Upper Extremity Injuries in Young Athletes

Contemporary Pediatric and Adolescent Sports Medicine Series Editor: Lyle J. Micheli

Andrea S. Bauer Donald S. Bae Editors

Upper Extremity Injuries in Young Athletes

Contemporary Pediatric and Adolescent Sports Medicine Series Editor Lyle J. Micheli, Boston, MA, USA

More information about this series at http://www.springer.com/series/11729

Andrea S. Bauer  •  Donald S. Bae Editors

Upper Extremity Injuries in Young Athletes

Editors Andrea S. Bauer Department of Orthopedic Surgery Boston Children’s Hospital Boston, MA USA

Donald S. Bae Department of Orthopedic Surgery Boston Children’s Hospital Boston, MA USA

ISSN 2198-266X     ISSN 2198-2678 (electronic) Contemporary Pediatric and Adolescent Sports Medicine ISBN 978-3-319-56650-4    ISBN 978-3-319-56651-1 (eBook) https://doi.org/10.1007/978-3-319-56651-1 Library of Congress Control Number: 2018958000 © Springer International Publishing AG, part of Springer Nature 2019 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

The Micheli Center for Sports Injury Prevention

The mission of The Micheli Center for Sports Injury Prevention is at the heart of the Contemporary Pediatric and Adolescent Sports Medicine series. The Micheli Center uses the most up-to-date medical and scientific information to develop practical strategies that help young athletes reduce their risk of injury as they prepare for a healthier future. The clinicians, scientists, activists, and technologists at The Micheli Center advance the field of sports medicine by revealing current injury patterns and risk factors while developing new methods, techniques, and technologies for preventing injuries. v

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The Micheli Center for Sports Injury Prevention

The Micheli Center, named after Lyle J. Micheli, one of the world’s pioneers in pediatric and adolescent sports medicine, had its official opening in April 2013. Thus far, The Micheli Center has served more than 2800 athletes and has published more than 100 studies. Dr. Micheli is the series editor of Contemporary Pediatric and Adolescent Sports Medicine. Consistent with Dr. Micheli’s professional focus over the past 40  years, The Micheli Center conducts world-class medical and scientific research focused on the prevention of sports injuries and the effects of exercise on health and wellness. In addition, The Micheli Center develops innovative methods of promoting exercise in children. The Micheli Center opens its doors to anyone seeking a healthier lifestyle, including those with medical conditions or illnesses that may have previously limited their abilities. Fellow clinicians, researchers, and educators are invited to collaborate and discover new ways to prevent, assess, and treat sports injuries.

Series Editor Biography

Dr. Lyle J. Micheli  is the series editor of Contemporary Pediatric and Adolescent Sports Medicine. Dr. Micheli is regarded as one of the pioneers of pediatric and adolescent sports medicine, a field he has been working in since the early 1970s when he co-founded the USA’s first sports medicine clinic for young athletes at Boston Children’s Hospital. Dr. Micheli is now director of the Division of Sports Medicine at Boston Children’s Hospital and Clinical Professor of Orthopaedic Surgery at Harvard Medical School. He is a past president of the American College of Sports Medicine and is currently the secretary-general for the International Federation of Sports Medicine. Dr. Micheli co-chaired the International Olympic Committee consensus on the health and fitness of young people through physical activity and sport. In addition to many other honors, Dr. Micheli has served as chairperson of the Massachusetts Governor’s Committee on Physical Fitness and Sports, on the Board of Directors of the United States Rugby Football Foundation, as chairman of the

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USA Rugby Medical and Risk Management Committee, and on the advisory board of the Bay State Games. He served as attending physician for the Boston Ballet from 1977 to 2016 and is medical consultant to the Boston Ballet School. Dr. Micheli received his undergraduate degree from Harvard College in 1962 and his medical degree from Harvard Medical School in 1966. As an undergraduate student, Dr. Micheli was an avid athlete, competing in rugby, gridiron football, and boxing. Since graduating, Dr. Micheli has played prop for various rugby clubs, including the Boston Rugby Football Club, the Cleveland Blues Rugby Football Club, the Washington Rugby Football Club, and the Mystic Valley Rugby Club, where he also served as team coach. Dr. Micheli has authored over 300 scientific articles and reviews related to sports injuries, particularly those sustained by children. His present research activities focus on the prevention of sports injuries in children. Dr. Micheli has edited and authored several major books and textbooks.

Series Editor Foreword

It gives me great pleasure to introduce Upper Extremity Injuries in Young Athletes. It is an important new addition to our book series, Contemporary Pediatric and Adolescent Sports Medicine, which is being published under the imprimatur of The Micheli Center for Sports Injury Prevention. The time is certainly right for a new entry in the literature on this topic. Andrea Bauer and Andrea Stracciolini make this clear in Chap. 1, “Early Specialization and the Rise of Upper Extremity Injuries in Young Athletes.” As Drs. Bauer and Stracciolini report, sports injuries in young athletes are on the rise due to increased sports participation – and upper extremity injuries make up a considerable portion of these injuries. Drs. Bauer and Bae are valuable members of our team of orthopedists at the Division of Sports Medicine at Boston Children’s Hospital. I am grateful but not surprised they managed to assemble such a first-rate slate of contributors. I am especially pleased to see overuse injuries being covered so thoroughly in this volume. Acute injuries have always been part of the medical care of children and youth. Overuse injuries are a relatively recent phenomenon that we can trace to the increase in organized sports. Understanding how to diagnose and treat overuse injuries is so very important to us as sports medicine doctors treating young athletes and, of course, so is preventing overuse injuries. Any project like this is a major undertaking. I know what a full schedule Drs. Bauer and Bae have, and undertaking and completing such a large project is testament to their commitment to the care of young athletes. Waltham, MA, USA

Lyle J. Micheli, MD

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Contents

1 Introduction: Early Specialization and the Rise of Upper Extremity Injuries in Young Athletes����������������������������������������������������    1 Andrea S. Bauer and Andrea Stracciolini 2 Footballer’s Shoulder������������������������������������������������������������������������������    7 Dennis E. Kramer and Timilehin Wusu 3 The Thrower’s Shoulder��������������������������������������������������������������������������   21 Robert L. Parisien and Benton E. Heyworth 4 Swimmer’s Shoulder��������������������������������������������������������������������������������   45 Alton W. Skaggs and Brian M. Haus 5 The Pitcher’s Elbow��������������������������������������������������������������������������������   61 Donald S. Bae 6 Gymnast’s Wrist��������������������������������������������������������������������������������������   79 Elspeth Ashley V. Hart and Kate W. Nellans 7 Tennis and Golf Wrist������������������������������������������������������������������������������   95 Ameya V. Save and Felicity G. Fishman 8 Carpal Injuries in Sport��������������������������������������������������������������������������  109 Katherine C. Faust and Allan E. Peljovich 9 Common Sports Hand Injuries��������������������������������������������������������������  139 Julie Balch Samora 10 The Jammed Finger��������������������������������������������������������������������������������  165 Anna M. Acosta and Suzanne E. Steinman

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11 Upper Extremity Nerve Injuries������������������������������������������������������������  189 Andrea S. Bauer 12 Musculoskeletal Ultrasound in Treating and Preventing Upper Extremity Injuries in Young Athletes����������������������������������������  209 Andrea Stracciolini, Sarah S. Jackson, and Pierre d’Hemecourt Index������������������������������������������������������������������������������������������������������������������  231

Contributors

Anna M. Acosta, MD  Department of Orthopedics and Sports Medicine, Seattle Children’s Hospital, Seattle, WA, USA Donald  S.  Bae, MD  Department of Orthopedic Surgery, Boston Children’s Hospital, Boston, MA, USA Andrea  S.  Bauer, MD  Department of Orthopedic Surgery, Boston Children’s Hospital, Boston, MA, USA Pierre  d’Hemecourt, MD  Department of Sports Medicine, Boston Children’s Hospital, Boston, MA, USA Katherine C. Faust, MD  Private Practice, New Orleans, LA, USA Felicity G. Fishman, MD  Department of Orthopedic Surgery and Rehabilitation, Loyola University Medical Center, Maywood, IL, USA Elspeth Ashley V. Hart, PA-C, ATC, MS, BS  Department of Sports Medicine/ Orthopedics, Boston Children’s Hospital, Boston, MA, USA Brian M. Haus, MD  Department of Orthopedic Surgery, University of California, Davis Medical Center, Sacramento, CA, USA Benton E. Heyworth, MD  Department of Orthopedic Surgery, Division of Sports Medicine, Boston Children’s Hospital, Boston, MA, USA Sarah S. Jackson, MD, CSCS  Department of Orthopedics and Sports Medicine, Boston Children’s Hospital, Boston, MA, USA Dennis  E.  Kramer, MD  Department of Orthopedic Surgery, Boston Children’s Hospital, Boston, MA, USA Kate  W.  Nellans, MD, MPH  Department of Orthopedic Surgery, Northwell Health, Hofstra-Northwell Medical School, Great Neck, NY, USA Robert  L.  Parisien, MD  Department of Orthopedic Surgery, Boston University Medical Center, Boston, MA, USA xiii

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Contributors

Allan  E.  Peljovich, MD, MPH  Department of Orthopedic Surgery, Children’s Healthcare of Atlanta, The Hand and Upper Extremity Center of Georgia, Children’s Hospital of Atlanta, Atlanta, GA, USA Julie  Balch  Samora, MD, PhD, MPH  Department of Orthopedics Surgery, Nationwide Children’s Hospital, Columbus, OH, USA Ameya V. Save, MD  Department of Orthopedic Surgery, Yale New Haven Hospital, New Haven, CT, USA Alton  W.  Skaggs, BS  School of Medicine, University of California, Davis, Sacramento, CA, USA Suzanne  E.  Steinman, MD  Department of Pediatric Orthopedics and Sports Medicine, Seattle Children’s Hospital, Seattle, WA, USA Andrea  Stracciolini, MD, FAAP, FACSM  Department of Orthopedics, Boston Children’s Hospital, Boston, MA, USA Timilehin  Wusu, BA, MD  Department of Orthopedics, Massachusetts General Hospital, Boston, MA, USA

Chapter 1

Introduction: Early Specialization and the Rise of Upper Extremity Injuries in Young Athletes Andrea S. Bauer and Andrea Stracciolini

Sports play a central role in the lives of youth worldwide. Over 46 million children participate in youth sports in the United States annually, nearly 8 million of these at the high school level [1, 2]. For most children, the social, academic, and health benefits of sports outweigh the risk for injury, including injury to the upper extremity. With increased participation in organized sports, however, comes increased sports-related injuries. In 2013, there were over 1.3 million US emergency room visits by children aged 6–19 years due to sports-related injuries. These accounted for 20% of all injury-related emergency room visits in this age group [3], with an annual cost of nearly 1 billion dollars per year [4]. Upper extremity injuries in the young athlete make up a considerable portion of overall injuries. Andrish et al. reported that 15% of all injuries to skeletally immature athletes occurred in the upper extremity (UE), and, notably, 45% of the UE injuries involved the shoulder [5]. Injuries to the UE occur more often in sports that place increase stress and demand on the UE. For example, in a single season, 35% of baseball pitchers between 9 and 14 years of age report shoulder pain [6]. Furthermore, UE injury patterns vary according sex, sport, and age. For example, in gymnastics, injuries to female participants are sustained primarily to the lower extremity, ankle, and knee, whereas in male participants the most commonly injured body part is the upper extremity, specifically the shoulder and wrist [7–10].

A. S. Bauer (*) Department of Orthopedic Surgery, Boston Children’s Hospital, Boston, MA, USA e-mail: [email protected] A. Stracciolini Department of Orthopedics, Boston Children’s Hospital, Boston, MA, USA © Springer International Publishing AG, part of Springer Nature 2019 A. S. Bauer, D. S. Bae (eds.), Upper Extremity Injuries in Young Athletes, Contemporary Pediatric and Adolescent Sports Medicine, https://doi.org/10.1007/978-3-319-56651-1_1

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Specialization Versus Diversification As youth sports participation continues to increase, there is an emerging concern surrounding early sports specialization and its link to overuse injury and burnout in children [11]. Recently, the association between specialization and overuse injury in young athletes has been defined. In a landmark study on this topic, Jayanthi et al. discovered that youth athletes who train >8 months per year are more likely to be injured. These same authors also found that youth who maintain an organized sport-­ to-­free play ratio greater than 2:1 were more likely to be injured and to develop a serious overuse injury [12]. The American Academy of Pediatrics (AAP) recommends that children play a variety of sports to decrease the chance of injury as well as burnout and that they limit participation to only one team per season. In addition, the AAP recommends one to two rest days per week and 3 months per year (recommended as 1 month at a time, three times per year) completely off from sports for young athletes to recover and recharge [13]. Similarly, the American Orthopaedic Society for Sports Medicine (AOSSM) Consensus Statement in 2016 concluded that there is no evidence to support the benefit of early specialization in the majority of sports but did acknowledge the link between early specialization and overuse injury and athlete burnout [14]. More sport-specific evidence-based guidelines are direly needed at this time. Formulating generalized youth sports specialization recommendations is not feasible. Athletes who participate at an elite level commonly participate in highly technical individual sports such as gymnastics, dance, swimming, and diving. The argument follows that for the elite gymnast or dancer, in order to obtain success, early specialization is required. Many coaches and families believe that early specialization in a single sport is the key to achieving success, which may be defined to include scholarship money, recognition, and participation on the national or international stage. In tennis, 70% of junior elite tennis players began specializing at a mean age of 10.4  years old, and 95% were specialized by the age of 18  years [15]. In gymnastics, the average age of the 2016 US women’s gymnastics team was 19 years, many of whom started participating in gymnastics at the age of 2–3 years and turned elite at age 12 years. For other sports, however, delaying specialization may increase the athlete’s chance of success in participating at the elite level. For example, of the 322 athletes invited to the 2015 National Football League (NFL) Combine, 87% had played more than one sport during their high school careers [16]. Similarly, a recent study of 102 current professional baseball players found that only 48% specialized in baseball earlier than high school and those players who had specialized early were more likely to have sustained a serious injury during their career [17].

Repetitive Stress Injuries of the Upper Extremity Repetitive and overuse injuries are a common problem in young athletes. Players with at least one prior injury have two to three times greater risk of sustaining a subsequent injury than those who have never been injured [18]. Overuse injuries

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have been described as presenting in four stages: (1) pain in a particular area after physical activity; (2) pain during the activity, without restricting performance; (3) pain during the activity that restricts performance; and (4) chronic pain even at rest [19]. This is a useful framework for understanding any overuse injury, regardless of anatomic location. Using this classification, providers can teach young athletes how much pain is too much to “push through” during a season. It is advisable to instruct patients to report to parents and coaches any pain that occurs during activities and to increase rest time if pain after practice persists into the next day. This is particularly important for patients attempting to return to sport after injury. Overuse injuries are generally believed to be related to overtraining and single-­ sport specialization, although data is severely limited at this time. A recent systematic review of literature pertaining to injury risk and early single-sport specialization found three relevant studies, which demonstrated associations between sports specialization and overuse injuries [20]. Since that review, a prospective study has been published which focused on lower extremity injury rates in 1544 high school athletes. Athletes were stratified by extent of specialization and followed for several seasons. The authors found that those athletes with moderate to high specialization were more likely to sustain lower extremity injuries than those with low specialization [21]. Many organizations are attempting to combat the ill effects of overtraining and early specialization by providing guidelines to protect young athletes; providers should be aware of existing guidelines, as many families and coaches often lack awareness prior to the onset of injury. For UE athletes, perhaps the best-known guidelines surround limiting pitch counts in youth baseball. Monitoring pitch counts, delaying initiation of “breaking pitches” (such as the curveball), and teaching pitchers to not pitch through arm fatigue and pain can help parents and coaches protect their young athletes from injury [22, 23]. We will discuss baseball injuries and techniques for prevention and treatment more specifically in Chap. 5. Another good example of overuse to the UE is gymnast wrist. This injury occurs from repetitive compressive loading and shearing forces on an extended wrist and represents a disruption to the radial growth plate. As such, it is an injury unique to the growing skeleton [24–26]. We will discuss gymnast wrist and other gymnasticsspecific injuries more specifically in Chap. 6.

Summary There are strong and lasting benefits of participation in youth sports. In addition to the enjoyment and stress relief provided, sports help young children develop gross motor and socialization skills, while older children benefit from learning teamwork and leadership. As organized sports participation increases, however, the risk of sports-related injury also increases. As described, many children now specialize in a single sport at a young age, which may additionally increase the risk of overuse injuries. Pediatric health-care providers should be familiar with the diagnosis and treatment of the most common acute and chronic upper extremity sports-related injuries.

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The chapters in this book will describe upper extremity injuries common to the young athlete. Just as we associate ACL tears with downhill skiing, characteristic upper extremity injury patterns exist for many sports. We will highlight these sports-­ specific injury patterns as well as identify injuries those that are uniquely pediatric, such as physeal injuries. Each chapter will detail specific UE diagnoses in youth sports and address nonoperative and operative treatment. Finally, authors will provide evidence-based recommendations when possible for rehabilitation and return to sport after UE injury. Seemingly benign injuries such as a mild sprain to the elbow, or small fracture of the finger, may be the first sidelining injury for a youth athlete. Providing timely, accurate, and comprehensive care of the young athlete with an UE injury will serve to minimize time loss from play, decrease emotional strife, and promote long-term participation in sport and physical activity.

References 1. National Sporting Goods Association. 2011 vs 2001 Youth Sports Participation NhwnofpvYPwp. 2. National Federation of State High School Association. 2016–2017 High school athletics participation survey. www.nfhs.org/ParticipationStatistics/ParticipationStatistics/. Accessed 5 May 2018. 3. Healy M. 1.35 million youths a year have serious sports injuries. USA Today. 2013. http:// www.usatoday.com/story/news/nation/2013/08/06/injuries-athletes-kids-sports/2612429/. Accessed 14 May 2018. 4. Centers for Disease Control and Prevention, National Center for Injury Prevention and Control. Web-based Injury Statistics Query and Reporting System (WISQARS). www.cdc.gov/injury/ wisqars. Accessed 27 May 2018. 5. Markiewitz AD, Andrish JT. Hand and wrist injuries in the preadolescent and adolescent athlete. Clin Sports Med. 1992;11(1):203–25. 6. Lyman S, Fleisig GS, Waterbor JW, et al. Longitudinal study of elbow and shoulder pain in youth baseball pitchers. Med Sci Sports Exerc. 2001;33(11):1803–10. 7. Caine DJ, Nassar L. Gymnastics injuries. Med Sport Sci. 2005;48:18–58. 8. Saluan P, Styron J, Ackley JF, Prinzbach A, Billow D. Injury types and incidence rates in precollegiate female gymnasts: a 21-year experience at a single training facility. Orthop J Sports Med. 2015;3(4):2325967115577596. 9. Westermann RW, Giblin M, Vaske A, Grosso K, Wolf BR. Evaluation of men’s and women’s gymnastics injuries: a 10-year observational study. Sports Health. 2015;7(2):161–5. 10. Kerr ZY, Hayden R, Barr M, Klossner DA, Dompier TP.  Epidemiology of national collegiate athletic association women’s gymnastics injuries, 2009–2010 through 2013–2014. J Athl Train. 2015;50(8):870–8. 11. Brenner JS.  Overuse injuries, overtraining, and burnout in child and adolescent athletes. Pediatrics. 2007;119(6):1242–5. 12. Jayanthi NA, LaBella CR, Fischer D, Pasulka J, Dugas LR. Sports-specialized intensive training and the risk of injury in young athletes: a clinical case-control study. Am J Sports Med. 2015;43(4):794–801. 13. Brenner JS.  Sports specialization and intensive training in young athletes. Pediatrics. 2016;138(3):e20162148. 14. LaPrade RF, Agel J, Baker J, et al. AOSSM early sport specialization consensus statement. Orthop J Sports Med. 2016;4(4):2325967116644241.

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15. Jayanthi NDA, Durazo R, Dugas L, Luke A. Training and sports specialization risks in junior elite tennis players. J Med Sci Tennis. 2011;16:14–20. 16. TrackingFootball.com. https://twitter.com/trckfootball. Accessed 15 Dec 2017. 17. Wilhelm A, Choi C, Deitch J. Early sport specialization: effectiveness and risk of injury in professional baseball players. Orthop J Sports Med. 2017;5(9):2325967117728922. 18. Kucera KL, Marshall SW, Kirkendall DT, Marchak PM, Garrett WE Jr. Injury history as a risk factor for incident injury in youth soccer. Br J Sports Med. 2005;39(7):462. 19. Mellion MB, Walsh WM, Madden C, Putukian M, Shelton GL. Team physician’s handbook. 3rd ed. Philadelphia: Hanley & Belfus; 2002. 20. Fabricant PD, Lakomkin N, Sugimoto D, Tepolt FA, Stracciolini A, Kocher MS.  Youth sports specialization and musculoskeletal injury: a systematic review of the literature. Phys Sportsmed. 2016;44(3):257–62. 21. McGuine TA, Post EG, Hetzel SJ, Brooks MA, Trigsted S, Bell DR. A prospective study on the effect of sport specialization on lower extremity injury rates in high school athletes. Am J Sports Med. 2017;45(12):2706–12. 22. Pitchsmart USA Baseball. Guidelines for youth and adolescent pitchers. http://m.mlb.com/ pitchsmart/pitching-guidelines/. Accessed 14 May 2018. 23. Olsen SJ 2nd, Fleisig GS, Dun S, Loftice J, Andrews JR. Risk factors for shoulder and elbow injuries in adolescent baseball pitchers. Am J Sports Med. 2006;34(6):905–12. 24. DiFiori JP, Puffer JC, Aish B, Dorey F. Wrist pain in young gymnasts: frequency and effects upon training over 1 year. Clin J Sport Med. 2002;12(6):348–53. 25. DiFiori JP, Puffer JC, Aish B, Dorey F. Wrist pain, distal radial physeal injury, and ulnar variance in young gymnasts: does a relationship exist? Am J Sports Med. 2002;30(6):879–85. 26. DiFiori JP, Caine DJ, Malina RM. Wrist pain, distal radial physeal injury, and ulnar variance in the young gymnast. Am J Sports Med. 2006;34(5):840–9.

Chapter 2

Footballer’s Shoulder Dennis E. Kramer and Timilehin Wusu

Introduction The clavicle is an important structure involved in support, mobility, and function of the upper extremity. It functions as the structural transition point between the shoulder girdle and the axial skeleton. The medial clavicle takes part in the only bony articulating connection between the upper extremity and the axial skeleton through the sternoclavicular (SC) joint. The lateral clavicle articulates with the acromion of the scapula at the acromioclavicular (AC) joint. Injuries to the clavicle and its articulations follow three main mechanisms of injury. These mechanisms occur during every play in an American football game. The most common mechanism occurs indirectly through a direct forceful impact to the shoulder, such as falling onto the shoulder or collision through the shoulder with another player while blocking or tackling. The second most common mechanism of injury is through direct anterior impact on the clavicle itself. Finally, a fall onto an outstretched arm can also produce indirect injuries to the clavicular structures [1]. Outside of football, the overall most common cause of clavicle injuries is motor vehicle collisions followed by sports-related collisions and falls [1, 2].

D. E. Kramer (*) Department of Orthopedic Surgery, Boston Children’s Hospital, Boston, MA, USA e-mail: [email protected] T. Wusu Department of Orthopedics, Massachusetts General Hospital, Boston, MA, USA © Springer International Publishing AG, part of Springer Nature 2019 A. S. Bauer, D. S. Bae (eds.), Upper Extremity Injuries in Young Athletes, Contemporary Pediatric and Adolescent Sports Medicine, https://doi.org/10.1007/978-3-319-56651-1_2

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Adolescent Athlete There are a number of special considerations for evaluation and management of clavicle-related injuries in the adolescent athlete compared to similar injuries in the mature adult. The most salient is that adolescent athletes in contact sports are more likely to return to a competitive sport that will directly and repeatedly challenge the injured limb through the same or similar mechanism that caused the initial injury. Furthermore, the anatomy of the clavicular structures continues to change until 20–25 years of age. Clavicle joint articulations transition from hyaline to fibrocartilage by age 17 on the acromion and age 24 on the clavicular side of the AC joint [2]. Furthermore, the medial clavicular physis remains open until 25 years of age.

AC Joint Injuries Introduction AC joint injuries are commonly referred to “shoulder separations.” The AC joint is injured far more frequently than the SC joint, accounting for 9–10% of all shoulder girdle injuries [1, 3]. In the athletic population, AC joint separations account for 40% of shoulder girdle injuries [1]. Though the vast majority of these injuries can be treated non-operatively, surgical intervention may be required for more severe injuries with higher degrees of separation and joint instability. There are two typical mechanisms of injury to the AC joint, direct and indirect. Direct AC joint injuries are caused by a forceful blow to the shoulder, such as with a shoulder tackle or fall directly onto the shoulder. Indirect AC joint injuries occur through a fall onto an outstretched arm where the force is transmitted through the humeral head to abut the overlying acromion. AC joint separations are primarily evaluated with a detailed physical exam followed by plain radiographs. Physical exam should consist of visual inspection of the AC joint region assessing for asymmetry, skin tenting, and swelling over the AC joint with comparison to the non-injured side. The shoulder and clavicle should be palpated for tenderness and deformity. The distal clavicle can be depressed to see if it elevates once the depressive force is released (piano key sign) to get a sense of joint AC stability, once again in comparison to the contralateral side. Neurovascular examination should also be performed. Radiographic imaging may include bilateral Zanca views (upright anteroposterior (AP) radiographic views of the clavicles with the beam pointed 10–15° cephalad) which best demonstrate the AC joint. A glenohumeral axillary view and a Stryker notch view can also be useful for evaluating for Type IV AC separations (in which the clavicle herniates posteriorly) and coracoid fractures, respectively [2]. It can sometimes be difficult to distinguish between distal clavicle physeal fractures and AC joint injuries in skeletally immature patients based on radiographs.

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In cases where the injury is mild and radiographs show no clear abnormalities, no further imaging is indicated as the treatment would be the same (nonsurgical) and both injuries should heal without issue over time. Advanced imaging with CT or MRI is indicated in more severe injuries associated with swelling and bruising at the posterior shoulder where posterior dislocation of the clavicle or posteriorly displaced physeal fractures are suspected. The MRI or CT in these cases would better classify the extent of injury and determine if operative intervention is necessary. Anatomy The AC joint is a diarthrodial joint with a fibrocartilage meniscal disk between the articular surfaces of the medial acromion and the lateral clavicle. The AC joint is stabilized by both static and dynamic stabilizers. The static stabilizers include the acromioclavicular (AC) and coracoclavicular (CC) ligaments. The AC ligaments surround the AC joint capsule, with the primary function to resist anterior/posterior translation of the clavicle compared to the acromion. The CC ligaments are found medial to the AC joint and anchor the clavicle to the coracoid process just inferior to it. Their primary function is to prevent elevation of the clavicle in relation to the acromion. The dynamic stabilizers of the AC joint include the fibrous attachments of the deltoid and trapezius muscles. As the AC joint progresses through increasing severity of injury and instability, the static stabilizers are disrupted first through the AC ligaments followed by the CC ligaments, followed by the dynamic stabilizers [3]. As a general rule, if the deltotrapezial fascia remains intact, the AC joint separation can likely be treated non-operatively [3]. Classification System AC joint separations have been classically described using the Rockwood and Green classification system, which evaluates the radiographic appearance of the clavicle in relationship to the acromion [4]. Type I injuries are AC joint “sprains” in which radiographs are negative but physical exam is positive for tenderness over the AC joint. Type II injuries are injuries to the AC joint ligaments, while the CC ligaments remain intact. Radiographs may show slight widening of the AC joint without significant superior elevation of the distal clavicle (less than 30%). Type III injuries represent injury to both the AC and CC ligaments, such that the distal clavicle is elevated relative to the acromion 30–100% on radiographs. Types IV-V-VI injuries are rare. Type IV injuries occur when the distal clavicle herniates through the trapezius posteriorly. These are best seen on axillary radiographic views or cross-­ sectional imaging. Type V injuries show major elevation (100–300% of the distal clavicle) and occur with detachment of the deltoid and trapezius muscles. Type VI injuries show inferior dislocation of the clavicle.

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Treatment The Rockwood classification [4, 5] also helps to determine the course of treatment. Type I and II AC separations are treated non-operatively with analgesics, cryotherapy, and sling wear for 5–10 days, followed by progressive range of motion and activity as pain and swelling permit. Most athletes return to play in 2–4 weeks as they become asymptomatic, but it can take up to 12 weeks before painless return to play can be achieved [3]. Type IV, V, VI AC joint separations require surgical fixation. There are multiple options for operative fixation: • • • •

Primary fixation across AC joint with pins, screws, rods, or plate + screw Fixation between clavicle and coracoid with screw, suture, fiber wire Dynamic muscle transfer in which conjoint tendon is transferred to clavicle Ligament transfer of coracoacromial ligament (detached from acromion and transferred to distal clavicle) • Ligamentous reconstruction of CC and AC ligament with allograft Type III AC joint dislocations are somewhat controversial. Though the majority of Type III injuries can be treated non-operatively, there are specific populations that warrant surgical consideration. Younger active patients, thinner patients with marked prominence of the lateral clavicle, heavy laborers, and overhead-throwing athletes should be evaluated on in individual basis. There is some variation among orthopedic surgeons regarding treatment plans for these cases. We typically do not advocate acute surgical treatment of Type III AC joint injuries. Surgical management of these injuries in our practice is reserved for patients who are persistently symptomatic following a period of rest and rehabilitation. Return to play following operative management of an AC joint injury can vary but involves a period of time to allow the surgical repair to heal followed by physical therapy to regain strength and mobility, and the process can take 3–4 months. Figure 2.1 presents an algorithm for Type III injuries in athletes [2].

SC Joint Injuries Sternoclavicular (SC) joint injuries are uncommon, accounting for only 1% of all dislocations and 3% of dislocations involving the shoulder girdle [6]. There are two types of SC joint dislocations: anterior and posterior. Anterior dislocations are two to three times more common than posterior dislocations; however, most of the SC joint literature focuses on posterior dislocations because of the risk of serious and potentially life-threatening injuries to the mediastinal structures that lie beneath the SC joint. In the young athletic population, many presumed SC joint dislocations are actually Salter-Harris I or II fractures through the medial clavicle physis, which remains open until 25 years of age. The most common causes of SC joint dislocations occur from motor vehicle collisions, followed by athletic injuries and falls [3].

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In-season athlete?

Yes

Consider intra-articular injection and return to sport

No

Functional rehab for 3 months

Residual pain, loss of function, or inability to perform at previous level of activity/sport? No

Return to full activity

Yes Surgery

Fig. 2.1  An algorithm that can be used when treating a patient with an acromioclavicular joint injury. (Reproduced from Bontempo and Mazzocca [2], with permission from BMJ Publishing Group Ltd.)

The mechanism of injury involves either a direct blow to the clavicle or, more commonly, an indirect force to the clavicle applied through the shoulder. Anterior SC dislocations occur when an anterolateral force on the shoulder acts to compress the clavicle medially, while the shoulder is pushed backward. Posterior SC dislocations usually occur when a direct force is applied to the anteromedial clavicle. Posterior SC dislocations also occur when a posterolateral force on the shoulder acts to compress the clavicle medially while the shoulder is thrust forward [2, 3]. The position of the arm may also affect the direction of the dislocation when a medially directed force is applied to the shoulder. There is a cantilever effect on the clavicle through the medially positioned costoclavicular ligament. If the arm is abducted, such as when a quarterback is tackled onto their side with their arm outstretched, an anterior dislocation is more likely to occur. If the arm is adducted and flexed, such as under a football “dog pile,” a posterior dislocation is more likely to occur [1]. Anatomy The sternoclavicular (SC) joint is the only bony articulation between the upper limb and the axial skeleton. Yet, the saddle-shaped bony articular surface provides very little intrinsic stability. Instead, the joint capsule, ligaments, and soft tissue connections provide tremendous stability for the joint, making dislocations fairly rare.

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Furthermore, the superior and posterior aspects of the SC joint capsule are reinforced and thickened, adding additional protection from posterior dislocations as compared to anterior dislocations. The costoclavicular (rhomboid) ligament provides the greatest stability to the joint [7]. It connects the inferomedial aspect of the clavicle to the superior cartilaginous aspect of the first rib. The costoclavicular ligament also acts as a pivot point for force transmission from the shoulder girdle to the SC joint. This helps to explain why a posteriorly directed force on the shoulder (and associated lateral clavicle) causes an anterior SC joint dislocation, and conversely, an anteriorly directed force on the shoulder causes a posterior SC joint dislocation [3]. The SC joint surfaces of the clavicle and manubrium are lined with fibrocartilage in fully mature adults. A single meniscal disc acts as a cushion from compressive forces transmitted from the shoulder through the clavicle [3]. Just behind the SC joint lies the structures of the superior mediastinum. The structures most frequently encountered just posterior to the SC joint, in descending order, are the left and right brachiocephalic veins, right and left common carotid arteries, aortic arch, trachea, superior vena cava, pleura, left internal mammary artery, and left subclavian vein. Nearly 75% of patients have at least one of these structures within 10  mm of the SC joint [8]. The immediate proximity of these structures has implications when evaluating trauma-related injuries to this area as well as the potential for iatrogenic injuries from surgical intervention. Evaluation/Imaging While most SC joint injuries are sprains, anterior and posterior dislocations can occur and must be identified. The patient will complain of medial clavicle pain made worse with any extremity movement. Classically, lying supine will intensify the medial joint pain. On exam, anterior dislocations will demonstrate a prominent medial clavicle. Posterior dislocations have more subtle physical findings, but the examiner may be able to appreciate a recessed medial clavicle, which may be obscured by increased soft tissue swelling in the area. It is important to check for other signs of posterior impingement of underlying structures: tachypnea, dyspnea, dysphagia, and venous congestion. Suspected injuries to the SC joint and proximal 1/3 of the clavicle warrant a serendipity radiographic view of the bilateral clavicles as well as computed topography (CT) imaging of the chest. The serendipity view radiograph is an AP of the clavicles taken with the radiographic beam pointed 40° cephalad [3]. This makes it easier to appreciate anterior to posterior displacement of the clavicle. CT imaging with contrast is used to evaluate mediastinal structural relationships to the displaced clavicle, to assess vascular injuries, and to help differentiate between SC joint dislocation and proximal clavicle fractures [1, 9]. Treatment Treatment for SC joint injuries depends on the direction of the dislocation and the severity of the joint instability. SC joint injuries can be categorized as Type I (mild), II (moderate), and III (severe). Mild SC joint injuries are essentially sprains with

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stable joints and maintained ligamentous integrity. Moderate SC joint injuries have joint subluxation due to partial ligamentous disruption, but do not frankly dislocate. Severe SC joint injuries involve anterior or posterior dislocation of the joint with complete ligamentous disruption [2]. The goal of SC joint injury treatment is to manage pain, stabilize the joint, restore functional capacity to the shoulder girdle, address associated injuries, and minimize the potential complications. As previously described, Type I and Type II SC joint injuries maintain a level of stability that lends itself to conservative management. Since there is no frank dislocation, no reduction maneuver is required. Type I (mild sprain) SC injuries can be treated with NSAIDs, cryotherapy, and a sling for 3–4 days. Type II (partial ligamentous tear with subluxation) SC injuries are initially treated with NSAIDs, cryotherapy, and clavicle stabilization using a figure-­ of-­8 brace for 1 week, followed by a simple sling for 4–6 weeks. Unrestricted return to play typically occurs by 3 months. Type III (frank dislocation) SC joint injuries warrant an orthopedic consultation for potential surgical intervention. Posterior dislocations additionally warrant a cardiothoracic surgical consultation [2]. Anterior Type III SC joint dislocations can be initially treated with closed reduction in the emergency department under local anesthetic or conscious sedation or in the operating room under general anesthesia. Although anterior SC joint dislocations have a high rate of redislocation immediately after reduction, it is still recommended that at least one closed reduction be attempted [3]. The technique for reduction includes positioning the patient supine with a rolled towel between the scapulae. The ipsilateral arm is then abducted to 90° and extended posteriorly while traction is applied. A posteriorly directed force is then applied to the medial clavicle to achieve reduction [1, 3]. If the joint remains stable after closed reduction, the clavicle is immobilized with a figure-of-8 brace for 4–6 weeks. Elbow and glenohumeral joint range of motion exercises should be initiated by week 3. If the joint remains unstable after reduction attempts, the deformity is accepted, and the patient can be given a splint for comfort until acute symptoms resolve. Studies have shown that stability of the SC joint is not necessary to ensure normal painless function of the involved shoulder [10]. Operative intervention for chronic anterior SC joint instability is considered for patients that have residual pain and instability after conservative management [3]. The author’s preferred technique for these cases involves joint reduction followed by SC joint ligament reconstruction using a figure-­ of-­8 tendon graft reconstruction through drill holes through the medial clavicle and manubrium [11]. If there is significant articular cartilage damage to the medial clavicle, medial clavicular resection can be considered. Following surgical reconstruction, patients are immobilized in a sling and swathe for 4–6  weeks, and contact sports are avoided for 3–6 months postoperatively. Posterior Type III SC joint dislocations are much less common than anterior dislocations but are a much more serious and potentially life-threatening injury. The close proximity of important nearby mediastinal structures has implications for both urgent evaluation and potential surgical intervention after initial workup. The force required to cause a posterior dislocation can cause abutment of the medial clavicle against at least one or more of the nearby structures, potentially injuring that structure. Accordingly, all posterior SC joint dislocations require a CT of the chest to evaluate associated injuries, and these patients are generally kept in hospital until

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definitive management [9]. Many posterior SC joint Type III dislocations are actually posteriorly displaced fractures through the medial clavicle epiphysis. These injuries are treated similarly with the exception of the location of surgical repair as discussed below. In addition to an orthopedic consult, the cardiothoracic team should be contacted and readily available to assist with life-preserving surgical intervention if complications are encountered before or during joint reduction. Closed reduction of the posterior SC joint dislocation or posteriorly displaced medial clavicle physeal fracture has been proposed; however while an initial reduction may be achieved, recurrent instability is very common [12, 13]. We therefore advocate for formal open reduction and suture fixation of acute posterior SC joint fractures and dislocations [13, 14]. The patient is brought to the operating room and, under general anesthesia with appropriate general or thoracic surgery backup, is positioned in the modified beach chair position with a bump between the scapula. The ipsilateral arm is prepped into the sterile field so that it is fully free for intraoperative manipulation. A transverse incision centered over the SC joint is made, and the platysma is divided in line with the incision. Careful subperiosteal dissection of the clavicle is then done in a lateral-­ to-­medial fashion to expose the medial clavicle and SC joint [14]. Inspection is then done to determine if the injury was a medial clavicle physeal fracture with posterior clavicular displacement (more common) or a true posterior SC joint dislocation. If a medial clavicle physeal fracture is encountered, the medial clavicle is carefully manipulated anteriorly to reduce the fracture, and suture fixation with heavy nonabsorbable sutures is accomplished in a figure-of-8 fashion utilizing drill holes in the medial clavicle metaphysis and epiphysis [14]. If a posterior SC joint dislocation is noted, the medial clavicle epiphysis is carefully manipulated anteriorly back to the SC joint (with careful attention to anatomy—the clavicular head is normally only partially seated into clavicular notch of the manubrium), and the repair is accomplished similar to above with a figure-of-8 repair using sutures through drill holes between the medial clavicle epiphysis and sternum [14]. Stability is then assessed intraoperatively with shoulder range of motion. After surgery, patients are immobilized in a sling and swathe for 4–6 weeks. Active assisted range of motion exercises are started at week 6, followed by active motion and strength progression beginning at 12 weeks [3]. Contact sports are avoided for 3–6 months postoperatively [13, 14].

Glenohumeral Instability Introduction Shoulder injuries have become more common in young athletes as participation in high-demand contact sports has become more widespread at younger ages. Injury patterns in the adolescent shoulder generally are specific to the sport. One of the most common acute traumatic shoulder injuries in football players is a glenohumeral dislocation [15]. For these injuries, two traumatic instability patterns have

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been described: anterior (most common) and posterior. Anterior glenohumeral joint dislocations typically follow a traumatic injury and present with the affected arm held in abduction and external rotation with the humeral head palpable anteriorly. The typical mechanism of dislocation is a forced external rotation moment in the abducted arm. This can occur with a forceful collision, such as when a wide receiver reaching for a pass has his abducted arm pulled backward, or during a fall on an outstretched arm, such as when a running back dives for more yardage and lands on his shoulder. This causes the humeral head to dislocate anterior to the glenoid. Posterior dislocations are much less common. These occur from posteriorly directed forces onto the glenohumeral joint with the arm forward flexed such as when a lineman is blocking. These injuries can be subtle and typically present with the arm held in adduction and internal rotation.

Anatomy The glenohumeral joint allows the greatest arc of motion and is the most commonly dislocated joint in adolescents and adults [16, 17]. The bony anatomy of the glenohumeral joint has been described as a “golf ball on a tee” whereby the humeral head (golf ball) has tremendous flexibility with limited bony restraints from the glenoid (tee). Stability is thus achieved through a combination of static (ligamentous) and dynamic (muscular) soft tissue forces. The dynamic stabilizers include the rotator cuff muscles, long head of the biceps, deltoid, and scapulothoracic muscles and are functional during midrange of motion. These serve to compress the humeral head against the relatively flat glenoid (concavity compression) [18]. The static stabilizers include the glenohumeral ligaments, capsule, and labrum and function at end range of motion to limit abnormal humeral head translation. The glenoid labrum serves as an anchor point for insertion of the glenohumeral ligaments, doubles the anteroposterior depth of the glenoid socket, increases surface area for humeral head contact, and also deepens the concavity of the relatively flat glenoid [18]. The static stabilizers are typically injured in glenohumeral dislocations. The inferior glenohumeral ligament (IGHL) functions as a hammock with three parts including the anterior band, axillary pouch, and posterior band, with the anterior band being the most common ligament injured during anterior shoulder dislocations. Injury to static and dynamic restraints creates a unique pattern of disability that can limit normal shoulder function in the young athlete [16, 17, 19].

Evaluation/Imaging On presentation, following assessment of neurovascular status, radiographs including anteroposterior (AP), scapular-Y view, and axillary views will help make the diagnosis by depicting the location of the humeral head in relation to the glenoid.

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For subtle bony injuries, the West Point axillary view and Stryker notch view can be helpful to identify glenoid rim (bony Bankart lesions) and/or humeral head fractures (Hill-Sachs lesions) [20]. Gentle reduction should be performed promptly utilizing one of a number of reduction maneuvers. Following reduction of an anterior dislocation, patients will often have a positive “apprehension test” (symptoms of glenohumeral instability are reproduced by placing the arm in the abducted externally rotated position) and “relocation test” (improvement in instability symptoms occurs with a posteriorly directed force on the glenohumeral joint with the arm in the abducted, externally rotated position) [21]. These tests are not done in the acute setting as they will universally be positive and cause undue pain for the patient. In our practice, these tests are reserved for assessing shoulder stability following rehabilitation of an acute glenohumeral dislocation, typically at least 6 weeks following injury. In the setting of a first-time shoulder dislocation without acute bony pathology on radiographs in which the treating physician is planning on non-operative management, an MRI is not necessary. Indications for MR imaging following an acute first-time shoulder dislocation are controversial but may include bony pathology noted on radiographs, high-energy injury, nerve injury, suspected rotator cuff pathology, or patients at high risk of recurrence in whom surgical intervention may be considered. If the MRI is obtained in the acute setting soon after dislocation, an arthrogram may not be necessary as the likely glenohumeral joint effusion can assist with diagnosis of common tear patterns. If the MR is obtained later, an MR arthrogram is preferred to help assess for capsulolabral injuries. The most common injury pattern following anterior shoulder dislocations is a tear of the anterior inferior labrum off the glenoid (Bankart tear) at the attachment point of the anterior band of the IGHL.

Treatment Conservative management begins with a period of sling immobilization (1–3 weeks) although there is no evidence that sling immobilization is superior to early joint mobilization [22]. Controversy exists regarding the optimal position of immobilization (internal vs. external rotation) [23, 24]. A randomized controlled trial comparing immobilization in external rotation vs. internal rotation for 3 weeks noted a 40% decrease in recurrent rates in the external rotation group [23]. Results of this study have not been duplicated, and another randomized control trial suggested that both positions offered similar outcomes [25]. Following immobilization, a course of physical therapy is initiated focusing on periscapular and rotator cuff strengthening exercises. Return to contact sports is generally restricted until full shoulder range of motion and full return of strength has been achieved. High rates of recurrent instability (50–100%) following first-time dislocation have been reported in patients less than 20 years old [26–29]. Younger patients, males, and those involved in contact sports such as football are at the highest risk of redislocation [30, 31]. Participation in a contact sport such as football can increase the risk of redislocation by seven times [30]. The majority of these redislocations occur in the 1st year following treatment.

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Controversy exists regarding surgical versus nonsurgical management for adolescent with a first-time shoulder dislocation [26, 28, 29, 32]. A meta-analysis concluded that in young males performing high-demand activities, early surgical stabilization reduces recurrence and may be preferred [26]. A recent systemic literature review included over 700 shoulders in patients age 18 and under and showed significantly lower recurrence rates following operative treatment (17.5% vs. 71.3%) [33]. Return to sport rate was also significantly higher in the surgical group [33]. Patients with bony Bankart injuries (fractures of the anterior inferior glenoid labrum in association with anterior shoulder dislocations) may also do better with initial operative management within 3 months of injury [34]. In a randomized trial of first-time dislocators treated with arthroscopic repair vs. arthroscopic lavage, the risk of redislocation was reduced by 76%, and functional scores, treatment costs, return to previous activity level, and patient satisfaction were all improved in the repair group although arthroscopic lavage in the non-repair group may have impeded healing and worsened their outcome compared to non-operative management [32]. Other studies have shown that very young patients may be at lower risk of redislocation. In a recent analysis of shoulder dislocations in patients aged 10–16 years, the overall rate of recurrent dislocation was 38.2%, higher among 14–16-year-olds but actually substantially lower in patients aged 10–12 years [31]. Surgical treatment for glenohumeral instability involves repair of the anterior-­ inferior capsulolabral injury (Bankart repair) typically with an additional capsulorrhaphy. Both arthroscopic and open techniques have been described. Recurrence rates following arthroscopic repair have recently become equal to the classic open Bankart procedure likely due to newer techniques, equipment, and implants [35– 38]. A meta-analysis (which evaluated reports using older arthroscopic techniques and included adults and children) noted that open approaches were more reliable for restoring stability and returning patients to work or sports, but better subjective Rowe scores were seen following arthroscopic repair likely due to less stiffness and better function [39]. Reports on arthroscopic repair in purely adolescent groups are rare. One retrospective report on 32 shoulders in patients aged 11–18 who underwent arthroscopic repair at 2 years follow-up noted 5 redislocations (15% rate)—2 of which occurred in one patient with familial hyperlaxity [40]. All patients returned to sports, and high SANE (Single Assessment Numeric Evaluation) scores were noted. Other papers have reported good results in adolescent patients as part of larger adult series [36, 37, 41, 42]. More complex techniques such as a Latarjet shoulder stabilization (transfer of the coracoid to the glenoid) may be indicated in the setting of significant glenoid bone loss and recurrent instability. Return to play following non-operative management of a shoulder dislocation is variable. In a patient who sustains a first-time shoulder dislocation in whom non-­ operative management is planned, a longer period of rest is recommended to allow the soft tissue injury to heal. These patients are kept out of sports for approximately 6 weeks. In an in-season athlete with either first time or recurrent shoulder instability in whom surgical stabilization is planned for the off-season, return to play can be as short as a few days pending return of full shoulder range of motion and strength. These athletes may benefit from shoulder bracing to restrict abduction/external rotation upon return to sport. Figure 2.2 presents an algorithm for treatment of shoulder dislocations in athletes.

