23. Shoulder MRI showing supraspinatus tendon tear with muscle retraction.

DISCUSSION: Given the type of injury, the profound changes on examination, and the risk of an acute tendon rupture, MRI was the test of choice in this laborer with profound loss of shoulder function on the dominant side. The patient underwent acute surgical intervention to repair the torn tendon. Criteria for surgical treatment of rotator cuff tears include dramatic loss of function, weakness of external rotation or abduction that approaches 50% and that is not exaggerated by concurrent rotator cuff tendonitis pain, acute traumatic tears (a more favorable outcome than the chronic mucinoid degenerative tears of older adults), dominant side, and no medical contraindications.

SHOULDER

BICEPITAL TENDONITIS Acute inflammation of the long head of the biceps causes anterior shoulder pain, bicipital groove tenderness, and pain aggravated by resisting flexion at the elbow. Chronic inflammation of the biceps tendon can lead to bicipital tendon rupture.

PALPATION SUMMARY: Local tenderness is located directly over the bicipital groove and is palpable approximately 1 inch down from the anterolateral tip of the acromion. Tenderness is invariably present but not absolutely necessary for the diagnosis. MANEUVER: The bicipital groove is identified by placing a finger on the anterolateral humeral head between the greater and lesser tubercles. Passive rotation of the arm aids in the identification as the greater and lesser tubercles are felt moving under the fingertip.

FIGURE 2–24. Palpation of the bicipital groove for bicipital tendonitis.

ADDITIONAL SIGNS: Pain aggravated by flexion of the elbow, isometrically performed; a positive passive painful arc maneuver if impingement is present (see Figure 2–6); a bulge in the antecubital fossa, signifying long head tendon rupture; and preserved strength of elbow flexion despite tendon rupture. The strength of the unaffected short head of the biceps and the brachioradialis muscles combine to make up 80% of the strength of elbow flexion. INTERPRETATION: Each patient is examined for swelling and inflammation of the long head of the biceps in the bicipital groove, for signs of tendon rupture, and for associated subacromial impingement. Bicipital tendonitis is less common than rotator cuff tendonitis.

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BICIPITAL TENDONITIS SUMMARY: The ribbon-like long head of the biceps lies in the bicipital groove and is susceptible to inflammation and tendon rupture. It is the third most common form of tendonitis at the shoulder. It ranks behind tendonitis of the supraspinatus and infraspinatus tendons. POSITIONING: the leg.

Sitting, relaxed shoulder, hand on

SURFACE ANATOMY: Anterior humeral head, lesser and greater tubercles, anterolateral corner of the acromion. POINT OF ENTRY: Between the lesser and greater tubercles of the humerus, 1 inch below the anterolateral corner of the acromion. ANGLE OF ENTRY: NEEDLE: DEPTH: FIGURE 2–25. Bicipital tendonitis confirmed by local anesthetic placed at the bicipital groove.

Perpendicular to the skin.


ANESTHESIA: Ethyl chloride, skin: 1 mL, deltoid; 1 mL, bicipital groove.

BICIPITAL TENDON RUPTURE CASE: This 64-year-old man on coumarin had a “spontaneous” rupture of the right long head of the biceps. He denies injury, a fall to an outstretched arm, or unusual lifting. Note the extensive bruising from his coumarin. His international normalized ratio was 3.7 at the time of presentation. DIAGNOSIS: Acute rupture of the long head of the biceps on the right side and an old bicipital rupture on the left.

FIGURE 2–26. Bicipital tendon rupture confirmed by clinical examination.

DISCUSSION: Complete bicipital tendon ruptures cause the typical “Popeye” deformity in the antecubital fossa and often are associated with extensive ecchymosis. Although dramatic in appearance, these are rarely repaired. The short head of the biceps and the brachioradialis are responsible for 80% to 85% of the strength of elbow flexion.

SHOULDER

AC JOINT OSTEOARTHRITIS AND SEPARATION The

diagnosis of AC arthritis or separation is readily made based on its characteristic focal tenderness; in fact, patients readily identify the AC joint by pointing directly to it when describing their anterior shoulder pain. Osteoarthritis is a nearly universal occurrence with advancing age. Injury to its supporting ligaments is called shoulder separation.

PALPATION OF THE AC JOINT SUMMARY: The diagnosis of AC osteoarthritis or shoulder separation—injury to the supporting ligaments—is based on the demonstration of focal tenderness over the anterosuperior portion of the joint. Arthritis is further characterized by the degree of bony enlargement. AC separation is defined as first, second, or third degree based on the radiographic measurement of bony separation. MANEUVER: The anterior, lateral, and posterior edges of the acromion are marked with a pen. The AC joint is located along the anterior portion of the acromion, approximately 13⁄4 inches from its lateral edge. FIGURE 2–27. Palpation of the AC joint.

ADDITIONAL SIGNS: Bony enlargement defines the degree of osteoarthritis. Downward pressure on the arm to displace the joint defines the degree of AC separation. Pain can be reproduced by passively adducting the arm across the chest, forcing the ends of the articulating bones together. If the condition is severe, pain can be reproduced by actively resisting the biceps; the action of the biceps generates traction across the joint. INTERPRETATION: Local tenderness combined with bony enlargement defines the degree of osteoarthritis. Local tenderness occurring after injury but with the normal alignment of the acromion and clavicle defines first-degree AC separation. Local tenderness occurring after injury with widening of the joint when downward traction is placed on the joint defines a second-degree AC separation. Third-degree separations are obvious to inspection; the clavicle is abnormally positioned above the plane of the acromion.

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AC JOINT OSTEOARTHRITIS CASE: This middle-aged plywood mill worker complained of anterior shoulder pain and pointed to the AC joint as the most sensitive area of his shoulder. He has pain with reaching overhead and when he rolls onto his right side during the night. DIAGNOSIS: AC joint osteoarthritis with inferiorly directed osteophytes.

FIGURE 2–28. AC joint osteoarthritis is confirmed by plain x-rays.

DISCUSSION: Osteoarthritis of the AC joint is a universal condition, developing in nearly all patients older than 50 years. However, only 5% ever develop symptoms. The diagnosis is suggested by anterior shoulder pain, focal tenderness directly over the joint, and bony enlargement. The diagnosis is confirmed by x-ray or by anesthetic placed just over the joint. Large inferiorly directed osteophytes can cause rotator cuff tendonitis; the supraspinatus tendon is positioned directly under the AC joint.

LOCAL ANESTHETIC BLOCK OF THE AC JOINT SUMMARY: Occasionally patients present with a combination of symptoms suggesting simultaneous involvement of the AC joint and rotator cuff tendonitis, two common shoulder conditions. Local anesthetic block is used to determine the role of the AC joint in the patient’s clinical presentation. The needle enters just over the end of the clavicle (11⁄2 inches medially to the lateral edge of the acromion). NEEDLE:


5

DEPTH: ⁄8 to 5⁄8 inches, down to the periosteum of the clavicle. 3

VOLUME:

FIGURE 2–29. Local anesthetic block of the AC joint to confirm osteoarthritis and first-degree separation.

1 mL anesthetic and 1⁄2 mL K40.

NOTE: The needle does not enter the joint directly. The injection is placed just under the synovial membrane attached to the distal clavicle.

SHOULDER

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THIRD-DEGREE AC SEPARATION CASE: This 35-year-old mountain biker fell forward over the handlebars after striking a rock. His shoulder struck the ground. The direct blow to the anterior shoulder caused immediate shoulder pain and deformity. DIAGNOSIS:

Third-degree AC separation.

DISCUSSION: The acromioclavicular, coracoclavicular, and coracoacromial ligaments are attached tightly to the periosteum and hold the acromion, clavicle, and coracoid together. Falls to an outstretched arm, a dramatic blow to the anterior shoulder (tackling in football), or a fall landing directly on the anterior portion of the shoulder can cause the ligaments to be sprained, partially torn, or completely disrupted (first-degree sprain and secondand third-degree AC separations, respectively). FIGURE 2–30. Third-degree AC separation confirmed by plain x-rays.

GLENOHUMERAL OSTEOARTHRITIS Osteoarthritis of the glenohumeral joint is an uncommon problem. Most cases are preceded by a history of shoulder injury, either recent or remote. The diagnosis often is overlooked because of its similarity to frozen

shoulder on examination. The diagnosis is made by the characteristic changes seen on routine x-rays, including asymmetrical narrowing of the cartilage, increased bony sclerosis, and the unique osteophyte formation that projects inferiorly off the humeral head.

ANTERIOR SHOULDER SWELLING SUMMARY: Active arthritis of the glenohumeral joint is not common. MANEUVER: The coracoid process, the AC joint, and the humeral head are palpated and marked. Glenohumeral joint swelling and its accompanying joint line tenderness are located in the infraclavicular fossa just lateral to the coracoid process. Swelling ranges from subtle filling in of the fossa to anterior enlargement, often seen best by inspecting the shoulder from above, looking down.

FIGURE 2–31. Anterior shoulder swelling characteristic of a swollen glenohumeral joint.

ADDITIONAL SIGNS: The range of motion in all directions can be limited, depending on the acuteness of the process. Joint line tenderness located just under the coracoid process can be elicited by palpation in a superior and slightly lateral direction. Crepitation is evident with active movement of the shoulder either passively or against resistance (osteoarthritis). Signs of inflammation are notably absent because of the depth of the joint. INTERPRETATION: Osteoarthritis and rheumatoid arthritis are the most common causes of glenohumeral joint swelling. The severity correlates directly with the loss of range of motion, particularly in external rotation and abduction. Septic arthritis is rare. Patients with acute bacterial infections cradle their arm and do not allow any movement in any direction.

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GLENOHUMERAL JOINT OSTEOARTHRITIS CASE: A 67-year-old rancher’s wife presents with anterolateral shoulder pain and stiffness over several years. She denies any history of fracture, dislocation, or severe injury. However, she states, “People say I’ve always done a man’s work. It doesn’t surprise me that it is arthritic, since arthritis runs in my family.” DIAGNOSIS:

Glenohumeral osteoarthritis.

DISCUSSION: Arthritis of the glenohumeral joint is characterized by a loss of articular cartilage between the humeral head and the glenoid, osteophyte formation extending from the inferior portion of the humeral head, and humeral head sclerosis. Note that the combination of the loss of articular cartilage and osteophyte formation transforms the normally round humeral head into the characteristic clublike deformity.

FIGURE 2–32. Glenohumeral joint osteoarthritis confirmed by plain x-ray of the shoulder.

GLENOHUMERAL JOINT OSTEOARTHRITIS SUMMARY: Intra-articular injection enters 1⁄2 inch below the coracoid process and is directed outward toward the medial portion of the humeral head. Err toward the superior aspect of the joint to avoid the neurovascular bundle of the axilla. NEEDLE: 11⁄2 inch to 31⁄2 inch spinal needle, 22 gauge. DEPTH: 11⁄2 to 21⁄2 inches, down to periosteum of the humeral head or glenoid. VOLUME:

3 to 4 mL anesthetic and 1 mL K40.

NOTE: Fluoroscopy is strongly recommended in obese patients.

FIGURE 2–33. Glenohumeral joint osteoarthritis confirmed by aspiration of the shoulder.

SHOULDER

SUBLUXATION A loose glenohumeral capsule, a poorly developed deltoid muscle, and insufficiency of the rotator cuff tendons all contribute to the instability of the ball-and-socket joint and its suscep-

tibility to dislocation. Patients often describe a general looseness to the joint, anxiety when the shoulder is placed in the extremes of range of motion, and variable degrees of subluxation or frank dislocation.

SULCUS SIGN SUMMARY: The deltoid muscle arises from the acromion and attaches to the midhumerus. The supraspinatus tendon attaches to the greater tubercle. Downward movement of the humeral head is restricted by the tone and bulk of the deltoid, the tone and thickness of the supraspinatus tendon, and the redundancy of the glenohumeral capsule. This maneuver is used to assess the looseness of the shoulder joint, the looseness of the subacromial space (subluxation), and the patient’s potential tolerance of the pendulum stretch exercise. MANEUVER: The patient is asked to relax the shoulder. One hand is placed atop the acromion, and one hand is placed in the antecubital fossa. Downward pressure is applied to the arm to open the subacromial space. The examiner assesses the looseness of the shoulder and the discomfort of the maneuver.

FIGURE 2–34. Subluxation or hypermobility is confirmed by the sulcus sign on clinical examination.

INTERPRETATION: A tight shoulder—no movement with downward pressure—is seen with extreme guarding or tension due to pain, frozen shoulder, fibromyalgia, or an overly developed deltoid. Downward movement of 1⁄4 inch is considered average looseness. Downward movement of more than 1 ⁄2 inch indicates hypermobility (subluxation). When this downward displacement is accompanied by an abnormal movement of the humeral head in the anteroposterior direction, the term multidirectional instability is applied.

APPREHENSION TEST SUMMARY: The combination of an abnormal sulcus sign with an abnormal apprehension test (anterior movement of the humeral head) confirms the diagnosis of multidirectional instability. MANEUVER: The patient’s arm is carefully raised to the level of the shoulder. With one hand applying gentle pressure from behind, pressure is applied to the flexed elbow, rotating the shoulder externally. Apprehension experienced by the patient or anterior movement of the humeral head felt by the examiner strongly suggests anterior subluxation of the shoulder.

FIGURE 2–35. Apprehension test for multidirectional instability of the shoulder.

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ASSOCIATED SIGNS: Crepitation or a clicking can be demonstrated in some patients with passive circumduction of the shoulder. Anteroposterior movement of the humeral head (translation) can be demonstrated by forcefully grasping the humeral head and moving it in the anterior and posterior directions while holding the acromion in a fixed position. Extremely loose shoulders may be dislocated in the office.

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SUBSCAPULAR BURSITIS Exaggerated scapulothoracic

movement associated with loss of normal glenohumeral mobility causes friction between the bony thorax and the underside of the scapula. Subscapular bursitis is associated primarily with frozen

shoulder, glenohumeral osteoarthritis, or any other condition limiting the normal range of motion of the shoulder. The diagnosis is based on localized tenderness just under the superomedial angle of the scapula at the level of the second and third rib.

PALPATION OF THE SUBSCAPULAR BURSA OBJECTIVE: Local tenderness atop the second and third ribs directly under the superior medial angle of the scapula is the hallmark of subscapular bursitis. MANEUVER: The ipsilateral arm is fully abducted; the patient is asked to place the hand on the contralateral shoulder. The superior medial angle of the scapula and the center of the ribs are marked with a pen. Bursal tenderness is palpated directly over the rib closest to the angle of the scapula. ADDITIONAL SIGNS: Levator scapula, rhomboid, and trapezius muscle tenderness and spasm often accompany acute bursitis. A snapping sensation or popping may be evident with circumduction of the shoulder. Signs of primary shoulder or neck disorders may be present on exam.


INTERPRETATION: A half dollar–sized area of tenderness at the superior medial angle is most commonly caused by subscapular bursitis as opposed to the generalized muscular tenderness of the strain of the upper back muscles. Primary involvement of the rib or the scapula must be considered in the case of the patient with a known primary cancer (e.g., breast, lung, prostate).

LOCAL ANESTHETIC BLOCK SUMMARY: Local anesthetic block is used to distinguish subscapular bursitis from upper back muscular strain, referred pain from the neck, and primary involvement of the bony thorax. Enter directly over the second or third rib, whichever is closest to the superomedial angle of the scapula. NEEDLE:


DEPTH: 3⁄4 to 11⁄4 inch down to the periosteum of the rib. VOLUME:

1 to 2 mL anesthetic, 1 mL K40, or both.

NOTE: Place one finger above and one finger below the rib in the intercostal spaces and directly over the center of the rib. Never advance the needle more than 1 to 11⁄4 inches (pleura). FIGURE 2–37. Local anesthetic block of the subscapular bursa.

SHOULDER

SHOULDER PAIN REFERRED FROM THE NECK Trapezial

cervical strain and cervical radiculopathy account for 15% of patients who complain of shoulder pain.

BODY LANGUAGE SUMMARY: Approximately 15% of patients complaining of shoulder pain have a neck or upper back muscle source of their pain. Furthermore, patients with moderate to severe rotator cuff tendonitis, glenohumeral arthritis, or higher-degree AC separations can have concomitant cervical strain; the supporting muscles of the neck flare with the tension and pain caused by the shoulder. Patients whose pain is aggravated solely by neck rotation or lateral bending rather than shoulder reaching, pushing, pulling, and lifting usually have an isolated cervical strain or cervical radiculopathy. Note that each of the three lowest cervical roots can refer pain over the shoulder or the upper scapular area.

FIGURE 2–38. Body language of the patient complaining of primary neck symptoms.

CERVICAL SPINE MRI CASE: This 43-year-old woman complained of an acute onset of arm pain, numbness of the fingers, and stiffness of the neck. The pain radiated from the base of the neck, through the shoulder, down the arm, and into the hand. She experienced constant numbness and tingling of the first three digits. Her examination showed paraspinal tenderness between the spinous and transverse processes of the lower neck, endpoint stiffness with guarding when rotating the neck to the affected side, weakness of elbow flexion, and a diminished bicipital reflex. DIAGNOSIS: Cervical radiculopathy due to a C5–6 disk herniation. DISCUSSION: Cervical radiculopathy due to disk herniation should be suspected in the younger patient with acute symptoms, sensorimotor findings on neurologic examination, or cervical radiculopathy empirically treated with manual traction but with a poor response.

FIGURE 2–39. Cervical spine MRI confirming a herniated nucleus pulposus.

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SHOULDER PAIN REFERRED FROM THE CHEST OR ABDOMEN Referred pain to the shoulder from a medical condi-

tion in the chest or abdomen is nearly always distinguished by the characteristic associated symptoms of cough, nausea, and palpitation.

SHOULDER PAIN CASE: This 24-year-old suffered a fall from a ladder landing on the left side of the chest. Immediate pain developed along the chest wall, followed by chest and shoulder pain aggravated by deep breathing. DIAGNOSIS: Fractured ribs number 7 and 8, hemothorax, pneumothorax, and subcutaneous emphysema. DISCUSSION: Approximately 1% of shoulder pain is caused by primary involvement of the heart, great vessels, lungs, pleura, or upper abdomen. These nonskeletal diagnoses are readily identified by the associated symptoms that accompany the shoulder pain, reflecting the abnormal function of the major organ system.

FIGURE 2–40. Shoulder pain referred from the pleura and lung.

SHOULDER

2–1

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DIAGNOSIS


Isometrically performed resisted midarc abduction or external rotation

1. Rotator cuff tendonitis

Local anesthetic placed in the subacromial bursa; no significant muscle weakness

2. Impingement syndrome

Local anesthetic placed in the subacromial bursa

Rotator cuff tendonitis with tear

Local anesthetic placed in the subacromial bursa with persistent muscle weakness

Frozen shoulder

Local anesthetic placed in the subacromial bursa with persistent loss of range of motion

The passively performed painful arc maneuver Local subacromial tenderness The passively performed painful arc maneuver Local subacromial tenderness Weakness of midarc abduction or external rotation Isometrically performed resisted midarc abduction or external rotation The passively performed painful arc maneuver Local subacromial tenderness Loss of external rotation or abduction with endpoint stiffness Abnormal Apley scratch sign

No radiographic evidence of glenohumeral arthritis

Inability to reach overhead Loss of external rotation or abduction with endpoint stiffness

Glenohumeral osteoarthritis

Radiographic evidence of glenohumeral arthritis

Bicipital tendonitis

Local anesthetic placed in the bicipital groove

Rupture of the long head of the biceps

Examination

Multidirectional instability of the shoulder (subluxation)

Examination

AC joint arthritis

Shoulder series x-ray

Local tenderness at the AC joint

AC joint injury

Weighted views of the shoulder or local anesthetic placed over the AC joint

Pain aggravated by passive adduction

1st-degree separation

AC joint opens with traction applied at the elbow

2nd-degree separation

AC joint deformity: the clavicle is elevated above the acromion

3rd-degree separation

Local tenderness at the SC joint

SC joint arthritis

Apical lordotic views of the chest, local anesthetic placed over the SC joint


Local anesthetic placed over the adjacent 2nd or 3rd rib

Abnormal Apley scratch sign Inability to reach overhead Bicipital groove tenderness Pain aggravated by resisted elbow flexion “Popeye” deformity in the antecubital fossa Pain aggravated by resisted elbow flexion Inability to reach overhead ⫹Sulcus sign with downward traction applied at the elbow Abnormal anteroposterior movement of the humerus (translation) Apprehension with passive rotation of the shoulder Bony enlargement of the AC joint Local tenderness at the AC joint Pain aggravated by passive adduction

Pseudoenlargement of the clavicle Tenderness under the superior medial angle of the scapula No tenderness of the rhomboid or levator scapula muscles

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COMMON SHOULDER FRACTURES SUMMARY Fractures of the shoulder are not common, and those that do occur are seen in very specific age groups. Fractures of the humerus constitute approximately 2% of all fractures. The incidence increases with age and with osteoporosis (especially in the humeral neck). Humeral fractures are classified according to location: proximal neck, humeral shaft, and supracondylar. The proximal neck and humeral shaft fractures are grouped together, separate from the supracondylar fractures, because they are usually treated nonoperatively. Supracondylar fractures are more complex, can involve the elbow joint, and may necessitate open fixation.

Fracture of the clavicle is the most common fracture of childhood and is a very common fracture in shoulder girdle trauma in adults. These fractures are classified according to location (proximal-, middle-, and distal-third fractures), involvement of the adjacent articular cartilage of the SC or AC joint, and position of distal fractures relative to the coracoclavicular ligaments. Fracture of the middle third is the most common (80%). The second most common fracture is the interligamentous, nondisplaced fracture of the distal third (10%). Displacement of the clavical fracture fragments depends on the pull of the sternocleidomastoid muscles (the proximal fragments are pulled superiorly) and the pectoralis major muscles (the distal fragments drop forward).

SHOULDER DISLOCATION SUMMARY: Dislocation of the shoulder is not common. Multidirectional instability of the shoulder, rotator cuff insufficiency from chronic tendonitis, and rotator cuff tears are predisposing factors. Dislocations are classified as anterior, posterior, or inferior. The anterior dislocation is most common. Seventy percent occur in patients less than 30 years old. REDUCTION AND IMMOBILIZATION: The three methods for reduction are the traction–countertraction, Hennipen, and Stimson methods. All require intravenous sedation with narcotics and a muscle relaxant. After successful reduction, a shoulder immobilizer or sling and swath immobilization is used for 3 weeks. This is followed by range of motion exercises to prevent frozen shoulder.

FIGURE 2–41. Shoulder dislocation.

SURGICAL REFERRAL: Referral is necessary for rotator cuff tears, fracture of the greater tuberosity larger than 1 cm, and glenoid rim fractures displaced more than 5 mm. PROGNOSIS: The most common complication is recurrent dislocation (60%). Other complications include rotator cuff tears, greater tuberosity fracture, glenoid rim fracture, axillary nerve damage, brachial plexus damage, humeral head fracture, and biceps rupture.

SHOULDER

GREATER TUBERCLE FRACTURE SUMMARY: This 72-year-old woman fell and fractured the greater tubercle of the humeral head, which failed to heal, and normal anatomic alignment was not achieved. The abnormality has led to chronic impingement with an inability to abduct the shoulder more than 60 degrees. Surprisingly, she never developed any clinical episodes of rotator cuff tendonitis. IMMOBILIZATION: The patient was treated with a long arm hanging cast with collar and cuff followed by physical therapy exercises. SURGICAL REFERRAL: Acromioplasty is the treatment of choice for chronic impingement. PROGNOSIS: The patient declined surgical intervention; she has adjusted to her postfracture limitations.

FIGURE 2–42. Greater tubercle fracture of the humeral head.

FRACTURES OF THE HUMERAL NECK SUMMARY: Proximal neck fractures are classified as two-part, three-part, or four-part fractures with or without dislocation of the shoulder joint (Neer classification). Humeral shaft fractures are classified by fracture line (spiral, transverse, longitudinal, comminuted) and by location relative to the pectoralis and deltoid insertions. IMMOBILIZATION: Neck fractures are treated with a long arm hanging cast with collar and cuff followed by physical therapy exercises. The cast is adjusted by lengthening the sling and its position at the wrist to correct for any angulation.

FIGURE 2–43. Fractures of the humeral neck.

SURGICAL REFERRAL: Internal fixation is necessary for neck fractures showing dislocation of the shoulder, fragment displacement greater than 1 cm, or fragment angulation greater than 45 degrees and for shaft fractures that are open, severely comminuted, or transverse (where there is a higher degree of nonunion). PROGNOSIS: Complications include frozen shoulder (proximal neck fractures), chronic impingement (angulation of the greater tubercle), osteoarthritis of the shoulder (fracture or dislocation), radial nerve injury (lower-third shaft fractures), brachial artery injury (shaft fractures), nonunion (transverse and comminuted shaft fractures).

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CLAVICLE FRACTURES SUMMARY: Fractures of the clavicle are classified according to location: proximal, middle, and distal third. Fractures of the proximal third are classified as nondisplaced, displaced, or intra-articular. All middle-third fractures are grouped together. Fractures of the distal third are classified according to displacement, location relative to the coracoclavicular ligaments, and whether the fracture line enters the AC joint. IMMOBILIZATION: The shoulder is immobilized in a simple sling or figure-of-eight splint, and adjustments are made in order to maintain close approximation of the fragments.

FIGURE 2–44. Clavicle fractures.

SURGICAL REFERRAL: Surgery must be considered in the case of any fracture associated with first rib, pneumothorax, or neurovascular injury (less than 3%); in distal third fractures with displacement (because of the greater risk of nonunion); and in poorly healing fractures that are complicated by shoulder dysfunction or chronic pain. PROGNOSIS: Complications include dislocation of the AC or SC joint; head and neck injuries (displaced fractures); first rib fracture; pneumothorax (3%); brachial plexus injury (caused by severe and forceful blows in a downward direction); subclavian vessel or internal jugular vein injuries (caused by rare, severe blows); nonunion, which is rare; and malunion with cosmetic deformity, which is common.

SHOULDER

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CLINICAL PEARLS • Impingement is a universal problem. • Impingement syndrome, as a separate diagnosis, is determined by the two impingement maneuvers: the painful arc maneuver and subacromial tenderness. • Impingement signs are always present with active rotator cuff tendonitis. • Subtle impingement can be brought out by internally rotating the upper arm (thumb down), bringing the greater tubercle into closer contact with the undersurface of the acromion. • Active rotator cuff tendonitis is distinguished from pure impingement syndrome by the isometric resistance testing of the individual rotator cuff tendons (i.e., resisting midarc abduction, as in supraspinatus tendonitis). • The patient’s susceptibility to impingement correlates directly with the acromial angle. • The subacromial bursa and the synovial cavity of the shoulder are not connected. The two fluid-filled structures are separated by the rotator cuff tendons. Radiopaque dye injected into the synovial cavity will enter the subacromial bursa only when a full-thickness tear in the supraspinatus or infraspinatus is present. • Common shoulder tendonitis accounts for 70% of all shoulder diagnoses. • Common shoulder tendonitis most often affects the supraspinatus tendon; of the four rotator cuff tendons, it is the most susceptible to impingement because of its unique anatomic position between the acromial process and the humeral head. • Uncomplicated rotator cuff tendonitis is a tendon inflammation that is not complicated by frozen shoulder

•

•

•

•

• •

(10%), AC joint osteoarthritis (5%), rotator cuff tendon tear (1% to 2%), or glenohumeral arthritis (less than 1%). Risk factors for rotator cuff tendon tear include mucinoid degenerative thinning of the tendon, a narrowed subacromial space on plain x-rays of the shoulder, a fall to an outstretched arm or directly onto the shoulder, weakness of external rotation or abduction that is not attributable to pain, multiple episodes of recurrent or chronic tendonitis, a previous tendon rupture, systemic steroids, rheumatoid arthritis or other connective tissue disease, and improper placement of a corticosteroid injection. Four diagnostic tests are used to confirm a rotator cuff tendon tear: the subacromial lidocaine injection test, which relieves pain and demonstrates persistent weakness; arthrography of the glenohumeral joint; diagnostic ultrasound; and MRI. The clinical examinations of frozen shoulder and glenohumeral osteoarthritis are identical. Shoulder x-rays are normal with pure frozen shoulder and demonstrate cartilaginous wear, osteophytes, and subchondral sclerosis with osteoarthritis. Whereas osteophyte formation is variable in osteoarthritis of the hip, knee, back, and neck, 99% of patients with osteoarthritis of the glenohumeral joint demonstrate spurring off the inferior aspect of the humeral head. AC joint arthritis is a universal problem, increasing in frequency with increasing age. SC swelling and subluxation are nearly always misinterpreted as an enlarged proximal end of the clavicle.

CHAPTER 3: UPPER BACK DIFFERENTIAL DIAGNOSIS Diagnoses Upper back muscular strain (most common diagnosis) Stress Dorsokyphotic posture Fibromyalgia Scoliosis Reactive muscular strain Radiculopathy

Thoracic spine radiculopathy Vertebral body fracture Spinal cord injury or tumor Herniated nucleus pulposus Osteomyelitis or epidural process

Socioeconomic or psychological issues Typical posture seen in older adults or in patients with depression Confirmation by exam: multiple trigger points; normal lab Posteroanterior and lateral full-length spine x-rays The underlying spinal column, nerves, or cord pathology Neurologic testing Bone scan or magnetic resonance imaging (MRI)

X-ray: thoracic spine x-rays Bone scan or MRI MRI MRI MRI

Posterior chest wall Rib contusion or fracture Epidemic pleurodynia

Chest and tangential rib x-rays Local anesthetic block



Referred pain Cervical radiculopathy Primary lung disease (e.g., pneumonia, pulmonary embolus) Thoracic aortic aneurysm Takayasu’s arteritis Coronary arteries

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Confirmations

Neck x-rays, MRI, electromyography Chest x-ray, lung scan, computed tomography scan Chest x-ray Erythrocyte sedimentation rate, angiogram Electrocardiogram, creatine phosphokinase, angiogram

UPPER BACK

INTRODUCTION Upper back muscular strain is the dominant condition affecting the thoracic spine area. Muscular strain caused by tension, stress, dorsokyphotic posture, or whiplash is nearly as common as its analogous condition in the neck, cervical strain. This condition often overshadows the much less common intrinsic thoracic spine conditions. Less common conditions affecting the upper back pain include posterior rib and intercostal muscle injuries and the conditions that affect primarily the lung and pleura. As opposed to arthritis of the cervical and lumbar spine, arthritis of the thoracic spine is unusual outside the setting of primary scoliosis and the inflammatory spondyloarthropathies. The diagnosis of an uncomplicated upper back muscular strain caused by tension, stress, or poor posture is not difficult. Signs and symptoms are limited to the supporting muscles of the upper back, including the trapezius, levator scapula, and rhomboid muscles. The muscles are tender, and the movement of the upper back is limited by muscular spasm in the case of an uncomplicated muscular strain. There is a conspicuous absence of bony tenderness and radicular signs. This is in stark contrast to reactive muscular strain that is the direct result of an underlying threat to the spinal column. As with the intrinsic conditions affecting the cervical and lumbar spine, any condition threatening the bony integrity of the spinal column, the function of the spinal nerve, or the integrity of the spinal cord causes severe degrees of muscle spasm and focal midline tenderness. In assessing the patient with upper back muscular symptoms, the challenge to the primary care provider is to distinguish simple upper back muscular strain from the severe reactive muscle spasm that represents the body’s response to a serious underlying neurologic process. Intrinsic conditions affecting the upper back, including vertebral body compression fracture, osteomyelitis and epidural abscess, metastatic involvement of the vertebral body, and other fractures of the spinal column, are the most serious conditions in the differential diagnosis of upper back pain. Fortunately, these conditions are not common. They are identified by focal, midline tenderness over the spinous processes, severe reactive muscular strain, and radicular pain radiating around the chest wall. Pain referred to the upper back is common. Pneumonia, pulmonary embolus, thoracic aortic aneurysm, and rarely primary heart disease cause varying degrees of back pain. In addition, each of the lower cervical roots has an expression of pain over the scapula and posterior shoulder areas. The diagnosis of the early presentation of spinal nerve compression from spinal levels C5 through C7 can be very elusive. These minor sensory radiculopathies cause a vaguely described pain over the upper back that may not necessarily be accompanied by a significant degree of paresthesias or hypesthesias. Subscapular bursitis, a unique inflammation between the scapula and the underlying ribs, is an uncommon cause of upper back pain. It is typically secondary to loss of normal function at the shoulder or a reflection of intrinsic disease of the cervical spine.

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SYMPTOMS Conditions directly affecting the upper back cause pain, tension, and muscle spasm. Diffuse upper back pain is the most common pain pattern. This pattern results from the irritation and spasm of the one or both of the muscular layers that cover the bony thorax and scapula. The three divisions of the trapezius muscle—the superior, middle, and lower—form the outermost layer and the rhomboid major, rhomboid minor, and levator scapula muscles form the inner layer. The superior division of the trapezius is the most commonly affected muscle. Its characteristic pain is centered approximately halfway between the cervical spinous processes and the acromion. By contrast, the pain caused by spasm of the rhomboids or levator scapula muscles is deeper and described vaguely between the scapulae, typically centered between the spinous processes and the medial border of the scapula. This clinical presentation is nearly identical to the pain arising from muscle spasm from the middle and lower divisions of the trapezius. Most cases of upper back muscular spasm are caused by poor posture, stress, or fibromyalgia. In a minority of cases muscular symptoms reflect an underlying intrinsic process affecting the thoracic spine. Reflex muscular spasm may be a sign of structural disease of the spine (scoliosis, kyphosis, or compression fracture) or infiltrative disease (e.g., metastatic disease, osteomyelitis). Focal upper back pain, the size of a half dollar and located near the top of the scapula, is the classic presentation of subscapular bursitis. This is a friction point between the superior medial angle of the scapula and the underlying ribs. Its clinical presentation is identical to the pain pattern and local tenderness of levator scapula muscular strain. Local anesthetic placed either at the level of the rib or within the levator scapula muscle is necessary to distinguish the two conditions. Sharp pain aggravated by coughing or lying on the sides is characteristic of pain arising from the bony thorax (ribs, costal cartilage, or sternum). Pain arising from these local musculoskeletal areas must be distinguished from the pain arising from the underlying lungs (e.g., pleurisy, pneumonia, pulmonary embolus) or vascular structures (aortic aneurysm). Upper back pain without local tenderness (e.g., not aggravated by direct pressure, massage fails to identify a pressure point) is most often referred from the direct irritation of the cervical nerve roots. All three lower cervical spinal nerves refer pain over the scapula or posterior aspect of the deltoid muscle. This referred pain from cervical radiculopathy that is unassociated with hand paresthesias or an upper extremity lancinating pain often is overlooked by many health care providers and mistakenly diagnosed as a mild upper back muscular strain. Central upper back pain is characteristic of involvement of the spinal column. Compression fracture, osteomyelitis of the vertebral body, epidural abscess, or metastatic lesions involving the vertebral body present with varying degrees of pain and spinal nerve irritation. The combination of central back pain and pain that radiates around the chest wall should always suggest either thoracic radiculopathy or the preeruptive phase of shingles.

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BOX 3-1

ESSENTIAL EXAMINATION OF THE UPPER BACK 1. Note the patient’s posture, the ease or difficulty in moving from the chair to the exam table, and the patient’s breathing pattern. 2. Perform a complete exam of the lung, pleura, and heart if back pain is accompanied by shortness of breath, pleurisy, cough, hemoptysis, or palpitations. 3. Palpate the trapezius, levator scapulae, and rhomboid muscles.

EXAMINATION The examination of the upper back begins with general observations of the patient’s movement, resting posture, and breathing pattern. Cautious movement, poor posture, and labored breathing define the involvement of the chest wall. Labored breathing associated with cough, frank shortness of breath, hemoptysis, and pleuritic-like pain demands full evaluation of the lungs, pleura, heart, and great vessels. Palpation of the classic trigger points located between the medial border of the scapula and the vertebral spinous processes identifies the degree of upper back muscular strain involving the trapezius, levator scapulae, and rhomboid muscles. Palpation of the second and third ribs just under the superior medial angle of the scapula defines the degree of subscapular bursitis. Palpation of the spinous processes of thoracic spine suggests an intrinsic process involving the spinal column (vertebral body compression fracture, osteomyelitis and epidural abscess, metastatic involvement of the vertebral body, and other fractures of the spinal

4. Perform the chest compression test. 5. Measure the patient’s height. 6. Palpate the second and third ribs just under the superior medial angle of the scapula. 7. Perform an essential exam of the neck if radiculopathy is suggested.

column). Finally, referred pain from the lungs, pleura, heart, or great vessels or the lower cervical nerve roots should be considered if the upper back pain is unassociated with local tenderness over the muscles or the adjacent bones. ONE-MINUTE SCREENING EXAM: MANEUVERS ASSESSING OVERALL UPPER BACK FUNCTION AND DIFFERENTIAL DIAGNOSIS The next eight maneuvers represent the minimal examination of the patient presenting with upper back symptoms. Function testing, height measurement, and screening maneuvers for muscle spasm, conditions affecting the bony thorax, and intrinsic conditions to the vertebral column provide enough information to triage to x-ray, order appropriate labs, suggest general treatment recommendations, or proceed to more detailed examination and treatment.

GENERAL MOVEMENT SUMMARY: Movement difficulties in the exam room, difficulty in performing simple tasks such as removing a T-shirt, or the ease or difficulty in changing position on the exam table can be the first clue to the diagnosis of an upper back condition. MANEUVER: Without prompting, the patient’s general movement is observed, including the ease of movement and the consistency of the arm and torso motion. INTERPRETATION: Cautious movement, general stiffness, and restricted movement of the upper back and neck are characteristic of significant muscle irritation and spasm. Great disparities between the examiner’s first observations of posture and general movement and function can be the clue to malingering. FIGURE 3–1. General movement of the upper back.

UPPER BACK

INSPECTION SUMMARY: The normal curves of the back include cervical lordosis, thoracic kyphosis, and lumbar lordosis. The normal kyphotic curve can be affected by acute muscular spasm, scoliosis, and compression fracture. MANEUVER: The patient’s overall posture, the degree of thoracic kyphosis, and the position of the head, neck, and upper back are inspected from the side. Then, the patient is asked to sit up as straight as possible, and the positions of the head, neck, and upper back are reassessed. INTERPRETATION: Because age, depression, compression fracture, and scoliosis affect the normal thoracic kyphotic curve in the same way (exaggerating the curve), radiographic studies are necessary to define the exact underlying cause. FIGURE 3–2. Inspection of the patient’s upper back posture.

BREATHING PATTERN SUMMARY: Splinting, shallow breathing, and painful cough are clues to the conditions affecting the bony thorax (the sternum, the costal cartilages, the ribs), the vertebral bodies, and the underlying lung and pleura. MANEUVER: Observations with and without distraction are made of the patient’s ability to move about the exam room, the ability to adjust the examination gown, and the patient’s breathing pattern. INTERPRETATION: Shallow breathing or splinting indicates chest wall injury, most commonly to the bony ribs, but is also characteristic of pleurisy, pneumonia, pulmonary embolism, and inflammatory pleural effusion. FIGURE 3–3. Breathing pattern, splinting with injury to the thorax.

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PALPATION OF THE TRAPEZIUS MUSCLE OBJECTIVE: The trapezius muscle is divided into superior, middle, and lower third. Because of its intimate relationship with the neck and shoulder, muscular spasm most often affects the superior portion. Palpation of the upper third provides the optimal screening of muscular spasm. MANEUVER: Focal tenderness of the trapezius muscle usually is located halfway between the base of the neck and its attachment to the distal acromion. Firm pressure is applied at this site to determine the degree of tenderness and muscular spasm.

FIGURE 3–4. Palpation of the trapezius muscle.

INTERPRETATION: Acute trapezial spasm (intense local tenderness and moderate spasm) is seen with acute emotional or physical stress, cervical strain and radiculopathy, whiplash, and acute rotator cuff tendonitis. Chronic symptoms (mild tenderness and rock-hard muscular spasm) are characteristic of fibromyalgia, age-related dorsokyphotic posture, and chronic cervical radiculopathy.

PALPATION OF THE SUBSCAPULAR BURSA SUMMARY: The subscapular bursa is located underneath the scapula, acting as a natural protective pad between the ribs and scapula. For the examiner to palpate the bursa, the arm must be fully abducted, moving the scapula laterally and thus exposing the underlying bursa. MANEUVER: The superior medial angle of the scapula is marked with a pen. The patient is asked to place the hand on the contralateral shoulder (full adduction exposes the bursa). The ribs closest to the angle of the scapula are palpated for focal tenderness. INTERPRETATION: A half dollar–sized area of tenderness at the superior medial angle must be distinguished from strain of the trapezius muscle, spasm of the levator scapulae and rhomboid muscles, and primary involvement of the ribs. FIGURE 3–5. Palpation of the subscapular bursa.

UPPER BACK

HEIGHT MEASUREMENT SUMMARY: Height is determined by the curves of the back, the shape of the vertebral bodies, the intervertebral disk spaces, and posture. This is the most objective measurement of any condition that affects the structural integrity of the spinal column. MANEUVER: Serial heights should be performed in bare feet, with the patient standing as straight as possible. INTERPRETATION: Serial loss of height is seen with normal aging, degenerative arthritis, compression fracture, and scoliosis. A decrease in height of 1⁄2 inch over a 6- to 12-month period suggests that the patient’s spinal disorder is progressing. Patients with structural conditions affecting the spine, especially scoliosis, should undergo repeat standing radiographs if height continues to decrease.

FIGURE 3–6. Height measurement to assess the integrity of the spinal column.

CHEST COMPRESSION TEST SUMMARY: The bony thorax consists of the sternum, the costal cartilages, the ribs, and the vertebral bodies. Anteroposterior compression of the chest is the optimal screening maneuver to assess the integrity of the bony thorax. MANEUVER: Compression of the chest wall is first applied in an anteroposterior direction. The palmar eminences are placed over the middle of the sternum and over the spinous processes of T5 and T6 vertebra. The maneuver can be repeated with the palms placed obliquely across the chest or from side to side depending on response.

FIGURE 3–7. Chest compression test to assess the integrity of the bony thorax.

INTERPRETATION: A positive chest compression test is seen with any significant injury to the thorax, including rib contusions, rib fracture, nondisplaced rib fracture, costochondritis, and sternal fracture.

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PALPATION OF THE VERTEBRAL BODY SUMMARY: Patients with osteoporosis, known malignancy, or recent trauma are at the greatest risk of direct involvement of the vertebral body. Each individual spinous process must be palpated if the patient describes midline back pain. MANEUVER: Each spinous process is palpated with the index finger. This is followed by gentle fist percussion of each vertebral level if tenderness is not elicited by palpation.

FIGURE 3–8. Palpation of the vertebral body for focal tenderness.

ONE-MINUTE SCREENING EXAM: MANAGEMENT OPTIONS TRIAGE TO X-RAY The patient has a history of trauma, is at risk of bony injury, or has lost 1⁄2 inch of height in the last 6 to 12 months: • Order a chest x-ray and cardiogram if breathing is impaired (pneumonia, pulmonary embolus, angina, coronary artery disease). • Order a chest x-ray and tangential views of the ribs if the patient has sustained a blow to the chest wall (rib contusion, rib fracture). • Order a chest x-ray and thoracic spine views if focal vertebral pain and tenderness are noted on exam (compression fracture, bony metastasis, osteomyelitis, and epidural abscess). • Order posteroanterior and lateral films of the entire spine if the patient has lost 1⁄2 inch in height in the last 6 to 12 months (scoliosis, compression fracture). • Order a chest x-ray and thoracic spine films if the patient describes pain wrapping around the chest wall (compression fracture, metastatic disease, epidural abscess, primary disease of the spinal cord).

TRIAGE TO THE LAB For patients with back pain, fever, and significant respiratory insufficiency: • Order a chest x-ray, complete blood cell count, erythrocyte sedimentation rate, and blood cultures for patients with acute back or chest pain, exquisite vertebral body tenderness, or an acute change in respiratory function (pneumonia, acute osteomyelitis, epidural abscess).

INTERPRETATION: Primary involvement of the vertebral bodies is not common. Acute compression fractures occurring between thoracic level T12 and T7 are most commonly due to osteoporosis or blunt trauma. Compression fractures occurring above thoracic level T6 are uncommon and must be considered pathologic (due to malignancy) until proven otherwise.

CONSIDER A BONE SCAN For patients with acute vertebral body pain, persistent rib pain, or chest wall pain and a history of cancer (compression fracture, miscellaneous fractures of the spine, osteomyelitis, rib contusion or fracture, and metastatic disease). CONSIDER MRI For patients with focal vertebral body pain, radicular pain wrapping around the chest wall, or back pain and fever (compression fracture, miscellaneous fractures of the spine, osteomyelitis, and metastatic disease). RECOMMEND EMPIRICAL TREATMENT The patient has mild to moderate upper back pain and stiffness. Activities of daily living have not been affected. Symptoms have been present for less than 2 months. The breathing pattern is unaffected. • • • • • •

Limit reaching, lifting, pushing, and pulling. Attend to proper sitting posture. Avoid stress. Apply ice packs up to four times a day. Prescribe a muscle relaxer for 7 to 10 consecutive nights. Reexamine the patient if symptoms do not improve.

DETAILED EXAMINATION: SPECIFIC UPPER BACK DIAGNOSES Perform a detailed examination of the upper back if the following changes have occurred: The patient has persistent or chronic symptoms. There has been an injury. The patient’s height has decreased by 1⁄2 inch over the course of the last 6 to 12 months. Breathing is impaired, or respiratory function has deteriorated.

UPPER BACK

MUSCULAR STRAIN OF THE TRAPEZIUS, RHOMBOIDS, OR LEVATOR SCAPULA Acute muscular

strain is the dominant diagnosis in the upper thoracic area. The upper trapezius, rhomboids, and levator scapula are the most

commonly affected muscles. An exact anatomic diagnosis is based on the characteristic points of focal muscular tenderness combined with local anesthetic placed in the muscle belly.

PALPATION OF THE TRAPEZIUS MUSCLE SUMMARY: The trapezius muscle is divided into superior, middle, and lower thirds. The muscle originates from the spinous processes and inserts on the distal acromion process. MANEUVER: Focal tenderness of the trapezius muscle usually is located halfway between the base of the neck and its attachment to the distal acromion. Firm pressure is applied at this site to determine the degree of muscular spasm and tenderness. ASSOCIATED SIGNS: Passive ipsilateral rotation and contralateral bending of the neck place the trapezius under tension, aggravating the muscle spasm. Local tenderness involving the middle and lower thirds occurs with severe or chronic involvement.

FIGURE 3–9. Palpation of the trapezius muscle.

INTERPRETATION: Acute trapezial spasm (intense local tenderness and moderate spasm) is seen with acute emotional or physical stress, cervical strain and radiculopathy, whiplash, and acute rotator cuff tendonitis. Chronic symptoms (mild tenderness and rock-hard muscular spasm) are characteristic of fibromyalgia, age-related dorsokyphotic posture, and chronic cervical radiculopathy.

PALPATION OF THE LEVATOR SCAPULA AND RHOMBOID MUSCLES SUMMARY: The levator scapula originates from the uppermost spinous processes of the thoracic spine and angles inferiorly to the superior medial angle of the scapula. The rhomboids originate from the spinous processes, are located inferior to the levator scapula, and attach to the medial border of the scapula. MANEUVER: The patient is asked to sit up. The muscles are palpated halfway between the spinous processes and the medial scapular border, beginning just above the level of the superior medial angle of the scapula and extending to the level of the inferior angle. ASSOCIATED SIGNS:

FIGURE 3–10. Palpation of the levator scapula and rhomboid muscles.

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None.

INTERPRETATION: Irritation and spasm of the levator scapula and rhomboid muscles are the most common cause of interscapular pain and result from any of the causes of dorsokyphotic posture (e.g., aging, compression fracture, scoliosis).

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LOCAL ANESTHETIC BLOCK SUMMARY: Local anesthetic block is used to identify the muscle as a source of the upper back pain, rule out referred pain from the cervical spine, and rule out referred pain from the chest or abdomen. POSITIONING:

Sitting, relaxed shoulder.

SURFACE ANATOMY: Lateral edge of the acromion, the spinous processes, and the spine of the scapula. POINT OF ENTRY: Halfway between the distal acromion and the spinous processes. ANGLE OF ENTRY: NEEDLE:



DEPTH: 1⁄2 to 1 inch to the fascia and 1⁄4 inch into the muscle. FIGURE 3–11. Local anesthetic block placed in the superior division of the trapezius muscle.

ANESTHESIA: Ethyl chloride, skin: 1 mL at the dermal/fascia, 1 to 2 mL intramuscularly.

LOCAL ANESTHETIC BLOCK SUMMARY: Local anesthetic block is used to identify the muscle as a source of the upper back pain, rule out referred pain from the cervical spine, and rule out referred pain from the chest or abdomen. POSITIONING:

Sitting, relaxed shoulder.

SURFACE ANATOMY: The spinous processes and the medial border of the scapula. POINT OF ENTRY: Halfway between the spinous processes and the medial border of the scapula. ANGLE OF ENTRY: NEEDLE:


1 ⁄2 inch, 22 gauge. 1

DEPTH: ⁄2 to 1 inch to the fascia and 1⁄4 inch into the muscle. 1

FIGURE 3–12. Local anesthetic block placed in the rhomboid major muscle.

ANESTHESIA: Ethyl chloride, skin: 1 mL at the dermal–fascial interface, 1 to 2 mL intramuscularly.

UPPER BACK

SUBSCAPULAR BURSITIS Often overlooked because of its

hidden location under the superior medial angle of the scapula, this friction point between the undersurface of the scapula and the underlying ribs is easily diagnosed by local anesthetic placed just

over the adjacent rib. This focal inflammation usually results from the exaggerated shrugging that accompanies impaired mobility at the glenohumeral joint.

PALPATION OF THE SUBSCAPULAR BURSA OBJECTIVE: The scapula makes its closest contact with the underlying ribs at its superior medial angle. Exaggerated movement of the scapula (chronic shoulder conditions and C5 radiculopathy affecting the rotator cuff muscles) increases friction between the scapula and the ribs (subscapular bursitis). The subscapularis muscle originates from the undersurface of scapula and acts as a natural protective pad. MANEUVER: The superior medial angle of the scapula is marked with a pen. The patient is asked to place the hand on the contralateral shoulder (full adduction exposes the bursa). The ribs closest to the angle of the scapula are palpated for focal tenderness.


INTERPRETATION: A half dollar–sized area of tenderness at the superior medial angle must be distinguished from upper back muscular strain and primary involvement of the rib. If subscapular bursitis is diagnosed, it is necessary to identify the underlying cause, namely loss of the normal glenohumeral joint motion or cervical radiculopathy at C5 affecting the integrity of the rotator cuff muscles.

LOCAL ANESTHETIC BLOCK SUMMARY: Local anesthetic block is used to identify the subscapular bursa as the source of the upper back pain (as opposed to the trapezial or levator scapulae muscles), rule out referred pain from the cervical spine, and rule out referred pain from the chest or abdomen. POSITIONING: Sitting, relaxed shoulder, the ipsilateral hand placed on the contralateral shoulder. SURFACE ANATOMY: The underlying ribs and the superior medial angle of the scapula. POINT OF ENTRY: Directly over the rib that is closest to the superior medial border of the scapula. ANGLE OF ENTRY: NEEDLE: DEPTH: rib.



⁄2 to 1 inch down to the periosteum of the

1

ANESTHESIA: Ethyl chloride, skin: 1 to 2 mL at the level of the periosteum of the rib. FIGURE 3–14. Local anesthetic block placed in the subscapular bursa.

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SCOLIOSIS Midback pain is a common manifestation of scol-

iosis involving the thoracolumbar spine. The paraspinal muscles

are under constant tension, stretched beyond their normal length along the convexity of the curve.

HEIGHT MEASUREMENT SUMMARY: Scoliosis is defined as an S-shaped curvature of the spine over 10 to 15 degrees. All patients with significant curvature experience recurrent muscle spasm. Progressive increases in the angle of curvature cause increased muscular symptoms, progressive chest wall deformity, and gradual loss of height. MANEUVER: Serial heights should be performed in bare feet, with the patient standing as straight as possible. ADDITIONAL SIGNS: Paraspinal muscle spasm is nearly universal. If the curvature is associated with a rotational component, the paraspinal muscles on the convex side of the curve will appear enlarged. The paraspinal muscle enlargement can be enhanced by flexion at the waist (the paraspinal hump sign).

FIGURE 3–15. Height measurement to evaluate the progression of scoliosis.

INTERPRETATION: Serial loss of height is seen with normal aging, degenerative arthritis, compression fracture, and scoliosis. A decrease in height of 1⁄2 inch over a 6- to 12-month period suggests that the patient’s spinal disorder is progressing. Patients with structural conditions affecting the spine, especially scoliosis, should undergo repeat standing radiographs if height continues to decrease.

ANTEROPOSTERIOR SPINE X-RAY CASE: The patient has a family history of curvature of the back. She suffers episodes of middle and upper back pain that typically resolves slowly over several weeks. She describes her pain as a tightening of the back muscles. DIAGNOSIS: Congenitally acquired scoliosis with reactive muscle spasm. DISCUSSION: Muscular symptoms are the most common manifestation of scoliosis. The paraspinal muscles along the convex side of the curve are being stretched while the muscles on the concave side are foreshortened and susceptible to contracture.

FIGURE 3–16. Anteroposterior spine x-ray for measurement of the scoliosis curvature.

The curve is measured by extending parallel lines from the most involved vertebra, dropping perpendicular lines down to an intersection point, and using a protractor to determine the angle. After a baseline level is obtained at the time of presentation, a second measurement should be obtained at 1 year to see whether the process is stable or progressive. Repeat measurements are indicated if the patient’s height has decreased by 1 ⁄2 inch over the course of 6 to 12 months.

UPPER BACK

RIB CONTUSION AND FRACTURE Rib contusions or fractures involving the posterior ribs cause upper back pain. It is dramatically aggravated by deep breathing, coughing, sneezing, and direct pressure. The diagnosis is strongly suggested by focal tender-

ness over the affected ribs elicited by manual chest compression from the anteroposterior direction or pressure applied obliquely across the thorax.

CHEST COMPRESSION TEST SUMMARY: The bony thorax consists of the sternum, the costal cartilages, the ribs, and the vertebral bodies. MANEUVER: Compression of the chest wall is first applied in an anteroposterior direction. The palmar eminences are placed over the middle of the sternum and over the spinous processes of T5 and T6 vertebra. The maneuver can be repeated with the palms placed obliquely across the chest or from side to side depending on response. ADDITIONAL SIGNS: With the patient in the decubitus position, pressure applied over the mid- to lower thorax causes intense pain. Rib fracture associated with pneumothorax can produce subcutaneous emphysema (air dissecting into the soft tissues of the chest). Superficial bruising is variable. FIGURE 3–17. Chest compression test to assess the integrity of the bony thorax.


RADIOGRAPH OF THE CHEST CASE: This 55-year-old man fell 8 feet off a ladder and landed on concrete on his left side. There was immediate localized chest pain and local bruising. Because of a history of coronary artery disease with arrhythmia, the patient was admitted to the coronary care unit for observation. The patient complained of persistent left lateral chest pain aggravated by deep breathing, lying on the left side, and coughing. DIAGNOSIS: A displaced rib fracture is seen in the posterior aspect of the seventh rib. Serial chest x-rays looking for an accompanying pleural effusion (hemothorax) were negative. DISCUSSION: Because of the thinness of the bone and the overlying tissues, nondisplaced rib fractures (cracks) are difficult to identify on plain chest x-rays. Serial chest x-rays or special tangential rib views may disclose a fracture only when the fracture begins to heal (the osteoblastic phase). FIGURE 3–18. Chest x-ray demonstrating rib fracture.

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INTERCOSTAL NERVE BLOCK FOR RIB FRACTURE SUMMARY: Local anesthetic block is used to reduce the intense pain in patients with acute rib fracture, to palliate the pain of bony metastases, and as a local anesthetic block to determine the origin of the patient’s pain, thus helping to distinguish rib pain from soft tissue involvement. POSITIONING:

Sitting or lying down.

SURFACE ANATOMY: Superior and inferior edges of the rib, the intercostal space, and the muscle. POINT OF ENTRY: Just below the inferior edge of the rib on the proximal side of the fracture (i.e., between the fracture site and the spine). ANGLE OF ENTRY: NEEDLE:



DEPTH: ⁄2 to 3⁄4 inch to the rib and 1⁄4 inch further to the underside of the rib. 1

FIGURE 3–19. Intercostal nerve block for rib fracture.

VERTEBRAL BONY LESIONS Compression fractures due to

osteoporosis are common in the lower thoracic and lumbar spine and uncommon in the upper thoracic spine. Fractures affecting the

ANESTHESIA: Ethyl chloride, skin: 1 mL at edge of the rib and 1 to 2 mL underneath the rib.

T6–T1 vertebral bodies should be considered pathologic (metastatic or septic) until proven otherwise.

PALPATION OF THE SPINOUS PROCESSES SUMMARY: Patients with osteoporosis, known malignancy, or recent trauma are at the greatest risk of direct involvement of the vertebral body. Each individual spinous process must be palpated if the patient describes midline back pain. MANEUVER: Each spinous process is palpated with the index finger. This is followed by gentle fist percussion of each vertebral level if tenderness is not elicited by palpation. ADDITIONAL SIGNS: Percussion over the vertebral body may cause pain wrapping around the chest wall (radicular pain). Loss of sensation in a thoracic dermatome is seen with advanced vertebral body lesions.

FIGURE 3–20. Palpation of the spinous processes to assess vertebral bony tenderness.

INTERPRETATION: Primary involvement of the vertebral bodies is not common. Acute compression fractures occurring between thoracic level T12 and T7 are most commonly due to osteoporosis or blunt trauma. Compression fractures occurring above thoracic level T6 must be considered pathologic (due to malignancy) until proven otherwise. Shingles should be considered if the patient experiences dramatic radicular pain wrapping around the chest wall accompanied by minimal vertebral bony tenderness.

UPPER BACK

NUCLEAR BONE SCAN CASE: This patient fell from a ladder. He landed in a partially reclined position, striking his buttocks. Pain and acute muscle spasm developed immediately. Physical examination demonstrated intense muscle spasm, local tenderness over the spinous process of L1, and tenderness of the paraspinal muscles. DIAGNOSIS: Compression fracture of L1 with increased uptake on bone scan. DISCUSSION: The asymmetrical collapse of a vertebral body coupled with the intense paraspinal muscle spasm can cause an acquired scoliosis (as seen in this case). FIGURE 3–21. Nuclear bone scan demonstrating bony activity from an acute compression fracture.

MRI CASE: This industrial worker fell 20 feet, landing on his buttocks. Acute pain in the midback was followed by intense muscle spasm. In the days that followed, he suffered lancinating pain that wrapped around the chest wall and took his breath away. DIAGNOSIS: Lateral views of the thoracic spine demonstrate a fragmented T6 compression fracture leading to an exaggerated kyphosis (gibbus). Chest x-ray revealed no intrinsic lung or cardiac disease. DISCUSSION: Most compression fractures heal gradually over a period of 4 to 8 weeks. Few warrant surgical intervention. Indications for surgical referral include associated neurologic symptoms, instability, and persistent symptoms. With instability and nerve compression, stabilization is the procedure of choice. FIGURE 3–22. MRI demonstrating a fragmented compression fracture.

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REFERRED PAIN FROM CERVICAL RADICULOPATHY

Each of the lower cervical roots (C6–C8) refers pain over the scapula. The diagnosis of referred pain can be very difficult, espe-

cially when the symptoms of paresthesias or hypesthesias in the upper extremity are not prominent. The diagnosis should be suspected if the upper back pain is not accompanied by focal tenderness.

REFERRED UPPER BACK PAIN SUMMARY: Each of the lower three cervical roots can refer pain over the upper back and the scapula in particular. The pain is characteristically intense but unassociated with local tenderness. The diagnosis of cervical radiculopathy often is not considered because of the conspicuous absence of the typical associated paresthesias or hypesthesias of the upper extremity. MANEUVER: Full examination of the neck and upper extremity neurological exam are performed. ADDITIONAL SIGNS: Although there may be signs of muscular strain (trapezius and rhomboid muscles), the area of intense pain is not particularly tender (over the body of the scapula). The patient’s pain is most aggravated by the typical movement of the neck in rotation and lateral bending.

FIGURE 3–23. The patient describes pain around the scapula and shoulder but has no tenderness.

INTERPRETATION: This limited form of sensory cervical radiculopathy has a good prognosis. No motor involvement is present, making aggressive treatment rarely necessary.

OBLIQUE VIEW OF THE CERVICAL SPINE CASE: This 57-year-old man had a severe motor vehicle accident 20 years before presentation. He sustained a concussion and severe whiplash at the time. Over the last several years he has complained of intermittent stiffness of the neck and most recently of pain in the upper back. Examination disclosed limited rotation to 70 degrees, pain aggravated by downward compression of the head (Spurling maneuver), and partial pain relief with manual vertical traction on the neck. Neurologic exam of the upper extremities was normal. DIAGNOSIS: The oblique views of the neck demonstrate a reversed curvature of the neck, foraminal narrowing at multiple levels, and a dumbbell-shaped narrowing at the C6–C7 interspace (the seventh cervical root, named for the lower vertebra).

FIGURE 3–24. Oblique view of the cervical spine demonstrating the dumbbell-shaped foraminal encroachment causing radiculopathy.

DISCUSSION: The most common cause of cervical radiculopathy is foraminal encroachment by osteophytes from the paravertebral joints of Luschka and facet joints. Osteophytes project into the foramen, causing the dumbbell-shaped foraminal narrowing. Because the nerve is approximately 1⁄3 the size of the opening, a 50% narrowing of the normal foraminal shape can lead to radicular symptoms and signs.

UPPER BACK

3–1

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DIAGNOSIS


Local tenderness of the trapezius, levator scapulae, or rhomboid muscles

1. Upper back muscle strain, fibromyalgia

Local anesthetic placed into the involved muscle (optional)

Focal tenderness at the superior medial angle of the scapula (the arm fully adducted)


Local anesthetic placed in the bursa

Measure the patient’s height

Scoliosis

Chest x-ray for screening or a full-length anteroposterior spine to assess and measure the thoracic curves

Rib fracture, intercostal muscle spasm, ankylosing spondylitis

Local anesthetic placed over the intercostal nerve (optional) or chest x-ray

Compression fracture, vertebral body bony lesion, epidural process

Chest x-ray, MRI

Abnormal thoracic kyphosis Paraspinal muscle spasm or paraspinal muscle hump Abnormal chest compression

Less than 21⁄2-inch chest expansion Local tenderness of the spinous process

Percussion tenderness Muscle spasm

CLINICAL PEARLS • Muscle strain and spasm of the upper back muscles are the dominant conditions of the upper back. Chronic muscular symptoms affecting the upper back result from chronic stress, chronic poor posture, fibromyalgia, the dorsokyphotic changes of aging, or scoliosis. • Most cases of upper back muscular strain are benign. However, an underlying thoracic nerve or thoracic vertebral body lesion must be considered when the reactive muscular spasm is acute and severe or progressive or the response to treatment is poor. • Symptoms of upper back pain associated with cautious movement, general stiffness, and restricted movement of the neck should suggest the early presentation of a sensory radiculopathy arising from irritation of one of the lower cervical spinal nerves. • Patients with a history of lung, breast, or prostate cancer who present with focal tenderness in the scapular or

rib areas must undergo bone scanning or MRI to rule out metastatic involvement of the bone. Alternatively, if physical examination suggests a focal musculoskeletal process, local anesthetic block can be considered to confirm the exact anatomic location of their pain. • Periscapular pain that is associated with local tenderness arises in the supporting muscles of the upper back or in the subscapular bursa. Periscapular pain that lacks local tenderness usually arises from the cervical spine, referred from one of the lower cervical roots (C6, C7, or C8). • Osteoporosis occurring in the postmenopausal period is the most common cause of compression fracture. These fractures typically occur between vertebral levels T7 and L5. Any compression fracture above T7 should be considered pathologic (e.g., metastatic disease, tuberculous) until proven otherwise.

CHAPTER 4: ELBOW DIFFERENTIAL DIAGNOSIS Diagnoses

Confirmations

Lateral epicondylitis (most common)


Brachioradialis muscle strain

Examination

Medial epicondylitis


Olecranon bursitis Draftsman’s elbow Septic bursitis Bursitis secondary to gout Hemorrhagic bursitis secondary to chronic renal failure

Aspiration, Aspiration, Aspiration, Aspiration,

Olecranon spur fracture

X-ray: elbow series

Triceps tendonitis

Examination

Radiohumeral arthritis Osteochondritis dissecans Posttraumatic osteoarthritis Inflammatory arthritis Hemarthrosis

X-rays, magnetic resonance imaging (MRI), surgical exploration X-ray: elbow series Aspiration, cell count Aspiration, hematocrit

Cubital tunnel

Nerve conduction velocity testing

Bicipital tendonitis


Referred pain Cervical spine Carpal tunnel syndrome Shoulder tendonitis

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hematocrit Gram stain and culture crystal analysis hematocrit, chemistries

Neck rotation, x-ray, MRI Nerve conduction velocity testing Painful arc, subacromial tenderness, isometric testing of the tendons

ELBOW

INTRODUCTION Arriving at a specific diagnosis at the elbow is straightforward because lateral epicondylitis, olecranon bursitis, and medial epicondylitis represent more than 90% of the diagnoses. The pragmatic approach to the differential diagnosis emphasizes range of motion testing of the two compartments of the elbow joint to exclude arthritic involvement followed by specific testing for the common three conditions. Examining the elbow in this sequence allows the provider to rapidly arrive at the correct diagnosis. Lateral epicondylitis (tennis elbow) represents 70% of the diagnoses at the elbow. The quarter-sized attachment of the extensor carpi radialis tendons at the lateral epicondylar process of the distal humerus is susceptible to tension and traction when performing repetitious functions such as lifting, pushing, or pounding. In tennis the classic injury results from the single-grip backhand volley. The force of impact and the tension generated by all of these actions travel back from the wrist to the origin of the tendon at the lateral epicondyle. Pathologically, the tendon has been disrupted from its bony attachment on a microscopic level (microsplitting, microtearing, and microavulsion). Lateral epicondylitis is the quintessential type of mechanical tendon injury. Medial epicondylitis (golfer’s elbow) is one tenth as common as lateral epicondylitis. It is nearly identical to lateral epicondylitis in pathology, pathophysiology, examination, and treatment. As with lateral epicondylitis, successful treatment depends on the body’s ability to form a strong reattachment of the tendon to the periosteum of the elbow. Incomplete healing (poor reattachment) leads to recurrent episodes of tendonitis. Olecranon bursitis (draftsman’s elbow) is the third most common condition at the elbow. The olecranon is unique among the 200 bursae of the body in that it is susceptible to infection with Staphylococcus aureus and the deposition of uric acid with acute gout. However, the majority of cases are caused by repeated episodes of direct pressure over the elbow (traumatic bursitis). And because acute traumatic bursitis can appear just as inflamed as septic or gouty bursitis, it is imperative that every bursa undergo diagnostic aspiration and laboratory analysis of the fluid. Involvement of the elbow joint is uncommon. Posttraumatic osteoarthritis (e.g., trauma, osteochondritis dissecans, prior fracture) and rheumatoid arthritis are the two most common underlying causes. The diagnosis is always suspected if the patient has lost a significant degree of range of motion in extension or flexion. Fractures in adults are uncommon. Falls onto an outstretched arm lead to injures at the wrist and shoulder more often than at the elbow. Falls directly onto the olecranon or severe hyperextension injuries can lead to fractures of the ulna, fracture or dislocation of the radial head, or fracture or dislocation of the ulnar articulation with the humerus. Finally, pain can be referred to the elbow from the shoulder, cervical spine, or heart or may travel through the elbow,

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as in carpal tunnel syndrome and cervical radiculopathy. As with any referred pain, the range of motion of the elbow is maintained, and the anatomic structures surrounding the joint are free of local tenderness. SYMPTOMS Conditions directly affecting the elbow cause pain (epicondylitis), swelling (olecranon bursitis), or a loss of range of motion (radiocarpal joint). Lateral elbow pain is the most common complaint and arises from the lateral epicondyle or radiohumeral joint or is referred from the shoulder or neck. The pain of lateral epicondylitis typically is well localized (the patient often points to the lateral epicondylar process) and is aggravated by lifting or repetitious use of the forearm and wrist. Pain arising from the elbow joint is located slightly more posteriorly to the epicondyle (between the epicondyle and the olecranon process). It is not as well localized as the pain from the epicondyle and is readily distinguished by its effect on the range of motion of the elbow (lateral epicondylitis rarely affects the range of motion of the joint). Lateral elbow pain that is referred to the elbow is suggested by its vague localization and description, its lack of effect on elbow movement, its lack of local tenderness, and its more direct relationship to the movement of the shoulder or neck. Medial elbow pain is the second most common complaint and arises from the medial epicondyle, the ulnar nerve as it travels through the cubital tunnel, or rarely from the radiohumeral joint. As with lateral epicondylitis, the pain of medial epicondylitis is well localized and is aggravated by lifting or repetitious use of the forearm and wrist. The pain arising from the ulnar nerve is suggested by its radiation into the ulnar side of the hand and the associated affects on sensation in the fourth and fifth fingers. Posterior elbow swelling is the classic complaint of olecranon bursitis. The rapidity in which the warmth, redness, and swelling develop provides the most important clue to the underlying cause. Traumatic bursitis swells gradually and is mildly red and warm. By contrast, the swelling of septic and gouty bursitis develops rapidly, and the overlying soft tissues are dramatically inflamed, typically red and hot. Lateral elbow swelling is characteristic of a primary involvement of the joint. However, these symptoms are nearly always overshadowed by the universal complaint, “I cannot straighten my elbow.” Small effusions, whether due to trauma, osteochondritis dissecans, rheumatoid arthritis, or posttraumatic arthritis, cause an immediate loss of extension. Moderate to large effusions impair both extension and flexion. Finally, baseball players and gymnasts describe a loss of smooth motion of the elbow. This unique symptom is seen nearly exclusively in throwers, vaulters, and floor exercise gymnasts and is the strongest clue to osteochondritis dissecans of the humerus.

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BOX 4-1

DIFFERENTIAL DIAGNOSIS OF ELBOW PAIN BASED ON ANATOMIC AREA Lateral pain

Medial pain Posterior pain Anterior pain Referred pain

Lateral epicondylitis Brachioradialis strain Radiohumeral arthritis Inflammatory arthritis Posttraumatic osteoarthritis Osteochondritis dissecans Hemarthrosis Medial epicondylitis Cubital tunnel Olecranon bursitis Triceps tendonitis Biceps insertionitis Cervical radiculopathy Carpal tunnel syndrome Rotator cuff tendonitis

EXAMINATION The examination of the elbow begins with an evaluation of the range of motion of the two components of the elbow joint (radiohumeral and ulnarhumeral) followed by an evaluation of the epicondyles and olecranon bursa for local tenderness and swelling. Arthritis, joint effusion, and hemarthrosis involving the elbow are uncommon (except with rheumatoid arthritis or trauma). These are readily excluded by a normal range of motion in extension, flexion, supination, and pronation. The lateral and medial epicondyles are palpated to determine the degree of forearm extensor or flexor tendonitis, re-

spectively. Involvement of the olecranon bursa is assessed by inspection and direct palpation of the olecranon bursa. If these four anatomic areas are normal, the neck, shoulder, and wrist should be examined to determine a referral source of elbow pain. BOX 4-2

ESSENTIAL EXAMINATION OF THE ELBOW 1. Perform range of motion testing of the elbow joint (flexion, extension, pronation, and supination). 2. Palpate the extensor tendons at the lateral epicondyle and the flexor tendons at the medial epicondyle. 3. Inspect and palpate the olecranon bursa for swelling and chronic thickening. 4. Examine the neck, shoulder, and wrist for possible referred pain.

ONE-MINUTE SCREENING EXAM: MANEUVERS ASSESSING OVERALL ELBOW FUNCTION AND DIFFERENTIAL DIAGNOSIS The next five maneuvers represent the minimal examination of the patient presenting with elbow symptoms. Range of motion measurement and screening maneuvers for epicondylitis and olecranon bursitis provide enough information to triage to x-ray, order appropriate labs, suggest general treatment recommendations, or proceed to more detailed examination and treatment.

PASSIVE RANGE OF MOTION TESTING IN EXTENSION AND FLEXION SUMMARY: Arthritic involvement or acute effusion of the ulnarhumeral articulation causes loss of range of motion, initially extension followed by flexion. Conversely, full range of motion essentially rules out an active involvement of the joint. MANEUVER: Full arm extension and flexion are compared side to side. Loss of smooth motion (ratcheting, popping, or dramatic crepitation) suggests osteochondritis or loose body.

FIGURE 4–1. Passive range of motion testing in extension and flexion of the ulnarhumeral joint.

INTERPRETATION: The loss of full extension with endpoint stiffness suggests a small effusion or mild arthritis. The loss of full extension and flexion with endpoint stiffness suggests either an acute, large effusion or moderate to severe arthritis.

ELBOW

PASSIVE RANGE OF MOTION TESTING IN SUPINATION AND PRONATION SUMMARY: Injury or arthritis affecting the radial head causes a loss of smooth supination and pronation of the forearm. MANEUVER: Passive supination and pronation are compared side to side while palpating the radial head, located 1 cm distal to the lateral epicondyle. The radial head is tender to direct pressure and may exhibit popping or crepitation with passive motion. INTERPRETATION: The loss of full supination or pronation indicates previous fracture, dislocation of the elbow, or osteochondritis dissecans. FIGURE 4–2. Passive range of motion testing in supination and pronation of the radiohumeral joint.

LATERAL EPICONDYLAR TENDERNESS SUMMARY: All cases of lateral epicondylitis are characterized and require the demonstration of local tenderness directly over the epicondylar process. MANEUVER: With the elbow flexed at 90 degrees, the lateral epicondyle is readily identified and palpated for local tenderness. Swelling over the epicondyle is uncommon.

FIGURE 4–3. Lateral epicondylar tenderness to screen for lateral epicondylitis.

INTERPRETATION: Local tenderness over the lateral epicondyle must be distinguished from the local joint line tenderness located between the lateral epicondyle, the radial head, and the olecranon process indicative of ulnarhumeral joint arthritis or effusion and the local tenderness of a bony fracture.

MEDIAL EPICONDYLAR TENDERNESS SUMMARY: All cases of medial epicondylitis are characterized by local tenderness located 1⁄2 to 1 cm distal to the epicondylar process, directly over the tendon. MANEUVER: With the elbow flexed at 90 degrees, the common flexor tendons are readily identified and palpated for point tenderness. INTERPRETATION: Local tenderness over the common flexor tendons alone virtually makes the diagnosis of medial epicondylitis. FIGURE 4–4. Medial epicondylar tenderness to screen for medial epicondylitis.

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INSPECTION AND PALPATION SUMMARY: Swelling and variable degrees of inflammation characterize olecranon bursitis. MANEUVER: With the elbow flexed at 90 degrees, the bursa is inspected for the swelling, inflammation, and bursal wall thickening. INTERPRETATION: Acute bursitis is characterized by ballottable swelling and accompanying inflammatory changes of heat and redness. Chronic bursitis caused by unremitting inflammation is also characterized by swelling, but in addition the bursal wall tissues are palpably thickened.

FIGURE 4–5. Inspection and palpation of the olecranon bursa.

ONE-MINUTE SCREENING EXAM: MANAGEMENT OPTIONS TRIAGE TO X-RAY For patients with a history of trauma, risk of bony injury, possible joint involvement because of loss of normal range of motion: • Order three views of the elbow for patients with a history of fall onto the forearm, crush injuries, or direct blow (olecranon or radial head fractures). • Order three views of the elbow in patients with a loss of full range of motion (posttraumatic osteoarthritis, rheumatoid arthritis, or the arthritis accompanying spondyloarthropathy). • Order two views of the elbow for patients with recurrent olecranon pain (calcifications of the triceps tendon associated with triceps tendonitis or recurrent or chronic olecranon bursitis).

TRIAGE TO THE LAB acute septic arthritis:

For acute olecranon bursitis or

• Order a complete blood cell count, uric acid, and erythrocyte sedimentation rate for patients with acute olecranon bursal pain and swelling (traumatic, gouty, or septic bursitis). • Order a complete blood cell count, uric acid, erythrocyte sedimentation rate, and blood cultures for patients with acute pain, decreased range of motion of the joint, and inflammatory changes laterally (hemarthrosis from trauma or inflammatory or septic arthritis of the elbow).

CONSIDER A BONE SCAN For patients with vague bony pain and tenderness that does not correspond to the screening examinations of classic epicondylitis, olecranon bursitis, or radiohumeral arthritis (bony fracture or lesion). CONSIDER MRI For patients with incomplete or loss of smooth motion of the radiohumeral joint (osteochondritis dissecans). RECOMMEND EMPIRICAL TREATMENT For patients with mild to moderate elbow pain and stiffness, unrestricted movement of the joint, preserved forearm muscle tone, and preserved gripping and grasping strength: • Restrictions of lifting, gripping, grasping, and tooling (especially tools requiring torque). • Ice applied to the site of pain up to four times a day. • A pull-on neoprene elbow pad for bursitis or a forearm compression brace for epicondylitis. • A full-strength nonsteroidal anti-inflammatory drug for 10 to 14 days. DETAILED EXAMINATION: SPECIFIC ELBOW DIAGNOSES A detailed examination of the elbow is necessary if the patient has persistent or chronic symptoms, forearm muscle or hand strength is impaired, and the range of motion of the elbow is impaired.

ELBOW

LATERAL EPICONDYLITIS A presumptive diagnosis of ten-

nis elbow, the microtearing or microavulsion of the extensor carpi radialis brevis and longus tendons, is based on local tenderness directly over the lateral epicondyle, pain aggravated by resisted wrist

extension and radial deviation, and normal range of motion of the elbow. During the examination emphasis is placed on the close mechanical relationship of the wrist and elbow.

PALPATION OF THE LATERAL EPICONDYLE SUMMARY: Lateral epicondylitis is characterized by local tenderness directly over the epicondylar process. MANEUVER: With the elbow flexed at 90 degrees, the lateral epicondyle is readily identified and palpated for localized tenderness. ADDITIONAL SIGNS: Isometric resistance of wrist extension (extensor carpi radialis longus and brevis), loss of grip strength, and pain aggravated by passive supination and pronation are the additional signs of lateral epicondylitis.

FIGURE 4–6. Palpation of the lateral epicondyle for lateral epicondylitis.

INTERPRETATION: Mild lateral epicondylitis is characterized by local tenderness. Moderate involvement combines local tenderness with elbow pain reproduced by resisted wrist extension. Severe involvement is characterized by loss of grip strength. Local tenderness and pain aggravated by side-toside compression of the proximal forearm musculature suggests brachioradialis strain, a simple overuse of the muscle.

LATERAL EPICONDYLITIS SUMMARY: Local anesthetic placed at the interface of the subcutaneous fat and the outer fascia of the tendon is used to confirm the diagnosis and determine the severity of the condition. Grip strength measurement before and after local anesthesia is the best prognostic indicator of a successful treatment outcome. POSITIONING: Supine, elbow flexed to 90 degrees, hand tucked under the buttock. SURFACE ANATOMY: head. POINT OF ENTRY: epicondyle. FIGURE 4–7. Lateral epicondylitis confirmed by local anesthetic block. NOTE: To avoid a painful injection, the anesthesia is placed just outside the tendon, at the interface of the subcutaneous fat and the outer facia. If the needle is inserted at this proper depth, the needle should move back and forth when traction is applied to the skin.

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Lateral epicondyle, radial

Directly over the center of the

ANGLE OF ENTRY: Perpendicular if the patient has sufficient subcutaneous fat, 45-degree angle otherwise. NEEDLE: DEPTH:


5

⁄4 to 5⁄8 inch.

1

ANESTHESIA: Ethyl chloride, skin: 1⁄2 mL subcutaneous, 1⁄2 mL at the tendon–fat interface.

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MEDIAL EPICONDYLITIS A presumptive diagnosis of golfer’s elbow, a microtearing or microavulsion of the flexor carpi radialis tendons, is based on local tenderness just distal to the medial epicondyle, pain aggravated by resisted wrist flexion and

radial deviation, and normal range of motion of the elbow. Medial epicondylitis is the mirror image of its lateral counterpart, although 90% less common.

MEDIAL EPICONDYLAR TENDERNESS SUMMARY: Medial epicondylitis is characterized by local tenderness directly over the common flexor tendons 1⁄2 to 1 inch distal to the epicondyle. This differs from lateral epicondylitis, which is tender directly over its bony origin. MANEUVER: With the elbow flexed at 90 degrees, the flexor tendons are palpated for tenderness. ADDITIONAL SIGNS: Isometric resistance of wrist flexion (flexor carpi radialis longus and brevis), loss of grip strength, and pain aggravated by passive supination and pronation characterize the complete exam.

FIGURE 4–8. Palpation of the medial epicondyle for medial epicondylitis.

INTERPRETATION: Mild medial epicondylitis is characterized by local tenderness. Moderate involvement combines local tenderness with elbow pain reproduced by resisted wrist flexion. Severe involvement is characterized by loss of grip strength.

MEDIAL EPICONDYLITIS SUMMARY: Dramatic pain relief with local anesthetic placed at the interface of the subcutaneous fat and the outer fascia of the flexor tendons or a dramatic response to corticosteroid confirms the diagnosis of epicondylitis. Grip strength measurement before and after local anesthesia is the best prognostic indicator of a successful treatment outcome. POSITIONING: Supine, elbow flexed to 90 degrees, 90 degrees of shoulder rotation. SURFACE ANATOMY: non process. POINT OF ENTRY: epicondyle. FIGURE 4–9. Medial epicondylitis confirmed by local anesthetic block. NOTE: To avoid a painful injection, the anesthesia is placed just outside the tendon, at the interface of the subcutaneous fat and the outer facia. If the needle is inserted at this proper depth, the needle should move back and forth when traction is applied to the skin.

Medial epicondyle, olecra-

⁄2 inch distal to the medial

1

ANGLE OF ENTRY: Perpendicular if there is sufficient subcutaneous fat. NEEDLE: DEPTH:


5

⁄8 to 5⁄8 inch.

3

ANESTHESIA: Ethyl chloride, skin: 1⁄2 mL placed subcutaneously, 1⁄2 mL at the tendon–fat interface.

ELBOW

OLECRANON BURSITIS The diagnosis of acute olecranon

bursitis is readily made by noting the cystic swelling over the posterior olecranon process. However, bursal aspiration and lab analysis are necessary to distinguish the three common causes of bursal swelling: trauma (90%), sepsis (5%), or gout (5%).

