Disorders of the shoulder. Sports injuries. volume 2 [3 ed.] 9781451130584, 1451130589

Table of contents :
Prelims
Title page
Copyright
Dedication
Contents
Contributors
Preface
Acknowledgments
Part I: Introduction
1 The Athlete's Shoulder: Injury Patterns
and Evaluation
2 Anatomy and Biomechanics of Sports Injuries
3 Imaging of the Sports Injury:
Indications and Findings
4 Shoulder Motion and Sports-Specific
Rehabilitation
5 Arthroscopy Shoulder Surgery:
Anatomy, Setup, and Equipment
Part II: Glenohumeral Instability and Labral Tears
6 Shoulder Instability: Classification
and Diagnosis
7 SLAP Tears: Diagnosis and Management
8 Anterior Shoulder lnstability~Open
Repairs
9 Anterior Shoulder lnstabillty:Artb.
roscopic Repair
10 Posterior Instability: Open Repairs
11 Posterior Instability: Arthroscopic
Repairs
12 Multidirectional Instability
13 Evaluation and Oassification of Failed
Instability Repair
14 The Role of the Arthroscope
in Revision Instability Swgery
15 Swgical Management of Instability with
Bone Loss
16 Surgical Management of Glenohumeral
Instability with Soft-Tissue Deficiency
Part III:
Rotator Cuff and Biceps Tendon
17 Rotator CufF Tears: Classification
and Diagnosis
18 Rotator Cuff Repair: Open Management
19 Rotator CufF Repairs: .Arthroscopic
Management
20 Massive Cuff Tears: Open and Arthroscopic Approadhes
21 The Biceps Tendon Complex
Part IV: Muscle and Tendon Ruptures
22 Pectoralis Major Rupture: Diagnosis
and Treatment
23 Diagnosis and Management of
Latissimus Dorsi, Teres Major,
Pectoralis Minor, Short Head Biceps/
Coracobrachialis, Triceps and Deltoid
Tendon Ruptures
Part V: Acromioclavicular Joint Injuries
24 Acromioclavicular Joint Pathology:
Evaluation, Biomechanics,
and Classification
25 Arthroscopic Treatment for
Acromioclavicular Joint Injuries
26 Open Treatment of Ac.romioclavicu.lar
Injuries
Part VI: Glenohumeral Arthritis
27 Early Arthritis in the Athlete: Management Approaches
Part VII: Neurovascular Disorders
28 Diagnosis and Management
of Neurovascular Disorders About
the Shoulder in the Athlete
Part VIII: Sport-Specific Disorders
29 Common Shoulder lnjW'ies Associated
with Tennis and Baseball
30 Swimming Injuries in the Shoulder
31 Common Shoulder Injuries in Hockey
and American Football
32 Common Shoulder Injuries
in Volleyball
33 Shoulder Injuries in Skeletally
Immature Athletes
Index

Citation preview

Disorders ofthe

Shoulder Diagnosis and Management.· Sports Injuries THIRD EDITION

VOLUME 2

Disorders ofthe

Shoulder Diagnosis and Management: Sports Injuries THIRD EDITION VIIWIII! I!DII'III

Anthony Miniaci, MD, FRCSC Profeuor of S\11181Y

CIMiend Clinic Lerner College of Medi~ine CIMiand Clinic Garfield Heiahta. Ohio

_ . , ........~~. IIIJ:K

---..........._.... _... .... --___ .... 11.'-Dii_lf,... -~-

-m•

-.......

.lo,MD

. .....,no : • ...., ~

--""~;:::_

Ellii'OII

......... tw:4J:MI

....... D.lldaw•MD

.-.~~looiOIIIi..li.PIID

...... ,. , t...,..... ...

....,__. .... ...,.,

.__...........cw-

-·..

lllfBIM•trre a • ....,

-"tlllotu..--.t.p.~~

c..~-..-

r-~~

.......

lla.O...fallr.--

I

• Wolrers Kluwer Lippincott WIWams & Wilkins

.......

---------

ft.ll-'•:1• • '

a

, .....

•NM'ttlrlr•~

Acquisitii»>S EditfJr: Brian Brown PriJ~rtMflnllger: Dave Murphy

PrfJ~ctifJn ManAger: David Sahzberg

Marlteting ManAger: Lisa Zok.s Manuffl&turing ManAger: Beth Welsh Design Manager: Stephen Druding ProductifJn Services: Integra Software Services Pvt. Ltd. Printer: RR Donnelley Asia

© 2014 by llppincott Williams & Wilkins, a Wolters Kluwer Business Second edition © 2007 by llppincott Williams and Wilkins First edition © 1999 by llppincott Williams & Wilkins 351 West Camden Street Baltimore, MD 21201

Two Commcn:e Square 2001 Market Street Philadelphia, PA 19103 USA

Printed in China All rights reserved. This book is protected by copyright. No part of this book may be reproduced or transmitted in any form or by any means, including as photocopies or scanned-in or other electronic copies, or utilized by any information storage and retrieval system without written permission from the copyright owner, except for brief quotations embodied in critical articles and reviews. Materials appearing in this book prepared by individuals as part of their official duties as U.S. government employees are not covered by the above-mentioned copyright. To request permission, please contact Lippincott Williams & Wllkins at 2001 Market Street, Philadelphia, PA 19103, via email at [email protected], or via website at lww.com (products and services).

Libnuy of CoDgRA Cataloging-in-Pabllauion Data Disorders of the shoulder: diagnosis & management. - Third edition. P· ;em. Prcccded by: Disorders of the shoulder I editors, Joseph P. Iannotti, Gerald R. Williams Jr. 2nd cd. c2007. 2 v. (xii, 1364, 1-42 p.). Includes bibliographical references and index. ISBN 978-1-4511-2745-4 (v. 1)- ISBN 97S.1-4511-3058-4 (v. 2)- ISBN 978-1-4511-3057-7 (v. 3) I. Iannotti, Joseph P., editor of compilation. II. Williams, Gerald R., Jr., 1958- editor of compilation. III. Miniaci, Anthony, editor of compilation. N. Zuckerman, Joseph D. Ooseph David), 1952- editor of compilation. [DNLM: 1. Shoulder-surgery. 2. Athletic Injuries-diagnosis. 3. Athletic Injuries-surgery. 4. Joint Diseases-diagnosis. 5. Joint Discascs-sur~ry. 6. Shoulder Joint-sur~. WE 810] RD557.5 617.5 '72----dc23 2013020790 Care has been taken to confirm the accuracy ofthe information present and to describe generally accepted practices. However, the authors, editors, and publisher are not responsible for errors or omissions or for any consequences from application of the information in this book and make no warranty, expressed or implied, with respect to the currency, completeness, or accuracy of the contents of the publication. Application of this information in a particular situation remains the professional responsibility of the practitioner; the clinical treatments described and recommended may not be considered absolute and universal recommendations. The authors, editors, and publisher have aened every effon to ensure that drug selection and dosage set forth in this text are in accordance with the current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant £low of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any change in indications and dosage and for added warnings and precautions. This is particularly important when the recommended ~nt is a new or infrcquendy employed drug. Some drug~ and medical devices presented in this publication have Food and Drug Administration (FDA) clearance for limited usc in restricted research settings. It is the responsibility of the health care provider to ascenain the FDA status of each drug or device planned for use in their clinical practice. To purchase additional copies of this book, call our customer service department at (800) 638-3030 or fax orders to (301) 223-2320. International customers should call (301) 223-2300. Visit Lippincott Williams & Wilkins on the Internet http://www.lww.com. llppincott Williams & Wilkins customer service representatives arc available from 8:30 am to 6:00 pm, EST.

Dedication To my clinical and research colleagues, the students, residents, fellows, and my patients who together taught me all that I know about the shoulder and all that I will learn in the future.

-joseph P. Iannotti

To my parents Joe and Lina Miniaci, for the struggles, sacrifices, and risks that they endured to make a better life for their family. To my children Sara Lyn, Joseph, and Anthony, who have been a parent's dream and have always been there for me and shown an interest in what I did in my time away from home. And most of all to my wife Judy, my best friend and the love of my life; she has made anything we have ever accomplished possible.

-,Anthony Miniaci

I would like to dedicate the third edition of Shoulder Disorders to my patients, teachers, and students-past, present, and future-without whom this book would not be possible. In addition, I would like to thank Joe Iannotti for his friendship and mentoring over the years. Thanks also to Joe Zuckerman and Tony Miniaci for joining us on this project-it is vastly better because of you. Thanks to Bob Hurley and staff at Lippincott who have pushed us to finish this project. Finally, I would like to thank my wife, Robin, and my two children, Mark and Alexis, for their love and understanding.

-Gerald R WiUiams, Jr.

To my wonderful family-to my truly special wife Janet and my outstanding sons Scott and Matthew-you have been and always will be the most important and meaningful parts of my life.

-joseph D. Zuckerman

CONTENTS 9

-0.-

Antmt.rSiumld.r~c llq>eir 150

ei_A_

.III!ID!I."-I!r"""a....

HllGI-

PAn 1:

IAtrocJII':doe

1

1

Th.e .Ad!L:u'o Sb.aulda:: lilj wy P.•• ""'• :&1M!. £v.ai1Wioll 3

a..e.