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D. E. Kramer and T. Wusu Shoulder dislocation First time or recurrent?

Recurrent

First time Is the physician’s plan to treat the injury non-operatively?

Yes

No

In-season Yes

• Wear sling for 3 weeks • No sports for 6 weeks post-injury • Physical Therapy

• Return to sports in brace once shoulder range of motion and strength return

No

Surgery

• Surgery in off-season

Fig. 2.2  An algorithm that can be used when treating an in-season athlete with a shoulder dislocation

Summary Shoulder and clavicle injuries in the adolescent athlete are increasingly prevalent with increased participation in contact sports such as football. Injury patterns in younger patients are unique to the developing musculoskeletal system and can be specific to the involved sport. A prompt and accurate diagnosis coupled with proper treatment can prevent long-term sequelae and expedite return to play for the young athlete. While many injuries respond well to a conservative regimen of rest and rehabilitation, surgical management may be necessary in certain circumstances.

References 1. Balcik BJ, Monseau AJ, Krantz W. Evaluation and treatment of sternoclavicular, clavicular, and acromioclavicular injuries. Prim Care. 2013;40(4):911–23, viii–ix. 2. Bontempo NA, Mazzocca AD. Biomechanics and treatment of acromioclavicular and sternoclavicular joint injuries. Br J Sports Med. 2010;44(5):361–9. 3. Macdonald PB, Lapointe P. Acromioclavicular and sternoclavicular joint injuries. Orthop Clin North Am. 2008;39(4):535–45, viii. 4. Gorbaty JD, Hsu JE, Classifications in Brief GAO. Rockwood classification of acromioclavicular joint separations. Clin Orthop Relat Res. 2017;475(1):283–7.

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5. Rockwood CA Jr. Fractures of the outer clavicle in children and adults. J Bone Joint Surg. 1982;64B:642–9. 6. Little NJ, Bismil Q, Chipperfield A, et al. Superior dislocation of the sternoclavicular joint. J Shoulder Elb Surg. 2008;17(1):e22–3. 7. McArdle PJ, Kalbassi R, Ilankovan V. Stability of the sternoclavicular joint. A retrospective study. Br J Oral Maxillofac Surg. 2003;41(1):12–5. 8. Ponce BA, Kundukulam JA, Pflugner R, et  al. Sternoclavicular joint surgery: how far does danger lurk below? J Shoulder Elb Surg. 2013;22(7):993–9. 9. Mirka H, Ferda J, Baxa J. Multidetector computed tomography of chest trauma: indications, technique and interpretation. Insights Imaging. 2012;3(5):433–49. 10. Savastano AA, Stutz SJ. Traumatic sternoclavicular dislocation. Int Surg. 1978;63(1):10–3. 11. Bae DS, Kocher MS, Waters PM, et al. Chronic recurrent anterior sternoclavicular joint instability: results of surgical management. J Pediatr Orthop. 2006;26(1):71–4. 12. Goldfarb CA, Bassett GS, Sullivan S, et al. Retrosternal displacement after physeal fracture of the medial clavicle in children treatment by open reduction and internal fixation. J Bone Joint Surg Br. 2001;83(8):1168–72. 13. Waters PM, Bae DS, Kadiyala RK. Short-term outcomes after surgical treatment of traumatic posterior sternoclavicular fracture-dislocations in children and adolescents. J Pediatr Orthop. 2003;23(4):464–9. 14. Bae DS. Traumatic Sternoclavicular Joint Injuries. J Pediatr Orthop. 2010;30:S63–S8. 15. Culpepper MI, Niemann KMW. High school football injuries in Birmingharm Alabama. South Med J. 1983 1983/07;76(7):873–5. 16. Chen FS, Diaz VA, Loebenberg M, et al. Shoulder and elbow injuries in the skeletally immature athlete. J Am Acad Orthop Surg. 2005 2005/05;13(3):172–85. 17. Kocher MS, Waters PM, Micheli LJ. Upper extremity injuries in the paediatric athlete. Sports Med. 2000;30(2):117–35. 18. Levine WN, Flatow EL.  The pathophysiology of shoulder instability. Am J Sports Med. 2000;28(6):910–7. 19. Bigliani LU, Kelkar R, Flatow EL, et al. Glenohumeral stability. Clin Orthop Relat Res. 1996 1996/09;330:13–30. 20. Bankart ASB. The pathology and treatment of recurrent dislocation of the shoulder-joint. Br J Surg. 1938 1938/07;26(101):23–9. 21. Walton J, Paxinos A, Tzannes A, et al. The unstable shoulder in the adolescent athlete. Am J Sports Med. 2002;30(5):758–67. 22. Hovelius L, Eriksson K, Fredin H, et al. Recurrences after initial dislocation of the shoulder. Results of a prospective study of treatment. J Bone Joint Surg Am. 1983;65(3):343–9. 23. Itoi E, Hatakeyama Y, Sato T, et al. Immobilization in external rotation after shoulder dislocation reduces the risk of recurrence. J Bone Joint Surg (Am Vol). 2007 2007/10;89(10):2124–31. 24. Itoi E, Sashi R, Minagawa H, et al. Position of immobilization after dislocation of the glenohumeral joint. J Bone Joint Surg Am. 2001 2001/05;83(5):661–7. 25. Finestone A, Milgrom C, Radeva-Petrova DR, et al. Bracing in external rotation for traumatic anterior dislocation of the shoulder. J Bone Joint Surg Br Vol. 2009 2009/06/30;91-B(7):918–21. 26. Handoll HH, Almaiyah MA, Rangan A. Surgical versus non-surgical treatment for acute anterior shoulder dislocation. Cochrane Database Syst Rev. 2004;(1):CD004325. Review. PMID: 14974064. 27. Hovelius L, Augustini BG, Fredin H, et al. Primary anterior dislocation of the shoulder in young patients. A ten-year prospective study. J Bone Joint Surg. 1996 1996/11;78(11):1677–84. 28. Jakobsen BW, Johannsen HV, Suder P, et  al. Primary repair versus conservative treatment of first-time traumatic anterior dislocation of the shoulder: a randomized study with 10-year follow-up. Arthrosc: J Arthrosc Relat Surg. 2007 2007/02;23(2):118–23. 29. Kirkley A, Griffin S, Richards C, et al. Prospective randomized clinical trial comparing the effectiveness of immediate arthroscopic stabilization versus immobilization and rehabilitation

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in first traumatic anterior dislocations of the shoulder. Arthrosc: J Arthrosc Relat Surg. 1999 1999/07;15(5):507–14. 30. Sachs RA. Can the need for future surgery for acute traumatic anterior shoulder dislocation be predicted? J Bone Joint Surg Am. 2007 2007/08/01;89(8):1665. 31. Leroux T, Ogilvie-Harris D, Veillette C, et al. The epidemiology of primary anterior shoulder dislocations in patients aged 10 to 16 years. Am J Sports Med. 2015;43(9):2111–7. 32. Robinson CM, Jenkins PJ, White TO, et al. Primary arthroscopic stabilization for a first-time anterior dislocation of the shoulder. J Bone Joint Surg (Am Vol). 2008 2008/04;90(4):708–21. 33. Longo UG, van der Linde JA, Loppini M, et  al. Surgical versus nonoperative treatment in patients up to 18 years old with traumatic shoulder instability: a systematic review and quantitative synthesis of the literature. Arthroscopy. 2016;32(5):944–52. 34. Porcellini G, Paladini P, Campi F, et  al. Long-term outcome of acute versus chronic bony Bankart lesions managed arthroscopically. Am J Sports Med. 2007;35(12):2067–72. 35. Bottoni LCR, Smith MEL, Berkowitz MMJ, et al. Arthroscopic versus open shoulder stabilization for recurrent anterior instability: a prospective randomized clinical trial. Am J Sports Med. 2006 2006/07/21;34(11):1730–7. 36. Cole BJ, L’Insalata J, Irrgang JAY, et al. Comparison of arthroscopic and open anterior shoulder stabilization. J Bone Joint Surg (Am Vol). 2000 2000/08;82(8):1108–14. 37. Guanche CA, Quick DC, Sodergren KM, et al. Arthroscopic versus open reconstruction of the shoulder in patients with isolated Bankart lesions. Am J Sports Med. 1996 1996/03;24(2):144–8. 38. Brophy RH, Marx RG. The treatment of traumatic anterior instability of the shoulder: nonoperative and surgical treatment. Arthroscopy. 2009;25(3):298–304. 39. Lenters TR, Franta AK, Wolf FM, et al. Arthroscopic compared with open repairs for recurrent anterior shoulder instability. J Bone Joint Surg (Am Vol). 2007 2007/02;89(2):244–54. 40. Jones KJ, Wiesel B, Ganley TJ, et al. Functional outcomes of early arthroscopic bankart repair in adolescents aged 11 to 18 years. J Pediatr Orthop. 2007;27(2):209–13. 41. Gartsman GM, Roddey TS, Hammerman SM. Arthroscopic treatment of anterior-inferior glenohumeral instability. J Bone Joint Surg (Am Vol). 2000 2000/07;82(7):991–1003. 42. Gill TJ, Micheli LJ, Gebhard F, et al. Bankart repair for anterior instability of the shoulder. Long-term outcome. J Bone Joint Surg. 1997 1997/06;79(6):850–7.

Chapter 3

The Thrower’s Shoulder Robert L. Parisien and Benton E. Heyworth

Introduction Participation in organized sports in the United States has increased substantially in recent years, with nearly 45 million children and adolescents taking part in organized youth athletics. Nearly 11.5 million amateur baseball players compete at the high school and club level, with an increasing incidence of those specializing in baseball year-round [1]. As established by the National Center for Health Statistics, this trend has resulted in a 240% increase in the number of outpatient visits for shoulder-related symptoms and complaints over a 10-year period in patients under the age of 18 [2]. The intensity of today’s youth sports culture is increasingly problematic in the young overhead athlete, as the body is potentially most susceptible to overuse injury during rapid periods of pubertal growth, with closure of the proximal humeral physis occurring between 14 and 17  years of age in most females and 16–18 years of age in most males [3, 4]. Children and adolescents also have incomplete muscular development and increased joint laxity, allowing for potential mechanical imbalances and increased risk of injury [5]. Repetitive microtrauma and inadequate recuperation in young throwers may lead to fatigue, weakness, and breakdown of normal, healthy tissues [6]. A single prospective observational study reported that, over the course of a single baseball season, up to 35% of skeletally immature pitchers experienced shoulder pain, which was reportedly present in

R. L. Parisien Department of Orthopedic Surgery, Boston University Medical Center, Boston, MA, USA B. E. Heyworth (*) Department of Orthopedic Surgery, Division of Sports Medicine, Boston Children’s Hospital, Boston, MA, USA e-mail: [email protected] © Springer International Publishing AG, part of Springer Nature 2019 A. S. Bauer, D. S. Bae (eds.), Upper Extremity Injuries in Young Athletes, Contemporary Pediatric and Adolescent Sports Medicine, https://doi.org/10.1007/978-3-319-56651-1_3

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nearly 10% of pitching appearances [7]. In evaluation of baseball players 9–18 years of age, a separate study reported a nearly 70% incidence of shoulder pain when pitching [8]. The highest rates of arm fatigue and shoulder injury have been reported in baseball pitchers and positional softball players with baseball pitchers experiencing the greatest number of days lost from practice or competition [9, 10]. In the setting of this array of background data, the current chapter explores the pathophysiology and approaches to diagnosis and treatment of some of the most common conditions for adolescent overhead athletes, including little league shoulder, internal impingement, superior labrum tears and related conditions.

Biomechanics and Phases of Throwing Given the degree of intensity of torque, shearing, and compressive and translational forces during the arc of throwing motion, there must remain a fluid and symbiotic interrelation between the scapula and humerus to maximize throwing efficiency and glenohumeral stability and minimize risk of injury. The five well-described phases of throwing include (I) windup, (II) cocking (early and late), (III) acceleration, (IV) deceleration and (V) follow-through. The rapid progression from Phase I through Phase V takes roughly 2s with the majority (75%) occurring during windup and acceleration. During Phase I, the dynamic rotator cuff muscles are virtually inactive, as there is minimal force on the shoulder girdle. Phase II can be further broken down into two subphases, early cocking and late cocking. Early cocking represents a brief period of deltoid muscle activation followed closely by the high torque forces of late cocking. During late cocking, the arm is maximally externally rotated with concomitant activation of the rotator cuff muscles (supraspinatus, infraspinatus, and teres minor). Late cocking is most commonly associated with the shoulder pathologies of glenohumeral internal rotation deficit (GIRD) and internal impingement. Phase III may also be broken down into two distinct subphases, early and late acceleration. Early acceleration begins with the arm in maximal external rotation (ER) with rapid transition into late acceleration and ends with ball release. This period is denoted by early triceps activation, with late activation of the pectoralis major, latissimus dorsi, and serratus anterior muscles. The transition from late cocking to early acceleration represents the most injurious phase of the throwing arc of motion. During this phase, when the body is initiating forward motion, symptoms may arise at the pectoralis major insertion, the origin of the anterior deltoid, and the long head of the biceps, which may subluxate out of the bicipital groove [11]. The scapula also plays a vital role throughout the integrated phases of cocking and acceleration as it rotates to allow clearance of the acromion over the rotator cuff. Phase IV, or deceleration, is the highest torque phase, with eccentric contraction of all supporting musculature as the ball leaves the hand and the shoulder reaches a point of maximal internal rotation (IR). Deceleration is considered the second most injurious phase and is associated with a number of pathologic processes, such as superior labrum lesions as well as injury to the biceps tendon, brachialis, and teres minor. Phase V,

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or follow-through, is initiated when the shoulder is at maximal IR. It is the period of motion when muscle activity returns to resting levels and ends when the thrower reaches a balanced position. The act of throwing essentially represents the transition from potential to kinetic energy and has been carefully described from a biomechanical standpoint as a “sequential motion of a kinetic chain” [12] with peak forces generated between the phases of late cocking and early acceleration. These integrated phases impart high forces on the shoulder and elbow as the arm suddenly transitions from maximal ER to IR with angular velocities reportedly up to 7000°/s, representing the fastest recorded human motion [13–16]. Additional concomitant shear forces of up to 310N anteriorly and 250N superiorly are experienced at the interface of the glenoid and humeral head [16]. This process has also been commonly described as a “double pendulum,” with each body segment accelerating in order from caudal to cranial [17]. As the caudal segment (legs and trunk) moves forward, the cranial segment (arm and shoulder) lags behind, but eventually the distal elbow accelerates beyond the more proximal shoulder followed sequentially by the distal hand accelerating beyond the more proximal elbow at a much greater rate in a whip-like fashion. Within this kinetic chain, the primary force generators contributing to increased throwing directional velocity are a combination of leg, hip and trunk rotational velocity [17–19]. The scapula plays a pivotal role in shoulder function. Scapular dyskinesis is a well-described anatomic and biomechanical imbalance contributing to dis-­ coordination of the shoulder musculature and resulting in improper throwing mechanics. This power imbalance may lead to protraction of the scapula and altered glenohumeral mechanics, placing excessive stress on the anterior joint capsule and posterosuperior labrum. Kibler et al. [20] clearly elucidated five important roles of the scapula during throwing: (1) provide a stable glenohumeral articulation, (2) retraction and protraction, (3) elevation of the acromion, (4) base for muscular attachment, and (5) integral link in the kinetic chain. During the throwing motion, lack of scapular retraction on the thorax has a negative effect on the cocking phase, contributing to decreased explosive transition to early acceleration. Additionally, uncoordinated protraction through the acceleration phase will cause increased eccentric contraction of the musculature responsible for scapulothoracic deceleration causing altered concavity compression of the glenohumeral articulation [20]. Thus, the proper scapulothoracic coordination allows for optimal concavity compression through a stable center of rotation allowing for proper glenohumeral kinematics and decreased risk of injury during throwing [21].

“Little League Shoulder” (Proximal Humeral Epiphysiolysis) First described in 1953 [22], little league shoulder (LLS), or traction epiphysiolysis, is one of the most common overuse shoulder injuries in youth baseball players. The condition occurs as the result of repetitive torsional, traction and shear stresses

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placed on the immature proximal humeral physis, most commonly in youth baseball pitchers [5, 23]. One study retrospectively evaluated a cohort of 95 patients with a diagnosis of LLS at a single children’s hospital and reported that 97% were baseball players, in which 86% of whom were pitchers. Two of the 95 patients were female and 3% were tennis players [24]. Traction epiphysiolysis can be classified as a Salter Harris (SH) I pattern of injury with repetitive microtrauma damaging the hypertrophic zone, the weakest portion of the physis. The incidence of LLS has been increasing in recent years, with this trend contributing to nearly 11% of all youth athletes reporting shoulder injuries and up to 80% of pitchers aged 8–15 with findings of proximal humeral physeal widening of the throwing arm on plain radiographs [10, 24, 25]. In addition to high pitch counts and repetitive overhead stress, poor throwing mechanics have also been demonstrated as a direct risk factor for the development of LLS [26]. Adult throwers, in comparison, can better withstand a higher frequency of repetitive overhead activity but more commonly manifest intra-­ articular joint pathology with greater frequency of SLAP tears, labral tears and cartilage damage.

Diagnosis Pain is the most common presenting symptom of LLS, with patients typically reporting superolateral shoulder pain with increased throwing intensity and duration [27]. The pain is typically exacerbated in late cocking and early deceleration phases of the throwing cycle. Patients may also report decreased pitch velocity and control. As the condition worsens, patients may complain of constant pain that interferes with daily activities. Weakness, fatigue, and mechanical symptoms, such as clicking or catching, are less common but may be present in up to 10–30% of patients [24]. Instability and neurologic symptoms are atypical and, when present, should prompt the clinician to investigate alternative etiologies. Tenderness to direct palpation of the lateral-proximal humerus is the most common physical exam finding, with Heyworth et al. [24] reporting positive findings in 74% of patients. A complete physical examination of the shoulder girdle with proper attention to scapulothoracic and glenohumeral mechanics may demonstrate increased external rotation with the arm in 90° of abduction and associated pain and weakness with resisted active range of motion (ROM). Throwing athletes often demonstrate increased joint laxity, poor flexibility, and decreased passive ROM [28]. Glenohumeral internal rotation deficit (GIRD) has been reported in up to 30% of patients with LLS with a decreased rotational arc of motion, compared with the contralateral, non-throwing side [24]. Associated elbow pathology may be present in nearly 15% of patients, the most common of which being medial epicondyle apophysitis—“little league elbow”—and valgus extension overload. Plain radiographs classically demonstrate anterolateral physeal widening on true A-P and external rotation views (Fig. 3.1); contralateral comparison views can be helpful. Additional radiographic findings include sclerosis, physeal fragmentation,

3  The Thrower’s Shoulder Fig. 3.1 (a) Widening of the right proximal humeral growth, particularly the anterolateral aspect of the physis, as compared to the normal left side (b), as visualized on anteroposterior external rotation (AP-ER) views

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a

b

and calcification [29, 30]. MRI is not generally needed for diagnosis but may ­demonstrate associated physeal edema and is useful in evaluating or ruling out concomitant intra-articular pathology.

Treatment and Outcomes The mainstay of treatment for LLS has been conservative management, with a critical period of prolonged rest, followed by focused stretching and strengthening prior to a gradual return to overhead activity. Similar to the five well-defined “phases of throwing,” LLS can be considered to consist of five distinct “phases of recovery” consisting of rest, stretching, strengthening, throwing mechanics and progressive throwing. During the rest phase, the patient is expected to modify their activities with the recommended interval of rest consistently reported in the literature being

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2–3 months or until pain-free [5, 23, 31]. During the latter third of the rest phase, the patient should begin the stretching phase consisting of crossarm and sleeper stretches focusing on stretching static capsular structures with the intent of improving internal rotation of the shoulder. This allows for appropriate centralization of the humeral head within the glenoid during the arc of motion. As the pain resolves, the patient progresses into the strengthening phase with emphasis on strengthening the rotator cuff and periscapular musculature to restore dynamic stability. The next phase of recovery focuses on the evaluation of proper throwing mechanics intended to prevent recurrence of shoulder pain. Lastly, an appropriately structured and supervised progressive throwing program is crucial in gradually transitioning the athlete back into competition. Adequate conservative treatment of LLS results in complete resolution of shoulder pain in over 90% of throwers [5]. An early report of LLS by Carson and Gasser [32] in 1998 consisted of 23 cases. Patients were conservatively treated with rest from baseball throwing for an average of 3 months. All patients were ultimately followed for an average of 9.6 months. Complete symptom resolution occurred at an average of 7.7 months with 91% of throwers demonstrating an asymptomatic return to competitive baseball. The series by Heyworth et al. [24] consisted of 93 patients, 97% of whom were baseball players with 86% pitchers. Nearly 99% of patients were treated conservatively with rest and 79% of throwers underwent formal physical therapy. The authors reported an average time to resolution of 2.6 months with return to competitive throwing in 4.2 months. Symptoms recurred in 7% of throwers and were most commonly seen in patients with associated symptoms of GIRD. The authors therefore recommend close monitoring of young throwers diagnosed with LLS for up to 1 year following the initiation of conservative management. The most concerning complication reported in LLS is physeal arrest, which, although exceedingly rare, could be the result of repetitive stress with inadequate periods of rest.

Internal Impingement In the adolescent overhead athlete, persistent posterior shoulder pain is one of the more common presenting symptoms of a condition referred to as “internal impingement.” This pathologic process is characterized by repetitive contact of the greater tuberosity of the humeral head with the posterosuperior aspect of the glenoid when the arm is abducted and externally rotated, leading to a constellation of sequelae, including articular-sided rotator cuff tears, labral tears, biceps tendinitis, anterior glenohumeral micro-instability, an internal rotation deficit, and scapular dysfunction [11, 33, 34]. As described by Bennett [35] in the Annals of Surgery in 1947, the mechanism of posterior shoulder pain was proposed as a traction injury leading to inflammation of the posterior capsule and inferior glenohumeral ligament resulting in the classic “Bennett lesion” of the posteroinferior glenoid rim (Fig. 3.2). Exostosis of the posteroinferior glenoid is one of several radiographic findings in throwers with internal impingement that have been described, which also includes sclerosis of the greater

3  The Thrower’s Shoulder

a

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b

c Fig. 3.2  Heterotopic ossification on the infero-posterior aspect of the glenoid rim, also known as a “Bennett lesion” (short arrow), as seen in a T1-weighted MR arthrogram in the (a) coronal, (b) axial, and (c) sagittal planes in an adolescent pitcher with internal impingement syndrome and a concomitant Type 2 superior labrum anterior and posterior (SLAP) tear, with detachment of the superior labrum/biceps anchor from the superior glenoid rim (long arrow)

tuberosity, osteochondral lesions of the posterior humeral head, and rounding of the posterior glenoid rim. Multiple studies have substantiated the finding of extra-­ articular calcification in the region of the posteroinferior glenoid as a result of repetitive traction of the posterior capsule and PIGHL [36–38]. Lombardo et  al. [36] further described the presence of posterior shoulder pain and pathology as predominantly occurring during the late cocking phase of throwing. Additional analysis by Andrews et al. [39] and Walch et al. [40] of posterior shoulder pain in the throwing athlete identified associated superior labrum anterior and posterior (SLAP) lesions and articular-sided tears of the posterior supraspinatus (PASTA lesion) and anterior infraspinatus tendons at the margin of the posterosuperior glenoid. This constellation of findings, or some combination thereof, can be referred to as “internal impingement.”

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 iomechanics, Scapular Dyskinesis B and the Thrower’s Paradox The complex biomechanics of overhead throwing can predispose some athletes to shoulder dysfunction and resultant injury via shoulder remodeling, posterior capsular contracture, and scapular dyskinesis. The “thrower’s paradox” refers to a balanced equilibrium of mobility and stability allowing for a functional arc of motion that maximizes external rotation [16]. The normal internal-external arc of motion is 180° with the center of rotation shifted posteriorly in repetitive overhead throwing athletes which allows increased clearance of the greater tuberosity over the glenoid during rotation [41–43]. Additional physiologic adaptations of throwing that may predispose young throwers to internal impingement include increased external rotation with associated anterior laxity and increased humeral and glenoid retroversion [11]. In evaluation of 287 baseball players aged 6–18, Hibberd et al. [44] found that an “age-related increase in GIRD is primarily attributed to humeral retrotorsion rather than soft tissue tightness.” Additionally, the anterior and posterior bands of the inferior glenohumeral ligament have been shown to act as reciprocating cables responsible for balancing the humeral head in the glenoid during arm abduction [45]. Given this anatomical understanding, Burkhart et al. [43] proposed a pathophysiologic cascade leading to the loss of internal rotation and ultimate development of GIRD.  During this cascade, contracture of the posterior inferior glenohumeral ligament acts as a tether, shifting the central point of glenohumeral rotation in the posterosuperior direction. Anterior glenohumeral instability with repetitive shear stress during the phase transition of cocking-acceleration and recurrent microtraumatic events has also been described as a significant contributing factor leading to internal impingement [46, 47]. Paley et al. [48] further described dissociation of the glenohumeral and scapulothoracic articulations as the precipitating mechanisms leading to attenuation of the anterior glenohumeral ligament causing excessive anterior translation of the humeral head. Scapular dyskinesis has also been demonstrated to contribute significantly toward the development of glenohumeral instability associated with rotator cuff and labral injuries with a reported prevalence of 33–100% [49, 50]. It has been suggested that scapular dyskinesis is an independent risk factor contributing to internal impingement, with scapular dysfunction reported in up to 100% of throwers with signs and symptoms of internal impingement [20]. It has also been shown that scapular dyskinesis may result from shoulder fatigue, producing errors with regard to arm proprioception [51]. Such patients may complain of “dead-arm” symptoms with additional findings suggestive of SICK scapula syndrome, a muscular overuse pattern of pathology described as scapular malposition, inferior medial border prominence, coracoid pain, and scapular dyskinesis [52]. This lack of balanced scapular kinematics may lead to dynamic muscle imbalance, significantly impacting overhead throwing athletes. Myers et al. [53] have shown that with poor scapulothoracic rhythm, there is a trend toward scapular internal rotation and protraction

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around the rib cage resulting from inflexibility or imbalances in the periscapular musculature. The collective interplay of these biomechanical and pathophysiologic mechanisms may ultimately lead to development of the pathologic “peelback mechanism” with increased torsional loading of the posterosuperior labrum during late cocking and early acceleration. The 2013 consensus statement from the Scapular Summit states that scapular dyskinesis is most aptly viewed as a potential impairment to optimum shoulder function with scapular involvement playing an important, but not completely understood, role in creating or exacerbating shoulder dysfunction [54].

Glenohumeral Internal Rotation Deficit (GIRD) Glenohumeral internal rotation deficit shares an intimate relationship with the biomechanics and related pathology of internal impingement. GIRD is defined as the loss of internal rotation of the glenohumeral joint as compared to the contralateral side. Burkhart et al. [43] described how this loss of internal rotation may initiate the central pathophysiologic process in throwing athletes. This process results in the shifting of the central contact point of the glenohumeral articulation in the posterosuperior direction. This phenomenon was confirmed by Grossman et  al. [55] in a cadaveric model, in which GIRD and posterosuperior translation of the humeral head occurred during the late cocking phase of throwing. Soft tissue contributions of posterior and posteroinferior capsular contracture, anterior capsular stretch, and contracture of the inferior glenohumeral ligament leading to altered glenohumeral mechanics have been well-described [43, 45, 56]. Several studies suggest a positive correlation between the presence of humeral retrotorsion and throwers with GIRD. In evaluation of professional pitchers, Noonan et al. found that those with GIRD displayed significantly greater retrotorsion in their dominant arm as compared to those without GIRD.  Additionally, the pitchers with GIRD demonstrated a greater side-to-side difference in humeral torsion. Greenberg et al. [57] reported similar findings in an evaluation of youth baseball players, compared with age-­matched non-throwers. In another evaluation of youth athletes aged 6–18 years old, Hibberd et al. [44] reported that GIRD and humeral retrotorsion increased with age in youth/adolescent baseball players. However, upon closer investigation, total ROM and retrotorsion-adjusted GIRD remained constant across the age groups, thus indicating that this increase may not represent pathologic GIRD. Further understanding of elbow pathology in patients with GIRD may help to identify at-risk throwers, with Dines et al. [58] reporting on the association between ulnar collateral ligament insufficiency and GIRD with those throwers demonstrating a significantly greater internal rotation deficit as compared to throwers without a history of elbow pain.

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Diagnosis Young repetitive overhead throwing athletes with GIRD will typically present with vague shoulder pain and a decrease in overall throwing performance as consistent with other conditions associated with internal impingement. Throwers may also report the need for increased warm-up time, decreased velocity, and posterior shoulder pain in late cocking. The physical examination of a young thrower with shoulder pain is the most critical aspect of the diagnostic process. Importantly, most high-level throwing athletes, including asymptomatic throwers, will demonstrate altered shoulder internal and external ranges of motion, in which internal rotation is decreased and external rotation is increased in the dominant arm when compared with the nondominant arm. Thus, while there will be an equivalent total arc of motion in the two shoulders, the throwing side will show a shifted arc (toward the back of the shoulder or disproportionately in the externally rotated position). In contrast, patients with GIRD have such decreased internal rotation compared to their pre-overuse state that they develop decreased total arc of motion of their dominant throwing arm, as compared to the nondominant arm. Ruotolo et al. [59] found a 10° loss of internal rotation of the throwing shoulder in symptomatic collegiate baseball players as compared to asymptomatic controls. Most authors, however, cite a minimum 25° difference in the arc of motion to constitute GIRD. Rotational glenohumeral motion should be assessed with the arm at the side and at 90° of abduction while stabilizing the scapula to obtain a true measurement of glenohumeral rotation. This is easiest done in the supine position. A thorough investigation for scapular dyskinesis is necessary as well in evaluation of GIRD.  The scapula may demonstrate a prominent inferior medial border, and the throwing shoulder may appear to sag inferiorly compared to the non-throwing shoulder contributing to altered glenohumeral mechanics. An additional special test is the “posterior impingement sign.” This is a single maneuver proposed by Meister et  al. [60] to detect the symptoms and sequelae of GIRD. Forty-eight throwing athletes were evaluated for the presence of posterior shoulder pain with the arm in 90° of abduction, 10° of extension, and maximal external rotation. The authors reported a sensitivity and specificity of 95% and 100%, respectively. Standard anteroposterior, axillary, scapular-Y, and West Point views may be normal or demonstrate the classic Bennett lesion (as previously described), sclerosis of the greater tuberosity, posterior humeral head osteochondral cysts, and rounding of the posterior glenoid rim.

Superior Labrum Anterior and Posterior (SLAP) Lesions Superior labrum anterior and posterior lesions are a common labral injury in throwers, first described by Andrews et al. [61] in 1985. Five years later, Snyder et al. [62] further characterized these lesions of the superior labrum and biceps tendon origin. Cadaveric studies have demonstrated that over 70% of the anatomic biceps origins were either completely posterior or posterior dominant, while the biceps tendon insertion is most vulnerable to injury during the late cocking phase of throwing [63, 64].

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Table 3.1  Snyder classification of SLAP lesions Superior labrum anterior and posterior lesions Type I Degenerative fraying of the superior labrum with intact peripheral attachment and stable biceps tendon anchor Type II Degenerative fraying with detachment of the superior labrum and biceps from the glenoid Type III Bucket-handle tear of the superior labrum with an intact biceps tendon anchor Type IV Displaced bucket-handle labral tear with extension into the biceps tendon root

Contraction of the posterior band of the IGHL may increase shear forces on the superior labrum by shifting the contact point in a posterosuperior direction. Resultant SLAP lesions compromise shoulder stability by placing increased strain on the anterior band of the IGHL.  Various types of SLAP lesions have been described, with the classification by Snyder et al. [62] considered the most widely recognized with description of four major variants (Table 3.1). However, to avoid overtreatment of superior labral lesions, careful clinical correlation is warranted, as additional literature has demonstrated significant interobserver variability among experienced surgeons in diagnosing SLAP tears arthroscopically [65]. As previously described, Burkhart et al. [66] described the threshold of internal rotation deficit in GIRD to be >25° as compared to the contralateral, non-throwing shoulder. Studies have suggested that GIRD represents a risk factor for the development of SLAP lesions. However, these lesions are less commonly seen in youth throwers as compared to adults, with much of the literature on young people limited to case reports [67]. SLAP tears may be considered a spectrum of pathology typically developing in mature shoulders with repetitive stress to the posterosuperior aspect of the glenoid leading to the peel-back mechanism, which has been well-­ described by Burkhart and Morgan [66]. In evaluation of 490 baseball players with magnetic resonance imaging, Han et al. [68] reported a SLAP tear prevalence of 18% in high school baseball players as compared to a 4.8% prevalence among junior high players, suggesting a relative risk of 1.4. Heyworth et al. [69] evaluated 23 SLAP tears in a cohort of 177 adolescent athletes (ranging from 13 to 18 years of age) who underwent shoulder arthroscopy for any reason. The authors demonstrated that although SLAP tears are relatively rare in adolescent throwers, most superior labrum tears in this age group develop in conjunction with other instability patterns and labrum tears. Isolated tears (3.4% in their cohort), however, were most commonly seen in overhead athletes and patients presented with pain as their primary symptom.

Diagnosis SLAP tears can present a diagnostic challenge, both because of the relatively high rate of concomitant shoulder pathology and due to a lack of sensitivity and specificity in the physical examination maneuvers typically utilized to assess for superior labral pathology. In evaluation of 136 arthroscopically treated SLAP lesions, Kim

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et al. [70] discovered that 88% demonstrated coexisting pathology. The authors concluded that the type and severity of a SLAP lesion correlated with patient age and physical demands. Although SLAP tears may present following acute insult, the onset of symptoms in the throwing athlete is typically insidious, resulting from repetitive overhead activity. The most common presenting complaint is that of non-­ specific shoulder pain. As such, patients may report a spectrum of complaints including deep, sharp, or achy pain. However, all symptoms of SLAP lesions tend to be associated with and exacerbated by overhead activity. Patients will classically report decreased throwing velocity and pitch control associated with pain during the late cocking and early acceleration phases of throwing. Physical examination for SLAP tears should be multifaceted. Scapular mechanics should be closely assessed, as ROM and integrity of the rotator cuff are typically preserved with isolated SLAP lesions. O’Brien et  al. [71] reported sensitivity of 100% and specificity of over 98% with the active compression test. More typically referred to as “O’Brien’s test,” it is conducted with the arm forward flexed to 90° with the elbow in full extension, the arm adducted 10–15° medial to the sagittal plane of the body, and the thumb pointed downward in full pronation. The examiner, standing behind the patient, applies a uniform downward force to the arm (Fig. 3.3a). With the arm in the same position, the palm is then fully supinated, and the maneuver repeated (Fig. 3.3b). The test is considered positive if pain is elicited during the first maneuver and reduced or eliminated with the second. Despite promising results reported by O’Brien and colleagues, the active compression test remains controversial for the detection of SLAP pathology as additional studies have failed to predictably reproduce their results. The crank test is another exam described for the diagnosis of SLAP tears with Liu et  al. [72] reporting 91% sensitivity and 94% specificity. This test is performed with the patient upright or supine with the arm elevated to 160° in the scapular plane. The joint is loaded along the axis of the humerus while simultaneously internally and externally rotating the humerus. A positive test is indicated if there is reproduction of symptoms with or without a click (typically during ER). There is also some controversy surrounding the crank test, as additional studies [73–76] failed to realize the same promising results as that of Liu and colleagues. Additional proposed maneuvers include the anterior slide test [77], SLAPprehension Test [78], supine flexion resistance test [79] and the clunk test by Andrews et al. [61], with Hegedus et al. [80] reporting the biceps load II test as demonstrating the greatest level of sensitivity and specificity in their comprehensive systematic review and meta-analysis. However, a systematic review by Dessaur and Magarey [81] analyzed 26 tests for SLAP lesions from 17 published studies and concluded that no single test is sensitive or specific enough to accurately determine the presence or absence of a SLAP lesion. Magnetic resonance imaging (MRI) is the preferred modality when evaluating suspected SLAP tears. Indications for advanced imaging are non-specific but include persistent pain, mechanical symptoms, and patients with exam concerning for intra-articular pathology given the modalities described above. However, the accuracy of MR imaging remains controversial as compared to arthroscopic evaluation, in that reported sensitivity and specificity range from

3  The Thrower’s Shoulder Fig. 3.3  O’Brien’s test is positive when a patient reports significant pain when trying to resist a downward force on the affected extremity, with the arm in a forward flexed (90°), neutrally adducted (0°), and internally rotated position (thumb pointed downward) (a). In a positive test, this pain is decreased or eliminated when the arm is held in the same forward flexed position, but the arm is supinated, with the palm facing upward (b)

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a

b

84 to 98% and 6 to 91%, respectively. The need for MR arthrography versus MRI also remains in debate, with Connell et al. [82] demonstrating equivalent rates of sensitivity and specificity.

 artial Articular Supraspinatus Tendon Avulsion (PASTA) P Lesions Partial rotator cuff tears are a well-described entity dating back to 1934 with Codman’s first report [83]. Although partial-thickness tears have become increasingly recognized in the throwing athlete as a cause of pain and impairment, it

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remains unclear what the precise incidence may be, compared to full-thickness tears, particularly in the adolescent athlete, in whom it is likely much more rare [84]. The incidence in the general population has been reported to fall anywhere between 17% and 37% [85, 86]. The location of tear classically occurs at the myotendinous junction. Partial tears are classified as intratendinous, articular-sided or bursal-sided with one cadaveric model supporting intratendinous as the most common sub-type in the general population [87]. However, PASTA lesions appear to be more common in overhead throwing athletes, with Payne et  al. [88] reporting a 91% incidence of articular-sided tears in their cohort of athletes presenting with partial-­thickness tears. Work by Gartsman and Milne [89] provides further support for the notion of increased prevalence of PASTA lesions in the young overhead athlete population as they found articular-sided lesions comprising >90% of all partial-­thickness rotator cuff tears in their evaluation. Data suggests this phenomenon may be the result of relative hypovascularity of the articular side of the rotator cuff tendons, compared to the more robust vascularity feeding the bursal side of the tendon [90]. Data further demonstrates that excessive traction of the rotator cuff tendon during the late cocking phase is a critical etiologic factor in the development of articular rotator cuff tears in throwing athletes [39]. Although this proposed mechanism remains controversial, Burkhart et al. [43], in their evaluation of the biomechanics and associated pathology of the disabled throwing shoulder, report articular-sided tears as resulting from shear and torsional forces. Histologic and anatomic analysis has clearly demonstrated that collagen on the articular side of the rotator cuff is thinner and not as well organized compared to the bursal side, leading to increased ease of articular-sided tears during repetitive overhead throwing [90, 91]. Additional biomechanical and arthroscopic studies have proposed the mechanism of internal impingement as responsible for PASTA lesions in overhead athletes as the articular side of the supraspinatus and infraspinatus repetitively contacts the posterosuperior aspect of the glenoid during the late cocking phase of throwing [40].

Diagnosis Pain, weakness, and decreased throwing velocity are the classic presenting symptoms of partial-thickness rotator cuff pathology in overhead throwers. However, some evidence suggests that not all PASTA lesions are symptomatic [92]. Physical examination techniques designed to detect isolated partial articular lesions are relatively non-specific, as these lesions are often associated with concomitant shoulder pathology [40, 93]. The Jobe or empty can test is perhaps the most commonly used clinical examination technique, with the arm abducted to 90° in the plane of the scapula and forearm pronation with the thumb pointing down toward the floor. A positive test is determined by pain and/or weakness with resisted downward force. However, according to findings by Itoi et al. [94], the results produced by the full can test, with the forearm in supination, were not significantly different than that for

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the empty can. Although a classic sign of external or subacromial impingement, the Neer and Hawkins tests may reproduce symptoms with articular-sided tears. Partial articular-sided lesions are challenging to discern via physical exam alone as literature demonstrates that up to 30% of PASTA lesions occur in conjunction with other pathology, not in isolation [40]. Therefore, advanced imaging is invaluable in pursuit of an accurate diagnosis. Although plain radiographs are routinely obtained in athletes with symptomatic throwing shoulders, MRI remains the gold standard for investigation of rotator cuff pathology. Magnetic resonance arthrography (MRA) with gadolinium or saline is also commonly used, and many argue in favor of the MRA as compared with MRI. However, Potter and colleagues [95, 96] demonstrated equivalence of non-­ contrast MRI with use of specific sequences. However, clinicians must be careful not to pursue surgical treatment based solely on abnormal MR findings. In evaluation of the throwing and non-throwing arms of ten asymptomatic baseball players, Halbrecht et al. [97] reported signal changes representative of rotator cuff tendinosis or delamination in four of ten shoulders. Conversely, in analysis of 20 throwing athletes, Connor et  al. [98] reported rotator cuff tears in 40% of asymptomatic throwing shoulders as compared to 0% in the nondominant arm. These disparate reports in the literature support the notion that accurate diagnosis must hinge on the careful consideration of patient reported symptoms and physical examination along with advanced imaging.

 reatment and Outcomes of Internal Impingement T and Associated Pathology (GIRD, SLAP, PASTA) Nonoperative When the diagnosis of internal impingement is made, nonoperative management is the primary treatment of all associated pathology consisting of GIRD, SLAP, and PASTA lesions. Additionally, skeletal maturity must be considered when treating shoulder pathology in youth athletes, given that the unique anatomy of the skeletally immature athlete places them at an increased risk of recurrent injury [23]. The mainstay of conservative management of atraumatic shoulder pathology is rest and activity modification followed by organized physical therapy. The preferred method of pain management is with nonsteroidal anti-inflammatory medication, with appropriate conservative treatment methods based on the three clinical stages of internal impingement proposed by Jobe [99]. Stage I is characterized by patients reporting poorly localized pain with stiffness. These patients should be predominantly treated conservatively with rest and nonsteroidal anti-inflammatories. Stage II can be identified by posterior shoulder pain during the late cocking and early acceleration phases of throwing. Symptoms of instability and pain with normal activity are unusual. Patients with signs of Stage II internal impingement require prolonged rest

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followed by formal physical therapy. In prospective evaluation of 39 professional baseball pitchers with preseason GIRD, Levitz et al. [100] found that 60% sustained a spectrum of shoulder injuries that prevented them from completing the season. The sleeper stretch has thus been proposed as a mechanism to decrease posterior capsular contracture allowing for return to normal shoulder kinematics. The sleeper stretch is performed with the patient in the lateral decubitus position. The shoulders and elbows are positioned into 90° of flexion with the lateral border of the scapula positioned firmly against the treatment table (Fig. 3.4a). The patient then passively internally rotates the shoulder, with assistance of the contralateral arm, by grasping the distal forearm and slowly moving the arm toward the treatment table in a controlled manner (Fig.  3.4b). In a recent study of high school baseball pitchers by Reuther et  al. [101], it was demonstrated that the sleeper stretch accelerates the recovery of internal rotation loss and the authors further suggest that it may also mitigate the cumulative effects observed over the course of a season. In support of these findings, an evaluation of 33 National Collegiate Athletic Association (NCAA) Fig. 3.4  The “sleeper stretch” involves lying on one’s side with the affected/throwing arm in forward flexion, neutral adduction, and the elbow flexed to 90°. (a) The patient (or a physical therapist) applies a force against the dorsum of the wrist or forearm, pushing the shoulder into an internally rotated position, thereby stretching out the posterior capsule and external rotators of the shoulder (b)

a

b

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Division-I baseball players by Laudner et  al. [102] demonstrated a significant increase in internal rotation and posterior shoulder ROM with use of the sleeper stretch in the dominant throwing arm. In addition to sleeper stretches, attention should be given to scapular stabilization through exercises focusing on periscapular and rotator cuff strengthening. In evaluation of 96 overhead athletes treated with scapular stabilizing exercises for isolated SICK scapula syndrome, Burkhart et al. [52] reported a 100% rate of return to their pre-injury level of throwing. Data does not support the routine use of therapeutic injections for internal impingement and associated pathology. While a true risk of permanent tendon and chondral damage has not been substantiated for single injections or those spaced out over prolonged periods of many months, this modality is rarely recommended in youth throwers, despite the intended inhibition of the intra-articular inflammatory cascade.

Operative Given the relatively large spectrum of pathology associated with internal impingement, there are a variety of surgical treatment options. Typically, the integrated combination of surgical intervention and postoperative rehabilitation is necessary as data demonstrates that >50% of PASTA lesions will progress [103]. However, caution must be taken when considering surgical intervention in the youth shoulder. Appropriate surgical indications include failure to improve with conservative treatment or inability to return to competition despite a comprehensive and targeted rehabilitation program. Surgical intervention should be geared toward lesions that have been directly correlated with the patient’s symptoms. PASTA lesions represent the most commonly operative concomitant rotator cuff pathology in throwers with internal impingement. In the landmark series by Paley et al. [48], all 41 dominant throwing shoulders experienced contact between the posterosuperior glenoid rim and rotator cuff with the arm in the late cocking phase of abduction and external rotation with 93% demonstrating articular-sided fraying. A previous series by Walch et al. [40] reported articular-sided tears in 76% of throwing shoulders with 71% demonstrating posterosuperior labral fraying. It is generally accepted that tears involving >50% of the supraspinatus warrant surgical intervention. It is controversial whether completion of partial tears should be performed to mobilize the tendon for a better repair as this technique may portend a negative outcome in the throwing shoulder via unintended alterations in biomechanics [104]. It is clear, however, that isolated debridement is not an adequate treatment for overhead athletes with internal impingement associated with concomitant pathology such as anterior glenohumeral translation, posterior labral tears, and PASTA lesions [104, 105]. These studies reported poor results with low rates of return to the patient’s pre-injury level of throwing. Historical data suggests nonoperative management as a viable option in virtually all patients with SLAP tears; however, the superior labrum must always be assessed and adequately addressed surgically if symptoms persist. Burkhart et  al. [66]

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reported that 87% of throwers successfully returned to their pre-injury level of play for more than two seasons following repair. Multiple studies have supported these findings with suggestion of operative management of anterior laxity associated with internal impingement [58, 106]. Jobe retrospectively evaluated 25 overhead athletes treated with anterior stabilization and reported >90% good-to-excellent results. Corroborating these findings, an additional study reported on the utilization of open capsulolabral reconstruction with >95% good-to-excellent outcomes and 80% of overhead athletes successfully returning to their pre-level of competition [107]. However, these studies addressed anterior laxity via an open reconstruction which may result in decreased ROM secondary to capsular contracture, scarring, and overall morbidity. As such, Altchek and Dines [108] developed a less invasive technique whereby a horizontal incision is made in the anterior capsule and subsequently plicated with the goal of retaining pre-procedure ROM. This has become our preferred operative technique and follows a standard rehabilitation program for anterior instability surgery, with ROM and light strengthening pursued between weeks 2 and 12 postoperatively, followed by aggressive weight-based strengthening between 3 and 4 months, with initiation of a throwing program at 4 months and clearance to return to high velocity throws around 5–6 months postoperatively.