Chronic olecranon bursitis is characterized by palpable thickening to the bursal walls and variable degrees of cystic swelling.

INSPECTION AND PALPATION SUMMARY: The olecranon bursa is palpated for local tenderness, cystic swelling, and chronic thickening. The degree of acute inflammation and the extent of surrounding erythema are noted. MANEUVER: The optimal elbow position to evaluate the olecranon bursa is at 90 degrees. The bursa is palpated for ballottable fluid and bursal wall thickening. Any inflammatory changes are also noted. ADDITIONAL SIGNS: The range of motion of the elbow should be normal because the bursa is located extra-articularly.

FIGURE 4–10. Inspection and palpation of the olecranon bursa.

INTERPRETATION: Acute bursitis is characterized by ballottable swelling and accompanying inflammatory changes of heat and redness. Chronic bursitis caused by unremitting inflammation is also characterized by swelling, but in addition the bursal wall tissues are palpably thickened. Septic bursitis can be accompanied by diffuse erythema and redness (i.e., cellulitis).

NEEDLE ASPIRATION OF THE BURSA SUMMARY: Aspiration of the bursa is necessary to distinguish the three major causes of acute bursitis: traumatic (predominantly blood), septic (purulent and positive culture), and gout (positive for crystals). If the patient has minimal ballottable swelling, the needle is advanced to the periosteum of the ulna in the center of the bursa (the deep bursal wall is located at the level of the ulna). POSITIONING: Supine, elbow flexed to 90 degrees, forearm lying over the chest. SURFACE ANATOMY: epicondyle. POINT OF ENTRY: ANGLE OF ENTRY: FIGURE 4–11. Olecranon bursitis confirmed by needle aspiration of the bursa.

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NEEDLE: DEPTH:

Olecranon process, lateral

Distal, at the base of the bursa. Nearly parallel to the ulna.


Superficial, 3⁄8 to 5⁄8 inch.

ANESTHESIA: Ethyl chloride, skin: 1⁄2 mL subcutaneous.

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TRICEPS INSERTIONITIS Triceps insertionitis is an uncommon condition. Patients performing repetitive pushing, too many push-ups, or unaccustomed bench press exercises are at particular risk. The diagnosis is characterized by focal tenderness over the

insertion on the posterior olecranon process and pain aggravated by resisted elbow extension. A fractured olecranon spur is excluded by plain x-rays, and olecranon bursitis is excluded by exam and aspiration.

FOCAL TENDERNESS SUMMARY: All patients with triceps tendonitis have focal tenderness on the posterior aspect of the olecranon process. MANEUVER: The triceps insertion is palpated for local tenderness and swelling. ADDITIONAL SIGNS: Isometric resistance of elbow extension reproduces the patient’s elbow pain. The range of motion of the elbow should be normal. The olecranon bursa is not acutely inflamed. INTERPRETATION: The focal tenderness of olecranon bursitis, triceps insertionitis, and fractured olecranon spur overlap. Acute bursitis is characterized by ballottable swelling. Fractured olecranon spur is confirmed by x-ray. The diagnosis of triceps insertionitis is made by resisting elbow extension and by the exclusion of the other two diagnoses.

FIGURE 4–12. Focal tenderness of triceps insertionitis.

LATERAL X-RAY VIEW OF ELBOW SUMMARY: Olecranon spurring occurs in the body of the triceps tendon. Most exostoses off the olecranon process are completely asymptomatic. The larger 1⁄2-cm spurs are susceptible to fracture caused by a fall onto the elbow or direct blow. Focal tenderness with minimal swelling (none in the characteristic olecranon bursal area) is present on the proximal olecranon process.

FIGURE 4–13. Olecranon spur fracture confirmed by lateral x-ray view of elbow.

ELBOW

ULNARHUMERAL (ELBOW) JOINT ARTHRITIS Arthritis of the elbow is uncommon. Most cases are the result of previous trauma (intra-articular fracture), rheumatoid arthritis, or other systemic rheumatologic conditions. The diagnosis should always

be considered if the range of motion of the elbow is impaired (extension is preferentially affected in the early case). Confirmation requires joint aspiration or typical changes on x-ray.

PASSIVE RANGE OF MOTION SUMMARY: Arthritic involvement or acute effusion of the ulnarhumeral articulation causes loss of range of motion; initially extension is impaired, followed by flexion. MANEUVER: Full arm extension and flexion are compared side to side. ADDITIONAL SIGNS: Tenderness and swelling (the bulge sign) are located in the triangle formed by the radial head, the olecranon process, and the lateral epicondyle. Loss of smooth motion (ratcheting, popping, or dramatic crepitation) suggests osteochondritis or loose body. INTERPRETATION: The loss of full extension with endpoint stiffness suggests a small effusion or mild arthritis. The loss of full extension and flexion with endpoint stiffness suggests either an acute, large effusion or moderate to severe arthritis. FIGURE 4–14. Passive range of motion testing of the ulnarhumeral joint.

LATERAL X-RAY VIEWS OF THE ELBOW SUMMARY: This 48-year-old native Hawaiian had an acute injury to his elbow 32 years before presenting to the clinic with elbow pain and impaired range of motion. Every Saturday he delivered his father’s lunch to him on the job (his father drove the sugarcane train on the island of Maui). He always climbed a nearby palm tree to watch for the train’s arrival. At age 16 he fell from the tree, striking his whole weight on the right elbow. He did not seek medical attention at that time. Over the last few years he has gradually developed lateral elbow pain and progressive loss of range of motion. DIAGNOSIS: Osteoarthritis of the ulnarhumeral joint with hypertrophic spurring and loss of joint space.

FIGURE 4–15. Osteoarthritis of the ulnarhumeral joint confirmed by lateral x-ray views of the elbow.

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INTERPRETATION: The loss of full extension with endpoint stiffness suggests a small effusion or mild arthritis. The loss of full extension and flexion with endpoint stiffness suggests either an acute, large effusion or moderate to severe arthritis.

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RADIOGRAPHIC CHANGES OF RHEUMATOID ARTHRITIS SUMMARY: This 62-year-old Swedish American nurse developed polyarticular inflammatory small joint arthritis at age 32. Over the years involvement in the wrists, elbows, knees, ankles, and shoulders has developed. She presented with bilateral elbow effusions with painful, limited range of motion in her mid-fifties. DIAGNOSIS: Rheumatoid arthritis of the elbow confirmed by aspiration of an inflammatory effusion. The elbow has lost nearly all the articular cartilage in a symmetrical pattern. The bones demonstrate diffuse osteopenia. Minimal reactive osteophytes are present. DISCUSSION: Rheumatoid arthritis is characterized by a symmetrical loss of articular cartilage, as opposed to the typical asymmetrical loss of cartilage with osteoarthritis. FIGURE 4–16. Radiographic changes of rheumatoid arthritis involving the radiohumeral and ulnarhumeral joint.

ASPIRATION OF THE ELBOW JOINT SUMMARY: Aspiration of the elbow joint is indicated to differentiate traumatic hemarthrosis from inflammatory arthritis and the rare case of septic arthritis. POSITIONING: Supine, elbow flexed to 90 degrees, hand tucked under the buttock. SURFACE ANATOMY: Lateral epicondyle, radial head, and the olecranon process. POINT OF ENTRY: triangle.

In the center of the inscribed

ANGLE OF ENTRY: Perpendicular to the skin and parallel to the radial head. NEEDLE: DEPTH:

FIGURE 4–17. Aspiration of the elbow joint to determine the cause of the effusion.

1 inch, 21 or 22 gauge. ⁄4 to 1 inch.

3

ANESTHESIA: Ethyl chloride, skin: 1⁄2 mL subcutaneously, 1⁄2 mL at 3⁄4 inches or adjacent to bone.

ELBOW

Inflammation at the insertion of the biceps on the radial tubercle is an uncommon problem. Repeated lifting or an intense downward force on the arm causes microtear-

BICEPS INSERTIONITIS

ing and secondary inflammation to develop at the attachment site. Patients describe a deep ache in the antecubital fossa that is aggravated by direct pressure and isometric flexion of the elbow.

LOCAL TENDERNESS OF THE INSERTION OF THE BICEPS SUMMARY: The diagnosis of biceps insertionitis is difficult to make. The clinical signs overlap with those of muscular strain of the forearm muscles, strain to the ulnarhumeral joint, and the conditions that refer pain through the elbow (shoulder tendonitis, carpal tunnel, pronator teres syndrome, and cervical radiculopathy). MANEUVER: With the elbow flexed at 90 degrees, the biceps tendon is identified in the antecubital fossa and followed down to its attachment deep in the forearm adjacent to the radial tubercle. Focal tenderness at this exact location suggests biceps insertionitis. ADDITIONAL SIGNS: Isometric resistance of elbow flexion that reproduces the patient’s pain assists in the diagnosis. FIGURE 4–18. Local tenderness of the insertion of the biceps in the antecubital fossa.

INTERPRETATION: The long head of the biceps is much more susceptible to injury and inflammation than the combined distal biceps tendon.

ISOMETRICALLY RESISTED ELBOW FLEXION SUMMARY: The patient sustained a substantial injury and has felt a popping sensation in the antecubital fossa. Local tenderness is present along the distal portion of the combined short and long head biceps tendon. Resisting elbow flexion should reproduce the pain of this uncommon injury. MANEUVER: With the elbow flexed at 90 degrees, the examiner asks the patient to flex against resistance. Pain and weakness of flexion are noted. ADDITIONAL SIGNS: The range of motion of the elbow should be normal. No evidence of primary shoulder pathology, cervical radiculopathy, or median nerve compression from carpal tunnel or pronator teres syndrome should be present. FIGURE 4–19. Isometrically resisted elbow flexion to reproduce the patient’s biceps pain.

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INTERPRETATION: Definitive diagnosis requires surgical exploration and repair. Surgical referral is suggested if the patient has lost 30% to 40% of his or her strength on that side.

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CUBITAL TUNNEL SYNDROME Cubital tunnel syndrome is an entrapment neuropathy of the ulnar nerve as it courses through the bony channel of the proximal ulna. The diagnosis is suggested by a description of hypoesthesias or paresthesia in the hand (the fifth finger and half of the fourth finger) or neuritic-like pain trav-

eling through the elbow and forearm. Examination of the elbow should be normal except for a positive Tinel sign along the medial aspect of the proximal ulna, demonstrating ulnar nerve sensitivity. Unlike in carpal tunnel syndrome, muscular weakness is not a significant symptom of cubital tunnel syndrome.

TINEL SIGN FOR CUBITAL TUNNEL SYNDROME SUMMARY: The cubital tunnel is formed between the medial epicondyle and the olecranon process. The ulnar nerve lies in this bony groove. It provides sensation to the fifth finger and lateral half of the fourth finger. Cubital tunnel is the most common cause of ulnar neuropathy. MANEUVER: With the elbow flexed at 90 degrees and the arm externally rotated, the medial epicondyle and the olecranon process are identified. With firm pressure, the groove between the two bony prominences is tapped repeatedly with the tip of the finger.

FIGURE 4–20. Tinel sign tapped over the cubital tunnel suggests ulnar neuropathy.

ADDITIONAL SIGNS: The diagnosis of cubital tunnel is much more likely if sensation in the fourth and fifth fingers is diminished; the abductor digiti minimi muscle is weak; the examination of the neck is normal, excluding the diagnosis of cervical radiculopathy and brachial plexopathy; and the examination of the wrist is normal, excluding entrapment of the ulnar nerve in the intercarpal area. INTERPRETATION: A positive Tinel sign at the elbow should reproduce the lancinating pain down the forearm or cause the paresthesias in the fourth and fifth fingers. The response should be distinctly different from that of the opposite side. Abnormal responses should be confirmed with nerve conduction velocity testing.

NERVE CONDUCTION VELOCITY TESTING SUMMARY: The ulnar nerve function can be impaired at the elbow (cubital tunnel), at the wrist, or anywhere along the course of the nerve from trauma (e.g., supracondylar fracture, crush injuries of the wrist). A definitive diagnosis of cubital tunnel requires the demonstration of nerve conduction slowing across the elbow. Simultaneous electromyographic testing can be used to exclude significant lesions in the neck (brachial plexus lesions, thoracic outlet, or C8 radiculopathy).

FIGURE 4–21. Nerve conduction velocity testing to confirm ulnar neuropathy.

ELBOW

4-1


EXAMINATION SIGNS

DIAGNOSIS


Focal tenderness of the lateral epicondyle

1. Lateral epicondylitis

Local anesthetic block at the lateral epicondyle (optional)

2. Medial epicondylitis

Local anesthetic block at the medial epicondyle (optional)

Olecranon bursitis

Aspiration of the bursa for cell count, Gram stain, and crystal analysis

Triceps insertionitis

Local anesthetic block over the tendon

Radiohumeral arthritis

Aspiration of the joint from the lateral approach

Bicipital insertionitis

Examination

Cubital tunnel


Referred pain from the neck, shoulder, or carpal tunnel syndrome

Screening neck exam, screening shoulder exam, testing for carpal tunnel syndrome

Pain reproduced by resisted wrist extension Pain reproduced by resisted radial deviation of the wrist Diminished grip strength Focal tenderness of the medial epicondyle Pain reproduced by resisted wrist flexion Pain reproduced by resisted radial deviation of the wrist Diminished grip strength Cystic swelling or thickening over the olecranon process Normal range of motion of the elbow joint Tenderness of the triceps insertion on the ulna Pain reproduced by resisted elbow extension Full range of motion of the elbow Loss of full elbow extension Lateral bulge sign halfway between the lateral epicondyle and the olecranon process Loss of full flexion Loss of supination or pronation Antecubital fossa tenderness Pain aggravated by resisted elbow flexion History of ulnar hypesthesia and paresthesia ⫹Tinel sign at the elbow Normal neck exam (i.e., no evidence of C8 radiculopathy) Pain through the elbow

Normal range of motion of the elbow No focal epicondylar tenderness No olecranon swelling

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COMMON ELBOW FRACTURES SUMMARY Fractures of the elbow are not common in adults.

RADIAL HEAD FRACTURE SUMMARY: Displaced radial head fractures should be referred to an orthopedic surgeon for radial head excision. Nondisplaced radial head fractures can be treated medically. The preferred management with a sling and range of motion exercises is a classic example of the application of early physical therapy. It can be combined with aspiration of the hemarthrosis and intra-articular injection of local anesthetic to assist in early exercising. Note that associated injuries to the medial collateral ligament, interosseus membrane, and wrist should be excluded. IMMOBILIZATION: FIGURE 4–22. Radial head fracture.

A simple sling.

SURGICAL REFERRAL: placed fractures.

Surgery is reserved for dis-

PROGNOSIS: Patients are at risk for late-onset osteoarthritis.

ELBOW DISLOCATION SUMMARY: Elbow dislocation occurs mostly in the young (10 to 20 years) and in older adults. The elbow usually dislocates posteriorly. Neurovascular evaluation of the brachial artery, median nerve, and ulnar nerve is mandatory before reduction. Closed reduction involves distraction with or without hyperextension to unlock the olecranon, followed by anterior translation. Open reduction is rare.

FIGURE 4–23. Elbow dislocation without concomitant fracture.

REDUCTION: (1) The patient is to be in a prone position. (2) The arm is hung over the side of the examination table with weight applied to the wrist or with traction applied by the examiner. (3) With constant traction, and as the olecranon is felt to slip distally, the elbow is gently flexed. (4) The range of motion of the elbow in flexion to 30 degrees and in supination and pronation is performed to ensure the stability of the reduction. (5) A posterior splint is applied for 2 to 3 weeks. (6) Gentle, passive range of motion exercises are performed within 1 to 2 weeks to prevent contracture. (7) With improving motion, isometric toning exercises of elbow flexion and extension are begun. IMMOBILIZATION: 2 to 3 weeks.

A posterior splint is applied for

SURGICAL REFERRAL: PROGNOSIS:

Good.

Open reduction is rare.

ELBOW

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NONDISPLACED FRACTURES OF THE SHAFTS OF THE RADIUS AND ULNA SUMMARY: Fixed immobilization in a long-arm cast (axilla to metacarpals) with a collar and cuff suspension at the proximal forearm is the treatment of choice for a nondisplaced fracture. Displaced fractures must be evaluated by an orthopedic surgeon. IMMOBILIZATION: A long-arm cast (axilla to metacarpals) with a collar and cuff suspension at the proximal forearm.

FIGURE 4–24. Nondisplaced fractures of the shafts of the radius and ulna.

SURGICAL REFERRAL: Displaced fractures require open reduction and fixation in order to counteract the opposing muscular forces, restore the proper length of the bones, and achieve axial and rotational alignment. Similarly, open reduction and internal fixation is the preferred treatment for a Monteggia fracture in an adult (displaced fracture of the ulna with radial head dislocation). PROGNOSIS:

Good to excellent.

DISTAL HUMERAL FRACTURES: INTERCONDYLAR FRACTURE SUMMARY: Intercondylar fractures should be referred immediately to an orthopedic surgeon. The T- or Y-configuration fractures of the distal humerus are the most difficult to manage of fractures of the upper extremity. Open reduction with rigid internal fixation is the preferred treatment to optimize the alignment and continuity of the articular surfaces of the elbow.

FIGURE 4–25. Distal humeral fractures: intercondylar fracture.

CLINICAL PEARLS • Normal range of motion testing of the elbow rules out involvement of the joint. • Medial epicondylitis is a traction injury of the flexor carpi radialis tendon, occurring within 1 cm of the midpoint of the medial epicondyle. Local tenderness is the hallmark of medial epicondylitis. • Lateral epicondylitis is a traction injury of the extensor carpi radialis tendon occurring at the midpoint of the

lateral epicondyle. Local tenderness is the hallmark of lateral epicondylitis. • Epicondylitis and olecranon bursitis rarely affect the range of motion of the elbow. The only exceptions to this rule are cellulitis accompanying a septic olecranon bursitis and chronic lateral epicondylitis in the patient with an extremely low pain threshold.

CHAPTER 5: WRIST DIFFERENTIAL DIAGNOSIS Diagnoses The continuum of injuries at the wrist Simple wrist sprain (ligamentous) Sprain with chondral fracture Navicular fracture Perilunate dislocation Kienböck’s disease Triangular cartilage fracture of the ulnocarpal joint

Radiocarpal arthritis Posttraumatic osteoarthritis Rheumatoid arthritis Gout or pseudogout

Dorsal ganglion From the radiocarpal joint From the tenosynovial sheath

Tendonitis Dorsotenosynovitis De Quervain’s tenosynovitis

Referred pain to the wrist Carpometacarpal osteoarthritis Cervical spine Carpal tunnel syndrome (CTS) Pronator teres syndrome (mimicking CTS)

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Confirmations

Examination, normal x-rays Persistent loss of grip, decreased range of motion, and persistent tenderness Loss of 45% of the range of motion, sequential x-rays, positive bone scan Loss of the normal bony alignment A vascular necrosis of the lunate on serial x-rays of the wrist Magnetic resonance imaging (MRI) or arthroscopy

X-ray: wrist series Synovial fluid analysis, erythrocyte sedimentation rate, rheumatoid factor (RF) Crystal analysis

Aspiration Aspiration

Examination, associated signs of rheumatoid arthritis, gout, or gonorrhea Local anesthetic block

X-rays: thumb series Neck rotation, x-ray, MRI Nerve conduction velocity testing or local anesthetic block Nerve conduction velocity testing

WRIST

INTRODUCTION When approaching the differential diagnosis of wrist pain, the provider must first consider the role of injury. The joint is vulnerable to direct blows and to the twisting and compressive forces that result from falling onto an outstretched arm. This places tremendous strain on the supporting ligaments, the delicate cartilage, and the bones that make up the joint. Depending on the nature of the injury, the differential diagnosis can be seen as a continuum of injuries. Simple wrist sprain, the most common diagnosis, is a reversible stretching of the supporting ligaments. More substantial blows can cause fractures, cracks, and fissuring of the articular cartilage, or chondral fractures, a diagnosis that is often made only in retrospect when the apparent simple wrist sprain fails to improve in the typical 2- to 3-week interval. Greater twisting and compressive forces can cause rupture of the supporting ligaments. The perilunate dislocation is the most common example of ligament rupture. Rupture of the specialized triangular cartilage located between the ulnar styloid and the triquetrum occurs on the ulnar side of the wrist. The most dramatic torque and compression forces cause bony fractures. Navicular fracture, avascular necrosis of the navicular, and Kienböck’s avascular necrosis of the lunate occur on the carpal side of the joint. Distal radius fractures, including the most common form (Colles fracture), occur on the proximal side of the joint. The challenge that faces the primary care provider is to determine where to place the individual patient on the continuum of wrist injuries based on the type of injury, the effect on the range of motion of the joint, and the location of the patient’s pain. Despite the varieties of injuries that affect the wrist, direct involvement of the radiocarpal or ulnocarpal joint is uncommon. Late-onset osteoarthritis is uncommon. Arthritic involvement of the wrist is much more likely to be caused by a well-established rheumatic condition, such as rheumatoid or psoriatic arthritis, or a crystal deposition disease such as gout or pseudogout. However, subtle damage to the joint is not without consequences. Moderate to severe ligament and cartilage injuries can cause an overproduction of synovial fluid. Over time this excessive fluid can leak into the subcutaneous tissue surrounding the joint. The highly viscous fluid incites a fibrotic reaction, causing a thick-walled encapsulated cyst to form. These are called ganglion cysts or synovial cysts, which are a manifestation of an injured wrist joint. Tendonitis and tendon injuries are uncommon at the wrist as well. The diagnosis of dorsotenosynovitis, inflammation of the extensor tendons of the hand, is straightforward because it usually occurs as a secondary manifestation of rheumatoid arthritis, gout, or the systemic arthritis– dermatitis syndrome of gonorrhea. In addition, de Quervain’s tenosynovitis, an inflammation of the extensor and abductor tendons of the thumb, often is described as a wrist pain, although strictly speaking it is not directly related anatomically to the wrist. Pain referred solely to the wrist is uncommon. Median neuropathy from pronator teres syndrome or carpal tunnel can refer pain to the wrist, or pain can arise at the wrist and travel in a retrograde fashion but rarely affects the wrist exclusively.

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SYMPTOMS Conditions directly affecting the wrist cause pain with movement (e.g., simple sprain, radiocarpal arthritis, distal radius fracture), swelling (localized [ganglion cyst] or diffuse [extensor tenosynovitis or reflex sympathetic dystrophy]), or changes in sensation aggravated by use of the wrist (carpal tunnel). Dorsal wrist pain aggravated by flexion and extension is the most common complaint and can arise from the ligaments surrounding the joint, the synovium, the articular cartilage, or the bony structures of the radiocarpal joint. If these symptoms follow an injury (a fall to an outstretched arm or direct blow), the clinician must perform a comprehensive examination and radiographic studies to distinguish injury to the supporting ligaments (simple sprain and perilunate dislocation) from injuries affecting the articular cartilage (chondral fracture) and bones (navicular and distal radius fractures). If the symptoms are recurrent or chronic, radiographic studies and serologic testing are necessary to distinguish a rheumatic involvement of the joint from posttraumatic osteoarthritis. Focal dorsal wrist swelling arises from the wrist joint. Painless dorsal wrist swelling is the characteristic of a ganglion cyst. Note that a small number of patients experience pain when the cyst places pressure on the adjacent tendons or the superficial branch of the radial nerve. Painful dorsal wrist swelling over the navicular is characteristic of a swollen radiocarpal joint, although it may be too subtle to be noticed in mild or moderate cases. Diffuse dorsal wrist pain and swelling (extending from the wrist to the back of the hand) are much less common and is characteristic of extensor tenosynovitis, reflex sympathetic dystrophy (RSD), and metacarpal fractures. Involvement of the extensor tendons is likely if the pain is aggravated by

BOX 5-1

DIFFERENTIAL DIAGNOSIS OF WRIST PAIN BASED ON ANATOMIC AREA Dorsal pain

Radial pain Lateral pain Volar pain Referred pain

Wrist sprain Wrist sprain with chondral fracture Navicular fracture Perilunate dislocation Kienböck’s disease Radiocarpal arthritis Posttraumatic osteoarthritis Rheumatoid arthritis Gout and pseudogout Dorsal ganglion Dorsotenosynovitis CMC arthritis of the thumb De Quervain’s tenosynovitis Radial collateral ligament strain Lateral collateral ligament strain Triangular ligament strain Volar ganglion CTS Cervical radiculopathy

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movement of the fingers. RSD is characterized by vaguely defined but severe pain that is not influenced by any particular motion. Paresthesia and hypesthesia aggravated by wrist movement or position are characteristic of carpal tunnel syndrome (CTS). Finally, some patients complain of wrist pain and weakness of the thumb or grip. Although strictly speaking these patients have a primary condition affecting the thumb (de Quervain’s tenosynovitis or arthritis at the base of the thumb), a significant percentage of these patients describe their symptoms as arising from the wrist (see Chapter 6). EXAMINATION The examination of the wrist begins with the measurement of the range of motion of the radiocarpal joint in flexion and extension, the measurement or estimation of grip strength, and an estimation of the looseness of the supporting ligaments. These functional tests correlate directly with the severity of wrist sprain, fracture of the distal radius or carpal bones, and chronic arthritis. Involvement of the wrist joint is strongly suggested by local tenderness and swelling over the navicular and lunate bones. For patients complaining of pain across the radial side of the wrist, specific maneuvers identifying arthritis or tenosynovitis of the thumb must be performed. Approximately 25% of patients with carpometacarpal (CMC) arthritis or de Quervain’s tenosynovitis complain of wrist pain rather than thumb pain. Patients with diffuse swelling over the dorsum of the wrist and hand must be examined for the presence of cellulitis, extensor tenosynovitis, or RSD.

BOX 5-2

ESSENTIAL EXAMINATION OF THE WRIST 1. Evaluate the radiocarpal joint range of motion in flexion and extension and palpate the dorsum of the wrist for swelling. 2. Palpate the navicular and lunate bones, especially if trauma has occurred. 3. Inspect the wrist for the presence of a ganglion cyst over the dorsal wrist. 4. Perform the Tinel and Phelan maneuvers for CTS. 5. Examine the base of the thumb for degenerative arthritis or extensor tenosynovitis.

ONE-MINUTE SCREENING EXAMINATION OF THE WRIST The next eight maneuvers represent the minimal examination of the patient presenting with wrist symptoms. Functional testing, range of motion measurement, and screening maneuvers for dorsal swelling, conditions affecting the thumb, and carpal tunnel provide enough information to triage to x-ray, order appropriate labs, suggest general treatment recommendations, or proceed to more detailed examination and treatment.

RANGE OF MOTION AND ENDPOINT PAIN AND STIFFNESS SUMMARY: The distal radius, navicular, and lunate bones form the radiocarpal articulation. Ninety percent of the movement of the wrist occurs between these three bones. The wrist is supported by a thin joint capsule, a thick complex of criss-crossing ligaments, and the fascia covering the flexor and extensor tendons, the retinaculum. Passive movement of the wrist in flexion and extension defines the involvement of the wrist (normal flexion averages 90 degrees). The severity of the condition correlates directly with the loss of range of motion. MANEUVER: The patient is asked to relax the muscles of the forearm. While the examiner holds the distal forearm firmly, the wrist is passively flexed to its endpoint. Perform this cautiously in the acutely injured or inflamed wrist. INTERPRETATION: FIGURE 5–1. Measure the range of motion of the wrist joint and assess endpoint pain and stiffness in flexion (volarflexion).

See Figure 5-2 Interpretation.

WRIST

RANGE OF MOTION AND ENDPOINT PAIN AND STIFFNESS SUMMARY: Passive movement of the wrist in flexion and extension defines the involvement of the wrist (normal extension averages 80 degrees). The severity of the condition correlates directly with the loss of range of motion. MANEUVER: The patient is asked to relax the muscles of the forearm. While the examiner holds the distal forearm firmly, the wrist is passively extended to its endpoint. Perform this cautiously in the acutely injured or inflamed wrist.

FIGURE 5–2. Measure the range of motion of the wrist and assess endpoint pain and stiffness in extension (dorsiflexion).

INTERPRETATION: Mild symptoms and normal range of motion are seen with simple wrist sprains and mild arthritis. Moderate symptoms and a 20% to 50% loss of range of motion are characteristic of chondral fractures and moderate arthritis. Acute gout, navicular fracture, Colles fracture, and perilunate dislocation are characterized by severe symptoms and a loss of more than 50% of range of motion. Patients with a septic joint or displaced distal radius fractures refuse to move at all.

MANUAL GRIP STRENGTH MEASUREMENT SUMMARY: Grip strength measurement is the most objective but indirect measurement of the integrity and strength of the supporting muscles of the wrist. Gripping can be influenced by arthritis of the intrinsic joints of the hands and wrist, intrinsic muscles of the hand, and forearm flexor tendons and muscles. MANEUVER: Grip strength can be crudely estimated by manual gripping of the examiner’s fingers. However, physical measurement using a dynamometer is much more accurate and reproducible. An alternative method involves compressing a partially inflated blood pressure cuff. FIGURE 5–3. Manual grip strength measurement to assess forearm muscle strength.

INTERPRETATION: Grip strength is reduced in a consistent manner by disuse atrophy, wrist arthritis, CTS, hand arthritis, severe epicondylitis, and C8 cervical radiculopathy. Inconsistent measurement of grip strength is seen with malingering.

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GRIP STRENGTH MEASUREMENT SUMMARY: Grip strength measurement is the most objective but indirect measurement of the integrity and strength of the supporting muscles of the wrist. MANEUVER: The average of three consecutive readings using the dynamometer provides an accurate and reproducible measurement of gripping and forearm muscle strength. An alternative method involves compressing a partially inflated blood pressure cuff. INTERPRETATION: Grip strength is reduced in a consistent manner by disuse atrophy, wrist arthritis, CTS, hand arthritis, severe epicondylitis, and C8 cervical radiculopathy. Inconsistent measurement of grip strength is seen with malingering.

FIGURE 5–4. Grip strength measurement to assess forearm muscle strength.

STRENGTH ASSESSMENT OBJECTIVE: Strength assessment using resistance bands is another objective measurement of the integrity and strength of the supporting forearm muscles. It also educates the patient on the important role of physical therapy exercises in the recovery phase of treatment. MANEUVER: Forearm strength is measured in extension (depicted here) or in flexion (the opposite direction). A progressive number of standard 10-10 resistance bands are placed over the patient’s metacarpal phalangeal joints (extension) or the palm (flexion). The patient is asked to pull them apart, keeping the wrists perfectly straight. Side-toside comparisons are made. FIGURE 5–5. Strength assessment of the forearm muscles.

INTERPRETATION: Forearm muscle strength measurements are reduced in a consistent manner by disuse atrophy, wrist arthritis, CTS, hand arthritis, severe epicondylitis, and C8 cervical radiculopathy. Inconsistent measurement of grip strength is seen with malingering.

WRIST

INSPECT THE DORSUM SUMMARY: The dorsum of the hand is inspected for localized swelling arising from the joint, the focal swelling of a dorsal ganglion, and diffuse swelling over the extensor tendons. MANEUVER: Simple inspection of the dorsum of the wrist can be combined with palpation to define the characteristics of the swelling. INTERPRETATION: Radiocarpal joint swelling will localize directly over the joint, filling in the natural depression atop the navicular. The soft cystic swelling of a ganglion is similarly located but with more defined edges. The swelling accompanying dorsotenosynovitis and RSD extends over a greater area and obscures the dorsal tendons and carpal bones. FIGURE 5–6. Inspect the dorsum for wrist swelling, ganglion, or dorsotenosynovitis.

PALPATE THE RADIAL STYLOID AND COMPRESS THE CMC JOINT SUMMARY: The CMC joint of the thumb articulates with the trapezius bone of the wrist, and the extensor and abductor tendons of the thumb form the anatomic snuffbox, both of which are in close proximity to the radial side of the wrist. MANEUVER: The wrist is placed in neutral position, radial side up. The most distal portion of the radial styloid is identified, marked, and palpated for local tenderness. Similarly, the CMC joint is compressed in an anteroposterior direction to assess its involvement (see Figure 5-19).

FIGURE 5–7. Palpate the radial styloid and compress the CMC joint to screen for thumb involvement.

INTERPRETATION: Twenty percent to 25% of patients with de Quervain’s tenosynovitis or CMC joint osteoarthritis complain of wrist pain rather than thumb pain.

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TINEL SIGN COMBINED WITH A CONSISTENT HISTORY SUMMARY: The carpal tunnel is formed by the first row of carpal bones (navicular, lunate, pisiform, and triquetral) and the transverse carpal ligament. It contains nine flexor tendons and the median nerve. Because the Tinel sign is positive in only 70% of cases, it must be combined with a history of paresthesia or hypesthesia that is consistent with a median nerve distribution. MANEUVER: The wrist is placed in neutral position. Using the index finger, the wrist is vigorously tapped at the junction of the palmaris longus and the flexor creases. The tapping should encompass an area the size of a quarter.

FIGURE 5–8. Tinel sign combined with a consistent history to screen for CTS.

ONE-MINUTE SCREENING EXAM: MANAGEMENT OPTIONS TRIAGE TO X-RAY For the patient who has a history of trauma, is at risk of bony injury, or presents with a severe wrist sprain: • Order three views of the wrist for patients with a history of fall to an outstretched arm or direct blow to the wrist (distal radius or navicular fracture, perilunate dislocation, or triangular cartilage injury). • Order three views of the wrist for patients with significant loss of range of motion in extension and flexion (posttraumatic osteoarthritis or inflammatory arthritis, such as rheumatoid arthritis). • Order coned-down views of the navicular for a patient with a history of trauma, a loss of 50% of the range of motion of the wrist, and navicular tenderness (navicular fracture, greater anatomic detail). • Order the carpal tunnel view for patients with severe wrist sprain and concurrent development of CTS symptoms (perilunate dislocation). TRIAGE TO THE LAB For patients with severe limitation of wrist motion and signs of inflammation (gout, acute arthritis, or septic arthritis): • Order a complete blood cell count, uric acid, and erythrocyte sedimentation rate for patients with acute pain, exquisite tenderness, and poor range of motion of the wrist with signs of active inflammation (gout or acute arthritis); include blood cultures if the acute inflammatory changes are accompanied by significant fever or concurrent signs of infection elsewhere in the body (septic arthritis).

INTERPRETATION: For the Tinel sign to be considered positive, the patient’s pain must be reproduced, and the paresthesia should be distinctly different from the response on the contralateral side. Note that false positives occur in overly sensitive patients.

CONSIDER A BONE SCAN For patients with inconclusive exams but a suspicion of RSD, osteomyelitis, or subtle fracture accompanying severe wrist sprain.

CONSIDER MRI For patients with suspected navicular fracture to determine the integrity of the navicular bone or its blood supply (avascular necrosis) and to evaluate the triangular cartilage in patients with lateral wrist pain.

RECOMMEND EMPIRICAL TREATMENT For patients with mild to moderate wrist pain and stiffness, unrestricted movement of the joint, normal alignment, and normal grip strength. • Avoid the extremes of movement, keeping the wrist in neutral position. • Immobilize the wrist with a Velcro wrist splint. • Limit repetitious gripping and grasping. • Limit lifting to less than 10 pounds. • Avoid exposure to vibration and cold. • Apply ice over the dorsum of the wrist up to four times a day. • Perform gentle passive stretching exercises in flexion and extension daily. DETAILED EXAMINATION: SPECIFIC WRIST DIAGNOSES Perform a detailed examination of the wrist if injury has occurred. Symptoms are persistent or chronic. Wrist pain and stiffness are moderate to severe. Range of motion is impaired, or the patient’s grip is dramatically affected.

WRIST

WRIST SPRAIN Injuries to the wrist represent a spectrum of

conditions that include the simple wrist sprain (a strained ligament), perilunate dislocation (a torn ligament), chondral fracture,

and navicular fracture. Painful loss of range of motion is the key to distinguishing these conditions. Simple sprains rarely show more than a 10% loss of flexion and extension.

RADIOCARPAL JOINT LINE TENDERNESS SUMMARY: The junction of the distal radius, navicular, and lunate bones occurs directly under the intersection of the extensor tendon of the index finger and a line drawn perpendicular to the most distal aspect of the radius. MANEUVER: The wrist is placed in neutral position. The ulnar styloid is identified (x), and the extensor tendon of the index finger is identified (arrows). The navicular is palpated at the intersection of the distal radius and the first extensor tendon. The lunate is palpated between the ulnar styloid and the navicular bone. Tenderness may be enhanced by passively flexing and extending the wrist in an arc of 50 degrees. ADDITIONAL SIGNS: Mild swelling over the dorsum and a nearly normal range of motion of the wrist complete the examination.

FIGURE 5–9. Radiocarpal joint line tenderness for the diagnosis of wrist sprain.

INTERPRETATION: Radiocarpal joint line tenderness must be combined with range of motion measurements in flexion and extension to distinguish a simple wrist sprain from higher degrees of wrist trauma.

NORMAL X-RAYS SUMMARY: A sprained wrist is an injury to the supporting ligaments of the radiocarpal joint. Radiographs of simple wrist sprains are normal. With the exception of the nondisplaced navicular fracture, radiographs of the injured wrist (e.g., fracture, dislocation) or acute arthritic flare are abnormal. The posteroanterior, lateral, and oblique views are used to exclude fracture, perilunate dislocation, and underlying arthritis. DIAGNOSIS: Simple wrist sprain with a normal posteroanterior radiograph of the wrist. INTERPRETATION: The normal wrist is characterized by 2 mm articular width between the radius, navicular, and lunate bones (identical to the width of the intercarpal joints), normal bony position and alignment, and well-mineralized bone. FIGURE 5–10. Normal x-rays of the wrist are used to exclude fracture and arthritis.

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RADIOCARPAL JOINT ARTHRITIS Radiocarpal joint arthritis is an uncommon problem. Whether due to rheumatoid arthritis or the much less common posttraumatic osteoarthritis,

the severity of involvement of the joint is directly related to the loss of flexion and extension.

RADIOCARPAL JOINT DORSAL SWELLING AND TENDERNESS SUMMARY: Wrist swelling and tenderness preferentially affect the dorsum of the wrist, directly over the navicular bone. With progressive joint involvement, the normal concavity and bony firmness over the navicular bone are replaced by increasing domelike swelling and tenderness. MANEUVER: The wrist is placed in neutral position. The ulnar styloid is identified, and the extensor tendon of the index finger is identified. The navicular is palpated at the intersection of the distal radius and the first extensor tendon. The lunate is palpated between the ulnar styloid and the navicular bone. Tenderness may be enhanced by passively flexing and extending the wrist in an arc of 50 degrees. ADDITIONAL SIGNS: Increasing swelling over the dorsum and variable degrees of heat and redness complete the examination.

FIGURE 5–11. Radiocarpal joint dorsal swelling and tenderness.

INTERPRETATION: Wrist joint tenderness and swelling are moderate with osteoarthritis and severe with gout, Colles fracture, navicular fracture, perilunate dislocation, and septic arthritis.

RANGE OF MOTION OF THE RADIOCARPAL JOINT SUMMARY: The greater the involvement of the wrist with acute swelling and inflammation, the greater the impairment of range of motion. MANEUVER: The patient is asked to relax the muscles of the forearm. While the examiner holds the distal forearm firmly, the wrist is passively flexed and extended to its endpoints. Perform this cautiously in the acutely injured or inflamed wrist. Normal flexion and extension average 90 and 80 degrees, respectively.

FIGURE 5–12. Assess range of motion of the radiocarpal joint.

INTERPRETATION: Mild symptoms and normal range of motion are seen with simple wrist sprains and mild arthritis. Moderate symptoms and a 20% to 50% loss of range of motion are characteristic of chondral fractures and moderate arthritis. Acute gout, navicular fracture, Colles fracture, and perilunate dislocation are characterized by severe symptoms and a loss of at least 50% of range of motion. Patients with a septic joint or displaced distal radius fractures refuse to move at all.

WRIST

X-RAY CHANGES CASE: This 47-year-old high school basketball coach described a history of multiple wrist sprains over the last 20 years. The patient never had a documented fracture on previous x-rays of the wrist. His exam demonstrated mild dorsal swelling, flexion of 65 to 70 degrees, extension of 60 to 65 degrees, and mild endpoint stiffness and pain. DIAGNOSIS: Osteoarthritis of the radionavicular joint. The articular cartilage between the radius and the navicular bone is narrowed (single large arrow), and the gap between the navicular and lunate is widened (2 small arrows). The normal articular width between any of the carpal bones should be 2 mm. DISCUSSION: Osteoarthritis of the wrist is rare outside the setting of previous trauma. However, wrist involvement is common in well-established rheumatoid arthritis.

FIGURE 5–13. X-ray changes to confirm radiocarpal osteoarthritis.

LOCAL ANESTHETIC BLOCK OR ASPIRATION SUMMARY: In order to distinguish the various causes of wrist effusion, the radiocarpal joint is aspirated from the dorsal aspect. POSITIONING: The wrist is placed flat on the table with the palm side down. SURFACE ANATOMY: Distal radius, navicular, and extensor digitalis of the index finger. POINT OF ENTRY: In the angle made by the intersection of the radius and the extensor tendon. ANGLE OF ENTRY: NEEDLE: DEPTH:



5

⁄2 to 5⁄8 inch (1⁄4 inch is too superficial).

1

ANESTHESIA: Ethyl chloride, skin: 1⁄4 mL, extensor retinaculum; 1⁄4 mL intra-articularly.

FIGURE 5–14. Local anesthetic block or aspiration to confirm the involvement of the wrist joint.

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DORSAL GANGLION CYST Ganglion cysts are located in

the dermal layer of the skin. They are typically round, vary in circumference up to the size of a quarter, and can be multilobulated.

Their variability in size, shape, and firmness depends on the amount of excessive synovial or tenosynovial fluid produced by the adjacent joint or tendon.

DORSAL GANGLION SUMMARY: The diagnosis of a dorsal ganglion is made by simple inspection and palpation. More than 90% of dorsal ganglia result from an excess production of synovial fluid. A sinus tract connects the cyst to the joint located between the navicular and lunate bones. Ten percent of ganglia result from the excessive tenosynovial fluid produced by the extensor tendons. MANEUVER: The cyst is palpated for tension, fluctuance, and mobility. Passive movement of the fingers is performed to determine whether the cyst is attached to the tenosynovial sheath.

FIGURE 5–15. Dorsal ganglion inspection at the wrist.

ADDITIONAL SIGNS: Passive movement of the wrist should be normal unless underlying arthritis is present. If the ganglion moves with passive movement of the fingers, the ganglion probably arises from the extensor tendon sheath. INTERPRETATION: The excessive production of fluid represents overuse or previous injury to the joint or its supporting tendons.

DIAGNOSTIC ASPIRATION SUMMARY: The diagnosis is confirmed by the aspiration of the thick, tenacious, nonbloody fluid from the cyst. POSITIONING: down.

Wrist flat on the table, palm side

SURFACE ANATOMY: The four dorsal extensor tendons of the fingers are covered by the extensor retinaculum located below the subcutaneous layer. POINT OF ENTRY: ANGLE OF ENTRY:

At the base of the cyst. Parallel to the skin.

NEEDLE: 5⁄8 inch, 25 gauge for anesthesia and 1 inch, 18 gauge for aspiration. FIGURE 5–16. Diagnostic aspiration to confirm a dorsal ganglion.

DEPTH:

⁄4 to 3⁄8 inch.

1

ANESTHESIA: Ethyl chloride, skin: 1⁄4 mL subcutaneously.

WRIST

DORSOTENOSYNOVITIS Inflammation of the extensor tendons of the hand is called dorsotenosynovitis. It is characterized by dorsal pain, swelling, and acute inflammation. In addition, the pain of active tenosynovitis is uniquely aggravated by resisted ex-

tension and passive flexion of the fingers. The latter sign distinguishes it from the conditions that cause dorsal swelling (simple edema, cellulitis, fracture, and RSD).

DORSAL TENOSYNOVITIS CASE: This middle-aged office worker presented with acute swelling, pain, and warmth over the back of her hand that was aggravated by typing and other fine movements of the fingers. The patient had a history of hypertension treated with thiazide diuretics but no history of rheumatoid arthritis, gout, or other rheumatic diseases. She denied any direct trauma or unusual use of her wrist and hand. The localized pain and swelling were aggravated by resisting the extension of the middle three digits. Uric acid was elevated. DIAGNOSIS:

Acute dorsal tenosynovitis due to gout.

INTERPRETATION: Aspiration of fluid is not possible with acute tenosynovitis. Distinguishing it from RSD and cellulitis is based solely on clinical examination.

FIGURE 5–17. Dorsal tenosynovitis is characterized by diffuse dorsal swelling that is aggravated by movement of the fingers.

DIAGNOSIS OF DORSOTENOSYNOVITIS SUMMARY: No specialized testing is available to confirm the diagnosis of dorsotenosynovitis. The combination of dorsal swelling, pain reproduced by resisting finger extension, or pain aggravated by passive finger flexion remain the hallmarks of this local musculoskeletal process. MANEUVER: While holding the forearm fixed, the examiner places the other hand on the fingers and passively presses the extensor tendons downward. Bending the wrist 45 degrees enhances the active dorsotenosynovitis. This is combined with active resistance of the extensor tendons to confirm the diagnosis.

FIGURE 5–18. The diagnosis of dorsotenosynovitis is made strictly on clinical grounds.

INTERPRETATION: Whereas the swelling and inflammatory changes of cellulitis, RSD, and dorsotenosynovitis are indistinguishable, only the active inflammation of the extensor tendons is aggravated by the passive stretching and active resistance maneuvers.

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THUMB DIAGNOSES PRESENTING AS WRIST PAIN

The complete examination of the wrist requires an examination of the CMC joint and the extensor tendons of the thumb. Approx-

imately 25% of patients with de Quervain’s tenosynovitis and CMC arthritis describe their symptoms as wrist pain rather than pain in the thumb (see Chapter 6).

COMPRESSION OF THE BASE OF THE THUMB SUMMARY: Twenty percent to 25% of patients with de Quervain’s tenosynovitis or CMC joint osteoarthritis complain of wrist pain rather than thumb pain. MANEUVER: The wrist is placed in neutral position, radial side up. The examiner grasps the base of the thumb just beyond the anatomic snuffbox. The synovial lining and the base of the metacarpal are squeezed together using the thumb and finger. The compression can be enhanced by circumducting the thumb while continually holding pressure. ADDITIONAL SIGNS: Compressing the base of the thumb in the anteroposterior direction, noting crepitation with circumduction of the joint, and estimating the bony shelf sign suggest active arthritis of the base of the thumb.

FIGURE 5–19. Compression of the base of the thumb is the most effective maneuver to elicit pain from an osteoarthritis flareup of the CMC joint.

INTERPRETATION: Distinguishing CMC joint strain and osteoarthritis from primary involvement of the wrist requires local anesthetic block placed at the base of the thumb.

PALPATE THE RADIAL STYLOID SUMMARY: Twenty percent to 25% of patients with de Quervain’s tenosynovitis or CMC joint osteoarthritis complain of wrist pain rather than thumb pain. The extensor pollicis longus, extensor pollicis brevis, and abductor pollicis longus form the anatomic snuffbox. All three tendons course along the distal radial styloid to attach to the interphalangeal, metacarpal phalangeal, and CMC joints of the thumb, respectively. MANEUVER: The wrist is placed in neutral position, radial side up. The most distal portion of the radial styloid is identified, marked, and palpated for local tenderness. FIGURE 5–20. Palpate the radial styloid to assess the degree of de Quervain’s tenosynovitis.

ADDITIONAL SIGNS: Radial styloid tenderness, pain aggravated by resisting extension of the thumb, and pain aggravated by stretching the extensor tendons in flexion (the Finkelstein maneuver) suggests active de Quervain’s tenosynovitis. INTERPRETATION: Distinguishing de Quervain’s from primary involvement of the wrist requires local anesthetic block over the radial styloid (see Chapter 6).

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CARPAL TUNNEL SYNDROME Median nerve compression

at the wrist (CTS) or in the forearm (pronator teres syndrome) presents with a variety of symptoms depending on the extent of nerve compression, the length of time symptoms have been present, and previous surgical intervention. The symptoms include pares-

thesia or hypesthesia of the wrist and hand, variable degrees of subjective weakness, and true loss of strength and atrophy. If there is a history of neck pain, whiplash, arthritis of the neck, or neck surgery, studies should be obtained to evaluate for concurrent C6 radiculopathy.

TINEL SIGN SUMMARY: The carpal tunnel is formed by the first row of carpal bones (navicular, lunate, pisiform, and triquetral) and the transverse carpal ligament. It contains nine flexor tendons and the median nerve. Because the Tinel sign is positive in only 70% of cases, it must be combined with a history of paresthesia or hypesthesia that is consistent with a median nerve distribution. MANEUVER: The wrist is placed in neutral position. Using the index finger, the wrist is vigorously tapped at the junction of the palmaris longus and the flexor creases. The tapping should encompass an area the size of a quarter.

FIGURE 5–21. Tinel sign to assess the degree of CTS.

ADDITIONAL SIGNS: The Phelan sign, loss of twopoint discrimination of the fingertips, loss of light touch and pain sensation, weakness of thumb opposition, and thenar muscle atrophy are the additional signs of median neuropathy. INTERPRETATION: For the Tinel sign to be considered positive, the patient’s pain must be reproduced, and the paresthesia should be distinctly different from the response on the contralateral side.

NERVE CONDUCTION VELOCITY CASE: This professional hairdresser complained of numbness and tingling of the thumb and index finger. She feels her strength is normal. Nerve conduction velocity testing demonstrated a slowing of the median nerve across the wrist. DIAGNOSIS:

CTS from repetitious use.

DISCUSSION: Nerve conduction velocity testing is moderately sensitive in the diagnosis of persistent or progressive symptoms caused by median nerve compression. Approximately 70% of patients with CTS will have an abnormal test.

FIGURE 5–22. Nerve conduction velocity to confirm CTS and determine its severity.

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5–1



DIAGNOSIS

CONFIRMATION

Pain and stiffness at full wrist flexion or extension

1. Wrist sprain

Wrist series x-ray is normal

Minimal dorsal swelling

Resolves in 2 wk

Minimal tenderness over the navicular and lunate bones Loss of full wrist flexion and extension

Radiocarpal arthritis

Wrist series x-ray or local anesthetic placed in the radiocarpal joint

Dorsal swelling and tenderness Cystic swelling over the dorsum of the wrist

Dorsal ganglion

Simple aspiration of thick, gelatinous fluid

Hypesthesias or paresthesias by history

2. Carpal tunnel syndrome

Medial nerve block with anesthetic or nerve conduction velocity testing

Dorsal tenosynovitis

Anesthetic placed alongside the tenosynovial sheath

Triangular cartilage injury

MRI of the wrist or anesthetic placed in the ulnocarpal joint

Navicular fracture

Wrist series x-ray or bone scan

⫹ Tinel or Phelan sign Pain with resisted finger extension Diffuse swelling over the dorsum Point tenderness over the lateral wrist just distal to the ulnar styloid Pain with forced ulnar deviation Loss of full wrist flexion and extension Dorsal swelling and tenderness Point tenderness over the dorsum or in the snuffbox

WRIST

COMMON WRIST FRACTURES SUMMARY Because of its peripheral location and the injuries sustained during falls to an outstretched arm, fractures of the wrist are very common. The prevalence of wrist fractures is slightly

less than that of ankle fractures. Distal radius fractures and fractures of the navicular make up more than 90%. Of the variety of fractures that affect the distal radius, the Colles fracture is the most common. Most Colles fractures are either nondisplaced or show minimal displacement that is readily reduced and stable. The majority of these fractures can be managed by the primary care provider.

NONDISPLACED COLLES FRACTURE

FIGURE 5–23. Distal radius fracture: nondisplaced Colles fracture.

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SUMMARY: Fractures of the distal radius are classified according to the direction of angulation of the radius and whether the radiocarpal joint or radioulnar joint is involved. The Colles fracture involves the distal 2 cm of the radius, is angled dorsally, and may or may not involve the joint. The Smith fracture is identical to the Colles fracture except for the volar angulation. The Barton fracture is a fracture or dislocation with the predominant finding of wrist dislocation by clinical criteria and x-ray findings. Note the fracture of the ulnar styloid, the transverse, compacted fracture of the radius, and the oblique fracture extending proximally, all minimally displaced. IMMOBILIZATION: (1) Order x-rays, classify the type of fracture, determine the degree of displacement or dislocation of the adjacent joints, and assess the integrity of the median nerve. (2) Perform hematoma, axillary, or Bier block anesthesia. (3) Perform closed reduction using finger trap traction with proximal brachial countertraction. (4) Repeat the x-rays to ensure a slightly volar tilt and restoration of the length of the radius. (5) Use a sugar tong splint for the first 48 hours to allow room for swelling. (6) After 48 hours, replace the splint with a short arm cast for undisplaced fractures or a long arm cast with slight flexion and ulnar deviation for displaced fractures (if unstable, refer to surgery). (7) Repeat x-rays at 4 to 6 weeks to assess healing. (8) Use a Velcro wrist splint with a metal stay for 3 to 4 weeks after immobilization. (9) Start passive range of motion exercises of the wrist in dorsiflexion and volarflexion after fixed immobilization. SURGICAL REFERRAL: Colles fractures that are reducible but unstable, comminuted, or intra-articular, Smith fractures, and Barton fractures may require open reduction and internal fixation. These fractures should be managed by a fracture specialist. Pin fixation or open reduction is necessary for a fracture that remains unstable despite closed reduction, for a Barton fracture or dislocation, for a comminuted fracture, and for a displaced fracture (especially an intra-articular fracture).

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DISPLACED AND FORESHORTENED COLLES FRACTURE CASE: This older woman with advanced osteoporosis fell on an outstretched arm. She was unable to move the wrist in any direction. Her wrist showed dramatic dorsal angulation.

FIGURE 5–24. Distal radius fracture: displaced and foreshortened Colles fracture.

PROGNOSIS: The prognosis depends on the adequacy of reduction, the age of the patient, the presence of osteoporosis, and whether the fracture extended into the joint. Intra-articular and extraarticular fractures that result in a foreshortened or angled radius (⬎5 mm or 20 degrees, respectively) have a greater incidence of poor range of motion of the wrist, late-onset osteoarthritis, and median nerve damage.

NAVICULAR FRACTURE SUMMARY: The early diagnosis of navicular fracture must rely on a high index of suspicion, a comprehensive examination of the wrist, and serial radiographs. Because the fracture is small and often nondisplaced, it may not be detectable on initial plain radiographs. The diagnosis is suggested by dramatic local tenderness (either in the snuffbox or over the dorsum), the acute loss of 50% of flexion and extension, and dramatic dorsal swelling. IMMOBILIZATION: If the clinical findings suggest the possibility of navicular fracture, the thumb and wrist must be immobilized using a thumb spica short arm cast or at least a thumb spica Velcro wrist brace until the patient is seen by the fracture specialist. SURGICAL REFERRAL: Surgical referral to a hand specialist is strongly recommended. PROGNOSIS: Immobilization is imperative to avoid the potential complications of nonunion and avascular necrosis of the navicular. Incomplete recovery of range of motion and late-onset osteoarthritis of the wrist result when the fracture fails to heal.

FIGURE 5–25. Navicular fracture.

WRIST

AVASCULAR NECROSIS OF THE NAVICULAR CASE: This 52-year-old woman sustained a penetrating injury of her wrist while using an electric drill. The drill entered the dorsum of the wrist. Her examination demonstrated maximum tenderness over the navicular with moderate tenderness in the snuffbox and swelling over both areas. She was treated in a thumb spica short arm cast for 21⁄2 months. She never fully recovered her wrist range of motion or her grip strength. Months after the injury she manifested mild carpal tunnel symptoms. DIAGNOSIS:

FIGURE 5–26. Avascular necrosis of the navicular after fracture.

Avascular necrosis of the navicular.

SUMMARY: The navicular bone has a tenuous blood supply at best. When the bone is fractured, the proximal blood flow is interrupted, and the distal segment undergoes avascular necrosis. Approximately 5% to 10% of navicular fractures undergo collapse and subsequent sclerotic bony change. Loss of the normal integrity of the navicular leads to late-onset osteoarthritis of the radionavicular joint. Most patients with this complication fail to regain half the normal range of motion of the wrist joint.

PERILUNATE DISLOCATION SUMMARY: Perilunate dislocation results from a severe blow to the volar wrist and is characterized by severe wrist sprain. The supporting ligaments are torn, and the lunate rotates on its axis. The abnormal position distorts the carpal tunnel, leading to median nerve symptoms. IMMOBILIZATION: Initially, the patient is placed in a posterior splint to allow for swelling. REFERRAL:

Surgical referral is mandatory.

PROGNOSIS: The prognosis is good in most patients, although avascular necrosis and late-onset steoarthritis can result from this injury.

FIGURE 5–27. Perilunate dislocation associated with a severe wrist sprain.

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CLINICAL PEARLS • Loss of flexion of the wrist is the first sign of a developing effusion of the radiocarpal joint. • The absolute loss of flexion and extension is directly correlated with the severity of arthritis, wrist sprain, and the more advanced traumatic conditions, such as navicular fracture and perilunate dislocation. • Chronic irritation of the wrist causes an overproduction of synovial fluid. Because of the limited capacity of the synovial cavity, this excess fluid leaks out of the joint through a sinus and into the subcutaneous tissues. In this superficial location, the body isolates the fluid by encapsulation; a thick wall forms around the fluid, thereby creating the ganglion cyst. • Volar ganglia are uncommon and most often occur at the base of the thumb adjacent to the insertion of the flexor carpi radialis tendon and the radial artery.

• More than 90% of ganglia are located on the dorsum of the wrist, the majority of which arise from the radiocarpal joint. Fewer than 10% arise from the tenosynovial sheaths that envelop the extensor tendons of the thumb and fingers. • CTS can be graded as intermittent sensory loss, continuous sensory loss, combined sensorimotor loss, or sensorimotor loss with atrophy. Increasing pressure over the median nerve gives rise to increasing neurological impairment, typically beginning with paresthesia and progressing to hypesthesia, dysesthesia, motor weakness, and motor weakness with muscular atrophy.

CHAPTER 6: THUMB DIFFERENTIAL DIAGNOSIS Diagnoses Osteoarthritis Carpometacarpal joint Posttraumatic arthritis of the metacarpal phalangeal and interphalangeal joints Mucinoid cysts atop the joint

Confirmations

Examination; x-rays: hand series Examination; x-rays: hand series Examination, simple puncture

Extensor tendons De Quervain’s tenosynovitis

Examination, local anesthetic block

Flexor tendons Trigger thumb Fixed locked digit

Examination, local anesthetic block Examination

Gamekeeper’s thumb

Examination, local anesthetic block

Referred pain Carpal tunnel syndrome C5–C6 radiculopathy Reflex sympathetic dystrophy

Nerve conduction velocity testing, local anesthetic block Cervical spine x-rays, MRI, electromyography Examination, bone scan

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INTRODUCTION The differential diagnosis of thumb pain is dominated by the wear-and-tear arthritis of the base of the thumb, carpometacarpal (CMC) osteoarthritis. This is a universal condition that nearly everyone develops to some degree in the fifth and sixth decades of life. Despite its prevalence, patients may not necessarily develop symptoms significant enough to cause pain or interfere with overall hand function. By contrast, arthritis affecting the metacarpal phalangeal (MP) and interphalangeal (IP) joints is uncommon and almost always is the result of previous trauma. The second most common condition that affects the thumb is carpal tunnel syndrome. Most patients with mild to moderate median nerve entrapment develop varying degrees of thumb paresthesia, hypesthesia, or subjective thumb weakness. Patients with advanced nerve compression always experience objective thumb weakness and thenar muscle atrophy caused by the recurrent median nerve involvement. Repetitive use of the thumb also causes irritation and inflammation of the supporting tendons (tenosynovitis). Repetitive gripping and grasping with pressure over the palmar aspect of the MP joint cause flexor tenosynovitis (trigger thumb). Repetitive gripping and grasping with active movement of the wrist cause irritation and inflammation of the extensor and abductor tendons (de Quervain’s stenosing tenosynovitis). These periarticular conditions are characterized by their focality and unidirectional aggravation on examination of the thumb. Trigger finger is tender over the palmar aspect of the MP joint and aggravated by isometrically resisted flexion. De Quervain’s tenosynovitis is tender over the radial styloid and is aggravated by isometrically resisted extension and abduction. Contrast this with the exam of the CMC joint. Tenderness is over the entire joint, and the deep, poorly localizing pain is aggravated by movement in all directions. Injury to the thumb tendons is uncommon. Rupture of the extensor pollicis longus insertion leads to the mallet thumb deformity. Ligament injuries are exceedingly common. Simple sprains, partial dislocations, and repetitive stress to the supporting ligaments are for the most part benign. Unless the underlying cartilage is damaged (chondral fracture leading to late-onset posttraumatic osteoarthritis), these injuries are self-limited. The middle MP joint is most susceptible. The most common injury is gamekeeper’s thumb, an injury to the ulnar collateral ligament of the MP joint caused by repetitive twisting type movements or hyperextension injuries (ski pole injuries). The ligament can be stretched (first degree), partially torn (second degree), or completely torn or avulsed from the bone (third-degree injuries). Because of its peripheral location and its unique role in the hand, the thumb is susceptible to bony fracture. Nondisplaced fractures that do not involve the articular surfaces can be managed with simple immobilization. With the exception of third-degree gamekeeper’s thumb and Bennett and Rolando intra-articular fractures of the base of the metacarpal, most of these can be managed by nonsurgical means. Finally, carpal tunnel pain can be referred to the thumb. Similar to carpal tunnel syndrome, thumb pain, paresthesia, or hypesthesia is part of the clinical symptoms of C5–C6 cervical radiculopathy. Thumb pain is always part of the dif-

fuse hand pain seen with reflex sympathetic dystrophy. As with all referred types of pain, the examination of the thumb is free of local tenderness, loss of range of motion, or pain aggravation with movement. SYMPTOMS Conditions directly affecting the thumb cause symptoms of localized pain and sensitivity, swelling or deformity, and decreased gripping, grasping, and pinching. The latter impairments of function are nonspecific and can be caused by any condition affecting the thumb, individual fingers, or entire hand. Therefore, the key to establishing the correct diagnosis is the precise localization of the patient’s pain and swelling. Pain at the base of the thumb, the most common thumb complaint, reflects the nearly universal occurrence of arthritis of the CMC joint and the pain that accompanies simple sprains of the joint. Often, the patient points to the snuffbox or rubs along the proximal metacarpal when describing the condition. Patients also complain of the characteristic deformity (the “shelf sign” from the bony enlargement of the joint) or the swelling that forms in the anatomic snuffbox and distorts the radial side of the wrist. Pain over the distal radius that extends into the anatomic snuffbox is the classic pain pattern of de Quervain’s tenosynovitis. This pain can be felt over a wide area and can even travel in a retrograde fashion up the forearm. Pain over the flexor aspect of the MP joint is characteristic of the inflammatory stage of flexor tenosynovitis. This dime-sized area of pain is localized over the flexor creases in the palm (the same site as the local tenderness on examination of the flexor tendons). However, as the condition progresses, the pain may be overshadowed by the mechanical locking described at the distal IP joint (the mechanical stage of the condition). Patients with severe tendon swelling may complain of the end stage condition of flexor tenosynovitis, fixed locked digit. Pain along the inner aspect of the MP joint is seen with gamekeeper’s thumb, simple sprains, and partial dislocations. The ulnar collateral ligament is much more likely to be injured with repetitious use of the thumb, the twisting motions of a ski pole injury, or hyperextension sports injuries. Pain localized to the IP joint is the least common presentation. Tuft fractures and ligament injures are the most common causes of IP joint involvement. The joint is spared in most cases of rheumatoid arthritis. Osteoarthritis of the IP joint results almost exclusively from old and remote trauma. EXAMINATION Examination of the thumb begins with a functional assessment of gripping, grasping, and pinching and range of motion testing of its three joints. These maneuvers provide objective measurements of function, a preliminary assessment of the severity of the condition, and important clues to the specific diagnosis. Next, specific maneuvers for each diagnosis are performed based on the location and description of the pain and the clues provided by the functional screening tests. Pain at the base of the thumb, visible swelling in the anatomic snuffbox, or bony enlargement of the proximal metacarpal suggests osteoarthritis of the CMC joint. Pain

THUMB

aggravated by compression of the joint in the anteroposterior direction or reproduced by the mortar and pestle maneuver distinguishes active inflammation of the joint from simple sprains and the more common asymptomatic bony enlargement of the joint. Pain localized at the MP joint may arise from the active inflammation of flexor tenosynovitis (the inflammatory stage of trigger thumb), the injured ligament of gamekeeper’s thumb, simple ligament sprains of the MP joint, or the uncommon posttraumatic osteoarthritis of the MP joint. The pain and local tenderness of active flexor tenosynovitis (trigger thumb) are located directly over the flexor creases in the palm. Locking or clicking of the IP joint or a loss of the normal smooth motion of the IP joint with active flexion confirms this diagnosis. Tenderness located only on the ulnar side of the MP joint is characteristic of gamekeeper’s thumb (injury to the ulnar collateral ligament). This diagnosis is confirmed by reproducing the patient’s pain by valgus stress testing of the joint. Tenderness on both sides of the MP joint along with a loss of full flexion suggests either a strain of the MP joint (recent trauma) or posttraumatic arthritis. Pain experienced primarily over the distal radial styloid but often extending through the anatomic snuffbox to the base of the thumb strongly suggests de Quervain’s tenosynovitis. Distal radial styloid tenderness and pain aggravated by isometrically resisted thumb extension are necessary to distinguish involvement of the extensor tendons from involvement of the CMC joint. Finally, the examination of the thumb is completed with a screening maneuvers of the medial nerve for signs of carpal tunnel syndrome.

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BOX 6-1

ESSENTIAL EXAMINATION OF THE THUMB 1. Measure gripping and grasping and perform range of motion testing of flexion and extension of the CMC, MP, and IP joints. 2. Compress the CMC joint in the anteroposterior direction. 3. Palpate the lateral joint lines of the MP and IP joints. 4. Palpate the flexor tendons over the flexor creases in the palm (trigger thumb). 5. Palpate the extensor tendons over the radial styloid (de Quervain’s tenosynovitis). 6. Check the integrity of the ulnar collateral ligament of the MP joint (history of trauma). 7. Perform the Tinel and Phelan maneuvers for carpal tunnel syndrome.

ONE-MINUTE SCREENING EXAM: MANEUVERS ASSESSING OVERALL THUMB FUNCTION The next six maneuvers represent the minimal examination of the patient presenting with thumb symptoms. Range of motion measurements and screening maneuvers for CMC arthritis, trigger thumb, de Quervain’s tenosynovitis, and carpal tunnel syndrome provide enough information to triage to x-ray, order appropriate labs, suggest general treatment recommendations, or proceed to more detailed examination and treatment.

OPENING AND CLOSING THE HAND SUMMARY: Full function of the thumb requires normal movement of the three joints, normally functioning flexor and extensor tendons, and an intact recurrent median nerve and deep ulnar nerve. These maneuvers provide objective measurements of function, a preliminary assessment of the severity of the condition, and important clues to the specific diagnosis. MANEUVER: The patient is asked to open and close the hand, noting the patient’s ability to actively flex and extend the CMC, MP and IP joints. INTERPRETATION: Smooth, painless, and complete movement of the thumb rules out significant arthritis, trigger thumb, and de Quervain’s tenosynovitis. Patients with metacarpal and phalangeal fractures refuse to complete this maneuver.

FIGURE 6–1. Opening and closing the hand to assess the movement and range of motion of the three joints of the thumb.

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GRIP STRENGTH MEASUREMENT OBJECTIVE: Gripping can be influenced by arthritis of the intrinsic joints of the hands and wrist, intrinsic muscles of the hand, and flexor tendons and muscles of the forearm. Estimation of gripping and grasping strength provides the most objective measurement of the severity of the condition affecting the thumb. MANEUVER: Grip strength can be crudely estimated by manual gripping of the examiner’s fingers. However, physical measurement using a dynometer is much more accurate and reproducible. An alternative method involves compressing a partially inflated blood pressure cuff. FIGURE 6–2. Grip strength measurement using a partially inflated blood pressure cuff.

INTERPRETATION: Grip strength can be reduced by disuse atrophy, arthritis, carpal tunnel syndrome, de Quervain’s tenosynovitis, and cervical radiculopathy.

GRIP STRENGTH MEASUREMENT SUMMARY: The use of a dynamometer provides the most reproducible and objective measurement of the conditions affecting the thumb. It is the most effective means of assessing the severity of each condition and the best criterion to assess the effectiveness of treatment. Gripping can be influenced by arthritis of the intrinsic joints of the thumb, the thenar muscles, and the flexor tendons. MANEUVER: The strength of gripping can be accurately and reproducibly measured using a dynamometer, comparing one side with another. Three readings on each side are performed and averaged. Strength of the dominant side typically is 10% greater than that of the nondominant side, despite ambidexterity. INTERPRETATION: Grip strength can be reduced by disuse atrophy, arthritis, carpal tunnel syndrome, de Quervain’s tenosynovitis, and cervical radiculopathy.

FIGURE 6–3. Grip strength measurement by dynamometry.

THUMB

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INSPECTION OF THE THUMB SUMMARY: Simple inspection of the CMC, MP, and IP joints is used to screen for bony enlargement, swelling, or subluxation. Note the prominence of the left base of the thumb relative to the position of the distal radius, the shelf sign reflecting bony enlargement and subluxation. MANEUVER: The patient is asked to relax the muscles of the hands and forearms. The hands are placed in the anatomic position, radial side up. The widths of the joints in the anteroposterior direction are compared side to side.

FIGURE 6–4. Inspection of the thumb for CMC, MP, and IP joint swelling, subluxation, enlargement, or bony enlargement.

DISCUSSION: Osteoarthritis of the CMC joint is a nearly universal phenomenon. Osteoarthritis of the MP and IP joints almost always results from previous trauma.

RADIAL STYLOID PALPATION SUMMARY: In the absence of trauma to the radius, radial styloid tenderness is the definitive sign of de Quervain’s tenosynovitis. The extensor pollicis longus and brevis and abductor pollicis longus form the outer edges of the anatomic snuffbox. The tendons of these muscles become inflamed as they cross the radial styloid. MANEUVER: The wrist is placed in neutral position, radial side up. The most distal portion of the radial styloid is identified, marked, and palpated for local tenderness.

FIGURE 6–5. Radial styloid palpation to screen for de Quervain’s tenosynovitis.

INTERPRETATION: In the absence of trauma to the distal radius, radial styloid tenderness coupled with pain aggravated by resisting thumb extension is highly suggestive of active tenosynovitis.

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TINEL SIGN SUMMARY: The carpal tunnel is formed by the first row of carpal bones (navicular, lunate, pisiform, and triquetral bones) and the transverse carpal ligament. It contains nine flexor tendons and the median nerve. Because the Tinel sign is positive in only 70% of cases, it must be combined with a history of paresthesia or hypesthesia that conforms to a median nerve distribution. MANEUVER: The wrist is placed in neutral position. Using the index finger, the wrist is vigorously tapped at the junction of the palmaris longus and the flexor creases. The tapping should encompass an area the size of a quarter. INTERPRETATION: For the Tinel sign to be considered positive, the patient’s pain must be reproduced, and the paresthesia should be distinctly different from the response on the contralateral side. FIGURE 6–6. A localized history of thumb and finger pain, paresthesia, and hypesthesia combined with a Tinel sign to screen for carpal tunnel syndrome.

PALPATION OF THE FLEXOR TENDONS SUMMARY: Tenderness over the flexor tendons on the palmar aspect of the MP joint is the optimal screening maneuver for active flexor tenosynovitis. The flexor tendons are located in the midline and course down the finger to attach to the base of the middle and distal phalanges. Within the flexor tendon are two sesamoid bones located near the first flexor crease. MANEUVER: The flexor tendons are palpated over the palmar aspect of the MP joint (arrow).

FIGURE 6–7. Palpation of the flexor tendons on the palmar aspect of the MP joint.

INTERPRETATION: Active tenosynovitis is diagnosed by demonstrating flexor tendon tenderness at the base of the metacarpophalangeal joint combined with pain aggravated by passive stretching of the tendon in extension. If the tendon is sufficiently swollen, it will fail to move freely under the A-1 pulley of the tenosynovial sheath, resulting in mechanical locking at the IP joint.

THUMB

ONE-MINUTE SCREENING EXAM: MANAGEMENT OPTIONS TRIAGE TO X-RAY For patients with a history of blunt trauma or hyperextension injury, swollen or bony enlargement of one of the three joints, or severe impairment of gripping and grasping: • Order three views of the thumb for patients with a history of blunt trauma, dislocation, or hyperextension injury (Bennett or Rolando fractures, the eggshell tuft fracture, or phalangeal fractures). • Order three views of the thumb for patients with pain at the base of the thumb (CMC joint osteoarthritis or simple strain) to confirm and define the severity of the underlying injury. • Order three views of the thumb for patients with enlargement or swelling of the MP or IP joint (posttraumatic osteoarthritis or psoriatic arthritis). • Order three views of the thumb for patients with a history of hyperextension injury (tendon or ligament avulsion injury).

TRIAGE TO THE LAB For patients with acute swelling accompanied by inflammatory signs, order a complete blood cell count, uric acid, and erythrocyte sedimentation rate for patients with acute pain, exquisite tenderness, and inability to grip or grasp (gout or acute arthritis). CONSIDER A BONE SCAN For patients with diffuse pain, diffuse hand swelling, and possible accompanying

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discoloration and abnormal sweating (reflex sympathetic dystrophy). RECOMMEND EMPIRICAL TREATMENT For patients with mild to moderate thumb pain and stiffness, unrestricted movement of the three joints, normal alignment, and no tendon contractures: • • • • •

Avoid repetitious gripping and grasping. Avoid all vibration exposure. Avoid prolonged contact with cold. Wear thick leather gloves for protection. Perform gentle range of motion exercises in flexion and extension to prevent flexion contractures.

DETAILED EXAMINATION: SPECIFIC ANKLE DIAGNOSES Perform a detailed examination of the thumb if the thumb demonstrates palpable swelling, nodularity, or synovial thickening. Symptoms have been persistent or chronic. General function is moderately to severely impaired. Early joint contractures have begun to form. CMC JOINT OSTEOARTHRITIS “My thumb is getting larger,” “I can’t grip anymore,” “I get this achy pain in the base of my thumb,” “My thumbs used to hurt a lot but now they’re past the pain and are just ugly”: All of these patients have osteoarthritis of the base of the thumb.

COMPRESSION OF THE BASE OF THE THUMB OBJECTIVE: Anteroposterior compression of the CMC joint along its joint lines is a more sensitive sign of active arthritis or significant strain than palpation over the base of the metacarpal or in the snuffbox. MANEUVER: The wrist is placed in neutral position, radial side up. The examiner grasps the base of the thumb just beyond the anatomic snuffbox. The synovial lining and the base of the metacarpal are squeezed together using the thumb and finger. The compression can be enhanced by circumducting the thumb while continually holding pressure. ASSOCIATED SIGNS: Swelling filling the anatomic snuffbox, crepitation demonstrated by circumduction of the joint, and the bony shelf sign suggest active arthritis of the base of the thumb.

FIGURE 6–8. Compression of the base of the thumb is the most effective maneuver to elicit pain from an osteoarthritic flareup of the CMC joint.

INTERPRETATION: The examination of CMC strain overlaps greatly with the examination of osteoarthritis. X-rays are normal with simple thumb strain, helping to distinguish the two conditions.

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A


B FIGURE 6–9. X-rays to confirm the degree of arthritis of the CMC joint.

X-RAYS CASES: Case A is an example of the normal CMC joint demonstrating a 2-mm articular cartilage width and a normal alignment with the trapezium. Compare this with the abnormal narrowing and irregularities of the articular cartilage of the trapezial navicular articulation just below the CMC joint. Case B is an example of advanced osteoarthritis of the CMC joint. The articular cartilage has worn away, the trapezium has lost its saddle shape, and there is a 2- to 3-mm subluxation of the metacarpal bone. DISCUSSION: The diagnosis of osteoarthritis of the CMC joint can be confirmed with radiographic changes or by local anesthetic block.

THUMB

POSTTRAUMATIC ARTHRITIS OF THE MP OR IP JOINT

Osteoarthritis of the MP joint is uncommon and nearly always results from previous fracture or traumatic injury to the articular

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cartilage. The diagnosis is suggested by a combination of history of injury, lateral joint line tenderness, fusiform swelling, and lack of full flexion.

PALPATE THE LATERAL JOINT LINES SUMMARY: The MP joint is formed by the metacarpal and proximal phalangeal bones. The joint line is found 1⁄4 inch beyond the distal phalangeal head (knuckle) of the MP joint. The IP joint is formed by the proximal and distal phalangeal bones. The joint line is located 1⁄8 inch beyond the distal phalangeal head of the IP joint. MANEUVER: The lateral joint lines of each joint are palpated for local tenderness, bony enlargement, synovial thickening, and joint swelling. ADDITIONAL SIGNS: Full flexion is impaired, the joint may be deviated, and inflammatory signs complete the examination. The greater the degree of swelling and deformity, the greater the impairment of flexion. FIGURE 6–10. Palpate the lateral joint lines for posttraumatic arthritis.

INTERPRETATION: Bony enlargement with minimal synovial thickening and swelling is characteristic of posttraumatic arthritis. As the condition progresses, the ability to flex the joint is gradually impaired. Inflammatory arthritis can affect these joints as well but nearly always occurs as part of a polyarticular involvement.

X-RAYS CASE: The patient sustained a chip fracture of the thumb 10 years ago while playing baseball. Over the years the joint ached; more recently it began to swell. The examination demonstrated impaired flexion, bony enlargement, and early synovial thickening. DIAGNOSIS: Posttraumatic arthritis of the IP joint. X-rays show a loss of articular cartilage, bony osteophytes, and sclerotic bone. DISCUSSION: Most injuries to the small joints of the hand are simple sprains, reversible injuries to the supporting ligaments and synovial lining. Injury to the articular cartilage is much less common but can lead to varying degrees of osteoarthritis in subsequent years.

FIGURE 6–11. X-rays to confirm posttraumatic arthritis of the IP joint.

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DE QUERVAIN’S TENOSYNOVITIS “I can’t grip even my

pen”; “Every time I lift my baby I feel a sharp pain right here” (pointing to the radial styloid). The diagnosis of de Quervain’s

tenosynovitis is based on these classic descriptions and an examination demonstrating local tenderness directly over the radial styloid.

RADIAL STYLOID PALPATION SUMMARY: Radial styloid tenderness must be present to make the diagnosis of de Quervain’s tenosynovitis. The extensor pollicis longus and brevis and abductor pollicis longus form the outer edges of the anatomic snuffbox. The tendons of these muscles become inflamed as they cross the radial styloid to attach to the thumb. MANEUVER: The wrist is placed in neutral position, radial side up. The most distal portion of the radial styloid is identified, marked, and palpated for local tenderness. ADDITIONAL SIGNS: Pain aggravated by resisting thumb extension or abduction, pain aggravated by passively stretching the thumb in extension (Finkelstein maneuver), and the presence of cystlike swelling over the distal radius complete the examination. INTERPRETATION: In the absence of trauma to the distal radius, radial styloid tenderness coupled with pain aggravated by resisting thumb extension is highly suggestive of active tenosynovitis. FIGURE 6–12. Radial styloid palpation for de Quervain’s tenosynovitis.

LOCAL ANESTHETIC BLOCK SUMMARY: Local anesthetic block is necessary to confirm de Quervain’s tenosynovitis and distinguish it from CMC osteoarthritis and conditions affecting the radiocarpal joint. POSITIONING: side up.

Wrist in neutral position, radial

SURFACE ANATOMY: Styloid process of the radius, the anatomic snuffbox formed by the abductor and extensor pollicis longus tendons, and the proximal metacarpal. POINT OF ENTRY: ANGLE OF ENTRY: NEEDLE: DEPTH:

Directly over the radial styloid. 45 degrees.


5

⁄2 to 5⁄8 inch.

1

ANESTHESIA: Ethyl chloride, skin: 1⁄4 mL subcutaneous, 1⁄2 mL at the periosteum of the radial styloid. FIGURE 6–13. Local anesthetic block to confirm de Quervain’s tenosynovitis.

THUMB

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TRIGGER THUMB “My thumb hurts in the afternoon, and in

the morning it locks down” is the typical description of the painful tenosynovitis that occurs with repetitive use and the mechanical locking that results from the tendon swelling.

PALPATION OF THE FLEXOR TENDONS SUMMARY: The hallmark of flexor tenosynovitis is local tenderness located over the MP joint on the palmar aspect of the thumb. The flexor tendons are located in the midline and course along the thumb to the base of the middle and distal phalanges. Within the flexor tendon are two sesamoid bones located near the first flexor crease. MANEUVER: The flexor tendons are palpated over the palmar aspect of the MP joint (arrow). ADDITIONAL SIGNS: Passive stretching of the flexor tendons in extension, the demonstration of clicking or locking at the IP joint, and pain aggravated by resisting flexion (the least common sign) complete the examination. FIGURE 6–14. Palpation of the flexor tendons on the palmar aspect of the MP joint.

INTERPRETATION: Active tenosynovitis is diagnosed by demonstrating flexor tendon tenderness at the base of the metacarpal phalangeal joint combined with pain aggravated by passive stretching of the tendon in extension. If the tendon is sufficiently swollen, it will fail to move freely under the A-1 pulley of the tenosynovial sheath, resulting in mechanical locking at the IP joint.

LOCAL ANESTHETIC BLOCK SUMMARY: Local anesthetic block and a positive response to corticosteroid injection are used to confirm the diagnosis of trigger thumb and rule out involvement of the underlying MP joint. POSITIONING: Hand placed flat on the table in the palm-up position, thumb abducted. SURFACE ANATOMY: Flexor creases of the thumb, the MP joint, the flexor tendon sesamoid bone, and the flexor tendon. POINT OF ENTRY: Directly over the center of the tendon between the flexor creases. ANGLE OF ENTRY: NEEDLE: FIGURE 6–15. Local anesthetic block or empirical corticosteroid injection to confirm trigger thumb.



5

DEPTH: ⁄8 to 1⁄4 inch, just to the level of the tendon, the first tissue plane. 1

ANESTHESIA: Ethyl chloride, skin: 1⁄4 mL at the fat–tendon interface with or without 1⁄4 mL depomedrol (D80).

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GAMEKEEPER’S THUMB The middle joint of the thumb—the

MP joint—has sustained a torque-like injury; the collateral ligament on the ulnar side of the joint has been disrupted. The examination of gamekeeper’s thumb is characterized by local tenderness over the ligament, pain aggravated by valgus stress testing, and variable degrees of laxity depending on the extent of injury.