1

>1-n-t-

11

~1-biliry.~ lltp,.....AI 2 mm) and high T2 signals are seen in the subacromialsubdeltoid bursa indicate bursitis}3 Supraspinatus tendinosis may also develop, followed by bursal surf.lce panial-thickness or full-thickness rotator cuff tear. Other MR1 findings may include subacromial spur formation (Fig. 3-20a), osteophytes or capsular hypertrophy of the AC joint, intraanicular bicipital tendinosis, and os acromiale. 0• aaomiale I}'Bdrome is characterized by failure of fusion of one or more of the four secondary ossification centers of the acromion process, which usually appear by age 15 to 18 years and fuse by age 22 to 25 years. Os acromiale is seen in 1% to 15% of shouldersSS and is bilateral in 33% of cases. Seven types of os acromiale have been described accotding to the level of fusion &ilure.55 The os acromiale can rartge from a mobile fragment to fibrocartilaginous union to near complete union. This condition is usually asymptomatic but may occasionally be painful. Repetitive trauma in weighdifting or football or a single destabilizing injury can result in persistent motion at the growth center, preventing union and making it unstable. Degenerative effects with cystic changes and osteophytes may also be seen at the pseudarthrosis. Cuff impingement may be caused by ostcophytes at the margins of the os or by the downward pull of os acromiale by the deltoid muscle. Unstable os acromiale may also be associated with AC joint

•

PART I I INTRODUCTION

A

B

RGURE 3·20. Impingement syndromes. (A) Subacromial impingement syndrome: Coronal PD-weighted MAl shows a large subacromial spur which has low signal (arrow). In addition, tflere is bursal side fraying and intermediata signal in tfle supraspinatus tendon. consistent with tandinosis latrowhead}, consistent with subacromial impingement syndrome. (B) Os acromiale: Axial T2-w MRI in a 29 year old male shows an unfused ossification center of the acromion process (aiTOw). consistent with os acromiale. High signal is seen about the junction of tfle os acromiale with tfle acromion !synchondroses). consistent with stress changes caused by motion of tfle os acromiale secondary w deltoid contraction. This may result in subacromial bursitis and supraspinatus tandinosis due to impingement by tfle mobile os. {C) Subcoracoid impingement syndrome: Axial T2-weighted MRI image in a patient with narrowed coracohumeral interval(straight arro~ and subscapularis tandinosis !cutv9d aiTOW). suggestive of subcoracoid impingement.

c

Subcoracoid Impingement Syndrome

lesser tuberosity may predispose individuals to this condition, there is no evidence that these anatomical features predict subcoracoid impingt:ment. Dynamic evaluation can be performed with ultrasound to demonstrate the impingement of the subscapularis tendon. On axial MRI, a decreased coracohumeral interval may be demonstrated ( 10 mm in individuals without impingement) (Fig. 3-20c)30; however, this measurement can vary depending on positioning and can also be abnormal in patients with instability that causes anterosuperior translation of the humeQ} head (for instance, after a biceps pulley injury). A large coracoid process and lesser tuberosity of the humerus may also be seen. Other MRI features may include subscapularis tendinosis, panial- or full-thickness subscapularis tendon tear, subcoracoid bursitis, and anterior subacromial-subdeltoid bursitis.l7

In subcoracoid impingement, the subscapularis tendon and the subcoracoid bursa are compressed between the coracoid process and humeral head. which may result in anterior shoulder pain in throwing athletes. Although a long or prominent coracoid process, abnormal shape of coracoid, or prominent

Anterosuperior impingement (A.$1), seen with repetitive overhead activities and associated with pain during the followthrough phase of throwing, is characterized by impingement

degenerative changes.55,53 Os acromiale is best seen on axillary view radiographs or CT scans. On MRI, this condition is best visualized on axial images as a "double joint" appearance of a low signal intensity band traversing the acromion process at the same lcvd as that of the true AC joint (Fig. 3-20b). MR findings may be subtle on coronal and sagittal oblique images, and the pseudojoint can be confused with the true AC joint. Os acromiale can be distinguished from an unfused or fusing normal apophysis on the basis of morphologic features: an unfused or fusing normal apophysis has a rough, crescentic proximal border with multiple ossicles interdigitating with the proximal aspect of the acromion, whereas an os acromiale has a clean, linear orientation horizontal to the acromion a:xis.62

Anterosuperior Impingement

CHAPTER 3 I IMAGING OF THE SPORTS INJURY: INDICATIONS AND FINDINGS

Ell

of the subscapularis, anterior supraspinatus tendon, and biceps pulley complex: between the antedor humeral head and the anterosuperior glenoid labrum during adduction and internal rotation of the humerus. This condition can be physiologic,68 but lesions of the biceps pulley and cuff can predispose individuals to pathologic changes of impingement. A biceps pulley lesion and the resultant instability lead to anterior translation and superior ascent of the humeral head; this condition, along with partial subscapularis and supraspinatus tendon tears, predispose the individual to the development of ASI. Biceps subluxation by itselfcan also result in tearing of the distal subscapularis tendon, which further worsens the ASI.28 MRI in these individuals shows a constellation of findings, including biceps pulley injury with medial biceps subluxation, panialthickness anicular surface tear of the anterior supraspinatus tendon, partial-thickness tear of the distal subscapularis tendon (articular surface, bursal surface, or intrasubstance), and anterosuperior labral tear. Low Tl and T2 signal representing sclerosis may also be seen in the anterosuperior glenoid rim. Diagnosing an isolated anterosuperior labral tear can be very difficult, as several normal variants can occur in this location.

labrum, greater tuberosity, and superior glenoid.IO PSI occurs in the late cocking phase of pitching, volleyball serving and spiking, tennis serving, javelin throwing, and swimming. In individuals with this condition, MRI shows a constellation of findings? including articular surface fiaying/tears/tendinosis of the posterior supraspinatus and anterior infraspinatus tendons; posterosuperior labral tear or degeneration; and changes in the posterosuperior greater tuberosity such as cpt, erosions, flattening/indentation, edema, or sclerosis (Fig. 3-21a,b). MRl performed with the patient in the ABER position can demonst~te posterosuperior decentering of the humeral head, contact between the rotator cuff lesion and superior labrum/ glenoid, and even pinching of the supraspinatus tendon between the glenoid and greater tuberosity (Fig. 3-21c).2' MRl inABER may also show subluxation of the humeral head and anterior IGHL tear or attenuation. A thickened posterior or posteroinferior joint capsule may also be seen in individuals with associated GIRD. PSI is also highly associated with SLAP lesions, so overlap may be seen between the clinical findings of PSI and SLAP.

Posterosuperior Impingement

Although a number of the previously discussed abnormalities can occur in throwers, the throwing athlete can also develop a unique sequence of abnormalities. In the initial stages, the individual has posterior shoulder tighmess, which ma:y be seen on MRI as capsular thickening (Fig. 3-22a) and remodeled posterior glenoid rim with sclerosis. This is followed by a type 2 or posterior type 2 SLAP lesion. Subsequently, GIRD and SICK scapular syndrome occur. Articular surface partial-thickness tears of the posterior supraspinatus and anterior infraspinatus may be seen.67

Throwing Shoulder Posterosuperior impingement (PSI) is characterized by impingement of the posterior supraspinatus or anterior infra. spinatus tendon and the posterosuperior labrum between the greater tuberosity and the posterosuperior glenoid during the extreme abduction and external rotation of overhead movements. Although PSI is a physiologic finding in most individuals, humeral head instability and chronic repeti· tive impingement in the ABER position in overhead athletes can lead to tissue damage and abnormal findings in the cuff,

A

B

RGURE 3-21. PoSUlrosuperior impingement. (A) Axial T2-w MRI in a baseball pitcher with posterior sfloulder pain on pitching shows abnormal signal and morphology of the posterosuperior labrum, consistent with a tear (curved arrow!. There is also thickening and intermediate signal of the posterior supraspinatus and anterior infraspinatus tendon fibers, consistent with tendinosis (straight al7llw!. Multiple small cysts are seen in the posterior humeral head larrowhssd5i. {81 Coronal T2-W MRI in another patient shows abnormal high signal in the anterior infraspinatus fibers consistent with tsndinosis/ partial tear (stmight arltMi. High signal is also seen in the adjacent greater tuberosity (curved arrow! due to posterosuperior impingement. (C) Axial image in the ABER position shows the posterosuperior impingement of the rotator cuff (arrow! between the glenoid and humeral head.

El

PART I I INTRODUCTION posterosuperior position on abduction and external rotation of the ann, increasing the arc of enernal rotation before the greater tuberosity contacts the posterior glenoid. Although this can increase throwing power, there is decreased internal rotation of the abduaed arm and additional stress on the bicepslahral anchor, superior labrum, rotator cuff, and muscles. In these individuals, MRI shows a thick. and shon posterior band of the IGHL, which is best seen on coronal or axial MR images as a low signal band {Fig. 3-22a). The posterior labrum may also be thickened, and the posterior lahrocapsular recess is small because oflahral and capsular thickening.72 Associated lesions include SLAP tears, partial articular surf.lce cuff teats, cystic ~ in the posterior humeral head, subarticular sclerosis, and cyst formation in the posterosuperior glenoid,70

Bennett Lesion

c FIGURE 3-21. (Ccntmued)

GIRD GIRD is the dccreasc: in internal rotation (in degrees) of the abducted ann ofa throwing athlete compared to the nonthrowing arm. The shoulder adapts to repetitive throwing by contracture of the posteroinferior capsule, which shifts the point of contact of the hum~ head with the glenoid to a more

The Bennett lesion is a bony prolifc:ration along the posteroinferior glenoid at the insertion of the posterior band of the IGHL that is seen in up to 22% of baseball pitchers.79 This lesion type is believed to be caused by chronic capsular traction as a result of repetitive throwing or posterior impingement; alternatively. this lesion may represent calcification of a POLPSA lesion. A superior Bennett lesion is a bony proliferation along the posterosuperior glenoid tim. This lesion subtype may be caused by fru:ture of the posterosuperior glenoid rim, particularly in throwers with internal impingement, or may arise from nonunion of a posterosuperior glenoid ossification center as a result of repetitive throwing. Radiographs, cr, and

A

B

FIGURE 3-12. Throwing shoulder. lA) GIRD: Axial T2-waightsd image in a pitcher with glenoid internal rotation deficit shows tflicl: posterior capsule (atroW} with areas of calcification and surrounding edema. Repetitive pitdling injures tfle posterior IGHL and posterior capsule at end of follow-through, resulting in thickening and contracture of these structures (arrow). This limits the degree of adduction and internal rotation of the humeral head. With abduction and external rotation. tfle thickened posterior capsule forms a sling under humeral head. causing posterosuperior subluxation. (B) Benn81:t lesion: Axial T2-weighted (B) and sagittal T1-weighted IC) MA images in a baseball pitt:her shows extensive ossification along the posteroinferior glenoid !stTOW} in an ext:raarticular location. consistent with tfle classic Bennett lesion.