Prevention Although patients with LLS or internal impingement respond well to conservative management, coaches, trainers, and parents should focus ardently on methods of prevention in young throwers to impede this pathologic process. Important tenants of prevention programs should include education, rapid identification of high-risk athletes, adequate rehabilitation of current and past injuries, and close monitoring for signs of overuse. Preseason screening is an important tool in the identification of at-risk athletes through attainment of an adequate patient history and thorough physical examination consisting of shoulder ROM and strength as well as lower extremity and core function [109]. The development of proper pitching mechanics and a focus on pitch type, count, and frequency are key components in the concept of safe throwing practices. Fleisig et al. [110] closely evaluated the biomechanics of throwing in youth, high school, collegiate, and professional pitchers and found that proper throwing mechanics can be learned at a young age. Dun et al. [111] evaluated the biomechanics of youth pitchers during delivery of the fastball, curveball, and changeup. The authors report that the curveball may not be more harmful than the fastball as they found internal rotation torque, varus elbow torque, and proximal force to be significantly less during delivery of the curve. Several studies have also suggested that high pitch counts, frequency, and pitch velocity may be the single greatest contributor to the development of shoulder and elbow pathology in the young thrower [112, 113]. As such, pitch count recommendations have been proposed for youth athletes, carefully taking into account pitch volume per game with correlation to frequency of mound appearances (Table  3.2). Furthermore, the

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Table 3.2  MLB and USA Baseball Pitch Smart guidelines Age 7–8 9–10 11–12 13–14 15–16 17–18 19–22

Daily max (pitches per game) 50 75 85 95 95 105 120

Required rest (pitches) 0 days 1 day 2 days 1–20 21–35 36–50 1–20 21–35 36–50 1–20 21–35 36–50 1–20 21–35 36–50 1–30 31–45 46–60 1–30 31–45 46–60 1–30 31–45 46–60

3 days N/A 51–65 51–65 51–65 61–75 61–80 61–80

4 days N/A 66+ 66+ 66+ 76+ 81+ 81–105

5 days N/A N/A N/A N/A N/A N/A 106+

N/A not applicable http://m.mlb.com/pitchsmart/pitching-guidelines/

National Athletic Trainers’ Association, supported by several studies, recommends avoidance of year-round participation in overhead throwing to allow for adequate rest to decrease risk of injury [114, 115]. Petty et al. [116] recommend careful consideration of the following safeguards to reduce the incidence of youth throwing injuries: breaking pitches should not be thrown in competition until the athlete has reached puberty, young throwers should focus on the development of proper throwing mechanics, no pitcher should be allowed back on the mound in the same game from which they have already been previously removed (one mound appearance per game), and pitchers should only pitch in one league at a time with at least 3 months of arm rest per year. Close monitoring, early recognition, and disciplined adherence to preventive protocols will help to reduce the development of overuse throwing injuries in young athletes. In addition, appropriately supervised interval throwing programs are invaluable in helping young athletes regain proper motion, strength and mechanics for optimal return to play post-injury while simultaneously minimizing the risk of reinjury.

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101. Reuther KE, Larsen R, Kuhn PD, Kelly JD 4th, Thomas SJ. Sleeper stretch accelerates recovery of glenohumeral internal rotation after pitching. J Shoulder Elb Surg. 2016;25(12):1925–9. 102. Laudner KG, Sipes RC, Wilson JT. The acute effects of sleeper stretches on shoulder range of motion. J Athl Train. 2008;43(4):359–63. 103. Yamanaka K, Matsumoto T.  The joint side tear of the rotator cuff. A followup study by arthrography. Clin Orthop Relat Res. 1994;304:68–73. 104. Payne LZ, Altchek DW. The surgical treatment of anterior shoulder instability. Clin Sports Med. 1995;14:863–83. 105. Meister K, Andrews JR, Batts J, Wilk K, Baumgarten T. Symptomatic thrower’s exostosis. Arthroscopic evaluation and treatment. Am J Sports Med. 1999;27:133–6. 106. Andrews JR, Dugas JR. Diagnosis and treatment of shoulder injuries in the throwing athlete: the role of thermal-assisted capsular shrinkage. Instr Course Lect. 2001;50:17–21. 107. Montgomery WH 3rd, Jobe FW. Functional outcomes in athletes after modified anterior capsulolabral reconstruction. Am J Sports Med. 1994;22:352–8. 108. Altchek DW, Dines DM. Shoulder injuries in the throwing athlete. J Am Acad Orthop Surg. 1995;3:159–65. 109. Shanley E, Thigpen C. Throwing injuries in the adolescent athlete. Int J Sports Phys Ther. 2013;8(5):630–40. 110. Fleisig GS, Barrentine SW, Zheng N, Escamilla RF, Andrews JR.  Kinematic and kinetic comparison of baseball pitching among various levels of development. J Biomech. 1999;32:1371–5. 111. Dun S, Loftice J, Fleisig GS, Kingsley D, Andrews JR. A biomechanical comparison of youth baseball pitches: is the curveball harmful? Am J Sports Med. 2008;36:686–92. 112. Lyman S, Fleisig GS, Andrews JR, Osinski ED. Effect of pitch type, pitch count, and pitching mechanics on risk of elbow and shoulder pain in youth baseball pitchers. Am J Sports Med. 2002;30(4):463–8. 113. Lyman S, Fleisig GS, Waterbor JW, et al. Longitudinal study of elbow and shoulder pain in youth baseball pitchers. Med Sci Sports Exerc. 2001;33(11):1803–10. 114. Valovich McLeod TC, Decoster LC, Loud KJ, Micheli LJ, Parker JT, Sandrey MA, et  al. National Athletic Trainers’ Association position statement: prevention of pediatric overuse injuries. J Athl Train. 2011;46(2):206–20. 115. Olsen IISJ, Fleisig GS, Dun S, Loftice J, JR A. Risk factors for shoulder and elbow injuries in adolescent baseball pitchers. Am J Sports Med. 2006;34(6):905–12. 116. Petty DH, Andrews JR, Fleisig GS, Cain EL.  Ulnar collateral ligament reconstruction in high school baseball players: clinical results and injury risk factors. Am J Sports Med. 2004;32(5):1158–64.

Chapter 4

Swimmer’s Shoulder Alton W. Skaggs and Brian M. Haus

Introduction With the unique ability to circumduct, the shoulder achieves the greatest range of motion of any joint in the human body. In contrast with other overhead throwing athletes, where force generation is shared both by the lower and upper limbs, this action is of critical importance to the competitive swimmer where circumduction of the upper limb provides 90% of the force required for water propulsion [1]. This increased range of motion, however, comes at a cost; the shoulder is also inherently unstable and prone to various chronic and acute injuries. Shoulder pathology in the competitive swimmer can be devastating and potentially career-ending [2]. From the recreational to the world-class Olympian, shoulder pain in swimmers is widely prevalent across all levels of expertise [3]. The so-called swimmer’s shoulder is an umbrella term used to describe a collection of pathologies caused by forceful, repetitive shoulder motions in avid swimmers. It is said that swimmers at elite levels may accumulate up to one million strokes per arm over the course of a year [4]. While morbidities in several joint systems are also prevalent among competitive swimmers, including pathology of the spine, elbow, and knee, given this remarkably heavy workload, it is no surprise that the shoulder is the most commonly injured joint among competitive swimmers [5].

A. W. Skaggs School of Medicine, University of California, Davis, Sacramento, CA, USA B. M. Haus (*) Department of Orthopedic Surgery, University of California, Davis Medical Center, Sacramento, CA, USA e-mail: [email protected] © Springer International Publishing AG, part of Springer Nature 2019 A. S. Bauer, D. S. Bae (eds.), Upper Extremity Injuries in Young Athletes, Contemporary Pediatric and Adolescent Sports Medicine, https://doi.org/10.1007/978-3-319-56651-1_4

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Definition The “swimmer’s shoulder” described by Kennedy and Hawkins in 1978 originally described the patient with supraspinatus impingement syndrome presenting with pain in the subacromial space [6]. Swimmer’s shoulder has since been expanded to encompass a spectrum of specific shoulder pathologies commonly incurred by competitive swimmers from overuse and fatigue. This may include pain from impingement, rotator cuff tendinopathy, labral pathology, suprascapular nerve entrapment, or any combination thereof [7]. These conditions are often caused or accompanied by structural abnormalities surrounding the glenohumeral joint, which may include scapular dyskinesis, glenohumeral hyperlaxity, instability leading to excess subluxation, glenohumeral internal rotation deficit (GIRD), or muscle strength imbalances. Regardless of the specific pathology, pain associated with swimmer’s shoulder can often be attributed to microtraumas from overuse, fatigue, and/or poor stroke mechanics. However, due to this considerable variance in etiology, the usefulness of the term “swimmer’s shoulder” in modern diagnosis is limited. It is imperative that the clinician correctly identify the cause of shoulder pathology in order to effectively manage symptoms while preventing unnecessary surgical intervention.

Epidemiology The shoulder is the most commonly injured joint in the swimming athlete. A study conducted by the University of Iowa in 2009 found that among Division I collegiate swimmers, the shoulder/upper arm accounted for 31% and 36% of all injuries in both male and female swimmers, respectively. Among injuries in swimmers, those of the shoulder are also the most likely to result in significant missed time [5]. Pain is most commonly reported in the anterior-superior region (44%), followed by the anterior-inferior (14%), posterosuperior (10%), and posteroinferior (4%). Diffuse pain occurs in 26% of athletes, although this is likely a result of broad inflammation and pathological progression [8]. The earliest epidemiological study, performed in 1978, found that of 2496 competitive swimmers in Canada, only 3% reported notable shoulder pain associated with training and competition [6]. More current literature suggests that this prevalence has risen dramatically over the past four decades, likely due to the increased training demand associated with organized swimming and increased intensity of competition. A large and more recent survey conducted in competitive swimmers found that shoulder pain was widely prevalent across age groups and skill level, with 47% of 13–14-year-olds and 66% of 15–16-year-olds reporting a history of interfering shoulder pain [3]. The risk of shoulder pain may be even more pronounced in elite swimmers, where training regimens are most demanding. A recent survey of 80 elite swimmers indicated unilateral or bilateral shoulder pain at a prevalence of 91% and 37%, respectively. Seventy percent of participants described pain in overhead movements, 68% complained of shoulder stiffness, and 28% reported pain while sleeping [9].

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Risk Factors Despite decades of research, the risk factors for chronic shoulder pain in swimmers remains somewhat unclear. A 2015 systematic literature review conducted by Hill et al. sought to investigate several perceived risk factors. However, due to limited available pooled data and poor study methodology, no risk factors with high level of certainty were identified. Risk factors found to have moderate certainty were clinical joint laxity and instability, GIRD, history of shoulder pain or injury, and competition level. In addition, years of experience, training load and intensity, female gender, age, scapular dyskinesia, and glenohumeral subluxation were classified as risk factors with a low level of certainty [10]. The development of shoulder pain in swimmers therefore appears to be a multifactorial process. A genetic predisposition has been suggested, although no studies have been conducted to date [10]. However, it has been proposed that individuals with shorter arm spans, which require a greater quantity of strokes, may be more prone to injuries of overuse [11]. What is clear is that microtrauma from fatigue and overuse is the primary cause of the symptoms associated with swimmer’s shoulder. To remain competitive, elite-level swimmers log up to 10,000–14,000 m per day, which equates to over 16,000 shoulder revolutions per arm over a single week [8]. Because swimming is a sport of endurance, periods of prolonged rest in training are particularly detrimental to one’s strength and performance [2]. Also, unlike athletes in most other sports, elite-level swimmers often train upward of 11  months in a given year, leaving little to no time for recovery and rehabilitation [3]. Aggressive training methods also increase the risk of shoulder pain in swimmers. McMaster’s 1993 survey reported that the use of hand paddles and kickboards and weight training and buddy stretching techniques were more likely to aggravate shoulder complaints in national-level swimmers with existing shoulder pain [3].

Etiology of Swimmer’s Shoulder Glenohumeral Internal Rotation Deficit Similar to other overhead athletes, including pitchers, tennis, water polo, and volleyball players, swimmers can develop adaptational changes in shoulder range of motion and subsequently acquire glenohumeral internal rotation deficiency (GIRD). GIRD is the result of recurrent and excessive external rotation during swimming, which causes a tightened posteroinferior capsule and leads to reduced internal rotation at the shoulder. When compared to nonswimmers, patients with GIRD average an extra 10° of external rotation with 40° less in internal rotation [7]. That is, GIRD is not simply a resetting of the arc of motion, but also a loss of total amount of shoulder rotation. This deficiency is typically more pronounced on the swimmer’s dominant side where they tend to breathe, which disproportionately increases body roll and causes excess unilateral strain [7]. The development of GIRD is thought to arise from thickening and contracture of the posteroinferior capsule in response to the demands of heavy training regimens and stretching techniques [12].

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Fig. 4.1  Glenohumeral internal rotation deficit (GIRD). Due to posterior shoulder capsular tightness, patients may have glenohumeral internal rotation deficit (GIRD). GIRD is diagnosed on physical examination where an affected shoulder (left in this patient) has decreased internal rotation relative to the opposite shoulder when it is placed at 90° of abduction

GIRD has been implicated in the development of shoulder pain in swimmers, particularly internal impingement syndrome and labral pathology [13]. A recent prospective 12-month cohort study of competitive swimmers who trained at least 5 days per week found that increased external rotation ROM is positively associated with shoulder injury and significant interfering pain, after adjusting for kilometers swam [14]. In addition, a 2005 cross-sectional study found that internal rotation was significantly reduced in swimmers aged 8–11 with shoulder pain when compared to swimmers with no pain [15]. GIRD is diagnosed by physical examination, where the patient’s shoulder is placed at 90° of abduction and then the shoulder is internally rotated. If there is a significant decrease in internal rotation, especially in the setting of the ability to excessively external rotate, the patient may have GIRD. If the problem is unilateral, then one can compare sides to demonstrate the differences in internal rotation (Fig. 4.1).

Glenohumeral Hyperlaxity Glenohumeral hyperlaxity,common among competitive swimmers, plays a key role in the development of swimmer’s shoulder. Shoulder laxity exists on a spectrum, from physiologic to major pathologic issues leading to frequent dislocation. Glenohumeral laxity occurs in both symptomatic and asymptomatic swimmers [16, 17]. The stability

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of the glenohumeral joint is provided both by static stabilizers (glenoid labrum and capsular ligaments) and dynamic stabilizers (muscles of the rotator cuff). Repetitive overuse from intense swim training leads to progressive attenuation of the static stabilizers, leading to glenohumeral joint hyperlaxity [7]. Some competitive swimmers perform the practice of “buddy stretching,” which is also believed to contribute to the development of hyperlaxity. “Buddy stretching” is a technique used in competitive swimming where another athlete or coach helps to forcefully extend and externally rotate another athletes shoulder in order to “stretch it out” before a competition [18]. Improper technique during weight training can also contribute to hyperlaxity. Excessive shoulder laxity is likely advantageous to the competitive swimmer, allowing for greater stroke length and improved body positioning with reduced drag—translating to greater overall speed [19]. The tendency for hyperlaxity in experienced swimmers may be more pronounced due to self-selection, given the intrinsic benefit to one’s swimming ability [20]. Despite the supposed positive effects of hyperlaxity, deficits in labral and capsular support must be compensated by the dynamic stabilizers of the rotator cuff. When subjected to fatigue and overuse during heavy training, the swimmer is liable to experience excessive subluxation, increasing risk for labral tears, subacromial impingement, and/or rotator cuff tendonitis [18]. Suspected shoulder laxity is diagnosed with clinical examination, which can be assessed by the apprehension (Fig. 4.2) and the relocation and/or load and shift tests (Fig. 4.3). The apprehension test is performed to test anterior shoulder instability Fig. 4.2  Apprehension test. The apprehension test is performed to test anterior shoulder instability due to ligamentous laxity or labral tears. The maneuver may cause the sensation of anterior shoulder subluxation. A positive test occurs when the patient experiences pain or apprehension when the shoulder is maximally externally rotated with the arm abducted to 90°. The maneuver may cause the sensation of anterior shoulder subluxation

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Fig. 4.3 Relocation/load and shift test for shoulder laxity/instability. The relocation and/or load and shift test is performed by placing the examiner’s fingers around the anterior and posterior aspect of the humeral head and then forcing it anteriorly or posteriorly to emulate laxity or instability. A positive test occurs when the humeral head can be felt subluxating out of the glenoid

due to ligamentous laxity or labral tears. The maneuver may cause the sensation of anterior shoulder subluxation. A positive test occurs when the patient experiences pain or apprehension when the shoulder is maximally externally rotated with the arm abducted to 90°. The maneuver may cause the sensation of anterior shoulder subluxation. The relocation and/or load and shift test is performed by placing the examiner’s fingers around the anterior and posterior aspect of the humeral head and then forcing it anteriorly or posteriorly to emulate laxity or instability. A positive test occurs when the humeral head can be felt subluxating out of the glenoid.

Scapular Dyskinesis Heavy training and overuse can also lead to another problem with swimmers: scapular dyskinesis. The term “SICK scapula” (scapular malposition, inferior medial border prominence, coracoid pain and malposition, dyskinesis of scapular motion) describes the loss of normal dynamic motion of the scapula due to muscular weakness in swimmers and other overhead athletes. Likely caused by overuse and poor

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Fig. 4.4  Scapular dyskinesis. In swimmers, scapular dyskinesis typically presents unilaterally and is characterized by an overtly protracted, abducted, and laterally positioned scapula due to muscular imbalance [13]. (Reprinted by permission from Springer Nature: Park and Hwang [39])

swimming technique, relative weakness and imbalance develops in the serratus anterior and lower latissimus muscles. When combined with a compensatory tight pectoralis muscle, abnormal motion develops in the scapula with motion [21]. In swimmers, scapular dyskinesis typically presents unilaterally and is characterized by an overtly protracted, abducted, and laterally positioned scapula (Fig. 4.4) [13]. In addition, excessive thoracic kyphosis also occurs in swimmers, which may lead to further apparent protraction of the scapula [22]. Excessive scapular protraction and dyskinesia increase stress on the anterior capsule and labral structures, impairing proper joint kinetics and contributing to injury [7]. Dyskinesis can also increase the risk of suprascapular neuropathy. While uncommon, entrapment of the suprascapular nerve within the suprascapular notch can cause dull pain and paresis and should be included on the differential when significant weakness or posterior shoulder pain is present [7]. Swimmers with scapular dyskinesis complain of pain and tenderness around the scapula with overhead motion, asymmetric posture, scapular snapping, or weakness. It can be diagnosed by examining either static or dynamic examination of the scapula. When examined from behind with the shoulder at rest, scapular dyskinesis

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can be detected when there is a prominence of the inferomedial border of the scapula. With dynamic motion, the scapula may wing with the inferomedial border of the scapula moving lower and protracted relative to the normal shoulder. There may also be pain with forward elevation and crepitus along the medial border with abduction and flexion. A topographic analysis of spinal and scapular deformity found that 64% of swimmers with shoulder instability and 100% of those with impingement syndrome exhibited significant dyskinesis, compared with 14% in pain-free swimmers [23]. While it is clear that these structural abnormalities are associated with the symptoms of swimmer’s shoulder, the role of dyskinesis as a causative factor or merely an adaptation to pain and underlying shoulder pathology has not been well defined [24]. Regardless, assessment of dyskinesis should play a key role in the management of swimmer’s shoulder.

Muscle Imbalances Range of motion deficiencies are often also accompanied by muscle strength imbalances because the muscles of the rotator cuff are not equally utilized while swimming. The teres minor and infraspinatus are generally weak in comparison to other muscles important in generating propulsion such as the supraspinatus, subscapularis pectoralis minor, deltoid, trapezius, and serratus anterior [20]. Such muscle imbalances may also contribute to increased shoulder laxity in swimmers. A study conducted by McMaster has shown that swimmers exhibit statistically significant increases in adduction, abduction, and internal rotation strength when compared to nonswimmers. However, no significant difference was found in external rotation strength [25]. Competitive swimmers have also been shown to possess increased adduction-to-abduction strength ratios. These unique strength characteristics likely arise from adaptations required for elite swimming but also may increase the risk of shoulder laxity, scapular dyskinesis, capsular strain, and subacromial impingement.

Labral Pathology The development of GIRD, muscle imbalances, scapular dyskinesia, and shoulder hyperlaxity is thought to predispose the competitive swimmer to labral tears. Swimmers suffering from labral pathology will often present with localized anterior shoulder pain accompanied by an audible click with circumduction of the shoulder. Common arthroscopic findings in swimmers include a torn labrum or anterior to posterosuperior labral (SLAP) tears [2]. SLAP tears are common among elite swimmers. One recent cross-sectional study found that of the 52 asymptomatic volunteer swimmers who underwent a voluntary MRI, 10 had an existing labral tear with SLAP tears being the most common (80%).

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While the specific pathophysiology of SLAP tears in swimmers has been a subject of debate, the mechanism of injury appears to be from repeated, forceful abduction and external rotation, leading to increased strain of the labral insertion [26]. Perhaps the most commonly accepted hypothesis regarding the etiology of SLAP tears in swimmers is similar in mechanism to the development of SLAP tears in baseball pitchers. The pathologic cascade of SLAP tears in overhead athletes is believed to first arise due to a tightened posteroinferior capsule due to thickening and contracture of the capsule in response to increased load. This posterior tightness leads to a hyperextensibility of the humeral head—a physiologic adaptation due to new rotational set point. Increased humeral extension increases the strain upon the biceps tendon anchor and the posterosuperior labral attachments, leading to a type 2 SLAP lesion [27]. As discussed previously, swimmers exhibit increased capsular laxity resulting in anterior subluxation of the glenohumeral joint. Subluxation in conjunction with hyperextensibility may exhibit synergistic effects, causing strain and lesions to labral attachments and increasing risk for SLAP-type tears.

Subacromial and Internal Impingement “Subacromial impingement syndrome,” first described by Neer in 1972, is perhaps the most traditionally thought-of etiology in the development of swimmer’s shoulder. Recently however, the ubiquity of subacromial impingement as a cause of interfering shoulder pain has been called into question [13]. Subacromial impingement occurs when the supraspinatus tendon, the bicipital tendon, or the subacromial bursa becomes inflamed in the space between the greater tuberosity and the inferior surface of the acromion [12]. Patients with subacromial impingement present with anterolateral pain commonly elicited with forward flexion and internal rotation [1]. This can be assessed clinically using the Neer and Hawkins tests (Figs. 4.5 and 4.6) [22]. The measured distance of the subacromial space generally lies between 5 and 10  mm [28]. Any pathologic narrowing of this space will increase the risk for impingement. Much like other causes of swimmer’s shoulder, this often is a multifactorial process which can involve shoulder hyperlaxity, chronic muscle fatigue, tendinous hypertrophy, formation of subacromial osteophytes, or a congenitally flattened acromial arch [20]. Increased glenohumeral laxity is also thought to increase the anterior translational capacity of the humeral head during overhead motion thus narrowing this space [20]. Additionally, muscle fatigue, particularly that of the serratus anterior, can contribute to subacromial impingement. The serratus anterior is of critical importance during the pull-through in generating propulsion. It also assists the scapula in upward rotation and protraction which maintains space to prevent impingement. Hence, overuse and fatigue can lead to impingement with associated shoulder pathology [12]. Finally, a shortened pectoralis minor leads to reduced posterior scapular tilt and reduction of subacromial space and has been suspected as an additional source of impingement [15].

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Fig. 4.5 Hawkins impingement test. The patient’s humerus is internally rotated with the shoulder at 90° of forward flexion and 90° of elbow flexion. A positive test is reproduction of pain

Fig. 4.6  Neer impingement test. The patient’s arm is forward flexed to 90° and the humerus is internally rotated (thumb facing down). The scapular border is stabilized to prevent rotation. A test is considered positive if the patient has pain with resisted forward flexion

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Fig. 4.7  Internal impingement. Internal impingement of the posterosuperior glenoid rim occurs due to excessive external rotation in abduction, causing degeneration and tears of the undersurface of the supraspinatus tendon, as well as labral tears. (From Walch et al. [30]:243, Fig. 5a. Reprinted with permission)

“Internal impingement” has also been described as a cause of shoulder pain in overhead athletes. In contrast with subacromial impingement, patients with internal impingement will present with posterior shoulder pain elicited during the recovery phase when the shoulder is maximally abducted and externally rotated [13]. This condition is often accompanied by posterior capsular tightness and involves pathologic contact of the posterosuperior glenoid rim with the articular surface of the supraspinatus or infraspinatus tendons wedged against the greater tubercle. Much like subacromial impingement, microtraumas from the repetitive contact of these structures can also result in tendinopathies and labral damage (Fig. 4.7) [29, 30].

Rotator Cuff Tendinopathies Tendinopathies most commonly involving the supraspinatus tendon are associated with chronic painful shoulder in swimmers. Much like etiologies discussed previously, tendinopathies arise due to microtraumas and overuse often in conjunction with glenohumeral hyperlaxity or impinging structures. Rotator cuff pathology is classically defined as a series of three progressive phases: acute tendinitis, followed by tendinosis with partial tears, and finally full-thickness ruptures—the latter being uncommon in swimmers [31]. While its title implies inflammation, histological analysis of rotator cuff tendinitis often shows little to no inflammatory cell infiltrates. Instead, rotator cuff pathology is characterized by apoptotic degeneration of structures caused by factors of extrinsic and intrinsic origin. Extrinsic factors include impingement or shear forces due to subacromial spurring or altered scapulohumeral kinematics. Intrinsic factors relate to degeneration caused by overuse, genetic predisposition, and normal aging [31]. Lesions of the rotator cuff appear to be quite common in swimmers. A cross-­ sectional study of competitive swimmers who underwent diagnostic MRI found that

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69% showed evidence of supraspinatus tendinopathy. Moreover, the incidence of tendinopathies in swimmers increased with skill level and training rigor. One hundred percent of those at the international level exhibited some level of tendinopathy compared with 89% at the national, 40% at the state level, and 0% at the club level. Supraspinatus hypertrophy was also observed in 27% of participant [9].

Prevention It is critical that training intensity, frequency, duration, and existence of pain are closely monitored in order to limit microtraumas and allow for proper recovery and rehabilitation. Swim coaches thus play a key role in the prevention of shoulder pathology in swimmers. Additionally, education of proper stroke mechanics, stretching techniques, and dry-land strength training is essential. Excessive training without stretching and cross-training causes hypertrophy and muscle shortening, particularly that of the pectoralis minor, which can lead to impingement and scapular dyskinesis. Stretching is essential in maintaining adequate muscle length and range of motion for proper stroke mechanics. Buddy stretching with an inexperienced partner, however, can increase stress in capsular structures and contribute to pathologic laxity [3]. As mentioned previously, the use of props in training, particularly hand paddles, can also aggravate shoulder pain and contribute to overuse injuries [3]. Additionally, muscle imbalances can be avoided with proper dry-land weight training exercises. Naturally, muscles involved in the pull-through phase when propulsion occurs require increased strength and are often the subject of focus in weight training. Failure to strengthen the opposing external rotators and abductors can lead to pathological muscle imbalances with associated shoulder pathology.

Management Nonsurgical The mainstay of treatment for swimmer’s shoulder is non-operative. Reduction in training, load, and periods of rest should be a part of any management plan. Ice, electrical stimulation (TENS), and cryotherapy can also be helpful in controlling inflammation [32]. Bak describes three phases of the non-operative management s of swimmer’s shoulder [22]. Phase I pertains to patients in early stages, with pain only present during swimming. Early stages of pathology should be managed conservatively, with an emphasis on reduced training, stroke correction, and proper stretching techniques, in addition to the preliminary assessment of GIRD, shoulder laxity, and scapular dyskinesis. The “sleeper stretch” and “roll-over sleeper stretch” are par-

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Fig. 4.8  Sleeper stretch. The sleeper stretch is performed to decrease posterior capsular tightness in patients with glenohumeral internal rotation deficit (GIRD). The stretch is performed while laying down on the affected shoulder with the elbow bent to 90°. The wrist of the affected arm is then pushed by the contralateral arm in internal rotation to stretch the posterior capsule

ticularly important in swimmers with reduced internal rotation deficiency caused by posterior capsule tightness (Fig. 4.8). Burkhart estimates that 90% of swimmers and baseball pitchers with symptomatic GIRD can reduce rotational impairments to acceptable levels with a 2–4-week course of posterior capsule stretching [27]. Phase II of management pertains to patients who have developed daily pain, present both in and out of the pool. Ice, stretching, and physical therapy are continued, although more restrictions are necessary at this stage of pathology. Swimmers should complete rest for 2-week periods in addition to 1-week courses of nonsteroidal anti-inflammatory medications. Corticosteroid injections may also be used [22]. However, the use of these modalities for the temporary relief of pain and inflammation should be used with caution, as overutilization can lead to atrophy and reduced healing capacity in addition to other systemic side effects [33]. In addition to physical therapy, patients with confirmed rotator cuff tendinopathies may undergo ultrasound-guided platelet-rich plasma (PRP) injections. This minimally invasive procedure is becoming increasingly more popular as alternatives to surgery. PRP involves injections of autologous plasma enriched with platelets and growth factors and has been shown to improve the healing capacity of vascularly deficient tissues including tendon, ligament, and bone [34]. Preliminary studies of these methods in individuals with shoulder pathology have been promising [35, 36]. However, focused studies pertaining to competitive swimmers have yet to be accomplished. According to Bak, swimmers with persistent pain that does not respond to conservative treatment efforts are classified under phase III and recommended to abstain from swimming for a period of no less than 3 months. If symptoms persist, surgery may be warranted [22].

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Surgical Patients who fail conservative treatment may be candidates for surgery. However, decisions for surgery must be made cautiously, as outcomes and return rates in competitive swimmers are suboptimal. A 2007 survey of competitive swimmers with various shoulder pathologies who opted for surgical treatment reported only a 56% return rate to preinjury level, with a mean recovery period of 4 months [2]. Still, proper diagnosis and directed surgical treatment can be highly beneficial in certain athletes with advanced symptoms of swimmer’s shoulder. Patients with apparent structural damage upon imaging, including labral tears, tendinous rupture, or suprascapular nerve entrapment, should undergo arthroscopy directed toward specific pathology. Instability and subluxation can be addressed with capsular plication or capsular shift procedures with labral repair. Swimmers with instability appear to have the most promising outcomes. There is an over 90% success rate in athletes who ­underwent capsular shift for multidirectional instability in regard to relief of pain and return to swimming [37]. Surgical treatment for impingement aims to increase the subacromial space and can include bursectomy, subacromial decompression, distal clavicle resection, and most commonly coracoacromial ligament release. Albertsson reported an 82% return to preinjury levels in overhead athletes with impingement after coracoacromial ligament release, though only 9/25 included were competitive swimmers [38]. For most operative procedures, the patients are placed in a sling for 6 weeks, and then passive range of motion and strengthening is initiated. Swimmers are taken out of swimming for 6 months after surgery to allow proper healing and progressive strengthening.

Conclusion The shoulder is the most common area of pain in the competitive swimmer. While its diagnostic value is limited, the term “swimmer’s shoulder” is commonly used clinically to describe chronic shoulder pain in swimmers. The etiology of this pain varies by individual and can include any combination of glenohumeral laxity and instability, GIRD, scapular dyskinesis, subacromial and internal impingement, labral tears, scapular nerve entrapment, and rotator cuff tendinopathies, among others. These etiologies appear however to have a common source, each arising from overuse along with improper stroke mechanics and stretching techniques. It is critical then that both coaches and clinicians are educated in the pathophysiology of swimmer’s shoulder, as early detection, monitoring of training intensity, and correction of improper mechanics can be successful, sparing the need for surgical procedures of often uncertain consequence.

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References 1. Wanivenhaus F, Fox AJS, Chaudhury S, Rodeo SA. Epidemiology of injuries and prevention strategies in competitive swimmers. Sports Health. 2012;4(3):246–51. 2. Brushøj C, Bak K, Johannsen H, Faunø P. Swimmers’ painful shoulder arthroscopic findings and return rate to sports. Scand J Med Sci Sports. 2007;17(4):373–7. 3. McMaster WC, Troup J. A survey of interfering shoulder pain in United States competitive swimmers. Am J Sports Med. 1993;21(1):67–70. 4. Richardson AB, Jobe FW, Collins HR. The shoulder in competitive swimming. Am J Sports Med. 1980;8(3):159–63. 5. Wolf BR, Ebinger AE, Lawler MP, Britton CL. Injury patterns in Division I collegiate swimming. Am J Sports Med. 2009;37(10):2037–42. 6. Kennedy JC, Hawkins R, Krissoff WB. Orthopaedic manifestations of swimming. Am J Sports Med. 1978;6(6):309–22. 7. Matzkin E, Suslavich K, Wes D.  Swimmer’s shoulder: painful shoulder in the competitive swimmer. J Am Acad Orthop Surg. 2016;24(8):527–36. 8. Pink MM, Tibone JE. The painful shoulder in the swimming athlete. Orthop Clin North Am. 2000;31(2):247–61. 9. Sein ML, Walton J, Linklater J, Appleyard R, Kirkbride B, Kuah D, et al. Shoulder pain in elite swimmers: primarily due to swim-volume-induced supraspinatus tendinopathy. Br J Sports Med. 2010;44(2):105–13. 10. Hill L, Collins M, Posthumus M. Risk factors for shoulder pain and injury in swimmers: a critical systematic review. Phys Sportsmed. 2015;43(4):412–20. 11. Bak K, Fauno P. Clinical findings in competitive swimmers with shoulder pain. Am J Sports Med. 1997;25(2):254–60. 12. Tovin BJ.  Prevention and treatment of swimmer’s shoulder. N Am J Sports Phys Ther. 2006;1(4):166–75. 13. Johnston TR, Abrams GD. Shoulder injuries and conditions in swimmers. In: Miller TL, editor. Endurance sports medicine: a clinical guide. Cham: Springer International Publishing; 2016. p. 127–38. 14. Walker H, Gabbe B, Wajswelner H, Blanch P, Bennell K.  Shoulder pain in swimmers: a 12-month prospective cohort study of incidence and risk factors. Phys Ther Sport. 2012;13(4):243–9. 15. Tate A, Turner GN, Knab SE, Jorgensen C, Strittmatter A, Michener LA. Risk factors associated with shoulder pain and disability across the lifespan of competitive swimmers. J Athl Train. 2012;47(2):149–58. 16. Zemek MJ, Magee DJ.  Comparison of glenohumeral joint laxity in elite and recreational swimmers. Clin J Sport Med. 1996;6(1):40–7. 17. Tibone JE, Lee TQ, Csintalan RP, Dettling J, McMahon PJ. Quantitative assessment of glenohumeral translation. Clin Orthop Relat Res. 2002;400:93–7. 18. McMaster WC, Roberts A, Stoddard TA. Correlation between shoulder laxity and interfering pain in competitive swimmers. Am J Sports Med. 1998;26(1):83–6. 19. Weldon EJ 3rd, Richardson AB. Upper extremity overuse injuries in swimming. A discussion of swimmer’s shoulder. Clin Sports Med. 2001;20(3):423–38. 20. McMaster WC. Shoulder injuries in competitive swimmers. Clin Sports Med. 1999;18(2):349– 59, vii. 21. Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology part III: the SICK scapula, scapular dyskinesis, the kinetic chain, and rehabilitation. Arthroscopy. 2003;19(6):641–61. 22. Bak K.  The practical management of swimmer’s painful shoulder: etiology, diagnosis, and treatment. Clin J Sport Med. 2010;20(5):386–90.

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23. Warner JJ, Micheli LJ, Arslanian LE, Kennedy J, Kennedy R. Scapulothoracic motion in normal shoulders and shoulders with glenohumeral instability and impingement syndrome. A study using Moire topographic analysis. Clin Orthop Relat Res. 1992;285:191–9. 24. Struyf F, Tate A, Kuppens K, Feijen S, Michener LA. Musculoskeletal dysfunctions associated with swimmers’ shoulder. Br J Sports Med. 2017;51:775–80. 25. McMaster WC, Long SC, Caiozzo VJ. Shoulder torque changes in the swimming athlete. Am J Sports Med. 1992;20(3):323–7. 26. Funk L, Monga P.  SLAP lesions part II: acute lesion versus chronic lesion resulting from repetitive motion (or microtrauma). In: Park J-Y, editor. Sports injuries to the shoulder and elbow. Berlin/Heidelberg: Springer Berlin Heidelberg; 2015. p. 109–16. 27. Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology part I: pathoanatomy and biomechanics. Arthroscopy. 2003;19(4):404–20. 28. Flatow EL, Soslowsky LJ, Ticker JB, Pawluk RJ, Hepler M, Ark J, et  al. Excursion of the rotator cuff under the acromion. Patterns of subacromial contact. Am J Sports Med. 1994;22(6):779–88. 29. Giaroli EL, Major NM, Higgins LD. MRI of internal impingement of the shoulder. AJR Am J Roentgenol. 2005;185(4):925–9. 30. Walch G, Boileau P, Noel E, Donell ST. Impingement of the deep surface of the supraspinatus tendon on the posterosuperior glenoid rim: an arthroscopic study. J Shoulder Elb Surg. 1992;1(5):238–45. 31. Seitz AL, McClure PW, Finucane S, Boardman ND 3rd, Michener LA. Mechanisms of rotator cuff tendinopathy: intrinsic, extrinsic, or both? Clin Biomech (Bristol, Avon). 2011;26(1):1–12. 32. Escamilla RF, Hooks TR, Wilk KE. Optimal management of shoulder impingement syndrome. Open Access J Sports Med. 2014;5:13–24. 33. Kennedy JC, Willis RB. The effects of local steroid injections on tendons: a biomechanical and microscopic correlative study. Am J Sports Med. 1976;4(1):11–21. 34. Foster TE, Puskas BL, Mandelbaum BR, Gerhardt MB, Rodeo SA. Platelet-rich plasma: from basic science to clinical applications. Am J Sports Med. 2009;37(11):2259–72. 35. Finnoff JT, Fowler SP, Lai JK, Santrach PJ, Willis EA, Sayeed YA, et al. Treatment of chronic tendinopathy with ultrasound-guided needle tenotomy and platelet-rich plasma injection. PM&R. 2011;3(10):900–11. 36. Khanna M, Wiederholz MH, Jimenez J, Rizkalla M.  A novel approach to the treatment of chronic tendon pathology using the FAST procedure: a pilot study. PM&R. 2013;5(9):S208. 37. Bak K, Spring BJ, Henderson IJP. Inferior capsular shift procedure in athletes with multidirectional instability based on isolated capsular and ligamentous redundancy. Am J Sports Med. 2000;28(4):466–71. 38. Albertsson M, Karlsson J, Peterson L, Westlin N.  Long-term results after resection of the coracoacromial ligament for shoulder impingement in athletes. Scand J Med Sci Sports. 1992;2(2):84–6. 39. Park JY, Hwang JT.  Chapter 15: Scapular dyskinesis: part II.  A new diagnostic modality  – three dimensional wing CT.  In: Park JY, editor. Sports injuries to the shoulder and elbow. Berlin: Springer-Verlag; 2015.

Chapter 5

The Pitcher’s Elbow Donald S. Bae

Introduction As participation in youth baseball and softball continues to grow, the incidence of overuse injuries to the young athlete’s elbow may be rising [1–3]. Younger participation, earlier sport specialization, year-round play, and greater awareness may all be factors leading to the perceived epidemic of overuse injuries. In the youth baseball pitcher, risk factors for elbow injuries include high pitch counts, year-round baseball participation, and suboptimal throwing mechanics [2, 3]. While limited data exists, similar risk factors may be presumed for softball and other overhead athletes. Familiarity with the clinical presentation, diagnostic work-up, and treatment principles of elbow injuries in the throwing athlete is critical for any pediatric orthopedic or sports medicine provider. The purpose of this chapter is to review the fundamentals of throwing mechanics, epidemiology of overuse injuries, and prevention strategies. Furthermore, specific detail will be provided regarding three common clinical conditions: medial epicondylar apophysitis, osteochondritis dissecans (OCD) of the capitellum, and ulnar collateral ligament (UCL) injuries. While information will be presented in the context of the pediatric and adolescent baseball player, similar conditions and treatment principles apply to softball players as well as other throwing and overhead athletes (e.g., gymnastics, tennis, water polo, volleyball).

D. S. Bae (*) Department of Orthopedic Surgery, Boston Children’s Hospital, Boston, MA, USA e-mail: [email protected] © Springer International Publishing AG, part of Springer Nature 2019 A. S. Bauer, D. S. Bae (eds.), Upper Extremity Injuries in Young Athletes, Contemporary Pediatric and Adolescent Sports Medicine, https://doi.org/10.1007/978-3-319-56651-1_5

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Throwing Mechanics The phases of throwing have been well characterized and historically divided into six phases separated by seven distinct points in the throwing motion (Fig. 5.1, Table 5.1) [4]. The motion begins with windup to the balance point. Stride is initiated until lead foot (e.g., left foot in a right-handed thrower) contact, during which the throwing arm goes through early cocking. Following this, the arm proceeds to late cocking until the point of maximal shoulder external rotation. Acceleration follows until the point of ball release, after which there is a rapid deceleration phase to the point of maximal shoulder internal rotation. Follow-through is the last phase and ends with the athlete in fielding position. All of these events occur within fractions of seconds, with tremendous angular velocities and forces imparted on the throwing limb. In both adult and youth baseball players, elbow injuries typically occur during late cocking and acceleration phases of throwing. With valgus stress, lateral structures are subjected to compressive forces, whereas medial structures undergo tensile forces. (Posterior structures, such as the triceps and olecranon, typically experience tensile stress later in the throwing cycle.) While there is a wealth of published information regarding the biomechanics of pitching in professional and collegiate throwers, less information exists relating to Foot Contact

Phases

Wind-up

Max ER

Arm cocking

Stride

Release

Arm Arm acceleration deceleration

Max IR

Follow-through

Fig. 5.1  Schematic representation of the phases of throwing. (Reprinted with permission from Kriz [46]) Table 5.1  The phases of throwing Phase Wind-up Early cocking (stride) Late cocking Acceleration Deceleration Follow-through

Initiation of phase Initial position Balance point Stride foot contact Max SER Ball release Max SIR

End of phase Balance point Stride foot contact Max SER Ball release Max SIR End (fielding) position

Max maximum, SER shoulder external rotation, SIR shoulder internal rotation

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Table 5.2  Examples of biomechanical parameters affecting elbow valgus loads in the youth pitcher [8] Mechanical parameter Phase Leading with hips Early cocking Hand-on-top Early cocking Arm in throwing position

Stride foot contact

Shoulder position Stride foot contact Stride foot Stride foot position contact

“Correct” performance Pelvis leading trunk Hand-on-top with forearm pronated Elbow at maximal height at lead foot contact Lead shoulder closed Stride foot pointed to target

“Incorrect” performance Pelvis vertical below trunk Hand below ball, forearm supinated Elbow fails to achieve maximal height by foot strike Lead shoulder open Stride foot not pointed to target

youth and adolescent athletes. Cosgarea et al. previously assess throwing kinematics in youth, adolescent, and adult (collegiate or professional) pitchers and noted similar pitch duration, stride length, and arm abduction angles across age groups, though ball velocity was higher in older athletes participating at higher levels of competition [5]. With “normal” throwing, elbow varus torque across the elbow in young throwers approaches 50 Nm or more [6, 7]. As these forces exceed the native strength of the osteocartilaginous capitellum, medial epicondylar physis, and UCL, proper mechanics as well as the dynamic stabilizing forces of the flexor-pronator muscles are critical in avoiding acute and chronic overuse injuries. Prior work has tried to elucidate biomechanical “errors” in the throwing motion that might subject the elbow to greater valgus loads and thus theoretically higher risks of injury. Identification and correction of these biomechanical issues might therefore improve throwing efficiency and reduce the risk of injury. For example, Davis et al. performed quantitative motion analysis of 169 baseball pitchers between 9 and 18 years of age and identified 5 such parameters (Table 5.2) [8]. Other studies have implicated excessive trunk lean, side arm throwing with reduced arm-trunk angle, and high shoulder external rotation torque at late cocking, perhaps due to suboptimal timing of trunk rotation [9, 10]. Further investigation of optimal throwing mechanics is needed to inform athletes, coaches, and parents regarding performance optimization and injury prevention.

Epidemiology As noted above, elbow injuries are exceedingly common in youth and adolescent baseball players. In the classic prospective longitudinal study of 298 youth pitchers followed over two seasons, elbow pain was reported in 26% of athletes. Identified risk factors in that cohort included baseball play outside the league, arm fatigue during pitching, and throwing more than 600 pitches during the season [11].

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A follow-­up analysis by Lyman et al. also identified increased risk of elbow pain with throwing sliders [12]. More recent investigations have further characterized the scope of the problem. Saper et al. recently evaluated 150 elbow injuries in over 1.7 million high school athlete exposures derived from the National High School Sports-Related Injury Surveillance Study [13]. The incidence of elbow injury was found to be 0.86 per 10,000 athlete exposures, the majority affecting pitchers and sustained during competition. While the vast majority of athletes were treated nonsurgically, over 10% of injuries resulted in medical disqualification and over a third of athletes did not return within 3 weeks. Softball athletes similarly sustain elbow injuries, though perhaps at a lower rate than their baseball counterparts. The reported incidence of elbow injuries in softball players is 0.43 per 10,000 athlete exposures; as anticipated, softball pitchers are far less commonly affected, given the underhand or windmill pitching motion [14]. In addition to pain and time out of sport, recent published information suggests that excessive throwing and overuse result in real structural changes in the elbow. Okamoto and colleagues, for example, reported on the magnetic resonance imaging (MRI) screening of 62 baseball players between 9 and 12 years of age. Forty-two percent of athletes had discernable abnormalities in the UCL [1]. High rates of medial epicondylar apophyseal changes have similarly been seen in ultrasound screening of youth and adolescent baseball players [15].