VALGUS STRESS TESTING SUMMARY: Pain aggravated by valgus testing of the ulnar collateral ligament of the MP joint of the thumb is needed for the diagnosis of this ligament injury. The MP joint is held together by its joint capsule, the collateral ligaments, and to a lesser extent the flexor and extensor tendons that cross the joint. MANEUVER: The CMC joint and metacarpal bone of the proximal thumb are securely grasped by one hand, and the middle phalanx is firmly grasped by the other. The examiner presses with two thumbs on the radial side, applying stress across the ulnar collateral ligament.

FIGURE 6–16. Valgus stress testing for gamekeeper’s thumb.

ADDITIONAL SIGNS: Excessive movement of the ulnar side to the joint defines the higher, secondand third-degree ligament injuries. Degenerative osteoarthritic changes of the MP joint occur late. INTERPRETATION: The ligament can be strained (pain without abnormal movement), partially torn (pain and increased movement), or completely disrupted (pain and unstable joint).

LOCAL ANESTHETIC BLOCK SUMMARY: Local anesthetic block is used to distinguish simple sprain from a torn or avulsed ulnar collateral ligament. Once adequate pain control is achieved, valgus stress testing can be performed. POSITIONING: Hand placed flat on the table in the palm-down position, thumb abducted. SURFACE ANATOMY: POINT OF ENTRY: line. ANGLE OF ENTRY: NEEDLE:

MP joint and joint line.

Midplane, directly over the joint Perpendicular to the skin.


5

DEPTH: ⁄4 to 3⁄8 inch, just to the level of the ligament, the first tissue plane. 1

ANESTHESIA: Ethyl chloride, skin: 1⁄4 mL at the fat–ligament interface. FIGURE 6–17. Local anesthetic block to confirm gamekeeper’s thumb and determine the degree of ulnar collateral ligament injury.

THUMB

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PAIN REFERRED TO THE THUMB FROM THE CARPAL TUNNEL Paresthesia or hypesthesia of the thumb that is unasso-

ciated with local tenderness or loss of range of motion of any of the joints of the thumb suggests either carpal tunnel syndrome or the less common C6 radiculopathy.

TINEL SIGN SUMMARY: The carpal tunnel is formed by the first row of carpal bones (navicular, lunate, pisiform, and triquetral bones) and the transverse carpal ligament. It contains nine flexor tendons and the median nerve. Because the Tinel sign is positive in only 70% of cases, it must be combined with a history of paresthesia or hypesthesia that conforms to a median nerve distribution. MANEUVER: The wrist is placed in neutral position. Using the index finger, the wrist is vigorously tapped at the junction of the palmaris longus and the flexor creases. The tapping should encompass an area the size of a quarter.

FIGURE 6–18. Tinel sign to assess carpal tunnel syndrome.

ADDITIONAL SIGNS: The Phelan sign, loss of twopoint discrimination of the fingertips, loss of light touch and pain sensation, weakness of thumb opposition, and thenar muscle atrophy are the additional signs of median neuropathy. INTERPRETATION: For the Tinel sign to be considered positive, the patient’s pain must be reproduced, and the paresthesia should be distinctly different from the response on the contralateral side.

LOCAL ANESTHETIC BLOCK SUMMARY: Local anesthetic block or the response of symptoms to corticosteroid injection can be used to identify carpal tunnel syndrome as the primary cause of thumb pain or source of the patient’s paresthesia. POSITIONING: Wrist in the palm-up position, dorsiflexed to 30 degrees. SURFACE ANATOMY: Palmaris longus, pisiform bone, and navicular bone. POINT OF ENTRY: On the ulnar side of palmaris longus at the most distal volar wrist crease. ANGLE OF ENTRY: NEEDLE: DEPTH: FIGURE 6–19. Local anesthetic block to confirm medial nerve compression neuropathy (carpal tunnel syndrome).

45 degrees.


5

⁄2 to 5⁄8 inch.

1

ANESTHESIA: Ethyl chloride, skin: 1⁄4 mL in the subcutaneous tissue, 1⁄2 to 1 mL beneath the transverse carpal ligament with or without 1⁄2 mL K40.

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6–1



EXAMINATION SIGNS

DIAGNOSIS

CONFIRMATION

Pain with anteroposterior compression of the CMC joint

1. CMC osteoarthritis

Thumb series x-ray, local anesthetic placed at the trapezium bone

Trigger thumb

Local anesthetic placed at the flexor tenosynovial sheath (optional)

Posttraumatic arthritis or sprain of the MP or IP joints

Thumb series x-ray will be normal with the acute sprain as opposed to the narrowed articular cartilage and osteophyte formation seen with posttraumatic arthritis

De Quervain’s tenosynovitis

Local anesthetic placed at the radial styloid

Gamekeeper’s thumb

Anesthetic placed at the ligament will distinguish simple strain from advanced ligament tears

2. Carpal tunnel syndrome

Medial nerve block with anesthetic or nerve conduction velocity testing

Shelf sign Swelling at the base of the thumb and the anatomic snuffbox Crepitation with the mortar and pestle maneuver Loss of smooth motion of the IP joint (triggering) Tenderness over the flexor tendons at the flexor creases in the palm Pain reproduced by passive extension of the thumb Pain, stiffness, and incomplete movement of the MP or IP joints Palpable swelling along the sides of the joints Tenderness of the radial styloid Pain with resisted thumb extension + Finkelstein maneuver Tenderness along the ulnar side of the MP joint aggravated by valgus stress testing Swelling in the MP joint Loss of opposition strength Hypesthesias or paresthesias by history +Tinel or Phelan sign Loss of sensation in the first 3 digits Diminished opposition strength

THUMB

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COMMON THUMB FRACTURES AND DISLOCATION

FRACTURE OF THE BASE OF THE METACARPAL Transverse or oblique fractures of the shafts of the metacarpal (totally extra-articular in all views) can be treated with closed reduction with good results. The fracture is immobilized for 4 weeks in a wellmolded thumb spica cast and followed by passive range of motion exercises of the thumb. Comminuted metacarpal fractures or fractures that involve the CMC joint are inherently unstable and must be managed surgically. A Bennett fracture is a fracture or dislocation of the base of the metacarpal and is unstable because of the dorsal and radial pull of the abductor pollicis longus. A Rolando fracture is a comminuted fracture of the base of the thumb and is even more unstable than the Bennett fracture. Both fractures should be managed by an orthopedic surgeon because of the difficulty in maintaining anatomic reduction without internal pin fixation. FIGURE 6–20. Fracture of the base of the metacarpal.

TUFF FRACTURE OF THE DISTAL PHALANGES SUMMARY: Fractures of the distal phalanx are classified as longitudinal, transverse, or crushedeggshell types. They account for 50% of all hand fractures. IMMOBILIZATION: Simple protective splinting for 3 to 4 weeks using a fingertip guard or Stack splint is combined with specific treatment of the soft tissue injuries (e.g., laceration, subungual hematoma). The splint should not be placed close to the proximal IP joint so as to avoid joint stiffness. SURGICAL REFERRAL: Fractures associated with soft tissue injuries requiring debridement. PROGNOSIS:

FIGURE 6–21. Tuff fracture of the distal phalanges.

Excellent.

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DISLOCATION OF THE MP JOINT SUMMARY: Dislocations of the MP joint occur as a result of hyperextension injuries (falling or striking the end of the thumb). These are classified as incomplete, simple complete, or complex complete. The incomplete is the most common and with the best prognosis (depicted here). The simple complete is angled at a 90-degree angle. The complex complete creates the bayonet deformity. IMMOBILIZATION: An aluminum metal splint is used for 3 weeks for the incomplete injuries. SURGICAL REFERRAL: Ligament and volar plate injuries are more complicated with the simple compete and complex complete types and should be evaluated by the hand surgeon. PROGNOSIS: The prognosis is guarded. Late-onset osteoarthritis and recurrent dislocations are the rule for the more advanced injuries.

FIGURE 6–22. Dislocation of the MP joint.

DISLOCATION OF THE IP JOINT SUMMARY: Simple dislocation without significant injury to the articular cartilage or the supporting ligaments has a uniformly good prognosis. Dislocation with permanent damage to the cartilage or the supporting ligaments can cause an accelerated wear pattern leading to osteoarthritis years later. Mallet thumb results from a rupture of the extensor pollicis longus insertion. Treatment with IP joint splinting and operative repair provides similar results.

FIGURE 6–23. Dislocation of the IP joint can lead to osteoarthritic changes years later.

THUMB

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AVULSION OF THE LATERAL COLLATERAL LIGAMENT OF THE MP JOINT SUMMARY: Avulsion of the lateral collateral ligament of the MP joint is analogous to gamekeeper’s thumb. The injury is staged as simple, partially torn, or completely torn with or without avulsion fracture. Local anesthetic block is used to distinguish the simple sprain from a torn or avulsed lateral collateral ligament. Once adequate pain control is achieved, varus stress testing can be performed. Simple and partially torn ligaments can be managed with 3 weeks of fixed immobilization (dorsal hood splint, thumb spica cast, or Velcro thumb spica splint). Complete tears should be evaluated by the hand surgeon.

FIGURE 6–24. Avulsion of the lateral collateral ligament of the MP joint.

CLINICAL PEARLS • Osteoarthritis of the CMC joint is a universal problem, developing to some degree in nearly everyone over age 60. Fortunately, only 5% to 10% develop arthritic flares, consisting of pain and loss of function. • The examination of a sprained CMC joint overlaps with that of the examination of the osteoarthritic joint. The pain and lateral joint line tenderness and the soft tissue swelling are identical. However, the simple sprain lacks bony enlargement, subluxation, and the x-ray changes demonstrating arthritic changes. • In the absence of direct trauma, soft tissue swelling that fills the anatomic snuffbox probably is caused by a severely sprained or osteoarthritic CMC joint. • Local anesthetic block is necessary to distinguish de Quervain’s tenosynovitis from an arthritic flare of the CMC joint; the pain pattern, impairment of thumb

function, and abnormal signs on examination overlap greatly. Note that the Finkelstein maneuver (stretching the extensor and abductor tendons of the thumb while passively moving the wrist in ulnar deviation) can be positive in either condition; a positive maneuver is not synonymous with de Quervain’s tenosynovitis. • Examination of the acutely injured gamekeeper’s thumb alone cannot distinguish the simple sprain from the more advanced torn ligament. Local anesthetic block is necessary to control the patient’s pain, allowing proper valgus stress testing. • Although the mechanisms causing the loss of smooth movement are similar, the mechanical symptom of trigger thumb (locking at the IP joint) is distinct from that of the trigger finger (locking at the proximal IP joint).

CHAPTER 7: HAND DIFFERENTIAL DIAGNOSIS Diagnoses

Confirmations

Osteoarthritis (most common) Heberden’s and Bouchard’s nodes Posttraumatic monoarticular osteoarthritis Mucinoid cysts atop the joint Erosive subtype of osteoarthritis

Examination, x-rays: hand series Examination, x-rays: hand series Examination, simple puncture X-ray: hand series

Rheumatoid arthritis

Flexor tendons Trigger finger or flexor tenosynovitis Fixed locked digit Tendon cyst Benign giant cell tumor

Synovial fluid analysis, erythrocyte sedimentation rate, rheumatoid factor (RF)

Examination Examination Examination, simple puncture Surgical removal, pathology

Palmar fascia Palmar fibromatosis without contracture Dupuytren’s contracture Limited joint mobility syndrome (in long-standing diabetes)

Examination Examination Examination

Posttraumatic metacarpophalangeal joint arthritis

Examination, local anesthetic block, x-rays

Extensor tendons Mallet finger Carpal tunnel Cervical radiculopathy Reflex sympathetic dystrophy

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Examination Nerve conduction velocity, local anesthetic block Cervical series, magnetic resonance imaging, electromyography Examination, bone scan

HAND

INTRODUCTION The conditions occurring in the hand can be conveniently divided into diagnoses affecting the joints (the arthritides), the tendons (injuries and tendonitis), and the peripheral nerves (carpal tunnel and ulnar neuropathy). The arthritides are further classified based on the number of joints affected, the distribution of the affected joints, and the degree of inflammation. The conditions affecting the tendons are classified based on type (flexor or extensor tendons injuries), acuity of the process, and mechanism of injury. Multiple joint involvement in the hands is caused most often by osteoarthritis, rheumatoid arthritis, or psoriatic inflammatory arthritis. Osteoarthritis is by far the most common form of arthritis affecting the hands. This wear-andtear arthritis is characterized by bony enlargement of the lateral aspects of the joint, modest swelling, and gradual loss of range of motion and deformity. With age-related osteoarthritis the distal interphalangeal joints (DIPs) are affected preferentially, with lesser involvement of the proximal interphalangeal joints (PIPs); metacarpophalangeal (MCP) or wrist joint involvement is unusual. Secondary complications include bony ankylosis, fixed deformity, and mucinoid cyst formation atop the dorsal aspect of the joint. By contrast, rheumatoid arthritis, the quintessential inflammatory arthritis, is characterized by soft, fusiform swelling of the joints, moderate loss of range of motion, and moderate to severe inflammatory changes. Involvement of the PIP joints, the MCP joints, and the wrists predominates; DIP joint involvement is unusual, with the exception of psoriatic arthritis. A symmetrical pattern of joint distribution is the rule. Secondary complications consist of ulnar deviation, especially at the MCP joints and wrist, swan neck deformities of the DIP joints, boutonnière deformities of the PIP joints, and dorsal tendon rupture. Single joint involvement in the hands is almost always the result of previous and often remote trauma. Posttraumatic arthritis is characterized by bony enlargement, modest swelling, gradual loss of range of motion, and joint deformity. The DIP joints are most susceptible to injury, followed by the PIP and MCP joints. Because gripping and grasping are the dominant functions of the hand, it follows that repetitive and unaccustomed use leads to injury and inflammation of the flexor tendons. Direct pressure over the palm, especially over the heads of the distal MCP joints, leads to the acute swelling and pain (flexor tenosynovitis), loss of smooth motion (mechanical locking or triggering), loss of function (the fixed locked digit), and cystic degeneration of the tendon (tendon cyst formation). Chronic pressure over the flexor tendons of the palm leads to the gradual scarring of the palmar fascia (palmar fibrosis or Dupuytren’s contracture). By contrast, the extensor tendons of the hand are more susceptible to traumatic injury rather than overuse or pressure. Damage to the profundus extensor tendon causes mallet finger. Damage to the central slip of the extensor tendon combined with tearing of the triangular ligament on the dorsum of the middle phalanx causes the acute boutonnière deformity. Diffuse hand pain typically accompanied by hypesthesia or paresthesia can be caused by carpal tunnel, cervical radiculopathy, brachial plexopathy, or reflex sympathetic dystrophy. The particular diagnosis usually is obvious based

119

on the associated symptoms and signs at the wrist, neck, or shoulder, respectively. SYMPTOMS Conditions directly affecting the joints and soft tissues of the hand cause a loss of general function (reduced gripping, grasping, and pinching), pain, swelling, deformity, stiffness, loss of range of motion, or a combination of these symptoms. In general, multiple joint involvement probably is the result of osteoarthritis or a generalized rheumatologic condition. Involvement of one or two digits or joints suggests a focal soft tissue condition. Pain, stiffness, and bony enlargement of multiple DIP joints suggest the common, wear-and-tear osteoarthritis that accompanies aging. Bony enlargement rather than synovial thickening or swelling is the key physical finding when one palpates the lateral joint lines. Pain, swelling, and fusiform enlargement of multiple hand joints is the classic presentation of an inflammatory arthritis. Involvement of the DIP joints is seen with psoriatic arthritis. Involvement of the PIP and MCP joints is seen with rheumatoid arthritis. Compressible synovial thickening and swelling are the key physical findings when one palpates the lateral joint lines. Localized tenderness over a single MCP joint in the palm with or without the loss of smooth motion of the digit is the classic physical finding of flexor tenosynovitis. Persistent inflammation causes the tendon to gradually swell, preventing the smooth motion of the two flexor tendons under the A-1 pulley of the tenosynovial sheath. Mechanical symptoms of clicking or trigger phenomenon result. Tendon cysts and Dupuytren’s contracture present as painless nodules that form in or along the flexor tendons in the palm. A firm nodule located adjacent to a single MCP joint is characteristic of a benign tendon cyst. Despite their size, these rarely interfere with the function of the digit or hand. By contrast, multiple nodules adjacent to several MCP joints in the palm are characteristic of Dupuytren’s contracture. This progressive scarring of the palmar fascia affects finger function, gradually interfering with the ability to fully extend of the digit. Mallet finger presents as a characteristic deformity after trauma. Pain is rarely a significant issue after the initial injury heals. Pain localized to the dorsum of a single MCP joint typically is caused by posttraumatic arthritis. Finally, the examination of the hand is completed with a screening maneuvers of the medial nerve for signs of carpal tunnel syndrome. EXAMINATION Examination of the hand begins with an assessment of active function (gripping, grasping, and pinching) and range of motion testing of all 17 joints. These maneuvers combine to provide an objective measurement of function, a preliminary assessment of the severity of the condition, and important clues to the specific diagnosis. Next, specific maneuvers for each diagnosis are performed based on the location and description of the pain and the clues provided by the functional screening tests. Pain, stiffness, and bony deformity of the DIP or PIP joints are the characteristic signs of the common age-related

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BOX 7-1

ESSENTIAL EXAMINATION OF THE HAND 1. Observe the general movement of the hand joints (opening and closing the fist). 2. Estimate or measure grip strength (dynamometric measurements). 3. Inspect the DIP, PIP, and MCP joints for swelling, synovial thickening, and bony enlargement. 4. Examine the flexor and extensor tendons for inflammation, nodules, or nodular thickening. 5. Perform screening tests for carpal tunnel syndrome.

arthritis (osteoarthritis). Pain, stiffness, and synovial swelling of the PIP or MCP joints are the characteristic signs of inflammatory arthritis, with rheumatoid arthritis being the most common form. Pain and local tenderness located directly over the flexor creases in the palm are characteristic of a flexor tendon cyst or active flexor tenosynovitis (trigger finger). Locking or clicking of the PIP joint or a loss of the normal smooth motion of the PIP joint with active flexion indicate trigger finger. Painless thickening of the palm associated with impaired extension of the affected digit is the classic finding of Dupuytren’s contracture. This must be distinguished from the swelling that occurs in an isolated tendon; tendon cysts occur at the base of the digit rather than in the central area of the palm.

Pain and swelling over an isolated MCP joint are typical for posttraumatic osteoarthritis. Symmetrical involvement of several MCP joints is seen with inflammatory arthritis. Swelling over the extensor aspect of the DIP joint is specific for a mucinoid cyst. Painless loss of extension of the DIP joint is the characteristic abnormality of mallet finger, or traumatic rupture of the distal extensor tendon. Paresthesia or hypesthesia of selected fingers is characteristic of compression neuropathy. Sensory loss of some combination of the first three fingers is the classic distribution of carpal tunnel syndrome. Sensory loss of the fourth and fifth fingers is the classic distribution of ulnar neuropathy. Loss or abnormal sensation affecting all fingers simultaneously can be caused by hyperventilation (if bilateral), brachial plexus lesions, multilevel spinal stenosis, peripheral neuropathy, or the rare combination of ulnar and medial nerve compression neuropathies. ONE-MINUTE SCREENING EXAM: MANEUVERS ASSESSING OVERALL HAND FUNCTION The next six maneuvers represent the minimal examination of the patient presenting with hand symptoms. Range of motion measurement and screening maneuvers for osteoarthritis, Dupuytren’s contracture, trigger finger, and carpal tunnel syndrome provide enough information to triage to x-ray, order appropriate labs, suggest general treatment recommendations, or proceed to more detailed examination and treatment.

GRIPPING AND GRASPING SUMMARY: Full function of the hand requires the normal function of the MCP, PIP, and DIP joints on all four fingers, intact flexor and extensor tendons, and an intact recurrent median nerve and ulnar nerve. MANEUVER: The patient is simply asked to open and close the fist while the examiner notes the patient’s ability to actively flex and extend the MCP, PIP, and DIP joints of each finger and thumb. INTERPRETATION: Arthritis from any cause or any condition affecting the flexor tendons (finger and Dupuytren’s contracture) or the extensor tendons (mallet finger and dorsotenosynovitis) can impair overall hand function.

FIGURE 7–1. Gripping and grasping to assess overall hand function.

HAND

121

MANUAL GRIP STRENGTH MEASUREMENT SUMMARY: Grip strength measurement is the most objective, albeit indirect, measurement of the integrity and strength of the intrinsic and supporting muscles of the hand. Gripping can be influenced by arthritis of the intrinsic joints of the hands, intrinsic muscles of the hand, and flexor and extensor tendons. MANEUVER: Grip strength can be crudely estimated by manual gripping of the examiner’s fingers. However, physical measurement using a dynamometer is much more accurate and reproducible. An alternative method involves compressing a partially inflated blood pressure cuff. FIGURE 7–2. Manual grip strength measurement.

INTERPRETATION: Grip strength is reduced in a consistent manner by disuse atrophy, hand arthritis, carpal tunnel syndrome, severe tenosynovitis, Dupuytren’s contracture, and C8 cervical radiculopathy. Inconsistent measurement of grip strength is seen with malingering.

GRIP STRENGTH MEASUREMENT SUMMARY: Grip strength measurement is the most objective, albeit indirect, measurement of the integrity and strength of the intrinsic and supporting muscles of the hand. Gripping can be influenced by arthritis of the intrinsic joints of the hands, intrinsic muscles of the hand, and flexor and extensor tendons. MANEUVER: The average of three consecutive readings using the dynamometer provides an accurate and reproducible measurement of gripping and forearm muscle strength. An alternative method involves compressing a partially inflated blood pressure cuff (see Figure 7-2). INTERPRETATION: Grip strength is reduced in a consistent manner by disuse atrophy, hand arthritis, carpal tunnel syndrome, severe tenosynovitis, Dupuytren’s contracture, and C8 cervical radiculopathy. Inconsistent measurement of grip strength is seen with malingering.

FIGURE 7–3. Grip strength measurement.

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INSPECT THE SMALL JOINTS OF THE HAND SUMMARY: The DIP, PIP, and MCP joints, the extensor tendons, and the intrinsic muscles of the hand are readily inspected with the palms down. MANEUVER: The hands are inspected for alignment, fusiform swelling, bony enlargement, joint deformity including ankylosis and contracture, and the presence of cysts or nodules in the palms-down position.

FIGURE 7–4. Inspect the small joints of the hand for swelling, bony enlargement, and deformity.

INTERPRETATION: Osteoarthritis affects the DIP and PIP joints, producing bony enlargement, mild swelling, and deformity. Rheumatoid arthritis affects the PIP and MCP joints and is characterized by fusiform swelling in a symmetrical pattern and normal alignment. Atrophy of the intrinsic muscles of the hand occurs with chronic arthritis and chronic C8 cervical radiculopathy.

INSPECT THE PALM SUMMARY: The flexor tendons of the hand are covered by a tenosynovial sheath, which in turn is covered by a thick palmar fascia. Abnormal thickening of this fascia is called palmar fibromatosis. MANEUVER: The position of each of the four fingers is noted (incomplete extension of the fifth fingers is depicted here). All four fingers are passively stretched in full flexion, followed by passive stretching in extension.

FIGURE 7–5. Inspect the palm for swelling, tendon thickening, and deformity.

INTERPRETATION: Lack of full extension typically is caused by the nodular thickening of the palmar fascia. Several discrete nodules can be palpated along the course of the flexor tendons in the palm. Single ganglion cysts arising from the tenosynovial sheaths typically do not restrict full extension of the fingers.

HAND

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TINEL SIGN COMBINED WITH A COMPATIBLE HISTORY SUMMARY: The carpal tunnel is formed by the first row of carpal bones (navicular, lunate, pisiform, and triquetral) and the transverse carpal ligament. It contains nine flexor tendons and the median nerve. Because the Tinel sign is positive in only 70% of cases, it must be combined with a history of paresthesia and hypesthesia that conforms to the median nerve distribution. MANEUVER: The wrist is placed in neutral position. Using the index finger, the wrist is vigorously tapped at the junction of the palmaris longus and the flexor creases. The tapping should encompass an area the size of a quarter.

FIGURE 7–6. Tinel sign combined with a compatible history to screen for carpal tunnel syndrome.

ONE-MINUTE SCREENING EXAM: MANAGEMENT OPTIONS TRIAGE TO X-RAY The patient has a history of trauma, the exam demonstrates osteoarthritic bony enlargement or joint swelling, rheumatoid arthritis is suspected, or the patient is at risk for reflex sympathetic dystrophy: • Order three views of the fingers for patients with a history of hyperextension injuries, crush injuries, or a direct blow (ligament injury due to dislocation, phalangeal fracture, tendon avulsion, or tuft fracture). • Order arthritic views of both hands for patients with suspected arthritis (osteoarthritis, rheumatoid arthritis, or psoriatic arthritis). • Order a posteroanterior view of both hands for patients with diffuse hand pain, swelling, and discoloration (reflex sympathetic dystrophy). • Order a carpal tunnel view for patients with wrist trauma and acute median nerve loss (perilunate dislocation and acute carpal tunnel syndrome). TRIAGE TO THE LAB For patients with acute inflammatory arthritis or patients with recent penetrating injury and acutely inflamed joint: • Order a complete blood cell count, erythrocyte sedimentation rate, and C-reactive protein for patients with acute pain, swelling, and signs of active inflammation (inflammatory arthritis). • Order a complete blood cell count, erythrocyte sedimentation rate, and blood cultures for patients with acute inflammatory changes and significant fever.

INTERPRETATION: For the Tinel sign to be considered positive, the patient’s pain must be reproduced and the paresthesia should be distinctly different from the response on the contralateral side.

CONSIDER A BONE SCAN For patients with diffuse hand pain, swelling, and discoloration (reflex sympathetic dystrophy). CONSIDER A NERVE CONDUCTION VELOCITY TEST For patients with advanced carpal tunnel symptoms involving motor weakness and atrophy. RECOMMEND EMPIRICAL TREATMENT For patients with mild to moderate hand pain and stiffness, unimpaired gripping and grasping, normal joint alignment, and no contractures or deformities: • • • • • •

Avoid repetitious gripping and grasping. Avoid all vibration exposure. Avoid prolonged contact with cold. Wear thick leather gloves for protection. Apply direct heat (wax treatments in a crock pot). Perform gentle range of motion exercises in flexion and extension to prevent contractures.

DETAILED EXAMINATION: SPECIFIC HAND DIAGNOSES Perform a detailed examination of the hand if the joints of the hand demonstrate palpable swelling, nodularity, or synovial thickening. Symptoms have been persistent or chronic. Overall hand function is moderately to severely impaired, or early joint contractures have developed.

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OSTEOARTHRITIS OF THE HAND Osteoarthritis of the hand is characterized by bony enlargement of the DIP and PIP joints (Heberden’s and Bouchard’s nodes). It is one of the most

common forms of arthritis, and most patients complain more about the bony deformity and unattractive appearance than the pain or loss of function.

PALPATE THE BONY ENLARGEMENT SUMMARY: As the articular cartilage gradually wears down, the body responds by forming osteophytes along the joint margins. These hard bony prominences are called Heberden’s nodes at the DIP joints and Bouchard’s nodes at the PIP joints. As the process continues, the joint gradually loses range of motion. MANEUVER: After the hands are inspected, individual joints are palpated along the joint lines for bony enlargement, synovial thickening, and swelling. ADDITIONAL SIGNS: Mucinoid cysts may be present on the dorsum of the DIP joints. Advanced arthritis leads to deformity and loss of full flexion. FIGURE 7–7. Palpate the bony enlargement of the DIP joints.

INTERPRETATION: The bony enlargement along the lateral joint lines readily distinguishes osteoarthritis from rheumatoid arthritis. The severity of the process is determined by the bony enlargement and the effect on joint alignment and on the ability to fully flex the fingers.

X-RAY OF THE HANDS CASE: The patient has had painful hands with the gradual loss of the fine motor skills over the last 20 years. The family history is remarkable for arthritis. Examination of the hands demonstrates bony enlargement of the DIP and PIP joints with very little palpable swelling or thickening. Range of motion is severely limited, especially at the DIP joints; the patient is unable to make a complete fist. X-rays demonstrate complete loss of articular cartilage, large bony osteophytes, and ankylosis. The middle finger is especially affected. DIAGNOSIS:

Advanced osteoarthritis of the hands.

DISCUSSION: Osteoarthritis of the hands is a clinical diagnosis. X-rays usually are not necessary to confirm the diagnosis. However, X-rays are indicated when inflammatory arthritis is suspected.

FIGURE 7–8. X-ray of the hands to confirm the degree of osteoarthritic wear and tear.

HAND

RHEUMATOID ARTHRITIS Of the five forms of rheumatoid arthritis (classic, monarthritic, pauciarticular, systemic, and palindromic), only the classic form consistently affects the hands.

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Classic rheumatoid arthritis is characterized by loss of full grip, morning stiffness, symmetrical joint swelling of the PIP and MCP joints, and boggy synovial thickening.

PALPATION SUMMARY: The synovial lining of the small joints of the hand extends 5 to 6 mm above and below the joint line. Excessive amounts of joint fluid cause the characteristic fusiform shape. MANEUVER: The examiner places two fingers of one hand on the lateral joint lines and two fingers from the opposite hand on the top and bottom of the joint. The examiner applies pressure from the top and bottom while palpating the joint for synovial thickening and excessive joint fluid. The maneuver can be enhanced by alternating the pressure from one set of fingers to the other.

FIGURE 7–9. Palpation of the PIP joint synovial thickening of inflammatory arthritis.

ADDITIONAL SIGNS: Measurement of grip strength is always impaired with active disease. The MCP, wrists, and intrinsic joints of the feet may be involved. Advanced cases may show the palpable purpura of vasculitis. INTERPRETATION: Inflammatory arthritis is characterized by swelling and synovial thickening, as opposed to the bony enlargement and deformity caused by osteoarthritis.

X-RAY OF THE HANDS CASE: The patient has a long history of psoriatic arthritis. Fusiform swelling of the PIP and DIP joints is noted on physical examination. X-rays of the hands demonstrate mild osteoarthritic changes at the DIP joints and inflammatory changes at the DIP and PIP joints. Large erosive changes are particularly notable at the DIP joints of the index and middle fingers (arrows). DIAGNOSIS:

FIGURE 7–10. X-ray of the hands to evaluate the severity of inflammatory arthritis.

Psoriatic arthritis of the IP joint.

DISCUSSION: X-rays of the hands of patients with inflammatory arthritis often are normal in the early stages of the disease. Juxta-articular osteoporosis, reflecting the increased blood flow to the joints, is the earliest radiographic finding. Late findings include symmetrical wear of the articular cartilage, generalized osteopenia, erosive changes, angulation, and ankylosis.

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MCP SQUEEZE SIGN SUMMARY: The MCP joints are formed by the distal metacarpal bones and the proximal phalanges. When a fist is made, the joint lines are located 1⁄4 to 3⁄8 inch from the center of the knuckle (the distal metacarpal head). Rheumatoid arthritis commonly affects the MCP joints in a symmetrical pattern. MANEUVER: With one hand placed over the middle of the metacarpal bones to hold them in line, the examiner applies pressure across the second and fifth metacarpal heads, forcing all four metacarpal joints together. ADDITIONAL SIGNS: Grip strength is impaired with active involvement of the MCP joints. Swelling may obliterate the normal hills and valleys between the knuckles. Advanced disease may show ulnar deviation. FIGURE 7–11. MCP squeeze sign to assess the involvement of the MCP joints.

INTERPRETATION: Posttraumatic arthritis of the MCP is the likely diagnosis if a single joint is involved. Multiple joint involvement is almost always an indication of active rheumatoid arthritis.

DECREASED AND PAINFUL LOSS OF RANGE OF MOTION SUMMARY: Bilateral wrist involvement is characteristic of the classic form of rheumatoid arthritis. As the condition progresses, the wrists become painful, swell, and subsequently lose full range of motion. MANEUVER: With one hand grasping the forearm, the examiner passively flexes and extends the wrist, noting the patient’s pain, the tendency to resist the maneuver, the degree of endpoint stiffness, and the range of motion, measured in degrees of flexion and extension (normal range of motion is 90 degrees of flexion, 80 degrees of extension, and approximately 45 degrees of radial and ulnar deviation). ADDITIONAL SIGNS: With advanced disease the wrist gradually drifts into ulnar deviation.

FIGURE 7–12. Decreased and painful loss of range of motion suggest involvement of the wrist.

DIFFERENTIAL DIAGNOSIS: Rheumatoid arthritis can present in innumerable ways. The symmetrical involvement of the PIPs, MCPs, and wrist is the classic pattern.

HAND

TRIGGER FINGER Minor trauma and repetitive gripping and grasping compress the flexor tendons as they course over the MCP head in the palm. This pressure and friction cause the tendon to gradually swell within the unyielding tenosynovial sheath, an in-

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flammatory reaction that leads to a loss of smooth motion of the tendons under the A-1 pulley of the tenosynovial sheath. The diagnosis can be made by identifying active tenosynovitis or by documenting the mechanical triggering phenomenon.

MECHANICAL DYSFUNCTION SUMMARY: Smooth motion of the finger requires the free movement of the two flexor tendons through the tenosynovial sheath. MANEUVER: The hands are placed in the palms-up position, and the patient is asked to flex and extend the fingers. Alternatively, if active triggering is not present, the examiner places his or her fingers on the PIP joint as the finger is actively flexed and extended, noting the loss of smooth motion or a clicking sensation. ADDITIONAL SIGNS: Passive stretching of the finger is painful with active tenosynovitis. Less commonly, resisting finger flexion isometrically is painful. A small percentage of patients have a palpable nodule in the flexor tendon located over the MCP head.

FIGURE 7–13. Mechanical dysfunction (triggering or clicking) of trigger finger.

INTERPRETATION: The three stages of trigger finger are active tenosynovitis, mechanical triggering, and the fixed locked digit.

LOCAL ANESTHETIC BLOCK OVER THE FLEXOR TENDON SUMMARY: Swelling of the flexor tendons (tenosynovitis) always precedes the mechanical locking of trigger finger. Left untreated, the triggering phenomenon can persist and cause the fixed locked digit. POSITIONING: extended.

Hand flat, palm-up position, fingers

SURFACE ANATOMY: Flexor tendon, metacarpal head, and proximal finger crease. POINT OF ENTRY: Over the metacarpal head, proximal to the finger crease. ANGLE OF ENTRY: NEEDLE: FIGURE 7–14. Local anesthetic block placed over the flexor tendon to confirm the tenosynovitis accompanying trigger finger.

DEPTH:



5

⁄8 to 1⁄2 inch.

3

ANESTHESIA: Ethyl chloride, skin: 1⁄4 mL subcutaneous, 1⁄4 mL at the flexor tendon.

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TENDON CYST Intratendon and peritendinous cysts typically are pea-sized nodules located in or adjacent to the flexor tendons in the palm. Minor trauma or repeated heavy pressure over the

MCP joints incites excessive production of the tenosynovial fluid. In contrast to the mechanical locking of trigger finger, active and passive movement of the digit is unimpaired.

PALPATION SUMMARY: The majority of tendon cysts occur within a centimeter of the flexor crease of the palm. On average, they are pea-sized and firm to hard in consistency. MANEUVER: With the hand placed palm up and the fingers extended, the flexor tendon is palpated along its entire course from DIP joint to the palm. Passive movement of the finger is performed to determine whether the cyst moves with the finger (intratendinous) or independently of it (peritendinous). ADDITIONAL SIGNS: Finger movement should be normal. Inflammatory reactions are unusual. INTERPRETATION: The tendon cyst is sensitive to direct pressure. Active tenosynovitis (pain aggravated by passive stretching or isometrically resisted flexion) is unusual.

FIGURE 7–15. Palpation of the flexor tendon for tenderness or cyst formation.

SIMPLE PUNCTURE SUMMARY: Tenosynovial cysts are located within the tendon or adjacent to it. Minor injury to the tendon leads to an overproduction of tenosynovial fluid. POSITIONING: extended.

Hand flat, palm-up position, fingers

SURFACE ANATOMY: Flexor tendon, metacarpal head, and proximal finger crease. POINT OF ENTRY: Over the metacarpal head, proximal to the finger crease. ANGLE OF ENTRY: NEEDLE: DEPTH:



5

⁄8 to 1⁄2 inch.

3

ANESTHESIA: Ethyl chloride, skin: 1⁄4 mL subcutaneous, 1⁄4 mL at the flexor tendon. FIGURE 7–16. Simple puncture to confirm the benign tenosynovial cyst.

HAND

DUPUYTREN’S CONTRACTURE Dupuytren’s contracture is

a progressive fibrosis of the flexor tendons in the palm. Painless, palpable nodules (palmar fibrosis) most commonly form over the

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fourth and fifth flexor tendons. Although it is associated with alcoholic cirrhosis, the majority of cases (95%) are inherited; patients of northern European descent are at greater risk.

SIMPLE INSPECTION OF THE PALM SUMMARY: The two flexor tendons course through the palm to attach to the middle phalanges (superficialis tendon) and to the distal phalanges (profundus tendon) of each finger. The tendons are enveloped by a tenosynovial sheath, which in turn is covered by the thick palmar fascia.

FIGURE 7–17. Simple inspection of the palm is used to diagnose advanced Dupuytren’s contracture.

MANEUVER: The hands are placed in the palmsup position. Each of the four digits is passively stretched in extension, and the examiner notes any differences in flexibility and any palmar scarring. Triangular puckering at the base of the finger may be the only sign of early palmar scarring. Next, the tendons are palpated for thickening or nodularity along their course through the palm. ADDITIONAL SIGNS:

None.

INTERPRETATION: Loss of full extension is the functional consequence of Dupuytren’s contracture. Clicking, catching, and triggering, as with trigger finger, do not occur with this pathologic scarring process.

PASSIVE EXTENSION OF THE FINGER AND PALPATION SUMMARY: Most cases of Dupuytren’s contracture go unnoticed for years. The earliest finding is a puckering of the skin in the palm when attempting to stretch the fingers passively in extension. This early scar formation limits extension during passive movement of the fingers. MANEUVER: The hands are placed in the palms-up position. Each of the four digits is passively stretched in extension, and the examiner notes any differences in flexibility and any palmar scarring. Triangular puckering may be the only sign of early palmar scarring. Next, the tendons are palpated for thickening or nodularity along their course through the palm. FIGURE 7–18. Passive extension of the finger and palpation of the palmar fascia for nodularity are used to detect the early stage of palmar fibrosis.

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TRAUMATIC ARTHRITIS OF THE MCP JOINT Months to years after a substantial injury to the articular cartilage of the metacarpal joint (e.g., direct blow, fist injury, crush), an accelerated wear-and-tear arthritis develops. On examination, the MCP

squeeze sign is painful, and the involved MCP joint fails to fully flex. As the condition progresses, x-rays will confirm greater degrees of articular cartilage wear, osteophyte formation, and sclerotic bone formation.

MCP JOINT SWELLING SUMMARY: The distal metacarpal heads articulate with the proximal heads of the phalanges to form the MCP joints. Swelling of these joints obliterates the impression formed between the MCP joints (i.e., the hills and valleys of the knuckles are lost). MANEUVER: The patient is asked to make a partial fist, and the MCP joints are inspected for swelling. ADDITIONAL SIGNS: Substantial swelling impairs the ability to fully flex the MCP joints. Grip is impaired by pain. The MCP squeeze sign is painful.

FIGURE 7–19. MCP joint swelling.

DISCUSSION: Single MCP joint involvement usually is due to previous trauma (monarthritic traumatic arthritis). Symmetrical involvement of multiple MCP joints is characteristic of inflammatory arthritis, particularly rheumatoid arthritis.

LOCAL ANESTHETIC SUMMARY: Isolated involvement of a single MCP joint usually follows bony fracture or injury to the articular cartilage. Often the seemingly minor injury goes unnoticed because symptoms develop months or even years later. POSITIONING: down.

Wrist flat on the table, palm side

SURFACE ANATOMY: Metacarpal heads, web space, extensor tendons. POINT OF ENTRY: In the web space between the metacarpal heads. ANGLE OF ENTRY: NEEDLE: DEPTH: FIGURE 7–20. Local anesthetic is placed adjacent to the MCP joint to confirm involvement of the joint.

45 degrees.


5

⁄4 to 3⁄8 inch.

1

ANESTHESIA: Ethyl chloride, skin: 1⁄4 mL subcutaneously.

HAND

MALLET FINGER Mallet finger is the deformity associated with the complete detachment of the extensor longus tendon from

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the base of the distal phalanx. The diagnosis is based on the characteristic deformity and the loss of full extension of the DIP joint.

INSPECTION SUMMARY: The profundus tendon attaches to the base of the distal phalanges just past the joint line of the DIP joint. MANEUVER: The affected finger is grasped with one hand and the finger of the second hand is placed atop the distal phalanges. The patient is asked to actively extend the DIP joint. ADDITIONAL SIGNS:

None.

DISCUSSION: Direct blows to the tip of the extended finger are the most common mechanism of tendon rupture.

FIGURE 7–21. Inspection of the finger deformity caused by a rupture of the distal extensor tendon.

X-RAYS CASE: The patient sustained an acute injury while playing basketball. Initially, the symptoms were too acute for a full examination of the finger. In the follow-up period, the patient was unable to fully resist extension of the distal phalanx. DIAGNOSIS: Avulsion fracture accompanying the rupture of the extensor profundus tendon, leading to the mallet finger deformity.

FIGURE 7–22. X-rays to confirm the rupture of extensor profundus, leading to the mallet deformity.

DISCUSSION: The mallet finger deformity can result from stretching or partial tearing of the extensor tendon, complete rupture, or rupture with avulsion fracture of the distal phalanx. Treatment consists of splinting the DIP joint in full extension or slight hyperextension for 1 to 2 months, using a dorsal aluminum splint and tape or a Stack splint. The patient should be advised that function may be impaired in up to 30% of cases, especially in patients over age 60, in patients with rheumatoid arthritis or peripheral vascular disease, if treatment is delayed more than 4 weeks, or if immobilization lasts fewer than 4 weeks. Patients with large avulsion fractures should be evaluated by an orthopedic surgeon.

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Mucinoid cysts result from the excessive production and subsequent leakage of synovial fluid from osteoarthritic DIP or PIP joints. The fluid leaks

MUCINOID CYST OF THE DIP JOINT

out of the small synovial cavity into the subcutaneous tissues, forming 4- to 5-mm diameter, faint gray cysts. Simple puncture demonstrates the highly viscous synovial fluid.

INSPECTION SUMMARY: Arthritic DIP or PIP joints that are exposed to repetitious use or prolonged vibration produce excessive amounts of lubricating synovial fluid. Because the synovial cavity is limited in size and distensibility, some of the excessive fluid leaks into the subcutaneous tissue; then, the body isolates the fluid by forming a cyst. MANEUVER: The size, shape, and compressibility of the cyst are determined by physical measurement and palpation. ADDITIONAL SIGNS: The underlying osteoarthritic changes are always detectable by exam or x-ray. DIFFERENTIAL DIAGNOSIS: Herpetic whitlows and subcutaneous abscesses are red, hot, and swollen. The fibrosis that accompanies foreign body reactions and dermatofibromas are firm to hard in consistency, as opposed to the cystic quality of the mucinoid cyst.

FIGURE 7–23. Inspection of the dorsum of the hand for mucinoid cysts.

SIMPLE PUNCTURE SUMMARY: Mucinoid cysts result from an overproduction of synovial fluid from an arthritic DIP. Fluid in this small-capacity joint leaks into the subcutaneous tissues, forming a 4- to 6-mm diameter cyst. POSITIONING:

Finger flat and fully extended.

SURFACE ANATOMY: POINT OF ENTRY: ANGLE OF ENTRY: NEEDLE: DEPTH:

Cyst, DIP joint, and nail bed.

At the base of the cyst. Perpendicular to the skin.

⁄8 inch, 25 gauge or 1 inch, 22 gauge.

5

Superficial.

ANESTHESIA: Ethyl chloride is sprayed on the skin. 1 ⁄4 cc of local anesthetic is placed just under the skin.

FIGURE 7–24. Simple puncture to confirm the benign nature of a mucinoid cyst.

HAND

7–1

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EXAMINATION SIGNS

DIAGNOSIS


Bony enlargement of the DIP or PIP joints

1. Osteoarthritis

X-ray series of the hand (optional)

Inflammatory arthritis, psoriatic (DIP joints) rheumatoid arthritis

Clinical diagnosis, erythrocyte sedimentation rate, x-ray series of the hand, serology testing (optional)

2. Trigger finger

Local anesthetic block placed at the flexor tenosynovium (optional)

Tenosynovial cyst

Simple aspiration of the cyst

Dupuytren’s contracture

Examination

Monarticular posttraumatic arthritis of the MCP joint

Lidocaine injection of the joint

Inability to fully extend the DIP joint and the characteristic flexion deformity

Mallet finger

Clinical diagnosis

Pale gray, 3- to 5-mm cyst over the DIP or PIP joint

Mucinoid cyst

Clinical diagnosis

Stiffness and decreased flexion or extension Minimal signs of inflammation Synovial thickening, swelling of the DIP, PIP, and MCP joints Stiffness and decreased flexion or extension Loss of smooth motion of the PIP joint; triggering Tenderness of the flexor tendons over the MCP joint in the palm Pain reproduced by passive extension of the finger Cystic swelling of the flexor tendons near the MCP joint Normal range of motion of the finger Thickening of the flexor tendons the palm Loss of full extension of the fingers due to contracture Tenderness of the MCP joint to palpation

MCP joint squeeze sign

Associated osteoarthritic signs of the adjacent joint

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COMMON HAND FRACTURES

FRACTURE OF THE PROXIMAL AND MIDDLE PHALANGES SUMMARY: Fractures of the phalanges are classified by location, configuration (transverse or oblique), and effects of the fracture on the rotation and foreshortening of the digit. The majority of these fractures can be managed nonsurgically. IMMOBILIZATION: Extra-articular fractures that do not exhibit displacement, rotation, or angulation can be treated with buddy taping and active range of motion exercises. Nearly all transverse fractures can be managed in this fashion. In addition, small chip fractures of the collateral ligaments, dorsal chip fractures of the central slip of the extensor tendon at the base of the middle phalanx, and nondisplaced marginal fractures of the base of the proximal phalanx can be managed with buddy taping. FIGURE 7–25. Fracture of the proximal and middle phalanges.

SURGICAL REFERRAL: Transverse fractures at the base or neck of the proximal phalanx, nearly all spiral oblique fractures, and all comminuted and condylar (intra-articular) fractures must be evaluated by an orthopedic surgeon for possible open reduction and internal fixation. PROGNOSIS: All phalangeal fractures must be assessed for late complications, including malrotation, lateral deviation, recurvatum angulation, shortening, intra-articular malunion, nonunion, tendon adherence, joint stiffness, and nail bed interposition.

HAND

ACUTE BOUTONNIÈRE INJURY Finger injuries leading to an acute boutonnière deformity (tissue disruption of the central slip of the extensor tendon combined with tearing of the triangular ligament on the dorsum of the middle phalanx) can be treated by closed reduction as long as no bony chip fracture is present. The PIP joint is immobilized in full extension with a PIP splint, and active and passive range of motion exercises are performed daily. As with all finger and thumb injuries, postimmobilization stiffness must be guarded against.

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RUPTURE OF THE FLEXOR DIGITORUM PROFUNDUS TENDON This is an uncommon injury caused by forced hyperextension of the DIP joint. Early surgery is the treatment of choice.

DISLOCATION OF THE PIP JOINT SUMMARY: There are three types of dislocation of the PIP joint: dorsal, volar (rare), and rotatory (uncommon). The dorsal or volar plate injury (with or without a small volar avulsion fracture) is the most common type of dislocation and is the result of hyperextension of the joint. Reduction is accomplished by closed means. IMMOBILIZATION: The PIP joint is immobilized with a PIP splint for 2 weeks (no more than 15 degrees of flexion) or with buddy taping for 3 to 6 weeks. Buddy taping has the advantage of allowing early active motion (guarding against residual joint stiffness) while preventing hyperextension. Range of motion exercises are continued for several weeks after immobilization. SURGICAL REFERRAL: Surgical consultation is strongly recommended for dorsal dislocations associated with volar lip fractures involving more than 20% of the articular surface and for nonreducible dislocations. FIGURE 7–26. Dislocation of the PIP joint.

PROGNOSIS: Guarded. Full range of motion may not be recovered, and late-onset osteoarthritic changes can develop.

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FRACTURE OF THE DISTAL PHALANX SUMMARY: Fractures of the distal phalanx are classified as longitudinal, transverse, or crushedeggshell types. They account for 50% of all hand fractures. IMMOBILIZATION: Simple protective splinting for 3 to 4 weeks using a fingertip guard or Stack splint is combined with specific treatment of the soft tissue injuries (e.g., laceration, subungual hematoma). The splint should not be placed close to the PIP joint so as to avoid joint stiffness. SURGICAL REFERRAL: Fractures associated with soft tissue injuries requiring debridement. PROGNOSIS:

Excellent.

FIGURE 7–27. Fracture of the distal phalanx.

CLINICAL PEARLS • A comprehensive hand examination is the most important method of evaluating generalized hand arthralgia, especially if the patient is overly concerned about a family history of arthritis. Radiographic and serologic testing is nearly always normal unless the specific maneuvers of the hand demonstrate objective findings of bony enlargement, synovial thickening, or joint swelling. • An efficient screening examination for classic rheumatoid arthritis includes the following maneuvers: general hand inspection, grip measurement, palpation of the PIP joints for tenderness, the MCP squeeze sign, extension and flexion of the wrists, observation of gait and walking on tiptoes, and the metatarsophalangeal squeeze. If the combination of these signs does not show loss of range of motion or synovial thickening, rheumatoid arthritis is unlikely. • The earliest sign of Dupuytren’s contracture is a triangular puckering of the dermal tissue over the flexor tendon just proximal to the flexor crease of the finger. As

•

•

• •

scarring progresses, nodules form, and the finger gradually loses its flexibility. Patients of northern European descent are at the greatest risk for Dupuytren’s contracture. Less than 5% of Dupuytren’s contractures occur in patients with chronic liver disease. Tenosynovitis of the flexor tendons always precedes the mechanical symptoms of triggering. However, not all patients demonstrate active tenosynovitis at the time they are examined. As the patient tries to avoid the triggering phenomenon (by using the finger less and less), the tenosynovial signs gradually subside, leaving the patient with a painless mechanical triggering. Flexor tenosynovitis and mechanical triggering can be so dramatic as to preclude movement of the finger from a flexed position. This is called a fixed locked digit. Despite their size, tendon cysts rarely lead to mechanical dysfunction.

CHAPTER 8: CHEST DIFFERENTIAL DIAGNOSIS Diagnoses

Confirmations

Rib cage (most common) Costochondritis Sternochondritis Tietze’s syndrome Epidemic pleurodynia Rib fracture, nondisplaced Rib fracture, displaced

Local anesthetic block Local anesthetic block Examination Examination, local anesthetic block Chest compression sign, chest x-ray, or bone scan Chest compression sign, chest x-ray

Sternum and sternoclavicular joint Strain Inflammatory arthritis Septic (intravenous drug abuse)

Referred pain to the chest wall Hiatal hernia Cholelithiasis Splenic flexure syndrome Coronary artery disease Aortic aneurysm Pneumonia Pulmonary embolism

Local anesthetic block Local anesthetic block, abnormal erythrocyte sedimentation rate, exam correlations Aspiration and culture

Gastrointestinal cocktail taken orally, barium swallow, endoscopy Liver chemistries, ultrasound Examination, abdominal x-ray Electrocardiogram, creatine phosphokinase, troponin, or angiogram Computed tomography of the chest, angiogram Chest x-ray, complete blood cell count, cultures O2 saturation, d-dimer, lung scan, computed tomography scan, angiogram

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INTRODUCTION The initial evaluation of the patient who complains of anterior or anterolateral chest pain must include a thorough examination of the chest for evidence of coronary, pulmonary, pleural, major vascular, or upper abdominal disorders. At times, this entails full physical, radiographic, and electrophysiologic evaluation in the patient with significant risk factors for major heart, lung, vascular, or abdominal disease, despite a strong suspicion of chest wall abnormality. By contrast, if the patient is young and has a low risk of major chest disorders, and symptoms are described as superficial, localized, and aggravated by direct chest wall pressure or chest movement in general, a local musculoskeletal process should be considered and unequivocally suggested to the patient to avoid unnecessary anxiety. Of the various structures of the chest wall, the ribs and costal cartilages are the most susceptible to injury and inflammation. Rib contusions and nondisplaced rib fractures commonly occur after mild chest wall trauma. Costochondritis and its analogous condition, sternochondritis, involve local irritation and inflammation of the junctions of the cartilaginous portions of the thorax cage with the ribs and sternum, respectively. Although the condition can result from minor trauma or follow open heart surgery, the majority of cases are idiopathic. Major trauma to the chest from falls, motor vehicle accidents, and blunt trauma is more likely to cause displaced rib fractures. Patients with multiple displaced fractures must be observed closely for possible hemothorax or pneumothorax. In addition, severe decelerating injuries to the upper chest can cause fractures of the sternum or proximal clavicle or fracture or dislocation of the sternoclavicular joint. The amount of blunt trauma or force associated with these fractures is so great that life-threatening associated injuries to underlying great vessels and lung parenchyma should be sought. Epidemic pleurodynia is an irritation and resulting spasm of the intercostal muscles, commonly known as the devil’s grip. This is a rare condition thought to be of viral origin, occurring in sporadic outbreaks. Xiphodynia is a rare but unique cause of anterior chest pain. Irritation and inflammation of the junction between the sternum and the xiphoid process cause a localized pain and tenderness and an unusual sensitivity. Pressure placed directly over the xiphoid can incite an autonomic reaction consisting of nausea, vomiting, abdominal pain, and sweating. SYMPTOMS Chest pain can arise from the chest wall or internal organs. In general, musculoskeletal chest pain is characterized by superficial, focal tenderness and is aggravated by chest wall movement (lying on the side, chest expansion with a deep breath, or reaching overhead with outstretched arms). Chest pain arising from the heart, lungs, pleura, major vessels, or upper abdomen is more often accompanied by additional symptoms, such as palpitations, shortness of breath, pleuritic pain, or nausea and vomiting. Any of the structures that make up the chest wall can cause chest pain, including the ribs, costal cartilage, costochondral junctions, intercostal muscles, sternum, xiphoid process, and sternoclavicular joints. The chest pain arising from these structures typically is described as a focal irritation unless more

than one rib or costochondral junction is involved. Rib contusions and fractures are tender directly over the affected bone. Patients with costochondritis describe discrete tenderness at the junction of the rib and costal cartilage in a line extending from the sternoclavicular joint through the nipples. Patients with sternochondritis experience focal tenderness approximately 1 inch from the midline directly over the junction of the sternum and the costal cartilage. Xiphodynia, or inflammation between the lower sternum and the xiphoid process, is characteristically tender over a dime-sized area at the very end of the sternum. Contrast these with epidemic pleurodynia. Inflammation of the intercostal muscles causes a linear type of pain following the course of the intercostal muscle between two adjacent ribs. The pain is intermittent and cramplike at intervals of 15 to 20 minutes. Pain arising from the sternum tends to be more persistent, especially when caused by infection. As with other structures of the chest wall, the pain is aggravated by deep breath, coughing, and direct pressure. Pain arising from the sternoclavicular joint is always focal. However, unlike pain in other structures of the chest wall, it is not consistently aggravated by chest wall expansion or compression. Movement of the arms is much more aggravating. Any of these conditions, with the exception of the sternoclavicular joint disorders and xiphodynia, can lead to splinting of respiration and a sense of shortness of breath when the pain is severe. True oxygen deprivation and desaturation are not typical and suggest primary involvement of the lungs or heart. EXAMINATION General observations are made of the movement of the upper torso and the patient’s posture. The patient’s breathing pattern and the general movement of the bony thorax are used to assess the restrictive conditions affecting the chest wall (e.g., scoliosis, rib trauma). These observations are combined with an assessment of the patient’s vital signs and degree of oxygenation. If the pulse is irregular or more than 110 beats per minute or the respiratory rate is more than 20 per minute with signs of labored breathing or poor color, further evaluation of the patient’s oxygenation and vital organ function is mandatory. If the vital signs, coloration, and level of distress are unremarkable, then the physician proceeds with an examination of the chest wall and associated musculoskeletal structures. Rib fracture, rib contusion, and costochondritis are assessed by direct palpation of the affected areas and by the chest compression maneuver. Palpable tenderness and swelling of the chondral junctions is highly suggestive of costochondritis and sternochondritis. Focal tenderness over the lowest part of the sternum suggests xiphodynia. Tenderness and swelling directly over the sternoclavicular joint with or without pseudoenlargement of the clavicle are characteristic of arthritis of the articulation between the upper sternum and the proximal end of the clavicle. Pain along the course of an intercostal muscle suggests endemic pleurodynia, shingles, or radiculopathy from a thoracic vertebral lesion. Epidemic pleurodynia is characterized by local muscular tenderness. Shingles and thoracic radiculopathy

CHEST BOX 8-1

ESSENTIAL EXAMINATION OF THE CHEST WALL 1. Observe the general movement of the chest. a. Observe the movement of breathing. b. Measure chest expansion. 2. If the patient is short of breath, is coughing, has palpitations, or is nauseated, then perform a thorough examination of the chest for evidence of coronary, pulmonary, pleural, major vascular, or upper abdominal disorders. 3. Palpate the integrity of the bony thorax (ribs and sternum). 4. Assess the degree of chest wall inflammation, especially the junctions of the costal cartilages.

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lack focal tenderness. However, the skin corresponding to the thoracic dermatotome is hypesthetic or exhibits some degree of heightened sensation caused by nerve irritation. In the case of shingles, tenderness occurs when the rash appears. ONE-MINUTE SCREENING EXAM: MANEUVERS ASSESSING OVERALL CHEST WALL FUNCTION The next six maneuvers represent the minimal examination of the patient presenting with chest symptoms. Range of motion measurement and screening maneuvers for epicondylitis and olecranon bursitis provide enough information to triage to x-ray, order appropriate lab, to suggest general treatment recommendations, or proceed to more detailed examination and treatment.

GENERAL UPPER BODY MOVEMENT AND BREATHING PATTERN SUMMARY: Difficulties in moving in the exam room, performing simple tasks such as removing a T-shirt, or changing position on the exam table can be the first clue to the diagnosis of a chest wall condition. MANEUVER: Without prompting the patient, the examiner observes the patient’s general movement, noting the ease of movement and the consistency of arm and torso motions. INTERPRETATION: Cautious movement, general stiffness, and restricted movement of the chest are characteristic of conditions affecting the bony thorax. Inconsistencies between the examiner’s first observations of posture, general movement, and function and the patient’s behavior during examination can indicate malingering. FIGURE 8–1. Observe the patient’s general upper body movement and breathing pattern.

BREATHING PATTERN SUMMARY: The bony thorax consists of the sternum, the costal cartilages, the ribs, and the vertebral bodies. Chest wall splinting is a nonspecific symptom but is typical in patients with true chest wall disorders. MANEUVER: Observations with and without distraction are made of the patient’s ability to move about the exam room, ability to adjust the examination gown, and breathing pattern. INTERPRETATION: Shallow breathing or splinting indicates chest wall injury, most commonly to the bony ribs, but is also characteristic of pleurisy, pneumonia, and inflammatory pleural effusion. FIGURE 8–2. Breathing pattern, splinting with injury to the thorax.

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CHEST COMPRESSION TEST SUMMARY: The chest wall consists of the sternum, the costal cartilages, the ribs, and the vertebral bodies. Anteroposterior compression of the chest is the optimal screening to assess the integrity of the bony thorax. MANEUVER: Compression of the chest wall is first applied in an anteroposterior direction. The palmar eminences are placed over the middle of the sternum and over the spinous processes of T5 and T6 vertebra. The maneuver can be repeated with the palms placed obliquely across the chest or from side to side depending on response.

FIGURE 8–3. Chest compression test to assess the integrity of the chest wall.


PALPATION SUMMARY: Irritation and inflammation of the junctions between the costal cartilage and the adjacent rib and sternum is called costochondritis and sternochondritis, respectively. Most cases are idiopathic. MANEUVER: The intercostal spaces are palpated and marked with a pen. The rib is located halfway between the two spaces. Sternochondral tenderness is located 1 inch from the midline. Costochondral tenderness is located along the line between the sternoclavicular joint and the center of the nipple. INTERPRETATION: Most patients with costochondritis or sternochondritis have one irritated and inflamed junction. When multiple junctions are tender, the centralmost junction usually is responsible for the patient’s symptoms. FIGURE 8–4. Palpation of the costochondral and sternochondral junctions.

CHEST

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CHEST WALL EXPANSION SUMMARY: Chest wall expansion measurements are the most objective means of assessing impaired chest wall movement. Originally, this measurement was used suggested as an objective means of assessing the stiffness associated with ankylosing spondylitis. From a practical point of view, this measurement can be used to define the severity of the condition in question and assess the success of treatment. MANEUVER: The measuring tape is placed at the level of T6 and the lower sternum. The patient is asked to fully exhale, and the examiner records the circumference of the chest. The patient is then asked to inhale fully and then hold the breath in. The chest expansion is measured once again, and the difference in the two measurements is recorded. INTERPRETATION: to 21⁄2 inches.

The normal chest expansion is up

FIGURE 8–5. Use a tape measure to assess the patient’s chest wall expansion.

PALPATION SUMMARY: Epidemic pleurodynia, shingles, and thoracic radiculopathy cause pain that wraps around the chest wall, following the course of an intercostal space. MANEUVER: The intercostal spaces are palpated and marked with a pen. The intercostal muscle is palpated for local tenderness and spasm. Light touch and pain sensation are tested along the course of the intercostal space. INTERPRETATION: Tenderness over the muscle suggests epidemic pleurodynia. Hypersensitivity or loss of sensation is seen with shingles and vertebral body lesions at thoracic levels T7–T1. Shingles is characterized by a grouping of erythematous vesicular lesions along the course of the intercostal space.

FIGURE 8–6. Palpation of the intercostal muscles to assess epidemic pleurodynia.

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ONE-MINUTE SCREENING EXAM: MANAGEMENT OPTIONS TRIAGE TO X-RAY For patients with a history of blunt trauma to the chest, those with osteoporosis, acute chest pain, and severe paroxysms of cough, or those with chest pain and associated symptoms including palpitations, dizziness, productive cough, pleurisy, nausea, and vomiting: • Order a chest x-ray and cardiogram if breathing is impaired (pneumonia, pulmonary embolus, angina, coronary artery disease). • Order a chest x-ray and tangential views of the ribs if the patient has sustained a blow to the chest wall (rib contusion, rib fracture). • Order a chest x-ray and tangential views of the ribs if the patient has osteoporosis and has acute pain in the chest after paroxysms of coughing (rib contusion, rib fracture). • Order chest x-ray and special views of the sternum if the patient has persistent pain over the sternum (fracture, osteomyelitis after open heart surgery). • Order a chest x-ray and thoracic spine films if the patient describes pain wrapping around the chest wall (compression fracture, metastatic disease, epidural abscess, primary disease of the spinal cord).

CONSIDER A BONE SCAN For patients with focal chest wall pain and a history of malignancy, with persistent rib pain, or with radicular pain wrapping around the chest wall (compression fracture, miscellaneous fractures of the spine, osteomyelitis, rib contusion or fracture, and metastatic disease). CONSIDER MRI For patients with radicular pain wrapping around the chest wall (compression fracture, miscellaneous fractures of the spine, osteomyelitis, and metastatic disease). RECOMMEND EMPIRICAL TREATMENT For patients with mild to moderate chest wall pain and stiffness, unrestricted movement, and normal breathing: • Avoid vigorous exercise, lifting, twisting, pushing, and pulling. • Avoid lying on either side. • Apply ice to the tender areas of the chest wall. • Use a nonsteroidal anti-inflammatory medication for 10 to 14 days with a taper over 7 days at the end. • Recommend an Ace wrap, wide bra, or a rib binder, but only if there are no risks of pulmonary complications (optional).

TRIAGE TO THE LAB For patients with chest pain, cough, fever, and significant respiratory insufficiency: • Order a chest x-ray, complete blood cell count, erythrocyte sedimentation rate, and blood cultures for patients with acute chest pain, cough, fever, and an acute change in respiratory function (e.g., pneumonia, pulmonary embolus, pleural effusion, pneumothorax).

DETAILED EXAMINATION: SPECIFIC CHEST WALL DIAGNOSES Perform a detailed examination of the chest if the patient has persistent or chronic symptoms, moderate to severe chest wall pain, severe bony tenderness, significant breathing impairment, intense paraspinal muscle spasm, or radiculopathy.

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COSTOCHONDRITIS Inflammation between the costal cartilage and the end of the rib is called costochondritis. Inflammation between the costal cartilage and the bony sternum is called sternochondritis. Inflammation and bulbous enlargement of the costochondral junction is called Tietze’s syndrome.

PALPATION SUMMARY: Inflammation of the junctions of the costal cartilage and the ribs and sternum is called costochondritis and sternochondritis, respectively. When the inflammatory reaction is complicated by a unique bulbous enlargement of the joint, the condition is called Tietze’s syndrome. MANEUVER: The intercostal spaces are palpated and marked with a pen. The center of the rib is located halfway between the two spaces. Sternochondral tenderness is located at the junction of the cartilage and the sternum, approximately 1 inch from the midline. Costochondral tenderness is located at the junction of the cartilage and the rib that follows a line extending from the sternoclavicular joint through the center of the nipple.

FIGURE 8–7. Palpation of the local tenderness of costochondritis and sternochondritis.

INTERPRETATION: Most patients with costochondritis or sternochondritis have one irritated and inflamed junction. When multiple junctions are tender, the centralmost junction usually is responsible for the symptoms.

LOCAL ANESTHETIC BLOCK SUMMARY: Enter atop the center of the rib; angle the syringe perpendicular to the skin. The injections should be placed flush against the cartilage adjacent to the costochondral junction using mild pressure. NEEDLE:


5

DEPTH: ⁄2 to 1 inch, depending on the location on the chest. 1

VOLUME: 1 to 2 mL local anesthetic, 1⁄2 mL D80 or K40, or both. FIGURE 8–8. Local anesthetic block to confirm costochondritis or sternochondritis.

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NONDISPLACED RIB FRACTURE Simple nondisplaced rib

fractures (cracks) result from a minor blow to the chest or a fall onto the bony thorax. Focal tenderness, a positive chest compres-

sion sign, and relief with local anesthesia are useful in making a presumptive diagnosis. Chest radiographs are normal in most cases.

PALPATION SUMMARY: The anterolateral and posterolateral ribs are the areas of the chest wall that are most vulnerable to injury. Ribs 6 through 10 are most often fractured. MANEUVER: The patient is placed in the lateral decubitus position. The center of the ribs are palpated and marked with a pen. The length of the rib is palpated for local tenderness and deformity. ADDITIONAL SIGNS: The rib compression sign is positive. Palpable deformity suggests a displaced fracture. Signs of pneumothorax may be present. If pneumothorax has occurred, subcutaneous emphysema may be present.

FIGURE 8–9. Palpation of the rib.

INTERPRETATION: Patients with bruised ribs have tenderness without deformity. Patients with displaced fractures have tenderness and deformity.

LOCAL ANESTHETIC BLOCK SUMMARY: The intercostal nerve and vascular bundle are located on the undersurface of the rib. Local anesthetic block is placed between the area of injury and the vertebral column. Before placing the anesthetic at the undersurface of the rib, the examiner determines the depth of injection by inserting the needle directly over the center of the rib. NEEDLE:


DEPTH: 1⁄2 to 1 inch, depending on the location on the chest wall. VOLUME: 1 to 2 mL local anesthetic, 1⁄2 mL D80, or both.

FIGURE 8–10. Local anesthetic block to confirm costochondritis or sternochondritis.

NOTE: Never advance the needle more than 1⁄2 inch further than the depth of the rib.

CHEST

Sternoclavicular joint strain from seat belt injuries or falls to an outstretched arm and its long-term sequela, sternoclavicular joint arthritis, are characterized by local tenderness and pseudoenlargement of the proxi-

STERNOCLAVICULAR JOINT ARTHRITIS

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mal end of the clavicle. The prominence of the clavicle, often mistakenly diagnosed as a bony tumor, is due to joint swelling and displacement, which create the appearance of an enlarged clavicle.

PALPATION SUMMARY: The sternoclavicular joint is formed by the upper portion of the sternum and the proximal clavicle. When the joint swells, the proximal clavicle projects anteriorly. The anterior position of the clavicle causes a pseudoenlargement of the clavicle. MANEUVER: The sternal notch, proximal clavicle, and center of sternum are palpated and marked with a pen. The sternoclavicular joint is palpated at the junction of the sternum and the proximal clavicle, approximately 3⁄4 to 1 inch from the midline. ADDITIONAL SIGNS: Swelling in the sternoclavicular joint gives the false impression of an enlarged clavicle, the pseudoenlargement of the clavicle. The patient’s pain can be reproduced by passive adduction of the shoulder across the chest. FIGURE 8–11. Palpation of the sternoclavicular joint.

INTERPRETATION: Sternoclavicular joint involvement is uncommon. Sternoclavicular joint strain is characterized solely by local tenderness. Sternoclavicular joint local tenderness and pseudoenlargement of the clavicle are seen with sternoclavicular joint arthritis, most commonly Reiter’s disease. A red, hot, swollen joint is a unique complication of intravenous drug abuse (septic arthritis usually is due to Staphylococcus aureus or Gram-negative bacilli).

LOCAL ANESTHETIC BLOCK SUMMARY: Enter atop the center of the proximal clavicle with the needle perpendicular to the skin. The injection should be placed flush against the proximal end of the clavicle, just adjacent to the center of the joint, using mild pressure. NEEDLE: DEPTH:


5

⁄8 to 1⁄2 inch.

3

VOLUME: 1 mL local anesthetic, 1⁄2 mL K40, or both.

FIGURE 8–12. Local anesthetic block to identify the sternoclavicular joint as the source of the patient’s pain.

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EPIDEMIC PLEURODYNIA Epidemic pleurodynia, or the devil’s grip, is an acute inflammation of the muscles of the chest wall. The presumptive diagnosis is suggested by focal pain, muscle

tenderness, and chest wall irritation between two adjacent ribs. The diagnosis can be confirmed by placing local anesthetic directly into the affected intercostal muscle.

PALPATION SUMMARY: Epidemic pleurodynia is characterized by dramatic local tenderness and spasm of the intercostal muscles. Often one intercostal space is affected more than another, although the patient may describe a wide area of discomfort. MANEUVER: The intercostal spaces are palpated and marked with a pen. The intercostal muscle is palpated for local tenderness and spasm. ADDITIONAL SIGNS: The chest compression sign is negative. The sensory testing of the intercostal space should be normal. The overlying skin is free of rash.

FIGURE 8–13. Palpation of the intercostal space.

INTERPRETATION: Tenderness over the muscle suggests epidemic pleurodynia. Hypersensitivity or loss of sensation is seen with shingles and vertebral body lesions at thoracic levels T7–T1. Shingles is characterized by a grouping of erythematous vesicular lesions along the course of the intercostal space.

LOCAL ANESTHETIC BLOCK SUMMARY: The intercostal muscle is located at the same depth as the adjacent ribs. Local anesthetic block is placed in the most proximal portion of the irritated area, closest to the vertebral column. Before placing anesthetic at the undersurface the of the rib, the examiner determines the depth of injection by inserting the needle directly over the center of the rib. NEEDLE:


DEPTH: 1⁄2 to 1 inch, depending on the location on the chest wall. VOLUME: 1 to 2 mL local anesthetic, 1⁄2 mL D80, or both. NOTE: Never advance the needle more than 1⁄2 inch further than the depth of the rib.

FIGURE 8–14. Local anesthetic block to confirm involvement of the intercostal muscle.

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XIPHODYNIA Xiphodynia is a rare cause of chest pain. Focal

inflammation and pain are located at the junction of the xiphoid and lower sternum. Direct pressure causes pain and a visceral response (nausea and abdominal discomfort).

PALPATION SUMMARY: The xiphoid process is an inch-long bone attached to the inferior aspect of the sternum. Injury and inflammation occur at the junction of these two bones. MANEUVER: The inferior aspect of the sternum is identified and marked. The xiphoid process extends approximately 1 inch inferior to the sternum in the midline between the medial aspects of the ribs. The maximum tenderness is located at the junction of the sternum and xiphoid process. ADDITIONAL SIGNS: Firm pressure over the xiphoid causes tenderness and an autonomic response consisting of nausea, abdominal discomfort, and sweating.

FIGURE 8–15. Palpation of the xiphoid process.

INTERPRETATION: Local tenderness in the midline directly over the xiphoid process unequivocally defines xiphodynia. The local tenderness of sternal injury, fracture, or osteomyelitis typically is more diffuse and extends over a large area of the bone. The local tenderness of sternochondritis is always off the midline.

LOCAL ANESTHETIC BLOCK SUMMARY: Enter directly over the junction of the sternum and the xiphoid process in the midline. Maintain the angle of the syringe perpendicular to the skin. The injection should be placed flush against the firm to hard bone adjacent to the junction, on the sternal or xiphoid side of the articulation. NEEDLE:


5

DEPTH: 1⁄2 to 1 inch, depending on the location on the chest. VOLUME: 1 to 2 mL local anesthetic, 1⁄2 mL D80, or both.

FIGURE 8–16. Local anesthetic block to confirm xiphodynia.

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8–1




DIAGNOSIS


Focal tenderness over the cartilage

Costochondritis or sternochondritis

Local anesthetic block at the junction of the cartilage with the rib or sternum, respectively

#1: Rib fracture or contusion

Rib x-rays

+ Chest wall compression sign Diminished chest expansion Focal tenderness over the rib after injury + Chest wall compression sign

Local anesthetic block over the rib

Diminished chest expansion (pain) Enlargement and focal tenderness of the sternoclavicular joint

Sternoclavicular joint injury or arthritis

Pain aggravated by passive adduction of the shoulder Focal tenderness and spasm of an intercostal muscle

Apical lordotic views of the chest MRI of the upper chest

Epidemic pleurodynia

+ Chest wall compression sign

Chest x-ray Local anesthetic block in the intercostal muscle

Diminished chest expansion (pain) Focal tenderness over the xiphoid

Xiphodynia

Local anesthetic block over the junction of the sternum and the xiphoid

Focal tenderness over the sternum

Sternal injury or infection

Sternum x-rays

+ Chest wall compression sign

Abnormal bone scan

Diminished chest expansion

CLINICAL PEARLS • Patients with inflammation of the chest wall (costochondritis or sternochondritis) often present with tenderness over more than one rib. In most cases the rib that manifests the greatest sensitivity to palpation is the focus of the patient’s pain. The sensitivity of the adjoining ribs often is referred pain. Local anesthetic placed at the most involved rib often is sufficient to control the chest wall inflammation. • Swelling of the sternoclavicular joint causes subluxation of the clavicle, leading to what appears to be an enlargement of the bone, or pseudoenlargement of the clavicle.

• Epidemic pleurodynia often is misdiagnosed as rib contusion. The classic signs of rib contusion and rib fracture— chest wall compression and direct rib palpation—are not seen with pleurodynia. Pleurodynia is characterized by intercostal muscle tenderness and spasm located between the ribs. • Sternal infection is rare outside the setting of open heart surgery. • Chest wall compression should be performed in several different directions to rule out rib fracture.

CHAPTER 9: LUMBOSACRAL SPINE DIFFERENTIAL DIAGNOSIS Diagnoses

Confirmations

Lumbosacral back strain (most common) Unaccustomed or improper use

Examination: local tenderness, Schober measurement

Reactive lumbosacral back strain Osteoarthritis Scoliosis Spondylolisthesis Herniated disk

X-ray: routine back series X-ray: standing scoliosis views X-ray: routine back series and the oblique views Computed tomography (CT) scan or magnetic resonance imaging (MRI)

Compression fracture

X-ray: lateral view of the back, bone scan, MRI

Epidural process

MRI

Lumbosacral radiculopathy (sciatica) Herniated disk Osteoarthritis (spinal stenosis) Intra-abdominal process Wallet sciatica Cauda equina syndrome

CT scan or MRI CT scan or MRI Ultrasound or CT scan History MRI

Sacroiliac joint strain Sacroiliitis

Local anesthetic block X-ray: standing anteroposterior pelvis; the oblique views of the sacroiliac joints; bone scan

Coccydynia


Referred pain Kidney (e.g., pyelonephritis, stones) Aorta Colon (e.g., appendicitis, cecal carcinoma, rectal carcinoma) Pelvis (e.g., tumor, pregnancy)

Urinalysis, intravenous pyelogram, ultrasound Ultrasound, CT scanning Hemoccult, barium enema, sigmoidoscopy, colonoscopy Examination, ultrasound

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INTRODUCTION The back is the most complicated and misunderstood area of the skeleton. With a variety of conditions, a systematic approach to the differential diagnosis of low back pain involves separation of these conditions into five general categories: structural, radiculopathic, sacroiliac, traumatic, and medical. Structural causes of low back pain dominate the differential diagnosis and include irritation or injury to the supporting paraspinal muscles, the complex network of supporting ligaments, facet joint cartilage, and the vertebral bones. Of the various structural elements of the spinal column, the paraspinal muscles are most susceptible; therefore, low back strain is the most common cause of structural back pain. Reversible strain of the paraspinal muscles results from overuse of improperly stretched and toned muscles. However, recurrent or chronic muscle strain and spasm can result from any condition that threatens the structural integrity of the lower back (abnormal alignment from scoliosis, kyphosis, and spondylolisthesis, chronic inflammation from spondylitis, wear of the facet joint cartilage and disk from degenerative arthritis, or loss of normal alignment from compression fracture). As with the cervical spine, the irritation and spasm of the paraspinal muscles are the body’s protective reflex whenever the spinal column, spinal cord, or spinal nerve is in jeopardy. Lumbar radiculopathy is the next most common problem affecting the lower back. Compression of the spinal nerves, spinal roots, or spinal cord causes localized low back strain (reflexive paraspinal muscle spasm to protect the spinal elements) or radicular symptoms in the lower extremities (sciatic pain and numbness). Degenerative disk disease, herniated nucleus pulposus (HNP), and degenerative arthritic narrowing of the lateral recesses are the primary causes. Spinal stenosis (the most extreme case of degenerative changes), epidural abscess, epidural metastatic disease, and primary involvement of the spinal cord are less common causes. Lumbar radiculopathy is graded according to the degree of nerve compression. Progressive pressure causes sensory symptoms first, followed by sensorimotor and sensorimotorvisceral (cauda equina syndrome) symptoms. The sacroiliac joint is a unique cause of low back pain. Most patients describe a well-localized area of irritation over the sacral area, although some patients describe low back pain similar to that due to the structural causes of pain, especially when the paraspinal muscles react dramatically. Injury and strain to the supporting iliolumbar and iliosacral ligaments (sacroiliac strain) and inflammation of the joint (sacroiliitis) in the setting of active spondyloarthropathy are the two most common causes. Nearly all traumatic injuries to the spine demand the attention of the orthopedic or neurosurgical specialists with the exception of the less severe compression fractures. It is not uncommon for an osteoporotic patient to present to the primary care provider with a cough or minor injury induced by partial collapse of a vertebral body. Finally, if the four intrinsic causes of low back pain are not identified, a thorough search for a medical cause of

referred pain must be sought. Common causes include pyelonephritis, nephrolithiasis, gynecological disorders, ascending and descending lesions of the colon, and atherosclerotic involvement of the abdominal aorta. Associated symptoms of dysuria, hematuria, menometrorrhagia, bowel irregularity, and claudication are clues to the presence of a medical cause of back pain. SYMPTOMS Conditions directly affecting the back cause lower back pain, muscle spasms, stiffness and impaired movement, radicular symptoms, or a combination of these symptoms. Diffuse low back pain is one of the most common symptoms because of the universal occurrence of lumbosacral strain (acute irritation and spasm of the paraspinal muscles). Although the pain can be poorly localized, vague in description, and variable in intensity, the diagnosis of lumbosacral strain is strongly suggested by aggravation caused by specific movements of the back. Most episodes of acute back strain result from poor posture, improper lifting, or unaccustomed use of these supporting muscles. However, it is also the body’s final common pathway for any process that threatens the integrity of the structure of the spinal column, spinal nerves, or spinal cord. Unexplained lumbosacral strain (i.e., unassociated with an obvious physical event), should alert the clinician to an underlying structural abnormality, radiculopathy, or sacroiliac joint disorder. Focal low back pain is encountered much less commonly. Pain along either side of the spine is most often caused by paraspinal muscle spasm that accompanies scoliosis, osteoarthritis, or sacroiliac strain. On the other hand, pain localized to the center of the spine suggests involvement of the vertebral column (fracture, tumor, infection, or herniated disk). In either case, if the process is severe, radicular pain may accompany the clinical presentation. Low back pain accompanied by pain or paresthesia referred down the leg (sciatica) is the classic presentation of lumbar radiculopathy. The severity of these symptoms varies from patient to patient and depends on the underlying cause, the acuteness of the process, the degree of nerve compression, and the degree of reactive paraspinal muscle spasm. These factors tend to be quite dynamic, changing over time, interacting, and compounding one another. For example, sensory radiculopathy (impairment limited to the sensory branches of the spinal nerve) can progress to sensorimotor radiculopathy (impairment of both sensory and motor nerves) as the reactive paraspinal muscle spasm places greater localized pressure on the spine. Focal low back pain localized below the iliac crest is the classic location of sacroiliac joint irritation or inflammation. Focal low back pain localized in the midline of the gluteal crease is classic for coccydynia. Low back pain that is unassociated with focal back tenderness, a change in mobility, stiffness, or radicular symptoms suggests referred pain from the abdomen. Pyelonephritis and renal colic are the most common med-

LUMBOSACRAL SPINE BOX 9-1

BOX 9-2

DIFFERENTIAL DIAGNOSIS OF BACK PAIN BASED ON ANATOMIC AREA Structural back disease

Radiculopathy

Sacroiliac joint Coccyx Referred pain

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Low back strain Scoliosis Spondylolisthesis Osteoarthritis of the back Compression fracture Herniated disk Spinal stenosis Cauda equina syndrome Epidural abscess Epidural metastasis Compression fracture Sacroiliac strain Sacroiliitis Coccydynia Nephrolithiasis, pyelonephritis Aortic aneurysm Disease of the colon Pelvic tumor, pregnancy

ical causes of back pain. However, any retroperitoneal process (e.g., retrocecal appendix, cecal carcinoma, pelvic tumor, abdominal aneurysm) can mimic the pain of low back strain. EXAMINATION Conditions affecting the lumbosacral spine are exceedingly common and can range from the inconvenience of a minor back strain to the severe incapacitation of a compression fracture or spinal stenosis. The examination of the back should always begin with assessment of the patient’s overall function. This is accomplished by observing the patient’s posture and gait, the ability to climb onto the exam table, and the ease or difficulty in reclining and sitting up. Next, the examiner assesses the integrity of the spinal column by inspecting the lumbosacral curve, palpating the spinous processes, and palpating and percussing each individual vertebra. Palpation of the paraspinal muscle groups and measurement of lumbar flexion using the Schober test are used to assess the degree of reactive muscle strain and overall spinal mobility. The straight leg raise maneuver and a detailed neurologic exam of the lower extremities are used to determine the degree of lumbar radiculopathy.