CHAPTER 3 I IMAGING OF THE SPORTS INJURY: INDICATIONS AND FINDINGS

Ell

AC Injuries AC Joint Separation

c RGURE 3-Zt !CootinUBd) MRI in patients with Bennett lesions show a crescentic area of calcification or ossification along the posteroinferior glenoid in an extraanicular location. On MRI. the lesion has low signal on all pulse sequences if the lesion is calcified and has marrow signal if the lesion is ossified (Fig. 3-22b,c). Associated posterosuperior labral tears and posterior undersurface cuff tears may also occur in patients with these lesions; these conditions may account for patients' pain.45l

AC joint separation accounts for 10% ofshoulder injuries and is common in contact sports such as football. rugby, and icebased sports. I AC joint separation has been classified into six types (Rockwood classification) based on the involvement of various ligamentous structures.! Radiographs are commonly diagnostic for this condition; however, MRI is highly sensitive and accurate in assessing the AC joint ligaments (AC, coru:oclavicular. and coracoacromial) and often demonstrates a higher grade of injury than was evident clinically or radiographically. With MRI, the AC joint ligaments can be seen on sagittal oblique images from a regular shoulder protocol but are best visualized on dedicated coronal oblique images acquired parallel to the AC joint. Although normal ligaments are best visualized on Tl-weighted images. changes of acutely disrupted ligaments are best seen on PD- or T2-weighed images, and subtle sprains may only be detectable on f.lt-suppresscd PD- or T2-weighted images. Radiographic findings may be subtle in patients with grade 1 injury (sprain of AC ligament), in which AC joint widening (>7 mm in men; >6 nun in women) may be seen only in stress views.57 MRl is more sensitive. often demonstrating tear of the supetodorsal AC ligament with edema around the AC joint as well as subtle marrow edema (Fig. 3-23a,b). MRI also can distinguish low-grade injury from normal variation and age-related changes. In patients with grade 2 injury, the AC ligament is completely torn. Radiographs in these patients show AC joint widening in routine views and MRI shows complete tear of the AC ligaments (both superior and

A

B

RGURE 3-23. Acromioclavitlllar joint injuries. (A) Coronal 12-weighted MR image shows edematous signal about the acromioclavicular joint Iarrow) with normal signal witflin tfle bone marrow. consistent witfl capsular edema in patient witfl AC sprain. (8) Sagittal T2-w MRI image in tfle same patient shows an intact coracoclavitlllar Iigament !curved arttM? in addition to the AC edema !straight atrowl. consistent with a Grade 1AC joint injury. (C) AP radiograph in another patient shows widening of the AC joint, consistent with Grade 3 AC joint injury. Coracoclavicular distance is normai.ID) Sagittal 12-weighted image in another patient shows near-tolal tear of tfle coracoclavicular ligament with only small fibers remaining attached to tfle undersurface of clavicle Iarrow) and the space filled with edematous signal. The AC ligaments were also tom (not shown here).

m

PART I I INTRODUCTION injury, even in the absence of radiographic coracoclavicular widening, MR1 often upgrades the injury severity. which can help to determine the treatment course and allows for a more accurate prediction of when the patient will be able to return to play. Grade 4 to 6 injuries are associated with injuries to several non-AC structures, as can be demonstrated on MRl.l MIU can also assess the integrity of the coracoacromialligament, which can potentially be used as a surgical substitute for the coracoclavicular ligament. In chronic AC injuries, the AC and coracoclavicular ligaments are thickened with low signal intensity on all pulse sequences.

Distal Clavicular Osteolysis Distal clavicular osteolysis can be seen after acute trauma or chronic repetitive stress, particularly in young male weightlifteB. Patients with this condition present with pain over the AC joint and weakness on arm abduction, symptoms that can mimic a fracture or rotator cuff tear. Distal clavicular osteolysis is believed to be the sequel of a distal clavicular subchondral fracture that undergoes osteolysis and delayed union as a result of instability caused by lack of impaction between bones on either side of the fracture plane; this process is typically the result of associated AC joint microuaumatic instahility.39 Radiographs in these patients show irregularity of the distal clavicle at the AC joint (Fig. 3-24a) with subchondral cysts and, in later stages, widening from bony resorption (Fig. 3-24b).37 MIU, which is more sensitive than radiographs in these patients, usually shows edema localized to the distal

c

D

FIGURE 3-21. (Ccntmued)

i.nkrior). Edema--like signal in the coracoclavicular ligament and marrow edema in the clavicle and acromion may also be s=n in MR1. In grade 3 injury, the coracoclavicular ligament is tom along with the AC ligament. Radiographs show dislocation of the joint and elevation of the distal clavicle {> 11 to 13 mm) (Fig. 3-23c), with the inferolateral clavicular border often lying above the infi:romedial acromial border. MRI shows edema and complete tear of the AC and coracoclavicular ligaments (Fl.g. 3-23d). Clinical and radiographic studies are often not accurate in distinguishing between grade 2 and grade 3 injuries. By demonstrating coracoclavicular ligament

A

RGURE 3-24. Distal clavicular osteolvsis. lA) Radiograph in a 17-yearold waigh1liftsr sbows subtle erosion of the distal clavicle. suggestive of distal clavicular ostaolysis. IB) Follow-up radiograph perfurmed 1 week later shows worsening erosion of the distal clavicle and widening of the erosion of the distal clavicle and widening of the acromioclavicular joint space. (C) Coronal 12-w MRI image shows lvsis of the distal clavicle, with high T2 signal, which is extending to the AC joint, which is wider than normal.

CHAPTER 3 I IMAGING OF THE SPORTS INJURY: INDICATIONS AND FINDINGS

m

visualized on fluid-sensitive MRI sequences such as T2-weighted and short tau inversion n:covery (SilR) sequences. In grade 1 (mild) mucle injury, microswpic injury without significant macroscopic fiber disruption occurs. MRI shows high signal in the muscle that traclcs along the muscle fascicles in a feathery appearance without any architl'!ctural distortion, and pe~ cial Buid may track around a muscle belly or group of muscles (F'tg. 3-25a).ln grade 2 (mod~) injury, macroswpic-partial

A

c RGURE 3-24. !Continued)

clavicle (Fig. 3-24 c).23 Edema may also be seen on either side of the AC joint but is never isolated to the acromion. A hypointense subchondral fracture line may be seen in the clavicle.3!1 Cortical irregularity, erosion, bone fragmentation, and AC joint widening with fluid in the AC joint (F'tg. 3-24c) and capsular distension may also be seen, particularly if the offending activity is not stopped.l8 In the setting of chronic injury, intermediate Tl and low T2 signal may appear surrounding the AC joint because offibrous tissue.l8

Muscle Injuries Injuries can be seen in various muscles around the shoulder joint, including the pectoralis major, supraspinatus, infraspinatus, teres minor, subscapularis, biceps, latissimus dorsi, pectoralis minor, and triceps. Muscle injuries occur after excessive fora:fUJ. contraction and are most common at the inherently weak myotendinous junction (M1J). Muscle injums are best

B

RGURE 3-2:5. Muscle injuries. (A) Sagittal T2-weighted MRI in a patient who got injurad during an yoga session shows faatflel'( edema in tfle teres minor muscle (arrow!. consistent witfl Grade 1 strain. (B) Axial T2-weighted MRI in another patient witfl posterior shoulder dislocation shows high signal hematoma in tfle teras minor muscle. consistent witfl Grade 2 strain.

m

PART I I INTRODUCTION

tl:ar is seen in the muscle, which can be fUrther classified as low (> 1/3 fibers tom), m.ockrate (1/3 to 2/3 fibers tom), or high (>2/3 torn) grade. High T2 and Tl signal is seen at the myo-tendinous jWlction as a result of hemorrhage or edema, and per~ i&scial fluid may also be seen (Fig. 3-25b). In gnde 3 (leVCft) injury, there is complete muscular or musculotendinous disru~ tion with or without retraction, and the gap is filled with fluid. Intra- or intermuscular hematoma ma:y be seen in the acute stages. Approximately 75% of muscle injuries are first-degtet: injuries.6 Remote or chronic strains are mon: difficult to detect with MRl, which demonstrates thinning of the myotendinous unit and low-T2 signal because of hemosiderin and fibrosis in such cases. A direct blow to the muscle may cause contulion or a mass-like hematoma with no evidence of fiber disruption. In these patients, MR1 may show increased muscle girth with~ out fiber discontinuity or laxity. Diffuse or geographic high signal is also seen, often with a feathery margin. Contusions are generally largt:r than strains but are associated with a faster recovery. Low-grade contusions are difficult to distinguish from strains on the basis of imaging alone and often require clinical history. With dUtraction or •hearing injuria, sharply demarcated fiber discontinuity is seen with or without fOcal edema or hemorrhage. Delayed-onset mutc:le .ozmea is muscular pain, soreness, and swelling following unaccustomed eccentric muscle contr.ctions, as a result of reversible cellular structural damage. Symptoms begin 1 to 2 days after exercise, peak in 2 to 3 days, and subside in I week. MR1 appearance of these injuries is similar to the appearance of a grade 1 strain, with high signal ofinterstitial edema and occasional perifascial fluid collections. The clinical history distinguishes these injuries from strains.6

heads can also be challenging on MR1. In a complete tear, com~ plete discontinuity of all the fibers occurs at the site of injury; with or without rett&Ction of either the tendon at the enthesis (Fig. 3~26a) or the muscle at the myotendinous jWlction (F~g. 3-26b). In acute stages, the gap is filled with high-T2 signal fluid/hematoma; in chronic stages, fibrosis and scarring lead to low signal. Intermediate-to--high signal may be seen superficial to the cortex. at the humeral insertion site as a result of periosteal stripping (Fig. 3~26a). Hyperintense edema may appear in the clavicle, sternum, or ribs. Occasionally, in acute tean, defining the precise location of the tear may be difficult, as the site of maximal edema may be remote fi:om the site of acrual tear, due to tendon retraaion. Diagnosing a chronic tear is often difficult, as the imaging finding5 may be subtle and no signal abnormality may be seen on fluid-sensitive sequences. In partial tears, high-signal fluid/hemonhage is seen at the myo~ tendinous junction or enthesis without complete discontinu-ity or retraction (Fig. 3-26c).ll Distinguishing complete fi:om partial tear is essential, as wmplete tears are managed surgically, particularly in high-perfonnance athletes, whereas partial tears can be managed conservativdy.