Prevention Given the high prevalence of elbow injuries in the throwing athlete, great efforts have been made to incorporate preventative strategies within guidelines and rules of play [16]. In youth baseball, rules have been established to limit the quantity of throwing and therefore mitigate the risks of elbow injury (Table 5.3). In addition to limiting the number of pitches per game, youth baseball rules stipulate a minimum number of days of rest between outings, oft referred to as the “4-3-2-1 rule” (Table 5.4). Understanding that field position players—particularly catchers—also are at risk of elbow injury due to throwing volume, guidelines have been implemented regulating pitching and catching. A pitcher who has thrown more than 41 pitches is not permitted to play catcher for the rest of the calendar day, nor is a player who has caught more than 4 innings allowed to pitch in that calendar day. Table 5.3 Guidelines regarding the number of pitches permitted per day in youth baseball pitchers, according to age [16]

Age (years) 7–8 9–10 11–12 13–16

Pitches permitted per day 50 75 85 95

5  The Pitcher’s Elbow Table 5.4  Youth baseball rest requirements for pitchers age 14 years and younger [16]

65 Pitches thrown 66+ 51–65 36–50 21–35 1–20

Number of subsequent calendar days of rest 4 3 2 1 0

Softball guidelines employ similar principles. Youth softball players currently are limited to 12 innings of pitching per day. Any athlete who pitches more than 7 innings must rest a calendar day before returning to pitching. While these rules and guidelines represent important steps toward injury prevention, a number of other considerations exist. First, preventative measures should not be limited to on-field pitch counts during competition. Stretching and strengthening regimens are important for elbow health; indeed, prior studies have demonstrated the efficacy of stretching and conditioning programs to prevent elbow injuries in young throwers [17, 18]. Second is recognition that cumulative exposure can also lead to overuse injury. Indeed, prior studies indicate that throwing more than 8 months during the calendar year increases the risk of injury and potential surgical intervention fivefold [19]. Furthermore, each athlete’s symptoms should be carefully weighed. Continued pitching and/or throwing with pain is perhaps the greatest risk of injury; indeed, the risk for injury requiring surgery may increase 3600% with regular pitching despite persistent arm fatigue [20]. Finally, guidelines and policies are only as effective as their implementation. Recent published information suggests that pitching rules are not universally followed, exposing young throwers to avoidable risk. Prior surveys, for example, indicate suboptimal coaching compliance as well as athletes continuing to participate with pain [21, 22]. Only with continued education and enforcement will the maximal benefit of these preventative strategies be realized.

Medial Epicondylar Apophysitis Given the valgus forces seen during throwing –particularly during cocking and acceleration phases—as well as the traction forces imparted by the flexor-pronator muscles, the medial epicondylar apophysitis is a common source of elbow pain in the young thrower. This is particularly true in patients age 10–14, in which the secondary center of ossification has formed but the underlying physis remains open. As it is most common in this young age group, medial epicondylar apophysitis is sometimes referred to as “little leaguer’s elbow.” Athletes will typically present with medial elbow pain, often of insidious or gradual onset. On physical examination, tenderness is elicited with direct palpation over the bony epicondyle (Fig.  5.2). Resisted wrist flexion or forearm pronation may similarly elicit discomfort, given the muscular origin on the medial epicondyle.

66 Fig. 5.2 (a) Palpable landmarks on the medial side of the right elbow. The medial epicondyle is marked with “ME.” The attachment of the ulnar collateral ligament on the sublime tubercle of the ulna is marked “ST.” The ulnar collateral ligament traverses in the path of the parallel lines. (b) Palpation directly upon the medial epicondyle will often elicit tenderness in patients with medial epicondylar apophysitis. (c) Resisted forearm pronation and wrist flexion will similarly provoke pain with medial epicondylar apophysitis. (Images copyright © Children’s Orthopaedic Surgery Foundation and used by permission. All rights reserved)

D. S. Bae

a

b

c

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Fig. 5.3 Anteroposterior radiograph of the right elbow in a patient with medial epicondylar apophysitis. Note is made of abnormal widening of the physis. (Image copyright © Children’s Orthopaedic Surgery Foundation and used by permission. All rights reserved)

Elbow range of motion is typically unaffected, and patients do not typically endorse symptoms of locking, catching, or giving way. In any throwing athlete with elbow pain, careful evaluation of the entire kinematic chain is critically important [23]. Assessment of glenohumeral range of motion is particularly important. Often an internal rotation deficit is identified, which may contribute to suboptimal throwing mechanics (e.g., reduced arm-trunk angle or “sidearm” throwing). While predominantly a clinical diagnosis, radiographs may aid in confirming the diagnosis and ruling out other associated conditions (Fig. 5.3). As the medial epicondyle is a posteromedial structure, external rotation radiographs are needed to bring the bony structures in profile and provide optimal visualization of the underlying growth plate. Comparison views of the unaffected non-throwing elbow may be useful. Radiographic findings typically include relative irregularity or widening of the epicondylar physis, with or without fragmentation or ossification changes to the epicondyle itself.

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Fig. 5.4  Radiograph after reduction and surgical fixation of a left displaced medial epicondyle fracture, sustained during pitching. (Image copyright © Children’s Orthopaedic Surgery Foundation and used by permission. All rights reserved)

Treatment typically consists of rest and cessation from throwing, followed by physical therapy focusing on flexor-pronator stretching and strengthening. As with all athletes, concomitant issues throughout the kinematic chain (e.g., glenohumeral internal rotation deficit) as well as suboptimal throwing mechanics should be addressed during rehabilitation and subsequent return-to-play programs. In rare situations, acute medial epicondylar apophyseal fractures may occur during throwing [24]. Patients will report vague prodromal medial elbow pain, likely due to apophyseal stress. With continued pitching, patients will report a sudden “painful pop” as the medial epicondyle is avulsed. Physical exam will reveal swelling, tenderness, ecchymosis, and limited elbow range of motion. Given the proximity of the ulnar nerve to the medial epicondyle, a careful distal evaluation of sensation and motor function should be performed to identify associated ulnar nerve injury. Plain radiographs will confirm the diagnosis (Fig. 5.4). In throwing or overhead athletes with displaced medial epicondyle fractures, surgical reduction and fixation is typically advised. Though these fractures are extra-­ articular, the fragment is often small, and the attached flexor-pronator mass generally pulls the fragment anterior and distal to its usual location, making true bony healing

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unlikely for displaced fractures. Surgical treatment restores the origin of the flexor-­ pronator mass, minimizes the risk of persistent valgus instability, and allows for early range of motion which may minimize risk of post-injury stiffness. Multiple studies have demonstrated that reduction and fixation of medial epicondyle fractures is safe and effective in this young athletic population [25, 26]. Following ­surgical fixation of medial epicondyle fractures, however, there is a risk of elbow stiffness. For this reason, patients are immobilized for only a short period of time following surgery, followed by an early return to elbow motion as part of a supervised physical therapy program.

Osteochondritis Dissecans Osteochondritis dissecans (OCD) of the capitellum is a characteristic condition of adolescent throwers and overhead or weight-bearing athletes. Typically affecting patients between 10 and 14 years of age, repetitive compressive forces across the lateral elbow leads to injury of the capitellum. Given the relative hypovascularity of the developing capitellum in the skeletally immature patient, there is inability to heal after such repetitive microtrauma, ultimately leading to subchondral fracture, articular cartilage failure, and loose body formation [27]. Patients will typically present with lateral elbow pain. While lateral elbow pain is often dismissed as lateral epicondylitis (“tennis elbow”), this condition is uncommon in the younger throwing or overhead athlete; indeed, lateral elbow pain in an adolescent pitcher should be considered capitellar OCD until proven otherwise. In more advanced stages, there will be notable loss of elbow motion. Up to 25% of patients will present with symptoms of locking, catching, or giving way, suggesting intra-articular loose body formation. The hallmark of clinical diagnosis is tenderness with direct palpation on the capitellum (Fig.  5.5). This is best achieved by hyperflexing the elbow, thereby moving the radial head away from the typical area of involvement. Palpation directly on the capitellum will typically elicit pain in patients with OCD. Plain radiographic findings may be subtle and include lucencies, cystic and/or sclerotic changes of the capitellum, or even radiographic opacities correlating with unstable osteochondral fragments. Increasingly, MRI is utilized to make the diagnosis, characterize the extent of fragment instability, and guide treatment (Fig. 5.6) [28]. In general, stable OCD lesions in which the affected articular cartilage and underlying subchondral bone remain localized and connected to the distal humerus are treated non-operatively. Non-operative management consists of elbow rest and cessation from baseball activities, with serial clinical and radiographic evaluation to monitor healing. Given the inherent issues of vascularity as well as the heterogeneity in clinical presentation, prior studies have determined that healing rate is 50–90% with rest, which may take up to 12–15 months [29]. In patients presenting with or progressing to unstable OCD lesions, surgical treatment is recommended. A host of surgical treatment options have been ­proposed,

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a

b

Fig. 5.5 (a, b) In patients with capitellar OCD, tenderness is elicited with direct palpation of the capitellum with the elbow hyperflexed. (Images copyright © Children’s Orthopaedic Surgery Foundation and used by permission. All rights reserved)

1

2

3

4

Fig. 5.6  Sagittal T2-weighted MRI sequences depicting the stages of osteochondritis dissecans [28]. Stage 1: Bony edema but intact cartilaginous surface. Stage 2: High signal breach of articular cartilage. Stage 3: Thin rim of high signal extending behind the osteochondral fragment. Stage 4: Loose body. (Image copyright © Children’s Orthopaedic Surgery Foundation and used by permission. All rights reserved)

ranging from in situ fixation to loose body removal and microfracture to osteochondral autologous transplantation surgery (OATS) (Fig.  5.7). Historically, return to baseball throwing at the same level of competition has ranged from 40% to 80% following surgical fixation or debridement and microfracture [30–33]. Recent information suggests that osteochondral grafting may provide advantages over other surgical techniques, as it replaces necrotic subchondral bone and restores hyaline

5  The Pitcher’s Elbow

a

71

b

Fig. 5.7 (a) Preoperative MRI depicting an unstable OCD lesion. (b) Postoperative MRI following osteochondral grafting. Note is made of restoration of a smooth, congruent articular surface and healthy subchondral bone. (Images copyright © Children’s Orthopaedic Surgery Foundation and used by permission. All rights reserved)

articular cartilage to the capitellum. Indeed, recent case series and meta-analyses have suggested improved healing rates and patient outcomes with osteochondral grafting [34–37]. Regardless of treatment method, however, recovery after surgery consists of a prolonged period of rest from baseball activities.

Ulnar Collateral Ligament Injuries In older adolescents, UCL rupture is a cause of acute medial elbow pain and compromised performance, typically manifested as reduced pitch velocity. Patients with acute UCL tears will report a “painful pop” during throwing, often preceded by arm soreness or fatigue. These prodromal symptoms indicate that the dynamic stability conferred by the flexor-pronator muscles is being lost, after which the UCL must bear more valgus load with throwing, The UCL is then subjected to valgus strains exceeding its ultimate strength, resulting in acute rupture. Range of motion is not typically affected, and distal neurological symptoms are uncommon. On examination, tenderness may be elicited with direct palpation along the course of the UCL, particularly at its insertion at the sublime tubercle of the ulna (Fig.  5.8). Pain or apprehension may be elicited with valgus stress of the elbow flexed 30° with the forearm pronated. As instability and medial joint line gapping are difficult to evoke with static valgus stress, the dynamic moving valgus stress test has been proposed to reproduce symptoms throughout the arc of elbow motion (Fig. 5.9) [38].

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a

b

Fig. 5.8 (a) Clinical photograph depicting palpation of the sublime tubercle of the ulna, the insertion of the ulnar collateral ligament. This point may be found by placing the interphalangeal joint of the examiner’s thumb on the medial epicondyle; the tip of the thumb will lie near the sublime tubercle. (b) Valgus stress testing of elbow stability may be performed with the elbow flexed 30° and forearm pronated. (Images copyright © Children’s Orthopaedic Surgery Foundation and used by permission. All rights reserved)

a

b

Fig. 5.9 (a, b) The dynamic or moving valgus stress test [38]. With the shoulder abducted 90° and externally rotated, the examiner grasps the patients thumb and imparts a valgus load to the elbow (arrow). The patient’s elbow is then brought through an arc of flexion and extension, with the examiner’s other thumb feeling the medial joint line for gapping or instability. (Images copyright © Children’s Orthopaedic Surgery Foundation and used by permission. All rights reserved)

Plain radiographs are evaluated to assess for other pathology, particularly medial epicondylar apophyseal stress injuries or avulsion fractures. Valgus stress radiographs have been advocated by some, though the sensitivity of these specialized views in determining UCL insufficiency has been limited [39]. Currently, MRI or MRI arthrog-

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Fig. 5.10  Coronal MRI scan depicting a proximal tear of the ulnar collateral ligament in a skeletally immature baseball pitcher. (Image copyright © Children’s Orthopaedic Surgery Foundation and used by permission. All rights reserved)

raphy provides the most accurate means of determining UCL tears (Fig. 5.10) [40, 41]. The author’s preference is to utilize a 3-T MRI without intra-­articular contrast. Non-operative treatment after acute injury consists of rest and physical therapy, focused on improving flexor-pronator strength and optimizing other elements of the kinematic chain. Careful analysis of pitching technique may provide insight into modifications in throwing mechanics. Prior reports suggest that up to half of athletes will be able to return to prior level of competition with non-operative care, though admittedly there may be difficulty in achieving the same pitch velocity from the pre-injury state [42]. In patients who have persistent pain and/or functional limitations despite non-operative treatment, surgical reconstruction may be considered. While a host of surgical techniques have been proposed, all seek to reconstruct the anterior band of the UCL, the primary restraint to valgus stress with elbow flexion. Typically the ligament is reconstructed with tendon graft, passed or secured through bony tunnels at the anatomic footprints of the UCL origin (anteroinferior medial epicondyle) and insertion (sublime tubercle) [43]. Rehabilitation following ligament reconstruction is lengthy, often spanning 9–12 months postoperatively. With meticulous surgical technique and diligent postoperative rehabilitation, UCL reconstruction has been highly successful in adult professional- and collegiate-­ level pitchers in restoring elbow stability and returning athletes to their prior level of participation (Fig. 5.11) [43]. Great care, however, must be taken before extrapolating the published outcomes of UCL reconstruction in adults to children and adolescents. For example, in their report of 10-year outcomes following UCL reconstruction, Osbahr and colleagues reported that high school baseball athletes participated in baseball for mean 2.9 years after surgery, with 21% unable to return to the same or higher level of competition [44].

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Fig. 5.11 Intraoperative photograph depicting a completed ulnar collateral ligament reconstruction with tendon graft. (Image copyright © Children’s Orthopaedic Surgery Foundation and used by permission. All rights reserved)

Table 5.5  The “soreness rules” of return to throwing rehabilitation [45] No soreness Soreness during warm-up; pain-free within first 15 throws Soreness more than 1 h after throwing Soreness during warm-up and persistent after first 15 throws

Advance one step every throwing day Repeat previous workout Take 1 day off and repeat prior workout Take 2 days off, move back one step in program

Rehabilitation and Return to Throwing Following non-operative or surgical treatment, initial emphasis is placed upon pain relief, regaining elbow motion and restoring normal strength. Once these clinical parameters have been achieved, return to baseball activities—and pitching in particular—is best achieved through an interval throwing program. The goal of any interval throwing program is to progress the athlete back to full baseball participation gradually, safely, and with proper mechanics. A host of interval throwing programs have been proposed, yet all encompass the same fundamental principles [45]. First, they are age-, sport-, and position-specific. Functional rehabilitation using baseballs on the field or pitching mound provides opportunity for realistic progression, allows for more effective instruction and compliance, and facilitates patient engagement. Second, interval throwing programs provide specific guidance on how to gradually increase intensity and quantity of throwing. Detailed scripted programs ensure compliance, help the patient to maintain proper mechanics, and avoid recurrent injury from too rapid or overzealous return. Finally, most interval throwing programs provide precise instructions on how to handle recurrent pain or symptoms. “Soreness rules” are commonly utilized to allow transparent communication among athletes, coaches, parents, and care providers, managing both progression and expectations. An example of an interval throwing program is provided in Tables 5.5 and 5.6.

5  The Pitcher’s Elbow Table 5.6  Example of first two phases of an interval throwing program for 13- and 14-year-old pitchers [45]

75 Phase I: Return to throwing

Step 1

2

3

II: Return to pitching

4

5

6

III: Intensified pitching

Program Warm-up toss 60′ 15 throws at 30′ × 3 20 long tosses to 60′ Warm-up toss to 75′ 15 throws at 45′ × 3 20 long tosses to 75′ Warm-up toss to 90′ 15 throws at 60′ × 3 20 long tosses to 90′ Warm-up toss to 105′ 20 fastballs at 50% 16 fastballs at 50% × 2 25 long tosses to 105′ Warm-up toss to 120′ 20 fastballs at 50% × 3 25 long tosses to 120′ Warm-up toss to 120′ 16 fastballs at 50% 20 fastballs at 50% × 2 16 fastballs at 50% 25 long tosses to 120′

7–16

References 1. Okamoto Y, Maehara K, Kanahori T, Hiyama T, Kawamura T, Minami M. Incidence of elbow injuries in adolescent baseball players: screening by a low field magnetic resonance imaging system specialized for small joints. Jpn J Radiol. 2016;34:300–6. 2. Fleisig GS, Andrews JR, Cutter GR, Weber A, Loftice J, McMichael C, Hassell N, Lyman S. Risk of serious injury for young baseball pitchers: a 10-year prospective study. Am J Sports Med. 2011;39:253–7. 3. Fleisig GS, Andrews JR. Prevention of elbow injuries in youth baseball pitchers. Sports Health. 2012;4:419–24. 4. Fortenbaugh D, Fleisig GS, Andrews JR. Baseball pitching biomechanics in relation to injury risk and performance. Sports Health. 2009;1:314–20. 5. Cosgarea AJ, Campbell KR, Haggod SS, McFarland EG, Silberstein CE. Comparative analysis of throwing kinematics from Little League to professional baseball pitchers. Med Sci Sports Exerc. 1993;25:S131. 6. Dun S, Loftice J, Fleisig GS, Kingsley D, Andrews JR. A biomechanical comparison of youth baseball pitches: is the curveball potentially harmful? Am J Sports Med. 2008;36:686–92. 7. Nissen CW, Westwell M, Ounpuu S, Patel M, Solomito M, Tate J.  A biomechanical comparison of the fastball and curveball in adolescent baseball pitchers. Am J Sports Med. 2009;37:1492–8. 8. Davis JT, Limpisvasti O, Fluhme D, Mohr KJ, Yocum LA, ElAttrache NS, Jobe FW. The effect of pitching biomechanics on the upper extremity in youth and adolescent baseball pitchers. Am J Sports Med. 2009;37:1484–91.

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9. Aguinaldo AL, Chambers H. Correlation of throwing mechanics with elbow valgus load in adult baseball pitchers. Am J Sports Med. 2009;37:2043–8. 10. Anz AW, Bushnell BD, Griffin LP, Noonan TJ, Torry MR, Hawkins RJ. Correlation of torque and elbow injury in professional baseball pitchers. Am J Sports Med. 2010;38:1368–74. 11. Lyman S, Fleisig GS, Waterbor JW, Funkhouser EM, Pulley L, Andrews JR, Osinski ED, Roseman JM. Longitudinal study of elbow and shoulder pain in youth baseball pitchers. Med Sci Sports Exerc. 2001;33:1803–10. 12. Lyman S, Fleisig GS, Andrews JR, Osinski ED. Effect of pitch type, pitch count, and pitching mechanics on risk of elbow and shoulder pain in youth baseball pitchers. Am J Sports Med. 2002;30:463–8. 13. Saper MG, Pierpoint LA, Liu W, Comstock RD, Polousky JD, Andrews JR. Epidemiology of shoulder and elbow injuries among United States high school baseball players: school years 2005–2006 through 2014–2015. Am J Sports Med. 2018;46:37–43. 14. Pytiak AV, Kraeutler MJ, Currie DW, McCarty EC, Comstock RD. An epidemiological comparison of elbow injuries among United States high school baseball and softball players, 2005– 2006 through 2014–2015. Sports Health. 2018;10:119–24. 15. Otoshi K, Kikuchi S, Kato K, Sato R, Igari T, Kaga T, Konno S.  Age-specific prevalence and clinical characteristics of humeral medial epicondyle apophysitis and osteochondritis dissecans: ultrasonographic assessment of 4249 players. Orthop J Sports Med. 2017;5:2325967117707703. 16. Little League Baseball. Regular season pitching rules  – baseball and softball. https://www. littleleague.org/playing-rules/pitch-count/. Accessed 14 May 2018. 17. Sakata J, Nakamura E, Suzuki T, Suzukawa M, Akaike A, Shimizu K, Hirose N. Efficacy of a prevention program for medial elbow injuries in youth baseball players. Am J Sports Med. 2018;46:460–9. 18. Shitara H, Yamamoto A, Shimoyama D, Ichinose T, Sasaki T, Hamano N, et  al. Shoulder stretching intervention reduces the incidence of shoulder and elbow injuries in high school baseball players: a time-to-event analysis. Sci Rep. 2017;7:45304. 19. Olsen SJ II, Fleisig GS, Dun S, et al. Risk factors for shoulder and elbow injuries in adolescent baseball pitchers. Am J Sports Med. 2006;34:905–12. 20. Kerut EK, Kerut DG, Fleisig GS, Andrews JR.  Prevention of arm injury in youth baseball pitchers. J La State Med Soc. 2008;160:95–8. 21. Pamias-Velázquez KJ, Figueroa-Negrón MM, Tirado-Crespo J, Mulero-Portela AL. Compliance with injury prevention measures in youth pitchers: survey of coaches in Little League of Puerto Rico. Sports Health. 2016;8:274–7. 22. Makhni EC, Morrow ZS, Luchetti TJ, Mishra-Kalyani PS, Gualtieri AP, Lee RW, Ahmad CS.  Arm pain in youth baseball players: a survey of healthy players. Am J Sports Med. 2015;43:41–6. 23. Sgroi T, Chalmers PN, Riff AJ, Lesniak M, Sayegh ET, Wimmer MA, Verma NN, Cole BJ, Romeo AA. Predictors of throwing velocity in youth and adolescent pitchers. J Shoulder Elb Surg. 2015;24:1339–45. 24. Osbahr DC, Chalmers PN, Frank JS, Williams RJ, Widmann RF, Green DW. Acute, avulsion fractures of the medial epicondyle while throwing in youth baseball players: a variant of Little League elbow. J Shoulder Elb Surg. 2010;19:951–7. 25. Canavese F, Marengo L, Tiris A, Mansour M, Rousset M, Samba A, Andreacchio A, Dimeglio A.  Radiological, clinical and functional evaluation using the quick disabilities of the arm, shoulder and hand questionnaire of children with medial epicondyle fractures treated surgically. Int Orthop. 2017;41:1447–52. 26. Pace GI, Hennrikus WL. Fixation of displaced medial epicondyle fractures in adolescents. J Pediatr Orthop. 2017;37:e80–2. 27. Kobayashi K, Burton KJ, Rodner C, Smith B, Caputo AE. Lateral compression injuries in the pediatric elbow: Panner’s disease and osteochondritis dissecans of the capitellum. J Am Acad Orthop Surg. 2004;12:246–54.

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28. Brittberg M, Winalski C. Evaluation of cartilage injuries and repair. J Bone Joint Surg Am. 2003;85–A:58–69. 29. Matsuura T, Kashiwaguchi S, Iwase T, Takeda Y, Yasui N. Conservative treatment for osteochondrosis of the humeral capitellum. Am J Sports Med. 2008;36:868–72. 30. Byrd JW, Jones KS. Arthroscopic surgery for isolated capitellar osteochondritis dissecans in adolescent baseball players: minimum three-year follow-up. Am J Sports Med. 2002;30:474–8. 31. Takahara M, Mura N, Sasaki J, Harada M, Ogino T. Classification, treatment, and outcome of osteochondritis dissecans of the humeral capitellum. J Bone Joint Surg. 2007;89:1205–14. 32. Hennrikus WP, Miller PE, Micheli LJ, Waters PM, Bae DS. Internal fixation of unstable in situ osteochondritis dissecans lesions of the capitellum. J Pediatr Orthop. 2015;35:467–73. 33. Lewine EB, Miller PE, Micheli LJ, Waters PM, Bae DS.  Early results of drilling and/or microfracture for grade IV osteochondritis dissecans of the capitellum. J Pediatr Orthop. 2016;36:803–9. 34. Bae DS, Ingall EM, Miller PE, Eisenberg K. Early results of single-plug autologous osteochondral grafting for osteochondritis dissecans of the capitellum in adolescents. J Pediatr Orthop. 2018. [epub ahead of print]. 35. Westermann RW, Hancock KJ, Buckwalter JA, Kopp B, Glass N, Wolf BR. Return to sport after operative management of osteochondritis dissecans of the capitellum: a systematic review and meta-analysis. Orthop J Sports Med. 2016;4:2325967116654651. 36. Kirsch JM, Thomas J, Bedi A, Lawton JN.  Current concepts: osteochondritis dissecans of the capitellum and the role of osteochondral autograft transplantation. Hand (N Y). 2016;11:396–402. 37. Iwasaki N, Kato H, Ishikawa J, Masuko T, Funakoshi T, Minami A. Autologous osteochondral mosaicplasty for osteochondritis dissecans of the elbow in teenage athletes. J Bone Joint Surg Am. 2009;91:2359–66. 38. O’Driscoll SWM, Lawton RL, Smith AM. The “moving valgus stress test” for medial collateral ligament tears of the elbow. Am J Sports Med. 2005;33(2):231–9. 39. Azar FM, Andrews JR, Wilk KE, Groh D.  Operative treatment of ulnar collateral ligament injuries of the elbow in athletes. Am J Sports Med. 2000;28:16–23. 40. Nakanishi K, Masatomi T, Ochi T, Ishida T, Hori S, Ikezoe J, Nakamura H. MR arthrography of elbow: evaluation of the ulnar collateral ligament of elbow. Skelet Radiol. 1996;25:629–34. 41. Timmerman LA, Schwartz ML, Andrews JR. Preoperative evaluation of the ulnar collateral ligament by magnetic resonance imaging and computed tomography arthrography. Evaluation in 25 baseball players with surgical confirmation. Am J Sports Med. 1994;22:26–31; discussion 32. 42. Rettig AC, Sherrill C, Snead DS, Mendler JC, Mieling P. Nonoperative treatment of ulnar collateral ligament injuries in throwing athletes. Am J Sports Med. 2001;29:15–7. 43. Raducha JE, Gil JA, Harris AP, Owens BD. Ulnar collateral ligament injuries of the elbow in the throwing athlete. JBJS Rev. 2018;6(2):e1. 44. Osbahr DC, Cain EL, Raines T, Fortenbaugh D, Dugas JR, Andrews JR.  Long-term outcomes after ulnar collateral ligament reconstruction in competitive baseball players: minimum 10-year follow-up. Am J Sports Med. 2014;42:1333–42. 45. Axe M, Hurd W, Snyder-Mackler L. Data-based interval throwing programs for baseball players. Sports Health. 2009;1:145–53. 46. Kriz P. Throwing sports and injuries involving the young athlete’s spine. In: Micheli L, Stein C, O’Brien M, d’Hemecourt P, editors. Spinal injuries and conditions in young athletes. Contemporary pediatric and adolescent sports medicine. New York: Springer; 2018.

Chapter 6

Gymnast’s Wrist Elspeth Ashley V. Hart and Kate W. Nellans

Introduction Gymnastics demands strength, flexibility, grace, and artistry in young and typically skeletally immature athletes. It is one of the only sports that uses the upper extremity as a weight-bearing surface, thus creating a spectrum of wrist injuries specific to gymnastics. Gymnastics is one of the oldest sports dating back to the ancient Greeks [1]. USA Gymnastics (USAG), the governing body of US gymnastics, reports 102,295 athlete members, including 86,800 artistic gymnasts [2]. There are five main types of gymnastics: artistic (the most common), tumbling and trampoline, rhythmic, acrobatic, and Gymnastics for All (TeamGym, HUGS—Hope Unites Gymnastics with Special Athletes). There are four events for women in artistic gymnastics: vault, uneven bars, balance beam, and floor exercise. There are six events for men in artistic gymnastics: floor exercise, vault, high bar, pommel horse, rings, and parallel bars. There are different levels of competitive gymnastics: recreational classes (beginner level), competitive teams (Junior Olympic levels 1–10, with 10 being the highest, and Excel/Prep-Optional), and Elite (Olympic-level training). Training time and volume in gymnastics depend upon the level. For example, recreational or beginner level gymnasts may train between 1 and 4 h per week, while elite gymnasts may

E. A. V. Hart Department of Sports Medicine/Orthopedics, Boston Children’s Hospital, Boston, MA, USA K. W. Nellans (*) Department of Orthopedic Surgery, Northwell Health, Hofstra-Northwell Medical School, Great Neck, NY, USA e-mail: [email protected] © Springer International Publishing AG, part of Springer Nature 2019 A. S. Bauer, D. S. Bae (eds.), Upper Extremity Injuries in Young Athletes, Contemporary Pediatric and Adolescent Sports Medicine, https://doi.org/10.1007/978-3-319-56651-1_6

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train between 30 and 50 h per week, often split into two practice sessions daily [3]. Competitive gymnasts train year-round, and sports specialization (participation in only gymnastics) by 8–10 years of age is common. Sports specialization sets the stage for repetitive use injuries. In the 1970s, 1980s, and early 1990s, 13- and 14-year-old gymnasts were pushed into international competitions, raising concerns about appropriate training and development of these athletes. In response, the International Gymnastics Federation prohibited participation in the Olympics for those younger than 16 years after the 1996 Olympics. There is not yet data to show that this specific change has reduced the incidence of injury in the youngest elite level gymnasts. However, with increased importance placed on equipment safety measures between 1990 and 2005, there was an associated 25% decline in the rate of overall injury rate in young gymnasts [4]. There are multiple injuries that can occur in gymnastics. The most common body part injured in gymnastics is the ankle, followed by the knee, with injuries to the wrist being the third most common type of injury [2, 5]. This chapter will discuss the most common injuries encountered in a gymnast’s wrist and specifically address “gymnast wrist” and the sequelae of this injury. Gymnast wrist is often a diagnosis that mimics other chronic wrist injuries including dorsal capsular irritation, occult ganglions, scaphoid impingement, and even fractures of the scaphoid. These will be presented in detail related to gymnasts to help the reader discern between these conditions. The sequelae of untreated gymnast wrist including ulnar impaction syndrome will be highlighted to underscore the fact that early recognition of gymnast wrist can prevent long-term consequences requiring major surgical intervention. This article will also discuss a more traumatic wrist injury known as “grip lock” as a specific entity in gymnasts using dowel grips and present ways to avoid this catastrophic injury.

Upper Extremity Overview for Gymnastics Gymnastics involves multiple skills that result in considerable forces imparted to the upper extremity and is one of the only sports to use the upper extremity as both a high impact and weight-bearing limb. In men’s gymnastics, the proportion of upper extremity injuries (53.4%) are greater than lower extremity (32.8%) injuries [6]. The most common location of injuries in the upper extremity in men’s gymnastics is the shoulder, followed by the wrist [7]. Among female gymnasts, the wrist is the most commonly affected structure of the upper extremity, followed by the elbow [3, 7]. The annual rate of upper extremity injuries resulting in missed practice time in gymnasts ranges from 11% to 53% [7]. Multiple prospective observational studies have suggested, however, that in the course of a single season, over 80% of athletes will experience some wrist and elbow pain, though this will not necessarily result in a missed practice or competition [8–11].

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The force across the wrist is 16 times the gymnast’s body weight [12]. The prevalence of isolated wrist pain ranges from 46% to 79% of gymnasts; however, there are reports that as many as 70–88% of gymnasts will experience wrist pain over their career [3, 12, 13]. In men’s gymnastics the most common events causing wrist pain include the floor exercise and pommel horse, whereas in women’s gymnastics, the floor exercise and vault are the most common causes [12]. A number of external factors can increase the risk of wrist pain in an individual including very soft mats/training surfaces (causing increased wrist extension), twisting elements on the upper extremity with fixed forearms, improper technique, and repetitive skills performed with the wrist loaded in extension. Risk factors unique to the individual would include a previous injury, a delay in skeletal maturity compared to age and training level, and high-intensity training during a growth spurt, which may all result in transient weakness in the physis (or “growth plate”) [3, 12]. Recently, there has been a slight decrease in wrist pain seen with vaulting due to the change in the vaulting table, which is now larger and wider [14]. A larger vaulting surface allows for multiple “sweet spots” and thus is more forgiving of alterations in preflight approach and hand positioning compared to the prior smaller vaulting tables.

Anatomy of the Upper Extremity When discussing wrist injuries in gymnastics, it is important to understand the anatomy of the wrist. The osseous “wrist” consists of the forearm (radius and ulna) and hand (carpal bones, of which the scaphoid is the most commonly injured, and metacarpals) (Fig. 6.1). The majority of the growth of the forearm originates from the physes of the distal radius and ulna, which remain open until approximately 15 years of age in girls and 16 years in boys. The length relationship between the radius and ulna at the wrist is referred to as ulnar variance.

Factors that Lead to Wrist Pain in Gymnasts Sports Specialization at an Early Age  Gymnastics is a sport known for athletes who specialize in only gymnastics at a very young age [15]. Without time away from the sport, chronic wrist injuries or weaknesses have little time to heal, as all events in artistic gymnastics require full weight-bearing on the upper extremity. Volume of Training and Skills Performed  Gymnasts’ training time and volume in gymnastics depend upon the level and can vary greatly. For example, recreational or beginner-level gymnasts may train between 1 and 4 h per week, while higher levels such as elite gymnasts may train between 30 and 50 h per week and sometimes two times a day. Intense training for the gymnast involves year-round training.

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Fig. 6.1  Bony anatomy of the wrist

id

ho

ap

Sc

Radial physis

Ulnar physis Radius

Ulna

Age of Training  Unlike many other high-level athletes who expect peak performance in later years, female gymnasts peak in their abilities between the ages of 13 and 18 years old. This peak occurs during rapid periods of growth for gymnasts; thus, their growth plates are open and vulnerable to overuse and trauma. Improper Technique  Gymnasts who continually use improper technique are at a higher risk for wrist injuries. Wrist extension range of motion should be greater than 90° to bear weight consistently and without placing additional strain across the radial physis [12].

Radial Physeal Inflammation/“Gymnast Wrist” Overview  The term “gymnast wrist” was first published in 1981 [16]. Gymnast wrist refers to stress injury of the distal radial physis and results from repetitive compressive loading and shearing forces on an extended wrist [5, 12]. As the distal radius

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typically bears 80% of the axial load imparted on the extended wrist, the distal radius physis is much more likely to be injured than the distal ulnar physis [12]. Signs and Symptoms  Gymnasts will commonly present with chronic dorsal (or radialsided) wrist pain with no one event of acute trauma [5, 12]. This will usually be most painful while tumbling and vaulting, on pommel horse for men or with back handsprings on beam for women. Generally, pain while on bars (either uneven or high bar) is not a major symptom because the wrist is not hyperextended. A focus group of sports medicine physicians recommended using terms such as “sore,” “aching,” or “tenderness” when trying to elicit a history from a gymnast about wrist pain, as well as other symptoms like swelling and limited range of motion, to fully evaluate the wrist of a gymnast. The gymnast should locate his/her pain to the radial growth plate, not at the joint itself [3]. The gymnast will have pain with extreme wrist extension and axial loading, along with possible swelling/inflammation, and decreased grip strength [3]. Physical Exam  Physical examination will show tenderness to palpation along the dorsal and radial distal radial physis, minor swelling in the distal forearm, decreased grip strength, and pain with hyperextension and axial loading. The wrist pain may not be present with just the examiner hyperextending the wrist and may require the gymnast to bear weight. This can be done easily in an exam room by having the gymnast sit at the edge of the table or chair and lift their body weight off the edge from a seated position (called an “L-seat,” Fig. 6.2). A “plank” position can also be used on the exam table to test for pain at the radial physis (Fig. 6.3).

Fig. 6.2  “L-seat” testing in office for distal radial physeal inflammation and pain

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Fig. 6.3  “Plank” testing in office for distal radial physeal inflammation and pain

Diagnostics  Radiographic findings on X-ray include abnormalities at the distal radial physis which may include widening or haziness of the physis, especially on the volar and radial aspects, cystic changes, a beaked distal volar and radial physis, and sometimes positive ulnar variance [11, 17] (Fig. 6.4). An MRI may be ordered if X-rays are normal, and the clinical suspicion is high, but is not usually necessary to make the diagnosis if changes are seen on X-ray. Caine et al. estimate that there are radiographic abnormalities on MRI consistent with distal radius physeal stress reaction in 10–85% gymnasts, even in asymptomatic patients [6]. Treatment  Current treatment recommendations include rest from gymnastics, physical therapy, and sometimes immobilization with bracing or casting. Typically, complete rest (no weight-bearing at all) is recommended for 6 weeks, until the distal radius physis is completely non-tender. A brace or cast may be needed to “slow down” the gymnast, but is not an absolute necessity. DiFiori et al. explained specific return to gymnastics criteria stating that if the physical examination is unremarkable and the imaging studies demonstrate resolution of physeal injury, training may resume and that compression-loading activities (i.e., handstands, tumbling) should be gradually reintroduced [12]. This group came up with the 75% reduction rule, meaning that gymnasts should return at 25% of their previous skill level and then each week reassess and increase the amount of load gradually by 25%. Follow-up X-rays at 6–12 months following the initial treatment can help identify changes in ulnar variance due to growth arrest.

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Distal radial physeal widening

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Late Gymnast Wrist

Premature distal radial physeal closure

Ulnar overgrowth

Fig. 6.4  X-rays showing early gymnast wrist changes as well as late effects

Prevention  Prevention strategies for gymnast wrist includes working on proper technique for weight-bearing upper extremity skills, proper equipment usage, the use of wrist guards and/or supportive braces, and decreasing repetition of elements on the wrist during periods of significant growth. Wrist guards/braces (like Tiger Paws™, Skids™, and Ten-O™ braces) are worn by many gymnasts; however, no studies have been done to prove the efficacy of the use of wrist guards/braces in reducing axial loads on the distal radial physis or the incidence of distal radial physeal disturbance.

Ulnar Impaction Syndrome Overview  Ulnar impaction syndrome or ulnocarpal abutment occurs when the ulna bears additional force across the wrist with weight-bearing activities [18]. The distal end of the ulna typically bears 20% of force across the wrist with the radius bearing 80% of the force in normal, neutral ulnar variance [18]. However, when the ulna is 1 mm longer than the radius (ulnar positive), it bears 30% of the forces, and this increases to 40% of the forces when the variance is 2 mm ulnar positive. Non-­gymnasts and growing athletes typically have an ulnar-negative

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variance, meaning that their ulna is shorter than their radius [18]. In gymnasts however, there is a higher incidence of positive ulnar variance compared with a nonathletic population [19]. It is felt that with loading and repetitive microtrauma, the radial epiphysis may prematurely close. Consequently, this can predispose toward positive ulnar variance, placing gymnasts at a high risk for ulnar impaction syndrome [19]. Signs and Symptoms  The gymnast will report pain on the distal ulna. He/she may have also had a history of gymnast wrist. Similar to gymnast wrist, the gymnast will complain of pain with tumbling and vaulting, on pommel horse for men or with back handsprings on beam for women. Physical Exam  The gymnast will have tenderness to palpation/touch of the distal ulna. Similar to gymnast wrist, the wrist pain may not be present with just the examiner hyperextending the wrist but may require the gymnast to bear weight, such as with the “plank” or “L-seat” on the exam table. Diagnostics  Radiographic findings on X-ray include positive ulnar variance and possible cyst formation or sclerosis in the ulnar head or within the portion of the lunate touching the ulnar head [11]. An MRI may be warranted for surgical planning and to assess the ulnar side for further injury such as a triangular fibrocartilage complex tear (TFCC) injury. The TFCC may become “pinched” between the lunate and the ulnar head and develop central tearing and degeneration. This type of tearing is quite different from acute, peripheral tears and generally does not require repair as long as the ulnar variance is addressed. Treatment  Current treatment recommendations include complete rest from impact for 6 to 12 weeks depending on resolution of symptoms, anti-inflammatory medications, injections, and possible surgical intervention. The procedure may include shortening the ulna to shift forces back to the radius (Fig. 6.5). Generally, more than 2 mm of ulnar-positive variance at baseline is unlikely to resolve completely without episodes of recurrence once the gymnast returns to full activities. For these gymnasts, an ulnar shortening osteotomy may be considered early on as rest alone is unlikely to provide reliable pain relief. Postoperatively, the bone healing following the osteotomy can take 8–10  weeks, and full return to gymnastics may take 16 weeks or more. Prevention  To prevent this condition, early treatment and diagnosis of wrist pain is needed. It has been surmised that the high rate of ulnar-positive variance in gymnasts results from undertreated gymnast wrist, but this had not yet been causally linked. Studies have demonstrated that decreased grip strength can predispose gymnasts to this injury, suggesting that grip strengthening may be area for additional strength and conditioning work in young gymnasts [18].

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Fig. 6.5  Wrist X-ray of an ulnar-positive wrist in a 14-year-old gymnast, treated with ulnar shortening osteotomy to decrease forces at ulnar head

Scaphoid Impaction Syndrome/Dorsal Capsular Irritation Overview  This occurs in the gymnast due to impaction of the dorsal rim of the scaphoid against the dorsal lip of radius that is caused by forced hyperextension of the wrist [3]. There can be direct bony contact, but there can also be compression of the dorsal wrist capsule at the radiocarpal joint, causing progressive inflammation and irritation of the dorsal capsule. Signs and Symptoms  The gymnast will complain of insidious onset of scaphoid and dorsal-sided wrist pain. It may wax and wane based on intensity of training. Physical Exam  The gymnast will present with pain in the proximal snuffbox, especially when the wrist is placed in an extended and radially-deviated position. There

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Fig. 6.6  X-ray showing dorsal distal radius impingement on proximal pole of scaphoid with wrist hyperextension

may be some comparative weakness of the muscles responsible for flexion and ulnar deviation, allowing the wrist to collapse into a hyperextended, radially deviated position with weight-bearing. Diagnostics  X-rays are needed and can present with a small ossicle or hypertrophic ridge at the dorsal scaphoid rim (Fig. 6.6) [11]. Treatment  The wrist should be allowed to rest until pain-free, typically 3–6 weeks. Should the pain return upon resumption of activities, a steroid injection can be considered to reduce the swelling of the dorsal tissues. Operative debridement of the dorsal capsule and any hypertrophic bony ridges or ossicles, along with neurectomy of the posterior interosseous nerve innervating the dorsal capsule of the wrist, may improve recalcitrant cases. Prevention  Proper stretching of the wrist and strengthening of volar and ulnar muscles. Wrist guards may be used to prevent the wrist from extending to the point where the dorsal lip of the radius and scaphoid touch.

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Grip Lock Overview  Grip lock is a dangerous acute injury. Though rare, it is an important injury that is unique to gymnastics. Dowel grips are used in gymnastics to decrease the shear forces created between the palm and the bar and to improve grip strength [17]. Grip lock occurs while wearing grips that are too long on the following events: uneven bars, high bar, or the rings (Fig. 6.7a). While the gymnast performs a circling element (i.e., giant, clear hip), the leather grip overlaps/folds over causing the hand to stay in place, while the forearm continues to rotate (Fig. 6.7b) [17, 20]. This may result in an acute forearm fracture and possible tendon and muscle injury as well [3, 21]. The gymnast is then either suspended from the bar with the handgrip locked in place or sometimes released and flung from the bar. This injury is more common in men’s gymnastics than women’s gymnastics, in part because the high bar has a smaller diameter, allowing the dowel portion of the grip to fold over and touch the portion of the wrist or the wristband worn beneath the grip [20]. The most at-risk position while wearing grips is known as an “eagle grip” when the position of the shoulder is maximally internally rotated with the forearm in hyperpronation as the grip slips to the ulnar aspect of the hand [17]. Signs and Symptoms  Acute onset pain and visible deformity of the forearm or wrist. Physical Exam  Gross deformity at the wrist, extreme pain. The skin should be examined for lacerations as the force of this injury can lead to an open forearm fracture. Distal neurovascular status must be checked as the neurovascular structures can become kinked with significant forearm deformity. Diagnostics  Once transferred to a local emergency department, X-rays will be performed. Treatment  Covering medical staff and coaches need to be aware of this issue and the proper techniques to stabilize the athlete after such an injury. If the gymnast is still on the bar, stabilization techniques of the fractured arm need to be in place prior to “unlocking” and removing the grip. If a gymnast is flung from the apparatus, basic emergency planning should be in place, which may include attention to the airway, breathing, and circulation, as well as cervical spine stabilization and transfer techniques. Often the forearm and wrist fractures occurring from grip lock-type injuries will require surgical reduction and fixation.

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Good Fit

Too large: At risk for grip lock

b

Good Fit: Significant space between dowel and wrist band of grip

Poor Fit: Very small gap between dowel and wrist band of grip

Fig. 6.7 (a) Appropriate dowel grip fit compared to grip that is too large. (b) Difference between a dowel grip with a good fit and a grip that is too large when gripping the bar

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Prevention  Prevention techniques for this injury include the proper fitting of grips, making sure they are not too long or worn too close to the hand on the wrist. Grips that are worn and/or stretched are more vulnerable to locking [17].

Gymnastics Specific Training with a Wrist Injury Gymnastics is a year-round sport, and taking months off from this sport can lead to a gymnast falling significantly behind in his/her training, being unable to return to the same level. If cleared by medical providers, gymnasts can still go into the gymnastics gym with a cast, splint, or wrist injury. The gymnast, parents, and coaches must be clear that the gymnast is only allowed in the gym doing modified gymnastics, avoiding any weight-bearing or traction on the injured wrist. Collaboration between the physician and coach can be helpful to specifically tailor the exercises and return to full practices based on the gymnast’s skill level and competition schedule/season. For example, an 11-year-old gymnast with radial physeal inflammation should be treated very conservatively with full rest for 6–8 weeks or until pain-free owing to the long-term consequences of incomplete treatment of gymnast’s wrist. However, a collegiate gymnast with chronic dorsal capsular impingement could try a short rest of a few days to a week or so and progressive return to upper extremity weight-bearing, using pain as a guide. Gymnasts may work on leaps, jumps, and turns on the beam and floor, and the gymnast can do any lower body, core, and back conditioning, as well as stretching. Skills not involving the wrist should be done in a conservative manner (i.e., low beam) if there is a chance the gymnast may fall and reach out onto the injured wrist to catch themselves.

Conclusion Wrist injuries in gymnastics are common as it is used as weight-bearing joint seeing high loads on nearly all events. While some injuries are acute (grip lock), most are chronic, resulting from overtraining and failure to address early pain with appropriate treatment. This article summarizes some of the most common overuse injuries, with tips to help correctly diagnose these conditions (Table 6.1). A break in training using that arm may allow early injuries to heal without surgery. We encourage medical providers, coaches, parents, and gymnasts to work collaboratively to keep the gymnast strong, flexible, and engaged at the gym while recovering from these injuries.