ESSENTIAL EXAMINATION OF THE LUMBOSACRAL SPINE 1. Observe the patient’s general movement, including gait, difficulties in changing positions, and posture. 2. Palpate the paraspinal muscles and perform a Schober test. 3. Define the degree of radicular pain and perform a straight leg raise maneuver. 4. Palpate and percuss each of the five spinous processes. 5. Palpate the sacroiliac joint and perform a Patrick maneuver. 6. Palpate the sacrococcygeal junction. 7. Examine the abdomen for a medical cause of low back pain.

Irritation and inflammation of the sacroiliac joint are assessed by direct palpation of the joint and by Patrick maneuver (recreating the patient’s pain by applying torque to the sacroiliac joint; forced abduction and external rotation of the hip). Finally, the abdomen and pelvis are examined when the examination of the back does not demonstrate localized tenderness, impaired mobility, or evidence of radiculopathy. ONE-MINUTE SCREENING BACK EXAM: MANEUVERS ASSESSING OVERALL BACK FUNCTION The next six maneuvers represent the minimal examination of the patient presenting with back symptoms. Observation of general function, range of motion measurement, and screening maneuvers for lumbosacral strain, radiculopathy, and sacroiliac strain provide enough information to triage to x-ray, order appropriate labs, suggest general treatment recommendations, or proceed to more detailed examination and treatment.

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GAIT SUMMARY: Walking with upright posture requires an intact lumbosacral spine, spinal nerves, and spinal cord as well as flexible and strong lower extremity muscles. MANEUVER: The patient is asked to walk through the exam room while the examiner observes heel–toe walking and general coordination, watching for antalgic gait and spasticity. INTERPRETATION: Full upright posture will be affected by an abnormal alignment of the spine (scoliosis), osteoarthritis of the spine (spinal stenosis), paraspinal muscle spasm (lumbosacral strain), and disorders of the spinal nerves and spinal cord (lumbar radiculopathy). Observation of the patient’s gait is useful in determining the severity of the underlying process.

FIGURE 9–1. Observe the patient’s gait.

SCHOBER TEST SUMMARY: Bending forward at the waist combines the movement of the facet joints, the lumbosacral ligaments, and the paraspinal muscles of the lumbosacral spine; movement of the sacroiliac joint; and flexion of the hips. The Schober test objectively measures the contribution of the lumbosacral back to flexion. The Schober measurement is considered normal if the distance between the marks increases by 50% (from 10 to 15 cm), the marks gradually and smoothly move apart, and the maneuver does not incite back pain. MANEUVER: The maneuver begins with the patient standing. Two marks are made over the spine, one at the level of the iliac crests and one at 10 cm. Then the patient is asked to bend forward slowly and to report when symptoms are felt. The tape is held at the upper mark. As the patient actively bends, the point at which pain occurs and the point of maximum flexion are measured.

FIGURE 9–2. Perform a objective measurement of back flexion using the Schober test.

INTERPRETATION: The Schober test provides a rough gauge of the severity of the underlying condition affecting the lumbosacral spine. Its most practical use is to rule out significant structural and spinal disorders. A 50% increase in the measurement effectively excludes significant back disease and is consistent with sacroiliac strain, medical causes of back pain, or drug-seeking patients feigning back pain.

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153

PARASPINAL MUSCLES SUMMARY: The erector spinae muscles (the paraspinal muscles) arise from the thoracolumbar fascia, attach to each spinal level, and extend up the spine to the base of the skull. MANEUVER: The patient is asked to sit up as straight as is comfortable with attention to posture. Local tenderness and muscle spasm are compared side to side. The optimal site of palpation is approximately 2 inches from the midline. The irritability and spasm can be enhanced by asking the patient to rotate to the right and then to the left at the waist. INTERPRETATION: Paraspinal muscle spasm can be unilateral with common back strain, scoliosis, disk herniation, or an epidural process. Bilateral paraspinal spasm is more common and can occur with any underlying back process. FIGURE 9–3. Palpate the paraspinal muscles to assess irritability and spasm.

SPINOUS PROCESSES OF THE VERTEBRAL BODIES SUMMARY: The spinous process, the most accessible portion of the vertebra to palpation, connects to the vertebral body through the posterior elements of the neural arch. MANEUVER: The patient is asked to sit up as straight as is comfortable with attention to posture. The individual spinous processes are palpated with firm pressure. If simple palpation does not recreate the patient’s pain, then percussion of each individual spinous process is performed. Percussion can be accomplished using a reflex hammer or the ulnar side of the fist. INTERPRETATION: Focal tenderness implies a more involved process such as acute disk herniation, compression fracture, or epidural process. FIGURE 9–4. Palpate and percuss the spinous processes of the vertebral bodies.

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STRAIGHT LEG RAISE MANEUVER SUMMARY: The straight leg raise maneuver is the most important screening maneuver for acute radiculopathy. It is much less sensitive when the patient has chronic nerve irritation (e.g., spinal stenosis, spondylolisthesis). When the leg is straightened, the sciatic nerve is placed under tension. An abnormal response should reproduce the patient’s radiating sciatic pain. MANEUVER: The maneuver can be performed in the seated position or while supine. With the hip flexed at 90 degrees, the leg is gradually straightened. Adding passive dorsiflexion of the foot can enhance the stretch. FIGURE 9–5. Perform the straight leg raise maneuver to screen for radiculopathy.

INTERPRETATION: The straight leg raise maneuver usually is positive in patients with acute symptoms, occurring with acute HNP, compression fracture, epidural abscess or hemorrhage, or acute muscle spasm atop spondylolisthesis or lateral recess encroachment. Patients with chronic low back pain, uncomplicated osteoarthritis of the back, spinal stenosis, scoliosis, and minor disk bulges rarely have a positive response.

PALPATE THE SACROILIAC JOINT SUMMARY: The sacroiliac joint is hidden under the wing of the iliac crest. In order to create enough pressure over the joint to cause pain, the joint must be palpated from a slightly medial position. MANEUVER: The patient is placed prone. The PSIS and the midline are marked with a pen. The area of maximum tenderness is 1 inch medial and 1 inch inferior to the PSIS. Pressure is directed slightly laterally at a 70-degree angle. INTERPRETATION: Tenderness directly over the sacroiliac joint is virtually pathognomonic of sacroiliac strain and sacroiliitis. This must be distinguished from the tenderness of the thoracolumbar fascia located superior to the sacroiliac joint and the sacral bony tenderness that is more midline and inferior of the sacroiliac joint.

FIGURE 9–6. Palpate the sacroiliac joint for local tenderness.

LUMBOSACRAL SPINE

ONE-MINUTE SCREENING EXAM: MANAGEMENT OPTIONS TRIAGE TO X-RAY For a patient who has a history of trauma, has focal tenderness over a single vertebra, has severely impaired flexion by Schober measurement, has lost 1⁄2 inch in height within 1 year, has a progressive neurodeficit on exam, or has acute back pain: • Order posteroanterior (PA) and lateral views of the spine for patients with a history of trauma or acute pain after paroxysms of cough (fracture dislocation, transverse process fracture, compression fracture). • Order PA and lateral views of the spine for patients with impaired flexion or abnormal Schober measurement (ankylosing spondylitis, spinal stenosis). • Order PA and lateral views of the spine for patients with focal tenderness over a single vertebra (metastatic disease, epidural abscess, benign bony tumor). • Order PA and lateral full spine views for patients with scoliosis who have lost 1⁄2 inch in height in 6 months (progressive scoliosis curve). • Order PA, lateral, and oblique view of the spine for patients with spondylolisthesis and worsening low back pain, sciatica, or both (progressive spondylolisthesis slippage). • Order a standing anteroposterior (AP) pelvis for patients with chronic low back pain and a short leg (low back strain, sacroiliac strain, or degenerative arthritis aggravated by leg length discrepancy). TRIAGE TO THE LAB • Order a complete blood cell count, erythrocyte sedimentation rate, blood cultures, and nuclear medicine scan of the sacroiliac joints for patients with acute sacroiliac low back pain and peripheral arthritis (inflammatory spondylitis). • Order a complete blood cell count, erythrocyte sedimentation rate, and blood cultures for patients with acute pain, fever, and rapidly progressive neurologic deficit (vertebral body osteomyelitis or epidural abscess). CONSIDER A BONE SCAN For patients with focal spinous process tenderness, severe low back pain, progressive neurologic deficit, and a history of trauma or cancer (compression fracture, epidural metastasis).

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CONSIDER MRI For patients with sensorimotor radiculopathy, cauda equina, increased symptoms from old compression fractures, advanced osteoarthritis with radiculopathy (large HNP, spinal cord tumor, compression fracture progression, spinal stenosis). CONSIDER ELECTROMYOGRAPHY For patients with advanced lower extremity neurologic deficits that are vague in distribution or encompass more than one spinal level or that are complicated by peripheral neuropathy (radiculopathy). RECOMMEND EMPIRICAL TREATMENT For patients with mild to moderate low back pain and stiffness, minimally impaired overall movement of the back, intermittent mild sciatica, and a normal Schober test: • Avoid lifting, twisting, and other physically demanding work. • Maintain straight, upright posture. • Apply ice to the muscle groups in spasm. • Perform daily passive stretching exercises in flexion. • Recommend a muscle relaxer over 7 consecutive nights. • Use a Velcro lumbosacral back brace during the daytime (optional). DETAILED EXAMINATION: SPECIFIC BACK DIAGNOSES For patients with persistent or chronic symptoms, severe back pain and stiffness, focal spinous process tenderness, Schober measurement demonstrating less than 50% of normal spinal flexion, intense paraspinal muscle spasm, or radiculopathy with motor involvement. LUMBOSACRAL MUSCLE STRAIN Lumbosacral strain is caused most often by the unaccustomed or improper use of the muscles that support the back (“back strain”). However, in the absence of an obvious precipitating event, intense muscle spasm suggests the possibility of a potentially severe underlying spinal process. Any perceived threat to the integrity of the spinal column, nerves, or spinal cord initiates the protective spinal reflex, which activates the reactive muscle spasm. The Schober measurement of spinal flexion combined with the direct palpation of the paraspinal muscles provides the most objective means of determining the degree of lumbosacral strain.

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SCHOBER MEASUREMENT SUMMARY: Bending forward at the waist combines the movement of the lumbar spine including facet joints, the lumbosacral ligaments, and the paraspinal muscles of the lumbosacral spine; movement of the sacroiliac joint; and flexion of the hips. The Schober test objectively measures the contribution of the lumbosacral back to flexion. The Schober measurement is considered normal if the distance between the marks increases by 50% (from 10 to 15 cm, or 5 to 71⁄2 inches depicted here), the marks gradually and smoothly move apart, and the maneuver does not incite back pain. MANEUVER: The maneuver begins with the patient standing. Two marks are made over the spine, one at the level of the iliac crests and one at 10 cm. Then, the patient is asked to bend forward slowly and to report when symptoms are felt. The tape is held at the upper mark. As the patient actively bends, the point at which pain occurs and the point of maximum flexion are measured. ADDITIONAL SIGNS: Paraspinal muscle tenderness and spasm, paraspinal muscle prominence, inability to lateral bend to the same degree side to side, and painful rotation of the lower back complete the assessment of lumbosacral strain. INTERPRETATION: The Schober test provides a rough gauge of the severity of the underlying process affecting the lower spine. Its most practical use is to rule out significant structural and spinal pathology. A 50% increase in the measurement effectively excludes significant back disease and is consistent with sacroiliac strain, medical causes of back pain, or drug-seeking patients feigning back pain. Measurements up to 14 cm are consistent with mild to moderate lumbosacral strain from back strain, scoliosis, spondylolisthesis, or moderate osteoarthritis. Measurements up to 11 cm are consistent with ankylosing spondylitis, spinal stenosis, severe spinal nerve or spinal cord compression, and severe reactive lumbosacral strain.

FIGURE 9–7. Perform a Schober measurement to assess spinal flexibility and lumbosacral strain.

LUMBOSACRAL SPINE

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LOCAL ANESTHETIC BLOCK SUMMARY: Local anesthetic block is used to identify the paraspinal muscles as the source of the patient’s lumbosacral pain. POSITIONING:

Prone on the exam table.

SURFACE ANATOMY: Spinous processes, PSIS, paraspinal muscles, thoracolumbar fascia. POINT OF ENTRY: Two inches from the midline directly over the point of maximum tenderness. ANGLE OF ENTRY:

1 ⁄2 inch, 21 gauge.

NEEDLE: DEPTH:

90-degree angle.

1

⁄8 to 11⁄2 inch.

3

ANESTHESIA: Ethyl chloride, skin: 1⁄2 mL over the outer fascia of the muscle, 1⁄2 to 1 mL intramuscularly.

FIGURE 9–8. Local anesthetic block of the paraspinal muscles to confirm lumbosacral muscle strain.

LUMBAR RADICULOPATHY The diagnosis of lumbar

radiculopathy is based on the patient’s description of “sciatica,” that is, a lower extremity lancinating pain accompanied by vary-

ing degrees of neurodeficit (e.g., paresthesia, hypesthesia); an examination demonstrating impaired neurologic function; and abnormalities on CT or MRI that correlate with the neurologic findings.

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STRAIGHT LEG RAISE SUMMARY: The sciatic nerve arises from the lumbosacral plexus and travels through the buttocks, behind the hip joint, within the body of the piriformis muscle, through the popliteal fossa, and down into the lower leg. At the level of the knee it branches as the tibial and common peroneal nerves. Any pressure along the course of the nerve causes sciatica.

FIGURE 9–9. Perform a straight leg raise maneuver to evaluate for acute or subacute sciatica or lumbar radiculopathy.

MANEUVER: The maneuver can be performed in the sitting or supine positions. The leg is gradually extended either at the knee (while seated) or at the hip (while lying flat). The angle at which the patient’s radicular pain is reproduced is noted. Calf tightness or pain or pain behind the knee is not considered a positive response. ADDITIONAL SIGNS: The patient often sits with extended arms to reduce the pressure over the back. Percussion over the affected vertebra may reproduce the patient’s pain. Neurologic abnormalities can include loss of sensation in the foot, reflex asymmetry, motor weakness and atrophy, and loss of bowel and bladder function. INTERPRETATION: The straight leg raise maneuver usually is positive in patients with acute symptoms occurring with acute HNP, compression fracture, epidural abscess or hemorrhage, or acute muscle spasm atop spondylolisthesis or lateral recess encroachment. Patients with chronic low back pain, uncomplicated osteoarthritis of the back, spinal stenosis, scoliosis, and minor disk bulges rarely have a positive maneuver.

CT IMAGING CASE: The patient experienced acute low back pain after lifting a large audio speaker. Flexibility gradually decreased. Within 36 hours the patient complained of pain radiating down the left leg accompanied by numbness of the bottom of the foot. DIAGNOSIS: Acute disk herniation at L5–S1 with compression of the S1 nerve root in the lateral recess.

FIGURE 9–10. CT imaging to confirm the cause of lumbar radiculopathy.

DISCUSSION: Lumbar radiculopathy is graded according to the degree of neurologic deficit. Seventyfive percent to 80% of cases are limited to impairment of sensation in a dermatomal distribution (sensory deficit only), 20% to 25% involve impairment of both sensation and motor function (sensorimotor deficit), and less than 1% of patients have impairment of bowel and bladder function (sensorimotorvisceral or cauda equina syndrome). CT imaging is indicated for persistent or progressive sensory loss or sensorimotor loss with or without cauda equina syndrome.

LUMBOSACRAL SPINE

CAUDA EQUINA SYNDROME Cauda equina syndrome is the neurologic condition affecting the lowermost segments of the cord, the sacral nerves. Large herniated disks, disk fragments, sacral tumors, and primary spinal cord tumors cause loss of

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sensation in the perineal area (“saddle anesthesia”), loss of bowel and bladder control, or neurogenic bladder. The definitive anatomic diagnosis always includes CT or MRI.

RECTAL SPHINCTER TONE AND WINK SIGN AND PERINEAL SENSATION SUMMARY: The combination of loss of sensation in the perineal area (saddle anesthesia), loss of bowel and bladder control, and bilateral lower extremity neurologic impairment is called cauda equina syndrome. Large herniated disks at the lower lumbar areas can cause the complete syndrome. Sacral tumors and primary spinal cord tumors can present with isolated bowel and bladder impairment. MANEUVER: The patient is placed in the lateral decubitus position with the hips and knees flexed to 90 degrees. Rectal sphincter tone is performed on rectal examination. The rectal sphincter wink sign is performed by scratching the perianal skin and observing or feeling the reflex contraction of the rectal sphincter. FIGURE 9–11. Rectal sphincter tone and wink sign and perineal sensation are used to define impairment of the lower sacral nerves.

ADDITIONAL SIGNS: Sensory testing of the skin of the perineal areas shows diminished light touch and pain sensation. Reactive paraspinal muscle spasm may be present. Evidence of lower extremity neurologic deficit may be present. Abnormalities of bladder function are present on cystometrograms. INTERPRETATION: Patients suspected of having cauda equina syndrome should undergo immediate radiographic imaging and emergent referral to the neurosurgeon. Delay in evaluating patients with bowel and bladder involvement increases the risk of permanent loss of control of these vital organ functions.

CT IMAGING CASE: The 53-year-old patient had a history of chronic low back pain and intermittent sciatica down the right leg. His symptoms changed acutely after a violent episode of coughing. The exam showed bilateral sensory deficits, weakness of both legs, urinary incontinence, and decreased rectal sphincter tone with bowel leakage. DIAGNOSIS: Acute disk herniation at L5–S1 with compression of the S1 nerve root in the lateral recess. DISCUSSION: The three stages of cauda equina syndrome include chronic backache, sciatica, and acute bilateral leg weakness and incontinence. Most cases are caused by large extruded disk herniation with fragmentation. Emergent CT or MRI is mandatory in the third stage. FIGURE 9–12. CT imaging to confirm the cause of lumbar radiculopathy.

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OSTEOARTHRITIS OF THE LUMBOSACRAL SPINE

Osteoarthritis of the lumbar spine is a universal phenomenon. The mildest forms are associated with chronic back ache (“lumbago”) and early morning stiffness. However, severe involvement—diffuse idiopathic skeletal hyperostosis, spinal stenosis, and osteoarthritic

scoliosis—are associated with dramatic loss of mobility, chronic muscle strain, and lumbar radiculopathy. The diagnosis often is assumed based on age and stiffness, but confirmation includes plain x-rays, CT scanning, or MRI.

FUNCTIONAL STIFFNESS SUMMARY: Observation of the patient’s general movement often provides the most important clue to overall back function. Ever greater degrees of osteoarthritis create ever greater difficulties in changing position, flexing at the waist, and arising from a sitting position. MANEUVER: Simple observations are made of the patient’s ability to stand, walk in the room, climb onto and off of the exam table, and change from a lying to a sitting position. ADDITIONAL SIGNS: The Schober test provides the most objective measurement of the loss of flexibility of the back. The normal lumbar lordosis is replaced with a straightening of the lumbar curve or a replacement with a scoliosis curve. Paraspinal muscle spasm can be intense. Various degrees of impaired neurologic function of the lower extremity may be present. FIGURE 9–13. Osteoarthritis of the spine does not have a specific sign; it is more of a functional stiffness suggested by the mannerisms of the patient.

INTERPRETATION: Observations on the general movement of the back and measurement of the Schober test provide the best overall assessment of the impact of lumbosacral osteoarthritis. However, plain x-rays are needed to distinguish the degree of osteoarthritic change from the impairment of function caused by reflex muscle spasm.

LUMBOSACRAL SPINE

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POSTEROANTERIOR RADIOGRAPH OF THE LUMBOSACRAL SPINE CASE: This 63-year-old salesperson complained of low back pain over many years and a gradual loss of flexibility. He denied any prior trauma. He had not experienced any pain down the leg, loss of lower extremity sensation, coordination, or strength, or difficulties with bowel and bladder function. The patient exhibited a general stiffness when moving in the exam room. He used his arms to push against his upper thigh when arising from a seated position. The paraspinal muscles were rock hard, and his Schober measurement was 10 to 11 cm, or only 20% of normal. DIAGNOSIS: Forestier’s disease or diffuse idiopathic skeletal hyperostosis (DISH syndrome). FIGURE 9–14. PA radiograph of the lumbosacral spine to confirm degenerative osteoarthritis.

SPINAL STENOSIS The diagnosis of spinal stenosis is suggested by a history of extensive osteoarthritis, chronic lumbosacral symptoms, and documentation of extreme limitation of motion, with the Schober test demonstrating a loss of more than 75% of flexion. Confirmation of the diagnosis includes MRI that demon-

DISCUSSION: DISH is characterized by the exuberant formation of osteophytes along four contiguous vertebra. Contrast this with the bridging syndesmophytes of ankylosing spondylitis leading to the bamboo spine deformity. Osteophytes extend laterally before turning up or down to the adjacent vertebra. Syndesmophytes (paravertebral ossifications) extend vertically, following the course of the ligaments.

strates the following: a narrowed AP diameter (less than 10 mm), deformed lateral recesses (loss of the normal heart-shaped canal), and spinal cord compression at the spinal level that correlates with the patient’s symptoms and signs.

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SCHOBER TEST SUMMARY: Facet joint osteophyte formation, hypertrophy of the ligamentum flavum, and the irregularities caused by the collapse of the vertebral disks combine to cause a gradual stenosis of the spinal column and a gradual impairment of lumbar flexibility. MANEUVER:

See Figure 9–7 for details.

ADDITIONAL SIGNS: The straight leg raise maneuver often is equivocal because of the slowly progressive chronic process. The normal lumbar lordosis is replaced with a straightening of the lumbar curve. Paraspinal muscle spasm can be intense. Percussion over the affected vertebra may reproduce the patient’s pain. Neurologic abnormalities include loss of sensation in the foot, reflex asymmetry, motor weakness, and atrophy but rarely cauda equina symptoms.

FIGURE 9–15. Spinal stenosis is strongly suggested by a Schober test combined with plain x-rays of the back demonstrating advanced osteoarthritic changes.

INTERPRETATION: MRI is needed to confirm the diagnosis of spinal stenosis and distinguish it from ankylosing spondylitis, DISH syndrome, and the severe reflex muscle spasms that can accompany advanced scoliosis or spondylolisthesis.

MRI SUMMARY: MRI is used to measure the AP diameter of the spinal column and determine which lumbar level has the greatest spinal cord or spinal nerve compression. CASE: This 73-year-old retired nurse complained of severe intermittent right lower leg pain whenever she stood too long or walked. Her symptoms occurred predictably after 20 minutes of standing or walking approximately 1 block. Her straight leg raise maneuver was negative. Her dorsiflexion was weak, and the circumference of her calf was 3⁄4 inches smaller on the right side. DIAGNOSIS: levels.

Spinal stenosis at L4–L5 and L5–S1

INTERPRETATION: The indication for decompression laminectomy requires a documentation of spinal stenosis on MRI, a correlation of the patient’s pain pattern with the neurologic deficits found on examination, and a correlation of the neurodeficits on exam with the objective radiographic findings. FIGURE 9–16. MRI to confirm spinal stenosis.

LUMBOSACRAL SPINE

SCOLIOSIS Patients with significant thoracolumbar scoliosis

are examined for a change in height, the degree of reactive muscle strain, the presence of radiculopathy, and impairment of pul-

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monary function. A decline in height of 1⁄2 inch or more in a 6- to 12-month period of time is the primary indication for repeat, fulllength, standing radiographs of the spine.

SERIAL HEIGHT MEASUREMENT SUMMARY: The patient’s height is determined by posture, vertebral body and vertebral disk integrity, alignment of the thoracic and lumbosacral spines, and the presence of a scoliosis curve. MANEUVER: Serial measurements of height are taken at 6- to 12-month intervals. Ideally, the same scale or wall measurements should be used over time. ADDITIONAL SIGNS: The normal lumbar lordosis is replaced with a straightening of the lumbar curve. Paraspinal muscle spasm can be intense. The Schober test of lumbar flexibility is reduced. Typically the patient has measurements of 10 to 13 cm, depending on the degree of muscle spasm. If the patient has a rotatory component to the curve, flexion at the waist will cause a paraspinal hump (prominent paraspinal muscles along one side of the spine).

FIGURE 9–17. Serial height measurement is the single most important objective measurement for the patient with scoliosis.

INTERPRETATION: Progressive angulation of the scoliosis curve leads to an inevitable loss of overall height.

POSTEROANTERIOR LUMBOSACRAL SPINE X-RAYS SUMMARY: Serial PA lumbosacral spine films are used to assess the stability or progression of the scoliosis curve. Repeat x-rays are indicated whenever the patient’s height decreases by 1⁄2 inch. TECHNIQUE: Standing full-length x-rays including the sacrum, lumbar vertebra, and thoracic vertebra are obtained. Lines are drawn parallel to the endplates of the vertebra at the each end of the curve. Next, perpendicular lines are drawn so that they intersect close to the vertebral column. The scoliosis angle is measured between these intersecting lines. INTERPRETATION: Progressive angulation warrants referral to the spine specialist for possible stabilization.

FIGURE 9–18. Full-length posteroanterior lumbosacral spine x-rays are used to measure the S-shaped curvature of scoliosis.

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SPONDYLOLITHESIS Spondylolisthesis causes varying degrees of recurrent and chronic low back pain, lumbosacral muscle strain, or slowly progressive radiculopathy. The diagnosis is suggested by a palpable step-off sign at the spinous processes, but stan-

dard radiographs of the lumbosacral spine are needed to confirm the diagnosis. The step-off sign correlates with the anterior slippage of one vertebral body relative to another, as seen on the lateral projection of the spine.

INSPECT AND PALPATE THE SPINOUS PROCESSES SUMMARY: Spondylolisthesis, an anterior slippage of one vertebral body on another, is caused by a defect in the pars interarticularis portion of the vertebrae. Although this condition can be acquired through injury, most cases are congenital. The signs and symptoms are nonspecific. Confirmation of the diagnosis depends on objective x-ray changes. MANEUVER: Advanced cases may show spinous process tenderness (depicted here) or the classic step-off at the site of the spondylolisthesis.

FIGURE 9–19. Inspect and palpate the spinous processes of the lumbosacral curve for the step-off sign of spondylolisthesis.

ADDITIONAL SIGNS: The Schober test provides the most objective measurement of the loss of flexibility of the back. The normal lumbar lordosis is replaced with a straightening of the lumbar curve or replacement with a scoliosis curve. Paraspinal muscle spasm can be intense. Various degrees of impaired neurologic function of the lower extremity may be present. INTERPRETATION: Grading of spondylolisthesis can be based on function, flexibility, the presence or absence of accompanying radiculopathy, or radiographic criteria. Repeat x-rays are necessary for patients with progressive loss of flexibility, greater degrees of paraspinal muscle spasm, and progressive radicular symptoms. Progression from one grade to the next is an indication for surgical stabilization.

X-RAYS CASE: This 40-year-old man suffered chronic low back pain for years. The patient denied radicular pain, loss of muscular strength, or change in bowel and bladder symptoms. The Schober measurement of flexion was 10 to 13 cm. DIAGNOSIS: Grade II spondylolisthesis of L5 on S1. Secondary osteoarthritic changes in the facet joints of L4 and L5. DISCUSSION: Spondylolisthesis is graded according to the degree of anterior displacement: Grade I, up to 1⁄4 of the length of the vertebral body; Grade II, between 1⁄4 and 1⁄2; Grade III, more than 1⁄2; and Grade IV, anterior to the vertebral body.

FIGURE 9–20. X-rays to measure the anterior migration of the vertebral body and stage the degree of spondylolisthesis.

LUMBOSACRAL SPINE

COMPRESSION FRACTURE Compression fracture of the

vertebral body is characterized by focal tenderness directly over the spinous process, severe lumbosacral muscle spasm, and dramatic

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loss of spine flexibility. Bone scanning or MRI is needed to distinguish an acute fracture from a previous healed fracture.

COMPRESSION FRACTURE SUMMARY: The vertebral body is susceptible to the compressive forces that result from falls, hyperflexion injuries, or paroxysms of cough, especially when the patient suffers from generalized osteoporosis. MANEUVER: Each of the five spinous processes is palpated. If the patient’s pain is not reproduced by simple palpation, then each of the five lumbar levels is percussed using a reflex hammer or the blunt side of the fist.

FIGURE 9–21. Palpate the spinous process for the focal tenderness of compression fracture.

ADDITIONAL SIGNS: As with any acute process, the following signs may be present. The Schober test demonstrates severe impairment of flexibility; typical measurements of 10 to 11 cm. Paraspinal muscle spasms can be unilateral or bilateral and usually are intense. Neurologic abnormalities including loss of sensation in the foot, reflex asymmetry, motor weakness and atrophy, and cauda equina symptoms can accompany the fracture. INTERPRETATION: Because the abnormal signs on examination of the back overlap with those of osteomyelitis, epidural abscess, and metastatic cancer of the vertebral body, it is imperative to confirm the diagnosis of simple compression fracture by special radiographic studies. If the compression fracture occurs after coughing, hyperflexion injury, or minor trauma, the patient should be evaluated for osteoporosis by bone densitometry.

BONE SCANNING OR MRI CASE: The patient experienced acute low back pain after falling directly on the buttock in the shower. The pain remained in the center of the back. Movement of any kind became progressively more painful and stiff. Point tenderness was present at L1. DIAGNOSIS: Acute compression fracture of L1 with reactive paraspinal muscle spasm causing an acquired S-shaped curve. DISCUSSION: Point tenderness over a spinous process after trauma usually is caused by compression fracture. Plain x-rays will demonstrate the percentage loss of vertebral height (measured along the anterior portion of the vertebral body). Radiographic imaging with bone scanning or MRI will confirm whether this is a new or old fracture.

FIGURE 9–22. Plain x-rays cannot distinguish an old fracture from an acute fracture. Bone scanning or MRI is used to determine whether the compression fracture is new.

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EPIDURAL PROCESS The epidural space can be compromised by tumor, infection, or hemorrhage. Acute swelling in this small, confined area causes localized deep pain, focal spinous process ten-

derness, severe lumbosacral muscle spasm, and neurologic signs that can evolve rapidly. In order to avoid irreversible neurologic damage, the diagnosis must be made promptly by MRI.

PALPATE AND PERCUSS THE SPINOUS PROCESSES SUMMARY: The posterior spinous processes are the only accessible bony prominences available for direct palpation. MANEUVER: Each of the five spinous processes is palpated. If the patient’s pain is not reproduced by simple palpation, then each of the five lumbar levels is percussed using a reflex hammer or the blunt side of the fist. ADDITIONAL SIGNS: The Schober measurement demonstrates severe impairment of flexibility; typical measurements are 10 to 11 cm. Unilateral or bilateral paraspinal muscle spasms, often in cramplike waves are present. Neurologic abnormalities including loss of sensation in the foot, reflex asymmetry, motor weakness and atrophy, and cauda equina symptoms can evolve rapidly. FIGURE 9–23. Palpate and percuss the spinous processes for intrinsic disease of the spinal column.

INTERPRETATION: Painful spinous processes are seen with fracture, primary and secondary bony disorders, and rarely osteoarthritis. Percussion pain is more characteristic of radiculopathy from HNP or spinal stenosis.

MRI CASE: The patient was diagnosed with large cell carcinoma of the lung. During the course of chemotherapy he developed low back pain that became progressively more severe. After a severe coughing episode, he suddenly became paralyzed below the waist. Prompt institution of radiation therapy to the back failed to reverse the paralysis. DIAGNOSIS: Metastatic large cell carcinoma of the lung to the L2 and L3 vertebral bodies with extension into the epidural space and compression of the spinal cord. DISCUSSION: Patients with a known history of cancer presenting with new back pain must be evaluated emergently and undergo radiographic imaging expeditiously.

FIGURE 9–24. MRI is the test of choice if an epidural process is suspected on clinical grounds.

LUMBOSACRAL SPINE

Symptoms arising from the sacroiliac joint vary widely and consist of localized low back pain, secondary lumbosacral muscle spasm, referred pain mimicking radiculopathy, or a combination of these

SACROILIAC STRAIN AND SACROILIITIS

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symptoms. The diagnosis requires the demonstration of focal tenderness over the joint. The area of maximum tenderness is located 1 inch medial and 1 inch inferior to the posterior superior iliac spine (PSIS).

SACROILIAC JOINT SUMMARY: The sacroiliac joint is located 1 inch medial and 1 inch inferior to the PSIS. In order to reproduce the patient’s pain, pressure is applied over the joint and directed in a downward and slightly outward direction (the ilium lies directly over the joint). MANEUVER: The patient is placed in the prone position. Local tenderness over the sacroiliac joint is compared with the adjacent bones (sacrum and iliac crest) and the origin of the erector spinae muscle. ADDITIONAL SIGNS: The Patrick maneuver, also called the Faber maneuver (flexion, abduction, and external rotation of the hip), can reproduce the pain of moderate to severe sacroiliac strain and sacroiliitis. Compression of the pelvis against the exam table with the patient in the lateral decubitus position occasionally is positive. FIGURE 9–25. Palpate the sacroiliac joint for tenderness.

INTERPRETATION: Local tenderness is mild to moderate with sacroiliac strain, the most common condition affecting the joint. Moderate to severe tenderness is characteristic of sacroiliitis seen with the inflammatory spondyloarthropathies (e.g., Reiter’s disease, ankylosing spondylitis).

LOCAL ANESTHETIC BLOCK OBJECTIVE: Local anesthetic block is used to confirm involvement of the sacroiliac joint. TECHNIQUE: Enter 1 inch caudal to the PSIS and 1 inch lateral to the midline; advance at a 70degree angle to the firm resistance of the posterior supporting ligaments. NEEDLE: DEPTH:

11⁄2 inch or 31⁄2 inch, 22 gauge. 11⁄2 to 21⁄2 inches.

VOLUME: both.

1 to 2 mL local anesthetic, 1 mL K40, or

NOTE: The injection should be placed flush against the periosteum at the junction of the sacrum and the ileum at the maximum depth.

FIGURE 9–26. Local anesthetic block to confirm the involvement of the sacroiliac joint.

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COCCYDYNIA

Focal tenderness at the sacrococcygeal junction (by direct palpation or bimanual rectal examination) is the hallmark feature of coccydynia. However, before concluding that this is a local muscu-

loskeletal condition, it is necessary to rule out rectal or pelvic disorders by performing a complete examination of the lower colon, rectum, and pelvis.

PALPATE THE SACROCOCCYGEAL JUNCTION OBJECTIVE: The majority of cases of coccydynia occur in women. Most cases are the result of childbirth. The remaining cases usually are the result of direct trauma from falls. MANEUVER: The patient is placed in the lateral decubitus position with the hips and knees flexed to 90 degrees. The sacrum is identified, and the examiner palpates down the sacrum until the sacrococcygeal junction is met. Tenderness should be maximum at this point. ADDITIONAL SIGNS: Bimanual examination of the coccyx with one finger in the rectum and one finger grasping the coccyx is extremely painful. In place of the normal curvature of the sacrum and coccyx, the coccyx can be acutely angulated. The remaining examination of the rectum and pelvis is normal.

FIGURE 9–27. Palpate the sacrococcygeal junction to evaluate coccydynia.

INTERPRETATION: The diagnosis of coccydynia is straightforward. The only pitfall in evaluating the patient with a painful coccyx is making sure the lower colon and pelvis are thoroughly evaluated before concluding that the process is of a local musculoskeletal origin.

LOCAL ANESTHETIC BLOCK SUMMARY: Local anesthetic block is used to confirm the sacrococcygeal joint as the source of the patient’s buttock pain. TECHNIQUE: Enter 1 inch caudal to the sacrococcygeal junction in the midline; the needle is advanced at a 70-degree angle to the firm resistance of the posterior supporting ligaments or the hard resistance of bone. NEEDLE: DEPTH:


VOLUME: both.

1 to 2 mL local anesthetic, 1 mL D80, or

NOTE: The injection should be placed flush against the supporting ligaments or the periosteum of the sacrum.

FIGURE 9–28. Local anesthetic block to confirm involvement of the sacrococcygeal joint.

LUMBOSACRAL SPINE

BACK PAIN REFERRED FROM THE ABDOMEN Low

back pain unassociated with focal back tenderness, impairment in flexibility, low back stiffness, or radicular symptoms suggests the

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possibility of referred pain from the retroperitoneum (e.g., pyelonephritis, renal colic, retrocecal appendix, cecal carcinoma, pelvic tumor, abdominal aneurysm).

PALPATE THE ABDOMEN SUMMARY: Any of the retroperitoneal structures can cause back pain. Pyelonephritis and nephrolithiasis are the two most common conditions presenting with a significant component of back pain. With the exception of the early presentations of tumors of the retroperitoneum (including ascending and descending colon cancer) and abdominal aortic aneurysm, most of the conditions have associated symptoms that suggest a medical cause of referred pain to the back.

FIGURE 9–29. Palpate the abdomen for dilation and tenderness of the abdominal aorta.

MANEUVER: A full examination of the abdomen and pelvis is necessary if a medical cause of referred pain to the back is suspected. Examination of the entire vascular tree including the abdominal aorta (for local tenderness and bruits), the iliac and common femoral arteries, and the foot and ankle arteries should be performed if the patient has risk factors for peripheral vascular disease. INTERPRETATION: Any patient who lacks local back tenderness, paraspinal muscle spasm, impaired flexibility, or sacroiliac tenderness should be evaluated for a medical cause of referred back pain.

SPIRAL CT IMAGING CASE: This 50-year-old woman presented with acute, cramplike back pain. The pain was so severe that she could not find a comfortable position on the exam table. Examination disclosed tenderness at the right costovertebral angle, moderate pain to percussion over the paraspinal muscles, but no tenderness or loss of flexibility in the back. Urinalysis demonstrated microscopic hematuria without signs of active infection. DIAGNOSIS: Right urethral stone with secondary hydronephrosis of the right kidney. Normal size abdominal aorta. DISCUSSION: The colicky pain of nephrolithiasis mimics the cramplike pain of an epidural abscess. However, renal colic does not cause paraspinal muscle spasm or dramatic loss of lumbar spine flexibility as measured with the Schober test. FIGURE 9–30. Spiral CT imaging to evaluate the retroperitoneal structures.

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9–1



Examination Signs

Diagnosis

Confirmation

Tender paraspinal muscles

1. Lumbosacral strain

Local anesthetic placed within the paraspinal muscles (optional)

2. Lumbar radiculopathy

CT or MRI demonstrating nerve compression (necessary if motor signs are present)

Cauda equina syndrome

MRI, cystometrogram

Osteoarthritis

X-rays, CT, or MRI of the back

Spinal stenosis

CT or MRI of the back

Scoliosis

AP view of the entire back for scoliosis curve measurement

Spondylolisthesis

Lumbosacral back x-ray

Compression fracture, metastatic bony lesion, epidural abscess

Lumbosacral back x-ray, MRI

Epidural abscess

MRI

Sacroiliac strain, sacroiliitis

Oblique views of the pelvis, scan of the sacroiliac joints

Coccydynia

Local anesthetic placed at the sacrococcygeal junction

Schober: 60–70% of normal spinal flexion Painful and limited flexion and lateral bending No evidence of radiculopathy or structural back disease ⫹ Straight leg raise maneuver Schober: 20–40% of normal spinal flexion Painful and limited flexion and lateral bending Abnormal lower extremity neurologic exam Incontinence Perineal hypesthesia Loss of rectal tone Spastic bladder Chronic stiffness with an otherwise normal exam Schober: impairment or flexion depends on the extent of the arthritis Paraspinal muscle spasm with a minor degree of tenderness Chronic sciatica with equivocal straight leg raise; progressive Schober: 10–20% of normal spinal flexion Rigid paraspinal muscles with a minor degree of tenderness S-shaped curve to the back Paraspinal hump when flexing Decreasing height measurements Variable degree of lumbosacral strain Loss of the normal lumbosacral lordotic curve with step-off Variable degrees of lumbosacral strain Focal percussion tenderness over a single vertebral body Schober: 10–20% of normal spinal flexion Severe muscle tenderness and spasm Focal percussion tenderness over a single vertebral body Schober: 10–20% of normal spinal flexion Severe muscle tenderness and spasm Low-grade fever, mildly elevated complete blood cell count, prostration Local tenderness over the sacroiliac joint Patrick maneuver produces pain over the sacroiliac joint when acute or severe Lateral pelvic compression causes pain over the sacroiliac joint when acute or severe Tenderness at the sacrococcygeal junction Normal rectal, pelvic, and colon exams

LUMBOSACRAL SPINE

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CLINICAL PEARLS • The diagnosis of lumbar radiculopathy relies heavily on the patient’s description of pain. Sciatica must be distinguished from the referred pain of hip arthritis and trochanteric bursitis. The pain of classic sciatica radiates from the buttocks, past the knee, to the foot. In most cases it is associated with paresthesia or hypesthesia in the foot. Referred pain from the hip rarely extends past the knee. In general, any pain that crosses two consecutive joints is neurogenic in origin until proven otherwise. • Assessment of the patient presenting with lumbar radiculopathy entails identification of the nerve root that is most responsible for the patient’s symptoms. To this end, the patient’s description and location of the sciatic pain is one of the best clues used in correlating symptoms and the exact anatomic process. The L5 root, located at the L4 and L5 level, radiates down the lateral aspect of the leg. The S1 root, located at the L5 and S1 level, radiates down the posterior aspect of the leg. • The straight leg raise maneuver is the most consistent sign of acute or subacute nerve root irritation. A negative straight leg raise maneuver rules out an acute process involving compression of a nerve root or spinal cord. In contrast, the straight leg raise maneuver must be interpreted with caution in the case of chronic lumbar radiculopathy. The maneuver often is negative with spinal stenosis or the radiculopathy associated with spondylolisthesis. • Greater degrees of spinal nerve root compression cause a progressive lower extremity neurodeficit. Loss of sensation in the foot is followed by dysesthetic pain, loss of the reflex arc, loss of resting muscle tone and weakness, muscle atrophy, and loss of bowel and bladder sensation and muscle tone. Similarly, recovery of neurologic function usually follows the same order, just in reverse.

• Seventy-five percent to 80% of lumbar radiculopathy is limited to sensory symptoms. The prognosis in these cases is uniformly favorable, as opposed to that of patients with motor involvement or bowel and bladder dysfunction. Therefore, emphasis is placed on determining subtle changes in the reflex arc, motor strength, and bowel and bladder tone. The earliest change in reflex arc testing is a difference in the thresholds of the reflex. The earliest change in muscle strength is an inability to perform repeated dorsiflexion or plantarflexion (i.e., a loss of endurance). • Patients with lumbar radiculopathy with symptoms and signs limited to sensory changes respond to conservative treatment with rest, ice, stretching, a muscle relaxer, and time. Special testing usually is not indicated unless symptoms and signs fail to improve over several weeks. • Patients with lumbar radiculopathy involving motor, bowel, or bladder symptoms and signs should be evaluated with special imaging studies. If symptoms and signs are acute and evolving (e.g., large disk, epidural process, hemorrhage), imaging must be performed immediately and neurosurgical consultation made emergently. • A normal Schober measurement combined with average tone of the paraspinal muscles of the lumbosacral spine virtually rules out a significant structural or neurologic process. Attention is then turned to evaluating the retroperitoneal area as a source of the patient’s complaint (e.g., pyelonephritis, nephrolithiasis, pancreatitis, aortic aneurysm, pelvic pathology). • The sequential height measurement is the single most important variable when following a patient with scoliosis, spondylolisthesis, osteoporosis, or spinal stenosis.

CHAPTER 10: HIP DIFFERENTIAL DIAGNOSIS Diagnoses

Confirmations

Hip bursa (most common) Trochanteric bursitis Gluteus medius bursitis Ischiogluteal bursitis Iliopectineal bursitis Snapping hip

Local anesthetic Local anesthetic Local anesthetic Local anesthetic Examination

Hip joint Osteoarthritis Inflammatory arthritis Septic arthritis Shallow acetabulum Subluxation or dislocation

X-ray: standing anteroposterior (AP) pelvis Aspiration and synovial fluid analysis Aspiration, synovial fluid analysis, and culture X-ray: standing AP pelvis X-ray: AP pelvis

Hip prosthesis Loosening Prosthesis fracture Subluxation or dislocation

X-ray: bone scan X-ray: hip series X-ray: hip series

Meralgia paresthetica

History, sensory examination

Bony disorders Avascular necrosis of the hip Occult fracture of the femoral neck Malignancy

Bone scan, magnetic resonance imaging (MRI) Bone scan, MRI Bone scan, MRI

Referred pain Lumbosacral spine Sacroiliac joint Vascular occlusive disease Inguinal hernia

Neurologic exam, computed tomography scanning X-ray, bone scanning Examination, Doppler study Examination

172

block block block block

HIP 173

INTRODUCTION The hip is a ball-and-socket joint formed between the proximal end of the femur and the acetabular fossa of the pelvis. It is supported by a synovial membrane, a layer of supporting ligaments, and the largest group of muscles of the body: the gluteus muscles posteriorly, the quadriceps and iliopsoas muscles anteriorly, and the adductors medially. Understanding the conditions that affect the hip entails an appreciation of four unique characteristics of the joint: the unusual 135-degree angle between the femur and the acetabulum (the asymmetrical pressure placed over the articular cartilage increases the risk of osteoarthritis), the skeletal friction created between the femur and the body’s largest group of supporting muscles (the friction is countered by the body’s largest aggregate concentration of lubricating bursal sacs, the trochanteric, gluteus medius, ischiogluteal, and iliopectineal bursitis), the dependence of the movement of the hip on the adjacent sacroiliac (SI) joint and lower back (the common overlap of hip bursitis and lower back disorders), and the hip’s unique and precarious dual blood supply (interference of the ligament teres supplying the proximal third of the femoral head or the haversian system located in the medulla of the femur supplying the distal third of the femur can lead to osteonecrosis of the femoral head). Bursitis dominates the differential diagnosis of hip pain. Trochanteric and gluteus medius bursitis are caused by the friction between the gluteus medius tendon, the tensor fascia lata, and the trochanteric process of the femur. Ischiogluteal bursitis is caused by the friction between the biceps femoris and the ischium of the pelvis. Iliopectineal bursitis, the least common of the four bursal inflammations, is caused by the friction between the iliopsoas and the iliopectineal line of the pelvis. Osteoarthritis of the hip is the second most common condition. Patients with genetic predisposition (positive family history of arthritis), previous hip or femur fractures, dislocations, rheumatoid arthritis, or shallow acetabuli are at particular risk. The 135-degree angle of articulation creates an uneven pressure over the acetabular surface. Meralgia paresthetica, a compression neuropathy of the lateral femoral cutaneous nerve, causes dysesthetic pain or hypesthesia over the upper outer thigh. It is included as a hip condition simply because of the location of its symptoms. Strictly speaking, it is not directly related to the intrinsic conditions affecting the hip. In general, trauma does not play a major role in the pathogenesis of most of the common conditions affecting the hip. Osteoarthritis, the various forms of hip bursitis, and meralgia paresthetica rarely result from direct trauma. However, patients with significant osteoporosis who fall are at risk for occult hip fracture, a nondisplaced crack through chronically weakened bone. If occult fracture is suspected, the patient must be evaluated and treated just as is the patient with major trauma and referred to the fracture specialist. Finally, pain can be referred to the hip knee from the lower lumbar nerve roots, from the SI joint, or from occlusive disease of the distal aorta and iliac arteries. Lumbar level L4–L5 and lumbar level L5–S1 cause pain and numbness that typically course through the hip either laterally or posteriorly, respectively. Moderate to severe sacroiliitis often refers pain into the lower buttocks and upper outer

thigh areas. Aortoiliac occlusive disease (Leriche’s syndrome of buttock claudication and impotence) classically refers pain into the buttock and upper outer thigh areas. SYMPTOMS The description, character, and location of the patient’s pain are the key elements in the differential diagnosis of hip pain. Patients with bursitis and meralgia paresthetica complain of pain and irritation over a welldefined area of the lateral thigh. By contrast, patients with primary involvement of the hip joint describe “groin” pain located in a ill-defined area anteriorly. Diffuse posterior hip pain is the least common pain pattern and is most commonly referred from the gluteus medius bursa, lumbosacral spine, or SI joint. Lateral hip pain aggravated by direct pressure is the classic pain pattern of trochanteric and gluteus medius bursitis. Because all bursae are pressure sensitive, greater degrees of inflammation and swelling result in more intense pressureinduced symptoms. Pressure sensitivity ranges from mild morning pain and stiffness to intolerance of sleeping on the affected side. Progressive lateral hip pain aggravated by direct pressure and weight bearing can also be seen with the involvement of the bony femur. Although bursitis is 100 times more common than involvement of the bone, patients with a history of adenocarcinoma who present with lateral hip pain must be evaluated by special radiographic testing (e.g., bone scanning, MRI). Lateral hip pain associated with paresthesia and hypesthesia is the classic combination of symptoms seen with meralgia paresthetica. Meralgia paresthetica is characterized by a localized area of a pain (often described as a burning pain or a uncomfortable heightened sensation) that is not influenced by direct pressure, movement of the hip, or movement of the lower back. By contrast, lumbar radiculopathy, particularly at the L4 spinal root (L4–L5 disk space), causes lateral hip pain and sensory abnormalities that commonly extend over a much wider area including the knee, calf, and foot. Anterior hip pain (“groin pain”) is the classic condition affecting the hip joint. When anterior pain is associated with the gradual loss of internal and external rotation, osteoarthritis is the most likely diagnosis. By contrast, when anterior pain develops acutely, weight bearing is poorly tolerated, and internal and external rotation are dramatically impaired, special testing must be performed for the following conditions: AVN (vascular risk factors), occult fracture (trauma), acute synovitis (known as inflammatory arthritis), or the uncommon septic arthritis (when systemic symptoms are present). Anterior hip pain that is aggravated by neither direct pressure nor flexion of the hip suggests inguinal hernia, lower abdominal disorders, or the uncommon referred pain from the higher lumbar spinal nerve roots (L2 and L3 spinal levels). Posterior hip pain (“gluteal”) is the least common pain pattern and is either caused by gluteus medius bursitis or referred from lumbosacral nerve roots, the SI joint, or the nerve infected by herpes zoster (shingles). Patients describing pain in the gluteal area should undergo a thorough examination of the lumbosacral spine, SI joint, and hip. This

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BOX 10-1

BOX 10-2

DIFFERENTIAL DIAGNOSIS OF HIP PAIN BASED ON ANATOMIC AREA Lateral hip pain

Anterior hip pain (groin)

Posterior hip pain Referred pain

Trochanteric bursitis Gluteus medius bursitis Meralgia paresthetica Snapping hip Osteoarthritis of the hip Inflammatory arthritis Avascular necrosis Septic arthritis Iliopectineal bursitis Dislocation of the hip Prosthesis fracture or loosening Occult fracture of the hip Ischiogluteal bursitis Hamstring pull Lumbar radiculopathy SI strain Vascular occlusive disease Inguinal hernia

often includes special radiographic testing of these areas in order to define the exact anatomic cause. Finally, patients presenting with anterior hip or thigh pain localized to the midthigh pose the greatest clinical challenge. Primary disease of the hip joint, primary and secondary lesions of the upper femur, stress fracture of the femoral neck, and radiculopathy arising from the higher lumbar roots can refer pain to the midthigh or even as far as the anterior knee. Unless the patient’s pain can be reproduced by passive rotation (hip joint), reproduced by torque applied to the thigh (femur bone), or reproduced by specific signs in the back (radiculopathy), most patients with this pattern of pain need special radiographic procedures to determine the exact anatomic process. EXAMINATION Because all significant diagnoses at the hip can affect the patient’s ambulation, the first priority in the hip examination is to evaluate the patient’s gait, tolerance of squatting, and general ability to move in the exam room. These simple screening tests allow rapid assessment of the severity of the process. Next, assess the integrity of the hip joint by performing passive internal and external rotation, noting the patient’s tolerance of the maneuver and

ESSENTIAL EXAMINATION OF THE HIP 1. Observe the general function of the hip. a. Observe the patient’s normal gait with or without heel and toe walking. b. Observe changing positions (sitting to standing, squatting, climbing onto the exam table). 2. Measure internal and external rotation of the joint and note pain and endpoint stiffness. 3. Palpate the trochanteric and gluteus medius bursae for tenderness. 4. Perform a straight leg raise maneuver and, if abnormal, include a lower extremity neurologic exam. 5. Palpate the SI joint 1 inch inferior and 1 inch medial to the posterior superior iliac spine. 6. Palpate the lower extremity pulses and, if abnormal, measure capillary fill times for vascular insufficiency.

any endpoint stiffness. If the range of motion is impaired and the endpoints cause severe pain, immediate evaluation for AVN, occult fracture, acute synovitis, metastatic lesion of the femur, and so forth must be initiated. If the range of motion of the joint is normal, then the trochanteric and gluteus medius bursae are palpated at the middle and superior portions of the greater trochanter, respectively. Finally, because the lumbar spinal nerves, SI joint, lateral femoral cutaneous nerve, and lower abdominal vascular structures can refer pain through the hip, the examiner concludes by performing the straight leg raise maneuver (lumbar radiculopathy), palpating the SI joint (SI joint strain or inflammation), assessing the sensation of the upper outer thigh (meralgia paresthetica), and palpating the lower extremity pulses (aortoiliac occlusive disease). ONE-MINUTE SCREENING HIP EXAM: MANEUVERS ASSESSING OVERALL HIP FUNCTION The next six maneuvers represent the minimal examination of the patient presenting with hip symptoms. Function testing, range of motion measurement, and screening maneuvers for bursitis and lumbar radiculopathy provide enough information to triage to x-ray, order appropriate labs, suggest general treatment recommendations, or proceed to more detailed examination and treatment.

HIP 175

GAIT SUMMARY: The ability to walk easily depends on a flexible hip joint, a strong iliopsoas muscle, a strong quadriceps muscle, and normal lumbosacral nerve roots. MANEUVER: The patient is asked to walk in the exam room. Any significant gait abnormalities can be enhanced by asking the patient to toe and heel walk. INTERPRETATION: Impairment of ambulation and inability to change position smoothly can be affected by severe hip arthritis, involvement of the bony femur (AVN or metastatic disease), dramatic loss of muscular support, or dramatic loss of lumbosacral nerve function. In general, meralgia paresthetica, mild hip arthritis, and most cases of bursitis have a minimal impact on ambulation.


SQUAT SUMMARY: The ability to squat is influenced by the supporting musculature, the hip joint, and the lubricating bursae over the trochanteric bursa. MANEUVER: The patient is asked to squat as far as his or her pain level allows. Patients suspected of having an advanced hip condition should be instructed to perform the maneuver while holding on to the exam table. INTERPRETATION: The squatting maneuver can be impaired by moderate to advanced arthritis of the hip, moderate to severe bursitis, and any condition reducing the effective strength of the supporting muscles.

FIGURE 10–2. Observe the patient’s ability to squat.

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CLIMB ONTO THE EXAM TABLE SUMMARY: The ability to climb easily onto the exam table depends on a flexible hip joint, a strong iliopsoas muscle, a strong quadriceps muscle, and normal lumbosacral nerve roots. MANEUVER: The patient is asked climb onto the exam table. INTERPRETATION: Inability to change position smoothly can be affected by severe hip arthritis, involvement of the bony femur (AVN or metastatic disease), dramatic loss of muscular support, or dramatic loss of lumbosacral nerve function. In general, patients with meralgia paresthetica, mild hip arthritis, and most types of bursitis have little difficulty performing this task.

FIGURE 10–3. Observe the patient’s ability to climb onto the exam table.

RANGE OF MOTION SUMMARY: The hip joint is capable of moving in all directions, a range of motion that is surpassed only by that of the glenohumeral joint of the shoulder. As with its companion ball-and-socket joint, early involvement of the joint is identifiable by loss of internal and external rotation. MANEUVER: The range of motion can be evaluated while the patient is seated (depicted here) or recumbent. Internal and external rotation are much more reproducible in the seated position because the movement of the buttocks is restricted. The patient is asked to keep the ischial tuberosities fixed on the exam table. Internal rotation is measured as the leg swings out (normal 45 degrees), and external rotation is measured as the leg swings inward (normal 45 degrees). Pain and endpoint stiffness are noted. FIGURE 10–4. Evaluate the range of motion of the hip joint.

INTERPRETATION: Young women and patients with shallow acetabula may have 60–70 degrees of internal and external rotation. Patients with osteoarthritis have a preferential loss of internal rotation. The greater the degree of arthritis, the greater the loss of rotation (mild, 35–45 degrees; moderate, 15–30 degrees; severe, less than 10 degrees of internal rotation). Avascular necrosis, occult hip fracture, metastatic bony lesions with fracture, and acute synovitis cause severe pain and severe loss of rotation.

HIP 177

TROCHANTERIC AND GLUTEUS MEDIUS BURSAE SUMMARY: The trochanteric process is the most prominent portion of the femur. The trochanteric and gluteus medius bursae are located over the middle and superior portion of the trochanteric process, respectively. They lubricate and reduce friction between the gluteus medius tendon, the tensa fascia lata, the iliotibial band, and the underlying periosteum of the bone. MANEUVER: The trochanter can be palpated with the patient in the sitting position or the lateral decubitus position. In either case, the hip must be flexed to 90 degrees for the examiner to adequately identify the superior aspect of the trochanteric process. Firm pressure must be applied to determine local tenderness in the obese patient. INTERPRETATION: Bursitis is the most common cause of local pain and tenderness over the trochanteric process. However, tenderness is also seen with occult fracture, stress fracture, and metastatic disease. FIGURE 10–5. Palpate the trochanteric and gluteus medius bursae.

STRAIGHT LEG RAISE SUMMARY: The sciatic nerve arises from the lumbosacral plexus, exits the pelvis through the sciatic notch, and travels down the posterior aspect of the leg, forming the common peroneal and popliteal nerves. Straightening the leg while the hip is flexed at 90 degrees causes traction on the nerve. MANEUVER: The maneuver can be performed in the sitting or lying position. The leg is gradually moved to the fully extended position. Ankle dorsiflexion can be added in full extension to bring out the subtle case.

FIGURE 10–6. Perform the straight leg raise maneuver.

INTERPRETATION: A positive straight leg raise maneuver must reproduce the patient’s neuritic pain. The test is inconclusive if tightness or pain is felt only in the hamstring area. Acute spinal root and spinal nerve irritation caused by herniated nucleus pulposus, trauma, compression fracture with fragmentation, spondylolisthesis, epidural abscess, and epidural metastasis have a positive maneuver. The test usually is negative with lumbosacral osteoarthritis and spinal stenosis despite nerve compression.

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ONE-MINUTE SCREENING EXAM: MANAGEMENT STRATEGIES TRIAGE TO X-RAY For patients with a history of trauma or risk of bony injury, those in whom hip arthritis or leg length discrepancy is suspected, or those with risk factors are present for avascular necrosis: • Order three views of the hip to assess injuries or direct blows to the trochanteric process (fractures of the femoral head, neck, intertrochanteric crest, and shaft) or to obtain baseline films for possible occult fracture in the patient with osteoporosis. • Order a standing AP pelvis film for patients with a gradual loss of internal or external rotation (to assess osteoarthritis of the hip joint or to obtain baseline films for possible avascular necrosis). • Order a standing AP pelvis for patients with trochanteric bursitis and a suspicion of a short leg (leg length discrepancy). • Order a standing AP pelvis for patients with recurrent subluxation and ill-defined groin pain (shallow acetabulum). TRIAGE TO THE LAB For patients with severe hip pain, impaired ambulation, or extremely guarded rotation, with or without fever: • Order a complete blood cell count, uric acid, erythrocyte sedimentation rate, and blood cultures (osteomyelitis, septic arthritis, inflammatory arthritis, or pseudogout). CONSIDER A BONE SCAN For patients with a history of trauma, deep groin or ill-defined thigh pain, severe pain with internal or external rotation, or known history of cancer (stress fracture, avascular necrosis, occult fracture of the femur, or metastatic bony involvement is suspected). CONSIDER MRI For patients with acute pain, impaired gait, and impaired internal and external rotation (avascular necrosis, occult fracture of the femur, or metastatic bony lesions).

RECOMMEND EMPIRICAL TREATMENT For patients with mild to moderate hip pain and stiffness, normal gait, and normal range of motion of the hip joint: • Minimize weight-bearing activities (limit walking, standing, and impact). • Avoid physically demanding work, especially work that involves repetitious bending or twisting at the waist. • Avoid direct pressure over the outer hip. • Sleep with a pillow between the legs. • Perform daily cross-leg, passive stretching exercises. • Apply ice over the affected area four times a day (if the patient is thin). • Recommend an anti-inflammatory medication for 10 to 14 days at full dosage. • Use crutches with touch-down weight bearing for 5 to 7 days (optional). • Use a Velcro lumbosacral back brace during the day (optional). DETAILED EXAMINATION: SPECIFIC HIP DIAGNOSES Perform a detailed examination of the hip for patients with persistent or chronic symptoms, moderate to severe hip pain and stiffness, antalgic gaits, moderate to severe trochanteric bursal tenderness, and acute loss of range of motion at the hip joint.

TROCHANTERIC BURSITIS Trochanteric bursitis, the most common condition affecting the hip, is a common complication of lumbosacral spine stiffness, leg length discrepancy, knee arthritis, and ankle sprain. These diagnoses are characterized by gait impairment, which leads to an exaggerated movement and increased friction of the gluteus medius tendon and the tensor fascia lata over the trochanteric process of the femur. Treatment focuses on reducing inflammation and measures to restore or at least improve the abnormal gait. If the condition is untreated, the normally paper-thin bursal wall thickens, undergoes fibrosis, and gradually loses its ability to lubricate the outer hip.

HIP 179

PALPATE THE MIDPORTION OF THE GREATER TROCHANTERIC PROCESS SUMMARY: The trochanteric process is the most prominent portion of the femur. The trochanteric bursa is located over the midportion of the process and lubricates and reduces friction between the gluteus medius tendon, the tensa fascia lata, the iliotibial band, and the periosteum of the bone. MANEUVER: The trochanter can be palpated with the patient in the sitting position or the lateral decubitus position. In either case, the hip must be flexed to 90 degrees for the examiner to adequately identify the superior aspect of the trochanter process. Firm pressure must be applied to determine the local tenderness in the obese patient.

FIGURE 10–7. Palpate the midportion of the greater trochanteric process for bursal tenderness.

ASSOCIATED SIGNS: The range of motion of the hip should be normal, with minimal endpoint stiffness. The back is examined for loss of flexibility (abnormal Schober test). The alignment of the pelvis is inspected for possible short leg. The ankle and knee are examined for conditions that could alter the patient’s gait. Neuropathy, previous stroke, and other neurologic abnormalities that could contribute to an altered gait are sought. INTERPRETATION: Bursitis is the most common cause of local trochanteric tenderness. However, tenderness is also seen with occult fracture, stress fracture, and metastatic disease.

LOCAL ANESTHETIC BLOCK SUMMARY: The trochanteric bursa is located between the gluteus medius tendon and the femur. Its deepest portion is part of the periosteum of the femur. A local anesthetic block is placed below the gluteus medius tendon and just above the periosteum of the trochanteric process. POSITIONING: Lateral decubitus position, hip and knees flexed to 90 degrees. SURFACE ANATOMY: Middle and superior portions of the greater trochanter (crown). POINT OF ENTRY: ANGLE OF ENTRY:

Mid-trochanter. Perpendicular to the skin.

NEEDLE: 1 ⁄2 inch, 22 gauge or 22-gauge spinal needle. 1

DEPTH:

FIGURE 10–8. Local anesthetic block of the mid-trochanteric process to confirm trochanteric bursitis.

11⁄2 to 31⁄2 inches.

ANESTHESIA: Ethyl chloride, skin: 1 mL at the interface of the subcutaneous fat and tendon; 1 mL at the periosteum.

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GLUTEUS MEDIUS BURSITIS The clinical presentation of bursitis of the gluteus medius (the lubricating sac located atop the superior portion of the trochanteric process) is nearly identical to that of trochanteric bursitis. Although gluteus medius bursitis is much less common, the gluteus medius bursa is just as important

as the trochanteric bursa in maintaining the smooth movement of the gluteus medius tendon and tensor fascia over the lateral femur. This condition differs from trochanteric bursitis in the location of the discomfort (“gluteal” area) and the location of the palpable tenderness (directly over the superior trochanter).

PALPATE THE SUPERIOR TROCHANTERIC PROCESS SUMMARY: The trochanteric process is the most prominent portion of the femur. The gluteus medius bursa is located over the superior portion of the process and lubricates and reduces friction between the gluteus medius tendon, the tensa fascia lata, the iliotibial band, and the periosteum of the bone. MANEUVER: The trochanter can be palpated with the patient in the sitting position or the lateral decubitus position. In either case, the hip must be flexed to 90 degrees for the examiner to adequately identify the superior aspect of the trochanter process. Firm pressure must be applied to determine local tenderness in the obese patient.

FIGURE 10–9. Palpate the superior trochanteric process for bursal tenderness.

ASSOCIATED SIGNS: The range of motion of the hip should be normal, with minimal endpoint stiffness. The back is examined for loss of flexibility (abnormal Schober test). The alignment of the pelvis is inspected for possible short leg. The ankle and knee are examined for conditions that could alter the patient’s gait. Neuropathy, previous stroke, and other neurologic abnormalities that could contribute to an altered gait are sought. INTERPRETATION: Bursitis is the most common cause of local trochanteric tenderness. However, tenderness is also seen with occult fracture, stress fracture, and metastatic disease.

HIP 181

LOCAL ANESTHETIC BLOCK SUMMARY: The gluteus medus bursa is located between the gluteus medius tendon and the superior aspect of the trochanteric process of the femur. Its deepest portion is part of the periosteum of the femur. A local anesthetic block is placed below the gluteus medius tendon and just above the periosteum of the trochanteric process. POSITIONING: Lateral decubitus position, hip and knees flexed to 90 degrees. SURFACE ANATOMY: Superior portion of the greater trochanter (crown). POINT OF ENTRY:

Superior trochanter.

ANGLE OF ENTRY:

45-degree angle.


DEPTH:


ANESTHESIA: Ethyl chloride, skin: 1 mL at the interface of the subcutaneous fat and tendon; 1 mL at the periosteum.

FIGURE 10–10. Local anesthetic block to confirm gluteus medius bursitis.

OSTEOARTHRITIS OF THE HIP Osteoarthritis is the second most common condition affecting the hip. It is characterized by deep groin pain that often radiates down the anterior leg to the knee, pain that is aggravated by weight bearing and that limits the ability to walk fixed distances, local tenderness 1 inch below the

inguinal ligament and deep to the femoral artery, impairment of internal rotation (best measured in the seated position), and loss of articular cartilage, demonstrated on weight-bearing films of the hip (a standing AP pelvis x-ray).

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MEASUREMENT OF INTERNAL AND EXTERNAL ROTATION SUMMARY: Progressive osteoarthritis of the hip directly and preferentially affects the rotation range of motion. Internal rotation is affected to a greater degree in most patients. Range of motion measurements can be more accurately reproduced if the pelvis is fixed in position (with the patient sitting with the ischial tuberosities flat against the exam table) rather than while the patient is lying down. MANEUVER: The patient is asked to keep the pelvis flat and not to roll the buttocks when rotation is applied. With the leg in the dependent position (0 degrees), internal and external rotation are measured, and the endpoint symptoms of pain and stiffness are noted.

FIGURE 10–11. Measurement of internal and external rotation to evaluate the severity of hip arthritis.

ADDITIONAL SIGNS: The patient cannot perform a full squat. The patient with advanced arthritis cannot reach his or her feet to remove shoes or socks. With ever greater impairment of rotation, reduced hip flexion and abduction are noted (the Patrick maneuver [flexing, abducting, and externally rotating the hip] causes groin pain). Groin tenderness is variable and is located 1 inch inferior to the midpoint of the inguinal ligament. INTERPRETATION: The greater the degree of arthritis, the greater the loss of rotation (mild, 35–45 degrees; moderate, 15–30 degrees; severe, less than 10 degrees of internal rotation). Patients with osteoarthritis have moderate pain and mild to moderate endpoint stiffness. By comparison, patients with avascular necrosis, occult hip fracture, metastatic bony lesions with fracture, and acute synovitis have severe pain, severe endpoint pain, and severe limitation of rotation.

WEIGHT-BEARING AP PELVIS X-RAY SUMMARY: A standing, weight-bearing AP pelvis x-ray is an excellent way to compare right and left hip joints for osteoarthritic wear. The articular width of the hip joints is measured between the superior head of the femur and the superior acetabulum. Because osteophyte and subchondral cyst formation vary from patient to patient, the degree of wear is based strictly on the width of the articular cartilage. In general, the width correlates reasonably well with the degree of rotation impairment seen on examination. MANEUVER: The x-ray is performed in the standing position with the shoes off. FIGURE 10–12. Weight-bearing AP pelvis x-ray to confirm the presence of osteoarthritis of the hip.

INTERPRETATION: The normal articular width is 4 to 5 mm.

HIP 183

ACUTE ARTHRITIS OF THE HIP Acute arthritis is an uncommon condition affecting the hip. It is characterized by severe deep groin pain that often radiates down the anterior leg to the knee, intolerance of weight bearing (patients often use a cane, walker, or crutches), dra-

matic local tenderness 1 inch below the inguinal ligament and deep to the femoral artery, severe pain with even 5 to 10 degrees of internal rotation and external rotation (best measured in the seated position), and inflammatory exudates, demonstrated on aspiration of the joint.

MEASUREMENT OF INTERNAL AND EXTERNAL ROTATION SUMMARY: Acute synovitis from pseudogout, inflammatory arthritis, or the rare case of septic arthritis (gonorrhea or Staphylococcus aureus) is characterized by severe groin pain, severe intolerance of weight bearing, and severe pain and loss of range of motion during internal and external rotation of the hip. MANEUVER: All directions of motion are impaired and painful, especially in the case of septic arthritis.

FIGURE 10–13. Measurement of internal and external rotation to assess the integrity of the hip joint.

ADDITIONAL SIGNS: Weight bearing is impaired with acute synovitis and impossible with septic arthritis. The patient may assume a position in bed with the hip partially flexed (relaxing the hip capsule). Groin tenderness varies from moderate to severe (1 inch inferior to the midpoint of the inguinal ligament). The Patrick maneuver (flexing, abducting, and externally rotating the hip) causes severe groin pain or is impossible to perform depending on the acuteness of the process. INTERPRETATION: The greater the degree of arthritis, the greater the loss of rotation (mild, 35–45 degrees; moderate, 15–30 degrees; severe, less than 10 degrees of internal rotation). Patients with osteoarthritis have moderate pain and mild to moderate endpoint stiffness. By comparison, patients with avascular necrosis, occult hip fracture, metastatic bony lesions with fracture, and acute synovitis have severe pain, severe endpoint pain, and severe loss of rotation.

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ASPIRATION OF THE HIP JOINT SUMMARY: Synovial fluid analysis is necessary to distinguish septic arthritis from the acute synovitis caused by crystal deposition disease or inflammatory arthritis (rheumatoid arthritis). If fluid is not obtained from the lateral approach, consultation with an interventional radiologist or orthopedic surgeon is necessary. POSITIONING: Lateral decubitus position, hip and knees flexed to 90 degrees. SURFACE ANATOMY: Superior portion of the greater trochanter (crown). POINT OF ENTRY: trochanter.

1 inch above the superior

ANGLE OF ENTRY:


NEEDLE: DEPTH:

FIGURE 10–14. Aspiration of the hip joint to obtain fluid to confirm acute synovitis or septic arthritis.

3 ⁄2 inch, 22-gauge spinal needle. 1


ANESTHESIA: periosteum.

Ethyl chloride, skin: 1 mL to the

HIP 185

MERALGIA PARESTHETICA

The lateral femoral cutaneous nerve, a pure sensory nerve, is susceptible to compression as it courses from the lumbosacral nerve plexus, through the abdominal cavity, under the inguinal ligament, and into the subcutaneous tissue of the thigh. Symptoms

range from numbness and tingling (hypesthesia) to burning pain (paresthesia) over the upper outer thigh. Pain referred beyond the upper outer thigh or pain accompanied by impaired reflexes or muscular weakness suggests either trochanteric bursitis or lumbar radiculopathy.

SENSATION OF THE ANTEROLATERAL THIGH SUMMARY: The lateral femoral cutaneous nerve enters the upper thigh 1 inch medial to and approximately 1 inch inferior to the anterior superior iliac spine and innervates the skin of the lateral and to a lesser extent the anterior mid- to upper thigh. It is most susceptible to compression in the inguinal area but can be irritated by pathologic conditions in the pelvis. MANEUVER: The skin is tested for light touch, pinprick, and deep pain sensation with a cotton ball, a sharp point, and pinching. ADDITIONAL SIGNS: The range of motion of the hip is normal. Any pain or paresthesia extending down the leg should be ascribed to lumbar radiculopathy rather than the lateral femoral cutaneous nerve.

FIGURE 10–15. Assess the sensation of the anterolateral thigh for meralgia paresthetica.

INTERPRETATION: Loss of sensation (hypesthesia) or a feeling of heightened sensation (dysesthesia or hyperesthesia) is characteristic of the condition. Because the nerve provides only sensation to the skin, changes in motor function suggest lumbar radiculopathy.

LOCAL ANESTHETIC BLOCK SUMMARY: A local anesthetic block is placed over the lateral femoral cutaneous nerve just above the fascial plane of the quadriceps to distinguish meralgia paresthetica from referred pain from the lumbosacral roots. POSITIONING:

Supine.

SURFACE ANATOMY: Anterior superior iliac spine, inguinal ligament, and symphysis pubis. POINT OF ENTRY: One inch medial and 1 inch inferior to the anterior superior iliac spine. ANGLE OF ENTRY: NEEDLE:



DEPTH: ⁄2 to 11⁄2 inches to the subcutaneous fat– fascia interface. 1

ANESTHESIA: Ethyl chloride, skin: 1 mL at the interface of the subcutaneous fat and the fascia. FIGURE 10–16. Local anesthetic block of the lateral femoral cutaneous nerve to confirm meralgia paresthetica.

186


AVASCULAR NECROSIS OF THE HIP Avascular necrosis

of the hip (osteonecrosis) results from an impairment of the blood supply to the head of the femur. Risk factors for ischemia include trauma, diabetes, alcoholism, iatrogenic Cushing’s disease, and hematologic states causing high viscosity. Patients presenting with severe groin pain, an antalgic gait, and acute loss of internal and

external rotation must avoid all weight bearing while emergent radiographic studies are performed. Failure to make this diagnosis in a timely fashion places the patient at risk for the complications of the ischemic process: collapse of the femoral head, coxa plana, and premature osteoarthritis.

RANGE OF MOTION TESTING SUMMARY: Avascular necrosis is an acute process that presents with dramatic changes on examination of the hip. The pain typically is severe enough to impair normal weight bearing. Patients often refuse to walk and come in with crutches or in a wheelchair. MANEUVER: The patient is asked to keep the pelvis flat and not to roll the buttocks when rotation is applied. With the leg in the dependent position (0 degrees), internal and external rotation are measured, and the endpoint symptoms of pain and muscular guarding are noted. Most patients are unwilling to allow rotation beyond 30 degrees.

FIGURE 10–17. Range of motion testing in the evaluation of avascular necrosis.

ASSOCIATED SIGNS: The Patrick maneuver is poorly tolerated (flexion, abduction, and external rotation, the figure-of-four position). The anvil test typically is painful (fist percussion at the heel with the leg held perfectly straight, transmitting the shock to the fracture site). INTERPRETATION: Severe pain and limited rotation of the hip are seen with avascular necrosis, occult fracture of the hip, metastatic disease with fracture, and acute synovitis. Radiographic and laboratory tests are necessary to distinguish these conditions with similar clinical presentations.

PLAIN X-RAYS, BONE SCAN, OR MRI SUMMARY: Plain x-rays of the hip may demonstrate the classic collapse of the femoral head, leading to a loss of the normal round configuration, the classic step-off areas at the cortex, and the sclerotic bone where the proximal third impacts into the distal two-thirds of the femoral head. Comparative views of the right and left side can be obtained with a standing AP pelvis (if the patient can bear weight). Unfortunately, these changes occur days to weeks later, and therefore plain x-rays cannot be used as a screening test.

FIGURE 10–18. Plain x-rays, bone scan, or MRI to confirm avascular necrosis.

HIP 187

OCCULT FRACTURE OF THE HIP Occult fracture of the hip, a nondisplaced fracture of the neck of the femur, is difficult to detect and should be suspected whenever the injured patient’s examination demonstrates severe anterolateral hip tenderness, severe pain with even partial weight bearing, and intolerance of passive

hip rotation. Routine x-rays of the hip and pelvis are notoriously difficult to interpret because of osteoporosis. If the diagnosis is suspected, the patient must avoid weight bearing (to avoid completion of the fracture) until MRI or serial radiographs of the hip rules out this difficult diagnosis.

INTERNAL AND EXTERNAL ROTATION OBJECTIVE: Patients with known osteoporosis are at high risk for occult fracture of the hip. Older adults who have fallen, are intolerant of weight bearing, and have significant loss of rotation should be evaluated by special radiographic testing to exclude occult fracture. MANEUVER: The examiner places one hand at the ankle and one hand at the knee. The lower leg is rotated laterally to test internal rotation and medially to test external rotation. The patient is instructed to avoid rolling the buttocks during the maneuver. If the patient is unable to sit, the leg can be rolled from side to side while lying (the log roll maneuver) to evaluate the tolerance of rotation.

FIGURE 10–19. Measure internal and external rotation to assess the integrity of the femur.

ADDITIONAL SIGNS: Other than the anvil sign (fist percussion of the heel with the leg in the straight position, transmitting pressure through a potential fracture site), there are no other specific signs of bony involvement. INTERPRETATION: Older adults with osteoporosis are a high risk for hip fracture. Initial plain films of the hip are notoriously inaccurate in detecting subtle cracks in the bone from trauma. It may take several weeks for osteoporotic bone to demonstrate a fracture line in severely osteopenic bone. Bone scanning or MRI is the test of choice to rule out occult fracture of the hip.

BONE SCAN OR MRI CASE: This 75-year-old woman with osteoporosis fell out of bed and immediately developed hip pain. Bedside plain x-rays performed in the nursing home were interpreted as normal, without fracture. The patient’s hip pain persisted. Turning in bed became progressively more painful. She refused to get up to use the bathroom. Examination disclosed severe pain with any attempts to rotate the hip joint. MANEUVER: Approximately 20 MCi technetium99m is injected into the patient’s forearm. Four hours after the injection of the isotope, bone flow and postperfusion radioactivity images are recorded.

FIGURE 10–20. Bone scan or MRI to evaluate occult fracture.

INTERPRETATION: Radioisotopic bone scanning is a more sensitive test for the identification of occult fractures than the initial screening plain films.

188


METASTATIC DISEASE AFFECTING THE FEMUR

Metastatic involvement of the femur must be diagnosed and treated in a timely fashion in order to avoid the disastrous complication of secondary fracture. Patients with a history of malignancy, severe, deep thigh pain, and apprehension with weight bearing and an examination demonstrating severe thigh tenderness, severe pain with

even partial weight bearing, and intolerance of passive rotation of the hip must undergo special studies to exclude bony involvement. Routine x-rays of the hip and pelvis are notoriously difficult to interpret. If the diagnosis is suspected, the patient must avoid weight bearing (to prevent completion of the fracture) until bone scanning, MRI, or serial x-rays rule out this elusive diagnosis.

INTERNAL AND EXTERNAL ROTATION SUMMARY: Patients with known metastatic disease of the prostate, breast, kidney, thyroid, or lung (the five types known to metastasize frequently to bone) must be evaluated in a timely fashion whenever pain in or around the hip develops. Thinning of the cortical bone thickness leads to an unacceptable risk of bony fracture. MANEUVER: The examiner places one hand at the ankle and one hand at the knee. The lower leg is rotated laterally to test internal rotation and medially to test external rotation. The patient is instructed to avoid rolling the buttocks during the maneuver. ADDITIONAL SIGNS: Other than the anvil sign (fist percussion of the heel with the leg in the straight position, transmitting pressure through a potential fracture site), there are no other specific signs of bony involvement. FIGURE 10–21. Severe pain with internal and external rotation of the hip.

INTERPRETATION: Early metastatic disease involving the femur may remain asymptomatic and undetectable for weeks. Periodic bone scanning may demonstrate preclinical disease. Dramatic symptoms arise when the weakened femur microcracks and then fractures. Any patient with early involvement of the femur on bone scan must have periodic plain x-rays to determine the integrity of the cortical bone. ROUTINE X-RAYS OF THE FEMUR OR BONE SCANNING CASE: This 45-year-old woman had breast cancer diagnosed a year earlier. Shortly thereafter, she developed skeletal pain in a wide number of areas including her hips. Plain x-rays disclosed erosion of the cortical bone on the right side. Prophylactic rodding of the femur was performed. MANEUVER: Approximately 20 MCi technetium99m is injected into the patient’s forearm. Four hours after the injection of the isotope, bone flow and postperfusion radioactivity images are recorded. INTERPRETATION: Radioisotopic bone scanning is a more sensitive test for the identification of stress fractures, occult fractures, osteoblastic tumors, and infected bone.

FIGURE 10–22. Routine x-rays of the femur or bone scanning to look for primary or secondary bony involvement of the femur.

HIP 189

HIP PAIN CAUSED BY AORTOILIAC VASCULAR OCCLUSIVE DISEASE Claudication caused by aortoiliac oc-

clusive disease at or just distal to the bifurcation of the aorta (Leriche’s syndrome) can mimic intrinsic disease at the hip (gluteus or upper thigh pain that is aggravated by walking). This di-

agnosis should be considered whenever significant risk factors for atherosclerosis are present, the vascular examination of the lower extremities is impaired, and the hip joint and soft tissues are normal on examination.