Pectoralis Major Injuries Injuries to the pectoralis major muscle and tendon are more common in young athletic men after extreme tension and eccentric contraction of the muscle. These injuries are usually seen in weightlifting (after bench press), and less commonly in football, waterskiing, and wrestling. Partial tears are more common than complete tears; these tears are seen at the myotendinous junction and tendon-bone interface, respectively. Intrasubstance tears of the muscle are less common and are caused by direct uauma in contact sports. Combined sternal and clavicular head injuries are more common than isolated head injuries, although in wn:stlers; isolated injury of the superior clavicular portion may be seen. Clinical examination may be limited in distinguishing a tear from normal muscle and distinguishing partial rupture from complete rupture, particularly in the acute and subacute phases because of hemorrhage, tenderness, and spasm. Radiographs may show only subtle signs of these injuries, such as loss of muscle outline and avulsed bony fragment. On MRl, T1-weighted images are used to identify the tendon and the position of the myotendinous jWlction, and T2-weighted images are used to evaluate the fluid and hematoma. Axial oblique images oriented along the tendon and coronal oblique imaga along the plane of the myotendinous unit an: helpful in ddineating the anatomy.l6 The myotendinous junction may not be dearly defined because of twisting and radiating fibers and distinguishing the sternal and clavicular

A

RGURE 3-2&. Pectoralis major injuries. (A} Complete avulsion: Axial 12-weighted MRI shows a large complete tear of the pectoralis major tandon from tfle humerus. witfl retraction of tfle tendon up to tfle deltopactoral groovalstraight afit1VI?. The tandon gap is filled with high signal intensity fluid {curved arrowt. The long head biceps tendon can be seen anterior to the humerus with greater separation of the tendon from tfle bone due to tfleloss of the overlying pactoralis tendon. (B) Myotendinous junction tear: Axial oblique 12-W MRI in another patient shows a small area of hemormage and edema {arrow! at tfle lateral aspect of tfle pectoralis major muscle, just medial to tfle mid-axillary line. The distal attachment of the tendon at the humerus was normal. This is consistent witfl a tsar at tfle mvotsndinous junction with medial retraction. (C) Partial tear: 12-W axial image in anotfler patient showing edema tracking along tfle mvotendinous junction {aJTOw). but no fluid-tilled gap was identified distallv and tflere is no tendon retraction, consistent with a partial tear.

CHAPTER 3 I IMAGING OF THE SPORTS INJURY: INDICATIONS AND FINDINGS

Ell

is isointense to muscle on Tl-weighted images (Fig. 3-27b) and hyperintense on T2-weighted images (Fig. 3-27c).51 This abnormal signal may extend into the metaphysis and, less commonly, into the epiphysis and periosteum.32 Cessation of the provoking physical activity may result in regrowth of vessels and growth plate remodeling. 51

B

A

c RGURE 3-26. !CootinUBd)

Miscellaneous Little League(s Shoulder Little Leaguer$ shoulder is seen in adolescent overhandthrowing athletes (11 to 16 years of age), particularly baseball pitchers. It is believed to be caused by repeated torque and distraction on the proximal humeral physis, resulting in injury to the hypertrophic zone that leads to disruption ofblood supply to the physis. This process causes chondrocyte proliferation and impaired endochondral ossification, leading to ph:yseal wid.ening.66 Radiographic findings ma:y be subtle, particularly in the first 3 weeks after onset. Widening of the lateral humeral ph~ plate is the most common finding (Fl.g. 3-27a).25 Less common findings include physeal fragmentation, paraphyseal demineralization, and proximal metaphpeal sclerosis and cystic changes. MRI in these patients shows a widened physis, which

B

RGURE 3-Z'I. Little leaguers' shoulder. (A) Radiograph shows widened and irregular lateral physeal plate {arrow!. (B) Coronal T1-wuighted image shows irregular widening and low signal in the lateral aspect of the growth plate la~rowJ.IC) Coronal T2·weighted images sflow high signal edema in tile growth plate extending into the proximal humeral metaphysis {arrow).

m

PART I I INTRODUCTION anterosuperior humeral head and very rarely in the glenoid (Fig. 3-28). Affi:cted patients have a history ofa single traumatic event or repetitive microuawna. Chondral shearing injuries can also occur in patients with acute or recurrent instability.45 Osteochondral lesions of the humeral head have been noted in up to 17% ofhigh-level overhead-throwing athletes with internal impingement.54 Cartilage lesions are also seen in patients with rotator cuff pathologies and subacromial impingement: 13% of patients with fUll-thickness tears have cartilage lesions,26 29% of patients with subacromial impingement have humeral canilage lesions, and 15% of patients with subacromial impingement have glenoid c:artilage lesions.31 Cartilage lesions are best visualized on PD- and T2-weightcd images. MR arthrogram increases the contrast between joint Ruid and articular cartilage, resulting in a sensitivity of76.5%/69% and 75%/65% in the detection of humeral and glenoid cartilage lesions, respectivdy.31

CONCWSION c FIGURE 3·21. {lmtmuedl

ChondraVOsteochondrallnjury Ostwchondritis dissecans is an uncommon type of cani.lage lesion in the glenohumeral joint, in which the primary pathology is in the subchondral plate, with secondary injury to the overlying articular cartilage. This lesion, which is most commonly seen in young to middle-aged men, occurs along the

Sports injuries to the shoulder involve complex biomechanical mechanisms and abnormalities. Imaging plays an important role in the evaluation of these injuries, including diagnosis, characterization, presurgical planning, and determination of when the patient will be able to return to play.

ACKNOWLEDGMENT The authors thank the staff of the Musculoskeletal Imaging Section, Cleveland Clinic and Megan Griffiths, scientific writer for the Imaging Institute, Cleveland Clinic, for their help in the preparation of this manuscript.

A

B

FIGURE 3·21. Osteochondral injury. Axial (A) and coronal (B) T2-w MR images sbow an ostsochondrallesion measuring 1B X 8 X 5 mm in 1he central ponion of glenoid anicular surface {arrow), with a cleft of fluid-like signal intensity separating 1he fragment from the rest of 1he glenoid, suggesting an unstable fragment