Acute onset wrist/forearm pain, often unable to let go of bar

Gross deformity of the forearm/wrist

Wrist/ forearm

Grip lock

The dowel of the grip becomes caught against the wristband, “locking” the hand to the bar, while the body continues to rotate

Mild swelling of Repetitive impact on Pinching extended wrist sensation with dorsal wrist at joint upper extremity line weight-bearing

Dorsal wrist joint

Dorsal capsular irritation/ scaphoid impaction

Tender at ulnar fovea, pain with ulnar deviation and loading

Tender at ulnar fovea, pain with ulnar deviation and loading

Ulnar head impacts lunate, resulting in central TFCC tears, cysts in lunate

Physical exam Pain with weight-­ bearing, not necessarily painful with wrist hyperextension

Signs and symptoms Tenderness at the radial metaphysis, not at joint, no acute injury

Pain at ulnar head/ fovea

Location of pain Mechanism of injury Repetitive impact on Dorsal radial wrist, extended wrist just proximal to the joint

Ulnar impaction syndrome

Injury Gymnast wrist

X-rays showing an acute fracture of both forearm bones

X-rays to rule out fracture, MRI to look for dorsal capsular inflammation or occult ganglion

Diagnostic workup X-rays showing increased space in the radial growth plate, MRI showing inflammation at physis X-rays showing ulna longer than radius, MRI with edema at ulnar head and ulnar lunate

Table 6.1  Summary table of common injuries to the wrist in gymnasts and defining characteristics

Rarely indicated

Conservative treatment Rest from upper extremity impact for 6–8 weeks, brace or cast, physical therapy (PT) to maintain motion Rest from upper extremity impact 6–12 weeks, avoid loading wrist in ulnar-deviated position Short course of rest until pain-free, possible steroid injection to reduce swelling

Dorsal capsular debridement, proximal retinaculum excision, posterior interosseous neurectomy Open reduction and internal fixation of forearm fractures in an urgent fashion

Operative treatment No surgical intervention unless growth is arrested, and there is overgrowth of the ulna Ulnar shortening osteotomy, possibly with wrist arthroscopy and TFCC debridement

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References 1. Hecht SS, Burton M. Medical coverage of gymnastics competitions. Curr Sports Med Rep. 2009;8(3):113–8. 2. USA Gymnastics. Start here, go anywhere. https://usagym.org. 2017. [Cited 2017 August 10th]. 3. Webb BG, Rettig LA. Gymnastic wrist injuries. Curr Sports Med Rep. 2008;7(5):289–95. 4. Chawla A, Wiesler ER. Nonspecific wrist pain in gymnasts and cheerleaders. Clin Sports Med. 2015;34(1):143–9. 5. Poletto ED, Pollock AN.  Radial epiphysitis (aka gymnast wrist). Pediatr Emerg Care. 2012;28(5):484–5. 6. Caine DJ, Maffulli N. Epidemiology of pediatric sports injuries. Basel, Switzerland: Karger Medical and Scientific Publishers; 2005. 7. Overlin A, Chima B, Erickson S.  Update on artistic gymnastics. Curr Sports Med Rep. 2011;10(5):304–9. 8. Caine D, Roy S, Singer KM, Broekhoff J. Stress changes of the distal radial growth plate: a radiographic survey and review of the literature. Am J Sports Med. 1992;20(3):290–8. 9. DiFiori JP, Puffer JC, Aish B, Dorey F. Wrist pain in young gymnasts: frequency and effects upon training over 1 year. Clin J Sport Med. 2002;12(6):348–53. 10. Mandelbaum BR, Bartolozzi AR, Davis CA, Teurlings L, Bragonier B. Wrist pain syndrome in the gymnast: pathogenetic, diagnostic, and therapeutic considerations. Am J Sports Med. 1989;17(3):305–17. 11. DiFiori JP, Puffer JC, Aish B, Dorey F. Wrist pain, distal radial physeal injury, and ulnar variance in young gymnasts: does a relationship exist? Am J Sports Med. 2002;30(6):879–85. 12. DiFiori JP, Caine DJ, Malina RM. Wrist pain, distal radial physeal injury, and ulnar variance in the young gymnast. Am J Sports Med. 2006;34(5):840–9. 13. Keller MS. Gymnastics injuries and imaging in children. Pediatr Radiol. 2009;39(12):1299. 14. Marshall S, Covassin T, Dick R, Nassar L, Agel J.  Descriptive epidemiology of collegiate women’s gymnastics injuries: National Collegiate Athletic Association Injury Surveillance System, 1988–1989 through 2003–2004. J Athl Train. 2007;42(2):234. 15. Guerra MRV, Estelles JRD, Abdouni YA, Falcochio DF, Rosa JRP, Catani LH.  Frequency of wrist growth plate injury in young gymnasts at a training center. Acta Ortopedica Bras. 2016;24(4):204–7. 16. De Smet L, Claessens A, Lefevre J, Beunen G. Gymnast wrist: an epidemiologic survey of ulnar variance and stress changes of the radial physis in elite female gymnasts. Am J Sports Med. 1994;22(6):846–50. 17. Bezek EM, VanHeest AE, Hutchinson DT. Grip lock injury in male gymnasts. Sports Health. 2009;1(6):518–21. 18. Amaral L, Claessens A, Ferreirinha J, Maia J, Santos P. Does ulnar variance change with age and what is the influence of training and biological characteristics in this change? A short-term longitudinal study in Portuguese artistic gymnasts. Clin J Sport Med. 2014;24(5):429–34. 19. Caine D, Howe W, Ross W, Bergman G. Does repetitive physical loading inhibit radial growth in female gymnastics. Clin J Sport Med. 1997;7(4):302–8. 20. Samuelson M, Reider B, Weiss D. Grip lock injuries to the forearm in male gymnasts. Am J Sports Med. 1996;24(1):15–8. 21. Wolfe MR, Avery D, Wolfe JM. Upper Extremity Injuries in Gymnasts. Hand clinics. 2017;33(1):187–97.

Chapter 7

Tennis and Golf Wrist Ameya V. Save and Felicity G. Fishman

Wrist injuries are commonly encountered in the young athlete. The developing musculoskeletal system of the young athlete presents a unique profile of injuries, which range from acute fractures and physeal injuries to overuse syndromes [1, 2]. As discussed in Chap. 1, as pediatric and adolescent participation in competitive sports has increased, the incidence of injuries has also increased [3, 4]. In particular, overuse injuries have increased in prevalence as young athletes participate in sports activities and training programs occurring year-round [3, 5–7]. Recent studies have demonstrated that young athletes dedicating increasing time to participation in an organized sport have a higher risk of overuse injury [1, 5, 8, 9]. Highly specialized sports training that focuses on a single motor pattern may lead to the development of muscle imbalances and repetitive loading of structures, which can independently lead to a higher risk of overuse injury [5]. In this chapter, we focus on common overuse injuries of the wrist in the young athlete involved in the sports of tennis and golf. The majority of the injuries that occur to the upper extremity in tennis are overuse injuries and not the result of an acute traumatic event [10]. The forehand stroke in tennis places the dominant hand of the player in wrist flexion, ulnar deviation, and full supination. Additionally, after the racket makes contact with the tennis ball, both wrist flexion and extension play key roles in the completion of the swing [11]. In golf, the dominant wrist requires a large arc of motion in the flexion-extension plane, whereas the non-dominant wrist moves from ulnar deviation to radial deviation and then returns to full ulnar deviation until the impact of the club on the golf A. V. Save Department of Orthopedic Surgery, Yale New Haven Hospital, New Haven, CT, USA F. G. Fishman (*) Department of Orthopedic Surgery and Rehabilitation, Loyola University Medical Center, Maywood, IL, USA © Springer International Publishing AG, part of Springer Nature 2019 A. S. Bauer, D. S. Bae (eds.), Upper Extremity Injuries in Young Athletes, Contemporary Pediatric and Adolescent Sports Medicine, https://doi.org/10.1007/978-3-319-56651-1_7

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ball [12]. The repetitive nature of these sports can lead to specific injuries, including extensor carpi ulnaris tendonitis and instability, injuries to the triangular fibrocartilage complex, DeQuervain’s tenosynovitis, intersection syndrome, flexor carpi radialis tendinitis, and dorsal impingement syndrome. These overuse injuries of the wrist can be grouped into those affecting the radial side of the wrist or the ulnar side of the wrist.

ECU Tendonitis and ECU Instability Ulnar-sided wrist pain can be caused by intra-articular pathology, including TFCC injuries and ulnocarpal impaction, as well as extra-articular pathology, such as extensor carpi ulnaris (ECU) tendinopathy and instability. Pathology of the ECU tendon is a common cause of ulnar-sided wrist pain in the young athlete. The ECU muscle originates on the lateral epicondyle of the distal humerus and crosses the wrist joint to attach on the dorsal aspect of the base of the fifth metacarpal. Its function is to provide extension and ulnar deviation at the wrist. At the level of the wrist, the ECU tendon travels through a fibro-osseous tunnel within the ECU groove of the distal ulna for approximately 15–20  mm [13, 14]. Given this intimate anatomic relationship, distal ulna morphologic features such as increased ulnar-negative variance (an ulna that is shorter than the radius at the level of the articular surface) and shallower and shorter ECU tendon grooves have been shown to be associated with ECU pathology [13]. The ECU fibro-osseous tunnel is covered superficially by the dorsal wrist extensor retinaculum, which reaches over the ulna to attach onto the pisiform and triquetrum bones, and prevents bowstringing of the tendon with muscle contraction [15]. Deep to the extensor retinaculum is the ECU subsheath, which attaches to the ulna and prevents subluxation of the tendon with wrist motion. ECU tendon pathology can range from tendinopathy and longitudinal tears to frank subluxation or dislocation. ECU tendon rupture without penetrating trauma is rare, and documented cases in the literature have been preceded by corticosteroid injection. Repetitive wrist motions during sports activities with or without tendon instability can lead to ECU tenosynovitis, consisting of irritation and inflammation of the tendon sheath, seen most commonly at the location at which the ECU tendon exits the fibro-osseous tunnel to attach onto the fifth metacarpal. This can further progress to tendinopathy, which is an adaptive response of the tendon to repetitive trauma. The early stages of tendinopathy can result in increased tendon thickness and stiffness and can lead to degradation of the tendon matrix, increased vascularity, and neuronal ingrowth. Ultimately, this may result in collagen matrix breakdown and the development of partial tears [14]. The ECU subsheath can also be acutely disrupted during sports activities, allowing the ECU tendon to subluxate over the ulna underneath an intact extensor retinaculum. Patients typically report a sensation of a pop or tear during the injury, with immediate pain at the ulnar aspect of the wrist. The mechanism for this injury involves sudden forced wrist flexion and ulnar deviation with forearm supination, often seen in tennis play, such as in the dominant

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Fig. 7.1  ECU synergy test

wrist when hitting a low forehand or the non-dominant wrist when hitting a ­two-­handed backhand [16–18]. This and other ulnar-sided injuries are more likely in players using a western or semi-western grip for topspin heavy strokes [19]. In golf players, this injury can occur in the leading hand after impact, when the wrist is forcibly flexed, ulnarly deviated, and supinated [20]. Examination of players with ECU pathology can show tenderness along the ECU tendon from its attachment on the fifth metacarpal extending proximally through the fibro-osseous sheath. Given the diagnostic challenge of evaluating patients with ulnar-sided wrist pain, the ECU synergy test can be utilized to distinguish between ulnar intra-articular and extra-articular pathology [21]. The ECU synergy test is performed with the affected forearm in full supination and the elbow flexed to 90°. The patient is asked to abduct the thumb against resistance, while the ECU tendon is directly palpated (Fig.  7.1). Pain along the ECU tendon with this maneuver is diagnostic of ECU tendinopathy. In cases of frank instability, the tendon can be seen and palpated as it moves over the ulna with active ECU contraction. In more subtle cases, subluxation can be felt with maximal wrist flexion and ulnar deviation, with

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active resisted forearm supination. Players typically describe severe pain as the ­tendon moves over the ulna. Diagnostic imaging can be obtained to evaluate the morphology of the distal ulna and any associated injuries. Ultrasound evaluation carries the benefit of dynamic examination of the tendon with wrist motion. In uninjured asymptomatic individuals, ultrasound examination has shown that the ECU tendon can displace up to 50% within the ulnar groove with forearm supination, wrist flexion, and ulnar deviation [22]. Treatment of ECU tendinopathy should begin with nonsurgical options such as rest, ice, activity modification, and splinting [14]. Persistent symptoms can be treated with wrist immobilization in a short-arm cast with the wrist in extension for 3 weeks, followed by initiation of physical therapy [23]. An corticosteroid injection into the ECU subsheath can be considered for both diagnostic and therapeutic purposes, as this can confirm the diagnosis as well as temporarily help with symptoms [24]. Surgical management for chronic ECU tendinopathy is rare but can consist of release of the inter-compartmental septum between the fifth and sixth dorsal wrist compartments [14]. Initial treatment for ECU instability consists of rest and immobilization of the affected wrist in a long-arm or Muenster-type cast with the wrist in extension and slight radial deviation and the forearm in pronation for a period of 4–6 weeks [17, 25, 26]. Surgical management for ECU instability is reserved for patients who fail conservative management and have continued symptoms. In those cases, surgical repair or reconstruction of the tendon sheath can be considered depending on the exact pathology of the injury [27]. In acute cases in which the fibrous sheath is disrupted from either its radial or ulnar-sided attachment, direct repair can be considered. However, in cases where the sheath is not repairable, a sling reconstruction can be performed [26]. In some instances where there is periosteal separation of the sheath from the ulnar side of the bone but the sheath is otherwise intact, the false pouch can be closed down and secured with suture anchors [28]. Additionally, an ulnar groove deepening can be considered concurrently with repair of the sheath in order to allow the tendon to be seated deeper within the distal ulna and discourage subluxation [29] (Figs. 7.2, 7.3, and 7.4). Postoperative care after surgical reconstruction consists of cast immobilization for 6 weeks, followed by limited activities and physical therapy for up to 3–4 months prior to return to play.

TFCC Injuries Injuries to the triangular fibrocartilage complex (TFCC) are another cause of ulnar-­ sided wrist pain in young players. The TFCC consists of the triangular fibrocartilage disk, the radioulnar ligaments, the ulnomeniscal homolog, the ulnar collateral ligament, the ECU tendon subsheath, and the ulnotriquetral and ulnolunate ligaments [30, 31]. This group of structures provide stability to the distal radioulnar joint and assist with transmission of 20% of the load from the carpus to the distal ulna in a patient with neutral ulnar variance [32]. In players with positive ulnar variance, the

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Fig. 7.2  Axial MRI, extensor carpi ulnaris tendon (white arrow) subluxated volarly with associated fluid and attenuation of subsheath

Fig. 7.3  Surgical repair of ECU subsheath

load through the carpus to the ulna increases and can predispose players to injuries to the TFCC as well as ulnocarpal abutment. Injuries to the TFCC can occur due to repetitive motions associated with sports activities. Players typically complain of ulnar-sided wrist pain and/or mechanical symptoms with axial loading, forearm pronation/supination, and wrist ulnar deviation [32]. Examination will demonstrate tenderness to palpation along the ulnar aspect of the wrist within the sulcus between the pisiform and the ulnar styloid [18]. Some patients may have a palpable click with forearm rotation. As previously noted, the ECU synergy test can be used to distinguish ulnar-sided intra-articular pathology from ECU tendonitis [21]. Provocation tests to elicit symptoms associated with TFCC pathology include the

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Fig. 7.4 Intraoperative fluoroscopic image of wrist after repair of ECU subsheath with suture anchors and supplementary suture

ulnar grind test, which consists of wrist extension and ulnar deviation with axial loading, and the piano key test, which involves applying volar and dorsal directed forces to the distal ulna and evaluates for distal radioulnar joint instability [33]. Additionally, the fovea test, consisting of the examiner manually palpating the interval between the FCU and ulnar styloid along the volar surface of the ulnar head and pisiform, can elicit tenderness indicative of a foveal disruption of the distal radioulnar ligaments [34]. Radiographs of the wrist can be used to evaluate for acute fractures and characterization of bony anatomy including ulnar variance, DRUJ morphology, and any associated degenerative changes. The proper position in which to obtain a radiograph to assess ulnar variance places the shoulder in 90° of abduction, the forearm in neutral rotation, and the wrist at neutral. MRI arthrogram is most sensitive for diagnosing TFCC injuries, although a non-arthrogram MRI done on a 3.0 T machine with a wrist coil can distinguish TFCC pathology without the need for arthrogram [35]. Typically an MRI is obtained if physical examination is suggestive of TFCC pathology and the patient and physician are considering surgical intervention. Despite the improved sensitivity of MRI evaluation of the wrist, the gold standard remains wrist arthroscopy [35]. Initial management of TFCC injuries consists of rest, immobilization, therapy, and potentially an ulnocarpal corticosteroid injection. Wrist arthroscopy is a treatment option for players who have failed non-operative management and have persistent symptoms. Arthroscopy provides direct ­visualization and confirmation of the pathology and potential dynamic evaluation of

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the distal radioulnar joint. Injuries to the central disk are typically treated with debridement due to limited healing potential of this relatively avascular region of the disk. Peripheral tears can be repaired with open or arthroscopic-assisted techniques [36]. Postoperative care after surgery includes immobilization for 4–6 weeks, followed by range of motion exercises, with return to play typically after 3 months [23].

DeQuervain’s Tendonitis Common causes of radial-sided wrist symptoms in the young athlete include DeQuervain’s tenosynovitis, intersection syndrome, and flexor carpi radialis (FCR) tendinopathy. The most common cause of tendonitis in players of racket sports is DeQuervain’s tenosynovitis [37]. This overuse injury involves the abductor pollicis longus (APL) and the extensor pollicis brevis (EPB) tendons within the first dorsal compartment on the radial side of the wrist. These two tendons form the volar border of the anatomic snuffbox. There is considerable variability in the anatomy of the first dorsal compartment, including the presence of septations within the compartment and presence of multiple slips of the APL [38]. DeQuervain’s tenosynovitis is associated with overuse and repetitive motions such as thumb abduction and wrist ulnar deviation that are associated with racket sports and golf. In particular, radial-­ sided pathology, such as DeQuervain’s tenosynovitis, is more commonly seen in tennis players who use the Eastern grip [19]. Repetitive motion contributes to swelling and thickening of the tendon sheath, leading to friction and pain with wrist motion. Players typically complain of insidious onset of radial-sided wrist pain, which is worsened with gripping and wrist ulnar deviation. Examination will demonstrate tenderness to palpation along the APL and EPB tendons on the radial and dorsal aspect of the wrist. Provocative tests for DeQuervain’s include the Finkelstein test, Eichoff’s maneuver, and the wrist hyperflexion and abduction of the thumb (WHAT) test. The Finkelstein test is performed by holding the patient’s thumb and ulnarly deviating the wrist, while checking for pain along the first dorsal compartment. Eichoff’s maneuver consists of making a fist over the flexed thumb within the palm and ulnarly deviating the wrist (Fig. 7.5). The WHAT test is performed with the wrist in hyperflexion, while the examiner resists the patient’s thumb in abduction and full extension of the metacarpophalangeal and interphalangeal joints (Fig. 7.6) [39]. Initial treatment for DeQuervain’s tenosynovitis consists of rest, activity modification, ice, and anti-inflammatory medications [18]. Players who continue to have symptoms can be treated with cast immobilization or injection [24]. Corticosteroid injections are the most effective non-operative treatment for patients, with a high rate of success [40]. However, patients who have positive clinical provocative tests and an ultrasound finding of an intra-compartmental septum between the tendons have been shown to be more likely to fail conservative measures and require s­ urgical intervention [41]. Surgical management consists of release of the first dorsal

102 Fig. 7.5 Eichoff’s maneuver

Fig. 7.6 Wrist hyperflexion and abduction of thumb (WHAT) test

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c­ ompartment to relieve symptoms. The extensor retinaculum is released on the dorsal aspect of the compartment to prevent iatrogenic volar subluxation of the tendons over the radial styloid. Great care is taken during surgery to avoid injury to the superficial sensory branch of the radial nerve. After a release of the extensor retinaculum, the compartment is evaluated for the presence of a sub-compartment between the APL and EPB tendons, which also requires decompression to prevent residual or recurrence of symptoms [42]. After surgical decompression of the first extensor compartment, hand therapy is beneficial to help restore range of motion and strength as well as decrease residual inflammation. Once the athlete is asymptomatic in daily activities as well as during strengthening activities at therapy, consideration may be given to return to sport, typically 6–8 weeks from the time of the operative intervention.

Intersection Syndrome Intersection syndrome is a less common cause of radial-sided wrist pain, but can be seen in young tennis and golf players [18]. Similar to DeQuervain’s, it is a tenosynovitis involving the extensor tendons but occurs at the crossing point of the abductor pollicis longus (APL) and extensor pollicis brevis (EPB) in the first dorsal compartment and the extensor carpi radialis longus and brevis (ECRL and ECRB) tendons in the second dorsal compartment. Players typically present with pain, swelling, and crepitus on the dorsum of the wrist, about 4–8 cm proximal to Lister’s tubercle [43, 44]. The differential diagnosis for these symptoms otherwise also includes DeQuervain’s tenosynovitis and Wartenberg’s syndrome, which is a neuritis of the radial sensory nerve. Diagnosis is typically made based on history and physical examination; however, MRI of the wrist and forearm can be obtained to confirm the diagnosis. Typical findings on MRI with intersection syndrome include peri-tendinous fluid within the first and second dorsal compartments, muscle edema, tendon thickening, loss of normal tendon architecture, and juxtacortical edema [45, 46]. Corticosteroid injection can be considered for diagnostic and therapeutic purposes. Initial management of intersection syndrome includes rest, activity modification, and NSAIDs. Persistent symptoms can be treated with wrist splinting, typically in about 15° of wrist extension [42]. Surgical management, which is rarely undertaken, consists of release of the second dorsal compartment.

Flexor Carpi Radialis Tendinitis The FCR originates from the medial epicondyle and inserts on the second metacarpal. As the tendon travels across the wrist crease toward its insertion, it deviates obliquely through a fibro-osseous tunnel adjacent to the trapezium. Due to this

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anatomy, the tendon may become irritated by the repetitive wrist flexion and extension motions that occur during both golf and tennis. The young athlete will typically complain of pain at the level of the radial wrist crease. Their discomfort is worsened by resisted wrist flexion and radial deviation [42]. Non-operative treatment consists of splinting, ice, stretching, activity modifications and NSAIDs. In cases of recalcitrant symptoms despite a trial of non-operative treatment, surgical release of the fibro-osseous tunnel may lead to symptomatic relief and eventual return to sport [12].

Dorsal Wrist Impingement Tennis and golf players are also predisposed to dorsal wrist impingement due to the complex biomechanics of the golf swing and tennis strokes [47]. Repetitive wrist extension can lead to impingement of the dorsal wrist capsule against the extensor carpi radialis brevis tendon and distal radius, resulting in thickening and scarring of the capsule [48]. Secondary inflammatory changes to the extensor retinaculum and dorsal extensor tendons can also be noted. Cadaveric analysis has identified the thickened distal border of the extensor retinaculum as a predisposing factor to development of dorsal wrist impingement [48]. A secondary cause for dorsal wrist impingement is scapholunate instability. With scapholunate instability or scaphoid rotatory subluxation, when load is applied to the scaphoid, the proximal pole traps the capsule against the ECRB as it shifts dorsally, causing indirect impingement [49]. Patients with dorsal wrist impingement complain of dorsal wrist pain associated with wrist extension and load bearing. Examination is significant for swelling and tenderness along the dorsal aspect of the wrist with worsening of symptoms upon provocative wrist hyperextension [48]. Radiographs and MRI may play a role in ruling out other causes of wrist pain as well as evaluation of more advanced degenerative changes include formation of osteophytes and dorsal cysts. CT scan, specific radiographic views (lateral radiograph with the hand flexed and supinated 30–40°), and potentially a corticosteroid injection into the carpometacarpal joint may help to differentiate between dorsal wrist impingement and a symptomatic carpal boss. Initial management for dorsal impingement, like most other overuse syndromes, includes rest, nonsteroidal anti-inflammatory medications, and splinting. Corticosteroid injections can be considered in an attempt to decrease inflammation and provide temporary relief of symptoms. Cases that fail conservative management can progress to surgical intervention, although this varies based on the specific pathology. Surgical options include arthroscopic debridement and excision of hypertrophic synovium versus open partial resection of the thickened extensor retinaculum with a tenosynovectomy of the affected extensor tendons [48–50].

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In summary, wrist injuries that are associated with the young athlete involved in golf and tennis are typically due to repetitive strain and are overuse in nature. Acute injuries, such as traumatic ECU dislocations, can occur, but are less commonly seen than overuse injuries such as ECU tendinopathy, DeQuervain’s tendinitis, and FCR tendinitis. Initial treatment of these injuries is generally non-operative with surgical intervention reserved for those with persistent symptoms despite conservative management. Return to sport may be considered for these patients when range of motion and strength is restored and the patient remains asymptomatic with both therapy and activities of daily living.

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18. Wang S, Hausman M.  Elbow, wrist, and hand injuries in the young tennis athlete. In: The young tennis player. Cham: Springer International Publishing; 2016. p. 167–182. 19. Tagliafico AS, et al. Wrist injuries in nonprofessional tennis players: relationships with different grips. Am J Sports Med. 2009;37(4):760–7. 20. Ek ETH, Suh N, Weiland AJ. Hand and wrist injuries in golf. J Hand Surg. 2013;38(10):2029–33. 21. Ruland RT, Hogan CJ. The ECU synergy test: an aid to diagnose ECU tendonitis. J Hand Surg. 2008;33(10):1777–82. 22. Lee KS, et al. Ultrasound imaging of normal displacement of the extensor carpi ulnaris tendon within the ulnar groove in 12 forearm–wrist positions. Am J Roentgenol. 2009;193(3):651–5. 23. Avery DM, Rodner CM, Edgar CM. Sports-related wrist and hand injuries: a review. J Orthop Surg Res. 2016;11(1):99. 24. Wysocki RW, Biswas D, Bayne CO. Injection therapy in the management of musculoskeletal injuries: hand and wrist. Oper Tech Sports Med. 2012;20(2):132–41. 25. Patterson SM, et al. Conservative treatment of an acute traumatic extensor carpi ulnaris tendon subluxation in a collegiate basketball player: a case report. J Athl Train. 2011;46(5):574–6. 26. Burkhart SS, Wood MB, Linscheid RL. Posttraumatic recurrent subluxation of the extensor carpi ulnaris tendon. J Hand Surg. 1982;7(1):1–3. 27. Hunt TR.  Operative techniques in hand, wrist, and elbow surgery. Switzerland: Lippincott Williams & Wilkins; 2016. 28. Inoue G, Tamura Y. Surgical treatment for recurrent dislocation of the extensor carpi ulnaris tendon. J Hand Surg [Br]. 2001;26:556–9. 29. MacLennan AJ, et al. Diagnosis and anatomic reconstruction of extensor carpi ulnaris subluxation. J Hand Surg. 2008;33(1):59–64. 30. Palmer AK.  Triangular fibrocartilage complex lesions: a classification. J Hand Surg. 1989;14(4):594–606. 31. Skalski MR, et al. The traumatized TFCC: an illustrated review of the anatomy and injury patterns of the triangular fibrocartilage complex. Curr Probl Diagn Radiol. 2016;45(1):39–50. 32. Crosby NE, Greenberg JA.  Ulnar-sided wrist pain in the athlete. Clin Sports Med. 2015;34(1):127–41. 33. Ahn AK, Chang D, Plate AM. Triangular fibrocartilage complex tears: a review. Bull NYU Hosp Jt Dis. 2006;64(3–4):114–8. 34. DaSilva MF, et  al. Evaluation of ulnar sided wrist pain. J Am Acad Orthop Surg. 2017;25(8):E150–6. 35. Anderson ML, et al. Diagnostic comparison of 1.5 tesla and 3.0 tesla preoperative MRI of the wrist in patients with ulnar-sided wrist pain. J Hand Surg. 2008;33(7):1153–9. 36. Buterbaugh GA, Brown TR, Horn PC. Ulnar-sided wrist pain in athletes. Clin Sports Med. 1998;17(3):567–83. 37. Eric C, et  al. Imaging of sports-related hand and wrist injuries: sports imaging series. Radiology. 2016;279(3):674–92. 38. Júnior PRP, et al. Surgical and anatomical studies on De Quervain’s tenosynovitis syndrome: variations in the first extensor compartment. Hand Microsurg. 2016;5(2):50–5. 39. Goubau J, et al. The wrist hyperflexion and abduction of the thumb (WHAT) test: a more specific and sensitive test to diagnose de Quervain tenosynovitis than the Eichoff’s test. J Hand Surg (E). 2014;39E(3):286–92. 40. Richie Iii CA, Briner WW. Corticosteroid injection for treatment of de Quervain’s tenosynovitis: a pooled quantitative literature evaluation. J Am Board Fam Pract. 2003;16(2):102–6. 41. De Keating-Hart E, et al. Presence of an intracompartmental septum detected by ultrasound is associated with the failure of ultrasound-guided steroid injection in de Quervain’s syndrome. J Hand Surg (Euopean Volume). 2015;41(2):212–9. 42. Adams JE, Habbu R.  Tendinopathies of the hand and wrist. J Am Acad Orthop Surg. 2015;23(12):741–50. 43. Jain SK, Agarwal V, Naik S. Intersection syndrome: how, why and role of imaging. Int J Health Sci Res (IJHSR). 2016;6(3):325–8.

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44. Draghi F, Bortolotto C.  Intersection syndrome: ultrasound imaging. Skelet Radiol. 2014;43(3):283–7. 45. Shiraj S, et al. Intersection syndrome of the wrist. Orthopedics. 2013;36(3):165–227. 46. Lisle DA, et al. MR imaging of traumatic and overuse injuries of the wrist and hand in athletes. Magn Reson Imaging Clin N Am. 2009;17(4):639–54. 47. Partington KJ, McNally EG. Imaging of golf and racquet injuries. In: Guermazi A, Roemer FW, Crema MD, editors. Imaging in sports-specific musculoskeletal injuries. Cham: Springer International Publishing; 2016. p. 359–80. 48. VanHeest AE, et  al. Extensor retinaculum impingement in the athlete. Am J Sports Med. 2007;35(12):2126–30. 49. Henry M.  Arthroscopic management of dorsal wrist impingement. J Hand Surg. 2008;33(7):1201–4. 50. Jain K, Singh R. Short-term result of arthroscopic synovial excision for dorsal wrist pain in hyperextension associated with synovial hypertrophy. Singap Med J. 2014;55(10):547–9.

Chapter 8

Carpal Injuries in Sport Katherine C. Faust and Allan E. Peljovich

Introduction Approximately 30 million pediatric patients participate in “organized sport” in America; therefore, approximately 60 million pediatric wrists are at risk of athletic injury in the United States [1]. The frequency of injury to the more vulnerable neighboring distal radius physis makes injuries to the carpus itself much less common. Challenges to diagnosis include a progressive ossification pattern whereby not all the bones are present on radiographs until age 9–10 years and incomplete ossification until about 12–14 years. Ossification follows a predictable clockwise pattern: capitate (2–3  months of age), hamate (4  months), triquetrum (2  years), lunate (4 years), scaphoid, trapezium (5 years), and pisiform (9–10 years) (Fig. 8.1d) [2].

Fractures Thick cartilage covers the ossifying carpus, protecting the bone from fracture. Because ossification is incomplete until skeletal maturity, magnetic resonance imaging (MRI) may be necessary to diagnosis fractures in pediatric patients that would be visible on radiographs in adults. Various sports have hand positions and uses that predispose carpal bones to fracture, such as the hammer fist in martial arts, gripping a club in golf, holding a baseball bat/lacrosse stick/hockey stick, and flat-­hand grab position in diving. K. C. Faust Private Practice, 2633 Napoleon Ave, Suite 600, New Orleans, LA, USA A. E. Peljovich (*) Department of Orthopedic Surgery, Children’s Healthcare of Atlanta, The Hand and Upper Extremity Center of Georgia, Children’s Hospital of Atlanta, Atlanta, GA, USA e-mail: [email protected] © Springer International Publishing AG, part of Springer Nature 2019 A. S. Bauer, D. S. Bae (eds.), Upper Extremity Injuries in Young Athletes, Contemporary Pediatric and Adolescent Sports Medicine, https://doi.org/10.1007/978-3-319-56651-1_8

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Fig. 8.1  These X-rays are from a 16-year-old high school football player. He presented to the ED during spring practices after a fall on an extended wrist with focal pain along the radial wrist and snuffbox tenderness. (a) Initial views interpreted as normal. He was splinted and allowed to return to sport as tolerated. Pain subsided after spring football. (b) He presented to the office with radial wrist pain that recurred once summer football workouts began. Radiographs clearly demonstrate a proximal pole nonunion. (c) Surgery was required to stabilize and ultimately heal this injury. (d) The average onset of radiographic ossification is labelled on this x-ray

Scaphoid Fractures The most frequently fractured carpal bone is the scaphoid, and even its occurrence is rare in young children. By definition, a pediatric scaphoid fracture occurs in a patient with an open distal radius physis [3]. Ossification of this carpal bone begins distally as early as age 4 years and ends proximally by age 12–14 years. Peak incidence of fracture in children occurs between 12 and 15 years of age [4]; fractures within the first decade of life are relatively rarer [5]. Original reports of this injury in children cited distal pole fractures as more common in younger patients [6, 7]. However, Gholson et al. found that scaphoid fracture patterns in children today actually mirror adult trends with a preponderance of waist fractures [8]. The authors hypothesized their findings as the result of children participating in more “adult-­like” sports and

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activities, as well as increased body mass indices. Stress fractures are insufficiency fractures, and athletes with high repetitive loads on the wrist are at risk for scaphoid stress fractures. These types of fractures have been documented in gymnasts, platform divers, tennis players, and shot putters [9–13]. Diagnosis of scaphoid fractures is critical due to the high risk of nonunion in unrecognized scaphoid fractures. Complications of scaphoid nonunion include persistent pain and premature traumatic arthritis. The challenge is that recognition is not straightforward, as plain X-rays are often negative initially. The fall on an outstretched rotated wrist is memorable, but not necessarily very painful. A high index of suspicion is therefore warranted to make the diagnosis early. The various findings on physical exam include volar tubercle tenderness, snuffbox tenderness, pain with radial deviation of the hand, and pain with wrist motion [14]. None of these findings are specific enough to make a definitive diagnosis. Parvizi et al. found that the combination of snuffbox tenderness, volar tubercle tenderness, and pain at the snuffbox with axial compression of the thumb was 100% sensitive and 74% specific for a true scaphoid fracture [15]. The pronated lateral and ulnar deviated PA radiographs added to the routine posteroanterior (PA) and lateral wrist radiographs improve the sensitivity in acute diagnosis. Even when these X-rays are negative, however, clinical suspicion of a scaphoid fracture warrants immobilization and further workup given the high degree of false-negative plain films (Fig. 8.1). Immobilization of the wrist in a thumb spica cast is recommended with repeat clinical and radiographic evaluation in 2–3 weeks. Thirty percent of pediatric patients with positive physical exam findings for scaphoid fracture but normal radiographs on presentation will show radiographic findings at 2 weeks [16]. An alternative to consider is to use advanced imaging early. MRI and computed tomography (CT) scans both have been shown to improve the sensitivity of diagnosis and are recommended if the athlete strongly desires immediate return if the bone is not fractured (Fig. 8.2). The relative utility of MRI over CT scan is the absence of radiation and the improved diagnostic accuracy as the differential diagnoses are more thoroughly evaluated, i.e., soft tissue injury and bone contusion. MRI finding of bone bruising without fracture should still be treated as a fracture, as 2% can progress to complete fracture even with immobilization [17]. For those scaphoid fractures diagnosed on plain films, CT scan is performed to assess for displacement, given the association of displacement with nonunion and the consequences of malunion. Cast immobilization for avulsion fractures, incomplete fractures, and non-­ displaced fractures of the scaphoid may range from 4 to 12 weeks depending on the location of the fracture [3]. Gholson et al. found that open physes correlated with a longer time to union [8]. The healing rate in the pediatric and adolescent populations is more than 90% in non-displaced fractures treated acutely. The need for a longversus short-­arm cast, and whether to incorporate the thumb in the cast, continues to be assessed with clinical studies. Gellman and colleagues found that the union rate for non-­displaced scaphoid waste fractures was not negatively affected with a simple short-­arm cast; but, rotation of the forearm does stress the scaphoid in biomechanical studies [18, 19]. The authors’ preference is to immobilize in a long short-arm cast with i­ nterosseous mold to reduce rotation and incorporate the thumb

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Fig. 8.2  A 9-year-old football player presented with radial-sided wrist pain and discrete snuffbox tenderness. (a) Initial radiographs were normal. (b) Parents strongly desired return to play if able, so an MRI was ordered which demonstrated a distal pole fracture

across the metacarpophalangeal (MCP) joint only, leaving the thumb interphalangeal joint free. Children are seen approximately every 3–4 weeks with repeat radiographs until there is clear clinical and radiographic evidence of healing. In cases where healing is suspected, but not clear, a CT scan is used to make a final determination. Children can run and work on lower extremity and core strengthening

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with their cast, but are not cleared for release to fully train and/or participate in sport until healing is confirmed. Once healed, a removable wrist splint is provided to help the transition along with therapy to expedite strengthening of the arm. Acute displaced scaphoid fractures should be treated with surgical reduction and fixation to reduce the risk of nonunion and prevent the consequences of malunion. In addition, fractures within the proximal third of the fracture (known as “proximal pole fractures”) are usually offered surgery given the high rate of nonunion without surgery (Fig. 8.1) [2]. There is also the option of early stabilization of non-displaced scaphoid fractures with a compression screw to allow athletes an earlier return to play, depending on their sport. It is important to note however that early surgery requires the athlete to assume the risks of surgery and does not improve the healing rate, although it may shorten the healing time. It is quite common for children to present for first-time evaluation with a chronic scaphoid nonunion (Fig.  8.1). While there are case reports of pediatric scaphoid nonunion healing with immobilization alone, the generally accepted recommendation is surgical fixation often with bone graft to stimulate healing [20–24].

Capitate, Hamate, Triquetral, Trapezial, and Pisiform Fractures Carpal fractures other than the scaphoid are rare injuries in children. Isolated capitate fractures in younger children are almost reportable, and one case report demonstrated impressive remodeling potential in a young child treated in a cast [25]. A high-energy injury is usually required to fracture the capitate, and this may explain its more common association with perilunate injuries and Fenton syndrome (scaphocapitate fracture). Triquetral fractures are typically avulsion-type injuries seen in perilunate injuries. Trapezial fractures may be seen in combination with thumb metacarpal base fractures. Pisiform fractures and dislocations have been seen in combination with distal radius fractures in 12- and 13-year-old patients; in described cases, they healed with closed reduction and immobilization [26]. A more recognized carpal injury involves the hamate and more specifically its palmar projection called “the hook.” Hook of hamate fractures are typically the result of forceful direct impact seen in athletes who play “stick” sports, i.e., baseball, golf, hockey, tennis, etc. When injured, there is immediate pain along the ulnar base of the palm and often a sudden electrical shock along the small and ring finger due to the proximity of the ulnar nerve to the hook. Diagnosis of carpal bone fractures requires recognition of the possibility and a high index of suspicion when there is tenderness over any of the carpal bones after an injury. Palpation of the carpus is the best examination maneuver to identify the fracture, but some pediatric patients are not cooperative or able to be examined in such a fashion. As with scaphoid fractures, short-term immobilization for suspected injuries with repeat evaluation is an option. Similarly MRI or CT scans might be necessary if plain radiographs are inconclusive but pain persists. The authors’

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Fig. 8.3  A 16-year-old golfer presented with persistent pain along the ulnar base of his palm. His pain resulted from a memorable swing that caught the turf hard. His clinical findings included point tenderness along the hook of the hamate. (a) Initial plain films including a carpal tunnel view does not demonstrate any obvious fracture or instability pattern. (b) Representative CT scan view of his carpus clearly demonstrates a fracture through the base of the hook of the hamate. The hook was excised surgically, and he was able to return to sport approximately 6 weeks later

preference is to use MRI when assessing for a radiographically negative carpal fracture due to both its precision and ability to evaluate more than the bone [27]. The hook of hamate fracture is particularly confirmed with a combination of tenderness over the hook and a fracture seen on the carpal tunnel view radiograph. If no fracture is visible on plain film, which is more often the case than not, MRI can confirm the diagnosis (Fig. 8.3). Treatment varies based on the carpal injured and the severity of injury. Stable avulsion-type injuries of the triquetrum might only require a removable splint, while non-displaced body fractures should be casted until osseous union. Capitate ­fractures, especially at the neck, warrant consideration for surgical fixation due to the risk of nonunion and avascular necrosis. And, while the hook of the hamate fracture can heal closed with many weeks of casting, even adolescent athletes may be offered early surgery to excise the hook for earlier return to sport [28].

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Children can also present with nonunited fractures, especially for the hamate hook. Excision of the hook is the surgical option for this situation. One relative advantage of excision is a fairly rapid return to sport quoted as short as an average of 6 weeks in one study of amateur athletes and a median of 6 weeks in a study including amateur and professional athletes [28, 29]. Treating nonunions of the other carpals ranges from temporary cast immobilization to bone grafting with fixation [30].

Combined Carpal Fractures Multiple carpal fractures are the result of higher-energy injury and come with greater potential for negative consequences. Fenton’s syndrome, otherwise labeled “scaphocapitate syndrome,” occurs when the capitate impinges on the distal radius and fractures in the setting of a scaphoid fracture [31, 32]. There are also cases of scaphoid fractures in combination with distal radius and triquetral fractures [33, 34]. It remains important to recognize these possibilities as these combined injuries almost always require surgical fixation.

Carpal Contusions Distinct from either stress fractures or traumatic fractures, bone contusion represents an intermediate injury: enough acute energy to injure but not fracture. Never visible on plain films, this diagnosis is made from a combination of the clinical history supporting pain from a discrete injury and advanced imaging demonstrating a discrete area of edema within the bone in the absence of a fracture line or other findings that could support vascular necrosis and stress response [35]. A bone contusion is a result of subcortical microfractures with intraosseous hemorrhage and inflammation [36]. These injuries most often present with unresolving pain following an injury where radiographs are normal and clinical exam suggests a discrete location of pain (Fig. 8.4). The challenge in treating these injuries is the length of time for pain resolution which can be months. And, there is one prospective study that evaluated scaphoid contusions in which 1 of 50 converted to a true fracture [17]. While casts to protect scaphoid contusions have been reported, it is unclear that anything more than supportive bracing and patience is required for treatment [17, 37, 38]. Follow-up plain films and MRI are warranted if pain worsens or persists beyond about 2 months [17, 38].

Sprains Sprains, or ligamentous injuries, are likely much more common than appreciated. Many physeal fractures and torus fractures of the distal radius are often misdiagnosed clinically as a wrist sprain; however, real injury involving the ligaments of the wrist is not uncommon.

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Fig. 8.4  A 13-year-old basketball player presented with nearly 2 months of wrist pain following a fall during a game. Initial wrist radiographs at an urgent care were normal. Pain has persisted, and he has played through it wearing a brace after games and taking nonsteroidal anti-inflammatory medications for discomfort. He had focal tenderness in his scaphoid and scapholunate ligament but no clinical instability. (a) Representative radiographs of a dynamic series of films demonstrate the profile of his scaphoid and lunate and the scapholunate relationship. (b) Representative views of MRI ordered to evaluate the carpus demonstrate edema within the scaphoid and the lunate without discrete fracture lines or ligamentous disruption consistent with contusions of the scaphoid and lunate. In time, and with supportive care, his pain resolved

I ntercarpal Ligament Injury, Including Scapholunate Interosseous Ligament (SLIL) Tears In adults, scapholunate ligament injuries are generally identified by scapholunate interval widening on plain radiographs. Because the scaphoid ossifies from distal to proximal, the scapholunate interval closes radiographically as patients skeletally mature. Kaawach et al. analyzed 119 radiographs of children age 6–14 years and found that the typical adult scapholunate interval of 2 mm is not reached by girls until age 11 years and by boys until age 12 years [39]. Contralateral wrist films can be helpful, but advanced imaging is in order if there is a question of SLIL injury with normal radiographs (Fig. 8.5). Complete SLIL tears are generally operative, but which surgical technique to employ is controversial, and guidance in the

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Fig. 8.5  A 15-year-old basketball player presented after she fell on her wrist during a game. She initially came out of the game but then returned with her wrist taped. Persistent pain and stiffness led her to a formal evaluation after about 1 week. (a) Radiographs, including stress views, suggest only dorsal lunate tilt. (b) MRI arthrogram, ordered due to focal SL pain, led to the diagnosis of a complete SL tear. (c) She underwent surgery to repair the SL and stabilize the carpus anatomically

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pediatric population is limited. Families should be counseled that lengthy rehabilitation may be needed and that return to play may not be allowed for several months.