LOWER EXTREMITY PULSES SUMMARY: The aorta branches to form the iliac arteries, which in turn branch to form the femoral arteries. MANEUVER: The dorsalis pedis (dorsum) and the posterior tibialis (medial ankle) arteries are palpated, and the capillary fill times of the toes are compared with those of the fingers. ADDITIONAL SIGNS: Poor perfusion of the foot can change coloration. Loss of hair over the dorsum of the foot or up the pretibial surface is common. Severely restricted blood flow can cause ulceration of the skin and chronic osteomyelitis.

FIGURE 10–23. Palpate the lower extremity pulses and check capillary fill times.

INTERPRETATION: Atherosclerotic disease affecting the bifurcation of the aorta (Leriche’s syndrome) or the iliac arteries can cause exercise-induced pain in the buttock or upper thigh.

DOPPLER ULTRASOUND OR ANGIOGRAPHY SUMMARY: Atherosclerotic narrowing of the aorta or iliac arteries cause upper thigh or buttock claudication. Leriche’s syndrome (obstruction of the bifurcation of the aorta) causes bilateral buttock claudication and impotence (insufficiency of the pudendal artery). Vascular insufficiency can be documented by poor capillary fill in the feet, decreased pulses, and abnormal flow by Doppler ultrasound. Radiographic angiography is necessary to confirm the exact anatomic area of obstruction.

FIGURE 10–24. Doppler ultrasound or angiography to confirm vascular insufficiency.

190


HIP PAIN REFERRED FROM THE LUMBOSACRAL SPINE OR SI JOINT The back and SI joints commonly refer

pain to or through the hip. The lower lumbar roots refer pain through the gluteus and posterolateral thigh areas. The SI joints refer pain into the gluteal area. Referred pain from the lumbosacral

spine or the SI joint should be considered whenever back symptoms accompany the pain, the pain extends past the knee, paresthesia or hypesthesia accompanies the pain, and the examination of the hip joint and soft tissues is unremarkable.

SI JOINT SUMMARY: The SI joint is located 1 inch medial and 1 inch inferior to the posterior superior iliac spine. In order to reproduce the patient’s pain, pressure is applied over the joint and directed in a downward and slightly outward direction (the ilium lies directly over the joint). MANEUVER: The patient is placed in the prone position. Local tenderness over the SI joint is compared with the adjacent bones (sacrum and iliac crest) and the origin of the erector spinae muscle. ADDITIONAL SIGNS: The Patrick maneuver, also called the Faber maneuver (flexion, abduction, and external rotation of the hip), can reproduce the pain of moderate to severe SI strain and sacroiliitis. Compression of the pelvis against the exam table with the patient in the lateral decubitus position is occasionally positive. FIGURE 10–25. Palpate the SI joint.

INTERPRETATION: Local tenderness is mild to moderate with SI strain, the most common condition affecting the joint. Moderate to severe tenderness is characteristic of sacroiliitis seen with the inflammatory spondyloarthropathies (e.g., Reiter’s disease, ankylosing spondylitis).

LOCAL ANESTHETIC BLOCK SUMMARY: When paraspinal muscle spasm or radiculopathy coexists with focal findings at the SI joint, local anesthetic block is used to confirm the exact source of the patient’s pain. TECHNIQUE: Enter 1 inch caudal to the posterior superior iliac spine and 1 inch lateral to the midline; advance at a 70-degree angle to the firm resistance of the posterior supporting ligaments. POSITIONING:

Lying prone, completely flat.

SURFACE ANATOMY: Spinous processes, the paraspinal muscles, and the iliac crests. NEEDLE: DEPTH:

11⁄2 inch or 31⁄2 inch, 22 gauge. 11⁄2 to 21⁄2 inches.

VOLUME: both.

FIGURE 10–26. Local anesthetic block to confirm the involvement of the SI joint.

1 to 2 mL local anesthetic, 1 mL K40, or

NOTE: The injection should be placed flush against the periosteum at the junction of the sacrum and the ileum. If the SI joint is responsible for the patient’s pain, the general function and pain should improve after local anesthetic is placed over the joint.

HIP 191

LOWER EXTREMITY NEUROLOGIC EXAM SUMMARY: The patient describes a lancinating pain through the hip that extends down the leg, through the knee, and into the foot. The examination of the hip is unremarkable (normal mobility, 45 degrees of internal and external rotation, and no localized tenderness). MANEUVER: A full neurologic examination of the lower extremities is necessary. The straight leg raise maneuver is performed on the right and left sides. Sensory testing of the feet for light touch, pinprick, and deep pain sensation is combined with reflex testing and motor testing of dorsiflexion and plantarflexion. FIGURE 10–27. Perform a lower extremity neurologic exam.

ANATOMY: The nerves of the lumbosacral plexus provide sensation and motor function to the lower extremities. The 5th lumbar root (L4–L5 disk) is responsible for sensation over the top of the foot and dorsiflexion. The S1 root (L5–S1 disk) is responsible for sensation on the bottom of the foot and plantarflexion. INTERPRETATION: Impairment of the L5 or S1 root can cause pain through the buttock, into the leg (lateral thigh [L5] or posterior thigh [S1]), and down the leg to the foot. The L5 dermatome extends to the dorsum of the foot and the S1 dermatome on the plantar surface.

CT SCANNING OF THE LUMBAR SPINE SUMMARY: If an intrinsic condition of the hip is unlikely and the patient describes a posterior hip pain that radiates down the leg beyond the knee, the lumbosacral spine is scanned for possible nerve root compression. In addition, CT scanning of the lumbar spine is necessary to identify the underlying cause of recurrent or chronic hip bursitis. More than 60% of patients with hip bursitis have significant disorders in the lumbosacral spine. These include spinal stenosis, subclinical disk disease, chronic lumbosacral muscle spasm from osteoarthritis, scoliosis, or spondylolisthesis.

FIGURE 10–28. CT scanning of the lumbar spine to determine the cause of lumbar radiculopathy.

ANATOMY: The spinal column is formed by the vertebral bodies and vertebral disks anteriorly, the lateral recesses and facet joints laterally, and the posterior elements. In this case, a large disk herniation (arrows) is compressing the right S1 nerve root against the facet joint. INTERPRETATION: In the evaluation of lumbar radiculopathy, the neuroanatomic abnormalities seen on CT scan must be correlated directly with the neurologic findings on examination of the lower extremities.

192


10–1


EXAMINATION SIGNS

DIAGNOSIS

CONFIRMATION

Tender mid-trochanter

#1: Trochanteric bursitis

Local anesthetic block of the at the mid-trochanteric process

#2: Gluteus medius bursitis

Local anesthetic block at the superior trochanteric process

Osteoarthritis of the hip

Standing AP pelvis x-ray

Meralgia paresthetica

Examination

Avascular necrosis of the hip, acute arthritis, septic arthritis

MRI, AP pelvis x-ray, or aspiration of the hip by fluoroscopy

Occult fracture of the hip

MRI, AP pelvis x-ray

Vascular insufficiency

Doppler study, angiogram

Lumbar radiculopathy

CT or MRI demonstrating nerve compression (necessary if motor signs are present)

Primary or secondary involvement of the femur

Full x-ray of the femur, bone scan

Associations: stiff back, short leg, ankle or knee disorders, stroke Normal range of motion of the hip with minimal endpoint stiffness Tender superior trochanter Associations: stiff back, short leg, ankle or knee disorders, stroke Normal range of motion of the hip with mild endpoint stiffness Stiffness and mild pain with internal or external rotation Tenderness over the anterior hip Abnormal Patrick maneuver Hypesthesia or paresthesia over the anterolateral thigh No evidence of lumbar radiculopathy No evidence of hip disease Acute loss and severe pain with internal or external rotation Limping with an antalgic gait Tenderness over the anterior hip Abnormal Patrick maneuver Acute loss and severe pain with internal or external rotation after an injury Severe antalgic gait or refusal to bear weight Tenderness over the anterior hip Abnormal Patrick maneuver Diminished dorsalis pedis and posterior tibial pulses Delayed capillary fill times ⫹ Straight leg raise maneuver reproducing the radicular pain Schober test: 20–40% of normal spinal flexion Painful and limited flexion and lateral bending Abnormal lower extremity neurologic exam Pain aggravated by torque applied to the femur

Localized bony tenderness ⫹ Anvil sign

HIP 193

COMMON HIP FRACTURES

PELVIS FRACTURE SUMMARY: The successful management of a fractured pelvis requires the combined clinical skills of the primary care provider, the orthopedic surgeon, and the urologist. Blunt trauma severe enough to fracture the sacrum, ilium, ischium, or pubic bones often leads to injury of the underlying organ systems. Life-threatening hemorrhage; injury to the bladder, urethra, or ureters; or gastrointestinal injury to the colon must be assessed quickly for possible emergent treatment.

FIGURE 10–29. Pelvis fracture.

After the patient has been stabilized medically, specific x-rays should be obtained to determine the severity and classification of the injury. The x-rays should include cervical spine, chest, posteroanterior pelvis, and inlet and outlet views of the pelvic ring. If the acetabulum is involved, special iliac and obturator views or a CT scan of the entire pelvis must be obtained. With these x-rays, the fractures can be classified according to the degree of pelvic ring disruption, the involvement of the acetabulum, and the degree of displacement and instability of the bony fragments in the vertical and rotational directions. Hospitalization, sling traction, and close observation for the first 24 to 48 hours, including hemodynamic monitoring, are combined with early pin placement for external fixation or open reduction and internal fixation. Unstable patients with ongoing retroperitoneal hemorrhage should be evaluated by pelvic angiography and treated with embolization.

DISLOCATION OF THE HIP SUMMARY: Dislocation of the hip is an uncommon problem. Immediate surgical referral is necessary. The prognosis for complete recovery is guarded. Recurrent dislocation, avascular necrosis of the femoral head, sciatica from direct compression, and late-onset osteoarthritic wear are the most common complications. The patient must be reexamined frequently, with serial examinations and radiographs monitoring for avascular necrosis in the days and weeks after reduction.

FIGURE 10–3O. Dislocation of the hip.

194


HIP FRACTURE SUMMARY: Fractures of the femur are divided into fractures involving the hip joint and fractures of the femur. Hip fractures are further subdivided into impacted, occult, avascular necrosis, stress, and nondisplaced and displaced neck fractures. Fractures of the femur are further subdivided into intertrochanteric, trochanteric process, subtrochanteric, shaft, and supracondylar fractures (although the latter traditionally is grouped with fractures of the knee). All of these fractures are treated surgically (internal fixation, hemiarthroplasty, or total hip replacement), with the exception of certain impacted and occult fractures, stress fractures of the femoral neck, and avascular necrosis. The primary care physician must be able to diagnose and initiate the early treatment of these four fractures.

FIGURE 10–31. Hip fracture and fractures of the femur.

EMERGENCY DEPARTMENT TREATMENT FOR HIP FRACTURE: The patient presents with a displaced femoral neck fracture with a foreshortened leg that is externally rotated. The extremity must be supported carefully during transfers. The patient must be evaluated for a cardiovascular event that could have caused the fall. Appropriate intravenous analgesia should be provided. Traction should be applied at 5 to 10 pounds, depending on the size of the patient and the bulk of the quadriceps. Consultation with an orthopedic surgeon should be made emergently.

CLINICAL PEARLS • Progressive involvement of the hip joint is characterized by a loss of internal rotation followed by loss of external rotation. The severity and progression of osteoarthritis of the hip can be estimated by the loss of internal rotation. • Avascular necrosis of the hip, occult fracture of the hip, metastatic disease affecting the femur with fracture, and acute synovitis of the hip are all characterized by severe pain and limitations of internal and external rotation. • The classic position of comfort with acute swelling of the hip joint (hemorrhage, acute synovitis, or septic arthritis) is with the leg partially flexed to 45 degrees. This relaxes the tension of the distended capsule. • Patients who describe pain through the gluteal area but limited to the upper thigh have either gluteus medius bursitis or referred pain from the SI joint. • Meralgia paresthetica is inflammation of the lateral femoral cutaneous nerve, a pure sensory nerve. Any accompanying symptoms extending past the knee or involving the motor function of the lower extremity arise from the lumbar roots (lumbar radiculopathy).

• Severe episodes of trochanteric bursitis can refer pain down the leg to the knee (following the course of the femur and the accompanying iliotibial band). Pain that refers from the hip and extends beyond the knee to the foot is much more likely to be caused by lumbar radiculopathy. • Trochanteric and gluteus medius bursitis rarely coexist with osteoarthritis of the hip. A loss of movement from hip arthritis nearly precludes the development of hip bursitis. • Persistent trochanteric or gluteus medius bursitis can cause enough of a gait disturbance to cause contralateral hip bursitis. Chronic bursitis (either trochanteric or gluteus medius bursitis) is the main common cause of iliopectineal bursitis. • Ten percent of trochanteric and gluteus medius bursitis is caused by the gait disturbance caused by leg length discrepancy. • If trochanteric or gluteus medius bursitis is diagnosed, then next immediate step is to identify the cause of the underlying gait disturbance (stiff back, SI strain, short leg, knee or ankle disorder, or chronic neurologic disease).

CHAPTER 11: KNEE DIFFERENTIAL DIAGNOSIS Diagnoses

Confirmations

Patella (most common) Subluxation or dislocation Patellofemoral syndrome Dashboard knee (chondral fracture) Patellofemoral osteoarthritis Patella alta

Examination; x-ray: sunrise views Examination; x-ray: sunrise views Arthroscopy (optional) X-ray: sunrise view X-ray: lateral view of the knee

Main joint Osteoarthritis: medial compartment or lateral compartment Inflammatory arthritis Septic arthritis Hemarthrosis

Bursa Prepatellar (“housemaid’s knee”) Anserine bursitis Baker’s cyst Infrapatellar (superficial or deep)

X-ray: bilateral standing anteroposterior knees Aspiration and synovial fluid analysis Aspiration, synovial fluid analysis, and culture Aspiration, synovial fluid analysis, and hematocrit

Aspiration, bursal fluid analysis, crystal analysis, and culture Local anesthetic block Aspiration or ultrasound Local anesthetic block

Ligaments Medial collateral injury: 1st, 2nd, 3rd degree Lateral collateral injury: 1st, 2nd, 3rd degree Anterior cruciate injury Posterior cruciate injury

Exam, Exam, Exam, Exam,

Meniscal tear Traumatic or degenerative

MRI, arthroscopy

Iliotibial band syndrome Snapping knee

Exam, local anesthetic block Exam

Referred pain Trochanteric bursitis Hip joint Femur Lumbosacral spine radiculopathy

local anesthetic block local anesthetic block magnetic resonance imaging (MRI) MRI

Exam, local anesthetic block X-ray: standing anteroposterior pelvis Bone scan Computed tomography (CT) scan, MRI, electromyography

195

196


INTRODUCTION The knee’s unique anatomy consists of three separate joint compartments (medial, lateral, and patellar), the body’s largest and strongest muscles (quadriceps and hamstrings), four main ligaments (medial collateral ligament [MCL], lateral collateral ligament [LCL], anterior cruciate ligament [ACL], and posterior cruciate ligament [PCL]), five major bursal sacs, and the body’s largest synovial cavity. Because of this level of complexity, the knee has the greatest range of conditions, including a variety of injuries, the most susceptibility to age-related wear, and the most common episodes of inflammatory arthritis and septic arthritis, a variety of conditions that is unmatched by any other joint in the body. In order to manage this diverse group of conditions, physicians categorize patients presenting with knee pain by degree of trauma, age, pain location, and the presence of effusion and inflammatory change. The differential diagnosis of knee pain varies with age. The active stage of Osgood–Schlatter epiphysitis occurs exclusively in teenagers. Athletic patients under age 40 are more likely to develop patellofemoral syndrome, patellar tendonitis (“jumper’s knee”), iliotibial band syndrome (mostly affecting runners), prepatellar and infrapatellar bursitis, and the ligament and cartilage injuries seen with mild to moderate trauma. With advancing age and decreasing activity, osteoarthritis and its consequences (effusion, anserine bursitis, secondary MCL strain, and degenerative meniscal tear) and inflammatory arthritis dominate the differential diagnosis. Knee pain location is very helpful in narrowing the differential diagnosis. Medial knee pain is the most common pattern and is associated with medial compartment osteoarthritis, anserine bursitis, MCL strain, medial meniscal tears, and large knee effusions. Anterior knee pain is typical of patellofemoral syndrome (especially when bilateral), knee effusion, prepatellar and infrapatellar bursitis, patellar tendonitis, and Osgood–Schlatter disease. Posterior or popliteal pain typically reflects the pressure of an acute effusion or the compressive effects of a Baker cyst. Lateral knee pain, the least common pattern, is seen with iliotibial band syndrome, the much less common isolated lateral compartment osteoarthritis, LCL strain, and lateral meniscal tear. Knee effusion and prepatellar bursitis are the two conditions characterized by significant swelling and inflammatory change. Patients with acute knee effusion complain of anterior or popliteal pain and an inability to fully flex the knee. By contrast, patients with prepatellar bursitis describe anterior pain and minimal impairment of knee flexion; mobility is preserved because the swelling is extra-articular. Because both conditions can be caused by trauma, acute inflammation, or infection, aspiration and laboratory analysis are necessary to determine the exact cause. Trauma plays an important role in the origin of many of the conditions affecting the knee. Minor trauma is a contributing factor in flareups of osteoarthritis, traumatic prepatellar bursitis, dashboard knee, and MCL strain. Injury plays an even greater role in hemarthrosis. The dramatic injuries that lead to hemarthrosis include tears of the cruciates and collateral ligaments, meniscal cartilage tears, disruption of the synovial capsule, and tibial plateau fractures. Major trauma (direct blows, falls onto the

anterior knee, and severe torque injuries) cause patellar, tibial, and distal femur fractures. Finally, pain can be referred to the knee from the lower lumbar nerve roots, from the hip, or from the femur. Lumbar level L4–L5 and lumbar level L5–S1 cause pain and numbness over the outer knee and popliteal areas, respectively. Moderate to severe trochanteric bursitis commonly refers pain to the lateral knee. Occasionally pain is referred to the lower femur and anterior knee from conditions affecting the hip joint. Rarely, primary and secondary lesions of the femur manifest pain at the knee. A referred pattern of pain should always be considered when local signs of knee swelling, tenderness, and impaired motion are absent. SYMPTOMS In order to arrive at a specific diagnosis, the physician divides the patient’s knee symptoms into the following three categories: symptoms that reflect the change in overall function, including loss of muscular support (weakness, giving out, collapsing), loss of smooth movement (catching, “something is wrong inside”), and difficulty with ambulation (limping, fatigue, favoring); symptoms that suggest the presence of a joint effusion, including descriptions of swelling and impaired bending (e.g., “I can’t squat,” “My knee doesn’t flex”), and popliteal tightness or fullness; and anatomically related symptoms such as pain location, inflammatory change, and abnormal noise (clicking, popping, and grinding). The first two categories of symptoms are helpful in determining the severity of the condition. Larger joint effusions, impaired ambulation, and muscular weakness correlate directly with the severity of the process. The most commonly described pattern of pain is along the medial aspect of the knee. Medial knee pain is the classic pain described by patients with medial compartment osteoarthritis, anserine bursitis (the most common inflamed bursa), MCL strain (the most common injured ligament), and medial meniscal tear (the meniscus with the greatest vulnerability to injury). Medial joint line pain is characteristic of osteoarthritis, second- and third-degree MCL injuries, medial meniscal tears, and fractures of the tibial plateau. Medial tibial plateau pain, localized 1 to 11⁄2 inch below the joint line, is characteristic of anserine bursitis and mild MCL injuries. A wide variety of conditions present with anterior knee pain, the second most common location of knee pain. This is the classic area of pain associated with injury to the quadriceps mechanism (the quadriceps muscle, its tendons, the patella, and the insertion of the patellar tendon on the tibial tubercle) and large knee effusions. Bilateral anterior knee pain is characteristic of patellofemoral syndrome, particularly in patients under age 45, and also of advanced osteoarthritis involving all three compartments of the knee. Anterior knee pain accompanied by swelling and inflammatory change is the characteristic presentation of acute prepatellar bursitis. Focal anterior knee pain at the inferior pole of the patella, the origin of the patellar tendon, is characteristic of patellar tendonitis, or jumper’s knee. As the name implies, this diagnosis is seen almost exclusively in athletes. Focal anterior knee pain at the tibial tubercle, the insertion of the patellar tendon, is characteristic of Osgood–Schlatter disease. This epiphysitis is seen exclusively in young men and woman under age 19 whose

KNEE

growth centers are still active. Diffuse anterior knee pain accompanied by swelling and inflammatory change is seen with inflammatory arthritis (e.g., rheumatoid arthritis, gonorrhea, gout, pseudogout) or septic arthritis. Although its symptoms are similar to those of acute prepatellar bursitis, patients presenting with acute inflammatory arthritis have dramatically impaired flexion. Lateral knee pain is the least common pain pattern. Lateral compartment osteoarthritis, injuries to the LCL, and lateral meniscal tears are much less common than their medial counterparts. Lateral knee pain located at the joint line suggests lateral compartment osteoarthritis, injury or tear of the LCL, or a lateral meniscal tear. Focal lateral knee pain at the femoral condyle is the characteristic site of inflammation of the iliotibial band syndrome. This diagnosis is practically certain when the pain is accompanied by palpable or even audible snapping. Popliteal pain or pressure can accompany any of the aforementioned pain patterns. It is most commonly caused by the buildup of pressure caused by a large, acute effusion. When the patient flexes the effused knee, the quadriceps mechanism forces the fluid posteriorly. Pressure is exerted on the gastrocnemius muscles, vascular structures, and branches BOX 11-1

DIFFERENTIAL DIAGNOSIS OF KNEE PAIN BASED ON ANATOMIC AREA Anterior knee pain

Medial knee pain

Posterior knee pain Lateral knee pain

Referred pain

Patellofemoral syndrome Patellar dislocation Dashboard knee Patellofemoral osteoarthritis Patella alta Knee effusion Prepatellar bursitis Osgood–Schlatter syndrome Infrapatellar bursitis Jumper’s knee Hemarthrosis Cruciate ligament injuries Osteoarthritis of the medial compartment Inflammatory arthritis Septic arthritis Anserine bursitis Medial collateral ligament injury Medial meniscal tear Tibial plateau fracture Knee effusion Baker’s cyst Lateral compartment osteoarthritis Lateral collateral ligament injury Iliotibial band syndrome Lateral meniscal tear Lumbar radiculopathy Trochanteric bursitis Femur bone Hip bone

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of the sciatic nerve, leading to local pain, lower extremity edema, and even sciatica, respectively. If the effusion persists, over time this hydraulic pressure leads to the formation of a Baker cyst, a natural extension of the chronic knee effusion. Patients often describe a variety of noises arising at the knee, including crepitation, clicking, grinding, popping, and snapping sounds. These often accompany osteoarthritis and patellofemoral syndrome but also accompany meniscal tears and the iliotibial band syndrome. These are nonspecific with the exception of the snapping sound along the lateral femoral condyle that is characteristic of the iliotibial band syndrome. EXAMINATION The examiner assesses the general function of the knee by observing the patient’s gait and the ability to squat, duck waddle, and change positions in the exam room. In addition, the examiner assesses muscular support by estimating the strength of the quadriceps muscle either by lifting the unweighted leg off the exam table or actively resisting leg extension. To assess patellofemoral syndrome, the most common condition under age 45, the examiner vigorously compresses the patella firmly against the femur, attempting to recreate the patient’s retropatellar pain and determine whether the crepitation or clicking arises from the patellofemoral articulation. Knee effusion is suggested by general fullness anteriorly, loss of the peripatellar dimples, tightness with passive flexion, and an abnormal heel-to-buttock distance. Osteoarthritis of the knee is suggested by joint line tenderness and crepitation but must be confirmed with weight-bearing radiographs. Anserine bursitis, often accompanying larger knee effusions, has a unique quarter-sized area of tenderness in the midline of the medial tibial plateau. The stability of the knee is assessed by varus and valgus stress testing and by the anterior and posterior drawer signs. Meniscal tear and other conditions causing internal BOX 11-2

ESSENTIAL EXAMINATION OF THE KNEE 1. Observe the general function of the knee and lower extremities. a. Observe the patient’s gait, ability to squat, and ability to duck waddle. b. Observe the difficulties in changing position, especially climbing onto the exam table. c. Estimate the strength and tone of the quadriceps muscle. 2. Perform patellar compression and assess the tracking of the patellofemoral joint. 3. Check for signs of effusion, such as general fullness, loss of flexion, and abnormal heel-to-buttock distance. 4. Palpate medial and lateral joint line tenderness. 5. Palpate anserine bursa tenderness at the medial tibial plateau. 6. Perform varus and valgus stress testing and the anterior and posterior drawer signs. 7. Assess for joint line popping and loss of smooth motion.

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derangement (uncommon in the nontraumatized knee) are suggested by a history of loss of smooth function, locking in the advanced case, and an examination showing focal joint line tenderness, popping, or simply a vague indefinable sense of something not being quite right with passive movement of the joint. Finally, the back, sacroiliac joint, and the hip commonly refer pain to the knee. The S1 root and sacroiliac joint refer pain down the back of the leg to the popliteal space. The L5 root, the trochanteric bursa, and the femur refer pain down the outer thigh to the lateral area of knee. The hip joint and the femur refer pain down the front of the thigh to the anterior knee.

ONE-MINUTE SCREENING KNEE EXAM: MANEUVERS ASSESSING OVERALL KNEE FUNCTION The next nine maneuvers represent the minimal examination of the patient presenting with knee symptoms. Functional testing, measurement of knee flexion for the presence of an effusion, and screening maneuvers for patellofemoral syndrome, prepatellar bursitis, osteoarthritis, and anserine bursitis provide enough information to triage to x-ray, order appropriate labs, suggest general treatment recommendations, or proceed to more detailed examination and treatment.

GAIT SUMMARY: The ability to walk easily depends on a flexible knee joint, intact supporting ligaments, a strong quadriceps muscle, and normal lumbosacral nerve roots. MANEUVER: The patient is asked walk in the exam room. Symptoms can be enhanced by asking the patient to toe and heel walk. INTERPRETATION: This maneuver is used as a screening for the more severe conditions (acute effusion, acute flare of osteoarthritis, acute inflammatory arthritis, and septic arthritis).


SQUAT SUMMARY: The ability to squat is influenced by the supporting musculature and ligaments, the knee joint, and the prepatellar bursa. MANEUVER: The patient is asked to squat as far as his or her pain level allows, either standing freely or holding on to the exam table. INTERPRETATION: The ability to squat can be impaired by any cause of an effusion, moderate to advanced arthritis of the knee, insufficiency or injury to the supporting ligaments, and any condition reducing the effective strength of the supporting quadriceps mechanism.

FIGURE 11–2. Observe the patient’s ability to squat.

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ABILITY TO DUCK WADDLE SUMMARY: The ability to duck waddle depends on a well-supported knee free of significant meniscal disorders, effusion, or arthritis and with intact collateral and cruciate ligaments. MANEUVER: The patient is asked to squat and then move forward, transferring the weight back and forth from the right side to the left. INTERPRETATION: The ability to duck waddle rules out significant ligamentous instability, joint effusion, and significant damage to the meniscal cartilage.

FIGURE 11–3. Observe the patient’s ability to duck waddle.

STRENGTH OF THE QUADRICEPS SUMMARY: Active leg extension depends on an intact patellar tendon, patella, and quadriceps tendon and a reasonably toned quadriceps muscle. Resisting leg extension isometrically estimates the strength of the quadriceps muscle. MANEUVER: The patient is asked to extend the leg against the resistance placed at the lower leg. INTERPRETATION: Inability to extend the leg is seen with quadriceps tendon rupture, advanced osteoarthritis of the knee, and anterior loose bodies. Weakness of the quadriceps muscle is seen with any chronic knee condition.

FIGURE 11–4. Estimate the strength of the quadriceps by resisting leg extension.

HEEL-TO-BUTTOCK MEASUREMENT SUMMARY: The heel-to-buttock distance is used to assess the patient’s ability to flex the knee. This maneuver is an objective, easy to perform, and reproducible way to estimate knee flexion. MANEUVER: The knee is passively flexed. The patient’s tolerance of the maneuver is noted. The distance between the posterior heel and the buttocks is measured.

FIGURE 11–5. Perform the heel-to-buttock measurement to assess knee effusion.

INTERPRETATION: Knee flexibility may be reduced by bulky musculature and tightness or contracture of the quadriceps. Intrinsic knee conditions that impair flexion include effusion of the knee, a Baker cyst, large bony osteophytes, tight collateral ligaments, and previous knee surgery (total knee replacement, ACL repair).

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PATELLAR COMPRESSION SUMMARY: The patella is the largest sesamoid bone of the body, centered over the distal femoral groove and embedded in the large tendon of the quadriceps muscle. MANEUVER: The patella is grasped firmly and moved back and forth and up and down in the groove of the femur. Retropatellar pain and crepitation are noted. INTERPRETATION: Focal chondromalacia begins in the inferior aspect of the femur. To identify the early presentation of this condition, emphasis is placed on compression of the patella in the inferior aspect of the femoral groove. As the condition progresses, pain and crepitation can be demonstrated over the entire groove. FIGURE 11–6. Perform patellar compression to assess patellofemoral syndrome.

JOINT LINES SUMMARY: The joint lines are formed by the femoral condyles and the tibial plateaus. The meniscal cartilage is located in the space between the two bones, and these are covered by the synovial membrane and the collateral ligaments. MANEUVER: With the leg fully extended, the superior and inferior poles of the patella are identified and marked. The joint lines are located at the level of the inferior pole of the patella in the midplane. INTERPRETATION: Tenderness at the joint line is most commonly caused by irritation of the synovial membrane (e.g., osteoarthritis, inflammatory arthritis). However, meniscal and collateral ligament injuries cause tenderness at the same location. FIGURE 11–7. Palpate the joint lines to assess the medial and lateral compartments of the knee.

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INSPECT THE PREPATELLAR BURSA SUMMARY: The bursa is one of four synovial lined structures that lubricate the quadriceps mechanism. The other three are the suprapatellar pouch (a part of the synovial cavity) and the two infrapatellar bursae, one located above and one located below the patellar tendon. MANEUVER: The prepatellar bursa is palpated for warmth, focal tenderness, and swelling, and the walls are squeezed between the fingertips to assess for bursal wall thickening. After the acute and chronic inflammatory changes are noted, the range of motion of the knee is assessed. INTERPRETATION: Acute bursitis is characterized by cystic swelling and varying degrees of tenderness, warmth, and redness. Chronic bursitis is characterized by palpable thickening of the bursal walls. The range of motion of the knee should be preserved unless a secondary cellulitis complicates the case of septic bursitis.

FIGURE 11–8. Inspect the prepatellar bursa for swelling and thickening.

ANSERINE BURSA SUMMARY: The anserine bursa is located between the MCL and the conjoined tendon formed by the gracilis, sartorius, and semitendinosus tendons. The entire tibial plateau is palpated to distinguish the localized tenderness of anserine bursitis from the more extensive tenderness of the MCL. MANEUVER: The patella and the tibial tubercle are marked with a pen. Medial midline tenderness at the level of the tibial tubercle is compared with tenderness at the medial joint line and medial femoral condyle.

FIGURE 11–9. Palpate the anserine bursa for local tendeness.

INTERPRETATION: A quarter-sized area of tenderness in the concavity of the medial tibial plateau and at the level of the tibial tubercle is the classic location of anserine bursitis. Tenderness that extends from the anserine bursal area to the joint line probably is caused by irritation or injury to the MCL.

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ONE-MINUTE SCREENING EXAM: MANAGEMENT STRATEGIES TRIAGE TO X-RAY For the patient who has sustained an injury or is at risk of bony injury or the patient in whom patellofemoral syndrome or osteoarthritis is suspected on clinical grounds: • Order posteroanterior and lateral views of the knee for patients with a history of injuries or direct blow to the knee (distal femur fractures, patellar fracture, tibial plateau or proximal tibial fracture, or proximal fibular fracture). • Order bilateral standing anteroposterior x-rays for patients at risk for accelerated wear (to define the degree of osteoarthritic changes in the medial and lateral compartments). • Order bilateral sunrise or Merchant views of the patella for younger patients with bilateral anterior knee pain (patellar subluxation and patellofemoral syndrome). • Order specialized tunnel views for patients with mechanical symptoms (osteochondritis dissecans or intra-articular loose body). TRIAGE TO THE LAB For patients suspected of having inflammatory or septic effusion or suspected gouty or septic prepatellar bursitis: • Order a complete blood cell count, uric acid, erythrocyte sedimentation rate, blood cultures, and screening cultures for gonorrhea for patients with acute pain, exquisite tenderness, inability to weight bear, and large, actively inflamed knee effusions (e.g., rheumatoid arthritis, gout, pseudogout, gonorrhea, septic arthritis). • Order a complete blood cell count, uric acid, erythrocyte sedimentation rate, and blood cultures for patients with acute inflammatory or septic prepatellar bursitis (gout, pseudogout, Staphylococcus aureus). CONSIDER A BONE SCAN To investigate suspected metastatic involvement of the femur or tibia or to evaluate for subtle bony fracture. CONSIDER MR IMAGING For patients with dramatic athletic injuries, acute hemarthrosis following trauma, and significant mechanical symptoms such as loss of smooth mo-

tion or an inability to duck waddle (loose body, meniscal tear, cruciate ligament injury, or osteochondritis dissecans). RECOMMEND EMPIRICAL TREATMENT For patients with mild to moderate knee pain and stiffness, full range of motion, normal alignment, normal gait, and no more than a mild effusion: • Limit walking, standing, and impact. • Avoid bending the knee more than 90 degrees (sitting, sleeping, exercising). • Wear comfortable, properly fitted shoes with padded insoles to reduce the effects of impact. • Apply ice and elevate the knee four times a day. • Perform gentle daily straight leg raise to enhance the quadriceps and hamstring muscle tone. • Use a patellar restraining brace with fabric stays during the day (optional). • Recommend an anti-inflammatory medication for 10 to 14 days at full dosage. • Use crutches with touch-down weight bearing for 5 to 7 days (optional). DETAILED EXAMINATION: SPECIFIC KNEE DIAGNOSES Perform a detailed examination of the knee for patients with persistent or eluonic symptoms, moderate to severe knee pain and stiffness, antalgic gait, and acute loss of range of motion. PATELLOFEMORAL SYNDROME The diagnosis of patellofemoral syndrome, the leading cause of knee pain in patients under age 45, is based on a history of anterior knee pain exacerbated by repetitious flexion and an exam that demonstrates retropatellar pain and crepitation (e.g., grinding, clicking) when the patella is vigorously compressed against the walls of the femoral groove. Irritation to the patellar cartilage is caused by uneven tracking of the patella in the femoral groove (lateral subluxation). The sunrise view of the patella is used to determine the severity of subluxation and degree of chronic wear.

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PATELLAR COMPRESSION SUMMARY: The patella is the largest sesamoid bone of the body, normally centered over the distal femoral groove and embedded in the large tendon of the quadriceps muscle. Patellofemoral syndrome, the constellation of signs and symptoms resulting from subluxation, results from the overly developed vastus lateralis muscle and the lateral forces caused by the quadriceps (the Q-angle). MANEUVER: The patella is grasped firmly and moved back and forth and up and down in the groove of the femur. An abnormal response should reproduce the patient’s pain. Crepitation can be reproduced when the patella is compressed forcefully against the femur. FIGURE 11–10. Perform patellar compression to assess patellofemoral syndrome.

ADDITIONAL SIGNS: Anterior knee clicking with passive flexion of the knee is felt over the patella. The patient either refuses or hesitates to perform the Insall maneuver, a nonspecific sign recreating the abnormal patellofemoral tracking (the quadriceps is relaxed, the patella is forced into the inferior portion of the femoral groove, and then the patient is asked to contract the quadriceps, dragging the patella through the groove). The range of motion of the knee is unaffected unless a knee effusion is present. INTERPRETATION: Focal chondromalacia begins in the inferior aspect of the femoral groove. To identify the early presentation of this condition, emphasis is placed on compression of the patella in the inferior aspect of the groove. As the condition progresses, pain and crepitation can be demonstrated over the entire articulation (pan patellar disease).

BILATERAL SUNRISE X-RAYS SUMMARY: Bilateral x-rays allow comparison of the alignment of the patellae in the femoral grooves (subluxation), the articular width of the medial and lateral cartilage, and evaluation of subchondral bony thickening. CASE: Bilateral sunrise views demonstrate moderate subluxation, thinning of the lateral patellar cartilage, thickening of the subchondral bone, and the rare finding of osteochondritis dissecans on the left.

FIGURE 11–11. Bilateral sunrise x-rays to confirm patellofemoral subluxation, arthritis, and so forth.

INTERPRETATION: X-rays of the early presentation of patellofemoral syndrome are normal. As the condition progresses, lateral subluxation develops, followed by progressive wear of the cartilage, subchondral bony thickening, osteophyte development, and in rare cases osteochondritis dissecans with loose body.

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MEDIAL COMPARTMENT OSTEOARTHRITIS Of the three

compartments of the knee (medial, lateral, and patellofemoral) the medial compartment is most susceptible to age-related wear. This mildly inflammatory arthritis is characterized by medial joint line tenderness, joint line crepitation, palpable tibial plateau spurs,

and varying degrees of knee effusion. The diagnosis can be confirmed by measurement of the medial articular width obtained from a weight bearing posteroanterior view of the knee or by direct visualization using arthroscopy.

JOINT LINES SUMMARY: The normal carriage angle of the knee is 8 to 10 degrees valgus, a necessary angle to allow the femur to articulate with the pelvis at 135 degrees. This angle causes an asymmetrical pressure on the medial compartment of the knee. MANEUVER: The superior and inferior poles of the patella are identified and marked. The joint lines are located at the level of the inferior pole of the patella in the midplane of the femur. Local tenderness medially is compared with the joint line tenderness laterally.

FIGURE 11–12. Palpate the joint lines to assess the medial and lateral compartments of the knee.

ADDITIONAL SIGNS: Passive flexion and extension of the knee can cause a grinding sensation (crepitation). Full flexion may be limited by advanced arthritic changes or the presence of an effusion. Secondary anserine bursitis or a mild MCL strain is suggested by more widespread areas of tenderness along the medial side of the knee. Lack of full extension suggests advanced arthritic change or the presence of a degenerative meniscal tear or loose body. The varus–valgus rocking maneuver of the tibia against the femur is loose because of the thinning of the medial cartilage. INTERPRETATION: Tenderness at the joint line is most commonly caused by irritation of the synovial membrane (e.g., osteoarthritis, inflammatory arthritis). However, the local tenderness characteristic of meniscal and collateral ligament injuries overlaps with the joint line tenderness of arthritis.

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BILATERAL WEIGHT-BEARING X-RAYS SUMMARY: Bilateral posteroanterior weight-bearing views of the knee performed on a single cassette allow a direct comparison of the degree of arthritic wear of the main knee joint. Normally, the width of the medial compartment cartilage, measured at the center of the femoral condyle, should be equal to or 1 mm greater than the width of the lateral compartment cartilage. CASE: This x-ray demonstrates advanced narrowing of the medial compartment, a loss of the normal 8- to 10-degree valgus carrying angle (measured here at 0 degrees), and mild subchondral bony thickening. Notice the absence of osteophytes. FIGURE 11–13. Bilateral weight-bearing x-rays to determine the degree of medial and lateral compartment osteoarthritis.

KNEE EFFUSION Of the various maneuvers used to detect the presence of a knee effusion, estimation of the lost of flexion by the heel-to-buttock measurement is the most reliable because it can be applied to all patients regardless of size. Full flexion of the knee is impaired whenever a knee effusion develops acutely. A 1- to

INTERPRETATION: The severity of osteoarthritis correlates directly with the width of the articular cartilage. The presence of joint line osteophytes, subchondral sclerosis or cystic degeneration, and meniscal calcification vary from patient to patient and are not necessary to confirm the diagnosis. The normal medial cartilage width averages 6 to 8 mm depending on sex, body frame, and so forth.

2-inch difference between the right and left heel-to-buttock measurements correlates directly with the presence of an acute effusion. Other much less common causes of impaired flexion include prior surgery, an intra-articular fracture, advanced osteoarthritis, or a large, palpable Baker cyst.

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HEEL-TO-BUTTOCK MEASUREMENT SUMMARY: Loss of flexion is the most reliable means of evaluating the knee for the presence of excess synovial fluid. The heel-to-buttock distance is a convenient and easy method to distinguish side-to-side differences in flexion. Of all the means of assessing excess fluid production, this is the only method that is reliable enough to use in obese patients. MANEUVER: The knee is passively flexed. The patient’s tolerance of the maneuver is noted. The distance between the posterior heel and the buttocks is measured. ADDITIONAL SIGNS: Loss of the peripatellar dimples, ballottement of fluid, the side-to-side milking maneuver, and suprapatellar fullness are additional signs of excess fluid.

FIGURE 11–14. Perform the heel-to-buttock measurement to assess knee effusion.

INTERPRETATION: In the asthenic patient the first sign of access fluid is the general fullness about the knee and the loss of the peripatellar dimples. With increasing amounts of fluid the ballottement signs and milking maneuvers become abnormal. Only the largest fluid accumulations extend above and distend the suprapatellar extension of the synovial cavity.

ASPIRATE THE KNEE JOINT SUMMARY: The evaluation of the knee accompanied by joint effusion is incomplete until the synovial fluid is obtained for laboratory analysis. The lateral approach to the knee is preferred because the synovial cavity distends laterally in 75% of patients. POSITIONING:

Supine.

SURFACE ANATOMY: Lateral patella, superior patellar pole, iliotibial band, and distended synovial cavity. POINT OF ENTRY: Laterally, halfway between the undersurface of the patella and the middle of the iliotibial track. FIGURE 11–15. Aspirate the knee joint to determine the cause of the knee effusion.

ANGLE OF ENTRY:

70 degrees.


DEPTH:

⁄2 to 3 inches.

1

ANESTHESIA: Ethyl chloride, skin: 1 mL to the lateral retinaculum; 1 mL intra-articularly.

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PREPATELLAR BURSITIS Acute prepatellar bursitis (inflammation of the largest knee bursa) is characterized by varying degrees of palpable swelling, focal tenderness, erythema, and warmth, all centered over the lower half of the patella. Because the swelling is completely extra-articular, the range of motion of

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the knee is unimpaired. In approximately 5% of these acute cases, the inflammatory process fails to resolve. Chronic prepatellar bursitis is characterized by palpably thickened bursal walls, focal tenderness, and less dramatic signs of inflammation.

PALPATE THE PREPATELLAR BURSA SUMMARY: The bursa is one of four synovial lined structures that lubricate the quadriceps mechanism. The other three are the suprapatellar pouch (a part of the synovial cavity) and the two infrapatellar bursae, one located above and one located below the patellar tendon. MANEUVER: The prepatellar bursa is palpated for warmth, focal tenderness, and swelling, and the walls are squeezed between the fingertips to assess for bursal wall thickening. ADDITIONAL SIGNS: The range of motion of the knee is unaffected unless a secondary cellulitis is present.

FIGURE 11–16. Palpate the prepatellar bursa for swelling and thickening.

INTERPRETATION: Acute bursitis is characterized by cystic swelling and varying degrees of tenderness, warmth, and redness. Chronic bursitis is characterized by palpable thickening of the bursal walls. These changes are located over the lower third of the patella, in contrast to the infrapatellar bursa, which is located exclusively over the patellar tendon.

ASPIRATE THE BURSA SUMMARY: Aspiration and laboratory analysis of the fluid are necessary to distinguish bursitis caused by trauma, crystal deposition disease (gout), or infection. POSITIONING:

Supine.

SURFACE ANATOMY: Lateral patella, superior patellar pole, iliotibial band. POINT OF ENTRY: Laterally, halfway between the undersurface of the patella and the middle of the iliotibial track. ANGLE OF ENTRY: FIGURE 11–17. Aspirate the bursa to distinguish the three common causes of prepatellar bursitis.

70 degrees.

NEEDLE: 11⁄2 inch, 22 gauge or 22-gauge spinal needle. DEPTH:

⁄2 to 3 inches.

1

ANESTHESIA: Ethyl chloride, skin: 1 mL to the lateral retinaculum; 1 mL intra-articularly.

LATERAL COMPARTMENT OSTEOARTHRITIS Although lateral compartment osteoarthritis commonly accompanies medial compartment osteoarthritis, isolated involvement does occur but almost always results from a previous injury (lateral meniscal tear,

tibial plateau fracture, or grade-three ligament tears). The diagnosis is suggested by a history of injury, lateral joint line tenderness and crepitation, palpable spurring along the lateral tibial plateau, and varying degrees of joint effusion.

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LATERAL JOINT LINE TENDERNESS SUMMARY: Lateral knee pain encompasses irritation of the lateral compartment of the knee, injury to the LCL, lateral meniscal disorders, or iliotibial band inflammation. Local tenderness limited to a dime-sized area at the level of the inferior pole of the patella is caused by intrinsic conditions affecting the lateral compartment of the knee or the lateral meniscus. MANEUVER: The superior and inferior poles of the patella are identified and marked. The joint lines are located at the level of the inferior pole of the patella in the midplane of the femur. Local tenderness laterally is compared with the joint line tenderness medially.

FIGURE 11–18. Lateral joint line tenderness suggests lateral compartment osteoarthritis.

ADDITIONAL SIGNS: Passive flexion and extension of the knee can cause a grinding sensation (crepitation). Full flexion may be limited by advanced arthritic changes or the presence of an effusion. Secondary anserine bursitis or a mild LCL strain can accompany the arthritic flareup. Lack of full extension suggests advanced arthritic change or the presence of a degenerative meniscal tear or loose body. The varus–valgus rocking maneuver of the tibia against the femur is loose because of the thinning of the lateral cartilage. INTERPRETATION: Tenderness at the joint line is most commonly caused by irritation of the synovial membrane (e.g., osteoarthritis, inflammatory arthritis). However, meniscal and collateral ligament injuries have local tenderness that overlaps with the joint line tenderness.

WEIGHT-BEARING X-RAYS SUMMARY: Less than 5% of patients with osteoarthritis have exclusive involvement of the lateral compartment. CASE: This 54-year-old former lineman for the Oregon State University football team injured his lateral meniscus at age 20. Meniscectomy was performed, and the patient was able to return to active play. Over the last several years the patient has had chronic knee pain, an occasional giving-out sensation, and intermittent swelling. INTERPRETATION: The absolute criterion for osteoarthritis of the lateral compartment is a loss of articular cartilage measured on weight-bearing x-rays of the knee. The presence of joint line osteophytes, subchondral sclerosis or cystic degeneration, and meniscal calcification confirm the diagnosis of osteoarthritis but do not universally accompany thinning of the articular cartilage. The normal width of the articular cartilage is 5–7 mm. FIGURE 11–19. Weight-bearing x-rays confirm lateral compartment osteoarthritis.

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ANSERINE BURSITIS The diagnosis of anserine bursitis requires local tenderness confined to a quarter-sized area of the medial tibial plateau, approximately 11⁄2 inches below the medial joint line; a negative valgus stress maneuver (indicating an intact MCL);

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and a normal x-ray of the tibia (no underlying bony disorder). The diagnosis can be confirmed by placing 1⁄2 mL local anesthetic between the medial collateral ligament and the conjoined tendon, approximately 3 to 4 mm above the periosteum of the tibia.

ANSERINE BURSA SUMMARY: The anserine bursa is located between the MCL and the conjoined tendon formed by the gracilis, sartorius, and semitendinosus tendons. MANEUVER: The patella and the tibial tubercle are marked with a pen. Bursal tenderness at the level of the tibial tubercle is compared with tenderness at the medial joint line and medial femoral condyle. The tenderness of the bursa should be limited to a quartersized area, as compared with the local tenderness of the MCL, which extends several centimeters from the joint line down to the area of the anserine bursa. ADDITIONAL SIGNS: Valgus stress applied to the joint should be pain free. Range of motion of the knee should be normal, and the joint line should be painless unless anserine bursitis is a complication of osteoarthritis (a common occurrence).

FIGURE 11–20. Palpate the anserine bursa for local tenderness.

INTERPRETATION: A quarter-sized area of tenderness at the level of the tibial tubercle is the classic location of anserine bursitis. Tenderness that extends from the anserine bursal area to the joint line probably is caused by irritation or injury involving the MCL

LOCAL ANESTHETIC BLOCK SUMMARY: Local anesthetic block is used to determine the contribution of bursitis to the patient’s overall pain level (anserine bursitis often accompanies osteoarthritis, joint effusion, or any primary diagnosis that causes an impaired gait). POSITIONING:

Supine.

SURFACE ANATOMY: Tibial tubercle, medial tibial plateau, and medial joint line. POINT OF ENTRY: Midplane, at the level of the tibial tubercle or 1.5 inches below the medial joint line. ANGLE OF ENTRY: Perpendicular to the curvature of the tibial plateaus. NEEDLE: DEPTH:

11⁄2 inch, 22 gauge. ⁄2 to 5⁄8 inch.

1

ANESTHESIA: Ethyl chloride, skin: 1⁄2 mL 3 to 4 mm above the tibial periosteum. FIGURE 11–21. Local anesthetic block to confirm anserine bursitis.

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MCL INJURY All MCL injuries are characterized by local tenderness extending from the medial femoral condyle across the joint line to its attachment to the medial tibial plateau, pain and varying degrees of laxity during valgus stress testing (first degree, no

laxity; second degree, mild to moderate laxity; third degree, disruption and unstable), and pain with passive external rotation (variable).

VALGUS STRESS TEST SUMMARY: Medial knee stability is maintained by the quadriceps muscle, the joint capsule, and the MCL. The valgus stress test is used to determine the integrity of the MCL. MANEUVER: One hand is placed above the knee along the lateral thigh, and one hand is placed along the medial gastrocnemius muscle. The upper hand is used to stabilize the thigh while the lower hand exerts outward pressure on the calf. Pain, movement of the medial joint space, and elasticity of the ligament are noted. ADDITIONAL SIGNS: Local tenderness extends from the upper tibial plateau (the same area as the anserine bursa), across the joint line, and to the medial femoral condyle. FIGURE 11–22. Valgus stress test of MCL injury.

INTERPRETATION: Pain without abnormal movement of the joint indicates a first-degree sprain. Pain with opening of the joint but rapid return to normal position characterizes a second-degree sprain or partial tear. Pain and persistent looseness or frank instability of the joint are characteristic of a third-degree sprain or complete tear. A false positive test can be seen with wear of the medial articular cartilage (medial compartment osteoarthritis with ligament laxity caused by compartmental narrowing).

LOCAL ANESTHETIC BLOCK SUMMARY: This procedure is nearly identical to the injection of the anserine bursa, with the exception of the point of entry. It is used to distinguish MCL injury from involvement of the medial meniscus, osteoarthritis of the medial compartment, and anserine bursitis. POSITIONING:

Supine.

SURFACE ANATOMY: Tibial tubercle, medial tibial plateau, medial joint line. POINT OF ENTRY: Enter in the midline over the tibial plateau just below the joint line. NEEDLE:

⁄8 inch, 25 gauge or 11⁄2 inch, 22 gauge.

5

DEPTH: 1⁄2 inch (thin patients) to 3⁄4 inch, or 1⁄8 inch just above the periosteum of the tibia. FIGURE 11–23. Local anesthetic block to confirm MCL injury.

VOLUME:

1 to 2 mL anesthetic.

NOTE: Never inject between the MCL and the bone, and always brace after injection.

KNEE

LCL INJURY LCL injuries are uncommon. The diagnosis is

suggested by an injury involving dramatic varus stress, an exami-

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nation demonstrating tenderness along the lateral joint line, and pain or laxity that is aggravated by varus stress testing of the knee.

VARUS STRESS TEST SUMMARY: Lateral stability of the knee is maintained by the quadriceps muscles, the joint capsule, and the LCL. The varus stress test is used to determine the integrity of the LCL. MANEUVER: One hand is placed above the knee medially, and one hand is placed along the lateral gastrocnemius muscle. The upper hand is used to stabilize the thigh while the lower hand exerts inward pressure on the calf. Pain, movement of the lateral joint space, and the elasticity of the ligament are noted. ADDITIONAL SIGNS: Local tenderness is present along a line extending from the fibular head, across the joint line, to the lateral femoral condyle. The range of motion of the knee should be normal. FIGURE 11–24. Varus stress test of LCL injury.

INTERPRETATION: Pain without abnormal movement of the joint indicates a first-degree sprain. Pain with opening of the joint but rapid return to normal position characterizes the second-degree sprain or partial tear. Pain and persistent looseness of the joint are characteristic of a third-degree sprain or complete tear.

LOCAL ANESTHETIC BLOCK SUMMARY: This procedure is used to distinguish LCL injury from involvement of the lateral meniscus and osteoarthritis of the lateral compartment. POSITIONING:

Supine.

SURFACE ANATOMY: Fibular head, lateral joint line, the iliotibial band demarcating the level of the midplane. POINT OF ENTRY: Enter in the midplane just above the fibular head and just below the joint line. NEEDLE:

⁄8 inch, 25 gauge or 11⁄2 inch, 22 gauge.

5

DEPTH: 1⁄2 inch (thin patients) to 3⁄4 inch, or 1⁄8 inch just above the ligament. Volume:

FIGURE 11–25. Local anesthetic block to confirm LCL injury.

1 to 2 mL anesthetic.

NOTE: Never inject between the LCL and the bone, and always brace after injection.

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ACL INJURY ACL injuries are uncommon in the nontraumatized patient. The diagnosis should be suspected if the patient has sustained a significant injury, describes symptoms of instability

(e.g., looseness, unexplained giving out), and experiences pain and laxity with the Lachman maneuver or the anterior drawer sign.

ANTERIOR DRAWER SIGN SUMMARY: The ACL is located in the intercondylar notch of the femur and is named for its attachment at the anterior tibial spine. Its function is to prevent the anterior movement of the tibia relative to the femur. MANEUVER: The proximal tibia is grasped firmly with both hands. While stabilizing the foot, the examiner forcefully pulls the tibia anteriorly, noting any pain, laxity, or abnormal movement compared with the contralateral side. ADDITIONAL SIGNS: The Lachman maneuver should corroborate a positive drawer sign. A tense hemarthrosis may be present. Additional injuries such as an MCL or meniscal tear may be present.

FIGURE 11–26. Anterior drawer sign to evaluate the integrity of the ACL.

INTERPRETATION: A difference of 1 cm between the anterior drawer signs suggests complete tear of the ligament. Partial tears are characterized by pain, loss of elasticity, and poor springback with the Lachman maneuver (the latter maneuver is identical to the anterior drawer sign with the exception of holding the foot fast to the exam table).

MRI OR ARTHROSCOPY SUMMARY: The cruciate ligaments are named for their attachments to the tibial spines. The photograph depicts the posterior cruciate ligament (arrow). Both ligaments originate from the distal femur and traverse the intercondylar notch. CASE: The 28-year-old patient sustained a hyperextension injury and describes a vague, unstable sensation with knee flexion. The patient presented with a tense effusion of the knee, which on aspiration was a hemarthrosis. The drawer and Lachman maneuvers were equivocal. Based on the injury, the presence of intra-articular bleeding, and the subtle irregularities on MRI, the patient underwent arthroscopy, which demonstrated a partially torn PCL.

FIGURE 11–27. MRI or arthroscopy to confirm injury to the cruciate ligaments.

INTERPRETATION: Depending on the severity of the injury, the persistence of symptoms, and the subtle changes on the knee exam, the clinician must choose between MRI and arthroscopy to evaluate the integrity of the cruciate ligaments. The direct visualization of the ligaments by arthroscopy has a greater sensitivity in determining the integrity of the cruciate ligaments.

KNEE

BAKER’S CYST A Baker’s cyst, also called a popliteal cyst, is

a direct result of excessive synovial fluid production (chronic knee effusions associated with rheumatoid arthritis, advanced osteoarthritis, and so forth). Large cysts (more than 4 cm long) inter-

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fere with full flexion of the knee. Patients who complain of popliteal tightness, fullness behind the knee, or impairment of bending have a large knee effusion, a Baker’s cyst, or both.

POPLITEAL FOSSA SUMMARY: All synovial fluid is produced anteriorly by the joint capsule. As excess fluid accumulates, the peripatellar dimples begin to fill in, the patella floats above the femoral groove, and eventually the fluid extends into the suprapatellar portion of the synovial cavity. Repetitive flexing of the knee forces the fluid through a sinus into the popliteal fossa, distending the semimembranosus bursa. With continued distension and the hydraulic pressure of flexion, the bursa gradually enlarges and eventually seals itself off from its connection with the synovial cavity. When the sinus finally collapses, a true Baker’s cyst forms. MANEUVER: Two hands are used to palpate the medial side of the popliteal fossa for a cystic or pulsatile mass.

FIGURE 11–28. Palpate the popliteal fossa for a Baker’s cyst.

ADDITIONAL SIGNS: Signs of the underlying effusion and its primary cause are present in most cases. If the Baker’s cyst has ruptured, calf tenderness and bruising may be present at the ankle (the crescent sign located behind the malleolus). INTERPRETATION: A sensation of pressure or fullness in the popliteal fossa is most often associated with a joint effusion. The differential diagnosis of popliteal mass includes large posterior fat pads, Baker’s cyst, and popliteal aneurysm.

ASPIRATION SUMMARY: A painless mass is palpable in the popliteal fossa. Needle aspiration is used to confirm the diagnosis and to reduce the pressure on the structures of the popliteal fossa. POSITIONING:

Prone.

SURFACE ANATOMY: Popliteal fossa and knee creases, semimembranosus and semitendinosus tendons. POINT OF ENTRY: palpable cyst. ANGLE OF ENTRY: FIGURE 11–29. Aspiration to confirm a Baker cyst.

NEEDLE: Depth:

Directly over the center of the Perpendicular to the skin.


⁄2 to 3⁄4 inches.

1

ANESTHESIA: Ethyl chloride, skin: 1⁄2 mL subcutaneously. MENISCAL TEAR The symptoms and signs of meniscal tear often are vague and nonspecific. The pain is not well localized or defined. The exam may demonstrate a loss of smooth motion, a

small, bland effusion of the knee, and minor joint line tenderness, symptoms that overlap with those of other conditions. After a thorough examination of the knee, MRI or diagnostic arthroscopy

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can be considered in patients who have sustained an injury, complain of persistent impairment of function (giving out, a sense of

instability, or a loss of smooth motion), and demonstrate the subtle abnormalities on examination.

MCMURRY MANEUVER SUMMARY: The McMurry maneuver attempts to trap the torn meniscus between the tibia and the femur. A positive maneuver occurs when the cartilage suddenly dislodges, causing a popping at the joint line. Unfortunately, it screens only for posterior or posterolateral meniscal tears. The McMurry maneuver cannot detect anterior or anterolateral tears, making this test inherently difficult to interpret. MANEUVER: The examiner’s thumb and index fingers are placed on the medial and lateral joint lines. The knee is passively flexed. While applying torque to the foot, the examiner rotates the knee medially to trap the lateral meniscus or laterally to trap the medial meniscus. The knee is passively extended. The examiner repeats the maneuver in a smooth back-and-forth motion, feeling for a popping sensation along the joint line. FIGURE 11–30. Perform a McMurry maneuver to assess for meniscal tear.

ADDITIONAL SIGNS: Joint line tenderness is invariably present. Knee effusion accompanies the more significant meniscal tears. ACL and MCL injuries can accompany meniscal tears. Large, fragmented meniscal tears can cause locking or incomplete extension of the knee. INTERPRETATION: The sensitivity of the McMurry maneuver is limited because the maneuver is incapable of trapping most anterior and anterolateral tears. A negative test cannot be used to rule out a meniscal tear.

MRI OR ARTHROSCOPY SUMMARY: The disk-shaped meniscal cartilages are composed of fibrocartilage and provide smooth motion between the two bones. Patients with substantial injuries to the cartilage often describe a vague sense of instability, especially with repeated knee flexion. Occasionally the patient complains of loud popping sounds when attempting to squat. Depending on the severity of the injury, the persistence of symptoms, and the subtle changes on exam of the knee, the clinician must choose between MRI and arthroscopy to evaluate the integrity of the meniscal cartilage. DIAGNOSIS: A complex medial meniscal cartilage tear extending to the articular surface of the tibia.

FIGURE 11–31. MRI or arthroscopy to confirm a meniscal tear.

INTERPRETATION: Mucinoid degeneration of the meniscal cartilage develops with age. These appear as increased signal arising from the center of the meniscus on MRI. This age-related phenomenon must be distinguished from the much more significant traumatic meniscal tears that extend to the articular surface (arrow).

KNEE

ILIOTIBIAL BAND SYNDROME Iliotibial band syndrome is seen almost exclusively in runners. The diagnosis should be considered in an athletic patient with focal tenderness with or without

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palpable clicking over the lateral femoral condyle. X-rays of the femur usually are normal, and the knee exam is otherwise normal.

LATERAL FEMORAL CONDYLE SUMMARY: The iliotibial band is a broad, thick fascia that forms the distal portion of the tensor fascia lata and the vastus lateralis fascia. It crosses the prominence of the lateral femoral condyle to attach to the fibular head. It blends with the lateral patellar retinaculum near the lateral joint line. MANEUVER: The superior, inferior, and lateral poles of the patella are palpated and marked with a pen. The iliotibial band is palpated over the lateral femoral condyle, located at the same level as the superior pole of the patella. The inch-wide band is best identified by palpation in a downward direction toward the popliteal area. ADDITIONAL SIGNS: Passive flexion and extension of the knee can be associated with a snapping sensation of the band across the femoral condyle.

FIGURE 11–32. Palpate the lateral femoral condyle to assess the iliotibial band.

INTERPRETATION: Local tenderness over the lateral femoral condyle in a nontraumatized patient is nearly always caused by iliotibial band syndrome. Plain x-rays are used to exclude primary or secondary bony lesions of the condyle. However, these bony lesions rarely have the same precise area of tenderness at the intersection of the band and the femoral condyle as seen with iliotibial band syndrome.

LOCAL ANESTHETIC BLOCK SUMMARY: The quarter-sized area of tenderness at the lateral femoral condyle usually is diagnostic of iliotibial band syndrome. When the tenderness lacks the characteristic location or size, local anesthetic block is performed to distinguish the symptoms arising from the iliotibial band from involvement of the LCL and lateral compartment of the knee. POSITIONING:

Supine.

SURFACE ANATOMY: Lateral patella, superior patellar pole, iliotibial band, and lateral femoral condyle. FIGURE 11–33. Local anesthetic block to confirm iliotibial band injury.

POINT OF ENTRY: ANGLE OF ENTRY:

Over the lateral femoral condyle. Perpendicular.


DEPTH:

⁄2 to 11⁄4 inches.

1

ANESTHESIA: Ethyl chloride, skin: 1 mL above and below the iliotibial band.

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PAIN REFERRED TO THE KNEE The back, sacroiliac joint, and hip commonly refer pain to the knee. The L5 root and sacroiliac joint refer pain down the back of the leg to the popliteal space. The S1 root, the trochanteric bursa, and the femur refer pain down the outer thigh to the lateral area of knee. The hip

joint and the femur refer pain down the front of the thigh to the anterior knee. Referred pain is suggested whenever the patient’s pain is not well localized, the knee exam is free of local tenderness or inflammatory changes, and the flexion and extension of the knee are normal.

STRAIGHT LEG RAISE MANEUVER SUMMARY: Lumbar level L4–L5 and lumbar level L5–S1 cause pain and numbness over the outer knee and popliteal areas, respectively. Moderate to severe trochanteric bursitis commonly refers pain to the lateral knee. Occasionally pain is referred to the lower femur and anterior knee from conditions affecting the hip joint. Rarely, primary and secondary lesions of the femur manifest pain at the knee. A referred pattern of pain should always be considered when local signs of knee swelling, tenderness, and impaired motion are absent (see Chapter 9 for details). FIGURE 11–34. Straight leg raise maneuver to evaluate for lumbar radiculopathy.

CT OR MRI SUMMARY: CT scanning or MRI is necessary to define the anatomic process causing lumbar radiculopathy. CASE: This 62-year-old man complained of pain running down the back of the leg to the knee and a tingling sensation on the bottom of the foot. The ankle reflex was diminished, but motor strength of dorsiflexion and plantarflexion were normal. DIAGNOSIS:

FIGURE 11–35. A definitive diagnosis of radiculopathy requires direct correlation of the neurodeficits defined by examination and CT or MRI studies.

Herniated disk at the L5–S1 level.

11–1


EXAMINATION SIGNS

DIAGNOSIS

CONFIRMATION

Pressure of the patella against the femur causing retropatellar pain and crepitation

#1: Patellofemoral syndrome

Bilateral sunrise views taken on one cassette to evaluate for patellar subluxation and arthritic changes

Patellar apprehension sign with lateral subluxation

Patellar subluxation or dislocation

Clinical diagnosis

Medial joint line tenderness or spurring

#2: Medial compartment osteoarthritis

Standing anteroposterior knees on one cassette, showing narrowing of the articular cartilage

Knee effusion

Aspiration and lab analysis for cell count, differential, crystals, glucose, Gram stain, and culture

Prepatellar bursitis

Aspiration and lab analysis for cell count, differential, crystals, glucose, Gram stain, and culture

Chronic prepatellar bursitis

Local anesthetic block in the bursa

Lateral compartment osteoarthritis

Standing anteroposterior knees on one cassette showing narrowing of the articular cartilage

Anserine bursitis

Local anesthetic block in the 2–3 mm above the periosteum

Medial collateral ligament injury

Empirical treatment with 3–4 wk of straight leg mobilization; local anesthetic block placed just over the ligament (optional)

Lateral collateral ligament injury

Improvement with 3–4 wk of straight leg immobilization; local anesthetic block placed just over the ligament (optional)

Anterior cruciate ligament injury

Arthroscopy or MRI

Baker’s cyst

Characteristic aspirate

Meniscal tear

Arthroscopy or MRI

Iliotibial band syndrome


Patellar clicking with passive flexion and extension ⫹ Insall maneuver; retropatellar pain with quadriceps contraction

Stiffness or incomplete flexion Crepitation with passive flexion and extension Heel-to-buttock measurement differs side to side Loss of the peripatellar dimples Synovial milking sign Ballottement sign for large effusions Distension of the suprapatellar pouch Cystic swelling over the anteroinferior portion of the patella No loss of range of motion Thickening of the prepatellar bursa No loss of range of motion Lateral joint line tenderness or spurring Stiffness or incomplete flexion Crepitation with passive flexion and extension Tenderness over the medial tibial plateau, 11⁄2 inch below the joint line No pain with valgus stress testing Normal range of motion of the knee Line of tenderness over the medial tibial plateau extending up to or above to the medial joint line Pain aggravated by valgus stress testing Pain aggravated by external rotation of the tibia on the femur Tenderness over the lateral tibial plateau extending along a line to the lateral joint line Pain aggravated by varus stress testing Pain aggravated by internal rotation of the tibia on the femur Painful anterior drawer sign Pain or inability to fully squat and duck waddle Palpable cyst in the medial side of the popliteal fossa Incomplete range of motion if the cyst is large Distal edema Joint line tenderness and mechanical locking or joint line popping Inability to duck waddle Popping with squatting Lateral femoral condyle tenderness Normal lateral collateral ligament exam No active evidence of lateral compartment osteoarthritis

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COMMON KNEE FRACTURES

DISTAL FEMUR AND PROXIMAL TIBIAL KNEE FRACTURES SUMMARY: Because of the variety of fractures that occur at the knee (tibial plateau) and the distal femur (supracondylar), the intra-articular extension of a large proportion of these fractures, the associated injuries to the supporting ligaments, and the need for specialized traction and cast-bracing, most patients with these fractures should be referred to an orthopedic surgeon for management. Fractures that can be treated nonoperatively include avulsion fractures at the joint line (MCL and LCL injuries), nondisplaced osteochondritis dissecans fractures that do not cause mechanical locking, minimally depressed tibial plateau rim fractures (depression less than 10 degrees), and certain patellar fractures.

FIGURE 11–36. Distal femur and proximal tibial knee fractures.

FRACTURES OF THE PATELLA SUMMARY: Patellar fractures are classified as transverse, stellate, longitudinal, marginal, and, rarely, osteochondral. More than half of the fractures are transverse, and the majority of these are the result of a direct blow to the patella that is magnified by the tremendous pull of the quadriceps mechanism. Most show little or no separation of the fragments because of the intact medial and lateral quadriceps muscle “expansions.” IMMOBILIZATION: Nonoperative management includes hemarthrosis aspiration and intra-articular anesthesia to accurately assess the integrity of the quadriceps mechanism, followed by long-leg casting and gradual restoration of weight bearing (nondisplaced fractures).

FIGURE 11–37. Fractures of the patella.

SURGICAL REFERRAL: Refer to a surgical orthopedist if the quadriceps mechanism is ruptured or the fragments are separated by more than 2 mm. Surgery involves cerclage wiring or lag screw internal fixation for displaced fragments or total patellectomy for the severely comminuted fracture. PROGNOSIS: Severely displaced fractures increase the risk of late-onset osteoarthritis.

KNEE

219

OSTEOCHONDRITIS DISSECANS SUMMARY: Osteochondritis dissecans is an osteochondral fracture, a defect of cartilage and bone on the articular surface. As to its exact cause, direct trauma, ischemia, and true avulsion are theorized. Patients present with nonspecific knee complaints or with mechanical locking caused by an associated loose body. SURGICAL REFERRAL: Patients with large fragments, persistent knee effusion, and mechanical locking should be referred to orthopedic surgery to consider PCL repair, drilling of the fragment (to stimulate revascularization), or repair of any other associated injuries to ligaments or meniscal cartilage. PROGNOSIS: Large defects cause an accelerated wear-and-tear osteoarthritis.

FIGURE 11–38. Osteochondritis dissecans of the femur.

FRACTURES OF THE TIBIAL SHAFT SUMMARY: Because of the complexity, the need for specialized casting, and the potential complications, most tibial shaft fractures should be managed by an orthopedic surgeon. IMMOBILIZATION: Fractures with no more than 1 cm of shortening, 5 degrees of varus or valgus angulation, or 10 degrees of anteroposterior or rotational angulation can be managed nonoperatively. After closed reduction using intravenous sedation, a long-leg cast with suprapatellar and medial tibial molding is applied. The foot and ankle are kept in the neutral position, and the knee is flexed to 5 degrees. Healing time averages 5 months. Cast wedging is used to correct any postreduction angulation. When adequate callus formation is noted on x-rays, the cast can be replaced with a patellar tendon–bearing cast or brace to complete the healing process.

FIGURE 11–39. Fractures of the tibial shaft.

PROGNOSIS: During the recovery period, the patient must be carefully monitored for deep venous thrombosis, anterior compartment syndrome, and distal ischemia.

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TIBIAL STRESS FRACTURE SUMMARY: Stress fractures of the tibia result from repeated microtrauma to the proximal third of the bone, often occurring in the section of the tibia with the smallest cross-sectional area. The condition is seen almost exclusively in runners, professional ballet dancers, and military recruits, although patients with severe osteoporotic bones are also susceptible. Radiographically, the periosteum of the tibia is thickened in the proximal third of the bone in runners and in the middle third of the bone in ballet dancers. A true fracture line is seen rarely. Stress fracture must be distinguished from the more common shin splints, anterior compartment syndrome, and localized pain or paresthesia of the outer lower leg caused by lumbosacral radiculopathy. IMMOBILIZATION: Running and other impact sports must be avoided for several weeks. Patients with severe pain should be advised to use crutches. Persistent cases can be treated with fixed immobilization with an air cast or short leg walking cast. In the recovery phase, nonimpact muscle toning exercises are strongly recommended, and padded arch supports are suggested for long-term prevention. FIGURE 11–40. Tibial stress fracture.

SURGICAL REFERRAL:

None.

TIBIAL AND FIBULAR FRACTURES SUMMARY: This combined fracture should be referred to an orthopedic surgeon because of the presence of instability, angulation, or major soft tissue injury. IMMOBILIZATION: Isolated fibular shaft fractures are much less common than the combined tibial and fibular fracture. It usually occurs as a result of a direct blow. Immobilization is used for pain control only. The fracture can be treated with a shortened stride, decreased weight-bearing activities, or immobilization with a short leg walking cast. Fixed immobilization with casting is recommended when weight-bearing pain is troublesome.

FIGURE 11–41. Combined tibial and fibular fractures.

KNEE

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CLINICAL PEARLS • Lateral subluxation of the patella is the hallmark and major cause of patellofemoral syndrome, accounting for half the diagnoses in patients presenting with knee pain. • The quadriceps mechanism, including the quadriceps muscle, the patellar tendon, and the patellofemoral articulation, needs the greatest degree of lubrication in the body. The largest synovial cavity, the prepatellar bursa, and the infrapatellar bursae surround these structures to protect against friction and wear. • Patients with osteoarthritis of the medial compartment of the knee most often manifest symptoms when the underlying arthritis is complicated by effusion, anserine bursitis, MCL injury, or degenerative meniscal tear. • The earliest sign of osteoarthritis on weight-bearing x-rays of the knee is an equalization of the widths of the medial and lateral compartment cartilages (normally the medial compartment cartilage is 1 mm wider than the lateral compartment width, measured at the midfemoral condyle). • Osteoarthritis limited to the lateral compartment almost always occurs as a long-term sequela of previous trauma (fracture, meniscal tear, or ligament injury). • The synovial cavity of the knee is the largest of all of the joints of the body. Large effusions, ranging from 15 to 60 mL, cause a loss of the peripatellar dimples (knee fullness), lift the patella off the femur (ballotable patella), distend the superior pouch of the cavity up to 4 inches above the superior pole (fullness above the patella and a lateral bulge), and interfere with flexion of the knee (reduction of the heel-to-buttock distance, especially when effusions develop acutely). • Ten percent of all knee effusions are accompanied by a distension of the semimembranosus bursa and a true Baker cyst when the sinus connecting the bursa and the synovial cavity closes. • Rupture of a true Baker cyst can cause symptoms identical to the signs and symptoms of deep venous thrombosis of the calf. The exception is the crescent sign at the ankle, a collection of blood below the malleoli indicative of blood dissecting down the tissue planes of the calf to the ankle. • Large knee effusions that extend into the popliteal space can cause lower extremity edema by compressing the popliteal veins, and symptoms can mimic sciatica through pressure on the neurovascular bundle. • Anserine bursitis results from any primary condition affecting the knee that alters the normal mechanics of gait, mostly commonly, any diagnosis that leads to the development of a significant knee effusion. Because anserine bursitis develops secondarily, emphasis should be placed on treating the main joint.

• It is impossible to distinguish acute, traumatic prepatellar bursitis from the inflammatory changes associated with septic or gouty bursitis. Therefore, all bursae must be aspirated for laboratory studies to avoid the difficulties in clinical decision making when empiric treatment with antibiotics fails to resolve the condition. • Tendonitis of the patellar tendon (jumper’s knee) is seen almost exclusively in athletes such as basketball and volleyball players and high jumpers. • Ninety-five percent of patients with acute hemarthrosis have an underlying injury to ligament, meniscal cartilage, or adjacent bone and therefore need MRI and referral to a knee arthroscopist. The remaining patients have bloody effusions caused by synovial capsule tears or a bleeding diathesis caused by oral anticoagulation or hemophilia, all of which are reversible. • Traumatic meniscal tears are distinctly different from the degenerative tears associated with aging and osteoarthritis. The latter often respond to conservative management of the knee, whereas the traumatic tears (often in younger athletic patients) warrant evaluation with MRI and arthroscopy if function is impaired dramatically. • Meniscal tears rarely cause true mechanical locking. Most patients describe a loss of smooth mechanical function, complain of “something just not right inside my knee,” or develop an unexplained knee effusion after injury. • McMurry and Apley maneuvers are quite specific for meniscal disorders but lack sensitivity (30% false negatives). MRI often overestimates meniscal disorders because of the high incidence of mucinoid degenerative changes. The decision to use diagnostic arthroscopy should be predicated on the impairment of overall knee function, the need to define the cause of an unexplained knee effusion (especially with normal radiographs of the knee), or in some cases, the demands of the athletic patient. • Local anesthetic block is an integral part of the evaluation of the patient with ligament injury. The acute pain of the injury and motion guarding must be controlled in order to distinguish second-degree sprains (partial tears) from third-degree sprains (complete, surgically repairable tears). • Patients with advanced medial compartment osteoarthritis of the knee are susceptible to MCL injuries and medial meniscal tears. The MCL gradually loosens as the medial compartment cartilage wears away, causing ever greater loosening of the joint (wobbling). • ACL and PCL injuries are rare in patients with advanced osteoarthritis.

CHAPTER 12: ANKLE DIFFERENTIAL DIAGNOSIS Diagnoses Ligaments (most common) Ankle sprain (1st, 2nd, 3rd degree) Ankle sprain with fibular avulsion Ankle sprain with peroneus tendon avulsion fracture Ankle sprain with osteochondritis dissecans or chondral fracture Ankle sprain with interosseus membrane disruption Ankle sprain with instability

Confirmations

Examination, x-ray (if indicated) Examination, x-ray: ankle series Examination, x-ray: ankle series Examination, x-ray, magnetic resonance imaging (MRI) Examination, x-ray: stress views Examination, x-ray: stress views

Joint Osteoarthritis, posttraumatic Inflammatory or septic arthritis Subtalar arthritis

X-ray: ankle series Aspiration and synovial fluid analysis Examination, local anesthetic block

Posterior heel Achilles tendonitis Achilles tendon rupture Pre-Achilles bursitis Retrocalcaneal bursitis Os trigonum syndrome

Examination, MRI Examination, MRI Local anesthetic block Local anesthetic block X-ray

Plantar heel Heel pad syndrome Plantar fasciitis Calcaneal stress fracture Sever’s disease (age less than 18 years)

Examination Local anesthetic block X-ray or bone scanning X-ray: ankle series

Tendons Peroneus tenosynovitis Posterior tibialis tenosynovitis

Local anesthetic block Local anesthetic block

Tarsal tunnel syndrome


Referred pain Lumbosacral spine radiculopathy Compartment syndrome or shin splints Baker’s cyst Ankle fractures

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Computed tomography (CT) scan, MRI, electromyelography Calf examination Knee examination, ultrasound X-ray, bone scan, or MRI

ANKLE

INTRODUCTION The conditions affecting the ankle can be divided into three distinct areas—the true ankle joint, the posterior heel, and the plantar heel—based on the patient’s description and location of their pain, the mechanism of injury, and the anatomic structures most susceptible to injury. Of the structures that make up the ankle joint, the supporting ligaments and tendons are most susceptible to injury; injury to the joint or its supporting soft tissues causes true ankle pain. Of the anatomic structures of the back of the ankle, the Achilles tendon mechanism is most susceptible to injury; injury to any of the structures of the back of the ankle causes posterior heel pain. And of the bones and ligamentous structures that form the arch of the foot, the plantar fascia is most susceptible to injury; injury to any of the structures forming the arch cause plantar heel pain. Injury to the lateral supporting ligaments of the ankle is the most common ankle condition. In most cases, the diagnosis of ankle sprain is not difficult. However, distinguishing simple first- and second-degree ankle sprains from the complex third-degree ankle sprain remains the greatest challenge. The primary care provider must remain vigilant to the complications that accompany the higher-degree sprains, including incomplete ligament healing and recurrent ankle sprain, ankle instability, fibular avulsion fracture, peroneus avulsion fracture, peroneus tendonitis, talar dome osteochondritis dissecans, and chondral fracture of the articular cartilage of the talus. Less common conditions at the ankle include arthritis of the true ankle joint, subtalar joint arthritis, and os trigonum syndrome. Despite the fact that the ankle carries nearly all the body’s weight, osteoarthritis of the ankle is uncommon. Inflammatory arthritis (chiefly rheumatoid arthritis) eventually will affect the ankle joint in its progressive forms and is the most common cause of subtalar arthritis. Plantar fasciitis is the most common cause of plantar heel pain. It must be distinguished from the traumatic conditions affecting the heel, namely heel pad syndrome (the stone bruise of the calcaneus) and the common conditions affecting the calcaneus bone, stress fracture in adults and epiphysitis in children (Sever’s disease). Injury to the Achilles tendon mechanism with or without partial or complete rupture dominates the differential diagnosis of posterior heel pain. Achilles tendonitis, partial tear of the tendon, and complete rupture must be distinguished from the less common and often misdiagnosed pre-Achilles bursitis (the pump-bump) and the uncommon inflammation of the bursal sac located between the tendon and the posterior aspect of the ankle joint, retrocalcaneal bursitis. Unlike the other joints of the skeleton, trauma is a major cause of the conditions affecting the ankle. For example, simple and complicated ankle sprains, Achilles tendonitis and tendon rupture, and ankle arthritis all result directly from injury or are long-term sequelae of it. The primary care physician must remain familiar with the types and mechanisms of the injuries associated with these common conditions in order to effectively triage the patients suffering more severe trauma. Early consultation with the fracture specialist is necessary for patients sustaining ski injuries, vertical falls from significant heights, and crushing injuries from motor vehicle accidents, who are at greater risk for calcaneal and talar dome fractures, distal fibular fractures,

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interosseous membrane rupture, and the bimalleolar and trimalleolar fractures. Finally, pain and numbness can be referred to the ankle from the lower lumbar nerve roots, from tarsal tunnel syndrome, or from the lower leg. Lumbar level L4–L5 and lumbar level L5–S1 cause pain and numbness over the dorsum and plantar surfaces, respectively. Compression and irritation of the posterior tibial nerve as it wraps around the medial malleolus cause pain to course through the ankle and down to the plantar surface of the ball of the foot. Tibial stress fractures, primary bony lesions of the tibia, and shin splints occasionally refer pain to the ankle. SYMPTOMS Patients with intrinsic conditions affecting the ankle most often complain of pain or difficulty with ambulation. The location of the pain is the most useful fact in narrowing the possible anatomic diagnoses. The type and mechanism of injury and the effect of the injury on ambulation are used to determine the overall function of the ankle and severity of the process. Anatomically, patients typically describe their pain as arising from the general area of the ankle or the heel. Patients with ankle pain accurately define their pain as lateral, anterior, or medial. Similarly, patients with heel pain accurately define their pain as arising from the bottom of the heel (plantar) or behind the heel (posterior location). Lateral ankle pain is the most commonly described pattern of pain. It is the classic area described by patients with injury to the lateral ankle ligaments. The degree of injury to the ligaments is defined by the effect on function. Patients with uncomplicated, simple ankle sprains are able to bear weight or ambulate with little difficulty. By contrast, patients with higher-degree ligament tears with or without avulsion fracture at the lateral malleolus or the base of the fifth metatarsal (the insertion of the peroneus tendon) have dramatic impairment of ambulation and weight bearing. Peroneus tenosynovitis and arthritis of the ankle are much less common causes of lateral ankle pain. Anterior ankle pain is the classic location of pain arising from ankle arthritis, dorsotenosynovitis of the extensor tendons, and referred pain from shin splints or the tibia bone. Medial ankle pain is the location of pain described with subtalar arthritis (most often from advanced rheumatoid arthritis), posterior tibial tenosynovitis, and tarsal tunnel syndrome. Posterior heel pain is the location of pain arising from the Achilles tendon, the pre-Achilles bursa, the retrocalcaneal bursa, and os trigonum syndrome. Plantar heel pain is caused by plantar fasciitis, heel pad syndrome, calcaneal stress fracture, and Sever’s disease. Referred pain to the ankle is uncommon. Sciatica is the most common cause. Rarely, a intrinsic condition affecting the knee can cause pain down the anterior lower leg. Occasionally shin splints refer pain over the anterior aspect of the ankle joint. EXAMINATION The examiner assesses the general function and integrity of the ankle by observing the patient’s ankle alignment while standing, the patient’s ability to bear weight, and the ability to perform normal heel–toe

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BOX 12-1

BOX 12-2

DIFFERENTIAL DIAGNOSIS OF ANKLE PAIN BASED ON ANATOMIC AREA Lateral ankle pain

Anterior ankle pain Medial ankle pain

Posterior heel pain

Plantar heel pain Referred pain

Ankle sprain Ankle sprain with instability Ankle sprain with chondral fracture Ankle sprain with interosseous membrane rupture Ankle sprain with osteochondritis dissecans of the talus Avulsion of the peroneus tendon Avulsion fracture of the fibula Peroneus tendonitis Ankle osteoarthritis Inflammatory arthritis Dorsotenosynovitis Posterior tibialis tendonitis Deltoid ligament strain Subtalar arthritis Tarsal tunnel Achilles tendonitis Achilles tendon rupture Pre-Achilles bursitis Calcaneal stress fracture Retrocalcaneal bursitis Os trigonum syndrome Plantar fasciitis Heel pad syndrome Calcaneal stress fracture Lumbar radiculopathy Tarsal tunnel Baker’s cyst

walking. These simple maneuvers provide a rapid assessment of the severity of the condition affecting the ankle. For patients presenting with true ankle pain, the first priority is to assess the integrity of the tibiotalar joints by evaluating the range of motion of the joint, comparing flexion and extension from side to side. Normal range of motion is 30 degrees of dorsiflexion and 60 to 70 degrees of plantarflexion. To evaluate the subtalar joint, the examiner compares passively performed inversion and eversion from side to side. The examiner assesses ankle joint stability by stress testing the deltoid ligaments medially, the interosseous membrane, and the talofibular and fibulocalcaneal ligaments laterally. The examiner assesses ligament integrity by assessing local tenderness, passively stretching the ligaments in inversion and eversion, and noting endpoint stiffness and pain. Inflammation or rupture of the supporting tendons of the ankle is evaluated by palpation and isometric stress testing of the tendons. By resisting inversion isometrically and palpating just under the medial malleolus, the examiner assesses the posterior tibial tendon. To assess the peroneus tendons, the examiner resists eversion isometrically and palpates just under the lateral malleolus.