CHAPTER 3

I IMAGING OF THE SPORTS INJURY: INDICATIONS AND FINDINGS •

REFERENCES 1. Alyas F, Curtis M, Speed. C, Saifuddin A, Conndl D. MR Imaging appeamnces of acromioclavicular joint dislocation. RMiitlfT•phia 2008;28:463-479. 2. Beggs I. Ultrasound of the shoulder and dbow. OrthDp Clin N Am 2006;37:266-285. 3. Beo..nett WF. Correlation of SlAP Ienon with lesions of the medial sheath of the biceps u:ndon and intra-articular subscapularis tendon. In4Un J Orthf1J12009;43:342-346. 4. Bergin D. Imaging shoulder instability in the athleu:. Mlllfl &son imllfinl Clin N Am 2009;17:585-615. 5. Bigliani LU, Pollock RG, Soslowsky LJ, Flatow EL, Pawluk RJ, Mow VC. Tensile properties of the inferior glenohumeral ligament. J OrthDp Res 1992;10:187-197. 6. Boutin RD, Fritz RC, Steinbach l..S. Imaging of sports related muscle injuries. Rtulwl Clin N Am 2002;40:333-362. 7. Bud.offJE, Nirschl RP, llahi OA, ct al. lnt=lal impingement in the etiology of rotator cuff u:ndinosi.s revisited. ArthrotCtJpy 2003; 19:810-814. 8. Bui-Mans6eld LT, Taylor DC, UhorchackJM, TenutaJJ. Humeral avulsioo..s of the glenohumeral ligament: imaging features and a review of the literature. AJR Am J RDmtt;mol2002;179(3}:659-655. 9. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to the failure of arthroscopic Bankart tepairs: significance of inverted-pear glenoid and humeral ~ Hill-Sachs lesion. ArthromiJIJ 2000;16(7}:677-694. 10. Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spcctru.m of pathology. Pan 1: pathoarwomy and biomcch.anic.s. ArthroJcopy 2003;19:404-420. 11. Carrino JA. Chando.anni VP, Mitchell DB, Choi-Ch.in.n K. DeBeracdino TM, Millder MD. Pectoralis major muscle and tendon tears: diagnosis and grading using magnetic cesoo.ao.ce imaging. Slukt4J Rdwl 2000;29:305- 313. 12. Catalano OA, Manfredi R. Vanzulli A, et al. MR arthrography of the glenohumeral joint: modified posu:rior approach without imaging guidance. Rtu/iqf4D 2007;242(2}:550-554. 13. Chang 0 , Mohana-Borges A, Borso M, Chung CB. SLAP lesions: arwomy, clinical presentation, MR imaging diagnosis and chacacrcriz.ation. Eur] .R.tJW/2008;68:72-87. 14. Chung CB, Dwck JR. Fend S, Resniclr. D. MR arthrography of the glenohumeral joint: a tailored approach. AJR Am J Rom1fmol 2001;177(1}:217-219. 15. Cohen SB, Towers JO, Bradley JP. Rotator cuff contusions of the shoulder in professional fOotball players: epidemiology and magnetic resonance imagingftodings. Am] Spfl111 Mtlt2007;35(3}:442-447. 16. Connell DA, Potu:r HG, Sherman NF, WickicwiczTL. Injuries of the pectoralis major muscle: evaluation with MR imaging. RAJjqltJo 1991;210:785- 791. 17. Cowdecoy GA, Li.sle DA. O'Connell PT. Overuse and impingement syndromes of the shoulder in the athlete. Mlllfl Reron lmllfint Clin N Am 2009;17:577-593. 18. De La Puente R. Boutin RD, Theodorou OJ, Hooper A, Schweitzer M, Resnick D. Post traumatic and. stress induced osteolysis of the distal clavicle: MR imaging in 17 patients. SJ:ekt4J .R.tJW/1999;28:202- 208. 19. De Macsenccr M, Van Roy F, Lcnchik L, ct a!. CT and MR arthrography of the normal and pathologic anterosuperior labrum and labralbicipital compla. RdiOf7WPhia 2000;20:567-581. 20. DeJesusJO, Parker L, Frangos A}, NazacianLN. Accuracy ofMRI, MR arthrography. and ultrasound in the diagnosis of rotator cuff tears: a meta-analysis. AM] Romlfpffll2009; 192(6}:1701-1707. 21. Escobedo EM, Richardson ML, Schulz YB, er al. Increased risk of posterior glenoid labrum tears in footha.ll players. AJR Am ] Romtt.mol 2007;188(1):193-197. 22. Farmer KD, Hughes PM. MR arthrography of the shoulder. Fluoroscopically guided technique using a posterior approach. AJR Am J Ramtfmo/2002;178:433-434. 23. FioreUa 0 , Hdms CA, Speer KP.Increased T2 signal in the distal clavicle; incickncc and clinical implications. Skelmd Rdio/2000;29:697-702. 24. Fitzpatrick 0, Waltz OM. Shoulder MR imaging normal vacian!3 and imaging artifacts. Shoulder MR imaging normal v.uiants and imaging artifacts. M•lfl &son lm4fint Clin N Am 2010;18(4}:615-632.

25. Fleming JI, Hollingswonh CL, Squire DL, ct a!. Little leaguer's shoulder. Skekt4J Rtu/jq/2004;33:353-354. 26. Gactsman GM, Tavana E. The incideoce of glenohumeral joint abnormalities associated with full-thickness, reparable rotator cuff tears. ArthrtHCfiPJ 1997;13:450-455. 27. George MS. Fractures of the greater tuberosity of the humerus. JAm Ac.J Orthop S111f 2007; 15:607-613. 28. Gerber C, Sebesta A. Impingement of the deep surface of subscapularis tendon and the reflection pulley on the anterosuperior glenoid rim: a prdiminacy repon. J Shou/Jer EIJJIJW Su'f 2000;9:483-490. 29. Giacoli EL, Major NM, Higgio..s LD. MRI of internal impingement of the shoulder. AJR Am J Romt{mo/2004;183 (4}:969-974. 30. Giacolli EL, Major NM, Lemley DE, ct a!. Coracohumeral interval imaging in subcoracoid impingement syndrome on MRI. A]R Am ] Ramtfeno/2006; 186:242-246. 31. Guntcrn DV. Pficrmann CW. Schmid MR. ct al. Articular cartilage lesions of the glenohumeral joint: diagnostic effectiveness of MR arthrography and prevalence in patients with subacromial impingement syndrome. Rtuliowo 2003;226:165-117. 32. Hau:m SF, Recht MP. Profitt B. MRI of the little leaguer's shoulder. SJ:ekul Rtulio/2006;35(2}:103-106. 33. Holsbeeclr. M, Strouse PJ. Sonography of the shoulder: evaluation of the subacromial-subdeltoid bursa. A]RAm] Rom'fmo/1993;160:561-564. 34. lliu YC, Pan RY, Shih YUI, ct al. Superior capsulae elongation and its significance in atraumatic posteroinfcrior multidirectional shoulder instability in magnetic resonance arthrography. Acu Rlllli11l 2010;51 (3);302-308. 35. ltoi E, Lee SB, Berglund LL, Berge LL, An KN. The effect of glenoid defect on antcroinferior stability of the shoulder alter Banlr.act repair: a cadaveric study. J Bone Joint Su'f Am 2000;82:35-46. 36. JungJY, Yoon YC, Yi SK, Yoo J, Choe BK. Comparison stUdy of indirect MR arthrography and direct MR arthrography of the shoulder. Skekt.t R.Jjq/2009;38(7):659-667. 37. Kaplan PA, Resnick D. Stccs.s-induccd osteolysis ofthe clavicle. Rdiowo 1986;158:139-140. 38. Kassarjian A, Bcncacdino JT, Palmer WE. MR imaging of the rotator cuff. M•lfl Resrm lm#fint Clin N Am 2004;12:39-60. 39. KassarjianA, Uopis E, Palmer WE. Distal clavicular osteolysis: MR evidence for subchondral fracture. Skekul RM/io/2007;36:17-22. 40. Kassacjian A, Torriani M, Ouellette H, Palmer WE. Intramuscular rotator cuff cysts: association with tendon rcacs on MRI and arthroscopy. Amj Ran11fmol2005;185:160-165. 41. l..coouvct FE, Simoni P, .Koutaissoff S, Venade Berg BC, Malghem J, Dubuc JE. Multidetector spiral CT arthrography of the shoulder. Oinical applications and limits, with MR arthrography and arthroscopic corrdations. Eur J IW/jq/2008;68(1):120-136. 42. Lo IK, Burkhart SS. Triple labrallesions: pathology and surgical repair technique. Report of seven cases. Arthrostvpy 2006;21 (2}: 186-193. 43. Magee T, Shapiro M, Williams D. Comparison of high-fidd-strength versus low-field-strength MRI of the shoulder. A]R Am J &m1f.m111 2003;181(5):1211-121 5. 44. Magee T. 3-T MRI of the shoulder: is MR arthrography necessary? AJR Am J Romtt.mo/2009;192:86-92. 45. McCarty PL II, Cole BJ. Non arthroplasty treatment of glenohumeral cactibgc lesions. Arthroscopy 2005;21(9}:1131- 1142. 46. Meister K. Thesing J, Montgomery WJ, Indelicato PA. Walczak S, Fontenot W. MR arthrography of pactial thickness tears of the undersurface of the rotator cuff. an arthroscopic correlation. SJ:ekul Rllliifll 2004;33:136-141. 47. Mohana-Borgcs AYR. Chung CB, Resnick D. Supcrioc labral anteroposterior rcac: classification and diagnosis on MRI and MR arthrography. AJRAm] Rom'fmo/2003;191:1449-1462. 48. Morgan CD, Burkhart SS, Palmeri M, ct al. Type ll SlAP lesioo..s, three subtypes and their relatioruhips to superior instability and rotator cuff tears. ArthromJpy 1998; 14(6}:553-565. 49. Nalcigawa S, Yoncda M, Hayashida K, Mizuno N, Take Y. Superior Bennett lesion: a bone fragment at the posterosuperior glenoid rim in 5 athletes. ArthroJcopy 2007;23(10): 1135 el-c4. 50. Nak:igawa S, yoncda M, Mizuno N, et al. Throwing shoulder injury involving the anterior rotator cuff. Concealed tears not as uncommon as previously thought. ArthroJcopy 2006;22(12}: 1298-1303.

•

PART I

I INTRODUCTION

51. Obembc: 00, Gaskin CM, Taffuni MJ, Anderson MW. Little leaguer's .shoulder (proximalhurneral epiphysiolysis): MRI findings in four boys. Petliatr &tdiol2007;37(9):885-889. 52. Oudlette H, Kassarjian A, Tretteault P, Palmer W. Imaging of the overhead throwing athlete. Scmin Musculoskdet Radio! 2005;9:316-335. 53. Pagnani MJ, Mathis CE, Solman CG. Painful os acromi2le in athletes. J Shoultin Elbow Su'f 2006; 15:432-435. 54. Paley KJ, Jobc: FW. Pink MM, Kvitne RS, E!Attrache NS. Arthroscopic findings in the overhead throwing athlete: evidence for posterior internal impingement of the rotator cuff. Arthrosmpy 2000; 16:35-40. 55. Park JG, Lee JK, Phdps CT. Os acromiale associated with rotator cuff impingement: MR imaging of the shoulder. Rdioloo 1994;193: 255-257. 56. Petchprapa CN, beltran LS, Jauawi LM, Kwon Jw. Babb JS, Recht MP. The rotator interval: a review of anatomy, function and normal and abnormal MRI appearances. AJR 2010; 195:567-576. 57. Petersson CJ, Redlund-Jonnell I. Radiographic joint space in normal acromioclavicular joints. .Actlt Orthop SC4nti 1983;54:431-433. 58. Polster JM, Schickendantz MS. Shoulder MRI: what do we miss? AJR Am] Romtgmo/2010;195(3):577-584. 59. Pricket WD, Teefey SA, Galatz LM, et al. Accuracy of ultrasound imaging of the rotator cuff in shoulders that are painful post operativdy. f Bone joint Su1f Am 2003;85-A: 1084-1089. 60. Reinus WR, Hatem SF. FractUreS of the greater tUberosity presenting as rotator cuff abnormality: magnetic resonance demonstration. J Trttum4 1998;44 (4):670-675. 61. Rutten MJCM, Jager GJ, Blickman JG. US of the rotator cuff; Pitf.d!s, limitations and artifacts. &tdiotr•phia 2006;26:589-604. 62. Sammarco VJ. Os acromiale: frequency, anatomy, and clinical implications. J Bone joint Su'X' Am 2000;82:394-400. 63. Sanders TG, Tirman PFJ, Linares R, Fdler JF, Richardson R The glenolabral articular disruption lesion: MR arthrography with arthroscopic corrdation. AJRAmf Romtgmol1999;172:171-175. 64. Smith DK, Chopp TM, Aufdemorte TB, et al. Sublabral recess of the superior labrum: stUdy ofcadavers with conventional non-enhanced MR imaging, MR arthrography, anatomic dissection and limited histologic examination. Rdliioloo 1996;171:235-238. 65. Snyder SJ, Karzc:l RP, Dd Pizzo W, Ferkd RD, Friedman MG. SLAP lesions of the shoulder. Arthroscopy 1990;6:274-279. 66. Song JC, Lazarus ML, Song AP. MRl findings in Little lc:aguc:r's shoulder. 5/rekul Rdtiio/2006;35(2):107-109.