Triangular Fibrocartilage Complex (TFCC) Tears Ulnar-sided wrist pain in the athlete can result from a number of issues. Probably the most commonly injured structure is the triangular fibrocartilage (TFCC), which sits atop the distal ulna attached to the radius, the carpus, and the extensor carpi ulnaris (ECU). The TFCC is comprised of the articular disc, the dorsal and volar radioulnar ligaments, the ulnocarpal ligaments, the meniscus homologue, and the ECU tendon sheath. It functions to share load across the wrist with the distal radius and serves as the primary stabilizer to the distal radioulnar joint (DRUJ). The TFCC is injured with rotational injuries to the wrist and has been associated with distal radius fractures in children and adults [40]. Tears are classified by location, with ulnar-peripheral (type B) tears being the most common in adolescents [2], in contrast to adults in whom central tears are more common. Athletes with TFCC tears present with pain that is primarily ulnar-sided, right around the soft spot between the pisiform and the ulnar styloid. Those patients who had an associated distal radius fracture may present with ulnar-sided pain that persists after the radial-sided pain resolves. The “ulnar foveal sign” describes tenderness in an area highly diagnostic for injury to the TFCC (Fig. 8.6a) [41]. Swelling, bruising, and other externally visual markers of injury are mostly absent. Other symptoms include a perceived or audible click, pain with wrist rotation, and pain when loading the wrist, especially in extension and ulnar deviation. Stressing the DRUJ is critical; one should look for a discrepancy compared to the uninjured side that would indicate a significant injury. The standard radiographs for the wrist are a PA and lateral; TFCC injuries are suspected with fractures of the ulnar styloid or a type 2 lunate, which can be a hint of lunate-hamate impaction. When assessing the TFCC, the ulnar variance is determined by a PA radiograph done with the shoulder abducted to 90°, the elbow flexed at 90°, and the forearm in neutral [42, 43]. An additional view particularly helpful in the setting of TFCC pain is a pronated clenched fist view which estimates the functional ulnar variance under conditions similar to activity [44]. Advanced imaging is recommended when there is either gross instability or failure to improve with conservative management. MRI is the preferred modality, and an arthrogram is often added to the procedure to enhance the visualization of the TFCC and assess for disruptions, but arthroscopy remains the gold standard for diagnosis of TFCC tear given the high rate of false-negative studies (Fig. 8.6b) [40]. Initial management includes casting or splinting acute injuries and splinting and activity restriction for injuries that present later than about 3–4 weeks. The need for a long-arm cast is determined by whether short-arm immobilization with or without interosseous molding to minimize rotation is enough to eliminate pain. Acutely, immobilization is continued for 3 weeks. Following cast removal, athletes are sent

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Fig. 8.6  Diagnosing and treating a TFCC injury. (a) The ulnar foveal soft spot is found just palmar and distal to the ulnar styloid and just proximal to the palpable triquetrum. (b1) MRI arthrogram of a patient with suspected TFCC tear. The TFCC is not a uniform color, and the dye passes into the area where the TFCC typically connects to the ulnar side of the capsule. (b2) MRI demonstrates a tear off the radial attachment of the TFCC with dye passing directly into the DRUJ compartment. (c) Braces and taping options to stabilize the wrist and limit extremes of motion that could lead to pain

for physiotherapy to work on a gradual strength and mobility program. As pain improves, immobilization transitions to DRUJ support taping. Transition to sport depends upon sufficient strength and sports simulations that demonstrate the athlete can participate without pain. DRUJ support is often continued as athletes transition back to sport (Fig. 8.6c). Athletes and their parents should be advised that return to sport even with nonoperative management can take 2–3 months. Athletes who are struggling to progress with therapy can consider receiving a corticosteroid injection. Surgery is indicated for all athletes with gross instability and those who fail to progress with conservative treatment. While there is no data concerning the natural history of TFCC injuries, it is the authors’ impression that most will improve without the need for surgery. Surgery consists of either repairing or debriding the TFCC, depending upon the specific location of the injury within the TFCC, and is usually accomplished with arthroscopic techniques (Fig. 8.7). Ulnar shortening osteotomy should be considered in the presence of static ulnar positivity. Young athletes return to sport an average of 3–4 months after surgery [45].

120 Fig. 8.7 Arthroscopic view of a TFCC tear. (a) A view of the peripheral TFCC detachment with synovitis. (b) The synovitis is debrided along with the peripheral TFCC. The tear is more visible. (c) An arthroscopic repair demonstrates the TFCC periphery now abuting the ulnar capsule. The arthroscopic knot/suture is visible

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Dislocations The wrist joint is stabilized by as many as 18 extrinsic and 5 intrinsic ligaments, making this joint and its articulations highly complex. Dislocations by their nature involve rupturing of ligaments with associated instability and disruption of articulations. The energy required to cause a wrist dislocation is high enough that there can be associated fractures. In the acute phase, there is risk to the neurovascular structures and the possibility of compartment syndrome. Treatment is immediate reduction and often surgery to help the ligaments heal anatomically. Consequences of these injuries include significant contracture, chronic instability, avascular necrosis, and traumatic arthritis. The representative injury for the carpus is the perilunate dislocation, which is the result of high-energy axial loading of the wrist with torsional moments. It is rare but described in pediatric patients [46–50]. Perilunate injuries are dramatic. The athlete will cease play; swelling or deformity is apparent; and paresthesias to the fingers may be present. Radiographs will demonstrate a combination of incongruity, ­dislocation, and possible extrusion of the lunate away from the distal radius. Careful attention to the radiographs are required, considering up to 25% of these injuries have been missed on initial evaluation in one study (Fig. 8.8a–b) [51]. Carpal fractures can be easily overlooked on standard radiographs but be very apparent on MRI or CT scan, which can be obtained after reduction [52]. Treatment is prompt reduction and ligamentous repair, in addition to temporary immobilization with smooth pins and casting (Fig. 8.8c). Return to sport is not guaranteed, and the process can take months to a year.

Repetitive Stress Injuries Various sports place large repetitive forces across the wrist, and open physes in pediatric athletes may have altered growth as a result. Physeal arrest of the distal radius is discussed in detail in the “Gymnast Wrist” chapter.

Hyperligamentous Laxity and Carpal Instability Ligamentous laxity is more commonly known by the phrase “double jointed.” Various authors have attempted to quantify loose-jointedness, but a true objective and reliable measure is lacking [53–55]. A common measure, called the Beighton Score, seeks to determine the general state of ligamentous laxity in an individual by noting mobility in the knees, elbows, wrists, and fingers with an increasing score indicative of hypermobility (Table 8.1) [55, 56]. Repetitive stress loosens hypermobile joints which can lead to chronic pain as well as joint clunking. Ligamentous

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Fig. 8.8  This 16-year-old football player, a defensive back, needed to come off the field for acute wrist pain following a fall on an outstretched wrist during a play. (a) His initial X-rays at the referring facility prior to transfer. As is typical for these painful injuries, getting views in the right position is difficult for the injured athlete, and the significance of the injury is easily misinterpreted as the views are off-plane. (b) An extra cross table lateral clearly demonstrates the volar lunate dislocation in this variant of a perilunate dislocation. (c) Radiographs after open reduction, carpal fixation, and ligament repair

Table 8.1  The Beighton-Horan score for measuring joint hypermobility. A combined score ≥4 reflects hypermobility [55, 56] The Beighton-Horan criteria for generalized hypermobility Maximum Joint examination points Passive hyperextension of the small finger (measured 2 bilaterally) Passive thumb apposition to the forearm (measured 2 bilaterally) Elbow hyperextension (each elbow) 2 Knee hyperextension (each knee) 2 Standing trunk flexion with knees fully extended 1

Criteria for positive sign >90° Thumb touches forearm >10° >10° Both palms flat on floor

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laxity in the wrist can produce a pattern of symptoms sometimes referred to as the “snapping wrist.” This pattern is due to incompetence of the ulnar triquetrohamatocapitate ligament volarly and the dorsal radiocarpal ligament dorsally [57]. Complaints include ulnar and midcarpal wrist pain, associated with ulnar to radial deviation and other forceful wrist motions. Patients complain of a snap or clunk in their wrist that is particularly painful. General ligamentous laxity is more frequent in young females especially around puberty, and the sports that seem to bring out wrist pain include stick and racquet sports [55]. The most extreme cases manifest from congenital conditions that result in pathologically lax collagen, namely, Ehlers-Danlos syndrome and Marfan’s syndrome. Diagnosis truly requires recognition of this condition and is frequently undiagnosed or misdiagnosed for a long time due to the nebulousness of the symptoms and the difficulty in bringing out symptoms in a normal physical exam without special stress maneuvers. Patients are sometimes written off as being hypochondriacs or as having secondary gain, i.e., desire to leave a sport they feel pressured to continue. Measuring ligamentous laxity is critical, and the Beighton scale or the Garcia-Elias method can be employed [53, 58]. The midcarpal shift test is the physical examination maneuver that reproduces the pain and sometimes even a clunk [59]. Radiographs will often depict a palmar sag to the carpus visible on the lateral with an associated volar tilt to the lunate (Fig. 8.9). This pattern is often referred to as a

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Fig. 8.9  The radiographs of a young field hockey player with progressive wrist pain. She had several suspect radiographic findings: (a) normal alignment but pronounced trabeculae on PA. (b) VISI on lateral, type 2 lunate articulating with the hamate, and slight ulnar positivity. Examination was consistent with ligamentous laxity, and her pain was reproduced with a midcarpal clunk test. A course of therapy to strengthen the extrinsic muscles, and supportive taping, proved sufficient for sport

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palmar midcarpal instability. Rarely the opposite is seen where the lunate is dorsally tilted and the capitate appears to subluxate dorsally [60, 61]. Treatment is geared to strengthening the muscles and tendons that cross the wrist, proprioceptive retraining, athletic orthoses including taping and pisiform boost splints, and generalized sport fitness [61, 62]. Surgery is reserved for exceptional cases where the athlete cannot otherwise continue and understands that the results of the operation may still not allow return to sport. Capsular tightening procedures have been shown to be helpful, but not always reliable; they have been reported in at least one child with success [63, 64]. Partial fusions of the midcarpal joint have also been utilized with some modest success but are associated with a fairly substantial loss of motion [64–66]. Nonoperative treatment is the authors’ preferred choice, including switching sports. While partial wrist fusions are considered in adults with midcarpal instability failing conservative measures, the authors would start with a soft tissue procedure to “tighten” the midcarpal joint, such as a capsulodesis procedure, in the pediatric patient if surgery was the only reasonable option.

Ulnocarpal Impaction Ulnar-sided wrist pain due to the repetitive loading of an ulnar-positive wrist, known as ulnocarpal impaction, is a common source of pain in young athletes. Another common label for this same phenomenon is ulnocarpal abutment syndrome, and it is the cause of secondary TFCC disruptions. This condition results from a mismatch in the relationship between the length of the radius and ulna where the ulna is “taller” than the radius. Ulnar positivity is a normal anatomic finding for some but in children can also result from premature closure of the distal radial physis that can occur as either the consequence of a periphyseal fracture or a chronic gymnast wrist (distal radial physeal stress fracture). Athletes typically present with insidiously worsening ulnarsided wrist pain. Symptoms are exacerbated with loading in wrist extension, ulnar deviation, and forearm rotation. Physical findings are similar to that of TFCC injury. Treatment always starts conservatively. Physically reducing the ulnar variance via ulnar-shortening osteotomy remains the surgery of choice for recalcitrant cases [67].

Stress Fractures Young athletes with stress fractures of the carpus will present with pain in the wrist, sometimes vague, without any real discrete history of trauma. Tendinosis, synovitis, repetitive stress, and secondary gain are all in the differential diagnoses. The athlete may have already had a set of normal X-rays and may have tried rest, braces, and even therapy with only short-term improvement. Case studies in the literature point to the scaphoid as the most commonly reported carpal with stress fracture, but the hook of hamate has also been involved [11, 68–71]. These reports concerning carpal stress fractures in children and adolescents illustrate some consistencies in

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presentation: males aged 15–18 years with insidious onset of pain and regular training of multiple hours per day in their sport. Findings on examination included discrete carpal tenderness, reduced range of motion, and reduced strength. Plain films demonstrated nonunion in some, but were unremarkable in others. The diagnosis of stress fracture is generally made by MRI, with edema of the affected bone. Stress fracture should be included in the differential diagnosis when a young athlete presents with a history of insidious and worsening activity-related pain in the wrist. Signs of other issues like tendinosis are likely to be lacking. Plain films should be obtained. In addition, the authors certainly advocate for MRI when pain has been present for months; symptoms are worsening; and stress fracture is a consideration. If diagnosed, rest and immobilization are the mainstay of treatment, with surgical treatment a possibility on a case-dependent basis. Furthermore, vitamin d levels are checked to ensure they are not low, and if low, vitamin d supplementation is part of the treatment [72–75]. The authors have also employed bone stimulation in the hopes of expediting recovery and healing.

Lumps and Bumps Benign growths and prominences are relatively common pediatric conditions that are often asymptomatic. In the setting of repetitive stress, especially the kind of high stress and loading with athletics, these lesions can become a nuisance. In some cases, as with occult ganglions, the lesion is symptomatic long before it is visible or palpable. Any growth or prominence deserves attention and a workup that could occasionally require advanced imaging, such as ultrasound or MRI, and possibly surgery. Ganglions Ganglions are benign pseudocysts that commonly arise from either the dorsal or volar wrist capsule or tendons. Dorsal ganglions can become painful in the setting of repetitive wrist extension and loading as the lesion located about the scapholunate interval becomes impacted. Volar ganglions can be painful too depending upon sport, but less commonly so. The etiology of ganglions is largely unknown. Not clearly associated with injury, there does appear to be a statistical association between ligamentous laxity and painful dorsal wrist ganglions [76]. Wrist ganglions in children seem to have a different natural history then adults, with a spontaneous resolution rate reported as greater than 80% within a year of diagnosis [77, 78]. Both these studies evaluated young children with an average age of 3.2 years in one study and 10.2 years in the other. Whether the resolution rate reduces as children move into or past puberty is unclear. Ganglions are often straightforward to diagnose by a combination of their specific location in the wrist, their surprising firmness, and their response to a pen light (transillumination) (Fig. 8.10). Flexing the wrist can help visualize a dorsal wrist

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a

b

c

Fig. 8.10  Wrist bumps. (a) The volar wrist ganglion is most often encountered in the area of the wrist creases radial to the position of the flexor carpi radialis tendon. (b) The dorsal wrist ganglion is most often encountered over the dorsoradial wrist in the area of the scapho-luno-capitate interval. Flexing the wrist can help expose an otherwise “hidden” prominence. (c) The “carpal boss” radiograph profiles the protuberant and painful index CMC joint

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ganglion. Doubts can be confirmed either with ultrasound or MRI, where their features are diagnostic. Painful occult ganglions will occasionally present with dorsoradial wrist pain specific to the scapholunate interval and no obvious physical findings. Advanced imaging is often utilized in the case of persistent pain in the scapholunate location with negative radiographs and failure to respond to splinting, activity modification, and rest [79]. Treatment is initially conservative given the natural history [80]. Painful ganglions may improve with splinting and rest. If persistent symptoms occur, aspiration and/or injection can palliate the athlete during season. Recurrence following aspiration runs around 60% however [81]. Surgery is reserved for those young athletes for whom pain persists despite an appropriate period of treatment and observation. Surgery is also considered for athletes about to start an important season or after the completion of an important season when symptoms persist. Excision during season is avoided given that many athletes will have wrist pain for 3–8 weeks following excision. Recurrences are not infrequent in these younger patients and reported as high as 36% in one study [82]. Su et al. have found success in methylene blue staining of the ganglion intraoperatively to aid in complete resection and found their recurrence down to 6% [83].

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Carpal Bosses Carpal bosses present like dorsal wrist ganglions over the dorsal-radial aspect of the wrist. They are relatively easy to differentiate from ganglions as their location is over the index or long carpometacarpal (CMC) joint as opposed to the carpus. Diagnosis can be confirmed with plain films, including a particular modified lateral “carpal boss” view (Fig. 8.10c) [84]. Current opinion is split on whether these bony prominence of the index and sometimes long CMC joint represent degenerative changes from a chronically lax joint or the consequence of a congenital extra ossicle, an os styloideum [84, 85]. When symptomatic, it may be from a combination of degenerative changes that occur in the dorsum of the abnormal CMC joint, a secondary ganglion, or sometimes irritation of the wrist extensors [86, 87]. Repetitive loading in extension can stimulate pain, especially in stick and racquet sports. Children and adolescents will present with a painful bump on the dorsum of the hand. The location over the CMC joint and the characteristic appearance on plain films help confirm the diagnosis. Initial treatment is geared to a combination of rest, splinting, taping, NSAIDS, and even corticosteroid injections and is often successful. If pain persists, however, surgery to remove the boss and degenerative portion of the joint is often successful [88, 89]. There is some controversy regarding the potential indications for arthrodesis of the joint, but the authors prefer in children to utilize arthrodesis only if excision fails [90, 91].

Congenital Conditions While many congenital differences are apparent at birth, there are some which only manifest clearly later during preadolescence and adolescence. These differences are internalized within the skeletal anatomy and can alter the typical mechanics of the wrist to produce pain under conditions of activity, repetitive stress, and load bearing. We will mention these conditions briefly as they may present in the young athlete.

Madelung’s Deformity Madelung’s deformity refers to an alteration in the skeletal anatomy of the wrist secondary to premature closure of the volar and ulnar portion of the distal radial physis. The result is a spectrum of deformity that leads to an exaggerated alignment of the distal radius, subluxation of the distal radioulnar joint, ulnar positivity, and loss of lunate support [92, 93]. Madelung’s deformity is associated Leri-Weil dyschondrosteosis, which is a heritable condition of short stature and short forearms and can be assessed with genetic testing [94, 95]. Gymnast wrist, pseudohypoparathyroidism, and multiple hereditary exostoses can all produce deformities that mimic Madelung’s [96–98].

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Young athletes may present with insidious onset of central to ulnar vague wrist pain associated with sport and activity. The location of reported pain is not the same as for TFCC injuries or ulnar-positive wrists, but not too far off either. There is also less than average forearm rotation, especially supination. The forearm may look “short,” and the ulnar head is generally prominent. Careful inspection of the hand from the lateral view will reveal a wrist that appears volarly translated or volarly collapsed. The wrist may be tender about the radiolunate articulation, and loading the wrist, especially the ulnar side, will produce pain. Plain films will generally reveal the skeletal deformity, and no further imaging is required (Fig. 8.11). Parents are given the option to pursue genetic testing if they wish. Treatment starts with rest, bracing, and then physiotherapy to help return to sport. If successful, this approach may be repeated as episodes of pain recur due to the altered wrist mechanics. If this fails to make appropriate improvements, the athlete can consider surgery. The authors feel that if the athlete only has pain during sport, and is willing to either change sport or discontinue sport, then surgery can be avoided. Surgical options include physiolysis and release of Vickers ligament (an extra-articular capsular ligament thought to be a deforming force in Madelung’s) in very young patients or osteotomies of the radius and/or ulna in patients in older children and teenagers (Fig. 8.11) [98–104]. a

Fig. 8.11  A 16-year-old female elite tennis player presents with worsening left central wrist pain associated with tournaments and practice. Rest helps, but pain returns with sport. (a) Clinical appearance of her left wrist. There is forearm shortening, a prominent ulnar head, and increased girth of her wrist associated with the DRUJ subluxation. (b) Radiographs of her left wrist demonstrate the classic appearance of Madelung’s deformity. (c) She underwent surgery to realign her distal radius using a dome osteotomy to bring coverage under the lunate, redistribute the load across the wrist, and realign the DRUJ. Once healed, she was able to return to her previous level of competitiveness after a course of physiotherapy

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Carpal Coalition Incomplete separation of a cartilaginous connection among the carpal bones during the 4th to 8th weeks of fetal development leads to varying degrees of connection called carpal coalitions. Congenital carpal coalitions may vary by their completeness and the nature of the connection: fibrous, cartilaginous, or bony. Coalitions of

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the lunate-triquetrum, the capitate-hamate, and the capitate-trapezium are the most common [105–108]. Based upon data published by Pruszczynski et al. [108], the overall prevalence is low, 0.5%, and coalitions are more prevalent in African American children. Coalitions are usually diagnosed incidentally through radiographs taken for another purpose. The incomplete coalitions have been more commonly associated with pain with sport, trauma, or skeletal maturity [109, 110]. The theory is that incomplete coalitions, especially those with fibrous connections, may lead to development of painful pseudarthroses since the normal cartilage layer is absent. Athletes will present with insidious onset of pain in the region of the coalition. Careful palpation may tip off to the possibility of a coalition as the tender area will be intercarpal. It may be mistaken for a sprain, especially if radiographs do not show a clear bony coalition. Sometimes the only hint on a radiograph is a focal area between a carpal segment where the space narrows, which is easily missed. An MRI will ultimately reveal a fibrous coalition in the cases where a bony connection is not present. Treatment should initially consist of rest, bracing, and temporary cessation of activity. Gradual return to sport is initiated after an asymptomatic period. Failure of relief of pain and failure to return to sport are indications to consider performing an intercarpal arthrodesis [105, 107, 109].

Avascular Necrosis Avascular necrosis is the general term describing a bone, or segment thereof, that loses its circulation. There is a typical progression of events that results from this insult that follows the body’s natural attempt to heal the avascular portion of bone by re-establishing circulation and remodeling the dead bone. In this process, the bone segment softens as sclerotic bone is first resorbed; then, depending upon the bone, the segment, and its position, it collapses. If the segment involves subchondral bone, then the overlying cartilage suffers, and traumatic arthritis can set in through a combination of cartilage cellular death and joint deformity from collapse. The condition is often painful in its earliest stages as the weakening bone during early resorption fatigues under the stress of load. Pain progresses with the ultimate development of arthritis, unless the bone is able to heal and maintain its shape. The most common carpal example of this process involves the lunate; in adults, this condition is known under its eponym, Kienböck’s disease. It is rare in children and adolescents, typically diagnosed in patients from 20 to 40 years of age [111]. While avascular necrosis can affect any bone, the second most commonly described carpal bone involved is the scaphoid, also known as Preiser’s disease [112]. This latter condition has only been rarely reported. Whether these terms are appropriate when the condition affects children is unclear, and some researcher have argued to a separate terminology because the condition often behaves very differently in adults compared to children [113].

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Pediatric Kienböck’s Disease, aka, Lunatomalacia Risk factors for the development of this condition are not entirely known. Negative ulnar variance results in increased loading of the lunate across the wrist which creates greater stress. Lunate morphology and variations in blood supply have also been implicated [114]. The Lichtman classification follows the radiographic progression of disease from lunate sclerosis to collapse and eventual arthritis, which aids in guiding treatment [115]. In adults, treatment depends upon the stage of disease and utilizes a combination of reducing stress on the lunate by unloading it, expediting remodeling, or reconstructing the bone and joints. Irisarri et al. noted that children seem to experience a completely different natural history of disease compared to adults; they found that many pediatric patients, especially younger children, will heal the insult with immobilization alone and experience complete resolution [113]. The authors advocated changing the name of this condition in children to “lunatomalacia” and further subdividing it into infantile (≤12 years of age) and juvenile (≥13 years through skeletal maturity) lunatomalacia given the differences in natural history [113]. They did not believe that mechanical factors such as negative ulnar variance and activities played a role in pediatric patients developing the disorder. In infantile lunatomalacia, even with lunate deformity, clinical outcomes are still good. Children up to age 14 years have a good prognosis, and those juvenile cases requiring surgery prior to age 15 do better than adults, they found. Athletes will present with insidious and somewhat vague central wrist pain that progresses over time. Examination might only suggest synovitis and might reveal relative stiffness of the involved wrist. In its earliest stages, radiographs will be negative, but an ulnar-negative wrist and/or persistent symptoms should lead to MRI evaluation. Intravenous contrast can be used to elicit enhancement associated with revascularizing bone. With a diagnosis established, the athlete’s age and radiographic stage are considered. Infantile lunatomalacia can be treated with cast immobilization alone even with carpal collapse. Similar treatment can be applied to juvenile cases in the absence of collapse [116]. Juvenile cases with collapse should be considered for operative intervention. Traditional procedures include radial shortening osteotomy for ulnar-negative wrists, limited carpal fusions to unload the lunate, and vascular grafting into the lunate to expedite remodeling. Complications of treatment unique to children include radial overgrowth following shortening osteotomy and recurrence of disease [117–119]. Regardless of age and alignment, the athlete and their family should understand that this condition can result in carpal changes that can limit any future athletic participation and even spill over into regular life activities and that the data to guide treatment is lacking.

Conclusions Many young athletes sustain carpal and carpal-related injuries that are straightforward to diagnose and treat with an associated expectation of return to sport. On the other hand, there are several injuries and conditions that are neither obvious nor

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always easy to treat. The diagnoses we fail to make are linked to the diagnoses of which we are unfamiliar. Incumbent upon the healthcare team is to recognize the various problems young athletes can face and remain diligent in pursuing problems that simply do not present as expected, resolve as anticipated, and impede the young athlete’s return to play.

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73. Ogan D, Pritchett K.  Vitamin D and the athlete: risks, recommendations, and benefits. Nutrients. 2013;5(6):1856–68. 74. Villacis D, Yi A, Jahn R, Kephart CJ, Charlton T, Gamradt SC, Romano R, Tibone JE, Hatch GFR III. Prevalence of abnormal vitamin D levels among division 1 NCAA athletes. Sports Health. 2014;6(4):340–7. 75. Giffin KL, Knight KB, Bass MA, Vlliant MW. Predisposing risk factors and stress fractures in division 1 cross country runners. J Strength Cond Res. 2017. 76. McKeon KE, London DA, Osei DA, Gelberman RH, Goldfarb CA, Boyer MI, Calfee RP. Ligamentous hyperlaxity and dorsal wrist ganglions. J Hand Surg Am. 2013;38A:2140–3. 77. Calif E, Stahl S, Stahl S. Simple wrist ganglia in children: a follow-up study. J Pediatr Orthop B. 2005;14(6):448–50. 78. Wang AA, Hutchinson DT. Longitudinal observation of pediatric hand and wrist ganglia. J Hand Surg Am. 2001;26A(4):599–602. 79. Steinberg BD, Kleinman WB. Occult scapholunate ganglion: a cause of dorsal radial wrist pain. J Hand Surg Am. 1999;24(2):225–31. 80. Wang AA, Hutchinson DT. Longitudinal observation of pediatric hand and wrist ganglia. JHS Am. 2001;26(4):599–602. 81. Head L, Gencarelli JR, Allen M, Usher-Boyd K. Wrist ganglion treatment: systematic review and meta-analysis. JHS Am. 2015;40(3):546–53. 82. Satku K, Ganesh B. Ganglia in children. J Pediatr Orthop. 1985;5(1):13–5. 83. Su Y, Xie Y, Qin J, Nan G. Visualization of the wrist ganglion capsule by methylene blue staining as an aid for complete resection in children. J Hand Surg Am. 2015;40(4):685–7. 84. Park MJ, Namdari S, Weiss AP. The carpal boss: review of diagnosis and treatment. J Hand Surg Am. 2008;33(3):446–9. 85. Alemohammad AM, Nakamura K, El-Sheneway M, Viegas SF. Incidence of carpal boss and osseous coalition: an anatomic study. J Hand Surg Am. 2009;34(1):1–6. 86. Williams MR, Fullilove SM. Re: a carpal boss leading to extensor tendon ruptures—a case report. J Hand Surg Eur. 2008;33(2):223. 87. Ghatan AC, Carlson EJ, Athanasian EA, Weiland AJ. Attrition or rupture of digital extensor tendons due to carpal boss: report of two cases. J Hand Surg Am. 2014;39(5):919–22. 88. Vermeulen GM, de With MC, Bleys RL, Schuurman AH. Carpal boss: effect of wedge excision depth on third carpometacarpal joint stability. J Hand Surg Am. 2009;34(1):7–13. 89. Capo JT, Orillaza NS, Lim PK. Carpal boss in an adolescent: case report. J Hand Surg Am. 2009;34(10):1808–10. 90. Clarke AM, Wheen DJ, Visvanathan S, Herbert TJ, Conolly WB. The symptomatic carpal boss. Is simple excision enough? J Hand Surg Br. 1999;24(5):591–5. 91. Lorea P, Schmitz S, Aschilian M, Chirila-Dobrea A, Petrea A.  The preliminary results of treatment of symptomatic carpal boss by wedge joint resection, radial bone grafting and arthrodesis with a shape memory staple. J Hand Surg Eur. 2008;33(2):174–8. 92. Zebala LP, Manske PR, Goldfarb CA. Madelung’s deformity: a spectrum of presentation. J Hand Surg Am. 2007;32(9):1393–401. 93. Tuder D, Frome B, Green DP. Radiographic spectrum of severity in Madelung’s deformity. J Hand Surg Am. 2008;33A:900–4. 94. Ross JL, Scott C Jr, Marttila P, Kowal K, Nass A, Papenhausen P, Abboudi J, Osterman L, Kushner H, Carter P, Ezaki M, Elder F, Wei F, Chen H, Zinn AR. Phenotypes associated with SHOX deficiency. J Clin Endocrinol Metab. 2001;86(12):5674–80. 95. Binder G, Renz A, Martinez A, Keselman A, Hesse V, Riedl SW, Hausler G, Fricke-Otto S, Frisch H, Heinrich JJ, Ranke MB. SHOX haploinsufficiency and Leri-Weill dyschondrosteosis: prevalence and growth failure in relation to mutation, sex, and degree of wrist deformity. J Clin Endocrinol Metab. 2004;89(9):4403–8. 96. Brooks TJ.  Madelung deformity in a collegiate gymnast: a case report. J Athl Train. 2001;36(2):170–3.

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97. Sanchez J, Perera E, Jan de Beur S, Ding C, Dang A, Berkovitz GD, Levine MA. Madelung-­ like deformity in pseudohypoparathyroidism type 1B.  J Clin Endocrinol Metab. 2011;96(9):E1507–11. 98. Kozin SH, Zlotolow DA. Madelung deformity. J Hand Surg Am. 2015;40(10):2090–8. 99. Vickers D, Nielsen G.  Madelung deformity: surgical prophylaxis (physiolysis) during the late growth period by resection of the dyschondrosteosis lesion. J Hand Surg Br. 1992;17(B):401–7. 100. Bruno RJ, Blank JE, Ruby LK, Cassidy C, Cohen G, Bergfield TG. Treatment of Madelung’s deformity in adults by ulna reduction osteotomy. J Hand Surg Am. 2003;28A:421–6. 101. Harley BJ, Brown C, Cummings K, Carter PR, Ezaki M.  Volar ligament release and distal radius dome osteotomy for correction of Madelung’s deformity. J Hand Surg Am. 2006;31(9):1499–506. 102. de Paula EJL, Cho AB, Junior RM, Zumiotti AV. Madelung’s deformity: treatment with radial osteotomy and insertion of trapezoidal wedge. J Hand Surg Am. 2006;31A:1206–13. 103. Steinman S, Oishi S, Mills J, Bush P, Wheeler L, Ezaki M. Madelung deformity correction: long-term follow-up. JBJS Am. 2013;95-a(13):1198–204. 104. Imai Y, Miyake J, Okada K, Murase T, Yoshikawa H, Moritomo H. Cylindrical corrective osteotomy for Madelung deformity using a computer simulation: case report. J Hand Surg [Am]. 2013;38(10):1925–32. 105. Simmons BP, McKenzie WD.  Symptomatic carpal coalition. J Hand Surg Am. 1985;10(2):190–3. 106. Delaney TJ, Eswar S. Carpal coalitions. J Hand Surg Am. 1992;17(1):28–31. 107. Defazio MV, Cousins BJ, Miversuski RA Jr, Cardoso R. Carpal coalition: a review of current knowledge and report of a single institution’s experience with asymptomatic intercarpal fusion. Hand (NY). 2013;8(2):245. 108. Pruszczynski B, Saller J, Rogers KJ, Holmes L, Ty JM. Incidence of carpal coalition in the pediatric population. J Pediatr Orthop. 2016;36(8):e106–10. 109. Ritt MJ, Maas M, Bos KE. Minnaar type 1 symptomatic lunotriquetral coalition: a report of nine patients. J Hand Surg Am. 2001;26A(2):261–70. 110. Peters S, Colaris JW. Carpal coalition: symptomatic incomplete bony coalition of the capitate and trapezoid—case report. J Hand Surg Am. 2011;36A:1313–5. 111. Ando Y, Yasuda M, Kazuki K, Hidaka N, Yoshinaka Y. Temporary scaphotrapezoidal joint fixation for adolescent Kienböck’s disease. J Hand Surg Am. 2009;34(A):14–9. 112. Hsu PA, Light TR. Disorders of the immature carpus. Hand Clin. 2006;22(4):447–63. 113. Irasarri C, Kalb K, Ribak S.  Infantile and juvenile lunatomalacia. J Hand Surg Eur. 2010;35E(7):544–8. 114. Lichtman DM, Pientka WF 2nd, Bain GI. J Hand Surg Am. 2016;41(5):630–8. 115. Lichtman DM, Degnan GG. Staging and its use in the determination of treatment modalities for Keinbock’s disease. Hand Clin. 1993;9(3):409–16. 116. Herzberg G, Mercier S, Charbonnier JP, Got P. Keinbock’s disease in a 14-year-old gymnast: a case report. J Hand Surg [Am]. 2006;31(2):264–8. 117. Edelson G, Reis ND, Fuchs D. Recurrence of Kienbock disease in a twelve-year-old after radial shortening. Report of a case. J Bone Joint Surg Am. 1988;70(8):1243–5. 118. Herdem M, Ozkan C, Bayram H. Overgrowth after radial shortening for Keinbock’s disease in a teenager: a case report. J Hand Surg Am. 2006;31A:1322–5. 119. Matsuhashi T, Iwasaki N, Oizumi N, Kato H, Minami M, Minami A. Radial overgrowth after radial shortening for skeletally immature patients with Kienböck’s disease. J Hand Surg Am. 2009;34(A):1242–7.

Chapter 9

Common Sports Hand Injuries Julie Balch Samora

Introduction The hand is the most common location of injuries sustained in the pediatric and adolescent population [1]. Because of increasing sports participation, there is an increased incidence of hand injuries [2, 3]. Remodeling of skeletal deformity is dependent on location and type of injury as well as the age of the patient. Early diagnosis and treatment are of paramount importance to allow for proper healing and restoration of function.

 alter-Harris III Fracture of Thumb Proximal Phalanx S (“Bony UCL Injury”) Background Pediatric Salter-Harris III fractures of the thumb proximal phalanx occur with a similar mechanism as seen in adult ulnar collateral ligament injuries of the thumb, also known as “Skier’s thumb” [4]. Although frequently observed in skiing injuries, any athlete that incurs a forceful valgus load to an abducted thumb can sustain this type of injury. In children and adolescents, this mechanism most often results in a bony avulsion of the ulnar collateral ligament (UCL) which is attached to the epiphysis, resulting in a Salter-Harris III intra-articular fracture. This is due to the relative strength of the ligament when compared with the physis. Rarely, in skeletally mature adolescent J. B. Samora (*) Department of Orthopedic Surgery, Nationwide Children’s Hospital, Columbus, OH, USA e-mail: [email protected] © Springer International Publishing AG, part of Springer Nature 2019 A. S. Bauer, D. S. Bae (eds.), Upper Extremity Injuries in Young Athletes, Contemporary Pediatric and Adolescent Sports Medicine, https://doi.org/10.1007/978-3-319-56651-1_9

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individuals, a soft tissue avulsion of the UCL can occur. The ulnar collateral ligament is the primary stabilizer of the thumb metacarpophalangeal (MP) joint and helps resist valgus stress, and therefore improper or delayed treatment of either a soft tissue or bony injury could lead to debilitation and perhaps preclude athletic participation.

Diagnosis The diagnosis is made with clinical and radiographic evaluation. On exam, patients will have soft tissue swelling and pain around the ulnar aspect of the thumb MP joint. Oftentimes, a mobile bony fragment can be palpated in this region. If the patient will permit testing of the stability of the MP joint, valgus stress at full extension and at 30° of flexion will demonstrate laxity and will not display a solid endpoint. If there is any question of laxity, a contralateral valgus stress exam provides a good control exam. Radiographs will demonstrate an intra-articular fracture usually with some rotation of the epiphyseal fragment (Fig. 9.1a). If plain radiographs fail to demonstrate a Salter-Harris III fracture, yet there is instability of the MP joint, a soft tissue UCL rupture may have occurred. In this case, it is important to assess for the presence of a Stener lesion, which is a soft tissue “mass” that occurs when the distal portion of the ruptured UCL displaces proximally and is trapped under the proximal edge of the intact adductor a­ poneurosis [5]. If there is any question about the diagnosis in a high-level athlete (concern for a

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Fig. 9.1  Displaced Salter-Harris III fracture of the proximal phalanx of the thumb (bony UCL) with the fragment rotated (a). Exposure is through a lazy “S” incision on the ulnar aspect of the thumb MP joint (b). One option for fracture stabilization is to place one pin perpendicular to the fracture line and one parallel to the joint line (c)

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Stener lesion, increased laxity on exam), an ultrasound or MRI can be performed for further evaluation [6–8]. Milner and colleagues [9] created a treatment-oriented MRI classification of thumb UCL injury based on the degree of displacement.

Treatment Because thumb proximal phalanx Salter-Harris III fractures may result in articular incongruity, instability, and deformity, displaced fractures should be treated with surgery. For minimally displaced fractures, closed reduction and percutaneous pinning can be attempted. To ensure articular congruity of displaced fractures, an open reduction is performed. Utilizing an incision over the dorsal-ulnar aspect of the thumb MCP joint (Fig. 9.1b), the radial sensory nerve is protected, and the adductor pollicis fascia is released from the extensor tendon. The ulnar collateral ligament is normally intact and should be protected. Usually the MP joint can be exposed through the fracture site, but occasionally the dorsal capsule must be entered. Kirschner wires are placed from ulnar to radial then driven through to emerge completely through the skin radially, where they can then be bent and cut (Fig. 9.1c). A tension-band wire technique or suture anchors can also be utilized [10, 11]. A layered closure is performed, and a thumb spica splint or cast is then applied. In the event of a soft tissue UCL avulsion, if there is no Stener lesion, this can be managed with immobilization [12], although some surgeons advocate for early surgical treatment for any complete rupture of the UCL [4, 13–16]. If there is a Stener lesion, however, this should be treated with surgical intervention [4, 15]. In the case of chronic UCL injuries, reconstruction with various techniques can be performed [17–20], all with good outcomes [21].

Rehabilitation For bony UCL injuries, patients remain in the thumb spica cast for 4  weeks, at which time the pins are pulled. Depending on radiographic healing and sport participation, patients can either transition into a waterproof thumb spica cast or a thumb spica Velcro brace at the 4-week visit. Once there is clinical and radiographic evidence of fracture healing, which usually occurs by 6 weeks, slow integration into activities is initiated. Usually a home exercise program is all that is necessary. For soft tissue UCL avulsion injuries treated surgically, patients are usually immobilized for 4  weeks and then usually transitioned to a hand-based thermoplastic thumb spica orthosis, from which they will wean over the following 4 weeks [16].

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Complications Surgical complications can include harm to the sensory nerve, infection, hardware complications, and inaccurate reduction leading to malunion, instability, and arthrosis. Delayed or missed diagnosis or inadequate treatment may lead to an incongruent or unstable joint, pain, and limitations of strength, motion, and function. In the absence of MP joint arthrosis, nonunions may be treated with open reduction, bone grafting, and internal fixation. If there is a thin or miniscule fracture fragment, it may be excised with ulnar collateral ligament advancement, repair, or reconstruction. Persistent instability may be treated with ulnar collateral ligament reconstruction with various techniques [18, 22]. With prompt diagnosis and appropriate treatment, patients can expect to demonstrate good motion, stability, and function.

In-Season Considerations This intra-articular fracture should be treated in an expeditious fashion, but once the pins are removed, a player may return to sport with a thumb spica cast in place, which could occur as early as 4 weeks. Depending on the sport requirements, those patients with soft tissue injuries could possibly play with a cast after surgery once pain allows [16].

Case Example A 16-year-old lacrosse player sustained an abduction injury to his thumb and was found to have a displaced Salter-Harris III fracture (Fig. 9.2). Surgery was recommended for this displaced intra-articular fracture. He underwent open reduction and pinning using parallel pins placed from ulnar to radial and was cast immobilized for 4 weeks. At 4 weeks, the pins were pulled, and he was placed in a waterproof cast and returned to lacrosse. At 6  weeks, he demonstrated clinical and radiographic healing (Fig. 9.2d). He returned to sport without restriction at 8 weeks, once full opposition of the thumb was achieved.

Proximal Phalanx Base Fractures Background The incidence of phalanx fractures has been reported to be 27 per 1000 patients aged 0–19 years and is highest in children ages 10–14 years [23, 24]. Males account for 2/3 of all phalangeal fractures [25]. Proximal phalangeal base fractures are one

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Fig. 9.2  Displaced and rotated Salter-Harris III fracture of the proximal phalanx of the thumb (bony UCL injury) (a) with attempted closed reduction in the emergency department (b). Intraoperative fluoroscopy image demonstrating good alignment of the fracture fixated with two parallel Kirschner wires (c). Radiographic healing at 6 weeks with well-aligned joint (d)

of the most common injuries, with the small finger the most frequently injured digit [23, 24, 26, 27]. The term “extra-octave” fracture describes the ulnar deviation of the small finger, which increases the distance from the thumb to the small finger, enabling a pianist to play an “extra-octave” on the keyboard [11]. Pediatric phalangeal base fractures can either be physeal or juxta-epiphyseal injuries, as classified by Al-Qattan et  al. [27] (Table  9.1). The most common fracture is the juxta-­ epiphyseal type II fracture (Fig. 9.3). The mechanism of base fractures is often an abduction type deformity, beyond the normal limits of the metacarpophalangeal joint.

Diagnosis Clinical evaluation and radiographic assessment are utilized to diagnose these fractures. The skin should be evaluated for abrasions or open injuries, and digital cascade is evaluated for overlapping or malrotation. A neurovascular exam should be documented and tendon function assessed. Plain radiographs should include at a minimum an anteroposterior and lateral radiograph of the injured finger, but oblique radiographs often are beneficial as well (Fig. 9.3a, b).

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Table 9.1  Classification of pediatric fractures at the base of the proximal phalanx of the fingers Fracture type Salter-Harris (involving the physis)

Juxta-epiphyseal (1–2 mm distal to growth plate)

Metaphyseal fractures (distal to the juxta-epiphyseal fracture line)

Fracture subtype SH I: only the growth plate (physis) is involved SH II: involves the growth plate as well as a small metaphyseal fragment at the ulnar or the radial corner (also called the Thurston–Holland fragment or corner sign) SH III: a vertical fracture line that runs from the articular surface through the epiphysis and growth plate SH IV: the fracture line runs from the articular surface through the epiphysis growth plate and a small metaphyseal fragment (Thurston–Holland fragment) SH V: growth plate crush injury juxta-epiphyseal JE I: the fracture line is transverse along the metaphyseal subchondral bone JE II: similar to type I but there is involvement of a Thurston– Holland metaphyseal fragment at the ulnar or radial corner of the metaphysis T: transverse metaphyseal fracture O: short oblique metaphyseal fracture

Reprinted from Al-Qattan et  al. [27]. Sage Publications. Reproduced under STM permissions guidelines Classification of pediatric proximal phalanx base fractures, as proposed by Al-Qattan et al.

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Fig. 9.3  AP (a) and oblique (b) radiographs of an “extra-octave” fracture that is a juxta-epiphyseal type II fracture with a Thurston-Holland metaphyseal fragment, as described by Al-Qattan et al. [27]. A closed reduction is performed in the emergency department with a digital block and use of fluoroscopy (c)

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Treatment These fractures can most often be treated with closed reduction and immobilization [28]. A digital block can be performed, although sometimes the local anesthetic is more painful than the actual reduction maneuver. A reduction technique that can sometimes be utilized is to place a writing utensil (pen/pencil) deep in the webspace as a lever and arcing the finger over the utensil to effect a reduction. This is not always successful, however, because oftentimes the webspace is not deep enough to accommodate the utensil, thereby rendering it ineffective as a true lever. Buddy taping of the fingers helps maintain reduction, and then either a cast or splint is applied. There is a great potential for bony remodeling due to the location of the fracture in relation to the physis, and healing is expected within 3–4  weeks. A recent study demonstrated that functional-conservative casts or Lucerne casts (LuCa) effectively treat extra-articular physeal fractures of the proximal phalanges [29]. The functional-­ conservative cast blocks the metacarpophalangeal joints in 70–90° of flexion, and the fractured finger is buddy-taped to the neighboring finger. Patients are encouraged to flex the interphalangeal joints. The LuCa cast allows free mobilization of the interphalangeal joints and also the wrist joint while buddy taping the affected finger and protecting the metacarpophalangeal joints. Closed reduction and percutaneous pinning are indicated for the occasional unstable fracture which has failed closed reduction [30]. Rarely, open reduction and internal fixation might be indicated in base fractures with soft tissue entrapment within the fracture site [28].

Rehabilitation Rarely is rehabilitation indicated for these injuries.

Complications Functional outcomes are nearly universal after closed management of phalangeal base fractures. However, malrotation, skin issues, stiffness, and physeal arrest can occur with nonoperative treatment. When proximal phalanx base fractures are treated surgically, there is a 4.8% complication rate, including infection, pin site complications, stiffness, and malunion [30].

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In-Season Considerations Athletes with these fractures can generally safely participate either in a standard or functional cast [29].

Metacarpal Fractures Background Metacarpal fractures are common injuries treated by hand surgeons [31]. Fractures are variable and include injuries to the head, neck, shaft, and base. Treatment is dependent on location of injury, skin integrity, fracture pattern, malrotation, and displacement. The vast majority of metacarpal fractures can be treated conservatively.

Diagnosis Diagnosis is made with a good history and clinical as well as radiographic evaluation. Careful examination for any open injuries (as can be seen in fight bites) is of paramount importance to prevent infection. Physical examination includes tenodesis to evaluate for overlapping of digits which indicates malrotation that may be underappreciated on radiographs (Fig. 9.4). Neurovascular status and tendon function are assessed. Plain radiographs should include anteroposterior, oblique, and lateral radiographs. Fractures of the thumb metacarpal can be better visualized with the Robert’s view, which requires hyperpronation to enable the dorsum of the thumb

Fig. 9.4  Clear overlapping of the left ring and long fingers due to a ring metacarpal shaft fracture

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to lie on the radiographic plate. Bett’s view, with the hand pronated 20–30° and the imaging beam directed obliquely at 15° in distal-to-proximal direction, enables a true lateral of the carpometacarpal joint [32].

Treatment Treatment varies based on the location of the fracture, the remodeling potential (age of the patient and proximity to the physis), and the rotational alignment. Metacarpal head fractures are rare, usually resulting from an axial force to a flexed MCP joint. Open reduction and internal fixation should be performed for fractures with intra-­ articular displacement [33], and patients should be counseled on the risk of avascular necrosis after these injuries, regardless of treatment plan. Metacarpal neck fractures can often be treated with casts or splints (Fig. 9.5). In high-level pediatric athletes, hand-based thermoplastic splints may permit quicker return to sport and have previously been shown to result in improved early range of motion and grip strength, without complications compared with conventional ulnar gutter splints [34]. Occasionally, malrotation can be seen with metacarpal neck fractures, and closed reduction with percutaneous pinning or open reduction is indicated (Fig. 9.6). Locked plating has been described for small metacarpal neck fractures, but when compared with percutaneous pinning, it does not appear to offer any advantages [35]. Antegrade vs retrograde intramedullary pinning have been advocated as Fig. 9.5  An ulnar gutter removable brace (a) dorsal view, (b) volar view can be utilized to treat most small metacarpal neck fractures

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Fig. 9.6  Ring and small metacarpal neck fractures with malrotation of the digits (a). Intraoperative fixation with closed reduction and retrograde percutaneous pinning (b, c)

treatment options to treat displaced small metacarpal neck fractures, and antegrade pinning has been recommended for the treatment of athletes to enable them to return to sport earlier [36]. Delayed presentation of a malrotated metacarpal neck fracture may require osteoclasis or open reduction with internal fixation (Fig. 9.7). Metacarpal shaft fractures can often be managed with closed reduction and immobilization. When instability or unacceptable deformity is present, or in the presence of multiple metacarpal shaft fractures (Fig. 9.8), percutaneous pin fixation, elastic stable intramedullary nailing, and open reduction internal fixation are all acceptable options [31, 37, 38]. Percutaneous pinning of metacarpal shaft fractures is simple and offers the advantage of not retaining hardware (Fig. 9.9). The advantage of open plating or intramedullary fixation of metacarpal fractures is the opportunity to participate in early motion (Fig. 9.10). The thumb metacarpal allows more tolerance of angulation than the neighboring metacarpal bones due to the degree of mobility at the carpometacarpal joint. Up to 40° of angulation can be accepted for extra-articular fractures [39]. However, occasionally, closed reduction of these fractures fails, and surgery is indicated (Fig. 9.11). Metacarpal base fractures of the ulnar digits are relatively uncommon but may require internal fixation to restore alignment, joint congruity, and stability. Thumb metacarpal base intra-articular fractures include Bennett and Rolando fractures and are unstable. Bennett fractures are two-part, whereas Rolando fractures are three-­ part fractures with either a Y- or T-configuration [40]. Due to the deforming forces of the abductor pollicis longus, extensor pollicis longus, extensor pollicis brevis, and the adductor pollicis tendons, there is flexion, supination, and proximal metacarpal migration [32]. While minimally displaced fractures can be treated nonoperatively, operative fixation is indicated for those fractures with displacement at the articular surface [41]. Closed reduction with intermetacarpal fixation to the second metacarpal, closed reduction with percutaneous pinning, oblique traction pinning,

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Fig. 9.7  AP (a), oblique (b), and lateral (c) radiographs demonstrate callus formation in a small metacarpal neck fracture in a 19-year-old male who presented 4 weeks after punching a wall with a clinically malrotated small finger. Osteoclasis attempts were unsuccessful. AP (d), oblique (e), and lateral (f) fluoroscopic images after open callus removal and retrograde percutaneous pinning

external fixation, or open reduction and internal fixation can be performed [42–44]. A recent article demonstrated good results with open reduction internal fixation and an early active rehabilitation program [45]. In the case of late presentation, a fusion may be indicated (Fig. 9.12).