SCREENING EXAMINATION OF THE ANKLE EMPHASIZING FUNCTION 1. Observe the general function of the ankle. a. The patient’s stance. b. The patient’s ability to bear weight. c. The patient’s gait. 2. Perform passive stretching (stress testing) in eversion for the deltoid ligament (medially) and in inversion for the lateral ankle ligaments. 3. Measure the range of motion of the tibiotalar joint (extension and flexion) and the subtalar joint (inversion and eversion) and compare with the unaffected side. 4. Palpate the posterior heel (Achilles tendon, calcaneus, and pre-Achilles bursa). 5. Palpate the plantar heel (plantar fascia, heel pad, and calcaneus). 6. Perform a Tinel maneuver for tarsal tunnel syndrome.

For patients presenting with posterior heel pain, the examiner evaluates the Achilles tendon by palpating the length of the tendon and by isometric stress testing. The examiner assesses the pre-Achilles bursa by noting any swelling and palpating the area over the superior aspect of the calcaneus, and the examiner evaluates the retrocalcaneal bursa by noting any swelling between the Achilles tendon and the talus and compressing the bursa by forced, passive plantarflexion. For patients presenting with plantar heel pain, the examiner palpates the plantar fascia heel at its insertion on the calcaneus. To assess injury and irritation of the heel pad, the examiner squeezes the specialized fat from side to side, and to assess the integrity of the calcaneus, the examiner compresses the bone from side to side. ONE-MINUTE SCREENING EXAM: MANEUVERS ASSESSING OVERALL ANKLE FUNCTION AND DIFFERENTIAL DIAGNOSIS The next seven maneuvers represent the minimal examination of the patient presenting with ankle symptoms. Functional testing of ambulation and stance, range of motion measurement of the joint, and screening maneuvers for ligament injuries, posterior heel pain, and plantar heel pain provide enough information to triage to x-ray, order appropriate labs, suggest general treatment recommendations, or proceed to more detailed examination and treatment.

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ABILITY TO BEAR WEIGHT SUMMARY: The ability to walk easily depends on a flexible ankle joint; intact supporting ligaments; strong Achilles, posterior tibialis, and peroneus tendons; and normal lumbosacral nerve roots. MANEUVER: The patient is asked to walk in the exam room. Symptoms can be enhanced by asking the patient to toe-and-heel walk. INTERPRETATION: This maneuver is used as a screening for the more severe conditions (fractures, third-degree ligament sprains, acute gouty or septic arthritis, and Achilles tendon rupture)

FIGURE 12–1. Observe the patient’s ability to bear weight.

STANCE AND ANKLE ALIGNMENT WHEN STANDING SUMMARY: Ankle alignment depends on a normal joint, intact supporting ligaments, well-toned medial and lateral tendons, and tarsal bones free of degenerative arthritic change. MANEUVER: The patient is asked to stand, placing an equal amount of weight on each side. INTERPRETATION: Pes planus, pes cavus, and pes plano-valgus are readily identified by inspection of the foot and ankle. In addition, anterior joint swelling, dorsal edema, and color changes reflecting vascular insufficiency or reflex sympathetic dystrophy should be readily apparent by simple inspection of the dorsal and anterior aspects of the ankle. FIGURE 12–2. Observe the patient’s stance and ankle alignment when standing.

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FLEXION AND EXTENSION SUMMARY: The range of motion of the main ankle joint can be compromised by joint fluid, synovial thickening, bony osteophytes, bony fracture, an inflexible Achilles tendon, and tight calf muscles. Ankle effusion often is difficult to detect. Moderate to large effusions cause a bandlike swelling, several centimeters wide around the ankle, obliterating the normal bony contours of the malleoli. MANEUVER: The range of motion, stiffness, and crepitation are assessed by passive stretching of the ankle joint in flexion and extension. INTERPRETATION: This maneuver is used primarily to screen the main ankle joint for effusion, arthritis, and associated bony disorders.

FIGURE 12–3. Flexion and extension range of motion testing to assess the main ankle joint.

PASSIVE STRETCHING IN INVERSION AND EVERSION SUMMARY: Ankle inversion and eversion occur at the subtalar joint. Passive stretching assesses the integrity of the joint, its joint capsule, and the medial and lateral collateral ligaments that support the main ankle joint. MANEUVER: Both ankles are passively stretched in inversion and eversion. The mobility, looseness, and sensitivity are compared side to side. INTERPRETATION: Because subtalar arthritis is uncommon outside the setting of rheumatoid arthritis, this maneuver is used to screen the collateral ligaments of the main joint for integrity, looseness, or acute injury.

FIGURE 12–4. Passive stretching in inversion and eversion is used to assess the integrity of the lateral and medial collateral ligaments and the integrity of the subtalar joint.

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PALPATE THE POSTERIOR HEEL SUMMARY: The three main structures of the posterior heel include the Achilles tendon, the preAchilles bursa located above the insertion of the tendon, and the retrocalcaneal bursa located in the space between the Achilles tendon and the posterior aspect of the talus. MANEUVER: The entire length of the Achilles tendon is palpated from the calcaneus to the musculotendinous juncture, several inches above the insertion. The thickness and integrity of the tendon are noted. The pre-Achilles bursa is palpated at the insertion of the calcaneus. The retrocalcaneal bursa is palpated, with pressure directed against the posterior aspect of the talus. FIGURE 12–5. Palpate the posterior heel for Achilles tendonitis, pre-Achilles bursal swelling, thickening for Achilles tendon disruption, retrocalcaneal bursitis, and os trigonum syndrome.

INTERPRETATION: The pre-Achilles bursal swelling and tenderness is located at the superior aspect of the calcaneus. True Achilles tendonitis and rupture occur 3 to 4 cm above the insertion of the tendon on the calcaneus.

PALPATE THE PLANTAR HEEL SUMMARY: The plantar aspect of the ankle consists of the calcaneus, the specialized fat tissue protecting the calcaneus (the heel pad and its overlying thick covering of epidermis), and the arch, consisting of the plantar fascia. The plantar fascia originates from the undersurface of the calcaneus in the midline. MANEUVER: The entire heel is palpated for local tenderness. INTERPRETATION: Bony lesions of the calcaneus and the fat pad syndrome are characterized by diffuse tenderness. By contrast, plantar fasciitis is characterized by focal tenderness at the origin of the arch in the midline or slightly medial to the midline.

FIGURE 12–6. Palpate the plantar heel for local tenderness.

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TINEL SIGN SUMMARY: Pain that is referred to the ankle or foot can arise from compression of the posterior tibial nerve or from the lower lumbar roots. In either case the patient describes a neurogenic type of pain (burning, tingling, or numbness) that is unassociated with local ankle tenderness, impaired mobility, or a loss of ankle range of motion. MANEUVER: The patient is asked to relax the foot. A Tinel tapping sign is performed just posterior to the malleolus.

FIGURE 12–7. Perform a Tinel sign to assess for tarsal tunnel.

ONE-MINUTE SCREENING EXAM: MANAGEMENT OPTIONS TRIAGE TO X-RAY For a patient who has a history of trauma, is at risk for bony injury, or has sustained a typical inversion ankle sprain type of injury: • Order three views of the ankle for patients with a history of inversion injuries, crush injuries, or direct blow to the ankle (fibular, tibial, calcaneal, or talar dome fractures). • Order three views of the ankle for patients with impaired ambulation and a loss of range of motion of the true ankle joint (posttraumatic osteoarthritis, rheumatoid arthritis, or the arthritis accompanying spondyloarthropathy). • Order calcaneal views for patients with recurrent or chronic heel pain unresponsive to initial treatment (a calcaneal stress fracture, large heel spur with plantar fasciitis, or pre-Achilles bursitis with large calcification). • Order anteroposterior and inversion stress views of the ankle in patients with persistent symptoms after injury to the supporting ankle ligaments (instability of the ankle after severe ankle sprain). • Order three views of the foot for patients with persistent lateral ankle pain and pain at the base of the fifth metatarsal (peroneus avulsion fracture complicating ankle sprain). • Order a lateral ankle view for patients with persistent posterior ankle pain and limited plantar flexion (os trigonum syndrome). TRIAGE TO THE LAB For patients with acute pain, exquisite tenderness, inability to bear weight bear, and signs of active inflammation, order a complete blood cell count, uric acid, and erythrocyte sedimentation rate (gout or acute arthritis) and include blood cultures if the acute inflamma-

INTERPRETATION: A positive response reproduces the patient’s pain. Typically the pain or paresthesia is referred down across the bottom of the foot or up the leg (retrograde conducted pain is almost always caused by a compression neuropathy). Pain that is localized just to the area of tapping probably is caused by posterior tibialis tendon irritation or injury.

tory changes are accompanied by significant fever or concurrent signs of infection elsewhere in the body (septic arthritis). CONSIDER A BONE SCAN For patients with persistent but vague, poorly localized, or ill-defined ankle or heel pain (calcaneal stress fracture, reflex sympathetic dystrophy, osteomyelitis, or fracture accompanying severe ankle sprain). CONSIDER MRI For patients with chronic symptoms or severe injuries to the Achilles (tendon rupture or chronic Achilles tendonitis) or patients with recurrent or chronic swelling of the ankle joint after injury (osteochondritis dissecans of the talar dome accompanying severe ankle sprain). RECOMMEND EMPIRICAL TREATMENT For patients with mild to moderate ankle pain and stiffness, unrestricted movement of the joint, normal alignment, and normal gait: • Limit walking, standing, impact, and repetitive movement. • Wear comfortable, high-top shoes with padded insoles or padded insoles with arch supports. • Apply overlap taping of the ankle joint or strapping of the plantar fascia. • Apply ice and elevate the foot four times a day. • Perform gentle daily passive stretching exercises in extension and flexion only. • Recommend an anti-inflammatory medication for 10 to 14 days at full dosage. • Use crutches with touch-down weight bearing for 5 to 7 days (optional).

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DETAILED EXAMINATION: SPECIFIC ANKLE DIAGNOSES ANKLE SPRAIN The degree of local swelling and bruising,

the patient’s ability to bear weight, the presence of bony tenderness

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(the Ottawa criteria), and the mechanism of injury are used to assess the extent of ligament injury. The clinical challenge is to assess whether the ligaments have been simply overstretched, partially torn, or completely ruptured and to determine the risk of accompanying bony fracture.

PASSIVE STRETCHING IN INVERSION SUMMARY: The three lateral ligaments of the ankle are named for their bony attachments: anterior talofibular, calcaneofibular, and posterior talofibular. The anterior talofibular and calcaneofibular ligaments are the most susceptible to injury. There are three grades of ligament injuries: simple sprain (first degree), partially torn (second degree), and completely torn (third degree). MANEUVER: The ankle is passively inverted, and the patient’s pain tolerance, looseness, endpoint stiffness, and guarding are noted. ADDITIONAL SIGNS: Each ligament is palpated for local tenderness. Swelling and bruising over the lateral ankle are noted. Flexion and extension of the ankle are evaluated to assess concomitant ankle injury and effusion. The distal fibula, the inferior malleolus, and the base of fifth metatarsal are palpated for bony tenderness.

FIGURE 12–8. Passive stretching in inversion to assess the degree of ligament injury.

INTERPRETATION: The first-degree ankle sprain is characterized by mild restriction of ankle inversion, mild to moderate tenderness, mild swelling, and minimal bruising. Partial tears are characterized by poor tolerance of weight bearing, moderate tenderness, moderate to severe guarding with inversion, and mild to moderate swelling with bruising. Thirddegree ankle sprains are characterized by intolerance of weight bearing, severe tenderness, inversion guarding, dramatic swelling, and extensive bruising.

LATERAL LIGAMENT TENDERNESS AND SWELLING SUMMARY: The bleeding associated with the partial and complete tears of the lateral ligaments pools below the lateral malleolus. The force of gravity causes the blood to flow down the tissue planes of the ankle and foot to form the classic crescent sign. MANEUVER: The lateral ankle and foot are inspected for bruising. The crescent sign is not painful. All tenderness is located over the lateral ligaments. ADDITIONAL SIGNS:

FIGURE 12–9. Lateral ligament tenderness and swelling suggest higher-grade ligament injury.

See Figure 12–8.

INTERPRETATION: The crescent sign is a nonspecific sign of disrupted tissue. Calf muscle tears, plantaris tendon rupture (at the knee), fracture of the tibia or ankle, or second- and third-degree ankle sprain all cause significant bruising. However, the combination of local tenderness over the lateral ligaments and the crescent signs confirms a partial or complete ligament tear.

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INSTABILITY COMPLICATING ANKLE SPRAIN Ankle instability is the most common complication of ankle sprain. Recurrent ankle sprain is exceedingly common after partial and complete tear of the supporting ligaments. Signs of instability are performed after the acute symptoms of pain, swelling, and im-

paired weight bearing have resolved. The anterior and posterior drawer signs, the passive range of motion of the ankle, and the talar knock signs are performed to assess the degree of ligament laxity and ankle instability.

ANTERIOR DRAWER SIGN SUMMARY: The patient has sustained a second- or third-degree ankle sprain, and the acute symptoms have resolved. The anterior drawer sign assesses the integrity and laxity of the anterior talofibular ligament. MANEUVER: The examiner stabilizes the lower leg by firmly grasping the tibia. With the other hand placed over the tarsal bones, the examiner applies anterior force to the ankle joint. An abnormal response consists of an excessive anterior movement compared with the opposite side. Pain or apprehension that manifests during the maneuver strongly suggests insufficiency of the anterior talofibular ligament.

FIGURE 12–10. The anterior drawer sign to assess instability of the ankle.

ADDITIONAL SIGNS: The posterior drawer sign may be abnormal, suggesting insufficiency of the posterior talofibular ligament. If the interosseous membrane between the tibia and fibula has been disrupted, the talar knock sign will be abnormal (forced inversion and eversion causing the talus to knock into the tibia). If the calcaneofibular ligament has been torn, the affected ankle may have greater degrees of inversion movement. If any of the three lateral ligaments is completely torn, a concavity may remain in its place. INTERPRETATION: Patients with mild ankle instability often comment, “My ankle doesn’t feel right.” Other patients simply describe multiple episodes of recurrent ankle sprain. These patients rarely have abnormal instability signs. Only the severely traumatized ankle demonstrates an unequivocal abnormal drawer sign, indicating either a complete anterior or posterior talofibular ligament rupture.

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STRESS VIEWS OF THE ANKLE SUMMARY: Manually applied inversion and anterior stress placed across the ankle are used to demonstrate the abnormal widening of the tibiotalar joint on plain x-rays of the ankle. CASE: The patient is a 25-year-old avid basketball player who injured his ankle on many separate occasions. He has been unable to play because of the fear and apprehension his ankle “will give out once again.” Examination disclosed a depression over the calcaneofibular ligament and excessive inversion compared with the unaffected ankle. DIAGNOSIS: ligament.

FIGURE 12–11. Stress views of the ankle to confirm ligament instability.

Insufficiency of the calcaneofibular

INTERPRETATION: The lateral ankle joint demonstrated abnormal widening when inversion stress was placed across the joint. A lateral view of the ankle with anterior force placed across the ankle was normal; thus, the anterior talofibular ligament was intact.

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Rheumatoid arthritis is the most common cause of arthritis of the ankle. Osteoarthritis is much less common and occurs almost exclusively as a result of a previous injury (fracture or severe sprain). The diagnosis is

ARTHRITIS OF THE ANKLE

suggested by anterior joint line tenderness, impairment of flexion and extension, and impaired weight bearing. The diagnosis can be confirmed by x-ray, intra-articular anesthetic block, or joint fluid analysis.

ANTERIOR BALLOTTEMENT SUMMARY: Effusion at the ankle must be distinguished from simple edema and the swelling of dorsotenosynovitis. MANEUVER: The examiner places two fingers behind each malleolar process. Forward pressure is exerted on the back of the ankle to force any posterior fluid anteriorly. With thumbs on either side of the extensor tendons, the examiner uses back-andforth compression to feel for excessive fluid accumulation. Normally the bony structure should be easily palpated with the thumbs. A spongy feeling or a sense of fullness is appreciated when excess fluid is present. ADDITIONAL SIGNS: The range of motion in flexion and extension may be impaired with large or extremely inflammatory effusions. Large effusions present with a bandlike swelling extending around the joint, obliterating the bony prominences of the malleolar processes. FIGURE 12–12. The anterior ballottement sign to assess for ankle effusion.

INTERPRETATION: Patients with simple edema and the swelling of dorsotenosynovitis should maintain normal and painless range of motion of the ankle. Patients with dorsotenosynovitis have pain with passive movement of the toes.

INTRA-ARTICULAR ANESTHETIC BLOCK AND ASPIRATION SUMMARY: Enter just medial to extensor hallucis longus (anteromedial approach) or just lateral to extensor digiti minimi (anterolateral approach). Because the lateral synovial cavity extends over a larger area, it is the preferred site of entry. NEEDLE:


DEPTH: 1 to 11⁄4 inch through either the tibionavicular ligament medially or the fibulonavicular ligament laterally. VOLUME:

2 to 3 mL anesthetic, 1⁄2 mL K40, or both.

NOTE: If bone is encountered, withdraw back through the ligament, use skin traction to redirect the needle either toward the midline or inferiorly, and advance again. FIGURE 12–13. Intra-articular anesthetic block with or without aspiration of the joint.

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SUBTALAR ARTHRITIS Arthritis affecting the subtalar joint is uncommon. Rheumatoid arthritis and previous fracture or injury to the talus are the most common causes. X-ray interpretation is difficult. Confirmation of this diagnosis requires local anesthetic block.

PASSIVE INVERSION AND EVERSION SUMMARY: The subtalar joint allows the ankle to invert and evert. Progressive arthritis leads to progressive loss of inversion and eversion. MANEUVER: The examiner stabilizes the lower leg by firmly grasping the tibia. With the opposite hand the examiner passively inverts and everts the ankle and foot while preventing flexion and extension of the main ankle joint. The range of motion is compared side to side. ADDITIONAL SIGNS: Tenderness may be present when firm pressure is applied just under the malleolar processes. INTERPRETATION: In the absence of trauma (acute fracture, ankle sprain, or injury to the supporting peroneus and posterior tibialis tendons), loss of inversion and eversion is attributed to arthritis of the subtalar joint. FIGURE 12–14. Perform passive inversion and eversion to assess the integrity of the subtalar joint.

INTRA-ARTICULAR ANESTHETIC BLOCK SUMMARY: The subtalar joint can be injected from a lateral or medial approach. Laterally, the joint line is located 1 cm below the most inferior point of the lateral malleolus. The injection is placed flush against the talus or calcaneus, adjacent to the joint line. NEEDLE: DEPTH:


5

⁄8 to 1⁄2 inch.

3

VOLUME:

1 to 2 mL anesthetic, 1⁄2 mL D80, or both.

NOTE: Because the peroneus tendon follows a course very close to the lateral malleolus, the point of entry should err more toward the heel than the malleolus. To ensure the safest possible injection, the bevel of the needle should be kept parallel to the fibers of the tendon.

FIGURE 12–15. Intra-articular anesthetic block to confirm subtalar arthritis.

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ACHILLES TENDONITIS AND RUPTURE Achilles tendonitis is characterized by tenderness, swelling, and thickening at the musculotendinous junction, located 2 to 3 inches above the insertion of the tendon on the calcaneus. The pain is characteristi-

cally reproduced by passively performed dorsiflexion and actively resisted plantarflexion. Complete tendon rupture is characterized by a loss of active plantarflexion, a palpable defect 2 to 3 inches above the calcaneal insertion, and varying degrees of bruising.

ACHILLES TENDON SUMMARY: The Achilles tendon is susceptible to injury, irritation, inflammation, and tendon rupture. Risk factors include tight, inflexible calf muscles, plantar fasciitis, sports involving repetitive jumping, an improperly placed corticosteroid injection, and the rare case of chronic fluoroquinolone exposure. MANEUVER: The Achilles tendon is palpated for tenderness, swelling, thickening, or disruption along its length from the calcaneus to the musculotendinous juncture. ADDITIONAL SIGNS: The pain of active tendonitis can be reproduced by passively dorsiflexing the ankle, stretching the tendon, or by isometrically resisting plantarflexion. Patients with true tendon rupture cannot actively plantarflex the ankle. If tendon rupture has occurred, a defect in the tendon is palpable at that site.

FIGURE 12–16. Palpate the Achilles tendon for swelling, thickening, or disruption.

INTERPRETATION: Acute Achilles tendonitis is characterized by localized swelling, exquisite tenderness, and mild thickening. Chronic Achilles tendonitis is characterized by minimal tenderness and thickening. Tendon rupture usually follows a traumatic injury, followed by immediate inability to plantarflex the ankle and the palpable defect in the tendon.

MRI SUMMARY: All cases of Achilles tendonitis are characterized pathologically by microtearing of the tendon with secondary inflammation. With further injury the weakened tendon can proceed to complete tear. CASE: This 35-year-old weekend baseball player had a violent slide into second base. All of his body weight struck the base with his leg in the extended position. Symptoms waxed and waned over the next several weeks, with progressive posterior heel pain and tendon swelling. On exam the tendon was 21⁄2 times normal width. CASE: Acute Achilles tendonitis with mucinoid degenerative swelling in the center of the tendon. INTERPRETATION: MRI is the test of choice to distinguish Achilles tendonitis from partial tears and complete rupture. FIGURE 12–17. MRI to assess Achilles tendon inflammation, partial tear, or complete tendon rupture.

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PRE-ACHILLES BURSITIS Pre-Achilles bursitis (the “pump bump”) is an inflammation of the bursal sac located at the Achilles tendon insertion on the calcaneus. It develops as a reaction to the pressure and friction created by tight-fitting shoes. The diagnosis is based on the specific site of local tenderness and

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swelling over the calcaneus and confirmed by local anesthetic block. Anesthetic is injected in the subcutaneous tissue, 1/4 inch below the skin, centered over the calcaneus, and just above the fibers of the Achilles tendon.

PALPATE THE PRE-ACHILLES BURSA SUMMARY: The pre-Achilles bursa provides lubrication between the skin and the insertion of the Achilles tendon. It is a pressure-sensitive sac aggravated by tight-fitting shoes and repetitive flexion and extension of the ankle. MANEUVER: The quarter-sized bursa is located in the midline directly over the center of the attachment of the Achilles tendon to the superior calcaneus. Tenderness, swelling, and thickening are noted. ADDITIONAL SIGNS: The bursa should be soft and compressible unless chronic thickening or calcification has developed. Haglund’s deformity is a large calcification arising from the superior calcaneus.

FIGURE 12–18. Palpate the pre-Achilles bursa for swelling and bony thickening.

INTERPRETATION: Pre-Achilles bursitis often is confused with Achilles tendonitis. The two conditions are not related. Bursal inflammation always occurs at the insertion of the tendon, whereas true Achilles tendonitis occurs several centimeters above the insertion.

LOCAL ANESTHETIC BLOCK SUMMARY: A presumptive diagnosis of pre-Achilles bursitis can be made based solely on the typical swelling and tenderness located directly over the superior calcaneus. Local anesthetic block may be necessary in the uncommon event that bursitis occurs concomitantly with Achilles tendonitis. Enter over the posterior–superior aspect of the calcaneus, directly in the midline. NEEDLE: DEPTH:


5

⁄4 to 3⁄8 inch.

1

VOLUME: both.

⁄2 to 1 mL anesthetic, 1⁄2 mL D80, or

1

NOTE: The injection should be superficial to the tendon; high pressure during injection suggests an intratendinous position.

FIGURE 12–19. Local anesthetic block to confirm preAchilles bursitis.

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RETROCALCANEAL BURSITIS Retrocalcaneal bursitis is an

uncommon problem. Patients complain of posterior ankle pain and swelling located between the Achilles tendon and the posterior of the talus. The normal concavity behind the ankle is filled in

with soft tissue swelling. The diagnosis is suggested by these subjective changes and confirmed with local anesthetic placed just posterior to the talus.

LOCAL TENDERNESS OF THE RETROCALCANEAL SPACE SUMMARY: The retrocalcaneal bursa is located in the soft tissue space between the Achilles tendon and the posterior aspect of the ankle. Its function is to lubricate the posterior ankle structures in extreme plantarflexion. MANEUVER: The posterior aspect of the ankle is inspected for swelling and compared with the opposite side. Local tenderness is palpated using two fingers compressing the soft tissues in the space between the Achilles tendon and the talus. ADDITIONAL SIGNS: The patient’s pain should be reproduced by passive plantarflexion of the ankle, compressing the bursa between the Achilles tendon, the calcaneus, and the talus. INTERPRETATION: Simple edema should not be painful to direct palpation of the compressive effects of forced plantarflexion. Swelling large enough to fill in the bony contours of the posterior ankle should be present anteriorly and reduce the overall range of motion of the ankle. FIGURE 12–20. Local tenderness of the retrocalcaneal space detected by manual compression of the soft tissue between the posterior ankle and the Achilles tendon.

LOCAL ANESTHETIC BLOCK SUMMARY: Local anesthetic block is used to distinguish the local bursal irritation from simple edema, the swelling that accompanies ankle arthritis, and the pain caused by os trigonum syndrome. The safest point of entry is on the lateral side of the Achilles tendon, 1 inch above the calcaneus. This avoids the neurovascular bundle containing the posterior tibialis artery, vein, and nerve. NEEDLE:


DEPTH: 3⁄4 to 1 inch (1⁄2 inch posterior to the tibia and talus). VOLUME:

⁄2 mL anesthetic, 1⁄2 mL D80, or both.

1

NOTE: Place the medication adjacent to the talus rather than the Achilles tendon.

FIGURE 12–21. Local anesthetic block is used to confirm retrocalcaneal bursitis.

ANKLE

OS TRIGONOM SYNDROME Os trigonum syndrome is an uncommon problem. The patient describes posterior ankle pain that is aggravated by movement of the big toe. The diagnosis de-

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pends on x-ray confirmation of a well-circumscribed accessory bone at the junction of the flexor hallucis longus tendon and the posterior aspect of the talus.

OS TRIGONUM TENDERNESS SUMMARY: Os trigonum syndrome consists of the mechanical sequelae of the presence of the accessory bone located just posterior to the talus. The bone is in intimate contact with the flexor hallucis longus tendon. Tenosynography of the flexor hallucis tendon shows a constriction of the sheath at the level of the accessory bone. MANEUVER: Tenderness is elicited by placing firm pressure in the space between the Achilles tendon and the posterior aspect of the talus. The pressure is directed against the talus. ADDITIONAL SIGNS: Resisting flexion of the great toe should reproduce the posterior ankle pain. Full plantarflexion may be impaired with the larger accessory bones. Otherwise the range of motion of the ankle usually is well maintained. INTERPRETATION: The symptoms of os trigonum syndrome overlap with those of retrocalcaneal bursitis. The tenderness is in the same exact location. However, bursitis typically has a greater degree of soft tissue swelling. A lateral x-ray view of the ankle will readily distinguish the two conditions. FIGURE 12–22. Os trigonum tenderness over the posterior aspect of the talus in the midline.

LATERAL X-RAY VIEW OF THE ANKLE SUMMARY: Patients with a history of trauma to the ankle, especially in severe plantarflexion, should undergo plain x-rays or CT scanning to rule out fracture of the posterior process of the talus. The os trigonum syndrome cannot be made until fracture has been excluded by radiography. CASE:

Os trigonum syndrome.

INTERPRETATION: Fracture of the talus is characterized by ill-defined and irregular bony borders. On the other hand, the os trigonum bone should be spherical with well-demarcated borders. The definitive treatment for os trigonum syndrome is resection of the accessory bone.

FIGURE 12–23. Lateral x-ray view of the ankle readily identifies the accessory bone.

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PLANTAR FASCIITIS The diagnosis of plantar fasciitis, an inflammation of the longitudinal or “arch” ligament of the foot, requires midline tenderness localized to a dime-sized area at the calcaneal attachment. Severe cases are characterized by calcaneal

bony irritation (compression of the calcaneus from side to side) and pain aggravated by forced ankle dorsiflexion. Gastrocnemius muscle tightness, pes planus, pes cavus, ankle pronation, and obesity are predisposing factors.

PLANTAR FASCIA SUMMARY: The plantar fascia originates from the calcaneus and forms the arch of the foot. The fibers fan out to attach to four of the metatarsals. MANEUVER: The patient lies prone on the exam table. The origin of the plantar fascia is palpated at the base of the arch in the midline. If tenderness is not obtained directly in the midline, the examiner palpates the medial side of the origin. ADDITIONAL SIGNS: Side-to-side compression of the calcaneus is painful in moderate to severe cases. Severe cases may be aggravated by forced dorsiflexion of the ankle, stretching the fascia. Uncommonly, pressure over the origin can cause swelling along the medial aspect of the heel. Sideto-side compression of the fat pad is not painful. FIGURE 12–24. Palpate the origin of the plantar fascia for local tenderness.

INTERPRETATION: Plantar fasciitis has a characteristic focal tenderness. Diffuse heel tenderness is most often caused by heel pad syndrome. Patients with calcaneal stress fractures or Sever’s epiphysitis have focal plantar surface tenderness. However, these patients characteristically have greater bony pain with side-to-side compression than direct tenderness from palpation.

LOCAL ANESTHETIC BLOCK SUMMARY: When plantar fascial signs accompany possible stress fracture of the calcaneus or signs of the fat pad syndrome, local anesthetic block is used to distinguish the three conditions. The needle is passed through the plantar surface in the midline, approximately 3⁄4 inch distal to the origin of the plantar fascia. NEEDLE: DEPTH:

11⁄2 inch, 22 gauge. 1 to 11⁄2 inch.

VOLUME:

1 to 2 mL anesthetic, 1 mL D80, or both.

NOTE: The injection must be at a depth greater than 1 inch to avoid injecting steroid in the specialized fat of the heel pad.

FIGURE 12–25. Local anesthetic block to confirm plantar fasciitis.

ANKLE

HEEL PAD SYNDROME Patients with heel pad syndrome, a trauma-induced irritation of the specialized fat of the heel, present with symptoms identical to those of plantar fasciitis. However, the exam of the heel is distinctively different. The entire heel is tender

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to palpation. The pain is readily reproduced by side-to sidecompression of the fat pad. Side-to-side compression of the calcaneus is not painful; the bone is unaffected.

COMPRESSION OF THE CALCANEAL HEEL PAD SUMMARY: The calcaneus is protected by specialized fat that is compartmentalized by thick fascial tissue. Traumatic injuries can break down the normal fascial septa, leading to a diffuse pain and tenderness over the entire heel. This injury often is called the stone bruise of the heel. Simple protection with a padded insole or heel cup should resolve the irritation within 2 to 3 weeks. MANEUVER: The heel pad is compressed from side to side, recreating the patient’s pain. ADDITIONAL SIGNS: The entire heel is tender. Compression of the calcaneus does not elicit pain. The origin of the plantar fascia is no more tender than the rest of the heel. FIGURE 12–26. Compression of the calcaneal heel pad for tenderness.

INTERPRETATION: The combination of diffuse heel tenderness and pain reproduced by side-to-side compression of the heel pad confirms the diagnosis.

HEEL PAD SYNDROME SUMMARY: Simple padding used continuously over 2 weeks should resolve an uncomplicated case of heel pad syndrome. Calcaneal stress fracture and plantar fasciitis rarely resolve in this short time period. CASE: The patient stumbled while walking down a flight of stairs. The patient missed the last step and came down hard on the right heel. The heel was diffusely tender. The pain was reproduced by sideto-side compression of the heel pad. Within 2 weeks the condition resolved with heel pads. DIAGNOSIS:

FIGURE 12–27. The diagnosis of heel pad syndrome is made when symptoms improve after 2 weeks with simple padding.

Heel pad syndrome.

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CALCANEAL STRESS FRACTURE Microfracturing of the

posterior aspect of the calcaneus is an uncommon condition, seen almost exclusively in long-distance runners or patients with severe osteopenia. The diagnosis should be suspected whenever the side-to-

side compression of the calcaneus elicits a greater degree of pain than direct palpation of the heel, just the opposite of the findings of plantar fasciitis. The diagnosis is confirmed by bone scanning.

CALCANEAL COMPRESSION SUMMARY: Calcaneal stress fractures are uncommon. Tibial and metatarsal stress fractures are much more common. However, when athletes (runners especially) present with diffuse pain and tenderness over the heel and the diagnosis of plantar fasciitis is not likely, evaluation for calcaneal stress fracture should be considered. MANEUVER: The hands are cupped over the sides of the calcaneus bone. With the fingers locked in place, the sides of the calcaneus are compressed between the heels of the palms. Bony lesions, fractures, and stress fractures typically are more sensitive to compression than simple palpation of the plantar aspect of the heel. ADDITIONAL SIGNS: The bottom of the heel usually is diffusely tender. The origin of the plantar fascia is no more sensitive than the rest of the heel. Squeezing the fat pad from side to side typically does not elicit pain. FIGURE 12–28. Perform a calcaneal compression sign to assess the integrity of the calcaneus.

INTERPRETATION: In the absence of direct trauma to the heel, focal compression tenderness over the calcaneus strongly indicates a stress fracture.

SERIAL X-RAYS OR NUCLEAR BONE SCAN SUMMARY: The proximal third of the body of the calcaneus is most susceptible to the repeated trauma of running and jumping. Stress fractures can occur in the nonathlete with severe osteopenia. CASE: This 54-year-old woman with chronic renal failure on dialysis developed bilateral heel pain that progressed over several weeks. Initial x-rays were normal. Her exam demonstrated pain when the calcaneus was compressed from side to side. The patient had secondary hyperparathyroidism. DIAGNOSIS: Calcaneal stress fracture. Repeat x-rays demonstrated a band of sclerotic bone over the proximal third of the calcaneus. The entire calcaneus was active on nuclear bone scan.

FIGURE 12–29. Serial x-rays or nuclear bone scan to confirm calcaneal stress fracture.

INTERPRETATION: Initial plain x-rays are notoriously inaccurate in the first 2 to 3 weeks. The diagnosis can be confirmed by the demonstration of the typical sclerotic bone (osteoblastic activity of a healing fracture) on serial ankle x-rays. Nuclear bone scanning has the advantage of confirming the diagnosis in the first few weeks.

ANKLE

POSTERIOR TIBIAL TENOSYNOVITIS The posterior tibial tendon is susceptible to friction as it passes under the medial malleolus bone. Inflammation of this tendon and its overlying sheath is suggested by a history of medial ankle pain and an exam demon-

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strating medial ankle tenderness that is reproduced by resisted inversion and plantarflexion. However, a definitive diagnosis requires local anesthetic block placed along the tendon, just inferior to the tip of the medial malleolus.

ISOMETRIC RESISTANCE OF INVERSION SUMMARY: The posterior tibialis tendon is located just under the medial malleolus of the ankle and attaches distally to the navicular, talus, three cuneiforms, and three middle metatarsals. Contraction of the muscle causes the ankle to plantarflex, adducts and inverts the foot, and supports the arch. MANEUVER: The patient is asked to maintain the ankle in neutral position, avoiding stretching the supporting ligaments and joint capsule during the maneuver. Then the patient is asked to invert the foot against the resistance of the examiner’s hand. The patient’s pain at the malleolus should be reproduced by the maneuver. ADDITIONAL SIGNS: Isometric resistance of plantarflexion may be equally painful. Maximum tenderness is present over the tenosynovial sheath located just below the malleolus. Range of motion of the ankle should be normal.

FIGURE 12–30. Isometric resistance of inversion to assess posterior tibial tenosynovitis.

INTERPRETATION: The local tenderness of medial collateral ligament injuries, bony lesions of the talus, and tibial bony fractures overlaps with the local tenderness of posterior tibialis tenosynovitis. However, only the tenosynovitis is aggravated by isometric testing of the tendon in inversion and plantarflexion.

LOCAL ANESTHETIC BLOCK SUMMARY: Enter just below the posterior edge of medial malleolus. The layers down to the posterior tibialis tendon include skin, subcutaneous fat, retinacular fascia, tenosynovial sheath, tendon, and talus bone. NEEDLE: DEPTH:


5

⁄8 to 1⁄2 inch.

3

VOLUME:


NOTE: Keep the bevel of the needle parallel to the tendon, allowing the fibers to separate and avoiding cutting through the fibers. Use the least amount of anesthetic in the superficial layers, injecting just enough anesthetic for comfort. Inject the majority of the anesthetic at the level of the tendon or talus in order to maximize the local anesthetic block. FIGURE 12–31. Local anesthetic block is needed to confirm the diagnosis of posterior tibialis tendonitis.

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Peroneus tenosynovitis, an inflammation of the tendon as it passes under the lateral malleolus bone, is an uncommon complication of ankle sprain. The diagnosis is suggested by persistent lateral ankle tenderness that is consis-

PERONEUS TENOSYNOVITIS

tently aggravated by isometrically resisted eversion and plantarflexion. Because the symptoms and signs closely mimic those of ankle sprain, the diagnosis requires local anesthetic block placed just inferior to the tip of the lateral malleolus.

ISOMETRIC RESISTANCE OF EVERSION SUMMARY: The peroneus tendons evert the foot and plantarflex the ankle. The peroneus tertius and brevis tendons attach to the base of the fifth metatarsal. The peroneus longus attaches to the first cuneiform and the first metatarsal. MANEUVER: The patient is asked to maintain the ankle in neutral position, avoiding stretching the supporting ligaments and joint capsule during the maneuver. Then the patient is asked to evert the foot against the resistance of the examiner’s hand. The patient’s pain at the malleolus should be reproduced by the maneuver. ADDITIONAL SIGNS: Isometric resistance of plantarflexion may be equally painful. Maximum tenderness is present over the tenosynovial sheath located just below the malleolus. Range of motion of the ankle should be normal.

FIGURE 12–32. Isometric resistance of eversion to assess for peroneus tenosynovitis.

INTERPRETATION: The local tenderness of lateral ligament injuries, bony lesions of the talus, and fibular bony fractures overlaps with the local tenderness of peroneus tenosynovitis. However, only the tenosynovitis is aggravated by isometric testing of the tendon.

LOCAL ANESTHETIC BLOCK SUMMARY: Enter just below the posterior edge of lateral malleolus. The layers down to the peroneus tendon include skin, subcutaneous fat, retinacular fascia, tenosynovial sheath, tendon, and talus bone. NEEDLE: DEPTH:


5

⁄8 to 1⁄2 inch.

3

VOLUME:


NOTE: Keep the bevel of the needle parallel to the tendon to avoid cutting the fibers of the tendon. Use the least amount of anesthetic in the superficial layers, injecting just enough anesthesia for comfort. Inject the majority of the anesthetic at the level of the tendon or talus in order to maximize the local anesthetic block.

FIGURE 12–33. Local anesthetic block to confirm peroneus tenosynovitis.

ANKLE

TARSAL TUNNEL SYNDROME Tarsal tunnel syndrome is a compression neuropathy of the posterior tibial nerve. The diagnosis is strongly suggested if the patient’s electric-like pain, either up the leg or into the plantar aspect of the foot, is reproduced by the

243

Tinel sign, tapping just under the medial malleolus bone. Severe ankle pronation, previous ankle fracture, and severe ankle synovitis from inflammatory arthritis are predisposing factors.

TINEL SIGN SUMMARY: The posterior tibial nerve courses around the medial malleolus, branches to form the medial and lateral plantar nerves, and provides sensation to the plantar surface of the foot. MANEUVER: The medial malleolus is identified and the inferior point is marked. Using the index finger, vigorous tapping is performed just under the medial malleolus. ADDITIONAL SIGNS: Because tarsal tunnel syndrome results from severe pronation, previous ankle fracture, or advanced arthritis of the ankle, the exam is completed with evaluation of stance, range of motion of the ankle joint, and radiographic studies to assess the integrity of the underlying tarsal bones. FIGURE 12–34. A positive Tinel sign reproducing the patient’s pain strongly suggests tarsal tunnel.

INTERPRETATION: The Tinel sign is considered positive if the patient’s plantar symptoms or pain traveling in a retrograde direction up the leg are reproduced. Tenderness and pain localized to the area around the medial malleolus arise from the posterior tibial tendon or the underlying tarsal bones.

NERVE CONDUCTION VELOCITY TESTING SUMMARY: The manifestation of tarsal tunnel syndrome includes paresthesia and hypesthesia on the plantar surface of the foot or pain that travels in a retrograde direction up the leg. Weakness of the intrinsic muscles of the foot is rarely affected. The definitive diagnosis depends on demonstration of nerve transmission slowing across the ankle by electrophysiologic testing.

FIGURE 12–35. Nerve conduction velocity testing for tarsal tunnel syndrome.

12–1


EXAMINATION SIGNS

DIAGNOSIS


Severe pain with ankle passive inversion

#1: Severe ankle sprain, fibular fracture, interosseous membrane disruption, osteochondritis dissecans

Examination, ankle series x-ray

Instability of the ankle

Examination, stress views of the ankle

Ankle arthritis, hemarthrosis, osteochondritis dissecans

Aspiration of the cell count, differential, crystals, Gram stain, culture, and ankle series x-ray

Subtalar arthritis

Intra-articular anesthetic block

Achilles tendonitis

Examination, MRI of the ankle (optional)

Achilles tendon rupture

MRI of the ankle (optional)

Tender and swollen Achilles tendon insertion on the calcaneus

Pre-Achilles bursitis

Anesthetic block in the bursa

Retrocalcaneal swelling and local tenderness

Retrocalcaneal bursitis

Anesthetic block placed just posterior to the talus

Os trigonum syndrome

Lateral x-ray of the ankle

Plantar fasciitis

Anesthetic block placed at the origin

Heel pad syndrome

Examination, resolution in 2 weeks with simple padding with heel cups

Calcaneal stress fracture

Bone scan or serial x-rays of the ankle

Posterior tibialis tendonitis

Anesthetic block in the tenosynovial sheath

Peroneus tendonitis

Anesthetic block in the tenosynovial sheath

Tarsal tunnel syndrome


Local tenderness over the affected ligament Dramatic swelling over the lateral ankle Inability to bear weight or walk naturally Exaggerated movement ⫹Anterior or posterior drawer sign ⫹Talar knock sign Inability to heel or toe walk Pain, swelling, and decreased range of motion of the tibiotalar joint Anterior joint line tenderness Decreased flexion and extension Inability to bear weight or walk naturally Pain, swelling, and decreased range of motion of the subtalar joint Decreased inversion and eversion Tenderness below the medial and lateral malleoli Tender and enlarged Achilles tendon 2 inches above the calcaneal insertion Pain aggravated by resisted plantarflexion Pain aggravated by passive dorsiflexion Tender Achilles tendon and a defect 2 inches above the calcaneal insertion Total loss of plantarflexion Pain aggravated by passive dorsiflexion

Pain aggravated by passive plantarflexion compressing the bursa Retrocalcaneal local tenderness Pain aggravated by passive extension of the big toe Pain aggravated by isometric flexion of the big toe Tenderness at the origin of the plantar fascia Mild pain with calcaneal compression applied medially to laterally Mild pain with forced dorsiflexion of the foot Tenderness over the entire plantar heel Pain aggravated by compression of the fat pad Severe pain with compression of the calcaneus History of running or heavy exercise Medial ankle pain aggravated by resisted inversion Tenderness and swelling just inferior to the medial malleolus Pain aggravated by passive eversion Lateral ankle pain aggravated by resisted eversion Tenderness and swelling just inferior to the lateral malleolus Pain aggravated by passive inversion ⫹Tinel sign over the medial ankle Subjective numbness over the plantar aspect of the foot

ANKLE

COMMON ANKLE FRACTURES

SUMMARY

Fractures of the ankle probably are the most difficult of all fractures to manage, in part because of the complexity of the ankle joint but also because of the variety of fractures that can occur. Various combinations of injuries to ligaments, the interosseous membrane, and surrounding bone are possible. Classification is based on the injury pattern, the affected bones and ligaments, the degree of fragment

displacement, and the degree of incongruity of the articular surface. The Henderson system identifies malleolar, bimalleolar, and trimalleolar fractures. Lauge–Hansen classifies according to injury forces; and the supination–adduction injury pattern corresponds to the classic turned-in ankle sprain. Danis–Weber classifies the fractures according to the location of the fibular fracture relative to the syndesmosis, which correlates well with fracture instability.

ANKLE FRACTURE ALIGNMENT SUMMARY: The primary care physician’s goal is to accurately diagnose the extent of the injury by assessing the severity of the injury, the radiographic abnormalities, and the stability of the fracture and joint. The posteroanterior, lateral, and mortise x-rays are used to define the number and locations of the fractures. Measurements of the tibiofibular line, talocrural angle, talar tilt, and medial clear space from these views are used to determine fracture stability and displacement. Angle measurements on stress views of the ankle are used to determine ligamentous injuries. CT scans are used to define complex fracture patterns.

FIGURE 12–36. Ankle fracture alignment and stability are measured using the mortise view.

FIBULAR AVULSION FRACTURE SUMMARY: Severe inversion injuries of the ankle can cause the avulsion of a fleck of bone from the most distal portion of the fibula. The calcaneofibular ligament detaches a small portion of cortex when the ankle is turned in. IMMOBILIZATION: A short leg walking cast is the treatment of choice. Immobilization should be continued for 3 to 4 weeks to allow the ligament to reattach securely to the fibula. SURGICAL REFERRAL:

Unnecessary.

PROGNOSIS: Excellent unless accompanied by a chondral fracture, incomplete healing of the lateral ligaments, osteochondritis dissecans, or peroneus tendon injury.

FIGURE 12–37. Fibular avulsion fracture associated with severe ankle sprains.

245

246


NONDISPLACED FIBULAR FRACTURE SUMMARY: Nondisplaced single malleolar fractures and stable bimalleolar fractures can be treated nonoperatively. IMMOBILIZATION: Initially, a Jones compression dressing with plaster splint reinforcement is used until swelling begins to resolve. Subsequently, a short leg walking cast, fracture brace, or walking boot is prescribed. Weight bearing is limited until fracture healing is documented. SURGICAL REFERRAL: necessary.

Surgical intervention is not

PROGNOSIS: Excellent unless accompanied by a chondral fracture, incomplete healing of the lateral ligaments, osteochondritis dissecans, or peroneus tendon injury. FIGURE 12–38. Nondisplaced fibular fracture treated with a short leg walking cast.

DISPLACED FIBULAR FRACTURE SUMMARY: Most fractures at the syndesmosis, all fractures above the syndesmosis, and fractures with significant displacement (radiographically, by line measurement or stress views) should be referred to the fracture specialist. Note the abnormal widening of the talofibular space. IMMOBILIZATION: Initially, the patient is placed in a Jones dressing, given crutches, and instructed to avoid weight bearing. SURGICAL REFERRAL: Surgical referral is necessary for definitive open reduction and internal fixation. PROGNOSIS: The prognosis depends on the degree of reduction, the age of the patient, and the underlying associated injuries to the ligaments, tendons, and articular cartilage.

FIGURE 12–39. Displaced fibular fracture warrants surgical referral.

ANKLE

247

DISPLACED TIBIAL FRACTURE SUMMARY: This displaced tibial malleolar fracture is unstable and has a unacceptable risk of posttraumatic osteoarthritis of the ankle. Note the abnormal widening of the tibiotalar space and the widening of the syndesmosis (interosseous membrane disruption). IMMOBILIZATION: The patient should be placed in a Jones dressing, given crutches, and instructed to avoid weight bearing until seen by the fracture specialist. SURGICAL REFERRAL: Surgical referral is necessary for definitive open reduction and internal fixation. PROGNOSIS: The prognosis depends on the degree of reduction, the age of the patient, and the underlying associated injuries to the ligaments, tendons, and articular cartilage.

FIGURE 12–40. Displaced tibial fracture warrants surgical referral.

FRACTURE OF THE TALUS SUMMARY: Inversion injury with extreme equinus or extreme dorsiflexion positioning can cause a injury to the talus, including fracture of the lateral process of the talus, fracture of the posterior process of the talus, and osteochondritis dissecans (depicted here). The fracture of the posterior process must be distinguished from the os trigonum, an accessory bone that is located posterior to the talus. A mortis view or posteroanterior tomograms usually are necessary to demonstrate the fracture line. IMMOBILIZATION: Small and minimally displaced fragments can be treated with a compressive dressing or a short leg walking cast for 4 to 6 weeks. SURGICAL REFERRAL: If the fragments are large, surgical referral for internal fixation is needed. PROGNOSIS: These injuries carry a significant risk of posttraumatic arthritis. FIGURE 12–41. Fracture of the talus accompanying severe ankle sprain.

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AVULSION FRACTURE OF THE BASE OF THE FIFTH METATARSAL SUMMARY: Inversion injury with rotation can cause excessive pressure on the peroneus brevis tendon and result in an avulsion fracture of the base of the fifth metatarsal. IMMOBILIZATION: Small and minimally displaced fragments can be treated with a short leg walking cast for 4 to 6 weeks. SURGICAL REFERRAL: unnecessary.

Surgical referral is

PROGNOSIS: The prognosis is excellent unless the fracture is accompanied by a chondral fracture, incomplete healing of the lateral ligaments, or osteochondritis dissecans.

FIGURE 12–42. Avulsion fracture of the base of the fifth metatarsal.

CALCANEAL FRACTURES SUMMARY: The calcaneus is the tarsal bone that is most commonly fractured. Most fractures result from vertical falls and twisting injuries. Fractures are classified as extra-articular or intra-articular. Extra-articular fractures are further subdivided into anterior, tuberosity, medial process, sustentacular, and body fractures (depicted here). Radiographically, posteroanterior, lateral, axial-calcaneal, and oblique views are combined with CT scans to define the location and intraarticular extension of the fragments.

FIGURE 12–43. Calcaneal fractures, extra-articular and intraarticular.

IMMOBILIZATION: Most extra-articular fractures can be treated nonoperatively. Initially, Jones compression dressing is applied for 2 to 3 days and combined with 5 to 6 days of strict bed rest with leg elevation. If pain and swelling have been controlled, a short leg walking cast is applied. Ambulation is restricted to non–weight-bearing crutches until union is definitely seen on repeat x-rays (typically several weeks). Subsequently, weight bearing is increased through partial to full weight bearing, as tolerated. SURGICAL REFERRAL: Surgical referral is indicated for nonunion of the anterior process fracture, for displaced posterior process fractures (to restore the integrity of the Achilles tendon), and for all intraarticular fractures. PROGNOSIS: Intra-articular fractures heal unpredictably. The clinician must apprise the patient of the potential of long-term complications, including subtalar joint pain, subtalar posttraumatic arthritis, peroneus tendinitis, bone spur formation, calcaneocuboid osteoarthritis, or entrapment of the medial and lateral plantar nerves.

ANKLE

249

FRACTURES OF THE TALUS SUMMARY: The incidence of talus fractures is second only to that of calcaneal fractures. Classically, these are the result of hyperdorsiflexion injuries (e.g., from hitting the brakes). Fractures are classified as chips, avulsions, or nondisplaced or displaced neck fractures. IMMOBILIZATION: Nondisplaced fractures respond to 8 to 12 weeks of immobilization with a short leg walking cast in a slightly equinus position for the first month, followed by 1 to 2 months in the neutral position. As soon as union is documented on repeat x-rays, range of motion exercises can be started. SURGICAL REFERRAL: Surgical referral is advisable for the displaced neck fracture (depicted here), which is often accompanied by subtalar joint dislocation, because a favorable outcome demands a perfect reduction of the articular cartilage. PROGNOSIS: Unfortunately, despite perfect reduction, healing can be complicated by avascular necrosis of the body in as many as 50% of cases.

FIGURE 12–44. Fractures of the talus.

CLINICAL PEARLS • A patient with a first-degree ankle sprain that does not heal within 3 weeks or a second- or third-degree sprain that does not heal within 6 weeks should be evaluated for potential ankle sprain complications including instability due to poor healing, avulsion of the peroneus tendon, avulsion of the calcaneofibular ligament, interosseous membrane rupture, talar dome osteochondritis dissecans, or chondral fracture of the talus with associated ankle effusion. • The anterior talofibular ligament is most commonly injured by the inversion injuries that occur with running.

• Because of the nearly identical pain pattern and location, os trigonum syndrome often is confused with fracture of the posterior process of the talus and retrocalcaneal bursitis. A history of injury is seen with the talar fracture. Pain reproduced by resisted flexion of the great toe is seen exclusively with os trigonum syndrome. Plain x-rays are normal, and movement of the great toe is painless with retrocalcaneal bursitis. • Pre-Achilles bursitis is a separate condition from true Achilles tendonitis. Bursal tenderness is located at the upper portion of the calcaneus. True Achilles tendonitis occurs several centimeters above the calcaneus.

CHAPTER 13: FOOT DIFFERENTIAL DIAGNOSIS Diagnoses

Confirmations

1st metatarsophalangeal (MTP) joint Osteoarthritis Hallux valgus (bunion) Hallux rigidus Prebunion bursa Gout (podagra) Sesamoiditis Turf toe

X-ray: foot series X-ray: foot series Local anesthetic block Synovial fluid analysis X-ray: sesamoid view Examination

Bunionette of the 5th MTP joint

Examination; x-ray: foot series

Metatarsalgia Tight extensor tendons or hammer toe deformity (most common) Corns and calluses Morton’s neuroma Rheumatoid arthritis Plantar warts

Swelling over the dorsum of the foot Dorsal tenosynovitis Dorsal bunion Stress fracture of the metatarsals Reflex sympathetic dystrophy Cellulitis Anatomy: pes planus and pes cavus

Referred pain Lumbosacral spine radiculopathy Tarsal tunnel syndrome

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Examination Examination Local anesthetic block Examination, rheumatoid factor Examination

Examination X-ray: foot series X-ray, bone scanning Bone scanning Examination, complete blood cell count Examination

Computed tomography scan, magnetic resonance imaging, electromyography Nerve conduction velocity testing

FOOT

INTRODUCTION The nontraumatic conditions affecting the feet can be divided into three distinct anatomic areas based on the affect on ambulation, the location of pain, and the degree of swelling and inflammation: the metatarsophalangeal (MTP) joint area of the ball of the foot, the metatarsal area of the dorsum of the foot, and the longitudinal ligament and plantar aponeurosis of the arch. For each area, unique maneuvers for examination and specific testing are needed to confirm the diagnosis. Conditions affecting the MTP joint area are most common. The pressure exerted over the ball of the foot, the greater degree of motion, and the adverse consequences of ill-fitting shoes cause MTP joint wear (osteoarthritic changes), gradual loss of normal alignment, and secondary inflammatory reactions. The first MTP joint, the great toe, has the greatest susceptibility. Hallux valgus, hallux rigidus, prebunion bursitis, gout, turf toe, and sesamoiditis affect the first MTP joint. The bunionette deformity affects the fifth MTP joint. Hammer toes and Morton’s neuroma affect the minor MTP joints. Combined, these conditions dominate the differential diagnosis of foot pain. Conditions affecting the dorsum are less common and include simple edema, cellulitis, dorsotenosynovitis, reflex sympathetic dystrophy (RSD), and the swelling that accompanies metatarsal stress fracture. All of these diagnoses are characterized by varying degrees of pain and diffuse swelling over the dorsum of the foot. Conditions affecting the arch, pes cavus, pes planus, and pes planovalgus are common but rarely are the primary cause of foot pain. The variations in the configuration of the tarsals, metatarsals, and longitudinal ligament more often play a secondary role, potentially aggravating the primary cause of foot pain and dysfunction. The primary care provider is likely to encounter many of the minor traumatic conditions affecting the feet. Mild to moderate direct blows to the foot can result in nondisplaced metatarsal fractures, minor Jones fractures of the fifth metatarsal, fractures of the proximal phalanges, and the classic eggshell fractures of the tuft. The majority of these can be readily managed with short-term restrictions in ambulation, boot immobilization, or simple splinting with tape. Similarly, the stubbing-like injuries to the supporting ligaments of the phalanges are also managed with simple taping methods. Finally, pain and numbness can be referred into the foot from the lower lumbar nerve roots, from tarsal tunnel syndrome, or from the progressive loss of sensation accompanying peripheral neuropathy. Lumbar radiculopathy and tarsal tunnel syndrome are the two most common extrinsic conditions that cause symptoms in the feet. Lumbar level L4–L5 and lumbar level L5–S1 cause pain and numbness over the dorsum and plantar surfaces, respectively. Compression and irritation of the posterior tibial nerve as it wraps around the medial malleolus causes pain and numbness over the plantar surface. Peripheral neuropathy from any cause (e.g., diabetes, alcoholism) causes a diffuse loss of sensation in a stocking–glove distribution. SYMPTOMS Patients diagnosed with intrinsic conditions affecting the foot most often complain of pain, deformity, or functional symptoms (difficulties with shoe

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wear or impaired ambulation). Pain ranges from the inconvenience of tired arches to the exquisite pain of gout. The MTP joints, the dorsal of the foot, and the arch are the most commonly affected areas. Less commonly, patients complain of a progressive deformity (bunions, bunionette, dorsal bunion) accompanied by functional symptoms. The patient’s description of the pain combined with its anatomic location provides the most important clues to the anatomic diagnosis. Metatarsalgia, pain in the ball of the foot, is the most common pain pattern in the foot. It is a descriptive term and not a diagnosis. Any condition that directly affects the MTP joints causes either a localized or more generalized metatarsalgia. Pain is localized to the first MTP joint with hallux valgus, hallux rigidus, prebunion bursitis, and gout. Pain localized between two adjacent toes is most often caused by Morton’s neuroma. Pain localized to the fifth MTP joint is most often caused by underlying osteoarthritis, the bunionette deformity. In contrast, pain affecting multiple MTP joints is caused by either the gradual development of hammer toes or the progressive effects of chronic inflammation seen with inflammatory arthritis. The second most common group of symptoms involves the consequences of progressive foot deformity and how it affects shoe wear. Patients complain of the cosmetic effects of progressive arthritic deformity and how it leads to illfitting shoes. The slowly progressive and deforming forms of osteoarthritis of the foot (hallux valgus, hallux rigidus, the bunionette deformity, and dorsal bunions) and the various causes of swelling over the dorsum (dorsotenosynovitis, march fracture, dorsal bunion) distort the normal contours and alignment of the foot precluding a comfortable shoe fit. Impairment of ambulation is a universal foot symptom for patients with significant foot disorders. Tired feet at the end of the day, favoring of the affected side, and the inability to bear weight directly over the foot correlate directly with the degree of acute inflammation. The greatest degree of impairment is seen with acute gout, severe dorsal tenosynovitis, infection, and acute inflammatory arthritis. Pes planus and cavus, hammer toes, and the various forms of osteoarthritis cause more functional impairment (limiting prolonged standing and extended walking) than actual foot pain. Foot pain accompanied by dorsal swelling is the classic location of pain arising from simple edema, cellulitis, the dorsal bunion deformity, dorsotenosynovitis of the extensor tendons, and the dramatic dorsal swelling of the march fracture or underlying osteomyelitis of the tarsals or metatarsals. Referred pain into the foot is common. Sciatica is the most common cause. The L5 root refers pain over the dorsal aspect. The S1 root refers pain over the plantar aspect of the foot. Tarsal tunnel syndrome, a much less common cause of referred pain, also causes paresthesia and hypesthesia over the plantar aspect of the foot. EXAMINATION The efficient examination of the foot focuses on three distinct anatomic areas: the MTP joints (metatarsalgia), the dorsum of the foot (the metatarsals and extensor tendons), and the arch (plantar aponeurosis and longitudinal ligaments).

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BOX 13-1

BOX 13-2

DIFFERENTIAL DIAGNOSIS OF FOOT PAIN BASED ON ANATOMIC AREA Metatarsal pain

Dorsal pain and swelling

Arch of the foot

Referred pain

Hallux valgus Hallux rigidus Gout Prebunion bursa Hammer toes Inflammatory arthritis of the metatarsals Morton’s neuroma Bunionette Edema Cellulitis Dorsal bunion Reflex sympathetic dystrophy Metatarsal stress fracture Pes planus Pes planovalgus Pes cavus Plantar fibromatosis Lumbar radiculopathy Tarsal tunnel syndrome Peripheral neuropathy

The exam should always begin with assessment of the general function of the foot. The patient’s alignment when standing, the patient’s ability to bear weight, and the ability to perform normal heel–toe walking not only indicate overall foot function but also define the severity of the condition. Next, the MTP joints are inspected for proper alignment, and the MTP squeeze maneuver is performed to determine the degree of metatarsalgia. If the MTP squeeze sign is positive, joint range of motion is assessed, bony osteophytes are palpated, extensor tendon flexibility is assessed, and the interdigital spaces are palpated for Morton’s neuroma. Attention is then turned to inspection and palpation of the dorsum of the foot. An assessment of dorsal swelling and degree of inflammation combined with the tarsal squeeze sign and passive flexion and isometric extension of the toes allows the examiner to distinguish between simple edema or cellulitis and the reactive swelling of the march fracture and extensor tenosynovitis. Finally, the configuration and integrity of the arch are assessed by direct palpation of the arch for size and nodular thickening while the patient is standing. If an intrinsic condition affecting the foot is not readily diagnosed, the examiner evaluates the patient’s vascular status or seeks a referred cause of pain. Older adults with significant risk factors for peripheral vascular disease are assessed by capillary fill time measurement and palpation of the dorsalis pedis and posterior tibialis vessels. Patients with vague descriptions of pain and numbness are assessed with the straight leg maneuver, a detailed neurologic exam, and Tinel signs at the medial malleolus.

ONE-MINUTE SCREENING EXAMINATION OF THE FOOT 1. Assess the general function of the foot. a. The patient’s stance. b. The ability to bear weight. c. The ability to walk heel to toe. 2. Evaluate the MTP joints for osteoarthritis and acute swelling and inflammation. a. The MTP squeeze maneuver. b. Joint alignment. c. Toe flexibility. 3. Evaluate the dorsum of the foot: MT squeeze sign, inflammatory changes, and deformity. 4. Evaluate the arch of the foot. 5. Palpate the digital nerve between two metatarsal joints. 6. Measure capillary fill times and palpate the dorsalis pedis and posterior tibialis arteries. 7. Perform Tinel sign at the medial malleolus or assess for sciatica if referred pain is suspected.

ONE-MINUTE SCREENING FOOT EXAM: MANEUVERS ASSESSING OVERALL FOOT FUNCTION The next five maneuvers represent the minimal examination of the patient presenting with foot symptoms. Observation of the patient’s ability to bear weight and walk, inspection of the patient’s stance, and screening maneuvers for metatarsalgia, dorsal pain and swelling, and arch abnormalities provide enough information to triage to x-ray, order appropriate labs, suggest general treatment recommendations, or proceed to more detailed examination and treatment.

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ABILITY TO BEAR WEIGHT AND WALK SUMMARY: The ability to walk easily depends on a normal ankle joint with intact supporting tendons, flexible toe joints, intact extensor and flexor toe tendons, and a solid bony skeleton (tarsals, metatarsals, and phalangeal bones). MANEUVER: The patient is asked to walk in the exam room. Symptoms can be enhanced by asking the patient to toe and heel walk.

FIGURE 13–1. Observe the patient’s ability to bear weight and walk.

INTERPRETATION: Weight bearing is mildly impaired with hallux valgus and rigidus, turf toe, sesamoiditis, hammer toes, dorsotenosynovitis, rheumatoid arthritis, and metatarsal stress fracture. The patient’s gait is severely affected by gout and fractures affecting the foot. Morton’s neuroma, dorsal bunion, and tarsal tunnel rarely have a significant effect on weight bearing and gait.

ALIGNMENT AND DEFORMITY, DORSAL SWELLING SUMMARY: Several of the common conditions affecting the foot can be readily diagnosed by simply inspecting the arch of the foot, the ankle alignment, the alignment and positions of the toes, and the presence of inflammatory changes and swelling. MANEUVER: The patient is asked to stand on the exam platform, applying equal weight on each foot. INTERPRETATION: Loss of the normal alignment of the tibia, ankle, and foot is called pronation or supination (eversion or inversion, respectively). Enlargement of the MTP joint of the great toe is seen with hallux rigidus and hallux valgus. Dorsal bunion is characterized by bony prominence over the articulation of the first cuneiform and the first metatarsal. Enlargement of the fifth metatarsal is called the bunionette deformity. Exaggerated flexion of the toes is seen with hammer toes. FIGURE 13–2. Have the patient stand and inspect the toes for proper alignment and deformity and the top of the foot for dorsal swelling.

Swelling and inflammatory changes over the dorsum of the foot are seen with extensor tenosynovitis, metatarsal stress fracture, RSD, and cellulitis. Acute inflammation is seen with gout, rheumatoid arthritis, or acute prebunion bursitis.

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ASSESS THE PATIENT’S ARCH SUMMARY: The arch is formed by the metatarsal and tarsal bones, the ligaments that support them, the plantar aponeurosis, and the longitudinal ligament. The patient must stand while the examiner assesses the configuration of the arch. MANEUVER: The patient is asked to stand on the exam platform. The examiner palpates the arch using the middle finger. INTERPRETATION: The examiner’s finger can be inserted up to the distal interphalangeal crease in the average arch. Flattening of the arch is called pes planus, and an exaggerated arch is called pes cavus. When ankle pronation is combined with pes planus, the condition is called pes planovalgus. Discrete nodular thickening of the arch is called plantar fibromatosis (compare this to palmar fibromatosis, Dupuytren’s contracture of the hand).

FIGURE 13–3. Assess the patient’s arch.

MTP SQUEEZE SIGN SUMMARY: The ball of the foot is formed by the five MTP joints. The prebunion bursa is located medial to the great toe. The digital nerves course between the heads of the MTP joints (Morton’s condition). Pain over the ball of the foot is called metatarsalgia. MANEUVER: All five MTP joints are compressed from side to side. The sign can be enhanced by holding the MTP joints of the middle, lesser toes in line with the examiner’s other hand, especially for patients with very flexible toes.

FIGURE 13–4. Perform the MTP squeeze sign.

INTERPRETATION: Any of the conditions that affect the MTP joints will have a positive MTP squeeze sign, including prebunion bursitis of the great toe, arthritis of the great toe, MTP joint inflammation from hammer toes, the bunionette deformity, and Morton’s neuroma. If the squeeze sign is positive, then the next step is to palpate the individual joints and periarticular areas to define the anatomic structure responsible for the symptoms.

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MT JOINT SQUEEZE SIGN SUMMARY: The midfoot consists of the cuboid, the three cuneiform, and five metatarsal bones. They are covered by a thick network of ligaments and the extensor tendons above and the arch ligaments below. MANEUVER: The midfoot is compressed at two levels: at the level of the midshaft of the metatarsal bones and along the joint line between the tarsal bones with the metatarsals. INTERPRETATION: This maneuver is used to screen for pathologic involvement of the tarsal and metatarsal bones (stress fractures, true fractures, osteoarthritis of the first cuneiform and the first metatarsal bones [dorsal bunion], and the rare case of osteomyelitis).

FIGURE 13–5. Perform the MT joint squeeze sign.

ONE-MINUTE SCREENING EXAM: MANAGEMENT STRATEGIES TRIAGE TO X-RAY For a patient who has a history of trauma or is at risk of bony injury, stress fracture, hallux valgus, hallux rigidus, dorsal bunion, bunionette, or sesamoiditis: • Order three views of the foot for patients with a history of crush injuries or direct blow to the dorsum of the foot (metatarsal fractures, the Jones fracture of the fifth metatarsal, fracture of the proximal phalanges, the eggshell fracture of the tuft, or dislocation). • Order three views of the foot for patients with suspected underlying osteoarthritis (hallux valgus, hallux rigidus, the dorsal bunion deformity, and the bunionette deformity). • Order a posteroanterior view of the foot for athletic patients or patients with known osteoporosis with swelling of the dorsum of the foot (metatarsal stress fracture). • Order a sesamoid view for patients with pain over the plantar surface of the great toe (differentiate sesamoiditis from bipartite sesamoid and true fracture). • Order three views of the foot for the athletic patient with pain on the plantar surface of the great toe (flexor tendon avulsion fracture complicating turf toe). • Order three bilateral views of the foot for patients with diffuse foot pain and dorsal swelling and discoloration (RSD).

TRIAGE TO THE LAB For patients with dramatic degrees of swelling and inflammation: • Order a complete blood cell count, uric acid, and erythrocyte sedimentation rate for patients with acute pain, exquisite tenderness, inability to bear weight, and signs of active inflammation (gout or acute dorsotenosynovitis). • Order a complete blood cell count, uric acid, erythrocyte sedimentation rate, and blood cultures for patients with diffuse dorsal swelling accompanied by acute inflammatory changes and significant fever. CONSIDER A BONE SCAN For patients suspected of having stress fracture, RSD, or osteomyelitis. RECOMMEND EMPIRICAL TREATMENT For patients with mild to moderate foot pain and stiffness, unrestricted movement of the joints, normal alignment, and normal gait: • Limit walking, standing, and impact. • Wear comfortable, properly fitted shoes with padded insoles with or without arch supports. • Apply ice and elevate the foot four times a day. • Perform gentle daily passive stretching exercises of the toes in extension and flexion. • Recommend an anti-inflammatory medication for 10 to 14 days at full dosage. • Use crutches with touch-down weight bearing for 5 to 7 days (optional).

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DETAILED EXAMINATION: SPECIFIC FOOT DIAGNOSES HALLUX VALGUS (BUNIONS) The common term bunion

is used to describe osteoarthritis of the MTP joint of the great toe accompanied by valgus angulation. The diagnosis is suggested by

local swelling and inflammation, moderate pain with movement of the joint, and the characteristic changes of asymmetrical wear of the articular cartilage documented on x-rays. It must be distinguished from hallux rigidus (osteoarthritis without valgus angulation) and gout, which is much more acute, inflamed, and painful.

SIMPLE INSPECTION OF THE FOOT SUMMARY: Simple inspection of the foot reveals an enlarged and angulated first MTP joint. The metatarsal head is prominent, and the great toe is angled toward the lesser toes. MANEUVER: Simple inspection readily identifies the enlargement and angulated first MTP joint. ASSOCIATED SIGNS: The MTP squeeze sign is painful when the joint is acutely inflamed. Flexion and extension of the toe are limited by pain and stiffness. A bony ridge (osteophyte) can be felt at the joint line over the dorsum. The medial aspect of the joint is discolored (irritated) or acutely swollen and inflamed (adventitial bursitis).

FIGURE 13–6. The diagnosis of hallux valgus can be made by simple inspection of the foot.

INTERPRETATION: Hallux valgus and hallux rigidus are two forms of the same process: osteoarthritis of the first MTP joint. They differ only in the angulation of the joint. In either case, inflammation may complicate the osteoarthritic changes but not to the degree seen with gout.

PLAIN X-RAYS SUMMARY: Symptoms arising from hallux valgus are the most common cause of metatarsalgia. Women are 10 times more likely to develop osteoarthritis than men. The role of improper shoe wear (pointed toe box) is illustrated by the fact that men develop hallux rigidus and women develop hallux valgus. DIAGNOSIS: Plain x-rays of the foot demonstrate osteoarthritic changes at the MTP joint and valgus angulation of the joint. TREATMENT: Wide–toe box shoes; padded insoles; cotton, foam, or rubber spacers; bunion shields; ice; gentle flexion and extension range of motion; and local injection of 1⁄2 mL Kenalog 40 mg/mL. REFERRAL: Surgical referral is based on the following criteria: poor shoe fit, recurrent prebunion bursitis, severe valgus angulation, and patient preference.

FIGURE 13–7. Plain x-rays to confirm and determine the severity of hallux valgus.

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HALLUX RIGIDUS Hallux rigidus is osteoarthritis of the first MTP joint (loss of range of motion of the great toe caused by wear of the articular cartilage and reactive osteophyte formation). It is analogous to the findings of bunions but without valgus angulation.

JOINT ENLARGEMENT AND DECREASED RANGE OF MOTION SUMMARY: Arthritis of the first MTP joint is not common. Most cases are a result of previous injury to the articular cartilage from a simple strain or bony fracture. MANEUVER: Simple inspection of the great toe reveals bony enlargement along the medial and superior aspects of the great toe and mild degrees of joint inflammation. Flexion and extension of the toe are limited by pain and bony osteophyte formation. ASSOCIATED SIGNS: The MTP squeeze sign is mildly painful. Crepitation may be present when the joint is passively flexed and extended. A bony ridge (osteophyte) can be felt over the dorsum. Ambulation is mildly impaired by the loss of full motion of the great toe.

FIGURE 13–8. A presumptive diagnosis of hallux rigidus is made by documenting joint enlargement and decreased range of motion.

PLAIN X-RAYS SUMMARY: Plain x-rays of the foot demonstrate osteoarthritic changes at the MTP joint (narrowed articular cartilage, bony osteophytes at the margin, and bony sclerosis) with a normal angulation of the joint. DIAGNOSIS: Moderate osteoarthritis of the first MTP joint, hallux rigidus. TREATMENT: Wide–toe box shoes; padded insoles; cotton, foam, or rubber spacers; ice; gentle flexion and extension range of motion; and local injection of 1⁄2 mL Kenalog 40 mg/mL. REFERRAL: Surgical referral is considered when symptoms persist and at least 50% of the normal range of motion has been lost.

FIGURE 13–9. Plain x-rays to confirm the diagnosis of hallux rigidus.

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PREBUNION BURSITIS The prebunion bursa, an adventitial bursa, develops as a result of constant pressure over the medial aspect of the great toe. Friction between the valgus angulated metatarsal head and the shoes causes dramatic swelling and

inflammation. The condition often is confused with acute gout. However, the bursal tenderness is restricted to the medial joint line, in contrast to the generalized and severe tenderness characteristic of gout.

SIMPLE INSPECTION SUMMARY: Prebunion bursa is an adventitial bursa that forms as a result of repeated friction of tight fitting narrow–toe box shoes. MANEUVER: Simple inspection demonstrates cystic swelling located directly over the medial aspect of the first MTP joint. Inflammation is limited to a quartersized area over the angulated metatarsal head. ASSOCIATED SIGNS: The MTP squeeze sign is painful. The range of motion is limited by the underlying osteoarthritic changes but not to the extreme degree seen with acute gout. All the physical findings of the underlying hallux valgus are present. INTERPRETATION: By contrast, acute gout is characterized by diffuse tenderness and swelling over the entire MTP joint.

FIGURE 13–10. Simple inspection readily identifies the swelling and inflammation of prebunion bursitis.

LOCAL ANESTHETIC BLOCK AND INJECTION OF RADIO-OPAQUE DYE SUMMARY: Because the physical signs of hallux valgus and prebunion bursitis are nearly identical, a definite diagnosis requires local anesthetic block or the aspiration of fluid from the bursa. Enter the bursal sac medially over the point of maximum swelling (over the distal head of the metatarsal). DIAGNOSIS: Hypaque radio-opaque dye outlining the extent of the prebunion bursa. NEEDLE: DEPTH:


5

⁄4 to 3⁄8 inch (1⁄8 inch above the bone).

1

VOLUME: both.

⁄2 to 1 anesthetic, 1⁄4 to 1⁄2 mL K40, or

1

NOTE: The bursa lies between the subcutaneous fat layer and the synovial membrane. FIGURE 13–11. Local anesthetic block and radioopaque dye injection to confirm the diagnosis of prebunion bursitis.

GOUT In the absence of a penetrating injury, prior surgery, or

significant risk factors for infection (e.g., diabetes, peripheral vascular disease, immunodeficiency states), an empirical diagnosis of acute gout is strongly suggested by acute swelling and inflamma-

REFERRAL: Surgical referral is predicated more on the severity of the underlying hallux valgus rather than the involvement of the bursa. tion and exquisite tenderness of the first MTP joint. If risk factors are present for infection, it is necessary to aspirate the joint for synovial fluid analysis: cell count, crystals, Gram stain, and culture.

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GOUT SUMMARY: Gout is an acute, crystal-induced, monarthric arthritis of the MTP joint of the great toe. Acute swelling, redness, and heat develop as an inflammatory response to the precipitation of monosodium urate crystals in the synovial fluid. The synovial fluid becomes supersaturated with uric acid crystals as a result of overproduction of uric acid (hemolytic anemia, leukemia, psoriasis, tumors with rapid cell turnover, and other causes of overproduction account for 10% of cases) or undersecretion of uric acid (diuretics, renal disease, aspirin, and niacin are the most common drugs that account for nearly 90% of cases). MANEUVER: The great toe is red, hot, and swollen. Any attempts to move the joint are resisted. Compression of the joint from any direction is extremely painful. FIGURE 13–12. The empirical diagnosis of gout is suspected when the first MTP joint is acutely inflamed, motion of the joint and ambulation are severely limited, and the patient has no risk factors for infection (e.g., diabetes, vascular insufficiency, or venous ulceration).

ASSOCIATED SIGNS: The MTP squeeze sign is exquisitely painful. Joint swelling is most prominent medially but often extends between the first and second MTP joints. Tophaceous deposits may be present at other joints or along the outer ear. INTERPRETATION: Infection in the first MTP joint is rare in patients with normal immunity and no risk factors for infection. A presumptive diagnosis of gout can be made based on the physical findings described here and the documentation of an elevated blood uric acid level (90% of cases of gout have an elevated level).

MTP JOINT ASPIRATION SUMMARY: A definitive diagnosis of gout is based on the demonstration of uric acid crystals in the synovial fluid by polarized light microscopy. Enter medially on the metatarsal or phalangeal side of the joint line. NEEDLE: 5⁄8 inch, 25 gauge for anesthesia or 21 gauge for aspiration. DEPTH:

⁄8 to 1⁄2 inch (depending on swelling).

3

VOLUME:

⁄2 to 1 mL anesthetic, 1⁄4 mL K40, or both.

1

NOTE: Multiple attempts to enter the joint may be damaging; with the needle flush against the periosteum (under the synovial membrane) the needle is intra-articular; manual pressure may yield sufficient fluid for analysis.

FIGURE 13–13. MTP joint aspiration to confirm acute gout.

REFERRAL: Rheumatology referral is considered for atypical presentations of gout. Surgery is not indicated.

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SESAMOIDITIS Sesamoiditis is a chronic irritation of the sesamoid bones in the flexor tendons of the first MTP joint. Repeated minor trauma causes pain and localized tenderness on the plantar aspect of the great toe. The diagnosis is suggested by the

plantar location of the pain and tenderness that is consistently aggravated by passive stretching of the toe in extension. Bilateral sesamoid views of the forefoot are used to rule out bony fracture and congenital bipartite sesamoid.

LOCAL PLANTAR TENDERNESS OF THE GREAT TOE SUMMARY: The two sesamoid bones are located within the bodies of the flexor tendons of the great toe. Repeated microtrauma causes a localized inflammatory reaction. MANEUVER: The first MTP joint is palpated on the plantar surface, directly over the sesamoid bones. Passive flexion and extension of the toe can facilitate finding the exact location of the two small bones. ASSOCIATED SIGNS: Passive stretching of the great toe in extension is painful at the extremes of range of motion. Swelling typically is too subtle to appreciate. The range of motion of the toe is normal. INTERPRETATION: Major trauma to the first MTP joint can cause sesamoid bone fracture. X-rays demonstrate an irregular fracture line. This is in stark contrast to the well-demarcated line seen with bipartite sesamoid bone, which is often bilateral. FIGURE 13–14. Local plantar tenderness of the great toe in a patient with a history of repeated minor trauma.

SESAMOID VIEW OF THE FOOT SUMMARY: The sesamoid view of the foot demonstrates ill-defined irregularities of one or both of the sesamoid bones. DIAGNOSIS:

Sesamoiditis.

TREATMENT: Non–weight-bearing activities, wide–toe box shoes, padded insoles, metatarsal bar, and ice. REFERRAL:

FIGURE 13–15. Sesamoid view of the foot to confirm the diagnosis of sesamoiditis.

Surgery is not indicated.