67. Stoller DW, Wolfe EM, LiAE, Nottage WM, Tirman PFJ. The shoulder. In Stoller DW, ed. M~~.pait &JtJ,.,u lm~~~fint in Orthopetiits IZ1IIl Sports Metlicm~, 3rd ed. LWW publishers. Philaddphia 2006:1261-1290. 68. Struhl S. Anterior internal impingement. An arthroscopic observation. Arthroscopy 2002; 18:2-7. 69. Sugaya H, Kon Y, Tsuchiya A Arthroscopic repair of glenoid fractures using sutUre anchors. Arthroscrpy 2005;21 (5):635-640. 70. Tehranzadeh AD, Fronek J, REsnick D . Posterior capsular fibrosis in professional baseball pitchers. Case series of MR arthrographic findings in six patients with glenohumeral internal rotation deficit. Clin JmtWng 2007;31 (5):343-348. 71. Tirman PF, Fdler JF, Palmer WE, Carroll Kw; Steinback LS, Cox I. The Buford complex- a variation of normal shoulder anatomy: MR arthrographic imaging featUres. AJRAmf RomtgmD/1996;166(4):869-873. 72. Tuite MJ, Petersen BD, Wise SM, et al. Shoulder MR arthrography of the posterior labrocapsular complex in overhead throwers with pathologic internal impingement and internal rotation deficit. 5/re/md Rllliiol 2007;36{6):495-502. 73. VanderWoude H-J, Vanhoc:nacker FM. MR arthrography in lenohumeral instability.}BR-BTR 2007;90:377-383. 74. Vmson EN, Major NM, Higgins LD. Magnetic resonance imaging findings associated with surgically proven rotator interval lesions. Slt&t41 &tdio/2007;36(5):405-410. 75. Waldt S, Burkart A, Imhoff AB, Bruegd M, Rurnmeny EJ, Woertler K Anterior shoulder instability: accuracy of MR arthrography in the evaluation of anteroinlerior labroligamentous injuries. &zdioloo 2005;237(2):578-583. 76. Wintzell G, Larsson H, Larsson S. Indirect MR arthrography of anterior shoulder instability in the ABER and the apprehension test positions: a prospective comparative study of two clifierent shoulder positions during MRI using intravenous gadodiamide contrast for enhancement of the joint fluid. SJ:elmd RM/io/1998;27(9):488-494. 77. Woertler K, Waldt S. MR imaging in sporu-rdated glenohumeral instability. Eur Rdiol2006; 16(12):2622-2636. 78. Wolf EM, Siparsky PN. Glenoid avulsion of the glenohumeral ligaments as a cause of recurrent anterior shoulder instability. Arthroscopy 2010;26(9):1263-1267. 79. Wright RW, Paletta GA Jr. Prew.lcnce of the Bennett lesion of the shoulder in major league pitchers. Am] Sports M~J 2004;32(1):121-124. 80. Yanny S, Toms AP. MR patterns of denervation around the shoulder.

A]RAm] Rom~fmol2010;195(2):W157-W163.

CHAPTER W. Ben Kllller

Shoulder Motion and Sports-Specific Rehabilitation

_.......... ....

.....,._n

...,.....

IN'I'IIODUcnCIN

,_

Sltnllsllj.., tl lupulor Rot• 81 ....... ..., 13

Slill\rlllllJct;o ~ ~ . . ohcrcldor ""~""",.... a.c ~ .ID.Ddaoa Df the ~ ecHilpoacDt& of doc~ . . dl!daot,.mu-... . Pthoary- ..... ..... _ .... ...,..,.0&6 ........ «< ... ,.. ..U........t (GoH) jol.al. c...p; .. oE ...... ...,;, ;. ""

....,..., D!ll*&olo • Coli- h...,. fllr S•lll•llr llylld•. . " lpocif.c Pm'lo"" in flo n..-1.11111110 14

l..ollrolllljoy 14

Ga.ribc .......~. tE cllr.bl ...tualioe. .wf. ...dloc ......

-Sifw.....,...I~I'NIII•II

~

•

II

. . .. . ,

.......-12

t

II

lllaall IIIP dt r ,_..._._.

11 l'rol:toiort of s ...........

•••••dlecbt

- - 8Rl•d1110lrln 73 -8RludTROM D An Nrrt 7ll Dolioilion of GIRD llld 1110MD 73 -C-IIIIIe•d ,_DI 73 H-1• ~ R-crr Aleu-ly 111-IMI :M Trwrdr"rrl at IIRD llld 11101110 74 • 11 0

...,..., llplriMII Pr••t ll Alulo "'"' N••tr 11 Rloo..-,f'IMMl31r 11W.Ibl71 ftoltllo..II'IWII !8 .. ID Wloobl 71

o"' a_..,

"'!""

"""""'-~ podoauooo aedl« !lvz I dol. nil dorpr 'Will .......! _do .. ol-.rlror _ .... c.H-....... ..,.... 0&6. . ..... - -· !twill --oltaa~UouUr. coral>lklt. fio< II oooaic!u-.1 po~ alwolio•~ ..,....,._,, C-H ' " - I - . cl.s. cit (GilD), aarl taW ,.... oE .mo--.... ,. ...... _

J!D41lt 1114 m~,it.rcto·suideli..,,

•

PART I

I INTRODUCTION

Three-Dimensional Movements

Results for SHR and Shoulder and Arm Function

The scapula exhibits motion in three planes and translations in two dire50

0.82

Note that for most of the tests the positive and negative likelihood ratios are close to 1.0. As such they have little effect on the probability that the patient has or does not have a rotator cuff tear. Lag signs and the rent test have the highest positive likelihood ratios and when positive increase the probability that the patient has a rotator cuff tear substantially.2.3,Z4.25,Z7,3D,36,39.47

tests are not very helpful. The best test would have very high positive likelihood ratios. Lag signs are physkal exam tests where the arm is placed in a position that requires rotator cuff function, and the patient is asked to hold the arm in that position. If the patient is unable to hold the arm, and the arm lags back to the starting position, the test is positive. Lag signs for rotator cuff tears of the supra and infraspinatus include the drop arm test, external rotation with the arm at the side, and external rotation ofthe abducted arm. Lag signs for the subscapularis can be done by internally rotating the arm with the arm behind the back. Lag signs have very high positive likelihood ratios, whicil. means when the test is positive, it increases the probability of having a rotator cuff tear significantly. Unfortunatdy, the negative likdihood ratios were close to 1.0, whicil. means if the test is negative the probability that the patient has a rotator cuff tear is not cil.anged mucil.. The rmt test was originally described by EA. Codman, in an era before advanced imaging. The examiner palpates the rotator cuff through the deltoid, while internally and externally rotating the arm feding for a defect in the rotator cuff tendon. Wolf evaluated this test and found it to have very favorable likelihood ratios.62

Precision of Physical Examination Tests for Rotator Cuff Tears Physical exam tests should be accurate and should have high precision. Inter- and intraobserver agreement studies are one way to assess the precision of a test. Two studies have evaluated the precision ofphysi4 days • No breaking pitches until puberty(~ 13 years of age) • No multiple pitching appearances in a single game • Avoid pitching "showcases" • Players should NOT participate in leagues with overlapping seasons • Baseball pitchers should be limited to 100% superior displacement of the lateral clavicle with periosteal tube disruption, and type VI.inkrior subcoracoid dislocation of the lateral clavide.l41 Nonoperati.ve treatment is typically the cornemone of treatment in children under 13 years of age. especially fOr type I-III injuries; however, degree of displacement alone is an important factor to considcr.l0.42,44,120.141 As these injuries are almost always physeal fractures instead of true ac.rom.ioclavicular joint injuries, they have great remodeling and healing potential, which usually stems from the maintained continuity of the periosteal tube with the supporting ligamentous structures (i.e., acromioclavicular and coracoclavicular ligaments). Treatment of type III injuries remains controversial; however, most authors still recommend initial nonoperative management.M9,83 Initial operative management is usually reserved for type IV-VI injuries, especially in cases of significant displacement. Of note, the periosteal sleeve in children is extremely osteogenic and severely displaced distal clavicle fractures, with

intact i.n&rior periosteum can occasionally result in clavicular duplication necessitating subsequent resection. Older children, including adolescents, tend to sustain adult type acromioclavicular joint injuries and are typically treated in the same manner.42 Nenopoulos and colleagues reviewed distal clavicular fractures and acromioclavicular dislocations in 75 skeletally immature patients (ages 3 to 16 years) at an average of8 years follow-up.112 The authors reponed cosmetic complaints in those patients with displaced fractures; however, they had no limitations in tange of motion. To improve cosmesis and prevent clavicular duplication, they concluded that surgical intervention may be considered fOr patients older than 8 years of age with significantly associated displacement of the distal clavicle fracture or acromioclavicular joint.