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Fig. 9.8  AP (a), oblique (b), and lateral (c) radiographs demonstrating multiple midshaft metacarpal fractures. Intraoperative AP (d) and oblique images (e) demonstrating closed reduction and retrograde pin fixation

Rehabilitation Rarely do young athletes need formalized therapy after sustaining metacarpal fractures, regardless of the type and location of the fracture. However, each fracture type and athlete is treated on an individual basis.

Complications In rare instances, an injury to the metacarpal head and physis may result in growth arrest and late deformity. Malrotation, stiffness, arthrosis (if an intra-articular fracture), hardware complications, and weakness can occur [31, 32].

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Fig. 9.9  AP (a), oblique (b), and lateral (c) radiographs of a small metacarpal shaft fracture. Fixation is with closed reduction, percutaneous pinning using retrograde smooth Kirschner wires (d, e)

In-Season Considerations Many metacarpal fractures can be treated nonoperatively and are stable enough in a cast that athletes can still participate in their sports activities. However, fractures that undergo surgical fixation may delay return to sport. Athletes should not participate in contact activities if there are temporary pins in place. Once the pins are removed, however, they can be protected with either casting or splinting. Consideration may be given to open fixation using a plate and screws or intramedullary screw to allow earlier return to play for some in-season athletes. Each fracture pattern and athlete is treated uniquely.

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Fig. 9.10  Ring and small metacarpal shaft fractures with shortening and rotation (a). Open reduction internal fixation with a plate construct (b), which allows for early motion. AP (c) and lateral (d) fluoroscopy images of an index metacarpal fracture fixed with a T-plate configuration

Case Example A 16-year-old high-level competitive dancer injured her hand while performing a back handspring and presented with a malrotated long finger secondary to a metacarpal shaft fracture (Fig. 9.13). Her goal was to compete in an important national dance competition within 4 weeks. She underwent open reduction and internal fixation with lag screws and a neutralization plate. One week after surgery, she had an OT orthosis made, initiated early motion, and began dance rehearsals in the orthosis. She competed without the orthosis at 4 weeks after surgery and was back to full motion and strength at 8 weeks without restriction.

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Fig. 9.11  AP (a) and lateral (b) radiographs of a displaced epibasal thumb metacarpal fracture that underwent closed reduction but still demonstrates excessive angulation. Manipulation should include axial traction, extension, and pronation to reduce the fracture. Intraoperative AP (c) and lateral (d) fluoroscopy images demonstrating improved alignment. AP (e) and lateral (f) radiographs with good position and healing at 6 weeks

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Fig. 9.12  An 18-year-old male with a 4-month-old Bennett fracture with daily subluxation, pain, and weakness. Plain radiographs (a, b) and computed tomography (c) images demonstrate chronic subluxation and fracture. Upon direct visualization in the OR, the CMC joint was found to have early arthrosis, so a fusion was performed. Final radiographic healing was obtained, and the patient demonstrated good strength and function with elimination of pain

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Fig. 9.13  AP (a) and oblique (b) radiographs demonstrating a spiral comminuted metacarpal shaft fracture in a high-level competitive dancer. She did have a pronation deformity to her finger and was treated with lag screws and a neutralization plate (c, d). She began early range of motion at 1 week and participated in a national dance competition at 4 weeks

Flexor Digitorum Profundus Avulsion (“Jersey Finger”) Background The most common type of closed flexor tendon injury in the finger is a traumatic rupture of the flexor digitorum profundus (FDP) from the distal phalanx. Commonly referred to as a “Jersey finger” [46], the usual mechanism is a forced hyperextension of the distal interphalangeal (DIP) joint that is being held in a flexed posture, such as when a finger is caught in another player’s jersey. Athletes that play football, flag football, or rugby are most at risk for sustaining an FDP avulsion injury [47].

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Although any finger can sustain an FDP traumatic rupture, the ring finger is most often affected (75% of the time), as it is the longest finger when the hand is in a closed fist position, placing it at greatest risk [48]. Leddy and Packer created a classification system that not only describes the injury pattern but also guides treatment options [49, 50]. Injuries can be soft tissue only, avulsion with a small bony fragment, or avulsion with a large intra-articular fracture at the DIP joint. The level of retraction affects the healing potential, as the further retracted the tendon, the further disrupted the blood supply.

Diagnosis Early diagnosis is of paramount importance, as delayed presentation will negatively affect the outcome and can severely alter the treatment options. The diagnosis can be made with physical examination alone. The affected finger will be painful, swollen, and will have altered tenodesis (Fig.  9.14). It is usually relatively extended

Fig. 9.14  Clinical photo with clearly altered tenodesis of the ring finger in a 17-year-old football player hoping to play in college. He could not actively flex his distal interphalangeal joint

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Fig. 9.15  Evaluation of ring flexor digitorum superficialis (FDS) tendon function (a), holding the neighboring digits in extension. Evaluation of the ring flexor digitorum profundus tendon (FDP) holding the proximal interphalangeal (PIP) joint in neutral (b)

compared to the neighboring digits and does not move in sync with the other digits when the wrist is passively flexed and extended. Palpation along the finger can be used to detect tenderness or fullness, which may give the examiner an idea of where the tendon has retracted. The flexor digitorum superficialis (FDS) and FDP tendons must be evaluated individually (Fig. 9.15). Isolated DIP flexion tests FDP function, and isolated PIP flexion with the other digits held in extension tests FDS function. Radiographs should be obtained at the initial evaluation. Bony involvement can be seen at the DIP joint and/or along the tendon sheath (Fig. 9.16).

Treatment Treatment involves surgical repair of the tendon and/or bone, depending on the injury. The Bunnell pullout suture technique is the traditional treatment approach for soft tissue FDP avulsions, but complications can include infection and nail deformity (Fig.  9.17). Suture anchors can be used, but there is risk of physeal injury depending on the age of the athlete, and the available anchors are often too large to be utilized in the younger, more petite athletes. Three figure-of-eight sutures with early active mobilization have demonstrated 100% excellent outcomes (Fig. 9.18) [51].

158 Fig. 9.16  AP (a) and lateral (b) radiographs of a patient with a Jersey finger. The lateral view demonstrates mild hyperextension at the distal interphalangeal joint and a small fleck of bone just distal to the proximal interphalangeal joint, indicating the tendon is likely maintained in this area

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Rehabilitation Therapy is an essential component of flexor tendon repair success. However, rehabilitation protocols remain an area of controversy, particularly in the pediatric population. Whereas some surgeons recommend postoperative immobilization [52–56], others contend early mobilization should be utilized [52, 57]. In a retrospective review of pediatric flexor tendon injuries, 96% of patients who underwent tendon repair with a postoperative immobilization protocol had an excellent outcome, as assessed by TAM scores [52]. In a multicenter comparison study assessing early motion protocols and immobilization for 3–4 weeks after zone I and zone II flexor tendon repairs, there was no difference in digital motion [55]. If patients were immobilized past 4 weeks, however, there was clearly a worsening of function. In a study of 28 children less than 16 years of age with a total of 45 flexor tendon injuries treated with an early active motion program, there were no ruptures in multistrand repairs, but three 2-strand core sutures failed within 1 month of the repair [58]. In this study, there were good to excellent results in all 45 fingers.

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Fig. 9.17  The flexor digitorum tendon is easily identified and pulled through the A4 pulley (a). Intraoperative fluoroscopy is utilized to ensure good positioning of the Keith needles through the distal phalanx (b). Clinical photo of the Keith needles through distal phalanx, which has been roughened up to promote tendon to bone healing (c). Size 2-0 Prolene suture is placed through the tendon. Small hypodermic needles are utilized to keep the tendon in position as the suture is tied over a Xeroform pad (d)

Fig. 9.18  Figure-of-8 suture repair as described by Al-Qattan [51]

If there is a solid surgical repair, and early motion is deemed appropriate for the athlete (based on presumed compliance and reliability), therapy is initiated within 3–5 days after surgery. A removable dorsal blocking splint is fashioned by the occupational therapist. For those patients treated with immobilization rather than early

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motion, therapy begins at 4 weeks. The button or pullout sutures are removed at 6 weeks. Resistance is initiated around 8 weeks, with all steps of the therapeutic process individualized to patients’ progress. Therapy is progressed, and full activity is usually allowed between 10 and 12 weeks.

Complications Rupture of repair can occur, particularly if the athlete has returned too early to athletic endeavors [59]. Infection, nail bed injury, physeal injury, stiffness, and contractures of the DIP or PIP joint can occur. Indications for tenolysis are an imbalance between passive and active motion, failure of conservative approaches to improve motion, and a cooperative patient that can actively participate in postoperative rehabilitation protocols, with preserved joint motion [60, 61]. Flexor tenolysis yields better results in older children (ages 11–16 years) than those under 11 years of age [60, 62].

In-Season Considerations Whereas some orthopedic injuries can be treated in delayed fashion to enable an athlete to finish her season, if a primary repair is to occur, surgical treatment needs to be performed urgently and the season must be truncated early. There is chronic disability associated with undertreatment or delayed treatment of FDP ruptures. Return to full grasping in sports before 10–12 weeks can result in rerupture of the tendon [59]. In some sports, including some football positions where grasp is not required, a fist-type or gauntlet-type cast can be applied to allow earlier return to play after repair, but this is a patient- and surgeon- specific decision.

Case Example A 17-year-old healthy male presented acutely after sustaining an injury while playing football when he caught his right ring finger in another player’s jersey (Fig. 9.19). He presented with pain, swelling, and an inability to flex his ring DIPJ. He went on to have an immediate repair, was cast immobilized for 4  weeks, and initiated a modified Duran protocol at that time. The surgical button was removed at 6 weeks, and he returned to sports at 10 weeks. He had nearly full motion with a subtle DIP contracture of the ring finger.

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Fig. 9.19  A 17-year-old male with acute soft tissue Jersey finger due to a football injury with tendon retraction to the level of the A1 pulley (a). A size 5 pediatric feeding tube is utilized to move the tendon through the pulley system without opening up at the decussation (b). Final intraoperative appearance with a surgical button and good tenodesis (c). Nicely healed incision (d), with a small extensor lag of the ring finger (e), but great grip strength (f)

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Conclusion Hand injuries are common in athletes, and their incidence is increasing due to greater participation in sports. Common sports hand injuries include Salter-Harris III fractures of the thumb, phalangeal base fractures, metacarpal fractures, and jersey fingers. Guidelines for injury treatment include physical examination for malrotation, nonoperative treatment for minimally displaced fractures, and surgery for anatomic reduction of articular fractures. Return-to-play decisions are individualized for each athlete and injury depending on the stability of the fracture and its fixation.

References 1. Hastings H, Simmons BP. Hand fractures in children: a statistical analysis. Clin Orthop Relat Res. 1984;188:120–30. 2. de Putter CE, van Beeck EF, Looman CW, Toet H, Hovius SE, Selles RW. Trends in wrist fractures in children and adolescents, 1997–2009. J Hand Surg Am. 2011;36:1810–5. 3. Nellans KW, Chung KC. Pediatric hand fractures. Hand Clin. 2013;29(4):569–78. 4. Ritting AW, Baldwin PC, Rodner CM. Ulnar collateral ligament injury of the thumb metacarpophalangeal joint. Clin J Sport Med. 2010;20(2):106–12. 5. Stener AK. Displacement of the ruptured ulnar collateral ligament of the metacarpo-­phalangeal joint of the thumb: a clinical and anatomical study. J Bone Joint Surg Br. 1962;44:869–79. 6. Hergan K, Mittler C. Sonography of the injured ulnar collateral ligament of the thumb. J Bone Joint Surg. 1995;77B:77–83. 7. Shinohara T, Horii E, Majima M, et  al. Sonographic diagnosis of acute injuries of the ulnar collateral ligament of the metacarpophalangeal joint of the thumb. J Clin Ultrasound. 2007;35:73–7. 8. Mahajan M, Tolman C, Würth B, Rhemrev SJ. Clinical evaluation vs. magnetic resonance imaging of the skier’s thumb: a prospective cohort of 30 patients. Eur J Radiol. 2016;85(10):1750–6. 9. Milner CS, Manon-Matos Y, Thirkannad SM. Gamekeeper’s thumb-a treatment-oriented magnetic resonance imaging classification. J Hand Surg. 2015;40(1):90–5. 10. Stahl S, Jupiter JB. Salter-Harris type III and IV epiphyseal fractures in the hand treated with tension-band wiring. J Pediatr Orthop. 1999;19(2):223–35. 11. Cornwall R, Ricchetti ET.  Pediatric phalanx fractures. Unique challenges and pitfalls. Clin Orthop Relat Res. 2006;445:146–56. 12. Landsman JC, Seitz WH Jr, Froimson AI, et al. Splint immobilization of gamekeeper’s thumb. Orthopedics. 1995;18(12):1161–5. 13. Downey DJ, Moneim MS, Omer GE Jr. Acute gamekeeper’s thumb: quantitative outcome of surgical repair. Am J Sports Med. 1995;23(2):222–6. 14. Kato H, Minami A, Takahara, et al. Surgical repair of acute collateral ligament injuries in digits with the Mitek bone suture anchor. J Hand Surg Br. 1999;24:70–5. 15. Chuter GS, Muwanga CL, Irwin LR. Ulnar collateral ligament injuries of the thumb: 10 years of surgical experience. Injury. 2009;40:652–6. 16. Werner BC, Hadeed MH, Lyons ML, et al. Return to football and long-term clinical outcomes after thumb ulnar collateral ligament suture anchor repair in collegiate athletes. J Hand Surg Am. 2014;39(10):1992–8. 17. Hogan CJ, Ruland RT, Levin LS. Reconstruction of the ulnar collateral ligament of the thumb metacarpophalangeal joint: a cadaver study. J Hand Surg Am. 2005;30(2):394–9.

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18. Rettig A, Rettig L, Welsch M. Anatomic reconstruction of thumb metacarpophalangeal joint ulnar collateral ligament using an interference screw docking technique. Tech Hand Up Extrem Surg. 2009;13(1):7–10. 19. Glickel SZ, Malerich M, Pearce SM, et al. Ligament replacement for chronic instability of the ulnar collateral ligament of the metacarpophalangeal joint of the thumb. J Hand Surg Am. 1993;18:930–41. 20. Mitsionis GI, Varitimidis SE, Sotereanos GG. Treatment of chronic injuries of the ulnar collateral ligament of the thumb using a free tendon graft and bone suture anchors. J Hand Surg Br. 2000;25:208–11. 21. Samora JB, Harris JD, Griesser MJ, et al. Outcomes after injury to the thumb ulnar collateral ligament- a systematic review. Clin J Sport Med. 2013;23:247–54. 22. Lee SK, Kubiak EN, Lawler E, Iesaka K, Liporace FA, Green SM. Thumb metacarpophalangeal ulnar collateral ligament injuries: a biomechanical simulation study of four static reconstructions. J Hand Surg Am. 2005;30(5):1056–60. 23. Naranje SM, Erali RA, Warner WC Jr, Sawyer JR, Kelly DM.  Epidemiology of pediatric fractures presenting to emergency departments in the United States. J Pediatr Orthop. 2016;36(4):e45–8. 24. Chew EM, Chong AK. Hand fractures in children: epidemiology and misdiagnosis in a tertiary referral hospital. J Hand Surg Am. 2012;37(8):1684–8. 25. Worlock PH, Stower MJ. The incidence and pattern of hand fractures in children. J Hand Surg Br. 1986;11(2):198–200. 26. Rajesh A, Basu AK, Vaidhyanath R, Finlay D. Hand fractures: a study of their site and type in childhood. Clin Radiol. 2001;56(8):667–9. 27. Al-Qattan MM, Al-Zahrani K, Al-Boukai AA. The relative incidence of fractures at the base of the proximal phalanx of the fingers in children. J Hand Surg Eur. 2008;33E(4):465–8. 28. Al-Qattan MM. Juxta-epiphyseal fractures of the base of the proximal phalanx of the fingers in children and adolescents. J Hand Surg Br. 2002;27:24–30. 29. Franz T, Jandali AR, Jung FJ.  Functional-conservative treatment of extra-articular phy seal fractures of the proximal phalanges in children and adolescents. Eur J Pediatr Surg. 2013;23:317–21. 30. Boyer JS, London DA, Stepan JG, Goldfarb CA. Pediatric proximal phalanx fractures: outcomes and complications after the surgical treatment of displaced fractures. J Pediatr Orthop. 2015;35(3):219–23. 31. Bloom JCP, Hammer WC.  Evidence-based medicine: metacarpal fractures. Plast Reconstr Surg. 2014;133:1252–60. 32. Carlsen BT, Moran SL. Thumb trauma: Bennett fractures, Rolando fractures, and ulnar collateral ligament injuries. J Hand Surg Am. 2009;34(5):945–52. 33. Light TR, Oden JA. Metacarpal epiphyseal fractures. J Hand Surg Am. 1987;12(3):460–4. 34. Davison PG, Boudreau N, Burrows R, et  al. Forearm-based ulnar gutter versus hand-based thermoplastic splint for pediatric metacarpal neck fractures: a blinded, randomized trial. Plast Reconstr Surg. 2016;137:908–16. 35. Facca S, Ramdhian R, Pelissier A. Fifth metacarpal neck fracture fixation: locking plate vs K-wire? Orthop Traumatol Surg Res. 2010;96:506–12. 36. Kim JK, Kim DJ. Antegrade intramedullary pinning versus retrograde intramedullary pinning for displaced fifth metacarpal neck fractures. Clin Orthop Relat Res. 2015;473:1747–54. 37. Lieber J, Härter B, Schmid E, Kirschner HJ, Schmittenbecher PP. Elastic stable intramedullary nailing (ESIN) of pediatric metacarpal fractures: experiences with 66 cases. Eur J Pediatr Surg. 2012;22(4):305–10. 38. Lee SK, Kim KJ, Choy WS.  Modified retrograde percutaneous intramedullary multiple Kirschner wire fixation for treatment of unstable displaced metacarpal neck and shaft fracture. Eur J Orthop Surg Traumatol. 2013;23:535–43. 39. Huang JI, Fernandez DL. Fractures of the base of the thumb metacarpal. Instr Course Lect. 2010;59:343–56.

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40. Gedda KO.  Studies on Bennett’s fracture; anatomy, roentgenology, and therapy. Acta Chir Scand Suppl. 1954;193:1–114. 41. Stern P. Fractures of the metacarpals and phalanges. In: Green DP, Hotchkiss RN, Pederson WC, editors. Green’s operative hand surgery. 5th ed. Philadelphia: Elsevier Churchill Livingstone; 2005. p. 711–71. 42. Lutz M, Sailer R, Zimmermann M, Gabl M, Ulmer H, Pechlaner S. Closed reduction transarticular Kirschner wire fixation versus open reduction internal fixation in the treatment of Bennett’s fracture dislocation. J Hand Surg Br. 2003;28B:142–7. 43. Greeven AP, Alta TD, Scholtens RE, de Heer P, van der Linden FM. Closed reduction intermetacarpal Kirschner wire fixation in the treatment of unstable fractures of the base of the first metacarpal. Injury. 2012;43(2):246–51. 44. Kjaer-Petersen K, Langhoff O, Andersen K. Bennett’s fracture. J Hand Surg. 1990;15B:58–61. 45. Uludag S, Ataker Y, Seyahi A, Tetik O, Gudemez E. Early rehabilitation after stable osteosynthesis of intra-articular fractures of the metacarpal base of the thumb. J Hand Surg Eur Vol. 2015;40(4):370–3. 46. Boyes JH, Wilson JN, Smith JW. Flexor tendon ruptures in the forearm and hand. J Bone Joint Surg Am. 1960;42:637. 47. Goodson A, Morgan M, Rajeswaran G, Lee J, Katsarma E.  Current management of Jersey finger in rugby players: case series and literature review. Hand Surg. 2010;15(2):103–7. 48. Stamos BD, Leddy JP.  Closed flexor tendon disruption in athletes. Hand Clin. 2000;16(3):359–65. 49. Leddy JP. Avulsion of the flexor digitorum profundus. Hand Clin. 1985;1:77–83. 50. Leddy JP, Packer JW.  Avulsion of the profundus insertion in athletes. J Hand Surg Am. 1977;2:66. 51. Al-Qattan MM.  Zone I flexor profundus tendon repair in children 5–10 years of age using 3 “figure of eight” sutures followed by immediate active mobilization. Ann Plast Surg. 2012;68(1):29–32. 52. Sikora S, Lai M, Arneja JS. Pediatric flexor tendon injuries: a 10-year outcome analysis. Can J Plast Surg. 2013;21(3):181–5. 53. Berndtsson L, Ejeskar A. Zone II flexor tendon repair in children. A retrospective long-term study. Scand J Plast Reconstr Hand Surg. 1995;29:59–64. 54. Fitoussi F, Lebellec Y, Frajman JM, Penneçot GF. Flexor tendon injuries in children: factors influencing prognosis. J Pediatr Orthop. 1999;19:818–21. 55. O’Connell SJ, Moore MM, Strickland JW, et al. Results of zone I and zone II flexor tendon repairs in children. J Hand Surg Am. 1994;19:48–52. 56. Elhassan B, Moran SL, Bravo C, Amadio P. Factors that influence the outcome of zone I and zone II flexor tendon repairs in children. J Hand Surg Am. 2006;31:1661–6. 57. Moehrlen U, Mazzone L, Bieli C, Weber DM. Early mobilization after flexor tendon repair in children. Eur Pediatr Surg. 2009;19:83–6. 58. Nietosvaara Y, Lindfors NC, Palmu S, Rautakorpi S, Ristaniemi N. Flexor tendon injuries in pediatric patients. J Hand Surg Am. 2007;32(10):1549–57. 59. McCue FC, Wooten SL.  Closed tendon injuries of the hand in athletics. Clin Sports Med. 1986;5:741. 60. Birnie RH, Idler RS. Flexor tenolysis in children. J Hand Surg Am. 1995;20:254–7. 61. Strickland JW.  Flexor tendon injuries. Part 5: flexor tenolysis, rehabilitation and results. Orthop Rev. 1987;16:33. 62. Cannon NM. Enhancing flexor tendon glide through tenolysis and hand therapy. J Hand Ther. 1989;2:122–37.

Chapter 10

The Jammed Finger Anna M. Acosta and Suzanne E. Steinman

Introduction The hand is the most commonly injured area of the body in pediatric and adolescent trauma [1, 2]. Within the hand, injury to the phalanx occurs most often. As early participation in contact sports among adolescents becomes increasingly popular, the incidence of hand and phalangeal injuries continues to rise. Hand injuries in the pediatric population follow a bimodal distribution. The greatest incidence occurs in children between the ages of 0 and 2 years and adolescents between the ages of 12 and 16 years [3]. Seventy-nine percent of all accidents resulting in hand injuries in children occur in the home or during sport activities. Toddlers and preschool age children usually have injuries that occur at home, whereas adolescents more often have injuries occur outside the home. The most commonly injured locations are the base of the proximal phalanx (67.3%) of the border rays (little finger 52.2% and thumb 23.5%) [4]. Up to 16% of all pediatric hand injuries are related to sporting incidents. The majority of these patients (76%) are male, and two-thirds of those are adolescents between the ages of 12 and 16 years old. Sport-related hand injuries tend to present in a delayed fashion to the emergency department compared to other hand injuries. On average, sport-related hand injuries present more than 12  h after the injury occurred [3].

A. M. Acosta Department of Orthopedics and Sports Medicine, Seattle Children’s Hospital, Seattle, WA, USA S. E. Steinman (*) Department of Pediatric Orthopedics and Sports Medicine, Seattle Children’s Hospital, Seattle, WA, USA e-mail: [email protected] © Springer International Publishing AG, part of Springer Nature 2019 A. S. Bauer, D. S. Bae (eds.), Upper Extremity Injuries in Young Athletes, Contemporary Pediatric and Adolescent Sports Medicine, https://doi.org/10.1007/978-3-319-56651-1_10

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The “jammed finger” is a common sports injury seen by coaches, trainers, and primary care and emergency room providers. Although a seemingly common and innocuous injury at times, the “jammed finger” may have underlying pathology that can range greatly in severity. These patients are often referred to the Orthopedic Surgeon in a delayed fashion after stiffness and deformity continue to plague them for an extended period of time. This chapter will address the possible underlying etiologies that can occur with a “jammed finger,” recommendations for evaluation and diagnostic imaging, treatment plans, and possible complications that can occur.

The “Classic” Jammed Finger The “classic” jammed finger usually results in one of three common injuries: a phalangeal neck fracture, an intraarticular fracture of the phalangeal head or base, or a volar plate injury with avulsion fracture of the epiphysis. All three injuries present with a swollen, painful, and stiff finger and appear equivalent clinically. Radiographic imaging will help to delineate the underlying injury and help guide the provider down the correct treatment path.

Phalangeal Neck Fracture Phalangeal neck fractures occur most often in the proximal phalanx but can also be seen in the middle phalanx. The phalanx fractures are just proximal to the collateral ligament recess, maintaining the blood supply to the condyles, which originates within the collateral ligaments. It is imperative these fractures are recognized early so that the appropriate treatment, which is often operative, may be pursued. Clinical examination should include not only skin assessment and neurovascular exam but also assessment of rotation, sagittal and coronal alignment, and range of motion at the injured joint. This can be difficult in pediatric patients secondary to pain and anxiety around moving the digit. Passive flexion and extension of the wrist can be a useful way to evaluate finger motion and rotation using the tenodesis effect (passive wrist extension causes passive flexion of the fingers and passive wrist flexion causes passive extension of fingers) [5]. Additionally, squeezing the musculature at the proximal forearm will cause passive finger flexion. Assessment of rotation is an important focal point in this injury. All fingers should point to the scaphoid tubercle. Underlap, overlap, or deviation of a digit may signify malrotation of bony etiology (Fig. 10.1). Comparison to the contralateral hand is also important as some patients naturally have some overlap between digits. Imaging should include AP, lateral, and oblique X-rays with the finger in question isolated. Phalangeal neck fractures often fall into extension with dorsal translation of the distal segment, leaving an uncovered proximal volar cortical spike (Fig. 10.2) [1, 6]. Al-Qattan [7] defined a classification system for extra-articular

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Fig. 10.1 (a, b) Clinical exam showing malrotation of the ring finger following a phalangeal neck fracture

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Fig. 10.2 (a, b) Lateral and AP X-rays of phalangeal neck fracture of the proximal phalanx. Lateral X-ray shows extension and dorsal translation of the fracture with cortical bone spike in subchondral fossa

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phalangeal neck fractures to guide treatment decisions and assist with prognosis. Type I refers to a nondisplaced phalangeal neck fracture. Type II is a phalangeal neck fracture that is displaced but has some remaining cortical contact. In a Type III, the phalangeal neck fracture is displaced and has additional rotational deformity. Type III is further divided into Types IIIa–d describing the specific displacement of the distal fragment. Treatment is based on the amount of displacement. Type I fractures may be treated non-operatively with cast immobilization for 3–4 weeks [1, 5, 7]. These fractures must be followed closely for loss of reduction with repeat X-rays out of cast at 1 week. Type II and III fractures are inherently unstable and carry a high risk for loss of reduction into extension and dorsal translation. Fracture instability in this pattern is due to the lack of tendinous attachments on the cartilage cap of the skeletally immature phalanx. Type II and III fractures treated with closed reduction and casting often return for follow-up with a late loss of reduction and block to flexion secondary to the proximal volar cortical spike mentioned above (Fig. 10.3). This loss of reduction is problematic, as there is little potential for these fractures to remodel even in young children. This inability to remodel stems from the fact that the physis is located proximally on the phalanx, while the fracture occurs distally [5]. Operative fixation is recommended for all phalangeal neck fractures with any displacement. The preferred treatment is a closed reduction using traction, angular/ rotational correction, and hyperflexion at the PIP joint (or DIP joint if the middle phalanx is involved) and then retrograde cross pinning using 0.028/0.035 K-wires (Fig. 10.4) [1, 2, 5, 7]. Pins can be removed after 3 weeks followed by 3 weeks of buddy taping to begin early motion before return to sports. Displaced late-­presenting fractures often require percutaneous osteoclasis with subsequent reduction and pinning. For fractures where an appropriate reduction is unable to be obtained by closed means, an open reduction with internal fixation may be used as a last resort. Open reduction of phalangeal neck fractures carries a high risk for osteonecrosis of the phalangeal condyles. Extreme diligence should be used not to disrupt collateral ligament tissue and attachments during open reduction, as these tissues contain the blood supply to the phalangeal condyles. The fracture is again fixed with retrograde cross pinning and cast immobilization for 3–4 weeks until healing is noted at the fracture site. The patient is then converted to buddy taping for another 3 weeks once pins are removed to start early motion. Contact and ball sports are restricted for at least 6 weeks until the patient has return of pain-free motion. Complications of phalangeal neck fractures include loss of motion, malunions in rotational, sagittal and coronal planes, and osteonecrosis of the condyles [1]. Established malunions in the sagittal plane can be observed for remodeling under specific circumstances. Case reports have demonstrated that there can be functional remodeling if there is no rotational or coronal malalignment, the adjacent interphalangeal joint is congruent, bony union of the fracture is achieved, there is significant growth remaining in the child, and the child and family can tolerate restricted motion during the remodeling process which can be prolonged [8]. The best outcomes of remodeling occur when the middle phalanx is involved, as the DIP joint requires less motion for function. In patients with phalangeal neck fractures of the proximal phalanx (PIP), sufficient remodeling to regain adequate range of motion is less

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Fig. 10.3 (a, b) AP and lateral X-rays of missed phalangeal neck fracture. This patient presented late with subsequent healing of their phalangeal neck fracture. The outcome resulted in malrotation of the digit and a block to flexion secondary to dorsal translation of the distal fragment and a subchondral spike within the fossa

likely. Late corrective osteotomy for malunited fractures is technically challenging and increases the risk of osteonecrosis of the condyles. For this reason, surgical reconstruction of the subchondral fossa has been proposed to improve motion, but this is a salvage procedure that will not return joint motion to normal [2].

Intraarticular Phalanx Fractures Intraarticular phalanx fractures can occur at either end of the phalanx (head or base). Fractures of the head of the phalanx are more commonly referred to as phalangeal condyle fractures. These tend to be the more common injury seen with a jammed

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Fig. 10.4 (a, b) AP and lateral X-ray cross pinning of a proximal phalanx phalangeal neck fracture

finger and can be unicondylar or bicondylar. All condylar fractures are secondary to a shear force mechanism and can present with or without joint subluxation [1]. Intraarticular fractures of the base of the phalanx are less common in the setting of a jammed finger and are most often lateral avulsion fractures through the corner of the epiphysis. Most fracture patterns are simple; however, rarely an intraarticular fracture may present with significant comminution. Comminuted fractures are usually due to a high energy mechanism, rather than the typical shear or avulsion force [2]. Patients with intraarticular phalanx fractures present with a swollen, painful, and stiff finger, often in a delayed fashion. Clinical exam should again include neurovascular and skin assessment as well as angular and rotational profile of the finger. Imaging should include AP, lateral, and oblique X-rays of the finger in question. Fractures involving the head of the phalanx may show a double density sign or “double bubble” on lateral X-ray, indicating articular displacement (Fig. 10.5) [1, 6]. Fractures at the base of the phalanx are usually a Salter-Harris Type III injury and represent an avulsion injury mechanism. Treatment for phalangeal condyle fractures is based on the amount of fragment displacement. As these are articular injuries, only a small amount of displacement

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Fig. 10.5 (a) AP and lateral X-ray of phalangeal condyle fracture. A. Intraarticular fracture of the proximal phalanx seen on the AP X-ray as a loss of height in the third digit proximal phalanx radial condyle. (b) The condylar fracture can be seen with the classic sign of a “double bubble”

may be accepted (up to 1–2  mm). Nondisplaced fractures can be treated non-­ operatively with cast immobilization for 3–4 weeks. However, we advise caution and close weekly follow-up to evaluate for loss of reduction. Follow-up imaging should be done out of cast immobilization to visualize articular detail. In-office fluoroscopy can be useful if plain radiographs are difficult to interpret. Displacement of the fragment >1–2 mm or rotational deformity >5–10° is an indication for operative fixation. Closed reduction and percutaneous pinning using 0.028/0.035/0.045 K-wires remain the preferred treatment (Fig. 10.6). Percutaneous reduction of the fracture fragment using a towel clip or a K-wire joystick may be helpful [1]. Anatomic reduction of the articular surface is imperative to decrease long-term joint complications. If the fracture cannot be reduced by closed means, open reduction with internal fixation (small screw or K-wires) may be required. Open reduction of phalangeal condyle fractures may also be required for late-­ presenting fractures that are irreducible by closed means. Open treatment, however, carries a high risk for osteonecrosis. This should be performed with extreme caution using a dorsal incision to visualize the articular surface while maintaining hypervigilance to preserve the collateral ligaments and surrounding soft tissues that ­contain the blood supply to the condyles [5]. Postoperatively, patients should remain immobilized for 4 weeks before pins are removed. Resumption of range of motion (ROM) exercises with buddy taping can then ensue and is continued for 2–3 weeks before the patient may return to sports. Although extremely rare in pediatric patients, if a comminuted intraarticular phalanx fracture is found, distraction treatment with a mini ex-fix may be the most appropriate treatment [2]. Postoperative ROM in the ex-fix is recommended after the initial healing of the fracture fragments.

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Fig. 10.6 (a, b) Reduction and cross pinning of the proximal phalanx condyle fracture

Complications of phalangeal condyle fractures can include osteonecrosis, decreased range of motion, and late traumatic arthritis from malunion. The highest risk for osteonecrosis results from open reduction and internal fixation due to the tenuous blood supply through the collateral ligaments. Malreduction can lead to a mechanical block at the subcondylar fossa causing decreased range of motion. Failure to anatomically reduce a condylar fracture fragments can result in an uneven articular surface and may lead to long-term traumatic arthritis.

Volar Plate Injuries Volar plate injuries in pediatric patients are very common in the setting of a jammed finger. Forced hyperextension after direct axial load of an external object, such as a ball, causes disruption of the volar capsule at the PIP or DIP joint. In the skeletally immature, this most often results in an avulsion fracture from the volar lip of the epiphysis on the middle or distal phalanx, as this is the weakest link in the

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attachment of the volar plate [2]. In skeletally mature patients, this mechanism more likely results in disruption of the volar plate with or without collateral ligament injury and subluxation or dislocation of the joint (see Dislocation section below). Volar plate avulsion fractures may result in joint subluxation as well, depending on the amount of joint surface involved (see Intraarticular Phalangeal Fractures, Base Fractures). Clinical exam will be typical of a “jammed finger” as mentioned above. Patients present with a painful, swollen, and stiff finger. Often these patients present in a delayed fashion to orthopedic providers after pain and swelling have failed to resolve over time. Imaging should include AP, lateral, and oblique X-rays of the finger in question. A small avulsion fracture from the volar portion of the epiphysis will be present on radiographs (Fig. 10.7). Loss of volar plate attachment on the epiphysis may result in joint subluxation, which can also be seen on the lateral X-ray. Joint reduction and evaluation of the stable arc of motion should be evaluated radiographically.

Fig. 10.7  Volar plate injury at the PIP joint. Lateral X-ray demonstrating an avulsion fracture of volar portion of the middle phalanx epiphysis. This is the skeletally immature equivalent to a volar plate injury in the adult

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Treatment consists of reduction and brief immobilization in flexion with a dorsal blocking splint for 5–10 days [2, 9]. Transition to buddy taping for an additional 3  weeks and progressive range of motion within the stable flexion-extension arc may start once healing has begun. Contrary to many other pediatric finger injuries, overtreatment with complete immobilization results in a stiff interphalangeal joint and is not recommended. If the joint is unstable after injury and reduction cannot be maintained with a flexed dorsal blocking splint, dorsal extension block pinning may be used [2]. Patients may return to play after 3–6 weeks of rest depending on the severity of the injury, but sport-specific considerations should be taken into account. Buddy taping for an additional 3 weeks during slow advancement back into sport play is advised. Custom gloves with internal finger splints are also an option in certain sports. Complications of volar plate injuries include early reinjury, hyperextension, stiffness, and periarticular swelling. It is important to avoid reinjury (hyperextension force) during the healing phase of the volar plate and collateral bands, as this may result in prolonged healing time or chronic instability [2]. Injuries that are treated with splinting in extension may fall into hyperextension at the IP joint and result in joint instability. Flexion of the dorsal blocking splint during initial immobilization and healing is an important component of early treatment. Counseling families on expectations of outcome should occur at the initial appointment. Periarticular swelling can be expected for 3–6 months and, in some cases, may last for life.

Other Injuries in the Jammed Finger Mallet Finger Although not as common, a mallet finger injury may occur in the setting of a jammed finger. A mallet injury occurs as a result of forced flexion to an extended DIP joint [10]. This injury falls into the category of extensor tendon injuries. The pathology of the injury is due to either an avulsion type fracture of the distal phalanx at the extensor tendon insertion or as an intra-substance tear of the extensor tendon [1, 2]. Adult mallet fingers are usually secondary to an intra-substance tear of the extensor tendon. However, in pediatric patients, the physis and epiphysis are weaker than the extensor tendon attachment to the distal phalanx. Mallet finger injuries in the pediatric population, therefore, are usually an intraarticular avulsion injury, Salter-Harris Type III or IV, at the base of the distal phalanx. There are several classification systems that can help guide treatment. Wehbe and Schneider [11] described a system based on the articular involvement of this injury. Type I is a fracture involving less than 1/3 of the articular surface and has no DIP joint subluxation. Type II involves between 1/3 and 2/3 of the articular surface and has DIP subluxation. Type III involves greater than 2/3 of the articular surface and includes injury to both the

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physis and epiphysis. A second classification proposed by Patel et al. [12] classifies patients based on injury acuity. Patients who present within 4 weeks of injury are classified as acute, and those presenting greater than 4 weeks from injury are classified as chronic [1, 11, 12]. Clinical exam will show a patient with a painful, swollen finger and a distal phalanx postured in a flexed position. An extensor lag of the DIP joint will be present on full finger extension (Fig. 10.8). Evaluation of the nail bed is important in this setting to delineate a mallet injury from a Seymour fracture (see Seymour Fracture section below). Nail bed should appear uninjured without subungual hematoma. Imaging should consist of AP and lateral radiographs of the finger in question. In the skeletally immature patient, most often an avulsion fracture from the dorsal portion of the epiphysis will be observed (Fig.  10.9). Depending on the amount of articular surface involved in the fracture, subluxation of the DIP joint may also be seen. Treatment for bony mallet finger injuries is based off of the adult literature due to a lack of studies within the pediatric population. The treatment goal is to prevent extensor lag and swan neck deformity. For Type I injuries with less than 1/3 of the articular surface involved, treatment should consist of reduction of the DIP joint and avulsion fracture fragment by bringing the DIP joint into hyperextension. The DIP joint is then splinted in hyperextension, leaving the PIP joint free (Fig. 10.10). This can be accomplished with either volar or dorsal splinting. Splinting should be full time for 6–8  weeks, followed by 2–4  weeks of nighttime splinting. Patients are brought back at 1 week for splint fit and skin check and to ensure the bony fragment is maintaining reduction. If patients are unable to tolerate the basic splint or keep it in position, combinations of plaster DIP splint under cast or custom DIP extension splint with a separate forearm component can be used. These are especially useful in small children. For patients in casts, families are given strict instructions that if there is increasing pain under the cast, this could indicate a skin issue, and they should come back for immediate examination. Fig. 10.8  Mallet finger demonstrated clinically as an extensor lag of the DIP joint

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Fig. 10.9  Lateral X-ray of a bony mallet finger injury

For Types II and III with greater than 1/3 of the articular surface involved, surgical management may be indicated. Any fracture with continued articular incongruence, volar joint subluxation persisting after reduction and splinting, or failure of bony contact after reduction and splinting, are also indications for surgical treatment. The most commonly used technique is percutaneous extension block pinning (Fig. 10.11). In this technique, the DIP joint is brought into full flexion with a wire placed dorsal to the fracture fragment through the extensor tendon. The DIP joint is then brought into full extension to reduce the fracture fragment, and a second wire is placed retrograde across the DIP joint to hold the reduction. Rarely, if reduction cannot be achieved by percutaneous means, open reduction with internal fixation such as tension band wiring, suture, direct pin fixation, or bone anchors is required [1].

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b

Fig. 10.10 (a) Clinical picture of dorsal hyperextension splint used for treatment of mallet finger injury. It is important to recognize the PIP joint is left free to allow range of motion. (b) Reduced bony mallet injury with dorsal hyperextension splinting

Although the incidence of soft tissue mallet injuries in the pediatric population is unknown [10], the treatment remains similar to that of the adult population. Soft tissue mallet injuries should be treated with DIP joint extension splinting full time for 6–8  weeks. Patients with delayed presentation or noncompliance with full-time splinting and extensor lag of greater than 40° may require surgical treatment. Shin and Bae [10] described the technique of tenodermodesis in pediatric patients. This involves advancement and repair of the extensor tendon in combination with skin and subcutaneous tissue and retrograde pinning across DIP joint. Although this technique may result in loss of flexion and possible nail plate deformity, it restores extension at the DIP joint preventing development of a swan neck deformity and avoiding fusion. Complications of mallet finger injury include stiffness and extensor lag which can ultimately lead to swan neck deformity. For every 1 mm of terminal extensor tendon lengthening, 25° of extensor lag results. On the contrary, operative fixation and terminal extensor shortening can result in severe restriction of DIP flexion [1, 2]. Currently, there are no studies looking at the long-term complications and outcomes of pediatric bony mallet fractures specifically. In general, the majority of these injuries heal well with good remodeling of the DIP joint. They often have an asymptomatic residual dorsal bump at the base of the distal phalanx, so it is good to counsel the family about that in the beginning. The majority of patients, even those with fibrous unions, return to full previous activities without restriction. Patients are held out of contact and ball sports until there is evidence of healing, usually at least 6  weeks. They may then return to full sport, but splint wear is ­recommended for usually 2 weeks during sport for protection until their motion has returned.

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d

Fig. 10.11  Step-by-step dorsal block pinning of bony mallet injury after failed non-operative splint treatment. (a) Lateral X-ray demonstrating bony mallet injury not reduced in splint. (b) Hyperflexion of DIP joint and pinning of the extensor tendon in place. (c) Lateral and (d) PA X-ray with extension of the DIP joint causing reduction of the dorsal epiphyseal fragment and pinning across the DIP joint to maintain reduction

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Seymour Fracture A Seymour fracture can also occur in the setting of a jammed finger. Seymour fractures were initially described as juxta-epiphyseal fractures of the distal phalanx in the skeletally immature patient with a concomitant disruption of the nail plate [13]. Seymour believed this type of fracture was inappropriately categorized as a type of mallet finger and was often mistreated. Today, we further describe Seymour fractures as a physeal injury, SHI or SHII, of the distal phalanx with an associated nail bed laceration making it technically an open fracture. It is usually seen as the result of a crush injury [1] but may also be seen in the setting of a jammed finger. The imbalance of the volar pull of the FDP attachment to the metaphysis versus the extensor tendon attached to the dorsal epiphysis causes these fractures to fall into a flexed posture at the physis [14, 15]. Seymour fractures may be confused for a mallet injury on clinical exam due to the flexion deformity at the distal phalanx [1, 2, 14], but no tendon disruption is present. On clinical exam, the patient will present with a painful finger that appears flexed distally. The nail bed laceration may not be visible initially, and the open injury may be dismissed as a closed mallet injury. However, if the nail remains intact, there is often a subungual hematoma present which should increase the provider’s suspicion of a Seymour fracture [16]. Other subtleties can include a break in the cuticle seal or a nail that appears longer that the other finger nails proximally, as the nail plate has pulled out from the eponychial fold. Other times, the nail bed laceration may be obvious with complete disruption of the nail and the distal edge of the fracture extruded through the nail bed (Fig.  10.12). Seymour fractures that present in a delayed fashion will often present with an eschar over the eponychial fold due to chronic pressure from the fracture apex. Evaluation for infection in fingers with delayed presentation is very important [1, 5, 16]. Diagnostic imaging should include AP and lateral X-ray of the finger in question. The AP image may appear normal or with slight gapping at the physis. A true lateral X-ray is important to demonstrate the flexion and apex dorsal displacement of the distal fragment at the physis (Fig. 10.13). Fig. 10.12 Seymour fracture. Clinical picture of an open SHII distal phalanx fracture with apex extruded through the nailbed. (Reprinted by permission from Springer: Pediatric Orthopedic Trauma Case Atlas by Christopher Iobst and Steven L Frick © 2017)

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Treatment is based on the open nature of the injury. Nondisplaced Seymour fractures may be treated with simple splinting or casting. Fracture displacement may mean that there is nail bed interposed at the fracture site and is therefore an indication for surgical treatment. If being treated closed, the patient should follow-up at 1 week for clinical exam and repeat X-rays to ensure that a more serious injury was not missed and that there is no evidence of infection. They should be immobilized for 4 weeks with an additional 2 weeks of protection while motion is regained. Seymour fractures are open fractures until proven otherwise. Open fractures must be managed surgically and in a timely manner (less than 24  h preferably). Surgical treatment should include nail plate removal, visualization of fracture through the nail bed, debridement and irrigation of the fracture site, removal of all incarcerated tissue, and reduction of the fracture. Failure to remove interposed tissue will result in inability to anatomically reduce the fracture and possible physeal arrest and/or late nail plate deformity. Fracture reduction should be performed by extension of the distal phalanx while holding the DIP joint stable. If stable after reduction, the nail bed should be repaired with 5-0/6-0 absorbable suture (Fig. 10.14) and then the nail plate secured back beneath the eponychial fold with interrupted

a

b

Fig. 10.13 (a, b) AP and lateral X-ray of the hand demonstrating a Seymour fracture of the fifth digit. (Reprinted by permission from Springer: Pediatric Orthopedic Trauma Case Atlas by Christopher Iobst and Steven L Frick © 2017)

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a

b

Fig. 10.14  Seymour fracture. (a) Nail bed laceration after surgical irrigation and debridement. (b) Nail bed repair with 6-0 chromic gut gut. (Reprinted by permission from Springer: Pediatric Orthopedic Trauma Case Atlas by Christopher Iobst and Steven L Frick © 2017)

sutures [5]. Foil wrapping from the suture package may also be used under the eponychial fold to maintain opening as the nail regrows, but original nail plate is preferred if available, as it will provide inherent stability to the fracture [14]. If the fracture is unstable after reduction, it should be percutaneously pinned using appropriately sized K-wires retrograde through the tip of distal phalanx and across the DIP joint. All patients should be given IV antibiotics initially in the emergency

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department and at the time of surgery. An additional 5–7 days of oral antibiotics should be given to patients on discharge given the high risk of infection [16]. Reyes and Ho [16] reported on the risk of infection for 34 patients with 35 Seymour fractures with delayed treatment. Those treated within 24 h after injury with irrigation and debridement, fracture reduction, stabilization, and antibiotics had no incidence of infection. Patients partially treated (missing one of the above steps for treatment) within 24 h returned with a 15% infection rate. Patients treated greater than 24 h post-injury had a 45% rate of infection. Other complications seen in Seymour fractures include osteomyelitis, early physeal arrest, nail bed deformity, or dorsal rotation of the epiphysis leading to extensor lag or articular deformity [1, 14–16]. Osteomyelitis is most often seen in missed injuries or those confused for mallet injury and not treated with surgical debridement and antibiotics (Fig. 10.15). After surgical treatment, the patient should be immobilized in a mitten cast, long arm if necessary, to protect the nail bed repair and to protect the pin if present. Cast and pin are usually removed at 4 weeks, and the finger can then be transitioned to a removable splint, so they may start working on motion. They may return to sport after 6 weeks if they are fully healed and have regained their motion.