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TURF TOE Young athletes playing on artificial turf are at risk for hyperextension injury of the first MTP joint, causing stretching of and strain on the capsule of the joint and the plantar plate. The patient describes a deep aching in the bone associated with local tenderness over the entire joint. This is in contrast to the tenderness

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localized to the plantar aspect of the joint suggesting sesamoiditis or fracture. Range of motion should be preserved, and x-rays should be normal unless avulsion fracture complicates the injury. Treatment includes buddy taping of the joint, stiff shoes, and a stiff orthotic for 2 to 3 weeks.

TURF TOE SUMMARY: Turf toe is seen almost exclusively in athletes performing on artificial turf. MANEUVER: The patient’s pain is reproduced by passive stretching of the first MTP joint in full extension. This places strain on the joint capsule, the flexor tendons, and the plantar plate. ASSOCIATED SIGNS: The plantar aspect of the first MTP joint may be diffusely tender to direct palpation. The range of motion in flexion and extension is minimally reduced, restricted more by discomfort than by an absolute loss of movement.

FIGURE 13–16. Turf toe is a diagnosis of exclusion. Before the diagnosis can be made in an athlete, fracture, hallux rigidus, sesamoiditis, and hallux valgus must be excluded by exam and radiographic studies.

INTERPRETATION: The symptoms of turf toe and sesamoiditis overlap. Turf toe occurs only in athletes subject to the trauma of artificial turf. The plantar tenderness of sesamoiditis is much more focal. X-rays are necessary to exclude tendon avulsion or true bony fracture.

HISTORY, CLINICAL FINDINGS, AND FOOT X-RAY SUMMARY: Plain x-rays of the foot and sesamoid views are used to exclude tendon avulsion, true bony fracture, and sesamoiditis. DIAGNOSIS: Normal posteroanterior x-ray of the foot in a patient with turf toe. Treatment: Wide–toe box shoes; padded insoles; cotton, foam, or rubber spacers; ice; gentle flexion and extension range of motion; and intra-articular injection of 1⁄2 mL Kenalog 40 mg/mL. REFERRAL: Surgical referral is recommended for tendon avulsion accompanying turf toe.

FIGURE 13–17. An appropriate history coupled with consistent clinical findings and a normal foot x-ray are necessary for a diagnosis of turf toe.

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BUNIONETTE The common term bunionette is used to describe

osteoarthritis of the fifth MTP joint complicated by varus angulation. The diagnosis is suggested by local swelling and inflammation, moderate pain with movement of the joint, and the characteristic changes of asymmetrical wear of the articular cartilage.

SIMPLE INSPECTION OF THE FOOT SUMMARY: Simple inspection of the foot reveals an enlarged and angulated fifth MTP joint. The metatarsal head is prominent, and the little toe is angled toward the other toes. MANEUVER: Simple inspection readily identifies the enlargement and angulated fifth MTP joint. ASSOCIATED SIGNS: The MTP squeeze sign is painful when the joint is acutely inflamed. Flexion and extension of the toe are limited by pain and stiffness. A bony ridge (osteophyte) can be felt at the joint line over the dorsum. The lateral aspect of the joint can be discolored (irritated) or acutely swollen and inflamed (adventitial bursitis). INTERPRETATION: As osteoarthritis progresses, the angle of the toe gradually increases. FIGURE 13–18. The diagnosis of bunionette can be made by simple inspection of the foot.

POSTEROANTERIOR X-RAY OF THE FOOT SUMMARY: Plain x-rays of the foot demonstrate osteoarthritic changes at the fifth MTP joint with a varus angulation of the joint. DIAGNOSIS: joint.

Bunionette deformity of the fifth MTP

TREATMENT: Wide–toe box shoes; padded insoles; cotton, foam, or rubber spacers; ice; gentle flexion and extension range of motion; and local injection of 1⁄4 mL Kenalog 40 mg/mL. REFERRAL: Surgical referral is based on the following criteria: poor shoe fit, recurrent skin irritation, severe varus angulation, and patient intolerance or preference.

FIGURE 13–19. Posteroanterior x-ray of the foot is used to confirm the diagnosis of bunionette.

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METATARSALGIA Metatarsalgia (pain over the ball of the foot) is the pain arising from the metatarsal joints or the surrounding soft tissues. Because metatarsalgia is a general term,

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a thorough search for a specific underlying diagnosis, such as hallux valgus, hallux rigidus, prebunion bursitis, hammer toes, gout, rheumatoid arthritis, or Morton’s neuroma, must be undertaken.

MTP SQUEEZE SIGN SUMMARY: Metatarsalgia is a descriptive term only, not a specific diagnosis. MANEUVER: The MTP squeeze sign is used to identify the ball of the foot as the source of the patient’s pain. ADDITIONAL SIGNS: Swelling and tenderness limited to the medial side of the great toe are diagnostic of prebunion bursitis. Loss of range of motion, bony enlargement, and variable degrees of inflammation are seen with hallux valgus and hallux rigidus. Intense pain and inflammatory change in the great toe are the classic presentation of gout. Lack of toe flexibility and generalized metatarsal pain are seen with hammer toes and rheumatoid arthritis. Pain and numbness limited to the third and fourth or second and third toes are consistent with Morton’s neuroma. Pain, deformity, and decreased range of motion in the fifth MTP joint are diagnostic of the bunionette deformity. FIGURE 13–20. MTP squeeze sign is used to screen the MTP joints or associated soft tissues as the source of the patient’s pain.

INTERPRETATION: The metatarsal squeeze sign is an excellent screening test to identify the ball of the foot as the source of the patient’s problem. However, additional testing is necessary to define the exact anatomic cause.

METATARSALGIA INVOLVING A SINGLE MTP JOINT SUMMARY: Occasionally one of the lesser toes sustains a remote injury (severe strain or fracture) that damages the articular cartilage and increases susceptibility to irritation and inflammation. MANEUVER: Selective MTP joint involvement is confirmed by direct palpation of the affected joint. Compression of the joint from above and below is tender or thickened. Passive flexion and extension are limited. Plain x-rays of the foot may demonstrate osteopenia, osteoarthritic changes, or normal findings. TREATMENT: Wide–toe box shoes; padded insoles; cotton, foam, or rubber spacers; ice; gentle flexion and extension range of motion; and local injection of 1⁄4 mL Kenalog 40 mg/mL. REFERRAL: FIGURE 13–21. Metatarsalgia involving a single MTP joint is seen with trauma, posttraumatic arthritis, or the selected inflammatory arthritis as a part of spondyloarthropathy.

Surgery is not indicated.

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HAMMER TOES The hammer toe deformity results from the

progressive loss of flexibility of the extensor tendons of the toes and is a specific cause of metatarsalgia. As the extensor tendons gradually tighten, subluxation of the tendons over the top of the proxi-

mal phalanges results in the characteristic deformity: abnormal flexion of the proximal interphalangeal joint and extension of the distal interphalangeal joint. Metatarsal pain, corns, and calluses often develop years before the deformity.

LACK OF FLEXIBILITY OF THE EXTENSOR TENDONS SUMMARY: The gradual tightening of the extensor tendons of the toes has predictable consequences. The gradual tendon contracture causes the toes to cock up and the metatarsal joints to project in a downward direction. Corns and calluses form as a result of the pressure atop the toes and below the metatarsal heads, respectively. Ultimately, the tendons slip off the sides of the toes, leading to the fixed contracture and hammer toe deformity. MANEUVER: Simple inspection with the foot in the plantar flexed position demonstrates the prominent extensor tendons, the cocked-up toes, and the associated hypertrophic skin changes (corns and calluses). The signs can be enhanced by passive flexion of the toes. FIGURE 13–22. Lack of flexibility of the extensor tendons of the toes characterizes hammer toes.

ADDITIONAL SIGNS: The MTP squeeze sign usually is positive. Individual joints may be selectively more sensitive to compression. The range of motion of the MTP joints is preserved (the joints have normal flexibility when the ankle is fully dorsiflexed, relaxing the tight tendons). INTERPRETATION: In the earliest stages of hammer toes, the physical findings overlap with the early signs of rheumatoid arthritis. X-rays of the foot may show juxta-articular osteoporosis with rheumatoid arthritis (the earliest radiographic finding) However, it may take serial examination, x-rays, and serological testing to distinguish the two conditions.

CLINICAL DIAGNOSIS OF HAMMER TOES SUMMARY: Patients with the classic hammer toe deformity do not need further testing. Plain x-rays demonstrate the cocked-up position of the toes in moderate cases. DIAGNOSIS:

Severe hammer toe deformity.

TREATMENT: Wide–toe box shoes; padded insoles; cotton, foam, or rubber spacers; hammer toe crests placed under the toes; paring of the associated corns and calluses; passive stretching of the extensor tendons; local injection of 1⁄2 mL Kenalog 40 mg/mL.

FIGURE 13–23. A clinical diagnosis of hammer toes is sufficient in most patients with classic findings. Further testing usually is not necessary.

REFERRAL: Surgical referral can be considered for the rigid, fixed hammer toe deformity that severely interferes with overall foot function and shoe wear.

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MORTON’S NEUROMA A presumptive diagnosis of Morton’s neuroma is suggested by a positive MTP squeeze sign, local tenderness, and hypesthesia between two adjacent toes. The

diagnosis can be confirmed by local anesthetic block placed at the level of the digital nerve, response to corticosteroid injection, or response to surgical intervention.

MTP SQUEEZE SIGN, LOCAL TENDERNESS, AND HYPESTHESIA SUMMARY: Morton’s neuroma, a digital neuroma located between the metatarsal heads of two adjacent toes, is caused by the constant compression of the nerve from the pressures of walking and the pressures of the adjacent metatarsal heads. MANEUVER: After the examiner screens the MTP joints with the MTP squeeze sign, the individual spaces between the metatarsal heads are compressed from above and below. A positive response is indicated by localized tenderness or by reproducing the patient’s hypesthesia along the inside of two toes.

FIGURE 13–24. The combination of a positive MTP squeeze sign and local tenderness and hypesthesia of two adjacent toes strongly suggests the diagnosis of Morton’s neuroma.

ASSOCIATED SIGNS: The MTP joints are not tender to compression. Long-lasting cases may show hypesthesia to light touch and pain sensation along the inner aspect of the adjacent toes. Rarely a palpable mass can be felt between the toes. Movement of the toes in flexion and extension is not painful. INTERPRETATION: The signs listed here are unique for Morton’s neuroma.

LOCAL ANESTHETIC BLOCK SUMMARY: Local anesthetic block of the digital nerve is placed below the transverse metatarsal ligament. The neurovascular bundle is located just under the ligament. The injection enters from above, 1⁄2 inch distal to the MTP joint. ⁄8 inch, 25 gauge.

NEEDLE:

5

DEPTH: 5⁄8 to 3⁄4 inch (below the transverse metatarsal ligament). VOLUME: NOTE:

⁄2 mL anesthetic, 1⁄4 mL K40, or both.

1

This injection is identical to a digital block.

REFERRAL: Surgical referral is indicated when two or three local injections within 1 year fail to control symptoms.

FIGURE 13–25. Local anesthetic block to confirm the diagnosis of Morton’s neuroma.

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METATARSAL STRESS FRACTURE (MARCH FRACTURE)

Microfracturing of the shafts of the metatarsal bones leads to a gradual thickening of the periosteum and the characteristic enlarge-

ment of the cortex. Although this stress fracture occurs most commonly in long-distance runners, military recruits, and ballet dancers, patients with severe osteoporosis are also at risk.

FOCAL METATARSAL PAIN AND DORSAL SWELLING SUMMARY: In the absence of major trauma, focal tenderness over a single metatarsal bone in a runner, military recruit, ballet dancer, or patient with known osteoporosis indicates stress fracture. MANEUVER: Each metatarsal shaft is palpated for local tenderness and bony prominence. ASSOCIATED SIGNS: The MT squeeze sign is moderately painful. The entire dorsum of the foot may be swollen, as long as peripheral edema, dorsotenosynovitis, RSD, and cellulitis are excluded. Inflammatory signs typically are not present. INTERPRETATION: The swelling of metatarsal stress fracture overlaps with the swelling of edema, cellulitis, and dorsotenosynovitis. Only stress fractures have a positive MT squeeze sign. Dorsotenosynovitis is aggravated by movement of the toes. Edema, cellulitis, and RSD are not aggravated by the MT squeeze sign or movement of the toes. FIGURE 13–26. Focal metatarsal pain and dorsal swelling consistent with metatarsal stress fracture.

SERIAL PLAIN X-RAYS OR BONE SCANNING SUMMARY: A definitive diagnosis can be made with plain x-rays or bone scanning. Patients with symptoms for several weeks demonstrate periosteal thickening along the shaft of the bone on plain x-rays. A true fracture line is not seen unless the patient suffers additional blunt trauma. By contrast, nuclear bone scanning demonstrates periosteal uptake within the first few weeks of symptoms. DIAGNOSIS: metatarsal.

Stress fracture affecting the second

TREATMENT: Wide–toe box shoes, padded insoles, restricted weight bearing (walking and standing), a shortened stride, and a short leg walking cast. REFERRAL: Surgical consultation is indicated if the bone fails to heal.

FIGURE 13–27. Metatarsal stress fracture is confirmed by serial plain x-rays or bone scanning.

FOOT

Inflammation of the extensor tendons of the foot is called dorsal tenosynovitis. It is characterized by dorsal pain, swelling, and acute inflammation. In addition, the pain of active tenosynovitis is uniquely aggravated by resisted

DORSAL TENOSYNOVITIS

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extension and passive flexion of the toes. The latter sign distinguishes it from the conditions that cause dorsal swelling (simple edema, cellulitis, march fracture, osteomyelitis, and RSD).

DORSAL INFLAMMATORY SWELLING SUMMARY: Dorsotenosynovitis can result from the friction of tight-fitting shoes, the migratory tenosynovitis of gonorrhea, the tenosynovitis of established rheumatoid arthritis, and the acute inflammation of gout or pseudogout. MANEUVER: Simple inspection of the dorsum of the foot extending from the base of the toes to the ankle is swollen, warm to the touch, and discolored. The entire area is tender to the touch. ASSOCIATED SIGNS: Dorsal foot pain is reproduced by resisted extension of the toes and passive flexion of the toes. The MT squeeze sign is minimally painful (compare with metatarsal fracture).

FIGURE 13–28. Dorsal inflammatory swelling of dorsal tenosynovitis.

INTERPRETATION: The swelling of dorsotenosynovitis overlaps with the swelling of edema, cellulitis, and metatarsal stress fracture. Only dorsotenosynovitis is aggravated by movement of the toes. Stress fractures have a positive MT squeeze sign. Edema and cellulitis are not aggravated by the MT squeeze sign or movement of the toes.

CLINICAL DIAGNOSIS OF DORSOTENOSYNOVITIS DIAGNOSIS: No specialized testing is available to confirm the diagnosis of dorsotenosynovitis. Dorsal swelling, pain reproduced by resisting toe extension, and pain aggravated by passive toe flexion remain the hallmarks of this local musculoskeletal process. TREATMENT: Loose-fitting shoes, double socks for extra padding, ice, a full-dose NSAID for 10–14 days, and treatment for gout or rheumatoid arthritis. REFERRAL:

FIGURE 13–29. Clinical diagnosis of dorsotenosynovitis is based solely on the examination.

Surgery is not indicated

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DORSAL BUNION

Osteoarthritic wear between the first cuneiform and the first metatarsal bone is manifested by a narrowing of the joint and reactive osteophyte formation. The firm to hard prominence palpable

over the dorsum of the foot is called a dorsal bunion. The diagnosis is confirmed by a lateral radiograph demonstrating the characteristic arthritic changes.

SIMPLE INSPECTION OF THE FOOT SUMMARY: Arthritis between the cuneiform and the metatarsal bones is uncommon. Previous fracture, pes planus, and pes cavus are risk factors. MANEUVER: Simple inspection readily identifies the localized arthritic changes on the medial side of the midfoot. The articulation between the first cuneiform and the first metatarsal bone is enlarged and bony hard to palpation. The surrounding skin, typically the size of a quarter, may show mild inflammation.

FIGURE 13–30. Simple inspection of the foot in the diagnosis of dorsal bunion.

ASSOCIATED SIGNS: The MT squeeze sign is mildly painful. Passive and resisted movement of the extensor tendons of the toes does not cause pain. INTERPRETATION: Bony enlargement over the articulation of the first cuneiform and first metatarsal is diagnostic of dorsal bunion.

PLAIN X-RAY OF THE FOOT SUMMARY: Plain x-rays of the foot demonstrate osteoarthritic changes at the articulation of the first metatarsal and the first cuneiform. Osteophyte formation on the dorsal side of the joint causes the bunion. DIAGNOSIS: Osteoarthritis of the first cuneiform and the first metatarsal bone with reactive osteophyte formation and near obliteration of the articular cartilage. TREATMENT: Loose-fitting shoes, double socks for extra padding, adhesive donut padding placed over the bunion, and ice. REFERRAL: Surgical referral is warranted when shoes fit poorly, skin irritation develops recurrently, or the patient requests it.

FIGURE 13–31. Plain x-ray of the foot confirms the diagnosis of dorsal bunion.

FOOT

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PES PLANUS, PES CAVUS Inspection of the medial aspect of the foot while the patient is standing and palpation of the longitudinal ligament and plantar aponeurosis for nodular thickening are the best means of evaluating these variations of the configuration of the arch.

SIMPLE INSPECTION OF THE ARCH CONFIGURATION SUMMARY: The arch is formed by the metatarsal and tarsal bones, the ligaments that support them, the plantar aponeurosis, and the longitudinal ligament. The patient must stand while the examiner assesses the arch configuration. MANEUVER: The patient is asked to stand on the exam platform. The examiner palpates the arch using the middle finger. The examiner’s finger can be inserted up to the distal interphalangeal crease in the average arch. ADDITIONAL SIGNS: The alignment of the ankle is most affected by pes planus. When ankle pronation is combined with pes planus, the condition is called pes planovalgus. Discrete nodular thickening of the arch is called plantar fibromatosis (compare with Dupuytren’s contracture of the hand or palmar fibromatosis). Plantar fasciitis and Achilles tendonitis can accompany the more severe arch abnormalities. FIGURE 13–32. Simple inspection of the arch configuration with the patient standing.

INTERPRETATION: Pes planus, pes cavus, and pes planovalgus are unique configurations of the foot and are readily diagnosed by inspection of the patient’s stance and palpation of the arch.

PALPATION OF THE ARCH SUMMARY: Flattening of the arch is called pes planus, and an above-average arch is called pes cavus. TREATMENT: Comfortable shoes, fatigue mat to stand on, padded insoles with arch supports for mild pes planus, and custom-made insoles for moderate to severe pes planus and pes cavus. REFERRAL: Patients are referred to a podiatrist most often for molding of the feet to make custom arch supports.

FIGURE 13–33. A definitive diagnosis of pes planus or pes cavus requires palpation of the arch.

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REFLEX SYMPATHETIC DYSTROPHY Any condition that reduces the normal movement of the lower extremity (e.g., injury, immobilization, surgery) alters the normal balance between the afferent and efferent system of nerves that innervate the lower extremity. Reduced movement of the leg, ankle, and foot decreases the

normal afferent activity (inhibitory to the sympathetic nervous system at the level of the spinal cord), which in turn increases the efferent activity and sympathetic tone. High sympathetic tone causes diffuse pain, edema, discoloration, vasodilation, and increased osteoclastic activity.

REFLEX SYMPATHETIC DYSTROPHY SUMMARY: RSD represents a combination of symptoms that result from an impairment of overall movement of the lower extremities. The lack of movement causes an imbalance between the afferent and efferent nervous systems, ultimately leading to an increase in sympathetic tone. MANEUVER: Simple inspection and palpation of the dorsum of the foot demonstrate diffuse edema, discoloration, skin sensitivity, and an unusual and widespread tenderness encompassing soft tissue, joints, and bone. ASSOCIATED SIGNS: The foot and ankle joints retain their normal range of motion. As the condition progresses, the foot takes on a reddishpurple, shiny hue. Capillary fill is delayed on the affected side. The foot may have a subtle difference in temperature.

FIGURE 13–34. A history of impaired lower extremity movement, diffuse pain involving the foot and ankle, and an exam demonstrating diffuse edema, discoloration, and sensitivity suggests reflex sympathetic dystrophy.

INTERPRETATION: RSD should be suspected in patients with impaired ambulation, diffuse ankle and foot pain, diffuse swelling of the dorsum, and diffuse tenderness throughout the ankle and foot. The diffuse pain pattern and widespread tenderness distinguish this neurogenic condition from the local musculoskeletal conditions including metatarsal stress fracture, edema, cellulitis, and dorsotenosynovitis.

SERIAL X-RAYS OR BONE SCANNING SUMMARY: Plain x-rays of the foot showing unilateral diffuse osteopenia (Sudeck’s atrophy of bone) is highly suggestive of RSD. However, the definitive diagnosis requires bone scanning. A diffuse unilateral uptake of the radioisotope over the entire foot on the perfusion phase of the scan is diagnostic of RSD. DIAGNOSIS:

Reflex sympathetic dystrophy.

TREATMENT: Physical therapy range of motion exercises and stimulation of the extremity, ice and elevation for swelling, a tapering dosage of prednisone from 30 to 40 mg/day, and progressive ambulation.

FIGURE 13–35. Serial x-rays or bone scanning are used to confirm the diagnosis of RSD.

REFERRAL: Patients with persistent symptoms over months despite physical therapy and oral prednisone can be considered for diagnostic sympathetic nerve block. If symptoms respond to nerve block, referral to the neurosurgeon for sympathectomy can be considered.

FOOT

13–1

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EXAMINATION SIGNS

DIAGNOSIS


Valgus deformity of the MTP joint

#1: Bunions

Osteoarthritic changes and valgus angulation of the MTP joint on anteroposterior x-ray of the foot

Hallux rigidus

Osteoarthritic changes with normal alignment of the MTP joint on anteroposterior x-rays

Prebunion bursitis

Local anesthetic block placed intrabursa

Acute gout (podagra)

Synovial fluid aspiration showing intracellular and birefringent uric acid crystals or prompt response to treatment with concurrent elevated uric acid

Sesamoiditis

Sesamoid view of the foot

Metatarsalgia, hammer toes

Diagnosis by clinical examination

Morton’s neuroma

Diagnosis by local anesthetic block placed between two MTP joints and below the transverse metatarsal ligament

Bunionette

Osteoarthritic changes and varus angulation of the MTP joint on anteroposterior x-rays of the foot

Metatarsal stress fracture

Periosteal thickening of the 3rd or 4th metatarsal bone or increased uptake on bone scan

Dorsal tenosynovitis


Dorsal bunion

Oblique view of the foot showing arthritic spurring between the first metatarsal and the first cuneiform

Pes planus, pes cavus


⫹ MTP squeeze (1st MTP pain) Loss of MTP range of motion Palpable dorsal spurring ⫹ MTP squeeze (MTP pain) Loss of MTP range of motion Palpable dorsal spurring Medial MTP joint swelling and acute inflammation ⫹ MTP squeeze sign (medial pain only) Underlying bunion Severe MTP joint swelling and acute inflammation

⫹ MTP squeeze (exquisite MTP joint pain) Severe pain with passive MTP joint movement Focal tenderness over the plantar surface of the MTP joint Pain aggravated by passive dorsiflexion of the flexor tendons Tight extensor tendons with the ankle in full plantarflexion ⫹ MTP squeeze (diffuse MTP pain) Normal MTP joint range of motion Secondary corns and calluses Hammer toe deformity (late) Focal tenderness in between two MTP joints ⫹ MTP squeeze sign (pain between two MTP joints) Hypesthesia along the inner aspect of the adjacent two toes Varus bony deformity of the fifth MTP joint ⫹ MTP squeeze sign (5th MTP joint pain) Focal tenderness and swelling directly over the midportion of the affected metatarsal ⫹ Metatarsal (midfoot) squeeze sign Diffuse dorsal swelling of the foot Pain with passive plantarflexion of the toes Diffuse dorsal swelling of the foot Pain with resisted toe extension Bony deformity over the dorsum of the foot Focal tenderness with or without swelling Mild erythema Flat or exaggerated arch while standing Associated ankle pronation

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COMMON FOOT FRACTURESCHARCOT OR NEUROPATHIC FRACTURES

FRACTURES OF THE MIDTARSALS SUMMARY: Midtarsal fractures are rare because of the rigidity of the midfoot. Most occur as a result of a direct blow to the dorsum of the foot. Point tenderness over the affected bone is accompanied by pain aggravated by side-to-side compression of the foot at the level of the tarsals or tarsal–metatarsal junction (the T or MT squeeze signs). DIAGNOSIS: Figure 13–36 depicts the Lisfranc fracture–dislocation at the first cuneiform and first metatarsal joint. REFERRAL: Surgical referral is indicated for all but the simple nondisplaced, well-aligned fractures.

FIGURE 13–36. Fractures of the midtarsals.

FOOT

CHARCOT OR NEUROPATHIC FRACTURES Patients with impaired sensation caused by peripheral neuropathy are at risk for fracture and impaired fracture healing. Often such patients present with localized swelling and ery-

273

thema that is disproportionate to the average amount of reactive soft tissue change for that particular fracture. The midfoot often is the site of these fractures. Nonunion and malunion of the fracture are common with delayed diagnosis.

FRACTURES OF METATARSALS 1–4 SUMMARY: A metatarsal fracture is most often caused by a direct blow to the top of the foot. Such fractures are classified according to the mechanism of injury (stress fractures), the location (base, neck, or shaft), the direction of the fracture line (transverse or spiral), and the displacement. DIAGNOSIS: Transverse fractures of metacarpals 2 through 4. IMMOBILIZATION: Nondisplaced fractures of the neck or shaft of metatarsals 2 through 4 can be treated with ice, elevation, analgesia, and a short leg walking cast. Nondisplaced fractures of the first metatarsal are treated similarly but with the addition of a 2- to 3-week period of non–weightbearing casting followed by a short leg walking cast to complete the 5-week immobilization.

FIGURE 13–37. Fractures of metatarsals 1–4.

SURGICAL REFERRAL: Displaced metatarsal fractures warrant referral to an orthopedic surgeon for reduction and internal fixation.

FRACTURES OF THE FIFTH METATARSAL BONE SUMMARY: Fractures of the fifth metatarsal are unique. The Jones fracture involves tuberosity of the base of the metatarsal. It should not be confused with a transverse fracture of the base, which has a very different prognosis. The Jones fracture is commonly located within 3⁄4 inch of the most proximal portion of the metatarsal. DIAGNOSIS:

Jones fracture of the fifth metatarsal.

IMMOBILIZATION: It is usually treated with a bulky Jones dressing for the first 24 to 36 hours and avoidance of weight bearing, followed by a short leg walking cast for 3 to 4 weeks. A transverse fracture of the shaft of the fifth metatarsal is treated with a short leg walking cast. SURGICAL REFERRAL: There is a high incidence of delayed union and of nonunion of this fracture despite proper immobilization. These patients need the expertise of the fracture specialist.

FIGURE 13–38. Fractures of the fifth metatarsal bone.

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FRACTURES OF THE GREAT TOE SUMMARY: Fracture of the proximal phalanx of the great toe occurs as a result of direct trauma (dropped objects) or a stubbing injury. Most fractures show minimal displacement. DIAGNOSIS: Minimally displaced fracture of the proximal phalanx of the great toe. IMMOBILIZATION: Treatment includes buddy taping, stiff shoes, or a short leg walking cast with a toe plate for 2 weeks. Displaced intra-articular fractures can be reduced with finger traps and then treated in the same fashion as nondisplaced fractures.

FIGURE 13–39. Fractures of the great toe.

FRACTURE OF THE SESAMOID BONE SUMMARY: Fractures of the sesamoid bone (medial aspect fractures are much more common than lateral aspect fractures) must be distinguished from the congenital bipartite sesamoid. True fractures have rough edges, are transverse in direction, and eventually show callus formation. Bipartite sesamoid fractures occur bilaterally and have smooth, sharply bordered edges. Most fractures occur as a result of direct trauma, avulsion forces, or repetitive stress. DIAGNOSIS:

Sesamoid fracture.

IMMOBILIZATION: Treatment with a short leg walking cast for 3 to 4 weeks is followed by a stiff shoe and a metatarsal bar or pad.

FIGURE 13–40. Fracture of the sesamoid bone.

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275

FRACTURES OF THE TOES SUMMARY: Fractures of the lesser toes are easily reduced with manual pressure or finger traps. Buddy taping to the adjacent larger toe with cotton placed in the toe web is the treatment of choice.

FIGURE 13–41. Fractures of the toes.

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ACCESSORY BONES OF THE FEET SUMMARY: The accessory bones occur in a variety of locations. Radiographically, they are sharply defined, well-circumscribed, oval or round ossifications adjacent to the tarsal or metatarsal bones. They are significant only because they are often misinterpreted as fractures. Their specific locations and distinctive anatomic features should differentiate them from avulsions and small fragment fractures of the bones of the feet.

FIGURE 13–42. Accessory bones of the feet.

ACCESSORY BONES OF THE FEET: The accessory bones of the feet are significant because they can mimic fractures. 1. Os trigonum 2. Os sustentaculum 3. Talus accessories 4. Os subcalcis 5. Os tibiotibiale 6. Calcaneus secundarium 7. Os supranaviculare 8. Os supratalare 9. Os tibiale externum 10. Os intercuneiforme 11. Os peroneum 12. Os vesalianum 13. Os intermetatarseum

CLINICAL PEARLS • Osteoarthritis of the great toe with normal alignment is called hallux rigidus and hallux valgus if the toe is angulated. The conditions are otherwise identical in symptoms, signs, and radiographic changes. • Acute prebunion bursitis often is misdiagnosed as acute podagra. Acute gout involvement of the great toe is characterized by diffuse swelling and inflammation and pain aggravated by motion of the joint in any direction. Acute prebunion bursitis is tender, swollen, and inflamed only along the medial aspect of the joint over the metatarsal head. • Metatarsalgia is a term describing pain arising from any of the structures of the ball of the foot (bunions, gout, prebunion bursitis, hammer toes, bunionette, rheumatoid arthritis, and Morton’s neuroma).

• The earliest manifestation of hammer toes is a tightening and loss of flexibility of the extensor tendons of the toes (the most common cause of metatarsalgia). • Cellulitis and acute inflammatory dorsal tenosynovitis present with similar dorsal swelling and acute inflammatory change. Cellulitis involves the dermis and therefore should not be aggravated by passive flexion of the toes and resisted extension of the toes. • The presence of corns and calluses over the metatarsal heads should alert the clinician to early hammer toes (loss of normal flexibility of the extensor tendons, metatarsalgia).

REFERENCES GENERAL Anderson BC. Stretching. Bolinas, California: Shelter Publications, 1980. Cyriax J. Textbook of Orthopedic Medicine, 8th ed. London: Baillière Tindall, 1982. Ellis RM, Hollingworth GR, MacCollum MS. Comparison of injection techniques for shoulder pain: results of a double-blind, randomized study. BMJ 287: 1339–1341, 1983. Gray RG, Tenebaum J, Gottlieb NL. Local corticosteroid injection treatment in rheumatic disorders. Semin Arthritis Rheumatol 10:231–253, 1981. Hill JJ, Trapp RG, Colliver JA. Survey on the use of corticosteroid injections by orthopedists. Contemp Orthop 18:39–45, 1989. Hollander JL, Brown EM, Jessar RA, Brown CY. Hydrocortisone and cortisone injection into arthritic joints: Comparative effects of and use of hydrocortisone as a local antiarthritic agent. JAMA 147:1629–1631, 1951. Hoppenfeld S. Physical Examination of the Spine and Extremities. New York: Appleton-Century-Crofts, 1976. Lapidus PW, Guidotti FP. Local injections of hydrocortisone in 495 orthopedic patients. Industr Med Surg 26: 234–244, 1957. Rockwood CA, Green DP, Bucholz RW. Fractures, 3rd ed. Philadelphia: JB Lippincott, 1991. Scott DB. Techniques of Regional Anesthesia. Norwalk, Connecticut: Appleton and Lange, 1989. Simon RR, Koenigsknecht SJ, Stevens C. Emergency Orthopedics, 2nd ed. East Norwalk, Connecticut: Appleton and Lange, 1987. Sivananda Yoga Vedanta Center. Yoga Mind and Body. New York: Dorling Kindersley Publishing, 1996. Tsauno JY, Lee HY, Hsu JH, et al. Physical exercise and health education for neck and shoulder complaints among sedentary workers. J Rehabil Med 36:253–257, 2004. NECK Cervical Strain Frost FA, Jessen B, Siggaard-Andersen J. A control, doubleblind comparison of mepivacaine injection versus saline injection for myofascial pain. Lancet 1:499–500, 1980. Goldenberg DL, Felson DT, Dinerman H. A randomized controlled trial of amitriptyline and naprosyn in the treatment of patients with fibromyalgia. Arthritis Rheumatol 29:1371–1377, 1986. Laporte C, Laville C, Lazennec JY, et al. Severe hyperflexion sprains of the lower cervical spine in adults. Clinic Orthop Relat Res 363:126–134, 1999. McMorland F, Suter E. Chiropractic management of mechanical neck and low-back pain: a retrospective, outcomebased analysis. J Manipulative Physiol Ther 23:307–311, 2000. Meyer HJ, Monticelli F, Kiesslish J. Fatal embolism of the anterior spinal artery after local cervical anagetic infiltration. Forensic Sci Int 10:149:115–119, 2005.

Pascarelli EF, Hsu YP. Understanding work-related upper extremity disorders: Clinical findings in 485 computer users, musicians, and others. J Occup Rehabil 11: 1–21, 2001. Peloso P, Gross A, Haines T, et al. Medicinal and injection therapies for mechanical neck disorders. Cochrane Database Syst Rev Apr 18;2:CD000319, 2005. Racette BA, McGee-Minnich L, Perlmutter JS. Efficacy and safety of a new bulk toxin of botulinum toxin in cervical dystonia: A blinded evaluation. Clin Neuropharmacol 22:337–339, 1999. Radanov BP, Sturzennegger M, Stefano GD. Longterm outcome after whiplash injury. Medicine 74: 281–297, 1995. Cervical Radiculopathy Cyteval C, Thomas E, Decoux E, et al. Cervical radiculopathy: Open study on percutaneous periradicular foraminal steroid infiltrations performed under CT control in 30 patients. Am J Neuroradiol 25:441–445, 2004. Dillin W, Booth R, et al. Cervical radiculopathy: A review. Spine 11:988–991, 1986. Honet JC, Puri K. Cervical radiculitis: Treatment and results in 82 patients. Arch Phys Med Rehabil 57:12–16, 1976. Joghataei MT, Arab AM, Khaksar H. The effect of cervical tractions combined with conventional therapy on grip strength on patients with cervical radiculopathy. Clin Rehabil 18:879–887, 2004. Kelly TR. Thoracic outlet syndrome: Current concepts of treatment. Ann Surg 190:657–662, 1979. Saal JS, Saal JA, Yurth EF. Nonoperative management of herniated cervical intervertebral disc with radiculopathy. Spine 21:1877–1883, 1996. Shen FH, Samartzis D, Khanna N, Goldberg EJ, An HS. Comparison of clinical and radiographic outcome in instrumented anterior cervical discectomy and fusion with or without direct uncovertebral joint decompression. Spine 4:629–635, 2004. Tsairis P, Dyck PJ, Mulder DW. Natural history of brachial plexus neuropathy: Report on 99 patients. Arch Neurol 27:109–117, 1972. Wang MY, Shah S, Green BA. Clinical outcomes following cervical laminoplasty for 204 patient with cervical spondylotic myelopathy. Surg Neurol 62:487–492, 2004. Greater Occipital Neuritis Ashkenazi A, Young WB. The effects of greater occipital nerve block and trigger point injection on brush allodynia and pain in migraine. Headache 45:350–354, 2005. Gille O, Lavignolle B, Vital JM. Surgical treatment of greater occipital neuralgia by neurolysis of the greater occipital nerve and sectioning of the inferior oblique muscle. Spine 29:828–832, 2004. 277

278


Hecht JS. Occiptal nerve block in postconcussive headaches: A retrospective review and report of ten cases. J Head Trauma Rehabil 19:58–71, 2004. Inan N, Ceyhan A, Inan Lk, et al. C2C3 nerve blocks and greater occipital nerve block in cervicogenic headache treatment. Funct Neurol 16:239–243, 2001. Kinney MA, Wilson JL, Carmichael SW, et al. Prolonged facial hypesthesia resulting from greater occipital nerve block. Clin Anat 16:362–365, 2003. Mosser SW, Guyuron B, Janis JE, Rohrich RJ. The anatomy of the greater occipital nerve: Implications for the etiology of migraine headaches. Plast Reconstr Surg 113: 293–297, 2004. Peres MF, Stiles MA, Siow HC, et al. Greater occipital nerve blockade for cluster headache. Cephalgia 22:520–522, 2002. Shields KG, Levy MJ, Goadsby PJ. Alopecia and cutaneous atrophy after greater occipital nerve infiltration with corticosteroid. Neurology 14:2193–2194, 2004. Vijayan N. Greater occipital nerve blockade for cluster headache. Cephalgia 23:323, 2003. Ward JB. Greater occipital nerve block. Semin Neurol 23:59–62, 2003. Temporomandibular Joint Ahlqvist J, Legrell PE. A technique for the accurate administration of corticosteroids in the temporomandibular joint. Dentomaxillofac Radiol 22:211–213, 1993. Alpaslan GH, Alpaslan C. Efficacy of temporomandibular joint arthrocentesis with and without injection of sodium hyaluranate in treatment of internal derangements. J Oral Maxillofac Surg 59:613–618, 2001. Boering G. Temporomandibular Joint Arthrosis: An Analysis of 400 Cases. Leiden: Stafleu, 1996. Broussard JS Jr. Derangement, osteoarthritis, and rheumatoid arthritis of the temporomandibular joint: Implications, diagnosis, and management. Dent Clin North Am 49:327–342, 2005. DeLeeuw R, Boering G, Stengenga B, et al. Clinical signs of TMJ osteoarthrosis and internal derangement 30 years after nonsurgical treatment. J Orofac Pain 8:18–24, 1994. Dolwick MF. Temporomandibular disorders. In Koopman WJ (ed): Arthritis and Allied Conditions. Philadelphia: Lippincott, Williams and Wilkins, 2001. Hepguler S, Akhoc YS, Pehlivan M, et al. The efficacy of intra-articular sodium hyalurnoate in patients with reducing displaced disc of the temporomandibular joint. J Oral Rehabil 29:80-60, 2002. Kopp S, Wenneberg B, Haraldson T, Carlsson GE. The short term effect of intra-articular injections of sodium hualuronate and corticosteroid on the temporomandibular joint pain and dysfunction. J Oral Maxillofac Surg 43: 429–435, 1985. Nyberg J, Adell R, Svensson B. Temporomandibular joint discectomy of treatment of unilateral internal derangement—a 5 year follow-up evaluation. Int J Oral Maxillofac Surg 33:8–12, 2004. Schindler C, Paessler L, Eckelt U, Kirch W. Severe temporomandibular dysfunction and joint destruction after intra-articular injection of triamcinolone. J Oral Pathol Med 34:184–186, 2005.

Suarex OF, Ourique SA. An alternate technique for management of acute closed locks. Cranio 18:233–234, 2000. Toller P. Use and misuse of intra-articular corticosteroids in treatment of temporomandibular joint pain. Proc R Soc Med 70:461–463, 1977. Vallon D, Akerman S, Nilner M, Peterson A. Long-term follow-up of intra-articular injections into the temporomandibular joint in patients with rheumatoid arthritis. Swed Dent J 26:149–158, 2002. Yura S, Totsuka Y, Yoshikawa T, Inoue N. Can arthrocentesis release intracapsular adhesions? Arthroscopic findings before and afftger irrigation under sufficient hydraulic pressure. J Oral Maxillofac Surg 61:1253–1256, 2003. Fibromyalgia Felson DT, Goldenberg DL. The natural history of fibromyalgia. Arthritis Rheum 29:1522–1526, 1986. Simms RW, Goldenberg DL, Felson DT, et al. Tenderness in 75 anatomical sites: Distinguishing fibromyalgia patients from controls. Arthritis Rheum 31:182–187, 1988. Wolfe F. Fibromyalgia: The clinical syndrome. Rheum Dis Clin NA 15:1–17, 1989. SHOULDER Anderson BC, Kaye S. Shoulder pain: Differential diagnosis. West J Med 138:268, 1983. Chuang TY, Hunder GG, Ilstrup DM, et al. Polymyalgia rheumatica: a 10-year epidemiologic and clinical study. Ann Intern Med 97:672–680, 1982. Codman EA. The Shoulder. Boston: Thomas Todd, 1934. Fiddian NJ, King RJ. The winged scapula. Clin Orthop 185:228–236, 1984. Kelley MJ, Ramsey ML. Osteoarthritis andtraumatic arthritis of the shoulder. J Hand Ther 13:148–162, 2000. Impingement Syndrome AlgunK, Birtane M, Akarirmak U. Is subacromial corticosteroid injection beneficial in subacromial impingement syndrome? Clin Rheumatol 23:496–500, 2004. Brox JI, et al. Arthroscopic surgery compared with supervised exercises in patients with rotator cuff disease (stage II impingement syndrome). Br Med J 307:899–903, 1993. Haahr JP, Ostergaard S, Dalsgaard J, et al. Exercises versus arthroscopic decompression in patients with subacromial impingement: A randomized, controlled study in 90 cases with a one year follow up. Ann Rheum Dis 64: 760–764, 2005. Koester MC, George MS, Kuhn JE. Shoulder impingement syndrome. Am J Med 118:452–455, 2005. Lozman PR, Hechtman KS, Uribe JW. Combined arthroscopic management of impingement syndrome and acromioclavicular joint arthritis. J South Orthop Assoc 4: 177–181, 1995. Neer CR. Impingement syndromes. Clin Orthop 173:70–77, 1983. Neer CS. Anterior acromioplasty for the chronic impingement syndrome of the shoulder. J Bone Joint Surg 73A:707–715, 1991.

REFERENCES

Neer CS II. Anterior acromioplasty for the chronic impingement syndrome in the shoulder. J Bone Joint Surg Am 87:1399, 2005. Neer CS II. Anterior acromioplasty for the chronic impingement syndrome in the shoulder: A preliminary report. J Bone Joint Surg. 54A:41–50, 1972. Rotator Cuff Tendinitis/Bursitis Arroll B, Goodyear-Smith F. Corticosteroid injections for painful shoulder: A meta-analysis. Br J Gen Pract 55: 224–228, 2005. Bosworth BM. Calcium deposits in the shoulder and subacromial bursitis. A survey of 12,222 shoulders. JAMA 116:2477–2482, 1941. Chard MD, Sattelle MD, Hazleman BL. The long-term outcome of rotator cuff tendonitis: A review study. Br J Rheumatol 27:385–389, 1988. Crisp EJ, Kendall PH. Treatment of periarthritis of the shoulder with hydrocortisone. Br Med J 1:1500–1501, 1955. Ellis RM, Hollingworth GR, MacCollum MS. Comparison of injection techniques for shoulder pain: Results of a double-blind, randomized study. BMJ 287:1339–1341, 1983. Fearnley M, Vadasz I. Factors influencing the response of lesions of the rotator cuff of the shoulder to local steroid injection. Ann Phys Med 10:53–63, 1969. Herrera JE, Stubblefield MD. Rotator cuff tendonitis in lymphedema: a retrospective case series. Arch Phys Med Rehabil 85:1939–1942, 2004. Petri M, Dobrow R, Neiman R, Whiting-O’Keefe Q, Seaman WE. Randomized, double-blind placebo-controlled study of the treatment of the painful shoulder. Arthritis Rheumatol 30:1040–1045, 1987. Valtonen EJ. Double-acting betamethasone (Celestone Chronodose) in the treatment of supraspinatus tendonitis. J Intern Med 6:463–467, 1978. White RH, Paull DM, Fleming KW. Rotator cuff tendonitis: Comparison of subacromial injection of a long-acting corticosteroid versus oral indomethacin therapy. J Rheumatol 13:608–613, 1986. Rotator Cuff Tendon Rupture Ahovuo J, Paavolainen P, Slatis P. The diagnostic value of arthrography and plain radiography in rotator cuff tears. Acta Orthop Scand 55:220–223, 1984. Codman EA, Akerson IV. The pathology associated with rupture of the supraspinatus tendon. Ann Surg 93:348–359, 1931. Darlington LG, Coomes EN. The effects of local steroid injection for supraspinatus tears. Rheumatol Rehabil 16: 172–179, 1977. Klinger HM, Steckel H, Ernstberger T, Baums MH. Arthroscopic debridement of massive rotator cuff tears: Negative prognostic factors. Arch Orthop Trauma Surg 125: 261–266, 2005. Millstein ES, Snyder SJ. Arthroscopic management of partial, full-thickness, and complex rotator cuff tears: indications, techniques, and complications. Arthroscopy 19 Suppl 1:189–200, 2003.

279

Nuber GW, Bowen MK. Arthroscopic treatment of acromioclavicular joint injuries and results. Clin Sports Med 22:301–317, 2003. Samilson RL, Binder WF. Symptomatic full-thickness tears of the rotator cuff. Orthop Clin North Am 6:449–466, 1975. Watson M. Major ruptures of the rotator cuff: The results of surgical repair in 89 patients. J Bone Joint Surg Br 67: 618–624, 1985. Biceps Tendinitis/Tear Erickson SJ, Fitzgerald SW, Quinn SF, et al. Long bicipital tendon of the shoulder: Normal anatomy and pathologic findings on MR imaging. Am J Roentgenol 158:1091–1096, 1992. Holtby R, Razmjou H. Accuracy of the Speed’s and Yergason’s tests in detecting biceps pathology and SLAP lesions: comparisons with arthroscopic findings. Arthroscopy 20:231–236, 2004. Mariani EM, Cofield RH, Askew LJ, Li GP, Chao EY. Rupture of the tendon of the long head of the biceps brachii: Surgical versus nonsurgical treatment. Clin Orthop 228:233–239, 1988. Murthi AM, Vosburgh CL, Neviaser TJ. The incidence of pathologic changes of the long head of the biceps tendon. J Shoulder Elbow Surg 9:382–385, 2000. Sethi N, Wright R, Yamaguchi K. Disorders of the long head of the biceps tendon. J Shoulder Elbow Surg 8: 644–654, 1999. Soto-Hall R, Stroot JH. Treatment of ruptures of the long head of the biceps brachii. Am J Orthop 2:192–193, 1960. Frozen Shoulder Andren L, Lundbery BJ. Treatment of rigid shoulders by joint distension during arthrography. Acta Orthop Scand 36:45–53, 1965. Bell S, Coghlan J, Richardson M. Hydrodilation in the management of shoulder capsulitis. Australas Radiol 47: 247–251, 2003. Bulgren DY, Binder AI, Hazleman BL, et al. Frozen shoulder: A prospective clinical study with an evaluation of three treatment regimens. Ann Rheumatol Dis 43:353–360, 1984. Gavant ML, Rizk TE, Gold RE, Flick PA. Distention arthrography in the treatment of adhesive capsulitis of the shoulder. J Vasc Interv Radiol 5:305–308, 1994. Jacobs LGH, Barton MAJ, Wallace WA, et al. Intra-articular distension and steroids in the management of capsulitis of the shoulder. Br Med J 302:1498–1501, 1991. Rizk TE, Pinals RS. Frozen shoulder. Semin Arthritis Rheumatol 11:440–452, 1982. Steinbocker O, Argyros TG. Frozen shoulder: Treatment by local injection of depot corticosteroids. Arch Phys Med Rehabil 55:209–212, 1974. Weiss JJ. Arthrography-assisted intra-articular injection of steroids in treatment of adhesive capsulitis. Arch Phys Med Rehabil 59:285–287, 1978.

280


Acromioclavicular Disorders Buttaci CJ, Stitik TP, Yonclas PP, Foye PM. Osteoarthritis of the acromioclavicular joint: A review of anatomy, biomechanics, diagnosis, and treatment. Am J Phys Med Rehabil 83:791–797, 2004. Dumonski M, Mazzocca AD, Rios C, et al. Evaluation and management of acromioclavicular joint injuries. Am J Orthop 33:526–532, 2004. Jacob AK, Sallay PI. Therapeutic efficacy of corticosteroid injections in the acromioclavicular joint. Biomed Sci Instrum 34:380–385, 1997. Mehrberg RD, Lobel SM, Gibson WK. Disorders of the acromioclavicular joint. Phys Med Rehabil Clin N Am 15: 537–555, 2004. Mestan MA, Bassano JM. Posttraumatic osteolysis of the distal clavicle: analysis of 7 cases and review of the literature. J Manipulative Physiol Ther 24:356–361, 2001. Mouhsine E, Garofalo R, Crevoisier X, Farron A. Grade I and II acromioclavicular dislocations: Results of conservative treatment. J Shoulder Elbow Surg 12:599–602, 2003. Shaffer BS. Painful conditions of the acromioclavicular joint. J Am Acad Orthop Surg 7:176–188, 1999. Slawski DP, Cahill BR. Atraumatic osteolysis of the distal clavicle. Results of open surgical excision. Am J Sports Med 22:267–271, 1994. Strobel K, Pfirrmann CW, Zanetti M, et al. MRI features of the acromioclaviculr joint that predict pain relief from intraarticular injection. Am J Roentgenol 181:755–760, 2003. Tao HM, Chen J, Ji YY, Yand DS. Post-traumatic osteolysis of the distal clavicle, pubis, and ischium in 7 patients. Chin J Traumatol 7:347–352, 2004. Walton J, Mahajan S, Paxinos A, et al. Diagnostic values of tests for acromioclavicular joint pain. J Bone Joint Surg Am 86:807–812, 2004. Weinstein DM, McCann PD, McIlveen SJ, Flatow EL, Bigliani LU. Surgical treatment of complete acromioclavicular dislocations. Am J Sports Med 23:324–331, 1995. Zawadsky M, Marra G, Wister JM, et al. Osteolysis of the distal clavicle: long-term results of arthroscopic resection. Arthroscopy 16:600–605, 2000. ELBOW Mair SD, Isbell WM, Gill TJ, et al. Triceps tendon ruptures in professional football players. Am J Sports Med 32:431–434, 2004. Lateral Epicondylitis Bowen RE, Dorey FJ, Shapiro MS. Efficacy of nonoperative treatment for lateral epicondylitis. Am J Orthop 30: 642–646, 2001. Boyd HB, McLeod AC. Tennis elbow. J Bone Joint Surg 55A:1183–1197, 1973. Day BH, Gavindasamy N. Corticosteroid injection in the treatment of tennis elbow. Practice Med 220:459–462, 1978. Fillion PL. Treatment of lateral epicondylitis. Am J Occup Ther 45:340–343, 1991. Nirschl RP, Pettrone FA. Tennis elbow: The surgical treatment of lateral epicondylitis. J Bone Joint Surg Am 61: 832–839, 1979.

Potter HG, Hannafin JA, Morsessel RM, DiCarlo EF, O’Brien SJ, Altchek DW. Lateral epicondylitis: Correlation with MR imaging, surgical and histopathologic findings. Radiology 196:43–46, 1995. Smidt N, Lewis MA, Hay EM, et al. A comparison of two primary care trials on tennis elbow: Issues of external validity. Ann Rheum Dis (in press). Olecranon Bursitis Berliner MN, Bretzel RG, Klett R. Successful radiosynoviorthesis of an olecranon bursitis in psoriatic arthritis. Ann Rheum Dis 61:187–188, 2002. Hassell AB, Fowler PD, Dawes PT. Intra-bursal tetracycline in the treatment of olecranon bursitis in patients with rheumatoid arthritis. Br J Rheumatol 33:859–860, 1994. Knight JM, Thomas JC, Maurer RC. Treatment of septic olecranon and prepatellar bursitis with percutaneous placement of a suction-irrigation system: A report of 12 cases. Clin Orthop 206:90–93, 1986. Stewart NJ, Manzanares JB, Morrey BF. Surgical treatment of aseptic olecranon bursitis. J Shoulder Elbow Surg 6:49–54, 1997. Weinstein PS, Canosos JJ. Long-term follow-up of corticosteroid injection for traumatic olecranon bursitis. Ann Rheum Dis 43:44–46, 1984. Elbow Arthritis Doherty M, Preston B. Primary osteoarthritis of the elbow. Ann Rheum Dis 48:743–747,1989. WRIST Allan CH, Joshi A, Lichtman DM. Kienbock’s disease: diagnosis and treatment. J Am Acad Orthop Surg 9:128–136, 2001. Papathanasiou ES, Loizides A, Panayiotou P, et al. Ulnar neuropathy at Guyon’s canal: Electrophysiological and surgical findings. Electomyogr Clin Neurophysiol 45:87–102, 2005. Wrist Sprain Adelaar RS.Traumatic wrist instabilities. Contemp Orthop 4:309–324, 1982. Cerezal L, del Pinal F, Abascal F. MR imaging findings in ulnar-sided wrist impaction syndromes. Magn Reson Imaging Clin N Am 12:281–299, 2004. Dorsal and Volar Wrist Ganglia Angelides AC, Wallace PF. The dorsa lganglion of the wrist: Its pathogenesis, gross and microscopic anatomy and surgical treatment. J Hand Surg 1:228–235, 1978. Crock HV. Large ganglia occurring in tendons. Br J Surg 47:319–321, 1959. Jacobs LGH, Govaers KJM. The volar wrist ganglion: just a simple cyst? J Hand Surg 15B:342–346, 1990. Kozin SH, Urban MA, Bishop AT, Dobyns JH. Wrist ganglia: Diagnosis and treatment of a bothersome problem. J Musculoskel Med 10:21–44, 1993.

REFERENCES

Limpaphayom N, Wilairatana V. Randomized controlled trial between surgery and aspiration combined with methylprednisolone acetate injection plus wrist immobilization in the treatment of dorsal carpal ganglion. J Med Assoc Thai 87:1513–1517, 2004. Lowden CM, Attiah M, Garvin G, et al. The prevalence of wrist ganglion in an asymptomatic population: Magnetic resonance evaluation. J Hand Surg Br 30:302–306, 2005. Ogino T, Minami A, Fukada K, et al. The dorsal occult ganglion of the wrist and ultrasonography. J Bone Joint Surg 13B:181–183, 1988. Park S, Iida T, Yoshimura K, Kawasaki Y. Phenol cauterization for ganglions of the hand, wrist, and foot: A preliminary report. Ann Plast Surg 48:582–585, 2002. Richman JA, Gelberman RH, Engber WD, et al. Ganglions of the wrist and digits. Results of treatment by aspiration and cyst wall puncture J Hand Surg 123A: 1041–1043, 1987. Thornberg LE. Ganglions of the hand and wrist. J Am Acad Orthop Surg 7:231–238, 1999. Carpometacarpal Osteoarthritis Berggren M, Joost-Davidsson A, Lindstrand J, et al. Reduction in the need for operation after conservative treatment of osteoarthritis of the first carpometacarpal joint: A seven year prospective study. Scand J Plast Reconstr Surg Hand Surg 35:415–417, 2001. Damen A, Dijkstra T, vand der Lei B, et al. Long-term results of arthrodesis of the carpometacarpal joint of the thumb. Scand J Plast Reconstr Surg Hand Surg 35:407–413, 2001. Hartigan BJ, Stern PJ, Kiefhaber TR. Thumb carpometacarpal osteoarthritis: Arthrodesis compared with ligament reconstruction and tendon interposition. J Bone Joint Surg 83A:1470–1478, 2001. Kriegs-Au G, Petje G, Fojti E. Ligament reconstruction with or without tendon interposition to treate primary thumb carpometacarpal osteoarthritis. A prospective randomized study. J Bone Joint Surg 86A:209–218, 2004. Kwasniewski CT. Basal joint osteoarthritis of the thumb: A prospective trial of steroid injection and splinting. J Hand Ther 18:51, 2005. Sachle T, Sande S, Finsen V. Abductor pollicis longus tendon interposisiton for arthrosis in the first carpometacarpal joint: 55 thumbs reviewed after 3 (1–5) years. Acta Orthop Scand 73:674–677, 2002. Schroder J, Kerkhoffs GM, Voerman HJ, Marti RK. Surgical treatment of basal joint disease of the thumb: Comparison between resection-interposition arthroplasty and trapezio-metacarpal arthrodesis. Arch Orthop Trauma Surg 122:35–38, 2002. Carpal Tunnel Syndrome Armstrong T, Devor W, Borschel L, Contreras R. Intracarpal steroid injection is safe and effective for shortterm management of carpal tunnel syndrome. Muscle Nerve 29:82–88, 2004. Braun RM, Rechnic M, Fowler E. Compications related to carpal tunnel release. Hand Clin 18:347–357, 2002.

281

Demirci S, Kutluhan S, Koyuncuoglu HR, et al. Comparison of open carpal tunnel release and local steroid treatment outcomes in idiopathic carpal tunnel syndrome. Rheumatol Int 22:33–37, 2002. Ellis J. Clinical results of a cross-over treatment with pyridoxine and placebo of the carpal tunnel syndrome. Am J Clin Nutr 32:2040–2046, 1979. Foster JB, Goodman HV. The effect of local corticosteroid injection on median nerve conduction in carpal tunnel syndrome. Ann Phys Med 6:287–294, 1962. Gelberman RH, Aronson D, Weisman MH. Carpal-tunnel syndrome: Results of a prospective trial of steroid injection and splinting. J Bone Joint Surg Am 62:1181–1184, 1980. Graham RG, Hudson DA, Solomons M, Singer M. A prospective study to assess the outcome of steroid injections and wrist splinting for the treatment of carpal tunnel syndrome. Plast Reconstr Surg 113:550–556, 2004. Hagebeuk EE, de Weerd AW. Clinical and electrophysiological follow-up after local steroid injection in the carpal tunnel syndrome. Clin Neurophysiol 115:1464–1468, 2004. Jimenez DF, Gibbs SR, Clapper AT. Endoscopic treatment of carpal tunnel syndrome: A critical review. Neurosurg Focus 3:e6, 1997. Leit ME, Weiser RW, Tomaino MM. Patient-reported outcome after carpal tunnel release for advanced disease: A prospective and longitundinal assessment in patients older than age 70. J Hand Surg (AM) 29:379–383, 2004. MacDonald RI, Lichtman DM, Hanon JJ: Complications of surgical release of carpal tunnel syndrome. J Hand Surg 7:70–76, 1978. Marshall S, Tardif G, Ashworth N. Local corticosteroid injection for carpal tunnel syndrome. Cochrane Database Syst Rev 4:CD001554, 2002. Michlovitz SL. Conservative interventions for carpal tunnel syndrome. J Orthop Sports Phys Ther 34:589–600, 2004. Nora DB, Becker J, Ehlers JA, Gomes I. Clinical features of 1039 patients with neurophysiological diagnosis of carpal tunnel syndrome. Clin Neurol Neurosurg 107:64–69, 2004. Phalen GS. Carpal tunnel syndrome: 17 years of experience in diagnosis and treatment. J Bone Joint Surg 48A:211–228, 1966. Phalen GS. The carpal tunnel syndrome: Clinical evaluation of 598 hands. Clin Orthop 83:29, 1972. Pierre-Jerome C, Bekkelund SI. Magnetic resonance assessment of the double-cruch phenomenon in patients with carpal tunnel syndrome: a bilateral quantitative study. Scan J Plast Reconstr Surg 37:46–53, 2003. Sevim S, Dogu O, Camdeviren H, et al. Long-term effectiveness of steroid injections and splinting in mild and moderate carpal tunnel syndrome. Neurol Sci 25:48–52, 2004. Shapiro S. Microsurgical carpal tunnel release. Neurosurgery 37:66–70, 1995. Solomons M, Singer M. A propective study to assess the outcome of steroid injections and wrist splinting for the treatment of carpal tunnel syndrome. Plast Reconstr Surg 113:550–556, 2004. Verdugo RJ, Salinas RS, Castillo J, Cea JG. Surgical versus non-surgical treatment for carpal tunnel syndrome. Cochrane Database Syst Rev 3:CD001552, 2003.

282


DeQuervain’s Tenosynovitis Anderson C, Manthey R, Brouns MC. Treatment of DeQuervain’s tenosynovitis with corticosteroids. Arthritis Rheumatol 34:793–798, 1991. Arons MS. De Quervain’s release in working women: A report of failures, complications, and associated diagnoses. J Hand Surg 12:540–544, 1987. Avci S, Yilmaz C, Sayli U. Comparison of nonsurgical treatment measures for de Quervain’s disease of pregnancy and lactation. J Hand Surg (AM) 27:322–324, 2002. Bjorkman A, Jorgsholm P. Rupture of the extensor pollicis longus tendon: a study of aetiological factors. Scan J Plast Reconstr Surg Hand Surg 38:32–35, 2004. Clark DD, Ricker JH, MacCollum MS. The efficacy of local steroid injection in the treatment of stenosing tenovaginitis. Plast Reconstr Surg 49:179–80, 1973. Faithful DK, Lamb DW: De Quervain’s disease: A clinical review. Hand 3:23–30,1971. Harvey FJ, Harvey PM, Horsly MW. DeQuervain’s disease: Surgical or nonsurgical treatment. J Hand Surg 15A: 83–87, 1990. Richie CA III, Briner WW Jr. Corticosteroid injection for treatment of de Quervain’s tenosynovitis: A pooled quantitative literature evaluation. J Am Board Fam Pract 16: 102–106, 2003. Distal Radius Fractures Cooney WP III, Dobyns JH, Linscheld RI. Complications of Colles’ fractures. J Bone Joint Surg 62A: 613–619, 1980. Dias JJ, Wray CC, Jones JM, Gregg PH. The value of early mobilization in the treatment of Colles’ fractures. J Bone Joint Surg 69B:463–467, 1987. Ladd AL, Pliam NB. The role of bone graft and alternatives in unstable distal radius fracture treatment. Orthop Clin North Am 32:337–351, 2001. Markiewitz AD, Gellman H. Five-pin external fixation and early range of motion for distal radius fractures. Orthop Clin North Am 32:329–335, 2001. Nesbitt KS, Failla JM, Les C. Assessment of instability factors in adult distal radius fractures. J Hand Surg Am 29: 1128–1138, 2004. Paksima N, Panchal A, Posner MA, et al. A meta-analysis of the literature on distal radius fractures: Review of 615 articles. Bull Hosp Jt Di 62:40–46, 2004. Ring D, Jupiter JB. Percutaneous and limited open fixation of fractures of the distal radius. Clin Orthop 375: 105–115, 2000. Simic PM, Weiland AJ. Fractures of the distal aspect of the radius: changes in treatment over the past two decades. J Bone Joint Surg 85A:552–564, 2003. Yajima H, Kobata Y, Shigematsu K, et al. Radiocarpal arthrodesis for osteoarthritis following fractures of the distal radius. Hand Surg 9:203–209, 2004. Navicular Fracture Bhat M, McCarthy M, Davis TR, et al. MRI and plain radiography in the assessment of displaced fractures of the waist of the carpal scaphoid. J Bone Joint Surg Br 86: 705–713, 2004.

Bohler L, Trojan E, Jahna H. The results of treatment of 734 fresh, simple fractures of the scaphoid. J Hand Surg 28:319–331, 2003. Magelvoort RW, Kon M, Schurman AH. Proximal row carpectomy: A worthwhile salvage procedure. Scand J Plast Reconstr Hand Surg 36:289–299, 2002. McAdams TR, Spisak S, Beaulieu CF, Ladd AL. The effect of pronation and supination on the minimally displaced scaphoid fracture. Clin Orthop 411:255–259, 2003. Merrell GA, Wlkfe SW, Slade JF III. Treatment of scaphoid nonunions: quantitative meta-analysis of the literature. J Hand Surg 27:685–691, 2002. Saeden B, Tornkvist H, Ponzer S, Hoglund M. Fracture of the carpl scaphoid. A propective, randomized 12-year follow-up comparing operative and conservative treatment. J Bone Joint Surg Br 83:230–234, 2001. Trumble TE, Salas P, Barthel T, et al. Management of scaphoid nonunions. J Am Acad Orthop Surg 12:33A, 2004. HAND General Belsky MR, Feldon P, Millender LH, et al. Hand involvement in psoriatic arthritis. J Hand Surg 7:203–207, 1982. Reginato AJ, Ferreiro JL, O’Connor CR, et al. Clinical and pathologic studies of twenty-six patients with penetrating foreign body injury to the joint, bursae, and tendon sheath. Arthritis Rheum 33:1753–1762, 1990. Trigger Finger Anderson BC, Kaye S. Treatment of flexor tenosynovitis of the hand (“trigger finger”) with corticosteroids. Arch Int Med 151:153–156, 1991. Fitzgerald BT, Hofmeister EP, Fan RA, Thompson MA. Delayed flexor digitorum superficialis and profundus ruptures in a trigger finger after a steroid injection: a case report. J Hand Surg Am 30:479–482, 2005. Gilberts EC, Wereldsma JC. Long-term results of percutaneous and open surgery for trigger fingers and thumbs. Int Surg 87:48–52, 2002. Gray RG, Kiem IM, Gottlieb NL. Intratendon sheath corticosteroid treatment of rheumatoid arthritis–associated and idiopathic flexor tenosynovitis. Arthritis Rheumatol 21: 92–96, 1978. Lyu SR. Closed division of the flexor tendon sheath for trigger finger. J Bone Joint Surg 74:418–420, 1992. Maneerit J, Sriworakun C, Buhraja N, Nagavajara P. Trigger thumb: Results of a prospective randomized study of percutaneous release with steroid injection versus steroid injection alone. J Bone Joint Surg Am 86:1103, 2004. Murphy D, Failla JM, Koniuch MP. Steroid versus placebo injection for trigger finger. J Hand Surg 20: 628–631, 1995. Park MJ, Oh I, Ha KI. A1 pulley release of locked trigger digit by percutaneous technique. J Hand Surg Br 29: 502–505, 2004. Stothard J, Kumar A. A safe percutaneous procedure for trigger finger release. J R Coll Surg 39:116–117, 1994.

REFERENCES

Dupuytren’s Contracture Abe Y, Rokkaku T, Ofuchi S, et al. Dupuytren’s disease on the radial aspect of the hand: Report on 135 hands in Japanese patients. J Hand Surg 29:359–362, 2004. Beltran JE, Jimeno-Urban F, Yunta A. The open palm and digital technique in the treatment of Dupuytren’s contracture. Hand 8:73–77, 1976. Beyermann K, Prommersberger KJ, Jacobs C, Lanz UB. Severe contracture of the proximal interphalangeal joint in Dupuytren’s disease: Does capsuloligamentous release improve outcome? J Hand Surg 29B:240–243, 2004. Khan AA, Rider OJ, Jayadex CU, et al. The role of manual occupation in the aetiology of Dupuytren’s disease in men in England and Wales. J Hand Surg 29:12–14, 2004. Larsen S, Frederiksen H. Genetic and environmental influence in Dupuytren’s disease amoung 6,105 males. J Hand Surg 28(Suppl 1):13, 2003. Leclereq C, Fernandez H. Complications following fasciectomy with primary closure in Dupuytren’s disease. J Hand Surg 28(Suppl 1):12, 2003. Meek RM, McLellan S, Reilly J, Crossen JF. The effect of steroids on Dupuytren’s disease: Role of programmed cell death. J Hand Surg 27:270–273, 2002. Rowley DI, Couch M, Chesney RB, Norris SH. Assessment of percutaneous fasciotomy in the management of Dupuytren’s contracture. J Hand Surg 9B:163–164, 1984. Skoff HD. The surgical treatment of Dupuytren’s contracture: a synthesis of techniques. Plast Reconstr Surg 113: 540–544, 2004. Tonkin MA, Burke FD, Varian JPW. Dupuytren’s contracture: A comparative study of fasciectomy and dermofasciectomy in one hundred patients. J Hand Surg 9:156–162, 1984. Rheumatoid Arthritis Arnett FC, Edwoarthy SM, Bloch DA, et al. The American Rheumatism Association 1987 revised criteria from the classification of rheumatoid arthritis. Arthritis Rheum 31:315–324, 1988. Fehlauer SC, Carson CW, Cannon GW. Two year follow up of treatment of rheumatoid arthritis with methotrexate: Clinical experience in 124 patients. J Rheumatol 16: 307–312, 1989. Fries JF, Spitz PW, Williams CA, et al. A toxicity for comparison of side effects among different drugs. Arthritis Rheumatol 31:121–130, 1990. Goemaere S, Ackerman C, Goethals K, et al. Onset of symptoms of rheumatoid arthritis in relation to age, sex, and menopausal transition. J Rheumatol 17:1620–1622, 1990. Kovarsky J. Intermediate-dose intramuscular methylprednisolone acetate in the treatment of rheumatic disease. Ann Rheumatol Dis 42:308–310, 1983. Kushner O. Does aggressive therapy of rheumatoid arthritis affect outcome? J Rheumatol 16:1–5, 1989. Schumacher HR. Palindromic onset of rheumatoid arthritis. Arthritis Rheum 31:519–525, 1992. Steere AC. Lyme disease. N Engl J Med 321:586–596, 1989.

283

Steere AC, Bartenhagen NH, Craft JE, et al. The early manifestations of Lyme disease. Ann Intern Med 99:76–82, 1983. Weiss MM. Corticosteroids in rheumatoid arthritis. Semin Arthritis Rheum 19:9–21, 1989. Williams HJ, Willkens RF, Samuelson CO Jr, et al. Comparison of low-dose oral pulse methotrexate and placebo in the treatment of rheumatoid arthritis. Arthritis Rheum 28:721–730, 1985. Zuckner J, Uddin J, Ramsey RH. Prolonged effect from intramuscular corticosteroids. Triamcinolone acetonide in rheumatoid arthritis. Acta Rheumatol Scand. 12:307–317, 1966. Zuckner J, Uddin J, Ramsey RH. Intramuscular administration of steroids in treatment of rheumatoid arthritis. Ann Rheumatol Dis 23:456–462, 1964. Complex Regional Pain Sndrome (Reflex Sympathetic Dystrophy) Adebajo A, Hazleman B. Shoulder pain and reflex sympathetic dystrophy. Curr Opin Rheumatol 2:270–275, 1990. Christensen K, Jensen EM, Noer I. The reflex dystrophy syndrome response to treatment with systemic corticosteroids. Acta Chir Scand 148:653–655, 1982. Crozier F, Champsaur P, Pham T, et al. Magnetic resonance imaging in reflesx sympathetic dystrophy syndrome of the foot. Joint Bone Spine 70:503–508, 2003. GrabowTS, Tella PK, Raja SN. Spinal cord stimulation for complex regional pain syndrome: An evidence-based medicine review of the literature. Clin J Pain 19:371–383, 2003. Harris J, Fallat L, Schwatz S. Characteristic trends of lower extremity complex regional pain syndrome. J Foot Ankle Surg 43:296–301, 2004. Karacan I, Aydin T, Ozaras N. Bone loss in the contralateral asymptomatic hand in patients with complex regional pain syndrome type 1. J Bone Miner Metab 22:44–47, 2004. Kemler MA, De Vet HX, Barendse GA, et al. The effect of spinal cord stimulation in patients with chronic reflex sympathetic dystrophy: two years’ follow-up of the randomized controlled trial. Ann Neurol 55:13–18, 2004. Kozin F, McCarty DJ, Dims J, Genant H. The reflex sympathetic dystrophy syndrome. I. Clinical and histologic studies: Evidence for bilaterality, response to corticosteroids and articular involvement. Am J Med 60:321–331, 1976. Kozin F, Ryan LM, Carerra GF, et al. The reflex sympathetic dystrophy syndrome (RSDS). III. Scintigraphic studies, further evidence for the therapeutic efficacy of systemic corticosteroids, and proposed diagnostic criteria. Am J Med 70:23–30, 1981. Macinnon SE, Holden LE: The use of three-phase radionuclide bone scanning in the diagnosis of reflex sympathetic dystrophy syndrome. J Hand Surg 9A:556–563, 1984. Mallis A, Furlan A. Sympathectomy for neuropathic pain. Cochrane Database Syst Rev 2:CD002918, 2003. Sandroni P, Benrud-Larson LM, McClelland RL, Low PA. Complex regional pain syndrome type I: Indicence and prevalence in Olmsted county, a population-based study. Pain 103:199–207, 2003.

284


Wasner G, Schattschneider J, Binder A, Baron R. Complex regional pain syndrome-diagnostic, mechanisns, CNS involvement and therapy. Spinal Cord 41:61–75, 2003. Zyluk A. Scoring system in the assessment of the clinical severity of reflex sympathetic dystrophy of the hand. Hand Clin 19:517–521, 2003. Zyluk A. Results of the treatment of posttraumatic reflex sympathetic dystrophy of the upper extremity with regional intravenous blocks of methylprednisolone and lidocaine. Acta Orthop Belg 64:452–456, 1998. CHEST WALL Costochondritis Disla E, Rhim HR, Reddy A, et al. Costochondritis, a prospective analysis in an emergency department setting. Arch Intern Med 154:2466–2469, 1994. Gregory PL, Biswas AC, Batt ME. Musculoskeletal problems of the chests wall in athletes. Sports Med 32:235–250, 2002. Kamel M, Kotob H. Ultrasonographic assessment of local steroid injection in Tietz’s syndrome. Br J Rheumatol 36:547–550, 1997. Mendelson G, Mendelson H, Horowitz SF, et al. Can (99m) technetium methylene diphosphonate bone scans objectively document costochondritis. Chest 111:1600–1602, 1997. Wise CM, Semble L, Dalton CB. Musculoskeletal chest wall syndromes in patients with noncardiac chest pain, a study of 100 patient. Arch Phys Med Rehabil 72:147–149, 1992. Sternoclavicular Arthritis Benitez CL, Mintz DN, Potter HG. MR imaging of the sternoclavicular joint following trauma. Clin Imaging 28: 59–63, 2004. Ernberg LA, Potter HG. Radiographic evaluation of the acromioclavicular and sternoclavicular joints. Clin Sports Med 22:255–275, 2003. Hiramuro-Shoji F, Wirth MA, Rockwood CA Jr. A traumatic conditions of the sternoclavicular joint. J Shoulder Elbow Surg 12:79–88, 2003. Noble JS. Degenerative sternoclavicular arthritis and hyperostosis. Clin Sports Med 22:407–422, 2003. Pingsmann A, Patsalis T, Michiels I. Resection arthroplasty of the sternoclavicular joint for the treatment of primary degenerative sternoclavicular arthritis. J Bone Joint Surg 84:513–517, 2002. Ross JJ, Shamsuddin H. Sternoclavicular septic arthritis: Review of 180 cases. Medicine 83:139–148, 2004. Xiphoidynia Howell J. Xiphoidynia: An uncommon cause of exertional chest pain. Am J Emerg Med 8:176, 1990. BACK Carette S, Graham DC, Little HA, et al. The natural disease course of ankylosing spondylitis. Arthritis Rheum 26:186–190, 1983.

Chen HC, Tzaan WC, Lui TN. Spinal epidural abscesses: A retrospective analysis of clinical manifestations, sources of infections and outcomes. Chang Gung Med J 27: 351–358, 2004. DeWald CJ, Vartabedian JE, Rodts MF, Hammerberg KW. Evaluation and management of high-grade spondylolithesis in adults. Spine 30(6Suppl):S49–S59, 2005. Khan MA, Khan MK. Diagnostic value of HLA-B27 testing in ankylosing spondylitis and Reiter’s syndrome. Ann Intern Med 96:70–76, 1982. Ogilvie JW. Complications in spondylolithesis surgery. Spine 30(6 Suppl):S97–S101, 2005. Stroebel RJ, Ginsburg WW, McLeod RA. Sacral insufficiency fractures: an often ussuspected cause of low back pain. J Rheumatol 18:117–119, 1991. Low Back Strain Akinpelu AO, Adeyemi, AI. Range of lumbar flexion in chronic low back pain. Cent Afr J Med 35:430–432, 1989. Basmajian JV. Acute back pain and spasm: A controlled multicenter trial of combined analgesic and antispasm agents. Spine 14:438–439, 1989. Benzon HT. Epidural steroid injections for low back pain and lumbosacral radiculopathy. Pain 24:277–295, 1986. Bogduk N, Cherry D. Epidural corticosteroid agents for sciatica. Med J Austral 143:402–406, 1985. Carette S, Marcoux S, Truchon R, et al. A controlled trial of corticosteroid injection into facet joints for chronic low back pain. N Engl J Med 325:1002–1007, 1991. Cullen AP. Carisoprodal (soma) in acute back conditions: A double-blind, radomized, placebocontrolled study. Curr Ther Res 20:557–562, 1976. Deyo RA, Diehl AK, Rosenthal M. How many days of bed rest for acute low back pain? A randomized clinical trial. N Engl J Med 315:1064–1070, 1986. Deyo RA, Walsh NE, Martin DC, et al. A controlled trial of transcutaneous electrical nerve stimulation (TENS) and exercise for chronic low back pain. N Engl J Med 322: 1627–1634, 1990. Garvey RA, Marks MR, Wiesel SW. A prospective, randomized, double-blind evaluation of trigger-point injection therapy for low-back pain. Spine 14:962–964, 1989. Huston CW, Slipman CW, Garvin C. Complications and side effects of cervical and lumbosacral selective nerve root injections. Arch Phys Med Rehabil 86:277–283, 2005. Jackson RP, Jacobs RR, Montesano PX. Facet joint injection in low back pain: A prospective statistical study. Spine 13:966–971, 1988. Kepes ER, Duncalf D. Treatment of back ache with spinal injections of local anesthetics, spinal and systemic steroids: A review. Pain 22:33–47, 1985. Macrai IF, Wright V. Measurement of back movement. Ann Rheumatol Dis 28:584–589, 1969. McLain RF, Kapural L, Mekhail NA. Epidural steroids for back and leg pain: mechanism of action and efficacy. Cleve Clin J Med 71:961–970, 2004. Rollings HE, Glassman JM, Joyka JP. Management of acute musculoskeletal conditions—thoracolumbar strain or sprain: A double-blind evaluation comparing the efficacy and safety of carisoprodol with cyclobenzaprine hydrochloride. Curr Ther Res 34:917–928, 1983.

REFERENCES

Vad VB, Bhat al, Lutz GE, Cammisa F. Transforaminal epidural steroid injection in lumboscaral radiculopathy: A prospective randomized study. Spine 27:11–16, 2002 Wang JC, Lin E, Brodke DS, Youssef JA. Epidural injections for the treatment of symptomatic lumbar discs. J spinal Disord Tech 15:269–272, 2002. Westbrook L, Cicala RJ, Wright H. Effectiveness of alprazolam in the treatment of chronic pain: Results of a preliminary study. Clin J Pain 6:32–36, 1990. Lumbosacral Disc Disease Cucler JM, Bernini PA, Wiesel SW, et al. The use of epidural steroids in the treatment of lumbar radicular pain: A prospective, randomized, double blind study. J Bone Joint Surg Am 67:63–66, 1985. Gajraj NM. Selective nerve root blocks for low back pain and radiculopathy. Reg Anesth Pain Med 29:243–256, 2004. Oliphant D. Safety of spinal manipulation in the treatment of lumbar disk herniations: A systematic review and risk assessment. J Manipulative Physiol Ther 27:197–210, 2004. Wiesel SW, Tsourmas N, Feffer HL, et al. A study of computer-assisted tomography. 1. The incidence of positive CAT scans in an asymptomatic group of patients. Spine 9:549–551, 1984. Wilson-MacDonald J, Burt G, Griffin D, Glynn C. Epidural steroid injection for nerve root compression. A randomized, controlled trial. J Bone Joint Surg Br 87: 352–355, 2005. Cauda Equina Bagley CA, Gokaslan ZL. Cauda equina syndrome caused by primary and metastatic neoplasms. Neurosurg Focus 16:e3, 2004. Kohles SS, Kohles DA, Karp AP, Erlich VM, Plissar NL. Time-dependent surgical outcomes following cauda equina syndrome diagnosis: Comments on a meta-analysis. Spine 29:1281–1287, 2004. Kostuik JP, Harrington, I, Alexander D, et al. Cauda equine syndrome and lumbar disc herniation. J Bone Joint Surg 68:386–391, 1986. Tussous MW, Skerhut HE, Story JL, et al. Caude equine syndrome of long-standing ankylosing spondylitis: case report and review of the literature. J Neurosurg 73:441–447, 1990. Sacroiliac Disease Ahlstrom H, Feltelius N, Nyman R, et al. Magnetic resonance imaging of sacroiliac joint inflammation. Arthritis Rheum 33:1763–1769, 1990. Arneet F. Seronegative spondyloarthropathies. Bull Rheumatol Dis 37:1–12, 1987. Burgos-Vargax R, Pineda C. New clinical and radiographic features of the seronegative spondyloarthropathies. Curr Opinion Rheumatol 3:562–574, 1991. Klein RG, Ech BC, DeLongWB, et al. A randomized double blind trial of dextrose-glycerine-phenol injections for chronic low back pain. J Spinal Disord 6:23–33, 1993.

285

Coccydynia De Andres J, Chaves S. Coccygodynia: A proposal for an algorithm for treatment. J Pain 4:257–266, 2003. Hodges SD, Eck JC, Humphreys SC. A treatment and outcomes analysis of patients with coccydynia. Spine J 4: 138–140, 2004. Malgne JY, Doursounian L, Chatellier G. Causes and mechanisms of common coccydynia: Role of body mass index and coccygeal trauma. Spine 25:3072–3079, 2000. Perkins R, Schofferman J, Reynolds J. Coccygectomy for refractory sacrococcygeal joint pain. J Spinal Discord Tech 16:100–103, 2003. Pyper JB. Excision of the coccyx for coccydynia: A study of the results in twenty-eight cases. J Bone Joint Surg Br 39:733–737, 1957. HIP General Carney BT, Weinstein SL, Noble J. Long-term follow-up of slipped cpital femoral epiphysis. J Bone Joint Surg 73:667–674, 1991. Lakhandpal S, Ginsberg WW, Luthra HS, Handen GG. Transient regional osteoporosis: A study of 56 cases and a review of the literature. Ann Intern Med 106:444–450, 1987. Smith RG, Appel SH. The Lambert-Eaton Syndrome. Hospital Practice 27:101–114, 1992. Soubrier M, Dubost JJ, Bolsgard S, et al. Insufficiency fracture. A surgey of 60 cases and review of the literature. Joint Bone Spine 70:209–218, 2003. Trochanteric Bursitis/Piriformis Syndrome Barton PM. Piriformis syndrome: A rational approach to management. Pain 47:345–352, 1991. Bird PA, Oakley SP, Shnier R, Kirkham BW. Prospective evaluation of magnetic resonance imaging and physical examination findings in patients with greater trochanteric pain syndrome. Arthritis Rheum 44:2138–2145, 2001. Brooker AF Jr. The surgical approach to refractory trochanteric bursitis. Johns Hopkins Med J 145:98–100, 1979. Cohen SP, Narvaez JC, Lebovits AH, Stojanovic MP. Corticosteroid injections for trochanteric bursitis: Is fluoroscopy necessary? A pilot study. Br J Anaesth 94:100–106, 2005. Ege-Rasmussen KJ, Fano N. Trochanteric bursitis: Treatment by corticosteroid injection. Scand J Rheumatol 14:417–420, 1985. Fishman LM, Zyber PA. Electrophysiologic evidence of piriformis syndrome. Arch Phys Med Rehabil 73:359–364, 1992. Fox JL. The role of arthroscopic bursectomy in the treatment of trochanteric bursitis. Arthroscopy 18:E34, 2002. Kagan A II. Clin Orthop Relat Res 368:135–140, 1999. Karpinski MR, Piggott H. Greater trochanteric pain syndrome. A report of 15 cases. J Bone Joint Surg Br 67: 762–763, 1985. Rothenberg RJ. Rheumatic disease aspects of leg length inequality. Semin Arthritis Rheumatol 17:196–205, 1988.