Proximal Humeral Physeal Fracture Proximal humerus fractures in the skeletally immature patient represent less than 5% of all pediatric fractures.l41 These fractures commonly involve the growth plate, as this region represents the weakest portion of the bone. As noted in the developmental shoulder anatomy section of this chapter, the proximal humerus has three ossification centers: the humeral head, greater tuberosity, and lesser tuberosity.27,118 By 5 to 7 years of age, the greater and lesser tuberosities fuse; however, the proximal humerus epiphysis remains open until approximately 14 to 17 years of age in females and 16 to 18 years of age in males.ll8 Physeal fractures are traditionally categor.ized by the Salter-Hanis classification system: Type I fractures occur through the physis within the hypertrophic wne, type II fractures involve the physis and enend into the distal metaphysis, type III fractures involve the physis and extend into the epiphysis, and type IV fractures involve the physis and atend into both the metaphysis and epiphysis (Fig. 33-4). Eighty percent of humeral growth occurs at the proximal humerus growth plate, which results from a rdativdy weak. metaphysis.

FIGURE 33-4. The most common type of proximal humerus fracture is the Salter-Harris type II seen here. These radiographs from a 6-year-old soccer player who fell from standing during sport clearly demonstrate the extensive remodeling potsntial of the proximal humerus. Injury films lA) show a nearly 90-degrae deformity, which gradually corrects at I B) 5montfls.IC) 11 months. and (D) 2 years to only an 18-degrae deformity. {Images courtesy of Dr. Roger F. Widmann at Hospital for Special Surge/}'.)

CHAPTER 33

I SHOULDER INJURIES IN SKELETALLY IMMATURE ATHLETES

AI; sudi, Salter-Harris II fraa:ures are most wmmon with the metaphyseal fragment, with a predilection toward the posteromedial aspect of the bone. Although, Salter-Harris type III and N fraa:ures are exceedingly unwmmon, they can be seen in after a dislocation.84 The medlanism of injury may be either direa: or indirect. Direa: trauma typically occurs from a blunt force, sudi as the impact of a football tackle; however, indirect trauma generally occurs from other medlanisms, including a fall onto an outstretclted arm or torsion during the throwing motion. In the throwing athlete, the injury may even occur during a single throw with or without preceding shoulder pain.l64 The physical examination should include observation (i.e., ecchymosis and swelling), palpation, neurovascular evaluation, and documentation of range of motion. Crepitation and blocks to range of motion should be noted. Concomitant tendinous injury is unwmmon in children but should be considered. Radiographic examination is critical in all skeletally immature patients and should include anteroposterior, scapular Y, and axillary views. Due to the variable nature of the proximal humeral physes, contralateral shoulder films can be useful for wmparison. Advanced imaging may include ultrasound, CT, and MRI, with the later being most useful for identifying non-displaced fractures and conwmitant pathology. CT examinations should be ordered only when necessary (i.e., during assessment of suspected intraarticular fractures) to avoid excessive radiation exposure in this population. Treatment modalities depend on fracture displacement and patient age. A large amount of displacement can be accepted in the proximal humerus, including up to 45 degrees of angulation and 50% displacement in c;hildren under 12 years of age. In the adolescent population, however, only 20 degrees of angulation and 30% displacement should be accepted. Closed reduction followed by temporary immobilization in a sling and swathe for 2 to 3 weeks is the mainstay of treatment. Closed reduction and percutaneous pinning may be indicated for unstable fraa:ure patterns. Pinning allows for a maintained reduction, while still allowing for relative preservation of the physeal growth potential. Open reduction and internal Hxation in the skeletally immature patient should be reserved for fracture patterns that involve the epiphysis (Salter-Harris III and IV) or nonreducible by closed maneuvers secondary to interposition of periosteum or other soft-tissue structures.

Chondral and Osteochondral Lesions of the Glenoid and Humeral Head Osteocltondrosis dissecans (OCD) of the glenoid or humeral head is a rare finding. Etiology of OCD in the adult population is thought to be multifactorial, attributed to microtrauma, ischemia, genetic predisposition, or abnormal patterns of ossification. 52 In the pediatric and adolescent population, the most wrnrnon cause of OCD about the shoulder is an acute traumatic event, resulting in focal necrosis of subdwndral bone. The wmpetency of overlying cartilage is variable from intact and stable to loose and unstable with secondary displacement. The clinical diagnosis may be difficult given the relatively subtle physical examination fmdings, such as nonlocalizable pain, swelling, and crepitus. In faa:, the diagnosis is more wmmonly noted upon radiographic examination, whic;h often necessitates obtaining advanced imaging with MRI or

~~

CT. MRI has a reported 97% sensitivity for unstable lesions36; however, CT is less sensitive because of limitations in evaluating the articular cartilage. While there is ample literature regarding OCD lesions about the distal femur, capitellum, and talus, there is a general paucity of evidence to guide surgical indications and treatment modalities for OCD lesions of the humeral head and glenoid fossa. This is especially true in the skeletally immature population. From studies evaluating the adult population, these lesions have been treated successfully by performing loosebody extraction and cltondroplasty with or without microfracture tedlniques29,52,81 (Fig. 33-5).

Shoulder Instability Skeletally immature athletes require a delicate balance of shoulder mobility and stability. The anatomic design of the shoulder, including the large humeral head articulation with a shallow glenoid fossa, affords significant mobility and versatility to the joint, but at the cost of inherent stability. This lack of bony stability accentuates the importance of the main static (labrum, capsule, glenohumeral ligaments, and negative intraarticular pressure) and dynamic (rotator cuff, biceps, and periscapular musculature) soft-tissue structures critical to joint stability.57,64,115,117,127 With the surrounding static and dynamic stabilizers, shoulder stability may be maintained throughout range of motion if the humeral head joint reaction force is directed into the glenoid fossa.63,147 Any injury that creates an abnormally directed humeral head joint reaction force can cause an imbalance of the osseous and nonosseous structures, with progression to overt subluxation and/or dislocation. As the physis is usually the weakest wmponent of the osseous and nonosseous strua:ures of the skeletally immature shoulder, injuries that typically cause a dislocation in an adult patient will usually result in a physeal fracture in a skeletally immature patient. In faa:, several studies report that skeletally immature patients only wmprise 1% to 5% of glenohumeral instability patients.61,93,137,160 Therefore, shoulder dislocations are rare in young dlildren (less than 12 years of age), but they become more wmmon in adolescents who present with more mature physes. Shoulder instability may be classified into two general categories: TUBS (traumatic, unilateral injury with associated Bankart lesion that usually requires surgery) and AMBRI (atraumatic, multidirectional, frequently bilateral injury that responds to rehabilitation, and rarely requires inferior capsular shift). The clinical and radiographic evaluations are essential to the successful diagnosis and management of shoulder instability, especially in establishing the direction of instability (anterior, posterior, or multidirectional). Overall, instability patients may present with a history of a frank dislocation, or they may describe more vague instability symptoms with the arm in certain positions of vulnerability, whic;h can provide important clues regarding the instability direction. The physical examination should include a wmplete instability examination, including load-and-shift, and apprehension/relocation tests with the goal of recreating their symptoms or pattern of instability. In addition, it is also critical to perform a thorough neurovascular examination, with special attention directed to the axillary nerve function. In the skeletally immature patient, generalized ligamentous laxity can be an important wmponent of

El

PART VIII

I SPORT-SPECIFIC DISORDERS

A

B

c RGURE 3:J.5. Arlhrostopic management of a glllf!oid ostsoooondrallesioo in a 17-year-old male overftead atfllete.IA) Note the relatively i~icuoos lesion at initial evaluation; howevet', (B) careful elevation of the ooondral fragment can prasant a significantly larger defact !black sf7tM1 with inadequate reparative fibrous tissue overlying the bone.(C) Choodral flap excision with isolated choodrnplasty may provide successful results in these patients. (Images courtesy of Dr. Daryl Osbahr at MedStar Union M9100tial Hospital.)

instability and potentially impact the treatment plan. TherefOre, it is important to assess generalized ligamentous laxity (e.g., hyperc:x:tension of the elbows, m.etacalpophalangeal joints, and knees) as well as specific shoulder laxity (sulcus sign, Gagey test, and CXCC$sive translation in multiple directions).5,26.48 The radiographic examination includes conventional radiographs, MRl, and possible CT scan. Conventional radiographs, including ax.illary and stryker notch views, are obtained to evaluate for dislocation as well as associated fractures. MRI is typically obtained, especially in cases ofdislocation, to evaluate the pattern of soft-tissue injury. This includes de.fining the extent oflabral injury and location ofcapsular injury (glenoidbased, midcapsular, or hwne.ral-ba.sed tears). Finally, CT scans, with and without humeral subtraction, can be used in suspected bone-loss cases to evaluate glenoid (e.g., bony Bankan lesion) and hwne.ral head (e.g., Hill-Sachs lesion) deficiency that can greatly affect the surgical treatment plan. After the diagnosis has been established as based on the clinical and radiographic evaluation, management principles are typically defined by the direction and pattern of instability. Patients with traumati(? anterior instability will most often present after a dislocation event that occurs with the shoulder in an abducted and cnernally rotated position. h previously discussed, the incidence of glenohwneral dislocation in children younger than 12 years of age is rdativdy rare. In fact, Wagner and Lyne reponed on 212 patients with traumatic anterior shoulder dislocations and reponed only a 4.7% incidence in patients with open phyxs.J60 Eighty percent of these patients initially treated nonoperatively sustained recurrence of overt dislocation while the remaining 20% reponed a history of"subluxation" at a later time point. The adult literature is fraught with evidence of high recurrence rates (50% to 100%) for patients with this injury, particularly in athletes younger than 30 years of age.5~1.136-139 Marans and colleagues reviewed 21 patients over 15 years of ~ with open physes and evidence of trawnatic anterior dislocation.93 All patients were treated with initial nonoperative management and were divided into two groups: 48% of the cohon underwent 4 to 6 weeks of sling immobilization and the remaining patients had physical therapy with early range of motion. Regardless ofthe physical therapy regimen, the authors reponed a 100% recurrence rate of dislocation and conclu25% bone loss), and humeral-based capsular tears (i.e., HAGL lesions) may necessitate open surgical management.72,105,124,126,128,129,155 No matter the operative treatment plan, postoperative rehabilitation is accomplished through a systematic physical therapy protocol with progression from immobilization and limited passive range of motion to more aggressive range of motion and strengthening_l,159,168 A spon-specific program may be initiated with eventual return to play once the athlete is asymptomatk with full range of motion and strength in the setting of appropriate stability.