DIP and PIP Dislocations Although less common than a volar plate avulsion injury in skeletally immature patients, DIP and PIP joint dislocations may also occur with a “jammed finger.” Again, the mechanism of injury is a forced hyperextension after direct axial load of an external object, such as a ball. This causes rupture of the volar capsule and volar a

b

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Fig. 10.15  Missed Seymour fracture. (a) Clinical photo of infected digit. (b) AP and (c) lateral X-ray demonstrating osteomyelitis at fracture site site. (Reprinted by permission from Springer: Pediatric Orthopedic Trauma Case Atlas by Christopher Iobst and Steven L Frick © 2017)

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plate injury, with or without collateral ligament injury (as discussed above in Volar Plate Injuries). Dorsally displaced dislocations are most common and are most often “uncomplicated” dislocations. Clinical examination of the finger usually reveals an obvious deformity about the DIP or PIP joint with significant pain and swelling. Imaging should include AP, lateral, and oblique X-rays of the finger in question. Most dislocations are dorsal but may also be volar (Fig. 10.16). “Uncomplicated” dislocations usually reduce easily and are stable after reduction. Most of these injuries will be reduced on the field by the patient, coach, or trainer prior to presentation to the provider. “Complex” dislocations will be irreducible on the field and in the emergency department. These are an indication of volar plate entrapment within the joint. An early sign of a complex dislocation is bayonet apposition on X-ray [2]. A rotatory dislocation of the PIP joint may also be irreducible due to buttonholing of a condyle of the proximal phalanx through a longitudinal defect in the extensor hood between the central slip and the lateral band. Clinical exam for stable range of motion and collateral ligament stability after reduction should always be completed prior to splinting. Postreduction repeat imaging should be obtained after the splint is placed to assure stable positioning of the joint.

a

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Fig. 10.16 (a, b) PA and lateral X-rays of a PIP dislocation

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Treatment of uncomplicated DIP and PIP joint dislocations involves reduction, brief immobilization, and early return to range of motion [2]. As with volar plate injuries, overtreatment with long-term immobilization can result in stiffness of the IP joints. After reduction of a DIP or PIP dislocation, the joint may continue to have some instability and fall into hyperextension (Fig.  10.17). Therefore, the injured digit should be immobilized in a flexed dorsal blocking splint for 5–10 days to allow soft tissues to heal around the joint (Fig. 10.18). This should then be followed by buddy taping to an adjacent finger for an additional 3  weeks for protection and a

b

Fig. 10.17 (a, b) PIP joint hyperextension instability at the joint after inadequate immobilization after reduction

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Fig. 10.18  Flexed dorsal blocking splinting stabilizing the hyperextension instability at the PIP joint

encouragement of active/passive range of motion. Complex dislocations will be irreducible in the emergency room setting. These require open reduction using a dorsal or volar approach to remove the interposed volar plate. Rotatory dislocations can be reduced with traction applied across the finger, while the PIP and MP joints are flexed 90°. The flexion relaxes the volarly displaced lateral band allowing it to slip back dorsally. If unsuccessful, then open reduction must be performed. For all dislocations, reduction must be confirmed with AP and lateral X-rays. Complications in DIP and PIP joint dislocations are similar to those in volar plate injuries (see Volar Plate Injury section above). Hyperextension of the joint

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during healing may cause reinjury and chronic instability. Athletes should be kept out of play for 3–6 weeks with buddy taping of digit on return to play. Periarticular swelling can be expected to last for several months to a year.

Central Slip Injuries Central slip injuries are relatively rare in the pediatric population but can occur in the setting of a jammed finger, especially as our pediatric population becomes more involved in high-intensity sporting activities at younger ages. Disruption of the central slip can be the outcome of a seemingly innocuous injury such as a jammed finger. Central slip injuries represent a zone 3 extensor tendon injury. They can be the result of forced hyperflexion to an extended finger, direct blunt or sharp trauma to the dorsum of the finger, or an injury due to volar dislocation at the PIP joint [17– 19]. Patients with central slip injuries present clinically with a swollen, painful, and often ecchymotic finger at the PIP joint. Imaging should include AP, lateral, and oblique X-rays of the affected digit to rule out fracture or dislocation. During the clinical examination, it is important to include the Elson test [17, 18]. To perform the Elson test, the examiner places the injured PIP joint in 90° of flexion. The patient is then asked to attempt to extend the digit, while resistance is applied to the middle phalanx. If the central slip is intact, then the DIP joint will remain flexed and without tension. If the central slip is disrupted, the DIP joint extensor tone will increase or the joint will extend. A digital block may be performed prior to examination of the digit, as movement is likely to cause discomfort. Treatment of a central slip injury is based off of the adult literature, as this continues to be a rare injury in the pediatric population. For acute, closed, central slip injuries without bony involvement, the PIP joint should be splinted in extension full time for 4–6 weeks, leaving the DIP joint free. DIP joint range of motion should be encouraged throughout the splinting treatment. This should then be followed by an additional 4 weeks of nighttime splinting. When evaluating for return to play, there are no universal guidelines [18]. Return to play is individualized with respect to age, hand dominance, position and sport involved, and performance level. Complications in central slip injuries include stiffness of the PIP joint and chronic boutonniere deformity due to volar subluxation of the lateral bands. Noncompliance with splinting or early return to play and reinjury can result in this chronic deformity. Chronic boutonniere deformities are treated surgically. It is important to council parents regarding periarticular swelling and joint stiffness, as it may continue for 3–6 months.

Gamekeeper’s Thumb A Salter-Harris III fracture at the ulnar base of the thumb proximal phalanx may occur as the result of a jammed thumb. This fracture is the pediatric equivalent of the adult gamekeeper’s thumb [2]. However, rather than a direct axial load, as in

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most jammed fingers, this injury occurs secondary to an abduction moment through the base of the thumb. For more information about Gamekeeper’s Thumb, please refer Chap. 9.

Salter-Harris II Fractures of the Phalanx Extra-octave fractures may occur as the result of a jammed finger injury. This injury refers to a Salter-Harris Type II injury to the base of the proximal phalanx. These fractures can usually be treated by closed reduction and immobilization. Pediatric patients have high potential for remodeling of these injuries and rarely require operative treatment. For further information regarding extra-octave fractures, please refer Chap. 9.

Summary Pediatric hand injuries are the most common injury seen in pediatric acute trauma. As these patients continue to become involved in high-intensity sports at earlier ages, the “jammed finger” will continue as one of the most common injuries seen by a variety of providers. Although the jammed finger often seems to be an innocuous injury, it may have a significant underlying injury requiring specific treatment by an orthopedic surgeon. The classic jammed finger is most often one of three diagnoses: phalangeal neck fracture, phalangeal condyle fracture, or a volar plate injury. These injuries are important to recognize in a timely fashion so that they may be treated appropriately to avoid complications. Other jammed finger injuries including mallet injury, Seymour fracture, DIP or PIP dislocation, central slip injury, game keepers thumb, and extra-octave fractures are also important to recognize in a timely fashion. Delayed treatment of the jammed finger can result in challenging complications for the orthopedic surgeon and may be avoided with early referral and treatment.

References 1. Abzug JM, Dua K, Baur A, Cornwall R, Wyrick TO. Instructional course lecture: pediatric phalanx fractures. J Am Acad Orthop Surg. 2016;24:e174–83. 2. Waters PM.  Surgical treatment of carpal and hand injuries in children. Instr Course Lect. 2008;57:515–24. 3. Fetter-Zarzeka A, Joseph MM. Hand and fingertip injuries in children. Pediatr Emerg Care. 2002;18(5):341–5. 4. Vadivelu R, Dias JJ, Burke FD, Stanton J. Hand injuries in children: a prospective study. J Pediatr Orthop. 2006;26:29–35. 5. Waters PM, Bae DS. Pediatric hand and upper limb surgery: a practical guide. Philadelphia: Lippincott; 2012. p. 439–52. 6. Nellans KW, Chung KC. Pediatric hand fractures. Hand Clin. 2013;29(4):569–78. 7. Al-Quattan MM. Phalangeal neck fractures in children: classification and outcome in 66 cases. J Hand Surg Br. 2001;26B(2):112–21.

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8. Cornwall R, Waters P. Remodeling of phalangeal neck fracture malunions in children: case report. J Hand Surg. 2004;29A(3):458–61. 9. Weber DM, Kellenberger CJ, Meuli M. Conservative treatment of stable volar plate injuries of the proximal interphalangeal joint in children and adolescents: a prospective study. Pediatr Emerg Care. 2009;25:547–9. 10. Shin EK, Bae DS.  Tenodermodesis for chronic mallet finger deformities in children. Tech Hand Upper Extrem Surg. 2007;11(4):262–5. 11. Wehbe MA, Schneider LH. Mallet Fractures. 1984;66(5):658–69. 12. Patel MR, Desai SS, Bassini-Lipson L. Conservative management of chronic mallet finger. J Hand Surg Am. 1986;11(4):570–3. 13. Seymour N. Juxta-epiphysial fracture of the terminal phalanx of the finger. J Bone Joint Surg Br. 1966;48(2):347–9. 14. Abzug JM, Kozin SH. Seymour fractures. J Hand Surg. 2013;38A:2267–70. 15. Krusche-Mandl I, Kottstorfer J, Thalhammer G, Aldrian S, Erhart J, Platzer P. Seymour fractures: retrospective analysis and therapeutic considerations. J Hand Surg. 2013;38A:258–64. 16. Reyes BA, Ho CA. The high risk of infection with delayed treatment of open seymour fractures: Salter-Harris I/II or juxta-epiphyseal fractures of the distal phalanx with associated nailbed laceration. J Pediatr Orthop. 2015;37:247; [epub]. 17. Lin JD, Strauch RJ. Closed soft tissue extensor mechanism injuries (mallet, boutonniere, and sagittal band). J Hand Surg Am. 2014;39(5):1005–11. 18. Grandizio LC, Klena JC. Sagittal band, boutonniere and pulley injuries in the athlete. Curr Rev Musculoskelet Med. 2017;10:17–22. 19. Izadpanah A, Izadpanah A, Sinno H, Williams B. Pediatric boutonniere deformity after blunt closed traumatic injury. Pediatr Emerg Care. 2011;27:1069–71.

Chapter 11

Upper Extremity Nerve Injuries Andrea S. Bauer

Introduction Upper extremity nerve injuries in sports are fortunately rare. Because they are rare, and in general have a different presentation than other musculoskeletal injuries, a high index of suspicion is required to make the correct diagnosis. Nerve injuries can be acute, due to a laceration or sudden traction injury, or they can be the result of chronic compression or strain. In order to understand peripheral nerve injuries of the upper extremity, a neuroanatomy review is in order. The peripheral nerves of the upper extremity are for the most part mixed motor/ sensory nerves. The motor pathway consists of a primary motor neuron, connecting the motor cortex in the brain to the spinal cord, and a secondary motor neuron, whose cell body resides in the anterior horn of the spinal cord (C5 to T1 levels), and connects the spinal cord to the target muscle. The sensory pathway begins in the sensory dermatome in the skin (C5-T1 dermatomes), with the cell body residing in the dorsal root ganglion just outside the spinal cord. The information is transmitted via the sensory axons to the thalamus and eventually the somatosensory cortex in the brain. Peripheral nerves as we encounter them in the extremity consist of axons surrounded by a layer of connective tissue called endoneurium. Axons are arranged into fascicles, and each fascicle is wrapped in a second layer of connective tissue termed perineurium. Finally, the fascicles are bundled together with a dense layer of connective tissue, the epineurium (Fig. 11.1). The spectrum of acute nerve injuries was first described in 1943 by Seddon as neurapraxia (stretch injury), axonotmesis (disruption of axons with outer structure of nerve intact), and neurotmesis (disruption of the entire nerve) [1]. This classifica-

A. S. Bauer (*) Department of Orthopedic Surgery, Boston Children’s Hospital, Boston, MA, USA e-mail: [email protected] © Springer International Publishing AG, part of Springer Nature 2019 A. S. Bauer, D. S. Bae (eds.), Upper Extremity Injuries in Young Athletes, Contemporary Pediatric and Adolescent Sports Medicine, https://doi.org/10.1007/978-3-319-56651-1_11

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Fig. 11.1  Illustration of the internal anatomy of a peripheral nerve. (Image copyright © Children’s Orthopaedic Surgery Foundation and used by permission. All rights reserved)

Fascicle

Axon Endoneurium Perineurium Epineurium

Table 11.1  Sunderland classification of peripheral nerve injuries Degree Description First Neurapraxia

Pathologic features Intact nerve

Second Axonotmesis

Axons not in continuity but remainder of nerve structure remain intact Internal architecture of nerve disrupted, but perineurium and epineurium intact Near-complete discontinuity of nerve, with only epineurium intact Complete discontinuity of nerve ends

Third

Axonotmesis + endoneurium disrupted

Fourth Axonotmesis + endoneurium + perineurium disrupted Fifth Neurotmesis

Recovery Spontaneous, weeks to months Spontaneous but requires axon regrowth over several months May require surgery

Usually requires surgery

Requires surgery

tion was expanded by Sunderland in 1951 to divide neurotmesis further by severity (Table  11.1). Sunderland differentiated between disruptions of the endoneurium only, disruption of the endoneurium and perineurium (with epineurium intact), and complete disruption of the nerve [2]. This distinction is important, as disruption of endoneurium may recover without surgical intervention, while disruptions of perineurium and epineurium generally require surgical repair. The severity of compression injuries is not as easily defined. Clinically, compression neuropathies begin with intermittent sensory symptoms such as burning, tingling, and numbness in the affected nerve distribution, often related to position or activity. Symptoms progress to persistent sensory symptoms and finally to motor weakness and muscle atrophy in the affected motor distribution. Because motor weakness and muscle atrophy may not recover even after surgical decompression, it

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is important to evaluate and treat compression neuropathies in the young athlete prior to the development of motor symptoms whenever possible. In this chapter, we will begin with an overview of the proper evaluation of the young athlete with a suspected nerve injury, followed by descriptions of specific injuries and their treatments, including burners and stingers, winging of the scapula, acute nerve lacerations, and the various compression neuropathies.

Evaluation of Nerve Injuries in Children Nerve injuries in children may present differently than in adults. Children have little experience with numbness and other sensory disturbances, so they may have difficulty describing their symptoms, making a careful history important. Altered sensation may be described as pain, achiness, sleepiness, or ants crawling on the skin. Children will often not mention the altered sensation at all, if not asked. For the hand specifically, if the location of altered sensation is in question, we find it helpful to ask, “Which finger is never involved?” If the thumb is reported as “never involved,” the suspicion is raised for ulnar nerve compression. If the small finger is never involved, that points toward median nerve compression. The Semmes-­ Weinstein test evaluates the sensory threshold by using a series of monofilaments designed to bend at a certain pressure. For cooperative children and teenagers, we find Semmes-Weinstein testing to be the most reliable for detecting sensory deficits, as well as for following changes over time. Recent literature has demonstrated that children can reliably comply with formal sensory testing from about age 5 and that Semmes-Weinstein may be easier for younger children to complete. Dua and colleagues examined nearly 200 subjects using both Semmes-Weinstein and 2-point discrimination tests. They found that 83% of 4-year-olds and all subjects 5 years and older could complete Semmes-Weinstein testing, while only 33% of 4-year-­ olds and 61% of 5-year-olds could complete 2-point discrimination tests successfully. Only for ages 9 and up could all children complete 2-point discrimination tests reliably [3]. For children who are unable to cooperate with formal sensory testing, two other options are available to evaluate sensation. First, simple inspection and palpation of the fingertips can give clues to a nerve injury. Since normal skin sweating is mediated by the sensory nerves, fingers in the distribution of an injured sensory nerve will feel drier than the other fingers, and the skin will have a dry appearance (Fig. 11.2). Second, it is possible to test for a median, ulnar, or digital nerve injury by immersing the hand in warm water. The skin wrinkling that occurs in water is mediated by afferent nerves, and so the fingers affected by the nerve injury will not wrinkle (Fig. 11.3) [4]. The skin wrinkling test should not be used to follow nerve recovery after repair, however, as the relationship between nerve recovery and the wrinkling test is not known. It is also important to note that finger wrinkling is related to the osmolar gradient between the water and the body, so that the same effect is not seen as readily when using normal saline in the hospital setting.

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Fig. 11.2  Dry skin in the distribution of an injured nerve. In this patient with a median nerve injury, notice that the thumb, index, and middle fingertips are drier appearing and less plump than the ring and small fingertips. (Image copyright © Children’s Orthopaedic Surgery Foundation and used by permission. All rights reserved)

Fig. 11.3  Lack of skin wrinkling in the distribution of an injured nerve. This photograph was taken after immersing the hand in water for several minutes. In this patient with an ulnar nerve injury, notice that the small finger did not become wrinkled after immersion in water. (Image copyright © Children’s Orthopaedic Surgery Foundation and used by permission. All rights reserved)

As described in Chap. 12, ultrasonography is a useful noninvasive tool in evaluating nerve compression. Normative and pathologic values for the cross-sectional area of the median nerve at the carpal tunnel and the ulnar nerve at the cubital tunnel have been established in adults to identify carpal and cubital tunnel on ultrasound [5]. A recent retrospective study of adult subjects who had undergone both ultrasound and electromyography found an ultrasound sensitivity of 77% for detecting electrodiagnostically confirmed cubital tunnel syndrome and a sensitivity of 84% for detecting electrodiagnostically confirmed carpal tunnel syndrome [6]. Ultrasound is appealing in children as it is fast and noninvasive, but more research is needed to confirm the accuracy of ultrasound diagnosis in children specifically. 3-Tesla magnetic resonance imaging (MRI) using newer sequences also has the ability to detect nerve abnormalities in a noninvasive manner. A recent retrospective study found the

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turbo spin-echo T2-weighted sequence on a 3-Tesla MRI to have 95% sensitivity at detecting a peripheral neuropathy [7]. Nerve conduction studies (NCS) and electromyography (EMG) remain the gold standard for evaluating the location and severity of nerve injury, as well as to follow recovery of a nerve [8]. Nerve conduction studies evaluate a nerve’s function by electrically stimulating the nerve and recording its response. EMG measures the intrinsic electrical activity of the muscle. The ability of a nerve to respond to an external stimulus is termed its excitability. A decrease in nerve excitability can be detected on EMG/NCS approximately 72  h after a severe acute nerve injury. As time goes on after an acute nerve injury, the affected muscle becomes denervated, leading to an increased sensitivity to acetylcholine. This hypersensitivity is seen as fibrillation potentials on needle EMG, which can be detected by 2 weeks after an acute injury. Therefore, EMG/NCS should not be performed prior to 2 weeks after an acute nerve injury. NCS and EMG evaluate the function of the motor unit, which is made up of the motor neuron, the axon, and all muscle fibers innervated by the motor neuron. A motor unit potential (MUP) is the action potential created by the voluntary contraction of the muscle in the motor unit, which is recorded by the EMG. Following denervation, high-amplitude MUPs can be seen as a sign of collateral reinnervation, as more muscle fibers are recruited by stimulation of a single motor unit. Compression neuropathies, which will be discussed in detail later in the chapter, lead to segmental demyelination of the affected nerve. This demyelination leads to slowing of the nerve conduction velocity (NCV), which is detected on NCS.  In addition, skin temperature, age, and height can all affect the recorded values for NCV and must be controlled for by the neurophysiologist performing the test. Compression neuropathies may be difficult to detect in the early stages on EMG/ NCS, and so a negative study, particularly in a young person, cannot rule out compression.

Burners and Stingers The brachial plexus consists of the C5 through T1 nerve roots as they exit from the cervical spine and travel through the neck and axilla and become the major motor and sensory nerves of the upper extremity. Burners and stingers are interchangeable colloquial terms for a brachial plexus injury sustained during sports activities. These injuries are rare, occurring most commonly in contact and extreme sports. They occur through a traction mechanism and are usually simple neurapraxias (Fig. 11.4). Symptoms include numbness and weakness in the unilateral affected nerve root distribution, usually C5 and C6. When the injury is a simple neurapraxia, symptoms typically resolve in minutes to hours, and players do not subsequently need medical attention. When they do present, physicians should be on the lookout for bilateral symptoms, which may indicate a cervical spinal cord injury. Evaluation of a burner starts with a thorough motor and sensory examination of the affected extremity, with comparison to the normal contralateral side. Horner’s syndrome, which is seen

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Fig. 11.4  Illustrative mechanism of a burner or stinger injury. (Image copyright © Children’s Orthopaedic Surgery Foundation and used by permission. All rights reserved)

on physical exam as ipsilateral ptosis, miosis, and anhidrosis, denotes an injury to the cervical sympathetic trunk and is pathognomonic for a severe brachial plexus injury. Treatment begins with rest and observation; players should not be allowed to return to play until complete resolution of symptoms. For those injuries that last beyond 1–2 weeks, physical therapy may be helpful to ensure motion is not lost and to assist with strengthening prior to return to play. Symptoms that last beyond 6 weeks should raise the suspicion for an injury that is more severe than a neurapraxia. If significant impairment in limb function exists beyond 6  weeks, EMG/ NCS is done at 6 weeks to evaluate the extent of the injury as well as to serve as a baseline for future reinnervation. In addition, MRI of the brachial plexus may be done at this time to evaluate for nerve root avulsions. Surgery is warranted if sufficient recovery has not occurred by 6 months after the injury and/or in the case of nerve root avulsions. Surgical options include nerve

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grafting, in which the injured segment of the brachial plexus is excised and replaced with autograft nerve, typically the sural nerve. Following nerve grafting surgery, the nerve repair heals in place in 3–4 weeks, but reinnervation can take 1–2 years, as the affected axons need to grow through the site of repair out to the appropriate muscle. Another option is nerve transfer, in which a portion of a nearby nerve that can be spared is redirected to the muscle which requires reinnervation. An example of a nerve transfer is the Oberlin transfer, in which a fascicle from the ulnar or median nerve is transferred to the biceps motor branch of the musculocutaneous nerve to reinnervate the biceps muscle (Fig. 11.5) [9]. Nerve transfers take place farther distally in the affected extremity, close to the motor end plate, which shortens the time to reinnervation substantially. Results from nerve transfers can be seen as early as 3  months after surgery. In general, nerve surgery is effective at reinnervation of antigravity strength in the shoulder and elbow, but reinnervation of more distal muscles is less reliable. Some injury patterns may also be amenable to later tendon transfers, in which a nearby muscle is detached from its insertion and redirected to Fig. 11.5 Intraoperative photograph of an Oberlintype nerve transfer. In this case, a fascicle of the median nerve was transferred to the biceps motor branch of the musculocutaneous nerve. (Image copyright © Children’s Orthopaedic Surgery Foundation and used by permission. All rights reserved)

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compensate for the denervated muscle. These transfers can be successful years after injury, but not all injury patterns have an appropriate nearby muscle to transfer. Therefore we recommend early referral to a brachial plexus specialist for all burners which do not resolve by 6 weeks after injury, so that any surgery, if warranted, can be done at the optimal time. Physical therapy following nerve and/or tendon transfer surgery is extensive, focusing on sensory and motor reeducation and functional activities of daily living. A brachial plexus injury severe enough to require surgery is typically a career-ending injury for a young athlete, although play may be considered in some cases 1–2 years after surgery.

Scapular Winging Scapular winging is the involuntary posterior protrusion of the scapula due to neuropathic loss of either serratus anterior muscle function or trapezius muscle function. This should be differentiated from scapular dyskinesis, which is an alteration in the normal movement pattern of the scapula that can be seen with repetitive overhead activity, as described in Chap. 3. There are two main categories of scapular winging based on the position of the superomedial corner of the scapula on exam. Medial winging of the scapula is due to dysfunction of the long thoracic nerve and/or serratus anterior muscle. In this scenario, the medial and superior pull of the rhomboid and trapezius muscles on the scapula is unopposed by the serratus anterior, so the scapula rotates superiorly and medially. Lateral winging of the scapula typically occurs when the spinal accessory nerve and/or trapezius muscle is injured, so that the unopposed lateral pull of the serratus anterior rotates the scapula out laterally (Fig. 11.6). Medial winging is far more common in sports, occurring most often in overhead sports such as volleyball. Evaluation consists of physical examination to visualize the function of the serratus anterior, rhomboids, and trapezius muscles along with the direction of scapular winging and overall range of motion of the shoulder and scapula. Nerve conduction studies can be helpful to grade the severity and chronicity of injury to the long thoracic or spinal accessory nerve [10]. Most scapular winging injuries are chronic and incomplete. Physical therapy is the mainstay of treatment, consisting of stretching, strengthening, and activity modification. Complete resolution of symptoms may take 1–2  years. Medial winging due to dysfunction of the long thoracic nerve can be treated with a nerve transfer from the thoracodorsal nerve in select cases within 1 year of injury [11]. Through an axillary approach, the lateral branch of the thoracodorsal nerve is isolated as it enters the latissimus dorsi and is transferred to replace the injured long thoracic nerve near where it innervates the serratus anterior muscle (Fig. 11.7). Rehabilitation is extensive following this transfer, with results seen at 6 months to 1 year after surgery.

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a

Spinal accessory n. Trapezius m.

Dysfunctional trapezius m.

Functional serratus anterior m.

Lateral scapular winging

b

Long thoracic n. Functional trapezius m. Dysfunctional serratus anterior m.

Serratus anterior m.

Medial scapular winging

Fig. 11.6 (a) Illustration of medial scapular winging. (b) Illustration of lateral scapular winging. (Image copyright © Children’s Orthopaedic Surgery Foundation and used by permission. All rights reserved)

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b

c

Fig. 11.7  Intraoperative photographs of thoracodorsal to long thoracic nerve transfer. (a) Surgical incision in the axilla (the arm is positioned over the head). (b) Branches of the thoracodorsal nerve isolated for transfer, along with the long thoracic nerve. (c) Branch of the thoracodorsal nerve coapted to the long thoracic nerve. (Image copyright © Children’s Orthopaedic Surgery Foundation and used by permission. All rights reserved)

For those patients who fail conservative management and are not appropriate candidates for a nerve transfer, other surgical options include transfer of the sternal head of the pectoralis major muscle for medial winging and the Eden-Lange transfer (transfer of the levator scapulae and rhomboid muscles from the medial border of the scapula to the lateral border) for lateral winging [12]. In severe cases, scapulothoracic fusion may be required. Although outcomes are generally good in terms of relief of pain and improvements in function, return to play following these surgeries is uncertain.

Nerve Lacerations Nerve lacerations in sports are rare but can be caused in figure skating and ice hockey by the blades of the skates, as well as by crashes in extreme sports such as motocross. In children, the concept of “topographic anticipation” dictates that sharp injuries over the expected paths of peripheral nerves and tendons be explored in the operating room for potential injury, even if obvious symptoms of that injury are not present. A review of 100 hand lacerations explored in the operating room found that even experienced hand surgeons missed up to 30% of injuries based on their clinical

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examination alone, and the authors recommended prompt referral to a hand surgeon for most hand lacerations, to consider formal exploration in the operating room [13]. Following nerve repair, patients are typically immobilized for 3–4 weeks, with return to play at 4–6 weeks depending on the exact injury and sport. Families should be aware, however, that recovery of the injured nerve may progress for 1–2 years.

Compression Neuropathies Thoracic Outlet Syndrome Thoracic outlet syndrome (TOS) describes compression of the brachial plexus and/ or subclavian vessels in the “thoracic outlet,” the interval from the clavicle to the first rib between the scalene muscles through which pass the brachial plexus and subclavian vessels. TOS is thought to result from a combination of anatomic predisposition combined with acute or repetitive trauma to the area. The dimensions of the thoracic outlet naturally change with arm position, with the narrowest dimensions occurring when the arm is in abduction (Fig. 11.8). In addition, scapular protraction and anterior tilt of the scapula can also narrow the thoracic outlet. The repetitive trauma can be sport, particularly those involving repetitive arm motions, such as swimming, rowing, and baseball [14]. Anatomic variations that are more common in TOS patients include the cervical rib, large C7 transverse processes, and the scalenus minimus, an accessory scalene muscle. TOS is divided into neurogenic a

b

Fig. 11.8  Coronal T1 post-contrast MRI images in a patient with right-sided vTOS, done with the arms down (a) and the arms abducted overhead (b). Notice that the subclavian vessels diminish in size on the left (blue arrows) in the arms overhead position versus the resting position, but there is comparatively more narrowing on the right side (red arrows), which correlated with this patient’s symptoms. (Image copyright © Children’s Orthopaedic Surgery Foundation and used by permission. All rights reserved)

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(nTOS), in which symptoms are more related to compression of the brachial plexus, and vascular (vTOS), in which symptoms arise from compression of the subclavian vessels. Up to 90% of cases of TOS are thought to be neurogenic [15]. Presenting symptoms of patients with TOS include pain and heaviness in the shoulder and arm, along with weakness, numbness, and/or paresthesias. Those with vTOS may also have swelling and/or cyanosis of the arm when the subclavian vein is involved or coolness and pallor when the artery is compressed. Physical examination begins with a generalized examination of the cervical spine and upper extremity. In addition, particular attention is paid to inspection of skin color and temperature, along with observing swelling/venous congestion or muscle atrophy, all of which may be signs of TOS.  Provocative maneuvers for TOS include the Roos test, in which the patient is instructed to hold their arms in 90° of abduction and 90° of elbow flexion while opening and closing the hands for 3 min. A positive test reproduces the patient’s usual symptoms. The Adson test consists of extending the arm and shoulder and turning the head toward the affected side while taking a deep breath (Fig. 11.9). A positive test consists of a diminished radial pulse in this position, although this may be a normal finding in as much as half the population [16]. Combining the Roos and Adson tests leads to a specificity of over 80% if both tests are positive, however [17]. Fig. 11.9 Provocative maneuvers to test thoracic outlet syndrome. (a) The Roos test. (b) The Adson test (Image copyright © Children’s Orthopaedic Surgery Foundation and used by permission. All rights reserved)

a

b

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Diagnostic tests for TOS include plain X-ray, which can identify a cervical rib, and EMG/NCS, which can rule out other conditions but are generally negative in TOS. Magnetic resonance angiography (MRA) with the same sequences repeated in neutral position and a provocative arm position (generally hyperabduction) can identify compression of the subclavian artery or vein [18]. In patients with nTOS, vessel compression will not necessarily be found, but anatomic abnormalities can be identified, and in some cases nerve compression can be seen. Treatment for TOS begins with activity modification and physical therapy, although for those patients with clear vascular compression, it may be appropriate to proceed directly to surgery. Activity modification includes complete rest from provocative sports. Physical therapy is tailored to the individual patient’s needs. Strengthening of the levator scapula, rhomboid, and serratus muscles along with postural correction techniques can provide more space in the thoracic outlet. In addition, therapists may address length deficits in the scalene and assist with range of motion and nerve gliding exercises. If symptoms do not improve following 6–12 months of conservative management, surgery may be warranted. Surgery consists of decompression via resection of the first rib, costoclavicular ligament, and/or any involved scalene muscles, along with neurolysis of the brachial plexus. This can be done via transaxillary, supraclavicular, and posterior approaches, with the transaxillary approach being the most commonly performed [19]. Potential complications of surgery include injury to the vessels, brachial plexus, and thoracic duct, although these are rare. More common is recurrence, with repeat surgeries ­representing nearly 25% of one surgical series [20]. There are several case reports and case series of TOS in competitive and professional athletes, but no clear advice on return to play, with some authors recommending that athletes do not return even after improvement and others documenting successful return to sport [21, 22]. As for the other complex and rare injuries described in this chapter, return to play must be discussed on a patient-specific basis.

Suprascapular Nerve Compression The suprascapular nerve arises from the posterior division of the upper trunk of the brachial plexus (C5 and C6 nerve roots) and supplies motor innervation to the supraspinatus and infraspinatus muscles. It is also thought to provide sensory branches throughout the shoulder, and thus suprascapular nerve compression can be a source of shoulder pain [23]. The most classic scenario for suprascapular nerve compression is a paralabral cyst which compresses the nerve at the spinoglenoid notch (Fig. 11.10). Overhead athletes, including volleyball and baseball players, are vulnerable to dynamic compression of the nerve due to repetitive overhead throwing/serving [24–26]. Because of this association, the diagnosis of suprascapular neuropathy should be considered for all overhead athletes who present with shoulder pain. Differentiating features include weakness of the rotator cuff and atrophy of the supraspinatus or infraspinatus fossa. Plain radiographs of the shoulder are

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Fig. 11.10 (a) Coronal and (b) axial MRI images demonstrating paralabral cyst at the spinoglenoid notch. (Image copyright © Children’s Orthopaedic Surgery Foundation and used by permission. All rights reserved)

generally normal, while MRI is a more useful modality to identify a paralabral cyst and atrophy of the supraspinatus and/or infraspinatus muscles. EMG/NCS can be used to directly examine the function of the suprascapular nerve and localize the area of compression, with a sensitivity and specificity of 74–91% [27]. For dynamic suprascapular compression in the overhead athlete, activity modification and physical therapy are the mainstays of treatment. Physical therapy consists of stretching and strengthening of the rotator cuff and deltoid and periscapular muscles along with scapular stabilization exercises. Results of nonoperative management are good, with one series reporting 12 of 15 subjects treated successfully without surgery [28]. A similar study of 38 competitive volleyball players found that 35 of 38 were also successfully treated conservatively [29]. For static compression with an identifiable cause on imaging, treatment consists of addressing the underlying problem, with or without concomitant decompression of the suprascapular nerve. In the case of a paralabral cyst, many authors argue that repair of the labral tear which caused the cyst is adequate treatment, while others advocate for formal decompression of the cyst and the nerve [30–33].

Ulnar Nerve Compression/Cubital Tunnel Syndrome The ulnar nerve arises from the medial cord of the brachial plexus, with contributions from the C8-T1 nerve roots. It has no branches above the elbow but continues past the elbow to supply motor function to the ulnar-sided long flexors of the wrist and fingers, as well as most of the intrinsic musculature of the hand. The sensory distribution of the ulnar nerve consists of the dorsal sensory branch, which innervates the dorsal aspect of the ring and small fingers and ulnar aspect of the hand, and the digital nerves to the ring and small fingers volarly. Given the elbow flexion and

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valgus moment imparted on the elbow during throwing, compression neuropathy of the ulnar nerve at the elbow is common in baseball pitchers. A recent study demonstrated that the same phenomenon can be present in women’s fast-pitch softball players as well. This small series identified six female softball pitchers with cubital tunnel symptoms, all of whom were successfully treated with subcutaneous transposition [34]. Cubital tunnel syndrome in athletes often presents in conjunction with other medial elbow pathologies, including medial epicondylitis and ulnar collateral ligament injuries, as the ulnar nerve is subject to the same tensile forces that lead to injury of these structures during the throwing motion. Furthermore, inflammation and valgus instability related to an ulnar collateral ligament injury may further compress the ulnar nerve in this area [35]. Initial treatment of cubital tunnel syndrome consists of rest from throwing, nighttime splinting with the elbow in 30–60° of flexion, and nerve gliding exercises to stretch the affected area. In those patients who do not improve with conservative management, NCS is typically performed prior to consideration for surgery. There are many techniques for cubital tunnel surgery including in situ decompression of the ulnar nerve either open or endoscopically, as well as anterior subcutaneous and anterior submuscular transposition. Although in older patients there is no clear best procedure, our preference in young patients with cubital tunnel syndrome is anterior subcutaneous transposition of the ulnar nerve (Fig. 11.11) [36–38]. Although symptom relief is generally rapid after ulnar nerve transposition, athletes should be prepared for significant time-out of sport, with one series demonstrating return to play at an average of 12 weeks [39].

Fig. 11.11  Intraoperative photograph of anterior subcutaneous transposition of the ulnar nerve. A sling is created from the fascia overlying the flexor-pronator mass and used to hold the ulnar nerve in its new anterior position. (Image copyright © Children’s Orthopaedic Surgery Foundation and used by permission. All rights reserved)

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Median Nerve Compression/Carpal Tunnel Syndrome The median nerve arises from the combination of the medial and lateral cords of the brachial plexus, with contributions from the C7 to C8 nerve roots. At the wrist, the median nerve travels through the carpal tunnel, an area bordered by the carpal bones radially, ulnarly, and dorsally, and the transverse carpal ligament volarly. The finger and thumb flexor tendons travel through the carpal tunnel along with the median nerve. Just prior to the carpal tunnel, the palmar cutaneous branch divides off the proper median nerve, supplying sensation to the palm of the hand. After it emerges from the carpal tunnel, the median nerve gives off a recurrent motor branch to the thenar muscles, as well as sensory branches to the volar thumb, index, and middle fingers. Thus, when the median nerve is compressed at the carpal tunnel, classic symptoms include numbness in the volar thumb, index, and middle fingers along with weakness of the thenar muscles, with preservation of palmar sensation. Carpal tunnel syndrome is not common in young athletes, although it can be seen more often in those sports with exposure to repetitive wrist motion and vibration, such as cycling, tennis, and wheelchair athletes [40]. Pediatric patients with carpal tunnel syndrome will often have a presenting complaint of wrist and hand pain, worse with writing and other activities. The typical adult complaint of waking up at night with paresthesias is not common in young people. Examination consists of sensory testing (as described above) as well as strength testing of the thenar muscles. Provocative tests for carpal tunnel include Tinel’s sign (examiner taps on the volar wrist over the carpal tunnel), Phalen’s test (patient flexes the wrist for 60 s), and Durkan’s compression test (examiner presses on the volar wrist over the carpal tunnel for 30 s). These provocative tests are considered positive if they elicit numbness or tingling in a median distribution. However, multiple studies have shown low sensitivities and specificities for the provocative tests, and there is no correlation between the results of provocative maneuvers and severity of EMG findings in patients with carpal tunnel syndrome [41, 42]. Injection of local anesthetic and corticosteroid into the carpal tunnel can be both a diagnostic and therapeutic procedure in young athletes with suspected carpal tunnel syndrome. This is particularly helpful in the young patient with an unclear diagnosis or the in-season athlete who cannot take off the time needed for surgery and recovery. A recent Cochrane review found that steroid injection offers reliable short-term relief for patients with carpal tunnel syndrome [43]. Carpal tunnel ­injections can be done safely in the office based on landmarks or under ultrasound guidance. To perform the injection using landmarks, the needle is inserted 1  cm proximal to the distal wrist flexion crease, at the ulnar border of the palmaris longus tendon, and angled 30° distally. If the patient does not have a palmaris longus tendon, the needle should be in line with the ring finger. The patient is instructed to report any paresthesias during the injection, and the needle is repositioned if paresthesias are reported. Conservative management includes splinting the wrist in neutral at nighttime as well as during activities as needed. Nerve gliding exercises, as described above for cubital tunnel syndrome, can also be helpful. Surgical treatment consists of release of the transverse carpal ligament through either an open or endoscopic approach. The risks and benefits of the two approaches have been studied

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extensively, with a recent meta-analysis demonstrating a higher risk of nerve injury with the endoscopic approach (usually transient neurapraxia), but a lower risk of scar tenderness and faster return of grip and pinch strength [44]. There is a learning curve for developing expertise with endoscopic carpal tunnel release, and so this procedure should only be done by hand surgeons who are well-versed in the technique [45]. However, it is an option that should be considered in the young athlete, particularly those, such as tennis players and rowers, who may wish to avoid having a scar on the palm. Postoperatively, patients are restricted from heavy lifting and gripping activities for 2 weeks, with return to play generally possible at 2–4 weeks depending on the sport.

Radial Sensory Nerve Compression/Wartenberg’s Syndrome The radial nerve divides into the posterior interosseous nerve and the superficial radial nerve at the level of the supinator. The superficial radial nerve (SRN) travels deep to the brachioradialis in the proximal forearm and then emerges between the brachioradialis and extensor carpi radialis longus (ECRL) approximately 9  cm proximal to the radial styloid. From there, it goes on to innervate the skin of the dorsal and radial aspect of the hand and thumb. The SRN can become irritated or entrapped between the brachioradialis and ECRL, known as Wartenberg’s Syndrome, which leads to pain and paresthesias in the dorsoradial forearm and hand. Patients often present with a vague radial-sided forearm pain, which can be confused with tendonitis. Symptoms are often exacerbated by repetitive motion involving wrist flexion and ulnar deviation, as can be seen in sports such as tennis and lacrosse, as well as by wearing a wristwatch. Provocative tests on physical exam include a Tinel’s sign over the RSN, Finkelstein’s test (reproduction of symptoms when examiner holds the thumb and ulnarly deviates the wrist), and a reproduction of symptoms when the wrist is held in flexion, ulnar deviation, and pronation for 1 min. The majority of Wartenberg’s syndrome cases improve with nonsurgical management [46]. This can include activity modification, wrist splints, and nonsteroidal anti-inflammatory medications. Injection of steroid along with local anesthetic in the area where the SRN emerges from beneath the brachioradialis can also be helpful. As with the other compressive neuropathies, this can be both diagnostic and therapeutic. Surgery is rarely indicated, but when needed, it consists of a release and neurolysis of the superficial radial nerve.

Digital Nerve Compression/Bowler’s Thumb Bowler’s thumb refers to development of a neuroma of the ulnar digital nerve of the thumb due to chronic irritation of the nerve, such as with bowling. This is a rare traction neuritis, with case reports in bowlers as well as baseball players [47, 48]. Patients present with numbness or paresthesias along the first web space and ulnar

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aspect of the thumb and may have a neuroma palpable on the ulnar aspect of the thumb. The diagnosis of bowler’s thumb can usually be made on history and physical examination alone, but EMG/NCS can be utilized to rule out carpal tunnel syndrome, and ultrasound or MRI can be used to evaluate those patients with a palpable mass in the thumb. Initial treatment is conservative, consisting of activity modification (including either rest from bowling or changing the grip, weight, and size of the bowling ball) and taping or wrapping the thumb to protect it from irritation. Many surgical techniques have been described, including transposition of the nerve and wrapping the nerve in either vein graft or commercial nerve wraps [49–51].

Conclusion Peripheral nerve injuries are rare in the young athlete. Because of their rarity, however, providers must be aware of these injuries in order to diagnose and treat them promptly. When young athletes present with an acute injury, including strength and sensory exams in a routine, age-appropriate manner can help detect a nerve injury even when the patient cannot easily describe the altered sensation or feeling of weakness. For those athletes presenting with vague and chronic symptoms in the upper extremity, the various compression neuropathies about the shoulder, elbow, wrist, and hand should be in the differential diagnosis. Adjuvant tests such as ultrasound and diagnostic injections can be helpful when the diagnosis is unclear. Fortunately, both nonoperative and operative treatments exist for most of these nerve injuries to allow successful return to play for our young athletes.

References 1. Seddon HJ. Three types of nerve injury. Brain. 1943;66(4):237–88. 2. Sunderland S. A classification of peripheral nerve injuries producing loss of function. Brain. 1951;74(4):491–516. 3. Dua K, Lancaster TP, Abzug JM.  Age-dependent reliability of Semmes-Weinstein and 2-point discrimination tests in children. J Pediatr Orthop. 2016. https://doi.org/10.1097/ BPO.0000000000000892. 4. Wilder-Smith EP. Water immersion wrinkling – physiology and use as an indicator of sympathetic function. Clin Auton Res. 2004;14(2):125–31. 5. Zaidman CM, Al-Lozi M, Pestronk A. Peripheral nerve size in normals and patients with polyneuropathy: an ultrasound study. Muscle Nerve. 2009;40:960–6. 6. Podnar S.  Contribution of ultrasonography to the evaluation of peripheral nerve disorders. Neurophysiol Clin. 2018;48(2):119–23. 7. Aggarwal A, Srivastava DN, Jana M, Sharma R, Gamanagatti S, Kumar A, Kumar V, Malhotra R, Goyal V, Garg K. Comparison of different sequences of magnetic resonance imaging and ultrasonography with nerve conduction studies in peripheral neuropathies. World Neurosurg. 2017;108:185–200. 8. Lee DH, Clauseen GC. Oh S. Clinical nerve conduction and needle electromyography studies. J Am Acad Orthop Surg. 2004;12:276–87.

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Chapter 12

Musculoskeletal Ultrasound in Treating and Preventing Upper Extremity Injuries in Young Athletes Andrea Stracciolini, Sarah S. Jackson, and Pierre d’Hemecourt

Pertinent Definitions Linear High-Frequency Probe  A higher frequency transducer or probe (10– 12 MHz) that provides the best image resolution for superficial structures. It has a limited depth of penetration (