286


Shbeeb MI, O’Duffy JD, Michet CJ Jr., et al. Evaluation of glucocorticosteroid injection for the treatment of trochanteric bursitis. J Rheumatol 23:2104–2106,1996. Slawski DP, Howar RF. Surgical management of refractory trochanteric bursitis. Am J Sports Med 25:86–89, 1997. Tortolani PJ, Carbone JJ, Quartararo LG. Greater trochanteric pain syndrome in patients referred to orthopedic spine specialists. Spine J 2:251–254, 2002. Hip Arthritis Gossec L, Tubach F, Baron G, et al. Predictive factors of total hip replacement due to primary osteoarthritis: A prospective two year study of 505 patients. Ann Rheum Dis. 64:1028–1032, 2005. Keener JD, Callaghan JJ, Goetz DD, et al. Twenty-fiveyear results after charnley total hip arthroplasty in patients less than fifty years old. J Bone Joint Surg Am 85: 1066–1072, 2003. Margules KR. Fluoroscopically directed steroid instillation in the treatment of hip osteoarthritis: Safety and efficacy in 510 cases. Arthritis Rheum 44:2449–2450, 2001. 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. Santos-Ocampo AS, Santos-Ocampo RS. Non-contrast computer tomography-guided intra-articular corticosteroid injections of severe bilateral hip arthritis in a patient with ankylosing spondylitis. Clin Exp Rheumatol 21:239–240, 2003. Meralgia Paresthetica Grossman MG, Ducey SA, Nadler SS, Levy AS. Meralgia paresthetica: Diagnosis and treatment. J Am Acad Orthop Surg 9:336–44, 2001. Lee CC. Entrapment syndromes of peripheral nerve injuries. In Winn HR: Youman’s Neurological Surgery, 5th ed. Philadephia: Elsevier, 2004. Sin TL, Chandran KN. Neurolysis for meralgia paresthetica: an operative series of 45 cases. Surg Neurol 63:19–23, 2005. Van Slobbe AM, Bohnen AM, Bernsen RM, et al. Incidence rates and determinants in meralgia paresthetica in general practice. J Neurol 251:294–297, 2004. Avascular Necrosis of the Hip Chan TW, Dalinka MK, Steinberg ME, et al. MRI appearance of femoral head osteonecrosis following core decompression and bone grafting. Skeletal Radiol 20:103–107, 1991. Colwell CW Jr. The controversy of core decompression of the femoral head for osteonecrosis. Arthritis Rheum 32:797–800, 1989. Ficat RP. Idiopathic bone necrosis of the fermoral heal: Early diagnosis and treatment. J Bone Joint Surg 67:3–9, 1985. Mitchesl DG, Rao VM, Dalinka MK, et al. Femoral head avascular necrosis: Correlation of MR imaging, radiographic staging, radionuclide imaging, and clinical findings. Radiology 162:709–715, 1987.

Zizic TM, Marcoux C, Hungerford DS, et al. The early diagnosis of ischemic necrosis of bone. Arthritis Rheum 29:1177–1186, 1986. Zizic TM, Marcoux C, Hungerford DS, et al. Corticosteroid therapy associated with ischemic necrosis of bone in systemic lupus erythematosus. Am J Med 79: 586–604, 1985. Osteitis Pubis Holt MA, Keene JS, Graf BK, Helwig DC. Treatment of osteitis pubis in athletes. Results of corticosteroid injection. Am J Sports Med 23:601–606, 1995. Johnson R. Osteitis pubis. Curr Sports Med Rep 2: 98–102, 2003. Morelli V, Smith V. Groin injuries in athletes. Am Fam Physician 64:1405–1414, 2001. Ross JJ, Hu LT. Septic arthritis of the pubic symphysis: review of 100 cases. Medicine 82:340–345, 2003. KNEE General Berman A, Espinoza LR, Diaz JD, et al. Rheumatic manifestations of human immunodeficiency virus infection. Am J Med 85:59–64, 1988. Espinoza LR, Aguilar JL, Berman A, et al. Rheumatic manifestations associated with human immunodeficiency virus infection. Arthritis Rheum 32:1615–1622, 1989. Fox JM, DelPizzo W, et al. Accuracy of diagnosis from MRI of the knee: A multicenter analysis of one thousand and fourteen patients. J Bone Joint Surg 73A:2–10, 1991. Krause BL, Williams JP, Catterall A. Natural history of Osgood-Slatter’s disease, J Pediatr Orthop 10:65–68, 1990. Pritchard MH, Jessop JD. Chondrocalcinosis in primary hyperparathyroidism. Ann Rhem Dis 36:146–151, 1977. Patellofemoral Syndrome Cox JS. Chondromalacia of the patella: A review and update—part I. Contemp Orthop 6:17–31, 1983. Insall J. Current concepts review patellar pain. J Bone Joint Surg 64A:147, 1982. Lun VM, Wiley JP, Meeuvisse WH, Yanagawa TL. Effectiveness of patellar bracing for treatment of patellofemoral pain syndrome. Clin J Sport Med 15: 235–240, 2005. Whittingham M, Palmer S, MacMillan F. Effects of taping on pain and functions in patellofemoral pain syndrome: A randomized controlled trial. J Orthop Sports Phys Ther 34:504–510, 2004. Osteoarthritis of the Knee Balch HW, Gibson JM, Eighorbarev AF, Bain LS, Lynch, MP. Repeated corticosteroid injections into knee joints. Rheumatol Rehabil 19:62–66, 1970. Bellamy N, Campbell J, Robinson V, et al. Viscosupplementation for the treatment of osteoarthritis of the knee. Cochrane Database Syst Rev Apr 18:CD005321, 2005.

REFERENCES

Bhattacharyya T, Gale D, Dewire P, et al. The clinical importance of meniscal tears demonstrated by magnetic resonance imaging in osteorarthritis of the knee. J Bone Joint Surg AM 85-A:4–9,2003. Chang RW, Falconer J, Stulberg SD, et al. A randomized, controlled trial of arthroscopic surgery versus closed-needle joint lavagge for patients with osteoarthritis of the knee. Arthritis Rheum 36:289–296, 1993. Friedman DM, Moore ME. The efficacy of intra-articular steroids in osteoarthritis: A double-blind study. J Rheumatol 7:850–855, 1980. Hernborg J, Nilsson BE. The relationship between osteophytes in the knee joints, osteoarthritis and aging. Acta Orthop Scand 44:69–74, 1973. Hollander JL. Intra-articular hydrocortisone in arthritis and allied conditions: A summary of two years’ clinical experience J Bone Joint Surg 35:983–990, 1953. Karakurum G, Karakok M, Tarakcioglu M, et al. Comparative effect of intra-articular administration of hyaluronan and/or cortisone with evaluation of malondialdehyde on degenerative osteoarthritis of the rabbit’s knee. Tohoku J Exp Med 199:127–134, 2003. Kehr MJ. Comparison of intra-articular cortisone analogues in osteoarthritis of the knee. Ann Rheumatol Dis 18:325–328, 1959. Lane NE, Block D, Jones A, et al. Running and osteoarthritis: A controlled study. Long distance running, bone density, and osteoarthritis. JAMA 255:1147–1151, 1986. Miller JH, White J, Norton TH. The value of intra-articular injections in osteoarthritis of the knee. J Bone Joint Surg 40B:636–643, 1958. Nakhostine M, Friedrich NF, Muller W, Kentsch A. A special high tibial osteotomy technique for treatment of unicompartmental osteoarthritis of the knee. Orthopedics 16:1255–1258, 1993. Panush RS, Schmidt C, Caldwell JR, et al. Is running associated with degenerative joint disease. JAMA 255: 1152–1154, 1986. Zitnan D, Sitaj S. Natural course of articular chondrocalcinosis. Arthritis Rheum 19(Suppl):363–390, 1976. Hemarthrosis Adalberth T, Roos H, Lauren M, et al. Magnetic resonance imaging, scintigraphy, and arthroscopic evaluation of traumatic hemarthrosis of the knee. Am J Sports Med 25: 231–237, 1997. Calmback WL, Hutchens M. Evaluation of patients presenting with knee pain: Part II. Differential diagnosis. Am Fam Physician 68:917–922, 2003. Casteleyn PP, Handelberg F, Opdecam P. Traumatic haemarthrosis of the knee. J Bone Joint Surg Br 70:404–406, 1988. Kocher MS, Micheli LJ, Zurakowski D, Luke A. Partial tears of the anterior cruciate ligament in children and adolescents. Am J Sports Med 30:697–703, 2002. Maffulli N, Binfield PM, King JB, Good CJ. Acute haemarthrosis of the knee in athletes. A prospective study of 106 cases. J Bone Joint Surg Br 75:945–949, 1993.

287

Sarimo J, Rantanen J, Heikkila J, Helttula I, et al. Acute traumatic hemarthrosis of the knee. Is routine arthroscopic examination necessary? A study of 320 consecutive patients. Scand J Surg 91:361–364, 2002. Shepard L, Abdollahi K, Lee J, et al. The prevalence of soft tissue injuries in nonoperative tibial plateau fractures as determined by magnetic resonance imaging. J Orthop Trauma 16:628–631, 2002. Anserinus Bursitis Forbes JR, Helms CA, Janzen DL. Acute pes anserinus bursitis: MR imaging. Radiology 194:525–527, 1995. Kang I, Han SW. Anserine bursitis in patients with osteoarthritis of the knee. South Med J 93:207–209, 2000. Rennie WJ, Saifuddin A. Pes anserine bursitis: incidence in symptomatic knees and clinical presentation. Skeletal Radiol 34:395–398, 2005. Yoon HS, Kim SE, Suh YR, Seo YI, Kim HA. Correlation between ultrasonographic findings and the response to corticosteroid injection in pes anserinus tendinobursitis syndrome in knee osteoarthritis patients. J Korean Med Sci 20:109–112, 2005. Repatellar Bursitis Bellon EM, Sacco DC, Steiger DA, Coleman PE. Magnetic resonance imaging in housemaid’s knee. Magn Reson Imaging 5:175–177, 1987. Kerr DR. Prepatellar and olecranon arthroscopic bursectomy. Clin Sports Med 12:137–142, 1993. Knight JM, Thomas JC, Maurer RC. Treatment of septic olecranon and prepatellar bursitis with percutaneous placement of a suction-irrigation system: A report of 12 cases. Clin Orthop 206:90–93, 1986. McAfee JH, Smith DL. Olecranon and prepatellar bursitis. Diagnosis and treatment. West J Med 149:607–610, 1988. Meniscal Tears Boyd KT, Myers PT. Meniscus preservation; rationale, repair techniques and results. Knee 10:1–11, 2003. Englund M. Meniscal tear—a feature of osteoarthritis. Acta Orthop Scand Suppl 75:1–45, 2004. Pearse EO, Craig DM. Partial meniscectomy in the presence of severe osteoarthritis does not hasten the symptomatic progression of osteoarthritis. Arthroscopy 19:963–68, 2003. Sethi PM, Cooper A, Jokl P. Technical tips in orthopaedics: meniscal repair with use of an in situ fibrin clot. Arthroscopy 19:E44, 2003. Zanetti M, Pfirrmann CW, Schmid MR, Romero J, et al. Patients with suspected meniscal tears: Prevalence of abnormalities seen on MRI of 100 symptomatic and 100 contralateral asymptomatic knees. AJR AM J Roentgenol 181: 635–641, 2003. Iliotibial Band Syndrome Barber FA, Sutker AN. Iliotibial band syndrome. Sports Med 14:144–148, 1992.

288


Ekman EF, Pope T, Martin DF, Curl WW. Magnetic resonance imaging of iliotibial band syndrome. Am J Sports Med 22:851–854, 1994. Faraj AA, Moulton A, Sirivastava VM. Snapping iliotibial band. Report of ten cases and review of the literature. Acta Orthop Belg. 67:19–23, 2001. Fredericson M, White JJ, Macmahon JM, Andriacchi TP. Quantitative analysis of the relative effectiveness of 3 iliotibial band stretches. Arch Phys Med Rehabil 83:589–592, 2002. Fredericson M, Wolf C. Iliotibial band syndrome in runners: innovations in treatment. Sports Med 35:451–9, 2005. Puniello MS. Iliotibial band tightness and medial patellar glide in patients with patellofemoral syndrome. J Orthop Sports Phys Ther 17:144–148, 1993. Richards DP, Alan Barber F, Troop RL. Iliotibial band Z-lengthening. Arthroscopy 19:326–329, 2003. Anterior Cruciate Ligament Injuries Fithian DC, Paxton LW, Goltz DH. Fate of the anterior cruciate ligament-injured knee. Orthop Clin North Am 33: 621–636, 2002. Nebelung W, Wuschech H. Thirty-five years of follow-up of anterior cruciate ligmanet deficient knees in athletes. Arthroscopy 21:696–702, 2005. Osteochondritis Dissecans Cahill BR. Current concepts review. Osteochondritis dissecans. J Bone Joint Surg 79-A:471–472, 1997. Cahill BR, Phillips MR, Navarro R. The results of conservative management of juvenile osteochondritis dissecans using joint scintigraphy. A prospective study. Am J Sports Med 17:601–606, 1989. Linden B. Osteochondritis dissecans of the femoral condyles: A long-term follow-up study. J Bone Joint Surg 59:769–776, 1977. Peterson L, Minas T, Brittberg M, Lindahl A. Treatment of osteochonidritis dissecans of the knee with autologous chondrocyte transplantation. J Bone Joint Surg 85-A:17–24, 2003. Septic Arthritis Blackburn WD, Alarcon GS. Prosthetic joint infections: A role for prophylaxis. Arthritis Rheumatol 34:110, 1991. Courtney P, Doherty M. Joint aspiration and injection Best Pract Res Clin Rheumatol 19:345–369, 2005. Gardner GR, Weisman MH. Pyarthrosis in patients with rheumatoid arthritis: A report of 13 years and a review of the literature from the past 40 years. Am J Med 88:503–510, 1990. Goldenberg DL, Reed JI. Bacterial arthritis. N Engl J Med 312:764–771, 1985. Vincent GM, Amirault JD. Septic arthritis in the elderly. Clinc Orthop 251:241–245, 1990. VonEssen R. Bacterial infections following intra-articular injection. Scand J Rheumatol 10:7–13, 1989.

LOWER LEG General Pineda C, Fonseca C, Martinez-Lavin M. The spectrum of soft tissue and skeletal abnormalities of hypertrophic osteoarthropathy. J Rheumatol 17:773–778, 1990. Tibial Fracture Aoki Y, Yasuda K, Tohyama H, Ito H, et al. Magnetic resonance imaging in stress fracture and shin splints. Clin Orthop 421:260–267, 2004. Boniotti V, Del Giudice E, Fengoni E, et al. Imaging of bone micro-injuries. Radiol Med (Torino) 105:425–435, 2003. Iwamoto J, Takeda T. Stress fractures in athletes: review of 196 cases. J Orthop Sci 8:273–278, 2003. Migrom C, Finestone A, Segev S, et al. Are overground or treadmill runners more likely to sustain tibial stress fractures? Br J Sports Med 37:160–163, 2003. Sonoda N, Chosa E, Totoribe K, Tajima N. Biomechanical analysis for stess fractures of the anterior middle third of the tibia in athletes: Nonliniear analysis using a three-dimensional finite element method. J Orthop Sci 8:505–513, 2003. ANKLE General Abramowitz Y, Wollstein R, Barzilay Y, et al. Outcome of resection of a symptomatic os trigonum. J Bone Joint Surg Am 85:1051–1057, 2003. Horton WA, Collins DL, DeSmet AA, et al. Familial joint instability syndrome. Am J Med Genet 6:221–228, 1980. Lektrakul N, Chung CB, Lai YM, et al. Tarsal sinus: Arthrographic, MR imaging, MR arthrographic, and pathologic findings in cadavers and retrospective study data in patients with sinus tarsi syndrome. Radiology 219:802–810, 2001. Oloff LM, Schulhofer SD, Cocko AP. Subtalar joint arthroscopy for sinus tarsi syndrome: A review of 29 cases. J Foot Ankle Surg 40:152–157, 2001. Ankle Sprain Anandacoomarasamy A, Barnsley L. Long term outcomes of insersion ankle injuries. Br J Sports Med 39:14, 2005. Bleakley C, McDonough S, MacAuley D. The use of ice in the treatment of acute soft-tissue injury: A systematic review of randomized controlled trials. Am J Sports Med 32:251–261, 2004. Boyce SH, Quigley MA, Campbell S. Management of ankle sprains: A randomized controlled trial of the treatment of inversion injuries using an elastic support bandage or an Aircast ankle brace. Br J Sports Med 39:91–96, 2005. Cetti R. Conservative treatment of injury to the fibular ligaments of the ankle. Br J Sports Med 16:47–52, 1982. Kerkhoffs GM, Handoll HH, de Bie R, et al. Surgical versus conservative treatment for acute injuires of the lateral ligament complex of the ankle in adults. Cochrane Database Syst Rev 3:CD000380, 2002. Kerkhoffs GM, Rowe BH, Assendelft WJ, et al. Immobilisation for acute ankle sprain. A systemic review. Arch Orthop Traum Surg 121:462–471, 2001.

REFERENCES

Kitsoaka HB, Lee MD, Morrey BF, Cass JR. Acute repair and delayed reconstruction for lateral ankle instability: Twenty-year follow-up study. J Orthop Trauma 11:530–535, 1997. Konradsen L, Bech L, Ehrenbjerg M, Nickelsen T. Seven years follow-up after ankle inversion trauma. Scand J Med Sci Sports 12:129–135, 2002. Konradsen L, Holmer P, Sondergaard L. Early mobilizing treatment for grade III ankle ligament injuries. Foot Ankle Int 12:69–73, 1991. Lamb SE, Nakash RA, Withers EJ, et al. Clinical and cost effectiveness of mechanical support for severe ankle sprains: Design of a randomized controlled trial in the emergency department (ISRCTN 37807450). BMC Musculoskelet Disord 6:1, 2005. Lindenfeld T, Parikh S. Clinical tip: Heel-thump test for syndesmotic ankle sprain. Foot Ankle Int 26:406–408, 2005. Lynch SA, Renstrom PA. Treatment of acute lateral ankle ligament rupture in the athlete. Conservative versus surgical treatment. Sports Med 27:61–71, 1999. Moller-Larsen F, Withelund JO, Jurik AG, de Cavalho A, Lucht V. Comparison of three different treatments for ruptured lateral ankle ligaments. Acta Orthop Scand 59: 564–566, 1988. Niedermann B, Andersen A, Andersen SB, Funder V, et al. Ruptures of the lateral ligaments of the ankle: Operation or plaster cast? Acta Orthop Scand 52:579–587, 1981. Pijnenburg AC, Bogaard K, Krips R, et al. Operative and functional treatment of rupture of the lateral ligament of the ankle. A randomized, propective trial. J Bone Joint Surg Br 85:525–530, 2003. Stiell IG, McKnight RD, Greenberg GH. Implementation of the Ottawa ankle rules. JAMA 271:827–832, 1994. Tochigi Y, Yoshinaga K, Wada Y, Moriya H. Acute inversion injury of the ankle: Magnetic resonance imaging and clinical outcomes. Foot Ankle Int. 19:730–734, 1998. Achilles Tendonitis/Rupture Astrom M. Partial rupture in chronic Achilles tendinopathy. A retrospective analysis of 342 cases. Acta Orthop Scand 69:404–407, 1998. Cowan MA, Alexander S. Simultaneous bilateral rupture of Achilles tendons due to triamcinolone. Br Med J 10: 1658, 1961. DaCruz DJ, Geeson M, Allen MJ, Phair L. Achilles paratendonitis: an evaluation of steroid injection. Br J Sports Med 22:64–65, 1988. Fox JM, Blazina ME, Jobe FW, et al. Degeneration and rupture of the Achilles tendon. Clin Orthop 107:221–224, 1975. Fredberg U, Bolvig L, Pfeiffer-Jensen M, et al. Ultrasonography as a tool for diagnosis, guidance of local steroid injection and, together with pressure algometry, monitoring of the treatment of athletes with chronic jumper’s knee and Achilles tendinitis: A randomized, double-blind, placebo-controlled study. Scand J Rheumatol 33:94–101, 2004. Gilcreest EL. Ruptures and tears of muscles and tendons of the lower extremity. JAMA 100:153–160, 1933.

289

Gill SS, Gelbke MK, Mattson Sl, et al. Fluoroscopically guided low-volume peritendinous corticosteroid injection for Achilles tendinopathy. A safety study. J Bone Joint Surg Am 86:802–806, 2004. Haunte G, Lloyd-Smith R. Topical glyceryl trinitrate for chronic Achilles tendinopathy. Clin J Sports Med 15: 116–117, 2005. Hugate R, Pennypacker J, Saunders M, Juliano P. The effects of intratendinous and retrocalcaneal intrabursal injections of corticosteroid on the biomechanical properties of rabbit Achilles tendons. J Bone Joint Surg Am 86:794–800, 2004. Khan KM, Forster BB, Robinson J, et al. Are ultrasound and magnetic resonance imaging of value int asseeement of Achilles tendon disorders? A two year prospective study. Br J Sports Med 37:149–153, 2003. Melmed SP. Spontaneous bilateral rupture of the calcaneal tendon during steroid therapy. J Bone Joint Surg 47B:104–105, 1965. Read MT. Safe relief of rest pain that eases with activity in achillodynia by intrasursal or peritendinous steroid injection: The rupture rate was not increase by these steroid injections. Br J Sports Med 33:134–135, 1999. Weber M, Nieman M, Lanz R, Muller T. Nonoperative treatment of acute rupture of the Achilles tendon results of a new protocol and comparison with operative treatment. Am J Sports Med 31:685–691, 2003. Pre-Achilles Bursitis Calder JD, Saxby TS. Surgical treatment of insertional Achilles tendinosis. Foot Ankle Int 24:119–121, 2003. Cozen L. Bursitis of the heel. Am J Orthop 3:372–374, 1961. Gerswter JC, Piccinin P. Enthesopathy of the heels in juvenile onset seronegative B-27 positive spondyloarthropathy. J Rheumatol 12:310–314, 1985. Ohberg L, Alfredson H. Sclerosing therapy in chronic Achilles tendon insertional pain—results of a pilot study. Knee Surg Sports Traumjatol Arthrosec 11:339–343, 2003. Posterior Tibialis Bare AA, Haddad SL. Tenosynovitis of the posterior tibial tendon. Foot Ankle Clin 6:37–66, 2001. Perry MB, Premkumar A, Venzon DJ, et al. Ultrasound, magnetic resonance imaging, and posterior tibialis dysfunction. Clin Orthop Relat Re 225–231, 2003. Plantar Fasciitis Acevedo JI, Beskin JL. Complication of plantar fascia rupture associated with corticosteroid injection. Foot Ankle Int 19:91, 1998. Barrett SL, Day SV. Endoscopic plantar fasciotomy for chronic plantar fasciitis/heel spur syndrome: Surgical technique—early clinical results. J Foot Surg 30:568–570, 1991. Blockey NJ. The painful heel: A controlled trial of the value of hydrocortisone. Br Med J 1:1277–1278, 1956. Buchbinder R. Clinical practice. Plantar fasciitis. N Engl J Med 350:2159–2166, 2004. Daly PJ, Kitaoka HB, Chao EY. Plantar fasciotomy for intractable plantar fasciitis. Foot Ankle Int 13:188–195, 1992.

290


DiGiovanni BF, Nawoczenski DA, Lintal ME. Tissuespecific plantar fascia-stretching exercises enhances outcomes in patients with chronic heel pain. J Bone Joint Surg Am 85:1270–1277, 2003. Furey JG. Plantar fasciitis. The painful heel syndrome. J Bone Joint Surg Am 57:672–673, 1975. Gould EA. Three generations of exotoses of heel inherited from father to son. J Heredity 33:228, 1942. Jerosch J, Schunck J, Liebach D, Filler T. Indication, surgical technique and results of endoscopic fascial release in plantar fasciitis. Knee Surg Sports Traumatol Arthrosc 12: 471–477 2004. Lapidus PW, Guidotti FP. Painful heel: Report of 323 patients with 364 painful heels. Clin Orthop 39:178–186, 1959. Newell SG, Miller SJ. Conservative treatment of plantar fascial strain. Physician Sports Med 5:68–73, 1977. Riddle DL, Pulisic M, Pidcoe P, Johnson RE. Risk factors for plantar fasciitis a matched case-control study. J Bone Joint Surg Am 85:872–877, 2003. Sellman JR. Plantar fascia rupture associated with corticosteroid injections. Foot Ankle Int 15:376, 1994. Wapner KL, Sharkey PF. The use of night splints for treatment of recalcitrant plantar fasciitis. Foot Ankle 12:135, 1991. Wolgin M, Dook D, Graham C, Mauldin D. Conservative treatment of plantar heel pain: Long-term followup. Foot Ankle Int 15:97–102, 1994. Tarsal Tunnel Syndrome Gondring WH, Shields B, Wenger S. An outcomes analysis of surgical treatment of tarsal tunnel syndrome. Foot Ankle Int 24:545–550, 2003. Kim DH, Ryn S, Tiel RI, Kline DG. Surgical management and results of 135 tibial nerve lesions at the Louisiana State University Health Sciences Center. Neurosurgery 53: 1114–1124, 2003. Lau JT, Stavrou P. Posterior tibial nerve-primary. Foot Ankle Clinc 9:271–985, 2004. McGuigan L, Burke D, Fleming A. Tarsal tunnel syndrome and peripheral neuropathy in rheumatoid arthritis. Ann Rheumatol Dis 42:128–131, 1983. Mondelli M, Morana P, Padua L. An electophysiological severity scale in tarsal tunnel syndrome. Acta Neurol Scand 109:284–289, 2004. Patel AT, Gaines K, Malamut R, Park TA, et al. Usefulness of electrodiagnostic techniques in the evaluation of suspected tarsal tunnel syndrome: An evidence-based review. Muscle Nerve 32:236–240, 2005. Sammarco GJ, Chang L. Outcome of surgical treatment of tarsal tunnel syndrome. Foot Ankle Int 24:125–131, 2003. Ankle Arthritis Thomas RH, Daniels TR. Current concepts review ankle arthritis. J Bone Joint Surg Am 85:923–936, 2003.

FOOT Allen LR, Flemming D, Sanders TG. Turf toe: Ligamentous injury of the first metatarsophalangeal joint. Mil Med 169:19–24, 2004. Bunions Coetzee JC, Resig SG, Kuskowski M, Saleh KJ. The Lapidus procedure as salvage after failed surgical treatment of hallux valgus. Surgical technique. J Bone Joint Surg Am 86 Suppl 1:30–36, 2004. Ferrari J, Higgins JP, Prior TD. Interventions for treating hallux valgus (abductovalgus) and bunions. Cochrane Database Syst Rev 1:CD000964, 2004. Menz HB, Munteaznu SE. Radiographic validation of the Manchester scale for the classification of hallux valgus deformity. Rheumatology May 18, 2005. Piggott H. The natural history of hallux valgus in adolescence and early adult life. J Bone Joint Surg 42:749–760, 1960. Sammarco VJ, Nichols R. Orthotic management for disorders of the hallux. Foot Ankle Clin 10:191–209, 2005. Schneider W, Aigner N, Pinggera O, Knahr K. Chevron osteotomy in hallus falgus. Ten year results of 112 cases. J Bone Joint Surg Br 86:1016–1020, 2004. Vanore JV, Christensen JC, Kravitz SR, et al. Diagnosis and treatment of first metatarsophalangeal joint disorders. Section 5: Hallux valgus. J Foot Ankle Surg 42:148–151, 2003. Viehe R, Haupt DJ, Heaslet MW, Walston S. Complications of screw-fixated chevron osteotomies for the correction of hallux abducto valgus. J Am Podiatr Med Assoc 93:499–502, 2003. Hallus Rigidus and Limitus Coughlin MJ, Shurnas PS. Hallux rigidus: dermographic, etiology, and radiographic assessment. Foot Ankle Int 24:731–743, 2003. Foukis TS, Jacobs PM, Dawson DM, et al. A prospective comparison of clinical, radiographic, and intraoperative features of hallux rigidus: short-term follow-up and analysis. J Foot Ankle Surg 41:158–165, 2002. Grady JF, Axe TM, Zager EJ, Sheldon LA. A retrospective analysis of 772 patients with hallux limitus. J Am Podiatr Med Assoc 92:102–108, 2002. Hammer Toes Cahill BR, Connor DE. A long-term follow-up on proximal phalagectomy for hammer toes. Clin Orthop 86: 191–192, 1972. Caterini R, Farsetti P, Tarantino U, et al. Arthrodesis of the toe joints with an intramedually cannulates screw for correction of hammertoe deformity. Foot Ankle Int 25: 256–261, 2004. Coughlin MJ, Kennedy MP. Operative repair of fourth and fifth toe corns. Foot Ankle Int 24:147–57, 2003. Myerson MS, Shereff MJ. The pathological anatomy of claw and hammer toes. J Bone Joint Surg Am 71:45–49, 1989.

REFERENCES

Newman RJ, Fitton JM. An evaluation of operative procedures in the treatment of hammer toe. Acta Orthop Scand 50:709–712, 1979. Sorto LA Jr. Surgical correction of hammer toes. A 5-year postoperative study. J Am Podiatry Assoc 64:930–934, 1974. Morton’s Neuroma Basadonna PT, Rucco V, Gasparini D, Onorato A. Plantar fat pad atrophy after corticosteroid injection for an interdigital neuroma: A case report. Am J Phys Med Rehabil 78:283–285, 1999. Diebold PF, Daum B, Dang-Vu V, Litchinko M. True epineural neurolysis in Morton’s neuroma: A 5-year follow up. Orthopedics 19:397–400, 1996. Dockery GL. The treatment of intermetatarsal neuroma with 4% alcohol sclerosing injections. J Foot Ankle Surg 38: 403–408, 1999. Fanucci E, Masala S, Fabiano S, et al. Treatment of intermetatarsal Morton’s neuroma with alcohol injection under US guide: 10-month follow-up. Eur Radiol 14:514–518, 2004. Nashi M, Venkatachalam A, Muddu BN. Surgery of Morton’s neuroma: Dorsal or plantar approach. JR Coll Surg Edinb 423:36–37, 1997. Okafor B, Shergill G, Angel J. Treatment of Morton’s neuroma by neurolysis. Foot Ankle Int 18:284–287, 1997. Ruushkanen MM, Niinimaki T, Jalovaara P. Results of the surgical treatment of Morton’s neuroma in 58 operated intermetatarsal spaces follwed over 6 (2–12) years. Arch Orthop Trauma Surg 113:78–80, 1994. Sharp RJ, Wade CM, Hennessy MS, Saxby TS. The role of MRI and ultrasound imaging in Morton’s neuroma and the effect of size of lesion on symptoms. J Bone Joint Surg Br 85:999–1005, 2003. Strong G, Thomas PS. Conservative treatment of Morton’s neurmoa. Orthop Rev 16:343–345, 1987. Thomson C, Gibson J, Martin D. Interventions for the treatment of Morton’s neuroma. Cochrane Database Syst Rev 3:CD003118, 2004. Vito GR, Talarico LM. A modified technique for Morton’s neuroma. Decompression with relocation. J Am Podiatr Med Assc 93:190–194, 2003. Wolfort SF, Dellon AL. Treatment of recurrent neuroma of the interdigital nerve by implantation of the proximal nerve into muscle in the arch of the foot. J Foot Ankle Surg 40:404–410, 2001. Younger AS, Claridge RJ. The role of diagnostic block in the management of Morton’s neuroma. Can J Surg 41: 127–130, 1998. Gout Agudelo CA, Weinberger A, Schumacher HR, et al. Definite diagnosis of gouty arthritis by identification of urate crystals in asymptomatic metatarsophangeal joints. Arthritis Rheum 22:559–560, 1979. Campion EW, Glynn RJ, DeLabry LO. Asymptomatic hyperuricemia. Risk and consequences in the normative aging process. Am J Med 82:421–426, 1987. Emmerson BT. The management of gout. N Engl J Med 334:445–451, 1996.

291

Fernandez C, Noguera R, Gonzalez JA, Pascual E. Treatment of acute attacks of gout with a small dose of intraarticular triamcinolone acetonide. J Rheumatol 26: 2285–2286, 1999. Grahame R, Scott JT. Clinical survey of 354 patients with gout. Ann Rheumatol Dis 29:461–470, 1970. Taylor CT, Brooks NC, Kelley KW. Corticotropin for acute management of gout. Ann Pharmacother 35:365–368, 2001. Werlen D, Gabay C, Vischer TL. Corticosteroid therapy for the treatment of acute attacks of crystal-induced arthritis: An effective alternative to nonsteroidal anti-inflammatory drugs. Rev Rheum Engl Ed 63:248–254, 1996. Sesamoiditis Allan MA, Casillas MM. The passive axial compression (PAC) test: A new adjunctive provocative maneuver for the clinical diagnosis of hallucal sesamoiditis. Foot Ankle Int 22:345–346, 2001. Ashman CJ, Klecker RJ, Yu JS. Forefoot pain involving the metatarsal regions: Differential diagnosis with MR imaging. Radiographics 21:1425–1440, 2001. Biedert R, Hintermann B. Stress fractures of the medial great toe sesamoids in athletes. Foot Ankle Int 24:137–141, 2003. Richardson EG. Injuries to the hallucal sesamoids in the athlete. Foot Ankle 7:229–244, 1987. Vanore JV, Christensen JC, Kravitz SR, et al. Diagnosis and treatment of first metatarsophalangeal joint disorders. Section 4: Sesamoid disorders. J Foot Ankle Surg 42: 143–147, 2003. MEDICAL DIAGNOSES, SUPPLEMENTS, MEDICATIONS Osteoporosis Barzel US. Estrogens in the prevention and treratement of postmenopausal osteoporosis: A review. Am J Med 85: 847–850,1988. Dawson-Hughes B, Dallal GE, Krall EA, et al. A controlled trial of the effect of calcium supplementation on bone density in postmenopausal women. N Engl J Med 323:878–883, 1990. Hui SL, Siemenda CW, Johnston CC. Age and bone mass as predictors of fractures in a prospective study. J Clin Invest 81:1804–1809, 1988. Lindsay R, Gallagher JC, Kleerekoper M, Pickar JH. Effect of lower doses of conjugated equine estrogens with and without medroxyprogesterone acetate on bone in early postmenopausal women. JAMA 287:2668–2676, 2002. Lukert BP, Raisz LG. Glucocorticois-induced osteoporosis: Pathogenesis and management. Ann Intern Med 112: 352, 1990. NIH Consensus Development Panel. Osteoporosis prevention, diagnosis, and therapy. JAMA 285:785–795, 2001. Raisz LG. Local and systemic factors in the pathogenesis of osteoporosis. New Engl J Med 318:818, 1988. Reid IR, Ames RW, Evans MC, et al. Effect of calcium supplementation onbone loss in postmenopausal women. N Engl J Med 328:460–464, 1993.

292


Tilyard MW, Spears GFS, Thomson J, et al. Treatment of postmenopausal osteoporosis with calcitriol or calosium. N Engl J Med 326:357–362, 1992. Speroff L, Rowan J, Symons J, et al. The comparative effect on bone density, endometrium, and lipids of continuous hormones as replacement therapy (CHART study): A randomized controlled trial. JAMA 276:1397–1403, 1996.

osteoarthritis. A 3-year, randomized, placebo-controlled, double-blind study. Arch Intern Med 162:2113–2123, 2002. Seroggie DA, Albright A, Harris MD. The effect of glucosamine-chondroitin supplementation on glycosylatedhemoglobin levels in patienst with type 2 diabetes mellitus: A placebo-controlled, double-blinded, randomized clinical trial. Arch Intern Med 163:1587–1590, 2003.

Corticosteroid Injection Side Effects Bedi SS, Ellis W. Spontaneous rupture of the calcaneal tendon in rheumatoid arthritis after steroid injection. Ann Rheumatol Dis 29:494–495, 1970. Gray RG, Tenenbaum J, Gottlieb NL. Local corticosteroid injection treatment in rheumatic disease. Seminars in Arthritis and Rheumatism. 10:231–254, 1981. Halpern AA, Horowitz BG, Nagel DA. Tendon ruptures associated with corticosteroid therapy. West J Med 127: 378–382, 1977. Hedner P, Persson G. Suppression of the hypothalamicpituitary-adrenal axis after a single intramuscular injection of methylprednisolone acetate. Ann of Allerg 47:176–179, 1981. Hollander JL, Jessar RA, Brown EM. Intra-synovial corticosteroid therapy: A decade of use. Bull Rheumatol Dis 11:239–240, 1961. Ismail AM, Balakrishnan R, Rajakumar MK. Rupture of patellar ligament after steroid infiltration: Report of a case. J Bone Joint Surg 51B:503–505, 1969. Kendall, PH. Untoward effects following local hydrocortisone injection. Ann Phys Med 4:170–175, 1961. Kleinman M, Gross AE. Achilles tendon rupture following steroid injection. J Bone Joint Surg 65A:1345–1347, 1983. Libanati CR, Baylink DJ. Prevention and treatment of glucocorticoid-induced osteoporosis: A pathogenetic perspective. Chest 102:1426–1435, 1992. Roseff R, Canoso JJ. Femoral osteonecrosis following several hundred soft tissue corticosteroid infiltrations. Am J Med 77:1119–1120, 1984. Rostron PKM, Calver RF. Subcutaneous atrophy following methylprednisolone injection in Osgood-Schlatter epiphysitis. J Bone Joint Surg 61A:627–628, 1979.

Hyluronic Acid Injections Dahlberg L, Lohmander LS, Ryd L. Intraarticular injections of hyaluronan in patients with cartilage abnormalities and knee pain. A one-year double-blind, placebo-controlled study. Arthritis Rheum 37:521–528, 1994. Evanich JD, Evanich CJ, Wright CA, et al. Efficacy of intraarticular hyaluronic acid injections in knee osteoarthritis. Clin Orthop 390:173–181, 2001. Leopold SS, Brigham BR, Winston J, et al. Corticosteroid compared with hyluronic acid injections for the treatment of osteoarthritis of the knee. J Bone Joint Surg 85A: 1197–1203, 2003.

Glucosamine Sulfate Bruyere O, Honore A, Ethgen O, et al. Correlation between radiographic severity of knee osteoarthritis and future disease progression. Results from a 3-year prospective, placebo-controlled study evaluating the effect of glucosamine sulfate. Osteoarthritiscartilage 11:1–5, 2003. McAlindon T. Glucosamine for osteoarthritis: Dawn of a new era. Lancet 357:247–248, 2001. Muller-Fassbender H, Bach GL, Haase W, et al. Glucosamine sulfate compared to ibuprofen in osteoarthritis of the knee. Osteoarthritis Cartilage 2:61–69, 1994. Noyszewski EA, Wriblewski K, Dodge GR, et al. Preferential incorporation of glucosamine into the galactosamine moieties of chondroitin sulfates in articular cartilage explants. Arthritis Rheum 44:1089–1095, 2001. Pavelka MD, Gatterova J, Olejarova M, et al. Glucosamine sulfate use and delay of progression of knee

Synovial Fluid Analysis Cohen AS, Brandt KD, Krey PR. Synovial fluid. In Cohen AS (ed.): Laboratory Diagnostic Procedures in the Rheumatoid Diseases, 2nd ed. Boston: Little, Brown, 1–62, 1975. Goldenberg DL, Reed JI. Bacterial arthritis. N Engl J Med 312:764–771, 1985. James MJ, Cleland LG, Rofe AM, Leslie AL. Intra-articular pressure and the relationship between synovial perfusion and metabolic demand. J Rheumatol 17:521–527, 1990. Krey PR, Bailen DA. Synovial fluid leukocytosis: A study of extremes. Am J Med 67:436–442, 1979. Ropes MW, Bauer W. Synovial Changes in Joint Disease. Cambridge: Harvard University Press, 1953.

Prolotherapy Yelland MJ, Mar C, Pirozzo S, et al. Prolotherapy injection for chronic low-back pain. Cochrane Database Syst Rev. 2:CD004059, 2004. Laboratory Testing Barland P, Lipstein E. Selection and use of laboratory tests in the rheumatic diseases. Am J Med 100:16S–23S, 1996. Cohen PL. What antinuclear antibodies can tell you. J Musculoskeletal Med April 10:37–46, 1993. Sox HC, Liang MH. The erythrocyte sedimentation rate: Guidelines for rational use. Ann Intern Med 104:515–523, 1986. White RH, Robbins DL. Clinical significance and interpretation of antinuclear antibodies. West J Med 147:210, 1987. Young B, Gleeson M, Cripps AW. C-reactive protein: A critical review. Pathology 23:2417–2420, 1992.

REFERENCES

NSAIDs Cheetham TC, Levy G, Spence M. Predicting the risk of gastrointestinal bleeding due to nonsteroidal anti-inflammatory drugs: NSAID electronic assessment of risk. J Rheumatol 30:2241–2244, 2003. Griffin MR. Epidemiology of nonsteroidal anti-inflammatory drug-associated gastrointestinal injury. Am J Med 104:23S–29S, 1998. Henry D, Lim LL, Garcia Rodriguez LA, et al. Variability in risk of gastrointestinal complications with individual non-steroidal anti-inflammatory drugs: results of a collaborative meta-analysis. BMJ 312:1563–1566, 1996.

293

Lewis JD, Bilker WB, Brensinger C, et al. Hospitalization and mortality rates from peptic ulcer diseases and GI bleeding in the 1990’s: Relationship to sales of nonsteroidal anti-inflammatory drugs and acid suppression medications. Am J Gastroenterol 97:2540–2549, 2002. Rashad S, Revell P, Hemmingway A, Low F, Rainsford K, Walker F. Effect of nonsteroidal anti-inflammatory drugs on the course of osteoarthritis. Lancet 2:519–22, 1989. Singh G, Triadafilopoulos G. Epidemiology of NSAID induced gastrointestinal complications. J Rheumatol 26S56:18–24, 1999. Wolfe MM, Lichtenstein DR, Singh G. Gastrointestinal toxicity of nonsteroidal anti-inflammatory drugs. N Engl J Med 340:1888–1892, 1999.

INDEX A Abdomen low back pain referred from, 169 palpation of, 169 shoulder pain referred from, 44 Achilles tendon rupture, 234, 244 Achilles tendonitis, 223, 234, 244, 249 Acromioclavicular joint differential diagnosis, 19 local anesthetic block of, 38 osteoarthritis of, 20, 25, 37–38, 45, 49 palpation of, 25, 37 separation of, 20, 37–38, 45 third-degree, 39, 45 Acute boutonnière deformity, 119, 135 Adhesive capsulitis, 20 Adson maneuver, 13, 14 Ambulation impairment, 251 Anesthetic blocks intra-articular, for ankle arthritis, 232 local. See Local anesthetic blocks Angiography, for aortoiliac vascular occlusive disease, 189 Ankle alignment of, 225 anterior talofibular ligament of, 249 arthritis of, 232–233, 244 description of, 223 differential diagnosis, 222 eversion of, 226, 233 isometric resistance of, 242 examination of, 223–224 extension of, 226 flexion of, 226 fractures of, 245–249 instability of, 230, 244 inversion of, 226, 233 isometric resistance of, 241 lateral ligament tenderness and swelling of, 229 one-minute screening examination of, 224–228 osteoarthritis of, 232–233, 244 passive stretching of, 226, 229 range of motion testing, 226 referred pain, 222 rheumatoid arthritis of, 232–233 stress views of, 231 traumatic injuries of, 222 weight bearing, 225 Ankle pain anterior, 223, 224 lateral, 223, 224 medial, 223, 224 posterior, 223, 224 symptoms of, 223, 224 Ankle sprain description of, 223, 249 diagnosis of, 229–231, 244 instability associated with, 230, 244 Anserine bursa, 201, 209 Anserine bursitis, 209, 217, 221 Antecubital fossa, 77 Anterior ballottement, 232 Anterior cruciate ligament injury, 212, 217 Anterior drawer sign, 212, 230 Anterior talofibular ligament, 249 Anterolateral thigh sensation testing, 185 Anteroposterior x-ray pelvic, for hip osteoarthritis evaluations, 182 spinal, for scoliosis, 60, 65, 163

Aortoiliac vascular occlusive disease, 189, 192 Apley scratch sign, 22, 31 Apprehension test, 41 Arch of foot, 251, 254 Arthritis ankle, 232–233 distal interphalangeal joint, 133 hip joint, 183–184 interphalangeal joint, 109 metacarpophalangeal joint, 102, 109, 114, 130 osteoarthritis. See Arthritis radiocarpal joint, 90–91, 96 rheumatoid. See Rheumatoid arthritis subtalar, 223, 233, 244 traumatic, of metacarpophalangeal joint, 130, 133 ulnarhumeral joint, 75–76 Arthrography of glenohumeral joint, 32 of rotator cuff, 34 Arthroscopy anterior cruciate ligament injury, 212 meniscal tears, 214 Aspiration of ankle, 232 for Baker’s cyst diagnosis, 213 of dorsal ganglion, 92 of elbow, 76 for glenohumeral joint osteoarthritis, 40 of hip joint, 184 of knee joint, 206 metatarsophalangeal joint, for gout diagnosis, 259 for olecranon bursitis diagnosis, 73 of prepatellar bursa, 207 for radiocarpal joint arthritis, 91 Avascular necrosis of hip joint, 186, 192 of navicular bone, 99

Boutonnière deformity, 119, 135 Breathing pattern assessments for chest evaluations, 139 for upper back evaluation, 53 Bunion diagnosis of, 256, 271 dorsal, 268, 271 Bunionette, 262, 271 Bursa anserine, 201, 209 gluteus medius, 177 olecranon, 70, 73 pre-Achilles, 235, 244 prebunion, 258 prepatellar, 201, 207 subscapular description of, 20 palpation of, 26, 54, 59 Bursitis anserine, 209, 217, 221 gluteus medius description of, 173, 194 diagnosis of, 180–181, 192 olecranon acute, 73 chronic, 73 description of, 67 needle aspiration for, 73 summary of, 79 pre-Achilles, 235, 244, 249 prebunion, 258, 271, 276 prepatellar, 207, 217 retrocalcaneal, 236, 244 subacromial, 20 subscapular, 42, 45, 59, 65 trochanteric description of, 173, 192 diagnosis of, 178–179 referred pain from, 194

B Baker’s cyst, 197, 213, 217, 221 Biceps insertionitis, 77, 79 Bicipital groove, 35 Bicipital tendon rupture, 36 Bicipital tendonitis, 35–36, 45 Bilateral sunrise x-rays, 203 Blocks, anesthetic intra-articular, for ankle arthritis, 232 local. See Local anesthetic blocks Bone scan for ankle conditions, 228 for avascular necrosis of hip joint, 186 for calcaneal stress fracture, 240 for chest conditions, 142 for compression fractures of lumbosacral spine, 165 for elbow conditions, 70 for foot conditions, 255 for hand conditions, 122 for hip conditions, 178 for knee conditions, 202 for lumbosacral spine conditions, 155 for metastatic disease of femur, 188 for neck conditions, 6 for occult hip fracture, 187 for reflex sympathetic dystrophy, 270 for shoulder conditions, 27 for thumb conditions, 107 for upper back conditions, 56 for wrist conditions, 88

C Calcaneal compression, 240 Calcaneal fractures diagnosis of, 248 stress, 240, 244 Calcaneal heel pad, 239 Carpal tunnel pain description of, 102 to thumb, 113 Carpal tunnel syndrome grading of, 100 nerve conduction velocity testing for, 95 summary of, 96, 114 symptoms of, 84 thumb pathology secondary to, 102 Tinel sign for, 78, 88, 95, 106, 113, 123 Carpometacarpal joint compression of, 87 osteoarthritis of, 94, 107–108, 114, 117 Cauda equina syndrome, 150, 159–160, 170 Cellulitis, 276 Cervical osteoarthritis description of, 2 examination for, 8, 14 lateral view of neck evaluation, 8 passive rotation of neck evaluations, 8 symptoms of, 2 Cervical radiculopathy classification of, 18 diagnosis of, 9 differential diagnosis of, 1

295

296


Cervical radiculopathy (Continued) examination for, 9–10, 14 herniated nucleus pulposus as cause of, 2 magnetic resonance imaging of, 10 manual cervical traction for, 9 oblique views of the neck for, 10 pain associated with, 5, 9 prognosis for, 18 radiographs for, 6 referred pain to upper back from, 64 signs of, 2 Spurling maneuver, 5, 9 Cervical spine cross-table lateral x-ray of, 17–18 magnetic resonance imaging of, 43 motor testing of, 16 oblique view of, 64 palpation of, 16 sensory testing of, 15 spinous processes of, 16 x-ray series for, 18 Cervical strain description of, 2 differential diagnosis of, 1 examination for, 14 reactive, 6, 17 signs and symptoms of, 2 Cervical traction, manual, 9 Charcot fracture, 273 Chest examination of, 138–139 one-minute screening examination of, 139–142 shoulder pain referred from, 44 Chest compression test, 55, 61, 140 Chest pain description of, 138 epidemic pleurodynia, 138, 141, 146, 148 symptoms of, 138 xiphodynia, 138, 147–148 Chest trauma, 138 Chest wall examination of, 139–142 expansion assessments, 141 Chest x-rays, for rib fractures, 61 Claudication, 189 Clavicle fractures, 46, 48 Coccydynia, 168, 170 Collateral ligaments, of knee lateral, 211, 217 medial, 210 Colles fractures description of, 83 displaced, 98 foreshortened, 98 nondisplaced, 97 Compression fractures of lumbosacral spine, 150–151, 165, 170 of thoracic spine, 62–63, 65 Computed tomography cauda equina syndrome evaluations, 159 low back pain referred from abdomen, 169 lumbar radiculopathy evaluations, 158, 191, 216 lumbosacral osteoarthritis evaluations, 161 Costochondral junction palpation, 140, 143 Costochondritis, 143, 148 Costothoracic syndrome, 20 Cross-table lateral x-ray of cervical spine, 17–18 Cubital tunnel syndrome, 78–79 Cysts Baker’s, 197, 213, 217, 221 dorsal ganglion, 92, 96 mucinoid, of distal interphalangeal joint, 132–133

Cysts (Continued) tendon, 128 tenosynovial, 133 D De Quervain’s tenosynovitis description of, 82, 102, 114 local anesthetic block for, 110, 117 radial styloid palpation for, 87, 94, 103, 105, 110 Diffuse idiopathic skeletal hyperostosis, 161 Dislocation elbow, 80 hip joint, 193 interphalangeal joint, 116 metacarpophalangeal joint, 116 patellar, 217 perilunate, 99 proximal interphalangeal joint, 135 shoulder, 46 Distal femur fracture, 218 Distal humeral fractures, 81 Distal interphalangeal joint arthritis of, 133 bony enlargement of, 124 inspection of, 122 mucinoid cyst of, 132–133 Distal radius fractures, 83 Doppler ultrasound, for aortoiliac vascular occlusive disease, 189 Dorsal bunion, 268 Dorsal ganglion cyst, 92, 96 Dorsokyphotic posture, 3 Dorsotenosynovitis of foot, 267, 271, 276 of wrist, 82, 93, 96 Draftsman’s elbow. See Olecranon bursitis Duck waddle, ability to, 199 Dupuytren’s contracture, 119, 129, 133, 136 Dynamometry, 104, 121 E Elbow aspiration of, 76 differential diagnosis, 66 dislocation of, 80 examination of, 68 flexion of isometrically resisted, 77 range of motion testing, 68 fractures of, 80–81 lateral x-ray of, 74–75 one-minute screening examination of, 68–70 range of motion testing in extension, 68 in flexion, 68 passive, 75 in pronation, 69 in supination, 69 swelling of, 67 symptoms involving, 66 Elbow pain anterior, 67, 68 description of, 67 differential diagnosis, 68 lateral, 67, 68 medial, 67, 68 posterior, 67, 68 referred, 67, 68, 79 Electromyography lumbosacral spine conditions, 155 upper extremity, 13, 14

Epicondylitis lateral description of, 67, 81 local anesthetic block for, 71 summary of, 79 tests for, 69 medial description of, 67, 81 local anesthetic block for, 72 summary of, 79 tests for, 69 Epidemic pleurodynia, 138, 141, 146, 148 Epidural process, 166, 170 Examination of ankle, 223–224 of chest, 138–139 of elbow, 68 of foot, 251–252 of hand, 119–120 of hip joint, 174 of knee, 197–198 of neck, 2–3 of shoulder, 21 of thumb, 102–103 of upper back, 52 Extensor tendons of foot, 264 of hand, 119, 131 F Femur distal, fracture of, 218 metastatic disease of, 188, 192 Fibular fractures avulsion, 245 description of, 220 displaced, 246 nondisplaced, 246 Finger(s) mallet, 119–120, 131, 133 passive extension of, 127 trigger, 127, 133, 136 Flexor digitorum profundus tendon rupture, 135–136 Flexor tendons of hand, 119 of thumb, 105 Foot accessory bones of, 276 arch of description of, 251, 254 inspection of, 269 palpation of, 269 description of, 251 dorsum of description of, 251–252 swelling of, 267 examination of, 251–252 extensor tendons of, 264 fractures of, 272–275 inspection of, 256, 258, 262, 268 one-minute screening examination of, 252–255 posteroanterior x-ray of, 262 referred pain to, 251 sesamoid view of, 260 swelling of, 253, 266 x-rays of, 256, 268 Foot pain differential diagnosis, 252 dorsal swelling associated with, 251 Forearm grip strength measurements, 85–86 strength assessments of, 86 Forestier’s disease, 161

INDEX Fractures ankle, 245–249 calcaneal, 240, 244, 248 Charcot, 273 clavicle, 46, 48 Colles, 83, 97–98 compression of lumbosacral spine, 150–151, 165, 170 of thoracic spine, 62–63, 65 distal femur, 218 distal humeral, 81 distal phalanx, 136 distal radius, 83, 97 elbow, 67, 80–81 fibular avulsion, 245 description of, 220 displaced, 246 nondisplaced, 246 foot, 272–275 great toe, 274 greater tubercle, 47 hand, 134–136 hip occult, 173, 187, 192 types of, 193–194 humeral, 46–47, 81 knee, 218–220 march, 266 metacarpal base, 115 metatarsal base, 248 midtarsal, 272 navicular, 96, 98 neuropathic, 273 nondisplaced, 81 patella, 218 pelvic, 193 proximal tibial, 218 radial head, 80 rib, 61–62, 65 sesamoid bone, 274 shoulder, 46–48 spinal column, 51 talus, 247, 249 thumb, 102, 115–117 tibial displaced, 247 of shaft, 219 stress, 220 toe, 274–275 tuff, 115 ulnar, 81 vertebral, 14 wrist, 97–99 Frozen shoulder Apley scratch sign, 22, 31 description of, 20, 49 examination for, 31–32, 45 glenohumeral joint arthrography for, 32 tests for, 31–32 G Gait, 152, 175, 198 Gamekeeper’s thumb diagnosis of, 112, 114, 117 symptoms of, 103 Glenohumeral joint abduction of, 22 anterior swelling of, 39 Apley scratch sign, 22, 31 arthrography of, 32 differential diagnosis, 19 osteoarthritis of, 20, 39–40, 45 rotation of, 22 swelling of, 39 touchdown sign, 22

Gluteus medius bursa palpation, 177 Gluteus medius bursitis description of, 173, 194 diagnosis of, 180–181, 192 Golfer’s elbow. See Medial epicondylitis Gout, 258–259, 271 Great toe fractures of, 274 local plantar tenderness of, 260 osteoarthritis of, 276 Greater occipital nerve focal tenderness of, 5 palpation of, 11 Greater occipital neuralgia description of, 2 diagnosis of, 14 focal tenderness, 5 headache associated with, 11 local anesthetic block for, 11, 14 Greater trochanteric process, 179 Greater tubercle fracture, 47 Grip strength measurements dynamometry for, 104, 121 of hand, 104, 120–121 of thumb, 104 of wrist, 85–86 H Hallux rigidus, 257, 271 Hallux valgus, 256 Hammer toe, 251, 264, 271, 276 Hand closing of, 103 differential diagnosis, 118 Dupuytren’s contracture of, 119, 129, 133, 136 examination of, 119–120 extensor tendons of, 119, 131 flexor tendons of description of, 119 local anesthetic block over, 127 fractures of, 134–136 grasping assessments, 120 grip strength assessments, 120–121 one-minute screening examination of, 120–123 opening of, 103 osteoarthritis of, 119, 124, 133 range of motion testing, 126 rheumatoid arthritis of, 119, 125–126, 136 small joints of, 122 x-rays of, 124–125 Hand pain diffuse, 119 symptoms of, 119 Head posture of, 3 trauma evaluations, 15–18 Headache cervical pain and, 2 greater occipital neuralgia and, 11 Heel plantar, 223, 224 posterior, 227 Heel pad syndrome, 239, 244 Heel-to-buttock measurement, 199, 206 Hemarthrosis, 221 Herniated nucleus pulposus cervical radiculopathy caused by, 2 magnetic resonance imaging of, 43 “High-riding humeral head” sign, 30, 33 Hip acute arthritis of, 183–184, 192 aspiration of, 184 avascular necrosis of, 186, 192 characteristics of, 173

297

Hip (Continued) description of, 173 dislocation of, 193 examination of, 174 external rotation testing, 182–183, 187–188 femur, metastatic disease of, 188, 192 internal rotation testing, 182–183, 187–188 one-minute screening examination of, 174–178 osteoarthritis of, 173, 181–182, 192 range of motion testing, 176, 186 referred pain, 173, 198 Hip fractures occult, 173, 187, 192 types of, 193–194 Hip pain aortoiliac vascular occlusive disease as cause of, 189, 192 description of, 173–174 from lumbosacral spine, 190 Humeral fractures, 46–47, 81 I Iliopectineal bursitis description of, 173 Iliotibial band syndrome, 215, 217 Impingement syndrome description of, 49 examination for, 21, 45 lidocaine injection test for, 28 passive painful arc maneuver for, 24, 28 symptoms of, 20 Infraspinatus tendon inflammation of, 20 isometric testing of, 29 Inspection of distal interphalangeal joint, 122 of dorsal ganglion, 92 of foot, 256, 258, 262, 268 of metacarpophalangeal joint, 122 of olecranon bursa, 70, 73 of palm, 122, 129 of proximal interphalangeal joint, 122 of thumb, 105 of upper back, 53 Intercostal muscles epidemic pleurodynia of, 146 palpation of, 141 Intercostal nerve block, for rib fractures, 62 Intercostal space, 141, 146 Interphalangeal joint arthritis of, 109 dislocation of, 116 distal bony enlargement of, 124 inspection of, 122 mucinoid cyst of, 132 x-rays of, 109 Intra-articular anesthetic block for ankle arthritis, 232 for subtalar arthritis, 233 Ischiogluteal bursitis, 173 Isometric testing, of shoulder description of, 23 infraspinatus tendon, 29 supraspinatus tendon, 29 J Joint. See specific joint K Kienböck’s disease, 82 Knee anatomy of, 196 anterior cruciate ligament injury, 212 aspiration of, 206

298


Knee (Continued) differential diagnosis, 195 examination of, 197–198 fractures of, 218–220 joint lines of, 200, 204 lateral femoral condyle, 215 ligaments of anatomy of, 196 anterior cruciate, 212, 217 injury to, 210–212 lateral collateral, 211, 217 medial collateral, 210, 217, 221 meniscal tears of, 197–198, 213–214, 217, 221 one-minute screening examination of, 198–202 osteoarthritis of description of, 197, 221 lateral compartment, 207–208, 217 medial compartment, 204–205, 217, 221 Knee effusion, 205–206, 217, 221 Knee pain age-related variations in, 196 anterior, 196–197 differential diagnosis, 196, 197 lateral, 197 medial, 196 referred, 196, 198, 216 symptoms of, 196–197 L Lateral collateral ligament injury, 211, 217 Lateral compartment osteoarthritis, 207–208, 217 Lateral elbow pain, 67, 68 Lateral epicondyle palpation, 69, 71 Lateral epicondylitis description of, 67, 81 local anesthetic block for, 71 summary of, 79 tests for, 69 Lateral femoral condyle, 215 Lateral joint line tenderness, 208 Lateral x-ray of ankle, 237 of elbow, 74–75 Leriche’s syndrome, 189 Levator scapula description of, 51 palpation of, 57 Lidocaine injection test for impingement syndrome, 28 for rotator cuff tendonitis, 31 Local anesthetic blocks diagnostic uses of acromioclavicular osteoarthritis and separation, 38 anserine bursitis, 209 carpal tunnel syndrome, 113 coccydynia, 168 costochondritis, 143 de Quervain’s tenosynovitis, 110, 117 gamekeeper’s thumb, 112, 114, 117 gluteus medius bursitis, 181 greater occipital neuralgia, 11, 14 iliotibial band syndrome, 215 intercostal muscles, 146 lateral collateral ligament injury, 211, 217 lateral epicondylitis, 71 low back strain, 157 medial collateral ligament injury, 210, 217 medial epicondylitis, 72 meralgia paresthetica, 185 metacarpophalangeal joint arthritis, 130 Morton’s neuroma, 265, 271 paraspinal muscles, 157

Local anesthetic blocks (Continued) peroneus tenosynovitis, 242 plantar fasciitis, 238 posterior tibial tenosynovitis, 241 pre-Achilles bursitis, 235 prebunion bursitis, 258, 271 radiocarpal joint arthritis, 91 reactive cervical strain, 6 retrocalcaneal bursitis, 236 rhomboids, 58 rib fracture, 144 sacrococcygeal junction, 168 sacroiliac joint conditions, 167, 190 sternoclavicular joint arthritis, 145 subscapular bursa, 59 subscapular bursitis, 42, 65 temporomandibular joint syndrome, 12, 14 trapezius, 58 trigger finger, 127 trigger thumb, 111 trochanteric bursitis, 179 xiphodynia, 147 intramuscular, for reactive cervical strain, 6 Low back pain differential diagnosis, 151 diffuse, 150 focal, 150 referred, 169 structural causes of, 150 Low back strain, 150, 155–157 Lower extremity. See also specific anatomy neurologic examination of, 191 pulse taking, 189 Lumbar radiculopathy description of, 150, 170–171 diagnosis of, 157–158, 191, 216 foot symptoms caused by, 251 Lumbosacral spine compression fractures of, 150–151, 165 differential diagnosis, 149 epidural process of, 166 examination of, 151 functional stiffness of, 160 hip pain referred from, 190 one-minute screening examination of, 151–155 osteoarthritis of, 160–161, 170 Schober test of, 152, 156, 162 scoliosis of. See Scoliosis spinous processes of, 164 stenosis of, 2, 161–162, 170 strain of, 150, 155–157, 170 M Magnetic resonance imaging Achilles tendon rupture, 234 ankle conditions, 228 anterior cruciate ligament injury, 212 avascular necrosis of hip joint, 186 cervical radiculopathy, 10 cervical spine, 43 chest conditions, 142 compression fractures of lumbosacral spine, 165 of thoracic spine, 63 elbow conditions, 70 epidural process, 166, 170 hip conditions, 178 knee conditions, 202 lumbosacral spine conditions, 155 meniscal tears, 214 neck conditions, 6 occult hip fracture, 187 shoulder, 34 shoulder conditions, 27

Magnetic resonance imaging (Continued) spinal stenosis, 162 upper back conditions, 56 wrist conditions, 88 Mallet finger, 119–120, 131, 133 Manual cervical traction, 9 March fracture, 266 McMurray maneuver, 214, 221 Medial collateral ligament injury, 210, 217, 221 Medial compartment osteoarthritis, 204–205, 217, 221 Medial elbow pain, 67, 68 Medial epicondyle palpation, 69, 72 Medial epicondylitis description of, 67, 81 local anesthetic block for, 72 summary of, 79 tests for, 69 Meniscal tears, 197–198, 213–214, 217, 221 Meralgia paresthetica, 173, 185, 194 Metacarpal base fracture, 115 Metacarpophalangeal joint dislocation of, 116 inspection of, 122 lateral collateral ligament of, avulsion of, 117 lateral lines of, 109 osteoarthritis of, 102, 109, 114 pain at, 103, 119–120 squeeze sign of, 126 swelling of, 130 traumatic arthritis of, 130, 133 Metastatic disease, of femur, 188, 192 Metatarsal fractures base, 248 fifth, 273 first, 273 fourth, 273 second, 273 stress, 266, 271 third, 273 Metatarsal pain, 266 Metatarsalgia, 251, 263, 271, 276 Metatarsophalangeal joint alignment of, 252–253 aspiration of, for gout diagnosis, 259 conditions that affect, 251 metatarsalgia of, 263, 276 squeeze sign of, 254–255, 263, 265 Midtarsal fractures, 272 Morton’s neuroma, 251, 265, 271 Motor testing of neck, 16 Mucinoid cyst of distal interphalangeal joint, 132–133 Multidirectional instability of shoulder, 41, 45 N Navicular avascular necrosis of, 99 fracture of, 96, 98 Neck differential diagnosis, 1 examination of, 2–3 general movement of, 3 lateral bending of, 2–3 lateral view of, 8 oblique views of, 10 one-minute screening examination of management options, 6 maneuvers, 3–6 passive rotation of, 4, 8 posture of, 3 rotation of, 2–3 sensory testing of, 15 supporting muscles of, 3, 4 trauma evaluations, 15–18

INDEX Neck osteoarthritis description of, 2 examination for, 8, 14 lateral view of neck evaluation, 8 passive rotation of neck evaluations, 8 symptoms of, 2 Neck pain description of, 2 treatment of, 6 Neck stiffness description of, 2 treatment of, 6 Nerve conduction velocity testing carpal tunnel syndrome evaluations, 95 cubital tunnel syndrome evaluations, 78 hand conditions, 122 tarsal tunnel syndrome evaluations, 243 ulnar neuropathy evaluations, 78 Neuropathic fracture, 273 Nuclear bone scan, for calcaneal stress fracture, 240 O Oblique view of cervical spine, 64 of neck, 10 Occult hip fractures, 173, 187, 192 Olecranon bursa inspection and palpation of, 70, 73 needle aspiration of, 73 Olecranon bursitis acute, 73 chronic, 73 description of, 67 needle aspiration for, 73 summary of, 79 Os trigonum syndrome, 237, 244 Osgood-Schlatter epiphysitis, 196 Osteoarthritic flare, 25 Osteoarthritis acromioclavicular joint, 20, 25, 37–38, 45, 49 ankle, 232–233 carpometacarpal joint, 94, 107–108, 113, 117 cervical description of, 2 examination for, 8, 14 lateral view of neck evaluation, 8 passive rotation of neck evaluations, 8 symptoms of, 2 glenohumeral joint, 20, 39–40, 45 great toe, 276 hand, 119, 124, 133 hip joint, 173, 181–182, 192 knee lateral compartment, 207–208 medial compartment, 204–205 lumbosacral spine, 160–161, 170 metacarpophalangeal joint, 102, 109 sternoclavicular joint, 45, 145, 148 ulnarhumeral joint, 75–76 Osteochondritis dissecans, 219 Osteoporosis, 65 P Pain ankle, 223, 224 carpal tunnel, 102 cervical radiculopathy, 5, 9 chest, 138, 141, 146–148 elbow, 67, 68, 79 foot, 251, 252 hand, 119 hip, 173–174, 189–190, 192 knee, 196–198, 216 low back, 150–151, 169 metacarpophalangeal joint, 103, 119–120

Pain (Continued) neck, 2, 6 periscapular, 65 popliteal, 197 referred. See Referred pain shoulder, 20, 21, 43–44 sternoclavicular joint, 138 thumb, 101–102, 113 upper back, 65 wrist, 82–83 Palm of hand, 122, 129 Palpation of abdomen, 169 of acromioclavicular joint, 25, 37 of arch of foot, 269 of bicipital groove, 35 of cervical spine, 16 of costochondral junction, 140, 143 of flexor tendons of hand, 128 of thumb, 105, 111 of gluteus medius bursa, 177 of greater occipital nerve, 11 of greater trochanteric process, 179 of intercostal muscles, 141 of intercostal space, 146 of lateral epicondyle, 69, 71 of levator scapula, 57 of medial epicondyle, 69, 72 of olecranon bursa, 70, 73 of paraspinal muscles, 17, 153 of plantar heel, 227 of pre-Achilles bursa, 235 of proximal interphalangeal joint, 125 of radial styloid, 87, 94, 103, 105, 110 of rhomboids, 57 of sacrococcygeal junction, 168 of sacroiliac joint, 154, 167 of spinous processes, 62, 164 of sternochondral junction, 140, 143 of sternoclavicular joint, 26 of subacromial space, 25 of subscapular bursa, 26, 42, 54, 59 of superior trochanteric process, 180 of temporomandibular joint, 6, 12 of trapezius, 4, 7, 54, 57 of trochanteric bursa, 177 of xiphoid process, 147 Paraspinal muscles local anesthetic block of, 157 palpation of, 17, 153 spasm of, 60 Paravertebral joints, 8 Passive painful arc maneuver, 24, 28 Passive rotation of neck, 4, 8 Passive stretching of ankle, 226, 229 Patella fracture of, 218 subluxation of, 221 Patellar compression, 200, 203 Patellar tendonitis, 221 Patellofemoral syndrome, 197, 202–203, 217 Pelvis fracture of, 193 weight-bearing anteroposterior x-ray of, 152 Perilunate dislocation, 99 Periscapular pain, 65 Peroneus tenosynovitis, 242, 244 Pes cavus, 251, 269, 271 Pes planovalgus, 251 Pes planus, 251, 269, 271 Phalanges distal, 115, 136 fractures of, 115, 134 middle, 134 proximal, 134

299

Plantar fasciitis, 223, 238, 244 Plantar heel pain of, 223, 224 palpation of, 227 Pleurodynia, epidemic, 138, 141, 146, 148 Popliteal fossa, 213 Popliteal pain, 197 Posterior tibial tenosynovitis, 241, 244 Posture dorsokyphotic, 3 of head, 3 of neck, 3 Pre-Achilles bursa, 235 Pre-Achilles bursitis, 235, 244, 249 Prebunion bursitis, 258, 271, 276 Prepatellar bursa, 201, 207 Prepatellar bursitis, 207, 217 Pronator teres syndrome, 95 Proximal interphalangeal joint dislocation of, 135 flexor digitorum profundus tendon rupture, 135–136 inspection of, 122 palpation of, 125 Proximal tibial fracture, 218 Puncture of mucinous cysts, 132 of tendon cysts, 128 Q Q-angle, 203 Quadriceps strength testing, 199 R Radial head fractures, 80 Radial styloid palpation, 87, 94, 103, 105, 110 Radiculopathy cervical classification of, 18 diagnosis of, 9 differential diagnosis of, 1 examination for, 9–10, 14 herniated nucleus pulposus as cause of, 2 magnetic resonance imaging of, 10 manual cervical traction for, 9 oblique views of the neck for, 10 pain associated with, 5, 9 prognosis for, 18 radiographs for, 6 referred pain to upper back from, 64 signs of, 2 Spurling maneuver, 5, 9 lumbar description of, 150, 170–171 diagnosis of, 157–158, 191, 216 foot symptoms caused by, 251 Radiocarpal joint arthritis of, 90–91, 96 dorsal swelling and tenderness of, 90 line tenderness evaluations, 89 local anesthetic block or aspiration of, 91 range of motion testing, 90 Radiographs. See X-rays Radiohumeral joint arthritis, 76, 79 Range of motion testing of ankle, 226 of elbow in extension, 68 in flexion, 68 passive, 75 in pronation, 69 in supination, 69 of hand, 126 of hip joint, 176, 186 of radiocarpal joint, 90 of wrist, 84–85

300


Reactive cervical strain, 6, 17 Rectal sphincter tone, 159 Referred pain to ankle, 222 from cervical radiculopathy, 64 to elbow, 67, 68, 79 to hip joint, 173, 190 to knee, 196, 198, 216 to low back, 169 from lumbosacral spine, 190 to neck, 1–2 from sacroiliac joint, 190 to shoulder, 19, 43–44 to thumb, 113 to upper back, 50–51, 64 to wrist, 82 Reflex sympathetic dystrophy, 270 Reiter’s disease, 145 Retrocalcaneal bursitis, 223, 236, 244 Retrocalcaneal space, 236 Rheumatoid arthritis of ankle, 232–233 of hand, 125–126, 136 of radiohumeral joint, 76, 79 of ulnarhumeral joint, 76 Rhomboids description of, 51 local anesthetic blocks in, 58 palpation of, 57 Rib contusion, 61–62, 65, 148 Rib fracture description of, 61–62, 65, 148 nondisplaced, 144 Rotation hip joint, 182–183, 187–188 passive, 4 Rotator cuff arthrography of, 34 differential diagnosis of, 19 high-riding humeral head sign, 30, 33 impingement syndrome. See Impingement syndrome tear of, 20, 33–34, 49 tendonitis of, 29–30, 45, 49 weakness of, 33 S Sacrococcygeal junction, 168 Sacroiliac joint palpation of, 154 referred pain from to hip, 190 to knee, 198 strain of, 150, 167, 170 Sacroiliitis, 150, 154, 167, 170 Schober test, 152, 156, 162 Sciatica, 150, 157, 171 Scoliosis anteroposterior spine x-ray for, 60, 65, 163 description of, 170 height measurements for assessing, 55, 60, 163 Sensory testing of anterolateral thigh, 185 of cervical spine, 15 of neck, 15 Sesamoid bone fractures, 274 Sesamoiditis, 260, 271 Shoulder. See also Acromioclavicular joint; Glenohumeral joint; Rotator cuff anatomy of, 20 anterior, 20 crepitation of, 41 differential diagnosis, 19 dislocation of, 46 examination of, 21 fractures of, 46–48

Shoulder (Continued) magnetic resonance imaging of, 34 one-minute screening examination of acromioclavicular joint palpation, 25 Apley scratch sign, 22, 31 isometric testing, 23 management options, 27 maneuvers for, 21–26 passive painful arc maneuver, 24 sternoclavicular joint palpation, 24 subscapular bursa palpation, 26 sulcus sign, 24, 41 touchdown sign, 22 weighted touchdown sign, 23 subluxation of, 41 trauma to, 20 Shoulder instability apprehension test for, 41 differential diagnosis, 19 multidirectional, 41, 45 sulcus sign for, 41 Shoulder pain anterior, 20, 21 description of, 20 posterior, 21 referred, 43–44 Spinal column fractures, 51 Spinal stenosis, 2, 150, 161–162, 170 Spine. See Cervical spine; Lumbosacral spine; Thoracic spine Spinous processes of lumbosacral spine, 164, 166 palpation of, 62, 164 of vertebral bodies, 62, 153 Spondylolisthesis, 164, 170 Sprain ankle description of, 223 diagnosis of, 229–231, 244 instability associated with, 230 wrist, 89, 96 Spurling maneuver, 5, 9 Squat, 175, 198 Squeeze sign of metacarpophalangeal joint, 126 of metatarsophalangeal joint, 254–255, 263, 265 Sternal injury, 148 Sternochondral junction palpation, 140, 143 Sternochondritis, 143, 148 Sternoclavicular joint differential diagnosis, 19 osteoarthritis of, 45, 145, 148 palpation of, 26 swelling of, 148 Sternoclavicular joint pain, 138 Straight leg raise maneuver, 153, 158, 171, 177, 216 Strain cervical description of, 2 differential diagnosis of, 1 examination for, 14 reactive, 6, 17 signs and symptoms of, 2 lumbosacral, 150, 155–157, 170 sacroiliac, 150, 167 trapezius, 57 upper back, 51, 65 Strength testing grip dynamometry for, 104, 121 of hand, 104, 120–121 of thumb, 104 of wrist, 85–86 quadriceps, 199

Stress fractures calcaneal, 240 metatarsal, 266, 271 Subacromial bursitis chronic, 20 description of, 20 Subacromial impingement description of, 20 passive painful arc maneuver for, 24, 28 Subacromial space narrowed, 30, 33 palpation of, 25 width of, 30 Subluxation patellar, 221 shoulder, 41 Subscapular bursa description of, 20 palpation of, 26, 54, 59 Subscapular bursitis, 42, 45, 51, 59, 65 Subtalar arthritis, 223, 233, 244 Sulcus sign, 24, 41 Superior trochanteric process, 180 Supraspinatus tendon inflammation of, 20 isometric testing of, 29 magnetic resonance imaging of, 34 Swelling of elbow, 67 of foot, 253, 266 of glenohumeral joint, 39 of lateral ligament of ankle, 229 of metacarpophalangeal joint, 130 of radiocarpal joint, 90 of sternoclavicular joint, 148 of wrist, 83–84 T Talus fracture, 247, 249 Tarsal tunnel syndrome description of, 222 diagnosis of, 244 foot symptoms caused by, 251 nerve conduction velocity testing for, 243 Tinel sign for, 228, 243 Temporomandibular joint, 6, 12 Temporomandibular joint syndrome, 12, 14 Tendon cysts, 128 Tendonitis Achilles, 223, 234, 244, 249 bicipital, 35–36, 45 rotator cuff, 29–30, 45, 49 Tennis elbow. See Lateral epicondylitis Tenosynovial cyst, 133 Tenosynovitis de Quervain’s description of, 82, 102, 114 local anesthetic block for, 110, 117 radial styloid palpation for, 87, 94, 103, 105, 110 dorsotenosynovitis, 82, 93, 96, 267, 271, 276 peroneus, 242, 244 posterior tibial, 241, 244 Third-degree separation, of acromioclavicular joint, 39, 45 Thoracic outlet syndrome Adson maneuver for, 13, 14 diagnosis of, 13 differential diagnosis of, 1 upper extremity electromyography evaluations, 13, 14 Thoracic spine arthritis of, 51 compression fractures of, 62–63, 65 radiculopathy of, 50

INDEX Thumb base of, compression of, 94, 107 differential diagnosis, 101–102 examination of, 102–103 flexor tendons of, 105, 111 fracture of, 102 fractures of, 115–117 gamekeeper’s, 103, 112, 114, 117 grip strength measurements of, 104 inspection of, 105 ligament injuries of, 102 one-minute screening examination of, 103–107 trigger, 111, 114 Thumb pain differential diagnosis, 101–102 referred, 113 symptoms of, 102 Tibial fracture displaced, 247 of shaft, 219 stress, 220 Tinel sign for carpal tunnel syndrome, 78, 88, 95, 106, 113, 123 for tarsal tunnel syndrome, 228, 241 Toe(s) fractures of, 275 hammer, 251, 264, 271, 276 Morton’s neuroma, 251, 265, 271 turf, 261 Torticollis, 3, 14 Touchdown sign, 22 weighted, 23 Trapezius function of, 6 local intramuscular anesthetic block of, 6, 58 palpation of, 4, 7, 54, 57 spasm of, 18 strain of, 57 superior division of, 51 upper portion of, 4 Trauma ankle, 222 chest, 138 head, 15–18 neck, 15–18 shoulder, 20 Traumatic arthritis of metacarpophalangeal joint, 130, 133 Triangular cartilage injury, 96 Triceps insertionitis, 74, 79 Trigger finger, 127, 133, 136 Trigger thumb, 111, 114

Trochanteric bursa palpation, 177 Trochanteric bursitis description of, 173, 192 diagnosis of, 178–179 referred pain from, 194 Tuff fracture, 115 Turf toe, 261 U Ulnar fractures, 81 Ulnar neuropathy, 78 Ulnarhumeral joint arthritis of, 75–76 passive range of motion testing, 75 rheumatoid arthritis of, 76 Upper back breathing pattern evaluations, 53 differential diagnosis, 50 examination of, 52 general movement of, 52 inspection of, 53 muscular strain of, 51, 65 one-minute screening examination of breathing patterns, 53 chest compression test, 55, 61 height measurements, 55, 60 management options, 56 maneuvers for, 52–56 subscapular bursa palpation, 54 trapezius palpation, 54 pain of, 65 Upper body movement, 139 Upper extremity. See also specific anatomy electromyography of, 13, 14 neurologic impairment of, 2 V Valgus stress test for gamekeeper’s thumb, 112 for medial collateral ligament injury, 210 Vertebral bodies of neck, 18 palpation of, 56 spinous processes of, 62, 153 of upper back, 56, 62–63 Vertebral bony lesions, 62–63, 65 Vertebral column injury, 18 Vertebral fracture, 14 Volar ganglia, 100 W Weight bearing during walking, 225, 253 Weight-bearing x-rays of knee, 205, 208 of pelvis, 152

301

Weighted touchdown sign, 23 Wink sign, 159 Wrist differential diagnosis, 82 dorsotenosynovitis of, 82, 93, 96 dorsum of, 87 examination of, 84 fractures of, 97–99 grip strength measurements, 85–86 one-minute screening examination of, 84–88 range of motion testing of, 84–85 stiffness of, 84–85 strength assessments of, 86 swelling of, 83–84 synovial fluid, 100 x-rays of, 89 Wrist pain differential diagnosis, 83 dorsal, 83 referred, 82 types of, 83 Wrist sprain, 89, 96 X Xiphodynia, 138, 147–148 Xiphoid process, 147 X-rays. See also specific x-ray avascular necrosis of hip joint evaluations, 186 bilateral sunrise, 203 calcaneal stress fracture, 240 of carpometacarpal joint, 108 cervical radiculopathy evaluations, 6 of foot, 256, 268 of hallux rigidus, 257 of hands, 124–125 of interphalangeal joint, 109 of mallet finger, 131 of metastatic disease of femur, 188 metatarsal stress fracture, 266 of radiocarpal joint, 91 for reflex sympathetic dystrophy, 270 spondylolisthesis evaluations, 164 subacromial width evaluations, 30 weight-bearing of knee, 205, 208 of pelvis, 152 of wrist, 89

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