Rotator Cuff Injuries and Subacromial Impingement Isolated rotator cuff injuries are far less common in skeletally immature athletes than in the older adult population, but they can occur in an isolated fashion or in conjunction with subacromial (external) impingement.6,50,149 However, throwing athletes, including children and adolescents, are equally susu:ptible to developing rotator cuff and other associated intraanicular pathology secondary to internal impingement, which will be fully discussed in the section on specific throwing shoulder injuries. When subacromial impingement occurs in the skeletally immature athlete, it usually occurs secondary to a muscular imbalance as opposed to a true external impingement.SO The clinical history should d ucidate a traumatk or overuse etiology. For example, traumatic causes of rotator cuff injury may occur secondary to a shoulder dislocation, and overuse rotator cuff pathology may be a result of internal impingement. Physical examination should include an assessment of atrophy (indicating chronidty) and signs ofmore acute trauma such as ecchymosis. Range of motion and rotator cuff strength should be fully tested to assess for possible defidendes. Conventional radiographs should be obtained but will typically be normal. In cases of trauma, evidence of anterior shoulder dislocation or subluxation might be present, including osseous avulsion injuries and impaction fractures involving the humeral head and glenoid. Advanced imaging with MRI may rarely be obtained if suspidous of rotator cuff injuries;

•

however, full-thickness rotator cuff tears are very uncommon. In an overhead athlete, an additional MRI sequence, ABER view may provide functional information when confirming internal impingement and may provide more detail in duddating panial and delaminated rotator cuff tears. The use of CT is rarely indicated for workup of suspected soft-tissue injuries and should be used sparingly in this young patient population to limit radiation exposure. When a young patient is diagnosed with rotator cuff tendonitis or subacromial impingement, nonoperative management is the mainstay of treatment and includes initial rest and nonsteroidal anti-inflammatory medications followed by a physical therapy protocol that targets underlying weakness or instability through early range of motion and progressive strengthening.168,169 Return to play is allowed only when the athlete is asymptomatic with a normal examination and will typically last approximately 8 to 12 weeks. Surgical intervention is rare in this young population and reserved for patients with initial full-thickness rotator cuff tears or refractive panial rotator cuff tears and subacromial impingement. Anhroscopy is preceded by an examination under anesthesia to accurately assess passive range of motion and instability signs. Rotator cuff tears are generally treated according to the depth of tear, with debridement for tears 50%. Subacromial decompression is rarely indicated in skeletally immature patients, as subacromial impingement in this population is typically secondary to a muscular imbalance and not external impingement.8.56,153,154 With either nonoperative or operative management, rehabilitation with restoration of range of motion and strength is a critical component to a successful recovery and return to play.

Lesser Tuberosity Avulsion Injury Subscapularis avulsion injuries of the lesser tuberosity in the pediatric and adolescent population are exceedingly uncommon and are described only in case reports and small case series.20,23,40,58,85,86,119,134,143,144 Nevenheless, such injuries often go undiagnosed or misdiagnosed for long periods of time (weeks to years), resulting in significant patient morbidity and lost activity.5B,B6,119 The mechanism of injury typically occurs during sponing activities and is frequently similar to that of the patient with anterior shoulder instability-forced ABER against resistance. The patient with a lesser tuberosity avulsion injury will be most comfonable with the arm in an adducted internally rotated position, as this is the position of comfon. Physical examination will be significant for positive "liftoff sign" such that the patient is unable to hold the hand away from their back when placed in this position, demonstrating weakness in internal rotation secondary to subscapularis avulsion. Other examination techniques that eluddate subscapularis weakness will also be markedly positive, including weakness with resisted internal rotation and a positive "belly-press test."5B,B5,B6,119,143,144 Conventional radiographs should be obtained first, but may be unrevealing in the skeletally immature patient given the variation in rates of ossification. MRI is the preferred imaging modality to evaluate this pathology, as it provides detailed visualization of the soft-tissue structures and simultaneously enables identification of concomitant pathoanatomy. When present, the bony avulsion is typically a thin piece of conical bone and has been described by some authors as a

m

PART VIII I SPORT-SPECIFIC DISORDERS

"crescent-shaped fragment ofbone" ranging from 3 to 6 nun in diameter and I to 2 mm in th.ickness.58 Treatment has historically been reported as either nonoperative with physical therapy or surgical with open reduction and internal .fixation of the small bony fragment. More recently, some authors have proposed early anhroscopic repair with suture anchors to achieve excellent results and minimize potential complications.58

SPECIFIC THROWING SHOULDER INJURIES Proximal Humeral Epiphysiolysis (i.e., Linle League Shoulder) Although typically referred to as Little League shoulder, proximal humeral epiphysiolysis is a disorder affecting skeletally immature throwing athletes and is most freq_uendy seen in male baseball pitchers between 11 and 16 years of age.25,38,6S.SO,l5G.l56 As Little League shoulder confers a negative association with Little League Baseball, we prefer not to use this tenn to describe this pathology. In fact, Little League Baseball has long maintained a supportive role in defining and shaping preventative strategies dedicated to decreasing the burden of injuries involving skeletally immature athletes. The patient with proximal humeral epiphysiolysis will typically present with progressive pain localized to the proximal humerus during the throwing motion, and most athletes will report a recent increase in throwing prior to the onset of symptoms.25,68,80 Although a complete physical e:wnination must be performed to exclude other potential sources of pathology, several keys findings can indicate a diagnosis of proximal humeral epiphysiolysis, most notably tenderness to palpation over the proximal humerus.25 Other less common and nonspecific findings on shoulder e:wnination can include swelling, weakness, atrophy. and motion loss.25 Conventional radiographs are obtained to evaluate for proximal humeral physeal widening and rule out other sources of pathology. Contralateral shoulder radiographs

are useful for comparison as pathology may be subtle, especially in the initial symptomatic period. Proximal humeral epiphysiolysis may not be an isolated fmding, especially in more severe cases, and other katures may include physeal irregularity, periosteal reaction and metaphyseal fragmentationl5,68,80 (Fig. 33-6A). As with all throwing shoulder injuries, it is critical to closely associate symptomatology with the imaging, as radiographic changes in the proximal humeral growth plate have also been noted in asymptomatic, youth baseball pitchers.l07 A high index. of clinical suspicion despite negative radiographs may wanant an MRI to confinn the diagnosis. MRI will typically demonstrate focal widening of the proximal humeral physis on Tl-weightcd and gradient echo imaging with possible extension of increased signal intensity into the metaphysis on T2-weighted sequences114,122 (Fig. 33-6B). MRI can also be used to rule out other potential sources of pathology. including rotator cuff' and labral tears. Although then: an: no comprehensive reports detaaing the constellation of MRI findings associated with proximal humeral epiphysiolysis in the skeletally immature throwing shoulder, the classic aforementioned clinical and radiographic features in the setting of no other reported pathology can be highly diagnostic. The first step in the successful management of proximal humeral epiphysiolysis is prevention. Education is the cornerstone of prevention and must involve the family, team, league personnel, and team physician. Once the diagnosis of proximal humeral epiphysiolysis has been established, treatment is almost always successful with nonoperative management consisting of activity modification and education. The nonoperative management program consists of an initial rest period with a progressive return to full activity with a focused a stepwise rehabilitation program. This includes activity modification for 3 months followed by institution of a well-established interval throwing program and continued adherence to USA Baseball Medical & Safety Advisory Committee established recommendations.91,158 In addition,

FIGURE 33-6. Physeal widening demonstrated on plain radiographs (AJ may be indicative of proximal humeral epiphysiolysis. MRI findings may include focal widening seen on a T1 sequence (not pictured), or an edema pattam extsnding into 1he metaphysis (B) on a fluid sensitive sequence. (Images courtesy of Dr. Daryl Osbahr at MedStar Union Memorial Hospital.)

CHAPTER 33

I SHOULDER INJURIES IN SKELETALLY IMMATURE ATHLETES

clinkal symptoms may be treated with the supplementation of over-the-counter nonsteroidal anti-inflammatory medications to further decrease pain and alleviate pain. Supervised physical therapy may be implemented during the rehabilitation period to maximize clinical goals, including range of motion and strength, improve throwing me~hanks, and prevent future injuries. If the athlete remains asymptomatic: throughout the rehabilitation period, including the interval throwing program, then return to ~tivity is typically successful. If clinical symptoms do not resolve or return at any point during the rehabilitation program, however, then the athlete should undergo an additional rest period with a follow-up clinical and radiographic: evaluation. Return to sports is almost universally s~sful and typically involves the loss of the ~;urrent season with return to play the following year.25,122 Unfortunately, there are ~;urrently a lad: of studies evaluating treatment protocols and outcomes involving the management of proximal humeral epiphysiolysis. In faa, the largest 1;a5e series evaluated only 23 patients but reported excellent results with asymptomati~; return to play in 91% of baseball players at 3 months (range: 1 to 12 months).25 Despite the la